Principles_and_Practice_of_Cardiopulmonary_Physical_Therapy__3rd_Edition.pdf

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PRINCIPLES AND PRACTICE OF

CARDIOPULMONARY

PHYSICAL THERAPY

THIRD EDITION


PRINCIPLES AND PRACTICE OF

CARDIOPULMONARY

PHYSICAL THERAPY

THIRD EDITION

Edited by: Donna Frownfelter, MA, PT, CCS, RRT

NovaCare, Inc.

Contract Services

Region 7

Northwestern University

Programs in Physical Therapy

Chicago, IJlinois

Committed to Excellence

Glenview, Illinois

Elizabeth Dean, PhD, PT

Associate Professor

University of British Columbia

School of Rehabilition Sciences

Vancouver, British Columbia

With 22 contributors and 40] illustrations

Mosby

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Vice President and Publisher: Don Ladig Editor: Martha Sasser Developmental Editors: Kellie White, Amy Dubin Project Manager: Deborah L. Vogel Production EdilOr: Mamata Reddy Designer: Pati Pye Manufacturing Supervisor: Linda Ierardi THIRD EDITION Copyright © 1996 by Mosby-Year Book, Inc. Previous editions copyrighted 1978, 1987 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Permission to photocopy or reproduce solely for internal or personal use is permitted for libraries or other users registered with the Copyright Clearance Center, provided that the base fee of $4.00 per chapter plus $.10 per page is paid directly to the Copyright Clearance Center, 27 Congress Street, Salem, MA 01970. This consent does not extend to other kinds of copying, such as copying for general distribution, for advertising or promotional purposes, for creating new collected works, or for resale. Printed in the United States of America Composition by Times Mirror Higher Education Group, Inc. Print Group Printinglbinding by RR Donnelley & Sons Company Mosby- Year Book, Inc. 11830 Westline Industrial Drive St. Louis, Missouri 63146 International Standard Book Number 0-8151-3340-5 96 97 98 99 00 / 9 8 7 6 5 4 3 2 1


CONTRIBUTORS

Anne Mejia Downs, PT, CCS

Michael Wade Baskin, PT, RRT OwnerlExecutive Director

Department of Physical and Occupational Therapy

GT Physical Therapy and Rehabilitation

Instructor, Division of Physical Therapy Department of Medical Allied Health Professions

West Point, Mississippi

School of Medicine

Jean K. Berry, PhD, RN

University of North Carolina

Senior Research Specialist

Chapel Hill, North Carolina

Medical-Surgical Nursing University of Illinois at Chicago

Willy E. Hammon, BSe, PT

Chicago, Illinois

Chief of Rehabilitative Services

Gary Brooks, MS, PT, CCS

Special Instructor in Physical Therapy

Associate Professor

College of Health

Health and Rehabilitation Sciences

Clinical Instructor, College of Nursing

The University Hospitals

The Sage Colleges

University of Oklahoma Health Sciences Center

Troy, New York

Oklahoma City, Oklahoma

Susan M. Butl er, MMSe, PT, CCS

Scott M. Hasson, EdD, PT

Division of Physical Therapy

Director

Department of Rehabilitation Medicine

Advanced Studies

Maine Medical Center

School of Physical Therapy

Portland, Maine

Texas Woman's University Houston, Texas

Margaret K. Covey, MS, RN Senior Research Specialist and Doctoral Candidate

Lyn Hobson, PT, RRT

Medical-Surgical Nursing

Rush-Presbyterian-St. Luke's Medical Center

University of Illinois at Chicago

Chicago, Illinois

Chicago, Illinois

Gail M. Huber, MHPE, PT L inda D. Cr ane, MMSe, PT, CCS

Instructor

Instructor

Programs in Physical Therapy

Division of Physical Therapy


University of Miami School of Medicine

Chicago, Illinois

Miami, Florida

v


vi

Preface

Thomas Johnson, MD

Claire Peel, PhD, PT

Associate Professor in Radiological Scienccs

Department of Physical Therapy and Allied Health Professions

University of Oklahoma Health Sciences Center

School of

Oklahoma Citv. Oklahoma

Creighton Omaha, Nebraska PhD

ArthurV. Associate Professor of Susan K.

MS, PT

Rush Medical

Rehabilitation T herapy Services

Illinois

Henry Ford Hospital Detroit, Michigan

Elizabeth J. Protas,PhD, PT, FACSM Assistant Dean and Professor School of

Mary lnaSS l" President,

Therapy

Texas Woman's University

Physical

Houston, Texas

Illinois

in

MD,

Michael


Assistant Professor of Medicine

Illinois

Rush Medical '-''''vU,,",V,

Illinois

Mary Mathews, BS, RN, CCRN,RRT MA,PT

Neonatal and Pediatrics Chest Coordinator

Assistant Professor Care Services

Physical

Luke's Medical Center

Program of Colorado Health Sciences Center

Denver, Colorado Lisa

Mendelson, MS,

Alexandra J.

CPAN

Practitioner-Teacher, College of

Education Coordinator

Luke's Medical Center

Rush Rush

Medical Center

University of Physical

Division

Physical Medicine and Rehabilitation

UIIC
Ann Arbor, Michigan Victoria A. Moerchen, MS,PT Doctoral Candidate in Motor Control of Kinesiology

Maureen

DNSc,R

, FAA

Satellite Site Coordinator Clinic

Early Intervention Waisman Center

Adjunct Clinical

Pediatric Consultant and Lecturer

Rush

Madison, Wisconsin

College of Nursing of Illinois College of

. of Wisconsin

Chicago, Illinois


To our students Present, and FutureFor T heir Inspiration, Inquiry, and Enthusiasm


CONTEMPORARY DEFINITION OF

CARDIOPULMONARY

PHYSICAL THERAPY

culation,

livery of noninvasive interventions in the

assessment, treatment, and follow-up) of patients with primary or secondary car

diopulmonary dysfunction

from acute, chronic, and acute-on-chronic

conditions, and the cardiopulmonary/cardiovascular manifestations of

disease. CPPT interventions include mobilization,

body positioning,

control, coughing and airway clearance maneuvers, and manual tech niques. Wherever possible and appropriate, CPPT is applied to and to

oxygen

or reduce the need for invasive medical including

Patient education and

patient-driven treatment planning are fundamental

of CPPT. In addi

tion, CPPT has an essential role in the promotion of optimal cardiopulmonary and cardiovascular health and fitness in the

population.

ix


FOREWORD

Donna Frownfelter and Elizabeth Dean have succeeded in creating a unique set of re sources for students and clinicians. The importance of the oxygen transport mecha nism is woven throughout this text and accompanying case study book, Clinical Case Study Guide. The disruption of the mechanism can create cardiopulmonary dysfunc tion and can result in reduced function, reduced functional work capacity, and death. A comprehensive understanding of oxygen transport and the factors that determine

and influence it is therefore essential in order to assess the deficits of the mechanism and determine treatment interventions. The third edition of Principles and Practice of Cardiopulmonary Physical Therapy is not simply a new edition of the former, Chest Physical Therapy and Pulmonary Re habilitation. It is a totally new textbook, encompassing both the cardiac and pul monary systems in health and dysfunction. The two previous editions have been praised for their clinical relevance. The new books go a long way to support the state of the art clinical practice with documented scientific literature. The authors have many years of experience teaching undergraduate students as well as consulting and teaching in professional postgraduate courses. These books have been written in response to questions and concerns raised by students and clinicians. This is the only text in which Mary Massery has published her work on neuropul monary rehabilitation. Several chapters emphasize positioning for respiratory success and ventilatory strategies to improve rehabilitation potential. The books are very user-friendly. Each chapter of the text has key terms and questions for discussion to help the reader focus on the important concepts presented in the chapter. The combination of the text and case study guide will be an asset in teaching cardiopul monary physical therapy. However, either book can be effectively used independently of the other. The case study guide can be of assistance to physical therapists in helping them focus on patient evaluation, cardiopulmonary dysfunction, and treatment approaches. I applaud the authors for these new books and would highly recommend them for stu dents and clinicians.

SaLLy C. Edelsberg, MS, PT Director and Associate Professor Programs in Physical Therapy Northwestern University Medical School

xi


PREFACE

The work that has gone into this third edition has resulted in a completely new book! When we first discussed the possibilities of a new edition, we knew it would be a total change from Chest Physical Therapy and Pulmonary Rehabilitation. We wanted to present a new approach, not just a revision. Elizabeth's research and study of oxygen transport mechanisms in relation to patient treatment highlighted this concept as the primary thread that would pull the new book together. The cardiopulmonary system must be viewed as a whole, interacting with other body systems for optimal function. Therapy interventions must incorporate cardiopulmonary goals as well as neuromus cuiar and musculoskeletal goals for patients to reach maximal rehabilitation potential. We have attempted to pull together physiological as well as clinical data to meet the changing needs of health care to provide objective documentation for our interven tions. Yet we were diligent in maintaining a text aimed at the undergraduate student or practicing therapist with minimal background in cardiopulmonary physical therapy. To that end we have tried to keep the material readable and very user-friendly. Our hope is that virtually any question that may arise about treating a patient with car diopulmonary dysfunction would have some answers in this book. We both teach undergraduate physical therapy students and thank them for their input, questions, and concerns about patients with cardiopulmonary dysfunction who have helped us focus this text to meet students' needs. In addition, through our contin uing education seminars with postgraduate physical therapists, we have been chal lenged to apply the concepts in light of the changing health care scene. How can we be most effective and scientifically correct in choosing treatment techniques that have demonstrated improvement in the oxygen transport mechanism and patient function? We always learn when we teach, and we hope to share that learning with others through this text. We are excited about being able to present an accompanying text, Clinical Case Study Guide. We are attempting to show the physiological principles presented in our text, by identifying real-life case studies that physical therapists deal with every day in their practice. Our hope is that this will be used widely in teaching physical therapy students and will facilitate their understanding of how to effectively integrate car diopulmonary concepts in each of their patients, not just in patients with a primary cardiopulmonary diagnosis. To our knowledge, this is the first international book written dealing with car diopulmonary physical therapy. It is a blend of physiology and international ap proaches to the patient with cardiopulmonary dysfunction. We have had the privilege of teaching and consulting internationally and have tried to make this text applicable to all therapists regardless of their situation and the degree of sophisticated equipment. xiii


xiv

Preface

hands-on therapy and positioning is the

We realize that in some Third-World only mode of

available. We believe that this is often all that is needed when

with the proper concepts and thought processes. We are new

with the way this edition has come together. We have many authors who have added

and direction for both cardiac and

monary foci. We are pleased this is finally completed and thank our families, friends, and colfor

us and

us

the rough times to see this book

Our hope is that this will be a welcome addition to your professional Ii and we welcome your comments and suggestions for future work.

Donna Frownfelter Elizabeth Dean


ACKNOWLEDGMENTS

There are so many people that I want to thank and acknowledge for their support and contributions to this book. First, my family, for their understanding and support dur ing stressful deadlines and crunch spots. My husband David has been there for me since I went to physical therapy school and has always encouraged me to do what my vision led me to do. My three teenagers, Lauren, Daniel, and Kristin, have helped keep my life on track and grounded in the reality of daily life while taking time to "smell the roses." You are special gifts to me, and I love you. To my students, I thank you for your questions, concerns, and wonderings about what this cardiopulmonary stuff really means to your patients. You wonder if you can really be a better therapist because you take these things into account in evaluation and treatment. Please remember the difference between ordinary and extraordinary is just that little "extra." I believe that is what incorporating cardiopulmonary attention does; it adds the little extra. Be an extraordinary therapist, no matter what the health care environment. To the contributing authors, I thank you for your time and significant effort in bringing together the literature and clinical aspects of cardiopulmonary physical ther apy. Your dedication to this project has made it much more than Elizabeth and I could have done alone. You know how important it is to convey the message of treat ing the whole patient and helping them reach his or her potential. To my colleague and soul mate Mary Masse!)/, who I have taught with, travelled with, given seminars with, laughed with, and cried with, I thank you for all you have taught me and how special it is to have someone you can always count on to discuss a difficult patient or a personal issue. We have become quite a team, and I value our professional and personal relationships. Your contributions to the clinical chapters we have done together this time have been significant. I look forward to many more pro jects and fun times together. There is no greater pleasure for a teacher than to see a former student travel in that teacher's tracks and surpass her. Thanks Spike! My deepest thanks go to Elizabeth Dean. You have been an incredible colleague who has given new life to this book. You have, in a gentle way, helped to ensure that physiologic and scientific evidence be paired with our clinical experience and treat ment techniques. You have truly brought about a book that I could never have com pleted alone. Words are not enough to thank you for your commitment to this project and the countless hours you have spent in a major revision of the former textbook. I am delighted at what you have done and the depth of knowledge you have brought in your content and organization of this book. I am honored that you chose this text in which to share your work, and I have enjoyed working with you and learning from you. We share a common bond in the relationships we have with our students and our xv


xvi

Acknowledgements

desire to spread the word about the importance of including cardiopulmonary con cerns in the patient's evaluation and plan of treatment. We have grown close in the last 10 years, and I value our friendship as well as our professional work together. T hank you hardly is enough, but 'Thanks!" To my friends, family, and fellow workers at NovaCare, Inc. Contract Services, I thank you for your patience and understanding of the demands on my time and your encouragement to continue and finish this project. Your support has meant a great deal and I hope you feel a part of this, for it is because of you this has really happened. I'm glad to have a work environment that supports personal and professional growth. To our Mosby staff: Martha Sasser, thanks for your ideas and vision for going with this new book. You saw the possibilities and were there with other suggestions to make it even better (even if some of them came when we thought we were donel). To Kellie W hite, you kept us on track and helped catch up with chapter authors who needed a nudge and still had time to have Julia Isabelle-quite an accomplishment! You will now find what we have, that motherhood is often harder than your other job! Best wishes! To Mamata Reddy and Amy Dubin, you have pushed us through the editing process with the gentle and firm hand that we needed and with much sup port and help. Thank you for your cooperation and critical eye in making this an ex cellent outcome. Finally, and most importantly, I thank God for the vision, strength, and energy to un dertake this book and see it through to completion. My involvement in spreading the word about the need for optimizing the cardiopulmonary system has always felt like a mission. It has been amazing to me how many therapists don't see the need and how they can have an "Aha!" experience in a seminar or class, or even just reading this book. If I can have a small part in that experience, my "mission" has been fulfilled, and for that I am grateful. Donna Frownfelter

To Donna, for having made this dream come true. Our working relationship and friendship began 10 years ago when I first approached Donna to review a manuscript entitled 'The Pulmonary Effects of Body Positioning," published in Physical Therapy in 1985. This publication was the stepping stone to a prolonged and ever-growing in terest in oxygen transport and how it is affected by cardiopulmonary interventions such as body positioning and mobilization. T he enthusiasm, interest, and support of Donna and my former graduate student, Jocelyn Ross, have fueled my energies in the exciting dynamic area of cardiopulmonary physical therapy. My heartfelt gratitude to you both. To Daniel Perlman, for your encouragement and support of my liaison with Donna at the outset and over the years. You knew a good thing when you saw it. To Doug Frost, for your support in getting this project into the end zone. Thank you for your support and for being there as the book continued to evolve.


Acknowledgements

To our dedicated contributors, for your expertise, which has contributed to a vol ume on the principles and practice of cardiopulmonary physical therapy that is on the cutting edge with respect to the scientific and physiologic literature. Thank you for your contributions and team effort. To my cardiopulmonary physical therapy colleagues and students for your inquisi tiveness and enthusiasm. T hank you all for your inspiration. And not to forget the Mosby crew-Martha Sasser, Kellie White, Mamata Reddy, and Amy Dubin-I thank each one of you for your commitment to making this book the best it can be.

Elizabeth Dean


xvii

CONTENTS

PARTI Chapter 1

CARDIOPUL MONARY FUNCTION IN HEALTH AND DISEASE, 1 Oxygen Transport: The Basis for Cardiopulmonary Physical

Elizabeth Dean

Therapy, 3

Chapter 2

Cardiopulmonary Anatomy, 23

Elizabeth Dean Lyn Hobson

Chapter 3

Cardiopulmonary Physiology, 53


Chapter 4

Cardiopulmonary Pathophysiology, 71

Willy E. Hammon Scott M. Hasson

Chapter 5

Cardiopulmonary Manifestations of Systemic Conditions, 99

PARTII

CARDIOPULMONARY ASSESSMENT, 1J5

Chapter 6

Measurement and Documentation, 1J7

Claire Peel

Chapter 7

History, 127

Willy E. Hammon

Chapter 8

Pulmonary Function Tests, 145

Donna Frownfelter

Chapter 9

Arterial Blood Gases, 153

Donna Frownfelter

Chapter 10

Principles of Chest X-Ray Interpretation, 159

Elizabeth Dean

Michael Ries Thomas Johnson

Chapter 11

Electrocardiogram Identification, 169

Gary Brooks

Chapter 12

Multisystem Assessment and Laboratory Investigations, 189

Elizabeth Dean

xix


XX

Contents

Chapter 13

Special Tests, 197

Gail M. Huber

Chapter 14

Clinical Assessment of the Cardiopulmonary System, 209

Susan M. Butler

Chapter 15

Monitoring Systems in the Intensive Care Unit, 229

Elizabeth Dean

PART III

CARDIOPULMONARY PHYSICAL T HERAPY INTERVENT IONS, 249

Chapter 16

Optimizing Treatment Prescription: Relating Treatment

Elizabeth Dean

to the Underlying Pathophysiology, 251

Chapter 17

Mobilization and Exercise, 265

Elizabeth Dean

Chapter 18

Body Positioning, 299

Elizabeth Dean

Chapter 19

Physiological Basis for Airway Clearance Techniques, 321

Anne Mejia Downs

Chapter 20

Clinical Application of Airway Clearance Techniques, 339

Anne Mejia Downs

Chapter 21

Facilitating Airway Clearance With Coughing

Mary Massery

Techniques, 367

Donna Frownfelter

Facilitating Ventilatory Patterns and Breathing

Mary Massery

Strategies, 383

Donna Frownfelter

Exercise Testing and Training: Primary Cardiopulmonary

Susan K. Ludwick

Chapter 22

Chapter 23

Dysfunction, 417

Chapter 24

Exercise Testing and Training: Secondary Cardiovascular

Phyllis G. Krug

Dysfunction, 425

Chapter 25

Respiratory Muscle Weakness and Training, 443

Maureen Shekleton Jean K. Berry Margaret K. Covey

Chapter 26

Patient Education, 453

Alexandra J. Sciaky


Contents

PART IV

GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: ACUTE CARDIOPULMONARY CONDITIONS, 467

Chapter 27

Acute Medical Conditions, 469

Elizabeth Dean Willy E. Hammon Lyn Hobson

Chapter 28

Acute Surgical Conditions, 495

Elizabeth Dean Mary Mathews

PART V

GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL THERAPY: CHRONIC CARDIOPULMONARY CONDITIONS, 511

Chapter 29

Chronic Primary Cardiopulmonary Dysfunction, 513

Elizabeth Dean Donna Frownfelter

Chapter 30

Chronic Secondary Cardiopulmonary Dysfunction, 567

Elizabeth Dean Donna Frownfelter

PART VI

GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL THERAPY: INTENSIVE CARE, 565

Chapter 31

Comprehensive Patient Management in the Intensive

Elizabeth Dean

Care Unit, 567

Chapter 32

Intensive Care Unit Management of Primary

EI izabeth Dean

Cardiopulmonary Dysfunction, 579

Chapter 33

Intensive Care Unit Management of Secondary

Elizabeth Dean

Cardiopulmonary Dysfunction, 599

Chapter 34

Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure, 617


Elizabeth Dean

xxi

xxii

Contents

PART VII

GUIDELINE S FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL THERAPY: SPECIAL CASES, 633

Chapter 35

The Neonatal and Pediatric Patient, 635

Victoria A. Moerchen Linda D. Crane

Chapter 36 Chapter 37

The Aging Patient, 669

Elizabeth J. Protas

The Patient With Neuromuscular and Musculoskeletal

Mary Massery

Dysfunction, 679

Chapter 38

The Transplant Patient , 703

Susan Scherer

Chapter 39

The Patient in the Community, 721

Donna Frownfelter

PART VIII

RELATED ASPECTS OF CARDIOPULMONARY PHYSICAL THERAPY, 735

Chapter 40

The Art of Positioning and Moving Patients, 737

Mary Massery Donna Frownfelter

Chapter 41

Respiratory Care Practice Review, 749

Michael Wade Baskin

Chapter 42

Care of the Patient With an Artificial Airway, 761

Lisa Sigg Mendelson

Chapter 43

Respiratory and Cardiovascular Drug Actions, 775

Arthur V. Prancan

GLOSSARY, Gl INDEX, 11


PAR T

1

Cardiopulmonary Function in Health and Disease


CHAPTER

1

Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy Elizabeth Dean

KEY TERMS

Cellular respiration

Gravitational stress

Exercise stress

Oxygen transport pathway

INTRODUCTION

ceptual basis for cardiopulmonary physical therapy

Cardiopulmonary physical therapy is an essential non

practice. Oxygen transport is the basis for life. Impaired

invasive medical intervention that can reverse or miti

or threatened oxygen transport, hence, cardiopul

gate insults to oxygen transport. It can avoid, delay, or

monary dysfunction, is a physical therapy priority.

reduce the need for medical interventions, such as sup

In health, the oxygen transport system is normally

plemental oxygen, intubation, mechanical ventilation,

perturbed by movement and activity, changes in body

suctioning, bronchoscopy, chest tubes, surgery, and

position, and emotional stress. In disease, disruption

medications. A comprehensive understanding of oxy

of or threat to this system is always a medical priority

gen transpol1 and the factors that detelTnine and influ

because of the threat to life or impairment of func

ence it is therefore essential to the comprehensive as

tional capacity.

sessment of oxygen transport and optimal treatment prescription to effect these outcomes.

The fundamental steps in the oxygen transport pathway, and their function and interdependence are

This chapter details the oxygen transport system, the

described first. Special attention is given to cellular

pathway, and the component steps that provide a coo-

respiration and the utilization of oxygen during me 3


4

PART I


+VC02 +V02

Airways/lungs

('\

c

('\

.

C

a

4

a

g::J

g. ::J

FIGURE 1-1 Scheme of components of ventilatory-cardiovascular-metabolic doupling underlying oxygen transport. (Modified from Wasserman K et al: Principles of exercise tesling and interpretation, Philadelphia, 1987, Lea & Febiger.)

tabolism at the cellular level in muscle. Second, the

1992a; Goldring, 1984; Johnson, 1973; Ross, and

factors that normally perturb oxygen transport in

Dean, 1989; Weber et aI, 1983).

health are described, namely gravitational stress sec

Oxygen transpolt variables include oxygen delivery

ondary to changes in body position, exercise stress

(002),

secondary to increased oxygen demand of the work

hancement ratio (OER) or the utilization coefficient.

oxygen consumption

(V02)

and the oxygen en

ing muscles, emotional stress, and arousal. A thor

Oxygen demand is the amount of oxygen required by

ough understanding of the effects of those factors that

the cells for aerobic metabolism. Oxygen demand is

V02;

however, in cases of severe

normally perturb oxygen transport is essential to ac

usually reflected by

curately assess and treat deficits in oxygen transport.

cardiopulmonary dysfunction and compromise to oxy gen transport,

V02 can fall

short of the demand for oxy

gen. Oxygen transport variables, including the compo

OXYGEN TRANSPORT

nents of

Oxygen transport refers to the delivery of fully oxy

1-2.

002

002, V02,

and the OER, are shown in Figure

is determined by arterial oxygen content and

genated blood to peripheral tissues, the cellular up

cardiac output, oxygen consumption by the arterial and

take of oxygen, the utilization of oxygen from the

venous oxygen content, difference and cardiac output,

blood, and the return of partially desaturated blood to

and oxygen extraction by the ratio of

002 to

\'02.

the lungs. The oxygen transport pathway consists of

Measures and indices of oxygen transport that re

multiple steps ranging from the ambient air to the

flect the function of the component steps of the oxy

perfusion of peripheral tissues with oxygenated arter

gen transpolt pathway are shown in the box above.

ial blood (Figure

1-1).

Oxygen transport has become

the basis for conceptualizing cardiopulmonary func tion, and diagnosing and managing cardiopulmonary

Energy Transfer and Cellular Oxidation

dysfunction (Dantzker, 1983; Dantzker, Boresman,

Cellular metabolism and survival depend on the con

and Gutierrez, 1991; Dean, 1994a; Dean and Ross,

tinuous s y nthesis and degradation of adenosine


Measures and Indices of the Function of the Steps in the Oxygen Transport Pathway Control of Ventilation

Physiologic shunt Systolic and diastolic pulmonary artery pressures

PO. I (central drive to breathe)

Pulmonary capillary blood tlow

Ventilatory responses or hypoxia and hypercapnia

Pulmonary capillary wedge pressure

Pao} and Sa02 responses to exercise

Pulmonary vascular resistance

Inspired Gas

Pulmonary vascular resistance index Systemic hemodynamic variables

Alveolar oxygen pressure

Heart rate

Alveolar carbon dioxide pressure

Electrocardiogram (ECG)

Alveolar nitrogen pressure

Systemic blood pressure

Hematologic Variables

Mean arterial blood pressure

Hemoglobin

Systemic vascular resistance

Plasma proteins and their concentrations

Systemic vascular resistance index

Red blood cells and count

Central venous pressure

White blood cells and count

Pulmonary artery pressures

Platelets

Wedge pressure

Clotting factors

Blood volume

Clotting times

Cardiac output

Hematocrit

Cardi
Pao2

Stroke volume

Paco2 (eml tidal CO2)

Stroke index

P(A-a)o2

Shunt fraction

Cao2

Ejection fraction

CV02

Left ventricular work

C(a-v)o2 difference

Right ventricular work

HCo1

Fluid balance

Sa02

Renal output

pH

Creatinine clearance and blood urea nitrogen (BUN)

Paoe/PAo] Pao2/Flo2

Diffusion

Serum lactate

D (A-a)o2

Pulmonary Variables

Diffusing capacity Diffusing capacity/alveol
Minute ventilation Tidal volume

Gas Exchange

Respiratory rate

Oxygen consumption (Vo2)

Dead space volume

Carbon dioxide production (VCCl:)

Alveolar volume

Respiratory exchange ratio (Vco}iV02)

Alveolar ventilation

Ventilation and perfusion matching

Distribution of ventilation

Paol/PAol

Static and dynamic lung compliance

P(A-a)o2

Airway resistance Functional residual capacity

Oxygen Extraction and Utilization

Closing volume

Oxygen extraction ratio (V02/Do2)

Vital capacity

C(a-v)02 difference

Forced expiratory volumes and flows Other pulmonary volumes, capat:ities, and flow rates Inspiratory and expiratory pressures Work ofhreathing Respiratory muscle strength and endurance Pulmonary Hemodynamic Variables Cardiac output Total perfusion Distribution of perfusion

P(a-v)o2 differenc e SV02 Metabolic enzymes at the cellular level Oxyhemoglobin dissociation Adequacy of Tissue Perfusion and Oxygen Transport Tissue oxygenation

Tissue pH

Anatomic shunt


6

PART I


Oxygen delivery Arterial oxygen content

D02

Cardiac output

x

t

Oxyhemoglobin + Dissolved oxygen Hgb

x

t 1.34

x

5a02

II

Pa02

x

0.003

I

Oxygen consumption V02

=

(Arterial oxygen content - Venou s oxygen content)

t

Oxyhemoglobin Hgb

x

1.34

x

+

5v02

Cardiac output

x

Dissolved oxygen

II

Pa02

x

0.003

I

Oxygen enhancement ratio OER

Oxygen consumption

V02

Oxygen delivery

D02

FIGURE 1-2 FOlmulas for determining oxygen delivery

(002),

oxygen consumption

(Vo2),

and oxygen

extraction ratio (OER). (Modified from Epstein CD., Henning R.1.: Oxygen transport variables in the identification and treatment of tissue hypoxia, Heart Lung

triphosphate (A TP); the major source of energy for

22:328-348, 1993.)

that oxygen delivery is inadequate, nonaerobic (anaer

biological work. Work is performed in biological sys

obic or non-oxygen-requiring) energy-transferring

tems for contraction of skeletal, cardiac, and smooth

processes can also supply ATP. However, supplying

muscle (e.g., exercise, digestion, glandular secretion

energy anaerobically is more costly metabolically, that

and thermoregulation, and nerve impulse transmission)

is, it is not efficient, is limited, and cannot be slistained

(see box below). These processes require a continuous

because of the disruptive effects of lactate, a cellular

supply of A TP, which is made available by aerobic

byproduct of anaerobic metabolism, on physiological

(oxygen requiring) processes primarily. In the event

processes in general. Metabolic acidosis is a conse quence of lactate accumulation. In critically ill pa

Biological Work Requiring Continuous Oxygen Supply Contraction of skeletal muscle

tients, the presence of metabolic acidosis secondary to anaerobic metabolism can be life-threatening. Pro longed anaerobic metabolism is lethal in two respects. First, the patient is increasingly dependent on anaero

Contraction of cardiac muscle

bic metabolism because of inadequate oxygen delivery

Contraction of smooth muscle

to peripheral tissues, and second, acidosis interferes

Nerve impulse transmission Active cellular metabolic processes Active pumping mechanisms

with normal cellular processes and homeostasis, which require an optimal pH of 7.40. The ATP molecule consists of an adenine and a ri-


1

Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy

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te= wdale

Acetyl-Co-A -- Fatty acids -- 1 __ F t:_

Amino acids o

I

"Glycecol

)+

Citrate

-a

": ;

a

Ketoglutarate

CO2 + Energy FIGURE 1-3

Interrelationships among carbohydrate, fat, and protein metabolism and their points of entry into the Krebs cycle. (Printed with permission from Shepard R.J,:

of exercise,

Physiology and biochemistry

Phi ladelphia, 1985, Praeger Scientific.)

bose molecule with three phosphates attached. Split

electron transfer chain and then use this energy for

ting of the terminal phosphate bond or the two terminal

biological work (Ganong,

phosphate bonds generates considerable amounts of

Carbohydrates, fats, and proteins, ingested from

energy. This energy is used to power various chemical

foodstuffs in the diet, are oxidized to provide the en

1993; Shephard, 1985).

reactions associated with metabolism. These metabolic

ergy for phosphorylation of adenosine diphosphate

processes take place in specialized organelles in the

(ADP), that is, the formation of ATP by combining

cells called mitochondria. The primary pathways that

ADP with phosphate. These substances are broken

are responsible for the formation of ATP are the Krebs

down, and they access the Krebs cycle at the pyruvic

cycle and the electron transfer chain.

acid or acetyl coenzyme A (CoA) levels (Figure

The complex, enzymatically controlled chemical

1-3).

Some amino acids can enter the Krebs cycle directly.

reactions of metabolism are designed to form and

The Krebs cycle degrades acetyl CoA to carbon

conserve energy through the Krebs cycle and the

dioxide (C02) and hydrogen atoms (H2)' The primary


8

PART I


3ADP 3ATP

Mitochondrion Shuttle

Krebs cycle NADH etc.

FIGURE 1-4 Philadelphia, 1985,

and

purpose of this

(Printed with permission from

with the Krebs

Electron transfer chain and its

is to generate hydrogen ions for

the electron transfer chain by two principal electron

Scientific.)

by

energy is primarily

tivity and

aerobic metabolism. Oxygen for this process is pro

acceptors, nicotinamide adenine dinucleotide

vided by the oxygen transport pathway. Carbon com

and flavin adenine dinucleotide (FAD).

pounds that enter the

the numerous reactions of the Krebs

in the form of

and

Cellular oxidation or respiration refers to the func tion of the electron transfer chain to release energy in

oxidative metabolism

in the form of aerobic glycolysis in the mitochondria in the

of the cells.

small amounts and to conserve energy in the forma

The Krebs

tion of high energy bonds. It is this process that en

the biochemical

sures a continual energy supply to meet the needs of

cell responsible for harnessing the oxygen for aerobic

metabolism Three major supply energy durations

1-4).

metabolism and of energy transfer exist to

a continuous supply of oxy to produce two molecules of

ATP (glycolysis). Glucose is oxidized to

Katch, and Karch, I

though these systems are discrete they

in the mitochondria of the

gen for this process (Shephard, 1985). cose is

all-out exercise over

and the electron transfer chain are

Cellu

molecules of

yielding a net

lar ATP and creatine phosphate (CP) are immediate

molecules of ATP per molecule of

energy sources for the first 10 seconds of exercise.

pyruvate molecules enter the Krebs

From 30 to 60

are oxidized to

glycolysis

a short

where they

and water. This process

30

term energy source. The ATP-CP system and the

ATP molecules. Hydrogen ions released in the

colytic system are anaerobic processes. As exercise

process are transferred to the electron transfer chain

aerobic

yielding 4 ATP molecules for cellular metabolism.

system oredominates. Thus for sustained ohvsical ac-

Electrons are removed from hydrogen and funnelled

persists for several minutes, the



1

Sarcoplasmic reticulum

Triad j

A

9

Mitochondrion

i

Terminal Transverse tubule cisterns

Thick myofilament

Z line

M line

Z line

H zone I band I

I band

A band ,

Sarcomere I band

A band I Mi" .-!n ,n, ,,/ ' . ' .

I band

"

'--11 " ,'" .

B

,

:

"

'

' • •

,

,

.

'"'' " ' , , ,

.

.

.

: , : ::� :> ,'7:'> . • •• , •• '-" . ,

. ,

.

'"

. . . , .. .. , ' " / " . .

"

"

, ,

,•• " . ', ,' ' / / , " // , . .- . ... '/ " .

!

"

', :> ?::. .

.

' .

" "

'.' , ,

... ....

.

.

,", ' . , ",,',

.. . . _ _ .

"

.

...

:',', : . : : ' ::: . : :: :: : . .. . '.

,' ,

', 11/ . . .. "

.

_ ._ " "

" ' // , > '

.

, . .

. . ' ." " " ... ... , , , ..

- ... .. ...

."-"

Thin myofilament

I ' Thick myofilament Cross bridge H z one

,- .

.

.

.

,,,

. '

.

'''

, ...

/

Z line

FIGURE 1-5 Schematic of the ultrastructure of a muscle fiber. A, View of muscle mem brane structure and myofibril arrangement. B, A single functional unit (sarcomere) of a myofibril showing the interdigitation of the actin and myosin filaments. (Printe d with permission from Tortora, G.J., A nagnostakos N.P.: Principles of anatomy and physiology, New York, J 990, Harper & Row.)


10

PART I


Thin

Myosin (thick)

Thin

FIGURE 1-6 Arrangement of the thick and thin myofilaments. (From Hasson S.: Clinical exercise physiology, St. Louis, 1994, Mosby.)

down the electron transport chain by specialized elec

anaerobic metabolism can only serve as a shol1-term

tron carrier molecules, cytochromes 1 to S. It is only

energy source.

the last of these cytochromes, cytochrome oxidase, that can reduce molecular oxygen to water. This process is driven by a gradient of high-to-Iow poten tial energy. The energy transferred as electrons are

Muscle Contraction and Metabolism The basic mechanism for muscle contraction is excita

passed from H2 to O2, and is trapped and conserved

tion contraction coupl ing (Kirchberger,

as high energy phosphate bonds. Oxygen is only in

and Anagnostakos,

volved in these metabolic pathways at the end of the

centrally or through the spinal cord depolarize the

1991; T0I10ra, 1990). Action potentials mediated

electron transfer chain, where oxygen is the final

muscle cell membrane, the sarcolemma, and stimulate

electron acceptor and combines with H2 to form H20.

the release of calcium from the lateral sacs of the sar

More than

coplasmic reticulum, The sarcoplasmic reticulum is an

90% of ATP synthesis takes place through

the electron transfer chain by oxidative reactions

extensive network of invaginations and tubular chan

combined with phosphorylation, that is, oxidative

nels encasing the muscle fibers or myofibrils. The cal

phosphorylation. An individual's peak aerobic capac

cium floods over the myofilaments of the myofibrils.

ity is determined by the availability of oxygen at the

Myofilaments consist of thin and thick fibers, actin,

end of the electron transport chain.

and myosin protein, which interdigitate with each

For each molecule of glucose that is metabolized,

other giving the typical striated appearance to skeletal

1-6). Actin is a helical mole

36 molecules of ATP are produced; four molecules

muscle (Figures I-S and

from substrate phosphorylation (anaerobic), and 32

cule with tropomyosin intertwined along its length.

from oxidative phosphorylation (aerobic). The low

Tropomyosin normally inhibits the interaction of actin

ATP yield from anaerobic metabolism explains why

and myosin. Calcium causes a conformational change



of the tropomyosin molecule that enables troponin, also distributed along the actin molecule, to combine

11

Principles of Oxygen Transport A continuous supply of oxygen is needed to meet

with calcium. The combining of calcium and troponin

moment-to-moment demands for oxygen commensu

triggers the movement of actin and myosin. Contrac

rate with changing metabolic demands for energy at

tion involves the attaching and detaching of the

the cellular level in addition to basal metabolic de

myosin heads (cross bridges) to actin in a cyclical

mands (Cone, 1987; Dantzker, 1991; Samsel and

manner, which causes the actin and myosin filaments

Schumacker, 1991). Oxygen transport occurs either

to slide past each other. In this way, the muscle is

by convection or diffusion. Convection of oxygen

shortened without shortening of the myofilaments.

refers to the movement of oxygen from the alveoli to

The energy for muscle contraction in the form of

the tissue capillaries. Convection is primarily deter

ATP is generated within the mitochondria of the my

mined by the hemoglobin concentration, oxygen satu

ofibrils (Shephard, 1985). Myosin ATPase splits ATP

ration, and cardiac output. The diffusion of oxygen

so that the transfer of this energy can be used for

refers to the movement of oxygen from the capillaries

muscle contraction. Specifically, the enzyme ATPase

to the mitochondria. Diffusion is determined by

is activated when actin and myosin are joined. ATP is

metabolic rate, vascular resistance, capillary recruit

then available to bind with the cross bridge, causing

ment, tissue oxygen consumption, and extraction.

it to detach from actin. Relaxation occurs with the

Normally, D02 is regulated by tissue metabolism

cessation of electrical excitation and the rapid re

and the overall demand for oxygen. Typically, DOl is

moval or sequestration of calcium into the lateral sacs

3 to 4 times greater than oxygen demand, and V02 is

of the sarcoplasmic reticulum.

not directly dependent on Do2. In health, the increased

The specific metabolic properties of muscle de

metabolic demands of exercise constitute the greatest

pend on the constituent muscle fiber types (Fox,

challenge to the oxygen transport system. The V02 can

Bowers, and Foss, 1993). The three primary muscle

increase 20 times. In response to increased muscle

fiber groups are fast twitch fibers, slow twitch

metabolism, blood tlow increases to the peripheral

fibers, and intermediate fibers, which have proper

muscles through vasodilatation and capillary recruit

ties of both. The fast twitch fibers (fast glycolytic

ment, thereby increasing the availability of oxygen to

fibers) are recruited during short-term sprint type

the working tissues and its extraction from the arterial

exercise, which relies mainly on anaerobic metabo

blood. As D02 and V02 increase, venous return, stroke

lism. These fibers are well-adapted for rapid force

volume, and heart rate also increase, thereby increas

ful contractions, because they have large amounts

ing cardiac output (CO). The CO can increase more

of myosin ATPase, rapid calcium release and up

than five times in strenuous exercise.

take and high rate of cross bridge cycling. Slow

At rest, regional differences in the proportion of

twitch fibers (slow oxidative fibers) are recruited

CO normally delivered to the body organs reflects dif

during prolonged aerobic exercise. These fibers

ferences in organ functions and is not necessarily

have large amounts of myoglobin, mitochondria,

matched to the metabolic rate (Guyton, 1987). For ex

and myochondrial enzymes. Compared with the fast

ample, the distribution of CO to the kidneys is 20%,

twitch fibers, slow twitch fibers are fatigue-resis

and to the mesenteric, splenic, and portal tissues is

tant. The intermediate fibers have both anaerobic

20% to 30%. Comparatively, muscle at rest is 10% and the brain and myocardium are less than 5% each.

and aerobic metabolic enzymes, which make these fibers capable of both types of muscle work. Al though the characteristics of the fiber types are dis tinct, activity and exercise recruits both types of

Oxygen Content of the Blood

fibers. Depending on the particular activity or exer

Oxygen is transported in arterial blood to the tissues

cise, one fiber type may be preferentially recruited

in combination with hemoglobin (98%) a n d dis

over the others.

solved in plasma (2%) The majority of oxygen is


12

PART I


carried in the blood by hemoglobin, compared with a relatively minimal amount of oxygen that is dis solved in the blood. The oxyhemoglobin dissociation

150

curve represents the relationship between the affinity

A;

of hemoglobin for oxygen and arterial oxygen ten

c

sion. The affinity of hemoglobin for oxygen depends on the tissue oxygen demand. In health, exercising muscle increases the demand for oxygen. The heat of the working muscles and the acidic environment re sult in reduced oxyhemoglobin affinity, and in

:¥100 E E

d (/

l

N

o

0....

50

creased oxygen release. This is reflected by a shift to

Gal enp/

Diffusion

o An

Shunt

Tissues

the right of the oxyhemoglobin dissociation curve (see Chapter 9). The affinity of hemoglobin and oxy gen is increased with the cessation of exercise, which is reflected by a leftward shift of the curve.

o I�------

Atmosphere

•

Mitochondria

FIGURE 1-7 Scheme of oxygen partiaf pressures from air to tissue. The

Oxygen Delivery to the Tissues

cascade reflects the removal of oxygen by the pulmonary

The final steps in oxygen transport involve the disso ciation of oxygen from hemoglobin and the diffusion of oxygen from the capillaries to the cells (Schu macker, Samsel, 1989). Diffusion depends on the

capillary blood and the tissues. Depressions caused by the effects of diffusion and shunt are also illustrated. (Used with permission from West lB.: Respiratory p/7ysiology

the essentials, ed 5, Baltimore, 1995, Williams & Wilkins.)

quantity and rate of blood flow, the difference in cap illary and tissue oxygen pressures, the capillary sur face area, capillary permeability, and diffusion dis

mitochondria (Guyton, 1991). This decremental Pao2

t a n ce (West, 1 9 95). Wi t h i ncreased metabo lic

profile down the oxygen transport pathway, from the

demand of the tissues, capillary dilatation and recruit

airways to the tissues, is termed the oxygen cascade

ment increase capillary surface area and reduce vas

(Figure 1-7).

cular resistance to flow. Diffusion distance is de creased, the movement of oxygen into the cell is facilitated, and the tissue oxygen tension is increased.

Cardiac Output

The two diffusion gradients that determine effec

In addition to arterial oxygen content, CO is a primary

tive oxygen transpolt are between the pulmonary cap

determinant of D02 (Dantzker, 1991). The transport of

illaries and the alveoli, and between the peripheral

oxyhemoglobin to the tissues is dependent on convec

capillaries and the tissue cells. Diffusion of oxygen

tive blood flow by way of CO. The CO is the volume

occurs as the blood moves from the aorta to the arte

of blood pumped from the right or left ventricle per

rioles. The mean oxygen tension in the aorta is about

minute. The components of CO are stroke volume SV x HR.

95 mm Hg and in the arterioles is 70 to 80 mm Hg.

(SV) and heart rate (HR), that is, CO

The oxygen gradient between the arterioles and the

Stroke volume is the amount of blood ejected from the

=

cells is the most steep. The mean oxygen pressure is

left ventricle during each ventricular systole or heart

less than 50 mm Hg in the capillaries. The oxygen

beat and is determined by the preload, myocardial dis

tension in the capillaries detennines the rate of diffu

tensibility, myocardial contractility, and afterload. The

sion to the cells. An optimal diffusion gradient main

DDl is optimized in patients by increasing CO through

tains the oxygen tension in the cell between 1 to 10

the therapeutic manipulation of preload, myocardial

mm Hg; oxygen tension is less than 0.5 mm Hg in the

contractility, afterload, and heart rate.


1


Preload

13

to that consumed. The OER is calculated by dividing

Preload is the end diastolic muscle fiber length of the

V02 by 002. Normally, the OER is 23%.

ventricle before systolic ejection, and reflects the left ventricular end diastolic volume (LVEDV). The LVEDV is dependent on venous return, blood vol

Supply-dependent Oxygen Consumption

ume, and left atrial contraction. An increase in ven

Normally, a decrease in 002 does not reduce V02

tricular volume stretches the myocardial fibers and

(Phang, Russell, 1993). With a decrement in 002, the

increases the force of myocardial contraction (Star

tissues extract a proportionate amount of oxygen

ling effect) and stroke volume. This effect is limited

from the blood. In critically ill patients, the 002 may

by the physiologic limits of distension of the my- . ocardium. Excessive stretching such as in fluid over

be significantly limited to the point where basic 2 metabolic needs for oxygen (300 mllminJM ) are not

load of the heart leads to suboptimal overlap of the

being met (Fenwick et ai, 1990; Lorente et aI, 1991;

actin and myosin filaments, thus impairing rather

Phang, Russell, 1993). The critical level at which V02

than enhancing contractility.

falls is associated with tissue anaerobic metabolism and the development of lactic acidosis and decreased pH (Figure 1-8) (Mizock, Falk, 1992; Schumaker,

Afterload

Cain, 1987). Serum lactates correspondingly increase

Afterload is the resistance to ejection during ventricu

and provide a valid index of anaerobic metabolism in

lar systole. Afterload of the left ventricle is primarily

patients with multiorgan system failure.

determined by four factors: the distensibility of the aorta, vascular resistance, patency of the aortic valve, and viscosity of the blood.

The Oxygen Transport Pathway Oxygen transport is dependent on several intercon necting steps ranging from oxygen-containing air

Myocardial Contractility

being inhaled through the nares to oxygen extraction

Myocardial contractility reflects actin-myosin coupling

at the cellular level in response to metabolic demand

during contraction. Myocardial contractility is assessed

(see Figure I-I , p. 4). These steps provide the mecha

by the ejection fraction, rate of circumferential muscle

nism for ventilatory, cardiovascular, and metabolic

fiber shortening, pressure volume relationships, and the

coupling. In addition, blood is responsible for trans

rate of change of ventricular pressure over time.

porting oxygen within the body, thus its constituents and consistency directly affect this process.

Oxygen Debt Tissue oxygen debt or recovery oxygen consumption is

The Quality and Quantity of Blood

the difference between oxygen demand and oxygen

Although not considered a discrete step in the oxygen

consumption. In health, oxygen debt can be sustained

transpolt pathway, blood is the essential medium for

for short periods during intense exercise. Anaerobic me

transporting oxygen. To fulfill this function, blood

tabolism is stimulated to produce ATP under these con

must be delivered in

ditions. In patients, the degree of oxygen debt signifi

proportional to metabolic demands, and have the ap

cantly correlates with survival (Fenwick et aI, 1990).

propriate constituents and consistency. Thus consider

an

adequate yet varying amount

ation of the characteristics of the circulating blood vol ume is essential to any discussion of oxygen transport.

Oxygen Extraction Ratio or Utilization Coefficient

Blood volume is compartmentalized within the in

The oxygen extraction ratio (OER), or utilization co

travascular compartment such that 70% is contained

efficient, reflects the proportion of oxygen delivered

within the venous compartment, 10% in the systemic


PART I

14

arteries,


15% in the pulmonary circulation, and 5% In 1986). The large volume of

Blood is a viscous fluid composed of cells and

99% of the blood is red blood celis,

the capillalies (Sandler,

plasma. Because

blood contained within the venous circulation permits

the white blood cells play almost no role in determin

adjustments to be made as cardiac output demand

ing the physical characteristics of blood.

changes. The veins constrict, for example, when car

Hematocrit refers to the proportion of blood that is

diac output needs to be increased. When blood vol

38% for women and 42% for men. Blood is several times as viscous as

ume is normal and body fluids are appropriately dis

celis. The normal hematocrit is

t r i b u t e d b e t w e e n t h e i n t r a- a n d e x t r ava scular

water, which increases the difficulty with which

compartments, fluid balance is considered normal.

blood is pumped through the heart and flows through

When these are disrupted, a fluid balance problem

vessels; the greater the number of cells, the greater

exists. In addition, fluid imbalance affects the con

the friction between the layers of blood, which results

centration of electrolytes, and particularly sodium,

in increased viscosity. Thus the viscosity of the blood

which is in the highest concentration in the extracel

increases significantly with increases in hematocrit.

lular fluid. Four primary fluid problems that have im

An increase in hematocrit such as in polycythemia in

plications for oxygen transport are water deficit,

creases blood viscosity several times over. The con

water excess, sodium deficit, and sodium excess (see Chapter

15). Other ions that are often affected in

fluid and electrolyte imbalance deficits include potas sium, chloride, calcium, and magnesium (Figure

centration and types of protein in the plasma can also affect viscosity but to a lesser extent. In the adult, red blood cells are produced in the

1-8).

marrow of the membranous bones such as the verte

These electrolyte disturbances also contribute to im

brae, sternum, ribs, and pelvis. The production of red

paired oxygen transport by affecting the electrical

blood cells from these sites diminishes with age. Tis

and mechanical behavior of the heart and blood ves

sue oxygenation is the basic regulator of red blood

sels, and hence cardiac output and the distribution of

cell production. Hypoxia stimulates red blood cell

oxygenated arterial blood to the periphery.

production through erythropoietin production in bone (Guyton,

1991).

Viscosity of the blood has its greatest effect in the small vessels. Blood flow is considerably reduced in small vessels, resulting in aggregates of red blood ceils

c

.Q c... E

D02 Dependent

adhering to the vessel walls. This etlect is not offset by

D02 Independent

the tendency of the blood to become less viscous in

I I I I I

'" c o u c Q)

small vessels as a result of the alignment of the blood cells flowing through, which minimizes the frictional forces between layers of flowing blood cells. In addi

: Critical D02

g

tion, in small capillaries, blood cells can become stuck

I I I I

o

100

200

particularly where the nuclei of endothelial cells pro 300

Oxygen

400

500

600

700

delivery (ml/min)

from the lungs to the tissues. Red blood cells also

(Voz)

and

oxygen delivery (002)' The Dorindependent phase represents the normal metabolic state. The D02-dependent phase represents the dependency of Voz on 002 when 002 Falls below the critical 002. (Modified from Phang, P.T. and Russel, 1.A.: When does V02 depend on D02? Resp

Care 38:

618-630, 1993.)

The major function of the red blood cells is to transport hemoglobin, which in turn carries oxygen

FIGURE 1-8 Relationship between oxygen consumption

trude and momentarily block blood flow.

contain a large quantity of carbonic anhydrase, which catalyzes the reaction between COz and HzO. The ra pidity of this reaction makes it possible for blood to react with large quantities of CO2 to transport it from the tissues to the lungs for elimination. Hemoglobin is contained within red blood cells up to a concentration of


34 gmll 00 ml of cells. Each

1


gram of hemoglobin is capable of combining with

15

blood cells. These values vary according to gender,

1-2, p. 6). Therefore in

weight, and other factors. Normally, changes in blood

19 ml of oxygen and in healthy men,

volume reflect deficits and excesses of fluid through

21 ml of oxygen can be carried in the blood, given

imbalances created by losses through the skin and

that the whole blood of women contain

respiratory tract, and through urinary, sweat, and

1.34 ml of oxygen (see Figure healthy women,

of 14 gmll 00 ml of blood and

an average

16 gmll 00 ml of blood

in men.

fecal losses. Exercise and hot weather are major chal lenges to fluid balance in health.

Clotting factors of the blood are normally in a pro

The plasma contains large quantities of sodium

portion that does not promote clotting. Factors that

and chloride ions, and small amounts of potassium,

promote coagulation (procoagulants), and factors that

calcium, magnesium, phosphate, sulfate, and organic

inhibit coagulation (anticoagulants) circulate in the

acid ions. In addition, plasma contains a large amount

blood. In the event of a ruptured blood vessel, pro

of protein. The large ionic constituents of the plasma

thrombin is converted to thrombin, which catalyzes

are responsible for regulating intracellular and extra

the transformation of fibrinogen to fibrin threads.

cellular fluid volumes and the osmotic factors that

This fibrin mesh captures platelets, blood cells, and

cause shifts of fluid between the intracellular and ex

plasma to form a blood clot.

tracellular compartments.

The extreme example of abnormal clotting is dis seminated intravascular coagulation, where both he mOlThage and coagulation occur simultaneously. The acute form of this syndrome occurs in critically ill pa

Oxyhemoglobin Dissociation The demand for oxygen at the cellular level changes

tients with multiorgan system failure. The mechanism

from moment to moment. The properties of oxyhemo

appears to involve tissue factors, factors that damage

globin dissociation ensure that there is a continuous

the blood vessel wall, and factors that increase

supply of oxygen at the cellular level. Oxygen com

1990). The

bines with the hemoglobin molecules in the pul

chronic form of the syndrome occurs in chronic con

monary circulation and then is released in the tissue

platelet aggregation (Green and Esparaz, ditions such as neoplastic disease.

capillaries in response to a reduced arterial oxygen

Plasma is the extracellular fluid of the blood and contains

7% proteins, namely albumin, globulin, and

tension. The S-shaped oxyhemoglobin dissociation curve (see Chapter

9) shifts to the right in response to

fibrinogen. The primary function of the albumin and

reduced tissue pH, increased CO2, increased tempera

to a lesser extent, globulin and fibrinogen, is to create

ture and increased diphosphoglycerate (DPG), a con

osmotic pressure at the capillary membrane and to

stituent of normal blood cells.

prevent fluid leaking into the interstitial spaces. The

The delivery of blood and its ability to effectively

globulins serve as carriers for transporting substances

transport oxygen is central to all steps in the oxygen

in the blood and provide immunity as the antibodies

transport pathway and must be considered at each

that fight infection and toxicity. Fibrinogen is funda

step in clinical problem solving and decision making.

mental to blood clotting. The majority of blood pro teins, including hemoglobin, are also excellent acid base buffers and are res ponsi b Ie for

70% of a II

buffering power of whole blood.

(Q) depends on a pressure gradient (P) and vascular resistance (R), that is, Q PIR. Hence Blood flow

=

blood flow equals the pressure gradient divided by re

Steps in the Oxygen Transport Pathway Step One: inspired oxygen and quality

of the ambient air

In health, the concentration of inspired oxygen is rel

21 % unless the individual is at al

sistance. The length of a given blood vessel and the vis

atively constant at

cosity of the blood are also detelTninants of blood flow.

titude. In which case, the fraction of inspired oxygen

5,000 ml. Approxi 3,000 ml of this is plasma and 2,000 ml is red

The average blood volume is mately

is reduced the higher the elevation. Atmospheric air consists of


79% nitrogen, 20.97%

16

PART I


oxygen and 0.03% CO2. Because nitrogen is not ab

lined with cilia, fine microscopic hair-like projec

sorbed in the lungs, it has a crucial role in maintain

tions, which are responsible for wafting debris, cells,

ing the lung tissue patent. The constituents of the air

and microorganisms away from the lungs into larger

have become an increasingly important social, envi

airways to be removed and evacuated. The airways

ronmental, and health issue because of environmental

are also lined with mucus, which consists of two lay

hazards, pollution, and thinning of the ozone layer re

ers, the upper gel layer and the lower sol layer with

sulting in deterioration of air quality, an increase in

which the cilia communicate.

toxic oxygen free radicals and a reduction in atmos pheric oxygen pressure.

Step Three: lungs and chest wall

Many factors influence air quality, (e.g., geo

Air entry to the lungs depends on the integrity of the

graphical area, season, urban vs. rural area, high vs.

respiratory muscles, in particular, the diaphragm, the

Jow elevation, home environment, work environment,

lung parenchyma, and the chest wall. Contraction and

indoor vs. outdoor, level of ventilation, air condition

descent of the diaphragm inflates the lungs. The dis

ing, enclosed buildings, areas with high particu late

tribution of ventilation is primarily determined by the

matter, areas with gaseous vapors and toxic-inhaled

negative intrapleural pressure gradient down the

materials, and smoke-filled vs. smoke-free environ

lungs. The negative intrapleural pressure gradient re

ments). Poor air quality contributes to changes in the

sults in uneven ventilation down the lung, and inter

filtering ability of the upper respiratory tract, airway

regional differences (see Chapter 3). However, there

sensitivity, and lung damage, acutely and over time.

are other factors, intraregional differences, that con

Chronic irritation of the lungs from poor air quality

tribute to uneven ventilation within regions of the

can lead to allergies, chronic inflammatory reactions,

lung. These intraregional differences reflect regional

fibrosis, and alveolar capillary membrane thickening.

differences in lung compliance and airway resistance

At the alveolar level, the inspired air is saturated with

(Ross, Dean, 1992). In patients with partially ob

water vapor. In dry environments, however, the upper

structed airways, reduced lung compliance, and in

respiratory tract may become dehydrated, lose its

creased airway resistance increase the time for alveo

protective mucous covering, become eroded, and pro

lar filling. Gas exchange is compromised if there is

vide a portal of infection even though the air is ade

inadequate time for alveolar filling or emptying, that

quately humidified by the time it reaches the lower

is, increased time constants (West, 1995). Different

airways and alveoli.

time constants across lung units contribute to uneven patterns of ventilation during inspiration. A lung unit

Step Two: airways

with a long time constant is slow to fill and to empty,

The structure of the airways down the respiratory

and may continue to fill when sun'ounding units are

tract change according to their function. The main

emptying. A second factor is altered diffusion dis

airway, the trachea, consists of cartilagenous rings,

tance. In diseases where diffusion distance is i n

connective tissue, and small amounts of smooth mus

creased, ventilation along lung units is uneven.

cle. This structure is essential to provide a firm and

The lungs and the parietal pleura are richly sup

relatively inflexible conduit for air to pass from the

plied with thin-walled lymphatic vessels (Guyton,

nares through the head and neck to the lungs, and

1991). Lymphatic vessels have some smooth muscle

avoid airway collapse. As the airways become

and thus can actively contract to propel lymph fluid

smaller and branch throughout the lung tissue, they

forward. This forward motion is augmented by

consist primarily of smooth muscle. Airway narrow

valves along the lymphatic channels. The rise and

ing, or, obstruction and increased resistance to air

fall of the pleural pressure during respiration com

flow, is caused by multiple factors, including edema,

presses lymphatic vessels with each breath, which

mUCllS, foreign objects, calcification, particulate mat

promotes a continuous flow of lymph. During expi

ter and space-occupying lesions, as well as hyperre

ration and increased intrapleural pressure, fluid is

activity of bronchial smooth muscle. The airways are

forced into the lymphatic vessels. The visceral pleura



continuously drains fluid from the lungs. This cre ates a negative pressure in the pleural space, keeping

17

Step Five: perfusion The distribution of blood perfusing the lungs is pri

the lungs expanded. This pressure exceeds the elastic

marily gravity dependent, thus the dependent lung

recoil pressure of the lung parenchyma, which col

fields are perfused to a greater extent than the nonde

lapses the lungs.

pendent lung fields. In the upright lung, the bases are

The peritoneal cavity of the abdomen consists of a visceral peritoneum containing the viscera and a pari

better perfused than the apices (see Chapter

3). Venti

lation and perfusion matching is optimal in the mid

1985). In health,

etal peritoneum lining the abdominal cavity. Numer

zones of the upright lungs (West,

ous lymphatic channels interconnect the peritoneal

the ventilation to perfusion ratio is a primary determi

cavity and the thoracic duct; some arise from the di

nant of arterial oxygenation. In the upright lung this

aphragm. With cycles of inspiration and expiration,

ratio is

large amounts of lymph are moved from the peri toneal cavity to the thoracic duct. High venous pres

0.8 in the mid-zone.

Step Six: myocardial function

sures and vascular resistance through the liver can in

Optimal myocardial function and cardiac output de

terfere with normal flu id balance in the peritoneal

pends on the synchronized coupling of electrical ex

cavity. This leads to the transudation of fluid with a

citation of the heart and mechanical contraction. The

high protein content into the abdominal cavity. This

sinoatrial node located in the right atrium is the nor

accumulation of fluid is referred to as ascites. Large

mal pacemaker for the heart and elicits the normal

volumes of fluid can accumulate in the abdominal

sinus rhythm with its component P-QRS-T configura

cavity and significantly compromise cardiopul

tion. This wave of electrical excitation spreads

monary function secondary to increased intraabdomi

throughout the specialized neural conduction system of the atria, interventricular septum, and the ventri

nal pressure on the underside of the diaphragm. Optimal diaphragmatic excursion requires a bal

cles, and is followed by contraction of the atria and

ance between thoracic and intraabdominal pressures.

then the ventricles. Contraction of the right and left

Increases in abdominal pressure secondary to factors

ventricles ejects blood into the pulmonary and sys

other than fluid accumulation can impair diaphrag

temic circulations respectively.

matic descent and chest wall expansion, for example,

Cardiac output depends on several factors in ad

gas entrapment, gastrointestinal (GI) obstruction,

dition to the integrity of the conduction system and the adequacy of myocardial depolarization (dro

space-occupying lesions, and paralytic ileus.

motropic effect). The amount of blood returned to

Step Four: diffusion

the heart (preload), determines the amount ejected

Diffusion of oxygen from the alveolar sacs to the pul

(Starling effect). The distensibility of the ventricles

monary arterial circulation depends on five factors:

to accommodate this blood volume needs to be opti

the area of the alveolar capillary membrane, diffusing

mal, neither too restrictive nor compliant. The con

capacity of the alveolar capillary membrane, pul

tractility of the myocardial muscle must be suffi

monary capillary blood volume, and ventilation and

cient to eject the blood (inotropic effect). And

1993). The transit time of

finally, cardiac output is determined by the aortic

blood at the alveolar capillary membrane is also an

pressure needed to overcome peripheral vascular re

impoltant factor determining diffusion. The blood re

sistance and eject blood into the systemic circula

perfusion ratio (Ganong,

mains in the pulmonary capillaries for

0.75 seconds

tion (afterload).

at rest. The blood is completely saturated within one

The pericardial cavity, like the pleural and peri

third of this time. This provides a safety margin dur

toneal cavities, is a potential space containing a thin

ing exercise or other conditions in which cardiac out

film of fluid. The space normally has a negative

put is increased and the pulmonary capillary transit

pressure. During each expiration, pericardial pres

time is reduced. The blood can normally be fully

sure is increased, and fluid is forced out of the space

oxygenated even with reduced transit time.

into t h e me diastinal lymphatic channels. This


18

PART I


process is normally facilitated with increased volumes

sels, the greater their sensitivity to both exogenous

of blood in the hemt and each ventricular systole.

neural stimulation and endogenous stimulation by cir culating humoral neurotransmitters such as cate

Step Seven: peripheral circulation

cholamines and local tissue factors. This sensitivity is

Once oxygenated blood is ejected from the heart, the

essential for the moment-to-moment regulation of the

peripheral circulation provides a conduit for supply

peripheral circulation with respect to tissue perfusion

ing this blood to metabolically active tissue. Blood

and oxygenation, commensurate with tissue meta

vessels throughout the body are arranged both in se

bolic demands, and control of total peripheral resis

ries and in parallel. The arteries and capillaries are

tance and systemic blood pressure.

designed to advance blood to pelfuse the tissues with oxygenated blood. The vasculature is architected so that the proximal large al1eries have a higher propor

Step fight: tissue extraction

and utilization of oxygen

tion of connective tissue and elastic elements than

Perfusion of the tissues with oxygenated blood is the

distal medium and small arteries, which have a pro

p r i n c i p a l goal of t he oxygen transport system

gressively higher proportion of smooth muscle. This

(Dantzker, 1993). Oxygen is continually being used

structure enables the large proximal arteries to with

by all cells in the body, thus it diffuses out of the cir

stand high pressure when blood is ejected during ven

culation and through cell membranes very rapidly to

tricular systole. Considerable potential energy is

meet metabolic needs. Diffusion occurs down a gra

stored within the elastic walls of these blood vessels

dient from areas of high to low oxygen pressure. The

as the heart contracts. During diastole, the forward

distance between the capillaries and the cells is vari

propulsion of blood is facilitated with the elastic re

able, thus a significant safety factor is required to en

coil of these large vessels. The thin-walled muscular

sure adequate arterial oxygen tensions. Intracellular

arterioles serve as the stopcocks of the circulation and

P02 ranges from 5 to 60 mm Hg, with an average of

regulate blood flow through regional vascular beds

23 mm Hg (Guyton, 1991). Given that only 3 mm

and maintain peripheral vascular resistance to regu

Hg of oxygen pressure are needed to support metab

late systemic blood pressure. Blood flow through

olism, 23 mm Hg of oxygen pressure provide an ade

these regional vascular beds is determined by neural

quate safety margin. Thcsc mechanisms ensure an

and humoral stimulation, and by local tissue factors.

optimal oxygen supply over a wide range of varying

Blood pressure control is primarily regulated b y

oxygen demands in health and in the event of im

neural stimulation of the peripheral circulation and

paired oxygen delivery because of illness. Normally,

these vascular beds.

the rate of oxygen extraction by the cells is regulated

The microcirculation consists of the precapillary ar

by oxygen demand by the cells, that is, the rate at

teriole, the capillary, and the venule. The Starling effect

which ADP is formed from A TP and not by the

govems the balance of hydrostatic and oncotic pres

availability of oxygen.

sures within the capillary and the surrounding tissue. The balance of these pressures is 0.3

The adequacy of the quality and quantity of the mi

Hg; its net ef

tochondrial enzymes, required to support the Krebs

fect is a small outward filtration of fluid from the mi

cycle and electron transfer chain, and the availability

mrn

crovasculature into the interstitial space (see Chapter 3).

of myoglobin may be limiting factors in the oxygen

Any excess fluid or loss of plasma protein is drained

transport pathway secondary to nutritional deficits and

into the sun'ounding lymphatic vessels, which usually

muscle enzyme deficiencies. Myoglobin is a compara

has a small negative pressure as does the interstitium.

ble protein to hemoglobin that is localized within

The integlity of the microcirculation is essential to reg

muscle mitochondria. Myoglobin combines reversibly

ulate the diffusion of oxygen across the tissue capillary

with oxygen to provide an immediate source of oxy

membrane, and to remove CO2 and waste products. The greater the muscular component of blood ves

gen with increased metabolic demands and facilitate oxygen transfer within the mitochondria.



Normally, the amount of oxygen extracted by the

19

ergy expenditure, and thus increase rate of metabolism.

tissues is 23%, that is, the ratio of oxygen consumed

Several factors related to disease can significantly

to oxygen delivered. Thus this ratio ensures that con

increase oxygen consumption and metabolic rate over

siderably greater amounts of oxygen can be extracted

and above BMR. Such factors include fever, the dis

during periods of increased metabolic demand.

ease process itself, the process of healing and recov ery from injury or disease, thermoregulatory distur

Step Nine: return of partially desaturated

bance, reduced arousal, increased arousal resulting

blood and C02 to the lungs

from anxiety and pain, sleep loss, medical and surgi

Partially desaturated blood and CO2 are removed

cal interventions, fluid imbalance, and medications

from the cells via the venous circulation to the right

Dean, 1994b). These factors may contribute to a sys

side of the heart and lungs. C02 diffuses across the

temic increase in BMR or may reflect local changes in

alveolar capillary membrane and is eliminated from

tissue metabolism. Autoregulation of the regional vas

the body through the respiratory system, and the de

cular beds promotes increased regional blood flow in

oxygenated venous blood is reoxygenated. The oxy

accordance with their local tissue metabolic demand.

gen transport cycle repeats itself and is sensitively

Because gravitational stress and exercise stress are

tuned to adjust to changes in the metabolic demand of

fundamental to normal cardiopulmonary function and

the various organ systems, such as digestion in the GI

oxygen transport, the effects of gravity and exercise are

system, and cardiac and muscle work during exercise.

highlighted. It should be emphasized that the effects of

Factors that intelfere with tissue oxygenation and

gravity on fluid shifts and the systeIllic effects of exer

the capacity of the tissue to use oxygen include ab

cise are physiologically distinct, that is, exposing an in

normal oxygen demands, reduced hemoglobin and

dividual to a gravitational stress does not adapt that in

myoglobin levels, edema, and poisoning of the cellu

dividual to an exercise stress and vice versa. These two

lar enzymes (Kariman, Burns, 1985).

factors also augment arousal, through stimulation of the reticular activating system in the brain stem and the au tonomic nervous system (ANS), which when de

FACTORS THAT NORMALLY PERTURB

pressed, significantly compromises oxygen transport in

OXYGEN TRANSPORT

patient populations. The impact of emotional stress on

Basal metabolic rate (BMR) reflects the rate of me

oxygen transport is discussed briefly. These concepts

tabolism when the individual is in a completely

are described fUlther in Chapters 17 and L8.

rested state, that is, no food intake within several hours, after a good night's sleep, no arousing or dis tressing emotional stimulation, and at a comfortable ambient temperature. Normally, the BMR is constant

Gravitational Stress Humans are designed to function in a I G gravita

within and between individuals if measured under

tional field. Given that 60% of the body weigllt is

standardized conditions. This rate reflects resting en

fluid contained within the intra- and extravascular

ergy expenditure of the body's cells to maintain rest

compartments, and that this fluid has considerable

ing function, including the work of breathing; heart,

mass, changes in body position result in significant fluid shifts instantaneously and threaten hemody

renal, and brain function; and thermoregulation. Normally, over the Course of the day, the human

namic stability (Dean, Ross, 1992a; Dean, Ross,

body is exposed to fluctuations in ambient temperature

1992b). To maintain consciousness and normal body

and humidity, ingestion states, activity and exercise

function during changes in body position, the heart

levels (exercise stress), body positions and body posi

and peripheral vasculature are designed to detect

tion changes (gravitational stress), emotional states

these fluid shifts and accommodate quickly to avoid

(emotional stress) and states of arousal. These factors

deleterious functional consequences (e.g., reduced

significantly influence oxygen consumption and en

stroke volume, CO, circulating blood volume, and


20

PART I


cerebral perfusion). The preservation of the f1uid

The oxygen transport system is designed to deliver

regulating mechanisms is essential to counter the he

oxygen from the ambient air to every cell in the body

modynamic effects of changing body position. This

to support cellular respiration, that is, the metabolic

capacity is quickly lost with recumbency and is the

utilization of oxygen at the cellular level. Blood is the

primary cause of bed rest deconditioning in patient

essential medium in which cellular and noncellular

1966;

components transport oxygen from the cardiopul

1985). Restoration of gravitational stress

monary unit to the peripheral tissues. The fundamental

and older populations (Chase, Grave, Rowell, Winslow,

with upright positioning is the only means by which

steps in the oxygen transport pathway were described.

these fluid-regulating mechanisms can be maintained

These steps included the quality of the ambient air, the

and orthostatic intolerance and its short- and long

airways, lungs, chest wall, pulmonary circulation, lym

term sequelae averted.

phatics, he31t, peripheral circulation, and the peripheral tissues of the organs of the body. In health, the most significant factors that perturb

Exercise Stress

oxygen transport are changes in gravitational stress

Exercise constitutes the greatest perturbation to home

secondary to changes in body position, exercise stress

ostasis and oxygen transport in humans. Cardiac output

secondary to increased oxygen demand of working

can increase five times to adjust to the metabolic de

muscles, arousal, and emotional stress. A thorough

mands of exercise stress. All steps in the oxygen trans

understanding of the normal effects of gravitational

port pathway are affected by exercise stress. Ventilation

and exercise stress and arousal is essential to under

is increased, and ventilation and perfusion matching is

stand deficits in oxygen transport. In disease, numer

optimized to maximize oxygenation of blood. Heart

ous factors impair and threaten oxygen transport, that

rate and stroke volume are increased to effect greater

is, underlying pathophysiology, restricted mobility,

cardiac output of oxygenated blood to the tissues. At

recumbency, factors related to the patient's care, and

the tissue level, oxygen extraction is enhanced.

factors related to the individual (see Chapter

16).

Thus the physical therapist needs a detailed under standing of these concepts to diagnose these deficits

Emotional Stress

and prescribe efficacious treatments.

The body responds to emotional stress similar to ex ercise stress with the sympathetic stress reaction. Per ceived threat, the basis of emotional stress, triggers the fight, flight, or fright mechanism and a series of sympathetically mediated physiological responses. This reaction that prepares the body for flight in cludes an increase in heart rate, blood pressure, CO, blood glucose, muscle strength, mental alertness, cel

REVIEW QUESTIONS 1. Describe the oxygen transport pathway, its steps

and their interdependence. 2. Describe the physiological processes of energy

transfer and cellular oxidation. 3. Explain oxygen transport with respect to oxygen

lular metabolism, and increased local blood flow to

delivery, uptake and utilization and the interrela

specific muscle groups, as well as inhibition of invol

tionship among these processes.

untary function.

4. Outline the factors that perturb oxygen transport

in health.

SUMMARY This chapter described the oxygen transport system, its component steps, and their interdependence. This framework provides a conceptual basis for the prac tice of cardiopulmonary physical therapy.

References Chase, G.A., Grave,

c., & Rowell, L.B. (1966). Independence of

changes in functional and performance capacities attending prolonged bed rest,


Aerospace Medicille 37: 1232-1237.


Cone, lB. (1987). Oxyg.cn transport from capillary to cell. In Sny

21

Kariman, K., & Burns, S.R. (1985). Regulation of tissue oxygen

der, J.V., Pinsky, M.R. (eds). Oxygen transport in the criticailv

extraction in disturbed in adult respiratory distress syndrome,

ill, Chicago: Year Book.

A meri can Review Respi ratory Diseases 132: 109-1 14, 1985.

Dantzker, D.R. (1993). Adequacy of tissue oxygellation. Critical

Care M edicine 21:S40-S43.

Dantzker, D.R. (1991). CardiopulmonGl) , Critical Care, ed 2. Philadel phia: WE Saunders.

Kirchberger, M.A. (1991). Excitation and contraction of skeletal muscle. In West J.B., editor (1991). Best and Taylor's physiolog

ical basis of medical practice. Bahimore: Williams & Wilkins. Lorente, J.A., et al (J 991). Oxygen delivery-dependent oxygen con

Dantzker, D.R. (1985). The intluence of cardiovascular function on gas exchange. Clinical Chesl Medicine 4: 149-159.

sumption in acute respiratory failure, Critical Care Medicine

19.'770-775, 1991.

Dantzker, D.R., Boresman, B., & Gutierrez, G. (1991). Oxygen supply and utilization relationships. American Review of Respi

ratory Disorders 143:675-679.

MCArdle, W.D., Katch, F.l., & Katch, V.L. (1994). Essentials (j(

exercise physiology, Philadelphia: Lea & Febiger. Mizock, B.A., & Falk, J.L. (1992). Lactic acidosis in critical ill

Dean, E. (1994a). Oxygen transport: a physiologically-based con ceptual framework for the practice of cardiopulmonary physio

ness, Critical Core Medicine 20:80-93, 1992. Phang, P.T., Russell, J.A. (1993). When does V02 depend on D02

Respiratory Care 38:618-630.

therapy, Physiotherapy 80:347-355. Dean, E. (1994b). Physiotherapy skilis: positioning and mobiliza

Ross, J., & Dean, E. (1989). Integrating physiological principles

tion of the patient. 1 n Webber, B.A., Pryor, J.A., editors.

into the comprehensive management of cardiopulmonary dys

(1994b). Physiotherapy for respiralry and cardiac problems,

function. Physical Therapy 69:255-259, 1989. Ross, J" & Dean, E. (1992). Body positioning. In e.e. Zadai (Ed.).

Edinburgh: Churchill Livingstone. Dean, E., & Ross, 1. (1992a). Discordance between cardiopulmonary physiology and physical therapy. Chest 101:1694-1698, 1992a Dean, E., & Ross, 1. (1992b). Oxygen transport. The basis for con temporary cardiopulmonary physical therapy and its optimiza tion with body positioning and mobilization, Physical Therapy

Clinics in physical therapy. Pulmonary managemell1 in physi

cal therapy. New York: Churchill Livingstone. Samsel, R.W., & Schumacker, P.T. (1991). Oxygen delivery to tis sues, European Respiralry 10urna14: 1258-1267. Sandler, H. (1986). Cardiovascular effects of inactivity, [n Sandler, H., Vernikos, 1., (Eds.). Inactivity physiological effects. Orlando,

Practice 1:34-44. Epstein, e.D. & Henning, R.J. (1993). Oxygen transport variables in the identification and treatment of tissue hypoxia, Heart

Fla: Academic Press. Schumacker, P.T., & Cain, S.M.: The concept of critical oxygen delivery, Intensive Care Med i cine 13:223-229.

Lung, 22:328-348. Fenwick, J.e., et al: Increased concentrations of plasma lactate

Schumaker, P.T., & Samsel, R.W. (1989). Oxygen delivery and

predict pathologic dependence of oxygen consumption on oxy

uptake by peripheral tissues: physiology and pathophysiology,

gen delivery in patients with adult respiratory distress syn

Critical Care Clinics 5:255-269. Shephard, R.J. (1985). Physiology and biochemistry of exercise,

drome, lournal of Critical Care 5:81-86, 1990. Fox, E., Bowers R., & Foss M. (1993). The physiological basis for ex

ercise and sport, ed 5, Madison: Wis. 1993, Brown & Benchmark. Ganong, W.F.: Review of medical physiology, ed 16, Los Altos,

Philadelphia: Praeger Scientific. Tortora, G.J., & Anagnostakos N.P. (1990). Principles of anatomy and physiology, New York: Harper & Row. Wasserman, K., et al (1987). Principles of exercise testing and in

Calif: Lange Medical Publications. Goldring, R.M.: Specific defects in cardiopulmonary gas exchange,

American Review Respiratory Disorders 129:S57-S59, 1984. Green, D., & Esparaz, B. (1990). Coagulopathies in the critically-ill patient. [n Cane, R.D., Shapiro, B,A., & Davison, R. (Ed.). (1990).

Case sludies in critical care medicine, ed 2, Chicago: Year Book. Guyton, A.e. (1991). Textbook of medical physiology, ed 8,

terpretation, Philadelphia: Lea & Febiger. Weber, K.T., et al (1983). The cardiopulmonary unit: The body's gas exchange system, Clinics Chest Medicine 4:101-110. West, J. B. (1985). Respiratory physiology-the essentials, ed 5, Baltimore: Williams & Wilkins. West, J.B.: Ventilation, blood flow and gas exchange, (ed 4). Ox ford: Blackwell Scientific.

Philadelphia, 1991, WB Saunders. Guyton, A.e. (1987). Human physiology and mechanisms of dis

ease, ed 4, Philadelphia: WB Saunders.

Winslow, E.H. (1985). Cardiovascular conseq/./ences of bed rest,

Heart Lung 14:236-246.

Johnson, R.L. (1973). The lung as an organ of oxygen transport,

Bosic RespiralOry Diseases 2: 1-6, 1973.


Cardiopulmonary Anatomy


KEY TERMS

Cardiopulmonary unit

Peripheral circulation

Heart

Pulmonary circulation

Heart-lung interdependence

Respiratory muscles

Lymphatic circulation

Thoracic cavity

Parenchyma

Tracheobronchial tree

INTRODUCTION

This chapter presents the anatomy of the car

The heart lies in series with the lungs, constituting

diopulmonary system, including the skeletal features

the cardiopulmonary unit, the central component of

of t h e t horacic cavity; muscles of respiration;

the oxygen transport pathway (Scharf and Cassidy,

anatomy

1989; Weber et ai, 1983). Virtually all the blood re

parenchyma; basic anatomy of the heart; and periph

of t h e tracheobronchial tree; lung

turned to the right side of the heart passes through

eral, pulmonary, and lymphatic circulations (Berne

the lungs and is delivered to the left side of the heart

and Levy, 1992; Burton and Hodgkin, 1984; Ganong,

for ejection to the systemic, coronary, and bron

1993; Guyton, 1991; Katz, 1992; Murray, 1986; Mur

chopulmonary circulations. Because of this interrela

ray and Nadel, 1988; Nunn, 1993; West, 1991; West,

tionship, changes in either lung or heart function can

1995; and Williams et ai, 1989).

exert changes in the function of the other organ. A detailed understanding of the anatomy of the heart and lungs, and how these organs work synergisti

THORAX

cally is essential to the practice of cardiopulmonary

The bony thorax covers and protects the principal or

physical therapy.

gans of respiration and circulation, as well as the

23


24

PART I


FIGURE 2-2 The relationship of the lungs to the bony thorax (posterior view).

FIGURE 2-1 The relationship of the bony thorax and lungs to the abdominal contents (anterior view).

level with the second costal cartilages. The bifurca tion of the trachea into the right and left mainstem bronchi al s o occurs at t h e sternal ang le. The

liver and the stomach (Figures 2-1 and 2-2). The pos

manubrium and body are joined by fibrocartilage,

terior surface is formed by the 12 thoracic vertebrae

which may ossify in later life.

and the posterior part of the 12 ribs. The anterior sur

The body of the sternum is twice as long as the

face is formed by the sternum and the costal carti

manubrium. It is a relatively thin bone and can be

lage. The lateral surfaces are formed by the ribs. At

easily pierced by needles for bone marrow aspira

birth, the thorax is nearly circular, but during child

tions. The heart is located beneath and to the left of

hood and adolescence, it becomes more elliptical

the lower one third of the body of the sternum. Al

until adulthood. It is wider from side to side than it is

though it is attached by cartilage to the ribs, this por

from front to back.

tion of the sternum is flexible and can be depressed without breaking. This maneuver is used, with care, in closed cardiac massage to artificially circulate

Sternum

blood to the brain and extremities. The lower margin

The sternum, or breastbone, is a flat bone with three

of the body is attached to the xiphoid process by fi

parts: the manubrium, body, and xiphoid process.

brocartilage. This bone is the smallest of the three

The manubrium is the widest and thickest bone of the

parts of the sternum and usually fuses with the body

sternum. Its upper border is scalloped by a central

of the sternum in later life.

jugular notch, which can be palpated, and two clavic ular notches that house the clavicles. Its lower border articulates with the upper border of the body at a

Ribs

slight angle, the sternal angle or angle of Louis. This

A large portion of the bony thoracic cage is formed

angle can be easily palpated, is a landmark located

by 12 ribs located on either side of the sternum. The

between thoracic vertebrae T4 and TS, and is on a

first seven ribs connect posteriorly with the vertebral


2


25

B

FIGURE 2-3 The movements of the r ibs. A, "Bucket handle," lower rib. B, "Pump handle," first rib.

column and anteriorly through costal cartilages with

MOVEMENTS OF THE THORAX

the sternum. These are known as the true ribs. The re

The frequency of movement of the bony thorax joints

maining five ribs are known as the false ribs. The

is greater than that of almost any other combination

first three have their cartilage attached to the cartilage

of joints in the body. Two types of movements have

of the rib above. The last two are free or floating ribs.

been described-the pump-handle movement and the

The ribs increase in length from the first to the sev

bucket-handle movement (Figure 2-3) (Cherniack

enth rib, and then decrease to the twelfth rib. They

and Cherniack, 1983). The upper ribs are limited in

also increase in obliquity until the ninth rib and then

their ability to move. Each pair swings like a pump

decrease in obliquity to the twelfth rib.

handle, with elevation thrusting the sternum forward.

Each rib has a small head and a short neck that ar

This forward movement increases the anteroposterior

ticulate with two thoracic vertebrae. The shaft of the

diameter and the depth of the thorax and is called the

rib curves gently from the neck to a sudden sharp

pump-handle movement. In the lower ribs, there is

bend, the angle of the rib. Fractures often occur at

little antero-posterior movement. During inspiration,

this site. A costal groove is located on the lower bor

the ribs swing outward and upward, each pushing

der of the shaft of the ribs. This groove houses the in

against the rib above during elevation. This bucket

tercostal nerves and vessels. Chest tubes and needles

handle movement increases the transverse diameter

are inserted above the ribs to avoid these vessels and

of the thoracic cage. Thus during inspiration, the tho

nerves. The ribs are separated from each other by the

rax increases its volume by increasing its anteropos

intercostal spaces that contain the intercostal muscles.

terior and transverse diameters.


26

PART I


MUSCLES OF RESPIRATION Inspiration Inspiration is an active movement involving the con traction of the diaphragm and intercostals. Additional muscles may come into play during exertion in health. In disease, the role of these accessory muscles of inspiration may have an important role even at rest. The accessory muscles include the sternocleido mastoids, scalenes, serratus anterior, pectoralis major and minor, trapezius, and erector spinae. The degree to which these accessory muscles are used by the pa tient is dependent on the severity of cardiopulmonary distress (Clemente, and Williams et ai,

1985; Murray and Nadel, 1988; 1989).

Diaphragm The diaphragm is the principal muscle of respiration. During quiet breathing, the diaphragm contributes ap proximately two thirds of the tidal volume in the sit ting or standing positions, and approximately three fourths of the tidal volume in the supine position. It is also estimated that two thirds of the vital capacity in all positions is contributed by the diaphragm. The diaphragm is a large, dome-shaped muscle that separates the thoracic and abdominal cavities. Its

FIGURE 2-4

upper surface supports the pericardium (with which it

The diaphragm from below.

is partially blended), heart, pleurae, and lungs. Its lower surface is almost completely covered by the peritoneum and overlies the liver, kidneys, suprarenal

2-4). This large

lumbar vertebrae and extends upward to the central

muscle can be divided into right and left halves. Each

tendon. The central tendon is a thin, strong aponeuro

glands, stomach, and spleen (Figure

half is made up of three parts-sternal, lumbar, and

sis situated near the center of the muscle, somewhat

costal. These three parts are inserted into the central

closer to the front of the body. It resembles a trefoil

tendon, which lies just below the heart. The sternal

leaf with three divisions or leaflets. The right leaflet

part arises from the back of the xiphoid process and

is the largest, the middle is the next largest, and the

descends to the central tendon. On each side is a

left leaflet is the smallest.

small gap, the sternocostal triangle, which is located

Major vessels traverse the diaphragm through one

between the sternal and costal parts. It transmits the

of three openings (see Figure

superior epigastric vessels and is often the site of di

opening is located to the right of the midline in the

2-4). The vena caval

aphragmatic hernias. The costal parts form the right

central tendon and contains branches of the right

and left domes. They arise from the inner surfaces of

phrenic nerve and the inferior vena cava. The

the lower four ribs and the lower six costal cartilages.

esophageal opening is located to the left of the mid

They interdigitate and transverse the abdomen to in

line and contains the esophagus, the vagal nerve

sert into the anterolateral part of the central tendon.

trunks and branches of the gastric vessels. The aortic

The lumbar part arises from the bodies of the upper

opening is located in the midline and contains the


2

(


27

--------

? I t.

\ ff� '---

-----

FIGURE 2-5 When the patient is lying on side, the dome of the diaphragm on the lower side rises fUI1her in the thorax than the dome on the upper side.

aorta, thoracic duct, and sometimes the azygos vein.

in this POSItIon. On x-ray, the position of the di

The diaphragm is also pierced by branches of the left

aphragm can indicate whether the film was taken dur

phrenic nerve, small veins, and lymph vessels.

ing inspiration or expiration, and may also indicate

The position of the diaphragm and its range of

pathology in the lungs, pleurae, or abdomen.

movement vary with posture, the degree of distention

Each half of the diaphragm is innervated by a sep

of the stomach, size of the intestines, size of the liver,

arate nerve-the phrenic nerve on that side. Al

and obesity. The average movement of the diaphragm

though the halves contract simultaneously, it is pos

12.5 mm on the right and 12

sible for half of the muscle to be paralyzed without

mm on the left. This can increase to a maximum of

affecting the other half. Generally, the paralyzed half

in quiet respiration is

28 mm on the left during in

remains at the normal level during rest. However,

creased ventilation. The posture of the individual de

with deep inspiration, the paralyzed half is pulled up

30 mm on the right and

termines the position of the diaphragm. In the supine

by the negative pressure in the thorax. A special x

position, the resting level of the diaphragm rises. The

ray, moving fluoroscopy, is used to determine paral

greatest respiratory excursions during normal breath

ysis of the diaphragm.

ing occur in this position. Howevcr, the lung volumes

Contraction of the diaphragm increases the tho

are decreased because of the elevated position of the

racic volume vertically and transversely. The central

abdominal organs. fn a sitting or upright position, the

tendon is drawn down by the diaphragm as it con

dome of the diaphragm is pulled down by the abdom

tracts. As the dome descends, abdominal organs are

inal organs, allowing a larger lung volume. For this

pushed forward, as far as the abdominal walls will

reason, individuals who are short of breath are more

allow. When the dome can descend no farther, the

side-lying po

costal fibers of the diaphragm contract to increase the

sition, the dome of the diaphragm on the lower side

thoracic diameter of the thorax. This occurs because

rises farther into the thorax than the dome on the

the fibers of the costal part of the diaphragm run ver

comfortable sitting than reclining. fn

a

upper side (Figure 2-5). The abdominal organs have a

tically from their attachment at the costal margin.

tendency to fall forward out of the way, allowing

Thus contraction of these fibers elevates and everts

greater excursion of the dome on the lower side. fn

the ribs (Figure 2-6). If the diaphragm is in a low po

contrast, the upper side moves little with respiration

sition, it will change the angle of pull of the muscle's


28

PART I


.-;;/

"W.M

FIGURE 2-6 Contraction of the costal fibers of the diaphragm causes rib eversion and elevation.

costal fibers. Contraction of these fibers creates a

muscle forward to the sternum. There are II external

horizontal pull, which causes the lateral diameter to

intercostal muscles on each side of the sternum. They

become smaller as the ribs are pulled in toward the

are thicker posteriorly than anteriorly, and thicker

central tendon.

than the internal intercostal muscles. They are inner

As the diaphragm descends, it compresses the ab

vated by the intercostal nerves, and contraction draws

dominal organs, increasing intraabdominal pressure.

the lower rib up and out toward the upper rib. This

At the same time, the intrathoracic pressure decreases

action increases the volume of the thoracic cavity.

as the lung volume is increased by the descending di

There are also 11 internal intercostals per side.

aphragm. Inspiratory airflow occurs as a result of this

These are considered primarily expiratory in function.

decrease in intrathoracic pressure (see Chapter 3).

Studies have shown that the intercartilaginous or

The pressure gradient between the abdominal and

parasternal portion of the internal intercostals con

thoracic cavities also facilitates the return of blood to

tracts with the external intercostals during inspiration

the right side of the heart.

to help elevate the ribs. Besides their respiratory func

Movement of the diaphragm can be controlled to

tions, the intercostal muscles contract to prevent the

some extent voluntarily. Vocalists spend years learn

intercostal spaces from being drawn in or bulged out

ing to manipulate their diaphragms to produce the

during respiratory activity.

controlled sounds during singing. The diaphragm mo mentarily ceases movement when a person holds his

Sternocleidomastoid

or her breath. The diaphragm is invol untarily in

The sternocleidomastoids (SCMs) are strong neck

volved in parturition, bearing down in bowel move

muscles arising from two h e a d s , one from the

ments, laughing, crying, and vomiting. Hiccups are

manubrium and one from the medial part of the clavi

spasmodic, sharp contractions of the diaphragm that

cle (see Figure 2-7, p. 29). These two heads fuse into

may indicate disease (e.g., a subphrenic abscess) if

one muscle mass that is inserted behind the ear into the mastoid process. It is innervated by the accessory

they persist.

nerve and the second cervical nerve. There are two of

Intercostals

these muscles, one on each side of the neck. When one

The external intercostals extend from the tubercles

SCM contracts, it tilts the head toward the shoulder of

of the ribs, above, down, and forward to the costo

the same side and rotates the face toward the opposite

chondral junction of the ribs below, where they be

shoulder. If the two SCM muscles contract together,

come continuous with the anterior intercostal mem

they pull the head forward into flexion. When the head

brane (Figure 2-7). This membrane extends the

is fixed, they assist in elevating the sternum, increasing


2


29

Obllquus internus abdomlnis

Transversus abdomlnlS ......

FIGURE 2-7

Respiratory muscles (anterior view). the anteroposterior (AP) diameter of the thorax.

and inferiorly to the upper surface of the first two

The SCMs are the most important accessory mus

ribs (see Figure 2-7). They are innervated by related

cles of inspiration. Their contractions can be ob

cervical spinal nerves. These muscles are primarily

served in all patients during forced inspiration and in

supportive neck muscles, but they can assist in res

all patients who are dyspneic. These muscles become

piration through reverse action. When their superior

visually predominant in patients who are chronically

attachment is fixed, the scalenes act as accessory

dyspneic (sec Chapter 4).

respiratory muscles and elevate the first two ribs during inspiration.

Scalenes The anterior, medial, a n d posterior scalenes are

Serratus Anterior

three separate muscles that are considered as a func

The sen-atus anterior arises from the outer surfaces of

tional unit. They are attached superiorly to the trans

the first eight or nine ribs. It curves backward, forming

verse processes of the lower five cervical vertebrae

a sheet of muscle that inserts into the medial border of


30

PART I


the scapula. It is innervated by the long thoracic nerve

f"

(cervical nerves CS, C6, and C7). There are two of these muscles, one on each side of the body. Normally, they assist in forward pushing of the arm (as in boxing or punching). When the scapulae are fixed, they act as accessory respiratory muscles and elevate the ribs to which they are attached.

Pectoralis Major The pectoralis major is a large muscle arising from the clavicle, the sternum, and the cartilages of all the true ribs (see Figure 2-7, p. 29). This muscle sweeps across the anterior chest to insert into the intertuber cular sulcus of the humerus. It is innervated by the lateral and medial pectoral nerves and cervical nerves

CS, C6, C7, C8, and Tl. There are two of these mus

J

cles, one on each side of the body. This muscle acts to rotate the humerus medially and to draw the arm across the chest. In climbing and pull-ups, it draws the trunk toward the arms. In forced inspiration when the arms are fixed, it draws the ribs toward the arms, thereby increasing thoracic diameter.

Pectoralis Minor The pectoralis minor is a thin muscle originating from the outer surfaces of the third, fourth, and fifth ribs near their cartilages. It inserts into the coracoid process of the scapula. It is innervated by the pectoral nerves

FIGURE 2-8

Respiratory muscles (posterior view).

(cervical nerves C6, C7, and C8). There are two of these muscles, one on each side of the body. They con tract with the serratus anterior to draw the scapulae to ward the chest. During deep inspiration, they contract

the spine of the scapula. Its lower belly arises from the supraspinous ligaments and the spines of the

to elevate the ribs to which they are attached.

lower thoracic region, and runs upward to be in

Trapezius

serted into the lower border of the spine of the

The trapezius consists of two muscles that form a

scapula. This large muscle is innervated by the ex

huge diamond-shaped sheet extending from the head

ternal or spinal part of the accessory nerve and cer

down the back and out to both shoulders (Figure 2-

vical nerves C3 and C4. Its main function is to ro

8). Its upper belly originates from the external oc

tate the scapulae in elevating the arms and to control

cipital protuberance and curves around the side of

their gravitational descent. It also braces the scapu

the neck to insert into the posterior border of the

lae and raises them, as in shrugging the shoulders.

clavicle. The middle part of the muscle arises from a

Its ability to stabilize the scapulae makes it an im

thin

portant accessory muscle in respiration. This stabi

diamond-shaped

tendinous

s h e et,

the

supraspinous ligaments and the spines o f the upper

lization enables the serratus anterior and pectoralis

thoracic region, and runs horizontally to insert into

minor to elevate the ribs.


2

Cardiopulmonar)' Anatomy

31

Obliquus Intemus Abdominis

Erector Spinae The erector spinae is a large muscle extending from

This muscle originates from the lumbar fascia, the an

the sacrum to the skull (see Figure 2-8, p. 30). It orig

terior two thirds of the iliac crest, and the lateral two thirds of the inguinal ligament (see Figure 2-7, p. 29). Its post eri or fibers run almost vertically upward to in

inates from the sacrum, iliac crest,

and the spines of the lower thoracic and lumbar vertebrae. It separates into a lateral iliocostalis, an intermediate longissimus,

selt into the lower borders of the last three ribs. The

and a medial spinalis column. This muscle mass in

other fibers join an aponeurosis attached to the costal

serts into various ribs and vertebral processes all the

margin above, the linea alba in the midline and the

way up to the skull. It is innervated by the related

pubic crest below. It is innervated by the lower six tho

spinal nerves. These muscles extend, laterally flex,

racic nerves and the first lumbar spinal nerves.

and rotate the vertebral column. They are considered accessory respiratory muscles through their extension of the vertebral column. In deep inspiration, these

Transversus Abdominis The transversus abdominis arises from the inner sur

muscles extend the vertebral column, allowing fur

face of the lower six costal caltilages, the lumbar fas

ther elevation of the ribs.

cia, the anterior two thirds of the iliac crest, and the lateral one third of the inguinal ligament (see Figure

2-7, p. 29). It nms across the abdomen horizontally to

Expiration

insert into the ap one ur osi s extending to the linea alba. It is innervated by the lower si x thoracic nerves ,

Expiration is a passive process,

occurring when the in tercostals and diaphragm relax. Their relaxation al

and the first lumbar spinal nerves.

lows the ribs to drop to their preinspiratory position and the diaphragm to rise. These activities compress the lungs, raising intrathoracic pressure above atmos pheric pressure, and thereby contributing to air flow out of the lungs.

Action of the Abdominal Muscles These four muscles work together to provide a firm but flexible wall to keep the abdominal viscera in position. The abdominal muscles exert

a compressing force on

the abdomen when the thorax and pelvis are fixed. This

Rectus Abdominis

force can be used in defecation, urination, parturition,

The rectus abdominis rises from the pubic crest and

and vomiting. In forced expiration, the abdominal mus

extends upward to insert into the xiphoid process

cles help force the diaphragm back to its resting posi

and the costal margin of the fifth, sixth, and seventh

tion and thus force air from the lungs. If the pelvis and

costal cartilages (see Figure 2-7, p. 29). It is inner

vertebral column are fixed, the obJiquus externus abdo

vated by related spinal nerves, and its action is con

minis aids expiration further by depressing and com

sidered within the context of the other abdominal

pressing the lower part of the thorax. Patients with chronic obstructive pulmonary disease (COPD) have

muscles.

difficulty in exhalation, which causes them to trap air in

Ob/iquus Extemus Abdominis

their lungs. The continued contraction of the abdominal

This muscle arises in an oblique line from the fifth

muscles throughout exhalation helps them force this air

costal cartilage to the twelfth rib (see Figure 2-7,

from the lungs. The abdominal muscles also play an

p. 29). Its posterior fibers attach in an almost vertical

impOltant role in coughing. First, a large volume of air

line with the iliac crest. The other fibers extend down

is inhaled, and the glottis is

and forward to attach to the front of the xiphoid

muscles contract, raising intrathoracic pressure. When

process, the linea alba, and below with the pubic

the glottis opens, the large difference in intrathoracic

symphysis. It is innervated by the spinal nerves.

lower six thoracic

closed. Then the abdominal

and atmospheric pressure causes the air to be expelled forcefully at tremendous flow rates (tussive blast).


32

PART I


Patients with weak abdominal muscles (from neuro

upper ribs move forward and upward (Cherniack and

muscular diseases, paraplegia, quadriplegia or exten

Cherniack,

sive abdominal surgery) often have ineffective coughs (see Chapters

28 and 33).

1983).

Quiet expiration is passive and involves no mus cular contraction although some electrical activity

The four abdominal muscles have many other

can be detected. The inspiratory muscles relax, caus

nonrespiratory functions both individually and as a

ing intrathoracic pressure to be raised as the ribs and

group; these are not discussed here.

diaphragm compress the lungs by returning to their preinspiratory positions. This increased pressure al

internaiintercostais

lows air flow from the lungs.

There are II internal intercostal muscles on each side

In forced inspiration, a large number of accessory

of the thorax. Each muscle arises from the floor of

muscles may contract in addition to the normal in

the costal groove and cartilage, and passes inferiorly

spiratory muscles mentioned. The erector spinae

and posteriorly to insert on the upper border of the rib

contract to extend the vertebral column. This exten

below. These internal intercostals extend from the

sion permits greater elevation of the ribs during in

sternum anteriorly, around the thorax to the posterior

s piration. Va rious back muscles ( e .g., erector

costal angle. They are generally divided into two

spinae, trapezius, and rhomboids) contract to stabi

parts-the interosseous portion located between the

lize the vertebral column, head, neck, and scapulae.

sloping parts of the ribs, and the intercartilaginous

This enables accessory respiratory muscles to assist

portions located between costal carti lages. As dis

inspiration through reverse action. The SCM raises

cussed previously, the intercartilaginous portions are

the sternum. The scalenes elevate the first two ribs.

considered inspiratory in function. Contraction of the

The serratus anterior, pectoralis major, and pec

interosseous portions of the intercostals depresses the

toralis minor assist in elevating the ribs bilaterally.

ribs and may aid in forceful exhalation. This muscle

All these accessory muscles tend to elevate the ribs,

is innervated by the adjacent intercostal nerves.

thus increasing the AP diameter but not the trans verse diameter of the thorax. (In fact, the transverse diameter does increase slightly as a result of the in

SUMMARY OF RESPIRATORY MOVEMENTS

creased strength of the contraction of the normal in

In quiet inspiration, the diaphragm, external inter

spiratory muscles.) The marked increase in AP di

costals, and intercartilaginous portions of the internal

ameter in relation to transverse diameter creates an

intercostals are the primary muscles that contract.

impression of

The diaphragm contracts first and then descends, en

accessory muscles.

en

bloc breathing in the patient using

larging the thoracic cage vertically. When abdominal

In forced expiration, the interosseous portion of

contents prevent its further descent, the costal fibers

the internal intercostals and the abdominal muscles

of the diaphragm contract, causing the lower ribs to

contract to force air out of the lungs. Forced expira

swing up and out to the side (bucket-handle move

tion can be slow and prolonged (as in patients with

ment). This lateral rib movement is assisted by the

COPD) or rapid and expulsive (as in a cough). If the

external intercostals and the intercartilaginous portion

abdominal contractions are strong enough, the trunk

of the internal intercostals. The transverse diameter of

flexes during exhalation. This flexion further com

the thorax is increased by this bucket-handle move

presses the lungs, forcing more air from them.

ment. Finally, the upper ribs move forward and up ward (pump-handle movement) also through contrac tion

of

their

external

intercostals

and

the

intercartilaginous portions of the internal intercostals. This increases the AP diameter of the thorax. During

UPPER AIRWAYS Nose

quiet inspiration, the epigastric area protrudes, then

Noses vary in size and shape with individuals and na

the ribs swing up and out laterally, and finally the

tionalities. Its framework is comprised of bony and


2

cartilaginous parts. The upper one third IS primarily


33

are covered with a thin, yellow olfactory mucous

bony and contains the nasal bones, the fr ontal

membrane that consists of bipolar nerve cells that are

processes of the maxillae and the nasal part of the

olfactory in function. Only a portion of inspired air

frontal bone. Its lower two thirds are cartilaginous

reaches the olfactory region to provide a sense of

and contain the septal, lateral, and major and minor

smell. When people smell something specific, they

alar nasal cartilages. The nasal cavity is divided into

sniff

right and left halves by the nasal septum. This cavity

it comes in contact with the olfactory region.

This action lifts the inspired air so that more of

extends from the nostrils to the posterior apertures of

The anterior portion (vestibule) of the nasal cavity

the nose in the nasopharynx. The lateral walls of the

(Figure 2-9) is lined with skin and coarse hairs (vibris

cavity are irregular as a result of projecting superior,

sae) that entrap inhaled patticies. The rest of the cavity

middle, and inferior nasal chonchae. There is a mea

and sinuses (with the exception of the olfactory region)

tus located beneath or lateral to each choncha through

are lined with respiratory mucous membrane. This

which the sinuses drain. The chonchae increase the

membrane is composed of pseudostratified columnar

sUlface area of the nose for maximum contact w ith

ciliated epithelium (Figure 2-10). It contains goblet

inspired air. The superior chonchae and adjacent sep

cells, as well as mucous and serous glands that produce

tal wall are referred to as the olfactory region. They

secrete mucus and serous secretions. These secretions

Vestibule 01 nasal cavity

FIGURE 2-9 Sagittal section of the head and neck.


34

PART I


B

FIGURE 2-10 B, Normal movements of cilia.

A, Pseudostrmified columnar ciliated

and bacteria. This mucus is then

walls are lined

the cilia at a rate of 5 to 15

swept to the

The

where it is swallowed or

and stratified squamous in the oral parts.

mucous membrane is vascular, with arterial blood sup plied by branches of the internal and external carotid arteries. Venous

occurs

the anterior

The nasopharynx is a continuation of the nasal

2-9, p.

cavitIes

It lies behind the nose

facial veins. The mucous membrane is thickest over the

and above the soft palate. With the exception of the

chonchae. As air is inhaled, it passes around and over

soft

the chonchae, whose vascular moist surfaces heat, hu

never

its walls are immovable, so its

is

as is the oral and laryngeal phar

midify, and filter the inspired air. The mucous mem

ynx. The nasopharynx communicates with the nasal

brane may become swollen and irritated in upper

cavity

infections and may secrete copious amounts of

the posterior apertures of

the nose. It communicates with the

mucus. Because this membrane is continuous with si

pharynx through an opening, the

nuses, auditory tubes and lacrimal canaliculi, people

This opening is closed by elevations of the soft palate

isthmus.

suffering f r o m colds often complain of sinus headaches, watery eyes,

and other

The oral pharynx extends from the soft palate to

Secretions are often so copious that the nasal passages

p. 33). It opens into the

the ep!.r10ttis (see

become comDletelv blocked.

the oropharyngeal isthmus. walls lie on the bodies of the second and third cervical vertebrae. Laterally, two masses of

Pharynx

lymphoid tissue-the is an oval fibromuscular sac located

The

behind the nasal cavity, mouth, and larynx. It is ap

12 to 14 cm long and extends from the base of the skull to the esophagus below, at the level of the cricoid

the sixth cervical

be seen.

These tonsils form part of a circular band of lym into the diges

phoid tissue surrounding the t!ve and

tracts.

The laryngopharynx lies behind the larynx and ex tends from the

above to the inlet of the

vertebra. Anteriorly, it opens into the nasal cavity

esophagus below

(nasophar ynx), mouth (oral pharynx) and larynx

to sixth cervical vertebrae lie behind the laryngeal


Figure

p.

The fourth

2


35

a n d the cartilages of the larynx (e.g., thyroid, cricoid, epiglottic, right and left arytenoids, cornic ulates, and cuneiforms). The thyroid cartilage is the largest. It has a V-shaped notch in its upper one third, which projects forward, forming the "Adam's apple." The entire cartilage is pulled up in swal lowing, with the upper part of the cartilage passing beneath the hyoid bone. The cricoid cartilage is shaped like a signet ring, with the signet part facing the posterior. The anterior part of the carti lage is easily palpated just below the thyroid cartilage. It is thicker and more prominent than the tracheal rings, FIGURE 2-11

which lie below. It is the only cartilage that com

Visualization of the larynx via a laryngoscope.

pletely circles the airway. The cricoid cartilage is connected to the thyroid cartilage by the cricothy roid membrane. (This membrane is often punctured

pharynx. In front of the laryngopharynx are the

to establish an airway in an emergency when the

epiglottis, the inlet of the larynx and the posterior

upper airway is obstructed.) The epiglottic cartilage is the elastic skele ton of the epiglottis. It is a

surfaces of the arytenoid and cricoid cartilages.

leaflike structure attached by ligaments to the hyoid bone anteriorly and the thyroid cartilage below. It is

Larynx

considered a vestigial structure, and its removal

The larynx is a complex structure composed of carti

causes little effect. Finally, the arytenoid cartilages

lages and cords moved by sensitive muscles (Figure

are two small pyramid-shaped cartilages that articu

2-11), and is located between the trachea and laryn

late with the posterior part of the cricoid cartilage.

gopharynx, for which it forms an anterior wall. It acts

The vocal cords attach from these cartilages to the

as a sphincteric valve with its rapid closure, prevent

thyroid cartilage.

ing food, liquids, and foreign objects from entering

The true vocal cords (or vocal folds) are two

the airway. It controls airflow, and at times closes so

pearly white folds of mucous membrane that stretch

that thoracic pressure may be raised and the upper

from the arytenoid cartilage to the thyroid cartilage.

airways cleared by a propulsive cough when the lar

The space between the true vocal cords is called the

ynx opens. Expiratory airflow vibrates as it passes

rima glottidis. It changes shape with movement of the

over the contracting vocal chords, producing the

cords but is generally triangular when the cords are

sounds used for speech. (The larynx is not essential

open. The rima glottidis and the true vocal cords are

for speech. Humans can speak by learning to dilate

grouped together under the term glottis. The glottis is

the upper part of the esophagus so that air vibrates as

the narrowest part of the adult airway.

it passes over; this is called esophageal speech).

Just above the true vocal cords are two shallow

In adult men, the larynx is situated opposite the

grooves in the mucous membrane lining of the larynx.

third, fourth and fifth cervical veltebrae; it is situated

These grooves (ventricles of the larynx) contain nu

somewhat higher in women and children. In children,

merous glands that secrete the mucus that covers the

the larynx is essentially the same in girls and boys. At

larynx. The false vocal cords (vestibular or ventricular

puberty, the male larynx increases in size consider

folds) lie just above the venuicles of the larynx. They

ably until its AP diameter is almost doubled. All the

are two soft, pink masses of mucous membrane raised

cartilages enlarge, with the thyroid cartilage becom

slightly from the laryngeal wall. They extend from the

ing prominent anteriorly.

thyroid cartilage to the arytenoids. The false cords are

The laryngeal skeleton contains the hyoid bone

not as well developed as the true cords and do not


36

PART I


approximate completely during phonation. However, their closure can help protect the airway from aspira tion of foreign material. There are two main groups of muscles that control the opening and closing of the glottis-the abductors and adductors. The posterior cricoarytenoid muscle is the most important muscle in the larynx, since it is the only abductor of the vocal folds. It is vital for respira tion. Contraction of this muscle separates the vocal folds and widens the lumen of the glottis. There are eight adductors of the vocal folds: (I) aryepiglottic, (2) thyroepiglottic, (3) thyroarytenoid, (4) vocalis, (5) cricothyroid, (6) lateral cricoarytenoid, (7) trans verse arytenoid and (8) oblique arytenoid muscles. Contraction of these muscles results in approximation of the vocal cords and narrowing of the glottis. The adductors of the cords are important in protecting the lower airways. Their contraction prevents fluids, food, and other substances from being aspirated. All the in trinsic laryngeal muscles are innervated by the recur rent laryngeal nerve (a branch of the vagus nerve) with the exception of the cricothyroid muscle, which is supplied by the external branch of the superior la ryngeal nerve (also a branch of the vagus nerve). The mucous membrane of the larynx is continu ous with that of the laryngopharynx above and the trachea below. It lines the cavity of the larynx and the structures found within. On the anterior surface and upper h a l f of the posterior surface of the epiglottis, and the vocal folds, the mucous mem brane is stratified squamous epithelium. The rest of the laryngeal mucosa is ciliated columnar epithe lium. The mucous membrane of the larynx has many mucous glands. They are especially numerous in the epiglottis, in front of the arytenoid cartilages and in the ventricles of the larynx. Some taste buds are also located on the epiglottis and irregularly throughout the rest of the larynx.

LOWER AIRWAYS Trachea The trachea is a semi-rigid, cartilaginous tube approx imately 10 to II cm long and 2.5 cm wide. It lies in front of the esophagus, descending with a slight incli

nation to the right from the level of the cricoid carti lage (see Figure 2-11, p. 35, and Figure 2-12). It trav els behind the sternum into the thorax to the sternal angle (opposite the fifth thoracic veltebra), where it divides to form the right and left main-stem bronchi. The tracheal wall is strengthened by 16 to 20 horse shoe-shaped cartilaginous rings. The open P3lts of the tracheal rings are completed by fibrous and elastic tis sue and unstriated transverse muscle. This part of the ring faces the posterior and is very flexible. It indents or curves inward during coughing. which increases the velocity of expelled air. These cartilages lie hori zontally one above the other, separated by narrow bands of connective tissue. The trachea is lengthened during hyperextension of the head; swallowing, which raises the trachea; and inspiration, when the lungs ex pand and pull the trachea downward. Its cross-sec tional area becomes smaller with contraction of the unstriated transverse muscle fibers that complete the tracheal rings. The mucous membrane of the trachea also con tains columnar ciliated epithelium and goblet cells. Each ciliated epithelial eel I contains approximately 275 cilia. These structures beat rapidly in a coordi nated and unidirectional manner, propelling a sheet of mucus cephalad from the lower respiratory tract to the pharynx, where it is swallowed or expectorated. The cilia beat in this layer of mucus with a strong, forceful forward stroke, followed by a slow ineffec tive backward stroke that returns the cilia to their starting position. This propelling of mucus by the cilia (mucociliary escalator) is essential. When cilia are paralyzed by smoke, alcohol, dehydration, anes thesia, starvation, or hypoxia, mucus begins to accu mulate in distal, gravity-dependent airways, causing infiltrates and eventually localized areas of collapse referred to as atelectasis. The number of mucus-containing goblet cells is approximately equal to the number of ciliated epithe lial cells. Reserve cells lie beneath the ciliated and goblet cells. These reserve cells can differentiate into either goblet cclls or ciliated cells. Beneath the re serve cells lie the gland cells. There are approxi mately 40 times more gland cells than goblet cells. Mucus is composed of 95% water, 2% glycoprotein, I % carbohydrate, trace amounts of lipid, deoxyri


2


37

Apical

Apical

Anterior

Anterior

??'fjfjl;ff?-

Posterior

Apical-posterior

.

Llnguta

Posterior

Anterior

Anterior

Posterior

FIGURE 2-12 Tracheobronchial tree (a three-quarter view, rotated toward the right side).

dead tissue celis, phagocytes,

main-stem bronchus. The azygos vein arches over the

leukocytes, erythrocytes, and entrapped foreign parti

bonucleic acid

right main-stem bronchus, the right pulmonary artery

(DNA),

cles. Mucus lines the airways from the trachea to the

lies beneath. The right main-stem bronchus divides to

alveoli. Two separate layers have been observed-the

form the right upper lobe bronchus, the right middle

sol layer, which lies on the mucosal surface and con

lobe bronchus and the right lower lobe bronchus. The

tains high concentrations of water, and the gel layer,

right upp e r l o b e d i v i d e s i n t o th r e e s e gm e n t al

which is more supelficial and more viscous because

bronchi-apical, posterior, and anterior. The apical

of its lower concentration of water.

bronchus runs almost vertically toward the apex of

The right main-stem bronchus appears to be an ex

the lung. The posterior bronchus is directed posteri

tension of the trachea, being wider, shorter, and more

orly in a horizontal direction, while the anterior

vertical than the left main-stem bronchus. Its greater

bronchus is directed anteriorly in an almost horizon

width and more vertical course cause a majority of

tal direction. The right middle lobe bronchus divides

aspirated foreign material to pass through the right

about

10

mm below the right upper lobe bronchus


38

PART I


and descends downward anterolateraJly. The right

cross-sectional area increases because of the increased

lower lobe bronchus divides into five segmental

number of divisions of the airways. The mucous

bronchi. The apical or superior bronchus runs almost

membrane is essentially the same, with helical carti

horizontally, posteriorly. The medial or cardiac

laginous plates and cilia becoming more sparse. These

bronchus descends downward medially toward the

changes continue throughout the eighth to eleventh

heart. The anterior basal bronchus descends anteri

generations, which are referred to as bronchioles.

orly. The lateral basal bronchus descends laterally

The terminal bronchioles extend from the twelfth

and the posterior bronchus descends posteriorly. Note

to the sixteenth generation. The diameter of these air

that each segment describes its position.

ways is approximately I mm. Cartilage is no longer

The left main-stem bronchus is narrower and runs

present to provide structural rigidity. The airways are

more horizontally than the right main-stem bronchus.

embedded directly in the lung parenchyma, and it is

The aortic arch passes over it, while the esophagus,

the elastic properties of this parenchyma that keep

descending aorta, and thoracic duct lie behind it. The

these lower airways open. Strong helical muscle

left pulmonary artery lies anteriorly and above the

bands are present, and their contraction forms longi

left main-s t e m b r o n c h u s . T h e l e f t m a i n-stem

tudinal folds in the mucosa that sharply decrease the

bronchus has two major divisions-the left upper

diameter of these airways. The epithelium of the ter

lobe bronchus and the left lower lobe bronchus. The

minal bronchioles is cuboidal and no longer ciliated.

left upper lobe bronchus has three major segmental

The cross-sectional area of the airways increases

bronchi. The anterior bronchus ascends at approxi

sharply at this level, as the diameter of the terminal

mately a 45-degree angle. The apical-posterior

bronchioles ceases to decrease as markedly with each

bronchus has two branches; one runs vertically and

generation. All the airways to this level (I to 16 gen

the other posteriorly toward the apex of the left lung.

erations) are considered conducting airways, because

The lingular bronchus descends anterolaterally, much

their purpose is to transport gas to the respiratory

like the right middle lobe bronchus of the right lung.

bronchioles and alveoli, where gas exchange occurs.

The right lower lobe bronchus divides into four seg

The conducting airways receive their arterial blood

mental bronchi. The superior or apical bronchus runs

from the bronchial circulation (branches of the de

posteriorly in a horizontal direction. The anterior

scending aorta). Airways from below this point re

bronchus descends anteriorly. The lateral bronchus

ceive their arterial blood from the pulmonary arteries.

descends laterally, while the posterior bronchus de

The respiratory bronchioles extend from the sev

scends posteriorly. Again the segments describe their

enteenth to the nineteenth generation. They are con

anatomical position.

sidered a transitional zone between bronchioles and

The bronchi of the airways continue to divide until

alveoli. Their walls contain cuboidal epithelium inter

there are approximately 23 generations (Table 2-1).

spersed with some alveoli. The number of alveoli in

The main, lobar, and segmental bronchi are made up

creases with each generation. The walls of the bron

of the first four generations. The walls contain U

chioles are also buried in the lung parenchyma. The

shaped cartilage in the main bronchi. This cartilage

airways depend on traction of this parenchyma to

becomes less well-defined and more irregularly

maintain their lumen. Muscle bands are also present

shaped as the bronchi continue to divide. In the seg

between alveoli.

mental bronchi the walls are formed by irregularly

Alveolar ducts extend from the twentieth to the

shaped helical plates with bands of bronchial muscle.

twenty-second generation. Their walls are composed

The mucous membrane of these airways is essentially

entirely of alveoli, which are separated from one an

the same as in the trachea, but the cells become more

other by their septae. Septae contain smooth muscle,

cuboidal in the lower divisions.

elastic and collagen fibers, nerves, and capillaries.

The subsegmental bronchi extend from the fifth to

The twenty-third generation of air passages is

the seventh generation. The diameter of these airways

called alveolar sacs. They are essentially the same as

becomes progressively smaller, although the total

alveolar ducts, except that they end as blind pouches.


TABLE 2·1 Structural Characteristics of the Air Passages GENERATION (MEAN) NUMBER Trachea

0

MEAN DIAMETER AREA (MM) SUPPLIED 18

CARTILAGE

MUSCLE

Both lungs

13

4

7

EPITHELIUM

end of

Individual

2

EMPLACEMENT

Links open U-shaped

Main bronchi

NUTRITION

cartilage

lungs

Within connective

2 Lobar bronchi

Segmental bronchi

1

1

1

3

8

5

4 5

16 32

4 3

1

1

2,000 4,000

1 1

1

1

Small bronchi

1

Bronchioles

11 12

and terminal

1

bronchioles

16

65,000

tissue Lobes

Segments

sheath IlTegular

Helical

shaped

bands

and

Secondary

helical

lobules

plates

From the

Columnar ciliated

alongside

bronchial

arterial

circulation

vessels

Strong helical

0.5

muscle

Embedded

bands

Cubiodal

directly in the lung

17 Respiratory bronchioles

1

130,000

1

19

500,000

20

1,000,000

Muscle

0.5

Primary

Absent

lobes

Alveolar sacs

1 22 23

flat

between

between

Thin bands

1 4,000,000 8,000,000

ill

0.3 0.3

Alveoli

From Weibel MorphometlY of the human lung. New York, 1963, Springer. Used with permission.

w (0


Cubiodal to

band alveolar

Alveolar ducts

parenchyma

From the

the alveoli

pulmonary circulation

F01TI1S the

alveolar

lung

septa

parenchyma

Alveolar epithelium

PART I

40


(Actually, communication occurs between "blind

Other cells located in the distal airways that are

pouches" in the form of the pores of Kohn's, which

important in the defense of the lung are the lympho

are channels ill alveolar walls,. and Lambert's canals,

cytes a n d p o l y m o r p h o n ucl ear l e ukoc ytes. I m

which are communications between bronchioles and

murioglobulins (IgA, IgG, and IgM) in the blood

alveoli. These communications are thought to be re

serum appear to enhance the engulfing activity of the

sponsible for the rapid spread of lung infection. They

macrophages. There are two types of lymphocytes

also provide collateral ventilation to alveoli, whose

found in the lung-the B-Iymphocyte and the T-Iym

bronchi are obstructed. Although this ventilation does

phocyte. The B-lymphocytes produce gamma globu

little to arterialize blood, it does help prevent collapse

lin antibodies to fight lung infections, whereas the T

of these alveoli.) Each alveolar sac contains approxi

lymphoc ytes r e l e a s e a s u b s t a n c e that attracts

mately 17 alveoli. There are about 300 million alveoli

macrophages to the site of the infection. The poly

in an adult man, 85% to 95% of which are covered

morphonuclear leukocytes are important in engulfing

with pulmonary capillaries. Alveolar epithelium is

and killing blood-borne gram-negative organisms.

composed of two cell types. Type I cells, squamous pneumocytes, have broad thin extensions that cover about 95'!c of the alveolar surface. Type II cells, the

LUNGS

granular pneumocytes, are more numerous than type

Two lungs, each covered with its pleurae-the vis

I cells but occupy less than 5% of the alveolar sur

ceral pleura and the parietal pleura-lie within the

face. This is because of their small, cuboidal shape.

thoracic cavity. Each lung is attached to the heart and

These cells are responsible for the production of sur

the trachea by its root and the pulmonary ligament. It

factant, a phospholipid that lines the alveoli. SUlfac

is otherwise free in the thoracic cavity. The lungs are

tant keeps alveoli expanded by lowering their surface

light, soft spongy organs, whose color darkens with

tension. Type II cells have been shown to be the pri

age as they become impregnated with inhaled dust.

mary cells involved in repair of the alveolar epithe

They are covered with the visceral pleura, a thin, glis

lium. (This has been shown in experiments where O2

tening serous membrane that covers all sUlfaces of the

toxicity was induced in monkeys and in numerous

lung. The visceral pleura reflects and continues on the

other conditions where type I cells were destroyed.)

med iasti num and inner thoracic wall, where it be

Type III cells, alveolar brush cells, are rare and are

comes known as the parietal pleura. The space be

found only occasionally in humans.

tween the two pleurae is minuscule and contains a alveolar

negative pressure at all times, which helps keep the

macrophage, is found within the alveolus. These cells

lungs inflated. A small amount of pleural fluid lubri

An

additional

type

of

cell,

the

are thought to originate from stem cell precursors in

cates the two pleurae as they slide over each other

the bone marrow and reach the lung through the

during breathing. In disease, fluid, tumor cells. or air

blood stream. They are large, mononuclear, ameboid

may invade the pleural space and collapse the under

cells that roam in the alveoli, alveolar ducts, and

lying lung. Each lung ha an apex, base, arid three sur

alveolar sacs. They contain Iysosomes, which are ca

faces (costal, medial, and diaphragmatic). There are

pable of killing engulfed bacteria. (Studies show

also three borders (anterior, inferior, and posterior).

them to be most effective i n neutralizing inhaled

Each lung is divided by fissures into separate lobes. In

gram-positive organisms.) They also engulf foreign

the right lung the oblique fissure separates the lower

matter and are either transported to the lymphatic

lobe from the middle, whereas the horizontal fissure

system or migrate to the terminal bronchioles where

separates the upper lobe from the middle. The right

they attach themselves to the mucus. They are then

lung is heavier and wider than the left lung. It is also ' shorter because of the location of the right lobe of the

carried by the mucus to larger airways and eventually to the pharynx. Since cilia are not present below the

Jiver. The left lung is divided into upper and lower

eleventh generation of air passages, clearance of mat

lobes by the oblique fissure. It is longcr and thinner

ter and bacteria from these areas is largely dependent

than the right lung, because the hem1 and pericardium

on the macrophages.

are located in the left thorax. Numerous structures


2


41

enter the lung at the hilus, or root of the lung, includ

rior angle of the scapula with the arm at rest. The in

ing the main-stem bronchus, the pulmonary artery,

ferior border joins the posterior medial border of the

pulmonary veins, bronchial artelies and veins, nerves,

lung 2 cm lateral to the tenth thoracic vertebra. The

and lymph vessels. The root, or hilus, of the lungs lies

posterior medial border runs 2 cm lateral to the verte

opposite the bodies of the fifth, sixth, and seventh tho

bral column from the seventh cervical vertebra to the

racic veltebrae. The lungs are connected to the upper

tenth thoracic vertebra. The left lung is generally smaller than the right

airways by the trachea and main-stem bronchi.

and accommodates the position of the heart. The me dial border on the anterior aspect runs from the ster

Surface markings

noclavicular joint to the middle of the sternal angle,

Surface markings of the lungs can be outlined over

down the midline of the sternum to the fourth costal

the chest with a basic knowledge of bony landmarks

cartilage. A lateral indentation of about 1 \/2 in forms

and gross anatomy of each lung (Table 2-2, and Fig

the cardiac notch at the level of the fifth and sixth

ures 2-13, 2-14, and 2-15). The apices of both lungs

costal cartilages. The courses of the inferior and me

extend 1 in above the clavicles at the medial ends.

dial borders on the posterior aspect are similar in the

The anterior medial border of the right lung runs

left and right lungs. In the left lung, however, the in

from the sternoclavicular joint, to the sternal angle

ferior border crosses at the level of the tenth thoracic

downward to the xiphisternum. The inferior border

vertebra, not the twelfth observed in the right lung.

runs from the xiphisternum laterally to the sixth rib in

The position of the fissures of the lungs can be

the midclavicular line, the eighth rib in the midaxil

outlined over the chest wall. In both lungs, the

lary line, and the tenth rib in the midscapular line.

oblique fissure begins between the second to fourth

The midscapular line runs downward from the infe-

thoracic vertebrae. This can be roughly estimated by

Apical

Apical post.

AnI. basal

BRONCHOPULMONARY

SURFACE MARKINGS

SEGMENTS

FIGURE 2-13 Surface markings of the lungs (anterior aspect). The underlying bronchopulmonary segments are also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and

disease, ed 3, Philadelphia, 1983, WB Saunders.)


42

PART I


TABLE 2-2 Anatomical Arrangement of the Bronchopulmonary Se.gments LOBE

RIGHT LUNG: BRONCHOPULMONARY SEGMENTS

LOBE

LEFT LUNG: BRONCHOPULMONARY SEGMENTS

Upper

Apical-extends above the

Upper

Apical posterior-extcnds above the clavicle anteriorly; occupies

clavicle anteriorly; smaller area

comparablc area as the apical and

posteriorly

posterior segments of the right lung Anterior---occupies area between the

Anterior---occupies area between the

clavicle and horizontal fissure

clavicle and theborder of the lingula (comparable line to the horizontal fissure of the right lung)

Posterior-remainder of upper lobe on the posterior aspect down to the oblique fissure Middle

Lateral-extends medially

(Lingula)'"

from junction of the two fissures

Superior---occupies upper half of the lingula Inferior---occupies lower half of the

at the third intercostal space to

lingula

occupy one third the anterior SlIrface of the lobe Medial-occupies the remaining anterior surface of the lobe Lower (Base)

Anterior---occupics basal area

Lower

beneath the oblique fissure anteriorly

(Base)

Supelior---occupies half the area from

Anterior---occupies area inferior to the oblique fissure anteriorly Superior---occupic.' onc third of the

the oblique fissure downward*

basal area posteriorly from the oblique

on the posterior aspect

tissure downward

Lateral-extends from the junction

Lateral-occupies the lateral half of the

of the middle lobe over the

remaining two thirds of the left lower

midaxillary area to occupy one third

lobe beneath the superior scgment on

the area inferior to the superior

the posterior aspect

segment on the posterior a pect Posterior---occupies two thirds

Posterior---occupies the medial ponion

of the area posteriorly beneath

of the remaining two thirds of the left

the superior segment

ower lobe beneath the superior

Medial-occupies a space on

segment on the posterior aspect

the inner aspect of the righl base+

'This segmenl can be drained preferentially when the patient lies prone.

j"

Medial basal

segent has

therefore, cannot be directly auscultated. This segment s e gment because of the comparable angle ur its bronchus.

no direct exposure to the chest wall,

when the patienl is positioned for the left lateral basal

i:

Superiur segmenls abo called apical.

Lingula is not an anatomically uislinct area comp

is Hn
preferenlially dr
pari of the left upper lobe.

2

--

.....


- 4th rib -Xiphi

sternal

j u nc t io n i Mi d ax llary line

8th rib

-

SURFACE MARKINGS FIGURE 2·14 SUlface markings of the lungs (lateral aspect). (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and disease, ed 3, Philadelphia, 1983, WB Saunders.)

ji.'� J/J }:o l'

'-.r'

T2(spine)

v

Apical

u

I

l i

\

.

�-

Lat. basal BRONCHOPULMONARY

SURFACE MARKINGS

SEGMENTS

FIGURE 2·15 Surface markings of the lungs (posterior aspect). The underlying bronchopulmonary segments are also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and

disease, ed 3, Philadelphia, 1983, WB Saunders.)


43

44

PART I


following a line continuous with the medial border

heart is rotated to the left in the chest, resulting in the

of the abducted scapula, around the midaxillary line

right side of the heart being foremost. Thus joining

at the fifth rib, and terminating at the sixth costal

the two uppermost points outlines the level of the

cartilage anteriorly. The horizontal fissure of the

atria and joining the two lower points represents the

right lung originates from the oblique fissure at the

margin of the right ventricle.

level of about the fourth intercostal space in the mi

The heart as a whole is freely movable within the

daxillary line, and courses medially and slightly up

pericardial cavity, changing position during both con

ward over the fourth rib anteriorly. The left lung has

traction and respiration. During contraction, the apex

no horizontal fissure.

moves forward, strikes the chest and imparts the chest and apex beat, which may be felt and seen. Abnormal position of the apex beat can indicate cardiac enlarge

Bronchopulmonary Segments

ment or displacement. During breathing, the move

The bronchopulmonary segments lie within the

ments of the diaphragm determine the position of the

three lobes of the right lung and the two lobes of the

heart. This is because of the attachment of the central

left lung. There are 10 bronchopulmonary segments

tendon of the diaphragm to the pericardium. Changes

on the right and eight on the left. Brief anatomic de

in position during quiet breathing are hardly notice

scriptions of the position of each lobe are provided

able, but with deep inspirations, the downwal'd excur

in Table 2-2, p. 42. Figure 2-13, p. 41, illustrates the

sion of the diaphragm causes the heart to descend and

surface markings on the anterior view of the lungs

rotate to the right. The opposite occurs during expira

and the position of the various bronchopulmonary

tion. Pathology of the lungs can also change the posi

segments within the major anatomic divisions pro

tion of the heart. Atelectasis shifts the heart to the

vided by the fissures. Figure 2-14, p. 43, shows

same side. In tension pneumothorax, where air enters

some of these features from the lateral views. Figure

the chest usually through an opening in the chest wall

2-15, p.43 illustrates the surface markings and bron

and cannot escape, the positive pressure shifts the

chopulmonary segments of the posterior aspect of

heart away from the side of the pathology. The heart is enclosed by the pericardium, whose

the lungs.

two surfaces can be visualized by considering the heart as a fist that is plunged into a large balloon. The

HEART

outer surface, a tough fibrous membrane, is called the

The herut is a conical, hollow muscular pump enclosed

fibrous pericardium. It encases the heart and the or

in a fibroserous sac, the pericardium. Its size is closely

gans and terminations of the great vessels. This mem

related to body size and corresponds remarkably to the

brane is so unyielding that when fluid accumulates

size of an individual's clenched fist. It is positioned in

rapidly in the pericardial cavity, it can compress the

the center of the chest behind the lower half of the ster

heart and impede venous return. When this occurs

num. The largest portion of the heart lies to the left of

often, a window is cut in the pericardium, allowing

the midsternal line; the apex is found approximately 9

the fluid to escape. The inner surface, the serous peri

cm to the left in the fifth intercostal space.

cardium, is a serous membrane that lines the fibrous

The surface markings of the heart can be traced by

pericardium. Ten to 20 ml of clear pericardial fluid

joining four points over the anterior chest wall. On

separates and moistens the two pericardial surfaces.

the right, the heart extends from the third to the sixth

The pericardium with its fluid minimizes friction dur

costal caltilages at a distance of about to to 15 mm

ing contraction. It also holds the heart in position and

from the sternum. On the left, the heart extends from

prevents dilation. The serous pericardium consists of

the second costal cartilage to the fifth intercostal

an outer layer, the parietal layer, and an inner layer

space 12 to 15 mm, and 9 cm from the left sternal

the visceral layer, or epicardium.

border, respectively. Joining the two points on the

The heart is divided into right and left halves by an

left side outlines the left atrium and ventricle. The

obliquely placed longitudinal septum (Figure 2-16).


2


45

Superior vena cava ....... Pulmonary veins Pulmonary veins

Atrium

Pulmonary valve

t
..

FIGURE 2-16 Blood flow of the heart.

Each half has two chambers-the atrium, which re

amount of work they perform. The ventricles do more

ceives blood from veins, and the ventricles, which

work than the atria, and their walls are thicker. The

eject blood into the arteries. The sllperior vena cava,

pressure in the aorta is higher than that in the pul

inferior vena cava, and intrinsic veins of the heart de

monary trunk. This requires greater work from the

posit venous blood into the right atrium. Blood then

left ventricle, so its walls are twice as thick as those

passes through the tricllspid valve to the right ventri

of the right ventricle. The innermost layer, the endo

cle. The right ventticle projects the blood through the

cardium, is the smooth endothelial lining of the inte

pulmonary valve into the pulmonary arteries, which

rior of the heart. *

are the only arteries in the body containing deoxy genated blood. Pulmonary veins return the blood to the left atrium and from there, it passes through the

Heart Valves

mitral valve to the left ventricle. From the left ventri

The four valves of the heart, although delicate in ap

cle it is ejected through the aortic valve into the main

pearance, are designed to withstand repetitive clo

artery of the body-the aorta.

sures a g a i n st h i g h pressures (se e F i g u r e 2-16)

The heart is divided into three layers-the epi

(French, Criley, 1983). Normally, they operate for

cardium, myocardium, and endocardium. The outer

more than 80 years without need of repair or replace

most layer, the epicardium, is visceral pericardium

ment. The tricuspid and mitral valves function differ

and is often infiltrated with fat. The coronary blood

en tly from the other valves of the h e art. Bei n g

vessels that nourish tile heart run in this layer before entering the myocardium. The myocardium consists of cardiac muscle fibers. The thickness of the layers of cardiac muscle fibers is directly proportional to the

"For additional information o f tbe

refer

clinical aspects o f heart

And reol i et ai, 1991; Goldberger, 1990; Sokolow, Mcilroy, Cheitlin, 1990; and Gray s Anatomy.

anatomy,


10

'

46

PART I


located between the atria and ventricles, they must ef

free edges of these valves project into the lumen of

fect a precise closure within a contracting cavity.

the vessels. At the end of systole, blood in the aorta

During diastole, the two leaflets or cusps of the

and pulmonary artery forces the cusps of the valves

mitral valve and the three cusps of the tricuspid valve

shut. These valves are attached in such a manner

relax into the cavities of the ventricles, allowing

that they cannot be everted into the ventricles by in

blood to flow between the two chambers. As the ven

creased pressure in the vessels. During diastole, the

tricular chambers fill with blood, the cusps of the

cusps support the column of blood filling the ven

valves are forced up into a closed position. Fibrous

tricles. Contraction of the ventricles during systole

cords, the chordae tendinae, are located on the ven

increases pressure within the ventricular chambers,

tricular surfaces of these cusps. These cords connect

forcing the cusps to open and allow blood flow into

the cusps of the valve with the papillary muscles of

the vessels.

the ventricular walls. As pressure builds in the ven

The arterial supply of the heart muscle is derived

tricular chambers, contraction of these muscles pre

from the right and left coronary arteries, which

vents the cusps from being forced up into the atria.

arise from the aortic sinuses (Figure

Dysfunction or rupture of the chordae tendinae or the

coronary artery (LCA) divides into the anterior de

papillary muscles may undermine the SUppOlt of one

scending artery a n d the left circumflex artery.

2- 17). The left

or more valve cusps, producing regurgitation from

These arteries supply most of the left ventricle, the

the ventricles to the atria.

left atrium, most of the ventricular septum and, in

The pUlmonic and aortic valves are similar in ap

45% of people, the sinoatrial (SA) node. The right

pearance but the aortic cusps are slightly thicker

coronary artery (RCA) supplies most of the right

than the pulmo ic cusps. Each valve has three fi

ventricle, the atrioventricular (A V) node and, in

brous cusps, the bases of which are firmly attached

55% of people, the SA node. Infarction of these ar

to the root of the aorta or the pulmonary artery. The

teries or their branches can thus cause interruption

----

Circumflex branch

Interventricular branch (posterior descending) /

FIGURE 2-17 Blood supply of the heart.


2


47

or cessation of the conduction system and death of

node retains its position as pacer of the heru1 as long as

the myocardial muscle in the area supplied by the

it generates impulses at a faster rate than any other pru1

artery. The severity of the infarction is dependent

of the myocardium and as long as these impulses are

on the size of the artery and the importance of the

rapidly conducted from the atria to the ventricles. Nor

area it supplies.

mal impulse formation may be interrupted by vascular

The heart is drained by a number of veins. Most of

lesions (occlusion of the coronary arteries) or by car

the veins of the heart enter the coronary sinus, which

diac disease (pericarditis). The SA node is especiaUy

then empties into the right atrium. A small portion of

susceptible to pericarditis and all other surface cardiac

veins, the thebesian veins, empty directly into the

diseases because of its superticiaJ position immediately

right and left ventricles.

beneath the epicardium. The muscle fibers of the heart are self-excitatory, which enables the heart to rhythmically and automati

Innervation

cally contract. The normal pacemaker of the heart is

Innervation of the heart involves a complex balance be

the sinoatrial node located in the posterior wall of the

tween its intrinsic automaticity and extrinsic nerves

right atrium. The concentric waves of excitation sent

(Figure 2-18). The SA and A V nodes provide the heart

out by the SA node must travel through the A V node

with an inherent ability for spontaneous rhythmic initia

to reach the ventricles. This node is located in the floor

tion of the cardiac impulse. The rate of this impulse for

of the light atrium, just above the insertion of the tri

mation is regulated by the autonomic nervous system

cuspid valve. Its main function is to cause a 0.04 sec

(ANS), which also influences other phases of the car

ond delay in the atrioventricular transmissions. This

diac cycle. It controls the rate of spread of the excitation

has two advantages. It postpones ventricular excitation

impulse and the contractility of both atria and ventricles.

until the atria have had time to eject their contents into

The ANS extends its influence to the heaIl via the

the ventricles. It also limits the number of signals that

vagus nerve (parasympathetic) and upper thoracic nerves (sympathetic). These nerves mingle together around the root and arch of the aorta near the tracheal bifurcation, forming the cardiac plexus. Extensions from the cardiac plexus richly supply the SA and A V nodes. They are so well-mingled that scientists are un able to determine which nerves supply which parts of the heart. Stimulation of the sympathetic nervous sys tem causes acceleration of the discharge rate in the SA node, increase in A V nodal conduction, and increase in the contractile force of both atrial and ventricular muscles. Stimulation of the vagus nerve causes car diac slowing and decreased A V nodal conduction. Thus the parasympathetic system decelerates heart rate and the sympathetic system accelerates heart rate. Intrinsic innervation of the heart centers around the SA node, which lies near the junction of the superior vena cava and the right atrium. It is the normal pace maker of the heart, sending concentric waves of excita tion throughout the atrium. Without neural influence, impulse formation from this node would be greater than

100 beats/minute. However, vagal influence decreases

FIGURE 2-18

the impulse formation to 60-90 beats/minute. The SA

Electrical conduction of the heart.


48

PART I


can be transmitted by the A V node. The A V node also

tion, the QRS complex indicates ventricular depolar ization and the T-wave indicates ventricular repolar

has its own inherent rhythmicity, firing at a much

(40-60

beats/minute). Its

ization. There is no wave indicating atrial repolariza

main pathology is a result of occlusion of the right

tion, since this is embedded in the QRS complex

slower rate than the SA node

coronary artery, which supplies the AV node in

90%

(Andreoli et aI,

of the cases. From the A V node arises a triangular

of the Electtical Excitation of the Heart and ECG In

His. This bundle divides in the ventricular septum into

Conover,

group of fibers known as the AV bundle or bundle of

terpretation, Chapter II; Dubin,

1989;

Marriott,

1989; and Wagner, 1994.

two branches-the left bundle branch and the right bundle branch. Each of these bundles continues to di

SYSTEMIC CIRCULATION

vide into many fine strands that spread across the ven

The systemic vascular system is a complex series of

tricles. At the end of the bundle's ramifications are Purkinje's fibers, which are continuous with the car

blood vessels throughout the entire body. It conveys

diac muscle. The waves of excitation pass through the

nutrition and oxygen to all tissues of the body and car

bundle of His, down the bundle branches, and through

ries away their waste products. The driving force for

the Purkinje fibers, which permeate the ventricles and

this system is the heart. The vascular system can be

cause them to contract. This wave of depolarization

considered to have two major components-the periph

gives rise to the normal P-QRS-T configuration of the

eral and pulmonary circulations (Schlant et aI,

electrocardiogram (ECG) tracing (Figure 2- 19) (see

Chapter

II).

Blood vessels are designed to forward oxygenated blood from the heart during systolic ejection of the

The P-wave indicates atrial depolariza

1

1

b± =J==1--+-t----t-11r-I L-1-+-+--l--+++-+--i--t i-ll rQO.2 1. L-t-+ t-t-tTRl--r1!-t1l-r.o.4 l1 1 L -++rt ti T1 w 1 J lj 4-1 -titti-r rT- I· I .+ST m second s con

I

l-+-+----t-

PR se ment g

-rl II

I'

II I

'

PI

I I---+-+-+-t-.iI

-

1

T

I t- I i t-

5 mm 0.5 mv

mm

I

'

I_ I-.II I1 [ffiI l' It

I

se ment g I

r-

I

I ! 111 0

I I I l ]1 -+---r---,-,--: L-+r-� -t-"t-I-+-+1 \41 rr-4 PR interval I I !... I. I J 1 J -J IOR S.1nterva ' .1 1---+-+-+-t -1"-11T1 '1 II 1 l 1 1 I

I

1

, 1

1

U .

:

I, !I

I

I I

l ..l -J I

.

I I OTI interval L.i+-t--+-t-t i I I I

FIGURE 2-19

A normal ECG showing characteristic waves, intervals, and segments.


I

2


49

left ventricle, perfuse the vascular beds commensu

veins. These veins branch and become increasingly

rate with their metabolic needs and remove metabolic

larger. Blood flow through the veins is largely depen

excreta. Anatomically, the proximal vessels have a

dent on muscular or visceral action or pressures.

higher proportion of connective tissue and elastin to

These pressures are intermittent and, were it not for

withstand high pulse pressures (e.g., the aorta, which

double-cusp valves located within the veins, blood

carries blood to the head, viscera, and limbs). In addi

would flow backward when the pressure ceases. In the

tion, potential energy is stored in the walls of the

extremities, muscular contractions move blood into

larger vessels during systole. During diastole, the

the trunk. In the pelvic and abdominal region, blood

elastic recoil of these vessels maintains the forward

flow is dependent on intraabdominal pressure exceed

motion of the blood between ventricular systoles. The

ing intrathoracic pressure. Blood flows through the

medium-size blood vessels have comparable propor

trunk in veins that become increasingly larger until

tions of connective tissue and elastin to smooth mus

they finally enter the supelior and inferior vena cavae.

cle. As the blood vessels become smaller, smooth muscle predominates. The arterioles are primarily smooth muscle and their diameter can alter signifi

PULMONARY CIRCULATION

cantly. They regulate the blood flow to regional tis

The vena cavae empty directly into the right atrium.

sue beds and are also responsible for regulating total

Blood flow from the right side of the heart through

peripheral resistance and systemic blood pressure.

the lungs is known as the pulmonary circulation. The

They are called the stopcocks of the circulation.

quantity of blood flowing through the pulmonary cir

Many factors (e.g., nervous impulses, hormonal stim

culation is approximately equal to that flowing

ulation, drugs, oxygen, and carbon dioxide concentra

through systemic circulation. Blood flows from the

tions) determine the degree of contraction of vascular

right ventricle into the pulmonary artery, which di

smooth muscle and whether contraction occurs lo

vides into right and left branches 4 cm from the ven

cally or throughout the entire body.

tricle. These branches then separate, one going to

Arterioles branch to form the smallest vessels, the

each lung, where they continue to divide into smaller

capillaries, which consist of a single layer of endothe

arteries. The pulmonary arteries and arterioles are

lial cells forming lumen just large enough for the red

much shorter, have thinner walls and larger diame

blood cells to roll along. The capillary bed is enormous;

ters, and are more distensible than their systemic

its capacity far exceeding 5 L. Its network is finer and

counterparts. This gives the pulmonary system a

denser in active tissue like muscle and brain, and less

compliance as great as that of the systemic arterial

dense in less active tissue such as tendon. Gas ex

system, thereby allowing the pulmonary arteries to

change occurs in the capillary bed, where the red blood

accommodate the stroke volume output of the right

cells give up their oxygen, and blood plasma t:ransudes

ventricle. Pulmonary vascular resistance and arterial

capillary walls, carrying nutrition to tissue.

pressure are one sixth that of the systemic system

The microcirculation specifically consists of the metarterioles, the capillary bed, and the venules. The

20110 mm Hg com 120/80 mm Hg systemically).

(pulmonary arterial pressure is pared with

capillary wall is a semipermeable membrane that is re

P u l m o n a r y c a p i l l a r i e s are s h o r t a n d a r i s e

sponsible for the transfer of oxygen, nutrients, and

abruptly from much larger arterioles. They form a

waste between the circulation and the interstitial fluid

dense network over the walls of the alveoli, making

3). The capillary pores selectively

a minimum distance over which gas exchange oc

(see Chapters 1 and

allow different-size molecules to pass through them.

curs. The pulmonary veins are also very short but

This is an essential feature that regulates the move

have distensibility characteristics similar to those of

ment of fluid in and out of the intra- and extravascular

the systemic system. Unlike systemic veins, these

compartments. This process is fundamental to main

veins have no valves. Pulmonary veins act as a ca

taining and regulating normal hemodynamics.

pacitance vessel, or a blood reservoir for the left

Capillaries form venules, which are the smallest

atrium. Contraction of smooth muscle in the veins


50

PART I

Cardiopulmonal'Y Function in Health and Disease

makes the reservoir constrict. This increases blood

ture of the bony

volume in relation to the internal volume of the

sociated with the chest wall and of the diaphragm.

vessels. The pulmonary veins become larger until converge into two veins from each

which

the muscles of respiration as

The upper and lower scribed, a s well as the bronchial tree to the

then carry oxygenated blood to the left atrium.

The lung

is defined anatomically in terms of dis crete bronchopulmonary segments contained within

LYMPHATIC CIRCULATION

three major divisions of each

The lymphatic circulation

an additional

route for fluid t o be returned from the interstitium to the systemic circulation, and thus has a central of interstitial fluid

role in the

defined

The specific sur

the lung fissures and the

landmarks for the bronchopulmonary segments were emphasized. The basic anatomy of the heart was de and

scribed. The structure of the

the fluid that flows in the

Special ref

monary circulations was also

is interstitial fluid with similar composition t o tissue fluid. T h e lymphatics remove excess fluid, large

face

ns, and other large molecules away lit

from the interstitial spaces. Although

erence was made to the lymphatic circulation and its central role in the regulation of capillary fluid of cardiopulmonary

namics. A detailed anatomy is fundamental to the

base un

tle protein leaks from the capillaries into the sur

the assessment and management of car

rounding tissue. the absence of its immediate re

diopUlmonary dysfunction and impaired oxygen by physical therapists.

moval is all areas of the body drain into a network of

channels. From the lower portion of the

body, and left head and

excess tissue fluid and

drain into the thoracic duct, which empties into the venous circulation at the junction of the left

REVIEW QUESTIONS 1. Describe the thorax and its movements. 2. Describe the respiratory muscles and their func

internal jugular vein and subclavian vein. from the right side of the head, of the which tion of the

arm, and

thorax drain into the

from the monary and

of the body drains

into the inguinal and abdominal lymphatic channels. The pressure in the lymphatic which helps to

"dry." The lymph vessels are thin-walled with some

the heart to the pul circulations.

5. Describe the movement of deoxygenated blood from the oerioherv back to the heart.

is the interstitium

of oxygen from the atmos

4. Describe the movement of oxygenated blood

vein and subclavian

vein. Lymph from the lower

the

phere to the alveolar capillary membrane.

lymph duct,

into the venous circulation at the junc internal

tion.

3.

6.

\Jrnnh"tlr

circulation and

its physiological

smooth muscle and thus can contract to propel their contents. In addition,

vessels have valves to

facilitate the forward motion and to minimize retro movement of lymph.

References Andreoli,

K.G., Fowkes. Y.K., Zipes, D.P., & Wallace, A G, .

(199!). Comprehensive cardiac c are (7th ed,). Sl. LOllis: Mosby.

SUMMARY

Berne. R.M"

This chapter reviewed the anatomy of the cardiopul monary system. The anatomical features of the respi ratory pump were described with respect to the struc

& Levy, M.N. (1992). Cardiovascular physiology

(6th ed,). St Louis: CY Mosby,

G.G., & Hodgkin. J.E. (1984). Respiratorv care: A gllide 18 Lippincott. Chemiack, R.M., & Cherniack, L (1983), Respiration in Health and Disease (3rd ed,), Philadelphia: WB Saunders.

Bunon,

to clinical practice (2nd ed.). Philadelphia:


2

Clemente, CD. (Ed,). (1985), Anatomy of Ihe humon body (30th ed,), Philadelphia: Lea & Febiger.


51

Scharf, S,M & Cassidy. S,S. (Eds,), (1989). Hear/-lung interac tions in health and disease. New York: Marcel Dekker,

Dubin, D, (1989) Rapid interpretation of EKGs (4th ed,), Tampa,

Sokolow, M" McIlroy, M.B" & Cheitlin. M,D, (1990), Clinical cardiology (5th cd,). Norwalk, Conn.: Appleton & Lange,

Florida: Cover Publishing, French, W,G" & Criley, I.M, (Eds,). (1983), Practical cardiology:

Schlant, R,C" Alexander, R,W., O'Rourke, RA" Roberts, R

..

&

New York: John Wiley &

Sonnenblick, E,H, (Eds.). (1994), Hurst's lhe hearl, orteries

Ganong, W,F, (1993), Review of medical physiology (l6th ed,),

Wagoer, G,S, (1994), Marrioll's practical electrocardiography

Ischemic and valvular hearl

and veins (8th ed,). New York: McGraw,Hill.

Sons,

(9th ed.), Baltimore: Williams & Wilkins,

Los Altos, Calif.: Lange Medical Publications. Goldberger, E, (1990), Essentials of clinical cardiology, Philadel phia: JB Lippincott,

Weber, KT, Jaoicki, J.S" Shroff, S,G" & Likoff. MJ. (1983), The cardiopulmonary unit. The body's gas transport system, Clinics

Guyton, A,C, (1991), Textbook of medical physiology (8th cd,),

in chest medicille, 4, 101-110,

Weibel, E,R. (1963), Morphometry of the human lung, New York:

Philadelphia: WB Saunders, Katz, A.M. (1992), Physiology of the heart (2nd cd.). New York: Raven Press,

Springer-Verlag, West, lB, (Ed,), (199l), Best and Taylor's physiological basis of

Marriott, H.1.L, & Conover, M,B, (1989), Advanced concepts in

medical practice (12th cd,). Baltimore: Williams & Wilkins,

West, lB. (1995), Respiratory physiology-the essentials (5th ed,),

arrhythmias (2nd ed,), St. Louis: Mosby,

Murray, J,E (1986), Till? normal lung. Philadelphia: WE Saunders, Murray, J.P., & Nadel, I.A, (1988). Textbook of respiratory medi

Baltimore: Williams & Wilkins, Williams, P,L, Warwick, R., Dyson, M., & Bannister, LH, (1989), G r a y

cine, Philadelphia: WB Saunders,

Nunn, lE (1993), Applied respiratory physiology (4th ed.), Lon

Churchill Livingsione,

don: BUllerworths,


a n atomy (37th

E d i n b u r gh:

Cardiopulmonary Physiology


KEY TERMS

Control of breathing

Oxyhemoglobin dissociation

Control of the heart

Respiratory mechanics

Diffusion

Ventilation and petfusion matching

Electromechanical coupling

Ventilation perfusion

Gas exchange

INTROOUCTION

CONTROL OF BREATHING

This chapter reviews the basics of cardiopulmonary

The act of breathing is a natural process to which

physiology. A thorough understanding of normal

most of us give little thought. Unconsciously, it ad

physiology provides a basis for understanding the

justs to various degrees of activity, maintaining opti

deficits of cardiopulmonary dysfunction and adapta

mum arterial levels of POl and Peo2, whether we are

tion to it, and conducting a thorough assessment and

resting or physically active. Sighing, yawning, hiccup

prescribing treatment (Bates, 1989; Berne and Levy,

ing, laughing, and vo mitin g are all involuntary acts

1992; Clemente, 1985; Goldberger, 1990; Guyton,

using respiratory muscles. Br athing is also under our

1991; Katz, 1992; Murray and Nadel, 1988; Nunn,

voluntary control. A person can stop it temporarily by

1993, Sch31f and Cassidy, 1989; Schlant, Alexander,

holding his or her breath or can increase it by rapidly

O'Rourke, Roberts, and Sonnenblick, 1994; Sokolow,

panting until he or she faints (from cerebral vascular

McIlroy, and Cheitlin, 1990; and West, 1995.

constriction as a result of a decrease in arterial Peo2). 53


PART I

54


InhitJl/lon S/imv/olion

:;::rJ

MEDULLA .

:,

t ::"

',

Expir%ry -..Ce//s

yj jl

pulmonory streICh receptors

ororecePlors

emasenSilive Cells

--. -"

.--

to Insptrotory tnt

,

t

r

_ __ _ :d

g

iralOry Cells ______

--------===-

_

ca rotid and aortic cl1emoreceplors

to exptrotory tntereostols

I"

mo

FIGURE 3-1 Control of breathing. Exhalation is used in singing, speaking, coughing, and

longed inspiratory gasps (apneustic breathing) occur.

blowing, whereas inspiration is used for sniffing and

The pneumotaxic center is in the upper one third

sucking. Parturition, defecation, and the Valsalva ma

of the pons. It maintains the normal pattern of respi

neuver are all performed while voluntarily holding our

ration, balancing inspiration, and expiration by in

breath. These activities are directed by control centers

hibiting either the apneustic center or the inspiratory

located in the brain. The centers integrate a multitude

component of the medullary center.

of chemical, reflex, and physical stimuli before trans mitting impulses to the respiratory muscles. The cere bral hemispheres control voluntary respiratory activ i t y , whereas i n v oluntary respiratory activity i s controlled b y centers located i n the pons and medulla (Figure

3-1).

Central Chemoreceptors These receptors are located on the ventral lateral sur faces of the upper medulla. They are bathed in the cerebrospinal fluid (CSF), which is separated from blood by the blood-brain barrier. Although this bar rier is relatively impermeable to hydrogen (H) and bi

Medullary and Pontine Respiratory Centers

carbonate (HC03) ions. Carbon dioxide (C02) diffuses

The respiratory center in the medulla is in the reticu

through the barrier easily. Increased stimulation of

lar formation. It contains the minimum number of

central chemoreceptors by a rising arterial PC02 re

neurons necessary for the basic sequence of inspira

sults in increased rate and depth of ventilation.

tion and expiration. Although this center is capable of maintaining some degree of respiratory activity, these respirations are not normal in character.

Peripheral Chemoreceptors

The apneustic center is in the middle and lower

These receptors are located in the carotid bodies,

pons. If uncontrolled by the pneumotaxic center, pro

which lie in the bifurcations of the common carotid


3


55

artery and in the aortic bodies located above and

tory time. Receptors for this reflex are thought to

below the aortic arch. These bodies receive blood

lie in the smooth muscle of airways from the tra

from small branches of the vessels on which they are

chea to the bronchioles. In humans, it takes a lung

located. The receptors respond to an increase in arter

inflation of more than 800 ml above func tional

ial Peo2 by increasing ventilation but are much less

residual capacity to activate the reflex and delay the

important in their response to Peo2 than are the cen

next breath.

tral chemoreceptors. The main role of the peripheral chemoreceptors is to respond to hypoxemia by increasing ventilation. If

Cough Reflex

arterial Peo2 is normal, the P02 must drop to 50 mm

Mechanical or chemical stimuli to the larynx, trachea,

Hg before ventilation increases. A rising Pe02 causes

carina, and lower bronchi result in a reflex cough and

the peripheral chemoreceptors to respond more quickly

bronchoconstriction. The high velocity created by the

to a decreasing Po2. In some patients with severe lung

cough sweeps mucus and other irritants up toward the

disease, this response to hypoxemia (the hypoxic

pharynx (see Chapter 21).

drive) becomes very important. These patients often have a permanently elevated Peo2 (C02 retention). The CSF in these patients compensates for a chronically el

Stretch Reflex

evated arterial Peo2, by returning the pH of the CSF to

The intercostal muscles and the diaphragm contain

near normal values. When these patients have lost the

sensory muscle spindles that respond to elongation. A

ability to stimulate ventilation in response to an ele

signal is sent to the spinal cord and anterior horn

vated Peo2, arterial hypoxemia becomes the major

motor neurons. These neurons signal more muscle

stimulus to ventilation (hypoxic drive).

fibers to contract (recruitment) and thus increase the strength of the contraction. Theoretically, such a stretch reflex may be useful when there is an increase

REFLEXES

in airway resistance or a decrease in lung compliance. Stretching the ribs and the diaphragm may activate the

Hering-Breuer Reflex

stretch reflex and help the patient take a deep breath.

Hering and Breuer noted in 1868 that distention of

The fundamental pathways of the stretch reflex are

anesthetized animal lungs caused a decrease in the

shown in Figure 3-2. Research is needed, however,

frequency of inspiration and an increase in expira-

to establish the therapeutic role of propriocepti ve

SPINDLE

AFFERENT

MUSCLE SPINDLE FIGURE 3-2

Stretch reflex.


56

PART I


neurofacilitation techniques based on stretch reflex

creasing alveolar pressure. The increased alveolar

theory in altering pulmonary funclion.

pressure contributes to air flowing from the lungs. Normally, expiration is a passive process reflecting elastic recoil of the lung parenchyma.

Joint and Muscle Receptors Peripheral joints and muscles of the limbs are believed to have receptors that respond to movement and en hance ventilation in preparation for activity. Ventila tion has also been shown to be stimulated by a similar

Resistance to Breathing Compliance The inner walls of the thorax, lined with parietal

reflex in humans and anesthetized animals in response

pleura, and the parenchyma of the lung, enclosed in

to passive movement of the limbs. The precise path

visceral pleura, lie in close proximity to one another.

ways for these reflexes have not been well-established.

The pleurae are separated by a potential space con taining a small amount of pleural fluid. Muscular contraction of the intercostals and the diaphragm me

Mechanoreceptors

chanically enlarges the thorax. The lungs are en

Changes in systemic blood pressure cause correspond

larged at this time because of their close proximity to

ing changes in pressure receptors in the carotid and

the thorax. The healthy lung resists this enlargement

aortic sinuses. Increase in blood pressure causes me

and tries to pull away from the chest wall. The ease

chanical distortion of the receptors in these sinuses,

with which the lungs are inflated during inspiration is

producing reflex hypoventilation. Conversely, a reduc

known as compliance and is defined as the volume

tion in blood pressure can result in hyperventilation.

change per unit of pressure change. The normal lung is very distensible or compliant. It can become more rigid and less compliant in diseases that cause alveo

MECHANICAL FACTORS IN BREATHING

lar, interstitial or pleural fibrosis, and alveolar edema.

The flow of air into the lungs is a result of pressure

Compliance increases with age and in emphysema.

differences between the lungs and the atmosphere. In

The elastic recoil or compliance of the lung is also

normal breathing, for inspiration to occur, alveolar

dependent on a special surface fluid caJled surfactant,

pressure must be less than atmospheric pressure.

which lines the alveoli. This fluid increases compli

Muscular contraction of the respiratory muscles low

ance by lowering the surface tension of the alveoli,

ers alveolar pressure and enlarges the thorax (Gold

thereby reducing the muscular effort necessary to

man, j 979). The decreased pressure causes air to

ventilate the lungs and keep them expanded. It is a

flow from the atmosphere into the lungs. Patients

complex lipoprotein that is thought to be produced in

2). A decrease

who are unable to create adequate negative pressure

the type II alveolar cells (see Chapter

may have to be mechanically ventilated. The ventila

in surfactant causes the alveoli to collapse. Reex

tors create a positive pressure (greater than atmos

panding these alveoli requires a tremendous amount

pheric pressure) that forces air into the lungs where

of work on the part of the patient. The patient may

there is atmospheric pressure. The iron lung used dur

become fatigued and need mechanical ventilation.

ing the poliomyelitis epidemic of the 1950s assisted

This occurs in respiratory distress syndrome of the

ventilation using cycles of negative pressure to inflate

premature infant (previously called hyaline mem

the lungs.

brane disease) and in adult respiratory distress syn

Ex halation occurs when alveolar pressure is

drome. In another disease, alveolar proteinosis, there

greater than atmospheric pressure. At the cessation of

is excessive accumulation of protein in the alveolar

inspiration, the respiratory muscles return to their

spaces. This may be because of excessive production

resting positions. The diaphragm rises, compressing

of surfactant or deficient removal of surfactant by

the lungs and increasing alveolar pressure. As the in

alveolar macrophages.

tercostals relax, the ribs drop back to their preinspira

The elastic properties of the lung tend to collapse

tory position, further compressing the lungs and in

the lung if not counterbalanced by external forces.


3


57

FIGURE 3-3 Various relationships between the lungs and the thorax. At. The size the lungs would assume if they were not acted on by the elastic recoil of the thoracic wall. A2, nOlmal size of lungs within the thorax BI, The size the thorax would assume if it were not acted on by elastic recoil of the lungs. B2, Normal position of the chest wall when acted on by elastic recoil of the lungs C, The normal relationship of lung to thorax. 0, The positions assumed by the lung and thorax in a tension pneumothorax.

The tissues of the thoracic wall also have elastic re

posed by the usual elastic forces of the lungs, which

coil, which cause it to expand considerably if unop

have been damaged by disease.

posed. These two forces oppose each other, keeping the lungs expanded and the thoracic cage in a neutral position. If these forces are interrupted (as in pneu mothorax), the lung collapses and the thoracic wall expands (Figure

3-3). Similarly, the overinflated, bar

Pressure Volume Relationships Pressure volume curves help to define the elastic properties of the chest wall and lungs (Cherniack,

1983; Co m r o e, Fo r s t e r, Dub o i s , 1986). The elasticity of the

rel-shaped chest of the patient with chronic obstruc

Ch e r n i a ck,

tive pulmonary disease (COPD) is explained in part

Briscoe, and Carlsen,

by the elastic tension of the chest wall being unop

respiratory system as a whole is the sum of its two



PART I

58

and therefore functional residual 100 90

* (3

;t

a

curve also shows the range of lung volumes,

60

cally tidal volume, over which the energy

.f . }

'1

30

ff

0 f-

process. The pressure volume

70

50

Z :::> -' -'

is

lar work is required to effect inspiration,

80

>f-

is the rest

system. Active muscu

ing volume of the

20

RESIDU VOLUME --

10

-10

0

+10

+20

ture for breathing is most economicaL In other words, result from relatively small

volume ,U,C"ONAC

RESIDUAL CAPACITY

in pressure as noted from the sloDe of the curve over tidal volume, In lung

this balance of forces is disrupted More work and more energy are re-

to sustain the

+30

less able to

PRESSURE (em, H20)

chest

FIGURE 3-4

effort. The

or both.

put more energy into the

The relaxation pressure curve. The pressure in the lung at

is

on normal elastic recoil of either the to

function. The limits of respiratory excur

any volume reflects elastic forces of the lung and chest

sion are determined

wall.

both elastic and muscular

forces. At total lung

the elastic forces of the are balanced

the inspiratory

muscle force. At residual volume, the elastic forces of components, the

and the chest wall.

The so-called relaxation pressure curve is shown in

the chest wall are balanced

3-4. The curve illustrates the static pressure of the

the maximum

tory muscle force. This volume excursion from total capacity to residual volume reflects vital

chest wall, and the combination of the

the elastic forces

the curves

two measured at given lung volumes, Functional

of the lungs and chest wall are

residual capacity reflects the balance o f elastic

helpful in understanding the effect of lung dysfunction

forces exerted

the chest wall and the lungs, This

is an

and management of pa

The relaxation pressure curve

static

is determined

by the balance of forces between the chest wall and the lungs, The chest wall and

and Ket

the characteristic

the chest wall,

the excursion

111

lungs. At the other extreme is the effect of a

and the volume in the

in the

in

of the chest as a result of reduced elastic recoil of the

pressure measurements, This means that the muscles are

1983). For

barrel chest reflects the unopposed elastic forces of

tients with cardiopulmonary dysfunction.

at a

on pulmonary function and on the clinical presenta tion of the patient (Burrows, Knudson,

point with significant

for the clinical

they are

wound to the chest wall, which trapleural pressure

exert elastic

the in

that normally keeps the

and the chest wall contained. The re

forces that oppose each other. The chest wall at

sult of such a puncture is to produce a

tempts to pull the lung out and the lungs

where the lung collapses down to the hilum and the

to

recoil and pull in the chest wall. The curves labeled and chest wall are theoretical and illustrate the elastic force exerted

each when permitted to act

chest wall sorinQs outward (see FiQure 3-3, p. 57),

Airway ReSistance

unopposed by the other. Normally, these two forces

The flow of air into the lungs

are exerted together and

the pressure volume re

ferences and on the resistance to flow by the airways,

laxation curve, It can be seen that at functional resid

Resistance is defined as the pressure difference re

ual caoacitv (FRO. these forces are in equilibrium,

quired for one unit flow


on pressure dif

The air passages in

3


59

other obstructions. In normal lungs, airflow is a combi

LAMINAR

nation of laminar and turbulent flow and is known as

,)

( [)

tracheobronchial flow. The airways are distensible and compressible, and thus are susceptible to outside pressures. As these pres sures compress the airways, they alter the airway resis tance. Transmural pressure is the difference between

TURBULENT , ,;:

the pressures in the airways and the pressures sur

'-.=C)Jl 2,)

rounding the airways. In erect humans, there is a higher transmural pressure at the apices of the lungs than at the bases. This expands the alveoli at the apices relative to those at the bases. Although the alveoli in the apices have a greater volume at end expiration, the alveoli in the bases are better ventilated. This is be cause the alveoli in the bases operate at lower trans mural pressures and thus accommodate a greater vol ume during inspiration than those at higher pressures. Airway resistance decreases during inspiration as a

FIGURE 3-5

result of widening of the airways. During expiration,

The different types of airflow seen within the

airways narrow, thus increasing resistance. The posi

tracheobronchial tree.

tive alveolar pressure that occurs during expiration partially compresses the airways. If these airways have lost their structural support as a result of disease, they

humans are divided into upper and lower airways (see

may collapse and trap air distally (as in emphysema).

Chapter 2). The upper airways are responsible for 45% of airway resistance. The resistance to airflow by the lower airways depends on many factors and is there

VENTILATION

fore difficult to predict. The branching of the lower air

Ventilation is the process by which air moves into the

ways is irregular, and the diameter of the lumen may

lungs. The volume of air inhaled can be measured

vary because of external pressures, and contraction or

with a spirometer. The various lung capacities and

relaxation of bronchial or bronchiolar smooth muscle.

volumes are defined in chapter 8.

The lumen diameter may also decrease as a re.sult of

Regional differences in ventilation exist through

mucosal congestion, edema, or mucus. Any of these

out the lung. Studies using radioactive inert gas have

changes in the airway diameter may cause an increase

shown that when the gas is inhaled by an individual

in airway resistance. Flow of air through these airways

in the seated position, and measurements are taken

3-5). Lami

with a radiation counter over the chest wall, radiation

nar flow is a streamlined flow where resistance occurs

counts are greatest in the lower lung fields, interme

can be either laminar or turbulent (Figure

mainly between the sides of the tubes and the air mole

diate in the midlung fields, and lowest in the upper

cules. It tends to be cone-shaped, with the molecules in

lung fields. This effect is position or gravity depen

contact with the walls of the tubes moving more

dent. In the supine position, the apices and bases are

slowly than the molecules in the middle of the tube.

ventilated comparably, and the lowermost lung fields

Turbulent flow occurs when there are frequent molec

are better ventilated than the uppermost lung fields.

ular collisions in addition to the resistance of the sides

Similarly, in the lateral or sidelying position, the

of the tubes seen in laminar flow. This type of flow oc

lower lung fields are preferentially ventilated com

curs at high flow rates and in airways where there are

pared with the upper lung fields (see Chapter

irregularities caused by mucus, exudate, tumor, and

18).

The causes of regional differences in ventilation


60

PART I


can be explained in terms of the anatomy of the lung

greater volume change in relation to resting volume

and mechanics of breathing. An intrapleural pressure

which effects greater overall ventilation compared

gradient exists down the lung. In the upright position,

with the upper lung fields. In summary, ventilation is

the intrapleural pressure tends to be more negative at

favored in the lowermost lung fields regardless of the

the top of the lung, and becomes progressively less

position of the body.

negative toward the bottom of the lung. This pressure gradient is thought to reflect the weight of the sus pended lung. The more negative intrapleural pressure

DIFFUSION

at the top of the lung results in relatively greater ex

Once air has reached the alveoli, it must cross the

pansion of that area and a larger resting alveolar vol

alveolar-capillary (A-C) membrane (Figure

ume. The expanding pressure in the bottom of the

gases must cross through the surfactant lining, the

lung, however, is relatively small and hence has a

alveolar epithelial membrane and the capillary en

3-6). The

smaller resting alveolar volume. This distinction be

dothelial membrane. Oxygen has to travel further

tween the upper and lower lung fields is fundamental

through a layer of plasma, the erythrocyte membrane

to understanding differences in regional ventilation.

and intracellular fluid in the erythrocyte, until it en

The regional differences in resting alveolar volume

counters a hemoglobin molecule. This distance is ac

should not be confused with regional differences in

tually small in normal lungs, but in disease states, it

ventilation volume. Ventilation refers to volume

may increase. The alveolar wall and the capillary

change as a function of resting volume. The relatively

membrane often become thickened. Fluid, edema, or

higher resting volume in the upper lung fields renders

exudate may separate the two membranes. These

it stiffer or less compliant compared with the low

conditions are often first detected when arterial P02

lung volumes and greater compliance in the lower

becomes chronically lower than normal. Oxygen dif

lung fields. The lower lung fields therefore exhibit a

fuses slowly through the A-C membrane in compari-

".< .rlfflllll".

FIGURE 3-6 The components of the alveolar-capillary membrane.


3

son to CO2 diffusion. As a result, patients with diffu


61

or poorly oxygenated lung areas. Although hypoxic

sion problems frequently have hypoxemia with a nor

vasoconstriction may have an important role to im

mal Pe02. Sarcoidosis, berylliosis, asbestosis, sclero

prove the efficiency of the lungs as a gas exchanger,

derma, and pulmonary edema are some diseases that

this mechanism may be potentially deleterious to a

decrease the diffusing capacity of the gases. The ca

patient who has reduced arterial oxygen pressure sec

pacity may also decrease in emphysema because of a

ondary to pulmonary pathology. The acid base balance of the blood also affects

decrease in surface area for gas exchange.

pulmonary blood flow. A low blood pH or acidemia, for example, potentiates pulmonary vasoconstriction.

PERFUSION

Thus impaired ventilatory function can disturb blood

Pelfusion of the lung refers to the blood flow of the

gas composition and in turn, acid base balance. This

pulmonary circulation available for gas exchange.

effect can be amplified because of the cyclic reaction

The pulmonary circulation operates at relatively low

of pH on pulmonary vasoconstriction. Consideration

pressures compared with the systemic circulation. For

of these basic physiologic mechanisms are tanta

this reason, the walls of the blood vessels in the pul

mount to optimizing physical therapy intervention.

monary circulation are significantly thinner than comparable vessels in the systemic circulation. Pul monary arterial pressure is low, because perfusion of the top of the lung is the most distal area. Compared

Ventilation and Perfusion Matching It is essential that ventilated areas of the lung are in

with the systemic circulation, there is little require

contact with peIfused areas of the lung to effect nor

ment for significant regional differences in perfusion.

mal gas exchange. Conditions that alter the ventila

Hydrostatic pressure has a significant effect on per

tion or perfusion of part of the lung also affect the gas

fusion of the lowcr lobes. The hydrostatic pressure re

exchange in that portion of the lung. Uneven ventila

flects the effect of gravity on the blood, tending to

tion occurs where there is uneven compliance or un

favor peIfusion of the lower lung fields. This fact has

even airway resistance in different parts of the lung.

been substantiated using radioactive tracers in the pul

The lung is more compliant, that is, easier to inflate

monary circulation and measuring radiation counts

at low lung volumes. In the upright position, the

over the lung fields. The nonuniformity of peIfusion

apices have a higher resting volume because of a

reflects the interaction of alveolar, arterial, and venous

more negative intrapleural pressure than the bases,

pressures down the lung. Normally, blood flow is de

which renders the apices less compliant than the

termined by the arterial venous pressure gradient. In

bases with relatively low resting volumes. Ventilation

the lungs, there are regional differences in alveolar

as previously described is favored in the lower lung

pressure that can exert an effect on the arterial venous

regions rather than the apices. Uneven airway resis

pressure gradient. For example, in the upper lung

tance may result from airway narrowing (bron

fields, alveolar pressure approximates atmospheric

choconstriction in asthma, mucous plugs, edema,

pressure, which overrides the arterial pressure and ef

tumor,) or collapse from external pressures as with

fectively closes the pulmonary capillaries. In the lower

tumors or emphysema). Uneven compliance may also

lung fields, the opposite occurs. The relatively low vol

result from fibrosis, emphysema, pleural thickening,

ume of air in the alveoli is oveITidden by the greater

effusions, or pulmonary edema.

capillary hydrostatic pressure. Thus the capillary pres

Nonuniform peIfusion or blood flow can be a re sult of gravity, regional differences in intrapleural

sure effectively overcomes the alveolar pressure. Pulmonary blood vessels constrict in response to

pressure, regional changes in alveolar pressure, and

low arterial pressures of oxygen. This is termed hy

obstruction or blockage of part of the pulmonary cir

poxic vasoconstriction. Hypoxic vasoconstriction in

culation. Gravity increases blood flow in the depen

the lung is believed to serve as an adaptive mecha

dent portions of the lung and decreases it in the non

nism for diverting blood away from underventilated

dependent portions of the lung. Regional differences


62

PART [


ZONE I

ZONEm

FIGURE 3-7 The perfusion of the lung is dependent on posture. In the upright position three areas can be seen. Zone III has perfusion in excess of ventilation, in Zone II perfusion and ventilation are fairly equal and in Zone I ventilation occurs in excess of perfusion.

in intrapleural pressure change the transmural pres sure of blood vessels and thereby the amount of blood flowing through those vessels. Changes i n a lveolar pressure also affect the amount o f blood flowing through the vessels. Overexpanded alveoli can compress blood vessels, while underexpanded alveoli may allow more blood to flow through those vessels. Blood clots, fat, parasites, or tumor cells may constrict or block part of the pulmonary circulation. As discussed previously, gravity tends to pull blood into the dependent positions of the lung (Figure 3-7). In erect humans, therefore, there is greater blood flow at the bases of the lung. In places, the ar terial blood pressure exceeds the alveolar pressure and causes compression or collapse of the airways (Figure 3-8). Blood flow to the apices is decreased because of gravity. Alveoli in this region are more fully expanded as a result of high transmural pres

FIGURE 3-8 Relationship between the size of the airways and the amount of perfusion in the area in the upright position.

A, Perfusion is decreased in the apices due to gravity. This enables the alveoli to fully expand. This expansion may compress blood ves els and thereby fUl1her decrease blood

sures and may further decrease blood flow by com

flow. B, Perfusion is increased in the bases of the lungs due

pressing blood vessels. It follows that the areas of op

to gravity. The enlarged vessels prevent full expansion of

timal gas exchange occur where there is the greatest

alveoli and may in fact compress them to a smaller size.


3

CardiopuLmonary Physiology

\

FIGURE 3-9 The effect of positioning on perfusion of the lung. Note that gravity-dependent segments have the greatest amount of perfusion.

B A

c

FIGURE 3-10 A, Normal alveolus. B, Dead space. C, Shunt.


63

64

PART I

Cardiopulmonary Function in Healt.h and Disease

amount of perfusion and ventilation. This occurs to

ues of POl and PC02. Therefore the lungs must be able

ward the base of the lungs in erect humans. Changes

to supply four parts ventilation to about five parts

in posture cause changes in perfusion and ventilation.

perfusion. When the ratio is not uniform throughout

Generally, greater air exchange occurs toward the

the lung, the arterial blood cannot contain normal

gravity-dependent areas. In side lying, there is greater

blood gas values. Regions with low ratios (perfusion

gas exchange in the dependent lung (Figure

3-9).

in excess of ventilation) act as a shunt, while regions

In normal lungs, there is an optimal ratio or

with high ratios (ventilation in excess of perfusion)

matching of gas and blood. This ratio of ventilation to perfusion is

3-10). Hypoxemia results

act as dead space (Figure

0.8 to maintain normal blood gas val-

if regions of abnormal V:Q ratio predominate. An

\\tntilation-Perfusion Ratio o

2

4 v

Apex

Q

Blood flow

Base .05

Distance Down Lung

.10

1/min, % Lung

.15 Iume

FIGURE 3-11 The effect of gravity on ventilation, perfusion and ventilation-perfusion matching (V/Q ratio).

PO?

,W

ALVEOLAR

pco .L _ _ _ _

'

Apex Po,

'

A _

pco

_

-

:::'2:: Base

'd----

L

DEAD SPACE

t=oo NORMAL

*::::1:;

SHUNT

*=0

Distance Down Lung FIGURE 3-12 Schemata showing the effect of gravity on ventilation and perfusion down the upright lung.


elevation in arterial Peo2 may also occur unless the

65


3

COORDINATION OF CARDIAC EVENTS

patient increases ventilation. Therapists who are posi

The mechanical activity of the heart is precisely regu

tioning patients with cardiopulmonary pathology may

lated with the electrical activity of the heart to effect

find that their patients experience greater distress

optimal cardiac output to the organs of the body (An

when placed in certain positions. Such position-de

dreoli, Fowkes, Zipes, and Wallace,

pendent distress can be explained by ventilation-per

1991; Dubin, 1989; Wagner, 1994). The electrical and mechanical

fusion inequalities that cause poor gas exchange in

events of the cardiac cycle are summarized in Figure

the dependent lung.

3-13. These events include the spread of the wave of

The relationship of ventilation and perfusion in the

electrical excitation throughout the myocardium, the

lung is summarized in the following figures. Figure

resulting sequence of contraction of the atria and ven

3-11 shows increases in ventilation and peifusion down

tricles followed by dynamic changes in pressure and

the upright lung. Optimal ventilation and perfusion

blood volume in the heart chambers, the heart sounds

matching, V:Q occurs in the mid-lung zones. In the up right position, ventilation is in excess of pelfusion in the apices, and perfusion is in excess of ventilation in

0. 4 120

right lung, and their effect on alveolar gas. Specifically, Figure

(seconds)

TIME

the bases. Figures 3-12 illustrate the effects of shunt and physiologic dead space on V:Q matching in the up 0,

3-12 shows a schematic representation of re

100

I

gional differences in ventilation and perfusion in the upper, middle, and lower zones of the upright lung. These gradients are reflected in the alveolar P02 and

•

S

80

W a:

60

::J (/) (/)

Peo2 levels associated with alveolar dead space of the

W a: c..

apices, appropriate ventilation-perfusion matching in the mid-lung, and shunt in the bases.

0.6

0.8

.. . .. ....... . .. :: .... . . ... .. .

. b ..

E

E.

c I

.

.

Ventricle

40 d

20

Atrium DIASTOLE

a: ::s E

CARDIAC REflEXES The heart behaves automatically, thus is termed a functional syncytium. Three primary reflexes enable the heart to increase stroke volume and cardiac out put with moment-to-moment changes in myocardial demand (French and Ct'iley,

120

::J Ow 80 a: f-::J z..J wO 40 » HEART SOUNDS

1983).

-fl

__

__

________

4th R

The first reflex is the Starling effect which refers to the increased force of contraction that occurs with

ECG

increased venous return (preload). The second reflex,

Q

the Anrep effect, refers to the increase in ventricular contractile force as a result of an increase in aortic pressure (afterload). And third, the Bowdich effect refers to the corresponding increase in heart rate when myocardial contractile force increases. The in tegrated function of these three reflexes ensures that

FIGURE 3-13

Summary of electrical and mechanical events of the heart.

A, Atrial systole. B, Isovolumetric contraction. C, Ejection.

D, Isovolumetric relaxation. E, Rapid inflow, diastasis, and

active rapid filling. Note relationship of ventricular pressure

cardiac output adjusts as de mands on the heart

and volume.

change, that is in health, primarily in response to ex

(b)

ercise, body position and emotional stress.

semilunar valves;

(a) closure of the

atrioventricular valves;

opening of the semilunar valves;


(d)

(c) closure

of the

opening of the atrioventricular valves.

66

PART I


takes

of these events. The cardiac

and the

0.8 second in a heart

Myocardial Depolarization

l

l

l

at 75 beats/min. Ventric

ular systole or ejection takes about one-third of this

Ventricular Contraction

time. Its onset and termination are marked respec by closure and

of the atrioventricular

valves (mitral and tricuspid). Diastole, or the period

Tricuspid and Mitral Valves Close

between successive ventricular systoles in whieh the ventricles fill with blood, takes two thirds of the 0.8 second of each cardiac

Pressure Increases and Pulmonary Aortic Pressure

t

t

Phases of Systole and Diastole Ventricular systole normally has three phases: isovol period, and

umctric contraction a slower

Pulmonic and Aortic Valves Open

period. Ventricular diastole also has

three phases: passive slower filling

diastasis (a and active

is Completed; Pressure Below Pulmonary and Aortic Pressure

phase.

Heart Sounds

Pulmonic

A

duration sound (SI) followed by a slower duration sound

l

t

l

sounds of LUB-dub. S I is associated with closure of is associated with c1o

Tricuspid and Mitral

sure of the semilunar valves. In inspiration, the aortic valve closes several milliseconds before the pulmonic valve, resulting in a splitting of the second heart venous return and

increase, hence pulmonary

heart volume is prolonged in this

Myocardial Depolarization

and closure of the pulmonary valve is deOther variations in splitting of

occur with

pathology. The presence of a third (S3) or fourth heart sound is usually considered abnormal. associated with the

is usu

Open

Diastolic Filling

S2. During inspiration, intrathoracic pressure becomes more

tiC Valves Close

Ventricular Pressure Falls Below Atrial Pressure

that resembles the phonic

the atrioventricular valves.

t

t

The heart sounds are described as a low-pitched long

FIGURE 3-14 The sequence of pressure

in the hearl

the

cardiac

phase, and

with the active rapid-filling phase. heart are responsible for the

and

of the

valves. Coordinated valve opening and closure are im

Volume and Pressure Changes

portant in promoting the forward movement of blood

Changes in the ventricular volume curve and aortic

and

pressure wave reflect

in atrial and ventricular

pump resulting from valvular

of blood

and diastole (Ganong, 1993;

ventricular contraction.

of blood

pressure during

mechanical

of the heart

Guyton, 1991). The sequence of events appears in a

in the retrograde direction gives rise to heart murmurs

tlow chart in Figure 3-14. Pressure gradients within the

audible on auscultation of the heart (Goldberger. 1990).


3


67

fluid to be filtered out of the systemic circulation

TABLE 3-1

into the interstitium. Table

Balance of Forces Moving Fluid

3-1 illustrates the mean

pressures determining normal fluid dynamics across

In and Out of the Capillary

capillary membranes. mmHg

TRANSPORT OF OXYGEN BY THE BLOOD

Mean forces moving fluid out of capillary 17.0 6.3 5.0 28.3

Mean capillary pressure Negative interstitial pressure Oncotic interstitial pressure TOTAL OUTWARD PRESSURE

Plasma oncotic pressure

28.0 28.0

TOTAL INWARD PRESSURE

OUTW ARD PRESSURE - INW ARD =

with hemoglobin to form oxyhemoglobin (West,

1995). A small proportion of oxygen is dissolved in the plasma. The use of the hemoglobin molecule as

Mean forces moving fluid into capillary

PRESSURE

Once oxygen reaches the blood, it rapidly combines

NET OUTW ARD PRESSURE

0.3

an oxygen carrier allows for greater availability and efficiency of oxygen delivery to the tissues in re sponse to changes in metabolism. Saturation of the oxygen-carrying sites on the hemoglobin molecule is curvilinearly related to the partial pressure of oxygen in the tissues. This relationship is called the oxyhe moglobin dissociation curve and is a sigmoid or S

3-15). The hemoglobin of arter 98% or almost completely saturated with

shaped curve (Figure ial blood is

Peripheral Circulation

oxygen. Under normal circumstances, arterial blood

The purpose of the peripheral circulation including

is mixed with a small proportion of venous blood

the microcirculation at the tissue level is to provide

from the coronary and pulmonary circulation, result

100%. The graph

saturated oxygenated blood and remove partially de

ing in arterial saturation of less than

saturated blood. The microcirculation within each

shows a range of partial pressures of oxygen that may

organ regulated the blood flow both exogenously via

exist in the tissues. At relatively high arterial oxygen

the neurological system and endogenously via the hu

pressures, the oxygen saturation is high. This reflects

moral system commensurate with the metabolic

high association or low dissociation between oxygen

2). The four

and hemoglobin. Saturation does not fall significantly

needs of that tissue bed (see Chapter

80 50 mm Hg, al1er

principal factors that determine the movement of

until the partial pressure of oxygen falls below

fluid in the microcirculation include the following:

mm Hg. Even at P02 levels of 40 to

1. The capillary hydrostatic pressure from the blood pressure, which tends to move blood

ial saturation is still

75%. This suggests an enormous

capacity of the oxyhemoglobin dissociation system to

across the capillary membrane out of the circu

meet the varying needs of different tissues without

lation into the interstitium

severely compromising arterial saturation. A P02 of

2. The capillary oncotic pressure from the pro

less than

50%, for example, has a profound effect on

teins within the blood vessels, which tends to

arterial saturation. This demonstrates an adaptive re

retain fluid in the circulation

sponse of hemoglobin dissociation to respond to low

3. The interstitial hydrostatic pressure, which

oxygen tissue pressures by greater dissociation of

tends to move fluid back into the circulation

oxygen from hemoglobin as the need arises. As the

4. The interstitial oncotic pressure, which tends

P02 improves as a result of increased supply of oxy

to draw fluid out of the circulation into the

gen or decreased demand, the affinity between oxy

interstitium

gen and hemoglobin increases, and arterial saturation

The net forces acting on the capillary fluid are nearly in equilibrium with a slight tendency for

increases. Thus oxygen is not released unless there is a need for greater oxygen delivery to the tissues.


68

PART I


ARTERIAL OXYGENATION

C\J 0

75

Z 0

i= « 0::: ::J

(f) 0

20

27

80

60

40

PARTIAL

PRESSURE

100

02

FIGURE 3-15

The oxyhemoglobin dissociation curve.

Different conditions can increase or decrease he

Anemia (reduced red blood cell count and hemo

moglobin affinity for oxygen and thereby cause a shift

globin) and polycythemia (excess red blood cells and

in the oxyhemoglobin dissociation curve (West, 1995)

hemoglobin) produce changes in oxygen content of

(Figure 3-15). A shift to the right results in decreased

the blood as well as saturation. Anemia shifts the

oxygen affinity and greater dissociation of oxygen and

curve to the right and lowers the maximal saturation

hemoglobin. In this instance, for any given partial

achievable. Polycythemia has the opposite effect. The

pressure of oxygen, there is a lower saturation than

curve is shifted to the left and maximal saturation ap

normal. This means that there is more oxygen avail

proaches 100%.

able to the tissues. Shifts in the curve to the right occur with increasing concentration of hydrogen ions (i.e., decreasing pH), increasing Peo2, increasing tem

TRANSPORT OF CARBON DIOXIDE

peratures, and increasing levels of 2,3-DPG (diphos

CO2 is an acid produced by cells as a result of cell

phoglycerate), a byproduct of red blood cell metabo

metabolism. It is carried in various forms by venous

l i s m . W e s t ( 19 9 5 ) s u g g e s t s , "A simple way t o

blood to the lungs, where it is eliminated. Most of the

remember these shifts i s that an exercising muscle (in

CO2 added to plasma diffuses into the red blood cells,

creased metabolic demand), is acid, hypercarbic, (hy

where it is buffered and returned to the plasma to be

percapnic) and hot, and it benefits from increased un

carried to the lungs. The buffering mechanism is so . effective that large changes in dissolved CO2 can

loading of oxygen from its capillaries." A shift of the curve to the left results in increased

occur with small changes in blood pH.

oxygen affinity. Thus for any given partial pressure

The transport of CO2 has an important role in the

of oxygen, there is a higher saturation than normal.

acid-base status of the blood and maintenance of nor

This means that there is less oxygen available to the

mal homeostasis (Comroe, Forster, Dubois, Briscoe,

tissues. This occurs in alkalemia, hypothermia, and

and Carlsen,

decreased 2,3-DPG.

carbonic acid per day. (Carbonic acid is broken down


1986). The lung excretes 10,000 mEg of

3


69

into water and CO2. The CO2 is buffered and elimi

globin dissociation ensures adequate oxygen delivery

nated through the lungs.) The kidney can excrete only

to the tissues once oxygen has diffused through the

100 mEq per day of acids. Therefore alterations in

alveolar capillary membrane into the circulation.

alveolar ventilation can have profound effects on the

Transport of CO2 and its buffering mechanisms are

body's acid-base status. A decrease in the lung's abil

central to acid base balance and normal homeostasis.

ity to ventilate causes a sharp rise in Peo2 and a drop in pH. This causes an acute respiratory acidosis. If this change occurs gradually, the pH will remain

REVIEW QUESTIONS

within normal limits while the Peo2 is elevated. This

I. Describe the control of breathing.

is known as a compensated respiratory acidosis. Hy

2. Explain respiratory mechanics with respect to

perventilation or excessive ventilation causes rapid elimination of C02 from the blood. This results in a decreased Peo2 and an increased pH and is known as an acute respiratory alkalosis. Again, if the change occurs gradually, the pH remains within normal lim

airway resistance and lung compliance. 3. Describe the distributions of ventilation, perfu sion and diffusion. 4. Explain the determinants of ventilation and per fusion matching.

its even though the Peol is decreased. This is a com

S. Describe electromechanical coupling in the heart.

pensated respiratory alkalosis.

6. Describe oxyhemoglobin dissociation and the oxyhemoglobin dissociation curve.

SUMMARY This chapter presented an overview of cardiopul monary physiology with respect to breathing control, both central and peripheral mechanisms such as mus cle, joint, and lung and chest wall stretch receptors, in volved with the regulation of respiration. Mechanical factors of breathing, chest wall and lung compliance, and airway resistance are described. The elastic prop erties of the respiratory system, that is, chest wall and lungs, are ret1ected in the pressure volume relaxation curve. This curve has important implications for the clinical presentation of the patient with cardiopul monary dysfunction, and in particular, the efficiency and energy requirement of the respiratory system. Ventilation and pelfusion matching is the basis of gas exchange and the adequacy of lung function. Many factors in addition to disease, however, can affect ven

REFERENCES Andreoli, K.G., Fowkes, V.K., Zipes, D .P., Mosby. Bates, D.V. (1989). Respiratory Junction Berne, R.M.,

& Levy, M.N. (1992).

pling of electrical and mechanical events in the heart to effect cardiac output are described. Arterial P02 and Peo2 are normal! y maintained within certain prescribed limits. In health, oxyhemo

& Keitel, L.J. (1983).

Res

piratory disorders: A pathophysiologic approach (2nd ed.).

Chicago: Year Book Medical. Cherniack, R.M.,

& Cherniack, L. (1983).

Respiration in health

and disease ( 3rd ed.). Philadelphia : WB Saunders.

Clemente, C.D. (Ed.). (1985). Anatomy oj the human body (30th ed.). Philadelphia: Lea and Febiger. Comroe,

J.H., Jr., Forster, R.E., Il, Dubois, A.B., Briscoe, W.A., &

Carlsen, E. (1986). The lung; Clinical physiology and pul monary Junction tests (3rd ed.). Chicago: Year Book Medical.

Dubin, D. (1989). Rapid interpretation oj EKGs (4th ed.). Tampa,

FL: Cover.

diac output, hence, adequate oxygen delivery to the

Cardiovascular physiology

Burrows, B., Knudson, R.J., Quan, SF,

French, W.G.,

vital organs and peripheral tissues. The optimal cou

disease. (3rd ed.).

(6th ed.). St Louis: CV Mosby.

position, breathing at low lung volumes and smoking The purpose of the heart is to provide an adequate car

ill

Philadelphia: WB Saunders.

tilation and perfusion matching, including age, body history. The relationship of such factors are discussed.

& Wallace, A.G.

(Eds.). (1991). Comprehensive cardiac care (7th ed.). SI Louis:

& Criley, J.M. (Eds.). (1983).

Practical cardiology:

Ischemic and valvular heart disease. New York: John Wiley

and Sons. Ganong, W. F. (1993). Review oj medical physiology (16th ed.). Los Altos: Lange Medical Publications. Goldberger, E. (1990). Essentials oj clinical cardiology. Philadel phia: JB Lippincott. Goldman, M. (1979). Mechanical interaction between diaphragm and rib cage. American Review oj Respiratory Disease,

I 19(Part 2), 23-26.


PART I

70


Guyton, A,C, (l99J), Textbook of medical physiology. (8th ed,j, Philadelphia: WB Saunders. Raven Press. Murray, IF, & Nadel, l.A. (1988). Textbook of respiratory medi cine Philadelphia: W.s. Saunders,

ed.). Baltimore: Williams and Wilkins.

.

Nunn, J.F ([993). Applied respiralory physiology (4th ed,). Lon

West, 1.B. ([992), Pulmonary pathophysiology: The essenlials (4th

00.). Baltimore: Williams and Wilkins.

don: Butterworths. Scharf, S,M" & Cassidy S.S, (Eds,), (1989). Hearl-lung interac

in health and disease. New York: Marcel-Dekker, Inc.

West, .l.B. (1991). Best and Taylor's physiological basis of med ical praclice (12th ed.J. Baltimore: Williams and Wilkins.

Schlant, R,C., Alexander, R.W., O'Rourke, R.A., Robens, R., & Sonnenblick, E. H. (Eds.J. (1994). Hurst's lite heart: Arleries and

& Cheitlin, M.D. (1990), Clinical

(5th 00.), Norwalk: Appleton & Lange. Wagner, G.S. (J994), Marrioll's practical electrocardiography (9th ed,). Baltimore: Williams and Wilkins. West, J.B. (1995). Respiratory physiology-The essen/ials (5th cardiology

Katz, A,M, (1992). Physiology of Ihe hearl (2nd ed.) New York:

tions

Sokolow, M., McIlroy, M.B"

veins (8th ed.J. New York: McGraw-Hill.


Cardiopulmonary Pathophysiology

Willy E. Hammon Scott Hasson

KEY TERMS

Angina

Fibrosis

Bronchiectasis

Myocardial infarction

Coronary artery disease

Obstructive lung disease

Emphysema

Restrictive lung disease

INTRODUCTION

formance. The parameters affected by CAD can be the

The first part of this chapter, beginning with obstruc

volume of blood pumped and the heart rate. The

tive lung disease, describes the pathophysiology of

major purposes of this portion of the chapter are to de

chronic pulmonary disease. Chronic pulmonary dis

scribe the etiologic factors of clinical syndromes asso

ease can be categorized broadly into obstructive and

ciated with CAD, briefly describe medical treatment,

restrictive disorders.

and discuss issues of prognosis.

Obstructive disorders are characterized by a de creased rate of airflow during expiration (as a result of increased airway resistance). Restrictive disorders

OBSTRUCTIVE LUNG DISEASE

are conditions in which the inspiratory capacity of the

Several abbreviations can be found in the literature

lungs is restricted to less than the predicted normal.

for a pulmonary disorder characterized by increased airway resistance, particularly noticeable by a pro

Overlap between the two categories does exist. The second part of this chapter, beginning with

longed forced expiration. Some of these are chronic

coronary artery disease (CAD), describes the patho

obstructive pulmonary disease (COPD), chronic ob

physiology of cardiovascular disease. Cardiovascular

structive airway disease (COAD), chronic airway ob

disease is also known primarily as CAD, and is mani

struction (CAO), and chronic obstructive lung disease

fested in various clinical syndromes. CAD is an ather

(COLD) (Fishman,

1988).

osclerotic process that occurs in the right and left

The first part of this chapter describes chronic

coronary aJ1eries, which ultimately affects heart per-

bronchitis, emphysema, asthma, and bronchiectasis 71


72

PART I


individually. With the possible exception of asthma

susceptible to rcspiratory infections, and it takes them

and bronchiectasis, however, it is unusual in the clini

longcr to recovcr from these infections. In addition, the

cal setting to find a patient with only one of these con

ilTitation of smoke in the tracheobronchial trec causes

ditions. Most patients have some combination of

bronchoconstriction. Although smoking is the most

chronic bronchitis, emphysema, and asthma, and in

common cause of chronic bronchitis, other agents that

this chapter, these individuals are referred to as having

have been implicated are air pollution, bronchial infec

COPD. These patients have intermittent episodes of

tions, and certain occupations.

wheezing, along with a variable degree of chronic

These patients are referred to as "blue bloaters,"

bronchitis and emphysema (Hodgkin, 1975). Radio

because they usually have stocky body build and are

logically, they may have hyperinfiated lungs, flattened

"blue" as a result of hypoxemia (Dornhorst, 1955;

diaphragms, and an enlarged right ventricle as a result

Filley et ai, 1968; Fishman, 1988; Nash, Briscoe,

of increased pulmonary artery pressure. Other findings

and COUl·nand, 1965. Although many of these pa

vary from patient to patient, depending on the predom

tients have a high arterial partial pressure of carbon

inant disease process contributing to their COPD.

dioxide (Pac02), the pH is normalized by renal re

COPD is very common. In 1994 the American

tention of bicarbonate (HC03). In the patient with

Lung Association (ALA) estimated that 14.2 million

chronic bronchitis, bone marrow tries to compensate

Americans have COPD. In the United States alone,

for chronic hypoxemia by increased production of

health care costs for COPD exceed $7.6 billion annu

red blood cells, leading to p olycythemia (Snider,

ally. Deaths from COPD numbered more than 85,000

Faling, and Rennard, 1994). Polycythemia, in turn,

in 1991; it is the fourth leading cause of death in the

makes the blood more viscous, forcing the heart to

United States.

work even harder to pump it. Long-term hypoxemia leads to increased pulmonary artery pressure and right ventricular hypertrophy.

Chronic Bronchitis

Individuals with bronchitis often expectorate mu

Chronic bronchitis is a disease characterized by a

coid brownish-colored sputum. In an exacerbation,

cough producing sputum for at least 3 months and for 2

usually from infection, they have an even greater

consecutive years (American Thoracic Society, 1962).

amount of purulent sputum. Ventilation-perfusion ab

Pathologically, there is an increase in the size of

normalities are common, which increase hypoxemia

the tracheobronchial mucous glands (increased Reid

and Paco2 retention (Rochester and Brown, 1976).

index) and goblet cell hyperplasia (Mitchell, 1968;

The respiratory rate increases, as does the use of ac

Reid, 1960; Stoller and Wiedemann, 1990). Mucous

cessory muscles. The resultant increased work of

cell metaplasia of bronchial epithelium results in a

breathing requires greater oxygen consumption by

decreased number of cilia. Ciliary dysfunction and

these muscles, with a greater production of carbon

disruption of the continuity of the mucous blanket are

dioxide (C02) than the respiratory system can ade

common. In the peripheral airways, bronchiolitis,

quately meet. This contributes to a further drop in the

bronchiolar narrowing, and increased amounts of

arterial partial pressure of oxygen (Pao2) and a rise in

mucus are observed (Cosio, 1978; Wright, 1992).

Paco2. The hypoxemia and acidemia increase pul

The cause of chronic bronchitis is believed to be re

monary vessel constriction, which raises pulmonary

lated to long-term in-itation of the tracheobronchial tree.

artery pressure and ultimately leads to right heart fail

The most common cause of irritation is cigarette smok

ure (cor pulmonale).

ing (US Surgeon General, 1984). Inhaled cigarette

In the following example, a patient is admitted to

smoke stimulates the goblet cells and mucous glands to

the hospital with an exacerbation of chronic bronchi

secrete more mucus. This smoke also inhibits ciliary

tis and presents the following picture: he is of stocky

action. The hypersecretion of mucus and impaired cilia

body build, his color is dusky, and he breathes with

lead to a cllronic productive cough. The fact that smok

moderate-to-marked use of the respiratory accessory

ers secrete an abnormal amount of mucus makes them

muscles, depending on the degree of respiratory dis


4

tress.

may be audible or noted by ausculta

and Rennard,

on the degree of respiratory dis

sent, also

tress. Edema in the extremities

iJ"'''''''''U

in the

and neck vein distention reflect decom cor pulmonale. The

may report that w i th i n c r e a s e d

There are two main ular and panlobular

color) or decreased amounts of sputum

in

Arterial blood gases

creased retention of

Emphysema

a change in normal

this b r e athing difficu amounts o f secretions

of emphysema-centrilob

1976; ThurJbeck, I

It

that centrilobular

has been

20 times more common than panlobular both types are often found in the same pair

show the individual with bronchitis to have a lowered and a lowered

Pao2, a raised

function tests indicate a reduced vital forced

v o lume in I second

maximum voluntary ventilation and diffus capacity, as well as an increased functional resid ual

73

1983). Diuretics and

retractions may be pre

tion. Intercostal (or

ankle


and residual volume.

As its name implies, centrilobular emphysema is characterized

destruction of the respiratory bron

chiole, edema,

and thickened bronchi

olar walls. These changes are more common and more marked in the upper lobes and superior seg

an exacerbation, these

are usually

1963). This

ments of the lower lobes

fluids, antibiotics, bron

form of emphysema is found more often in men than

chodilator and low-flow oxygen. CO!1iocosteroids may

in women, is rare among nonsmokers, and is com

be administered. Some

mon among

treated with intravenous

with increased secre

tions respond to chest physical therapy and bronchial

A

with chronic bronchitis.

Pan lobular emphysema, on the other hand, is

Alveoli ___

FIGURE 4-1 A, Panlobular

is characterized by a destructive enlargement of the alveoli, B, A nonnal

respiratory bronchiole and alveoli. and destmction of the

Centrilobular emphysema is characterized bronchiole.


a selective

74

PART I


characterized by destructive enlargement of the alve oli, distal to the terminal bronchiole (Figure

4-1).

It

(Figure

1976).

4-2) (Reid, 1967; Thurlbeck, 1991; Thurlbeck,

It is thought that bullae develop from a coales

most often involves the lower lobes. This type of em

cence of adjacent areas of emphysema or an obstruc

physema is also found in subjects that have alphaJ

tion of the conducting airways that permits the flow of

antitripsin deficiency. Airway obstruction in these in

air into the alveoli during inspiration but does not

dividuals is caused by loss of lung elastic recoil or

allow air to flow out again during expiration. This

radial traction on the bronchioles. When individuals

causes the alveoli to become hyperinflated and even

with normal lungs inhale, the airways are stretched

tually leads to destruction of the alveolar walls with a

open by the enlarging elastic lung, and during exhala

resultant enlarged air space in the lung parenchyma.

tion the airways are narrowed as a result of the de

These bullae can be more than

creasing stretch of the lung. However, the lungs of

by compression, can compromise the function of the

10

cm in diameter, and

4-3).

patients with panlobular emphysema have decreased

remaining lung tissue (Figure

elasticity because of disruption and destruction of

surgical intervention to remove the bulla is often nec

If this happens,

surrounding alveolar walls. This in turn leaves the

essary. Pneumothorax, a serious complication, can re

bronchiole unsupported and vulnerable to collapse

sult from the rupture of one of these bullae.

during exhalation.

The emphysema patient's most common com

Bullae, emphysematous spaces larger than I cm in

plaint is dyspnea. Physically, these patients appear

diameter, may be found in patients with emphysema

thin and have an increased anteroposterior chest di-

B

FIGURE 4-2 A, AP chest film reveals bullous emphysema with multiple, thin, rounded fibrotic lucencies. B, The spot film bronchogram of the left midlung field shows intact bronchi and distal emphysematous blebs. (Courtesy of T. H. Johnson, M.D.)


4


75

ameter. Typically, they breathe using the accessory

heart (Figure 4-4). Pulmonary function tests show a

muscles of inspiration. These patients are often seen

decreased vital capacity, FEY"

leaning forward, resting their forearms on their knees

ventilation and a greatly reduced diffusing capacity.

or sitting with their arms extended at their sides and

The total lung capacity is increased, while the resid

pushing down against the bed or chair to elevate their

ual volume and functional residual capacity are even

maximum voluntary

shoulders and improve the effectiveness of the acces

more increased. Arterial blood gases reflect a mildly

sory muscles of inspiration. They may breathe

or moderately lowered Pao2, a normal or slightly

through pursed lips during the expiratory phase of

raised Pacol and a normal pH. These patients, unlike

breathing. These patients have been referred to as

patients with chronic bronchitis, normally will de

"pink puffers" because of the increased respiratory

velop heart failure in the end stage of the disease

work they must do to maintain relatively normal

(Figure 4-5).

blood gases (Dornhorst, 1955; Filley et aI, 1968;

Treatment of progressive emphysema that requires

Fishman, 1988; Nash, Briscoe, and Cournand, 1965).

hospitalization often includes IY fluids, antibiotics,

On auscultation, decreased breath sounds can be

and low-flow oxygen (Snider, Faling, and Rennard,

noted throughout most or all of the lung fields. Radi

1994). Some of these patients also receive bron

ologically, the emphysema patient has overinflated

chodilators, corticosteroids, diuretics, and digitalis.

lungs, a flattened diaphragm, and a small, elongated

Pursed-lip breathing can relieve dyspnea and improve

FIGURE 4-3 A, AP and B, lateral views of the chest of a patient with advanced bullous emphysematous changes. Note the bullae in the upper lung fields. The lateral film reveals an increased A-P diameter of the thorax, flattening of the diaphragms and in increased anterior clear space. (Collrtesy of T. H. Johnson,


M.D.)

76

PART I


FIGURE 4-4 A, AP chest film reveals the increased lucency of lung fields and flattening of the diaphragm of emphysema. The vascular structures are crowded mediaHy. B, Lateral chest film reveals an increased AP diameter and flattening of the diaphragms. There is an increase in the anterior clear space. These are all findings of emphysema. (Courtesy of T. H. Johnson,

M.D.)

arterial blood gasses (Muller, Petty, and Filley, 1970;

these and other factors in producing emphysema is

Petty and Guthrie, 1974).

still not well understood.

The cause of emphysema is uncel1ain. It is known that the incidence of emphysema increases with age. It

Prognosis of chronic bronchitis and emphysema

is most often found in chronic bronchitics, and there is

Chronic bronchitis and emphysema are marked by a

no question that emphysema is more prevalent in cig

progressive loss of lung function. At the end of 5

arette smokers than in nonsmokers (US Surgeon Gen

years, patients with COPD have a death rate four to

eral, 1984). The risk of developing COPD is 30 times

five times greater than the normal expected value.

greater in smokers than nonsmokers (Fielding, 1985).

Death rates reported by various studies depend on the

There also seems to be an hereditary factor, evident in

method of selection of patients, types of diagnostic

the severe panlobular emphysema that patients with

tests and other criteria (Anthonisen, 1989; Bousky et

an alpha,-antitrypsin deficiency develop relatively

ai, 1964; Kanner et ai, 1983; Kanner and Renzetti,

early in life, even though they m a y never h ave

1984). One study reported a 3-year overall mortality

smoked (Eriksson, 1965; Tobin, Cook, and Hutchin

rate of 23%, with patient age and the initial FEY I

son, 1983). Repeated lower respiratory tract infections

value being the most accurate predictors of death

may also play a role. However, the interrelationship of

(Anthonisen, Wright, and Hodgkin, 1986). In general,


4


77

gestive heart failure (CHF), which is secondary to cor pulmonale; respiratory failure; pneumonia; bronchi olitis; and pulmonary embolism.

Asthma Asthma is a disease characterized by an increased re sponsiveness of the trachea and bronchi to various stimuli, and is manifested by widespread narrowing of the airways that changes in severity either sponta neously or as a result of treatment. During an asthma attack, the lumen of the airways is narrowed or is oc cluded by a combination of bronchial smooth muscle spasm, inflammation of the mucosa, and an overpro duction of a viscous, tenacious mucus. Asthma is certainly a widespread disease in the world today. Its incidence is about 3% to 7% in adults (Barnes, 1993; National Asthma Education Program, 1991). It is found more often in individuals under age 25, where estimates of prevalence vary from 5% to 15% (Williams and McNicol, 1969).

FIGURE 4-5 The chest film reveals peripheral emphysematous lucency.

About 80% of children with asthma do not have

The hilar areas are tremendously enlarged by the

asthma after the age of 10.

pulmonary arteries in a typical cor pulmonale

Asthma that begins in patients under the age of 35

configuration. Cardiomegaly is also present. (Courtesy

is usually allergic or extrinsic. These asthma attacks

ofT. H. 10hnson, M.D.)

are precipitated when an individual comes in contact with a specific substance to which that person is sen sitive, such as pollens or household dust (see box 4-1

the death rates 5 years after diagnosis are 20% to

below). Often people with asthma are allergic to a

55%. Other investigators reported an overall mortal

number of substances, not only one or two.

ity of 47 percent at the end of 5 years (Burrows, and

If a patient's first asthma attack occurs after the

Earle, 1969). They believed a 5-year survival rate can

age of 35, usually there is evidence of chronic airway

be estimated as follows: 80% in patients with an

obstruction with intermittent episodes of acute bron

FEY I close to 1.0 L; and 40% for patients with an

chospasm. These individuals, whose attacks are not

FEY I less than 0.75 L. However, if the above flow

triggered by specific substances, are referred to as

rates are found in patients with complications of rest

having nonallergic or intrinsic asthma (see b o x

ing tachycardia, chronic hypercapnia and a severely

below). Chronic bronchitis i s commonly found i n this

impaired diffusing capacity, the survival rates should

group, and this is the type of individual often seen in

be reduced by 25%. Other factors that have been as

the hospital setting.

sociated with a poor prognosis are cor pulmonale,

The individual with an acute asthma attack usually

weight loss, radiologic evidence of emphysema, a

has been awakened at night or early in the morning with

dyspneic onset, polycythemia, and Hoover's sign (an

one or more of the following symptoms: cough, dysp

inward movement of the ribs on inspiration)

nea, wheezing, or chest tightness (McFadden, 1988). In

(Mitchell, Webb, and Filley, 1964; Renzetti, 1967).

fact, nocturnal awakenings are such a common occur

The most common cause of death in patients with

rence with asthma, that their absence from the history

COPD (in descending order of frequency) are con

causes even experienced clinicians to doubt the diagno


78

PART I


Factors That May Precipitate an Asthma Attack Allergic or extrinsic asthma Pollen (especially ragweed) Animals Feathers Molds Household dust Food Nonallergic or intrinsic asthma Inhaled irritants Cigarette smoke Dust Pollution Chemicals Weather High humidity Cold air Respiratory infections Common cold Bacterial bronchitis Drugs Aspirin Emotions Stress Exercise

FIGURE 4-6 A patient in respiratory distress during an acute asthma attack. Note the marked use of the stcrnocleidomastoids and other accessory muscles during inspiration.

sis (Turner-Warwick,

(988). The patient has a rapid

rate of breathing and is using the accessory respiratory muscle (Figure

4-6). The expiratory phase of breathing

high PacD2, a low Pao2, and a pH of less than Fadden and Lyons,

7.30 (Mc

1968).

Medical management of acute asthma has three

(2) mobilization of (3) maintenance of alveolar ventila

is prolonged with audible wheezing and rhonchi. How

goals: ( l ) relief of bronchospasm,

ever, when severe obstruction is present, the chest be

secretions, and

1976). The patient may cough

tion. Th e r e f ore m o s t hospitalized patients with

often, though unproductively, and may complain of

asthma are treated with IV fluids, bronchodilators,

tightness in his chest. Radiologically, the lungs may ap

supplemental oxygen, and corticosteroids.

comes silent (Gold,

pear hyperinflated or show small atelectatic areas from

An asthma attack that persists for hours and is unre

retained secretions. The degree of tachypnea, hyperin

sponsive to medical management is referred to as sta

flation, accessory muscle use, and pulsus paradoxus

tus asthmaticus. The patient may appear dehydrated,

(difference in systolic blood pressure during inspiration

cyanotic, and near exhaustion from labored breathing.

and expiration) are useful guides for determining the

In contrast to the audible whcczing and rhonchi heard

degree of airway obstruction present (Woolcock,

1994).

early in the attack, the chest now has greatly dimin

Early in the attack, arterial blood gases reflect slight hy

ished or absent breath sounds. Status asthmaticus re

poxemia and a low Paco2 (from hyperventilation). If the

sults in a significant death rate and is regarded as a

attack progresses, the PaD2 continues to fall as the PacD2

medical emergency. Bilateral manual lower chest com

climbs above the normal range. As obstruction becomes

pression assists expiration and has value as an emer

severe, deterioration of the patient occurs, evident by a

gency treatment of asthma (Fisher, Bowery, and Ladd


4


79

FIGURE 4-7 Gross specimen of lung showing large mucus plug within the bronchial tree of a patient who died from status asthmaticus. (Courtesy of J. J. Coalson, Ph.D.)

Hudson, 1989; Watts, 1989). Patients in respiratory

bronchial lumen, further contributing to the stasis of secretions. Although the alveoli are overinflated, the

failure may require mechanical ventilation. Studies that examine the lungs of patients who die from status asthmaticus find lungs that are signifi cantly hyperinflated and do not deflate even when the thorax is opened (Huber and Koessler, 1922;

permanent destructive changes found in emphysema are not present.

Prognosis of asthma

Dunnill, 1960; Saetta et ai, 1991). Examination of

Most studies following children with asthma for a

the airways reveals a mucosa that is edematous and

number of years report a death rate of about 1 %

inflamed. Characteristic of asthma, the basement

(Ogilvie, 1962). One large study of 1,000 people with

membrane is thickened. The mucous glands are en

asthma of all ages in England reported a mortality of

larged, and there is an increase in the number of gob

7% as a result of asthma or its complications. This

let cells. Evidence of bronchospasm is seen by the

study reported that 2% of the patients with intermit

hypertrophied and thickened smooth muscle. The lu

tent asthma died, compared with 9% of those with

mens of most bronchioles, down to the terminal

continuous asthma. During the 1960s, there was a

bronchioles, are filled with viscous, sticky mucus

sharp increase in the number of deaths among people

(Figure 4-7). It is evident that the occluded bronchi

with asthma reported by countries around the world.

oles have caused death by asphyxiation. Secretions

At the peak of this increase, England and Wales re

in the tracheobronchial tree of the patient with

ported that 7% of the deaths in children between 10

asthma are a combination of mucus, secreted by the

and 14 years of age were attributable to asthma. This

mucous glands, and an exudate from the dilated cap

reflected a 700% increase in only 7 years. Some med

illaries just below the basement membranae. It has

ical authorities feel this increase in deaths was related

been shown that cilia do not sweep the mucoserous

to widespread use or abuse of certain pressurized

t1uid nearly as effectively as pure mucus. In addition,

aerosol nebulizers containing isoproterenol, but this

sheets of ciliated epithelium have been shed into the

has been disputed (Gandevia, 1973). In 1987 there


80

PART I


were more than 4,300 deaths from asthma in the Un

bronchi to resemble varicose veins (Figure 4-8). Sac

tied States, 31% more than in 1980 (McFadden and

cular (or cystic) bronchiectasis refers to airways that

Gilbert, 1992).

have intermittent sphcrical ballooning (Figure 4-9). Bronchiectasis is usually localized in a few seg ments or in an entire lobe of the lung. Most com

Bronchiectasis

monly, it is unilateral (although 40% to 50% of the

Bronchiectasis is defined as an abnormal dilation of

cases are bilateral) and affects the basal segments of

medium-size bronchi and bronchioles (about the

the lower lobes. When the left lower lobe is involved,

fourth to ninth generations), generally associated with

it is not unusual to find bronchiectasis in the lingula of

a previous, chronic necrotizing infection within these

the left upper lobe as well. Interestingly, bronchiecta

passages. Ordinarily, there is sufficient cartilage

sis of the right middle lobe is relatively common in

within the walls of the larger bronchi to protect them

older adults and can contribute to both hemoptysis

from dilation.

and repeated infections of this lobe. Upper lobe

The airway deformities can be classified into three

bronchiectasis generally involves the apical and poste

types (Reid, 1950; Luce, 1994). Cylindrical (or longi

rior scgments and is usually caused by tuberculosis or

tudinal) bronchiectasis is the most common type,

bronchopulmonary aspergillosis.

with a uniform dilation of the airways. Varicose

Pathologically, the mucosa appears edematous and

bronchiectasis refers to a greater dilation than in

ulcerated. Destruction of the elastic and muscular

cylindrical bronchiectasis, causing the walls of the

structures of the airway walls is evident with resultant

FIGURE 4-8 A, AP chest film of a bronchogram with cylindrical and varicose bronchiectasis in the lower lung fields. B, Close-up view of cylindrical and varicose bronchiectatic changes in the left lower lobe. (Courtesy of T. H. Johnson, M.D.)


4


81

dilation and fibrosis. The walls are lined with hyper

Obstruction can cause bronchiectasis by collaps

plastic, nonciliated, mucus-secreting cells that have

ing lung tissue (atelectasis) distal to the obstruction

replaced the nOImal ciliated epithelium. This change

(Barker and Bardana, 1988). The increased negative

is significant, because it interrupts the mucociliary

pressure in the chest (from the collapsed lung) exerts

blanket and causes pooling of infected secretions,

a greater traction on the airways, causing them to ex

which further damage and irritate the bronchial wall

pand and to become distorted. Secretions are re

(Barker and Bardana, 1988; Currie et ai, 1987).

tained, and if the obstruction is prolonged, an infec

The etiology of bronchiectasis is related to ob

tio.u occurs that begins to destroy the walls of the

struction of the airways and respiratory infections

bronchi, as described above. There has been a signifi

(Luce, 1994; Simpson, 1975). Some 60% of the cases

c a n t reduction in the n u m b e r of p a t i e n t s w i t h

of bronchiectasis are preceded by an acute respiratory

bronchiectasis since the introduction o f antibiotics to

infection. The infection involves the bronchial walls.

treat respiratory infections.

Portions of the mucosa are destroyed and are re

Twenty-four-hour sputum volume has been used

placed by fibrous tissue. The radial traction of the

as an indicator of severity of disease to categorize pa

lung parenchyma on the damaged bronchi causes the

tients with bronchiectasis (Ellis et aI, 1981). Those

involved airways to become permanently dilated and

producing less than 10 ml per day have been catego

distorted (Barker and Bm·dana, 1988). These areas,

rized as having mild bronchiectasis, to to I SO ml as

devoid of normal ciliated cells, contain secretions

moderate bronchiectasis and greater than I SO ml as

that eventually become chronically infected.

having severe bronchiectasis.

FIGURE 4-9 A, AP chest film of a bronchogram shows saccular bronchiectasis. B, Close-up view of bronchiectatic areas with grapelike saccular bronchiectasis. (Courtesy of T. H. Johnson,


M.D.)

82

PART I


P atients w ith severe, diffuse, long-standing bronchiectasis are rare today. Physically, they are ema ciated, and as many as 25% of them may have clubbed fingers. A chronic cough, with expectoration of un pleasant-tasting, purulent sputum is typical in these pa tients. When this sputum is collected and allowed to stand, it may separate into three distinct layers: the up permost layer is frothy, the middle layer is serous or mucopurulent, and the lowest layer is purulent and may contain small grayish or yellowish plugs (Dit trich's plugs). Changes of body position, while sleep ing or on arising, often stimulate coughing as the pooled secretions again spill onto the mucosa of nor mal, larger airways. These individuals may have cor pulmonale from fibrosis that has extended to involve the pulmonary capillary bed. Patients with widespread bronchiectasis appear dyspneic and have increased work of breathing as a result of hypoxemia and hyper capnia from ventilation-perfusion mismatching. Anas tomosis of the bronchial and pulmonary vascular sys tems causes shunting of the systemic blood from the hypertrophied bronchial arteries. It also may contribute to a decreased capability to take oxygen into the in volved segments of the lung (Liebow, Hales, and Lind skog, 1949; Luce, 1994). Most patients complain of relatively few symp toms, except during a respiratory infection when they have an increased cough and sputum production. The amount of sputum expectorated and the severity of the cough vary from patient to patient, according to the amount of involvement. Hemoptysis does occur in about half of the older patients, evidently because of erosion of enlarged bronchial arteries that accom pany the dilated bronchi. Effective postural drainage, percussion, vibration, and the forced expiratory technique (FET) are impor tant in the management of bronchiectasis (Gallon, 1991; van Hengstum et aI, 1988; Sutton, 1983; Ver boom, Bakker, and Sterk, 1986) (see Chapter 20). ,It should be done as frequently as indicated in patients with a productive cough. Postural drainage should be done I hour before retiring at night to facilitate the ex pectoration of secretions that would interfere with rest by stimulating violent coughing when the patient changes positions. It should also be done on arising in the morning to clear the lungs of secretions that have

accumulated overnight. Therapists teaching the pa tient postural drainage positions devised to drain the involved segments should keep in mind that this dis ease causes distortion and dilation of the bronchi; hence the traditional positions found in books may be of limited value in determining the precise segment of the lung that is the source of the secretions. If the in volvement is in the lower lobes, the patient should be placed in the Trendelenburg position and should be gradually rotated from lying on one side, to supine, to lying on the opposite side, and prone, if tolerated, while doing the FET and/or receiving percussion and vibration 5 to to minutes per segment over all sur faces of the lower lobe being treated. A similar proce dure may be followed while sitting if the upper lobes require drainage, but these segments rarely require drainage, since they usually drain during the course of the day while the individual is in a more or less erect position. Positions that are especially productive should be emphasized and drained longer. The patient should be instructed to do the postural drainage even if the treatment seems unproductive. Secretions may be mobilized during treatment and it can take several minutes for the remaining cilia to sweep the mucus far enough up the tracheobronchial tree to be expecto rated or swallowed. Pulmonary function tests of patients with localized bronchiectasis show few or no abnormalities. How ever, in more widespread disease, there is a reduction in the FEV I, maximum midexpiratory flow rate, max imal voluntary ventilation (MVV), diffusing capacity, and an increase in the residual volume (Luce, 1994). Hospitalized patients with bronchiectasis may be treated with postural drainage, percussion, vibration, and/or the forced expiratory technique, intravenous fluids, antibiotics, supplemental oxygen and other medications (Stoller and Wiedemann, 1990; Luce, 1994). Long-term medical management may include a broad-spectrum antibiotic taken orally 10 to 14 days per month, low-flow oxygen for hypoxemia, postural drainage, avoidance of bronchial irritants (e.g., cigarette smoke and air pollution) and other measurers. Some patients may have surgical resection if their area of involvement is quite limited or to con trol hemoptysis. It is most important that these pa tients drink large volumes of water each day (2 to


4

3 L) to keep their secretions thin so they can be ex


83

spondylitis can cause lung restriction. Obesity and as

pectorated more easily (unless fluid intake is limited

cites, by limiting diaphragmatic movement, can also

for cardiac reasons).

produce a restrictive defect. Pulmonary function tests generally show a de

Prognosis of bronchiectasis

creased vital capacity, inspiratory capacity, and total

Before the antibiotic era, the prognosis for individuals

lung capacity, whereas the residual volume can be

with bronchiectasis was poor. As might be expected,

normal or reduced. If the restriction is pulmonary in

infection was usually the precipitating cause of death.

origin, there is a reduction in the lung compliance

However, at the present time, the prognosis of patients

and the diffusing capacity.

with proper medical management is much improved

Many of these restrictive disorders are discussed

(Sanderson et aI, 1974; Ellis et ai, 1981). Most studies

in Chapter 5. Since obstructive lung diseases are en

show that about 75% of the patients have an improved

countered much more often than restrictive disorders,

symptom complex since diagnosis and lead relatively

they have been discussed in greater detail. The fol

normal lives. Cor pulmonale, a complication of dif

lowing is a brief examination of some of the restric

fuse, long-standing bronchiectasis, accounts for about

tive lung diseases.

50% of the deaths (Konietzki, Carton, and Leroy, 1969). Pneumonia and hemorrhage are less common causes of death. With modern therapy, only a few pa

Diffuse Interstitial Pulmonary Fibrosis

tients succumb to respiratory infections or their com

This disease is known as diffuse interstitial pul

plications. Few children who develop bronchiectasis

monary fibrosis (IPF) in the United States and cryp

live beyond their 40s. Repeated bronchopulmonary in

togenic fibrosing alveolitis in Europe (Reynolds, and

fections can contribute to worsening pulmonary func

Matthay, 1990). IPF represents a common histologic

tion and an earlier death. Before the antimicrobial era,

response to a wide variety of insults (Weg, 1982).

most patients with untreated, widespread, severe

Initially, some type of injury to the pulmonary

bronchiectasis died within 25 years. Today prognosis

parenchyma causes an influx of inflammatory and

for each individual depends on the extent of the dis

immune cells, resulting in a diffuse inflammatory

ease process at the time of diagnosis and on proper

process distal to the terminal bronchiole (alveolitis).

medical management. Patients with moderate, local

This can progress to subacute interstitial disease with

ized disease, if treated properly, may have a relatively

the presence of acute and chronic inflammatory ceUs.

normal life expectancy.

Chronic disease is manifest by thickened alveolar walls and progression to fibrosis. The etiologic factors of this condition are uncer

RESTRICTIVE lUNG DISEASE

tain. Similar conditions can be produced by certain

A restrictive disease is characterized by lungs that are

drugs or poisons and are found in patients with

prevented from expanding fully. Normally during in

rheumatoid arthritis and systemic sclerosis. There

spiration, the diaphragm descends, the dimension of

appears to be a genetic factor, since twins, siblings,

the chest increases laterally and anteriorly, and the

and other members of the same family have been re

lung tissue expands as it fills with air. Hence an ab

ported with diffuse interstitial pulmonary fibrosis.

normality in any of these areas can produce a restric

This condition has also been reported in a few indi

tive pattern. For example, a decrease in compliance

viduals with Raynaud's phenomenon, ulcerative col

or elasticity of the lung parenchyma, such as intersti

itis, and other diseases, but their exact relationship

tial fibrosis, sarcoidosis, pneumoconiosis, and sclero

remains unclear.

derma, can produce this defect. Pleural abnormalities

The most common early symptoms are fatigue,

such as pleural effusion (by direct compression) can

dyspnea on exertion, and a chronic unproductive

prevent the lungs from expanding fully. Thoracic

cough. As the disease progresses, the patient becomes

changes such as kyphoscoliosis and ankylosing

steadily more dyspneic and cyanotic. On auscultation,


84

PART I


one notes sharply crackling rales. Chest expansion is

Since a pattern of DIP is commonly seen along with

reduced and clubbing of the digits is often present.

usual interstitial fibrosis (UIP) or IPF, some believe

The chest x-ray usually indicates diffuse reticu lar markings, most prominent in the lower lung

that DIP likely represents an earlier and more re versible stage of IPF.

fields. Sometimes, a gallium citrate Ga 67 isotope

Cortiocosteroids are the mainstay of treatment for

scan of the lungs is conducted to assess the overall

IPF (Reynolds and Matthay, 1990). A trial of im

inflammation of the lung parenchyma (Line et ai,

munosuppressive therapy is almost a l ways pre

1978; Turner-Warwick and Haslam, 1987).

scribed for a period of time. Obj ective measures

Pulmonary function tests show a reduced vital ca

such as blood counts, erythrocyte sedimentation rate,

pacity and total lung capacity with no impaired flow

pulmonary function testing, particularly exercise

rates (Keogh and Crys tal, 1980; Reynolds and

tests with measurement of arterial oxygen desatura

Matthay, 1990). Compliance is markedly reduced to

tion and diffusing capacity BAL fluid analysis and

less than half of the predicted value. A reduced diffus

the patient's symptoms must demonstrate improve

ing capacity is the earliest and most consistent change.

ment or the medication should be discontinued. A

At first, the arterial Pa02 may be normal at rest but

composite clinical roentgenographic, physiological

may drop significantly with exercise. The Paco2 is re

score (CRP score) of eight variables has been devel

duced as a result of hyperventilation, and the pH is

oped that allows quantification of the clinical course

kept normal by renal compensation. Later the Pao2 is

and the re sponse to therapy in individual patients

markedly reduced because of the thickened alveolar

(Watters et ai, 1986). If effective, medications are

membrane and ventilation-perfusion mismatching.

usually continued for a year and then a decision is

Bronchoalveolar lavage (BAL) is often used to as

made about continuing or tapering the dosage.

sess the amount of inflanunation and the accumulation

Individuals who are not responsive to corticos

of immune effector cells and proteins in the alveoli

teroids may be placed on other immunosuppressive

(Crystal, et ai, 1981; Rudd, Halslam, and Turner-War

drugs such as cyclophosphamide, azathioprine, or

wick, 198]). The technique consists of wedging a

penicillamine (Turner-Warwick, 1987; Reynolds and

fiberoptic bronchoscope in a sublobar airway, then in

Matthay, 1990). Penicillamine is more effective in

fusing 20 to 50 ml aliquots of saline into the periph

patients with connective tissue diseases and intersti

eral airway, which are immediately aspirated by sy

tial fibrosis other than those with IPF.

ringe. A total of 150 to 300 ml is ins tilled and

Patients should stop smoking at once. Supplemen

recovered. The fluid and cells are analyzed (Reynolds,

tal oxygen is important with exercise as there is a

1987). High-intensity alveolitis is defined by 10% or

characteristic significant fall in arterial oxygen ten

more polymorphonuclear granulocytes (PMNs) in

sion ( Pa02) (Hammon a n d Mc C a f f ree,

BAL cell differential counts; low-intensity alveolitis

Reynolds and Matthay, 1990). Individuals that re

consists of 10% PMNs or less (Reynolds, 1986).

quire more than 4 L flow/min by nasal prongs may

1985;

Lung biopsies that demonstrate an abundance of

prefer direct administration of oxygen into the tra

inflammatory cells suggest early disease, whereas a

chea. In addition to supplying higher concentrations

prevalence of fibrosis is indicative of advanced dis

of oxygen to the lungs, many patients prefer the cos

ease. A distinct category of IPF has been described

metic effective of not wearing obvious nasal prongs.

and may be clinically useful (Liebow, Steer, and

Patients that have refractory disease limited to the

Billingsley, 1965). Desquamative interstitial pneu

lungs may be candidates for single or double lung trans

monitis (DIP) is characterized by an intraalveolar ac

plantation. There have been significant advances in the

cumulation of mononuclear cells, relatively intact

success of lung transplantation in recent years (Toronto

alveolar walls without destruction or fibrinous exu

Lung Transplant Group, 1988) (see Chapter 38).

dates (numerous inflammatory cells with little or no

Individuals with the subacute form described by

fibrosis). This pattern has correlated with a more be

Hamman and Rich usually die within 6 months

nign course and a better response to corticosteroids.

(Hamman, 1944). Patients with the chronic form,


4

Cardiopulmonary Pathophysiolog)'

85

treated with steroids, may survive for as long as 15

complex. Over time, it can eventually result in a form

years. Untreated, these patients most often die within

of interstitial pu lmonary fibrosis with honeycombed

I to 4 years. Cause of death is usually related to res

lung changes on chest x-ray and a restrictive pattern

piratory or heart failure, although an unexpected

on pulmonary function tests.

number have died from adenocarcinoma and undif ferentiated or alveolar cell carcinoma of the lung.

This disease is more common in women (Seder linic, Sicilian, and Gaensler, 1988). Their symptoms include an acute respiratory illness with fever, night sweats, weight loss, and dyspnea. It can be confused

Pulmonary Infiltrates With Eosinophilia

with tuberculosis, but these patients deteriorate when

Eosinophils are commonly present in lung tissue as

treated with antituberculosis drugs. This disease must

part of the body's cellular response to a variety of

also be differentiated from eosinophilic granuloma

agents and systemic immunologic diseases (Butter

and the desquamative form of idiopathic interstitial

worth and David, 1981). They are present in the air

pneumonitis. Dense infiltrates located in the periph

ways and lung tissue of patients with idiopathic pul

ery of the lung on chest x-ray provide an important

monary fibrosis. In interstitial lung disease that

clue. Often, a lung biopsy is necessary to confirm the

appears to have an allergic component (e.g., hypersen

diagnosis. Treatment with cortiocosteroids produces

sitivity pneumonitis, drug-induced lung syndromes,

a striking improvement in the patient's symptoms and

sarcoidosis) eosinophils are a minor component of tis

chest x-ray in just a few weeks.

sue reaction. However, in certain primary or systemic diseases, eosinophils can be the most conspicuous in

Eosinophilic granuloma

flammatory cell present in the lung. These conditions

Eosinophilic granuloma (or histiocytosis X) can ei

can be grouped t o g ether and referred to a s

ther be a unifocal disease effecting only the lungs or

eosinophilic syndromes (Crofton e t aI, 1952). Consid

a multifocal disease involving the bones of the skull,

erable overlapping exists among these syndromes as

mandible, vertebra, pelvis, ribs, and extremities

their etiologic factors and pathogenesis remains

(Groopman and Golde, J 981; Marcy and Reynolds, 1985). Lung involvement is characterized by an inter

poorly understood (Reynolds and Matthay, 1990).

stitial granuloma composed of moderately large, pale

Simple pulmonary eosinophilia

histiocytes and eosinophils, and arteriolitis with

This is a self-limiting disease with chest x-ray

eosinophils. The histiocytic process with eosinophils

demonstrating migratory, fleeting areas of pulmonary

then involves bronchioles, alveolar ducts, and alveo

infiltrates located in the periphery of the lungs along

lar septa, which results in their destruction. The pro

with minimal respiratory symptoms and blood

liferative endarteritis causes necrosis.

eosinophilia (Crofton et aI, 1952). Certain drugs such

This disease most commonly effects men in their

as sulfonamides have been implicated as a cause

30s or 40s. They usually have symptoms of fatigue,

(Reynolds and Matthay, 1990). This disease is also

malaise, weight loss, a nonproductive cough, dyspnea

referred to as Loeffler's pneumonia and the PIE syr

on exertion, and chest pain, sometimes related to a

drome (peripheral infiltrates with blood eosinophilia)

pneumothorax or rib lesions. The chest radiograph

(Crofton et aI, 1952). If the Jisease is related to an al

often indicates a diffuse micronodular and interstitial

lergic rcsponse LO microfilaria, human parasites (e.g.,

infiltrate initially involving the middle and lower

Ascaris lum.briocoides, Strongyloides stercoralis), or

lung fields. In more advanced disease, small cystic

cat and dog parasites (ascarids) that produce visceral

areas develop in the infiltrate, producing a honey

larva migrans, it is termed tropical eosinophilia.

comb pattern. Spontaneous pneumothorax is a com plication in approximately 25% of cases.

Prolonged pulmonary eosinophilia

The course of the disease varies (Reynolds and

As implied by the name, this disease is more chronic

Matthay, 1990). Spontaneous regression with residual

than the simple form, with a more severe symptom

symptoms may occur in 10% to 25% of cases. In


86

PART I


many patients, the disease stabilizes or "burns out,"

findings may include fine inspiratory rales, dullness to

leaving them with a moderate pulmonary impairment

percussion and, in the later stages, cyanosis and club

as a result of fibrosis, cystic lung changes and a re

bing. Pulmonary function studies usually show a de

strictive defect on pulmonary function tests. Dyspnea

creased vital capacity, functional residual capacity arid

on exertion is common. Some patients have persistent

diffusing capacity. Arterial blood gases indicate a low

bronchitis. Cortiocosteroids are not particularly effec

Pao2, especially during exercise, with normal Paco2,

tive. Treatment is mainly symptomatic, with judicious

and pH (Rogers et aI, 1978).

use of antibiotics and bronchodilators. Occasionally,

The treatment of choice for patients with moderate

progressive pulmonary disease leads to cor pulmonale

to severe dyspnea on exertion from alveolar pro

and respiratory failure.

teinosis is bronchial alveolar lavage (Rogers and Tatum, 1970; Rogers, Graunstein, and Shuman

1972). The patient is taken to the operating room

Pulmonary Alveolar Proteinosis

where, after general anesthesia and placement of a

Pulmonary alveolar proteinosis is a rare disease of

double-lumen tube (which isolates each lung), the pa

unknown origin, characterized by alveoli filled with

tient is turned in the lateral decubitus position with

lipid-rich "proteinaceous" material and no abnormal

the lung to be lavaged downward. The double-lumen

ity of the alveolar wall, interstitial spaces, conducting

tube enables the patient to be ventilated by the upper

airways or pleural surfaces. Most often it is found in

most lung while the lower lung is carefully filled with

men between the ages of 30 and SO, although it has

saline to the functional residual capacity. Then an ad

been reported in patients of all ages and both sexes.

ditional 300 to 500 ml saline are alternately allowed

The most common symptoms are progressive dysp nea and weight loss, with cough, hemoptysis and chest pain reported less frequently (Claypool, Rogers, and Matuschak, 1984). Chest x-ray reveals diffuse bilateral (commonly perihilar) opacities (Figure 4-10). Physical

FIGURE 4-10

FIGURE 4-11

Pulmonary alveolar proteinosis. PA chest film demonstrates

A patient with pulmonary alveolar proteinosis in the

an irregular, patchy, poorly defined confluence of acinar

operating room undergoing bronchial alveolar lavage of her

shadows which are symmetrical in both lower lung fields.

left lung. Percussion is done over the left lung as the saline

The appearance is very similar to pulmonary edema.

runs out, increasing the amount of proteinaceous material

(Courtesy of T. H. Johnson,

M.D.)

removed during this procedure.


4


87

1990). If the patient is assessed during

to mn into and out of the ung by gravitational flow.

and Matthay,

As the saline flows out, percussion is done over the

an acute episode of pulmonary hemorrhage, fine rales

lung being lavaged, and this grcatly increases the

and dullness to percussion are present on physical ex-

amount of proteinaceous material washed from the

amination. An enlarged liver, spleen, and lymph

lung (Figure

4-1 J). The effectiveness of mechanical

nodes may be noted on palpation in

20% to 25% of

percussion, manual vibration, and manual percussion

cases. The chest x-ray during acute episodes show

in removing the material from involved lungs has

'Dac naI consolidation for 2 to 3 days, then a reticular pattern identical to other interstitial diseases. The

been compared and manual percussion has been found to be superior (Hammon,

1983; Hammon ,/'

'-i

chest x-ray usually returns to normal in lO to

12 days.

1986; Hammon, McCaf1993). In this procedure, a patient is usually lavaged with 20 to 30 L saline and is

However, after recurrent episodes with hemosiderin

then taken to the recovery room and later back to his

dicate a decreased diffusing capacity, with or without

Freeman, and McCaffree,

free, and Cucchiara,

or her own room. After

2 or 3 days, the procedure is

repeated on the opposite lung.

deposited in the interstitial spaces, there is progres sive interstitial fibrosis .. Pulmonary function tests ina fall in the patient's resting Pa02. The hemorrhage is ordinarily confined to the pe-

Most patients have significant clinical improve

ripheral airspaces. Interestingly, massive blood loss

ment following bronchial alveolar lavage, and many

into lung tissue can occur without hemoptysis or no-

have an improvement in their chest x-rays (Claypool,

ticeable blood in the trachea or major bronchi

Rogers, and Matuschak,

1984). After lavage, for rea

(Reynolds and Matthay,

1990). Sputum samples of

sons that are unclear, the material may reaccumulate

BAL

slowly o r not at all. Some patients d o have sponta

macrophages. After recurrent episodes of hemoptysis,

neous remissions without undergoing lavage.

interstitial fibrosis is present in most cases.

Before bronchial alveolar lavage was done on these patients, almost all children with alveolar pro-

f l uid

may

c o n t ain

hemosi d e r i n-l a d e n

The prognosis of IPH is variable with death occurring somewhere between

2Y2 to 20 years after the

20% to 25% of the adults died

onset of symptoms. Permanent remissions may occur

or cor pulmonale. Some

5 years, usually because of respiratory failure 60% to 70% improved

treatment has been shown to effectively alter the out-

greatly or recovered. The effect that bronchial alveo

come of this disease.

teinosis died, and within

with or without corticosteroid administration. No

lar lavage has on the long-term outcome remains to be seen, but present results are encouraging (Clay pool, Rogers, and Matuschak,

1984).

Sarcoidosis Sarcoidosis is a granulomatous disorder of unknown origin that can effect multiple body systems (Mitchell

IdiopathiC Pulmonary Hemosiderosis

and Scadding,

1974). Typically, initial findings can

Idiopathic pulmonary hemosiderosis (IPH) is a dis

include bilateral hilar adenopathy, pulmonary infiltra

ease of unknown origin and is characterized by re

tion and skin or eye lesions (Sharma,

peated episodes of pulmonary hemorrhage, iron-defi

lungs are the organs most often involved and some

1977). The

ciency anemia, and in long-term patients, pulmonary

20% to 50% of these patients first seek medical atten

1962). IPH is

tion because of respiratory symptoms. It affects

insufficiency (Soergel and Sommers,

10 to 20 times more often than whites and

most commonly found in children under the age of

blacks

10. In children, it is found with equal frequency in

women twice as often as men. It usually occurs in the

both genders, but in adults, it is twice as common in

third or fourth decade of life. The intrathoracic changes can be classified into

men as it is women. This disease has an insidious onset. The patient

four stages (Siltzbach et aI,

1974; Weg, 1982). In the

has symptoms of weakness, anemia, pallor, lethargy,

first stage, the patient is asymptomatic, with the chest

and occasionally, a nonproductive cough (Reynolds

x-ray showing bilateral hilar adenopathy and right


88

PART I


FIGURE 4-12 A, Sarcoidosis in its first stage is manifested by bilateral hilar adenopathy. Usually there are no significant physical symptoms. B, Disseminated sarcoidosis (third stage) reveals widespread parenchymal changes with scarring. The hilar adenopathy is usually decreased. (Courtesy of T. H. Johnson, M.D.)

paratracheal adenopathy (Figure 4- J 2, A). In the second

the lungs and pleurae. The most common thoracic

stage a diffuse pulmonary infiltration is found along

complication of RA is pleurisy, with or without

with the bilateral hilar adenopathy. Interstitial infiltra

pleural effusions. Although RA occurs twice as often

tion or fibrosis, without hilar adenopathy, characterizes

in women, pleuritis has a striking predilection for men

the third stage (Figure 4-12, B). In the fourth stage, em

(Reynolds and Matthay, 1990). Pleural disease is one

physematous changes, cysts, and bullae are found.

manifestation of RA, occasionaJJy causing fibrothorax

I n 60% to 90% of t h e s e p a t i e n t s w i t h h i l a r

and restrictive lung disease that requires decortication.

adenopathy, the disease spontaneously regresses over

Interstitial lung disease, indicated by abnormal pul

a period of I to 2 years. About one third of the pa

monary function tests demonstrating a restrictive venti

tients with sarcoidosis involving the lungs also have a

latory impairment and a reduced ventilatory capacity, is

spontaneous regression, usually leaving some resid

evident in about 40% of RA patients (Frank et ai,

ual fibrosis. The remaining two thirds that have

1973). It is also more prevalent in men. The chest x-ray

chronic sarcoidosis have progressive pulmonary im

demonstrates diffuse interstitial infiltrates, especially in

pairment, along with a variable degree of involve

the lung bases. Pulmonary nodules, which are patho

ment of the heart, liver, spleen, lymph nodes, mus

logically identical to the subcutaneous nodules found in

cles, bones, and central nervous system (CNS).

RA, may also oceur and cavitate (Weg, 1982).

Most patients with sarcoidosis need no treatment.

C o al miners with RA may have chest x - rays

Corticosteroids, although controversial, are the most

demonstrating rounded densities that evolve rapidly

effective forms of therapy for patients with sarcoido

and undergo cavitation (Caplan's syndrome) in con

sis that requires treatment (DeRemee, 1977; Turner

trast to the massive fibrosis found in coal miners'

Warwick et ai, 1986).

pneumoconiosis (Caplan, 1953).

Rheumatoid Arthritis

SystemiC lupus Erythematosus (SlE)

Rheumatoid arthritis (RA) is a systemic disease that

Although systemic lupus erythematosus (SLE) is a

principally involves the joints but also often affects

systemic collagen vascular disease, some 50% to


4

90% of these patients have pleural or pulmonary in volvement (Hunninghake and Fauci, 1979). Pleuritic


89

group, progression results in death after several years. Women seem to have a poorer prognosis than men.

chest pain often signals polyserositis associated with SLE. Pleural effusions are a manifestation of poly serositis and are present in

40% to 60% of individuals

with SLE. Most often they are bilateral.

Atherosclerosis

Patients with pulmonary involvement present with dyspnea on exertion and cough productive of mucoid sputum (Weg,

CORONARY ARTERY DISEASE

1982). Rarely do SLE patients com

Pathophysiology To discuss CAD the process of atherosclerosis must

plain of supine dyspnea, which suggests diaphrag

first be described. Although the specific pathogenesis

matic paralysis or a diffuse myopathy of the di

of atherosclerosis is not known, it is hypothesized

aphragm (Gibson, Edmonds, and Hughes,

1977).

that the process is initiated by trauma to the intima of

The chest x-ray usually indicates patchy, nonspe

the arterial wall. The trauma may be related to vari

cific densities and/or basilar linear or platelike atelec

ous primary risk factors such as: high blood pressure

tasis. Pleural effusions and pulmonary infiltrates are

and cigarette smoking.

common, whereas diffuse interstitial fibrosis is rarely seen (Hunninghake and Fauci,

1979).

High blood pressure has been indicated as a poten tial trauma inducer, since increased pressure and turbu

Pulmonary function tests often indicate a restric

lence may damage the endothelial cells of the intima,

tive pattem with a decreased diffusing capacity and a

thus exposing the media to the circulation. The media, which is composed primarily of smooth muscle is

reduced arterial oxygen saturation.

thought to be the origin of the atherosclerotic lesion. Cigarette smoking has also been indicated as a po

Progressive SystemiC Sclerosis (Scleroderma)

tential trauma inducer. However, the hypothesized

Progressive systemic sclerosis (scleroderma) is a rare

mode of injury is different than that observed with in

disease that causes thickening and fibrosis of the con

creased blood pressure. Cigarette smoke is high in

nective tissue of mUltiple parts of the body with re

carbon monoxide and hydrocarbons that are carried

placement of many elements of the connective tissue

by the red blood cells and the plasma. It is thought

by colloidal collagen. The skin is most often in

that the hydrocarbons or carbon monoxide bind to the

volved, although the lungs, heart, kidney, bones, and

endothelial cells, causing damage and possibly death

other parts of the body can also be affected.

to these cells.

Approximately one half to two thirds of the pa

Once the media is sufficiently exposed to the circu

tients with progressive systemic sclerosis have pul

lation the process of atherosclerosis is initiated.

monary involvement (Reynolds and Matthay,

1990).

Platelets aggregate at the injury site and release sub

Many of these patients with pulmonary involve

stances that induce endothelial and smooth muscle

ment are asymptomatic, although symptoms can in

cell replication. It is at this site that fatty streaks and

clude weight loss, progressive dyspnea, low-grade

fibrous plaques are developed. The cause of fatty

fever, and cough (sometimes producing mucoid spu

streak development is that low-density lipoproteins

tum). Chest x-ray shows a characteristic fibrosis of the

(LDLs) deposit fat into the smooth muscle of the

mid and lower lung fields. Auscultation often reveals

media. Why this occurs is unknown, but apparently is

bibasilar rales. Pulmonary function tests reveal a re

related to the smooth muscle cell proliferation and perhaps increased need for energy. The initial fatty

strictive defect with impaired diffusion. D-penicil lamine is the best treatment for pul

streaks are generally only slightly raised and do not

monary involvement in patients with progressive sys

imperil circulation. However, when a fibrous plaque

temic sclerosis (DeClerk et ai,

1987).

develops, the characteristic impingement of the vessel

Prognosis of patients with only skin and joint in

lumen occurs. The plaque is somewhat hard and con

volvement is much better than for those that have in

sists of connective "scar-like" tissue, smooth muscle

volvement of the heart, lungs and kidneys. In the latter

and fat. Finally, the plaque may undergo calcification


90

PART I


or lead to hemorrhaging if the vessel wall necroses.

angina, the episodes are more frequent and the dura

The result is decreased blood flow (ischemia) and

tion of each event is usually greater than 15 min

oxygenation (hypoxia), or complete lack of blood

utes. In addition the intensity or the pain may be

flow and oxygen (anoxia) to the target organ.

more severe. Unstable angina is usually an indicator of CAD progression. Individuals with unstable

Risk factors

angina are at greater risk to have

As described above high blood pressure, cigarette

farction

a

myocardial in

(MI). Unstable angina is less responsive to

smoking and hyperlipidemia are direct or primary

treatment using rest and sublingual nitrates. Often

risk factors for causing atherosclerosis. Secondary

times, the individual must be hospitalized and

risk factors are age, gender, race, obesity, stress, and

treated with IV nitrates.

activity level. Several risk factors are modifiable and i n c l u d e: (I) h y pertension,

(2) h y pe r l i p idemia,

Variant angina

(3) smoking, (4) obesity, (5) stress level, and activity

Variant angina occurs while the individual is at rest,

level. It is interesting to note that the "big three" pri

usually during waking and often at the same time pe

mary risk factors are all modifiable by the individual.

riod. Exertion does not influence variant angina.

Reducing risk factors can reduce the probability of

However, the angina may benefit from rest and sub

CAD by five- to ten-fold (Ornish et aI, 1990).

lingual nitrates. Like unstable angina the pain is in tense and of longer duration and likely to lead to an

CLINICAL SYNDROMES ASSOCIATED WITH CAD

MI. In addition, arrhythmias are more likely to occur with an individual who has variant angina, as com pared with exertion related angina (i.e., stable and un

Angina Pectoris

stable). Stable and unstable angina are believed to be

Angina pectoris is defined as chest pain that is related

caused primari Iy by progressive arterial occlusion

to ischemia of the myocardium. However, the pain

and ischemia. It is believed that variant angina is

referred from ischemia may be in the left shoulder,

caused by a combination of occlusion and coronary

jaw, or between the shoulder blades. Angina can be

artery spasm. Therefore variant angina has been suc

classified as stable, unstable, or variant.

cessfully treated with calcium channel blockers.

Prognosis of angina

Stable angina Stable angina generally occurs during physical effort

Individuals do not die from angina. The progression

but may be related to stress. The individual is able to

of atherosclerosis of coronary arteries is a change

describe what type and intensity of activity causes the

from the clinical signs of angina to MI, which is dis

angina. Stable angina is characterized by substernal,

cussed on p. 91. However, even though there is no

usually nonradiating pain that lasts between 5 to 15

risk for mortality from angina, an individual's

minutes after the offending incident. Care would in

lifestyle can change drastically. People with angina

volve sublingual nitrates and cessation of the activity

may be fearful of being active and may deny that

causing the angina. Usually the angina subsides com

they are having exertion-related chest pain. Denial of

pletely with treatment. However, angina brought

CAD, depression and anger are common manifesta

about by emotional stress is more difficult to treat,

tion for individuals with angina, though it has rarely

since the stress cannot be stopped as easily as cessa

been studied (Beckham et ai, 1994). The result of

tion of exercise.

angina (diagnosed or undiagnosed and denied) can be depression and potentially further decline in physical

Unstable angina

activity. Although rest is an important aspect of treat

Unstable angina also occurs during physical exer

ment, it is well-documented that even low levels of

tion or psychological stress. The major difference

activity can modify several risk factors and arrest the

between stable and unstable angina is the frequency,

progression of the disease process (Niebauer et ai,

duration and intensity of the pain. In unstable

1995). Research is sti II underway to determine if


4

CAD is reversible when lifestyle adjustments are ini tiated (Ornish et ai, 1990; Schuler et ai, 1992).

Myocardial Infarction MI is defined as necrosis of a portion of the my ocardium. The death of the myocardium occurs as a result of ischemia and anoxia. The vessels affected are the right and left coronary arteries. The right coronary artery supplies portions of the inferior sec tion of the left ventricle and the posterior section. The left coronary artery branches and forms the cir cumflex and anterior descending arteries. The cir cumflex supplies the lateral portion of the left ventri cle, while the anterior descending artery supplies the anterior portion. In addition, the right coronary artery supplies the right atrium atrial-ventricular (AV) bundle and the right ventricle. The left coro nary artery supplies the left atrium and the primary portion of the conduction pathway. Generally, the clinical symptoms are similar to that of angina, with emphasis on extreme pressure as well as tightness over the sternum region. In addition, pain can radiate to the jaw, upper back, and shoulders (with left more frequent than right). MIs can be classified into categories by size, loca tion, and degree of myocardial wall involvement. The terms small and large are often used to describe MIs. However, degrees of complication are also used in conjunction with size. MIs can be described as un complicated and complicated based on size of the MI and recovery of the patient. Location indicates the portion of the heart involved and also what coronary artery or branch that is at fault. As described above, the general regions of the heart are anterior, posterior, lateral, and inferior. Finally, MIs are classified by the extent of the wall damage. A transmural infarct (or full wall) extends from the endocardi um to the epi cardium. There is the potential that only a small por tion of the ventricle wall is affected, such as just below the epicardium (subepicardial) and just below the endocardium (subendocardial).

Uncomplicated myocardial infarction An uncomplicated MI is described as a small infarc tion with no complications during recovery. UsuaUy the result is full recovery without a significant de

Cardiopulmonat'y Pathophysiology

91

crease in cardiac performance at rest and during mini mal to moderate activity (Cahalin, 1994). However the location and the extent of the MI is also critical. MIs located in the inferior portion of the heart are the least significant, and partial wall thickness is less sig nificant than a transmural MY. Treatment, The treatment for an uncomplicated MI is initially like the complicated MI, where the patient is cared for in the coronary care unit. The medical treat ment is designed to decrease myocardial work and oxygen demand. Therefore patients are on oxygen and administered vasodilators (nitroglycerin) to in crease myocardial blood flow and analgesics to help further reduce ischemic pain. In addition, to reduce contractility of the myocardium, calcium channel blockers or beta-blockers are administered. Finally, antiarrhythmia medication may be prescribed if an aberrant cardiac rhythm is present or is highly proba ble to occur. Since the course is uncomplicated, this means that a patient's stay in the coronary care unit may be only 2 to 3 days, with a total hospital stay of 7 to 10 days. Treatment following leU discharge is oriented toward increasing physical activity and in educating the patient and family in risk factor reduction. This process is described as cardiac rehabilitation Phase 1.

Complicated myocardial infarction A complicated MI is different from an uncomplicated case since the patient may have one, a combination, or all four of the following conditions/complications: (I) arrhythmia, (2) heart failure, (3) thrombosis, and (4) damage to heart structures.

Arrhythmias. Arrhythmias occur in 95% of all pa

tients with MIs. The type and severity of the arrhyth

mia is dependent on the extent of myocardial damage

and the location of the damage. As described earlier,

the uncomplicated MI patient usually has a small area

of the myocardium involved; thus the potential ar

rhythmias are less dangerous and occurrence is less

common. Arrythmias that are life-threatening include

(I) complete A V heart block, (2) ventricular paced arrhytlImia, and (3) ventricular tachycardia, including ventricular flutter and fibrillation. In these conditions, either the heart rate is too slow and thus cardiac out put is impaired, or the heart rate is too rapid with


92

PART I


poor stroke volume and ejection fraction, and again

considered a distinct possibility in all surgical, MI,

impaired cardiac output. Treatment of the above con

and gunshot patients.

ditions is immediate and requires drugs and poten

Heart wall or mural wall thromhosis can lead to an

tially, electrical shock (for flutter/fibrillation). Usu

emboli lodging in the brain, intestine, kidney, artery

ally, an artificial pacemaker is implanted once the

to the extremities, or any location in the systemic ar

patient is stabilized.

terial circulation. Usually mural thrombosis do not

Heart failure. Another complication following MI is

affect the pulmonary system, since even the smallest

heart failure. Heart failure is a condition where the

fragments are caught in capillary beds and do not

heart is weakened and is unable to produce a signifi

enter into the venous system.

cant cardiac output to meet the bodies need for oxy

Structural damage. The last complication is structural

gen, nutrition, and removal of waste products. When

damage to critical myocardial tissue that affects heart

the heart experiences ischemia the myocardium con

function. If conductant pathway (bundle branch) tis

tracts with less force, and conduction abnormalities

sue located primarily at the septum is damaged, ar

may alter the mechanics of the contraction. If an area

rhythmias result. In addition, papillary muscles that

of the heart is infarcted, the affected myocardium

assist in closing valves can be infarcted. The result of

does not contract, thus affecting overall cardiac out

improper valve function is decreased cardiac output.

put. Another type of heart failure not directly related

Besides these two critical tissues, if significant full

to ischemia and infarction is congestive heart failure

thickness damage occurs to the myocardial wall car

(CHF) (see Congestive Heart Failure, p.

000).

diac function is compromised. HeaIt waJJ damage can

Immediately post-MI, cardiac output is reduced

result in venlricular aneurysms or ventricular wall

significantly. However, the compensatory response is

rupture. Ventricular aneurysm or bulging of the weak

to increase sympathetic innervation, resulting in in

ened ventricular wall oecurs in transmural (full wall

creased heart rate and myocardial contractility. The

thickness) infarcts. Ventricular wal I rupture, which

result of this compensation is a cardiac output that

can occur acutely following transmural infarction, but

may approach normal resting values. However, if the

more often occurs in the first to second week post-MI

damage has been great, the kidneys compensate by

following an aneurysm is usually fatal. Therefore fol

retaining sodium and water in an attempt to improve

lowing a n MI, it is critical to determine i f an

circulatory volume and venous return. Depending on

aneurysm has occurred in the myocardium so that ap

the amount of myocardial tissue death, the individual

propriate surgical intervention can be performed.

may survive with resulting chronic congestive heart

Treatment. The treatment for a complicated MI is

failure through persistent fluid retention and hypoten

initiaJly like the uncomplicated MI, where the patient

40% of the left ventricle is in

is cared for in the coronary care unit. The medical

farcted, the result is usually cardiogenic shock fol

treatment once again is designed to decrease myocar

sion. If grcater than

lowed by death of the individual.

dial work and oxygen demand. Patients are on oxy

Thrombosis. Another complication is increased inci

gen and administered vasodilators (nitroglycerin) to

dence of thrombosis from deep leg veins and from

increase myocardial blood flow and analgesics to

the damaged heart itself. Thrombosis from deep leg

help further reduce ischemic pain. Myocardium cal

veins occurs from lower limb inactivity and circula

cium channel blockers or beta-blockers are adminis

tory stasis. This is a complication that can be ob

tered to reduce contractility. Finally, antiarrhythmia

served for all surgical patients. Emboli from deep leg

medication are prescribed if an aberrant cardiac

vein thrombus usually result in pulmonary complica

rhythm is present.

tions. If the emboli are large or numerous the result

Individuals with a complicated MI have a much

can be pulmonary tissue infarction and potentially

longer stay in the coronary care unit, and their total

death. The incidence of pulmonary emboli has grown

hospital stay time is greatly increased when com

less since early ambulation is now the rule rather than

pared with the uncomplicated MI patient (Topol,

the exception. However, a pulmonary embolj must be

1988). The time in coronary care and total hospital


4

stay are dependent on the complications that occur


93

of pressure and resistance the heart must overcome to

following the MI. Individuals with heart failure,

eject blood into the systemic circulation (afterload);

thrombolytic events, or structural damage requiring

and myocardial contractility, which is the amount of

surgery may be in the coronary care unit for more

force the left ventricle can apply to the blood within

than 2 weeks. Total hospital stay time for compli

the chamber. If any of these three variables are nega

cated MI patients may exceed 2 to 3 weeks (Topol,

tively affected then cardiac output is reduced. The

1988). However, treatment following ICU discharge

cause of heart failure is often decreased contractility.

is similar to that of the uncomplicated MI patient with the goal of increasing physical activity and in

Acute heart failure

educating the patient and family in risk factor reduc

If an individual has a significant myocardial infarc

tion. The major difference in Phase I cardiac rehabili

tion, the contractility and pumping ability of the heart

tation for the complicated versus the uncomplicated

is immediately reduced. The initial result is decreased

MI patient is the initial workload intensity, duration,

cardiac output and damming of blood in the veins.

and frequency (i.e., much lower workload for compli

The result is increased systemic venous pressure.

cated MI patient) (Rowe, 1989). Progression is also

This acute phase, which may reduce cardiac output to

usually a bit more conservative, since the probability

40% of normal resting values is short-lived lasting

for a recurrent MI event is much greater in the com

only a few seconds before the sympathetic nervous

plicated MI patient (Rowe, 1989).

system is stimulated, and the parasympathetics be come reciprocally inhibited. Sympathetic innervation

Prognosis post-myocardial infarction

causes an increase in contractility of viable myocar

Prognosis following MI is dependent on many fac

dial tissue, and the increase in cardiac output may be

tors. Usually cardiovascular peliormance is reduced,

100%. In addition, sympathetic innervation also in

unless the structural damage to the ventricle is minor

creases venous return, since the tone of blood vessels

(as in the case of many uncomplicated MI patients).

is increased. The result is increased systemic filling

The most important factor is extent of ventricular

pressure, and thus increased preload. The sympa

damage. However, with early detection of transmural

thetic reflex following MI becomes maximally opera

infarction and improvement in surgical intervention

tional within 30 seconds; therefore, besides some

and coronary care, acute post-MI deaths have been

pain and fainting, an individual with a mild MI may

reduced (Wenger, 1984). Other critical factors in

not know they just suffered a heart attack! The sym

clude remaining cardiac capacity and status of CAD.

pathetic response can continue with cardiac output

Even though CAD mortality has declined in the

maintained at an adequate level for quiet rest. How

United States, the disease remains the top cause of

ever, the individual may still have persistent ischemic

sudden death in adults.

pain that should be assessed as quickly as possible.

Chronic heart failure Cong.estive Heart Failure

Following a MI several physiological responses

CHF is characterized by the inability of the heart to

occur besides sympathetic reflex compensation. The

maintain adequate cardiac output. The etiologic fac

kidney begins to retain fluid almost immediately fol

tors of heart failure is usually from ischemia and MI

lowing an MI. The reasons appear to be related to de

secondary to CAD. For the heart to maintain an ap

creased glomerular pressure secondary to decreased

propriate amount of blood flow to the pulmonary and

cardiac output. In addition, there is an increase in

systemic circulation, heart rate and stroke volume

renin output and therefore an increase in angiotensin

must be adequate. Usually, stroke volume is the criti

production. Angiotensin promotes reabsorption of

cal factor to maintain adequate cardiac output. Stroke

water and salt from the renal tubules. The effect of

volume is a function of the amount of blood in the left

moderate fluid retention is an increase in blood vol

ventricle at the end of diastole (preload); the amount

ume and an increase in venous return. This once


94

PART I


again increases preload and thus cardiac output.

result can be deterioration of the myocardium. As the

However, if the MI was severe, the result can be ex

heart weakens, not only is systemic blood flow com

cess fluid retention. This results in detrimental effects

promised, but so is the coronary system. The area

of edema and overstretching of the heart, since blood

most affected is the suhendocardial region. As these cells become infarcted, the heart weakens further

volume and venous return is too great. In addition to increased kidney retention of fluid, a

until other regions of the heart also become ischemic

second process that is activated immediately follow

and infarcted. The entire process described from the

ing an MI is recovery of the myocardium. New col

acute to chronic stages is congestive heart failure.

lateral arteries are formed to supply the peripheral portions of the infarcted region. This revasculariza

Prognosis

tion can assist cells that were marginally active to be

The result without pharmaceutical or surgical inter

come fully functional again. In addition, the unaf

vention (heart transplantation) is death. Pharmaceuti

fected myocardial cells hypertrophy. The result in a

cal intervention to halt or to delay heart failure is

mild to moderate MI is a great improvement in car

with diuretics to reduce fluid levels and cardiac gly

diac function that takes 6 weeks to several months,

cosides such as digitalis to improve myocardial con

depending on extent of injury.

tractility. This pharmacological treatment is com

Compensated and decompensated heart failure

bined with modification of salt and fluid intake. Finally, in cases when the heart has not compensated

The final state following acute and chronic physio

well and the myocardium has sufficiently weakened

logical changes is called compensated heart failure.

so that cardiac output is minimal, then heart trans

In this state, the heart is able to pump blood effec

plant is the only recourse. Since organ donors are not

tively, but at a reduced cardiac output compared with

readily available, the number of individuals who need

the pre-MI condition. The individuals cardiac reserve

new hearts far outnumber the donor organs. As de

has been greatly reduced. The cardiac reserve can be

scribed previously, once the heart has had enough tis

defined as the difference between the maximum car

sue damage to greatly reduce the cardiac reserve, the

diac output attainable minus the resting cardiac out

prognosIs IS poor.

put. When an individual exercises or is active at a heavy load, they experience the same symptoms of acute heart failure, because the heart is unable to sup ply the cardiac output required of the activity. The

SUMMARY The first portion of the chapter has described the es

symptoms include rapid heart rate, pallor, and di

sential pathophysiological features of obstructive and

aphoresis. Decompensated failure occurs when the

restrictive lung diseases. Obstructive disorders are

heart is so severely damaged or weakened that nor

characterized by a decreased rate of airflow during

mal cardiac output can not be attained. The result is

expiration (as a result of increased airway resistance).

that cardiac output is not high enough to allow for

Restrictive disorders are conditions in which the in

normal renal function. Fluid continues to be accumu

spiratory capacity of the lungs is restricted to less

lated and the heart is stretched more and weakened

than the predicted normal.

further so that only moderate-to-Iow quantities of

A knowledge of the pathophysiology of pulmonary

blood can be pumped. With unilateral left ventricle

dysfunction assists the practitioner in relating the

heart failure the left ventricle fails, while the right

pathophysiology to the clinical signs and symptoms,

ventricle continues to pump vigorously. The result

and the appropriate treatment goals and interventions.

can be increased blood volume and pulmonary capil

The second portion of this chapter has described

lary pressure in the lungs. If this occurs, fluid begins

the essential pathophysiological features of CAD.

to filter into the interstitial spaces of the alveoli re

CAD results from atherosclerosis. The clinical syn

sulting in pulmonary edema and suffocation. Even if

dromes associated with CAD are angina, MI, and

the heart does not have a unilateral dysfunction the

heart failure.


4


95

A knowledge of the pathophysiology of CAD en

Caplan, A. (1953). Certain unusual radiological appearanccs in

ables the clinical practitioner to relate the etiologic

chest of coal miners suffering from rheumatoid arthritis. Tho

factors and pathophysiology to the clinical signs and symptoms exhibited by this patient population, and prescribes treatment.

rax

8, 29-37.

Claypool, W., Rogers, R.,

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clinical diagnosis, management and pathogenesis of pulmonary alveolar proteinosis (Phospholipidosis). Chesl 85,550-558. Cosio, M. (1978). The relations between structural changes in small airways and pulmonary function tests. New England

REVIEW QUESTIONS

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RespiralOry Diseases 3, I.


CHAPTER

5

Cardiopulmonary Manifestations of Systemic Conditions Elizabeth Dean

KEY TERMS

Connective tissue dysfunction

Malnutrition

Endocrine dysfunction

Musculoskeletal dysfunction

Gastrointestinal dysfunction

Neurological dysfunction

Hematologic dysfunction

Obesity

Hepatic dysfunction

Renal dysfunction

Immunological dysfunction

Systemic disease

INTRODUCTION

lowing: musculoskeletal, connective tissue, neurolog

This chapter describes the cardiopulmonary conse

ical, gastrointestinal (GJ), hepatic, renal, hematologi

quences of systemic diseases. Systemic diseases can

cal, endocrine, and immunological systems. Finally,

significantly affect oxygen transport either directly or

the cardiopulmonary manifestations of nutritional

in combination with primary cardiopulmonary dys

d i s o r de r s , s pecifically o b e sity a n d s t a r v a t i o n

function. Although these effects can be as cata

(anorexia nervosa) are presented.

strophic as those resulting from primary cardiopul

Physical therapists (PTs) need to be able to predict

monary dysfunction, their presentation is often subtle

the impact of systemic disease on oxygen transport

and may elude detection until significant impairment

for a given patient to maximize the efficacy of their

is apparent. The pulmonary and pleural complications

treatment prescriptions. Compl ications of systemic

of cardiac disease and the cardiac complications of

disease appear to be increasingly prevalent. This may

pulmonary disease are described first. Then the car

reflect both the aging of the population and improved

diopulmonary complications of conditions involving

survival and prognosis of patients with multisystem

the following systems are described including the fol-

disease. Furthermore, PTs are treating an increasing 99


100

PART 1


number of patients without refelTal, and thus may not

whether treatment should be modified to avert an in

be alerted by a referring practitioner to the presence

cident, or whether treatment is contraindicated all to

and significance of underlying systemic disease.

gether, is essential.

Lastly, physical therapy by definition physiologically

Oxygen transport can be significantly affected by

stresses the patient, therefore, the PTs must be able to

dysfunction in the major organ systems of the body

identify all factors that compromise or threaten oxy

(see box below). The pulmonary and pleural compli

gen transport so that treatment can be prescribed

cations of heart disease and the cardiac complications

most effectively with minimal risk.

of pulmonary disease are usually predictable and

A comprehensive understanding of all factors that

therefore most readily detected clinically. The car

affect or threaten oxygen transport is essential particu

diopulmonary complications of conditions affecting

larly in those patients who are not obviously at risk,

other organ systems, however, can be more subtle, if

that is, those without overt cardiopulmonary disease.

not more devastating.

The PT must be able to "red flag" a patient with an un derlying problem for which physical therapy may be contraindicated or an untoward treatment response an

CARDIAC CONDITIONS

ticipated. Alternatively, treatment may need to be

The pulmonary complications of heart disease and the

modified or treatment responses monitored more often.

cardiac complications of pulmonary disease are well

Specific diagnosis of those factors that contribute

known (Scharf and Cassidy, 1989). The mechanically

to or threaten cardiopulmonary and cardiovascular

inefficient heart disrupts the normal forward propul

dysfunction is, therefore, tantamount to efficacious

sion of deoxygenated and oxygenated blood to and

treatment across all physical therapy specialties. The

from the lungs. Because the right and left sides of the

capacity of the oxygen transport system needs to be

healt are in series, a problem on one side inevitably

established to ensure that it can adequately respond to

has some effect, that can lead to a problem on the

changes in metabolic demand, including those im

other side, thus the healt and lung should be thought

posed by physical therapy treatment. Even though

of as a single functioning unit. Disruption of the car

cardiopulmonary dysfunction may not be the primary

diopulmonary circuit leads to backlogging of blood

problem, identifying whether cardiopulmonary dys

and an increased volume of blood in the capacitance

function can limit a patient's response to treatment,

vessels, or the veins. Right heart failure contributes to increased central venous pressure (i.e., right atrial pressure) and if sufficiently severe, leads to peripheral edema in the dependent body parts. Because blood is not being forwarded to the lungs adequately, hypox

Systems and Systemic Conditions That Affect the Cardiopulmonary System and Oxygen Transport

emia can result. In turn, hypoxic vasoconstriction of the pulmonary circulation leads to increased pul monary vascular resistance, and hence, illcreased right

Cardiopulmonary system Musculoskeletal system Connective tissue conditions Collagen vascular conditions

ventricular afterload and work. Left heart failure can result in inadequate forward movement of blood through the left heart, resulting in backlogging in the

Neurological system

pulmonary circulation

Gastrointestinal system

edema. Pulmonary edema alters lung mechanics and

Hepatic system Renal system Hematological system

nd cardiogenic pulmonary

lymphatic drainage, and in turn, these effects con tribute to an increased risk of infection secondary to

Endocrine system

impaired macrophage function and bacterial growth.

Immunological system

Excess pulmonary fluid arollnd the alveolar capillary

Nutritional disorders

membrane creates a diffusion defect. If fluid accumu lation is extreme, backlogging may be transmitted to


5

Cardiopulmonary Manifestations of Systemic Conditions

101

the right side of the heart and to the periphery. Com

the circulation, fluid balance in the lung is dependent

parable to excess fluid in the lungs, backup of fluid in

on Starling'S forces, that is, hydrostatic and oncotic

the peripheral circulation can impair tissue perfusion.

pressures. In health, several liters of fluid are ab

Other cardiovascular conditions such as systemic hy

sorbed from the pleural space, thus when the balance

peltension increases systemic afterload, which in turn

of these forces is disrupted in disease, considerable

increases the work of the heart thereby reducing its

fluid can accumulate in the pleural space. Impaired

mechanical efficiency.

alveolar expansion from pleural effusions is of clini

Pulmonary function can be significantly altered in

cal concern. There is some evidence, however, to

cardiac disease (Bates, 1989). Left heart failure, for

support that small effusions displace rather than com

example, is associated with accumulation of fluid in

press the lung (Anthonisen and Martin, 1977).

the pulmonary interstitium. This leads to reduced cal iber of the airways and early airway closure, air trap ping and increased residual volume. The fluid can

PULMONARY CONDITIONS

produce reflex constriction of bronchial smooth mus

Lung disease can contribute to cardiac dysfunction in

cle leading to the syndrome of cardiac asthma. The

several ways. First, lung disease invariably threatens

combination of airway collapse and bronchoconstric

oxygen transport by its effects on respiratory me

tion decreases total lung capacity, flow rates and

chanics, and ventilation and peliusion matching. To

forced expiratory volumes. Ventilation and peliusion

compensate, the heart attempts to increase cardiac

abnormalities are also associated with cardiac dis

output which produces a corresponding increase in

ease. Ventilation of underperfused lung zones con

cardiac work. Overall, ventilation and oxygen trans

tributes to increased ventilatory dead space, and per

port is less efficient. Hypoxemia secondary to inade

fusion of underventilated lung zones leads to a right

quate ventilation and perfusion matching may predis

to left shunt. In left heart failure, airway resistance

pose the patient to cardiac dysrhythmias.

contributes to inhomogeneous ventilation and perfu

Pleural complications can arise from either heart

sion. The normal pattern of increased ventilation to

or lung disease. Both heart and lung function can be

the bases is reversed in left heart failure, that is, the

compromised by altered fluid balance of the pleurae.

apices of the lungs are better ventilated (James,

Fluid balance in the pleural space is comparable in

Cooper, White, and Wagner, 1971).

terms of its regulation to that in the alveolar space.

With progression of the pulmonary edema, the alve

Both are determined by Starling forces. Specifically,

oli become flooded resulting in reduced ventilation, and

hydrostatic pressure pushes fluid into these space

significant ventilation and perfusion mismatching. The

while oncotic pressure counters the effect of the hy

alveolar-arterial gradient (A-ao2 gradient) is then in

drostatic forces. The net effect of these filtration and

creased, diffusing capacity decreased, and arterial par

absorption forces is a minimal net filtration pressure.

tial pressure of oxygen (Pao2) decreased. Lung compli

When the balance of these forces is disrupted, heart

ance is inversely related to pulmonary artery pressures

and lung function can be threatened. Excessive fluid

and interstitial fluid accumulation (Saxton, Rabinowitz,

floods the space usually reflecting both excessive hy

Dexter, and Haynes, 1956). The net effect of these ab

drostatic pressure and diminished oncotic pressure.

normalities is both obstructive and restrictive patho

The lymphatic vessels become overwhelmed and are

physiologic patterns of lung dysfunction, that is, re

unable to keep the pleural space dry. Pleural fluid ac

duced forced expiratory volumes and vital capacity,

cumulates and either displaces lung tissue (smaJ]-to

and an overall increase in the work of breathing.

moderate effusions) or restricts opening of adjacent

Pleural effusions can result from heart disease, in

alveolar sacs, causing atelectasis (severe effusions)

particular, congestive heart failure (CHF). Changes in

(Brown, Zamel, and Aberman, 1978), and if suffi

intravascular pressures lead to transudative pleural ef

ciently severe, may restrict cardiac filling. Pleural

fusions and cardiac injury leads to exudative effu

fluid accumulation poses a unique threat to oxygen

sions. Comparable to fluid balance in other parts of

transport as a result of its direct physical effect on the


102

PART I


lungs, heart, or both, thus it warrants special atten tion by PTs. Pulmonary lymphatics control fluid balance within the lung parenchyma. Lymphatic vessels arise within the pleurae and not within the alveolar capillary space. They drain fluid from the interlobular septae and subpleural areas, to the hilar vessels and the pri mary tracheobronchial lymph nodes. Problems aris ing within the heart or lungs can contribute to imbal ances in the major lymphatic inflow and outflow channels. This contributes to fluid accumulation, stagnation, and physical compression of the my ocardium and lungs (Guyton, 1991).

Cardiopulmonary Manifestations of Musculoskeletal Conditions General Manifestations Reduced alveolar venti/atio" Altered respiratory mechanics Chest wall rigidity Reduced chest wall excursion

Impaired IIlucocilary tra"sport Airflow obstruction Pulmonary restriction Atelectasis Inspissated secretions

Both heart and lung disease can produce deleteri ous hematologic changes to compensate for hypox emia. Increases in the number of red blood cells raise the hematocrit and the viscosity of the blood. This

Increased work of breatllillg Inefficient breathing pattern

Illcreased work of tile Ileart

phenomenon increases the work of the heart further.

Inefticient breatbing pattern

In addition, viscous blood increases the probability of

Constrictive pericorditis

thromboemboli. This risk is superimposed on the ex isting risk of thromboemboli in hypoeffective hearts. A thorough understanding of the interrelationship of the heatt and lungs is essential for diagnosis and op timal management. In addition, the cardiopulmonary and cardiovascular manifestations of other primary

Reduced aerobic capacity Manifestations in Specific Conditions Rheumatoid arthritis Pleuritis with or without effusion Diffuse interstitial pneumonitis and tibrosis Pulmonary arteritis

organ systems must be recognized and anticipated par

Bronchiolitis

ticularly in patients with multisystem disease.

Pleural effusions

Ankylosi"g spondylitis

MUSCULOSKELETAL CONDITIONS

Upper lobe fibrobullous disease

Musculoskeletal conditions impact on cardiopul

Chest wall restriction

monary function secondary to their effects on muscle, in particular, the diaphragm, muscles of the chest wall, oropharynx, larynx and abdomen, and on bones and joints (e.g., althritis, ankylosing spondylitis, kyphosco

22). The cardiopulmonary manifestation of muscu

liosis, and the deformity secondary to neuromuscular

loskeletal conditions are summarized in the box above.

diseases and chronic lung diseases). Additional effects

The cardiopulmonary deficits associated with

are imposed by inactivity, (i.e., muscle wasting and in

musculoskeletal disorders of the chest wall include

creased joint rigidity). Increased joint rigidity limits

reduced lung volumes consistent with pulmonary re

the amount of physical activity a patient may pelform,

striction, reduced flow rates, reduced inspiratory and

which contributes to cardiopulmonary compromise, in

expiratory pressures, increased atelectasis, increased

addition to the local effect of increased chest wall

dynamic airway compression, ventilation and perfu

rigidity and compromised bucket-handle and pump

sion mismatching, inefficient breathing pattern, im

handle motions. The normal three-dimensional move

paired cough and gag reflexes, increased risk of aspi

ment of the chest wall and normal pulmonary circula

ration, increased risk of obstruction secondary to

tion and lymphatic function is compromised (Chapter

impaired mucociliary clearance, restricted mobility,


5


103

compression of mediastinal structures and heart, and

connective-tissue changes in the skin can lead to

impaired lymphatic drainage which depends on nor

chest wall restriction. The cardiopulmonary mani

mal expiratory and inspiratory cycles (Bates, 1989).

festations of connective tissue conditions are sum marized in the box below.

CONNECTIVE TISSUE CONDITIONS Connective tissue/virgule collagen vascular disor

NEUROLOGICAL CONDITIONS

ders (e.g., scleroderma and systemic lupus erythe

Cardiopulmonary consequences of neurological dis

matosus [SLE]), invariably affect the cardiopul

ease reflects the specific pathophysiologic mechanisms

1979).

involved (Griggs and Donohoe, 1982). There are three

Inflammation. and tissue injury can affect the air

basic patterns of pathology: (1) involvement of the

way, lung parenchyma, pulmonary vasculature,

central nervous system (CNS), (2) the peripheral ner

monary

system

(Bagg

and

Hughes,

pleurae, respiratory muscles, heart and pericardium.

vous system, and (3) the autonomic nervous system.

Shrinking lung syndrome associated with chronic

The cardiopulmonary manifestations of neurological

connective tissue changes is a feature of advanced

conditions are summarized in the box on p. 104.

disease and is characterized by a significant loss of alveolar surface area, diffusion capacity, and lung volumes. Fibrotic changes increase the elasticity of

Involvement of the CNS

the lung parenchyma and reduce lung compliance,

The primary centers for breathing control and control

thereby i n c r e a s i n g work of b r e a t h ing. T h e s e

of the heart emanate from the midbrain. The genera

changes are comparable t o those i n idiopathic pul

tor for breathing control produces a regular respira

monary fibrosis. Both the electrical conduction sys

tory rate through modulation of inspiratory and expi

tem of the heart and its mechanical behavior are ad

ratory inhibitory and excitatory neurons.

versely affected by systemic connective tissue

Activity of the central generator is affected by

changes (Goldman and Kotler, 1985). Furthermore,

arousal and the general alerting reaction of the reticu lar activating system. In addition, breathing control is influenced by the hypothalamus, the orbital cortex,

Cardiopulmonary Manifestations of Connective Tissue/Collagen Vascular Conditions General Manifestations Acute injury to the alveolar-capillary unit Alveolar hemorrhage

forebrain, and amygdala (Hitchcock and Leece, 1967). Insult to the CNS can result in cardiovascular re sponses that precipitate neurogenic pulmonary edema. Such responses include systemic hyperten sion, pulmonary hypertension, intracranial hyperten sion and bradycardia. The medulla is believed to me

Interstitial pneumonitis

diate the cardiovascular responses associated with

Interstitial pulmonary fibrosis

neurogenic pulmonary edema. Marked sympathetic

Pulmonary hypertension Respiratory muscle dysfunction Pulmonary edema Pulmonary infection Abnormal diffusing capacity

stimulation, catecholamine release, and vagotonia ap pear to precipitate neurogenic pulmonary edema and the resulting leaking of the alveolar capillary mem brane and alveolar flooding (Col ice, 1985). However,

Chest wall restriction

the possibility of a primary pulmonary endothelial

Manifestations in Scleroderma

permeability abnormality has been suggested (Peter

Restrictive ventilatory impairment Decreased diffusing capacity

son, Ross, and Brigham, 1983). Cortical disturbances may have a direct effect on

Diaphragmatic dysfunction

cardiopulmonary function. Among the most common

Gastroesophageal reflux and aspiration

disturbances seen clinically are cortical infarction and seizures. Hemispheric infarction can lead to


Cardiopulmonary Manifestations of Neurological Conditions General Manifestations

Impaired mucociliary transport Reduced mobility Cilia dyskinesia Incrcased mucus accumulation Reduced cough and gag reflexes Impaired airway protection Increased airway resistance Increased risk of airway obstmction Impaired glottic closure Increased risk of aspiration

Impaired alveolar velltilation Reduced lung volumes and capacities, as well as now rates Weakness of pharyngeal and laryngeal structures Respiratory muscle weakness Reduced respiratory muscle endurance

Illcreased work of breathing Reduced aerobic capacity and decollditiollillg Manifestations in Specific Conditions M"ltiple sclerosis Respiratory muscle weakness Impaired ventilation secondary to spasm Increased oxygen consumption secondary to spasm Increased oxygen consumplion secondary to impaired posture and gait Impaired gag and cough reflexes Ineffective cough

Cerebral palsy Increased oxygen consumption secondary to increased muscle tone Significantly reduced mobility and activity Impaired movement economy Impaired swallowing Impaircd saliva control Reduced gag and cough reflexes Impaired coordination of thoracic and abdominal motion dUling respiration Ineffective cough and airway clearance mechanisms

Stroke Reduced movement economy Spasticity and increased oxygen demands Flaccidity of respiratory muscles Impaired respiratory muscle strength Impaired pulmonary function Asymmetric chest wall Weak and ineffective cough

Parkillsoll's disease Increased oxygen consumption secondary to increased muscle tone Reduced movement economy Chest wall restriction and impaired pulmonary function Ineffective cough

104


5


contralateral weakness of the diaphragm and other

105

creased muscle tone, which correspondingly increases

respiratory musc les. E pi l e ptic seizures disrupt

basal and exercise oxygen consumption, resulting in

breathing, which causes hypoxemia, respiratory aci

increased oxygen demands. Even though the demands

dosis, and a metabolic acidosis secondary to extreme

are increased in this condition, oxygen delivery is

muscle contraction and lactate accumulation. The as

compromised. For example, thoracic deformity and

sociated increase in sympathetic stimulation can pre

spasm of the muscles of the chest wall and abdomen

cipitate cardiac dysrhythmias and pulmonary edema.

impair breathing pattern and its efficiency (Fullford

Demyelinating diseases such as multiple sclerosis

and Brown, 1976). The airways of patients with cere

result in progressive deterioration of neuromuscular

bral palsy are vulnerable because of poor gag, cough,

function. The muscles of respiration become increas

and swallowing reflexes. In addition, these patients

ingly involved, resulting in respiratory insufficiency

often have poor saliva control, which increases the

(Cooper, Trend, and Wiles, 1985). In addition, with

risk of aspiration further. Mental retardation (Bates,

increasing debility cardiopulmonary conditioning is

1989) often complicates the presentation of cerebral

reduced. Weakness of the pharyngeal musculature

palsy and prevents these patients from responding ad

contributes to loss of airway protection in addition to

equately to their hydration needs or being able to co

the loss of cough and gag reflexes. Aspiration is prob

operate with life-preserving treatments. These patients

lematic for these patients as the disease advances.

harbor numerous microorganisms, which adds further

Stroke patients may have central involvement that

to their general risk of infection.

affects cardiopulmonary regulation and function, in

Patients with Parkinson's disease also exhibit sig

cluding reduced electrical activity of the respiratory

nificant cardiopulmonary deficits (Mehta, Wright,

muscles, or peripheral involvement such that weak

and Kirby, 1978). Oxygen demand is increased com

ness, spasticity, impaired biomechanics, and gait di

mensurate with increased muscle tone.

rectly affect respiratory muscle function and chest

to the patients described above, patients with Parkin

waJl excursion (DeTroyer, De Beyl, and Thirion,

son's also have reduced cardiopulmonary condition

Comparable

1981). Abdominal muscle weakness contributes to

ing levels as a result of compromised agility and abil

impaired cough effectiveness. Pharyngeal weakness

ity to be independently mobile in many cases. These

contributes to sleep apnea in these patients. The com

patients also have a restrictive pattern of lung disease

mon clinical presentation of unilateral involvement

with most lung volumes and capacities being re

leads to a posture listing to the affected side when re

duced. Chest wall rigidity impairs the normal pump

cumbent, sitting and during ambulation. This posture

handle and bucket-handle movements, thus it reduces

impairs ventilation and chest wall expansion on the

breathing efficiency. The energy cost of breathing is

affected side. Abdominal muscle involvement di

correspondingly increased. Respiratory insufficiency

rectly affects intraabdominal pressure and the effi

of Parkinson's disease likely reflects an increase in

ciency of diaphragmatic descent during contraction,

tone of the respiratory muscles, chest wall rigidity, as

that is, should the abdominal muscles become flaccid

well as increased parasympathetic tone and resulting

the efficiency of diaphragmatic contraction is signifi

airway obstruction.

cantly reduced. Lung volumes and flow rates are re

Patients with a history of poliomyelitis with or

duced proportionately giving a restrictive pattern of

without cardiopulmonary complications at onset, may

lung function. Reduced activity and exercise around

exhibit pulmonary limitation several decades later

the time of the stroke contributes to reduced car

(Dean, Ross, Road, Courtenay, and Madill, 1991;

diopulmonary conditioning and capacity of the oxy

Steljes, Kryger, Kirk, and Millar, 1990). These indi

gen transport system. Finally, a high proportion of

viduals are at risk for developing respiratory insuffi

patients with strokes are hypertensive and older, a

ciency as a result of respiratory muscle weakness,

population with a higher prevalence of heart disease

chest wall deformity, minor infection and periods of

and atherosclerosis (Chimowitz and Mancini, 1991).

relative immobility, or secondary to medical inter

Cerebral palsy is associated with significantly in

ventions, (e.g., anesthesia, sedation).


106

PART I


Diseases and lesions involving the brainstem can

the larynx, pharynx, and tongue can lead to upper

lead to various abnormal breathing patterns. Some

airway obstruction and increased airway resistance,

common breathing aberrations are Cheyne-Stokes res

and interfere with maintaining a clear airway. Aspi

piration, central neurogenic hyperventilation, ap

ration is a common and serious problem associated

neustic breathing, and ataxic breathing. Cerebellar and

with impaired motor control of the larynx, pharynx,

basal ganglia lesions may produce respiratory muscle

and tongue.

discoordination and dyspnea (Hormia, 1957; Neu, Connolly, Schwertley, Ladwig, and Brody, 1967). Spinal cord lesions have a variable effect on car

Involvement of the Autonomic Nervous System

diopulmonary function depending on the level of the

Cardiopulmonary consequences of disorders of the

lesion. Cervical lesions result in a high mortality rate

autonomic nervous system have been documented. Of

as a result of cardiopulmonary complications. All

those diseases with an autonomic component, auto

lung volumes are diminished with the exception of

nomic neuropathies, diabetes, and alcoholism have

total lung capacity (TLC), which over time returns to

been the most studied. MUltiple system atrophy ac

normal; tidal volume (TV), which is usually pre

companies autonomic failure affecting multiple sys

served (10% of TLC); and residual volume (RV),

tems. Because of the anatomic proximity of the auto

which is significantly increased (Estenne and De

nomic, respiratory and hypnogenic neurons and the

Troyer, 1987; Fugl-Meyer, 1971). Quadriplegic pa

degeneration of these structures in this condition, dys

tients tend to have a greater diaphragmatic contribu

function of the respiratory control mechanisms paral

tion to tidal ventilation compared with healthy people

lels autonomic and somatic dysfunction. The respira

(Estenne and DeTroyer, 1985). In addition, these pa

tory dysrhythmias that are seen in multiple system

tients have impaired cough as a result of loss of in

atrophy include central, upper airway obstruction, ir

nervation and paresis of the diaphragm in some cases,

regular rate, rhythm, and amplitude of respiration with

and abdominal and intercostal muscles. The contribu

or without oxygen desaturation, transient uncoupling

tion of accessory muscle activity to ventilation varies

of the intercostal and diaphragmatic muscle activity,

considerably (McKinley, Auchincloss, Gilbert, and

prolonged periods of apnea, Cheyne-Stokes respira

Nicholas, 1969). In quadriplegia, with only the acces

tion, inspiratory gasps, and transient sudden respira

sory muscles and diaphragm spared, platypnea (in

tory arrest (Bannister, 1989).

creased dyspnea when upright) may occur (Dantzker,

Patients with diabetes and autonomic neuropathies

1991). In the upright position, the diaphragm is flat

exhibit variable effects on cardiopulmonary status.

tened and less efficient when moved downward by

Postural hypotension is a complication of diabetic au

reduced abdominal pressures.

tonomic neuropathy and efferent sympathetic vaso

Thoracic lesions tend to have less effect on pul

motor denervation. Norepinephrine levels are gener

monary function (vital capacity and forced expiratory

ally reduced in these patients. The splanchnic and

volumes in particular) than cervical lesions, and the

peripheral circulations fail to constrict in response to

significance of this effect is reduced as the level of

standing, thus cardiac output falls. The postural effect

the lesion is reduced. Lumbar lesions may have mini

is exacerbated by reduced cardiac acceleration in pa

mal or no effect on pulmonary function; however, in

tients with diabetes. Insulin has been associated with

volvement of the abdominal muscles may limit cough

cardiovascular effects, including reduced plasma vol

effectiveness.

ume, increased peripheral blood flow secondary to va sodilatation, and increased heart rate. In the presence

Involvement of the Peripheral Nervous System

of autonomic neuropathies, insulin can induce pos tural hypotension. Diabetic diarrhea secondary to ab

Disorders of the peripheral nervous system include

normal gut motility can contribute to fluid loss and its

those of the motor neuron, peripheral nerve, neuromus

sequelae. Cardiopulmonary changes associated with

cular junction and muscle. Neuromuscular disorders of

autonomic neuropathy secondary to diabetes include


5


107

altered ventilatory responses to hypoxia and hyper

been associated with inflammatory bowel disease;

capnia, altered respiratory pattern and apneic episodes

however, their occurrence is not related to the activity

during sleep, altered bronchial reactivity and impaired

or therapy. Biopsy specimens have shown basement

cough (Bannister, 1989; Montserrat et aI., 1985).

membrane thickening, thickening of the epithelium, and infiltration of the underlying connective tissue with inflammatory cells (Higenbottom, et aI., 1980).

GASTROINTESTINAL CONDITIONS

The pulmonary manifestations of pancreatitis are

The cardiopulmonary manifestations of GI dysfunc

among the most important sequelae of this disease.

tion are summarized in the box below. Inflammatory

Of the deaths that occur in the first week of hospital

bowel disease and pancreatitis are principal exam

ization, 60% are associated with respiratory failure

ples of GI dysfunction that affects on cardiopul

(Renner, Savage, Pantoja, and Renner, 1985). Prob

monary function. Aspiration is a significant cause of

lems include elevated hemidiaphragms particularly

morbidity and mortality in patients with GI dysfunc

on the right side, basal atelectasis, diffuse pulmonary

tion, thus it should be prevented or detected early.

infiltrates appearing more often on the right side than

The pathophysiology, management, and outcome de

the left side, pleural effusions on the left side more

pend on the nature of the aspirate. Several predispos

than the right side, and pneumonitis. These findings

ing factors produce aspiration pneumonia including a

are not specific for pancreatitis and are probably sec

decreased level of consciousness, disorders of pha

ondary to localized peritonitis, subphrenic collec

ryngeal and esophageal motility, altered anatomy,

tions, ascitis, pain, and abdominal distension. In

disorders of gastric and intestinal motility, and iatro

chronic pancreatitis, abdominal symptoms may be re

genic factors such as surgery, nasogastric (NG) intu

duced and thoracic symptoms such as dyspnea, chest

bation, and general anesthesia.

pain, and cough may predominate. Chronic effusions

Inflammatory bowel disease can lead to the fol

may result in pleural thickening.

lowing cardiopulmonary pathologies: vasculitis, fi brosis, granulomatous disease, and pulmonary throm boembolism. Bronchitis and bronchiectasis have also

LIVER CONDITIONS Both acute and chronic liver conditions can predis pose a patient to cardiopulmonary and cardiovascular complications (see the box, on p. 108, at left). Hepatic

Cardiopulmonary Manifestations

failure can lead to hypoxemia secondary to intrapul

of GI Conditions

monary vascular dilatation and noncardiogenic pul monary edema. Hepatopulmonary syndrome, hall

Risk of aspiration

marked by intrapulmonary vascular dilatation,

Gastroesophageal reflux

produces both diffusion and perfusion defects in the

Increased airway resistance

Bronchospasm Reduced lung volumes Elevated hemidiaphragms Compression atelectasis Arterial hypoxemia Alveolar capillary leak and V/Q mismatch

I

Alveolar hemolThagc and consolidation worsen shunt Increased pulmonary vascular resistance

lungs and is the principal reason for severe hypoxemia (Sherlock, 1988). The origin of pulmonary edema is secondary to hepatic encephalopathy and cerebral edema (Trewby, et aI., 1978). With respect to chronic liver conditions, car diopulmonary manifestations have been associated with cirrhosis of the liver and hepatitis. The most common pulmonary abnormalities associated with these conditions are intrapulmonary vascular dilata tion with and without shunt, pulmonary hypertension, airflow obstruction, chest wall deformity, pleural ef fusions, pancinar emphysema, pleuritis, bronchitis,


108

PART I




of Liver COllditions

of Rellal Conditions

Intra pulmonary vascular dilatation

Alveo lar hemorrhage

Pulmonary hype11ension

Airway ohstruction

Expiratory airflow obstruction

Reduced lung volumes

Chest wall deformity

Reduced diffusing capacity

Pleural effusions

Panacinar emphysema Pleuritis

of these patients, physical therapy warrants being es

Bronchitis Bronchiectasis

pecially aggressive given the course of the pul

Impaired hypoxic vasoconstriction

monary-renal syndromes and the potential for re

Interstitial pneumonitis

lapses and irreversible organ damage.

Pulmonary fibrosis

HEMATOLOGIC CONDITIONS bronchiectasis, hypoxic vasoconstriction, and intersti

Hematologic disorders that can manifest cardiopul

tial pneumonitis, fibrosis. Hypoxemia results from

monary symptoms include abnormalities of the fluid

shunting, ventilation and perfusion mismatching and

and cellular components of the blood, and coagu

diffusion abnormalities.

lopathies (Bromberg and Ross, 1988). Cardiopul

Pleural effusions and ascites interfere with di

monary manifestations of hematologic conditions are

aphragm function and present unique problems in the

summarized in (the box on p. 109). The primary un

patient with Ii ver disease. Rich lymphatic connec

derlying mechanisms by which these conditions dis

tions exist between the abdominal and thoracic cavi

rupt gas exchange include hemorrhage, infection,

ties. Because of the rich lymphatic supply of the

edema, anemia, fibrosis, and malignancies.

pleural space, ascitic fluid can flow into the pleural

Abnormalities related to red blood cells and their

space. This effect is enhanced during inspiration

ability to transport hemoglobin and oxygen may pro

when the intraabdominal pressure is relatively posi

duce signs resembling pulmonary pathology, (e.g.,

tive and the intrapleural space is negative (Crofts,

tachypnea, dyspnea, and cyanosis). Abnormalities of

1954).

the deformability of red blood cells alter blood viscos ity and pulmonary blood flow. The interstitium can be disrupted by such factors as hemorrhage and malig

RENAL CONDITIONS

nancies. Coagulopathies disrupt the normal hemosta

Cardiopulmonary complications can result from renal

sis and clotting mechanisms of the blood. Pulmonary

disease and the category of disorders referred to as pul

hemorrhage and hemoptysis are common sequelae.

monary-renal syndromes (see the box above, at right).

The most common causes of pulmonary hemolThage

(Rankin and Matthay, 1982; Matthay, Bromberg, and

include vitamin-K deficiency, hemophilia, hepatic

Putman, 1980). The pathophysiologic characteristics

failure, and disseminated intravascular coagulation.

of these disorders include alveolar hemorrhage, inter

Pharmacologic agents such as platelet inhibitors and

stitial and alveolar inflammation, and involvement of

anticoagulants can also result in pulmonary hemor

the pulmonary vasculature. Pulmonary function testing

rhage. Pulmonary thromboemboli are common events

may detect both obstructive and restrictive abnormali

with symptoms including pleuritic chest pain, dysp

ties as a result of bronchial complications, and inflam

nea, and hemoptysis. Of the erythrocyte disorders sickle cell anemia is

mation and hemorrhage respectively. In systemic illness, pathology of the lungs and

probably the most common. Acute chest infection

kidneys often coexist. Like the medical management

and thrombosis leading to pulmonary infarction may



5

109

pending on the amount of plasma protein, particularly

Cardiopulmonary Manifestations of Hematologic Conditions

albumin, fluid is retained or lost from the circulation. With reduced protein and oncotic pressure within the vasculature, more fluid is filtered out of the circula

General Cardiopulmonary Manifestations

tion into the interstitium. In catabolic states in which

Hemorrhage

protein is broken down in the body, more protein

Edema

leaks through the capillaries taking water with it, thus

Polycythemia

leading to edema.

Anemia Infection AbnonnaJities of the Fluid Portion of the Blood

ENDOCRINE CONDITIONS

Abnormal blood volume Abnormal tluid balance

Endocrine and metabolic disorders can be associated

(water excesses and

with cardiopulmonary complications (see the box on

deficits)

p. 110). (Civetta, Taylor, and Kirby, 1989; Guyton,

Abnormal electrolytes Abnormal plasma proteins

1991). Disorders of the thyroid gland, pancreas (dia

Abnormal procoagulants and anticoagulants

betes mellitus [DM]) and adrenal glands are such disor

Abnormal clotting times

ders that are often seen clinically. Thyroid hormone in

Abnormalities of the Cellular Portion

fluences the central drive to breathe and surfactant

of the Blood Abnormal red blood cell

synthesis. Hypothyroidism can lead to sleep apnea, pleural effusions secondary to altered capillary perme

COllnt

Abnormal red blood cells

ability, and pericardial effusions. Decreases in vital ca

Abnormal deformability of the red blood cells

pacity have also been reported secondary to muscle

Abnormal hemoglobin Abnormal oxyhemoglobin dissociation

weakness. Hypelthyroidism increases cellular oxidative

(e.g., carbon

monoxide poisoning)

metabolism (the metabolic rate) leading to an increase

Abnormal white blood cells and antibodies

in oxygen consumption and CO2 production, and an

Blood dyscmsias

overall increase in minute ventilation. Vital capacity, lung compliance, and diffusion capacity can be reduced. In addition, maximal inspiratory and expiratory pres sures can be reduced secondary to muscle weakness. Patients with diabetes are prone to aspiration and

occur with clinical symptoms such as fever, pleuritic

respiratory infections. Late complications of diabetic

chest pain, cough, and pulmonary infiltrates. The pul

neuropathy include renal failure, which may be accom

monary function of patients with sickle cell anemia is

panied by pleural effusions and pulmonary edema. Au

abnormal with reduced TLC, vital capacity, diffusing

tonomic neuropathy may affect vagal activity and air

capacity, arterial oxygen tensions, and reduced exer

way tone. Ischemic heart disease and cardiomyopathies

cise capacity (Femi-Pearse, Gazioglu, and Yu, 1970).

are common in patients with diabetes and may cause

The hematologic malignancy disorders that can af

CHF and cardiogenic pulmonary edema. Patients with

fect pulmonary function include the leukemias and

diabetes have been reported to have reduced sensitivity

Hodgkin's disease. The three primary mechanisms by

to inspiratory loading (O'Donnell, Friedman, Russo

which these disorders can affect pulmonary function

manno, and Rose, 1988), which may impair their sub

include direct infiltration, increased risk of oppor

jective responses to exercise.

tunistic infection and secondary effects of treatment, such as interstitial pneumonitis and fibrosis.

Adrenal insuffiCiency can also compromise oxy gen transport (Civetta, Taylor, and Kirby, 1989). Re

Disorders of plasma proteins can have significant

duced aerobic capacity results from symptoms of

effects on the Starling'S forces maintaining normal

weakness, fatigue, and associated muscle and joint

fluid balance within the tissue vascular beds. De

complaints. Orthostatic intolerance primarily reflects


110

PART I


Cardiopulmonary Manifestations of Endocrine Conditions

Thyroid DisOI'ders

reduced inotrophic capacity of the heart and reduced systemic vascular resistance.

IMMUNOLOGICAL CONDITIONS

Hypothyroidism

H ypornetabolic

Congenital and acquired defects in the immunologi

Fatigue and excessive sleep

cal status of the lung lead to cardiopulmonary dys

Reduced conditioning

function, including infection and inflammation. In

Decreased vital capacity econdary to muscle weakness

addition, patients who are immunodeficient have an increased risk of pulmonary malignancies (Shackle

Slecp apnea

ford and McAlister, (975).

Decreased heart rate Decreased cardiac output

Acquired immunodeficiency syndrome (AIDS),

Decreased blood volume

an example of a primary disorder of cell-mediated

Pleural effusions

immunity, has reached epidemic proportions over

Pericardial effusions

the past 20 years. This syndrome leads to lympho

Hyperthyroidism

cyte death. The most serious pulmonary infections

Hypermetabolic

associated with AIDS is Pneul110cystis carinii pneu

Decreased vital capacity and diffusing capacity Fluid loss (diarrhea)

monia (Murray, Felton, and Garay, 1984). The fact that the patient with the human immunodeficiency

Respiratory muscle weakness

virus (HIV) is more likely to have recurrent pneu

Fatigue and inability to sleep

monia suggests that the infecting organisms persist

Reduced conditioning

in the lung despite treatment (Shelhamer, et aI.,

Pancreatic Disorders (Diabetes)

1984). The clinical presentation includes diffuse

Pulmonary endothelial thickening

pulmonary infiltrates, cough, dyspnea, and hemopt

Reduced TLC

ysis. These patients can also have symptoms of

Reduced vital capacity and forced expiratory

upper airway obstruction.

volumes Reduced airway vagal tone Increased risk of aspiration

NUTRITIONAL DISORDERS

Possible reduced elastic recoil Impaired hypoxic and hypercapnic responses Impaired ventilatory response to exercise

The two most common nutritional disorders seen

Defective neutrophil production

Western countries are obesity, and anorexia nervosa,

Colonization with gram-negative hacilli

which is akin to starvation. Obesity contributes in sev

Pleural effusions and pulmonary edema with

eral ways to impaired oxygen transport (Alexander,

diabetic nephropathy Reduced sensitivity to increases in inspiratory resistive loading Accelerated atherosclerotic vascular and cardiac changes Increased ischemic heart disease

of the increased weight of adipose tissue over the tho are increased. In addition, large abdomens, and abdom inal contents impinge on diaphragmatic motion, and

Increased risk of infection

can restrict diaphragmatic descent. This can lead to

Adrenal Insufficiency

compression of the dependent lung fields. Recumbency

Orthostatic symptoms

Reduced aerobic capacity secondary to anorexia.

weakness and fatigue Impaired breathing mechanics secondary to GI symptoms

1985; Bates, (989). These include alveolar hypoventi lation and impaired Pao2 and gas exchange as a result racic cavity. Systemic and pulmonary blood pressures

Cardiomyopathy

Tendency to retain fluid

111

can induce respiratory insufficiency, that is positional respiratory failure. Obese individuals have a higher in cidence of snoring and obstructive sleep apnea sec ondary to weakness, and increased compliance of the postpharyngeal structures. In addition, these patients often have weak ineffectual coughs resulting from expi


5

Cardiopulmon ary Manifestations of Systemic Conditions

ratory muscle weakness and mechanical inefficiency of these muscles. Work of breathing is markedly in

111

SUMMARY This chapter described the cardiopulmonary conse

creased. Furthermore, in chronic cases, reactive pul

quences of systemic diseases. Oxygen transport, the

monary vasoconstriction in response to chronic hypox

purpose of the cardiopulmonary system, can be sig

emia contributes to right ventricular insufficiency and

nificantly affected by dysfunction in virtually all

increased work of the heart and cardiomegaly.

organ systems of the body. The pathophysiological

The major cardiopulmonary manifestations of

consequences of diseases of the following systems on

anorexia nervosa relate to generalized weakness and

oxygen transport were presented: cardiac, pulmonary,

reduced endurance of all muscles, including the res

musculoskeletal, connective tissue/collagen vascular,

piratory muscles. Cough effectively is correspond

neurological, gastrointestinal, hepatic, renal, hemato

ingly compromised. Oxygen transport reserve is min

logic, endocrine, and immunological systems. In ad

imal. Because of poor nutrition and fluid intake, the

dition, the cardiopulmonary manifestations of nutri

patient is at significant risk of anemia, fluid and elec

tional disorders, i ncl ud ing obesi ty and anorex i a

trolyte imbalances, and cardiac dysrhythmias (Wil

nervosa, were described.

son, et ai, 1991). Common manifestations of nutri tional disorders are summarized in the box below.

A knowledge of these effects is essential to the practice of physical therapy across all specialties in that the prevalence of systemic disease appears to be increasing. The p r esentation of cardiopul monary consequences of systemic disease is often

Cardiopulmonary Manifestations of Nutritional Disorders

subtle or obscured, and is associated with a poor

Obesity

management is essential.

prog nosis, thus early detection and appropriate PTs need to be able to distinguish diagnostically

Al v eolar hypov entilat io n

cardiopulmonary manifestations of systemic dis

Obstructive sleep apnea Reduced outward recoil of the chest wall

eases to appropriately identify indications for physi

Increased abdominal contents

cal therapy, contraindications, side effects, and un

Increased llIass of the abdominal wall

usual treatment responses. In addition, detailed

Reduced functional re sidua l capacity Reduced expiratory

reserve vol

assessment of the patient's problems ensures that

ume

Marked reductions lung volumes, arterial oxygen tension (Pao2) and saturation

(Sao2) in

recumbency

Basal airway closure and resul t ing decrease in Pao2 Marked pulmonary abnormalities during sleep

problems amenable to physical therapy are appro priately treated, and those that are not are referred back to a physician.

Reduced ventilatory responses to CO2 Cardiomegaly Rotation and horizontal position of the heart Axis deviation Reduced myocardial pumping efficiency Reduced aerobic conditioning and oxygen transport reserve capacity

REVIEW QUESTION •

Describe the cardiopulmonary manifestions of:

1. Musculoskeletal dysfunction 2. Connective tissue dysfunction 3. Neurological dysfunction

Starvation or Anorexia Nervosa

4. Hepatic dysfunction

Generalized weakness, debility, and l os s of

S.

cardiopulmonary co nd itioning Impaired mucociliary transport Ineffective cough Fluid and elect rolyte dis turbance s Cardiac dysrhythmias

Renal dysfunction

6. Hematologic dysfunction 7. Endocrine dysfunction 8. Obesity

9. Malnutrition (e.g. anorexia nervosa)

Respiratory musc le weak ness


112

PART I


Griggs, R.C., & Donohoe, K.M. (1982). Recognition and manage

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(1991). Harri

PART

II

Cardiopulmonary Assessment


Measurement and Documentation

Claire Peel

KEY TERMS

Documentation

Reliability

Measurement

Subjective assessment

Objective assessment

Validity

INTRODUCTION

surements that relate to the cardiovascular and pul

Measurement and documentation are critical com

monary systems is essential for quality patient care.

ponents of the process of providing patient care.

Documentation of the results of measurements,

Measurements form the basis for deciding treat

the interpretation of the results and the patient care

ment strategies and therefore influence patients' re

plan is important not only for reimbursement but

sponses to therapeutic interventions. Measurements

also to assure communication among health care

are also used during treatment sessions to deter

team members. Timely and appropriate sharing of

mine rate of progression and appropriateness of ex

information on physiological responses to activity is

ercise prescriptions. Typically, therapists make a

often critical for optimal medical management. Doc

series of measurements and in combination with the

umentation needs to be written clearly and concisely,

results of measurements made by other health care

and to include objective findings that will facilitate

professionals, form an impression of the client. The

efficient and continuous care from all members of

impression includes both physical and psychosocial

the health care team.

aspects. If parts of the impression are incorrect be

This chapter provides a discussion of types and

cause of inaccurate measurements, then the course

characteristics of measurements that are common to

of treatment may be misdirected. The result could

cardiopulmonary physical therapy, followed by a dis

be treatment that is either not effective or unsafe.

cussion of the process of selecting, performing, and

Consequently, knowledgc of the qualities of mea-

interpreting measurements. A discussion of the pur 117


118

PART II


poses and types of documentation follows, including

function into those with obstructive lung disease, re

suggestions for providing objective and outcome-ori

strictive lung disease, or a combination of both types

ented information.

of dysfunction. The categories are mutually exclusive, that is, all patients fit into one and only one category. The categories of a nominal measurement scale

CHARACTERISTICS OF MEASUREMENTS

are defined Llsing objective indicators that are univer

The purpose of performing a measurement is to as

sally understood. For example, the classification of

sess or evaluate a characteristic or attribute of an in

patients with heart failure could be based on the pri

dividual. The characteristic to be measured first must

mary cause for the development of the condition (see

be defined, and the purpose of performing each mea

the box below, at left). In each case, the cause could

surement must be clear. Therapists then can select the

be determined by diagnostic testing such as angiogra

most appropriate method of measurement given the

phy or echocardiography. Clear descriptions of the

available resources and their clinical skills.

criteria for inclusion in each category facilitate clini cians' agreement on the assignment of patients to cat egories. A high percentage of agreement indicates

levels or Types of Measurements

high interrater reliability.

Measurements can be described according to their type or level of measurement. There are four levels of

Ordinal

measurements which are nominal, ordinal, interval

Ordinal measurements are similar to nominal measure

1993). Recognizing

ments with the exception that the categories are or

the level of measurement aids in the understanding

dered or ranked. The categories in an ordinal scale in

and ratio (Rothstein, Echternach, and interpretation of the result.

dicate more or less of an attribute. The scale for rating angina is an example of an ordinal scale (Pollock,

Nominal

Willmore, and Fox,

Objects or people are often placed in categories ac

1978) (see the box below, at right).

Each category is defined and a rating of grade I angina

cording to specific characteristics. If the categories

is less than a rating of grade 4. In an ordinal scale, the

have no rank or order, then the measurement is consid

differences between consecutive ratings are not neces-

ered nominal. An example of a nominal measurement is the classification of patients with pulmonary dys-

Allgina Scale Grade I:

Commoll Causes for the Developmellt of Heart Failure

Light-The discomfort that is cstablished, but j ust established

Grade 2:

Light moderate---Discom forl from -

which one can be distracted by a

Myoca rd ial infarction (Mf) or ischemia

noncataclysmic evcnt; it can be "pain"

Cardiac arrhythmias

but usually is not

Renal insufficiency Grade 3:

Cardiomyopathy

Moderate-sever

Discomfort or pain

that prevents distraction by a beautiful

Heart valve abnormalities Pericardial effusion or myocarditis

woman. handsome man. television

Pulmonary embolism or pulmonary hypertension

show, or other consuming interest;

Spinal cord injury

o nl y a tornado, earthq uake or expl osio n can distract one from a grade 3 discomfort or pain

Congenital abnormalities

Aging Grade 4: From Cahalin, L. P. (1994). Cardiac muscle dysfunction. In Hille gass, E.

A., &

Sadowsky,

H.

of cardiopul WB Saunders.

S. (Eds.). Essentials

monary pulmonary physicaltiJerapy. Philadelphia:


Severe---Discomfort that is the most excruciating pain experienced or imaginable

6


119

sarily equal. The difference between grade 1 angina

sured using either an interval or a ratio scale. The

and grade 2 is not necessarily the same as between

Fahrenheit temperature scale assigns the zero point to

grade 3 and grade 4 angina. Consequently, if num

the temperature at which water freezes, whereas the

bers are assigned to categories, they can be used to

Kelvin scale assigns the zero point to an absence of

represent rank, but cannot be subjected to mathemati

heat. The Fahrenheit scale is an example of an inter

cal operations. Averaging angina scores is incorrect

val level of measurement, and the Kelvin scale is a

because by averaging, it is assumed that there are

ratio level of measurement. Measuring force production using an isokinetic dy

equal intervals between categories. Categorical measurements are considered ordinal

namometer is an example of an interval measurement

if being assigned to a specific category is considered

commonly used in physical therapy. Patients may be

"better than" or "worse than" another category. For

able to generate muscle tension and move an extrem

example, patients with angina could be classified as

ity, but register a score of zero because they cannot

having either stable or unstable angina. This mea

move as fast as the dynamometer. Interval measure

surement would be considered ordinal, because stable

ments can have negative values, and can be subjected

angina usually is considered a better condition to

to some arithmetic operations. Adding and subtracting

have compared with unstable angina (Hurst, 1990).

values is logical. A patient who generates 10 ft-lbs at one session and 20 ft-Ibs at the following session in

Ratio

creased their torque production by 10 ft-Ibs. Interval

Ratio measurements have scales with units that are

values cannot be subjected to division or multiplica

equal in size, and have a zero point that indicates ab

tion. It cannot be stated that the patient generated

sence of the attribute that is being measured. Exam

twice as much torque on the second session compared

ples of ratio measurements that are used in cardiopul

with the first session because it cannot be assumed

monary physical therapy include vital capacity,

that a reading of zero indicated no torque production.

cardiac output, and oxygen consumption. Ratio mea surements are always positive values, and can be sub jected to all arithmetic operations. For example, an

Reliability

aerobic capacity of 4 Llmin is twice as great as an

Reliability is defined as the consistency or repro

aerobic capacity of 2 Llmin.

ducibility of a measurement. Ideally, if attempting to

When deciding if a measurement is ratio level or. not, the attribute that is being measured is defined.

measure a specific attribute, the value of the measure ment should change only when the attlibute changes.

If the zero point indicates absence of the attribute,

However, all measurements have some element of

then the scale would be considered ratio. For exam

error that contributes to the variability of the measure

ple, cardiac output can be defined as the amount of

ment. When the error is relatively high, the value of

blood in liters ejected from the left ventricle over a

the measurement can change, even though the attribute

I -minute period. A measurement of zero cardiac

has not changed. Believing that a change occurred

output would be absence of the characteristic, or no

when it did not could result in an inaccurate clinical

blood ejected from the left ventricle.

decision related to treatment planning or progression. Many factors contribute to variability in the results

Interval

of measurements. The characteristic being measured

Measurements that are at interval level have units on

may demonstrate a certain degree of variability. Both

a scale with equal distance between consecutive mea

blood pressure and heart rate vary depending on both

surements. Interval measurements are differentiated

mental and physical factors such as body position,

from ratio measurements, because the zero point is

hydration level, anxiety and time of day. For these at

arbitrary rather than absolute. An arbitrary zero point

tributes, multiple measurements often are used to

is one that does not mean an absence of the character

provide the best estimate of the patient's true heart

istic that is being measured. Temperature can be mea

rate and blood pressure.


120

PART II


Another factor that contributes to the variability of a

ment must possess a certain degree of validity. Mea

measurement is changes in the testing instrument.

surements can be reliable but not valid. For example,

Testing instruments may vary in their readings because

measurements made using bioelectrical impedance

of changes in environmental conditions or malfunction

analyses have been shown to be valid for the estima

of parts of the instrument. Instruments should be cali

tion of total body water, but uncertainty exists as to the

brated, that is, compared with a known standard, on a

validity of estimates of percent body fat made with this

regular basis to assure accuracy of the readings. Some

device (Kusher and Schoeller,

instruments are relatively easy to calibrate. For exam

1986).

There are various types of validity. Of importance

ple, values obtained using aneroid blood pressure de

in clinical practice are concurTent, predictive, and pre

vices can easily be compared with values obtained

scriptive validity. Concurrent validity is when a mea

using mercury manometers. Values obtained using ei

surement accurately reflects measurements made with

ther palpation or a heart rate monitor can be compared

an accepted standard. Comparing bioelectrical imped

with values obtained from BCG recordings. The mer

ance measurements for estimating percent body fat

cury manometer and the electrocardiograph (BCG)

with estimates made from hydrostatic weighing is an

would be considered the standard method of measure

example of determ.ining conCUITent validity. In this ex

ment. Other devices, such as cycle ergometers, are

ample, hydrostatic weighing would be considered the

more difficult to calibrate, and the usual approach is to

"gold" or accepted standard. Measurements with pre

rely on the manufacturer's specifications as to the ac

dictive validity can be used to estimate the probability

curacy of the work rate readings.

of occurrence of a future event. Screening tests often

A third factor contributing to measurement vari

involve measurements that are used to predict future

ability is differences in the methods that therapists

events. For example, by identifying people with risk

use to make measurements. If a result is consistent

factors for coronary artery disease (CAD),

when one therapist repeats a measurement, then the

is made that the likelihood of developing CAD is

a

prediction

measurement is said to have high intrarater reliabil

higher than normal. Measurements with prescriptive

ity. Measurements that are consistent when multiple

validity provide a guide to the direction of treatment.

therapists perform the measurement under the same

The categorical measurement of determining a per

conditions are said to have high interrater reliability.

son's risk for a future coronary event is a measurement

Often, measurements have high interrater reliability,

that would need to have predictive validity. By classi

but lower intrarater reliability because therapists vary

fying patients into high vs. low risk categories based

in the specific methods of making the measurement.

on the results of a diagnostic exercise test, the inten

For example, a slight variation in the anatomical site

sity, and rate of progression of treatment is determined.

used for measuring skinfold thickness can produce

The accuracy of various types of exercise tests

relatively large differences in percent fat estimates

often is described by reporting sensitivity and speci

1971). Interrater relia

ficity. Sensitivity is the ability of a test to identify in

(Ruiz, Colley, and Hamilton,

bility is important in clinical settings where a patient

dividuals who are "positive," or who have the charac

may be evaluated and treated by more than one thera

teristic that is being measured. Specificity is the

pist. If the interrater reliability of a measurement is

ability of a test to identify individuals who are "nega

low, then changes in the patient over time may not be

tive," or who do not have the characteristic. If a test

accurately reflected.

produces a high number of "false positive" results, then the sensitivity will be low. A false positive result means that the test result was positive but the charac

Validity

teristic was absent. Young women often have posi

Valid measurements are those that provide meaningful

tive stress test results but do not have CAD. The con

information and that accurately reflect the characteris

sequence of a false positive test result could be

tic for which the measurement is intended. For a mea

unnecessary treatment. A high number of "false neg

surement to be useful in a clinical setting, the measure

ative" results would produce a low specificity. A


6


121

false negative result would be a negative test result,

measurement, subjective measurements usually have

even though the disease or characteristic is present.

lower interrater reliability compared to objective mea

The consequence of a false negative test result is not

surements (Rothstein and Echtemach, 1993). Objective measurements are not affected by the per

receiving treatment when it is indicated.

son performing the measurement, that is, these mea surements do not involve judgement of the measurer.

Objective and Subjective Measurements

Heart rate measured by a computerized ECG system is

Measurements vary in degree of subjectivity vs. objec

an example of an objective measurement. Other exam

tivity. Subjective measurements are those that are af

ples include measurement of blood pressure using an

fected in some way by the person taking the measure

intraarterial catheter or oxygen consumption using a

ment, that is, the measurer must make a judgment as to

metabolic system. Objective measurements are not nec

the value assigned. The assessment of a patient's

essarily accurate, but usually have high intelTater relia

breath sounds is influenced by many factors including

bility (Rothstein, and Echtemach, 1993).

the therapist's choice of terminology for describing the

Most measurements cannot be classified as either

findings, their perception of normal breath sounds, and

objective or subjective. The quality of a measurement

their hearing acuity. The grading of functional skills

can be placed on a continuum based on the degree of

may be influenced by the therapist's interpretation of

reliability, as shown in Figure 6-\. The attribute or

what constitutes minimal vs. moderate assistance. Be

characteristic that is being measured also can be

cause of the influence of the person performing the

viewed as a subjective o r objective phenomena

Quality of the Measurement

Subjective

Objective

o

100 00

Phenomena Being Measured

Objective SO Reliability Continuum

Subjective o

100

SS

OS

FIGURE 6-1

Illustration of the relationship between the quality of a measurement as being subjective or objective, and the phenomenon being measured. The scales indicate that the objectivity of a measurement, or reliability, lies along a continuum. For example, a subjective phenomenon may be measured subjectively (subjective sign [SS]) or objectively (objective sign [OS]). (From Rothstein 1M: On defining subjective and objective measurements. Phys Ther 69:577-579, 1989.)


122

PART II


(Rothstein, 1989). A subjective attribute such as pain

stage post-MI could provide information to formulate

can be measured in either a subjective manner with a

an exercise prescription. However, the risks of per

low degree of reliability, or in an objective manner

forming this procedure at this time in the recovery

with a high degree of reliability.

period may outweigh the benefits.

SELECTING MEASUREMENTS

PERFORMING MEASUREMENTS

At the initial session with a client, how do therapists

When performing mcasurements, care must be

decide on the measurements to be performed? And

taken to use procedures that can be replicated for

what additional measurements need to be peltormed

future comparisons. Time must be taken to ensure

during the course of treatment and at follow-up evalu

that conditions are optimal and that the patient is

ations? Many factors influence the choice of the thera

informed of his or her part in the activity. For ex

pist, including information obtained from the medical

ample, measuring blood pressure in a noisy treat

record and the patient interview, and knowledge of

ment area immediately when the patient arrives for

available treatment options. Therapists also must

an appointment may not provide an accurate mea

strive for efficiency and not repeat tests that have been

surement of resting or baseline bJood pressure.

performed by other health care professionals. Charac

Documenting the conditions in which a measure

teristics or qualities of measurements, such as reliabil

ment was made also is important. Conditions may

ity and validity also influence the therapist's decision.

include, but are not limited to, time of day, room

Medical and personal information about the client will be a plimary factor guiding the selection of mea

temperature, recent activities performed by the pa tient, and type of measuring device.

surements. For example, appropriate measurements

Measurements should be made with an objective

differ for a patient with an acute MI vs. a patient who

and open mind, that is, without anticipating the result of

is 3 weeks post-MI. Other factors to consider include

the measurement. A measurement that is approached

the size of the infarction and associated complications

with a preconceived idea of the outcome may be af

such as an-hythmias, heart failure, or angina. Informa

fected by the therapist's expectations. Having confi

tion collected during the patient interview also may

dence in the results of one's measurements is impor

guide the selection. For example, for patients who dis

tant, and is developed as clinical skills are developed.

play anxiety when walking on a treadmill is discussed,

In clinics where more than one therapist is likely

another mode of exercise may be more appropriate.

to evaluate or treat a patient, written procedures for

Measurements need to be selected that are appropriate

performing measurements are needed. Therapists also

to the specific pathology, the severity of the condition,

need to review the written procedures on a regular

and other characteristics unique to the patient.

basis and practice performing the measurements as a

Another important factor to consider in selecting

group. Practicing together is especially important for

measurements is the application of the information.

therapists who are new to the clinic. The interrater re

Every measurement should contribute to the deci

liability for commonly used measurements then can

sions made by the therapist on the course and pro

be determined. If the reliability is low, the written

gression of treatment. Measurements that do not con

procedures may need to be revised to assure optimal

tribute to the assessment of the patient result in an

consistency of measurement.

inefficient use of the therapist's time and add unnec essary costs to medical care. Another factor that i nf! uences the selection of

INTERPRETING MEASUREMENTS

measurements is the risk-benefit ratio. How do risks

Interpreting the results of measurements often is a

of conducting a test or measurement relate to the

difficult task. Usually patients' problems are under

value of the information gained? Subjecting a patient

stood not by reviewing the results of a single mea

to a symptom-limited exercise test during the acute

surement, but by viewing the relationships between


6

the results of several measurements. For example,


123

and viewed in the context of the patient's personal

the finding that blood pressure does not increase

goals. Therapists develop a picture of the severity of the

with activity by itself may not be considered abnor

cardiopulmonary condition, the stage of recovery, and

mal, if the activity level is low and the patient is tak

the presence of coexisting conditions. A treatment plan

ing a beta receptor antagonist medication. The find

is developed based on the composite of findings. The

ing of no increase in blood pressure with signs and

plan is implemented and is continuously checked for

symptoms of exercise intolerance during moderate

appropriate direction by measurements made during

level activity in another patient may be indicative of

treatment sessions. Because of the progressive nature of many of the conditions that affect the cardiovascular

inadequate cardiac output. A knowledge of what is "normal" is important to be able to interpret the results of tests. For some mea

and pulmonary systems, each treatment session can be viewed as a reassessment.

surements, normal values are well-defined. Measure ments of resting blood pressure, cholesterol, and blood glucose have defined categories of normal,

PURPOSES OF DOCUMENTATION

borderline, and elevated. For other measurements,

To be useful, measurements need to be recorded or

population normative standards are not well-defined.

documented in a concise and organized manner.

For example, what is the normal increase in heart rate

Measurements that remain in the mind of the evalua

when walking at 3.5 mph on a level surt'ace? Values

tor often are forgotten or not remembered accurately.

for individuals differ, depending on age, medications,

Documentation is becoming more important to assist

fitness level, and walking efficiency. Results need to

and to maximize reimbursement, as well as to facili

be interpreted by considering these factors and patho

tate efficiency of care through communication be

logical conditions if present. Each individual has

tween health care professionals.

their own "normal" or usual response, and variations

Documentation includes information about evalua tive findings, the assessment of the patient's condi

from this value could be considered abnormal. Interpreting the results of tests is similar to putting the pieces of a puzzle together to create a picture of the patient and their limitations. Information is col

tion, and the plan for future care. Reasons for docu mentation include the following: I. To provide information for other therapists, as

lected from several sources, including the medical

sistants, or aides who may evaluate and/or treat

record, patient interview and physical therapy evalua

the client.

tion. Measurements performed and interpreted by other health care professionals can be obtained from

2. To provide data for comparison for follow-up

visits.

the medical record and include chest x-ray, blood

3. To provide data to determine treatment effec

analyses, and echocardiography. During an interview,

tiveness and efficiency through collection of in

the patient reports information about his cunent and

formation on the results or outcomes of various

past medical problems. It is important to be sensitive to the patient's feelings about his condition, noting

types of care. 4. To assist therapists in organizing findings to fa

his stage of emotional recovery. Detecting attitudes

cilitate logical decisions on the treatment ap

related to changing lifestyle habits also is important.

proach and overall care plan.

After the interview, the therapist should have a sense of the patient as a person and begin to plan a strategy for optimizing his or her physical function. Measurements made during the physical examina

TYPES OF DOCUMENTATION Systems for documenting information vary between

tion may include physiological responses to activity,

facilities. In acute care hospitals, physical therapy

breathing patterns, ventilatory capacity, and breath

notes may be included as a part of the patient's

sounds. The results of these measurements are inte

comprehensive medical record. In other facilities

grated with results collected during the chart review

such as private practice clinics the patient's record


124

PART II


may consist of physical therapy notes and medical

ambulation," and "abnormal tone." Written definitions

information that is relative to the physical therapy

of commonly used terms that include examples of

care plan. Whatever the system, notes can be classi

characteristics that illustrate the definition can help to

fied according to the timing and purpose of the doc

decrease confusion.

umentation, using the following categories:

Notes also need to clearly demonstrate the need

I. Initial evaluation, assessment, and plan

for professional skills if a physical therapist is per

2. Interim or progress notes

forming the evaluation and/or treatment. Activities

3. Discharge notes

that can be performed by physical therapists assis

4. Follow-up or reevaluation notes

tants, aides, nursing personnel or family members

The initial note usually is the longest, containing in

need to be delegated to the appropriate individual. In

formation on the reason for referral, other medical

addition, patients can be instructed in those activities

conditions and information that could affect physical

in which they can pelform independently.

therapy management, data collected during the pa

Another time in which documentation is essential

tient interview and physical examination, an assess

is when an unusual or adverse event occurs. For ex

ment or interpretation of the findings and the care

ample, abnormal responses to activity that may ap

plan. Interim or progress notes record short-term

pear relatively benign are important to record. Abnor

changes in the patient's status, and typically are writ

mal responses may include dizziness, anginal or

ten on a daily or weekly basis. The discharge note

musculoskeletal pain, or arrhythmias. An unusually

records the specific outcomes of treatment, the plan

high or low heart rate or blood pressure response also

for discharge, including home program, and the plan

should be noted. Combined with findings noted by

for follow-up. At follow-up visits, a note is written to

the patient or other health care professionals, these

assess changes since the time of discharge and plans

results may indicate significant changes in the pa

for additional treatment.

tient's cardiopulmonary status. The organization of documentation varies be tween facilities. Many facilities use the SOAP (sub

GENERAL GUIDELINES FOR CONTENT

jective, objective, assessment, plan) format (Ketten

AND ORGANIZATION

bach, 1990). Other facilities have modified this

Writing notes in a clear and concise format is impor

format, with the same information organized in a dif

tant so that information is conveyed accurately. Exam

ferent w a y . The following section presents an

ples of unclear notes are ones in which the handwriting

overview of relevant subjective and objective infor

is illegible, or that contain vague statements that could

mation, and a description of items to include in the

be interpreted in more than one way. Concise notes are

assessment and plan.

more likely to be read by other health care profession als. In most clinicians' schedules, time is not available to read through extensive information about a patient

Subjective Information

that may not be relevant. A concise note only includes

Subjective information contains a degree of judge

essential infOImation in a writing style that is clear and

ment or interpretation by the person reporting the in

does not include unnecessary phrases. Another impor

formation. The patient and family's perceptions of

tant rule is to use only standard or accepted abbrevia

their cardiac or pulmonary condition are considered

tions. Facilities have lists of approved abbreviations

subjective information. In the initial note, descrip

for that facility. The list should be available to those

tions of pain or discomfort that may be associated

who write, read, and review records. Within a physical

with either a cardiac event or a pulmonary complica

therapy department, common terms need to be clearly

tion are important to include. Some of the informa

defined and used in a consistent manner by all staff.

tion reported by the patient may be objective, such as

Terms that often generate confusion and carry multiple

blood cholesterol levels, resting blood pressure val

meanings include "minimally assisted," "functional

ues or number of cigarettes smoked per day.


6


125

In the interim note, it is impoltant to record the pa

The description of the evaluation and treatment

tient's responses to treatment including feelings of

results needs to include specific information on the

angina, dyspnea, or fatigue. Whether a prescribed home

activity, or exercise stress, and on the physiological

or ward activity program is performed and the patient's

responses. Components of the activity description in

subjective responses to the program also are important

clude the following:

to note. Any reported changes in the ability to function either at home or in the community are important to record. The most impoltant subjective finding to report in the discharge note is whether the patient believes

I. Mode of activity (corridor or track walking,

lower extremity cycling) 2. Work level or rate (mph, percent grade, esti

mated resting metabolic rate level) 3. Duration of activity at each work level

personal treatment goals were achieved.

The description of the activities should be written clearly so that the workload can be reproduced. The

Objective Information

responses to activity include changes in heart rate and

Measurable or observable information that is col

rhythm, blood pressure, respiratory rate, oxygen satu

lected during the interview, evaluation, and treat

ration levels, and heart and breath sounds as com

ment is considered objective. Information from the

pared with from preactivity to either during or imme

medical record may be included if it is relevant to

diately after activity. Signs of exercise intolerance,

the patient's current condition. To be relevant, the

such as changes in skin color, incoordination, and

information should have potential impact on the di

sweating, also need to be documented. Whether the

rection of the evaluation and treatment of the patient,

patient used oxygen during treatment, or required

such as current medications and results of diagnostic

physical assistance also should be noted. By objec

tests. Results uJ" tests and measurements conducted

tively recording the activity prescription and the

as a part of the initial evaluation are objective infor

physiological responses, therapists can estimate the

mation. A description of the treatment that is pro

patient's activity tolerance.

vided, and the patient's physiological responses to treatment also are considered objective information. When recording information collected during the

Assessment

evaluation, the results of various tests can be cate

The purpose of the assessment part of a note is to list

gorized as impairments or as functional limitations.

the client's major problem(s), identify treatment goals

An impairment is an abnormality of physiological

or outcomes, and provide an interpretation of the sub

function or anatomical structure at the tissue, organ

jective and objective findings. The problem list is lim

or body system level (Jette, 1994). Examples of im

ited to problems that can be addressed by physical

pairments include decreases in muscle strength or

therapy. Problems can be listed in order of priority

range of motion, or abnormal heart rate and blood

and stated in functional terms. For example, stating

pressure values. A functional limitation is a restric

"patient unable to c1imb stairs because of abnormal

tion in performance at the level of the whole person

ECG responses and dizziness," rather than stating

(Jette, 1994). Functional Ii mi tations can be attrib

"abnormal ECG response during activity."

uted to physical, social, cognitive, or emotional fac

Goals are the outcomes to be achieved by paltici

tors. Examples of functional limitations include the

pating in a physical therapy program and are generated

inability to dress, transfer, ambul ate, or climb

by the therapist and patient in consultation. Goals are

stairs. Improvements in functional status usually

stated in functional terms as to what the patient will be

are of primary interest to patients and families and

able to do at discharge. The following is an example:

to those who reimburse for health care. Measure ments of impairments arc important, because they

Patient will be able to carry one 25-lb. bag a distance of 50

assist therapists in deciphering the causes or rea

feet with appropriate heart rate and rhythm responses,

sons for limitations in function.

within 2 weeks.


126

PART II


To be able to detennine if a goal has been met, the ther

mation from records can be organized into sections

apist must be able to observe or to measure the activity.

describing subjective and objective information, as

Therapists also estimate the time that it will take to

sessment or interpretation of the findings, and the

achieve the outcome. In the discharge note, whether

care plan. Subjective and objective information is

each goal has been met is stated. If a goal has not been

collected during an interview, medical record review,

achieved, then a reason or explanation is provided.

and evaluation and/or treatment session. The assess

The assessment also includes a brief interpretation

ment provides an interpretation of the subjective and

of the subjective and objective findings. Therapists

objective findings, and states the desired treatment

can use this section to state their "clinical hypothe

outcomes. A specific plan to achieve the outcomes

sis," or explanation of the primary problem that pro

then is described. Documentation can be viewed as a

duces the objective and subjective findings. The ini

way to assist therapists to organize their findings, re

t i a l n o t e m a y i n c l u d e statemen t s

flect on the significance of the findings, and generate

about the

individual's potential t o succeed i n a rehabilitation

an efficient and comprehensive care plan.

program, or reasons for not performing tests that would typically be performed with individuals with similar diagnoses. Whether the patient needs to be re ferred to other health care professionals or to commu

REVIEW QUESTIONS l. Describe and give examples of nominal, ordinal,

nity services also can be included.

ratio and interval measurements. 2. Identify three factors that contribute to the vari ability of measurements.

Plan

3. Define sensitivity and specificity of tests.

The plan provides a description of the approach that

4. Differentiate between objective and subjective

will be taken to assist the patient in achieving the stated goals. The plan may include a description of

measurements. S. Identify four purposes for documenting the re

treatment that can be provided, education for the pa

sults of evaluation and treatment sessions.

tient and/or family, and referrals to other services. Descriptions of home or ward programs should be in cluded in the plan. At discharge from an inpatient unit, the plan includes where the patient will be resid ing and plans for follow-up. At discharge from an outpatient facility, the plan contains recommenda tions for follow-up care.

References Hurst, J.W.

(J 990). The recognition and treatment of four types of

angina pectoris and angina equivalents. In Hurst, J.W., Schlant, R.C., Rackley, C.E., Sonnonblick, E.H.,

& Wenger, N.K.

(Eds.). The hean Oth ed.). New York: McGraw-HilI. Jelle, A . M. (1994). Physical disablement concepts for physical therapy research and practice. Physical Therapy

74, 380-386.

Keuenbach, G. (J990). Writing S.O.A.P. notes. Philadelphia: FA Davis.

SUMMARY

Kusher, R.F.

Measurement and documentation are important com ponents of the process of providing patient care. Therapists select measurements because they reveal information about patient characteristics that is needed to determine appropriate directions for treat ment. Performing measurements in a consistent way allows comparison of patient characteristics at varied points in time. The recording, or documentation, of the results of measurements and other information about the patient serves as a legal record. Although

& Schoeller, D.A. (J986). Estimation of total body

water by bioelecu'ical impedance analysis. American Journal of Clinical Nutrition.

44, 417-424. & Fox, S.M. (1978).

Pollock, M.L., Wilmore, J.H.,

Health and it f

ness through physical activity. New York: John Wiley and Sons.

1.M. (J989). On defining subjective and objective mea 69, 577-579. Rothstein, J .M .. & Echternach, J. L. (1993). Primer on measure

Rothstein,

surements. Physical Therapy

ment: An introductory guide to measuremelll issues. Alexan

V A: American Physical Therapy Association. & Colley, J.R.T. & Hamilton, P.J.S. (1971). Measurement of triceps skin fold thickness: An investigation of sources of variation. British Joul11al of Preventive and Social Medicine 25, 165-167. dria,

Ruiz, L.,

documentation formats vary between facilities, infor


History

Willy E. Hammon

KEY TERMS

Cough

History

Dyspnea

Pain

INTRODUCTION

words and pace (Hurst, et ai,

1990). If the therapist ap

The value of the history depends in large part on the

pears hurried, distracted, preoccupied, irritated, or un

skill of the interviewer. When eliciting the history

caring; is often interrupted; or fails to be an attentive lis

from a patient, therapists must be alert to recognize

tener, the patient-therapist relationship will likely suffer.

the symptoms that are indicative of cardiac and pul

The interviewer must be careful not to allow per

monary disease. This information is then used in the

sonal feelings about the patient's grooming, appear

decision-making process to select the most appropri

ance, demeanor, and behavior during the interview to

ate intervention for the individual.

unduly question the validity of the chief complaints (Birdwell,

1993). By the time the patient is referred

for physical therapy, he or she may have seen one or

THE INTERVIEW

more physicians, have been subjected to a number of

Obtaining a thorough and accurate patient history is

noninvasive or invasive studies, or have been pre

truly an art. One imponant goal of histOlY taking is to

scribed oral or inhaled medications with variable or

establish a good patient-therapist rapport. The patient

unsatisfactory alleviation of symptoms. The patient is

must be allowed to explain the history in his or her own

likely to manifest a degree of anxiety and frustration. 127


128

PART n


Therefore the therapist's approach, history-taking and

2. Whether the treatment order is narrow or

interviewing style is important for gaining the pa tient's confidence and cooperation.

broad in scope. 3. The acuteness of the patient's illness, level of

The patient history interview can be divided into

consciousness, and his ability to provide ac

the data-gathering and interpretative sections (Snider,

curate information.

1994). The data-gathering segment begins with ask

This chapter presents a comprehensive approach to

ing why the patient has sought medical attention and

history taking. Therapists may find part or all of this

has been referred for physical therapy services. In

information applicable, depending on their particular

other words, what is the patient's chief complaint

circumstances.

the symptom that caused the patient to seek help? Each chief complaint should be carefully ex plored. Supplementary questions should be nonlead

QUESTIONNAIRES

ing, using words the patient can easily understand.

Printed symptom or medical questionnaires can be ben

This allows the interviewer to determine the signifi

eficial or detrimental to the patient-therapist relation

cance of the complaint. An in-depth knowledge of

ship, depending on how they are used. Questionnaires

cardiopulmonary pathophysiology allows the thera

can expedite the data-gathering portion of the initial

pist to almost simultaneously gather data about the

visit by allowing the patient to note in advance, all

patient's symptoms and to interpret the likely type of

symptoms, medical conditions, surgeries, occupalions,

cardiopulmonary dysfunction that exists. This in turn

medications, and other factors that may influence phys

serves as a basis for the therapist to begin to select

ical therapy intervention. They can reduce the amount

the appropriate assessment and treatment modalities

of nontreatment time therapists may otherwise spend

for the individual.

inquiring about irrelevant symptoms and conditions.

It is important to remember that patient satisfaction

Pri nted questionnaires also allow patients sufficient

is greatest if the patient is allowed to fully express

time to recall relevant informalion and respond more

major concerns without interrupting. In addition, the

accurately than they often do in an interview selting

risk of missing what is really of greatest concern to the

(Miller, 1980). Used in this way, a printed question

patient is reduced if the patient is allowed sufficient

naire can be a valuable tool for expediting a compre

time to describe it in his or her own words. Studies

hensive evaluation of cardiopulmonary patients.

have shown this usually only takes from I to 3 minutes.

However, if questionnaires are used improperly,

The patient's view of what is the problem and his or

they can depersonalize the history-taking portion of

her suggestions for addressing the problem should be in

the initial visit (Hurst, et ai, 1990). If the therapist al

cluded in the interview. Patient satisfaction is improved

lows the printed form to become a substitute for in

by his or her involvement in the interview as well as

teraction with the patient, patient satisfaction will be

later in the establishment of short- and long-term goals.

low and the patient-therapist relationship will suffer.

The depth of the history taken by the physical ther apist (PT) can vary according to the following factors:

1. Whether the individual is an inpatient or an

DYSPNEA

out patient. Many inpatients have detailed

Dyspnea, breathlessness or shortness of breath, can be

medical records available for the therapist to re

defined as the sensation of difficullY in breathing

view. This significantly reduces the amount of

(George, 1990). It is one of the most common reasons

information the therapist needs to obtain from

that patients seek medical attention. Dyspnea is difficult

the patient during an interview. If the informa

to quantitate, because it is subjective and at times is

tion in the chart is scant, or if the individual is

normal (i.e., at high altitudes, and during or following

an outpatient with only a treatment referral and

vigorous exercise). Dyspnea is a symptom of cardiac

little or no medical records available, the thera

and pulmonary diseases, as well as other conditions.

pist should obtain a more detailed history.

When a patient complains of shortness of breath or


7

MITOCHONDRIA

MUSCULOSKELETAL

CARDIOVASCULAR

History

RESPIRATORY

129

AIR

FIGURE 7-1 Schematic illustration of the oxygen transport system, which involves the interaction between the respiratory, cardiovascular, and musculoskeletal systems. (Reprinted with permission from Mahler D: Dyspnea: diagnosis and management. Clirz Chest Med 8 [2),215-230,1987.)

breathlessness, it should be noted that this complaint

in the work of breathing, and (3) an abnormality in the

is often unrelated to the patient's arterial oxygen

ventilatory system itself (George, 1990).

level (Pao2). Many times, it appears that altered me

An increased awareness of normal breathing is

chanical factors during breathing contribute to the

usually related to anxiety (Miller, 1980). The patient

sensation of breathlessness (Mahler, 1987). Numer

commonly complains of "not getting a deep enough

ous receptors that have a role in sensing dyspnea

breath," a feeling of "smothering," or "not getting air

have been identified and include vagal receptors

down in the right places" (Szidan and Fishman,

(e.g., irritant, stretch, and J-receptors), chemorecep

1988). These sensations have been designated as psy

tors, proprioceptive receptors (tendon organs, muscle

chogenic dyspnea. The patient's breathing pattern is

spindles, joint and/or skin receptors), and upper air

irregular, with frequent sighs. When severe, it is asso

way receptors (Snider, 1994).

ciated with tingling of the hands and feet, circumoral

Analyzing the oxygen transpOit system (Figure 7-1)

numbness, and lightheadedness. Coaching the patient

can help the therapist deterrrune the likely cause of each

to hyperventilate and to reproduce the symptoms may

patient's dyspnea and the most appropriate physical

help the patient better understand the cause of these

therapy intervention. The delivery of oxygen from am

symptoms and how to control them (Miller, 1980).

bient air to the mitochondrion within the cell depends

The hyperventilation syndrome is properly diagnosed

on the intact interaction of the respiratory, cardiovascu

only after organic causes have been excluded and

lar, and muscular systems. Also, carbOn dioxide (C02)

pulmonary function tests indicate normal respiratory

is eliminated in the opposite direction. Dyspnea can be

mechanics and Pao2. The second cause of dyspnea is an increase in the

caused by dysfunction in any of the systems. Dyspnea commonly occurs when the body's re

work of breathing. Greater inspiratory pressures must

quirement for breathing (ventilation) exceeds the

be generated by the respiratory muscles to move air in

body's capacity to provide (Snider, 1994). In other

and out of the lungs when the mechanical properties

words, the symptom varies directly with the body's

of the lungs have changed. This may be related to an

demand for ventilation and inversely with ventila

increase in lung water resulting from cardiac disease

tory capacity.

or the high cardiac output of anemia. A loss of com

There are three basic causes of dyspnea: (I) an in

pliance (increased lung stiffness) because of diffuse

creased awareness of normal breathing, (2) an increase

inflammatory or fibrotic lung disease often causes


130

PART II


shortness of breath. Small or large airways obstruction

I. Are you short of breath at rest? If the answer

as a result of bronchoconstriction, sputum, inflamma

is yes, it suggests a severe physiological dys

tion, and other effects commonly produces dyspnea.

function. The patient likely needs prompt eval

The third cause of dyspnea is an abnormality in

uation by a physician if this is of recent onset

the ventilatory apparatus or pump. The ventilatory apparatus consists of the thoracic cage, respiratory

and has not had a medical workup.

2. Do you have chest pain'? If so what part of

muscles, and nerves. Any of these may become dys

your chest? Unilateral localized chest pain

functional. Thoracic cage abnormalities include

raises the possibility of spontaneous pneumoth

kyphoscoliosis, extreme obesity, and large pleural ef

orax, pulmonary embolism, or chest trauma.

fusions. Diseases of the respiratory muscles include

3. What were you doing immediately before or

polymyositis and muscular dystrophy. Neurologic ab

at the time of onset of shortness of breath?

normalities include spinal cord injuries, phrenic nerve

Approximately 75% of spontaneous pneumotho

injuries, brachial plexus neuropathy, ascending

races occur during sedentary activity, 20% dur

polyneuritis (GuiJlain-Barre syndrome), myasthenia

ing some strenuous activity, and 5% are related

gravis, amyotrophic lateral sclerosis, poliomyelitis,

to coughing or sneezing. A history of immobi

neurotoxins, and exposure to paralytic agents.

lization of a lower extremity, recent surgery, bed

The time course of the appearance and progression

rest, travel requiring prolonged sitting, obesity,

of dyspnea should be identified (Sharf, 1989). Acute

CHF, venous disease of the lower extremities,

dyspnea is common in pulmonary embolism, pneu

are all risk factors for pulmonary embolism. If

mothorax, acute asthma, pulmonary congestion related

the patient's symptoms are related to chest

to congestive heart failure (CHF), pneumonia, and

trauma, the fact that a fall, a blow, or an accident occurred can usually be quickly established.

upper airways obstruction. Most of these conditions re quire immediate physician evaluation of the acute

4. Do you have any major medical or surgical

problem before physical therapy inlervention. Suba

conditions? Cystic fibrosis, chronic obstructive

cute or chronic progression of dyspnea generally pre

pulmonary disease (COPD), interstitial lung

sents as increasingly severe dyspnea with exertion over

disease, and malignancies are important causes

time. It occurs with emphysema, restrictive lung disor

of secondary spontaneous pneumothorax.

ders such as pulmonary fibrosis, chest wall deformi

If the therapist strongly suspects pneumothorax or

ties, respiratory muscle dysfunction, occupational lung

pulmonary emboli because of the history and physi

diseases, chronic CHF, or large pleural effusions.

cal assessment, the patient should be referred for im

Dyspnea may also be related to body position.

mediate medical evaluation.

Therefore when evaluating dyspnea, the patient should be asked if he or she has difficulty breathing when reclining horizontally. Is it necessary to be

Dyspnea on Exertion

propped up on several pillows to sleep at night (or

Dyspnea on exertion is a common complaint of pa

thopnea)? Does she have more difficulty breathing

tients with cardiopulmonary dysfunction. Dyspnea

when reclining on one side (trepopnea)? Does he ever

during exercise or exertion usually precedes dyspnea

wake up at night short of breath, and need to sit up or

at rest (Wasserman, 1982). It most often is a result of

walk around the room to "catch his breath" (paroxys

chronic pulmonary disease or CHF. Some causes of dyspnea during exertion or exercise are listed in

mal nocturnal dyspnea)?

Table 7-1. It is important to establish the amount of activity re

Acute Dyspnea

quired to produce dyspnea. Various scales (Borg, 1982;

The patient that has acute dyspnea requires a rapid and

Mahler and Harver, 1990) have been developed to cate

thorough history and physical assessment. The thera

gorize the level of dyspnea and impairment present in

pist should ask several important questions to address

patients (Figures 7-2, 7-3 and Table 7-2). The patient

the possible causes of acute dyspnea (Mahler, 1987):

should be asked about daily activity, and what activities


7

History

131

TABLE 7-1 Disorders Limiting Exercise Performance, Pathophysiology, and Discriminating Measurements*

DISORDERS

PATHOPHYSIOLOG Y

MEASUREMENTS THAT DEVIATE FROM NORMAL

Mechanical limitation to ventilation

VE maxlMVV, expiratory flow pattern, VDNT;

Pulmonary Airflow limitation

mismatching of VA/Q, hypoxic

V02 max, VEiVo2 VE response to hyperoxia,

stimulation to breathing

(A-a)po2

Restrictive

Mismatching V A/Q, hypoxic stimulation

Chest wall

Mechanical limitation to ventilation

VE max/MVV, Paco2 V02 max

Pulmonary circulation

Rise in physiological dead space as

Vo/VT, work-rate-related hypoxemia V02 max,

to breathing

VENo2, (a-ET)pco2, Orpulse

fraction of VT, exercise hypoxemia

Cardiac Coronary

Electrocardiogram (ECG), V02 max, anaerobic

Coronary insufficiency

threshold O2, VENo2 Orpulse, blood pressure (BP) (systolic, diastolic, pulse) Valvular

Cardiac output limitation (decreased

Myocardial

Cardiac output limitation (decreased

Anemia

Reduced O2 carrying capacity

02-pulse, anaerobic threshold Vo2, V02 max,


Inadequate O2 flow to metabolically

Anaerobic threshold V02, V02 max

Obesity

Increased work to move body;

effective stroke volume) ejection fraction and stroke volume) VEiVo2 active muscle V02-work rate relationship, Pao2, Paco2, Vo2max

if severe, respiratory restriction and pulmonary insufficiency Psychogenic

Hyperventilation with precisely regular

Breathing pattern, PC02

respiratory rate Breathing pattern, PC02

Hyperventilation and hypoventilation

Malingering

with irregular respiratory rate Deconditioning

02-pulse, anaerobic threshold Vo2, V02 max

Inactivity or prolonged bedrest; loss of capability for effective redistribution of systemic blood flow

*VA-alveolar ventilation; Q---pulmonary blood flow; MVV-max-imum voluntary ventilation; VoIV.-physiologic dead space/tidal volume ratio;

Or- oxygen: V02-02

consumption; (A-a)P02-alveolar-arterial P02 difference; (a-ET)pco2-anerial-end tidal Peo2

difference. (Reprinted with permission from Wasserman

© 1982

K:

Dyspnea on exertion:

Is

it the heart or lungs?

lAMA 248: 2039-2043, 1982.

American Medical Association.)

produce breathlessness (Constant,

1993). Does the pa

cent onset of dyspnea is more characteristic of heart

tient become short of breath climbing a flight of stairs

failure than chronic lung disease, which has a longer,

or walking uphill? Is the patient able to walk and talk

insidious onset. Acute pulmonary problems such as

simultaneously? Does walking slower affect the indi

pneumothorax, atelectasis, pneumonia, and other conditions superimposed on chronic lung disease can

vidual's dyspnea? In addition, when the patient began to notice an in crease in shortness of breath should be noted. A re

also explain a recent increase in symptoms. Is wheezing present with the dyspnea on exertion?


132

PART II


TABLE 7-2 American Thoracic Society Dyspnea Scale GRADE

0

I 2

3

DEGREE None

Not troubled with breathlessness except with strenuous exercise

Slight

Troubled by shortness of breath when hurrying on the level or walking up a slight hill

Moderate

Walks slower than people of the same age on the level because of breathlessness or has to

Severe

Stops for breath after walking about

Very severe

Too breathless to leave the house or breathless when dressing or undressing

stop for breath when walking at own pace on the level

4

100 yards or after a few minutes on the level

Reprinted with permission from Brooks SM (Chairman): Task group on surveillance for respiratory hazards in the occupational setting. Survei Ilance for respiratory hazards,

ATS News 12-16, 1982.

o 0.5

GREATEST BREATHLESSNESS

Nothing at all Very, very slight (just noticeable) Very slight

2

Slight

3

Moderate

4

Somewhat severe

5

Severe

6 7

Very severe

8 9

NO BREATHLESSNESS

10

Maximal

FIGURE 7-3

FIGURE 7-2 The visual analogue scale is a vertical line of

Very, very severe (almost maximal)

100 mm in

length. The patient is asked to make a mark along this line

The Borg category scale for rating breathlessness. (Reprinted with permission from Borg G: Psychophysical

that represents his level of breathlessness. The distance of

bases of perceived exertion, Med Sci Sports Exerc 14,

the patient's mark above zero represents the measurement

377-381,1982.)

of dyspnea. (Reprinted with permission from Mahler D: Dyspnea: diagnosis and management, Clin Chest Med

8

[2],215-230,1987.)


7

History

133

Has there been an associated weight gain? Does the

volume, the patient develops a rapid heart rate and a

patient have a positive smoking history and sputum

wide arteriovenous O2 difference (decreased capillary

production? If a positive response is received, these

P02) at an inappropriately low work rate. Therefore

suggest that COPD is the primary cause of symptoms

the exercising muscles (both skeletal and myocardial)

(Constant, 1993).

have increased difficulty getting an adequate oxygen

The basic defect that cardiac diseases produce dur

supply to perform the necessary work, which results

ing exertion is a limited cardiac output, primarily

in dyspnea, fatigue or pain. The lactic acidosis that

caused by a reduced stroke volume (Wasserman,

results from the low oxygen delivery to the muscles

1982). To compensate for the relatively low stroke

can be measured by either invasive or noninvasive

Functional and Therapeutic Classification of Patients with Heart Disease Functional Classification Class I Patients with cardiac disease but without resulting limitations of physical activity; ordinary physical activity does not l:ause undue fatigue, palpitation, dyspnea, or anginal pain.

Class II Patients with cardial: disease resulting in slight limitation of physical activity; they are comfortable at res£. Ordinary physical activity results ill fatigue. palpitation, dyspnea, or anginal pain.

Class III Patients with cardiac disease resulting in marked limitation of physical activity; they are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea. or anginal pain.

Class IV Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort; symptoms of cardiac insufticiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort increases.

Therapeutic Classification Class A Patients with cardiac disease whose physical activity need not be restricted in any way.

Class B Patients with cardiac disease whose ordinary physical activity need not be restricted but who should be advised against severe or competitive efforts.

Class C Patients with cardiac disease whose ordinary activities should be moderately restricted and whose more strenuous efforts should be discontinued.

Class D Patients with l:ardiac disease whose ordinary activity should be markedly restricted.

Class E Patients with cardiac disease who should be at complete rest, confined to bed or chair.

Reprinted with permission from the New York Heart Association (1964). Diseases of the heart and blood vessels; Nomenclature alld crite' ria for diagnosis. (6th ed.). Boston: Little, Brown.


134

PART II


gas-exchange methods during exercise testing. The

stenosis, it is probably related to an inadequate car

functional and therapeutic capacity of the patient with

diac output during exercise. Patients with tetralogy of

hean disease can be estimated based on the history

Fallot and other forms of cyanotic heart disease, ex

and symptoms (see box on p. 133).

perience both dyspnea and fatigue during exercise

Dyspnea in cardiac patients is usually related to metabolic acidosis-induced hydrogen ion stimulus.

when the aJterial oxyhemoglobin saturation has fallen appreciatively below the resting level.

Also, increased pressure in the right side of the heart and pulmonary circulation during exertion may stim ulate mechanoreceptors that increase ventilation and induce dyspnea.

Orthopnea Orthopnea is dyspnea brought on in the recumbent

Diseases that involve the lungs or thoracic cage

position (Hurst, 1990). The patient may state the need

generally prevent external respiration (ventilation)

for two or three pillows under the head to rest at

from keeping pace with internal respiration (in the

night. This symptom is commonly associated with

cells) (Wasserman, 1982). In other words, patients

CHF but may also be associated with severe chronic

outwalk or outrun their lungs during activities or ex

pulmonary disease.

ertion. The primary symptom that limits exercise in pulmonary patients is dyspnea because of the diffi culty they have eliminating CO2 produced by metab

Paroxysmal Nocturnal Dyspnea

olism. Some individuals such as those with pul

Paroxysmal nocturnal dyspnea (PND) is an impor

monary fibrosis and some with COPD do experience

tant type of shortness of breath. This symptom has

a decrease in P02 with exercise. Hence, dyspnea on

strong predictive value as a sign of CHF (Hurst, et

exertion in pulmonary patients is usually related to

ai, 1990). The patient usually falls asleep in the re

hypoxic or hypercapnic stimuli.

cumbent position, and 1 or 2 hours later, awakens from sleep with acute shortness of breath. The pa tient sits upright on the side of the bed or goes to an

Dyspnea in Cardiac Patients

open window to breathe "fresh air" to get relief from

The cause of dyspnea in cardiac patients depends on

shortness of breath.

whether an associated stiffness of the lungs (fall in

The mechanism of PND is the transfer of fluid

compliance) is also present (Szidan and Fishman,

from extravascular tissues into the bloodstream (or

1988). Dyspnea is the primary symptom of a decom

intravascularly) during sleep (Constant, 1993). The

pensating left ventricle (Marriott, 1993). As the ven

intravascular volume of fluid gradually increAses

tricle fails to eject the normal volume of blood, it pro

until the compromised left ventricle can no longer

duces chronic pulmonary venous hypertension,

manage it. The left atrial pressure rises when the rate

congestion, and pulmonary edema, resulting in stiff or

of lymphatic drainage from the lungs is unable to

less compliant lungs. This, along with modest hypox

keep up with the increased volume of tluid. The in

emia that augments the respiratory drive, increases

creased atrial pressure leads to a sufficiently elevated

ventilation and the work of breathing. Tachypnea is

pulmonary capillary pressure to produce interstitial

often seen at rest. Exercise exaggerates the pulmonary

edema. Patients who are light sleepers awaken early

congestion and edema, promotes arterial and mixed

with dyspnea. Deep sleepers may not awaken until

venous hypoxemia, which also increases the amount

they develop alveolar edema.

of dyspnea and tachypnea manifested. Fatigue, result

Classic PND cannot usually be eliminated by only

ing from low cardiac output, also affects the respira

elevating the trunk without lowering the legs. The pa

tory muscles, further increasing the sensation of

tient must pool blood in the extravascular tissues of

breathlessness.

the legs to get adequate relief, which usually takes at

Dyspnea in cardiac patients without stiff lungs is primarily seen during exertion or exercise (Szidan,

least 30 minutes. This is why the patient must sit up or stand up, and ambulate.

and Fishman, 1988). In uncomplicated pulmonic


The patient should be asked about the amount of

7

History

135

40, is 1990). When

exercise or work performed during the day before an

symptom, if first reported in patients over age

attack on PND. A true left ventricular failure episode

often related to heart failure (Hurst, et aI,

of PND is more likely to occur after a day of unusual

confilmed that the wheezing is because of heart dis

exertion, which has caused an increased amount of

ease, the patient is said to have cardiac asthma.

extravascular fluid to accumulate in the legs. If the

Wheezing in cardiac patients is a manifestation of nar

patient is participating in an exercise or rehabilitation

rowed airways and thickened bronchial walls as a re

program, the level of exercise may need to be re

sult of pulmonary edema (Szidan, and Fishman,

duced to prevent PND.

1988). However, if patients have a history of episodes of wheezing and dyspnea since childhood, COPD, or asthma is the likely cause. Other pulmonary condi

Platypnea

tions such as eosinophilic pneumonia, bronchopul

Platypnea is the onset of dyspnea when assuming the

monary aspergillosis, allergic granulomatosis, etc.,

sitting position from the supine position (Sharf,

can cause wheezing (Miller,

1989). This unusual phenomenon is often found in

differentiated from stridor, which is commonly caused

1980). Wheezing must be

patients with basilar pulmonary fibrosis or basilar ar

by laryngotracheal narrowing due to tracheostomy

teriovenous malformation. It can be related to the re

scar, trauma of intubation, laryngeal paralysis,

distribution of blood flow to the lung bases in the sit

epiglottitis, or tumors. Chronic pulmonary patients

ting position with resultant ventilation-perfusion

may also develop heart conditions, so it is good to re

mismatching and hypoxemia.

member patients that complain of wheezing may have both cardiac and pulmonary disease.

Trepopnea Trepopnea refers to dyspnea in one lateral position

COUGH

1994). It is often produced

Cough is a common symptom of pulmonary disease.

by unilateral respiratory system pathology such as

The cough mechanism consists of three phases:

lung disease, pleural effusion, or airway obstruction.

(1) an inspiratory phase, (2) a compressive phase, and (3) an expiratory phase (Irwin, 1977).

but not the other (Snider,

It also is commonly seen in patients with mitral

1993). Occasionally it may be the

There are numerous cough irritant receptors lo

result of a fall in blood pressure in the left lateral de

cated on the mucosa of the larynx, trachea, bronchi,

cubitus position. If the patient has ischemic heart dis

pleura, and external auditory canal. These receptors

stenosis (Constant,

ease, the reduction in coronary perfusion can cause

are most sensitive at the glottis and carina, and di

either angina or dyspnea.

minish rapidly beyond the fourth generation bronchi. A cough follows stimulation of these mucosal recep

tors by any of a number of factors including inflam

Functional Dyspnea

mation, sputum, foreign bodies, noxious gases or

Functional dyspnea is defined as shOltness of breath at

odors, chemical substances, endobronchial tumors,

1989). It is most

and extrabronchial pressure on the trachea or bronchi

rest but not during exertion (Shmf,

commonly seen in young women who complain of the

(Sharf,

1989).

need to take a deep breath or to sigh and interpret this

A productive cough is beneficial for clearing the

sensation as shortness of breath. The physical exami

airways of sputum and foreign material, and gener

nation and pulmonary function tests are negative. Re

ally should not be inhibited. However, a dry, hacking

assurance is usually all that is necessary.

cough is usually of no value and can have a self perpetuating irritant effect on the respiratory mucosa. A dry cough may be the initial symptom of certain

WHEEZING

interstitial lung diseases such as allergic alveoli tis,

Patients that complain of wheezing associated with

sarcoidosis, and pulmonary fibrosis. Some causes and

dyspnea may have pulmonary or cardiac disease. This

characteristics of coughs are listed in Table


7-3.

136

PART II


TABLE 7-3 Some Causes and Chnracteristics of Coughs CAUSE

CHARACTERISTICS

Acute infection of lungs Tracheobronchitis

Cough associated with sore throat, running nose, and eyes

Lobar pneumonia

Cough often preceded by symptoms of upper respiratory infection; cough dry,

Bronchopneumonia

Usually begins as acute bronchitis; dry or productive cough

Mycoplasma and viral pneumonia

Paroxysmal cough, productive of mucoid or blood-stained sputum associated

Exacerbation of chronic bronchitis

Cough productive of mucoid sputum becomes purulent

painful at first; later becomes productive

with influenza-like syndrome

Chronic infections of lungs Bronchitis

Cough productive of sputum on most days for more than 3 consecutive months and for more than 2 successive years; sputum mucoid until acute exacerbation, when it becomes mucopurulent

Bronchiectasis

Cough copious, foul, purulent, often since childhood; forms layer on standing

Tuberculosis or fungus

Persistent cough for weeks to months often with blood-tingling of sputum

Parenchymal inflammatory processes

J nterstitial fibrosis and infiltrations

Cough nonproductive, persistent, depends on etiologic factors

Smoking

Cough usually associated with injected pharynx; persistent, most marked in morning, usually only slightly productive unless succeeded by chronic bronchitis

Tumors Bronchogenic carcinoma

Nonproductive to productive cough for weeks to months; recurrent small

Alveolar cell carcinoma

Cough similar to bronchogenic carcinoma, except in occasional instance when

Benign tumors in airways

Cough nonproductive, occasionally hemoptysis

Mediastinal tumors

Cough, often with breathlessness, caused by compression of trachea and bronchi

Aortic aneurysm

Brassy cough

hemoptysis common large quantities of watery, mucoid sputum are produced

Foreign body Immediate, while still in upper airway

Cough associated with progressive evidence of asphyxiation

Later, when lodged in lower airway

Nonproductive cough, persistent, associated with localizing wheeze

Cardiovascular Left venuicular failure

Cough intensifies while supine along with aggravation of dyspnea

Pulmonary infarction

Cough associated with hemoptysis, usually with pleural effusion

Reprinted with permission from Szidon J, Fishman A: Approach to the pulmonary patient with respiratory signs and symptoms. In Fishman A, editor: Pulmol1{//y diseases alld disorders. New York, 1988, McGraw-Hill.


7

History

137

Cough may be the only presenting symptom of

deep breathing suggests asthma or interstitial lung

asthma. In asthmatics, cough is precipitated by inhal

disease. Allergens or irritant fumes at home or at

ing cold air or exercise, and is dry. Cough can precip

work may be a cause of cough. Postviral cough may

itate an asthma attack in sensitive patients and is

be present for weeks following a viral illness.

known as cough-induced bronchospasm.

Some medications can elicit coughing. Beta

It is important to determine the length of time

blockers prescribed to treat hypertension, migraine

cough has been present (Sharf, 1989). The most com

headaches, cardiovascular disease (CVD), or glau

mon cause of an acute cough is a viral respiratory in

coma may precipitate asthma. Many drugs, including

fection, which generally resolves within a few days

chemotherapeutic agents, can cause interstitial lung

or 2 to 3 weeks. Exposure to noxious gases also pre

disease and coughing.

cipitates acute coughing.

Cough and wheezing may result from COPD,

A cough that has persisted for more than 3 weeks

asthma, or early left heart failure. Early left heart fail

can be termed chronic (Snider, 1994). The most com

ure predisposes the patient to respiratory infections

mon cause of chronic cough is chronic bronchitis,

and may be responsible for chronic bronchitis.

and is present in up to 30% of cigarette smokers. The next most common cause is the postnasal discharge syndrome. Patients describe a sensation of secretions

Cough Complications

dripping from the back of the nose into the throat,

One of the more common complications of cough is

prompting throat clearing or coughing.

syncope. Tussive or cough-induced syncope, which is

Various cardiac conditions may stimulate receptors

more common in men than women, can be recognized

in the bronchi and provoke coughing (Goldberger,

through accurate history taking (Miller, 1980). It is

1990). Because the bronchial veins empty into the

typically reported by middle-age men who "smoke

pulmonary veins (leading to the left side of the heart),

hard, eat hard, drink hard, and cough hard." They ex

systemic veins, and the superior vena cava (leading to

perience fainting or near-fainting following cough

the right side of the heart), venous congestion and

paroxysms. The cause is obscure but may be related to

coughing may occur with either right- or left-side

vagal-induced cardiac slowing or vasodilatation, or

CHF. It is more common, however, with left-sided

high intrathoracic pressures that impair venous return,

CHF. The onset of a cough in a patient with paroxys

decrease cardiac output, increase intracranial pressure,

mal tachycardia or acute myocardial infarction (MI) is

and result in a reduced cerebral blood flow. Cough

often an early symptom of acute left-side heart failure.

syncope is often resolved by smoking cessation.

Coughing may be caused by other cardiovascular

Complications of cough include headache, back

conditions such as a large left atrium displacing the

pain, muscular tears, hematomas, rib fractures (along

left main-stem bronchus upward, aortic aneurysms

the posterior axillary line), occasionally vertebral

placing pressure on the bronchi, or a double aortic

compression fractures (in osteopenic patients), urinary

arch compressing the trachea.

incontinence (UI) (in women), and inguinal hernias

A specific diagnosis can be made in 80% of cases

(in men) may occur (Braman and Corrao, 1987).

of chronic cough by an appropriate history alone (Stulberg, j 985). Determining the precipitating causes or the time of onset points the clinician to a

CHEST PAIN

probable diagnosis. For example, does the patient

Taking an accurate history is crucial to the proper

cough primarily at night? If so, it points to heart fail

evaluation of chest pain (Snider, j 994). Although the

ure, esophageal problems, bronchiectasis or asthma

definitive cause of chest pain cannot be fully estab

as the potential cause. An early morning cough is

lished without diagnostic medical tests, it is usually

more common in bronchitis and individuals with

possible to determine whether the pain originates in

postnasal drip. Cough following meals suggests

the pleura, chest wall, or thoracic organs by means of

esophageal disease. Cough precipitated by exertion or

careful history taking.


138

PART II


Chest pain can be divided into two basic types:

palpated at the wrist. If a patient opens and

chest wall pain and visceral pain (George, 1990). The

closes a fist, pain will gradually appear and es

first arises from involved thoracic cage structures and

calate in the forearm. The causal mechanism of

tends to be superficial and well-localized. The latter

this pain is the same as that of myocardial pain:

arises from the heart, pericardium, aorta, medi

continuing muscular contraction in the absence

astinum, bronchi, or esophagus. It is described as

of an adequate oxygen supply. This type of pain requires several contractions of the my

deep and difficult to localize.

ocardium to reach its maximal intensity. In other words, there is a characteristic buildup or

Pleuritic

escalation of angina pain.

Pleuritic chest pain originates from the parietal pleura

2. Can you point to the area of pain with one

or endothoracic fascia, but not the visceral pleura,

finger? Anginal pain is characteristically

which has no pain receptors. The patient can usually

demonstrated by patients using their entire

identify it as being close to the thoracic cage (Szidan,

hand or closed fist against the anterior chest

Fishman, 1988). Pleuritic chest pain worsens sharply

wall. It is described as a sign of angina, because

with inspiration as the inflamed parietal pleura is

it is so typical (Marriott, 1993). By contrast,

stretched with chest wall motion. Deep breathing,

any pain that can be localized by pointing with a fingertip is unlikely to be angina.

coughing, or laughing are extremely painful, requir ing the patient to apply pressure over the involved

3. Is the pain deep inside your chest or does it seem as though it is close to the surface?

area to control the pain. Pleuritic chest pain is ordinarily found in patients

Anginal pain is visceral pain that may be re

that have other signs of respiratory illness, such as

ferred superficially but always has a deep inter nal component to it.

cough, fever, chills, malaise. Inflammation of the di aphragmatic pleura produces ipsilateral shoulder pain by way of the phrenic nerve (Miller, 1980).

Myocardial ischemia may be completely painless (silent ischemia). Angina may in fact not be painful

The onset of pleuritic chest pain varies according

but rather described as discomfort, pressure, squeez

to its cause (Snider, 1994). Sudden severe pleuritic

ing, a tight band, heaviness, burning, indigestion. It

chest pain suggest a spontaneous pneumothorax, pul

usually is located substernally and radiates into one

monary embolism, or infarct. Pulmonary embolism is

or both arms, neck, jaw, or back.

usually accompanied by sudden dyspnea, hemoptysis,

Angina is not limited only to patients with CAD

tachycardia, cyanosis, hypotension, anxiety, and agi

(Marriott, 1993). Individuals that have normal coro

tation (Marriott, 1993).

nary arteries but an insufficient oxygen supply for a given cardiac workload can also experience angina. These include individuals with anemia, hypertension,

Cardiac

tachycardia, and thyrotoxicosis. Hypertrophic and di

There are three cardinal features that are characteris

lated cardiomyopathy can produce typical angina

tic of cardiac chest pain. The patient should be asked

pain, although the latter tends to be intermittent, usu

the following questions (Marriott, 1993):

ally occurring with episodes of CHF. Aortic valve

I. Does the pain have maximal intensity from

the onset or does it build up for several sec

disease can cause angina as a result of impairment of adequate coronary artery blood tlow.

on ds? Ischemic cardiac pain or angina is

Angina is usually precipitated by exertion such as

caused by the myocardium contracting in the

walking uphill, against the wind, or in cold weather

absence of an adequate oxygen supply. The

(Marriott, 1993). It also is more likely to be brought

same type of pain can be produced by placing a

on after a meal or by emotional stress. The rapid

blood pressure cuff around the upper arm and

resolution of chest pain by rest

inflating it until the brachial pulse is no longer

glycerin strongly suggests a cardiac origin. The pain


or

sublingual nitro

7

History

139

produced by MI is longer, persisting more than 20

suggest an esophageal origin (Snider, 1994). Also,

minutes; occurs at rest; and is accompanied by nau

diffuse esophageal spasm is often associated with pain on swallowing (odynophagia), dysphagia, and

sea, diaphoresis, hypotension, and dyspnea.

regurgitation of stomach contents. Swallowing hot or cold liquids, or emotional stress tend to precipitate

Pulmonary Hypertension

this type of chest pain.

Chest pain related to pulmonary hypertension may mimic angina pectoris. It is usually found in patients with mitral stenosis or Eisenmenger's syndrome (pul

Chest Wall

monary hypertension related to an interventricular

Chest wall pain is the most common type of chest

septal defect, patent ductus arteriosus, or atrial septal

pain. Clues in the patient's history to this type of pain

defect). This type of chest pain is usually absent at

include intermittent occurrence, variable intensity,

rest, occurs during exertion, and is invariably associ

and local tenderness (Miller, 1980). Because it is

ated with dyspnea (Hurst, et ai, 1990). It is believed

often located on the anterior chest wall, many pa

to be because of dilation of the pulmonary artery or

tients believe it is heart pain. However, an important

right ventricular ischemia. The pain is not relieved by

differentiation from cardiac pain is that it does not

nitrates. Primary pulmonary hypertension may be ac

occur during but rather following exertion. It may

companied by syncope and Raynaud's phenomenon

worsen with inspiration, but its association with trunk

(Sharf, 1989).

motions (flexion, extension, rotation) distinguish it from pleuritic chest pain. Localized anterior chest pain as a result of costo

Pericardial

chondritis of the second to fourth costosternal articu

Pericardial chest pain is also midline, but because of its

lations (Tietze's syndrome) is described as tender to

anatomical relationship with the mediastinal pleura, it

touch (George, 1990). A complaint of rib tenderness,

has features that suggest pleural involvement (Snider,

together with a history of trauma, fall, long-term

1994). Deep breathing, coughing, swallowing, move

steroid use, coughing, or upper extremity exertion,

ment and lying down may make it worse. If the central

suggests rib fracture.

tendon of the diaphragm is involved, the pain may be

Degenerative disk disease and arthritis of the cervi

referred to the left shoulder or scapular area (Marriott,

cal or thoracic spine, thoracic outlet syndrome,

1993). The patient may report that each hemibeat af

spondylitis, fibromyalgia, kyphoscoliosis, and herpes

fects the pain. Sitting up and leaning forward, or lying

zoster can all produce chest wall pain (Epstein, Ger

on the right side often relieves the pain.

ber, and Borer, 1979; Miller, 1980; Pellegrino, 1990; Snider, 1994; Wise, Semble, and Dalton, 1992). Pri mary lung cancer that invades the adjoining chest

Esophageal

wall, ribs, or spine produces severe persistent local

Diffuse esophageal spasm or esophageal colic is a

ized pain (Snider, 1994). Pancoast's syndrome (supe

common cause of chest pain. It is often confused with

rior sulcus tumor), in which a primary lung tumor lo

cardiac pain because it is located substernally, has a

cated in the extreme apex of the lung invades the

squeezing or aching quality, and may radiate into one

brachial plexus and produces pain in the shoulder,

or both arms (George, 1990). Furthermore, diffuse

scapular region, or medial aspect of the arm and hand.

esophageal spasm may be relieved by sublingual ni

Chest wall pain may rarely be caused by thrombo

troglycerin as a result of its generalized function as a

sis of a superficial vein on the chest wall (Mondor's disease). It is a self-limiting condition of unknown

smooth muscle relaxant. Pain that radiates through the chest to the back,

origin and can last several weeks (Snider, 1994). The

pain that decreases by a change in position from

only physical finding is a subcutaneous cord that can

supine to upright, or relief by ingesting antacids, all

be palpated along the lateral chest wall.


140

PART II


FATIGUE AND WEAKNESS

HEMOPTYSIS is defined as coughing up blood. It can vary in amount from blood-streaked sputum to convirtually all blood. The

site may be

anywhere in the upper or lower respiratory tract. The timing and frequency of

as deter

mined in the history, can offer clues about its cause. since blood

A history of nosebleeds is

may be aspirated duling

and expecto

rated the following morning. Intermittent bouts of he is more characteristic of resoiratorv infec tions such as bronchiectasis, or broncholithiasis (Miller, blood-streaked basis is highly

of

hrr;,nf"hAfT"n

The lung receives its blood supply in two ways: the pulmonary arteries (a low pressure

and the

bronchial arteries (a high pressure

off of the may

aorta (Shalf, 1989). The appearance of vary according to which blood

is involved. If the

bronchial vessels are the source, there tends to be large or massive amounts of bright red blood. This is often

PEDAL EDEMA

the site of bleeding in bronchiectasis, since bronchial ar

CHF is a common cause of bilateral pedal edema

teries undergo enlargement and extensive anastomosis

(Marriott, 1993). Ifowever, several pounds of fluid

with the pulmonary artery system. where there is increased

in mitral steno-

(10 to 20 Ibs.) generally accumulate in the body be fore foot and ankle swell

I-IUJJJJ'-'JJ
tance, hemoptysis arises from

is evident. Therefore

weight gain is an even earlier indication of fluid re tention due to CHF. Occasionally, patients may only

mucosal bronchial veins Hemoptysis from the

complain about an increase in abdominal

artery system tends to occur in small amounts and is

ascites virtually

of dark or clotted venous blood It may arise from the

occurs after

present If the amount of ascites is

as in the case of the

vascular

found in the walls of

abscesses. These abscesses

tissue

that of constrictive

restrictive CardlOmyopatny or should be a consideration.

It is important to determine whether the

may be caused by infections such as or chronic irrita

anaerobic bacteria,

result

CHF. the onset of

ing from ascites. When caused

had dyspnea on exertion before the onset of lower-ex

tion from a fungus ball in an abscess cavity. If a

tremity edema. If the edema is a result of a

blood vessel ruptures in an abscess

functioning left

rhage tends to be massive, even

monale, it usually follows and

aortic aneurysm are also associated with hemoptysis (Hurst, et aI, 1990). Pink frothy with acute pulmonary edema. fully evaluate

of

or cor pul on exertion.

Patients with CHF and altered renal function

Cardiovascular conditions such as mitral pulmonary infarction,

mitral

commonly report edema of the ankle and lower legs while upright during the

but indicate a de

is often found

crease during the night (Hurst, et ai, 1990). This is

should care

a result of local hydrostatic factors related to the

and be certain

of its cause before cautiousIv conducting treatment.

upright position. Edema may be Dresent in nephrosis or starvation


7

when the total blood protein falls below 5 gmllOO ml (hypoproteinemia). Other causes of pedal edema in clude liver disease, kidney disease, and anemia. Edema of one leg is ordinarily because of local fac tors such as thrombophlebitis or varicose veins. HOARSENESS

Hoarseness, abnormal vocal cord motion during phonation, is a symptom of laryngeal dysfunction (Miller, 1980). It is usually associated with upper res piratory tract infections or allergies, and resolves in 1 to 2 weeks (Sharf, 1989). Trauma following intuba tion, laryngeal polyps, or tumors are other common causes of hoarseness. However, this symptom is also related to cardiopulmonary conditions. Because the recurrent laryngeal nerves pass through the upper thorax, intrathoracic pathology that involves one of these nerves can cause unilateral vocal cord paralysis, resulting in hoarseness (Shalf, 1989). These include lung or mediastinal tumors, granulomatous disease, enlarged mediastinal lymph nodes, and pericardial or mediastinal adhesions. Several cardiovascular conditions can produce hoarseness, because the left recurrent laryngeal nerve loops under the arch of the aorta and above the pul monary artery as it returns to the neck (Hurst, et ai, 1990). Therefore an aneurysm of the arch of the aorta, a dilated pulmonary artery or atrium resulting from an atrial septal defect, or mitral stenosis can cause hoarseness (Goldberger, 1990). Hence, if patients manifest hoarseness, it is neces sary to inquire about the length of time it has been present, the patient's smoking history, and any his tory of cardiac or pulmonary diseases. OCCUPATIONAL HISTORY

Taking an occupational history is particularly impor tant for pulmonary patients who arrive for physical therapy with little or no accompanying medical infor mation. The internal surface of the lung measures 50 to 100 m] and is in constant contact with the environment (Miller, 1980). Jobs that involve exposure to silica or silicates (e.g., miners, sandblasters, foundry workers, stone cutters, brick layers, or quarry workers) or other inorganic substances place workers at risk for combi

History

141

nations of obstmctive and restrictive lung disease (e.g., silicosis). Constmction workers, shipyard workers, pipefitters, and other industJial workers exposed to as bestos are at increased risk for developing a restrictive lung disease such as asbestosis (Varkey, 1983). Benign pleural plaques may be found on the diaphragmatic pleura and bilaterally between the sixth and tenth ribs on the anterolateral or posterolateral chest wall. Pro gressive pleural thickening rarely occurs. These indi viduals have an increased incidence of malignant neo plastic diseases such as bronchogenic carcinoma and malignant mesothelioma. Coal workers are exposed to coal mine dust. About 10% have simple pneumoconiosis, whereas a smaller proportion develop the complicated form progressive massive pulmonary fibrosis (Brandstetter and Sprince, 1982). A history of paroxysmal coughing, chest tightness, or dyspnea that is worse during the week but remits on weekends strongly suggests occupational asthma (Brandstetter, and Sprince, 1982). This condition is difficult to diagnose because symptoms often occur several hours after exposure to the provoking agent. Causal agents include grain dusts, wood dusts, forma lin, enzyme detergents, ethanolamines (in spray paints and soldering flux), nickel and hard metals (tungsten carbide). Workers exposed to cotton flax and hemp dusts may develop byssinosis, an obstmc tive lung disease. In the early stages, it is reversible, but long-term exposure over a number of years causes chronic irreversible obstructive lung disease. A history of fever, cough, shortness of breath, and recurrent pneumonias in farmers in the north ern United States suggests farmer's lung (Brand stetter, and Sprince, 1982). This is the most com m o n h y p e r s e n s i t i v e pneumonitis, c a u s e d b y inhaling fungal agents such a s thermophilic actino mycetes. Long-term exposure can lead to pul monary fibrosis. There are numerous occupations that expose workers to etiologic factors that cause hypersensitive pneumonitis. SMOKING HISTORY

The patient should be asked their tobacco-smoking history (Snider, 1994). The number of pack-years of cigarettes smoked may be calculated (average number


142

PART II

of packs/day

x


number of years smoked) as a relative

risk of lung cancer and COPD. Regular smoking of marijuana is more damaging to the lungs than ciga rette smoking.

REVIEW QUESTIONS 1. What are the basic causes of dyspnea? 2. What questions can be asked of a patient with

dyspnea to determine the likely cause? 3. What scales have been developed to quantitate

FAMILY HISTORY

dyspnea?

The family history is useful in evaluating the possi

4. What are the principal features of chest pain that

originate from the pleurae? The chest wall? The

bility of hereditary p ulmonary diseases such a s alphaj-antitrypsin deficiency, cystic fibrosis, allergic asthma, hereditary hemorrhagic telangiectasia, and others (Miller, 1980; Szidan, and Fishman, 1988). A family history of diabetes, hypertension, CAD, or

thoracic organs? 5. What are the cardinal features of cardiac chest

pain?

6. What occupations can place workers at rish for respiratory disease?

rheumatic fever raises the possibility of these condi tions existing in the patient as well (Marriott, 1993).

References PRIOR TREATMENT

Herbers, J., & Kroenke, K. (1 993). Eva lua ting chest s dia g n o s ti c a p p r oach . Arch ives of In/ernal Med i c ine, 153,

Birdwell, B.,

It is important to deterrnine what treatment(s) the pa tient has received for his or her condition. Specifically, has the patient ever received physical therapy for this or any other condition? What type of treatments were done? Were they helpful in improving or resolving the condition? In this way we determine what treatment modalities have been used, which of these the patient believes may have merit, and those with which the pa tient finds objectionable or lacks confidence, thus avoiding alienating the patient by not repeating what he or she believes to be ineffective therapy is avoided.

pain: the patient's presen tation style alte rs the phy si c ia n

'

1991-1995.

Borg, G. (1982).

Psyc ho physic al bases

of perce i ve d exertion. Merl

icine and Science in SPOrlS and t:rercise, 1 4,

Braman, S., Corrao,

W. (1 987) .

377-381.

Cough: differen/ial diagnosis and

8(2), 1 77-188. N. (1982). Occ u p at i on al lun g disease. June, 56-63.

/realinel1l. Clinical Ches/ Medicine

Brandsteller, R .. Sp rince, Medical Times,

Constant,

J.

(1993). The evolving checklist in history-taking. In

Bedside cardiology. Bo st on : Linle. Brown. Epstei n S., Gerber, L., & B o re r, J. (1979). Chest wall syndrome: a common cause of unexplained cardiac pai n . Journal of /he American Medical Associa/ion, 241, 2793-2797.

Constant

J.

,

George, R. (1990). History an d physical examination. In Geo rge

SUMMARY

ai/ical care medicine. Baltimore:

Obtaining an accurate and thorough history is the cornerstone of the physical t herapy e v a luation process. The probable cause and severity of many cardiopulmonary symptoms can be determined by careful history taking. This information enables ther apists to select the most appropriate evaluation and treatment techniques. When properly performed, ac curate h istory taking gains the patient's confidence and cooperation, and provides the basis for a good patient-therapist relationship.

,

R., et al (Eds.), Chest medicine: Essen/ials of pulmonary and

G o l dbe rger, E.

Wi l l ia ms and Wilkins.

(1990). Symptoms referable to the cardiovascular

E. Essentials of clinical cardiology. Phi la delp hi a: JB Lippincott. Irwin, R., Rosen, M., & Braman, S. (1977). Cough: a comprehen system. In Goldberger,

sive review. Arch h7lem Medicine 137,1186-1191. Hurst, 1., et al. (1990). The

h ist ory: past events and symptoms re J. (Ed.). The heall.

lated to cardiovascular disease. In Hurst,

N ew York: McGraw-Hili. Clin ics ill Ches/ Medicine. 8(2), 215-230. Mahler, D., & Harvel', A. (1990). Clinical measureme nt s of dysp nea. In Mah l e r, D. (Ed.). Dysp/1ea. Mount Kisco, NY: Futura. Marriol!, H. (1993). Taking the history. In Marriol!, H. Bedside cardiac diagnosis. Ph i ladelphia: JB Lippincott. Mahler, D. (1987). Dyspnea: diagnosis and management.


7

History

143

Miller, D. (1980). The medical history. [n Sackner, M. (Ed.).

Szidan, P., & Fishman, A. (1988). Approach to the pulmonary pa

Diagnostic techniques in pulmonary disease. New York:

tient with respiratory signs and symptoms. [n Fishman, A.

(Ed.). Pulmonary diseases and disorders. (2nd ed.). New York:

Marcel Dekker. Pellegrino, M. ( 1990). Atypical chest pain as an initial presentation of primary fibromyalgia. Archives of Physical Medicine and Rehabilitation

71, 526-528.

McGraw-HilI. Varkey, B., (1983). Asbestos exposure: An update on pleuropul monary hazards. Postgraduate Medicine, 74(4),93-103.

Sharf, S. (1989). History and physical examination. [n Baum, G.,

Wasserman, K., (1982). Dyspnea on exertion: is it the heart or the

& Wolinski, E. (Eds.). Textbook of pulmonary diseases. (4th

lungs? Journal of the American Medical Association, 248,

ed.). Boston: Lillie, Brown.

2039-2043.

Snider, G. (1994). History and physical examination. [n Baum, G.,

Wise, C., Semble, E., & Dalton, C. (1992). Musculoskeletal

& Wolinski, E. (Eds.), Textbook of pulmonary diseases. (5th

chest wall syndromes in patients with noncardiac chest pain: A study of 100 patients. Archives of Physical Medicine and

ed.). Little, Brown. SlUlberg, M. (1985). Evaluating and treating intractable cough

R eha bilitation,

Medical Staff Conference, University of California, San Fran cisco. West 1 Med, 143,223-228.


73, 147-149.

Pulmonary Function Tests

Donna Frownfelter

KEY TERMS

Expiratory reserve volume

Dead space

Inspiratory reserve volume

Lung capacities

Residual volume

Functional residual capacity

Tidal volume

Inspiratory capacity Total lung capacity

Obstructive component

Vital capacity

Predicted values Restrictive component

Lung volume

sis of pulmonary disease or dysfunction and improve

INTRODUCTION

ment with treatment win be evaluated as a result of in

Pulmonary function tests (PFfs) help in the evaluation

terpreting a patient's pulmonary function tests.

of the mechanical function of the lungs. (Cherniak, Crapo, and Youtsey, (992). They are based on re searched norms taking into account sex, height, and

DEAD SPACE

age. For example, there are predicted values for a

The most important function of the lungs is to supply

male, age 65 who is 6 feet tall. (Morris, Koski, and

the body with oxygen and to remove carbon dioxide

Johnson, (971). When the patient performs the test ac

(C02) produced as a waste product of metabolism.

tual results (observed) will be compared with the pre

As this continuous gas exchange takes place suffi

dicted value expected of a person of gender, height,

cient ventilation is needed to move the gases to the

and age to see if he falls within the "nonnal" range, or

alveoli. There is a series of conducting airways in the

has a restrictive or obstructive component based on the

lungs from the trachea down to the terminal bronchi,

tests. If the patient is not within the nonnal range, a

which do not participate in respiration but only move

bronchodilator is given, and the test will be repeated to

the gases to the alveoli. This is the volume known as

see if there is significant improvement with medica

anatomic dead space. Generally, the anatomic dead

tion. Basically, the pulmonary function tests are cate

space i s app r opria tely equal to the adult body

gorized as volume, flow, or diffusion studies. Diagno-

weight. For example, in a ISO-lb. person, there is an 145


146

PART II


approximately I SO mL anat(}mic dead space. A nor

functioning alveoli. This causes increased work of

mal tidal volume (TV), the breath normally taken,

breathing and may result in patient fatigue. Neurolog

needs to be large enough to reach the alveoli well

ical and neuromuscular weakness may result in an in

past the anatomic dead space. In a normal adult, the

ability to take a normal TV. Similarly, surgical proce

TV is generally 450 to 600 mL. The anatomic dead

dures

space would thus represent about one third TV vol

compromise a patient's ability to take a breath. As

or

p a i n f r o m fractured

r i b s c a n also

ume. The rest of the breath would reach the alveoli

the TV drops a large percentage of the breath is

and be considered "alveolar ventilation." With many

anatomic dead space. This results in increased work

neurologically impaired patients who have a limited

of breathing for the patient and may ultimately result

TV, it is important to note that little alveolar ventila

in respiratory failure if the patient is unable to pro

tion may be taking place when the patient is breath

vide alveolar ventilation.

ing in a rapid and shallow pattern. For example, if a p a t i e nt's TV w a s 200 mL,

IS O

mL w o u l d be

anatomic dead space and only SO mL of each breath

lUNG VOLUMES The lung has four volumes, TV, inspiratory reserve

would be alveolar ventilation. There are many diseases or conditions that can alter

volume (IRV), expiratory reserve volume (ERV), and

8-1).

the volume of dead space that needs to be ventilated. In

residual volume (RV) (Figure

some cases the dead space decreases, such as in a pneu

•

TV is the normal breath.

monectomy, where it is physically removed, or in

•

IRV is the maximal amount of air that can be in haled from the end of a normal inspiration.

asthma, where bronchospasm may narrow the airways. In other conditions such as pulmonary embolus, dead

•

be perfused. The alveoli continue to receive fresh gas, but there is no blood available for gas exchange. This type of dead space is known as physiologic dead space.

ERV is the maximal amount of air that can be ex pired after a normal exhalation.

space increases when ventilated areas of lung cease to •

RV is the volume of gas that remains in the lungs at the end of a maximum expiration. Changes in RV can help in the diagnosis of certain

When dead space is increased, a larger percentage

medical conditions. An increase in RV means that

of the tidal volume is ventilating the dead space,

even with maximum effort, the patient cannot exhale

leaving a smaller percentage for alveolar ventilation.

excess air from the lungs. This results in hyperin

The patient must work harder to get enough air to the

flated lungs and indicates that certain changes have

---I \tj

( C,\.'-'- '--

FIGURE 8-1 A

spirogram (pulmonary function testing).


8


147

occurred in the pulmonary tissue, which in time may

FRC is the volume of air remaining in the lungs at

cause mechanical changes in the chest wall (e.g., in

the resting expiratory level. It contains the ERV and

creased AP diameter, flattened diaphragms). These

the RV.

changes may be reversible in patients with partial

The FRC prevents large fluctuations in Pa02 with

bronchial obstruction, such as young asthmatics, or

each breath. An increase in FRC represents hyperin

irreversible, as in patients with advanced emphy

flation of the lungs. It causes the thorax to be larger

sema. Restrictive lung disease can cause a decrease in

than normal, which results in muscular inefficiency

residual volume, as can cancer of the lung, microat

and some mechanical disadvantage. Patients on me

electasis, or musculoskeletal impairment. (Smith and

chanical ventilators may increase their FRC with pos

Dickson, 1994).

itive pressure and by additional modes such as posi tive end expiratory (PEEP), or BiPap. Spontaneously breathing patients can also be on continuous positive

LUNG CAPACITIES

airway pressure (CPAP), which keeps the lungs at a

A lung capacity is two or more volumes added to

positive airway pressure to improve oxygenation.

gether (Figure 8-1). The capacities include total lung capacity (TLC), vital capacity (VC), inspiratory ca pacity (IC) and functional residual capacity (FRC). TLC is the amount of gas the lung contains at the

AIR FLOW MEASUREMENTS Forced Expiration

end of a maximum inspiration. It is made up of all four

When patients peIform a VC maneuver, it can either

lung volumes. An increased TLC is seen with hyperin

be slow or fast. During exhalation, the amount of air

flation such as emphysema. A decrease in TLC may be

exhaled over time can be measured. In a slow VC a

seen in restlictive lung disease such as pulmonary fi

patient with emphysema can take a great deal of time

brosis, atelectasis, neoplasms, pleural effusions, and

to empty his lungs. In a forced VC a normal individ

hemothorax, as well as in restrictive musculoskeletal

ual can exhale 75% of the VC in the first second of

problems such as spinal cord injury, kyphoscoliosis, or

exhalation (FEV I). Patients with emphysema often

as secondary to morbid obesity or pregnancy.

have greatly decreased VCs, only 40% of which are

VC is the maximum amount of gas that can be ex

predicted.

pelled from the lungs by forceful effort following a maximum inspiration. It contains the IRV, TV, ERV. A decrease in VC can occur as a result of absolute re

Flow Volume Curve

duction in distensible lung tissue. This is seen in

The flow volume curve is helpful in diagnosing lung

pneumonectomy, atelectasis, pneumonia, pulmonary

disease, since it is independent of effort. The curve in

congestion, occlusion of a major bronchus by a tumor

Figure 8-2 demonstrates that flow rises to a high

or foreign object, or restrictive lung disease.

value and then declines over most of expiration

A decrease in VC may also be seen without pri

(Rahn, et ai, 1946). In restrictive lung disease, the

mary lung disease or airway obstruction. In neuro

maximum flow rate is reduced, as is the total volume

muscular or musculoskeletal dysfunction, VC can be

exhaled. In obstructive lung disease, the flow rate is

compromised (Guillain-Barre, spinal cord injury,

low in relation to lung volume, and a scooped-out ap

drug overdose, motor vehicle accident with fractured

pearance is often seen (see Figure 8-2).

ribs, severe scoliosis, and kyphoscoliosis). Restrictive

Another diagnostic test that uses forced expiration

contributing factors such as morbid obesity, preg

is the flow volume loop. It is a graphic analysis of the

nancy, enlarged heart, and pulmonary effusion may

flow generated during a forced expiratory volume

involve the limitation of expansion of the lungs.

maneuver followed by a forced inspiratory volume

IC is the maximal amount of air that can be in

maneuver (Figure 8-3). This graph offers a pictorial

spired from the resting expiratory level. It contains

representation of data from many individual tests

the IRV and the TV.

(e.g., peak inspiratory and expiratory flow rates,


148

PART II


FLOW

VOLUME CURVES NORMAL

Z o wi= a:a.. :> X

U Q) II)

' :;>o w -.J o -.J<..9 u...Z 0::

OBSTRUCTIVE

=:J o

oI 10

r' ,.,.,.,.,.,.,.,\. """'·'·"""'T 8

9

.... .

6

7

/ 4

",

5

. . ..' 'j' xx;,i

",.",., ' '

3

2

LUNG VOLUME (Liters)

o

FlliURE 8-2 Comparison of tlow volume curves in the normal patient and in the patient with obstructive and restrictive lung disease.

+5

-r---- /\,.----;;;50% /

PFexp

\

j

EXPIRATION

U Q) II) ,

i 01

Ie

o -.J u...

-5

F;

\ INSPIRATION

PF insp

J

OBSTRUCTION __

_

o

2

4

6

VOLUME (Liters) FIGURE 8-3 Compatison of flow volume loops in the normal patient and in the patient with obstructive lung disease.


8

FVC, and FEV). The shape of the graph may also be helpful in diagnosing disease, again seeing a more scooped-out appearance with obstructive disease.

CLOSING VOLUME AND AIRWAY CLOSURE The assessment of closing volume is used to help di agnose small airway disease. A test called the single breath nitrogen (N2) washout is used for assessing closing volume and closing capacity of the small air ways. In this test, the patient takes a single VC breath of 100% oxygen. During complete exhalation, the N2 concentration can be measured. The characteristic tracing of N2 concentration can be measured. The characteristic tracing of N2 concentration vs. lung vol ume reflects sequential emptying of differentially ven tilated lung units, resulting in different expiratory N2 concentrations. Four phases can be identified (Figure 8-4). Phase I contains pure dead space and virtually none of the potential N2 from the RV. Phase Il is asso ciated with an increasing N2 concentration of a mix ture of gas from the dead space and alveoli. The plateau in N2 concentration observed in Phase III re flects pure alveolar gas emanating from the bases and middle lung zones. Phase IV occurs toward the end of expiration and is characterized by an abrupt increase


in N2 concentration. This high N2 concentration re flects closure of airways at the base of the lungs and expiration of gas from the upper lung zones, because in the single breath of 100% oxygen, less oxygen was initially directed to this area. Closing volume is the lung volume at which the inflection of Phase IV, the marked increase in N2 concentration after the plateau, is observed. Closing capacity refers to closing volume and RV. The same characteristic tracing of the single breath nitrogen washout test can be obtained with an inhalation of a bolus of tracer gas (e.g., argon, helium, xenon-133). The closing volume is 10% of the vital capacity in young, healthy individuals. It increases with age and is 40% of the vital capacity at age 65. Closing vol ume is used as an aid in the diagnosis of small airway disease and as a means of evaluating treatment or drug response.

MAXIMAL VOLUNTARY VENTILATION Maximal voluntary ventilation measures the maximal breathing capacity of the patient. It reflects strengths and endurance of the respiratory muscles. The patient is asked to pant for 15 seconds into the spirometer tub ing. This is often examined preoperatively with the

CLOSING VOLUA1E and CLOSING CAPACITY

z o (f)«f (9« 0::: f-f o:::Z WW ZU -z o U

I I I I I I I I

DEPENDENT AIRWAY BEGIN TO CLOSE ------,

TLC

149

VOLUME (Liters)

RV

Closing Vol. HCVl----!

FIGURE 8-4 The single breath nitrogen washout test to assess airway closure.


o

150

PART II


other results to determine a patient's prognosis for suc

ration). An obstructive component generally relates to

cess after surgery, such as his or her ability to cough,

problems in exhalation air flows and characteristic

to take deep breaths, and to enhance airway clearance.

patterns of obstruction, such as in the first second of expiration FEY I measurement). Patients do not often have only one primary disease process but many times

DIAGNOSIS OF RESTRICTIVE AND OBSTRUCTIVE LUNG DISEASE

have overlapping lung conditions (Clausen, 1984). A

Physicians use the results of pulmonary function tests

emphysema with bronchospastic component; good re

diagnosis may read: PFTs consistent with moderate

to diagnose lung disease or characteristic components

sponse to bronchodilators. A patient with an abnormal

of lung disease, such as bronchospasm. A restrictive

PFr is given a bronchodilator and retested. If there is

component describes conditions that limit the amount

a 15% to 20% increase in the PFr after bronchodila

of volume coming into the lungs (restriction to inspi

tors are administered, they will be a recommended

NORMAL

RESTRICTIVE

OBSTRUCTIVE

IRV IC

i

i

VC

IRV TLC TV

VC

IC

C TV

TI C

ERV ERV FRC

l

F

FRC

RV

RV

FIGURE 8-5 Examples of proportional changes of lung volumes and capacities characteristic of obstructive and restrictive lung diseases.


I

8


151

part of the patients' medications. However, some pa

a loss of intrapleural negative pressure. In older indi

tients are given a trial of bronchodilators, even if there

viduals, therefore, airway closure occurs at higher lung volumes. For example, closure has been reported to

is not such a dramatic response on PFfs). A pictorial demonstration of the differences in ob

occur at the age of 65 in the upright lung during nor

structive and restrictive lung disease is shown in Fig

mal breathing. In the supine position, where FRC is re

ure 8-5. Disease has a marked effect on pulmonary

duced, closure occurs at a significantly younger age

function, yet TV usually remains 10% of total lung

(about age 44). In addition to the often compounding

capacity until the disease is relatively severe. Physio

effect of age, the lung volume at which airway closure

logic pulmonary reserves in both disease processes

occurs increases with chronic smoking and lung dis

are limited and generally affect a patient's response

ease, and is changed with the alterations in body posi

to exercise. Exercise will be limited by the ventila

tion (Ben)" Pai, and Fairshter, 1990; Zadai, 1985).

tory status ratlier than by a cardiac end point. As ob structive lung disease progresses, TLC, FRC, and RV are markedly increased. In severe COPD, the in creased FRC can compromise the Vc. More energy

SUMMARY Pulmonary functions change as a patient's condition

is expended to breathe compared with that expended

gets better or worse (Emery et ai, 1991; Emerson,

by a normal individual. This effect can be dispropor

Lukens, Effron, 1994). There are normal declines in

tionally increased with minimal amounts of activity.

volumes and flows with aging as well as disease

In restrictive lung disease, restriction of the chest

processes. Basic bedside spirometry is often done to as

wall or lung tissue can produce a decrease in TLC. A

sess the patient's breathing mechanical ability. For ex

VC of 80% or less of predicted values for a patient is

ample, in a patient with Guillain Ban'e, as breathing be

considered a diagnostic feature. A residual decline in

comes labored, the VC is monitored to determine whether a ventilator is needed. On the other hand, a pa

FRC potentiates airway closure. The phenomenon of closing volume in the lungs is

tient with obstructed airways, such as the patient with

particularly significant to physical therapists (PTs)

cystic fibrosis, the pulmonary function tests will im

who prescribe breathing exercises and body position

prove (Versteegh, et ai, 1986). In patients with spinal

ing, and can thereby alter pulmonary mechanics and

cord injury or neuromuscular weakness, as their

gas exchange. These treatment interventions may

strength improves, their vital capacity increases. How

have a pronounced effect on the lung volumes and

ever, because of the lack of abdominal muscles, the

airway closure (Dean, 1985). At low lung volumes

flows may be reduced.

(e.g., breathing at FRC, Trendelenberg position, and in lung disease) intrapleural pressures are generally less negative and the pressure of dependent lung re

REVIEW QUESTIONS

gions may equal or exceed atmospheric pressure. In

1. What effect will an obstructive component have on

trapleural pressure is less negative because the lungs

exercise performance? What effect will a restric

are less expanded and elastic recoil is decreased. As a

tive component have on excercise peliormance?

result, airway closure is potentiated. In young indi

2. Why is it important to compare the patient's pre

viduals, closure is evident at RV; however, in older

dicted values with the actual observed values in a

individuals, closure is observed at higher lung vol umes, such as at FRC. Premature closure of the small airways results in uneven ventilation and impaired gas exchange with a given lung unit. Airway closure occurs more readily in chronic smokers and in pa

pulmonary function test? 3.

What response should you see to determine if bronchodilators have a positive effect on pul monary function?

4. How can pulmonary function tests be used to as sess patient improvement or decline?

tients with lung disease. Aging has a significant effect on airway closure. With aging, a loss of pulmonary elastic recoil results in

5. How valuable are pulmonary function tests if pa tients do not give maximal effort?


152

PART II


References Berry, R., Paj,

Rahn,

U. &

in !low rates and airway conductance after a deep breath, Jour

nal of Applied Physiology. 68, 635-{543. Cherniak, R,M, and

function in health

Pulmonary function tcstlng; guidelines and

Physical Therapy 65, 613-{5 J 8,

CL.,

in acute exacerbation of COPD, Chest, 105(6),

1709-1712,

c.E., J"

et a!. (1991). Psychological outcome of a pulmonary

Koski, A"

sis of

spine in patients who have idiopathic scoliosis.

76

BOI1<'

(I), I

Ven;tcegh, F.G,A., et a!. (1986), Relationship between pulmonary brosis. Advanced Cmdiology, cations,

Is

p"

lSI-ISS, 1986,

el aL (1992), Predicting postoperative compli

it a real problem

Archives

of /l1Icrnal Medicine,

Youtsey, J.W. (1990). Scanlon,

CL,

Basic

Spearman,

pulmonary function measurement In

CB., &

Sheldan, R.L. (Ed,.). Egan's

fundamentals of respiratory care. (5th ed.). SL Louis: Mosby.

Johnson,

L (1971),

Zadai,

Prediction nomograms

(BTPS) spirometric values in normal males and females. Am e r

ican Review of Respiratory

C (1985)

Pulmonary physiology of

The role of re

habilitation, Topics in CeriO/ric Rehabililation, 1,49-56,

rehab program. Ches/, 100 (3), 613-{517, Morris,

Dickson, R,A. (1994), Changes in residual volume

152 (6), 1209-12l3,

Lukens, T.W., Effron, D, (1994), Physician estima

I

&

Williams-Russe,

Dean, E. (1985). The effect of body position on pulmonary fUlle

tion of FEV

of the thorax

J 61.

function, O2 saturation during sleep and exercise with cystic

Pulmonary function testing, New England

Joumal of Medicine, 331 (I),

Emerson,

Smith, R.M.,

and Join! Surgo)'

controversies, London: Grune and Stratton, Crapo, R.O, (1

et aL (1946), The prcS'urc·volume

relative to vital capacity and total lung capacity after arthrode

(! 992J, Evaluation of respiratory Dis Man, (7),505-76,

J.L. (1984).

Clausen,

H"

lung, American Journal of Physiology, 146,

Fairshter, R, (1990). Effect of age on changes

Diseases, 163, 57-{57.


Arterial Blood Gases

Donna Frownfelter

KEY TERMS

Acid/base balance

Hypoxemia

Alveolar ventilation

Oxygen saturation

Arterial blood gas

Partial pressure of gases

INTRODUCTION

metabolites must be kept from accumulating in high

Arterial blood gases are assessment tools to help the

amounts, because the body's cardiovascular and ner

physical therapist (PT) understand the patient's

vous systems operate in a relatively narrow free H+

acid/base balance, alveolar ventilation and oxygena

ion range (narrow pH). Free H+ ion concentration is

tion status (Cherniak, 1992). They are valuable re

discussed as pH (-log [H+]). Maintenance of body

sources of information, from respiratory monitoring

systems requires an appropriate acid/base balance

in the intensive care unit to following outpatients to

(Shapiro, 1994). Approximately 98% of normal metabolites are in

evaluate the therapy and progress of their diseases. The purpose of this chapter is to help the clinician evaluate and interpret arterial blood gases more effec

the form of carbon dioxide (C02)' Carbon dioxide re acts readily with water to form carbonic acid:

tively and to integrate the information into treatment

CO2 + H20

planning and progression of the patient.

H2C03

Carbonic acid can exist either as a liquid or a gas. Be cause carbonic acid can change to CO2, much of the

ACID/BASE BALANCE

acid content can be excreted through the lungs during

Normal body metabolism consists of consumption of nutrients and excretion of acid metabolites. Acid

respiration. The Henderson-Hasselbach equation demonstrates 153


154

PART II


how the H+ ion concentration results from the disso

acidemia o r alkalemia. Acidosis i s a n abnormal

ciation of carbonic acid and the interrclationship of

acid/base balance where the acids dominate. Alka lemia is an abnormal acid/base balance where the

the blood acids, bases, and buffers: H2 0 + CO2

H2C03 H+ + HC03

bases dominate. When there is a decrease in the

Heo3-, it is seen in a negative base excess and referred to as a base deficit, which is usually seen as a negative

Renal Buffering Mechanisms

number on the blood gas report, that is, -3.

The kidneys are the mai n route of excretion for the

termine whether the patient's condition is acute or

normal metabolic acids. Hydrogen ions are excreted

chronic. Another method is to examine whether the

When interpreting a blood gas, it is helpful to de

in the urine and also resorbed by bicarbonate into

situation is uncompensated, partially compensated or

the blood. In this manner, the kidneys can respond

completely compensated. The pH is the key to mak

when there is an acid/base imbalance to return to

ing this determination. If the pH is not in the normal

normal homeostasis.

7.35 to 7.45 range, then the patient will be in an acute state. As it progresses back toward normal, it may be pa11ially compensated. When a normal pH exists, it is

Normal Blood Gas Values

compensated or chronic.

Acid/base is denoted by the pH. The pH values are

For example, in a patient who is retaining a CO2 of

normally 7.35 to 7.45. If the pH is below 7.35, the

55 mm Hg, the pH may read 7.25; this would be con

patient is considered to be in an acidotic state (more

sidered acute. As the body retains base, the pH will

acid). If the pH is above 7.45, the patient is consid

rise back toward the normal numbers. If the pH was

ered to be in an alkalotic state (more basic).

7.32 with a Peo2 of 55 and + 3 base excess, the read

Alveolar ventilation is reflected in the partial pres

ing would be partially compensated. When the pH is

sure of carbon dioxide (Peo2). Normal Peo2 values

within normal limits with the Peo2 of 55 and a pH of

are 35 mmHg to 45 mmHg. If the PC02 is below 35

7.35, the reading would be compensated or chronic.

mmHg the patient is said to be hyperventilating (in creased ventilation, blowing off more C02 than nor mal). If the Peo2 is above 45 mmHg the patient is hy

PARTIAL PRESSURE Of GASES

p o v e nt i l a t i n g , or not h a v i n g e n o u g h a l v e o l a r

To better understand blood gases, it is important to

ventilation o r not blowing off enough CO2 t o main

remember the properties of gases. The earth's surface

tain normal alveolar ventilation.

consists of gas molecules that have mass and are at

Arterial oxygen is measured as Po2, the partial pres

tracted to the earth's center of gravity. At the surface,

sure of oxygen. Normal values are 80 to 100 mm Hg. If

this atmospheric weight exerts a pressure that can

the P02 is below 80 mmHg in someone less than 60

support a column of mercury 760 mm high. Dalton'S law states that in a mixture of gases, the

years old, the patient is hypoxemic. A value of 60 to 80

total pressure is equaJ to the sum of the partial pres

mmHg would be considered moderate hypoxemia, and less

sures of the separate gases. Oxygen is 20.9% of the at

than 40 mmHg is severe hypoxemja (Chemiak, 1992).

mosphere, so it has a partial pressure of 159 (760 x

20.9%

159). Nitrogen is 79% of the atmosphere, so 600). Other gases make up 0.1% of the atmosphere. =

it has a partial pressure of 600 (760 x 79%

Base Excess/Base Deficit

=

The blood normally has a capacity to buffer acid

Diffusion of gases across semipermeable mem

metabolites. The normal level of base Heo3 in the

branes show gradients from higher concentrations to

blood is 22 to 26 milimoles per liter (mmollL). This

lower concentrations. Each gas moves independently

buffering capacity diminishes in the presence o f

from the others.


9

During respiration, oxygen and CO2 exchange


155

with no circulation, a dead unit is credited. Figure

across the alveolar capillary membrane. Special situa

9-1 demonstrates the regional differences seen In

tions may affect the normal progress of respiration

respiratory units.

and gas exchange. Normally, alveolar units ventilate and capillary

Hemoglobin

units bring oxygenated blood to the tissues, excret i n g C02 b a c k i nto t h e alveoli to be removed

Hemoglobin (Hgb) is the main component of the red

through the lungs. However, some abnormal situa

blood cell. It is crucial for oxygen transport. The nor

tions may occur, such as shunts and dead space

mal Hgb is 12 to 16 gmllOO mL blood. In patients that

units. In a shunt unit, the alveoli has collapsed, but

have lost blood through surgical procedures or dis

blood flow continues and is unable to pick up oxy

ease, the decreased hemoglobin can account for their

gen. An example of this is atelectasis, where a lung

extreme weakness as a result of decreased oxygen

segment or part of a segment has retai ned secre

transport capacity. In addition, patients with advanced

tions and lung tissue distal to the mucous plug col

chronic obstructive pulmonary disease (COPD) can at

lapses. Circulation continues but oxygenation does

times desaturate with exercise when their Po2s are

not occur and the POl decreases. On the other hand,

low; during exercise, they use increased oxygen.

a dead space unit can have ventilation but not per

Cyanosis, a bluish color to the skin, mucous mem

fusion. This occurs with pulmonary embolism,

branes, and nail beds, is indicative of an abnormal

blood clot obstructs the circulation. The

amount of reduced Hgb concentration, usually greater

oxygen is available in the ventilated alveoli, but

than 5 gm of reduced Hgb. The presence of cyanosis

where

a

B A

c

FIGURE 9-1 A, Normal alveolus. B, Dead space. C, Shunt.


156

PART II


suggests a high probability of hypoxemia; however, it

•

can occur without cyanosis. Two examples may be cited, one in which an anemic patient with hypox

For every 20 mm Hg increase in Peo2, the pH de creases by 0.10.

•

emia can have little cyanosis, and the other in which

For every 10 mm Hg decrease in PC02, the pH in creases by 0.10. There is also a relationship between the Peo2 and

a patient with polycythemia can have cyanosis with

the plasma bicarbonate:

minimal hypoxemia. There is a predictable relationship between the arter

•

sented in the oxyhemoglobin dissociation curve as fol

For every increase of 10 mm Hg in the Peo2, there is a decrease of I mmollL plasma bicarbonate

ial oxygen saturation of the Hgb and the POz. It is repre •

For every 10 mm Hg Peo2, there is a decrease in plasma bicarbonate of 2 mmollL.

lows. When oxygen saturation is monitored during exercise, saturation is kept at or above 90%. As the

Knowing these guidelines, it can be determined if

curve denotes at a level of approximately 60 mm Hg,

the changes in the arterial blood gases are in line with

the saturation is about 90%. As the P02 drops at the

respiratory problems vs. metabolic problems such as

sharp part of the curve, for every mm Hg POz, there is a

acidosis from diabetic ketoacidosis, where the base

marked decrease in oxygen saturation (Guyton, 1986).

deficit can be very low, the pH can be low (acidemic), but the Peo2 can be within normal limits (Shapiro, 1994; Shapiro, Peruzzi, and Templin, 1994).

Chemoreceptor Response to Hypoxemia The peripheral chemoreceptors, the carotid, and the aortic bodies, are located at the bifurcation of the in ternal and external carotid arteries and the arch of the

RESPIRATORY FAILURE Respiratory failure is defined as the failure of the pul

aorta. These receptors are nervous tissue that have a

monary system to meet the metabolic demands of the

high metabolic rate and an abundant oxygen supply.

body, that is, ventilation and oxygenation (Shapiro,

When tissue P02 decreases, their response to the brain

Peruzzi, and Templin, 1994). The blood gases usually

is to increase ventilation and cardiac output. When

have a pH below 7.30 and a Peo2 above 50. Generally

this is not sufficient to effect a normal POz, supple

the patient is also hypoxemic.

mental oxygen or increased mechanical assistance

During the acute phase, the kidneys have not

such as continuous positive airway pressure (CPAP)

started to compensate and the base HCO,- is within

is given (Tarpy, 1994).

normal limits. Later, a base excess can be noted as the kidneys try to compensate for the acidotic pH. Chronic respiratory failure can be noted by an in

BLOOD GAS INTERPRETATION

creased Peo2 with a pH within normal limits.

The norms for the pH, Peo2, Po2, and base have pre

In assessing the Po2, the following ranges are

viously been given and should first be considered. Is

used: mild hypoxemia less than 80 mm Hg, moderate

the value normal or not? Is the patient acute, that is,

hypoxemia 60 to 80 mm Hg, and severe hypoxemia

uncompensated, partially compensated, or fully com

below 40 mm Hg. Positional changes can affect the oxygenation sta

pensated (chronic)? There are also "acceptable" ranges to consider, as in the following:

tus. For example, unilateral right lower lobe atelecta

•

pH 7.30 to 7.50

sis with the patient lying on the right side causes in

•

Pe02 30 to 50 mm Hg

cre a s e d blood fl o w to the right lung, which i s

•

pH 7.45 alkalemia

collapsed. This causes increased shunting and a de

•

pH 7.35 acidemia

crease in oxygenation lying on the right side (differ

•

Pae02 45 respiratory acidosis (hypercapnia)

ential shunting). If the patient lies on the left side, the

•

Pae02 35 respiratory alkalosis (hypocapnea)

oxygenation will improve. Lying supine, a mixed P02

A relationship between the pH and the PC02 also

can be observed. When hypoxemia is noted, treatment consists of

exists. There is a predictable change caused by varia tion in carbonic acid:

oxygen therapy and alleviation of the cause of hypox


9


157

emia, if possible. This may be airway clearance tech

duced less O2 is available. This is particularly impor

niques or medication, in addition to the oxygen ther

tant if a patient already has a decreased P02 and is

apy. Oxygen therapy treats the hypoxemia, decreases

traveling to an area with lower barometric pressure.

the patient's work of breathing, and decreases my

Patients on oxygen will need an oxygen prescription

ocardial work.

based on the area in which they are living. Barometric pressure increases, such as a hyper baric oxygen chamber with higher barometric pres

FACTORS AFFECTING ARTERIAL BLOOD GASES

sure, can be helpful in delivering increased oxygen

There are many normal causes that have an affect on

for many patients. Wound-healing needs and carbon

arterial blood gases, such as extremes of age-neonatal

monoxide poisoning are two .such indications.

to geriatrics. The neonate has many changes going on

Increased temperatures (febrile state) can increase

in the initial life process; fetal circulation changes

metabolism and therefore increase oxygen consump

dramatically in the first hours and days of life. In the

tion. Decreased temperatures can decrease the oxy

geriatric patient, decreases in cardiac output (CO),

gen consumption, as seen in patients involved in cold

residual volume (R V) of the lungs, and maximal

water near drowning, where they survived several

breathing capacity gradually decrease P02 over the

minutes under the water, and were resuscitated and

life cycle. It is estimated that after 60 years of age,

resumed normal lives.

the P

It is important to note on the arterial blood gas

decreases by I mm Hg per year of age from

60 to 90 years.

report the status of the patient when the blood gas

Exercise or any increase in activity from rest may

was drawn. Usually patients are at rest when the is low at rest (60 mm

result in increased oxygen consumption for patients

blood gas is drawn. If the P

with cardiopulmonary dysfunction. In the normal

Hg) it is close to the sharp part of the oxyhemoglo

population, the human body compensate by increas

bin dissociation curve and the patient may desatu

ing oxygen consumption to meet the workload. Usu

rate with exercise. If the patient was on supplemental oxygen and the

ally, a plateau is reached and a constant oxygen con sumption for that activity is achieved. In patients with

P

cardiopulmonary dysfunction, oxygen consumption

with additional 02 (Carpenter, 1991). Similarly, if a

continues to increase even at the same workload in

patient is on mechanical ventilation, the blood gases

untrained patients. It is important to monitor oxygen

should be within or near normal limits.

was only 55 mm Hg, the P02 is still inadequate

saturation to prevent desaturation of these patients (Guyton, 1986). During pregnancy, hormonal and mechanical factors have a negative effect on car diopulmonary function. During the last trimester,

SUMMARY This cha pter discussed the normal arterial blood

women often observe shortness of breath and diffi

gases and what their values mean to the therapist.

culty taking a deep breath secondary to diaphrag

Relationships between pH and Pe02, Pe02 and He03-,

matic encroachment.

and O2 saturation and POz have been examined. We

During sleep, there is a decrease in minute ventila

saw predictable changes that are caused by respira

tion and a decreased responsiveness to CO2 and hy

tory changes were described. In addition we noted

poxemia. Many patients with spinal cord injury and

that metabolic changes can have marked effects on

COPD have been noted to have hypoxemia during

blood gases. Oxygen therapy and airway clearance

sleep studies. This should be considered in any tired

techniques can improve hypoxemia, and position

or groggy patient.

changes can be detrimental, causing differential

Low barometric pressure associated with high alti tude significantly decreases the amount of oxygen

shunting

or

i m p r o v i ng

the

P02

by

better

ventilatiOn/perfusion matching.

available to the individual. As noted before, the par

As PTs, it is necessary to be acutely aware of the

tial pressure 20% of oxygen is dependent on the total

respiratory monitors that can assess and progress pa

atmospheric pressure. When the total pressure is re

tients safely to their optimal rehabilitation potential.


158

PART II Cardiopulmonary Assessment

References

REVIEW QUESTIONS 1. Which factors affect arterial blood gases? 2. How can exercise have a deleterious effect on blood

3. What predictable

occur between pH and

and oxygen saturation? 4. What two theraDeutic t echniques can improve

K.D. (199]). Oxygen transport in the blood. !J (9), 20·33, Chernlak, R.M. (1992). Evaluation r<:'spiratory function in health and disease. Dis MOrl. (7),505-576. Guyton, A. (1986). Textbook of medical physiology (7th ed,), Philadelphia: WB Saunders. Shapiro, B.A. (1994), Evaluation blood gas monitors: pelfor-

Carpenter,

Care Nurse,

mance criteria, clinical impact, and cosrlbenefit (editorial com·

5. What affect can body position have on blood gases?

ment). Crilical Care Medicine, 22 (4), 546-548, Shapiro,

B,A" Peruai. W., & Templin, R, Clinical applicalion of

blood gases, (5th

St. Louis: Mosby,

& Farber. H,W, (1994), Chronic lung prescnbe home oxygen, Ceriatrics, 49 (2), 27-28,3

Tarpy, S,P"


Principles of Chest X-Ray Interpretation Michael Ries Thomas Johnson

KEY

TERMS

Air bronchogram

Hyperlucency

Air fluid levels

Mass formations

Atelectasis

Pneumonia

Densities

Radiograph

Diffuse patterns

Silouette sign

There are three general categories of radiographic

One of the first things to check before interpreting

studies of the chest-fixed-position studies, sus

the film is the quality of the film. An optimal PA

pended motion studies, and motion studies. The rou

chest film is one in which the dim outline of the ver

tine posteroanterior (PA) and lateral chest film is a

tebral bodies is seen through the mediastinum. Films

fixed-position, suspended motion study. The patient

may be overpenetrated (of increased density) or un

is positioned with chest against the x-ray film holder

derpenetrated (of decreased density) and still be ade

and is asked to hold his breath in deep inspiration.

quate for interpretation. Suboptimal films may also

The radiograph (x-ray) is named from the source

hide pathology and cause misinterpretation.

of the x-rays to the film. Thus a PA chest film is po

The purpose of a radiograph is to see inside the

sitioned so that the source of the x-rays is 72 in. be

otherwise opaque body by shifting the spectrum of

hind the patient and the film is in front. An antero

light to above the high ranges of the visible spectrum,

posterior (AP) chest film is the reverse, with the

thus converting the body structures into densities

back of the patient against the film. During interpre

rather than colors. The densities recorded on the x

tation, the conventional position of the fi 1m on the

ray film range in shades of gray to black depending

view box is as if the physical therapist (PT) were

on the amount of x-ray energy the structures of the

facing the patient.

body absorb as the x-ray passes through them. 159


160

PART II


c

FIGURE 10-1

(A and C) transform into two-dimensional (B and D). The pictures (A and C) also show a box of cherry tomatoes and a jar of bird seed (millet seed) and their x-rays. B, is the radiograph of A, and D, is the radiograph of C. Changes in position of the same objects from A to C illustrate the changes of shape in the corresponding x-rays. B to D, and emphasize the need for PA and lateral x-rays for evaluating Familiar fruits such as an apple, orange, pear and banana

objects when x-rayed

three-dimensional structures.

There are five basic densities, varying from very radiolucent to very radiopaque. The darkest or most

third dimension, which is used to interpret the inter nal problems of a patient.

radiolucent density is gas or air. Fat is moderately ra

The routine examination of the chest should in

diolucent. An intermediate or water density is seen

clude a PA and lateral chest film on maximum inspi

reflecting the connective tissues, blood, muscle, skin,

ration at least for the first examination. Without the

and other structures. Bone and deposited calcium are

lateral film, disease processes behind the heart and

moderately radiopaque. Metal is the most opaque

posterior in the thorax may be missed. Very ill pa

(white or clear). The structures of the body absorb

tients who cannot be transported to the radiology de

most of the x-rays as they pass through the body, and

partment must often be evaluated at the bedside from

the remainder of the rays expose the film.

a single PA or AP view (taken with the portable x-ray

An example of an x-ray is the familiar fruits or

unit). The size of the patient introduces mechanical

objects that have been converted into a two-dimen

limitations to the performance of a lateral chest film.

sional reproduction of densities in Figure

10-1.

These three-dimensional structures are reduced to two dimensions and only the edges or structures tan

Portable x-ray units are not as powerful as the sta tionary departmental machines. Additional radiographic views may be ordered to

gential to the beam of the x-rays are recorded. Thus

verify

two views, taken at 90° from each other (PA and lat

(I) oblique views, (2) apical lordotic views, (3) de cubitus views, (4) iaminograms, (5) inspiration and

eral), are required for a mental reconstruction of the


or e l u c i d a t e f i n d i n g s.

These i n clud e

10

Principles of Chest X-Ray Interpretation

161

FIGURE 10-2 These A, PA and B, lateral x-rays anatomically localize the basic structures that must be reviewed during chest x-ray evaluation. Some of the structures are seen in both views and others are seen in only one view. During evaluation, one should identify and see the foJlowing basic anatomical structures.

Soft /issues and ex/ralhoracic s/rucltlres: soft tissues (ST), breast shadows (BS), diaphragm (D). (L). and fundus of stomach (F). Bony /homx: ribs (RI), vertebrae (V), scapulae (5, seen best on PAl, clavicles (CL. seen best on PAl and sternum (SN. seen best on lateral). Medias/ina! s/rucll/res: mediastinum (M), trachea (T), carina (CA). aortic knob (AK). heart (H). anterior clear .'pace (ACS. seen on lateral) and hilus of lungs (HI). LUlIgjields: hilus of lungs (HI). pulmon;Jry vessels (arise from hilus and branch outward). costophrcnic angles (CPA) and lung apices (LA. seen best on PAl. liver

There arc many other structures that must be evaluated in addition to these basic ones, and pathologics must be identified.

ex.piration films,

since other pathologies may be present. All the

trast materials,

(6) special studies requinng con (7) physiologic mOlion evaluation with the fluoroscopc, (8) computed tomography (CT scan), and (9) magnetic resonance imaging (MRI).

anatomical structures on the film should be exam bones and soft tissues (including the abdomen), the

ined. A body system approach is recommended:

Film interpretation requires a solid knowledge of

mediastinum from larynx to abdomen, the cardiovas

gross anatomy and gross pathology. The PT is liter

cular system, the hila, and finally, the lungs (Figure

ally examining the internal structures of the body

10-2).

without an autopsy or surgical intervention. The structures of the body are thus converted into the den sities of air, fat, water, calcium, and metal. The PT

The tools of radiographic interpretation include the following: 1. The principle of bilateral symmetry ( when

should ex.amine the entire film, not just one area, and

structures are paired, then in general one should

should not get "tunnel vision." Once an abnormality

look like the other).

is found, the PT should continue to evaluate the re

2. The presence or absence of air fluid levels

mainder of the film and should not stop at that point,

(there are almost no straight lines in the chest).


162

PART II


If a line appears to be straight, then it must be

Bronchi are not usually seen unless they are sur rounded by fluid or have a disease causing thickening

explained.

3. The silhouette sign. When densities are next to

of the walls. The vascular pattern may be distorted,

each other, they obliterate normal margins and

blurred, increased, or decrcased by pulmonary dis

show no separation (normal silhouette of a

ease. Air space or alveolar disease is manifested by

structure is obliterated). When densities or

opacification (white appearance) of air-filled struc

structures are in front or in back of other densi

tures of the l ung. Thus pneumonia may appear as

ties or structures, then a margin is seen.

patchy coalescent areas of acini, or segmental and/or

4. An a i r b r o n c h o g r a m is seen w h e n t h e air

lobar consolidation. An air bronchogram is seen

around a bronchus is pathologically filled with

when the air-filled lung tissuc about the bronchus is

fluid or other material.

filled with fluid or other material and the bronchus is

5. Lobar and s e g mental collapse follows the

filled with air (Figure 10-3). Certain lung diseases cause a decrease (increase in

anatomy of the lung.

6. Pleural changes may be manifested by gas in a

translucency) , such as emphysema (generalized) or bUl

pneumothorax, fluid in a pleural effusion, cal

lae (localized). Interstitial pulmonary disease is mani

cium or soft tissue from scarring or mesothe

fested by distoltion or increase in volume of tissues sur

home. A hydropneumothorax demonstrates an

rounding the air spaces. An enormous number of

air fluid level.

diseases can produce interstitial roentgenographic

7. The presence or absence of mass formation as

changes. Sometimes a diagnosis is strongly suggested

in tumors, nodular changes or miliary changes.

by the roentgenographic appearance, but in most, a his

The conventional terminology depends on the

tologic evaluation is required for diagnosis. Enlarge

size of the abnormality.

ment of the bronchi may result in bronchiectasis (Fig

8. Air-containing spaces such as bullae or cysts.

ure 10-4). Bronchiectasis is characterized by tubular

FIGURE 10-3 A, There is total pneumonic consolidation of right upper lobe with complete alveolar and bronchial filling. B, Approximately 24 to 36 hours later, the consolidation has cleared markedly with patchy coalescent residual. A few air bronchograms are seen in the perihilar region.


10


FIGURE 10-4 A, Fibrosis and saccular bronchiectatic changes are present in the left lower lobe. A few cystic "circular" changes are present in the right upper lobe but are best seen on the bronchogram. B, The bronchogram demonstrates the dilated abnOImal bronchi of cystic and saccular bronchiectasis in the left lower I.obe with fibrosis around them. The right upper lobe reveals a few cystic changes.

FIGURE 10-5 A, The PA chest film demonstrates the water density of a pneumonic consolidation in the right lower lobe. The diaphragm is blurred. B, The lateral film shows obliteration of the posterior right diaphragm and the costophrenic angle by the pneumonic consolidation.


163

164

PART II


shadows that are double-line paraliel shadows follow ing the bronchovascular distribution. The shadows may branch similar to the bronchial tree. P n eu m on ias are u s u ally classified by their causative agents of anatomical distribution. A lobar pneumonia is one that involves the entire lobe, and a segmental pneumonia involves the anatomical seg ment of a lobe. Generalized pneumonic processes occur with aspiration of vascular spread of an infec tious agent (Figure 10-5). The roentgenographic find ings of bronchopneumonia are varied. The earliest manifestation may consist only of peribronchial cuff ing. The disease, however, spreads rapidly to the alveoli. More often, however, bronchopneumonia is manifested by multiple, ill-defined nodular densities (acinar nodules) that are patchy. As these acinar nod ules become confluent, airspace consolidation devel

FIGURE 10-6

ops. As the disease progresses, segmental and lobar

A 5-cm cavitary ahscess is seen on the le ft with an air fluid

pneumonias can be seen.

level and a relatively smooth wall. This patient was

Pulmonary abscesses and cavities may occur sec ondary to pneumonia. An abscess occurs when there is a breakdown of the tissues of the lung, with the area replaced by infectious materials (of water den

probably recumbent and lying slightly on the left side to aspirate materials to this area, which was first a pneumonic process in the superior segment of the left lower lobe and progressed to an abscess cavily.

sity). When the infectious materials empty into the bronchus and air communicates with the abscess, a cavity develops in that area of the lung. Lung ab scesses often result from aspiration and they are

catheters may result in a traumatic pneumothorax.

often found in the area s dependent at the time of the

The appearance is fairly characteristic, and there may

aspiration. Thus abscesses occur in the area that is

be an associated air fluid level with a hydropneu

downward by gravity, depending on the upright or

mothorax (secondary to minor bleeding from the

reclining position of thc individual (Figure 10-6). If

punctured lung). Pleural effwiions, or the accumula

the pleura is penetrated by the abscess, an empyema

tion of fluid between the lung and chest wall, can be

develops; and if a cavity communicates with the

seen in increased hydmstatic pressure (congestive

pleura, a pneumothorax de velops with a br on

heart failure [CHFJ), diseases of the pleurae (malig

chopleural fistula. A pneumothorax

nancies) or diseases of the lung (emphysema sec or

gas in the pleural space devel

ondary to pneumonia).

ops when the pleural .'pace communicates air through

Ale/ectasis is thc term used for incomplete expan

ei ther a defect in the chest wall or a defect in the

sion of a portion or all of the lung. A loss of air in the

pleural surface of the lung. As the air accumulates be

alveoli in the atelectatic area occurs. Atelectasis is a

tween the chest wall and the lung, the lung becomes

sign of disease, since it ·is always secondary to an

compressed and moves away from the chest wall

other lesion, such as (I) obstruction of a bronchus;

(separated by air) (Figure 10-7). Chronic interstitial

(2) loss of ability for pulmonary expansion as a result

disease and emphysema are often complicated by a

of pleural disease, diaphragmatic disease, and masses

spontaneous pneumothorax. Traumatic causes such

in the thorax; or (3) volume loss from local or gener

as automobile accidents or inseltion of central venous

alized pulmonary fibrosis. Atelectasis is a loss of vol


10


165

ume in the area involved and results in a decrease in size or a change in position of the surrounding struc tures (Figure 10-8). Congestive heart failure, uremia and pulmonary edema may be manifested by a "diffuse" pattern on the chest film (Figure 10-9). In CHF, there is a pro gression of roentgenographic changes as the disease evolves into pulmonary edema. The first manifesta tion is an increase in the antigravity vasculature of the lungs (redistribution of blood flow to the upper lobe vessels). The next stage is manifested by a loss of the distinct margins of the vessels. This is fol lowed by accumulation of fluid in the interstitial spaces (around the alveoli). Pulmonary edema is pre sent when the fluid seeps from the interstitium and makes the alveoli opaque. Pulmonary edema is radi ographically indistinguishable from diffuse pneumo nia. CHF usually is associated with cardiomegaly

FIGURE 10-7 The chest x-ray reveals separation of the visceral from the

(enlargement of cardiac silhouette) and may be asso

parietal pleural line and absence of vessels laterally. A

ciated with pleural effusions and/or pericardial effu

"straight line" is seen at the rIght base, indicating a gas

sions (Figure 10-10).

fluid level in a hydropneumothorax. Fibrotic and irregular pulmonary changes in the lungs indicate underlying interstitial disease, which was a pneumoconiosis (silicosis).

Pulmonary malignancies may be both primary and metastatic. Mass formation is characteristic, and there may be atelectasis when the mass o b s tructs a

FIGURE 10-8 A, The PA film demonstrates loss of the right heart border and the downward shift of the minor fissure, with atelectasis of the right middle lobe secondary to a radiolucent foreign body in the right middle lobe bronchus. No air remains in the middle lobe, thus it is dense. B, The

arrow

on the

lateral view points to the residual tissue density of the right middle lobe, which is atelectatic.


166

PART II


FIGURE 10-9

FIGURE 10-10

The central lung fields reveal increased density and there is

The chest film reveals cardiomegaly (enlargement of the

sparing of the peripheral areas in "butterfly" pulmonary

cardiopericardial silhouette) and bilateral pleural effusions

edema. The patient has had a thoracotomy, and chest tubes

are more marked on the right than on the left. Vascular

are in place.

structures are blurred with interstitial edema.

FIGURE 10-11 A, A mass is present in the left hilar area obstructing the left upper lobe bronchus. There is atelectasis of the left upper lobe and lingula secondary to the malignancy. B, The lateral view reveals an S-shaped curve of tumor mass and atelectasis.


10


167

articulating facets in rheumatoid arthritis of the spine. An obese individual may have severe difficulty with respiration, not only because of the excess fat and added weight on the thorax, but also because of the increased load on the cardiovasculature system. This increased load and hypoxemia may result in CHF.

REVIEW QUESTIONS 1. What are the three categories of radiographic studies of the chest? 2. How may the quality of the film impact interpre tation? 3. What are the five basic densities seen on a radi FIGURE 10-12

ograph?

This chest x-ray of a kyphoscoliotic patient reveals a markedly abnormal, reverse S-shaped curve of the thoracic spine deforming the mediastinal structures and ribs. This

4. What principles are used consistently to interpret radiographs? 5. How can lung disease cause a change in translu

patient is breathing primarily with the diaphragms.

cency of the Xray? 6. How can mediastinal deviation diagnose pneu mothorax or atelectasis?

bronchus (Figure 10-11). Secondary findings such as widening of the mediastinum, rib metastasis, pleural masses or pleural fluid, and encasement of vascula

Bibliography

ture with hyperlucency beyond the tumor may be

Felson, B. (1973). Fundamentals of chest roentgenology (2nd ed.).

seen. Alveolar cell carcinoma may appear like a

Philadelphia: WB Saunders. Fraser, R.G. & Pare, J.A. (I 988). Diagnosis of diseases of the chest (3rd ed.). Philadelphia: WB Saunders.

pneumonia. Involvement of the phrenic nerve may result in paralysis of the diaphragm with elevation. Thoracic deformities such as kyphoscoliosis may severely impair the respiration of an individual (Fig ure 10-12). The abnormal shape and direction of the spine interfere with the leverage necessary for move ment of the ribs with respiration. Severe impairment of respiration may occur when there is fusion of the

Freundlich, I.M. & Bragg, D.G. (I 992). A radiographic approach to diseases of the chest Baltimore: Williams and Wilkins. Meschan, I. (1976). Synopsis of analysis of roentgen signs in gen· eral radiology Philadelphia: WB Saunders.

Murray, J.F. & Jade, J.A. (1994). Textbook of respiratory medicine Philadelphia: WB Saunders. Paul, L.W. & Julll, J.H. The essentials of roentgen interpretation (3rd ed.). New York: Paul B Hober, 1972.


Electrocardiogram Identification

Gary Brooks

KEY TERMS

Arrhythmia

Electrocardiogram (ECG)

Artifact

Syncytium

Bradycardia

Supraventricular

Depolarization

Tachycardia

INTRODUCTION

The ECG is an essential tool in the physician's di

The heart is a vital link in the oxygen transport sys

agnosis and medical treatment of cardiac disease. In

tem, pumping blood to the pulmonary and peripheral

formation provided by the ECG may also assist the

circulation systems to supply oxygen and other nutri

physical therapist (PT) in the assessment of a pa

ents required for metabolism in all tissues. The beat

tient's readiness for and response to physical activity.

ing heart generates rhythmic, electrical impulses that

PTs in many different practice environments have ac

cause mechanical contraction, or the pumping action,

cess to information afforded by the ECG. For exam

of cardiac muscle. Some of the electrical current pro

ple, in an acute care or rehabilitation setting, a pa

duced by these rhythmic impulses is detectable by

tient's baseline ECG, with an interpretation, may be

electrodes that may be placed on the surface of the

available within the medical record. Documentation

skin. Current flow during the cardiac cycle is then

accompanying a referral for outpatient physical ther

recorded as the characteristic waveforms of the elec

apy may include a reference to the patient's ECG. In

trocardiogram (ECG). Mechanical events such as con

other settings such as an intensive care unit or cardiac

traction and relaxation of the myocardium are infelTed

rehabilitation program, ongoing monitoring of a pa

from the waveforms produced by the ECG.

tient's ECG may be performed during evaluation and 169


170

PART II


treatment procedures. It is therefore crucial that all

polarization, during which a stimulus of greater than

PTs have a basic understanding of the uses and limi

normal intensity is necessary to depolarize the cell

tations of the ECG in their practices.

again. The refractory period of atrial cells is signifi

This chapter briefly reviews the basic anatomy

cantly shorter than that of ventricular cells allowing a

and physiology of the myocardial conduction sys

more rapid intrinsic atrial rhythm than intrinsic ven

tem as it relates to the ECG. The configuration of

tricular rhythm. Therefore atrial rhythms pace the

the normal ECG is presented and discussed along

heart, including the ventricles, given intact atrioven

with several methods of quickly determining heart

tricular (AV) conduction.

rate a n d rhythm from an electro c a r d i o g r a p h i c

Closure of the slow Ca++ channels at onset of repo

record or "strip." Some o f the more common dys

larization is accompanied by opening of K+ channels,

rhythmias are examined, as are some other patho

causing a rapid outflow of K+, which restores resting

logic features. Throughout the chapter, the uses and

negative membrane potential. During the cell's resting

limitations of the ECG in physical therapy practice

phase, Na+ and Ca++ are actively pumped out of the

are highlighted.

cell, and K+ is pumped into the cell, restoring ionic gradients needed for repolarization (Shih, 1994; Guy ton, 1991; Smith and Kampine, 1990).

PHYSIOLOGY AND ANATOMY

It is the electrical current produced by ionic

OF THE CONDUCTION SYSTEM

flow that is transmitted through the conductive tis

Generation of the Action Potential

sues surrounding the heart. This current is de

The action potential, or cardiac impulse, is generated

tectable by surface electrodes, enabling the record

by ionic flow across myocardial cell membranes. In

ing of the ECG.

the cell's resting state, a negative membrane potential exists, based on the relative concentrations of sodium (Na+), Calcium (Ca++), and Potassium (K+) in the in

The Conduction System

ternal and external cellular environments. Membrane

Because myocardial cells are arranged as a syn

potential changes rapidly at the onset of depolariza

cytium, an impulse propagates, or spreads to adjacent

tion, with the opening of Na+ and Ca++ channels, al

cells, causing them to make contact also. This

lowing these ions to cross the membrane and enter the

arrangement alone does not pellllit the heart to func

cell. Calcium then becomes available for contraction

tion as an effective pump. It is the conduction system

of cardiac muscle myofibrils. During depolarization,

that initiates and rapidly transmits impulses to other

the membrane's potential becomes positive and the

locations within the myocardium, allowing for effec

cell contracts. As in skeletal muscle, the Na+ channels

tive, coordinated myocardial contraction and pump

are fast-opening and fast-closing mechanisms, allow

ing. The conduction system is comprised of special

ing Na+ to rapidly enter the myocardial cell on depo

ized cardiac muscle that contracts minimally, because

larization. Unlike skeletal muscle, however, cardiac

it contains few contractile myofibrils.

muscle has a prolonged depolarization phase as a re

Any portion of the conduction system is capable

sult of the slower and extended opening of the Ca++

of self-excitation and may act as a pacemaker, gener

channels. During depolarization, there is also a de

ating action potentials. However, because of the in

crease in membrane permeability to K+, for which

trinsically more rapid rate of spontaneous depolariza

there is an outward gradient. A plateau phase of the

tion of the sinoatrial (SA) node, it normally acts as

action potential exists, during which outward flow of

the heart's pacemaker. The rate of depolarization of

K+ ions is inhibited. This prolongs depolarization and

the SA node determines the heart rate. In the absence

delays return to the resting membrane potential.

of an impulse from the SA node, the atrioventricular

Each cell has an absolute refractory period during

(AV) node depolarizes spontaneously, taking over as

depolarization, meaning that an additional stimulus

pacemaker, with the important difference that the rate

will not cause an additional depolarization. A brief,

of depolarization is lower than that of the SA node.

but significant, relative refractory period follows de-


The pathway of a normal cardiac impulse may be

11


171

R R-R

o

I

s

I I I I I

FIGURE 11-1 Relationship of ECG complex to conduction pathway. (From Brown, K.R., & Jacobson. (1988).

MCI.I'lering dysrhYlhmias: A problem-soLving guide. Philadelphia: FA Davis.)

followed, highlighting its relationship to the cardiac

suiti ng in a dela y i n g of the impulse b ef o r e i t

cycle. Figure I I-I displays the association of the con

reaches t h e ventricular conduction system. This

duction system and its components with the ECG.

pause in impulse propagation allows the atria to

Atrial depolarization is initiated by a spontaneously

contract and fill the ventricles with blood_ The P-R

generated impulse that originates in the SA node. The

interval of the ECG represents this period between

impulse is then transmitted throughout the atrial mus

onset of atrial depolarization and the onset of ven

cle resulting in atrial contraction. This event is

tricular depolarization. Normally the P-R interval

recorded as the P-wave of the ECG. The impulse is

lasts between

also transmitted, via rapidly conducting internodal

Jacobson, 1988).

12 and

W seconds

(Brown and

pathways, to the A V node. Atrial repolarization is not

Following passage through the AV node, the im

recorded by the ECG, because it occurs during and is

pulse continues to the Purkinje's fibers, which trans

hidden by ventricular depolarization.

mit the impulse rapidly to the ventricular endo

Impulse conduction within the A V node and the

cardium. This initiates ventricular depolarization,

AV bundle (bundle of His) slows considerably, re

which is represented in the ECG by the QRS complex.


172

PART II


The depolarization wave propagates relatively slowly

U-wave may be seen. The U-wave was considered

throughout the ventricular myocardium. The span of

to have little physiologic or pathologic significance

1990).

However, U-wave in

time elapsing during ventricular depolarization is re

(Smith and Kampine,

flected by the

version may now be considered to correlate with

between

1988;

0.06

RS interval, which normally ranges

and

0.11

secon s

Smith and Kampine,

1990).

n an

Jacobson,

myocardial ischemia (American College of Sports Medicine,

Ventricular depo

1991).

Note that the ventricles remain in

larization originates in the interventricular septum,

a state of contraction until slightly after repolariza

creating the Q-wave, which is normally small or ab

tion. This period of contraction corresponds to the

sent. The depolarization wave next spreads to the apex

Q-T interval on the ECG. Diastole, therefore, begins

and then to the right and left ventricles, causing the R

subsequent to the end of the T-wave and continues

and S-waves. Depolarization also propagates in an en

until the next ventricular depolarization. Note also

docardial to epicardial direction within the ventricles

that atrial depolarization and contraction occur dur

(Lilly,

J993;

Guyton,

1991).

ing diastole.

The T-wave of the ECG represents ventricular re polarization. It is preceded by the S-T segment, dur

THE ELECTROCARDIOGRAM

ing which depolarization has been completed and

Recording the Electrocardiogram

repolarization is yet to begin. The configuration of the S-T segment is an important marker of myocar

Before examining the timing of the wave forms and

dial ischemia or infarction. Following the T-wave, a ----

the rhythms of the ECG, a basic understanding of the

I I n-- ilr-fi-r-.VR 1 IT '-l- I Tl vl I I' i - 1- · ITl-I-H-j 1 I I '

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! I ! I I

.

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-R

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Iffi1 rl- f I+H i ! ;ffft-TmTfFI' r: i}Tiii H {if ttl-mUll I I 111 1 ! i II ! 1I11I1II1I CB-8 i ± j LU i..Ult LI I I ttr I, ! !

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....

FIGURE 11-2

A normal 12-lead ECG tracing.


]1


173

-------

principles of

is needed. A stan

A VR. A VL, and A VF are derived from the electrical

12-lead

and

sum of the three standard limb leads. The transverse

medical management of cardiac conditions. An ex

plane leads are referred to as the precordial leads.

11

Imagine that each of the 12 leads "views" the heart

ample of a normal 12-1ead ECG is seen in 2. Six leads record the electrical

in the frontal

from a different angle, therefore

plane, and six leads record signals in the transverse

different locations of the heart

plane. The frontal plane leads include three standard limb II, and III. Three augmented limb leads,

(downward) when current travels away from a lead.

V6

V5

I-- V6

I- V5

,.i Vl

V2

-'\.

VA

V3

FIGURE 11-3 leads.


174

PART II


indicates appropriate conduction of impulses from

Other lead configurations may be used for exercise

testing (American College of Sports Medicine, 1991).

atria to ventricles.

Single-lead monitoring is commonly used during ex

•

What is the P-R interval? A P-R interval of greater than

ercise training or in acute care settings.

0.20

seconds indicates delay in conduction

from atria to ventricles.

Evaluating the ECG Strip

•

Is the QRS complex of normal duration and mor phology (shape)? A QRS complex greater than

The evaluation of an ECG should be approached in a

0.12

systematic fashion. The following questions are use

within a ventricle or was conducted abnormally through the ventricular conduction system.

ful to appreciate the information that is relevant to current clinical practice (Cummins, •

seconds indicates either that an impulse arose

1994).

By answering each of these questions, the tendency

What is the rate and pattern (regularity) of the

to "eyeball" the rhythm and make a quick but inaccu

rhythm? If the R-R interval, that is, the distance

rate assessment is avoided.

between successive R-waves, is inconsistent, is the

Determination of Heart Rate

pattern irregular? •

Does a P-wave precede every QRS complex? This indicates appropriate atrial activity.

Several quick methods estimate heart rate. Most

•

Is there a QRS complex after every P-wave? This

printed and displayed ECG recordings indicate a heart

I

J I

m =l-rIlIl_ L-J- -+ -- +-+--r-t-i R !-t- lr-r 0.2second 4s , .oo n +-+- -r1 L-+-t-t r1 rt lIlr

segment

I--H--+--t---t-I' t PR

,

,

-.l

I-+-

-r-rI, j

,

I

Ll"

!.i '

I

I!

segment I-++-t -nrmmnml 50.5mmmv. -+I I '

I

S

I! -'

',

111 i

0.1mv

!

I

, !

interval I ITi1 I 1 1 , aRS-.lInterva ' ..l

PR

1.--+-++ - -

I

ST

,

ll

, "

''

I I .:.. interla, a. T 1-' 1 1

!

1

1

J

FIGURE 11-4 A normal ECG showing characteristic waves, intervals, and segments, and some of the features of the traci ng paper.


11


175

rate. This must be interpreted with caution, however.

the rate would be estimated as falling between 100

The presence of artifact (extraneous deflections of the

and 75, or close to 80 beats per minute (BPM).

waveform caused by movement or electrical intelfer

In many clinics, rulers are available that are cali

ence) may render inaccurate the displayed or printed

brated so that heart rate may be estimated quickly by

heart rate. This is a common problem dUling activity

aligning markings on the ruler with features of the

or exercise, the circumstances during which many PTs

ECG strip. For example, after the arrow on the ruler

monitor patients. It is possible to calculate or to esti

is placed on an R-wave, count two R-waves to the

mate a heart rate from a printed ECG strip because, by

left and read the number at that position on the ruler.

convention, the recording paper is divided into I mm

In Figure 11-6, this method approximates the heart

squares and larger 5 mm squares, which are defined

rate as 74 BPM.

by heavier lines (Figure 11-4). Also by convention,

It is important to note that the preceding two

the standard paper speed for an ECG recording is a

methods are useful only if the rhythm of the ECG

rate of 25 mm/second. Each millimeter of length then

strip is regular, that is the R-waves are equally

represents 1125th, or 0.04 seconds, and each 5 mm

spaced, occurring at consistent intervals. Should the

block represents one fifth, or 0.20 seconds. Some

rhythm be irregular, with R-waves appearing at vary

monitor systems place a mark on the recording paper

ing intervals, another method must be employed to

at 25 mm, or I-second intervals.

estimate the heart rate.

There are several methods of estimating heart rate

Recall that the ECG graph paper is divided into

from a printed ECG strip. On a printed ECG strip,

boxes, with the horizontal spacing representing time

find an R-wave located on or near a heavy vertical

intervals of 0.04 seconds for each small (I mm) box

line. Proceeding to the left of that R wave, for each

and 0.20 seconds for each larger (5 mm) box. It fol

subsequent heavy vertical line, assign the following

lows that I second in time is represented by five

numbers: 300 for the first heavy line encountered,

larger boxes. A mark may be placed at 1- or 3-second

150 for the next followed by 100, 75, 60, 50, and 42

intervals, enabling quicker appraisal of heart rate

(Figure 11-5). Stop at the first heavy vertical line fol

based on a 6-second strip. The procedure is as fol

lowing the next R wave that is encountered. The

lows. Obtain a printed strip of sufficient length, cov

heart rate may be estimated as falling between the

ering more than 6 seconds. If l-second marks are not

two most recently assigned values. In Figure 11-5,

present, it may be convenient to place a mark at every

FIGURE 11-5 "Count-off" method of estimating heart rate.


176

PART II

,


, ' , f' f'z',

,J

+b '

V2

.. ... •

j

IfPL_, t. l

1 -.1

;:It"

-I '

r

- '

-

,

. tH-

.

'

I'

..

. .... +

I t

r.-- 'f' T ' 'r '4rf'

1.. ....11

t'.. ,.

II .

..; . t 't " ,.. • .r......

.•

.

.

..

.

"

.--

. .., .. 1..

,

;..

t

t

,

?r t_" 1" , '""' '/,j ._

,

'''lift'

-�

· 111111111 nil ] II r 1 1 II

"

'''t-,

fj7r'

. -F

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.

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1.

I " 1', :;-rt·

"

Heart rate (two cycles from reference arrow) chart rate (25 mm/ sec)

•

,".

.r

.!.•. t

"I

FIGURE 11-6 Using a rate-ruler to confirm heart rate.

FIGURE 11-7 Heart rale estimation in an irregular rhythm (atrial fibrillation).

fifth large block. Next, select a I-second mark or a heavy vertical line on the left side of the strip, and

Evaluation of Rhythms Electrocardiographic monitoring is an impOitant evalu

proceed to the right for a length corresponding to 6

ation tool during the treatment of individuals with his

seconds. If I-second marks are counted, do not count

tory of or potential for acute myocardial infarction (MI)

the starting mark or there will be only as-second

or myocardial ischemia. Most cardiac deaths are a re

strip. Count the number of R-waves within the 6-sec

sult of lethal arrhythmias, for which there is increased

ond recording, and multiply by lO. That is estimated

risk in the presence of infarction or ischemia. Rapid

heart rate. Several 6-second strips may be analyzed to

recognition of lethal an·hythmias, or arrhythmias that

document a heart rate range of an irregular rhythm

may deteriorate into lethal a.rrhythmias, is essential for

11-7). The rate of this irregular rhythm is es timated at 70 BPM.

all health professionals involved in the care of individu

(Figure

als with cardiac disease. The arrhythmias described in


11


177

FIGURE 11-8 Normal sinus rhythm.

this chapter are those that must be recognized by providers of Advanced Cardiac Life Support as deter mined by the American Heart Association (Emergency Cardiac Care Committee and Subcommittees, 1992). Normally, a cardiac impulse is generated by the SA node, causing atrial depolarization. This is fol lowed by a slight delay in the A V node, after which the impulse is conducted to the ventricles causing ventricular depolarization. These events are seen in their normal spatial and temporal sequence in normal sinus rhythm (Figure 1 1-8). A P-wave precedes every QRS complex and every P-wave is, in turn, suc ceeded by a QRS complex. This occurs within an in terval of 0.20 seconds (one large box), as determined by the P-R interval. The QRS complexes occur within a range of 0.04 to 0.11 seconds, indicating that ventricular impulse conduction and depolarization is occurring in a normal interval. The positively de flected T-wave indicates normal ventricular repolar ization. Because the SA node spontaneously depolar izes at a rate of between 60 and 100 BPM, the rate of normal sinus rhythm must fall within these limits. The identification of arrhythmias affects clinical decision making, particularly with regards to a pa tient's readiness for and/or response to activity. Clini cal significance of arrhythmias range from benign to lethal. The clinical significance of a given arrhythmia is determined by a number of considerations. Some of these considerations include the following: Is there evidence of hemodynamic compromise? Is the ar rhythmia a new or unusual finding? Might the ar

rhythmia be a precursor to a more serious or perhaps lethal arrhythmia? Is this an acute occurrence or a chronic arrhythmia pattern? The clinical response to a patient with an arrhythmia depends on the answers to these questions and the treatment setting. ARRHYTHMIA IDENTIFICATION Supraventricular Arrhythmias

Supraventricular arrhythmias arise from an abnormal ity of impulse generation or conduction "above" the level of the ventricles. The abnormality may occur in the atria or at the level of the A V junction. Supraven tricular arrhythmias may be categorized as sinus, atrial, or junctional alThythmias. A cardiac rhythm may be a sinus rhythm, but with an irregular or abnormally rapid or slow rate. Sinus ar rhythmia is an in'egular sinus rhythm with varying R-R intervals (Figure Il-9). This is a normal variant that is associated with the individual's respiratory pattern. Sinus bradycardia is a sinus rhythm occumng at a rate of less than 60 BPM (Figure 11-10). This rhythm may significantly reduce cardiac output, causing hemody namic compromise, manifested by hypotension or symptoms such as dizziness, lightheadedness, or syn cope. On the other hand, individuals taking beta-block ers, medication that slows the heart, may exhibit this as their normal rhythm, as may individuals who achieve a high level of physical conditioning. Sinus tachycardia is a sinus rhythm OCCUlTing at a rate of greater than 100 BPM (Figure 11- 1 1). Sinus tachycardia, or any other


178

PART II


ft' 'trr. " '' -,

.

.•

'

+t-;

. ,.. , '.

_",-,-::C' .

t

,.

.4

: '

f

t

. •

"

fr" ,t" " ,., ' L

L·

;

'

-

'

: .

,.

;

i' "

..

...:.·1._ t

.

_

.

.

4 ·

FIGURE 11-9 Sinus arrhythmia.

tt· "

.... . ..

"

: '!.'" L

FIGURE 11-10 Sinus bradycardia.

f

l , of fl I I (}t L,

1

l'"r

L

•

1

L..1-L r

t::°

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I, . .J.:... L

1"�1

FIGURE 11-11 Sinus tachycardia.


t

_

'· L t

L

'

.1' I

,

,

L

c

11


179

FIGURE 11-12 Premature atrial complex.

form of tachycardia, increases myocardial oxygen de

abruptly and spontaneously reconverting to the previ

mand, or the workload on the heart. This may initiate

ous rhythm within seconds or minutes. The P-wave is

or exacerbate ischemia in the presence of coronary

often not visible, making assessment of atrial or junc

artery disease (CAD).

tional origin difficult, but the duration of the QRS

A common form of arrhythmia is a "premature"

complexes occurs within an appropriate interval. The

complex, that is, a beat that occurs sooner than ex

R-R interval, however, is markedly shortened. Figure

pected given the established rhythm. A premature

11-13 demonstrates supraventricular tachycardia at a

atrial complex, or PAC, is an early beat of atrial origin

rate of [90 BPM. Other related forms of SVT include

(Figure [1-12). An R-wave appears closer to its pre

paroxysmal atrial tachycardia (PAT) and multifocal

ceding R-wave than the other R-waves in the estab

atrial tachycardia (MAT). Clinically, patients with

[ished rhythm. Closer inspection reveals the presence

SVT may perceive a "racing" heart rate, which may

of a P-wave associated with the QRS complex, mean

be quite distressing. At very rapid heart rates, for ex

ing that the impulse first depolarized the atria before

ample, greater than 170 BPM, diastolic ventricular

being conducted to the ventricles. Sometimes the AV

filling time is markedly reduced, which may cause

junction may initiate an early beat, causing a premature

hemodynamic compromise. Symptoms associated

junctional complex or PJc. When this occurs, the R

with inadequate cardiac output, such as dizziness,

wave appears earlier; however, there may be no associ

lightheadedness, and syncope may ensue. Some indi

ated P-wave, or there may be an unusual P-wave, one

viduals with SVT remain asymptomatic; the rhythm

that is inverted or following the QRS complex. An in

being detected incidentally, for example, during rou

verted or late P-wave indicates that the impulse was

tine pulse or telemetry monitoring.

conducted in retrograde (backward) fashion. Clinically,

Atrial fibrillation is the most common, clinically

a premature atrial or junctional complex may be pal

encountered arrhythmia, seen in more than 5% of pa

pated as a "skipped" or early beat during pulse taking,

tients over age 69. (National Heart, Lung and Blood

or the patient may perceive a palpitation or skipped

Institute, Working group on atrial fibrillation, 1993)

beat. Otherwise, these arrhythmias are usually of little

Atrial fibrillation is characterized by inconsistent, ir

clinical significance (Brown and Jacobson, [988).

regular R-R intervals with an absence of true P-waves.

A more serious supraventricular arrhythmia is

P-waves may be replaced by multiple, fibrillatory F

supraventricular tachycardia, or SVT. In this arrhyth

waves of varying configuration. This arrhythmia signi

mia, the healt rate is rapid, exceeding 150 BPM. The

fies that there is no established sinus or atrial pace

tachycardia may be sustained, lasting hours or even

maker, rather that many impulses are simultaneous[y

days, or may be "paroxysmal" (PSVT), appearing

generated from multiple locations within the atria. The


180

PART II


FIGURE 11-13 Supraventricular tachycardia.

atria, therefore, are not pumping effectively which, in

(Figure 11-15), the QRS complex is not preceded by

turn, may impair ventricular contraction. This is be

a P-wave. The AV node may generate an isolated

cause of the loss of the additional ventricular filling

"escape" beat, or it may take over as the heart's pace

supplied by atrial contraction. Impulses do conduct

maker. Sustained nodal

through the AV junction to the ventricles; however,

ally between 40 and 60 BPM, corresponding with the

this occurs inconsistently resulting in the irregular R-R

inherent rate of spontaneous AV node depolarization.

or

junctional rhythm is usu

interval. The ventricular response to atrial fiblillation is important. A rapid ventricular response, resulting in tachycardia, may cause hemodynamic compromise with associated symptoms or poor activity tolerance.

Ventricular Arrhythmias Ventricular arrhythmias result from spontaneous de

Of additional clinical significance is the association

polarization of a region within ventricular my

between atrial fibrillation and embolic cerebrovascular

ocardium; a region outside the normal pathway for

accidents. Figure 11-7 illustrates atlial fibrillation with

impulse generation. For this reason, the site of im

a "controlled," that is, less than 100 BPM, ventricular

pulse generation is called an ectopic focus. Ventricu

response. Pulse monitoring of an individual in atrial

lar arrhythmias may be distinguished from supraven

fibrillation reveals an irregularly irregular pattern. Another arrhythmia that is characterized by abnor

tricular arrhythmias, in that the QRS duration of a ventricular arrhythmia is longer than normal 0.12

mal atrial activity is atrial flutter, seen in Figure 11-

seconds. The appearance of ventricular arrhythmias

14. In this rhythm, P-waves are replaced by F-waves

may be characterized as being "wide and weird." It is

that have a distinctive morphology often referred to

important to point out that not all rhythms with a

as a "saw tooth" or "picket fence" appearance. Of

QRS duration greater than 0.11 seconds represent ec

clinical importance is the ratio of atrial to ventricular

topic ventricular beats; some widened QRS rhythms

conduction and whether or not the patient is hemody

result from d isturbances of impulse conduction

namically stable (Brown and Jacobson, 1988).

within the ventricles, rather than from impulse gener

Because the intrinsic rate of spontaneous depolar

ation within the ventricles.

ization of the AV node is less than that of the SA

The reason for the widening of the QRS complex

node, spontaneous AV node depolarization is nor

resulting from ventricular impulse conduction distur

mally prevented. However, in the absence of an atrial

bance or impulse generation is apparent when one con

impulse the AV node depolarizes spontaneously and

siders the normal conduction of a sinus impulse within

generates an impulse that then is conducted to the

the ventricles. An impulse normally is rapidly con

ventricles. Thus in junctional rhythm or nodal rhythm

ducted to ventricular myocardium via the Purkinje's


11

FIGURE 11-14

ff--


1

TI

"fir rtJ

181

hi:. f ,1t;f TT1 _n_1 ,_

l

Atrial fluller.

FIGURE 11-15 Junctional rhythm.

11-16).

fibers. This assures that the impulse reaches all regions

during an ectopic beat (Figure

of ventricular myocardium in a timely fashion, with

rhythm (bottom) is recorded simultaneously with the

An ECG

subsequent coordinated depolarization and contraction.

record of arterial blood pressure monitoring (top).

Within ventricular myocardium itself, however, propa

The appearance of the "wide and weird" complex re

gation of the depolarization wave proceeds more

sults in significant diminution of the corresponding

slowly, as a result of the syncytial anangement of my

arterial pressure wave.

ocm'dial cells.

The most common form of ventricular arrhythmia

An impulse generated within the ventricles, out

is a premature ventricular complex, or PVc. In Fig

11-16 the wide and weird QRS complex appears

side the normal conduction pathways, initially depo

ure

larizes surrounding local myocardium. The depolar

early, interrupting the established rhythm. A pause

ization wave then spreads outward from that focus,

often follows a PVC, after which the established

but is propagated at a slower velocity. Ventricular

rhythm resumes. Clinically, a PVC may be perceived

contraction, in this case, is not coordinated; some re

by a patient as a "skipped" beat or a palpitation. If

gions contract well b e fo re the depolarization wave

pulse monitoring occurs during a PVC, the examiner

reaches regions remote from the ectopic focus. It fol

will likely sense a "skipped" or irregular beat.

lows that the ventricular ejection of blood is reduced

PVCs sometimes happen in patterns, occurring at


182

PART II


l.L I

.... ' t' SPEEIJ)

If j

25

=

+ l L

Uti

1_-,-

I

.J.:.

L

.

.

I

I.

f t1 t�-r "

MM/SECOND I

1"""'j

I

LL

+- t .:]

FIGURE 11-16 Diminished arterial pressure wave following a PVc.

FIGURE 11-17 Ventricul ar bigeminy.

m!EulittIOOIOO·,

t1 '

IOOlfirkifmlffE[fffil

Tl-tffhtm flffimf!r.::17YrnCTftlTmrT];T1T ·Hfflt

regular i n t e rvals. A pye o ccurs in ventricular big eminy on every second b e a t, i n ventricular trigeminy on every third beat, and in ventricular quadrigeminy on every fourth beat. Figure 11-17 il lustrates ventricular bigeminy. With these rhythms, a regularly irregular pattern may be noted during pulse monitoring. pyes may also occur twice in succession as a ventricular couplet. seen in Figure 11-18. pyes that originate from more than one ectopic

rnl%'I@I#tllff#tmlL·'.r,· gMtmIff1F atffi lmmm..

focus are termed multifocal pyes. In this circum stance, the waveforms will have different morphol

FIGURE 11-18

ogy according to the locations of the ectopic foci. Re

Ventricular couplet.

member that the positive or negative deflection of the


11


183

FIGURE 11-19 Multifocal PVCs.

FIGURE 11-20 Ventricular tachycardia.

waveforms depends on the direction of depolariza

to most arrhythmias is beyond the scope of this chap

tion, as viewed by the lead used for monitoring. In

ter; however, some arrhythmias demand an immedi

Figure 11-19 the first pve seen has an initial positive

ate response if observed.

deflection, whereas the second pve seen has an ini

Ventricular tachycardia (V -tach, or VT) (Figure

tial negative deflection. Each of these pves comes

11-20) is defined as three or more consecutive pves at a rate greater than 100 BPM (Akhtar, 1990). This

from a different ectopic focus. The physical therapists's (PT's) decision-making

is a serious and potentially lethal arrhythmia that may

process in response to observation of ventricular ec

require emergency measures be undertaken. During

topic beats is complex and may not be easily grasped

v-tach all complexes are ventricular in origin. V-tach

by the entry-level practitioner. Factors such as pres

sometimes occurs in "runs" of three or more ectopic

ence or absence of symptoms, the acuity of the pa

complexes followed by reversion to the baseline

tient, and whether the rhythm is a new finding all in

rhythm, or it may be sustained. Effective circulation

fluence a clinical response. The presence of a pattern

may be preserved, or it may be seriously compro

such as bigeminy, couplets, or multifocality is also

mised or absent in sustained v-tach. A patient may be

considered. Further elucidation of clinical responses

asymptomatic, particularly if only a brief run of


184

PART II


. ::;

. : ;,' -r-±l t-f.,r.-f+-r"*, -'-!

+O-O

•1

L& 'I

'--o-rl-.-...-,b-4';""'-"-+. ' . J n

J /. . ,. ,. 1

: •

I

'

.

1\ ,

1 _tl_, ,..,t . .

. +-

' .

:- ..!r....

T

.

r

FIGURE 11-21 Ventricular fibrillation degenerating into asystole.

v-tach was experienced. If VT is sustained, the pa

ment artifact. Unwary therapists have hastily sum

tient may be asymptomatic, symptomatic, or uncon

moned help on observing v-fib or asystole, only to

scious and pulseless. The PT's response depends on

feel foolish when a lead is reattached to the patient.

the rhythm, regardless of whether it is sustained, and

These arrhythmias are always accompanied by loss of

the patient is symptomatic or conscious. Clinical re

consciousness and pulse; a clinician should assess the

sponses range from cessation of activity, ongoing pa

patient before taking action. Similarly, during activity

tient observation and immediate notification of a

or exercise, movement artifact may easily be mistaken for v-tach. By assessing the patient and asking him or

physician to a full code. Ventricular fibrillation (V-fib, VF) is a lethal ar

her to "hold still," the issue may be quickly resolved.

rhythmia accompanied by immediate loss of con sciousness and loss of circulation, that is, cardiac ar rest. It is characterized by disorganized, simultaneous

Conduction Blocks

firing of multiple, ectopic ventricular foci; there is no

Conduction blocks are another type of ECG abnor

organized rhythm (Figure 11-21). Effective ventricular

mality with which PTs should be familiar. The propa

contraction ceases and cardiopulmonary resuscitation

gation of a cardiac impulse may be inhibited or termi

is indicated until defibrillation is available. Death fol

nated along the conduction pathway. Blockage can

lows unless defibrillation successfully restores an ef

occur at the sinus node, between the atria and ventri

fective rhythm. Conditions that render the myocardium

cles, Or within the ventricular conduction system.

vulnerable to ventricular fibrillation include v-tach,

Sinus block occurs if the impulse cannot propagate

myocardial ischemia or infarction, dilatation of the

beyond the sinus node. In this case, the AV junction

heart, hyperkalemia, or electric shock (Guyton, 1991).

usually takes over as the pacemaker, and a junctional

If not successfully treated, v-fib may further de

rhythm is seen with the absence of P-waves.

generate into asystole, which indicates complete ab

More common are the AV blocks. They are ranked

sence of ventricular electrical activity (Figure 11-21).

as first-, secondo, or third-degree, depending on the

Asystole may also occur as a primary event. This is

extent of delay or obstruction of the cardiac impulse

known colloquially as "flat line" rhythm. Like ven

between the atria and ventricles. First-degree AV

tricular fibrillation, asystole requires that cardiopul

block is characterized by a prolongation of the P-R in

monary resuscitation begin immediately to save the

terval beyond its normal 0.2 seconds (Figure I 1-22).

patient's life.

Remember that the P-R interval is measured from the

Care must be taken to distinguish an apparent

beginning of the P-wave to the beginning of the QRS

lethal arrhythmia from lead disconnection or move

complex_ Each impulse is delayed between the atria


11


185

FIGURE 11-22 First degree A V block.

-,:.1 l fW' .,

.j.

.

',

,

:

-I--r

!t+t'

' -1 ��+*'-'+

FIGURE 11-23 Second degree A V block, Mobitz type I.

and ventricles but each eventually reaches the ventric

P-wave. The conduction ratio in Figure 11-24 is 3: I,

ular conduction system resulting in a normal QRS

or three P-waves for each QRS complex. Both first

complex. Thus for each P wave, there is a QRS com

and second-degree A V blocks are considered to be

plex; therefore the conduction ratio is 1: 1.

incomplete heart blocks.

Second-degree A V block takes two forms, al

Third degree A V block or complete heart block

though in each form, there are some sinus impulses

is also known as A V dissociation. In this rhythm

that are not conducted to the ventricles. In second

(Figure 11-25), P-waves are present, but there is no

degree block Mobitz type I, also known as Wencke

relationship between P-waves or QRS complexes.

bach, the P-R interval lengthens progressively uotil a

P-waves may be superimposed on QRS complexes,

P-wave fails to conduct to the ventricles (Figure 11-

but none of the sinus impulses are conducted to the

23). Notice how the first three P-R intervals lengthen

ventricles; the atria and ventricles are contracting

until, after the fourth P-wave, a QRS complex fails

independently of each other. In the absence of clini

to appear. The cycle then repeats itself. Second

cal intervention such as artificial pacing, ventricular

degree block Mobitz type 2 (Figure 11-24) is charac

depolarization is initiated by a junctional or ventric

terized by a fixed P-R interval with a "dropped"

ular pacemaker.

QRS f o llowing every seco nd, t h i r d, or f o u r t h

Clioically, A V blocks range in severity from benign,


186

PART II


'j.,�1

,. i' ' ; : .

L1Ji;! i

" . fi

/

l..r-�

t t 1L ?

M , +.·::;, .

..

• •: "

"

:;

:

L

......

.:

rr

"ti

....

+-....

FIGURE 11-24 Second degree A V block, Mobitz type 2,

. ,;;Y

t1ft

'

: I. t I

'

-�

FIGURE 11-25 Third degree A V block with ventricular pacing,

as is usually the case with first degree AV block, to po

often treat patients with coronary hearl disease, infor

tentially lethal. Whether hemodynamic compromise oc

mation regarding MI or myocardial ischemia is also

curs depends on the extent of impairment of cardiac

of interest. Although PTs do not medically diagnose

output caused by too slow of a rate of ventricular con

myocardial ischemia or MI, they should have a work

traction (Brown and Jacobson, 1988), Slow rates of

ing knowledge of its electrocardiographic evidence.

ventricular contraction may cause lightheadedness or

During myocardial ischemia, blood flow to a portion

syncope. In most cases of third degree block, treatment

of myocardium is compromised, resulting in alter

now includes implantation of an artificial pacemaker.

ation of myocardial metabolism. In MI, a portion of

In Figure 11-25, the needlelike spikes indicate that an

myocardium has died, but an adjacent zone of is

artificial pacemaker is depolarizing the ventricles at a

chemic myocardial cells endures. These ischemic

rate of 60 BPM.

cells may remain "leaky," and be unable to repolar ize. The persistent current flow from the "leaky" re

MYOCARDIAL ISCHEMIA OR INFARCTION

gion results in a current of injury, which is seen as a shifting of the S-T segment above or below the iso

The EeG provides much more information, beyond

electric line (Guyton, 1991; Lilly, 1993). S-T seg

that gleaned from arrhythmia analysis. Since PTs

ment shift has significant diagnostic value. For exam


11


FIGURE 11-26 S-T segment elevation during myocardial infarction.

pIe, S-T segment elevation (Figure 11-26) is associ ated with transmural Ml. whereas S-T segment de pression is associated with nOn transmural or suben docardial MI. Also, the O n s e t of S-T s e g m e n t depression during activity i s often considered diag nostic of myocardial ischemia. Figure 11-27 is an ex ample of exercise-induced S-T segment depression observed in one lead during exercise. The following is a brief discussion on other abnor malities of the ECG observed in coronary artery disease (CAD). A prominent, pathological Q-wave is indicative of a t.ransmural MI (Lilly, 1993). Indeed, "non-Q" is syn

FIGURE 11-27 S-T segment depression during exercise.

onymous with nontransmural concerning MI. The pres ence of a prominent Q-wave (Figure 11-28) does not, however, distinguish between an old or an acute event. The T-wave may also undergo changes during myocardial ischemia or MI. During ischemia, for example, the T-wave may invert as a result of pro longation of repolarization (Guyton, 1991). Simi l a r ly, d uring MI, c h a n g e s in the T - w a v e m a y "evolve" with the infarct, a t first becoming indistin guishable within an elevated S-T segment, then in verting, then perhaps reverting to original configu ration following the passage of time.

CONCLUSION Understanding the changes in the ECG during is chemia or MI may help PTs integrate all available in

FIGURE 11-28

formation to optimize patienl evaluation. This knowl

Significant Q wave.

edge, combined with astute arrhythmia recognition


187

188

PART II


and symptom assessment, provide entry-level PTs

7. What is the possible clinical significance of S-T

with important tools for management of patients at

segment depression, of S-T segment elevation?

risk for cardiopulmonary dysfunction.

What symptoms might be anticipated in the pres ence of those conditions?

REVIEW QUESTIONS 1. How may the following dysrhythmias be per ceived by a clinician without benefit of ECG monitoring? How may they be perceived by a atrial fibrillation

•

supraventricular tachycardia

•

premature ventricular contractions

•

third degree A V block

•

ventricular fibrillation

Cummins,

4. Does an impulse originating within ventricular myocardium generate an effective myocardial contraction? If not, why not? ocardial infarction?

6. What event is represented by each of the following:

T wave U wave

R.O.

(Ed.). (1994). Tex/book of advanced cardiac I'fe

Emergency Cardiac Care Committee and Subcommittees. (1992). Guidelines for cardiopulmonary resuscitation and emergency of/he American Medical Associa/ion, Guyton, A.C. (199

I).

268,

2199-224 I.

Tex/book oj medical physiology. Philadel

phia: WB Saunders. Lilly, L.S. (1993). POIhophysiology oj hear! disease. Philadelphia: Lea and Febiger. National Heart Lung and Blood Institute Working group on atrial fibrillation. (1993). Atrial fibrillation: Current understandings

5. Why is ECG monitoring indicated following my

•

Jacobson. S. (19 88). Mas/ering dysrhy/hmias: A

cardiac care, Ill: Adult advanced cardiac life support. Journal

tions of the conduction system act as pacemakers?

•

&

SUppOrl. Dallas: American Heart Association.

the heart? Under what conditions do other por

QRS complex

1561-1573.

problem solving guide. Philadelphia: FA Davis.

3. What propelty of the SA node allows it to pace

•

82,

Febiger. Brown, K . R . ,

arrhythmia?

P wave

Cireula/ioll,

cise /es/il1g and prescrip/ion. (4th ed.). Philadelphia: Lea and

2. What determines the clinical significance of an

•

Akhtar, M. (1990). Clinical spectrum of ventricular tachycardia. American College of Sports Medicine. (1991). Guidelinesfor exer

patient? •

References

and research imperatiws. Journal of AmericanCollege nfCar·

diologis/s, 22,

1830-1834.

Shih, H.T. (1994). Anatomy of the action potential in the heart.

Texas J-iear/lns/i/u/e lournal, 21, 30-41. & Kampine, J.P. (1990). Circula/OI)'

Smith, J.1.,

essentials. Baltimore: Williams and Wilkins.


physiology-/he

C HAP T E R

1 2

Multisystem Assessment and Laboratory Investigations Elizabeth Dean

KEY TERMS

Blood

Liver

Endocrine function

Lungs

Heart

Multisystem assessment

Immune function

Peripheral vascular circulation

Kidneys

INTRODUCTION

fected by virtually every organ system in the body.

The purpose of this chapter is to describe the ratio

The signs and symptoms of systemic disease can

nale for multisystem assessment in the patient man

mimic other conditions, including cardiopulmonary

aged for cardiopulmonary dysfunction and some

dysfunction treated by physical therapists. Therefore

common laboratory tests related to multisystem as

the physical therapist must be able to differentiate

sessment. The bases of tests to assess the function of

these presentations to determine what treatment, if

the following organ systems are presented: blood,

any, is indicated, and what treatments may be con

pulmonary, cardiac, peripheral vascular, renal, en

traindicated. Knowledge of multisystem function

docrine, liver, and immune systems. The information

helps confirm a diagnosis, as well as predict a pa

in this chapter is supplemental to the elements of car

tient's response to treatment and his or her recovery

diopulmonary and cardiovascular assessment and re

and prognosis. In addition, this information is crucial

lated laboratory investigations described in Part 2.

in refining and modifying treatment prescription.

The cardiopulmonary system affects and is af-

These abilities are particularly important in this era of

189


190

PART II


professional accountability and with the advent of di

response, recovery, and prognosis. The CBC includes

rect patient access.

the red blood cell count (RBC), a variety of red blood cell indices, white blood cell count (WBe), hematocrit

RATIONALE FOR MULTISYSTEM ASSESSMENT

(Hct), hemoglobin (Hgb), and platelet count. Tests of coagulation and hemostasis reflect bleeding

The cardiopulmonary system supports cellular respi

pathology, which often involves injury of blood vessels

ration and life. Thus every system and every cell in

and cells. Damage to the blood vessel wall leads to con

the body is affected by the adequacy of oxygen trans

striction, a primary mechanism of hemostasis. Circulat

port, which is dependent on cardiopulmonary and

ing platelets adhere to exposed subendothelial tissues,

cardiovascular function. In addition, these systems

which can predispose thrombus formation.

are affected by virtually every other system in the

The fluidity of the blood is regulated by the facili

body. The cardiopulmonary physical therapist (PT)

tation and the inhibition of thrombin formation.

therefore needs thorough knowledge of multisystem

When these two processes are in balance, the blood

function and the interdependence of the organ sys

has an optimal consistency; it is neither too thick nor

tems, an ability to assess multisystem function and to

too thin. This allows blood to flow optimally through

integrate this information into a comprehensive and

the circulation. Blood vessel injury can disrupt this

progressive treatment plan.

balance and can promote coagulation.

The lungs and heart are anatomically and physio

Disseminated intravascular coagulation (DIC) re

logically interconnected, and function as a unit to

sults from an imbalance between the formation and

transport oxygen via the peripheral circulation to per

deposition of fibrin, which leads to the formation of

fuse and nourish tissues. Tissue homeostasis is de

thrombi. The continuous production of thrombin

pendent on the adequacy of the anatomy and physiol

causes depletion of the coagulation factors and bleed

o g y of t h e b l o o d . T h e a d e q u a c y of p e r i p h e r a l

ing results. Tests used to assess bleeding capacity in

perfusion determines the adequacy o f the function of

clude thrombin time and fibrin clotting time (partial

all organ systems in the body. Therefore a knowledge

thromboplastin time [PTT]).

of the failure of the various organ systems can reflect

Proteins (amino acids) serve as regulators of me

impaired oxygen transport or may identify a threat to

tabolism. Much clinical information is obtained by

oxygen transport.

examining and measuring proteins, because proteins

The elements of laboratory evaluation and testing,

regulate many impoltant physiologic functions in the

as well as normal values, have been compiled from

body. Plasma proteins serve as a source of nutrition

Bauer (1982), Dean (1987), Fishbach (1988), Guyton

for the body tissues and function as buffers when

(1991 ), Jacobs et al. (1984), Le Fever Kee (1990),

combined with hemoglobin.

Pagan a and Pagana ( I 992), Siest et al. (1985), and Wallach (1986).

Albumin, a protein formed in the liver, maintains normal water distribution in the body (colloid os motic pressure). It transports blood constituents such

ELEMENTS OF MULTISYSTEM ASSESSMENT Blood

as ions, pigments, bilirubin, hormones, fatty acids, enzymes, and certain drugs. Approximately 55% of total protein is albumin. The remainder is globulin,

Some common blood tests are summarized in Table

which functions in antibody formation, and other

12-1 along with their normal values.

plasma proteins (fibrinogen and prothrombin) in

The average blood volume consists of 5 L of blood:

volved with coagulation.

3 L of plasma and 2 L of cells. Plasma is the medium

Lactic acid, a product of carbohydrate metabolism, is

which suspends and transpOIts blood cells. The com

produced when cells receive inadequate oxygen in rela

plete blood count (CBC) is one of the most commonly

tion to oxygen demand (anaerobic metabolism). When

ordered laboratory procedures. This basic screening

the production of lactic acid exceeds its removal from the

test helps to establish the patient's diagnosis, treatment

blood by the liver, lactic acid accumulates in the blood.


12

Multisystem Assessment and Laboratory Im'estigations

191

TABLE 12-1 Common Test'! of Multisystem Function and Their Normal Values: Blood Tests NORMAL VALUES (SI UNITS)

TEST Red blood cell count (RBC)

Hemoglobin (Hgb)

Hematocrit (Hcr)

Men

2.09-2.71 nmolfL

Women

1.86-2.48 nmolfL

Men

8.7-11.2 nmolfL

Women

7.4-9.9 nmolfL

Men

40% to 54%

Women

37% t047%

150.000-350.000/mm3

Platelet count Prothrombin time (PT)

10-14 seconds

Partial thromboplastin time (PTT)

60-85 seconds

White blood cell count (WBCC)

5-10

x

103/iJl

(Differential WBCC includes counts of neutrophils, eosinophils. basophils, lymphocytes. and monocytes) Erythrocyte sedimentation rate (ESR)

Men

0-15111m/hr

Women

0-20 mm/hr

Proteins Albumin

38-50 gm/L

Globulin

23-35 gm/L

Fibrinogen

2.0-4.0 gm/L

Lactate

Venous

0.5-2.2 mmolfL

Arterial

0.5-\.6 mmollL

Electrolytes (blood) Sodium (Na+)

135-148 mmollL

Potassium (K+)

3.5-5.0 mmol/L

Calcium (Ca++)

TOTAL

4.5-5.3 mmolfL

IONIZED

2. 1-2.6 mmolfL

Chloride (Cl-)

98-106 mmolfL

Cholesterol Creatine kinase

:-;OTI,:

3.63-6.48 mmollL Men

0.42-1.5 I mmol/sfL

Women

0.17-1.18 mmol/sfL

Normal values may vary depending on the laboratory performing the measurement. Within subject variation occurs from age, and

variations in the pre-test sLandardization procedures.

Cholesterol is used in the production of steroid hor mones, bile acids, and cell membr::mes. Cholesterol is

of cholesterol are associated with atherosclerosis and increased risk of coronary artery disease (CAD).

found in muscles, red blood cells, and cell membranes.

Electrolyte assessment is based on the electrolyte

Low-density and high-density lipoproteins (LDLs and

constituents of a b lood or urine sample. Although

HDLs) transport cholesterol in the blood. High levels

present in minute quantities, electrolytes are essential


192

PART II


in mainlaining normal cellular function and home

inspection of the integrity of the peripheral circulation

oslasis. The electrolytes that are routinely studied are

particularly to the eXlremities, palpation to assess pe

sodium, potassium, chloride, calcium, phosphorus,

ripheral pulses, and auscultation, which can be helpful

and magnesium.

in detecting bruits or areas of turbulent blood flow as sociated with arterial stenoses. Some common tests of peripheral vascular func

Pulmonary Function

tion are summarized in Table 12-2 along with their

See Chapters 8 and 14 for a detailed description of the

normal values.

assessment of the pulmonary system and its function.

Kidney Function Cardiac Function

Urine consists of the end products of cellular metabo

A detailed description of the assessment of the car

lism and is produced as large volumes of blood (ap

diac system and its function appears in Chapters 11

proximately 25% of the cardiac output [CO]) flow

and 14.

through the kidneys. When the kidneys are compro mised, death can ensue within a few days. Although fluid is lost through several routes, the kidneys are

Peripheral Vascular Function

primarily responsible for processing and regulating

Assessment of the peripheral vascular circulation is essential to provide information regarding central and

fluid balance in the body. Urea, the major nonprotein nitrogenous end product of protein catabolism, is measured in the blood as blood

peripheral hemodynam.ic tissue perfusion. This assessment is essential to estab

urea nitrogen (BUN). The urea is then carried to the

lish the integrity of the patient's hemodynamic status

kidneys by the blood to be excreted in the urine.

at rest and during physical and exercise stress which is

Creatinine is a byproduct in the breakdown of

associated with most physical therapy treatments.

muscle creatine phosphate resulting from energy me

Laboratory tests include segmental blood pressure

tabolism. Production of creatinine is constant as long

studies, skin temperature studies, pulse wave analysis,

as muscle mass is constant. Kidney dysfunction re

Doppler venous studies, and arteriography. The physi

duces excretion of creatinine resulling in increased

cal examination corroborates the results of the labora

levels of blood creatinine. Analysis of urine for crea

tory investigations and includes the patient's history,

tinine provides an index of kidney function.

TABLE 12-2 Common Tests of Multisystem Function and

TABLE 12-3

Their Normal Values: Tests of Peripheral Common Tests of Multisystem Function and

Vascular Function TEST

NORMAL VALUES

Skin temperature

Ranges from ambient temperature to 30DC

Ankle systolic pressures

97% of brachial pressure

Peri phera/ pu Ises

Apex heart rate

Capillary filling

Instantaneous filling following quick pressure over the nai I bed

Their Normal Values: Tests of Renalf'ullctioll NORMAL VALUES TEST

(SI UNITS)

Blood urea nitrogen (BUN)

3.6-7.1 mmollL

Creatinine

7.6-30.5 IlmollL

NO'll::

Normal values Jllay vary depending on the laboratory

performing the measureJllent. Within subject variation occurs from age, and variations in the pretest standardiz.ation procedures.


12

Multisystem Assessment and Laboratory Investigations

Increased osmolality stimulates the secretion of

193

marized in Table 12-4 along with their normal values.

anti-diuretic hormone (ADH) that acts on renal

Pancreatic function and insulin production

tubules. This results in the reabsorption of water, more concentrated urine, and less concentrated serum.

Insulin, a hormone produced in the pancreas by the beta

Some common tests of renal function are summa

cells of the islets of Langerhans, regulates the metabo

rized in Table 12-3 along with their normal values.

lism of carbohydrates along with liver, adipose tissue, muscle, and other target cells and is responsible for maintaining a constant level of blood glucose. The rate

Endocrine Function

of insulin secretion is determined primarily by the level

Endocrine glands are responsible for producing those

of blood glucose perfusing the pancreas and is also af

substances and neuromediators responsible for main

fected by hormonal status, the autonomic nervous sys

taining homeostasis and enabling the body to adapt

tem, nutritional status, smoking, restricted mobility,

when physically and psychologically challenged or

physical stress such as traumatic insult to the body dur

perturbed from a resting state. The key endocrine

ing illness and injury, and pharmacologic agents.

glands are the pancre as, thyroid gland, and the

Amylase is an enzyme produced in the salivary

adrenal glands. Endocrine glands regulate metabo

glands, pancreas, and liver, and c onverts starch to

lism and are responsible for increasing blood flow

sug ar. Inflammation of the pancreas or salivary

and pressure, and reducing vascular resistance when

glands results in more of the enzyme entering the

metabolic demands increase.

blood. The amylase test is used to diagnose and mon

Some common tests of endocrine function are sum-

itor treatment of acute pancreatitis.

TABLE 12-4 Common Tests of Multisystem Function and Their Normal Values: Tests of Endocrine Function NORMAL VALUES (SI UNITS)

TEST Thyroid Function

Total thyroxine (T4)

65-155 nmol/L

Total triiodothyronine (T3)

1.77-2.93 nmollL

Adrenal Function

0.0-81.9 nmoll24 hr

Epinephrine Norepinephrine

0.0-591 nmol/24 hr

Cortisol

Morning

138-635 nmollL

Evening

82-413 nmollL

Pancreatic Function

At I hl' glucose

Glucose tolerance test

1.1-2.75 mmollL

At 2 hl' glucose

0.2-0.88 mmol/L

Insulin

12 hr fasting

35-145 pmollL

Amylase

Blood level

25-125 UnitslL

N
Normal values may

vary

depending on the laboraLory peli'orming the measurement. Within subject variation occurs from age, and

variations in the pretest standarLiization procedures.


194

PART II


Thyroid

TABLE 12-5

The function of the thyroid gland is to take iodine

Common Tests of Multisystem Function and

from the circulating blood, combine it with amino

Their Normal Values: Tests of Liver Function

acid tyrosine, and convert it to the thyroid hormones thyroxine (T4), and triiodothyronine (T3). Thyroid hormones have a profound effect on metabolic rate. Increased metabolism causes more rapid use of oxy gen than normal and causes greater quantities of

Alkaline phosphatase Bilirubin (total)

metabolic end products to be released from the tis sues. These effects cause vasodilatation in most of the body tissues, thus increasing blood flow. Increase in the thyroid hormones increases cardiac output,

NORMAL VALUES (SI UNITS)

TEST

NOTl'.:

0.18-0.40 nmol/slL 5.1-I 7.1 fJmollL

Normal values may vary depending on the laboratory

performing the measurement. Within subject variation occurs from age and variations in the pretest standardization procedures.

heart rate, force of cardiac contraction, blood volume, arterial blood pressure, oxygen consumption, and car

TABLE 12-6

bon dioxide (C02) production, hence an increase in the rate and depth of breathing, increased appetite,

Common Tests of Multisystem FUllction

food intake and gastrointestinal motility. The thyroid

and Their Normal Values: Tests

gland also stores T3 and T4 until they are released

of Immunological Function

into the blood stream under the influence of thyroid stimulating hormone (TSH) from the pituitary gland.

Differential White Blood Cell Count

Adrenal function Catecholamines, epinephrine and norepinephrine, are

Neutrophils

produced by the adrenal medulla of the adrenal

Lymphocytes

glands. Urine samples are used to test for these im portant vasoactive neurotransmitters in the investiga tion of various disorders. In addition to their vasoac

MOllocytes Eosinophils Basophils

ABSOLUTE VALUE (No/uL)

RELATIVE VALUE (by Percent)

3,000-7,000 1,000-4,000 100-600 50-400 25-100

60-70 20-40 2-6 J-4 0.5-1

tive properties, the catecholamines are essential in stimulating the sympathetic response in the fight or with tests of liver enzymes such as amylase and al

flight mechanism. Cortisol is produced by the adrenal cortex of the

kaline phosphatase.

adrenal glands and is involved with metabolism of

Some common tests of hepatic function are sum

carbohydrate, protein, and fat. In addition, it inhibits

marized in Table 12-5 along with their normal values.

the action of insulin and thus the uptake of glucose by the cells. The normal secretion of cortisol varies diurnally, that is, high in the morning and low in the

Immunological Function Immunological function is dependent on the ade

evening.

quacy of the function of several tissues and organs, namely bone marrow, the thymus gland, lymph

liver Function

nodes, and vessels of the lymphatic system, spleen,

Liver function is especially important in that dys

tonsils, and intestinal lymphoid tissue. Immunologi

function of this organ can be life threatening. The

cal function can break down if insufficient protective

liver has a primary role in carbohydrate and protein

immune factors are produced, or the system is over

metabolism, it produces bile, and is responsible for

whelmed by an invading organism for which the

detoxification of the blood. Its function is assessed

body has inappropriate or insufficient resistance.


Multisystem Assessment and Laboratory Investigations

12

Some common tests of immunological function are summarized in Table 12-6 along with their normal values. Specific detailed accounts of immmunodiag nostic studies and tests for autoimmune deficiencies are beyond the scope of this chapter but can be re viewed in Fischbach (1988) and Le Fever Kee (1990).

SUMMARY This chapter described the rationale for multisystem

195

REVIEW QUESTIONS I.

Describe common tests of blood composition.

2. Describe pulmonary function tests. 3.

Describe tests of heart function.

4. Describe tests of peripheral vascular function. 5. Desacribe tests of renal function. 6.

Describe tests of endocrine function.

7.

Describe tests of liver function.

8. Describe tests of immune function.

assessment in the patient being managed for car diopulmonary dysfunction and some common tests of multisystem function. The cardiopulmonary system affects and is affected by virtually every organ system in the body. Thus primary cardiopulmonary dysfunc tion can lead to multiorgan system complications, and dysfunction of other organ systems can have car diopulmonary manifestations. In addition, the signs and symptoms of systemic disease can mimic other conditions treated by physical therapists. Therefore the PT must be able to differentiate these presenta tions to determine whether a pathology will respond to physical therapy management, what treatment is not indicated and what treatments may be contraindi cated. Multisystem monitoring provides fundamental information needed to refine and progress the treat ment prescription. These abilities are essential in this era of increased professional responsibility and with the advent of direct patient access.

References Bauer, J.D.

(1982).

Clinic allaboratOlY melhods (9th ed.). St.

Louis: Mosby. Dean,

E. (1987).

Assessment of the peripheral circulation: An up

date for practitioners. The Australian Journal of Physiotherapy,

33,

164-171.

(1988).

Fischbach, F.

A manual of laboratory diagnostic tests

(3rd

ed.). Philadelphia: J.B. Lippincott.

(1991).

Guyton, A.c.

Textbook of mediad physiology (6th ed.)

Philadelphia: W. B. Saunders. Jacobs, D.S., Kasten, B.L.,

(1984).

Le Fever Kee, J. tests

Demott,

W.R.,

&

Wolfson, W.L.

Laboratory test handbook. Stow: Lexi-Comp, Inc.

lVilh

(1990).

Handbook oflaboratOlY and diagnostic

nursing implications. Norwalk: Appleton and Lange.

Pagana, K.D.,

&

Pagana,

TJ. (1992). Mosby·s

diagno.Slic

and lab

ora/Ory leSI reference. St. Louis: Mosby. Siest, G., Henny, J., Schiele, F.,

&

Yonge, D.S.

(1985).

Inlerpretalion

ofclinical laboratory lests. Foster City: Biomedical Publications. Wallach, J.

(1986).

Interpretation of diagnostic tests. A synopsis of

laboratory medicine. Boston: Little, Brown.


Special Tests

Gail M. Huber

KEY TERMS

Echocardiography

Stunned myocardium

Ejection fraction

Thallium-201 scan

Hibernating myocardium

Ventilation-perfusion scan

Positron emission scans

INTRODUCTION

lungs, as well as determining cardiac anatomy, and

In assessing the cardiopulmonary patient, the physi

direct volume and pressure measures, it is without

cian uses many tools. The patient interview, physical

equal. Transesophageal echocardiography is another

examination, chest x-ray, and electrocardiogram

invasive test. Following the initial assessment of the

(ECG) provide information to make a diagnosis.

problem, these same special tests may be lIsed to as

When more information is needed, a variety of inva

sist in the determination of appropriate therapy and

sive and noninvasive tests can be pelformed. Nuclear

evaluate prognosis and response to treatment. The

medicine offers a variety of tools for evaluation of

noninvasive tests are most important in determining

cardiac and pulmonary function. EChocardiography is

ongoing surgical, interventional, or medical therapy.

a noninvasive method that offers information about

Physical therapists (PTs) need to understand these

the cardiovascular system, including valve function,

invasive and noninvasive tests for several reasons. It

ventricular performance, and estimation of filling

is useful to understand how the information is used

pressures. It is particularly useful with children.

to make a differential diagnosis and determine treat

At some point in a patient's workup, the physi

ment. These tests have helped to clarify our under

cian may need to use an invasive test. Pulmonary

standing of the physiology and pathophysiology of

and cardiac angiography is not without risk; how

the system. Therapists need to understand the patho

ever, for evaluating blood flow in the heart and

physiological basis f o r a p a t i e n t ' s m o v e m e n t 197


198

PART II


dysfunctions to select the most appropriate treat

moved from time to time for patient use (Kim, 1987).

ment strategies. Many special tests can and are

A generator system produces short-lived radionu

being used in research to evaluate treatment inter

clides (lskandrian, 1987).

ventions. For example, radiolabeled aerosols are

These elements are often attached to other sub

used to evaluate mucociliary clearance, providing a

strates for transport in the body to the particular tis

method to evaluate the effectiveness of pulmonary

sue of interest. The elements have differing character

hygiene techniques (Miller and O'Doherty, 1992).

istics such as energy output and half-life. Because of

C linically, PTs need to use information from the

their vaIied distribution in the body tissues, they pro

tests to develop a framework for predicting how the

vide different information.

patient may respond to a physical therapy interven

Detection of the radioactive energy emitted by a

tion. For example, nuclear imaging can provide in

specific radiopharmaceutical requires a camera.

formation about left ventricular ejection fraction.

When certain materials are struck by ionizing radia

This information helps the PT determine if the pa

tion, light is emitted. A scintillation detector detects

tient should be stratified into high-risk or low-risk

this light. A gamma camera is a scintillation detector

categories. Monitoring of an exercise session may

able to detect photons exiting the body. It uses a

depend on the risk level, and interpretation of the

large, collimated crystal monitored by an array of

patient's response to treatment may be effected.

photomultiplier tubes (Kim, 1987). A collimator is a device that allows only those photons traveling in an appropriate direction to reach the crystal. There are

NUCLEAR IMAGING SYSTEMS

several types of collimators: parallel-hole collima

AN 0 RAD I 0 PHARMACEUTI CALS

tors, pinhole collimators, and converging and diverg

A general view of how nuclear imaging systems work

ing collimators. The photomultiplier tube records the

should help the PT understand some of the differences

amount of light from the crystal and converts it into a

between the wide variety of tests used today. This

voltage, that is proportional to the intensity of the

area of medicine is experiencing rapid growth and

light (Kim, 1987).

change as technology changes the equipment used to

The camera system is connected to a computer

perform the test, the radiopharmaceuticals available,

that stores the light images. The computer is able to

and the computer's increasing ability to analyze data.

derive two dimensional images from the data. The

Radionuclide imaging allows for the noninvasive acquisition of images from a variety of body tissues.

computer can also quantify the data and perform a variety of data analyses (Iskandrian, 1987).

An imaging system requires three basic parts. The first requirement is a radiopharmaceutical that emits gamma radiation and is taken up by the body tissue

Planar Imaging

of interest. Next, a radiation detector or camera is

A single crystal camera (Anger) produces a two dimen

needed. FinalIy, computers are required to collect and

sional or planar image. Multicrystal cameras (Blau and

analyze the data.

Blender) also produce planar images but are able to per

Radionuclides are elements that are unstable; they

form fast dynamic imaging used in first pass and gated

gain stability by emitting particles or photons. This is

studies. Planar imaging may be the only option available

called radioactive decay, and gamma radiation is re

to obese patients who do not "fit" the single photon

leased. Radionuclides are either cyclotron- or genera

emission computed tomography (SPECT) camera.

tor-produced. The cyclotron accelerates alpha-parti cles, deuterons, and protons to energies suitable for the production of the required radionuclide (Kim,

1987). A radionuclide generator is a system of parent

Tomographic Imaging If a gamma camera is rotated about the patient and

and daughter radionuclides in equilibrium. The sys

mUltiple projections obtained, a three-dimensional

tem is constructed so that the daughter can be re

distribution of tracer is acquired. This is the basis for


13

Special Tests

SPECT (Kim, 1987). The s ame gamma-emitting

TESTS OF THE CARDIOVASCULAR SYSTEM

pharmaceuticals are used. Regular gamma cameras or

Radionuclide Imaging

specially designed systems can be used (Iskandrian,

1987). SPECT imaging produces higher spatial reso lution (Schwaiger, 1994), and increased sensitivity for coronary artery disease (CAD) over planar images (Beller, 1994). However, attenuation artifacts (ab sorption of the radioactive energy by other body tis sues such that the camera does not detect it) are greater than with planar images, particularly those images involving the inferior wall of the heart in men and the anterior wall in women, and may produce false-positive scans (Schwaiger, 1994). Quality of the images are dependent on the use of stringent quality control measures and experience of the staff. Image quality is also patient-dependent. Patients must be able to lie perfectly still for 15 to 20 minutes, with their hands over their heads, while data are collected. PTs can identify patients who would have diffi culty with arm movements or with remaining still. For these patients, other imaging modalities such as echocardiography may be appropriate. P o s itron e m i s s i o n t o m o g r a p h y (PET) u s e s positron-emitting radionuclides. The images ob tained by PET can provide information regarding metabolism in lung tissue and cardiac muscle, my ocardial perfusion, and myocardial receptor density (Maddahi, 1994). PET is valuable in delineating my ocardial areas with reversible and irreversible injury

199

Gated/ungated first pass scan In an ungated first pass study, data are collected on a radiolabeled bolus of blood as it passes through the car diac chambers. This allows for clear identification of the four cardiac chambers. During gated first pass stud ies, data are collected at specific periods in the cardiac cycle. Each R-wave of the EKG triggers the acquisition of data, thus the average cycle observed is the compila tion of several cycles. Gated equilibrium studies or multiple uptake gated acquisition (MUGA) scans aver age several hundred cardiac cycles. The quality of the image is best when the patient has a stable sinus rhythm. Patients with irregular heart rates, such as atrial fibrillation have images of poorer quality.

Exercise stress studies Many of the tests pert'ormed using radionuclides are coupled with an exercise test. A treadmill exercise test is pelformed, and at the peak of exercise, a tracer is injected. Shortly afterward, depending on the tracer, images are acquired. Exercise imaging en hances the identification of ischemic areas. These tests are then often compared with rest studies. Rest/stress or stress/rest protocols can be used.

Pharmacologic stress studies

and in assessing the feasibility of surgical revascu

Many patients are unable to exercise to an intensity

larization, coronary angioplasty, or thrombolysis

sufficient to produce stress on the cardiovascular sys

with respect t o potentially s a l v a g e a b le t i s s u e

tem. When patients are unable to exercise, pharmaco

(Niemeyer, 1992). Many o f the radionuclides used in

logic agents can be used to dilate the coronary arteries

PET scans require a cyclotron for generation and a

or incr e a s e t h e metab olic demand of the heart.

specialized detection system. PET images offer s u

Dipryridimole (Persantine) and adenosine are often

perior resolution compared with SPECT images

used. Pharmacologic stress tests can be coupled with

(Schwaiger, 1994). PET also allows greater correc

SPECT and PET nuclear imaging techniques or with

tion for attenuation artifact (Schwaiger, 1994). PET

echocardiography to determine regions of ischemic

imaging is a newer technology that offers improve

myocardium suggesting functionally significant block

ment in sensitivity and specificity when compared

age in the coronary artery supplying that territory.

with SPECT (Mullani, 1992). PET studies use short scanning times. Protocols

Nuclear-derived measurements

can last about I hour. The studies can be done at rest

Data derived from radionuclide images provide infor

or with a pharmacologic stress agent (Schwaiger,

mation about perfusion and function. Radionuclides

1994). Cost may prohibit the widespread use of this

taken up by the myocardium provide a picture of the

technology.

heart that includes wall thickness and an outline of


200

PART II


the chamber. In radionuclide angiography, which in cludes first pass and gated studies, the blood is high lighted as it passes through the chambers. Qualitative and quantitative measurements can be taken. The most important of these measurements, the ejection fraction (right and left ventricle) is a measure of my ocardial function. It is derived from quantitative counts of the ventricular area during diastole and sys tole (lskandrian, 1987): (End-diastolic counts - End-systolic counts) x 100 End-diastolic counts Left ventricu lar ejection fraction (L VEF) has been shown in several studies (Cass study and the Multi center Postinfarction Research Group Database) to be highly predictive of 1 year survival (Port, 1994; Mad dahi, 1994). Right ventricu lar ejection fracti o n (RVEF) has been found t o have a wide range o f nor mal values (35% to 75%) (Kinch, J 994) but is not that predictive of function without data about wall motion abnormalities. The strongest radionuclide pre dictor of outcome is the exercise LVEF. When pre dicting outcome, multivariate analysis of clinical data, catheterization data and radionuclide measure ments have shown that the radionuclide results (exer cise LVEF, resting end-diastolic volume, and change in heart rate [HR)) have the same prognostic power as the catheterization data (Port, 1994). Another important measurement is wall motion. Quantitative and qualitative evaluation of the move ment of the myocardium can be made. Wall thick ness, and movement are compared with systole and diastole. Assessments are made about akinesia, global or regional hypokinesia, and dyskinesia. Global left ventricular function is a strong predictor of survival. It can help clinicians differentiate a weak heal1 from one that is stiff, allowing the appropriate treatment. Regional wall function when correlated with knowledge of coronary artery anatomy allows for the identification of potential blockages or areas of infarct. Assessing wall thickness can provide in formation about hypertrophy or aneurysm but is done more reliably by echocardiography. Anatomical measurements can be made of cham ber size. From these data, chamber volume can be calculated, as well as stroke volume and cardiac out put (Table 13-1).

Tests to Evaluate Myocardial Perfusion Perfusion of the myocardium is a vital factor in the via bility and function of the heart. Information about my ocardial perfusion is used for diagnostic decisions, treatment decisions and prognosis. Peliusion of the my ocardium under rest and exercise conditions is impor tant in the diagnosis of CAD. Efficacy of reperfusion strategies, such as angioplasty and thrombolytic therapy must be evaluated. Identifying tissue that is viable but still at risk is one of the newer applications of myocar dial peliusion tests. Information gained from combined perfusion and metabolic studies has helped to increase the understanding of ischemic myocardium. Two types of contractile dysfunction have been delineated. Hiber nating myocardium is the result of prolonged ischemia. The contractility of the muscle fiber is effected so that there may appear to be regional wall motion abnonnali ties. The tissue is alive but not contracting. It is theo rized that this is a measure to reduce energy expendi ture and ensure myocyte survival. The second condition, myocardial stunning, occurs under condi tions of acute ischemia. In this case, there is contractile dysfunction during the acutc ischemic episode that per sists for some time after perfusion has returned to nor mal. Both conditions are reversible. Patients demon strating hibernating myocardium may benefit from revascularization procedures. Patients with stunned my ocardium may only require supportive care until con tractile function returns. (SchelbeI1, 1994). Thallium-201 Thallium-20l is the radioactive isotope most often u sed in myocardial perfusion studies (Wacker, 1994). It is a cyclotron-produced isotope that emits low-energy radiation (69 to 83 kiloelectron volt [keY)). Administered intravenously, its distribution throughout the body depends on blood flow. Thal lium concentrations in ·the myocardium depend on four processes. First, there is a linear relationship between thallium concentration and coronary blood flow. Second, extraction-transport across the cell membrane depends on active and passive transport mechanisms. Thallium is thought to be transported across the cell membrane through the sodium-potas sium ATPase pump (Maddahi, 1994). The third process is washout, also called redistribution. Thal


13

Special Tests

201

TABLE 13-1 Summary of Special Tests of the Cardiopulmonary System SPECIAL TESTS

CLINICAL FINDINGS

Cardiac Scans

Planar, SPEeT, MUGA, First pass Thallium-20I

Evaluates myocrdial perfusion, used in exercise stress studies and to assess

Technitium-99M-sestamibi

reversibility of defects. Quantitatively can be used to determine: EF, SV,

Technitium teboroxime

CO, regional function, ventricular volumes, intra-cardiac shunt, valvular regurgitation.

PET Scans IS-FOG

Assesses myocardial viability by evaluating glucose metabolism. Can

II C acetate

Assesses myocardial viability by evaluating oxidative metabolism. Can

identify areas that improve with reperfusiol1. identify areas that will improve with reperfusion.

Illfarct avid scans Technetium-99M-pyrophosphate Indium I II antimyosin

Identifies areas of infarction by binding with elements released by the death of myocardial tissue.

Pulmonary Scans

Perfusion scan MAB

Identifies regions of decreased pulmonary perfusion, used to identify pulmonary embolism.

Velltilation scall 99mTc OTPA I33-Xe Gallium scan

Identifies regions of decreased ventilation. Used in conjunction with perfusion scan to identify patients with pulmonary embolism. Identification of neoplastic or inflammatory pulmonary lesions

Echocardiography M-mode

Evaluates myocardial structure. 2- 0 used in exercise stress studies.

2 D

Quantitatively measures: chamber size, wall thickness, valve structure

TEE

and function, pressure and flow through valve, valve area, EF.

Doppler Angiography

Quantitative measures of pressure, resistance, flow, O2 consumption, arteriovenous oxygen difference EF, CO

Abbreviations: EF=ejection fracl.ion, CO=cardiac output, SV=stroke volume

lium enters the cell initially and then is redistributed

titatively evaluated. Normally perfused myocardium

until an equilibrium is attained based on a net bal

demonstrates uniform uptake of the tracer. Uniform

ance between Thallium-201 input through recircula

uptake can occur as long as blockages are less than

tion and intrinsic Thallium washout (Beller, 1994).

50% of the artery. Ischemic but viable myocardium

Finally, concentrations arc decay-related, dictated

initially appears as areas of decreased uptake, these

by the half-life of the isotope (Brown, 1994; lskan

areas fill in over time, a function of redistribution. Be

drian, 1987).

cause blood flow is decreased, clearance of Thallium

Thallium-201 images can be qualitatively and quan

201 from the defect region is slower (Maddahi, 1994).


202

PART II


In infarcted areas, these defects remain unchanged

in acutc situations. A patient with an acutc myocardial

over time. Qualitative evaluation requires visual in

infarction (MI) can be injcctcd with tracer, given

spection of the images. Quantitative evaluation is per

thrombolytics, stabilizcd, and scanned 4 hours later.

formed by computer. The computer analyzes the

The scan results show myocardial pert'usion at the time

amount of radioactivity taken up in a palticuJar region

of injection when the myocardium was ischemic. Later

of interest. It then quantifies this count so that regions

scans demonstrate the new perfusion situation.

can be compared with each other and with normalized data. In this way, unperfused or hypoperfused areas

Technetium-99M-teboroxime Another newer isotope is Technetium (Tc)-99M

can be identified. Thallium-201 is used to acquire planar and tomo

teboroxime. I t i s not yet widely accepted because of

graphic images (SPECT) for rest studies, exercise stress

its rapid washout and visualization problems related

studies, and pharmacologic stress studies. The tradi

to hepatic uptake (Berman et aI., 1991; Go, j 992).

tional Thallium-201 stress study calls for injection of

The half-life for teboroxime is 5 to 6 minutes (John

the tracer at the peak of exercise with collection of the

son, 1994). It has a myocardial extraction fraction

stress data shortly after. The redistribution study is com

higher than either sestamibi or thallium (Johnson,

pleted 4 hours later. Newer study protocols include rein

1994). Tc-99M-teboroxime uptake parallels myocar

jection of thallium before the 4-hour redistribution study

dial blood flow under both ischemic and nonischemic

(Go, 1992) and use in dual-isotope studies (Berman,

conditions (Johnson, 1994) and does not appear to

1994). Reinjection of thallium and repeat imaging 24

rely on active cellular processes.

hours after initial study can help identify severely is

Because of the short half-life, rapid acquisition

chemic (greater than 90% blockage) areas, which may

imaging systems are required so that the images do

take much longer to demonstrate redistribution.

not reflect washout. SPECT and first pass studies can be performed but Tc-99M-teboroxime does not per

Technetium-99M-sestamibi

mit gated SPECT acquisition (Berman, 1991). Proto

New isotopes were approved by the FDA for perfusion

cols using this isotope are designed to take advantage

imaging in 1990. Technetium (Tc)-99M-sestamibi was

of the rapid uptake and washout. When used with

developed because of the number of advantages it has

pharmacologic stress studies, a rest-stress study can

over thallium imaging. Sestamibi provides improved

be completed within minutes (Johnson, (994). This

SPECT image quality as a result of higher count rates

may have future application in studying reperfusion

and higher energy, in the 140 keY range. Tc-99M-ses

following balloon angioplasty or reperfusion therapy

tamibi is generator-produced. The isotope has a 6-hour

with thrombolytic agents (Johnson, 1994). PET trac

half-life (Berman et aI, 1994). Because of the short

ers are also used to evaluate perfusion and will be

half-life, higher doses can be injected, and although the

discussed below. They include, 13-N ammonia, 82

percentage of extraction is lower, sestamibi uptake in

Rb rubidium, or 15-0 water.

relation to flow is similar to that of thallium. These fac tors result in higher count rates, which thus allow the use of gated images and first pass acquisition studies.

Tests to Evaluate Myocardial Viability

Higher count rates are preferred when evaluating obese

Identification of the size of an infarct has traditionally

patients. One of the greatest limitations of Tc-99M-ses

been helpful in determining prognosis. Infarct avid trac

tamibi is that it does not readily redistribute; therefore

ers were used. The tracers bind with elements released

reversibility of defects cannot be ascertained as well as

by necrotic myocardial tissue.

with thallium. This factor is one reason thallium is

With the development of reperfusion strategies,

much more popular. Two-day protocols or dual isotope

angioplasty, bypass grafting, and thrombolytic ther

protocols can be used to overcome this limitation

apy it was noted that areas that appeared to be non

(Berman, 1994). Lack of redistribution has been ex

functional on perfusion scans regained function once

ploited in evaluating the impact of thrombolytic therapy

the area regained adequate blood supply, Tests were


13

developed that were able to distinguish these areas of stunned or hibernating myocardium. These tests of myocardial viability often look at metabolism. According to Maddahi, four different PET ap

Special Tests

203

revascularization (Scheiber!, 1994).

11-C-Acetate Another way to evaluate myocardial viability is to

proaches have been used for assessment of myocar

use an isotope that is incorporated into the meta

(I) perfusion-FOG metabolism imag

bolic pathways related to myocardial oxygen con

ing, (2) determination of oXidative metabolism with

sumption. II-C-acetate in its activated form, acetyl

dial viability:

(3) uptake and retention of 82-Rb and

CoA, represents the entry point for all metabolic

(4) the water perfusable tissue index (Maddahi, 1994).

pathways into the tricarboxylic acid cycle, which is

II-C-acetate,

tightly coupled to oxidated metabolism. It's advan

1BF-fluoro deoxyglucose

tage over 18-FOG, is that it does not rely on sub

18F-f1uoro-deoxyglucose (FOG) is a glucose ana

strate use (i.e., glucose vs. fat metabolism). It accu

logue that crosses the capillary and sarcolemmal

r a t ely r ef l e c t s o x i d a t i v e m e t a b o l i sm a n d c a n

membrane at a rate proportional to that of glucose. It

distinguish viable from nonviable myocardium in

becomes trapped in the myocardium, because it is not

b o t h a c u t e a n d c h r o ni c i s che m i c c o nd i t i o n s

a useful substrate in metabolic pathways. FOG distri

(Bergman, 1994.)

bution is relative to uptake of unlabeled glucose (Maddahi, 1994).

Technetium-99M-pyrophosphate

Identification of areas with normal metabolism,

Technetium-99M-pyrophosphate (TcPyp) identifies

altered metabolism or no metabolism is based on the

areas of myocardial infarction by forming a complex

use of glucose as an energy substrate. Normally,

with calcium, which is released when myocardial

perfused myocardial cells use fatty acids for adeno

cells die. TcPyp scans have the best results when ob

sine triphosphate (ATP) production when in a fast

tained 24 to 48 hours postinfarction. This time frame

ing state and use glucose as the primary energy

is obviously after reperfusion strategies would have

sour ce in the postprandial state. Ischemic m y

been employed. Sensitivity of this scan is high, but

ocardium uses glucose in the fasting state and the

specificity is low, since a number of other processes

postprandial state. Infarcted areas show no meta

can result in a positive scan (e.g., myocardial trauma,

bolic activity. Therefore increased uptake of FOG in

ventricular aneurysm, and uptake in skeletal struc

the postprandial state occurs in both hibernating and

tures) (Niemeyer, 1992).

normal myocardium, but in the fasting state, it oc curs only in the hibernating myocardium. Clinical

Indium-111-antimyosin

studies in infarct patients showed that area with per

Indium III antimyosin is a radiolabled monoclonoal

sistent thallium-20 I perfusion defects have evidence

antibody that identifies infarcted myocardial tissue. It

of remaining metabolic activity in 47% of regions

binds with myocardial myosin, which is released when

when studied with a PET scan, indicating overesti

the muscle cell dies. It can be used in conjunction with

mation of irreversible injury. Usc of reinjection and

thallium-20I to distinguish infarcted tissue from per

late redistribution imaging has significantly lowered

fused viable tissue. It is most reliable when performed

this number (Hendel, 1994). The implication de

48 hours after infarction (Niemeyer, 1992).

rived from this finding is that in areas with perfu sion defects, if glucose activity remains, the region is viable (mismatch pattern); conversely, if such ac

Echocardiography

tivity is absent, the area is likely to be infarcted or

Another noninvasive method of evaluating the heart

necrotic (match pattern) (Niemeyer, 1992). Viewed

uses the physical properties of sound. Echocardiogra

in functional terms, mismatch simply implies the

phy provides information about blood flow, structure,

potential for improvement; rnatch implies no poten

and function of the heart. Motion mode (M-mode)

tial for improvement in contractility after successful

and two-dimensional (2-0) images are highly reliable


204

PART II


methods of evaluation. Recent developments of tech

with indication of flow direction in real time (Wag

nique and technology include color flow Doppler

goner, 1990). Color is matched based on the direction

echo, transesophageal echo, and intravascular

of flow, and shading is indicative of intensity based

echocardiography. These techniques, when used in

on the mean velocity flow estimates (Waggoner and

combination can provide much of the information

Perez, 1990). It is primarily used to assess the extent

previously available only by cardiac catheterization

of regurgitant jets across "leaky valves," as well as to

(Hartnell, 1994).

indicate areas of abnormal shunts such as atrial septal defects. Turbulence created by narrowed valves cre

Physics of echocardiography

ates wide color shading.

Imaging systems that use ultrasound require a source

Measurements derived from echocardiography

for generation of the sound wave, a transducer, and a receiver to pick up the reflected sound waves. Sound

Echocardiographic results can be viewed qualita

is absorbed or reflected differentially by specific tis

tively and quantitatively. An experienced viewer can

sues. Therefore the sound wave reflected from mus

analyze the anatomical relationships and structure of

cle differs from that reflected from vascular space,

the heart, wall motion, valve movement and configu

or valvular structures. Returning signals are con

ration, and chamber size.

verted into electrical signals that generate an image.

Quanti tati ve measures are calculated from the

This is the basis for M-mode and 2-D echo. In M

Doppler frequency shifts. Velocity measures can be

mode echocardiography, the transducer transmits a

used in other equations to estimate pressure and valve

single sound wave through the chest wall. A thin

area. The modified Bernoulli equation is used to cal

slice of the heart, an "ice pick" view, directly under

culate pressure changes around the valve:

the sound wave, reflects the wave back to the trans L'1 P (mm Hg)

ducer. M-mode, though useful, is rarely used; 2-D is

=

4 X VIllax2 (m/second),

the primary diagnostic mode. In 2-D echocardiogra

where P is the pressure gradient across the valve and

phy, the transducer is able to pick up a wedge sec

V is the velocity of blood flow through the valve.

tion of the heart. In 2-D the transducer acts as the transmitter and receiver. A "real time" two-dimen

These measurements allow calculation of stenotic

sional picture of the heart is recorded on videotape.

valve gradients and right-sided filling pressures,

The heart can be viewed in motion, and wall motion

valve regurgitation, and ventricular septal defects

can be evaluated.

(Waggoner and Perez, 1990). Valve regurgitation and

Doppler echocardiography relies on the Doppler effect to determine velocity. W hen a sound wave is

shunt calculations are more complicated than the Bernoulli equation alone.

aimed at moving objects such as red blood cells,

Another important quantitative measure is the

the known transmitted frequency and the reflected

estimated area of the valve. The continuity equation

frequency differ, a phenomenon, known as a fre

is used to estimate valve area. It is based on the

q u e n c y s h i f t . The g r e a t e r the frequency s h i f t

principle of conservation of mass; that is, in a nor

the greater the speed o f the targeted object (Wag

mal heart, the volume of blood that enters the right

goner and Perez, 1990). The velocity of flow is

atrium should be conserved as it passes through the

the terminology used to express Doppler frequency

other chambers. Flow. volume at different sites is

shifts. Both continuous wave and pulsed wave

related to the flow velocity and the cross sectional

Doppler are used.

area of the site. Therefore AI x VI

=

A2 X V2,

Color flow Doppler echocardiography was intro

where VI is the velocity of flow at one side of the

duced in the mid-1980s. It is usually superimposed

valve and V2 is the flow velocity at the other side

on a two-dimensional image in real time but can be

of the valve, and A is the cross-sectional area

used with M-mode. It is a method that displays

(W aggoner and Perez, 1990) (Wilson, Va cek,

anatomic and spatial blood flow velocity estimates

1990).


13

Transesophageal echocardiography (TEE)

Special Tests

205

saturation can be obtained. When selective coronary

Because of consistent technical difficulties with

arteriography is performed, radiopaque contrast mate

transthoracic echocardiography, the technique of trans

rial is injected into the left main or right coronary

esophageal echo was developed to improve spatial res

artery. Cine recordings are made after the injection,

olution. The technique can obtain M-mode, 2-D, and

and injections are repeated until the entire coronary

color flow Doppler images by using a small probe

tree is visualized.

mounted on the tip of a modified gastroscope. The

Cardiac ventriculography is when dye is injected

probe is advanced into the esophagus and positioned so

into the ventricle and the entire chamber becomes

that multiple views of the heart are available (Kerber,

outlined. Several cardiac cycles are recorded on cine.

1988). Initially, the technique was performed intraoper

It provides valuable information about global and

atively on anesthetized patients and on intubated pa

segmental wall motion, valve motion, and the pres

tients in the intensive care unit. It is now used on awake

ence of abnormal anatomy (Grossman, 1986).

patients who are mildly sedated (Schneider, 1993). The semiinvasive nature of this test has slowed its adoption. It is most useful in ruling out thrombus or heart valve

TESTS OF THE RESPIRATORY SYSTEM

vegetation as a cause of transient ischemic attack (TIA)

Unlike the cardiovascular system, special tests of the

or stroke. Especially excellent views of the left atrium

respiratory system are less commonly used in the initial

and atrial appendage are seen. The atrial appendages

diagnosis and treatment of disease. This is the result of

cannot be visualized by traditional transthoracic echo. It

the generally high quality information obtained from

is also a good assessment of prosthetic valve function.

standard x-ray examination when combined with the patient's respiratory symptoms and the results of the physical examination (Lillington, 1987). When further

Cardiac Angiography

information is needed to refine the diagnosis or treat

The standard with which many of the noninvasive tests

ment decision several tests are available to clinicians.

are compared is that of cardiac catheterization. It is an

Radionuclide imaging of the chest is useful in the non

invasive test, with a small but serious risk to the pa

invasive evaluation of pulmonary embolism, whereas

tient. Complications include death, stroke, myocardial

pulmonary angiography is the invasive but definitive

infarction (MI), bleeding, arterial trauma or thrombus,

test. A computed tomography (CT) scan of the chest

renal dysfunction, and aIThythmias (Reagan, Boxt, and

also has a variety of applications (Webb, 1994). Al

Katz, 1994). The test is indicated in patients with a

though magnetic resonance imaging (MRI) provides

high risk of atherosclerotic heart disease whose stress

improved tissue contrast in comparison to a CT scan,

perfusion scans are positive. Patient's with diagnosed

imaging applications in pulmonary disease continue to

CAD with angina, unresponsive to medical therapy,

suffer from technical limitations (Mayo, 1994).

may also need catheterization.

Bronchoscopy Test Procedure

Bronchoscopy is often used as both a diagnostic and

The cardiac catheterization laboratory requires an x

therapeutic treatment modality (Mars and Ciesla,

ray generator tube and image intensifier/cine camera.

1993). It allows direct visualization of the trachea and

Data are stored using 35mm file (Reagan, Boxt, and

its major subdivisions. Fiberoptic bronchoscopy has

Katz, 1994).

virtually replaced bronchography (Lillington, 1987).

The procedure for cardiac catheterization of the

In fiberoptic bronchoscopy, a flexible tube is inserted

left side of the heart requires the threading of a

into the trachea of mildly sedated patients. This tude

catheter, guided by fluoroscopy, through the femoral

is able to enter small brochial subdivisions. Secre

artery or brachial artcry 10 thc aorta. Direct measure

tions can be removed for evalutation or as a treat

ments of chamber pressures, blood flow, and oxygen

ment. It is also possible to obtain biopsy samples


206

PART II


using tiny forcepts or cell brushings. Bronchoscopy is

standard against which ventilation/perfusion scans

particularly important in the diagmosis of bron

are compared (Juni, 1992). Contrast dye is injected

chogenic carcinoma (Price and Wilson, 1986).

into the pulmonary circulation through the pulmonary artery. Additional techniques such as balloon occlu sion, segmental injections, or increased magnification

RADIONUCLIDE IMAGING

improve the sensitivity of the test (Lillington, 1987).

Ventilation-Perfusion lung Scan

Interobserver reliability studies pelformed on the in

The ventilation-perfusion lung scan is a combination of

terpretation of pulmonary angiograms are 83% to

two separate imaging procedures. It is primarily used in

86% (Juni, 1992).

the diagnosis of pulmonary embolism, with limited use for other clinical problems (Lillington, 1987). The per fusion portion requires the injection of radioacti ve

Gallium SCintigraphy

tracer. Technetium-99M-macroaggregated albumin is

Gallium-67-citrate concentrates in neoplastic and in

(almost universally accepted as) the perfusion tracer of

flammatory lesions of the lung (Lillington, 1987).

choice (Juni and Alavi, 1991). The ventilation scan re

Gallium is more sensitive than normal chest x-ray in

quires the inhalation of radioactive gas, usually 133-XE

identifying infectious and noninfectious inflamma

gas or Tc-99M-diethylene triamine penta-acetic acid

tory processes. This is particularly important in iden

(DTPA) aerosol. Other isotopes can be used for ventila

tifying opportunistic infections in the immunocom

tion scanning (e.g. Kr-8IM, Xenon-I27) but they are

promised patient. In patients with acquired immune

more difficult to obtain.

deficiency syndrome (AIDS) the sensitivity of gal

A normal perfusion scan essentially rules out re

lium scanning for pneumocystis carinii pneumonia

cent pulmonary embolus. If the perfusion scan is ab

approaches 94% to 96% (Kramer and Divgi, 1991).

normal, it is compared with the ventilation scan for

The radioisotope is injected but it takes 48 to 72

match or mismatch of defects. An interpretation

hours before imaging can be pelformed (Miller and

scheme is used, such as Biello or Pioped, which clas

O'Doherty, 1992).

sifies the probability of pulmonary embolism into

Gallium is commonly used in the evaluation of pa

normal, low, intermediate (indeterminate), or high

tients with interstitial lung disease; this includes sar

(Juni, J 991; MiJJer and O'Doherty, 1992). Patients

coidosis, amiodarone toxicity, and following cyto

with high probability scans should begin anticoagula

toxic therapy with bleiomycin, as well as many other

tion therapy (Juni, 1991). Patients with intennediate

entities (Miller and O'Doherty, 1992). In conjunction

(indeterminate) scans may need to have a pulmonary

with neoplasms, the scan's use is limited to assessing

angiogram before beginning treatment (Miller and

tumor extent (Kramer and Divgi, 1991).

O'Doherty, 1992). Miller and O'Doherty (1992) note other applica tions of ventilation/perfusion scanning to include monitoring of response to radiotherapy and assess

Computed Tomography A computed tomography (CT) scan of the chest pro

ment of resectability of bullae. The scan is used to

vides a series of cross-sectional x-ray images. Com

predict whether someone can tolerate a pneumonec

pared with the standard x-ray, it is not commonly

tomy based on percent flow to the opposite lung and

used in the initial diagnQsis of pulmonary disease. CT

extent of disease present.

scan has been found to be a useful first-line diagnos tic tool in the evaluation of mediastinal disease, in cluding mediastinal masses, staging of mediastinal

Pulmonary Angiography

cancers, and identification of cysts (Lillington, 1987).

The diagnosis of pulmonary embolism is the primary

High-resolution computed tomography (HRCT)

indication for pulmonary angiography. It is the gold

has improved the documentation of morphologic


13

associated with chronic airflow obstruction. Webb's (

review of the application of this new identified the utility of this test in a vari

ety of obstructive diseases. HRCT is sensitive in the although

of

such as

used

Many tests are available t o

mines which tests are appropriate for the medical condition. When the tests are results are

HRCT demon

In the diagnosis of

to the selection of exercise and

It is the procedure of choice work loads the PT

tween the three different

PT reaches a certain

of abnormal bronchi

seen in bronchiectasis (cylindrical,

Until a

for the

level, as well as a

level of understanding and application of the test

but again there is l ittle clinical

treatment, it is

results to

1994). It can be used to differentiate

encouraged

that the PT discuss the test and results with the pa

spread of cancer versus heart failure when un

tient's physician. These discussions are excellent for learning both for the PT and to

clear clinically. HRCT also can be used to evaluate of

wiH apply to

function and response to exercise. This Ull

after plain chest X-rays. HRCT can discriminate be

(Webb,

and an evaluation of

the results are documented. PTs need to understand the results of the tests and how

well as waH thickness. strates a high

card

monary dysfunction. The attending physician deter

X

10 m m i n diameter, as

207

SUMMARY

HRCT is a b l e t o demonstrate cysts less than

Special Tests

the

Overall, HRCT has but the clinical

understand what physical ther

apy has to offer the

with

function is less clear.

REVIEW QUESTIONS Magnetic Resonance Imaging

Why is the sure of

mea function?

2. What i s the difference between

stunned my

ocardium and 3. embolism?

4, Which tests can be used to evaluate myocardial vjability? 5. Why is

a good choice for eval cardiac defects?

References Beller, G. (1994), Myocardial perfusion imaging with thallium 20 I. journal of Nuclear Medicine, 35, 674-680, Bergman,

S, (1994), Use and limitations of metabolic tracers la

beled with positron-emitting radionuclides in the identification of viable myocardium. journal oj Nuclear Medicine. 35, 15s-22s

D., Hosen, S" Van Train. K., Germano, G., Maddahi. J., Friedman, J. (1994). Myocardial perfusion imaging tech

Berman,

nitium-99M-sestamibi comparative analysis of available imag ing protocols, Journal of Nuclear .Medicine.


681-688,

208

PART II


Berman, D., Kim, H., Van Train, K., Garcia, E., Friedman, J., &

artery disease and left ventricular dysfunction. Jou rn al 0/ Nu

Maddahi, 1. (1991). Technetium, 99m sestamibi in the assess ment of chronic coronary artery disease. Setninars in Nuclear

clear Medicine, 35, 707-715. Mars, M., & Ciesla, N. (1993). Chest physical therapy may have prevented bronchoscopy and exploratory laparatomy-a case re

Medicine, 21,190-212.

port. Cardiopu lmonwy Physical Therapy Journal. 4: 1,4-6.

Brown, K. (1994), The role of stress redistribution thallium-201 myocardial perfusion imaging in evaluating coronary artery

Mayo, .J. (1994). Magnetic resonance imaging of the chest. Ad vances in Chesi Radiology, 32,795-809.

disease and perioperative risk. Journal of Nucfear Medicine,

Miller, KF., & 0' Doherty, M.l (1992). Pulmonary nuclear medi

35, 703-706.

cine. European Journal of Nuclear Medicine, 19, 355-368.

Go, R.T., Macintyre, W.J., Cook, S.A., Neumann, D.R. (1992). Myocardial perfusion imaging in the diagnosis of coronary

Mullani, N.A., & Volkow, N.D., (1992). Positron emission tomog raphy instrumentation: a review and update. A merican Journal

artery disease. Currelll Opinion in Radiology. 4(4). 23-33.

of Physiologic Im aging, 314, 121-135.

Grossman, W. (1986) Cardiac Catheterization and A ngiography. (3rd cd.) Philadelphia: Lea & Febiger.

Niemeyer, M.G., Van der Wall, E.E., Pauwels, E.KJ., van Dijk man, P.R.M., Blokland, .l.A.K., deRoos, A., & Bruschke,

Hartnell, G. (1994) Developments in Echocardiography. Radio

A.V.G. (1992). Assessment of acute myocardial infarction by

logic Clinics of Norlh America, 32,461-475.

nuclear imaging techniques. Angiology, 43, 720-733.

Hendel, R. (1994) Single-photon imaging for the assessment of myocardial viability. Journal of Nuclear Medicine, 35(4 suppl),

Port. S. (1994). The role of radionuc1ide ventriculography in the assessment of prognosis in patients with CAD. Journal of Nu

23s-3Is.

clear Medicil1e, 35,721-725.

lskandrian, A.S. (1987). Nuclear cardiac imaging: principles and app/icalions. Philadelphia: FA Davis. Johnson, L. (1994) Myocardial perfusion imaging with tech netium-99m-teboroxime. Journal of Nuclear Medicine, 35,

Price, S., & Wilson, L (1986). Pathol,hysi% gy: clinical concepts of disease processes. New York: McGraw-HilI. Reagan, K., Boxt, L., & Katz, J. (1994). Introduction to coronary ar teriography. Radiologic Clinics of Norlh America. 32,419-433.

689-692. Juni, J., & Alavi, A. (1991). Lung scanning in the diagnosis of pul

Schelbert, H. (1994). Metabolic imaging to assess myocardial via bility. Journal o/ Nuclear Medicine, 35(4 suppl), 8s-14s.

monary embolism: the emperor redressed. Seminars in Nuclear

Schneider, A., Hsu, T., Schwartz, S., & Pandian, N. (1993). Single,

Medicine, 21, 281-296.

biplane, multiplane, and three dimensional transesophageal

Kerber, R. (Ed.). (1988). Echocardiography in coronary arlery

echocardiography. Cardiology Clinics, II, 361-387.

disease. Mount Kisco, NY: futura Publishing. Kim, E. (1987). Nuclear diagnostic imaging: praClical clillical ap

Schwaiger, M. (1994). Myocardial perfusion imaging with PET. Journal of Nuclear Medicine, 35, 693-698.

plicaliolls. New York: Macmillan. Kinch, J., & Ryan, T. (1994). Right ventricular infarction. New

Wackers, FJ.T. (1994). Radionuclide evaluation of coronary artery disease in the 1990's. Cardiology Clinics. 12. 385-389.

England Journal o/Medicine, 330, 1211-1215. Kramer, E., & Divgi, c. (1991). Pulmonary applications of nuclear

Waggoner, A.D., & Perez, J. (1990). Principles and physics of

medicine. Clinics ill Chesl Medicine 12:1. 55-75.

doppler. Cardiology Clinics, 12, 385-389.

Lillington, G. (1987). A diagnos tic approach to chest disease. Bal

Webb, W.R. (1994). High-resolution computed tomography of ob structive lung disease. Radiologic Clinics of North A merica,

timore: Williams and Wilkins. Maddahi, 1., Schelbert, H., Brunken, R., & DiCarli, M. (1994). Role of Thallium-201 and PET imaging in evaluation of my

32, 745-757. Wilson, D., & Vacek, J. (1990). Echocardiography. Postgraduate

ocardial viability and management of patients with coronary


Medicine. 87. 191-202.

Clinical Assessment of the

Cardiopulmonary System

Susan M. Butler

KEY TERMS

Barrel-chest

Hyperresonant

Crackles

Resonant

Cyanosis

Wheeze

Dyspnea

Whispered pectoriloquy

Egophany

INTRODUCTION

the inpatient setting, a chart review is the first point

To develop an effective treatment program for the pa

of contact, whereas in the outpatient population, the

tient with a cardiopulmonary problem, it is essential

information may be only what is obtainable from the

that a thorough evaluation be peliormed by the physi

patient. Time management is an ever-present issue in

cal therapist (PT). This provides "baseline" data for

today's era of cost containment and health care re

comparison with subsequent reassessments that occur

form. Thus a medical chart review should be con

on a daily basis. Any progress or deterioration in sta

ducted in an organized fashion. Most PTs develop

tus can then be easily identified with appropriate ad

their own method.

justments made in the treatment plan.

One strategy to chart review is the following se quence: 1. Read the history and physical and admission

CHART REVIEW/PATIENT INTERVIEW

medical note (i.e., preadmission symptoms).

The first patient contact can be indirect, through the

2.

medical chart, or direct, through patient interview. In

3. Scan remainder of chart.

Read the last medical note.

209


210

PART II


4. Read any reports from medical specialists, con sultants, i.e., pulmonologist, neurologist, oncologist. 5. Review any pertinent lab tests. EXAMPI.ES: chest

and respiratory systems. These questions could in clude the following: What is the smoking history? Does the patient have a family history of premature

x-ray, arterial blood gases (ABG's), complete blood

coronary artery disease (i.e., a parent or sibling who

count (CBC).

had a myocardial infarction)? Can the symptoms pre

6.

Review medications, in particular, pulmonary

and cardiac drugs.

sented also be signs of a cardiovascular or pulmonary illness? Does the patient have an active versus a

7. Review the psychosocial information (i.e., fam

sedentary lifestyle? What activities precipitate symp

ily, architectural barriers).

toms? Do these symptoms include breathlessness?

This last step is crucial in this time of shortened hos

The patient should be seen as a human being with

pital stays. Any detail of the patient's background

multiple organ systems. The patient's prob.lem,

that would affect discharge planning is crucial to

whether oI1hopedic or cardiopulmonary, should not be

know even on the first day of treatment. Additional

viewed in isolation. An example is the outpatient with

information to review that may be helpful and falls

a physical therapy diagnosis of low back pain. When

into the cate gory of "as time allows" is the documen

questioned about limiting symptoms, the patient might

tation of other allied health professionals (i.e., nurs

describe cramping leg pain more suggestive of periph

ing, occupational therapy, speech pathology). Finally,

eral vascular disease (PYD).

when the initial chart review is finished, a mental pic ture of the patient should exist, even before the PT steps into the patient's hospital room.

PHYSICAL EXAMINATION

Details regarding the patient interview have been

The traditional components of a chest assessment are

covered in chapter 7. However, there are questions that should be posed to any patient regardless of

visual inspection, auscultation, percussion, and pal pation. The information provided by each of

whether their primary condition is cardiopulmonary.

these techniques, when integrated with the patient's

The patient whose referring problem is musculoskele

history and chal1 contents, allows the PT to piece to

tal or neurologic still must have operational cardiac

gether the pieces of the puzzle. For instance, to aus cultate breath sounds without observing the symme try of the chest wall fails to provide the needed clues

Anatomic Structures

to the total patient picture; thereby the development

Suprasternal /lotch-A depression palpable at the tip of the sternum Sternomanubrial angll'-A bony bump where the manubrium meets the body of the sternum; about 5 cm distal to suprasternal notch; also known as angle of Louis; palpating hlle.ral to this junction,

of an appropriate plan of care for the patient is maqe more difficult. Before each individual component of the assess ment is discussed, a review of the pertinent anatomical landmarks and topographical lines is to be discLlssed.

the .l'econd ribs is found and thus a reference point

Knowledge of the superficial anatomy arid its relation

for identifying intercostal spaces and successive

ship to the Llnderlying heart and lungs aids the therapist

ribs; also, a superficial marking for where the underlying trachea divides into right and left mainstem bronchi.

in decision making. The topographical lines allow for more accurate description of the physical findings.

Costal angle-The angle formed by the joining of the costal margins with the sternum; normally, no greater than 90 degrees. Vertebra prominens-The spinous process of the seventh ccrvical vertebra (C7); allows numbering of thoracic vertebra

TOPOGRAPHICAL ANATOMIC LANDMARKS Key anatomical structures include the following: •

Sternum

•

Clavicles


14

Clinical Assessment of the Cardiopulmonary System

211

-------

•

Suprasternal notch

•

Sternomanubrial angle (angle of Louis)

(MAL), and posterior axillary (PAL)-Like the

•

Costal angle

MCLs, these lines are also bilateral.

•

Vertebra prominens

•

The posterior chest has the following three lines:

See the box on p. 210 and Figures 14-1 and 14-2 for

•

thorax. Imaginary topographical lines are used to more clearly describe any physical findings (e.g., lo cation of surgical incisions, abnormal breath sounds, etc.) (Figure 14-3). The anterior view of the thorax has three vertical

-

runs through the

•

Mid-scapular lines (MSL)-lie parallel to the mid-spinal lines; bisect inferior angles of scapulae.

VISUAL INSPECTION Inspection is the foremost element of a chest assess ment. Not only should the features of the patient be

lines. These are the following: Mid-sternal line (MSL)-a vertical line bisecting . the sternum •

Vertebral or mid-spinal line

spinous processes of the vertebrae.

specific definitions and anterior and lateral views of

•

Anterior axillary line (AAL), mid-axillary line

observed, but also the equipment and any aspect of the patient's surroundings that would contribute to

Mid-clavicular fine (MCL)-lies parallel to the

delineating the true picture of that patient. Remem

MSL, bisects each clavicle; the lower lung borders

ber, the PT has speculated a preliminary picture of

cross the sixth rib at the MCL.

the patient based on chart review. Now, the ultimate

Laterally there are three vertical lines, originating

test: how realistic was this initial impression? What

in their respective axillary folds:

are the outward clinical signs that the therapist should

Clavicle

��-----1��n Manubrium ManubriostemaI junction (Angle of Louis)

Nipple

Costal angle

FIGURE 14-1 Topographical landmarks of the chest. (Adapted with permission from Seidel HM et al: Mosby's

guide to physical examination, ed 3, Boston, 1995, Mosby.)


212

PART II


Suprasternal notch Clavicle

/

\

'j,\

.1

'_=:,. c/:.Ay".J ,

Manubrium

Costal cartilages Ribs Xiphoid process

) FIGURE 14-2 Anterior view of the thorax. (With permission from Swartz MH: TeXfbook

ofphysical diagnoses

hi story and examination, ed 2, Philadelphia, 1994, WB Saunders.)

look for? It will be broken down into categories for

patient's build-stocky, thin or cachectic? Is the pa

clarity.

tient's mobility limited? Can the patient sit unsup ported? Should the assessment be performed in stages such

General Appearance

as

supine or alternate sidelying? Is there any extra

equipment in the patient's surroundings? Is the patient

Does the patient appear comfortable? Is there any facial

wearing supplemental oxygen? Is the oxygen delivered

grimacing? Is the patient awake and alert or disori

through a nasal cannula or a mask? What is the fraction

ented? Is there any nasal flaring or pursed-lip breath

of inspired oxygen (Fi02)? Are there any monitoring

ing? These are signs of respiratory distress. Nasal flar

lines and where are they located. For instance, if an ar

ing can be defined as the outward movement of the

terial line is present, is it placed in the radial or femoral

1994).

Are the accessory

artery? Are there electrocardiogram (ECG) leads? Is it a

muscles of respiration (i.e, sternocleidomastoid, trapez

"hard line" (directly connected to monitor) vs. teleme

ius) hypertrophied? How is the patient positioned? Is

try (through radio transmitter)? Are there intravenous

the patient resting comfortably or leaning forward over

(IV) sites? Are these peripheral (antecubital) or central

the bedside table and struggling for breath? What is the

(subclavian or jugular)? Is there a urinary catheter?

nares with inspiration (Swartz,


System

Clinical Assessment of the

14

L----j��::::- SuprasternaJ notch t---t----"1- SlernomanubriaJ angle t---;---/---'r--- Midsternal line r--+--t-..4f.1\\--::::---\--- Midclavicular lioe

I

1 A

/1 6"///

,"--4i If

--

Spinous process of C7

Anterior axillary liM --t----I

Midaxillary li ne ----+

+-_1

___

1--.....,..-+1-+---+----::>--+- Scapula line

dJ

pi

Posterior

line

---r----t-+--j

J/I F'

II---+--/!--":--- Midspinalline

FIGURE 14·3 lines. A, Anterior view. 8, Lateral view.

Posterior view. (Adapted with

and examination, ed 2,

permission from Swartz MH: Textbook Philadelphia, 1994, WB Saunders.)


213

214

PART II


Skin

desaturation has been noted, but this is not an exclu

Does the skin have a pink, healthy color versus a pal

sive phenomenon. Clubbing has been o bserved in

lor? Is cyanosis present? Cyanosis is a bluish tinge

non pulmonary diseases such as hepatic fibrosis and

that can be seen centrally or peripherally. Central

Crohn's disease. (George, Light, Matthay, and

cyanosis is a result of insufficient gas exchange

Matthay, 1990; Seidel, Ball, Dains, and Benedict,

within the lungs and is not usually seen unless oxy

1995; and Swartz, 1994).

gen saturation is less than 80%. A bluish tint may be seen at the mucous membranes (e.g., tongue, lips). Peripheral cyanosis, on the other hand, occurs when

Neck

oxygen extraction at the periphery is excessive. This

Are the accessory muscles of respirations being re

type is also more associated with low cardiac output

cruited for a resting breathing pattern? Do the stern

states. Areas to observe for peripheral cyanosis might

ocleidomastoid or trapezius muscles appear promi

be fingertips, toes, nose, or nail beds. A differentiat

nent? This is an early sign of obstructive lung disease

ing feature between central and peripheral cyanosis is

(Swam, (994).

that peripheral cyanosis occurs, usually in the cooler body parts such as nail beds and vanishes, usually when the part is warmed. In contrast, central cyanosis does not disappear when the area is warmed.

Jugular venous distension The jugular veins empty into the superior vena cava

Are any scars, bruises or ecchymoses observed?

and reflect right-sided heart function. Right atrial

Are there reddened areas suggestive of prolonged

pressure (RAP) is evident based on the extent to

pressure anywhere? Do the bony landmarks appear

which the jugular venous pulse (JVP) can be visual

more prominent than usual? Are there any signs of

ized. The more superficial external jugular veins may

trauma to the thorax or any other body parts? Does

be seen superior to the clavicles; the internal jugular

the skin appear edematous? Does this edema appear

veins, though larger, lie deep beneath the sternoclei

to limit joint motion? Are there any surgical inci

domastoids and are less visible. Jugular venous dis

sions, new and old? Do these incisions appear to be

tention (JVD) can be best seen when the patient lies

healed or seem reddened and swollen? Is there evi

with the head and neck at an optimal angle of 45 de

dence of clubbing of the digits? Clubbing can be de

grees (Figure 14-5). Symmetry of JVD should be

fined as the loss of angle between the nail bed and the

noted. The veins are distended bilaterally if there is a

distal interphalangeal joint (Figure 14-4). The cause

cardiac cause such as congestive heart failure (CHF).

of clubbing has a variety of theories, including in

A unilateral distention is an indication of a localized

creased perfusion. Its association with arterial oxygen

problem. (Seidel, Ball, Dains, and Benedict, (995).

CHEST WALL CONFIGURATION The normal thoracic cage is elliptically shaped when free of disease. The anteroposterior (AP) to lateral di ameter is 1:2 or 5:7. The angle of the ribs is less than 90 degrees. The ribs articulate with the vertebra, pos teriorly, at a 45-degree angle. The thorax should be

FIGURE 14-4 A, Clubbing of the fingers is best assessed by detemtining the ratio of the diameter at the base of the nail B, to the diameter at

observed both anteriorly and p osteriorly. With chronic obstructive pulmonary disease (COPD), the

the distal interphalangeal joint. This ratio is n ormally less than

ribs become more horizontal and the A-P diameter

I. (Reprinted with permission from George RB et al: Chest

increases, thus the term barrel chest is used. In in

medicine, ed 2, Baltimore, 1990, Williams and Wilkins.)

fants, the chest is round with the anteroposterior and


14


215

Carotid mCfY Internal jugular vein

-

Horiz nlal line FIGURE 14-5 Proper positioning to observe jugular venous distention. (Reprinted with permission from Seidel HM et al: Mosby's guide to physical examination, ed 3, Boston, 1995, Mosby.)

transverse or lateral diameters of about equal dimen

pathology. Again, any asymmetry should be observed

sions. As the child grows to adulthood, the chest be

from both anterior and posterior views.

comes more elliptical. Again, with the aging process,

Structural defects of the anterior chest may in

the chest returns to a more rounded appearance. The

clude the following: pectus excavatum, or funnel

increased anteroposterior diameter, in this population,

chest-a depressed lower sternum that usually causes

is a result of the multiple factors of decreasing lung

restriction only when severe; pectus carinatum, or pi

compliance, decreased strength of the thoracic and di

geon chest-a prominent upper sternum which does

aphragmatic muscles and skeletal changes of the tho

not restrict chest wall movement; and flail chest-the

racic spine. The sym metry of the thoracic cage

chest wall moves inward with inspiration, such as

should also be noted. Asymmetry can be the result of

with multiple rib fractures.

structural defects or an underlying intrathoracic

Other structural defects are spinal deformities.


216

.-

PART H

t \


J

.JPI4/1h

.

v

./

" / ./

/

\ 'I

)

(j>";-.

(";" \,\"'\\ Jilii/

I

\{

/' "',r- \ .

/(�

Kyphosis

"Barrel chest"

:Jil!

-

..:,:.-

A

Normal

} -\, .

Pectus excavatum

Pectus carinatum

FIGURE 14-6 Chest walJ configurations. (Reprinted with permission from Swartz MH: Textbook o/physical diagnoses-his/ol)! and examination, ed 2, Philadelphia, 1994, WB Saunders.)

These are best viewed posteriorly. Kyphoscoliosis is

Dyspnea describes the sensation of breathlessness

one example of how a posterior and lateral spinal devi

or shortness of breath and is seen in cardiopulmonary

ation can limit chest wall and lung expansion. Another

disorders. The level of dyspnea worsens as the sever

example is a patient with COPD, who usually has a

ity of the disease increases. An easy method to docu

forward head and thoracic kyphosis (Figure

14-6).

ment the level of dyspnea is to count the numbers of words that the patient is able to speak per breath. For instance, six-word dyspnea is not as significant as

BREATHING PATTERN

one-word dyspnea. The type of activities that elicit

Respiratory rate normally ranges between 12 and 20

shortness of breath should also be ascertained. For

breaths per minute (bpm). Eupnea is the term used to

example, is breathlessness precipitated by stair climb

describe a normal breathing cycle. Apnea is a tempo

ing, taking a shower, etc? The "normal" ratio of in

rary halt in breathing. Tachypnea is a rapid, shallow

spiratory time to expiratory time is j :2. As the respi

breathing pattern; this is an indicator of respiratory

ratory rate increases this ratio decreases to j: I. This

distress.

is seen in respiratory distress, as the patient struggles

Bradypnea exists when respiration is slowed, less

to breathe in, the expiratory phase is shortened, and a

than 12 bpm. Causes could be neurologic or metabolic.

vicious cycle continues. With pursed lip breathing,

Kussmaul's breathing is an increased rate and depth of

the idea is to prolong the expiratory phase and slow

respirations and is associated with metabolic acidosis.

the breathing pattern.


14

AUSCULTATION

Auscultation is the art of listening to sounds pro duced by the body. Lung and heart sounds are the focus of this chapter. Skill in auscultation is depen dent on the following four factors: I. A functional stethoscope 2. Proper technique 3. Knowledge of the different categories of lung sounds: normal, abnormal, and adventitious breath sounds and voice sounds 4. Knowledge of the different categories of heart sounds and murmurs Stethoscope

A stethoscope need not be fancy to be effective. A PT, skilled in auscultation, can use any basic stetho scope and be able to identify lung sounds. The stetho scope functions more as a filter to the extraneous noises than as an amplifier. A basic stethoscope con-

Tubing

FIGURE 14-7


217

sists of ear pieces, tubing, and a chestpiece. The bell portion of the chestpiece assesses low-pitched sounds, that is, heart sounds. The diaphragm portion discerns high pitched sounds (Figure 1 4-7). The tub ing should not be so long that sound transmission is not dampened. Length of tubing should be between about 30 cm (12 in) to 55 cm (21 to 22 in). The ear pieces should fit the PT's ears comfortably and allow tuning out of external sounds. Other considerations would be to position the ear pieces anteriorly or for ward toward the ear canals. Finally, an aside gained from the author's clinical experience: warming the diaphragm with the hands before placing it on the pa tient's skin is a first step in developing good patient rapport. Technique

Environment is another element in the correct pedor mance of auscultation. The room or cubicle should be as quiet as possible. Television and radio should be turned down or off. Any extraneous noises should be minimized or eliminated. This is especially important when auscultation is a new technique for the thera pist. The patient should be positioned sitting, if possi ble, for lung sounds. The anterior, lateral, and poste rior aspects of the chest should be auscultated both craniocaudally (apices to bases) and side to side (Fig ure 14-8). The PT places the diaphragm on the pa tient's skin so that it lies flat. The patient is instructed to breath in and out through the mouth. A slightly deeper breath than tidal breathing is suggested. A minimum of one breath per bronchopulmonary seg ment allows for a comparison of the intensity, pitch, and quality of the breath sounds. Movement of the di aphragm from one side to the other side while, at the same time, moving it craniocaudally, enables the PT to compare the right to the left chest. Clothing should be removed and/or draped so that it does not interfere in the assessment of the breath sounds. Chest Sounds

Stethoscope. (Replinted with permission from Wilkins RL, Hodgkin JE, Lopez B: Lung sOllnds, St. Louis, 1988, Mosby.)

Chest sounds may be divided into these categories:


218

PART II


A

B

FIGURE 14-8 Stethoscope placement for auscultation of breath sounds. A, The chest. B, The back. (From Buckingham EB: A

primer of clinical diagnosis,

I. Breath sounds-normal , abnormal, adventi

ed 2, New York, 1979, Harper & Row.)

piratory phase. A distinguishing feature is the pause that exists between the inspiratory and expiratory

tious 2. Voice sounds - egophany , bronchophany,

phases (Figure 14-9). This sound is also described as tracheal as its norma/ location is over the trachea.

whispered pectoriloquy 3. Extrapulmonary sounds-pl eural or friction

Brol1chovesicular suunds are similar in that these are

also high-pitched and have an equal inspiratory and

rubs 4. Heart sounds

expiratory cycles. However, a differentiating feature is the lack of a pause (Figure 14-9). Brol1chovesicular sounds are heard best wherever the bronchi or central

Breath Sounds

lung tissue is close to the surface. These include su

The terminology of breath sounds given in this chap

perior to the clavicles and suprascapular (apices), and

ter is a compilation of multiple resources and clinical

parasternal and interscapular (bronchi). The ATS

experience. Recognition of normal breath sounds is

AACP, in its 1977 recommendations for pulmonary

the key to the identification of abnormal and adventi

nomenclature, used the term bronchial to include

tious sounds by offering the listener a point of refer

both bronchial and bronchovesicular sounds. The fi

ence. Normal breath sounds can be broken down into

nite difference is minor (the pause between the inspi

bronchial, bronchovesicular, and ves icular_ The

ratory and expiratory phases). This recommendation

American Thoracic Society (ATS) and the American

is meant to provide uniformity to lung sounds tenni

College of Chest Physicians (ACCP) has attempted to

nology. Vesicular brealh suunds are heard over the

provide standardization of the nomenclature and con

remaining peripheral lung fields. These sounds have

tinues to conduct surveys of health care professionals

primarily an inspiratory component with only the ini

for use of this terminology in clinical practice.

tial one third of the expiratory phase audible. Their

Bronchial sounds can be described as high

intensity is also softer because of the dampening ef

pitched and are heard both in the inspiratory and ex

fect of the spongy lung tissue and the cumulative ef


14

BRONCHIAL loud, high pitched; hollow quality; heard over manubrium; louder on expiration; distinct pause between inspiration (I) and expiration (E)

~

BRONCHOVESICULAR mixture of bronchial and vesicular; I: E is 1: 1; heard over main-stem bronchi -- anteriorly: ICS # 1 and 2, posteriorly: between scapulae

/\


219

when it becomes airless-either partially or com pletely. In a consolidation type of pneumonia, the lung tissue is Hairless" because of the complete ob struction of segmental or lobar bronchi by secretions. Sound from the adjacent bronchi is enhanced and be comes more high-pitched and the expiratory compo nent louder and more pronounced. Compression of lung tissue from an extrapulmonary source also pro duces bronchial sounds. Examples include compres sion secondary to increased pleural fluid (pleural ef fusion) or tumor. Tubular breath sounds is a term used synonymously to describe abnormal bronchial

VESICULAR soft, low pitched; heard over peripheral lung tissue; no pause between I and E; ratio is 3: 1

FIGURE 14-9

/'

breath sounds. Decreased or absent breath sounds occur when sound transmission is diminished or abolished. De creased breath sounds are when the normal vesicular sounds are further diminished. Absent sounds are when no sounds are audible. Decreased or absent sounds can be caused by an internal pulmonary

Normal breath sounds.

pathology or can be secondary to an initially nonpul monary condition. Hyperinflation caused by emphy sema causes decreased sound transmission as a resull of the destruction of the acinar units and increased air as a result of loss of normal lung structure. The loss fect of the air entry from numerous terminal bronchi

of lung compliance resulting from pulmonary fibrosis

oles. The idea that vesicular sounds reflect air entry

also may produce decreased or absent breath sounds.

in the alveoli has been disproved. Thus as the thera

Extrapulmonary causes include tumors, neuromuscu

pist auscultates from top to bottom, the breath sounds

lar weakness (i.e, muscular dystrophy), and muscu

are quieter at the bases than at the apices. Infants and

loskeletal deformities (i.e., kyphoscoliosis). Pain is a

small children have louder, harsher breath sounds.

common cause for decreased or absent breath sounds.

This is as result of the thinness of the chest wall and

When the patient attempts to take a deep breath, the

the airways being closer to its surface.

volume is limited because of the onset of pain. The etiologic factors of the pain can be varied-from in cisional (i.e., midsternotomy) to traumatic (fractured

Abnormal Breath Sounds

ribs). Given that no underlying pathologies are pre

Abnormal breath sounds can be described as when

sent, decreased breath sounds may also be a reflec

the sound transmission changes as a result of an un

tion of the depth of respiration and/or the thickness of

derlying pathologic process. Sound is filtered by the

the chest wall (e.g., in obesity or with the presence of

lung tissues because these organs are air-filled; thus

bandages). The skill of auscultation lies in the differ

there is dampened sound transmission over the bases

entiation b etween normal and abnormal breath

versus the apices. On the other hand, sound transmis

sounds.

sion is enhanced when a liquid or solid is the medium. Certain lung pathologies produce abnormal lung sounds. Abnormal sounds can be divided into

Adventitious Breath Sounds

three types: bronchial, decreased, and absent.

Adventitious breath sounds are the extraneous noises

Bronchial sounds occur in peripheral lung tissue

produced over the bronchopulmonary tree and are an


220

PART II


indication of an abnormal process or condition. These

three." Egophany is also described when there is in

sounds may be more easily identifiable than abnor

creased transmission of the vocal vibrations. In this

mal sounds. Adventitious sounds are classified as

case, the patient is asked to say "eeee." The underly

c rackles (rales), rhonchi, and wheezes. Crackles

ing process distorts the "e" sound so that an "aaa"

(rales) are described as discontinuous, low-pitched

sound is heard over the peripheral area by the exam

sounds. They occur predominantly during inspiration.

iner. Egophany co-exists with bronchophany.

The sound of rubbing hair between the fingers or vel

Whispered voice sounds also produce low-pitched

cro popping simulates crackles. Crackles usually in

vibrations over the chest that are muftled by normal

dicate a peripheral airway process. Rhonchi are low

lung parenchyma. Whispered pectoriloquy describes

pitched but continuous sounds. These occur both in

when these whispered voice sounds become distinct

inspiration and expiration. Snoring is a term used to

and clear; "one, two, three" or "ninety-nine" are used

describe its quality. Rhonchi are attributed to an ob

to evaluate this sound. Whispered pectoriloquy can

structive process in the larger, more central airways.

be present when bronchophany and egophany are ab

Wheezes are continuous but high-pitched. A hissing

sent. This sign is helpful in identifying smaller or

or whistling quality is present. Wheezes predomi

patchy areas of lung consolidation.

nantly occur during expiration and are an indication

Voice sounds are a means of confirmation of the

of bronchospasm (i.e., asthma). However, wheezes

abnormal breath sounds. If a patient with significant

can also be caused by the movement of air through

atelectasis secondary to compression of lung tissue

secretions, thus inspiratory wheezes can be described.

presents with bronchial breath sounds, then egophany and bronchophany are also audible.

Extrapulmonary Sounds An adventitious sound that is nonpulmonary is the

HEART SOUNDS

friction rub. It can be described as a rubbing or leath

As with lung sounds, superficial topographical land

ery sound and occurs during both inspiration and ex

marks assist the therapist in auscultation of heart

piration. The sound is produced by the visceral

sounds and murmurs. The left ventricular apex is nor

(inner) pleural lining rubbing against the parietal

mally located at the MCL in the fifth intercostal

(outer) pleura and is a sign of a primary pleural

space (rCS). The cardiac apex is also known as the

process such as inflammation or neoplasm. Pain is

point of maximum impulse (PM/). There are four ref

usually associated with a friction rub.

erence areas for cardiac auscultation; these do not c o r r e s p o n d directly to the u n derlying cardiac anatomy. On the other hand, these areas do relate to

Voice Sounds

the events arising at the individual cardiac valves.

Voice sounds are vibrations produced by the speak

These four areas are defined as the following:

ing voice as it travels down the tracheobronchial tree

•

aortic: second rcs, at right sternal border

•

pulmonic: second ICS, at left sternal border

The transmission of these vocal vibrations can be in

•

tricuspid: fourth and fifth lCS, LSB

creased or decreased in the presence of an underlying

•

mitral: cardiac apex fifth ICS, MCL.

and through the lung parenchyma when heard with a

(RSB)

stethoscope. These sounds, over the normal lung, are low-pitched and have a muftled or mumbled quality.

(LSB)

pulmonary pathologic process. Bronchophany de scribes the phenomenon of increased vocal transmis sion. Words or letters are louder and clearer. Causes

Technique

are conditions where there is an increased lung den

An environment that is as quiet as possible is recom

sity as in consolidation from pneumonia. The patient

mended. Positions used for cardiac auscultation in

is usually asked to repeat "blue moon" or "one, two,

clude the following: supine-used for all areas; left


14


221

lateral decubitus (sidelying)-iistening to cardiac

ever, it is usually abnormal in individuals over age

apex or mitral area, bell usually used; and sitting

40. An extra effort must be made to auscultate S3; the

used for all the areas.

bell of the stethoscope should be used. The ideal po sition to hear S3 would be left side1ying; the bell would be placed over the cardiac apex. Causes of a

Heart Sounds

pathological S3 may include ventricular failure,

The first heart sound (Sl) signifies the closing of the

tachycardia, or mitral regurgitation. "Ken-TUCK'-y"

atrioventricular valves. Its duration is O. 10 seconds; it

is one sound that has been used to approximate the

is heard the loudest at the cardiac apex. The two com

sound sequencing of S3 in the cardiac cycle (SJ, S2,

ponents of Sl are tricuspid and mitral. Both the di

S3).

aphragm and the bell of the stethoscope can be used

The fourth heart sound (S4) signifies the rapid ven

to hear Sl. Its loudness is enhanced by any condition

tricular filling that occurs after atrial contraction.

in which the heart is closer to the chest wall (i.e., thin

When present, it is heard before Sl. S4 may be heard

chest wall) or in which there is an increased force to

in the "normal" trained individual with left ventricu

the ventricular contraction (e.g., tachycardia resulting

lar hypertrophy. Location of S4 is similar to S3' Its

from exercise).

sound can be described as dull because of the sudden

The second heart sound (S2) represents the clos

motion of stiff ventricles in response to increased

ing of the semilunar valves and the end of ventricu

atrial contraction. Pathologies eliciting an S4 may in

lar systole. Its components are aortic and pulmonic.

clude systemic hypertension, cardiomyopathies, or

During expiration, these two components are not

coarctation of the aorta. "TENN'-ess-ee" is a sound

distinct, since the time difference in the closure of

that approximates the sound sequencing when S4 is

the valves is less than 30 milliseconds. However,

present (S4, Sb Sz).

during inspiration, a splitting of S2 is audible. This physiological split results from the increased venous return to the right heart secondary to the decreased

Murmurs

intrathoracic pressure that occurs during inspiration.

Cardiac murmurs are the vibrations resulting from

The pulmonic valve closure is delayed as the right

turbulent blood flow. These may be described based

ventricular systolic time is lengthened. A split S2 is

on position in cardiac cycle (systole, diastole), dura

heard normally in children and young adults. The

tion, and loudness. SYSlolic murmurs occur between

diaphragm of the stethoscope shou ld be used to hear

Sl and S2; diastolic murmurs occur between Sz and

the split. The pulmonic component is the softer

SJ' A continuous murmur starts in SJ and lasts

sound and is best heard at the LSB, in the second to

through S2 for a portion or all of diastole. The loud

fourth ICS. The two components may be heard best

ness of a murmur is a factor of the velocity of blood

in the aortic and pulmonic areas, respectively. When

flow and the turbulence created through a specific

the split is heard both phases of respiration. an un

opening such as a valve. Grades I to VI are described

derlying cardiac abnormality is suspected. Causes

as folJows:

may include right bundle branch block and pul

•

monary hypertension. ( S w a r tz, 1994; T i lki a n ,

I: faint-requires concentrated effort to hear

•

II: faint-audible immediately

•

III: louder than II-intermediate intensity

•

IV: loud-intermediate intensity; associated with

•

V: very loud-thrill present

sound and reflects thc early (diastolic) ventricular

•

VI: audible wilhout stethoscope

filling that occurs after the atrioventricular valves

Murmurs that are Grade III or greater are usually as

open. S3 is normal in children and young adults; how

sociated with cardiovascular pathology.

Conover, 1993).

Gallops

palpable vibration (thrill)

The third heart sound (S3) is a faint, low frequency


222

PART II


MEDIATE PERCUSSION Mediate or indirect percussion allows the therapist to assess the density of the underlying organs. Striking the chest wall produces vibrations in the underlying structures which, in turn, gives rise to sound waves or percussion tones. The quality of that tone depends on the density of the tissue or organ, that is, it becomes louder over air-filled structures. These tones are de scribed by the following terms: •

resonant: loud or high amplitude, low-pitched, longer duration, heard over air-filled organs such as the lungs

•

dull: low amplitude, medium to high-pitched, short duration, heard over solid organs such as the liver

•

flat: high-pitched, short duration, heard over muscle mass such as the thigh

•

•

%

/.

FIGURE 14-10 Mediate percussion technique. (Reprinted with permission

tympanic: high-pitched, medium duration, heard

from Swartz MH:

over hollow structures such as the stomach

and examinaliol1, ed 2, Philadelphia, 1994, WB Saunders.)

Textbook of physical diagnoses-history

hyper-resonant: very low-pitched, prolonged duration, heard over tissue with decreased density (increased air: tissue ratio); abnormal in adults; heard over lungs with emphysema. to breathe deeply and hold that breath. The lowest

Technique

level of the diaphragm on maximal inspiration co

The middle finger of the nondominant hand is placed

incides with the lowest point where a resonant tone

firmly on the chest wall in an intercostal space and par

is heard. The patient is then asked to exhale, and

allel to the ribs. The top of the middle finger of the

mediate percussion is repeated. The lowest area of

dominant hand strikes the distal phalanx of the station

resonance now moves higher, as the diaphragm as

ary hand with a quick, sharp motion. The impetus of

cends with relaxation. The distance between these

the blow comes from the wrist versus the elbow and

two points is described as the diaphragmatic excur

has been likened to that of a paddle ball player (SWaItz,

sion; normal is three to five cm (Figure 14-11). Di

1994) (Figure 14-10). As with auscultation, the thera

aphragmatic movement is decreased in patients

pist must follow the sequence of apices to bases and

with COPO.

side to side so that comparisons can be made. This technique is not usually used in infants, since percus sion is too easily transmitted by a small chest.

PALPATION PTs use palpation in all areas of practice. Touch is an integral part of physical therapy. As part of the chest

Diaphragmatic Excursion

examination, palpation is used to assess: areas of ten

Assessment of diaphragmatic movement can b e

derness and/or abnormalities; chest wall excursion;

made with mediate percussion. The patient i s asked

edema; taclile fremitus; and tracheal deviation.


14


Inspiration

223

Expiration

FIGURE 14-11 Diaphragmatic excursion. (Reprinted with permission from Swartz MH: Textbook of physical diagnoses-history and examination, ed 2, Philadelphia, 1994, WB Saunders.)

Tenderness

is a crunchy sound often associated with articular

Specific superficial or deep landmarks are identified

structures. However, when bubbles of air occur

through palpation. Determination of gross spinal

within subcutaneous tissue, a crackling sensation can

alignment can be performed by tracing the spinous

be palpated. An air leak from a chest tube site is one

processes in a cephalocaudal direction. Structures can

cause when crepitus is palpated over the chest wall.

be identified, such as the T-4 vertebra or the sternal

Crepitus can also be secondary to a pleural or friction

angle, which only augment the PTs evaluation. Areas

rub.

of tenderness can be assessed for degree of discom fort and reproducibility. Differentiation of chest wall discomfort of an organic nature, such as with angina, from that of a musculoskeletal condition may b e

Edema Palpation allows the PT to assess petipheral edema.

made through palpation. I n a patient complaining of

Dependency of body parts can cause swelling from

chest pain, angina may be ruled out if the PT can re

cardiac and noncardiac conditions. Assessment of

produce or increase the discomfort with increased

edema is performed by pressing two fingers into the

tactile pressure. However, one must also determine

particular areas for 2 to 3 seconds. If an impression is

that corroborating symptoms (e.g., diaphoresis,

left once the fingers are removed, then pitting or de

tachycardia) are not present. Angina or chest pain

pendent edema is present. The degree of edema is

secondary to myocardial ischemia usuaJly results

based on the length of time that the indentation lasts.

from exertion and may be relieved by rest. Crepitus

I + is the least; 4+ is the worst.


224

PART II


Chest Wall Excursion

of the sternal angle and meet at the midline, slightly stretching the skin.

Evaluation of thoracic expansion allows the

4. The patient is asked to inhale.

to observe a "baseline" level by which to measure

5, The hands should be relaxed to allow for

progress or decline in a patient's condition. Chest

movement beneath,

wall movement can be restricted unilaterally as a re

6. The symmetry and extent of movement are

or a surgical incision. A

sult of lobar

assessed.

decrease in chest wall motion occurs in withCOPO. The hyperinflation associated withCOPO an increase in the

diameter with a pro-

loss of

excursion. Normal

chest wall excursion is about 3.25 inches

em) in a

young adult between 20 to 30 years of age. One method is to use a

measure at the level of the

xiphoid. However, the most common method involves in all

direct hand contact. This technique is

planes and from top to bottom. Symmetry and extent of movement are both noted. Procedures for this method are described in the or upper lobe motion

I. The PT faces the patient. The area to be examined is

2. The PT's hands are

and

as needed. over the anterior

chest. The heel of the hand is about the level of the fourth rib and the fingertips reach

FIGURE 14-13 Evaluation of middle lobe and lingula motion (anterolateral

excursion), (From Cherniak RM, et al: Respiration ill health

and disease, ed 2, Philadelphia, 1972, WB Saunders.)

toward the upper

3, The thumbs Jie horizontal at about the level

\

I

i

A

FIGURE 14-12

Evaluation of upper lobe motion. (From Cherniak RM, et al:

I

'

in health and disease. ed 2,

1972, WB Saunders,)

FIGURE 14-14

J±�

Evaluation of lower lobe motion (posterior

(From Cherniak RM, et al: Respiration in health and

disease. ed 2, Philadelphia, ]972, WB Saunders.)


14

•


225

Anterolateral or middle lobe/lingula motion (Figure 14-13) I. See above. 2. The PT's hands are placed with the palms distal to the nipple line with the thumbs meeting in the midline. The fingers lie in the posterior auxiliary foi' d. 3. See steps 4 to 6 above.

•

Posterior excursion/lower lobe motion (Figure 14-14) 1. The PT stands behind the patient. 2. The area to be examined is exposed with draping used as appropriate. 3. The PTs hands are placed flat on the posterior chest wall at the level of the tenth rib. The thumbs meet at the midline; fingers reaching toward the anterior axillary fold.

FIGURE 14-15

4. See steps 4 to 6 above.

Evaluation of fremitus, method one.

Tactile Fremitus Spoken word produces vibration over the chest wall.

aspect of the suprasternal notch. This is repeated on

Voice sounds have been previously discussed under

the opposite side. An equal distance between the

auscultation. With the PTs hands placed on the chest

clavicle and the trachea should exist bilaterally. Tra

wall, vibrations from spoken words can be felt and

cheal deviation may be caused by a pneumothorax,

are described as tactile fremitus. The presence or ab

atelectasis or a tumor among other conditions.

sence of tactile fremitus provides information on the

Whether the deviation will be ipsilateral or contralat

density of the underlying lungs and thoracic cavity

eral depends on the underlying cause. A right pneu

(Swartz, 1994).

mothorax or pleural effusion will deviate the trachea away (toward the left); a left lower lobe atelectasis, however, deviates the trachea toward the affected

Technique (Figures 14-15 and 14-16)

side, that is, the left.

Two methods can be used. The first technique is one in which the therapist uses the palmar surface of one or both hands. The second method involves the use of the ulnar border of one hand. With both techniques,

CASE STUDIES Case Study One

the sequence is, again, cephalocaudal and side to

A 30-year-old man with cystic fibrosis shows symp

side. In either method, the next step is to ask that the

toms of a one-week history of increased sputum pro

patient speak a predetermined phrase. The two most

duction, loss of appetite, fatigue, and 3-lb. weight

commonly used are "99" or "one, two, three." A light

loss. 'The results of the initial chest examination are

but firm touch is recommended.

as follows: Inspection: Forward head, kyphotic posture, increased anteroposterior diameter, appears thin

Tracheal Deviation (Figure 14-17) The trachea's midline position can be examined ante riorly. The PT places an index finger in the medial

and fatigued, no dyspnea observed, effective wet cough


226

PART II


:/"1\" , i ' f! '

\

"""- "'\

::--...

'.

-II . ..:--_ , :

'

'"

1J; FIGURE 14-17 Technique for determining the position of the trachea. (With permission from Swartz MH: TextboQk of physical diagnoses-history and examination. ed 2. Philadelphia,

1994, WB Saunders.)

FIGURE 14-16 Technique for evaluating tactile fremitus, method two. (With permission from Swartz MH: Textbook of physical diagnoses-history and examination, ed 2. Philadelphia,

1994, WB Saunders.)


14


227

Mediate percussion: dull over affected area

Auscultation: Decreased breath sounds with scattered crackles throughout all lung fields,

Palpation: trachea midline, markedly decreased

especially over right middle and lower chest

CWE on right side

Palpation: Limited chest wall excursion (CWE),

Case Study Three

especially laterally Mediate percussion: Dull over right middle and

A 72-year-old woman shows symptoms of persistent

lower chest, especially laterally

fevers, left chest wall discomfort, and history of fall I week ago. CT scan shows loculated pleural effusion

Case Study Two

on the left. Left chest tube is inserted for drainage;

An ll-year-old girl is admitted to Pediatrics with a 4-

working diagnosis is empyema. Patient is nonsmoker,

day history of recurrent fevers, shortness of breath, and lethargy. CXR showed an RML pneumonia. Inspection: tachypnea; respiratory rate (RR) of 44; Ratio of inspiration to expiration (I:E ratio

==

I: I;

Inspection: RR 30; l:E ratio

==

I:2; epidural

catheter for pain control Auscultation: Absent breath sounds halfway up left lower lateral chest wall

weak, shallow cough

Mediate percussion: flat over left lower lateral

Auscultation: bronchial over right midanterior

chest wall

chest, ego ph any also present

Palpation: trachea deviated to right, decreased

TABLE 14-1 Differentiation of Common Pulmonary Conditions Palpation

Inspection

Emphysema

Auscultation

Increased anteroposterior

Decreased tactile

Increased resonance;

Decreased lung

diameter; use of accessory

fremitus

decreased excursion

sounds; decreased

of diaphragm

vocal fremitus

Often normal

Often normal

Early crackJes

Increased tactile

Dull

muscles, thin individual Chronic bronchitis

Percussion

Possible cyanosis; short, stocky individual

Pneumonia

Possible cyanosis

Late crackles;

fremitus; splinting

bronchal breath

on affected side Pulmonary embolism

Sudden onset of dyspnea;

sounds

Usually normal

Usually normal

Usually normal

Absent fremitus;

Hyperresonant

Absent breath sounds

Dullnes s


Dullness


chest pain Pneumothorax

Rapid onset

trachea may be shifted to other side;

may have decreased chest wall excursion on affected side Pleural effusion

May be no outward

Decreased fremitus;

clinical sign

trachea shifted to other side; decreased

chest wall excursion on affected side Atelectasis

Often no outward

Decreased fremitus;

clinical sign

trachea shifted to same side; decreased chest wall excursion on affected side

Adapted with permission from

Swartz, MH:

Textbook ofphysical diag/Uises-history and examirulliOI1,


ed 2.

Philadelphia,

1994, WB

Saunders.

228

PART II


eWE on left, range of motion of left shoulder joint

7. Which components of the chest physical examina a physical therapist include in the initial

limited in flexion and abduction at about 90

tion

nP< maximum

assessment of a geriatric

the elements of a chest

with a recent left

total hio renlacement aud a history of COPD?

See Table 14-1 for a differentiation of Ul<11411U:>C;' examination.

References SUMMARY

Chemiak.

As demonstrated in the case

each element of

the chest physical examination contributes to the phys ical therapist solving the

of the individual pa

tient. It is through "putting all the

together that

au effective treatment program can be developed.

R.M., & Cherniak, L. ([983).

Respirmiorl in heailh and

disease. (3rd ed.). Philadelphia: WB Saunders.

Fraser, KG., Pare lA., Pare, P.O. Frazer,

R. S .. & Genereux, G.P.:

(1988). Diagnosis of diseases ill the chest. Philadelphia: WB Saunders. George,

R.B., Light, R.W. Matthay, M.A. & Matthay, RA ( l990).

Chesf medicine (2nd ed.). Baltimore: Williams and Wilkins.

Lehrer,

(1993). Understanding lung sound.," (2nd ed.). Philadel-

phia: WB Saunders. Mikami, et

REVIEW QUESTIONS

International symposium on

sounds, Chesl

92(2):342-345, 1987.

Describe the sequence for auscultation of lung sounds. 2. State the difference between oerioheral and cen

tral cyanosis.

3. How are normal bronchial breath sounds different from abnomUlI bronchial breath sounds?

& Benedict, G.W. (1995).

Mosby's guide 10 physical examinatioll (3rd ed.). Boston: Mosby.

Swartz, M.H. (1994). Textbook of physical diagnoses-llIslOry and examination (2nd ed). PhiJadeJphia: WB Saunders.

& Conover, M.D. (1993). Understanding heart ed.). Philadelphia: WB Saunders. Wilkins, R.I., Hodgkin, J.E., & Lopez, B. (1988). Lung sounds. Sl. Tilkian, A.G.,

sounds and murmurs (3rd

Louis: Mosby.

4. Name two causes for a oathollOl?:lC 5. Name two causes for decreased breath sounds.

6. Formulate a plan for evaluation of a patient with an acute Right Lower Lobe Pneumonia.

Seidel, RM., Ball, J.W., Dains, J.E.,

Wilkins, et al: Lung sound nomencla ture survey, C hest 98(4)886-889,1990. Willerson, J.T.,

& Cohn, J.N. ([995).

New York: Churchill Livingstone.


Cardiovascular medicine.

Monitoring Systems in the Intensive Care Unit Elizabeth Dean

KEY TERMS

Acid base balance

Intraaortic balloon counter pulsation

ECG monitoring

Intracardiac pressures

Fluid and electrolyte status

Intracranial pressure monitoring

Hemodynamic status

INTRODUCTION

may differ among intensive care units, the principles

The primary goal of the intensive care unit (ICU)

are similar and relate either directly or indirectly to the

team is the achievement of stable cardiopulmonary

foremost goal of optimizing oxygen transport.

function and optimal oxygen transport. This chapter

Cardiopulmonary status is often jeopardized with

presents an introduction to monitoring systems used

the ICU patient by fluid and electrolyte disturbances

in the evaluation of cardiopulmonary status in the

and acid-base imbalance. Regulation of these systems

ICU and describes some related elements of car

and the clinical implications of imbalance are de

diopulmonary regulation that are relevant to assess

scribed first with special reference to the JCU patient.

ment and treatment in physical therapy.

The principles of monitoring systems used in assess

ICUs are becoming more specialized. In major hos

ing cardiopulmonary sufficiency are presented in

pital centers, units are often exclusively designed and

cluding the electrocardiogram (ECG) monitor, moni

staffed for the management of specific types of condi

tors related to left- and right-sided heart function

tions e.g., medical, surgical, trauma, bums, and coro

utilizing arterial and venous lines, and the intracranial

nary and neonatal care. Although monitoring priorities

pressure (ICP) monitor. The intraaortic counter pulsa 229


230

PART II


FIGURE 15-1

General view of a typical leU.

tion technique used to augment myocardial efficiency is also described.

FLUIIJ AND ELECTROLYTE BALANCE When the normal regulation of fluid intake, utilization,

Familiarity with the extensive monitoring facilities

and excretion are disrupted, fluid, electrolyte, and acid

in the lCU allays some of the apprehensions the

base imbalances result. Essentially, all medical and

(PT) may have working in a critical

surgical conditions threaten these life-dependent mech

care. On introduction to the unit, the PT is immedi

anisms to some degree. Minor imbalances may be cor

ately struck by the high technology atmosphere.

rected by modification of the patient's nutrition and

physical therapist

Quality care in this setting depends on harnessing the

fluid intake. More major imbalances can be life-threat

potential of the monitoring equipment to optimize as

ening and can necessitate prompt medical attention.

sessment, treatment selection, and effectiveness, as

Imbalances are reflected as excesses, deficits, or as an abnormal distribution of fluids within the body

well as reduce untoward risk for the patient. For further detail on the monitoring topics pre

(1978), Burki and Albert (1983), Copel and Stolarik (1991), Cromwell, Weilbell, and Pfeiffer (1980), DeGowin and De Gowin (19 81), and W e i d e ma n n, M a t t h a y , and Matthay (1984). Figure 15-1 illustrates a general view of a typical sented refer to Barrell and Abbass

(Folk-Lighty,

1984; Phipps, Long, and Woods, 1991).

Excesses result from increased intake and decreased loss of fluid and electrolytes. Deficits result from ab normal shifts of fluid and electrolytes among the in travascular and extravascular fluid compartments of the body. Excesses occur with kidney dysfunction pro moting fluid retention and with respiratory dysfunction

lCU. A closer view of the patient at bedside indicates

promoting carbon dioxide retention. Deficits are com

to the PT the parameters that are being monitored, and

monly associated with reduced intake of fluids and nu

the types of lines, catheters, and leads in place (Figure

trition. Diaphoresis and wounds can also contIibute to

15-2). A closer view with the patient's gown removed

significant fluid loss. Diarrhea and vomiting drain the

demonstrates precisely where the various lines, leads,

gastrointestinal tract of fluid stores. Hemorrhage is al

and catheters are positioned, and identifies where cau

ways responsible for fluid and electrolyte loss. Deficits

tion must be observed. Treatments are modified ac

may be secondary to fluid entrapment and localized

cording to the types and positions of the lines and

edema within the body, making this source of fluid un

leads for each individual patient (Figure 15-3).

available for regulation of homeostasis.


15

Monitoring Systems in the Intensive Care Unit

231

FIGURE 15-2 A and B, Closer bedside views of patients in an ICU. Note that with all the equipment, the patient is almost lost. C, Note two IV lines with flow monitors. Blood infusion is also being received.

Continued.

Moderate to severe fluid imbalance can be re

with fluid overload. Normally, the jugular pulse is

flected in the systemic blood pressure and jugular ve

not visible 2 em above the sternal angle when the in

nous pressure (CVP). Elevated blood pressure can be

dividual sits at a 45-degree angle. If the jugular pulse

indicative of fluid overload, but an intravascular fluid

is noted, this can be a sign of fluid overload.

deficit of 15% to 25% must develop before blood

Fluid replacement is based on a detailed assess

pressure drops. The jugular vein becomes distended

ment of the patient's needs. Whole blood is preferred


232

PART II


FIGURE 15-2-conl'd D, Bedside oxygen and suction set-up. E, Close-up piped in O2 and suction units, F, Close-up IVs and drip monitoring flow devices (IMEO). G, Note IABP, ventilator, IVs, organization of unit at the head of the bed. ECG unit overhead, suctioning and airway care equipment at the right of the patient and "Ambu" bag at bedside.


IS


FIGURE 15·3 A, Patient after open heart surgery. Note insert of Swan Ganz, CV tubing connection taped to left chest. On ventilator with oral endotracheal tube, oral airway is in place. Note the nasogastric tube, ECG leads, and dressing covers sternal split incision site. B, Patient after open heart surgery. Note ECG leads. Patient is now weaned from ventilator and endou·acheal tube; pacemaker wires are held intact at upper abdomen in syringe area. Patient has a11erial Li ne in right forearm; Swan Ganz, CVP also removed. Patient is almost ready to leave ICU; he is receiving an aerosol treatment.


233

234

PART II


to replace blood loss. Plasma, albumin, and plasma

complaints of headache, thirst, and nausea, as well as

volume expanders such as Dextran can be used to

changes in dyspnea, skin turgor, and muscle strength.

substitute for blood loss and to help reestablish blood

More objective assessment is based on fluid intake,

volume. Albumin and substances such as Dextran in

output, and body weight. Fluid balance is so critical

crease plasma volume by increasing the osmotic pres

to physical well-being and cardiopulmonary suffi

sure of the blood, hence the reabsorption of fluid

ciency that fluid input and output records are rou

from the interstitial space. Low molecular weight

tinely maintained at bedside. These records also in

Dextran has the added advantage of augmenting cap

c l u d e f l u i d v o l u m e lost in w o u n d dra inage,

illary blood flow by decreasing blood viscosity, and

gastrointestinal output, and fluids aspirated from any

is therefore particularly useful in treating shock.

body cavity (e.g., abdomen and pleural space). A patient's weight may increase by several pounds before edema is apparent. The dependent areas mani

Clinical Picture

fest the first signs of fluid excess. Patients on bed rest

Excesses and deficits of fluids and electrolytes can be

show sacral swelling; patients who can sit over the

determined on the basis of laboratory determinations

bed or in a chair for prolonged periods tend to show

of serum levels of the specific electrolytes. Elec

swelling of the feet and hands.

trolyte levels and hematocrit are decreased with fluid

Decreased skin turgor can indicate fluid deficit.

excess (hemodilution) and increased with fluid loss

Tenting of the skin over the anterior chest in response to pinching may suggest fluid depletion. Wrinkled,

(hemoconcentration). Excess fluid can be managed by controlled fluid

toneless skin is more common in younger patients.

intake, normal diuresis, and diuretic medications. Re

Weight loss may be deceptive in the patient on IV

placement of fluid and electrolyte losses can be

fluids, who can be expected to lose a pound a day.

achieved by oral intake, tube feeding, intravenous

This sign should therefore not necessarily be inter

(IV) infusion, and parenteral hyperalimentation.

preted as underhydration.

Assessment of fluid and electrolyte balance is

The cardiopulmonary assessment can reveal

based on both subjective and objective findings

changes in fluid balance. Lung sounds are valuable in

(Table 15-1). At the bedside, the PT must be alert to

identifying fluid overload. Vesicular sounds may be-

TABLE 15-1 Assessment of Fluid and Electrolyte Imbalance FLUID EXCESSfELECTROL YTE IMBALANCE

FLUID LOSS/ELECTROL YTE IMBALANCE

Head and neck

Distended neck veins, facial edema

Thirst, dlY mucous membranes

Extremities

Dependent edema "pitting," discomfort from

Muscle weakness, tingling, tetany

AREA

weight of bed covers Skin

Warm, moist, taut, cool feeling when edematous

Dry, decreased turgor

Respiration

Dyspnea, orthopnea, productive cough, moist

Changes in rate and depth of breathing

Circulation

Hypertension, jugular pulse visible at 45-degree

breath sounds sitting angle, atrial dysrhythmias Abdomen

Modified

from

Increased girth, fluid wave

Phipps WJ, Long

Be,

Woods

NF,

Pulse rate irregularities. dysrhythmia, postural hypotension, sinus tachycardia Abdominal cramps

editors: Medical-surgical nursing: concepts in clinical practice, cd

Mosby.


4, SI.

Louis.

1991,

15


235

come more bronchovesicular in quality. Crackles

and collection system is shown in Figure 15-4. The

may increase in coarseness. In the presence of fluid

removal of thick fluids such as blood and organized

retention involving the pleurae, breath sounds dimin

exudates with chest tubes is often indicated to pre

ish to the bases. Dyspnea and orthopnea may also be

vent entrapment and loculation. Chest tubes are com

symptomatic of fluid excess.

monly inserted in the sixth intercostal space in the

An early sign of congestive heart failure (CHF)

mid or posterior axillary line. Chest tubes inserted

with underlying fluid overload is an S3 gallop (Ken

into the pleural space are used to evacuate air or exu

TUCK'-y) caused by rapid ventricular filling.

date. Chest tubes can also be inserted into the medi

Vigilance by the PT is essential in all areas of practice and not only the ICU. Fluid imbalance is

astinum after open heart surgery, for example, to evacuate blood.

common in older people and in young children, thus

Any collection system is designed to seal the

it needs to be watched for on the ward, in the home,

drainage site from the atmosphere and offer minimal

and community.

resistance to the drainage of fluid and gas. This is ac complished by immersing the end of the collection tube under water (Figure 15-4). This is referred to as

CHEST TUBE DRAINAGE AND FLUID

an underwater seal system. Additional reservoirs are

COLLECTION SYSTEMS

included to decrease the resistance to fluid leaving

Chest tubes are large catheters placed in the pleural

the chest. This resistance is greater in a single reser

cavity to evacuate fluid and air, and to drain into a

voir system in which the reservoir serves both as the

graduated collection reservoir at bedside (Phipps,

collection receptacle and underwater seal. A third

Long, Woods, 1991). A typical chest tube drainage

reservoir can be added to the system that is attached

FIGURE 15·4 A, Chest tube drainage. B, Anterior view, Mediastinal drains.


236

PART II


to the suction and serves as a pressure regulator. The

TABLE 15-2

more elaborate drainage systems are used to precisely measure fluid loss in patients following thoracic and

Signs and Symptoms of Common

cardiovascular surgery.

Acid Base Disturbances

The amount of exudate collected in the reservoir is measured every several hours or more often if the pa tient is losing considerable amounts of fluid or less

RESPIRA TORY ACIDOSIS

METABOLIC ACIDOSIS

Hypercapnia

Bicarbonate deficit

Hypoventilation

Hyperventilation

than the amount predicted. This information is incor

Headache

Headache

porated into the overall fluid balance assessment. In

Visual disturbances

Mental dullness

addition, changes in the quantity and quality of exu

Confusion

Deep respirations

date should be noted by the PT before, during, and after changes in position and therapeutic interventions.

Drowsiness

Stupor

Coma

Coma

Depressed tendon reflexes

Hyperkalemia

Hyperkalemia

Cardia dysrhythmias

Ventricular fibrillation

ACID-BASE BALANCE

(secondary to

Control of acid-base balance in the body is achieved by regulation of hydrogen ion concentration in the body fluids (Guyton, 1991; Shapiro, Peruzzi, and Kozelowski-Templin, 1994). The pH of the body is

(secondary to hyperkalemia)

hyperkalemia)

RESPIRATORY ALKALOSIS

METABOLIC ALKALOSIS

Hypocapnia

Bicarbonate excess

Lightheadedness

Depressed respirations

normally maintained within a range of 7.35 to 7.45,

Numbness/tingling of digits

Mental confusion

or slightly alkaline. When pH of the blood drops

Tetany

Dizziness

Convulsions

Numhm:ss/tingling of

Hypokalemia

Muscle twitching

Cardiac dysrhythmias

Tetany

below 7.35, a state of acidosis exists; above 7.45, a state of alkalosis exists. Regulation of pH is vital be cause even slight deviations from the normal range cause marked changes in the rate of cellular chemical

digits

(secondary to hypokalemia)

Convulsions Hypokalemia

reactions. A pH below 6.8 and above 8 are incompat

Cardia dysrhythmias

ible with life.

(secondary to

Acid-base balance is controlled by several regula

hypokalemia)

tory buffer systems; primarily carbonic acid-bicarbon ate, phosphate, and protein buffer systems. These sys tems act very quickly to prevent minute-to-minute changes in pH. In compensation, pH is returned to normal primarily by altering the component not pri marily affected. If the primary cause is respiratory, the

ume, potassium excess (hyperkalemia) is associated

compensating mechanism is metabolic. If the primary

with both respiratory and metabolic acidosis, and

cause is metabolic, the compensating mechanism is

neuromuscular hyperexcitability is associated with

respiratory. The lungs compensate for metabolic prob

both respiratory and metabolic alkalosis.

lems over hours, whereas the kidneys compensate for respiratory problems over days (Chapter 9).

BLOOD GASES Analysis of the composition of arterial and mixed

Clinical Picture

venous blood provides vital information about respi

A guide to the clinical presentation of acid-base im

ratory, cardiac, and metabolic function (Ganong,

balances is shown in Table 15-2. Besides the major

1993; Snider, 1973; Thomas, Lefrak, Irwin, Fritts,

distinguishing characteristics of acid-base imbalance

and Caldwell, 1974; Marini, 1987; West, 1995) (see

described in this chapter and elsewhere in this vol-

Chapter 9). For this reason, blood gases are usually


15

analyzed daily in the ICU. In cases where the pa tient's condition is changing for better or worse over


237

HYPOXEMIA In health, age and body position are factors that re

a short period of time or a specific treatment re

duce arterial oxygen tension (Oakes, 1988). Arterial

sponse is of interest, blood gases may be analyzed

oxygen levels diminish with age as a result of reduc

several times daily. With an arterial line in place,

tions in alveolar surface area, pulmonary capillary

frequent blood gas analysis ·is feasible and not trau

blood volume and diffusing capacity. Normal PaOz

matic for the patient. Should the patient be anemic,

levels in older people should exceed 110-0.5 age. In a

however, blood loss associated with repeated arter

young adult, Paoz ranges from 90 to 100 mm Hg in

ial blood sampling can be detrimental. Thus re

the upright seated position. In supine, this range is re

quests for arterial blood gas analysis need to be par

duced to 85 to 95 mm Hg and in sleeping, to 70 to 85

ticularly stringcnt in anemic patients.

mm Hg. These values are significant in that in older

Arterial saturation (Sao2) can be readily monitored noninvasively with a noninvasive pulse oximeter.

people, smokers, and people with pathology, these po sitional effects are accentuated.

The ear lobe or a finger is initially warmed by rub

Hypoxemia refers to reduced oxygen tension in

bing before attachment of the oximeter. Within a cou

the blood. Some common signs and symptoms of var

ple of minutes, the Sao2 can be directly read from the

ious degrees of hypoxemia in adults appear in Table

monitor. Pulse oximetry is a useful adjunct for rou

15-3. Although the brain is protected by autoregula-

tine evaluation of the effectiveness of mechanical ventilation, the effect of anesthesia and treatment re sponse. Continuous estimation of Saoz is particularly useful before, during, and after mobilization and ex ercise, position changes, and other therapeutic inter

TABLE 15-3 Signs and Symptoms of Hypoxemia Paoz

SIGNS AND SYMPTOMS

tients who are anemic, jaundiced, have heavily

80-100 mm Hg

Normal

pigmented skin, or have reduced cardiac output.

60-80 mm Hg

Moderate tachycardia, possible onset of

50-60 mm Hg

Malaise

ventions. The Sao2 may appear to be reduced in pa

Mixed venous oxygen saturation (SV02) provides a useful index of oxygen supply and utilization at the tis

respirat ory distress Lightheadedness

sue level (Copel, and Stolarik, 1991). Svoz is highly

Nausea

correlated to tissue oxygen extraction, and thus is a

Vertigo

good index of the adequacy of oxygen transport. The

Impaired judgment Incoordination

Sv0:2 is particularly useful as a significant warning sign,

Restless

a guide to myocardial function, and has been used as a tool to titrate positive end-expiratory pressure supp0l1.

Increased minute ventilation

35-50 mm Hg

Cardiac dysrhylhmias

NOImal values of SVD2 are 75%. SVD2 values less than 60% or a drop of 10% for several minutes are cause for concern. Excessive Svo2 values in excess of 80% are

Marked confusion

Labored respiration 25-35 m m Hg

Cardiac an-est Decreased renal blood flow

also cause for concern. High SV02 values may occur in

Decreased urine output

patients with left to right shunts, hyperoxia, hypother

Lactic acidosis

mia, cyanide toxicity, sepsis, anesthesia, and drug-in

Poor oxygenation

duced paralysis. Despite its general clinical usefulness,

Lethargy Maximal minute ventilation

SV02 is a nonspecific indicator of the adequacy of oxy gen transport, that is, of the balance between oxygen supply and demand. Abnormal Svoz values do not indi

Loss of consciousness

<25 mm Hg

cate precisely where the problem lies; thus other hemo dynamic variables need to be considered.


Decreased minute ventilation (secondary to depression of

respiratory center)

238

PART II


tory mechanisms, an arterial oxygen tension of 60

of nonpulmonary tissues is little altered. In the lung,

mm Hg produces signs of marked depression of the

high concentrations of oxygen replace nitrogen in

central nervous system (NS) reflecting the extreme

poorly ventilated regions. This results in collapse of

sensitivity of cerebral tissue to hypoxia.

areas with reduced ventilation perfusion matching.

H y poxemia is compensated primarily by in

Lung compliance is diminished.

creased cardiac output, improved perfusion of vital

High concentrations of oxygen (inspired oxygen

organs, and polycythemia. Secondary mechanisms of

fractions greater than 50%) directly injure bronchial

compensation include improved unloading of oxygen

and parenchymal lung tissue. The toxic effect of oxy

as a result of tissue acidosis and anaerobic metabo

gen is both time and concentration dependent. Very

lism, that is, rightward shift to the oxyhemoglobin

high concentrations of oxygen can be tolerated for up

dissociation curve.

to 48 hours. High concentrations of oxygen in combi

The progressive physiologic deterioration ob

nation with positive pressure breathing can predis

served at decreasing arterial oxygen levels will occur

pose the patient to oxygen toxicity. At concentrations

at higher oxygen levels if any of the major compen

of inspired oxygen less than 50%, clinically de

sating mechanisms for hypoxemia is defective. Even

tectable oxygen toxicity is unusual regardless of the

a mild drop in Pao2 for example, is poorly tolerated

duration of oxygen therapy.

by the patient with reduced hemoglobin and impaired cardiac output. Alternatively, the signs and symptoms of hypoxemia may appear at lower arterial oxygen

HYPOCAPNIA

levels, (e.g., in patients with chronic airflow limita

Acute reductions in arterial carbon dioxide levels

tion who have adapted to reduced Pao2 levels).

(hypocapnia) results in alkalosis and diminished cere bral blood flow secondary to cerebral vasoconstric tion. The major consequences of abrupt lowering of

HYPEROXIA

Paco2 are altered peripheral and central nerve func

Mean tissue oxygen tensions rise less than 10 mm Hg

tion. Mechanical ventilation may initially cause an

when pure oxygen is administered to a healthy sub

abrupt decrease in arterial PC02 and lead to a Iife

ject under normal conditions. Therefore the function

threatening situation. In addition to blood gas anaJy-

FIGURE 15-5 BCG oscilloscope, printout for BCG. Note defibrillator paddles and BP cuff on shelf.


Systems in the Intensive Care Vnit

15

end tidal

measurement is useful in that it

239

mal information regarding

chest to provide

in rhythm and heart rate, and thereby ensure

provides an index of

close patient monitoring. The positive electrode is positioned at the fourth intercostal space at the right

HYPERCAPNIA

sternal border. The

CO2, the principal end product of metabolism, is a relative benign gas.

has a key role in ventilation

and in

in cerebral blood

pH,

tone. Acute increases in

and

electrode is

at

the first intercosta l space in the left midclavicular electrode used to

line. The space in the

electrical

at the first intercostal

interference is often

the

midclavicular line,

wherever conve

capnia) depress level of consciousness

ground electrode may be

the effect of acidosis on the nervous

nient. Other electrode placements may be required,

but slowly

for

increases in

relatively well-tolerated. A high

is

in alveolar and arterial

with

Some patients with se

vere chronic airflow obstruction have been

rPT,r.rtp(,\

to be able to lead relatively normal lives with

Problems with the monitor faulty

Ie electrical interference. An erratic often results from

oxygen to

cause of any

disease, how

because it inteli'eres with the

hypoxic drive to breathe observed in these an increase in cardiac

and in pe

vascular resistance. These effects may help to offset the effect of excess

ward

and movement. The must be explained and unto

in electrical activity of the myocardium

ruled out. It is a dangerous practice for the PT to turn

enhances sympathetic stimula

Acute

and move

ment artifact. A thickened baseline can be caused

90 mm Hg if hypoxemia is countered

ever, may be

result from

electrical

with supplemental oxygen. Acute administration of with chronic

or in pa

secured to the patient's gown.

which causes a reduction

of alveolar

in excess of

in

tients with chest burns. The electrode wires are usu

ion on the car

off the ECG alarm system during treatment. Cardiac

can be broadly

into t a c h dy s r h y th m i a s a n d b radydysrhythmias. Tachydysrhythmias are subdivided into

diovascular system, allowing better tolerance of flow

ular and subjunctional tachycardias. Bradydysrhyth

than with metabolic acidosis of a similar degree.

mias are subdivided into sinus bradycardia, and those

At extreme levels of hypercapnia, muscle

related to heart block and conduction abnormalities.

and seizures may be observed. Trends in Paco2 can

The subjunctional

be monitored

rhythmias are

end tidal CO2 measurements.

or ventricular dys Ventricular

dia and ventricular fibrillation are medical emergen

MONITORING A

ECG

The characteristic features of are illustrated in Chapter

channel ECG monitor with an oscilloscope, at bedside in the lCU

\5-5). The ECG can often be observed both at bedside as well as at a central monitoring console, where the ECGs of all patients

11. PTs

in ICU management should be thoroughly famil

strip recorder, and digital heart rate display is cally located above the

and treatment.

immediate

cies

monitored can

be observed

iar with ECG interpretation and the implications of the various dysrhythmias for

management.

For further elaboration of ECG application and inter pretation refer to Andreoli, Fowkes, lace

and Wal

( 1991), Dubin (1989), and Fisher (1981).

The ECG monitor allows for continuous surveil lance of the

of

Low and

heart rates are determined below and above which the alarm will be

For routine moni

in the coronary care unit, a modified chest lead is often used. Three electrodes are positioned on the

Clinical Picture The clinical tivity of the heart

associated with dysrhythmic ac on the nature of the dys

rhythmia, the age and condition of the patient, and


240

PART II


TABLE 15·4 Clinical Picture of Common Dysrhythmias

DYSRHYTHMIA

IN HEALTHY INDIVIDUALS WITH NO UNDERLYING CARDIOVASCULAR DISEASE

IN INDIVIDUALS WITH UNDERLYING CARDIOVASCULAR DISEASE

No symptoms

May precipitate

I. Tachycardias A. Supraventricular tachycardia

Abrupt onset palpitations, light-headness nausea, fatigue

congestive heart failure, acute coronary insufficiency, myocardial infarction, pulmonary edema

1. Sinus tachycardia

Awareness of the heart on exertion or with anxiety

Secondary to some precipitating factor, e.g., fever, electrolyte imbalance, anemia, blood and fluid loss, infection, persistent hypoxemia in COPD, acute MI, congestive heart failure, thyrotoxicosis

2. Paroxysmal atrial tachycardia (PAT)

Prevalent, sudden onset, precipitated by coffee, smoking, and exhaustion

Common supraventricular tachycardia Spontaneous onset of regular palpitations that can last for several hours May be obscured by myocardial insufficiency and CHF in older patients Increased anxiety and report of fatigue

3. Atrial flutter

Rapid regular-irregular rate

Rare May be difficult to distinguish from PAT

Suggests block at AV node

May be precipitated by alcohol, smoking,

Atrial flutter waves in jugular venous

physical and emotional strain

pulse

4. Atrial fibrillation

Rare, occasionally with alcohol excess

5. Paroxysmal atrial

Rare

Common arrhythmia seen with

Rare

Usually related to MI, pulmonary

in the young

of cardiac disorders digitalis toxicity

tachycardia with block B. Subjunctional

Usually secondary to a variety

embolus, severe CHF Often unconscious, cyanotic, ineffective pulse, blood pressure and respiration

I. Ventricular tachycardia 2. Ventricular fibrillation

Rare

Predisposed to ventricular fibrillation

Rare

Ineffective cardiac Ol tpUt, unconscious, dusky, cardiac arrest threatens

II.

Bradycardias A. Sinus bradycardia

Physiologic in very fit young adults

In older patients may suggest sinus node and conduction system pathology; can produce syncope or congc:-;tive heart failure

B. Heart block

Hypotension, dizziness, Iight

Rare

headedness, syncope In chronic block with sustained bradycardia, congestive heart failure may be more frequent


15


241

TABLE 15-4 Clinical Picture of Common Dysrhythmias

DYSRHYTHMIA

IN HEAL THY INDIVIDUALS WITH NO UNDERLYING CARDIOVASCULAR

IN INDIVIDUALS WITH UNDERLYING CARDIOVASCULAR

DISEASE

DISEASE

Most common dysrhythmia iatrogenically produced with digitalis excess Associated with numerous cardiac conditions; commonly in age related degenerative disease in conducting system, inferior and occasionally anterior Mis

specifically the absence or presence of underlying

be measured directly from this line. A digital moni

heart disease. Distinguishing clinical features of com

tor displays systolic and diastolic blood pressures

mon atrial and ventricular dysrhythmias are outlined

above the patient at bedside. High and low blood

in Table IS-4.

pressure levels are set, above and below which the

The subjunctional or ventlicular dysrhythmias are

alarm will sound. Blood gas analysis can be per

typically associated with an extremely ill individual.

formed routinely with an intraarterial line in place

Cyanosis and duskiness of the mucosal linings and pe

without repeated puncturing of a blood vessel (Fig

riphery may be apparent. The patient is unresponsive,

ure IS-6).

the pulse if ineffective, and spontaneous respirations are likely absent. Defibrillation is initiated to restore an effective, more normal rhythm. The high incidence of myocardial conduction ilTegularities warrants a de

Pulmonary Artery Balloon Flotation Catheter (Swan Ganz Catheter)

fibrillator being present at all times in the lCU for

The pulmonary artery balloon floatation catheter or

rapid implementation of this commOn cardioversion

Swan Ganz catheter is designed to provide an accu

procedure by the medical personnel. Ventricular dys

rate and convenient means of hemodynamic assess

rhythmias may be tolerated better if ventricular rate is

ment in the lCU (Buchbinder, and Ganz, 1976; For

low, thereby improving cardiac output. Even in this

rester, Diamond, McHugh, and Swan, 1971; Swan,

circumstance, however, these dysrhythmias still pre

1975). The catheter is usually inserted into the inter

sent an emergency.

nal jugular vein, the subclavian vein, or a large pe

The ECG of a patient with a pacemaker will re

ripheral arm vein and directed by the flow of blood

flect either an imposed fixed or intermittent rhythm

into the right ventricle and pulmonary artery (see

and rate depending on whether a fixed rate or demand

Figure IS-3A (arrow), p. 233). The catheter is se

pacemaker has been inserted.

curely taped to the patient's anTI, which is splinted with an arm board to prevent dislodging. The proce dure is generally associated with little risk and dis

Intra-Arterial Lines

comfort. Some of the complications that have been

An arterial line is established by direct arterial punc

associated with pulmonary artery catheterization,

ture, usually of the radial artery. Blood pressure can

however, include infection, venous thrombosis, my


242

PART II


atrial pressure (LAP) and the pressure in the left ventricle (LVP). More elaborate catheters have pac ing wires, thermistors for cardiac output determina tion, and sensors for arterial saturation. Figure 15-7 shows the normal cardiac pressures in each heart chamber. Abnormal cardiopulmonary function may vary these readings. The PAP increases as a result of elevated pul monary blood flow, increased pulmonary arteriolar resistance secondary to primary pulmonary hyperten sion or mitral stenosis, and left ventricular failure. Measurement of PAP and PAWP in particular allows for more prudent management of heart failure and cardiogenic shock. The PAP, PAWP, and end diastolic LVP are di rectly related. Impaired left ventricular contractility that compromises normal emptying, (e.g., left ven tricular failure, mitral stenosis, or mitral insuffi ciency), result in an elevated end diastolic LVP, which in turn elevates PAWP and PAP. An end dias tolic PAP or PAWP greater than 12 0101 Hg is consid ered abnormal. The PAP and PAWP are low during hypotension secondary to hypovolemia. Infusion of normal saline,

FIGURE 15-6

whole blood, or low molecular weight Dextran ele

Intraarterial blood gas line.

vates the blood volume and blood pressure. Restora tion of blood volume returns end diastolic PAP and PAWP to normal. Elevation of the end diastolic PAP secondary to

ocardial irritation, air embolism, and pulmonary is

heart failure with pulmonary edema can typically

chemia or infarct to segmental lung tissue (Puri,

be reduced with appropriate medication. The effec

Carlson, Bander, and Weil, 1980).

tiveness of a drug and its prescription parameters

Complex catheters are available for monitoring a variety of parameters. In a two-lumen catheter, the

can be assessed by the observed changes in the end diastolic PAP.

first lumen is used to measure pulmonary artery

Deterioration of cardiovascular status and wors

pressure (PAP) and obtain mixed venous blood sam

ening of the clinical signs and symptoms of heart

ples. The second lumen terminates in a balloon with

failure elevate end diastolic PAP and PAWP, de

a volume of less than 1 011, which is inflated and de

crease cardiac output, decrease arterial and right

flated to obtain pulmonary artery occlusion or

atrial oxygen tension, a!ld increase the oxygen dif

wedge pressure (PAOP or PA WP). The average

ference between arterial and venous blood. As the

Hg, and

heart pump continues to fail, arterial oxygen ten

normally reflects right ventricular pressure (RVP).

sion decreases suggesting abnormal lung function

Hg and

and probably elevated LAP. Pulmonary dysfunction

range of the systolic PAP is 20 to 30

mOl

The diastolic PAP ranges from 7 to 12

mOl

reflects left ventricular pressure in the absence of

at this stage includes diffusion abnormalities, redis

pulmonary disease. The average range of PA WP is

tribution of pulmonary blood flow into the less

8 to 120101 Hg and gives an estimation of mean left

well-ventilated upper lobes, and right to left shunt


15


243

Pulmonary Artery

Aorta

Left Ventricle

Right Ventricle

FIGURE 15·7 Normal cardiac pressures in each heart chamber.

ing. All patients with acute infarction or shock have

MEASUREMENT OF CENTRAL VENOUS PRESSURE

reduced arterial oxygen tension. Pulmonary conges

Central venous pressure (CVP) is monitored by means

tion must be cleared before the patient responds to

of a venous line or catheter inserted into the subclavian,

15-3A, 233). The catheter is advanced to the right atrium by

basilic, jugular or femoral vein (see Figure

oxygen administration. Despite the enormous benefits of direct invasive

p.

hemodynamic monitoring to patient assessment and

way of the inferior or superior vena cava depending on

management, the benefits of basic hemodynamic as

the site of insertion. Minimal risk of phlebitis or infec

sessment are a fundamental part of the cardiopul

tion is associated with this procedure.

monary assessment regardless of whether the patient

Central venous pressure is the blood pressure mea

has an invasive line in or not (Kirby, Taylor, and

sured in the vena cavae or right atrium. Normal CVP

0 to 5 cm H20 and 5 to 10 cm H20

Civetta, 1990). Basic hemodynamic monitoring in

is approximately

cludes heart rate, ECG, blood pressure, and periph

if measured at the sternal notch and midaxillary line, respectively. Essentially the CVP provides informa

eral tissue pelfusion.

tion about the adequacy of right-sided heart function, including effective circulating blood volume, effec

INTRAVENOUS LINES

tiveness of the heart as a pump, vascular tone, and

IV lines are routinely established in the supelficial

venous return. Measurement of CVP is particularly

veins of patients, such as in the hand, usually before

useful in assessing fluid volume and fluid replace

admission to the ICU. These lines provide an imme

ment. If the patient has chronic airflow limitation,

diate route for fluids, electrolytes, nutrition, and med

ventricular ischemia, or infarction, the CVP will re

ications. The specific lines used depend on the pa

flect changes in pathology rather than fluid volume.

tient's individual needs determined by the history, laboratory tests, and physical examination.

Specifically, CVP provides an index of RAP. The relationship between RAP and end diastolic LVP is


244

PART II


unreliable; therefore end diastolic PAP and PA WP

into the femoral artery. To maintain proper placement

are used as the principal indicators of cardiopul

and good circulation, the leg must be extended. The

monary sufficiency in patients in failure and shock.

presence of an intraaortic balloon must be taken into consideration whenever the patient is being treated and positioned. Inflation and deflation of the balloon

INTRAAORTIC BALLOON COUNTER PULSATION (IABP)

with helium is correlated with the ECG. The intraaor tic balloon is deflated during venlricular systole and

Intraaortic balloon counter pulsation (Figure 15-8)

assists the emptying of the aorta. Stroke volume is

provides mechanical circulatory assistance with the

potentiated, afterload is reduced (hence, ventricular

use of an intraaortic balloon. The balloon is inserted

pressure), and myocardial oxygen delivery enhanced.

FIGURE 15-8 A, Patient near the window is receiving intraaortic balloon pump (lABP) support. B, Close-up of an IABP unit.


15


245

The balloon is inflated during diastole, thereby

neurons; progressive muscle weakness results. A con

restoring arterial pressure and coronary perfusion.

tralateral weakened hand grasp, for example, may

Counterpulsation improves cardiac output, reduces

progress to hemiparesis or hemiplegia. The Babinski

evidence of myocardial ischemia, and reduces ST

sign, hyperreflexia, and rigidity are additional motor

segment elevation. lntraaortic balloon counterpulsa

signs that provide evidence of decreasing motor func

tion is commonly used after open heart surgery, for

tion as a result of upper motor neuron involvement.

CHF, medically refractive myocardial ischemia, ven

Herniation can produce incoordinate respirations

tricular septal defects, and left main coronary stenosis

that are correlated with the level of brainstern com

in patients who have shock. The intraaortic balloon

pression. Cerebrate rigidity results from tentorial

pump provides protection for the myocardium in

herniation of the upper brainstem. This results in

many instances until surgery can be pelformed. Limb

blocking of the motor inhibitory fibers and the famil

ischemia, the most common complication, occurs in

iar extended body posture. Seizures may be present.

10% to 15% of patients.

These neuromuscular changes may further com

Left ventricular assist devices are used postopera tively in patients following open heart surgery who

pound existing cardiopulmonary complications in the ICU patient.

have developed cardiogenic shock and are unrespon

Clinically, increased rcp is best detected by altered

sive to conventional management. These devices take

consciousness, blood pressure, pulse, pupillary re

over the pumping action of the left ventricle and de

sponses, movement, temperature, and respiration

crease myocardial workload and oxygen consump

(Luce, 1985). The rcp monitor provides direct mea

tion. These types of assistive devices may have con

surement of ICP. A hollow screw is positioned through

siderable potential in the management of refractory

the skull into the subarachnoid space. The screw is at tached to a Luer-Lok, which is connected to a trans

heart failure.

ducer and oscilloscope for continuous monitoring. The prevention of further increase in rcp and a

MEASUREMENT OF INTRACRANIAL PRESSURE

corresponding reduction in cerebral perfusion pressure

rncreased intracranial pressure (ICP) resu Its from

is a treatment priority. High ICP and low cerebral per

many neurological insults including head injury, hy

fusion pressure are highly con-elated with brain injury.

poxic brain damage, or cerebral tumor, and may re

Measures to reduce venous volume are maintained

quire surgery. rn the adult, the cranial vault is rigid

until ICP has stabilized within normal range. Prudent

and noncompliant. rncreases in the volume of the cra

body positioning is used to enhance venous drainage

nial contents result in an elevated ICP and decreased

by elevating the bed 15 to 30 degrees and maintaining

cerebral perfusion pressure.

the head above heart level. Neck flexion is avoided.

Changes in consciousness are the earliest and most

Fluid intake and output are carefully monitored; the

sensitive indicators of increased rcp (Borozny, 1987;

patient may need to be fluid restricted. The Valsalva

Luce, 1985). Altered consciousness reflects herniation

maneuver is avoided, since intrathoracic pressure and

of the brainstem and compression of the midbrain.

rcp may increase correspondingly.

Compression of the oculomotor nerve and the pupillo

Normal range of ICP is 0 to \0 mm Hg for adults,

constrictor fibers results in abnormal pupillary reac

and 0 to 5 mm Hg for patients under 6 years of age.

tions associated with brain damage.

The ICP may reach 50 mm Hg in the normal brain;

The effect of rcp on blood pressure and pulse is

typically, however, this pressure returns to baseline

variable. Blood pressure may be elevated secondary

levels instantaneously. In patients with high levels of

to elevated rcp and hypoxia of the vasomotor cen

rcp and low cerebral compliance, extra care must be

ter. A reflex decrease in pulse occurs as blood pres

exercised during routine management and therapy. An ICP elicited by turning or suctioning up to 30 mm

sure rises. Compression of upper motor neuron pathways in

Hg may be acceptable provided the pressure drops

terrupts the transmission of impulses to lower motor

immediately following removal of the pressure


246

PART IJ


potentiating stimulus. Patients may be mechanically

bency. The selection of treatment and the assessment

hyperventilated to keep arterial PC02 at low levels,

of treatment response must be based upon quantita

since hypercapnia dilates c e rebral v e s sels and

tive evaluation of the parameters affecting oxygen

hypocapnia constricts them.

transport and cardiopulmonary function. Meticulous

To establish whether a patient will tolerate a treat

monitoring contributes substantially to more rational

ment that requires movement or body positioning, an

management of the lCU patient (i.e., the optimization

indication of cerebral compliance is needed. This can

of physical therapy efficacy, in addition to minimiz

be obtained by observing changes in ICP during rou

ing deleterious treatment outcomes).

tine nursing procedures or by titrating small degrees of movement or position change and observe the rate at which the ICP returns to baseline following the

REVIEW QUESTIONS

challenge. Rapid return to baseline minimizes the risk

1. Explain the determinants of fluid and electrolyte

of reduced cerebral perfusion pressure secondary to

balance, and factors that contribute to fluid ex

the increased lCP. A slow return to baseline or sus

cesses and deficits.

tained elevation of rcp is consistent with poor cere

2. Describe the basis of acid and base balance.

bral compliance and indicates treatment should be

3. Describe the physiological effects of hypoxia and hypercapnia.

modified or possibly not performed at all depending

4. Explain the physiologic basis of ECG monitoring

on the absolute level of the lCP.

and common supraventricular and ventricular dysrhythmias.

ELECTROENCEPHALOGRAM MONITOR

5. Explain (a) the physiologic basis of the pul

An electroencephalogram, or EEG, provides useful

monary artery balloon floatation catheter, and (b)

information about gross cerebral functioning and

what is represented by altered CYP, RAP (sys

changes in level of consciousness. A single-channel

tolic and diastolic), PAP (systolic and diastolic),

EEG monitor can be readily used in the lCU to reveal

and the PAOP.

evidence of posttraumatic epilepsy when the clinical

6. Describe the basis of intra aortic balloon counter pulsation.

signs may be inhibited by muscle relaxants. An EEG assessment may also be of some benefit to the PT in

7. Describe intracranial pressure monitoring, its physiological basis and clinical implications.

assessing the effects of arousal, treatment and senso rimotor stimulation on cerebral function.

References SUMMARY

V. K.. Zipes. D. P .. & Wallace.

Andreoli. K. G., Fowkes.

Monitoring cardiopulmonary function and oxygen transport is an essential component of the manage ment of the patient in the lCU. Regulation of home ostasis is disrupted in disease or following medical and surgical interventions. PTs working in the unit require a thorough understanding of homeostatic reg ulation and monitoring of fluid and electrolyte bal

Barrdl. S.

E. &

Abbas. H. M. (1978). Monitoring during physio

therapy after open heart surgery. Physiotherapy. 64(9). 272-273. Borozny. M. L. (1987). Intracranial hypertensi()n: Implications for the physiotherapist. Physiotherapy Cwwdu. 39. 360-366. Buchbinder, N. .

&

Ganz, W. (1976). Hemodynamic monitoring:

Invasive techniques. Anesthesi% Burkj. N. K..

&

45(2). \46-\55.

Noninvasive monitoring of

tory pathophysiology. Chest. 83(4).666-670. Copel L.

c.. &

Stolarik. A. (1991). Continuous Sv02 monitoring.

in patients requiring intensive care, using conserva

A research review.

tive, noninvasive approaches, in addition to averting

202-209.

the musculoskeletal, neuromuscular, and multisystem

gy.

R. K.'(1983).

Albert.

arterial blood gases. A report of the ACCP section on respira

ance, acid base balance, and blood gases. Physical therapy has an essential role in res tOling homeostasis

A. G. (Eds.)

(1991). Comprehensive cardilu: care (7th ed.). Sl. Louis: Mosby.

Cromwell, L.. Wei bell.

complications associated with immobility and recum


Dimensions of Cri/ica/ F. l, &

Pfeiffer.

E

C a re

Nursin!i. lO,

A. (1980). Biomedical

ins/rumentarion and measuremen/s (2nd ed.). Englewood

Cliffs: Prentice-Hall.

15

DeGowin, E, L, & DeGowin, R L (1981), Bedside diagnostic ex

247

Monitoring Systems ill the Intensive Care Unit

Oakes, D, F. (1988), Clincfal practitioners pocket

10

respira

lory care. Old Town: Health Educator Publications.

aminatioll (4th cd.). New York: Macmillan.

Dubin, D, (1989). Rapid illterprelatiotl of EKGs, (4th ed,), Tampa, Fl.: Cover.

Phipps, W. J., Long, B.

& Woods, N. F. (Eds,). (1991). Med

iced-surgical nursing: concepts and clinical practice (4th ed.).

Fisher, J, D, (1981). Role of electrophysiologic testing in the

St Louis: Mosby,

nosis and treatment of patients with known and suspected

Pmi, V. K, Carlson, R. W., Bander, J. J, & Wei!, M. H. (1980).

bradycardias and tachycardias. Progress in Cardiovascular

Complications of vascular catheterization in the critically ill. A prospective study. Critical Care Medicine. 8(9),495-499.

Diseases, 24(1),25-90.

Folk-Lighty, M. (1984). Solving the puzzles of patients' lluid im balances. Nursing, 14(2),34--41,

Shapiro, B. A., Peruzzi, W. T., & Kozelowski-Templin, R. (1994). Clinical application of blood gases (5th

Forrester, J. S., Diamond, G., McHugh, 1'. 1. (1971), Filling pres

SL Louis: Mosby.

Snider, G. L. (1973). Interpretation of the arterial oxygen and car

sures in the right and left sides of the heart in acute myocardial

bon dioxide partial pressures. A simplified approach for bed

infarction: A reappraisal of central-venous-pre5sure monitor

side use. Chest, 63(5), 801-806.

ing. New Englimd Journ al of Medicine, 285(4), 190--[93,

Swan,H. J, (1975), Second annual SCCM lecture. The role of he modynamic monitoring in the management of the critically ill.

Ganong, W. F. (1993), Review o.fmedical physiology, (16th Los Altos: Lange :Vledical Publications

Critical Care Medicine, 3(3),83-89,

Guyton, A. C. (l991). Textbook of medical physiology (8th ed.). Philadelphia: WB Saunders. paniol! Critical Care Immediate C once rns. Philadelphia: JB

in health and disease. Role of 2,3-diphosphoglycerate. Arneri Journal of Medicine, 57(3), 331-348.

West, J. B, (1995), Respiralory physiology-the essentials (5th

Lippincott. Luce, 1. M. (1985), Neurologic monitoring. Respiratory Care, 30,

ed.). Baltimore: Williams and Wilkins. Wiedemann, H, P , Mauhay,M. A" & Matlhay, R. A, (1984). Car

471-479. the house officer

.

Caldwell, P. R ([974). The oxyhemoglobin dissociation curve

Kirby, K R., Taylor, K W., & Civetta, J. M, (1990), Pocket Com

Marioi, J. J. (1987). Respiratory medicine and intensive

Thomas, H. M., 3rd, Lefrak, S. S., irwin, R. S., Fritts, H. W., Jr , &

for

diovascular-pulmonary monitoring in the intensive care unit (Part I) Chesr, 85(4), 537-549.


(2nd ed.). Baltimore: W

PART

III

Cardiopulmonary Physical Therapy Interventions


Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology Elizabeth Dean

KEY TERMS

Clinical decision making

Pathophysiological factors

Extrinsic factors

Problem definition

Intrinsic factors

Problem list

Oxygen transport deficits

Restricted mobility and recumbency factors

Oxygen transport threats

Treatment prescription

INTRODUCTION

I. What is the problem?

The purpose of this chapter is to provide a basis for clinical decision making and treatment prescription in

2. What is the treatment and why? 3. What is the course of treatment?

cardiopulmonary physical therapy (CPPT) for patients

This chapter focuses on the elements involved in

ranging from the medically unstable critically ill pa

addressing these questions when managing a patient

tient to the medically stable patient with cardiopul

with impaired to threatened oxygen transport. The

monary dysfunction living in the community. Clinical

basic principles for relating CPPT treatment to the pa

decision making and treatment prescription is based on

tient's underlying pathophysiologic problems (i.e., the

the answers to three primary clinical questions related

pathophysiological mechanisms responsible for im

to oxygen transport. With respect to a given patient,

pairment of oxygen transport and cardiopulmonary

the following must be considered:

function) are described. A physiologically based treat 251


252

PART III


Fundamental Knowledge and Expertise

Steps in Critical Problem-Solving De.flCits

to Critically Problem-Solve Deficits in

in Oxygen Transport

Oxygen Transport

I. De t ermine what factors are specifically con tributing to impaired oxygen transport and which

Norm al c a rd i o p u l m o n ary a n d c a r d i o v a s cul ar

steps in the pathway are affected

anatomy. as well as physiology and how these are affected by normal conditions such as aging and

2. Determine those factors that threaten oxygen

lifestyle habits (e . g .. smoking. stress. and the

transport and the steps in the pathway that are

physical environment)

involved

Physio lo gic adaptation to hypoxia and cardiopul

3. Determine the relative magnitude of the effect of

monary impairment

each factor either impairing or threatening oxygen transport, and prioritize the importance of each

Cardiopulmonary and cardiovascular pathophysiology and disease processes, and how these affect nonnal

4. Distinguish those factors that arc amenable and

cardiopulmonary and cardiovascular function

those that are not amenable to CPPT in that the latter will modify treatment and affect the moni

Multisystem and integrative pathophysiology that

toring that is needed

can have a secondary effect on cardiopulmonary function and oxygen transport

5. Giv en the answers to I through 4. select, priori tize, and apply specific treatments prescrip

Effects of medical. surgical, and nursing procedures

tively to address each factor that nmtributes to

on oxygen transport and gas exchange

cardiopulmonary dysfunction and is amenable

Investigative laboratory procedures and tests and

toCPPT

their effects on cardiopulmonary function Pharmacological effects on cardiopUlmonary function

ment hierarchy is presented, with the premise that

detailed understanding of the relevant anatomy and

physiologic function, including oxygen transport, is

physiology, multisystem and integrative pathophysiol

optimal when humans are upright and moving. Apply

ogy, the impact of medical, surgical, and nursing pro

ing a systematic physiologic approach to the analysis

cedures, the effect of various laboratory tests and pro

of the patient's problems, with respect to deficits in the

cedures, and the impact of pharmacological agents on

oxygen transport pathway, leads directly to the most

cardiopulmonary function (see box above, at left).

efficacious treatments. Such an approach provides a

For a given patient, the cardiopulmonary

PT pre

basis for modifying or discontinuing treatment based

scribes treatment by extracting the relevant information

on the use of appropriate treatment outcome measures.

from the history, laboratory tests and investigative pro cedures, and the assessment (see box above. at right). Problems are prioritized based on the relative magni

WHAT IS THE PROBLEM?

tude of each one's effect on impairment of oxygen

Oxygen transport is determined by a multitude of fac

transport. Once the mechanisms for the cardiopul

tors which affects different steps in the oxygen trans

monary and cardiovascular dysfunction have been iden

port pathway (see Figure I-I, p.

4) (Chapter I). For

tified, specific treatments are selected and prioritized.

treatment to be directed specifically to the underlying problems, the physical therapist

(PT) needs to consider

several levels of analysis of the deficits contributing to

The Problem list Impaired oxygen transport

impaired or threatened oxygen transport. To be profi

PT must have a thorough

Two levels of problems need to be identified. namely,

knowledge of the multiple factors that contribute to ab

functional and physiologic deficits. The functional

normal gas exchange. This knowledge base includes a

deficits are those that affect the patient's ability to

cient in such analysis, the


16

Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology

253

ExampLes of Deficits in and Threats to Steps in the Oxygen Transport Pathway Central Control of Breathing

Altered central nervous system (CNS) afferent input and control of breathing Impaired efferent pathways

Pharmacologic depression Substance abuse depression Airways

Aspiration related to lack of gastrointestinal (GI) motility Aspiration secondary to esophageal retlux Obstruction secondary to airway edema, bronchospasm, or mucus Inhaled foreign bodies Lungs

Altered breathing pattern secondary to decreased lung compliunce Ineffective breathing pattern related to decreased diaphragmatic function and increased lung volumes, respiratory muscle weakness, respiratory muscle fatigue, CNS dysfunction, guarding, reflex, fatigue, and re spirato ry inflam matory process Ineffective airway clearance related to restricted mobility, immobility, sedation, and pulmonary dysfunction sec

ondary to long smoking history, impaired mucociliary transport, absent cilia. or dyskinesia of cilia, retained secre tions, ineffective cough and mucociliary mechanisms, infection, inability to cough efficiently, artificial airway/in tubation and cndotracheal tube, drug-induced paralysis, and sedation Large airway ob:,truction secondary to compliant oropharyngeal structures Chest wall regidity and decreased compliance Loss of normal chest wall excursion movements (pump and bucket handle motions) and capacity to move appropri ately in all three planes of motion Chest wall and spinal deformity Impaired lung t1uid balance and acute lung injury

Blood

Bleeding abnormalities, altered body temperature (hypothermia, hyperthermia). fever, inflammation, hypermetabo lism secondary to mediator systems Altered body temperature related to integumentary disruption Low hematocrit secondary to GI bleed (more prone to hypoxia) Anemia Thrombocytopenia Dissemin ... ted intravascular coagulation Abnorm... 1 clotting faclOrs (i,e" halance between clotting and not c1olling, sludging of blood) Thromboelllboli Bleeding disorders with liver disease; ...bnormal clotting factors

Continued,


254

PART III


Examples of Deficits in and Threats to Steps ill the Oxygen Transport Pathway-cont'd Gas Exchange Alveolar collapse, atelectasis, intrapulmonary shunting or pulmonary edema, shallow breathing and tenacious mucus, body position, consolidation and alveolar collapse, ventilation/perfusion mismatch, airway constriction, t1uid vol ume excess, pleural effusions. breathing at low lung volumes. abdominal distension and guarding. ineffective air way clearance, pulmonary microvascular thrombi and altered capillary permeability secondary to circulating medi ators. closure of small airways secondary to dynamic airway compression. decreased functional residual capacity, and intrapulmonary shunting, increased lung surface tension Diffusion defects Respiratory Muscles Upper abdominal surgery. weakness, fatigue. neuromuscular discase. ileus related to gastric distension, mechanical dysfunction Myocardial Perfusion Coronary artery occlusion Tachycardia Potential for cardiac dysrhythmia related to reperfusion Cardiac dysrhythmia related to myocardial hypoxia Compression by edema or space-occupying lesions Heart Decreased venous return and cardiac output, secondary to volume deficit, ascites, myocardial ischemia, hemorrhage, and coagulopathies Conduction defects Mechanical defects Defects in electromechanical coupling Abnormal distension characteristics Abnomlal afterload Blood Pressure Volume deficit/bleeding Alteration in peripheral tissue perfusion related to acute myocardial infarction. myocardial depression, maldistribu tion of blood volume, and altered cellular metabolism Volume excess Tissue Perfusion Impaired cardiac output Impaired secondary to disseminated microvascular thrombi Atherosclerosis and thromboembolic events, decreased circulating blood volume. decreased circulating blood vol ume, decreased vascular integrity. and int1ammatory process Decreased cardiac output related to reduced venous return. impaired right ventricular function, dysrhythmias, in creased afterload, and bradycardia Low oxygen content in the blood Thromhoembolism. vasoconstriction secondary to toxins. sepsis, etc., blood flow alterations and hypermetabolism secondary to mediator systems


16


255

Examples of Deficits in and Threats to Steps in the Oxygen Transport Pathway-cont'd Fluid Volume Excess Related to excessive intravenous administration Related to impaired excretion Apparent hypervolemia secondary to restricted mobility and recumbency (e.g., resulting from hemodynamic instability) Renal failure Water intoxication Therapeutic volume expansion. acute myocardial infarction (MI) and acute renal failure. related to renal retention of sodium and water and increased levels of aldosterone, renin, angiotensin II, and catecholamines Fluid Volume Deficit Fluid volume deficit related to volume losses during surgery and inadequate oral intake, blood loss, internal injuries (e.g.. hematoma and third spacing phenomenon: hormonal imbalance; increased intestinal motility; vomiting; diar rhea: tluid sequestration in tissues; nasogastric (NG) suction and diarrhea: hypovolemia; sepsis and shock; surface capillary leak and fluid loss as in burns and excoriated wounds; tluid shifts) Tissue Oxygenation MultisysteJll organ failure with allered peripheral tissue perfusion and gas exchange at the cellular level

Indirect Factors That Contribute to Oxygen Transport Deficits Infection Pulmonary and nonpulmonaty infection increase the demands on the oxygen transport system Cognition Impaired neurological status and ccntral cardiopulmonary control Alleration in mental status secondary to inadequate cerebral perfusion with hypotension and cardiogenic shock Sleep pattern disturbance; altered blood gases and fatigue Anxiety and agitation relatcd to powerlessness and lack of knowledge, breathlessness, pharmacological paralysis, im paired verbal community secondary to intubation, paralysis etc. Psychosocial Factors Anxiety related to the condition, shllltncss of breath. hospitalization. et\:. So\:ial isolation second.uy to impaired wl11l11unication Fear and hopelessness Pain response Nutrition Altered nutritional needs secondlllY to greater need than resting state (i.e.. increased caloric need and nutrients asso ciated with illness, inability to ingest food, inability to absorb food) Restricted ingestion orders of food and water High caloric needs sen)l1dary to infectious process and protein catabolism


256

PART III


perform activities of daily living (ADLs) (e.g., re

Factors That Call Impair Oxygell Trallsport

duced activity or exercise tolerance as a result of re duced peripheral oxygenation, reduced mobility re

I. Cardiopulmonary pathophysiology

lated to deconditioning resulting from resting in bed,

primary (acute, chronic, acute on chronic)

extremity or internal injury, anticoagulant therapy,

secondary (chronic, acute on chronic)

drug-induced paralysis, impaired physical mobility re

Noncardiopulmonary pathophysiology that im

lated to muscle weakness and partial paralysis, paraly

pacts upon cardiopulmonary function

sis, depressed level of consciousness, and anemia).

2. Immobility-loss of physical exercise stress

Physiological deficits are those deficits in oxygen

Recumbency-loss of vertical gravitational stress

transport, specifically, at the individual steps in the

3. Extrinsic factors (i.e., those related to the pa

pathway, and oxygen transpolt overall. Examples of

tient's care)

deficits at each step in the pathway appear in the

4. Intrinsic factors (i.e .. those related to the patient)

boxes on pp. 253-255.

Threatened oxygen transport Although the complications of restricted mobility and static body positions are well understood, the precise prescription parameters for mobilization and body

(see box above), namely, the underlying cardiopul

positioning to avoid these complications have not

monary pathophysiology, restricted mobility (loss of

been defined in detail. With respect to cardiopul

physical exercise stress), recumbency (loss of vertical

monary complications, a one- or two- hourly turning

gravitational stress), extrinsic factors (i.e., those re

regi men is commonly accepted. For the flaccid or co

lated to the patient's care), and intrinsic factors (i.e.,

matose patient, range-of-motion (ROM) exercises

those related to the patient). These categories are ex

every several hours facilitates blood flow through de

panded and explained in detail in Chapter 17.

pendent areas and enhances alveolar ventilation as

Restricted mobility and recumbency:

special examples of extrinsic factors

well as mobilizes joints and muscles. Antiembolic stockings and pneumatic compression devices are routinely used to minimize circulatory stasis in the

Although bed rest can be considered an extrinsic

legs and the potential for thrombi formation.

factor (i.e., a therapeutic intervention that con

The PT has a major role in preventing infection of

tributes to cardiopulmonary dysfunction, the nega

all types but particularly cardiopulmonary infections.

tive sequelae of this intervention are often not fully

Both cardiopulmonary assessment and treatment in

appreciated clinically based on the widespread use

volves handling and close physical contact with pa

of rest in bed. Therefore to draw to the clinician's

tients. Thus the risk of nosocomial infection is high in

attention that the effects of this intervention need to

hospitalized patients. Some standard means of prevent

be considered in each patient, the effects of re

ing infection include meticulous hand washing before

stricted mobility and recumbency are analyzed sepa

and after every patient, and care of invasive lines and

rately (see Chapters 17 and 18).

catheters. The PT moves and repositions patients often, thus it is essential that lines, leads, and catheters are continuously monitored. The PT must consider when it is appropriate to gown, mask and glove to protect and

Treatment Goals Once the deficits and threats to oxygen transport have been determined, the goals of treatment fall into three

be protected from the patient adequately.

categories: short-term, long-term, and preventive.

Factors that contribute to or

threaten oxygen transport

Short-term treatment goals include the following. 1. To correct or reverse acute cardiopulmonary dysfunction

Those factors that can impair oxygen transport di rectly or threaten it fall into four primary categories,

2. To reduce the rate of deterioration


16


3. To avoid worsening the patient's condition.

257

Common Treatment Goals in the Management of

Long-term treatment goals include: I. To enhance the efficiency of the steps in the oxygen transport pathway overall

the Patient With Cardiopulmonary Dysfunction OVERALL GOAL: To optimize or preserve oxy

2. To enhance the efficiency of those specific

gen transport and gas exchange

steps in the oxygen transport pathway that com

Treatment directed at specific steps involved

pensate for impaired steps that may or may not

Object to enhance the efficiency of all steps in the

be reversibly affected

pathway

3. To maximize oxygen transport capacity to sus tain maximal functional activity.

Augment medical management Coordinate with nursing management (e.g., in criti

And preventive treatment goals include:

cal care)

I. To prevent cardiopulmonary dysfunction 2. To prevent multisystem organ complications and nonpulmonary infection that will lead to further restricted movement and recumbency, hence the potential for further deterioration

Goals Directed at Specific Steps in the Oxygen Transport Pathway

Maximize air entry and alveolar ventilation (mini mize airflow resistance) Maximize air distribution (optimize lung compli

3. To provide supportive palliative care.

ance and chest wall compliance) Maximize ventilation and perfusion matching

WHAT IS THE TREATMENT AND WHY?

Optimize diffusion

Clinical Decision Making

Optimize oxyhemoglobin saturation

The basis for clinical decision making in the man agement of the cardiopulmonary patient is to pair the most efficacious treatments specificall y with im paired or threatened steps in the oxygen transport

Reduce work of breathing (increased resistance, re duced or excessive compliance) Reduce work of the heart (increased preload, con traction. increased afterload)

pathway. In addition, the patient spends considerable

Maximize efficiency of heart mechanics

time between treatments, thus optimal therapeutic ef

Minimize electrocardiogram (ECG) irregularities

fect is dependent on the efficacy of "between treat ment" treatments (i.e., teaching the patient to carry

(identify factors that contribute to irregularities; anticipate problems)

out prescriptive treatment whenever possible and

Optimize blood flow distribution

eliciting the assistance of the patient's family or

Optimize oxygen extraction ratio

nursing staff). When confined to hospital, many patients spend considerable time recumbent and in restricted body

Reduce excessive or unnecessary energy expenditure Optimize carbon dioxide (C02) removal

positions, turn and move less frequently, and are up

Optimize blood volume

right and moving a smaller proportion of time. De

Optimize hydration

pending on the oxygen transport deficits, the body positions the patient assumes can have a positive, negative or neutral effect on oxygen transport. Thus, the positions the patient assumes and his or her re duced activity levels, must be monitored and any po tential ill effects anticipated and countered.

goals and specific treatments are prioritized accord

Some examples of some common treatment goals in managing the patient with cardiopulmonary dys

ing to the relative significance of the impact of each on oxygen transport.

function are shown in the box above. Specific treat

A physiologically based treatment hierarchy is

ments are identified to address these goals and for

shown in the box on p. 258 and 259, and the box on

threat to oxygen transport. Treatment

p. 260, top right. The treatment hierarchy is based on

each deficit

or


258

PART III


Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport PREMISE: Position of optimal physiological function is being upright and moving I. Mobilization and Exercise Goal: To elicit an exercise stimulus that addresses one of the three effects on the various steps in the oxygen trans

port pathway, or some combination

A. Acute effects B. Long-term effect C. Preventative effects II. Body Positioning Goal: To elicit a gravitational stimulus that simulates being upright and moving as much as possible i.e., adive. ac

tive assisted or passive

A. Hemodynamic effects related to fluid shifts B. Cardiopulmonary effects on ventilation anti its distribution, pelfusion. ventilation. and perfusion matching and gas exchange III. Breathing Control Maneuvers Goal: To augment alveolar ventilation, to facilitate mucociliary transport. and to stimulate coughing

A. Coordinated breathing with activity and exercise B. Spontaneous eucapnic hyperventilation C. Maximal tidal breaths and movement in three dimensions

D. Sustained maximal inspiration E. Pursed lip breathing to end tidal expiration

F. Incentive spirometry IV. Coughing Maneuvers Goal: To facilitate mucociliary clearance with the least effect on dynamic airway compression and adverse cardio

vascular effects A. Active and spontaneous cough with closed glottis B. Active assist (self-supported or by other) C. Modified coughing interventions with open glottis (e.g., forced expiratory technique, hulT) V. Relaxation and Energy Conservation Interventions Goal: To minimize the work of breathing. of the heart. and oxygen demand overall

A. Relaxation procedures at rest and during activity B. Energy conservation, (i.e., balance of activity to rest, performing activities in an energy) efficient manner. improved movement economy during activ:ty) C. Pain control interventions VI. ROM Exercises (Cardiopulmonary indications) Goal: To stimulate alveolar ventilation and alter its distribution

A. Active B. Assisted active C. Passive

Continued.


16


259

Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport-cont'd VII. Postural Drainage Positioning

Goal: To facilitate airway clearance using gravitational effects A. Bronchopulmonary segmental drainage positions VIII. Manual Techniques

Goal: To facilitate airway clearam;e in conj unction with specific body positioning A. Autogenic drainage B. Manual percussion C. Shaking and vibration D. Deep breathing and coughing

IX. Suctioning Goal: To fac ili tate the removal of airway secretions collected centrally A. Open suction system B. Closed suction system C. Tracheal tickle D. Instillation with saline

E. Use of manual intlation bag (bagging)

the premise that physiologic function, including oxy gen transport, is optimal when the human organism is

Treatment Plan

upright and moving. Thus the purpose of the hierar

The treatment plan consists of those interventions

chy is to exploit those treatments that are most physi

that will most expediently remediate the problems

ologic first (i.e., active mobilization and exercise in

that have been identified. These interventions are pri

the upright position). Therefore the hierarchy ranges

oritized according to the greatest effect they are pre

from the most physiologic interventions, that is, ac

dicted to have on remediating the oxygen transport

tive mobilization and exercise in the upright position,

deficit or minimizing any threat to oxygen transport,

to those interventions that are the least physiologic.

and on maximizing the benefit-to-risk ratio. Depend

The least physiological interventions, (i.e., conven

ing on the specific treatment goals and the adequacy

tional chest physical therapy techniques such as

of balance between oxygen supply and demand, coor

ROM, postural drainage and percussion) may simu

dinating physical therapy treatments with other care

late some of the physiologic effects of being upright

(e.g., nursing care and certain tests and procedures) is

and moving; however, their effects are more limited

often indicated.

and less scientifically well-substantiated, and affect fewer steps in the oxygen transport pathway. Thus they do not substitute for more physiologic interven

Treatment Prescription

tions higher up in the treatment hierarchy. All inter

Once the specific pathophysiological problems have

ventions featured in the hierarchy have some role in

been identified, they are differentiated as:

the management of cardiopulmonary dysfunction, but

that can be addressed by physical therapy (i.e., nonin

(I) those

(2) those that are

are recruited in descending order to ensure that the

vasive physical interventions) and

most physiological and efficacious interventions are

not amenable to physical therapy but need to be con

exploited first.

sidered during treatment to determine whether treat


260

PART III


ment is contraindicated or needs to be modified, and

Use of Modalities and Aids

specific outcome and treatment response measures are indicated.

Goal: To incorporate the use of those modalities and aids that enhance the ahove interventions

Problems amenable to physical therapy are priori tized, the treatment is indicated for each problem, and

Modalities

its parameters are defined. The treatment goals are

Treadmill, ergometer, rowing machine

identified, that is, to reverse pathophysiological

Weights

mechanisms contributing to impaired oxygen trans

Pulleys

port, to compensate for irreversible pathophysiologi cal deficits (improve efficiency of other steps in the

Nebulizers and aerosols

oxygen transport pathway), to decelerate deteriora

Flutter valve

tion, to avoid making patient worse palliative

BYPAP' and CPApt

care/support/comfort, and for prevention. Based on

Incentive spirometer

the goal of treatment, the parameters for the treatment prescription are defined. Treatment parameters in the

Pharmacologic Agents

management of a cardiopulmonary patient are shown

Oxygen

in the box below.

Bronchodilators Antiintlammatories

WHAT IS THE COURSE OF TREATMENT?

Mucolytics

Once a treatment has been prescribed, the prescrip

Surfactant

tion must be reviewed at each treatment and modified

Analgesics

accordingly, that is, change in the prescription para meters, as the patient's condition changes. In addi

"Bilevel positive airway pressure

tion, the parameters may be modified within a treat-

"'Continuous positive airway pressure

Parameters of the Treatment Prescription in the Management of the Cardiopulmonary Patient Define parameters of treatment based on history, laboratory investigations, tests, and assessment Treatment type Intensity (if applicable) Duration Frequency Instruct patient in "between treatment" treatment, and if applicable the nurse. a family member. or both Reassessment every treatment Modify as necessary within each treatment Progress between treatments as indicated Define treatment outcomes Determine when treatment is to be discontinued Request for additional supportive information. tests, and investigations as indicated Predict time course for optimal effects and course of treatment to determine treatment efficacy; modify as necess,u'y In conjunction with other interventions (e.g., medical, surgical, nursing, respiratory therapy (weaning» oxygen supplementation. sympathomimetic drugs, ADLs, balance with sleep and rest periods. peak of nutrition and feeds. peak energy times. peak of drug potency and effects (e.g., pain, reduced sedation. reduced neuromuscular blockade)


16


261

Assessment and Treatment Outcome Measures Used in the Management of Deficits in Oxygen Transport Pathway Central Control of 8reathing

8 Iood-cont 'd

Central drive to breathe test

Platelets


Hemoglobin

Cerebral perfusion

Coagulability

Ambient Air

Viscosity

Partial pressures of 02. Nl and CO2

Stasis

Air pollution and quality

Hydration

Humidity

Immunological status

Airways Clinical assessment including auscultation Pullllonary function tests Arterial blood gases Chest X-ray Histamine challenge exercise tests Lungs Clinical assessment including inspection. percussion. palpation and auscultation Pulmonary function tests Ventilation and perfusion scans Diffusion capacity test Arterial blood gases Chest X-my lmmunulogical status Respiratory muscle assessment Assessment of the structure and integrity of chest wall Lung water studies Blood Circulating blood volume and cardiac output

Pulmonary Circulation Pelfusion scan Pulmonary artery balloon t1oatation catheter to assess central venous pressure, pulmonary artery pres sures, wedge pressure Heart Clinical assessment including percussion. palpation. and auscultation Inspection and clinical observation tests including jugular venous distension test Heart rate, systolic and diastolic blood pressures, and rate pressure product ECG Hemodynamic studies to assess cardiac output, stroke volume, cardiac distensibility. and ejection fraction Ultrasound procedures to examine mechanical integrity Scans Coordination of electromechanical behavior of heart Coronary artery perfusion studies Stress test Hemodynamic monitoring including central venous pressure, pulmonary artery pressures and wedge pressure

Arterial oxygen content

Angiography

Venous oxygen content

Chest X-ray

Plasma volume

Peripheral Circulation

Red and white blood cell counts

Clinical assessment

Protein constituents

Segmental blood pressures of the extremities

Cun/iIlLted.


262

PART III


Assessment and Treatment Outcome Measures Used in the Management of Deficits ill Oxygen Transport Pathway-colll'd Peripheral Circulation--cont'd

Tissue-colll'd

Ultrasound studies

Vascularization of tissue

Arterial and venous lab studies and investigations

Adequacy and efficiency of aJterial ,Uld venous tissue

Adequacy and efficiency of lymphatic drainage system

Blood now

of the healt and lungs, and pelipheml circulation

Tissue fluid balance; hydrostatic pressure, oncotic

Stress test

pressure, and lymphatic pressure

Tissue

Blood work including serum lactates and SV02

Enzyme studies

Tissue oxygenation and pH

Tissue biopsies

Nutritional and hydration status

ment based on the patient's treatment response. The

sential that these measures have certain characteris

PT also bases the decision when to discontinue a

tics. For example, measurements must be objective

given treatment as well as what overall cardiopul

and their procedures standardized to maximize test va

monary physical therapy to employ, based on treat

lidity and reliability. Although PTs specialize in non

ment response and outcome.

invasive assessment procedures as well as treatments,

Measures to assess treatment response and out

noninvasive measures are prone to imprecision, and

come are selected that reflect (J) the status of oxygen

hence measurement error and unreliability. It is there

transport overall, and (2) the integrity of the step or

fore essential that assessment measurements are per

steps in the oxygen transport pathway that were iden

formed in a systematic manner according to measure

tified as being the primary problems contributing to

m e n t guid elines to maximize their quality and

cardiopulmonary or cardiovascular dysfunction in the

usefulness in guiding and directing treatment (Chapter

original assessment (see box on pp. 261-262.) (see

6). Assessment measurements always precede any

Part II of this text). Cardiopulmonary dysfunction is

treatment to ensure that treatment is appropriate, that

determined based on the history, assessment and lab

is, the baseline measurements. Measurements during

oratory investigations, such as, pulmonary function

treatment provides information about the patient's re

testing, breathing pattern, cardiac function testing,

sponses, both beneficial and detrimental. This feed

fluid balance and renal function, anerial blood gases,

back determines the parameters of treatment, and

arterial saturation, vital signs, and hemodynamic

whether the treatment should be modified in some

variables, including heart rate and ECG, blood pres

way, or possibly discontinued. The overall treatment

sure, and rate pressure product. Subjective repOits are

response is established by further monitoring and as

also clinically relevant, such as subjective ratings of

sessment at the termination of treatment, and often at

perceived exertion, breathlessness, angina, and fa

peliodic intervals posttreatment so that delayed effects

tigue. These same measures are used to detect im

can be monitored. Frequent and periodic measure

proved oxygen transport and gas exchange.

ments over time are refelTed to as serial measurements

Considering that clinical decision making is based

and provide useful trend data. The pre- and posttreat

largely on the results of tests and measures, it is es

ment responses and any noteworthy responses during


16


treatment are charted with sufficient information about the procedurcs that were used, that is, assess ment as well as treatment procedures. PTs often require the results of invasive tests such as blood work or invasive hemodynamic monitoring to establish treatment response and outcome; thus, these need to be requested as required.

263

REVIEWaUESTlONS I. Describe the use of the oxygen transport pathway as a conceptual model of cardiopulmonary prac tice and basis for defining problems related to cardiopulmonary dysfunction. 2. Distinguish between short-term goals, long-term goals and preventive goals of cardiopulmonary physical therapy management.

SUMMARY

3. Explain and distinguish the

This chapter has provided a framework for clinical problem solving and decision making based on oxygen transport. The process includes diagnosis and treatment prescription in the management of patients with car diopulmonary dysfunction ranging from the medically unstable critically ill patient to the medically stable pa tient with cardiopulmonary dysfunction living in the community. The purpose of a systematic approach to clinical decision making is to maximize treatment effi cacy and cost effectiveness by focusing on physiologi cal and evidence-based practice. The clinical decision making process involves diagnosis, that is, specific analysis of the patient's problems in relation to the physiology and underling pathophysiology, the contri bution of restricted mobility and recumbency, and ex

four

categories of

factors (i.e., pathophysiology, restricted mobility and recumbency, extrinsic, and intrinsic) that contribute to cardiopulmonary dysfunction. 4. Describe the factors that need to be considered in treatment prescription. 5. Desclibe the factors that must be considered In determining the course of treatment.

Bibliography & and

Barlow, D.H., Hayes, S.c., practitioner. Research

Nelson, R.O. (1984). The scientist accounlahiliry in clinical and edu

cational sellings. New York: Pergamon Press.

Cutler, P. (1985). Problem solving in clinical medicine. (2nd ed.). Baltimore: Williams and Wilkins. Dantzker, D.R. (1991). Cardiopulmonary critical care. (2nd ed.). Philadelphia: WB Saunders.

trinsic and intrinsic factors. Based on this analysis,

Dean, E. (1994). Oxygen transport: A physiologically-based con

treatment interventions and their parameters are pre

ceptual framework for the practice of cardiopulmonary physio therapy. Physiotherapy,

rameters should have a clear, justifiable rationale.

80, 347-355. & Henning R.1. (1993). Oxygen transpOlt variables in the identification and treatment of tissue h ypox i a Heart & L"ng, 22, 328-348.

Specific monitoring of the steps in the oxygen transport

Goldring, R.M. (1984). Specific defects in cardiopulmonary gas ex

sClibed that have the greatest physiological and scien tific justification. Treatments and their prescription pa

pathway that are impaired is essential to establish and confu'm the diagnoses, determine the most efficacious treatment, evaluate the treatment response, refine and progress the treatment, and determine when to discon tinue a given treatment and cardiopulmonary physical

Epstein, C.D.,

,

.

change. American Review of Respiratory Diseases,

Hillegass, E.A.,

&

129, S57-S59.

Sadowsky, H.S. (1994). Essentials of cardiopul

monary physical therapy. Philadelphia: WB Saunders. Irwin, S.,

& Tecklin, J.S. (1995).

Cardiopulmonary physical ther

apy (3rd ed.). SI. Louis: Mosby.

Patrick, D.E (1992). Clinical decision making. In Zadai C (Ed.).

therapy overall. The specific components of the treat

Clinics in physical therapy. P"lmonCllY management in physi

ment prescription include the treatment, its intensity (if

caltherapy. New York: Churchill Livingstone.

applicable), duration, and frequency, as well as its course and progression. A problem-solving approach to patient care has become essential in all health care pro fessions, given the prohibitive cost of such care and the need for all health care to be physiological, evidence based, cost-effective and ethically justifiable.

Riegelman, R.K. (1991).

Minimizing

medical mistakes. Boston:

Little, Brown. Schon, D.A. (1983). The rejlective practitioner. New York: Basic Books. Wasserman, K., Hansen,

J.E.,

Sue, D.Y.,

&

Whipp, B.1. (1987).

Principles of exercise testing and interpretation. Philadelphia:

Lea

& Fehiger.


Mobilization and Exercise

Elizabeth Dean

KEY TERMS

Exercise

Prescription

Metabolic demand

Recumbency factors

Mobilization

Restricted mobil ity

Oxygen transport

INTRODUCTION

port in a large proportion of patients. The sequelae of

The first purpose of this chapter is to define the terms

immobility and recumbency adversely affect all

mobilization and exercise and then to review the basis

steps in the oxygen transport pathway. An under

for prescribing mobilization and exercise as primary

standing of the effects of immobility and reduced ex

physical therapy treatment interventions to optimize

ercise stress on normal human physiological function

oxygen transport. The three distinct objectives of mo

provides the rationale for prescribing exercise for its

bilization and exercise for the purpose of maximizing

preventive effects.

oxygen transport are described. These include the ex ploitation of their acute, long-term, and preventive ef fects. Mobilization or exercise can be prescribed specifically to elicit whjch of these effects is indicated. The second purpose of this chapter is to review

DEFINITIONS Mobilization is defined as the therapeutic and pre scriptive application of low-intensity exercise in the

the negative effects of immobility and reduced exer

management of cardiopulmonary dysfunction usually

cise stress on multisystem function with special at

in acutely ill patients. Primarily, the goal of mobiliza

tention to cardiopulmonary and cardiovascular func

tion is to exploit the acute effects of exercise to opti

tion. Immobility and recumbency are major factors

mize oxygen transport. Even a relatively low-inten

contributing to impaired or threatened oxygen trans-

sity mobilization stimulus can impose considerable 265


266

PART III


metabolic demand on the patient with cardiopul

the submaximal exercise test have been less well-de

monary compromise. In addition, mobilization is per

fined (Dean and Ross, 1992a; Dean and Ross, 1993;

formed in the upright position, that is the physiologic

Shepherd et aI, 1968).

position (Chapter 18), whcnever possible, to optimize

The prescription of mobilization and exercise to

the effects of being upright on central and peripheral

optimize oxygen transport in the patient with acute

hemodynamics and fluid shifts. Thus mobilization is

cardiopulmonary dysfunction has been a relatively

prescribed to elicit both a gravitational stimulus and

neglected area of research compared with exercise

an exercise stimulus.

prescription in the management of chronic cardiopul

Exercise is the term used to describe the therapeu

monary dysfunction. This is surprising given that

tic and prescriptive application of exercise in the

"early mobilization" is a key component of car

management of subacute and chronic cardiopul

diopulmonary physical therapy in the management of

monary and cardiovascular dysfunction. Primarily,

acutely ill patients. Orlava (1959) was the first to re

the goal of exercise is to exploit the cumulative ef

port the beneficial application of mobilization in the

fects of and adaptation to long-term exercise and

management of acute cardiopulmonary compromise,

thereby optimize the function of all steps in the oxy

specifically, bronchopulmonary pneumonia. The

gen transport pathway.

physiologic literature supports an unequivocal role

In addition, mobilization and exercise can be pre

for therapeutic mobilization to maximize oxygen

scribed for their preventive effects. In this case, the

transport in patients with acute cardiopulmonary dys

parameters of the prescription focus on exploiting

function (Dean and Ross, 1992b). Despite this con

their multisystemic effects as well as their cardiopul

clusive body of literature, Orlava's work has not been

monary and cardiovascular effects.

extended significantly in the literature since her work was published more than 35 years ago. Unlike exercise prescription for the patient with

BASES FOR THE PRESCRIPTION

chronic cardiopulmonary and cardiovascular dys

OF EXERCISE STRESS

function, the acute patient cannot be exercise tested

The prescription of exercise is fundamental in the

in the conventional manner given the risks of an un

management of primary and secondary cardiopul

toward exercise response. Given the profound and di

monary and cardiovascular dysfunction. Exercise sci

rect effects of mobilization and exercise on car

ence has advanced exponentially over the past 30

diopulmonary and cardiovascular function, it is

years and is a primary basis for cardiopulmonary

essential that the physical therapist be able to identify

physical therapy. Guidelines have been developed for

the specific effects of exercise required and define the

prescribing exercise to maximize functional work ca

optimal therapeutic stimulus, ie, the stimulus that

pacity or aerobic capacity for healthy persons and in

yields the maximal benefit to oxygen transport with

dividuals with chronic heart and lung disease (Ameri

the least risk.

can College of Sports Medicine, 1994; Belman and

Acute and chronic cardiopulmonary and cardio

Wasserman, 1981; Blair, Painter, Pate, Smith and

vascular pathology have the additional problem of

Taylor, 1988; Froelicher, 1987; Hasson, 1994; Irwin

compromising functional capacity in two important

and Tecklin, 1985; Wasserman and Whipp, 1975;

ways. First, in acute illness, the patient tends to be re

Zadai, 1992). Exercise training is based on the find

cumbent in bed a greater propOition of time, and sec

ings of a maximum graded exercise test. Submaximal

ond, in both acute and chronic illnesses, the physical

exercise testing is often indicated for patients with se

activity of the patient is reduced. Recumbency and

verely impaired functional work capacity because of

immobility have physiologically distinct effects on

the inherent risks associated with maximal testing

oxygen transport and are the primary determinants of

(Compton, Eisenman, and Henderson, 1989). Guide

bed rest deconditioning (Chase, Grave, and Rowell,

lines for submaximal exercise testing, test interpreta

1966; Convertino, Hung, Goldwater, and DeBusk,

tion and prescription of exercise, however, based on

1982; Winslow, 1985). Thus dysfunction of oxygen


17

I

transport is further exacerbated in patients by the ad ditional factors of recumbency and immobility. The impact of these factors is further exacerbated in smokers, the young, older adults, obese individuals, and patients who are mechanically ventilated. Even though the prescription of mobilization and exercise for their acute effects ,is distinct from that for its long-term effects, the efficacy of the acute exer cise stimuli needs to be considered in terms of opti mizing long-term benefit to oxygen transport as well as the short-term acute effects. Both acute and long term exercise needs to be prescribed specifically for a given patient given the mechanisms of their underly ing pathology (American College of Sports Medicine, 1994). The prescription parameters should include (I) the type or types of mobilization or exercise, (2) specific intensity, (3) duration, and (4) frequency. These parameters are defined for each type of ex ercise being prescribed. In addition, (5) the course of the prescription, that is the time over which the pre scription is designed to produce its maximum benefit, and (6) the means of progression of the prescription are defined. Exercise has been reported to have beneficial ef fects in the management of a multitude of conditions. Its benefits range from enhancing all steps in the oxy gen transport pathway to other peripheral and central effects related to virtually every other organ system. The preventive effects of exercise are central to patient care across all conditions and physical therapy specialties. Exercise is advocated preventively to avoid the deleterious effects of immobility and to provide optimal systemic health protection secondary to cardiopulmonary conditioning. Mobilization and exercise are the physical thera pist's (PT's) "drug" with definable indications, con traindications, and side effects for each patient. The prescriptive parameters are determined by the effects needed to address the patient's underlying problems directly, whenever possible. Mobilization and exer cise constitute the most potent and direct interven tions affecting oxygen transport that are available to the PT in that, unlike other cardiopulmonary physical therapy interventions, they affect all steps in the oxy gen transport pathway. Thus they need to be pre scribed specifically as primary treatment interven


267

tions to remediate cardiopulmonary dysfunction, and their effects exploited first. OXYGEN TRANSPORT AND METABOUC DEMAND IN PATIENTS In health, when individuals have optimal physiologi cal reserve, both the acute and long-term responses to an exercise stimulus can be predicted. Specifically, minute ventilation (vE) and cardiac output (CO), hence oxygen delivery (002), increase commensu rate with work rate and oxygen demand. In patients, whose oxygen transport capacity is re duced or threatened, mobilization and exercise con stitute a significant additional metabolic demand that is superimposed on various other factors that con tribute to increased metabolic cost (see box on page 268). Hospitalized patients tend to be hypermeta bolic. In addition to their basal metabolic demands, their energy demands are increased secondary to such factors as an increased body temperature, healing and repair processes, increased work of breathing and of the heart, and in response to routine interventions and procedures including cardiopulmonary physical ther apy. The goal, therefore, in prescribing mobilization and exercise, is to ensure a safety margin wherein the patient's demand for oxygen does not exceed the available supply or delivery. In most situations, this would be indicated clinically by worsening of the pa tient's oxygen transport objectively and subjectively. Of the physical therapy related interventions, mobi lization, exercise, body positioning, arousal, breathing control maneuvers, coughing, postural drainage, man ual techniques, bagging, suctioning and range-of-mo tion (ROM) exercises can significantly increase oxy gen consumption and overall metabolic demand (Dean, Murphy, Parrent, and Rousseau, 1995; Weiss mann, Kemper, Darvask, Askanazi, Hyman, and Kin ney, 1984). Therefore, the capacity of the oxygen transport system to meet the patient's metabolic de mands needs to be established in the physical therapy assessment. Can the oxygen transport system support the patient's metabolic demands? If so, what reserve capacity is available to support a mobilization or exer cise stimulus? The exercise stimulus is designed to ex ploit the potential of the reserve capacity. Establishing


268

PART III


Factors That Contribute to Increased Metabolic Demand and Oxygen Consumption in Patient Populations Pathophysiological Factors Fever (e.g., secondary to an infectious agent or inflammation, surgery, multiple trauma, severe illness) Thermoregulatory challenges (i.e., too hot or too cold, altered ambient temperature and humidity) Healing and repairing (i.e., secondary to illness, trauma. surgery) Com hatting infection

Interventions Response to routine nursing, medical, and physical therapy inrerventions Feeding: cnterally or parenterally Physically being handled, e.g., by health care workers Body positioning Changing body position, i.e., passive. active assist, or active changes ROM exercises, i.e., passive, active assist, or active Mobilization and exercise Noxious stimulation, e.g., injections, insertion of lines, procedures, neurological checks Pharmacologic agents

Psychosocial Factors Social contact, e.g., health care workers, family Anxiety Discomf0l1 Pain Agitation

Miscellaneous Noises Disrupted circadian rhythms when ill, hospitalized or away from daylight

the availability of that reserve is essential to optimize

cedures need to be applied in the management of pa

the efficacy of the therapeutic exercise stimulus, that

tients with cardiopulmonary and cardiovascular dys

is, neither subthreshold or suprathreshold.

function in situations in which agitation, anxiety and

Metabolic demand and oxygen uptake are deter

pain contribute significantly to increased oxygen de

mined by multiple factors. In patients, the effect of

mand. This is especially true in intensive care, where

arousal, anxiety, pain, and noxious stimulation, in ad

oxygen transport is compromised or threatened in

dition to the hypermetabolic demands of recovery,

most patients (see Chapters 32 and 33).

contribute significantly to the energy cost and de mand on the oxygen transport system. Thus relaxing and calming patients is a central component of car diopulmonary physical therapy as these interventions

CElLULAR ENERGETICS IN RESPONSE TO MOBILIZATION AND EXERCISE

can minimize oxygen demand. Although relaxation,

The cardiopulmonary unit supports oxygen transport

often coupled with analgesia is central to physical

and cellular respiration (Weber, Janicko, Shroff, and

therapy management in other settings, relaxation pro

Likoff, 1983). Oxygen is continually being Llsed by


17

every cell in the body for oxidative phosphorylation


269

layed rather than eliminated. In disease states, anaer

and the synthesis of adenosine triphosphate (ATP).

obic metabolism occurs when a patient's oxygen

The splitting of a phosphate bond from ATP to form

transport system cannot meet the metabolic demand

adenosine diphosphate yields a considerable amount

required, e.g., patients with sepsis and multisystem

of energy for metabolism. The e nergy for this

organ failure. Serum lactate levels are significantly

process comes from the reduction of hydrogen in the

elevated in these patients, resulting in metabolic aci

formation of water and carbon dioxide, which is the

dosis, which is extremely unfavorable to the mainte

end products of the respiratory or electron transfer

nance of homeostasis.

chain. These metabolic processes which comprise

During exercise, the cellular P02 is lower than the

oxidative phosphorylation, take place in the mito

surrounding interstitial fluid P02. Oxygen diffuses

chondria of the cells (Chapter I).

rapidly through cell membranes. At the onset of

The balance of oxygen consumption to delivery

physical exercise, the increased metabolic demand of

is precisely regulated to ensure that there is not

the muscle and supporting tissues increases the oxy

only an adequate supply of oxygen, but also that

gen diffusion gradient. Feedback mechanisms are

under normal resting conditions approximately four

triggered to increase oxygen delivery, which de

times as much oxygen is delivered to the tissues as

pends primarily on arterial oxygen content and car

is used. This safety margin permits the immediate

diac output. The first line of defense is the response

availability of oxygen when the system is perturbed

to an increase in pericellular pH. The concentration

by physical, gravitational, and mental challenges

of carbon dioxide is increased which, as a result of

(see Chapter I).

the decrease in pH, facilitates the dissociation of

Anaerobic metabolism occurs during all out short

oxygen from hemoglobin, that is, it shifts the oxyhe

sprint type activities, e.g., hockey, soccer and volley

moglobin dissociation curve to the right. The cardiac

ball. Although PTs tend to focus on aerobic rather than

output (CO

anaerobic training, in conditions where oxygen deliv

with overall metabolic demand. The immediate re

=

SV x HR) increases commensurate

ery is significantly compromised, patients may rely on

sponse to oxygen deficit is an increase in CO to in

anaerobic metabolism to sustain ATP production and

crease oxygen delivery. This averts arterial desatura

break down to provide energy. Although anaerobic ex

tion which is not normally observed in health even

ercise implies that the exercise is pelformed in the ab

with extreme exertion.

sence of oxygen, anaerobic metabolism provides a

The increase in systemic CO results in increased

short-term means of supporting phosphorylation using

venous return and pulmonary CO. To oxygenate a

substrates other than oxygen to generate and split ATP.

greater volume of blood in the lungs, an increased

If insufficient oxygen is available, the amount of ATP

volume of air must be inspired. To effect an increase

that can be generated anaerobically is limited. Thus

in VE, tidal volume (VT) and respiratory rate (RR)

this process can only be sustained for a short period.

are increased. At low intensities of exercise, VT in

Lactic acid accumulates in the blood during anaerobic

creases disproportionately to RR, whereas at moderate

metabolism. In healthy, untrained individuals, lactic

to high intensities, VT plateaus and further increases

acid increases exponentially at an exercise intensity of

in VE are effected by an increase in RR (Jones and

about 55% of maximal aerobic capacity (McArdle,

Campbell, 1982). Exercise is associated with a small

Katch, and Katch, 1994). Anaerobic capacity and

but significant increase in airway diameter and length

specifically the anaerobic threshold can increase with

of pulmonary structures, hence, a reduction is airway

training, however, anaerobic training effects are less

resistance. Zone 2, that is, the zone of greatest ventila

significant compared with the training effects achieved

tion to pelfusion (V/Q) matching of the lungs, is in

with aerobic training.

creased as a result o

Anaerobic metabol ism is thought to be triggered

pulmonary capillary dilatation

and recruitment. Diaphragmatic excursion is enhanced

by tissue hypoxia. The term anaerobic is a misnomer

and the distribution of ventilation and perfusion is

in that oxygen is needed to pay the oxygen debt that

more uniform throughout the lung, which helps mini

it creates. Thus in health, the need for oxygen is de

mize atelectasis and airway closure. Exercise in


270

PART III


creases the excursion, hence, inflation of the lungs in three planes (i.e., anteroposterior, transverse, and cephalocaudal, particularly in the upJight positions). Rhythmic inflation and deflation of the lungs as

EFFECTS OF MOBILIZATION AND EXERCISE ON OXYGEN TRANSPORT In health, optimal function of oxygen transport de pends on the integrity of each step in the oxygen trans

sociated with physical activity has several clinically

port pathway and the interdependent function of all the

important physiologic effects. First, this action in

steps. As a result of cardiopulmonary and cardiovascu

creases alveolar ventilation by a primary increase in

lar dysfunction, one or more steps in the oxygen trans

tidal volume. Second, exercise-induced lung motion

port pathway can be affected. Because of the interde

facilitates lymphatic flow and drainage. Optimal

pendence of the steps in the pathway and the ability of

lymphatic drainage is essential to maintain optimal

functional steps to compensate for dysfunctional steps,

lung fluid balance with the increased volume of

gross measures of the efficacy of gas exchange and

blood being processed through the pulmonary circu

oxygenation can be normal. The number of steps af

lation and lung parenchyma. This action may ex

fected by disease and the severity of the disease deter

plain, in part, the beneficial effect of mobilization on

mines the degree of impairment of oxygen transport

the distribution and function of pulmonary immune factors (Pyne,

1994). The increased movement of the

overall and the degree to which this is reflected in gross measures of oxygen transport as a whole.

lungs during exercise has a primary effect on mu

To optimize the capacity of the various steps in the

cociliary transport and mucus clearance (Wolff,

oxygen transport pathway, the oxygen transport sys

1977). Related

tem needs to be exposed to two principal stressors:

to its effects on mucociliary transp0l1, physical activ

(I) gravitational stress and (2) exercise stress. These

Dolovich, Obminski, and Newhouse,

ity may help minimize bacterial colonization in the

stressors are tantamount to life in that they enhance

airways, hence, reduce the risk of pulmonary infec

the biochemical, physical and mechanical efficiency

1989). Finally,

of the various steps in the oxygen transport pathway,

tion (Skerrett, Niederman, and Fein,

lung movement stimulates surfactant production and

and the patient's ability to respond rapidly to changes

its distribution over parenchymal tissue. Surfactant is

in the physical environment.

essential for reducing surface tension in the alveoli,

The fact that the absence of gravitational stress

maintaining alveolar stability, maintaining lung com

and exercise stress are the two primary factors con

pliance, thereby, minimizing airway closure and

tributing to bed rest deconditioning supports the ex

areas of lung collapse.

ploitation of both gravitational and exercise stress in

The heart and peripheral circulation are primed

remediating cardiopulmonary dysfunction. Therefore

and respond to the increased demands of acute exer

mobilization and exercise are the two most physio

cise. Hemodynamic adjustments occur immediately

logic interventions available to the PT for remediat

with the onset of exercise stress. To maximize the

ing cardiopulmonary dysfunction.

CO available, blood moves from the venous capaci tance reservoirs such as the venous compartments of the gut and extremities, particularly the legs. At rest, most of the circulation,

70%, is contained within the

PRESCRIPTION OF MOBILIZATION AND EXERCISE: ACUTE RESPONSES

highly compliant venous circulation. The Starling

The clinical decision-making process involved in

Law of the heart regulates the forward movement of

defining the optimal mobilization and exercise stimu

blood commensurate with the volume of blood that is

lus is multifactorial. Based on the patient's history,

received. The heart chambers are normally distensi

history of the present illness, assessment, and results

ble and adjust to changing volumes of blood return

of the lab tests and procedures, the integrity of each

ing to the heart and pump more forcefully to eject it

step in the oxygen transport pathway is determined,

through the pulmonary and peripheral circulations. Muscle enzymes that extract oxygen at the cellular level are also primed and are produced commensurate

and the integrity of this system overall to preserve ar terial oxygenation and pH. The box on p.

271 shows

some common conditions associated with acute car

with chronic metabolic demand.


17


271

exploited are directed at each patient's specific

Acute Pathophysiological Conditions

pathophysiological deficits. Once the specific ef

That Benefit From the Acute Effects

fects of acute mobilization or exercise that are

of Mobilization alld Exercise

needed are identified and matched to the patient's

Atelectasis

pathophysiology, then the mobilization or exercise

Pulmonary consolidation

stimulus can be prescribed (see box on p. 273). The increased metabolic demand of acute exer

Pulmonary intiltrates

cise results in a slight increase in airway diameter,

Bronchopulmonary and lobar pneumonias

increased VE, alveolar ventilation (VA), VT, RR,

Bronchiolitis

air flow rates, CO, SV, HR, blood pressure (BP),

Alveolitis

rate pressure product (RPP), that is, product of heart

Pleural effusions

rate and systolic blood pressure (RPP is highly cor related with myocardial oxygen consumption, and

Acute lung injury and pulmonary edema

therefore myocardial work) oxygen consumption

Hemothorax

(V02), and carbon dioxide production (VC02). The

Pneumothorax

area of greatest ventilation to petfusion matching in

Cardiopulmonary insufficiency

the lungs, zone 2, is increased secondary to in

Cardiopulmonary sequelae of surgery

creased dilatation and recruitment of pulmonary

Cardiopulmonary sequelae of immobility

capillaries (West, 1995). The hemodynamic benefits of exercise are maxi mized in the upright position compared with recum bent positions in that exercise alone fails to counter the loss of volume regulating mechanisms associated with recumbency (Sandler, 1986) See Chapter 18 for

diopulmonary dysfunction for which a rational basis can be made for exploiting the acute effects of mobi

the effects of position changes. Mobilization and exercise stimulate the endocrine system. Catecholamines, released to support the car

lization as a primary treatment intervention. If the patient presents with acute cardiopul

diovascular system, sustain a given exercise work

monary dysfunction, then primarily the acute ef

rate. Increased sympathetic activity secondary to mo

fects of mobilization are indicated. These effects

bilization can help reduce the patient's need for sym

are distinct from those that occur on assuming the

pathomimetic pharmacologic agents (Bydgeman and

upright position. The majority of patients benefits

Wahren, 1974). Sympathetic nerve stimulation, for

most from a mobilization and exercise stimulus

example, is increased and sympathetic neurotransmit

when they are in the upright position. The effects of

ters are processed more efficiently. This is a signifi

being upright vs. exercise. however, need to be

cant effect that can be used as a goal for the prescrip

considered separately so that the benefits of their

tion of mobilization.

individual and combined contributions can be de

Central nervous system (CNS) responses to mobi

termined as well as any adverse reactions. The

lization include arousal and priming of the various

physiological benefits of acute exercise are shown

organ systems involved (Browse, 1965).

in the box on p. 272. The principal effects that re

The prescription of mobilization and exercise to

mediate acute cardiopulmonary dysfunction are in

stimulate their acute benefits parallels that of the pre

creased VE secondary to increased VT, RR, or

scription of exercise for its long-term, central and pe

both; improved air flow rates and mucus transport.

ripheral aerobic effects. The exercise parameters to

Cardiac output is increased secondarily to increased

achieve long-term adaptations in healthy people have

stroke volume (SV), heart rate (HR) or both, and

been well-defined by the American College of Sports

increased tissue perfusion. The particular benefits

Medicine (1994) (Table 17-1) and are well-accepted.

of acute mobilization and exercise that need to be

The individual engages in aerobic exercise at a heart


272

PART III


Acute Physiological Effects of Mobilization and Exercise Pulmonary System

Lymphatic System----
i

Regional ventilation

i

i

Regional perfusion

Hematologic System

i

Regional diffusion

i Circulatory transit times

i Zone 2 (i.e., area of ventilation perfusion matching) i Tidal i or !-

volume

Pulmonary lymphatic drainage

!- Circulatory stasis Neurological System

Breathing frequency

i

Arousal

i

Cerebral electrical activity

i

Minute ventilation

i

Efficiency of respiratory mechanics

!-

i

Stimulus to breathe

Airtlow resistance

i

Sympathetic stimulation

i

Postural reflexes

i Flow

rates

i

Strength and quality of a cough

i

Mucociliary transport and airway clearance

i

Distribution and function of pulmonary immune

Neuromuscular System

factors

Venous return

i

Stroke volume

i

Heal1 rate

i

Myocardial contractility

i i

Circulating blood volume

i Chest tube drainage Peripheral circulatory effects !- Peripheral vascular resistance i

Peripheral blood flow

i

Peripheral tissue oxygen extraction

Lymphatic System

i

Pulmonary lymphatic flow

di s t ribution,

and

degradation

of

catecholamines Genitourinary System

Stroke volume, heart rate and cardiac output

i Coronary perfusion

i Oxygen extraction i R e l e ase,

effects

i

flow

Endocrine System

Cardiovascular System

Hemodynamic

i Regional blood

i

Glomemlar tiltration

i

Urinary output

Gastrointestinal System

i

Gut motility

!- Constipation Integumentary System

i Cutaneous circulation for thermoregulation Multisystemic Effects

!-

Effects of anesthesia and sedation

!-

Deleterious cardiopulmonary effects of surgery

!-

Risk of loss of gravitational stimulus (when in con junction with the upright position) and exercise stimulus


17


273

Clinical Decision Making and Prescription of Acute Mobilization and Exercise

Step 1 Identify ALL factors contributing to deficits in oxygen transp0l1 (Chapter I), that is, those factors contributed to by:

I. The underlying pathophysiology of the disease or condition 2. Imillobility and recumbcncy 3. Extrinsic factors related to the patient's care, and 4. Intrinsic factors related to the individual patient Step 2 Determine whether mobilization and exercise are indicated, and if so, which form of either will specifically address the oxygen transport deficits identified in Step I.

Step 3 Match the appropriate mobilization or exercise stimulus to patient's oxygen transport capacity. EXAMPLES:

activities of daily living (ADLs). walking unassisted, standing erect with assist and taking a few steps,

transferring from bed to chair*, seated dangling position over bed side, moving in bedt

Step 4 Set the intensity within therapeutic and safe limits of the patient's oxygen transport capacity.

Step 5 Combine the various body positions especially in the erect position with the following maneuvers:

I. Thoracic mobility exercises. that is, flexion, extension, side tlexion, and rotation 2. Active. active assist, or passive ROM exercises 3. Breathing control exercises especially coordinated with body movements 4. Coughing, spontaneous and voluntary, supported by self or others Step 6 Set the dUnltion of the mobilization sessions based on the patient's responses (i.e., changes in measures and indices of oxygen transport) rather than time.

Step 7 Repeat the mobilization session as often

as

possible based on its beneficial effects and on is being safely tolerated by

the patient.

Step 8 Increase the intensity of the mobilization stimulus. duration of the session, or both comml!l1surate with the patil!nt's capacity to maintain optimal oxygen transport when confronted with an increased mobilization stressor, and in the absence of distress; monitored variables to remain within predetermined threshold range.

':'AII sitting positions requ i re upright ereci u pri gh t position are NOT physiologically

silting; propped up, semi recumbenl, slouched or slumped posit ions although approximaling the comparable

i-No amount of movement or activity is too sm.,lIlo derive benefits acutely or over long-Ierm


274

PART III


TABLE 17-1 Exercise Prescription Parameters to Elicit Long-Term Aerobic Benefits In Healthy Persons SPECIFICATIONS

Parameter Exercise Type

Rhythmic activity, involving the large muscle groups; the legs, arms or both

InLensity Duration

70% to 85% of the age predicted maximum heart rate or observed maximum heart rate 20 to 40 minutes

Frequency

Three to five times a week

Course

6 to 8 weeks

Adapted from the American Col lege of Sports Medicine, (1994). Guidelines for exerc ise testing and Williams and Wilkins .

prescription. (6th ed.). Philadelphia:

rate intensity of 70% to 85% of a maximum heart rate,

Mobilization Stimuli

for 20 to 40 times three to five times a week. Aerobic

Ambulation-independently, with one or more assisting

training effects are usually observed within 2 months. In severely deconditioned individuals and in some

Cycle ergomelly-Iower and upper extremity

patient populations, however, such a prescription

ADLs-independently, with one or more assisting

would not be realistic, ethical, or indicated. Thus exer

Standing-independently, with one or more assisting Transferring-independently, with one or more assisting Dangling-independently, with one or more assisting Cycle ergometry in bed (lower extremity)

cise is prescribed that is sufficient to elicit progressive physiological adaptation within defined limits of cer tain objective and subjective responses, such as per ceived exertion, shortness of breath, angina, discom fort/pain, and general fatigue. Considerable research, however, is needed to refine the prescription of mobi

Turning in bed

lization and exercise for their acute effects in patients

Bed exercises

with acute cardiopulmonary and cardiovascular dys

Supplemental Aids and Devices for Mobilization

For the patient: Walking aids, such as crutches, cane, intravenous (IV) pole, wheelchair, orthoses Weights Pulleys

function. Furthermore, the specifications for low level exercise needed to affect long-term acrobic adaptation have not been elucidated in dctail. However, based on physiological understanding of acute exercise re sponses and cardiopulmonary pathophysiology, prin ciples for prescribing mobilization for acute car diopUlmonary conditioning can be formulated.

Monkey bar Grab bars Grab rope

For the PT: Transfer belts Mechanical lifts for patients

Mobilization Testing Evaluating a patient's response to a mobilization stimulus can be assessed in two ways. First, the pa tient can be exposed to a mobilization challenge test. The patient is monitored before, during, and after mobilization activities (see box at left). Relatively low-intensity activities such as bed exercises, moving in bed, changing body position, sitting up, dangling


17

over bed side, transfer to chair, chair exercises, and


275

in the previous couple of hours, be as attentive and

short walks with assistance, constitute a sufficient

aroused as possible and be experiencing minimal

stimulus to elicit the acute effects of exercise. The de

pain or discomfort. Review of a patient's medication

gree of assistance required to perform the activity

schedule will ensure treatments are well-timed with

should be noted, since this significantly influences

respect to pain medications, and medications that in

the patient's individual effort. Second, if the patient's

terfere with a good treatment response, such as nar

status is unstable and oxygen transport is severely

cotics. The patient's clothing should not be restric

jeopardized, then monitoring a patient during stan

tive, and any lines, leads, and catheters should not be

dard care and procedures, such as turning the patient,

taut. Any equipment, monitors, and IVs need to be

ADLs, nursing and medical procedures, can provide

appropriately positioned to avoid disconnections or

an indication of the patient's physiological responses

mishaps. Mobilizing the patient in intensive care re

to mobilization and the capacity of the oxygen trans

quires positioning of the mechanical ventilator and

port system to meet the metabolic demands imposed.

other supports before moving the patient. The PT

No movement is too small. Any movement that is

must prepare personnel before moving a patient par

sufficient to perturb the oxygen transport system, no

ticularly if one or more assists are required. Despite

matter how minimal, is sufficient to elicit short- and

the number of persons assisting, the goal is usually

long-term gains.

to have the patient perform as much of the mobiliza tion activity as possible. Even small degrees of phys ical movement can provide sufficient stress to the

Monitoring

cardiopulmonary system to be beneficial.

Patients for whom mobilization is prescribed require

The basic components of the mobilization session

monitoring. Because of the stress to the oxygen trans

are comparable to the components of an exercise ses

port system that mobilization elicits, the following

sion described by the American College of Sports

variables in addition to the oxygen transport vari

Medicine for long-term training effects (Figure 17-1).

ables, are most useful to monitor: heart rate (HR),

Wherever possible, the session should include the

systolic and diastolic BP, RPP, RR, Sa02, arterial

following components: warm-up, steady-rate, cool

blood gases, ECG and subjective responses.

down, and recovery. These components are less dis tinct when a patient has minimal functional capacity or is being mobilized to remediate acute cardiopul

Mobilization Prescription

monary dysfunction. The rhythmic movement of

Prescribing a mobilization stimulus for its acute ef

large muscle groups is ideal. Prolonged static maneu

fects parallels the prescription of exercise for its long

vers are usually avoided particularly if the patient is

term effects with some important differences. In an

severely ill, because of their disproportionate hemo

acute patient, a mobilization or stimulus often results

dynamic response. The movements that are usually

in a greater response gain than such a stimulus in

considered when mobilizing a patient include: turn

subacute and chronic patients. In addition, to the

ing, sitting up, shifting, transferring, standing and

rapid favorable response an acute patient may have to

taking some steps. These can be extremely metaboli

acute exercise, the patient may exhibit a negative re

cally demanding for patients with significant acute

sponse just as quickly. Thus judicious monitoring of

cardiopulmonary dysfunction. Thus pacing the mobi lization session allows the patient to rest between

treatment response in these patients is essential. The scheduling of and preparation for a mobiliza

stages. The patient is reassured and encouraged to

tion session is crucial to the response that can be ex

relax and coordinate deep breathing and coughing

pected. The following conditions should be adhered

with the activity. Throughout the session, attention is

to as closely as possible; and their details should be

given to the patient's biomechanical alignment, and

recorded so that any factor that significantly influ

postural erectness and stability. Back extension or

ences the response to treatment can be identified.

body positioning minimizes slumping of the chest

The patient should be rested, not have eaten heavily

wall and compromised ventilation. In this way, chest


276

PART III


L """1J 0.. 1 200r .Q 1 ? L.. 1 E 1 0 L.. 1 8011 1 .:.c 1

c

'

1601-

u

0

-

g 1 U 1

Over time, exposure to an acute exercise stimulus of an appropriate intensity, for an appropriate duration

.:.c u

1

and at an appropriate frequency will stimulate long

I

I

120f-

,

I\

scribing the exercise stimulus results in less potent ef fects and overprescribing results in an excessive,

1

:\ :

I '

term exercise adaptation to that stimulus, Underpre

1

140r Trai in

100'

bility, or respiratory distress.

L..

"""1J 1

without arterial desaturation, hemodynamic insta

"""1J

1 .Q

deleterious effect. Although the latter may be toler ated in the short run, the patient's well-being may be

'01

\ I

1'>"

jeopardized, such as suboptimal treatment rc"ponse, ovettraining signs and symptoms, and injuries.

80

The duration of the session and the frequency of sessions should be response-dependent rather than

60

time-dependent. The optimal mobilization threshold, that is, physiological variables increased but not in o

Start exerCise

5

Time (minutes)

35 40 Stop exercise

45

FIGURE 17-1 Components of the exercise training session (i,e., stretching, warmup, training zone, cool down, and stretching,

excess of predetermined acceptable and safe limits, should be maintained for as long as possible within the patient's fatigue and comfort levels, and in the absence of adverse responses. The mobilization ses sion should be repeated as often as the patient can tolerate, that is, exhibits a beneficial response or no deterioration and adequately restores between treat men ts. Treatmen t sessions for acu te cardiopu 1monary dysfunction are usually shorter and more

wall expansion is maximized in three dimensions.

common than for the patient with chronic cardiopul

The erect position is efficient and requires the least

monary dysfunction. The patient's condition changes

amount of energy to maintain. Less demand is placed

rapidly both with respect to improvement as well as

on the accessory muscles of respiration in erect sit

deterioration. Progression of mobilization for its im

ting, and this effect is enhanced further with leaning

mediate acute effects is usually rapid. Progression of

forward and support of the arms.

exercise for its long-term effects may occur every several weeks whereas progression of mobilization for its acute effects may range from as frequently as

Mobilization Training

every treatment to every few days. Over time, expo

With respect to oxygen transport, the purpose of

sure to a progressive mobilization stimulus leads to

the mobilization session is to elicit the immediate

long-term physiological adaptations throughout the

effects of an exercise stimulus, no matter how min

oxygen transport pathway,

imal. The optimal therapeutic dose of the stimulus is based on the patient's presentation and history and the specific parameters are determined by the goals of the treatment and the acute effects of exer

Monitoring The more acute the patient's condition, the more

cise that are indicated. The intensity of mobiliza

physiologic variables usually need to be recorded,

tion for many patients, for example, is that intensity

More objective measures are available in special care

that elicits optimal tidal volumes and VA, increased

and intensive care units (ICUs), Subjective responses

breathing frequency and air flow rates, enhanced

are also vital components of determining the ade

mucocil i a r y transport, and cough stimulation,

quacy of the mobilization stimulus; however, se


17

verely ill patients are often unable to respond effec


277

a response-dependent duration and frequency, there is

tively. Compared with the condition of chronic pa

a cumulative adaptive response to that repeated stimu

tients, the condition of acute patients tends to vary

lation, or a long-term, training response. In decondi

more within and between sessions and afterward,

tioned individuals with low functional work capacity,

which necessitates greater monitoring.

or whose oxygen transport system has been compro

Monitoring needs to be performed continuously

mised by disease, the exercise intensity associated

for patients for whom acute mobilization has been

with relatively low-intensity mobilizing activities such

prescribed. First, a baseline of the patient's resting

as bed exercises, moving in bed, sitting up, dangling

metabolic state needs to be established. Second, the

over bed side, transferring to chair, chair exercises,

metabolic responses to stimuli that perturb oxygen

and short walks with assistance, constitute a sufficient

transport and the lability of this response needs to be

stimulus for long-term adaptation. However, optimal

established. Obtaining such a profile provides some

adaptation only occurs if these activities are pre

indication of the upper limit of the target intensity

scribed at a requisite intensity, duration, and fre

range for mobilization. The target intensity range can

quency and the exercise prescription progressed com

be defined in terms of an upper and lower level of

mensurate with the individual's adaptation.

various physiologic variables. The most commonly

Mobilization activities prescdbed to enhance oxy

used are HR, BP, RPP, RR, perceived exertion or

gen transport, can be coupled with resistive muscle

breathlessness. Monitoring during nursing procedures

work to increase muscle strength and endurance (e.g.,

and other types of routine care provides an indication

weights, use of a monkey bar for moving in bed and

of the patient's functional capacity without having to

sitting up, manual resistive exercise, the use of wrist

conduct a modified exercise test.

or ankle weights, ergometry, and walking). Coordi

Alternatively, a mobilization or exercise challenge

nating postural, thoracic mobility and upper extrem

can be given. The patient's response is compared

ity exercises with inspiratory and expiratory efforts

with resting baseline measures. The quality as well as

can be effective in stimulating increased VT, and im

the immediacy of the response is documented. The

proved ventilation and perfusion matching. Chapters

characteristics of the quality of response is also

2l and 22 illustrate how such movement and breath

recorded. Is the response commensurate with the in

ing patterns can be coupled to maximize oxygen

tensity of the exercise stimulus? With cessation of

transport in neurological patients. Such coordinated

exercise do the responses revert to baseline? If so,

exercise, however, can also be used with patients

how fast? Do the variables return to baseline or re

with acute cardiopulmonary conditions. Isometric

main above baseline?

type exercises, postures that require increased muscle

The variables to be measured depend on the pa

work for stabilization, and activities that elicit the

tient (see Chapters I and 16). Most commonly, HR,

Valsalva maneuver produces disproportionate hemo

ECG, BP, RPP, RR, and subjective symptoms, are

dynamic responses, which could be detrimental. The

basic measures and indices of exercise response that

capacity of the patient to respond appropriately to

require no invasive procedures. At the other end of

these loads needs to be established beforehand.

the spectrum is the critically ill patient who has vari

In the management of acute cardiopulmonary dys

ous invasive lines and monitoring equipment, includ

function, the parameters of mobilization stimuli in

ing hemodynamic monitoring and intracranial pres

clude a relatively low intensity (although often per

sure monitoring. This patient requires more specific

ceived as intense by the patient), short duration, and

and frequent measures of oxygen transport.

high frequency of sessions. If the patient is severely compromised (e.g., end-stage heart or lung disease) interrupted or interval training is indicated. This type

Adaptation to an Acute Mobilization Stimulus

of training is characterized by either on-off exercise,

When an individual is exposed to repeated exercise

which allows for rest in between bouts of exercise, or

stress, that is, of a specific threshold intensity, and for

high-low intensity of activity. The volume of work


278

PART III


TABLE 17-2 Relationships Among Mobilization and Exercise Prescription Parameters Activity and Relative Intensity SESSION DURAnON

SESSION FREQUENCY

Mobilization activities

5to 20 min

Interval continuous aerobic exercise

5to 20 min

Continuous aerobic exercise (light)

5to 20 min

Continuous aerobic exercise (moderate)

20 to 40 min 20 to 40 min

I time per I to 2 hours to 4 to 6 times per day I time per I to 2 hours to 4 to 6 times per day I time per I to 2 hours to 4 10 6 times per day 2 to 3 times daily to once daily Daily to 3 to 5times per week

Continuous aerobic exercise (heavy)

that can be achieved in an interrupted protocol by a

beds with lines and leads is crucial, because it is these

severely compromised patient, is significantly greater

patients who benefit significantly from exercise stress

than during continuous activity. With physiological

and also succumb most severely to its removal.

adaptation over time, the exercise period can be in

The goal is to adapt the patient to multiple ShOl1 mo

creased and the rest period decreased, and possibly

bilization sessions per day, as frequently as once per

eliminated. When high- and low-intensity exercise is

hour, and progressively increase the intensity of these

alternated the work load can be progressed by either

sessions, reduce the duration and conespondingly re

increasing the respective loads in each phase or by in

duce the frequency of sessions. Table 17-2 illustrates

creasing the duration of the higher load period. If the

the inverse relationsrup between mobilization and exer

patient has low functional work capacity but suffi

cise intensity, duration, and frequency of the sessions.

cient physiological reserve, adaptation can be rapid, necessitating small, frequent progressions. As the pa tient's aerobic capacity increases, the response gains

Multisystem Effects of Mobilization

are correspondingly smaller. If the patient has both

Acute exercise affects most organ systems in addition

poor functional capacity and poor physiological re

to the cardiopulmonary and cardiovascular systems.

serve capacity, progress would be correspondingly

The neurological system is primed for activity. To

slower and less significant.

counter postural perturbations, reflexes and postural

When mobilization activities are being prescribed

control adjustments are activated. Blood flow is in

to remediate acute cardiopulmonary dysfunction, par

creased to the working muscles commensurate with

ticularly in patients in the leU, extensive and often

the intensity and duration, and therefore overall meta

invasive monitoring is required. This permits detailed

bolic demand of the work. The endocrine system also

assessment, and ongoing metabolic assessment of the

adjusts to largely stimulate the cardiopulmonary and

patient's treatment responses and recovery. With

cardiovascular systems through a complex system of

these supports, mobilization and exercise can be pre

neurotransmitters to support the oxygen demands re

scribed effectively in these patients. Judicious moni

quired of the work rate imposed.

toring minimizes any inherent dangers of either under or over prescribing the intensity of the exercise stim ulus (Part II). Special consideration has to be given to the fact that various monitoring leads, lines, and

PRESCRIPTION OF MOBILIZATION AND EXERCISE: lONG-TERM RESPONSES

catheters may restrict certain body positions and ac

In health, the long-term effects of exercise occur in re

tivities. Such encumbrances, however, do not pre

sponse to a specific and sufficient exercise stimulus to

clude most activities including ambulation. Moving

which the individual is exposed for a finite period. With

relatively immobile patients who are tied to their

respect to aerobic training or adaptation, the essential


17


279

Long-Term Physiologic Effects of Mobilization and Exercise Cardiopulmonary System

Neuromuscular System

J,

Submaximal minute ventilation

Enhanced neuromotor control

i

Respiratory muscle strength and endurance

i

Efficiency of postural retlexes associated with type

i

Reflex control

i

Movement efticiency and economy

of exercise

i Collateral ventilation i

Pulmonary vascularization

Cardiovascular System

i Myocardial muscle mass

Musculoskeletal System

i

i

Muscle vascularization

i

Myoglobin

Myocardial efficiency

Exercise-illduced bradycardia

J Stroke volume J, J..

at rest and submuximal work rates

Resting heart rate and blood pressure Submaximal heart rate. blood pressure, and rate pressure product

i

Muscle metabolic enzymes

i

Glycogen storage capacity

i

Improved biomechanical efficiency

i

Movement economy

J..

Submaximal perceived exertion and breathlessness

i

Efliciency of thermoregulation

J..

i

Muscle strength and endurance

Orthostatic intolerance when performed in the up-

i

Ligament tensile strength

Muscle hypertrophy

right position

Maintain bone dellSity

Hematologic System

i Circulating blood volume i Optimize number of red blood

Endocrine System

i Efficiency

cells

of hormone production and degradation

to support exercise

i

Optimize hematocrit

J..

Cholesterol

Immunological System

J..

Blood lipids

i

Resistance to infection

Central Nervous System

Integumentary System

i

Sense of well-being

i Efficiency

i

Concentration

i

of skin as a heat exchanger

Sweating efficiency

training parameters appear in the box above. As adapta

tion and hemodynamic responses to submaximal exer

tion to the exercise stimulus occurs, each step in the

cise are decreased. The subjective experience of exer

oxygen transport system becomes more efficient facili

cise stress is also reduced. These training effects are

tating oxygen delivery, uptake and extraction at the cel

commensurate with increases in the efficiency of oxy

lular level. The long-term effects of aerobic exercise

gen transport at each step in the pathway.

are summarized in the box above. In addition to an in

As the body adapts to the exercise training stimu

crease in maximal oxygen consumption, training results

lus, the intensity needs to be increased to elicit fur

in an exercise-induced bradycardia and increased stroke

ther training benefit. This is the basis for the physio

volume at rest and a reduction in the physiological de

logical adaptation to an exercise training stimulus.

mands of submaximal work rates. Specifically, ventila-

Depending on the goals of the exercise prescription, a


280

PART III


Chro1lic Pathophysiological Conditions That Benefit From the Long-Term Effects of Mobilizatio1l and Exercise Cardiovascular Conditions

Neurological Conditions-
Congenital heart disease

Multiple sclerosis

Acquired heart disease

Poliomyelilis

Postsurgical heart conditions

Endocrine Conditions

Angina

Thyroid dysfunclion

Hypertension

Diabeles mellitus

Hyperlipidemia

Neoplastic Conditions

Hypercholesterolemia

Conditions Requiring Organ Transplantation

Congesti ve heart failure

Pre- and postsurgical siages

Heal1 transplantation

Musculoskeletal Conditions

Peripheral vascular disease

OSleoarthrilis

Cardiopulmonary Conditions

Rheumatoid al1hrilis

Chronic obstructive pulmonary disease

Ankylosing spondylitis

Chronic ventilatory failure

Osteoporosis

Interstitial lung disease

Connective Tissue Conditions

Asthma

Systemic lupus erythelllatosis

Cystic fibrosis

Nutritional Disorders

Postthoracotomy conditions

Obesity

Lung transplantation

Anorexia

Neurological Conditions

Other Systemic Conditions

Siroke

Chronic fatigue syndrome

Parkinson's disease

Chronic depression

Quadriplegia

Alcoholism

Paraplegia

P regnanc y

Cerebral palsy

Renal disease

Down syndrome

Liver disease

decision is made after several weeks whether the ex ercise intensity needs to be increased to further in

EXERCISE TESTING AND TRAINING IN PATIENT POPULATIONS

crease aerobic capacity, or whether a maintenance

Numerous conditions including nonprimary car

program is indicated. The training program is pro

diopulmonary conditions have been shown to bene

gressed by establishing a new exercise intensity usu

fi t from the long-term effects of aerobic exercise

ally based on 70% to 85% of the maximal heart rate

(see box above). For eacll patient, however, with

achieved in a repeat of the initial exercise test.

each of these conditions, the exercise prescription


17


Common Indications for Exercise

Relative and Absolute Contraindications

Testing in Patient POpuUltiOIlS

to Exercise Testing

Diagnosis

Absolute Contraindications

Coronary artery disease and vasospasm

Congestive heart failure (CHF)

281

Hyperreactive airway disease

Acute EKG changes of myocardial ischemia

Cardiac vs. pulmonary limitation to exercise

Unstable angina


Ventricular or dissecting aneurysm

Assessment

Ventricular tachycardia

Maximal functional work capacity

Multifocal ectopic beats

Chest pain

Repetitive ventricular ectopic activity

Dyspnca

Untreated or refractory tachycardia

Endurance

Supraventricular arrhythmia

Ability to work

Recent thromboembolic event (pulmonary or other)

Employmelll options

Uncontrolled asthma

Cardiopulmonary and cardiovascular conditioning

Uncontrolled heart failure

Movement economy

Pulmonary edema

Limitations to exercise

Uncontrolled hypertension (above 250 mm Hg systolic, 120

Effect of medication

mm

Hg diastolic)

Acute infections

Adequacy of diabetes management

Relative Contraindications

Prescription

R e c e n t m y ocardial inf a rction (M!) (l e s s than

Exercise program

4 weeks ago)

Medications

Aortic valve disease Severe cardiomegaly Pulmonal), hypertension

differs. Comparable with prescribing mobilization in acute conditions, prescribing exercise for long

Resting tachycardia Resting electrocardiogram (ECG) abnormalities

term adaptations is based on the patient's presenta

Poorly controlled diabetes

tion, history, premorbid status and conditioning

Severe electrolyte disturbance

level, lab and investigative reports related to physio

Severe systemic hypertension

logic reserve capacity, the exercise test and the

Significant conduction disturbance

goals of the exercise prescription.

Complete atrioventricular block Fixed rate pacemakers

Exercise Testing

Acute cerebrovascular disease (CVD)

Exercise testing no matter how modified can pose a

Respiratory failure

potential risk to the patient, therefore exercise testing

Left ventricular failure

must have clear indications, and any contraindications

Epilepsy

must be ruled out. The indications for exercise testing are numerous (see box above, at left). They range from quantifying maximum functional capacity to as-

Adapted from Jones. N.L. (1988). Clinical Exercise Testing. (3rd Ed.). Philadelphia: WB Saunders.


282

PART III


TABLE 17-3

Subjective Scales of Exercise Responses Based on the Borg Scale of Rating of Perceived Exertion

0 0.5 1 2 3 4 5 6 7 8 9 10

PERCEIVED EXERTION

BREATHLESSNESS

DlSCOMFORTIPAIN

Nothing at all

Nothing at all

Nothing at all

Nothing at all

Very very weak

Very very light

Very very weak

Very very light

FATIGUE

Very weak

Very light

Very weak

Very light

Weak

Light

Weak

Light

Moderate

Moderate

Moderate

Moderate

Somewhat strong

Somewhat hard

Somewhat strong

Somewhat hard

Strong

Hard

Strong

Hard

Very strong

Very heavy

Very strong

Very heavy

Very very strong

Very very hard

Very very strong

Very very hard

Maximal

Maximal

Maximal

Maximal

sessing endurance during low level ADLs. Contraindi

the ratings can be used to compare the patient's sub

cations are classified as either relative or absolute (see

jective exercise responses over repeated tests.

box on p. 281, at right). Absolute contraindications

Depending on the functional impairments and ca

prohibit the safe conduction of an exercise test,

pacity of the patient, the exercise test can be one of

whereas the presence of relative contraindications re

various types depending on the objective of testing

quires that the test, protocol, physiological variables

and potential training. If exercise training is an objec

monitored, or the end point of the test be modified.

tive of the exercise test, the activity used in the test

Both the indications for the test and any contraindica

should be comparable with that to be used in training.

tions must be clearly established before performing an

Physiological responses and adaptation to exercise

exercise test.

are highly specific to the training stimulus (the speci

The guidelines used to test and train healthy peo

ficity of exercise principle). Thus if walking is to be

ple with no disease states are not directly generaliz

the training activity, the test should be a walking test

able to chronic medically-stable patient populations.

rather than cycling.

Because of functional impairments in these patients

There are numerous variants of standard exercise

(e.g., secondary to cardiopulmonary, cardiovascular,

tests (Table 17-4). These are categorized as continuous

neuromuscular, and musculoskeletal dysfunction) ex

and interrupted tests. Continuous tests include maxi

ercise testing and training must be modified. More

mal and submaximal incremental tests and steady-rate

over, patients who are physically challenged experi

tests, and interrupted tests include maximal interval

ence more subjective symptoms in response to

and submaximal interval tests. Interrupted tests are de

exercise compared with healthy people, therefore

signed for patients with low functional work capacity

monitoring the subjective responses to exercise is es

who cannot sustain prolonged periods of aerobic exer

sential. The Borg scale of rating of perceived exertion

cise. These patients can perform more work over time

can be modified for clinical use to score breathless

when the work load is administered in an interrupted

ness, discomfort, pain, and fatigue (Table 17-3)

or periodic manner. Specifically, the test alternates

(Borg, 1970; 1982). If the endpoints of the scale are

fixed periods of work and rest, or high and low intensi

well-described and understood by the patient, then

ties of exercise. The proportions of work-to-rest or


17


283

TABLE 17-4 Exercise Tests That Can Be Applied to Patient Populations TEST TYPE

INDICA TlONS

Continuous Tests Maximal

. Generally medically-stable patient No significant musculoskeletal abnormalities Test maximal functional capacity Basis for aerobic exercise program

Incremental

Incremental work rates usually 2 to 5 minutes in duration

Steady-rate

Endurance test at a given work rate; usually a comfortable walking or cycling speed

Submaximal

For patients for whom maximal testing is contraindicated

Incremental

Approximate maximal exercise testing Test of near maximal functional capacity or some significant propOition of maximum

Steady-rate

Establish baseline of response to steady-rate exercise usually at 60 to 75% of predicted maximum heart rate Establishes an index of endurance, cardiopulmonary conditioning and may give an index of movement economy

Interrupted Tests Maximal or Submaximal

Establish level of functional capacity in patients with extremely low functional work capacity On-off protocol or high-low intensity protocol, such as 5 min on to I min off; alternate high- and low-intensity exercise in cycles, such as I minute high to 15 seconds low

high-to-low exercise intensity is set according to the

treadmill or ergometer, which jeopardizes stringent

patient's level of impairment. One patient, for exam

test control (Dean and Ross, 1992a).

ple, may be able to tolerate 3 to 5 minutes of relatively

Like other diagnostic or testing procedures, the va

high intensity work to I to 2 rrlinutes of low-intensity

lidity and reliability of the exercise test depend on the

work, whereas another patient may be able to tolerate

quality of the procedures used. The preexercise test

only 1 minute of low intensity work to 10 to 20 sec

conditions and the preparation and testing procedures

onds of rest.

need to be standardized (see boxes on pp. 284-285).

For maximal standardization and the capacity to

The test is terminated as soon as the sign or symptom

perform more comprehensive monitoring, stationary

criteria for terminating the test is reached or the crite

exercise modalities such as the treadmill, ergometer,

ria for prematurely terrrlinating the test is reached (see

or step are recommended. However, there may be in

box on p. 286). Recording the test conditions and pro

dications to perform an exercise test without a modal

cedures in detail is essential. An example of an exer

ity, such as the 12-minute walk test or some variant

cise test data sheet that can be modified to any testing

like 6 or 3 minutes (McGavin, Gupta, and McHardy,

protocol using an exercise modality is shown in the

1976). Standardization of such tests, however, is

box on p. 287, at left. Many patients are unable to be

more difficult. Practice has a significant effect on the

exercise tested using a modality. These patients can

results of the 12-minute walk test, thus this test needs

walk on a marked circuit. An example of an exercise

to be repeated several times to achieve a valid test.

test data sheet is shown in the box on p. 287, at right.

Also, the instructions for this test are less well

Systematic and detailed record-keeping will maximize

standardized clinically compared with those for the

the test validity and its interpretation as well as ensure


284

PART III


Preexercise Test Conditions Establish the indications for an exercise test. Determine absolute and relative contraindications to conducting an exercise test.

Ensure patient is free of any acute illnesses including influenza and colds for 48 hours. Ensure patient understands the purpose of the test and provides signed consent. Ensure patient has not eaten heavil y . has avoided caffeinated beverages and has refrained frolll smoking for at least 3 hours before testing. Ensure patient is rested and has not e x ercised, or is not being excessively exerted for at least 24 hou rs before testing . Ensure patient is app ro priate ly dressed, for exampl e , shorts, n onbindi n g clothes, short-sleeve shil1. socks, running or walking shoes that have proper SliPPOI1, and secured laces or fastenings.

Orthoses should be worn unless the test is evaluating changes in functional capacity with and without nn orthosis. Ensure patient understands the subjective rating scales and is able to read them when held at an nppropr i ate distance. Select the type of exercise test, the pr otoc 01 and the exercise test termination criteria beforehand. Ensure the patient is familiar with and has practiced performing the test

or

test activity preferably before the test day

to reduce arollsal, improve movement efficiency . and maximize test validity.

that the same procedures are used in follow up tests

exercise capacity and are unable to tolerate being

thereby maximizing the abi Iity to compare test results.

tested on an exercise modality. A major disadvan

It is imperative that retests are conducted comparably

tage, therefore is that the patient cannot be as com

in every respect to the original test with respect to pa

prehensively monitored. Thus patients need to be se lected carefully to undergo a 12-minute walk test or

tient preparation and the procedures.

one of its variants. Knowledge of the patient's functional ability

Exercise Tests and Protocols

based on verbal report can be useful and can serve as

Depending on the functional capacity of the patient,

a guideline for determining the exercise test, its para

the exercise test can be a continuous maximal, sub

meters, and what tile patient's termination criteria

maximal incremental or steady-rate, or an interrupted

should be. Although these verbal reports do not re

maximal or submaximal test. The protocol for the test

place an exercise test, they can be used as an adjunct.

and the end points to be used in terminating the test

The oxygen cost diagram is shown in the box on p.

are determined beforehand depending on the indica

290, at left. This visual analog scale is constructed of

tions for the test and the objectives. Some commonly

a 100 mm line; the high end of the scale represents

used protocols are shown in Figure 17-2 along with a

strenuous activity, that is, walking briskly uphill, and

comparison of the energy expenditure of the various

the low end of the scale represents no activity, or

work stages in their protocols.

sleep. The patient crosses the line at the point where

The 12-minute w a lk test a n d i t s varian ts, 6

breathlessness does not allow continuation when at

minute- and 3 minute-walk tests, were designed to

the patient's best. Figure 17-3 shows an incremental

test patients with lung disease (McGavin, Gupta,

ladder of workloads associated with step increments

and McHardy, 1976). These tests have been favored

in metabolic cost, (hat is, multiples of resting or near

clinically, because they are functional and do not re

resting metabolic rate (resting metabolic rate

quire exercise equipment. However, these tests are

MET, or 3.5 ml 02/mink i g

often used for patients who have extremely impaired

of metabolic costs ranges from very light to very


=

I

17


285

PreparaJion and General Procedures for an Exercise Test Preparation Patient ch,mges into exercise clothes and shoes (not new); ensure laces are secure. If the ergometer is used. the seat-to-pedal distance must be established before the test, and the seat should be adjusted to allow for 15 degrees or knee extension when the foot is lowennost in the pedal in the revolution cycle; the knee must not extend fully. Patient sits quietly in a supported chair to establish a resting baseline. Monitors are allached (e.g., heart rate, ECG, blood pressure cuff, pulse oximeter) and the subjective rating scales are explained. Testing procedures are explained and demonstrated; the patient has an opportunity to answer questions.

General Procedures Unnecessary conversation and interaction with the patient is kept to a minimum throughout all stages of the test, in cluding postexercise recovery, to optimize the validity of the measurements and the test results overall. Resting baseline measures are taken over 5 minutes or ulltil they have plateaued. Patient stands

011

treadmill or sits erect on cycle ergometer with feet securely strapped into place on the pedals; the

metatarsal heads should be positioned comfortably over the pedals. Patient uses two fingers for balance on one side if possible when walking on the treadmill rather than a hand grip, or ir on the ergometer, not the excessively grasp the handle bar. Additional baseline measures are recorded in this position for 2 to 3 minutes or until the baseline is stable. The test timer is started. The warm-up portion of the protocol begins. The selected protocol is calTied out. Patient is monitored objectively and subjectively at least every couple of minutes throughout all stages of the test. in cluding postexercise recovery. The test is terminated when the preset exercise test termination criteria or any of the criteria for prematurely terminat ing an exercise test are reached. The cooldown begins. When the cooldown portion of the protocol is complete, the patient moves to the supported chair for the postexercise recovery phase with legs slightly elevated and uncrossed. Postexercise recovery continues until resting baseline measures have been reached or are within 5% to 10%. Obtain a report from patient about how patient feels. Disconnect the monitoring equipment. Continue to observe patient for any untoward postexercise signs or symptoms.

heavy actIVItIes. One limitation of such charts on

Monitoring

metabolic costs of various activities and exercise is

Common variables measured during an exercise test in

that they can only be used as a rough g uide in pa

clude HR, ECG, systolic and diastolic BP, RPP, RR,

tients with cardiopulmonary compromise, as they do

Sa02 and subjective responses such as perceived exer

not take into consideration the increased work of

tion, breathlessness, discomfort, pain, and fatigue. Mea

breathing and work of the heart observed in patients

sures are taken every few minutes after the patient has

with cardiopulmonary dysfunction.

been exercising at a given intensity for a few minutes.


286

PART III


Criteria/or Prematurely Terminating an Exercise Test Miscellaneous Wish of individual for any reason Failure of monitoring equipment

General Signs and Symptoms Fatigue Lightheadedness, confusion, ataxia, pallor. cyanosis, dyspnea, nausea, or peripheral vascular insufficiency Onset of angina

ECG Signs Symptomatic supraventricular tachycardia ST displacement (3

mm) horizontal or downsloping from rest

Ventricular tachycardia Exercise-induced left bundle branch block Onset of second- or third-degree atrioventricular block R=wave on T=wave premature ventricular contractions (one) Frequent multifocal premature ventricular contractions (frequent runs of three

or

more)

Atrial fibrillation when absent at rest Appearance of a Q wave

Cardiovascular Signs Any fall in blood pressure below the resting level Exercise hypotension

(> 20 mm Hg drop in systolic blood pressure)

Excessive blood pressure increase (systolic

220 or diastolic

110 111111 Hg)

Inappropriate bradycardia (drop in heart rate greater than 10 beats/minute with increase or no change ill work load)

Adapted from the American College of Sports Medicine, (1994). Guidelines for exercise testing and prescription. (6th ed.). Philadelphia: Williams and Wilkins.

Adapted from Jones, N.L. (1988). Clinical Exercise Testing. (3rd Ed.). Philadelphia: WE Saunders.

Exercise Training Prescription

tion of the heart rate response, or some other response,

One of the most conunon indications for exercise test

to a maximum or near maximum work i'ate that was

ing is to establish whether a training program is indi

safely tolerated during the exercise test. The training in

cated and, if so, what the training parameters should be.

tensity for a patient who is able to tolerate several in

The components of exercise training for patients is the

cremental work stages on a graded exercise test may be

same as for healthy people, specifically, selection of the

optimal between 70% to 85% of the peak heart rate

type of exercise. and its intensity, duration, and fre

achieved in the test. A patient who is unable to tolerate

quency; and the course of training and its progression.

a couple of increases in work stage, is more likely to

The selection of the type of exercise for training and

benefit from an exercise intensity range of 60% to 75%

that used in the exercise test, is based on the objectives

of the peak heart rate achieved. In some patients. heart

of training. The intensity is usually set at some propor

rate is an invalid indicator of exercise intensity either


17


Exercise Test Data Sheet for Treadmill

Exercise Test Data Sheet for a Walk Test

or Ergometer

on a Circuit

Patient name:

Patient name:

Patient number:

Patient number:

Date:

Date: Weight (kg)

Weight (kg)

Height (em)

Height (cm) Body mass index

Body mass index Reason for test:

FEY\

Reason for test:

Type of test:

Fye FEY\lFye

FEY\ Fye

Type of test:

FEY/Fye

Minute

287

Work rate

Minute

HR BP RPP RR Sa02 RPE

speed/grade

Work rate

HR BP RPP RR Sao2 RPE

speed/grade

(work/rpm)

(work/rpm)

o

o

2

2

I

3

3

4

4

5

5

6

6

Review of preexercise checklist

Review of preexercise checklist

Level of hand support

Level of hand support

Use of orthoses: type and side

Use of orthoses: type and side

How often docs the patient experience the level of

How often does the patient expelience the level of

exertion reached in the test (e.g., lx/ wee k ,

exertion r e a c h e d in t h e test (e.g., I x/week,

lx/month, 3x/day. etc.)

lx/month. 3x/day. etc.)

Reason for test termination

NOTE:

Reason for test termination

'Relevant notes and comments include abnormal ECG

NOTE:

'Relevant notes and comments i nclude abnormal ECG

changes, comments by patient, observations about coordination,

changes, comments by patient, observations about coordination,

and anxiety.

and anxiety.


I\) CD CD

Functional class

Clinical status

02 cost ml/kg/minute

::0 >-l -

Bicycle

Bruce 1 Watt 60 KPDS 3=minute stages mph %Gr For =

2::-

:

u

Normal and 1

0 Q) C> 0 c 0

56.0

C

52.5 49.0 45.5 42.0

-£

38.5

1-

35.0

>.. -£ -0

31.5

28.0

Q) ...r:::.

r->..

24.5

\..

2 3 4

5.5

.2

c Q) \J Q) V)

"] 'E

u 0"5

E .2

Cl..

E

-

>--V)

21.0

17.5

16 15

14

13

12 11

10 9 8 7

6

5

14.0 10.5

4

3.5

1

7.0

3

2

KPDS 1500 1350 1200 1050 900 750

600 450 300

150

5.0

%Gr at 3.3 MPH

1 20

4.2

1

18

1 16

3.4

1

2.5

1

14 12

1.7 1 10

1 1.7 1 1.7

5

Balke Ware

Kattus

ETS

"slow" Ellestad USAFSam McHENRY Stanford USAFSam 3/2/3= minute stages

Imph %Gr 4

1

4 4

1 18 1 14

4

1 10

3

1 1

2

6

1

15 mph %Gr

21 20 19 18 17 16 15 14 13 12 11 10 9 8 7 6 5 4 3 2

5

1

15

5

1 10

23 22

22

10 10 l-

I

0

4

1 10

3

1

1.7

10

1 10

o·

"0 =

3"

o ::J ., '<

-

26 25 24

3.3

1 25

3.3

1

3.3

l 15

mph %Gr

3.3

1 10

3.3

1

5

1 21 3.3 1 18 22.5 20.0 3.31 15 t---

mph %Gr

2

1 25 1 20 1 15 1 10

1

5

1

0

2 2 2

3.3

1

0

2

2.0

1

0

2

1 3.3 1 3.3 1

33 .

20 .

1

17.5 12 1 15.0

9 12.5 10.0 6 7.5 14

5.0 10.5 2.5 7

3

0.0 3.5

FIGURE 17-2 permission from Froehlicher YF: Exercise and the heart, ed 2, Chicago, 1987, Year-Book.)


'" ;:;. e:.. >-l

"0 '< ::J

-.lL -.!L.. 8

7

6

5

4

3 1

Oxygen cost of work stages of some commonly used exercise test protocols. (Reprinted with

'<

::J" ... .,

33 .

20

(j ., Q.

%Gr %Gr at at 2 3 mph mph

2=or3= minute stages

1 =minute stages mph %Gr

};

Q) \J c Q) Cl.. Q) \J >..

:c

70 kg bod weig t

-

Treadmill protocols

METS ergometer

" ., 0( ...

a o· 5l

17


FIGURE 17-3 Energy cost in METS of activity and exercise. (From Underhill, SL

et

at: Cardiac nursing, ed 2,

Philadelphia, 1989, JB Lippincott.)

9 METs

10 + METs Swimming (crawl,55 yard/minute Skiing, fast downhill Walking up hill,5 mph

8 METs

7 METs

Cycling, 13 MPH Swimming, 40 + yard/ minute Level ski touring, 4 MPH Cross-country running Walking on level,5 to 6 mph

6 METs

5 METs

Shoveling snow Digging vigorously Sawing wood Tennis Skiing Walking on level, 5 mph

4 METs

3 METs

Self-care washing dressing

Gardening (weeding) Ballroom dancing Canoeing, golF Bedmaking Woodworking (drilling, sawing) Walking on level ground, 4 mph

2 METs

Light calisthenics Driving (can be more MET under stressful conditions) light housework (sweeping, ironing, mopping) Walking, 2.2 mph

1 MET Resting Eating Writing Handsewing Knitting

Very light activity

Light activity

Moderate to heavy activity


289

Very heavy activity

290

PART 1II


Oxygen Cost Diagram Used to Assess

Patient's Check List Before Exercise Testing or

Breathlessness on Exertion

Training Session

Brisk walking uphill

Feeling well over the past 48 hours

Medium walking uphill

No cold or influenza No temperature

Brisk walking on the level Slow walking uphill

No unaccustomed muscle or joint discomf0l1 or pain Heavy shopping

No chest tightness or pain

Medium walking

No unaccustomed breathing difficulty or fatigue Adequate night's sleep

Bedlllaking

Have not eaten heav i ly within past 3 hours

Light shopping

Best time of day

Washing yourself Slow walking on the level

Wearing or using orthoses, walking aids. and devices

Sitting

Clothing appropriate for exercise conditions. such as indoors

Standing

well-fitting and secured laces
o

Have water within reach Taken preexercise medications at specified time

M, Naoe H, and McHardy GJR: Dysp

nea, disability, and distance walked: Comparison of estimates of ex ercise performance in respiratory disease. 8M}

outdoors

Appropriate socks and footwear that is comfonable.

Sleeping

From McGavin CR, Anvinli

or

Have nitroglycerine within reach (cardiac patients)

1:822-823, 1978.

Have inhaler within reach (pulmonary patients) Have sugar supply within reach (diabetics)

because of the pathology or medications (Dean, 1993;

ExerCise Training

Dean and Ross, I 992b). Thus other responses such as

General procedures

blood pressure, arterial saturation, or subjective para rating of perceived exertion or breath

Before an exercise session, the patient needs to review

lessness can be used. The duration and frequency of the

a checklist to ensure that exercise is not contraindi

exercise program are established based on the patient's

cated on that day. This is particularly important for

meters such

as

functional capacity, physiological reserve capacity and

patients whose conditions change rapidly or whose

exercise responses (see Table 17-2, for general guide

disease course tends to fluctuate, such as multiple

lines). Patients with low functional capacities but with

sclerosis, cystic fibrosis, and chronic fatigue syn

adequate physiologic reserve capacity respond to a

drome. The box above includes guidelines in prepara

training stimulus quickly (short training course), thus

tion for exercise testing and training sessions. Such a

need to be progressed accordingly. Patients with low

checklist, however, must be tailored to each patient.

functional capacities, however, with limited physio

Specific procedures

logic reserve capacity, adapt more slowly (long training course). The shorter the training course, the sooner a

In the supervised setting, the general procedures

retest is indicated to progress and reset the training pa

used in exercise training are comparable to those

rameters. To ensure that the patient continues to be

used for testing. Specifically, the patient prepares

trained safely and optimally, the training parameters

for the training session in a standardized manner,

should be progressed based on an exercise retest.

and is monitored according to his or her condition.


17

The components of the session are the same with re spect to a warm-up, cool-down, and recovery. The main part of the exercise program, however, will usually be steady-rate or interrupted exercise. Vary ing work rates may be indicated for some patients. In the majority of situations, the goal is to transfer the responsibility of surveillance and monitoring from the PT to the patient. Depending on the pa tient's pathology and ability to learn how to monitor


291

Physiological Consequences of Bed Rest I. Fluid volume redistribution Decreased plasma and blood volume Decreased total heart and left ventricular volumes Increased hematocrit and hemoglobin Diuresis and natriuresis

II. Muscular inactivity

exercise responses accurately, this process may take

Insulin resistance

varying amounts of time.

Loss of muscle mass

Monitoring

Loss of muscle strength

L(lSS of muscle endurance

For safety reasons and ensuring that the patient is

III. Altered distribution of weight and pressure

within the target training range of the variables selected

Venous stasis

to set exercise intensity, the patient must be closely

Urine stasis, retention. tendency toward calculus

monitored. This is particularly true if the patient has

formation

any risk of untoward or adverse reactions to exercise. If

Hyperca1ciuria

patients are considered to be at any fisk, then exercise training should only take place in a supervised setting. Stable patients may begin an exercise program in a su pervised setting, but with training and education they usually can be transfelTed to an unsupervised setting. Education includes self monitoring of exercise re sponses, maintaining exercise intensity within the ap

Bone demineralization

Local skin changes

IV. Mixed or unknown etiology Increased heart rate at rest and at all levels of activity Decreased resting and maximum stroke volume

propriate limits, and keeping a record of the details of

Decreased maximum cardiac output

their exercise sessions. When the patient is safely carry

Increased venous compliance

ing out the exercise program independently in the com

Increased risk of venous thrombosis and throm

munity some mechanism is needed to follow-up on the patient's progress. If the objective is continued condi tioning, then the patient needs to be rescheduled for a retest. If the patient is on a maintenance program, the PT is responsible for reminders about exercise and in

boembolism Decreased orthostatic tolerance Cardiovascular deconditioning Decreased V02 max

jury precautions, and notifying the PT or physician if

Anorexia

significant adverse effects are observed.

Constipation Increased sensitivity to thermal stimuli; increased sweating and hyperemia

PRESCRIPTION OF MOBILIZATION AND EXERCISE:

Alteration in clearance of some drugs

PREVENTATIVE EFFECTS

Increased anxiety, hostility, depression

Humans are designed to be upright and moving. When they are recumbent and inactive, gravitational stress (the vertical gravitational gradient) and exer cise stress are removed. Bed rest is one of the most

Increased auditory threshold Increase in focal point. decreased near point of visual acuity

commonly used yet unquestioned therapeutic prac tices. Despite its widespread acceptance, the body po

From Underhill SL. Woods SL. Froehlicher ES, and Halpenny

sitions it promotes, namely, being supine and immo-

Cardiac 1Illl'.I'illg,


ed 2. Philadelphia,

1989,18

Lippincotl.

CJ:

292

PART III


bile, is nonphysiologic (Chapter 18). The harmful se

1951). Thus alveolar-arterial oxygen difference and

quelae of this posture have been well-documented

arterial oxygen tension are reduced during periods

(Dean and Ross, I 992b) yet the more severely ill the

of bed rest (Cardus, 1967; Clauss, Scalabrini, Ray,

patient, the more-confined that individual is to the

and Reed, 1968; Ray et aI, 1974). Closing volumes

bed, and the greater the risk of multisystem complica

are increased precipitating arterial desaturation in

tions (see box on p. 291).

recumbent positions.

The immediate effects of immobility that are ob

Cardiovascular sequelae of prolonged recumbency

served are those associated with recumbency; these

include an increase in resting and submaximal heart

are followed within 24 to 48 hours by cardiopul

rate (Deitrick, Whedon, and Shorr, 1948), a decrease

monary and musculoskeletal changes. Within 24

in maximum oxygen uptake (Saltin et ai, 1968), and a

hours, significant fluid shifts occur and blood vol

decrease in total blood volume, plasma volume, and

ume is reduced by 10% to 15%. Within days, these

hematocrit (Deitrick et aI, 1948; Saltin et aI, 1968;

effects can significantly impair oxygen transport.

Friman, 1979). The combination of an increase in

These systemic effects are more profound in pre

blood viscosity and a decrease in venous blood tlow

mature infants, young and older people, smokers,

results in an increased risk of thromboemboli (Lentz,

obese and deconditioned individuals. These effects

1981; Wenger, 1982).

are further compounded when a patient has either

Musculoskeletal changes that occur with bed rest

primary or secondary cardiopulmonary and cardio

deconditioning include loss of muscle mass and

vascular compromise. The less aerobically fit an

strength, muscle and ligament shortening, joint contrac

individual, the less physiological reserve is avail

tures, skin lesions, and decubitus ulcers (Rubin, 1988).

able in the cardiopulmonary and cardiovascular

CNS changes include slowed electrical activity of

systems. In the event of a medical or surgical in

the brain, emotional and behavioral changes, slowed

sult, such a patient will have an increased risk of

reaction times, sleep disturbances, and impaired psy

morbidity and mortality than a more fit counter

chomotor performance (Rubin, 1988; Ryback, Lewis,

part. Thus tl1e importance of aerobic fitness cannot

and Lessard, 1971; Zubeck and MacNeil, 1966).

be overemphasized.

Metabolic changes that occur during periods of

A primary effect of mobilization and exercise on

bed rest include reduced insulin sensitivity and glu

the cardiopulmonary system is enhanced mucocililary

cose intolerance (Mikines, 1991), increased calcium

transport and clearance (Wolff, Dolovich, Obminski,

excretion from bone loss and increased nitrogen ex

and Newhouse, 1 977). Frequent body position

cretion secondary to protein loss from atrophying

changes are essential to maintain optimal bronchial

muscle (Deitrick et ai, 1948; Donaldson, Huliey, and

hygiene and avoidance of pooling and stagnation of

McMillan, 1969; Hulley, Vogel, Donaldson, Bayers,

bronchial secretions, hence, airway obstruction and

Friedman, and Rosen, 1971).

airt10w resistance (Chapter 18).

Bed rest has been associated with a reduction in

The primary effects of bed rest on the cardiopul monary system result from recumbency. Pulmonary

antibody counts, hence an increased risk of infection (Ahlinder, Birke, Norberg, and Plantin, 1970).

sequelae of recumbency included reduced lung vol

Of clinical significance is the fact that car

umes and capacities, particularly functional residual

diopulmonary and cardiovascular deterioration

capacity (FRC), residual volumes (RV) and forced

occur at a faster rate than musculoskeletal deterio ' ration, and that the rate of recovery from the ill ef

expiratory volumes (FEVs) (Blair and Hickman, 1955; Craig, Wahba, Don, Couture, and Becklake,

fects of bed rest is generalJ y slower than the rate of

1971; Hsu and Hickey, 1976; Powers, 1944; Risser,

impairment (Kottke, 1966; Sandler, Popp, and Har

1980; Svanberg, 1957). A reduction in FRC in

rison, 1988).

supine position compared with the sitting position

The negative effects of bed rest are accentuated in

has been attributed to both a decrease in thoracic

older adults (Harper and Lyles, 1988), and are likely

volume and an increase in thoracic blood volume,

to further compound the oxygen transport and other

hence pulmonary venous engorgement (Sjostrand,

deficits of patients with pathology.


17


293

tural alignment, stiffness, and soreness. Bed rest allo

HAZARDS OF BED REST The literature on the negative sequelae of bed rest has been unequivocal for 50 years (Chobanian, et aI., 1974; Dean and Ross, 1992b; Dock, 1944; Harrison, 1944; Ross and Dean, 1989). Thus the use of bed rest as a primary medical intervention requires consider able justification. The recumbent, immobile positions associated with bed rest adversely affect every organ system and palticularly compromise oxygen transport by its direct negative effects on the cardiopulmonary and cardiovascular systems. This is particularly signifi cant in that in conventional patient management there is a direct relationship between how sick the patient is and the amount of time confined to bed. In addition, the musculoskeletal and neurological systems are ad versely affected. The cardiovascular sequelae of bed rest primarily include the loss of fluid volume regulating mecha nisms, diuresis, and loss of plasma volume. In turn, the hematocrit is increased, and the risk of develop ing deep vein thromboses and thromboemboli is in creased. This is exacerbated by increases in blood viscosity, platelet count, platelet stickiness, plasma fibrinogen (Browse, 1965), and stasis of venous blood flow. The work of the heart is increased in the immobile, recumbent patient as is the work of breath

cates various body parts to being weight bearing. Skin breakdown most commonly occurs over boney prominences such as the sacrum, trochanters, elbows, scapulae, and heels. Muscles imbalance may result from poor postural alignment. Patients are at risk of bone demineralization. Of particular importance in older populations, patients with disabilities, post menopausal women, and patients on steroids is cal cium loss secondary to bed rest or sedentary lifestyle. Bed rest affects psychological status. Patients may become depressed, sensorily deprived, or develop a psychoneurosis with prolonged bed rest. The evidence supports the following: I. Evidence supporting the wide spread use of bed

rest as a therapeutic intervention is lacking. 2. Currently the use of bed rest is excessive and nonspecific. 3. Bed rest has multisystem negative effects and therefore must be used judiciously and specifically. 4. Alternative means of managing very ill pa tients, such as those in the intensive care, must be developed.

ALTERNATIVES TO THE NONSPECIFIC USE OF BED REST

ing. The work of the heart is increased as a result of

With respect to developing alternative means of man

the increased filling pressures and heart rate associ

aging very ill patients rather than in the recumbent

ated with recumbency, and increased blood viscosity.

immobile positions, physical therapists need to be

The work of breathing is increased by the decreased

come vocal in designing furniture and devices that

lung volumes secondary to visceral encroachment on

are better suited to the patient's normal physiologic

the underside of the diaphragm, increased intratho

functioning and to the needs of that patient's course

racic blood volume, and restricted chest wall motion.

of recovery. Such appliances would include a greater

With bed rest, the blood vessels of the muscles and

number of neurologic and cardiac chairs in ICUs,

splanchnic circulation dilate. With prolonged bed rest,

which enable easy transfer of patients from bed to

they may lose their ability to constrict. The ability of

chair and upright positioning, greater availability of

these vessels to constrict is essential to prevent the

patient-lifting devices, and increased number of or

pooling of blood and maintain circulating blood vol

derlies to assist with moving patients.

ume in the upright position. Thus following bed rest, a patient may feel lightheaded or dizzy, or may faint.

Rotating beds are electromechanical beds that turn the patient through an arc of about 30 degrees to ei

With only a few days of bed rest, skeletal muscle

ther side from supine over a 3-minute period (Schim

atrophies leading to weakness, discoordination and

mel, Civetta, and Kirby, 1977). These beds are used

balance difficulty (Lentz, 1981; Saltin, et aI., 1968).

for heavy care critically ill patients who are unable to

With severe weakness, excessive strain may b e

turn themselves or are difficult to turn. Even though

placed o n ligaments and joints. The limited position

studies have shown these beds can enhance oxygena

ing alternatives in bed may contribute to poor pos

tion in severely c o m promised patients such a s


294

PART III


patients with adult respiratory distress syndrome

agement of such patients. However, 30 years ago re

(Summer, Curry, Haponik, Nelson, and Elston, 1989;

striction to a chair was reported to be significantly

Yarnel, Helbock, and Schwiter, 1986), they need to

more beneficial than restriction to bed in heart dis

be used selectively to avoid reliance on passive posi

ease patients (Levine and Lowe, 1954). Despite this

tioning with the bed vs. more active and active as

finding, many coronary patients continue to recline in

sisted patient positioning.

beds rather than chairs. Mobilizing coronary patients

The use of tilt tables to promote mobilization can be

and permitting bathroom privileges has also been re

hazardous in that leg movement is minimal. Passive

ported to be less stressful than being confined to bed

standing on a tilt table constitutes a greater physiologi

and having to use

a

bedpan (Andreoli et ai, 1994).

cal stress than active standing. Upright sitting postures with the legs dependent may elicit greater physiologi cal benefit than passive standing with less risk.

Prescription of an Adequate Stimulus to Elicit the Preventative Effects of Exercise Although much is known about the protective bene

INDICATIONS FOR BED REST

fits of cardiopulmonary fitness and conditioning and

Despite the uni versal acceptance of bed rest as a

about the negative effects of bed rest and immobility,

medical therapeutic intervention, indications for its

little has been documented about defining the appro

therapeutic use have not been documented. FUlther

priate exercise stimulus to optimize the preventive ef

more, considerably more is known about the adverse

fects of exercise for a given patient. The preventive

and potentially life-threatening hazards of bed rest

effects of an exercise stimulus can be defined as that

than about its potential benefits. Bed rest should

exercise dose that will maintain the patient's condi

clearly be used as selectively as other medical inter

tioning level and prevent deterioration. At present,

ventions to ensure that specific benefits are being de

the presCliption of preventative mobilization and ex

rived and the multisystemic negative sequelae are

ercise is nonspecific. Research is needed to make ex

being minimized. Many procedures such as surgery

ercise prescription for the preventative effects of ex

are associated with considerable pain, thus being rel

ercise more scientifically based. For example, the

atively immobile and recumbent in bed is believed to

following questions need to be answered:

minimize postsurgical discomfort. In some cases,

•

however, relative immobilization rather than confine ment to bed may offer the same benefits without the

How do different types of exercise compare with respect to preventative aspects? Does exercising in some body positions elicit

•

dire risks. Patients who are severely limited are phys

better preventive effects than other body

ically supported by a bed and do not have to work

positions?

against the force of gravity. Minimizing the effects of gravity and the need to weight bear is often indicated

•

What principles establish which exercise intensity

•

What principles establish how often the patient

and duration are best?

in patients following orthopedic surgery. The bed en ables a patient with multiple wounds and fractures to be immobilized and supported in a fixed position that

should be mobilized or should petform exercise?

is believed to promote healing. Conditions that are

The question arises as to what constitutes an ade

associated with edema require minimizing the effect

quate stimulus to maximize the preventive effects of

of gravity on the affected limbs. Whether edema can

exercise for a given patient. Although the preventive

be controlled by localized elevation rather than bed

effects of exercise are accepted, this important ques

rest must be established. Some conditions particularly

tion has not been adequately researched. Some gen

in the acute stages to reduce the work of the heart,

eral practices, however, have become accepted clini

such as MI, require some activity restriction, thus the

cally. These include turning patients. The turning

use of the bed has been a mainstay of the early man

frequency that is widely accepted is every 2 hours.


17


295

There is no literature, however, to support greater

individual steps in the oxygen transport pathway

preventive effects turning a patient every 2 hours vs.

that are primarily affected, and oxygen transport as

hourly or every 4 hours. Sitting up and ambulation

a whole, such as oxygen delivery, oxygen consump

are two other practices that are also widely used. The

tion, and oxygen extraction at the tissue level, are

timing of these interventions, however, is often based

fundamental. Of considerable clinical relevance is

on convenience and what else may be happening with

the adequacy of tissue oxygenation; however, to

the patient, or on a once or twice daily regimen rather

date, there are no clinically expedient means of as

than on a prescriptive basis. Patients who are sitting

sessing tissue oxygenation.

or walking for preventive reasons often assume sub optimal and even deleterious slumped or malaligned postures. Patients and their caregivers need to be re

SUMMARY

minded about the importance of proper body position

This chapter described three distinct goals associated

at all times and be provided with appropriately sup

with the prescription of mobilization and exercise in

ported chairs, firm bolsters, and adjustable beds that

the management of impaired oxygen transport,

maintain optimal body positions.

namely, to exploit their acute, long-term, and preven

Like exercise prescribed for its beneficial acute and

tive effects.

long-term effects, exercise to elicit its optimal preven

The PT needs a comprehensive and detailed un

tive effects should be prescribed based on the individ

derstanding of how mobilization and exercise have

ual (e.g., age; premorbid functional work capacity; the

potent and direct effects on oxygen transport acutely,

type, distribution, and severity of disease; and within

in the long-term, and preventively. The specific mo

capabilities of patient). Such preventive mobilization

bilization or exercise prescription is based on a com

or exercise must also be prescribed to avoid any dele

prehensive multisystem assessment and the treatment

terious effects on the patient's overall condition.

goals for a given patient. If the acute effects of mobi

Frequent ambulation constitutes preventive exer

lization or exercise on oxygen transport are indicated,

cise. Provided the patient does not require undue

the prescription specifies the parameters of an appro

monitoring and has been cleared as a risk, preventive

priate mobilization or exercise stimulus, lIsually, of

exercise can be encouraged by all team members.

relatively low intensity, shOtt duration and high fre

This role of exercise is quite distinct and separate

quency. The treatment effects are often immediate.

from the therapeutic interventions of mobilization

Because treatment responses can be dramatic, the

and exercise for their specific acute and long-term ef

prescription is progressed relatively quickly based on

fects that are prescribed for the remediation of acute

the treatment response measures. Prescribing mobi

and chronic cardiopulmonary dysfunction. The appli

lization to remediate acute cardiopulmonary dysfunc

cation of mobilization and exercise for optimizing

tion requires the same precision and specificity as

oxygen transpott is the specific expertise and within

prescribing exercise for chronic cardiopulmonary

the unique domain of the PT.

dysfunction. If the long-term effects of exercise are indicated, the exercise stimulus is defined in an ap propriate prescription, i.e., generally higher intensity,

ASSESSMENT OF MOBILIZATION

longer duration, and less frequent compared with the

AND EXERCISE RESPONSES

/

prescription for the acute effects, and designed to be

To prescribe mobilization and exercise for optimal

followed for several weeks or more before significant

therapeutic effect, resting baseline measures of rele

physiologic adaptation can be observed and progres

vant physiologic oxygen transport responses need to

sion of the stimulus is indicated. If the preventive ef

be recorded so that any perturbation of oxygen

fects of mobilization or exercise are required, then

transport and homeostasis caused by exercise can be

the prescription focuses on maximizing these benefits

identified. Measures that rencct the function of the

for a given patient by prescribing exercise, that is of


PART III

296


sufficient intensity, duration, and frequency, to pre serve adequate aerobic capacity and endurance for a given patient. The principles for prescribing mobi lization and exercise for their optimal preventive ef fects have not been scientifically elucidated. These three levels of prescription of mobilization and exer cise are physiologically distinct and need to be pre scribed specifically for each patient.

Borg, G. (1982). Psychophysical basis of perceived exertion. Med ical Science in Sports and Exercise,

Borg, G.A.V.

(1970).

exertion. Scandinavian Journal of Rehabili/ation Medicine.

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Browse, N.L. (1965). The Physioiogy lind Pa/hol08Y of Bed Res/.

C. Thomas. Publisher J. (1974). Influence of body position

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02

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REVIEW QUESTIONS

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(j( Applied

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changes

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Rowell, L.B. (1966). Independence of

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prolonged bed rcst. Aerospace Medicine. 17, 1232-1237. Chobanian, A.V., Lillc, RD., Tercyak,A., Blevins, P (1974). The metabolic and hemodynamic cfT('cts of prolonged bed rest in

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Chase, G.A., Grave,

(2) chronic effects, and

normal subj ects . Circulation, Clauss, R.H.,

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551-559.

B.Y . , Ray,J.F.,

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37

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Compton, D.M., Eisenman, P.A., and Henderson, H.L. (1989). Ex ercise and fitness for persons with disabilities. Sports Medicine, 7,150-162.

(3) preventive effects. 4. Explain the effects of mobilization on enhancing the efficiency of oxygen transport. S. Explain the effects of exercise on enhancing the efficiency of oxygen transport.

Convertino, V.A., Hung, J .. Goldwater, D., and DeBusk, R.F. (1982). Cardiovascular responses 10 exercise in middle-aged men after 10 days of bedrest. Circulation,

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Orlava, O.E. (1959). Therapeutic physical culture in the complex

treatment of pneumonia. Physical Therapy Review, 39, 153-160.

& Likoff, M..r. ( 1 9 83)

.

The cardiopulmonary unit: the body's gas transport system. Clinics in Chest Medicine, 4,101-110.

surgery. Journal of the American Medical Associalion, 125,

Weissman, c., Kemper, M., Damask, M.C, Askanazi, J., Hyman, A.l., & Kinney, J.M. (1984). Effect of routine intensive care in teractions on metabolic rate. Chest, 86,8 I 5-8 I 8.

1079-1083.

Wenger, N.K. (1982). Early ambulation: The physiologic basis re

Powers. J.H. (1944). The abuse of rest as a therapeutic measure in

Pyne, D.B. (1994). Regulation of neutrophil Function during exer cise. Sports Medicine,

17, 245-258.

Ray, J.F., Yost, L., Moallem, S., Sanoudos, G.M., Villamena, P., Paredes, R.M.,

visitcd. Advances in Cardiology,

31, 138-141.

West, J.B. (1995). Respiratory Pilysiology-The Essentials. Balti

& Clauss, R.H. (1974). Immobility, hypoxemia,

and pulmonary arteriovenous shunting. Archives of Surgery,

more: Williams

& Wilkins.

Winslow, E.H. (1985). Cardiovascular consequences of bed rest. Heort Lung. 14,236-246.

109,537-541.


298

PART III


Wolff, R.K., Dolovich, M.B, Obminski, G , & Newhollse, M.T.

Osciilating Therapy: Research and Practical Applicaliol1s.

(1977). Effects of exercise and eucapnic hyperventilation on bronchial clearance in man. Journal of Applied Physiology, 43,

Miami: University of Miami Pr ",. Zadai, c.c. (ed). (1992). Pulmonary Management in Physical

46-50.

Therapy. New York: Churchill Livingstone.

Yarnel, l.R. Helbock, M., & Schwiter, E.1. (1986). Rotorest kinetic

Zubeck, J.P., & MacNeil, M. (1966). Effects of immobilization:

treatment table (Rotobed) in patients with acute respiratory

behavioural and EEG changes. Canadiall Journal of Psvchol

failure. In: Green, B.A., & Summer, W.R. (eds.). C ontil1uous

ogy, 20, 316-336.


Body Positioning Elizabeth Dean

KEY TERMS

Cardiopulmonary function

Prescriptive body positioning

Gravity

Routine body positioning

Oxygen transport

INTRODUCTION

prescriptions, because no specific patient is being con

The purpose of this chapter is threefold. First, thera

sidered. Understanding the physiological effects of

peutic body positioning, which is prescribed to opti

body position on oxygen transport and how patho

mize cardiopulmonary function and oxygeQ transport

physiology disrupts these normal processes is funda

is differentiated from routine

mental to prescribing body positioning. However, an

dY'l'ositioning. Sec

ond, the physiological effects of different body posi

optimal body position can only be prescribed based on

tions and changing body positions on cardiopulmonary

consideration of all the factors that impact on oxygen

function and oxygen transport, are described. And

transport, that is, effects of the patient's pathophysiol

third, the prescription of therapeutic body positioning

ogy and its specific presentation in that individual, the

is described. Body positions that simulate normal

effect of immobility, the effect of extrinsic factors re

physiological effects of gravity and position change on

lated to the patient's care and the effect of intrinsic

oxygen transport are the priority, that is, being upright

factors related to the patient (Chapter

and moving. A hierarchy of body positions ranging

an integrated analysis of these factors collectively that

from the most to the least physiological is presented. scribing therapeutic body positioning and body posi

(1) the most beneficial body positions can be pre (2) the least beneficial body positions can be identified and used minimally, and (3) the appropriate

tion changes. The chapter does not provide treatment

treatment outcome measures can be selected.

This chapter concentrates on the principles of pre

IS). It is only by

dicted,

299


300

PART III


GRAVITY AND NORMAL PHYSIOLOGIC FUNCTION: IMPLICATIONS FOR CARDIOPULMONARY PHYSICAL THERAPY The human is an orthograde animal. From moment to

-

J

O

-fl .> '0

(%)

moment, gravity exerts its influence on the human

(L minute)

body and importantly on oxygen transport. The com bined effects of gravity on the lungs, hea11, and pe ripheral circulation is central to their interdependent

I II / / I

Knowledge of the effects of gravity on cardiopul monary function in health and the deleterious effects of pathophysiological states on cardiopulmonary func tion provide a foundation for the clinical application of body positioning as a primary therapeutic interven tent and direct effect

011

oxygen transport, therapeutic

13

N O

N

Z 0....

u 0....

t0 U

therapy intervention that can augment arterial oxy genation so that invasive, mechanical, and pharmaco logical forms of respiratory support can be postponed,

/r-",

I\

\

I

I' t

" \

.\

\ \

\

\ f\ \ '\ / \ 1\

\

.82 1.29 0.63 89 1'42 582 19.21149 739 60 39 /' "'::j J.- \�..... V / "I "\ I

7

A patient is continually exposed to gravity, thus

be improved, maintained or worsened with changes in body position. Despite being essential to normal car diopulmonalY function, gravity is the principal contribu tor to signjficant inhomogeneity of physiological func tion down the lungs (West,

1995). Figure

8

\

I \ \

1'0

the singlemost important objec

gravity on oxygen transport, thus, oxygen transport can

U

in out (ml/minut

tive of cardiopulmonary physical therapy. every position the patient assumes reflects the effect of

0

N 0

:r: 0..

content (mil 100 ml)

(mm Hg)

/

N o

__

body positioning is a primary noninvasive physical

reduced, or avoided

N

o 0....

7 .24 .07 3.3 132 28 553 200 42 751 4

function and establishing normal oxygen transport.

tion to optimize oxygen transport. Because of its po

""-

. :;;

FIGURE 18-1 Regional physiologic differences down the upright lung.

VA

=

alveolar ventilation, Q

=

perfusion, V NQ

=

ventilation perfusion ratio. (Reprinted with permission from West JB: Respiratory physiology-rhe essenrials, ed 5, Baltimore, 1995, Williams & Wilkins.)

18-] illustrates

the effect of this gradient with respect to alveolar venti

hydrostatic, gravitational and compression forces act

lation (V A), perfusion (Q), ventilation and perfusion

ing on the heart, blood volume, lymphatic system,

ratio (V A/Q), Pao2, Peo2, PN2, oxygen content, CO2

lungs, and chest waJi, including the diaphragm, wiJi

content, pH, and the flow of oxygen and CO2 in and out

eventually compromise oxygen transport, and any ben

of the lungs. Thus the lungs should not be likened to

eficial effect will be offset. Therefore monitoring is es

balloons either physiologically or anatomically.

sential to ensure the patient is turned to another posi

Based on a thorough analysis of all factors con

tion before detrimental effects are observed. Frequent

tributing to impaired oxygen transport and gas ex

changes in body position and avoidance of prolonged

change (Chapter 16), those body positions that will

periods in any single position will minimize the risk of

have an optimal effect and those that may be deleteri

diminishing returns, which are inevitable. The time

ous must be discriminated. In this way, a greater pro

course differs according to pathology, type, severity,

portion of time can be spent in beneficial positions and

and other factors. The duration a patient assumes a

response-dependent

less time spent in deleterious body positions. When

body position should be primarily

beneficial positions are assumed for too long, however,

rather than time-dependent. Knowledge of the dekteri


18

ous effects of prolonged periods in a single position

Body Positioning

301

deleterious to oxygen transport. The side-lying positions

supports the prescription of both frequent body posi

have an effect that is intermediate between upright and

tion changes and extreme consecutive body positions.

supine. The prone position which is under utilized clini

These perturbations simulate the nOimal perturbations

cally, has such a significant beneficial effect on oxygen

that the cardiopulmonary and cardiovascular systems

transport that a good rationale should be made for not

are exposed to in health during normal mobility and

incorporating this position into the treatment prescrip

body position changes. The ability to weigh the rela

tion rather than for using this position.

tive beneficial and deleterious effects of each possible

The indications for therapeutic body positioning

body position, that is, over 360 degrees in the horizon

and the indications for frequent body position changes

tal plane and 180 degrees in the vertical plane (ranging

to optimize oxygen transp0l1 are shown in the boxes

from 20 degrees head down to 20 degrees lean for

on pp. 302-303. For each of the indications listed, an

ward) on a given patient's gas exchange, is critical in

optimally therapeutic body position can be selected

prescribing body positioning therapeutically.

for a given patient. A description of the physiological effects of several primary body positions follow, namely, the upright supine, side lying, head down,

PRESCRIPTIVE VS. ROUTINE BODY POSITIONING

and prone positions. This information, howevcr, can

The literature supports the benefits of frequent body po

not be applied out of context. The specific positions

sition changes particularly for the patient who is rela

prescribed for a patient are based on a consideration

tively immobile, severely debilitated, obtunded, breath

of the multiple factors that impair oxygen transport

ing at low lung volumes, obese, aged, very young or

(Chapter 16) in conjunction with a physiological

who has lost the sigh mechanism. The practice of rou

analysis of the most justifiable positions.

tinely turning patients every 2 hours is widely accepted.

Because of the potent and direct effects of body po

This practice is based on the belief that the deletelious

sitioning on various steps in the oxygen transport path

consequences associated with assuming a static posi

way in health and in disease, it is unknown whether the

tion for a prolonged period will be prevented. Recent

beneficial effects reported with the use of postural

evidence, however, supports that more frequent turning

drainage are attributable to enhanced mucociliary

can have greater physiological benefits in criticaJiy ill

transport, or to the direct effect of positioning the good

patients (Dean and Suess, 1995) which suggests less se

lung down on improving the gas exchange of that lung,

verely ill patients may also benefit. The preventive ef

by increasing alveolar volume of the affected, nonde

fects of a routine turning regimen are distinct from the

pendent lung, or both. Typically, studies evaluating

acute effects of body positioning on oxygen transport

conventional chest physical therapy, including postural

which is the primary focus of this chapter.

drainage, have failed to control for the direct effect of body positioning on cardiopulmonary function, or for the direct effects of increased arousal and mobilization

PHYSIOLOGICAL EFFECTS OF

that occur when changing a patient's body position

DIFFERENT BODY POSITIONS

(Dean, 1994a). This is an extremely serious method

Body positioning has potent and direct effects on most

ological problem that pervades the literature evaluating

steps of the oxygen transport pathway, thus can be pre

conventional chest physical therapy, and one that

scribed to elicit these effects specifically. Because hu

needs to be considered when interpreting the results of

mans function optimally when upright and moving,

studies on these procedurers. Unless these potent con

therapeutic interventions that elicit or simulate being

founding variables are controlled, the degree to which

upright and moving (i.e., elicit both gravitational and

conventional chest physical therapy had a beneficial

exercise stress) are most justified physiologically. The

effect over and above the effects of positioning as well

recumbent supine position, a common position assumed

as mobilization and increased arousal cannot be deter

by hospitalized patients, is nonphysiological, therefore

mined (Dean, I 994b).


PART III

302


Indications/or Body Positioning To Optimize Oxygen Transport Cardiopulmonary

Facililate viscerodiaphragmatic breathing

i Regional alveolar volume i

Change the pattern of breathing

Regional ventilation

Cardiovascular

i Regional perfusion i

..l. Preload and afterload

Regional diffusion

..l. Work of the heal1

Optimize area of optimal ventilation to perfusion matching

Improve systolic ejection fraction to pulmonary and systemic circulations

..l. Pulmonary shunting i Lung volumes and capacities particularly, functional

Alter venous return

..l.

residual capacity, vital capacity and tidal volume

..l. Closure of dependent airways

astinal structures. and lymphatic system

Alter breathing frequency

Optimize t1uid shift from central to dependent areas (extremities) and vice versa to maintain nuid vol

Alter minute ventilation

ume regulating mechanisms

Alter position of the hemidiaphragms

i

Other Systemic Effects

Respiratory muscle efticiency

..l.

Airway resistance

i

Lung compliance

i

Air now rates

Optimize chest tube drainage Facilitate urinary drainage Reduce posturally increased muscle tone Facilitate patient arousal

Stimulate cough

i

Gravitational. mechanical a n d compression forces on the myocardium. great vessels, medi

Biomechanical efficiency of cough, its strength

Promote relaxation Promote comfort

and productivity

..l. Work of breathing

Control pain

Improve arterial blood gases, gas exchange and oxy

Promote biomechanically optimal body positions

genation

lntraabdominal pressure

i Mucociliary transpOit and mucus clearance

Intracranial pressure

..l. Gravitational, mechanical and compression forces on the lungs, chest wall, diaphragm and the gut

Upright Positions

exercise stimulus. The upright standing position max

The physiological position for the human organism is

imizes lung volumes and capacities with the excep

the same as the anatomical position-upright. The

tion of closing volume, which is decreased (Svan

upright positions include walking, standing, and sit

berg, 1957). Functional residual capacity (FRC), the

ting. The upright position coupled with movement

volume of air remaining in the lungs at the end of a

(e.g., walking and cycling) optimizes oxygen trans

normal expiration, is slightly greater in standing com

port to the greatest degree in that ventilation and per

pared with sitting and exceeds that in supine by ap

fusion are more uniform than without the additional

proximately 50% (Figure


18-2). Maximizing FRC is

18

Indications for Frequent Changing of Body Position

Body Positioning

303

associated with reduced airway closure and maximal arterial oxygenation (Hsu and Hickey, 1976; Ray et ai, 1974). Figure 18-3 illustrates the relationship of

Cardiopulmonary

FRC and closing capacity as a function of age. Be

Alter chest wall configuration

cause of age-related changes, closing capacity of the

Shift distribution of alveolar volume Shift distribution of ventilation Shift distribution of perfusion Shift distribution of diffusion

dependent airways increases with age; this effect is further accentuated with recumbency. Airway closure is evident in supine in the healthy 45-year-old person, and in the upright position in the healthy 65-year-old person (Leblanc, Ruff, and Milic-Emili, 1970). These

Shift distribution of ventilation to perfusion matching

effects are further accentuated in patient populations,

Shift mechanical physical compression of the heart

thus the upright position is favored and the supine po

on adjacent alveoli Shift position of the heart thereby alter chamber end disastolic filling pressures. preload, afterload, and work of the heart

sition should be minimized to prevent airway closure and impaired gas exchange. With respect to pulmonary function testing, the up right sitting position with legs dependent is the stan

Shift distribution of mucus transport and accumulation

dard reference position (American Thoracic Society,

Stimulate effective and productive cough

1987). When upright, the diameter of the main air

Facilitate lymphatic drainage Perturb pattern of monotonous tidal ventilation Alter breathing pattern Shift gravitational, mechanical and compression forces on the lungs, chest wall. diaphragm, and the gut Simulate normal inflation-deflation sigh cycles Shift intraabdominal pressure

Cardiovascular Shift gravitational. mechanical, and compression forces on the myocardium, great vessels. medi astinal structures. and lymphatic system Stimulate fluid volume shifts particularly to the de pendent limbs

Other Systemic Effects Optimize chest tube drainage

ways increases slightly. If the airways are obstructed even small degrees of airway narrowing induced by recumbency can result in significant airway resistance (Figure 18-4). The vertical gravitational gradient is maximal when upright, the anteroposterior dimension of the chest wall is the greatest, and compression of the heart and lungs is minimal (Weber, Janicki, Sllroff, and Likoff, 1983). The shortened position of the diaphragmatic fibers is countered by an increase in the neural drive to breathe in the upright position (Druz and Sharp, 1982). The distribution of ventilation is determined pri ll)arily by the effect of gravity, which changes down the lung due to the anatomical position and suspen sion of the lungs within the chest. At FRC in the up right position, the intrapleural pressures at the apex is -10 cm H20 and at the base -2.5 cm H20 (Figure 18

Promote urinary drainage

5). The intrapleural pressure is less negative in the

Shift abnormal postural tone patterns

base because of the weight of the lung. Because of

Alter arousal state Promote relaxation Promote comfort Control of pain Prevent skin breakdown, risk of infection. and re sulting positioning limitations Limit lying on a preferred side

the greater negative intrapleural pressure in the apices, thus low compliance, these lung units have a larger initial volume, thus smaller volume changes occur during respiration. Because the lung units at the base have a smaller initial volume, thus high compli ance, larger volume changes occur during respiration. Therefore depending on their relative position with respect to gravity, different regions of the lung are at different parts of the pressure volume curve.


304

PART III


Mean height Cf) 0I a:I

1.S8

m

. 300 =-- 30. , ::i'::.__ ----- SO_:s:. 0

3.5 'u '" c.

B

3.0

'" :l 1:> 'v;

'" c

2. 5

.9 U

c :l u..

2.0

Bars indicate

:!: 1

standard deviation

---1

1.5 'L.. FIGURE 18-2

Changes in functional residual capacity in various body positions. (Data reprinted with permission from Nunn JF: Applied respiratory physiology, London, 1987, Butterworths.)

3

FRC upright

FRC supine '"

.. !;

2

.. E .2

o :> at c :l -'

OJ

__

30

________

40

______

________

50

______

60

__

70

Age yearsl

FIGURE 18-3 Functional residual capacity (FRC) and closing capacity as a function of age. (Data reprinted with permission from Nunn JF: Applied respiratory physiology. London, 1987, Butterworths.)


18

Erect

Body Positioning

305

-10 em H20

Supine

Intrapleural pressure

Bronchus 100%

<1l

Mucus

50%

§

FIGURE 18-4 Effect of body position on bronchiolar diameter. (Reprinted with permission from Browse NL: The physiology and

+10

pathology of bed rest, Springfield, III. 1965, Charles C.

o

Intrapleural pressure (cmH20)

Thomas.)

FIGURE 18-5 A common clinical concern is the patient breathing

Schematic of the regional differences in ventilation down

at low lung volumes (e.g., the patient in pain, the sur

the upright lung. (Reprinted with permission from West 18:

gical patient with thoracic or abdominal incisions,

Ventilation! bloodflow and gas excfumge,

older and younger patients, obese patients, pregnant

1985, Blackwell Scientific.)

ed 4, Ox ford,

patients, patients with gastrointestinal dysfunction -4 em H20

such as paralytic ileus and ascites, organomegaly, in trathoracic and intraabdominal masses, patients who are malnourished, mechanical ventilated patients and

Intrapleural pressure

patients with spinal cord injuries. Breathing at low

(RV)

lung volumes reverses the normal intrapleural pres sure gradient such that in the upright lung the apices

�-.,100%

have a negative intrapleural pressure compared with the bases, which have a positive intrapleural pressure, that is, exceeds airway pressure (Figure 18-6). This results in the apices being more compliant, thus better

<1l

E 50% .2

ventilated than the bases. The bases are prone to air way closure in patients breathing at low lung volumes. An other f a c t o r t h a t r e v e r s e s t h e n o r m a l in trapleural pressure gradient is mechanical ventilation. Despite its necessity in the management of patients in

o

respiratory failure, mechanical ventilation contributes to hypoxemia in several ways. First, it reverses the normal intrapleural pressure gradient so that the up permost lung fields are preferentially ventilated. Be

-30

Intrapleural pressure (cmH20) FIGURE 18-6 Schematic of the regional differences in ventilation at low

cause the dependent lung fields are preferentially per

lung volumes. (Reprinted with permission from West 18:

fused, ventilation perfusion mismatch is promoted.

Ventilation/ bloodflow and gas exchange,

Positive pressure ventilation has the additional com

1985, Blackwell Scientific.)


ed 4, Oxford,

306

PART III

Cardiopulmonary Physical Therapv Interventions

of

intrathoracic pressure and re-

the recruitment of pulmonary vessels. Arterial pres

venous return and cardiac output. These fac

sure exceeds alveolar pressure and blood flow. Zone

open the

to

pressure

tors in addition to the

3, in the lower area of the

reflects the blood

valve can increase the work of

flow from the distension of pulmonary vessels; arter

associated with mechanical ventilation

ial and venous pressures exceed alveolar pressure.

and Arcos, and Hiriart, 1984).

of the

gravity is the primary determinant of in differences in the distribution of ventila tion in the

secondary to differences in lung

has minimal to no pulmonary

blood flow because of interstitial pressure acting on the pulmonary blood vessels

1995). Ventilation (V) and

and resistance

and Abboud, 1992). These effects are eXa)!,)!,CI

Both V and Q increase down

(989).

V increases disproportion

The distribution of perfusion down the upright lung is also

(Figure 18-

gravity

The pressures affecting blood flow through the pulmonary capillaries and

(Q) matchl!1g re-

of the distributons of V and Q

also contribute

populations

a compression

force

lung, imrareg ional

of

in the most

zone 4

1990;

in the

18-8). As a

ately more than Q

the

mal area for VIQ matching is in the mid zone where the ratio is about 1.0 (West,

un

The uoril!ht position is associated with

even distribution of blood flow are alveolar pressure,

effects. These effects reflect primarily

and the arterial and venous pressures. Zone 1, at the

the central blood volume that is shifted from the tho

apex, alveolar pressure predominates arterial and ve

racic compartment to the dependent venous compart

nous pressures, thus has minimal to no blood flow.

ments on

Zone 2, in the

reflects the blood flow from

the

(Blomqvist and Stone,

position from Gauer and Thron,

---+

FIGURE 18-7 Schematic of pressures affecting the pulmonary permission from West 1B:

and blood flow. (Reprinted with

VentilaliOIl/bloodjlolV and gas exchange, ed 4, Ox ford, 1985,

Blackwell


18

15

Body Positioning

3

I/minute % Lung volume

10

Blood flow 2

Ventilation 05

Rib number

BaHam

Top

FIGURE 18-8 Distributions of ventilation and blood flow down the upright lung and the distribution of ventilation perfusion matching down the upright lung. (Reprinted with pennission from West JB:

Ventilationlbloodflow and gas exchange, ed 4, Oxford, 1985, Blackwell Scientific.)

4

5°

/ ° 45

15°

6

5

Blood 4 flow ml/minute/ 3 1 00 m l 2

,

Calf

Ai

,

,

0'

Foot

FIGURE 18-9 Effect of body position on peripheral blood flow. (Reprinted with permission from Browse NL: The physiology and pathology of bed rest, Springfield, 111., 1965, Charles C. Thomas.)


307

308

PART III


Erect

Supine

Stagnant area

FIGURE 18-10 Effect of body position on drainage from the pelvis of the kidney. (Reprinted with permission from Browse NL: The physiology and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)

Sandler, \986). End diastolic and stroke volumes are

Supine Position

decreased, which results in a compensatory increase

The supine position is clearly not a physiological

in heart rate (Thandani and Parker, 1978). Cardiac

position for humans unless sleeping, and is physio

output is correspondingly decreased. The net effect of

logically the least justifiable position for ill patients

these physiological changes is a reduction in myocar

regardless of whether they exhibit cardiopulmonary

dial work (Langou, Wolfson, Olson, and Cohen,

dysfunction (Dock, 1944; Moreno and Lyons, 1961;

1977). This finding in corroborated by the observation

Powers, 1944; Winslow, 1985). The nonspecific use

that anginal threshold is increased in cardiac patients

and overwhelming acceptance of bed rest has devel

in this position (Prakash, Parmely, Dikshit, Forrester,

oped historically over the past 130 years. In the

and Swan, 1973). Peripheral vascular resistance in

mid-1800s, that internal organs could be rested as a

creases and blood flow decreases, with the assumption

therapeutic intervention comparable with immobi

of the upright position greater than 45 degrees to off

lizing and resting injuries of the limbs was the pre

set dependent fluid shifts and potential blood pressure

vailing medical philosqphy. The injudicious appli

drop (Figure 18-9). Another important effect of body

cation and overuse of bed rest to cure all medical

position on fluid volume is the promotion of urinary

problems was critically challenged by Harrison

drainage from the renal pelvi to the bladder in the up

(1944) and Browse (1965). Although there has been

right positions as a result of the reduced area for uri

a significant decrease in use of prolonged periods of

nary stasis in this position compared with supine (Fig

bed rest based on innumerable studies of the nega

ure 18-10). Optimal renal function is essential in

tive sequelae of bed rest over t h e past several

preserving normal hemodynamic status.

decades (Dean and Ross, 1992b), the merits of bed


18

Body Positioning

309

rest as a therapeutic modality and the parameters for its prescription, that is, indications and specifica

Erect

Supine

tions to achieve healing and recovery without deteri oration, have not been scientifically established. This void in our scientific knowledge seems incon gruous given the exponential rate of medical re search and advances over the years in understanding obscure diseases and treatments. Because recum bency in bed is nonphysiologic and therefore associ ated with dire side effects, rest in bed needs to be as scientifically investigated and judiciously prescribed as any medication. The supine position alters the chest wall configu ration, the anteroposterior position of the hemidi aphragms, the intrathoracic pressure, and the intraab

o

0 0, , :.

:.. .:: "," . .:::.'.

dominal pressure secondary to the shifting of the abdominal viscera in this position (Behrakis, Baydur,

FIGURE 18-11

Jaeger, and Milic-Emili, 1983; Craig, Wahba, Don,

Effect of body position on the distribution of mucus within

Couture, and Becklake, 1971; Don, Craig, Wahba, and Couture, 1971; Druz and Sharp, 1981; Klingstedt et ai, 1990; Roussos, Fukuchi, Macklem, and Engel,

the bronchi. (Reprinted with permission from Browse NL: The physiology and pathology of bed rest, Springfield, IJI.,

1965, Charles C. Thomas.)

1976; Saaki, Hida, and Takishima, 1977). The normal anteroposterior configuration becomes more trans verse. The hemidiaphragms are displaced cephalad,

Several significant cardiovascular changes occur

which significantly reduces FRC in this position (Hsu

on assuming the supine position. A central shift of

and Hickey, 1976). Excess secretions tend to pool on

blood volume from the extremities to the central cir

the dependent side of the airway. Thus the upper side

culation initiates orthostatism (Sandler, 1986). This

may dry out, exposing the patient to infection and ob

fluid shift increases both the preload and afterload of

struction (Fig. 18-11).

the right side of the heart. This increased volume

An increase in intrathoracic blood volume also

tends to distort the interventricular septum, and re

contributes to a reduction in FRC, lung compliance,

duces left ventricular volume and preload. Prefaut

and increased airway resistance in the supine position

and Engel (1981) observed that hypoxic vasocon

(Nunn, 1987; Sjostrand, 1951). Collectively, these ef

striction secondary to closure of the dependent air

fects predispose the patient to airway closure and an

ways in the supine position contributed to preferential

increase in the work of breathing. Although a healthy

perfusion of the nondependent lung zones. The rela

person can accommodate to these physiological

tively increased central blood volume inhibits the re

changes, a healthy person does not assume this posi

lease of antidiuretic hormone. Ten to 15 percent of

tion for prolonged periods without shifting. A hospi

fluid is lost within 24 hours (Sandler, 1986), which

talized patient, however, is less likely to adapt to these

can manifest clinically as cardiac underfilling, ortho

immediate changes and their long-tenn effects. In ad

static intolerance, and a negative fluid balance (Dean

dition, they may be less responsive to the need to shift

and Ross, 1992a).

position or unable to respond to afferent stimuli

Because of a reduction in the vertical gravitational

prompting a need to change position. These effects are

gradient, and therefore the intrapleural pressure gra

accentuated in older people whose arterial oxygen ten

dient of the lung in supine, the distribution of V/Q

sions progressively diminish with age (Ward, Tolas,

matching appears more uniform and evenly matched

Benveniste, Hansen, and Bonica, 1966; Nunn, 1987).

in the supine position (Bates, 1989). These changes,


310

PART III


Erect

Supine

cm Above 20 iliac crest

15

FIGURE 18-12 Effect of body position on the level and movements of the diaphragm during respiration. (Reprinted with permission from Browse NL: The physiology and pathology of bed rest, Springfield. Ill.,

1965, Charles C.

Thomas.)

I

I 1.:I.::' /':-: ,..:-::L:': r:-::::,: (: :' :

---....

:: nnn rtn<..:< ,

Awake spontaneous

:':

r::::' j -:

· 7':

/

.:- -., ·:':::i

>1

....

/ nnnqn :

<

___

Anasthelized spontaneous

f

nn n\n Paratyzed

FIGURE 18-13 Position of the diaphragm in an awake spontaneously breathing subject, and in an anesthetized subject with and without paralysis. The broken line is the end-expiratory position of the diaphragm in the awake state in the supine position. The shaded area shows the excursion of the diaphragm during inspiration and expiration. (From Froese AB, Bryan AC: Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesrhesio[ogy

41 :242-255.)


18

however, must be considered in conjunction with

Body Positioning

311

Functional

other changes associated with supine, namely re

Maximal

residual

duced FRC, reduced vital capacity, reduced flow

inspiration

capacity

rates, increased area of dependent lung, and increased closure of the dependent airways. These deleterious factors offset any theoretical benefit of the supine po sition on VIQ matching (Ross and Dean, 1992). The position of the diaphragm and its function, is dependent on body position. Figure 18-12 illustrates the effect on body position on the level and movement of the diaphragm. In the supine position, the resting

Maximal

level of the diaphragm is influenced differentially by

inspiration

Functional residual

anesthesia and neuromuscular blockade (Froese and Bryan, 1974). Figure 18-13 illustrates these effects. In the spontaneously breathing subject, the excursion of the diaphragm is greater posteriorly because the de pendent viscera beneath the posterior portion of the diaphragm. During anesthesia with or without paraly sis, the diaphragm ascends 2 cm into the chest. When paralysis is induced, the loss of diaphragmatic tone re sults in greater excursion of the nondependent rather than the dependent part of the diaphragm.

FIGURE 18-14 Outlines of the lungs at two lung volumes in a conscious spontaneously breathing subject in the right side-lying

Side-Lying Positions Compared with the supine position, side lying is more physiological, thus a more justifiable position

position. (Reprinted with permission from Nunn JF: Applied respiratory physiology, London, 1987, Butterworths.)

in terms of i t s t h e r a p e utic b e n e f i t (Hu rewitz, Susskind, and Harold, 1 985; Ibanez, R a u r i ch, Abizanda, Claramonte, Ibanez, and Bergada, 1981;

right side lying. Although effective ventilation is en

Ross and Dean, 1992; Roussos, Martin, and Engel,

hanced to the dependent lung, inspiratory lung vol

1977). The side-lying position accentuates anteropos

ume and FRC are significantly reduced.

terior expansion at the expense of transverse excur

There is evidence to suggest that side lying results

sion of the dependent chest wall. In this position, the

in increased end diastolic ventricular pressure on the

dependent hemidiaphragm is displaced cephalad be

dependent side secondary to compression of the vis

cause of the compression of the viscera beneath it.

cera beneath the diaphragm, and reduced lung com

This results in a greater excursion during respiration,

pliance on that side (Lange, Katz, McBride, Moore,

and greater contribution to ventilation of that lung

and Hillis, 1988). Although such changes can be

and to gas exchange as a whole. The FRC in side

readily accommodated in health, for the patient with

lying falls between that in upright and supine. Simi

compromised oxygen transport, they may impair gas

larly, compared with supine, compliance is increased,

exchange fUl1her.

resistance is reduced, and the work of breathing re

Optimal V/Q matching occurs in the upper one

duced, whereas these are reversed when comparing

third of each lung in the side lying position (Kaneko,

this position with upright. Figure 18-14 illustrates the

Milic-Emili, Dolovich, Dawson, and Bates, 1966).

difference in lung volumes between maximal inspira

The total area therefore for optimal V/Q matching is

tion and FRC in a spontaneously breathing subject in

likely greater than that in the upright position, which


312

PART III


contributes to an improved V IQ matching. These ap

those with respiratory muscle fatigue may have in

parent improvements, however, are offset by reduced

creased respiratory distress in this posi tion due to

lung volumes and air flow rates in this position. In both healthy people and patients, arterial oxy

the resistive loading of the diaphragm from the weight of the viscera beneath.

gen tension is greater in side lying compared with supine (Clauss, Scalabrini, Ray, and Reed, 1968). This is true both for patients receiving supplemental

Prone Position

oxygen as well as those who are not. Thus sidelying

There is considerable physiological justification for

can be used to enhance the efficiency of oxygen

the use of the prone position to enhance arterial oxy

transport and thereby minimize or avoid the use of

genation and reduce the work of breathing in patients

supplemental oxygen. Arterial blood gases are im

with cardiopulmonary dysfunction. Specifically, the

proved in patients with unilateral lung disease (Re

prone position increases arterial oxygen tension, tidal

molina, Khan, Santiago, and Edleman, 1981; Sonnen

volume and lung compliance (Albert, Leasa, Sander

blick, Meltzer, and Rosin, 1983) when positioned

son, Robertson, and Hlastala, 1987; Schwartz, Fen

with the good lung down and worsened with the af

ner, and W o lfsdorf, 1975; Wagaman, Shutack,

fected lung down. When lung pathology is bilateral,

Moomjiam, Schwartz, Shaffer, and Fox, 1979). These

arterial blood gases are improved when patients lie

benefits have also been observed in critically ill pa

on the right side compared with the left. This can be

tients (Langer, Mascheroni, Marcolin, and Gattinoni,

explained by the greater size of the right lung and the

1988). In one study (Douglas, Rehder, Beynen,

reduced compression of the heart on the lung in this

Sessler, and Marsh, 1977), supplemental oxygen was

position compared with left side lying (Dean, 1985;

reduced in four out of five mechanically ventilated

Zach, Pontoppidan, and Kazemi, 1974).

patients whose positioning regimen included the prone abdomen-free position. The two common vari ants of the prone position are prone abdomen-re

Head Down Position

stricted and abdomen-free. Prone abdomen-restricted

The head down position augments oxygen transport

refers to lying prone with the abdomen in contact

in some palients by improving pulmonary mechan

with the bed, whereas in the prone abdomen-free po

ics. Patients with chronic airflow limitation, for ex

sition the patient's hips and chest are elevated so that

ample, tend to have hyperinflated chests and flat

the abdomen is free.

tened diaphragms in which the contraction of the

W h i le both prone positions augment gas ex

diaphragm is inefficient because of the position of

change, the prone abdomen-free position, comparable

its muscle fibers on the length tension curve. The

with the hands and knees position (Mellins, 1974),

head down position causes the v iscera to be dis

enhances lung compliance, tidal volume, FRC and di

placed cephalad beneath the diaphragm. The di

aphragmatic excursion to a greater degree. Although

aphragm is positioned more normally and rests at a

patients in respiratory failure have been shown to

higher and more mechanically efficient position in

benefit significantly from the prone position, certain

the chest (Barach and Beck, 1954; De Troyer,

precautions must be observed. The patient must be

1983). In this position, patients may experience re

positioned so that all pressure points particularly on

lief from dyspnea, reduced accessory muscle use,

the head and face, and stress on the mechanical venti

reduced upper chest breathing patterns and reduced

lator tubing and circuitry is minimized. The patient

minute ventilation. Patients with pathology to the

should be monitored continuously and not be unat

bases may also benefit from the head down position

tended. A semiprone position can provide many of

in that this position favors gas exchange in the more

the physiological benefits of a full prone position,

functional upper lung fields and promotes alveolar

and minimize some of the risks, particularly in me

distension of bases, which are uppermost in the head

chanically ventilated patients and patients with cervi

down position. Other patients, however, such as

cal spine pathology. In addition, the semiprone posi


18

Body Positioning

313

tion simulates the prone abdomen-free position. The

constituent distributions of ventilation, perfusion, and

scmiprone position may be more conservative, safer,

ventilation and perfusion matching. Areas of depen

and comfortable for the patient who is severely ill,

dent atelectasis, physiologic dead space and shunting,

potentially hemodynamically unstable, older, or who

and mucus distribution are dramatically shifted. The

has a protruding abdomen.

"stir-up" correspondingly s t i mulates lymphatic

For patients who are not able to be effectively mo

drainage, surfactant production and distribution, and

bilized some variant of the 'prone position is even

the distribution and function of pulmonary immune

more important. Excessive recumbency, particularly

factors (Pyne, 1994). Frequent physical perturbations

in patients who are being positioned through a re

also inhibit bacterial colonization (Skerrett, Nieder

stricted arc (e.g., supine and one-quarter turns to ei

man, and Fein, 1989). F r e q u e n t b o d y position

ther side) needs to be offst by some variant of the

changes redistribute compression forces acting on the

prone position and this position needs to be incorpo

diaphragm, myocardium, and mediastinal structures,

rated often. [nevitably, patients exposed to a re

and the compression of the lungs by the myocardium

stricted arc of positioning will develop atelectasis in

and mediastinal structures.

the dependent lung fields. The only means of pre

Frequent body position changes have significant

venting and countering compression and hydrostati

effects on stimulating the patient and increasing

cally induced atelectasis is by placing those depen

arousal and a more wakeful state (Figure 18-15). The more upright the patient is positioned the greater the

dent areas uppermost. The time course for the development of such hy

neurological arousal and greater the stimulus to

drostatic complications is dependent on the patient.

breathe; this effect is augmented by encouraging the

Although objective measures of oxygen transport and

patient to be self-supporting. Concomitant with an in

the adequacy of the steps in the oxygen trans[lort path

crease in arousal, the patient is stimulated to take

way are essential to monitor, functional changcs will

deeper breaths, and hence increase alveolar ventila

likely precede the appearance of objective changes.

tion. When body positioning is coupled with mobi lization, vasodilatation, and recruitment of the pul monary capillaries is stimulated, which in turn

PHYSIOLOGIC EFFECTS OF FREQUENT CHANGES IN BODY POSITION

improves the even distributions of ventilation and perfusion, and hence augments VIQ matching.

The box on p. 303 lists some of the significant physi ological effects of frequent changes in body position that are largely mediated through their effects on res piratory mechanics, cardiac mechanics, airway clo

PRESCRIPTION OF THERAPEUTIC BODY POSITIONS AND BODY POSITION CHANGES

sure, mucociliary transport, lymphatic drainage, and

Prescription of body positioning is based on an analy

altered neural activation of the diaphragm. These ef

sis of the factors that contribute to impaired oxygen

fects resulting from the changc in position are distinct

transport. Specific positions are selected to simulate

from the benefits derived from a particular body PoS!

as closely as possible the physiologic function of the

tion. The benefits of changing position can be en

normal healthy upright cardiopulmonary unit, and the

hanced by moving to an extreme position, ie, moving

perturbations and "stirring up" that occurs in the car

from supine to prone compared with supine to side

diopulmonary system during normal mobility and

lying. Extreme body position changes simulate, but

being upright. A hierarchy of body positioning alter

do not replace, the physiological "stir-up" and pertur

natives based on the physiologic justification of the

bations that occur with normal mobility and being

various positions, appears in the box on p. 3 14. These

upright. When the "stir-up" regimen was originally

positions range from the most to the least physio

proposed, Dripps and Waters ( 1941) did not appreci

logic. The hierarchy is based on the premise that oxy

ate fully its physiological implications. The net effect

gen transport is optimal when upright and moving.

of changing body position is a "stirring up" of the

Mobilization in the upright position increases tidal


314

PART III


Physiological Hierarchy of Body Positions Most Physiologic Therapeutic Body Positions Normally moving upright in a I G gravitational field and exposed to a range of body positions and body position changes over the course of several hours Relaxed erect standing (not too prolonged) Erect sitting (self supported or with assist) with feet moving (e.g., active, active assisted or passive cycling motion) Erect silting (self-supported or with assist) with feet dependent Lean forward sitting with arms supported and feet dependent

24S degree sitting with legs dependent Erect long sitting (legs non dependent) <

4S degrees sitting (legs non dependenl)

Prone and semiprone/side lying Supine

Least Physiological Therapeutic Body Positions

Provisos The upright erect position implies the back, head and neck are vertical and aligned with flexion only at the hips: the patient is not slumped

or

recumbent.

The less able the patient is to assist in positioning the greater the need for more extreme positions and greater the turning frequency.

If the patient is totally unable to move, that is, in coma or paralyzed, extreme body positions arc also indicated if not contraindicated because of hemodynamic instability or increased intracerebral pressure. The upright position is used as much as possible provided the patient is physically supported for safety and monitored in terms of treat ment response. Passive standing on a tilt table is hemodynamically questionable; preferably patients should be placed in

a

high Fowler's position with legs positioned dependently using the knee breaks in the bed.

Regimens of 360-degree horizontal tuming and ISO-degree vertical turning (ranging from 20 degrees head down to 20 degrees lean forward) are used unless contraindicated. Positioning through a maximal arc simulates as closely as possible three dimensional movement of the chest wall during normal respiration.

volume, respiratory rate, and hence minute volume,

right state. Furthermore, even the mobilized patient

flow rates, mucociliary transport, and clearance, and

can benefit from therapeutic body positioning be

enhances the efficiency and effectiveness of airway

tween mobilization sessions. Body position needs first to be exploited when

clearance and coughing. Thus incorporating active movement into the body position change is optimal. Despite the well-documented benefits of the judi

coupled with movement followed by the erect sitting positions with legs dependent. Figure 18-16 illus

cious application of therapeutic body positioning to

trates several variants of the sitting position. Each of

enhance oxygen transport, it does not replace the

these positions has distinct effects on oxygen trans

more physiological intervention of mobilization and

port, thus the specific upright position has to be pre

exercise to maximize oxygen transport. Rather, once

scribed specifically as the supported and "propped

the effects of mobilization/exercise have been ex

up" positions in bed do substitute for upright erect

ploited maximally, then body positioning is the next

sitting. These variants only have a role when the pa

best physiological approximation to a mobilized up

tient will deteriorate by attempting to position in the


18

Body Positioning

315

Asleep

Aroused

/

Cortical

activating

impulses

AFFerent impulses from

sense organs, with collateral

tracts to the reticular formation

FIGURE 18-15 Effect of arousal on cerebral activity. (Reprinted with permission from Browse NL: The physiology and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)

upright erect position, or the patient immediately de

prone or semiprone positions. Patients can be posi

teriorates once in the position. Sitting with the feet

tioned safely, with appropriate supervision and moni

down is preferable to long sit because of the hemody

toring, and comfortably in these full positions by ob

namic benefits associated with this position. Sitting

serving the normal precautions of passive positioning.

up in bed fails to position the patient in a perfectly

A common practice is to progressively turn pa

vertical upright position. Fowler's position in bed can

tients in one-quarter turns, such as supine to side

be maximized and the use of knee breaks in the bed

lying and back to supine and so forth. However, the

provides a gravitational stimulus to the circulating

use of extreme positions and extreme position

blood volume.

changes may yield greater benefit with respect to the

A major difficulty with positioning patients in bed is

degree of perturbation and "stir-up" elicited (Piehl

the tendency to lose the position. Patients lose optimal

and Brown, 1977). Extreme position changes result in

positions in bed very quickly and thus need to be moni

significant alterations in the distributions of V, Q,

tored to ensure the specific positions are maintained.

and V and Q matching. Mucociliary transport is stim

Pillows should not be used to maintain a body position,

ulated, and secretion accumulation and stagnation is

since these are easily compressed and shifted. Blankets

minimized. In addition, the more extreme the body

and sheets tightly rolled and secured with tape, and spe

position, the greater degree of arousal stimulated par

cially made bolsters are considerably more effective in

ticularly in the upright positions, which is essential in

maintaining a patient's body position.

critically ill patients.

Although there is a role for modified positions,

Another impo r t a n t consideration is the time

such as half side lying these positions are often

course of changes in ox.ygen

overused at the expense of full turns to each side, or

and position changes. There are three plausible out


316

PART III


1984; Fink, Helsmoor 1990; Gentillelo, Thomp

patients (Brackett and Condon,

f=4

Supine

HI h

Recumbent

Propped-up

hi

Sitting

FIGURE 18-16

Approximations of the upright position from supine. The recumbent and propped-up positons are not comparable physiologically to the upright sitting position. (Reprinted with

permission from Browse NL: The physiology and pathology of bed rest, Springfield, 111., 1965, Charles C. Thomas.)

tel, Stein, Lee, and Cohn,

1988; Gonzalez-Arias, Goldberg, 1983; Kelley, Vi b u l srest, Bell, a n d D u n c a n, 1987; Mein ig, Leininger, and Heckman, 1986; Summer, Curry, Haponik, Nelson, & Elston, 1989). These beds are in son, Tonnesen,

Baumgartner, Hoopes, and Rubin,

dicated for patients who are moderately hemodynami cally u nstable and on neuromuscular blockers, and thus tolerate manual turns poorly. Such turning frames are contraindicated, however, for patients who are less ill. Even for those patients who require multiple assis tants and extra caution and time to turn and position effectively, these issues should never deny a patient a much needed treatment with proven efi'icacy. The benefit of these beds on oxygen transport in critically ill patients has implications for the manage ment of less critically ill patients. The continuous me chanical rotation of the Rotobed® can be simulated by increasing the frequency and arc of positions when manually positioning patients.

PRACTICAL CONSIDERATIONS IN POSITIONING PATIENTS Prescriptive body positioning takes

a

significant

amount of the PTs time as well as other team mem bers' time. Such prescriptive positioning is based on clear indications and well-defined parameters; it is not to be confused with 'routine' positioning. For any hospitalized patient who is recumbent and inactive

comes: a favorable response, no response, an unfa

compared with being out of hospital, body position

vorable response. With the passage of time, all three

ing is a 24 hour concern, ie, a concern both during

outcomes will deteriorate. The specific time depends

treatment and between treatments. Such patients are

on the multitude of factors contributing to impaired

at risk of impaired oxygen transport.

oxygen transport.

Despite the time and labor involved in turning a pa

Because of the significant changes that can be ex

tient to prone, particularly if mechanically ventilated,

pected with positioning and positioning changes, the

the benefits of this position outweigh the time and ef

(PT) has a prime therapeutic oppor

fort required to prone a p tient even for short periods.

tunity to assess and treat the patient before, during,

Gi ven the considerable benefits that can be derived

and after position changes.

from the prone position, a good case needs to be made

physical therapist

for not turning a patient prone. Frequently, therapeutic body positioning can be effectively coordinated with

Mechanical Body Positioning

nursing interventions and other procedures.

Mechanical turning beds such as the Rotobed® have

Extreme body positions and body position changes

significant benefits On oxygen transport in severely ill

are the goal. However, when these are less feasible,


18

Body Positioning

317

modified positions may be used. Even though the

tient includes subjective and objective evaluation of

greatest benefits will be derived from extreme

indices of the adequacy of oxygen transp0l1 (Part II).

changes as these simulate the normal range o f

Among the most imp0l1ant are oxygen delivery, oxy

changes the human body is exposed to in health,

gen consumption, oxygen extraction, and gas ex

small changes can be effective in altering intrapleural

change indicators such as the A-a02 difference and

gradients slightly so that previously closed alveoli

Pa02/PA02. Subjectively, the patient's facial expres

will be opened even though· previously opened ones

sion, respiratory distress, dyspnea, anxiety, discomfort

may be prone to closure. Although modified posi

and pain are assessed. Objectively, heart rate, blood

tions and small degrees of position change should not

pressure, respiratory rate, Sa02, flow rates, beside

be relied upon their effects should not be minimized

spirometry are readily assessed. The appropriate stan

in patients for whom extreme positions are con

dardization and procedures need to be used to ensure

traindicated. Before and after every position change

that the measures are both valid and reliable (see

are prime opportunities to assess the patient, and to

Chapter 6). Because physiological variables are

encourage deep breathing and coughing, or suction

changing from moment to moment, serial measures over a period of time should be taken to establish an

the patient as indicated. Another important consideration is the time course of change in oxygen transport with positions and po

average value rather than using peak or discrete mea sures which may misrepresent a treatment effect.

sition changes. There are three possible outcomes: a

In order to interpret and compare various mea

favorable response, no response, an unfavorable re

sures, the Fi02 and any change in FI02 must be

sponse. With the passage of time, all these outcomes

recorded. The use of the ratio Pa02/Fl02 enables

will deteriorate. The specific time depends on the

comparison of gas exchange within and between pa

multitude of factors that contribute to the patient's

tients when patients Fi02s differ or are changed (Dean and Ross, 1992c). Similarly, for mechanically

oxygen transport and the patient's responses.

ventilated patients, any changes in the ventilatory pa rameters must also be noted, in addition to other in

MONITORING THE RESPONSE TO A BODY

POSITION OR POSITION CHANGES

terventions that have a direct effect on oxygen trans

The prescriptive parameters of body positioning and

conclude within reasonable doubt that the position or

port. Only in this way will the clinician be able to

body position changes include the positions selected,

position change was instrumental in enhancing car

the duration spent in each position, the sequence of

diopulmonary function.

position changes, the cycle of all positions, and posi

Measures are recorded before (pretreatment base

tion changes overall. Because a patient necessarily

line), during, and at periodic intervals following the

assumes a body position at all times, positioning pa

treatment. A valid stable pretreatment baseline is es

tients between treatments can contribute as much to

sential to determine the therapeutic effect of a given

the overall treatment response as the treatment itself

position on oxygen transport. Variables monitored

as the patient is likely to spend more time in the be

during the treatment are focused on ensuring that

tween-treatment positions than in the within-treat

the treatment is having a beneficial effect, in addi

ment positions.

tion to its not having any deleterious effect on the

The duration and frequency of the positions and

patient subjectively or with respect to any parameter

the frequency of body position changes are response

of oxygen transport. As long as beneficial effects

dependent rather than time-dependent. Monitoring is

are being recorded a position can be safely main

the basis for defining and modifying the body posi

tained, however, diminishing returns can be ex

tioning prescription. The physiological variables to be

pected as the period becomes prolonged. Patients

monitored depend on the patient's specific presenta

maintained in static positions for more than one to

tion, cardiopulmonary dysfunction, and its severity

two hours need to be monitored closely. A position

and distribution. Monitoring of the noncritically ill pa

change is physiologically defensible after this dura


318

PART III


tion rather than the risk of diminishing returns and

ations presented. Thus this chapter has presented prin

potentially worsening the patient's condition.

ciples that must be considered in the decision-making

Although sicker than a noncritically ill counter

process behind the prescription of therapeutic body

part, the critically ill patient has the advantage of

positioning, rather than a treatment prescription for a

having more monitoring lines in place. These lines

given patient.

give access to several measures and indices of oxy gen transport, and certain hemodynamic and pul monary variables are available continuously.

REVIEW QUESTIONS

In summary, the prescription of therapeutic body positions is based on a detailed analysis of each pa

I. Describe the effects of gravity on cardiopul monary function and oxygen transport.

tient's unique presentation and the factors contributing to impairment of oxygen transport or threatening it.

2. Distinguish between prescriptive and routine body positioning.

Then those positions that are predicted to result in the best therapeutic outcome are selected and applied, and

3. In reference to the seated upright position, describe

those that are predicted to lead to an adverse result are

the effects of different body positions (i.e., supine,

used minimally and with appropriate monitoring.

side lying, head down, and prone) on cardiopul

Monitoring is an essential component to body position

monary function and oxygen transport in health.

prescription in that it confirms the prediction of benefi

4. In reference to the seated upright position, describe

cial and deleterious positions, establishes when a posi

the effects of different body positions (i.e., supine,

tion change is indicated, and helps the PT anticipate

side lying, head down, and prone) on cardiopul monary function and oxygen transport in disease.

the point of diminishing returns of any given body po sitions. The specific physiological variables monitored

5. Explain how a physiologically ideal body posi

are those that reflect the steps in the oxygen transport

tion with respect to oxygen transport can be dele terious over time.

pathway that are most affected in a given patient.

6. Distinguish between the prescription of therapeu tic body positions and frequency of body posi

SUMMARY

tion changes.

The purpose of this chapter was to differentiate rou

7. Describe the principles of monitoring oxygen transport variables during body positioning.

tine and therapeutic body positioning designed to op timize oxygen transport. The physiological effects of different body positions and changing body positions on cardiopulmonary and cardiovascular function and oxygen transport, were described. The primary goal is to strive toward the physiological position for opti mizing oxygen transport, that is, upright and prefer ably moving. Issues related to optimizing the pre s c r i p t i o n of t h e r a p e u t i c b o d y p o s i t i o n i n g and monitoring treatment outcome were presented. This chapter focused on the physiological effects of body positioning, an intervention that has well-doc umented, direct and potent effects on oxygen trans port. Establishing a clear rationale for prescribing a specific body position or body position changes is es sential. The rationale, however, is based on multiple other factors in addition to the physiological consider

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Physiological Basis for Airway Clearance Techniques Anne Mejia Downs

KEY TERMS

Active cycle of breathing technique (ACBT)

Percussion

Airway clearance techniques (ACTs)

Positive expiratory pressure (PEP)

Autogenic drainage (AD)

Postural drainage (PD)

Flutter™

Shaking

Forced expiratory technique

Trendelenburg

High frequency chest compression (HFCC)

Vibration

Manual hyperventilation

INTRODUCTION

Research studying the results of airway clearance

Techniques for assisting the mobilization of secre

are often difficult to evaluate because the components

tions from the airways have long been advocated for

of a given treatment have not been standardized.

use in the patient with an impairment in mucociliary

Availability of equipment or education about a tech

clearance or an ineffective cough mechanism. The

nique as well as cultural differences in its application

goals of this therapy are to reduce airway obstruction,

confound the results. Differences in the outcome

improve mucociliary clearance and ventilation, and

measures for a given technique also occur-some

optimize gas exchange.

studies use wet or dry (dehydrated) sputum volume

Airway clearance techniques have been referred

or radioaerosol clearance, whereas other studies use

to in the literature in a variety of ways, including

pulmonary function tests, radiographic evidence or

chest p h y s i o t h e r a p y , c h esl ph y s i c a l t h e r a p y,

arterial blood gases to asses the effectiveness of an

bronchial drainage, postural drainage therapy, and

airway clearance technique. Although a treatment has

bronchial hygiene.

been shown to be effective in one cross section of pa 321


322

PART III


tients with pulmonary disease, care must be taken not

may interfere with this process. Retained secretions

to generalize the effectiveness of the treatment across

or mucus plugs in the airways may interfere with the

other groups of patients or differing time frame

exchange of oxygen. The secretions need to be mobi

(acute vs. chronic). The majority of secretion clear

lized from the peripheral or smaller airways to the

ance research has been focused on patients with cys

larger, more central airways where they may be re

tic fibrosis, as the need for ongoing secretion removal

moved by coughing or suction. The following conditions are indications for air

is apparent in this population. Recently the "gold standard" of airway clearance,

way clearance:

namely a combination of postural drainage, percus

I. Cystic fibrosis-In this multisystem genetic

sion, and vibration with cough, has been challenged

disease, copious (often purulent), thick secre

(Lapin, 1994). The indications for routine airway

tions and mucus plugs block the peripheral and

clearance with certain diagnoses have been ques

central airways. Even infants diagnosed with

tioned and the conditions leading to effective applica

cystic fibrosis, whether symptomatic or not,

tion have been examined. Postural drainage and per

show evidence of small airway obstruction in

cussion has been shown to be ineffective in some

the form of bronchial mucus casts (Wood,

cases, and in fact, to be detrimental to the pulmonary

1989). Recurrent bacterial infections combined

status of some patients. Caregivers have also been

with this mucus hypersecretion in the lungs

shown to suffer from the performance of percus

leads to destruction of the bronchial walls, or

sion-repetitive motion injuries of the wrists have

bronchiectasis. Airway clearance continues to

been documented as a result of regular performance

be an important therapy in the treatment of

of percussion (Ford, Godreau, Burns, 1991, MMWR

cystic fibrosis. This practice is supported by

Publication 1989).

evidence of deteriorating lung function when

Alternate techniques have arisen out of the need to

regular treatments of postural drainage and

find effective methods for those patients not respon

percussion have been stopped (Desmond,

1983, Reisman, 1988).

sive or not tolerant of traditional methods. A desire to increase compliance with airway clearance (Currie,

2. Bronchiectasis-This condition results in a

1986), especially in those patients approaching ado

breakdown of the elastic tissue in the bronchial

lescence and adulthood has led to an investigation of

walls, causing severe dilation. Inflamed mucosa

more independent techniques. Many of these tech

and copious, purulent secretions are present in

niques have been practiced for years in European

this condition. Airway clearance has been

countries, but are more recently being introduced to

shown to benefit patients with bronchiectasis in

practitioners in the United States.

the mobilization of sputum (Mazzocco, 1985, Gallon, 1991).

It is important to remember, however, that secre tion clearance is but one step to take toward realizing

3. Atelectasis-This condition is caused by the

effective gas exchange in the complex oxygen trans

collapse of an alveolar segment, often by re

port pathway (Dean, 1992). Airway clearance, when

tained secretions. It is a documented sequela of

indicated, should be integrated into a total approach

patients who have undergone surgery under general anesthesia, especially thoracic or ab

to optimize oxygen transport.

dominal surgery. Airway clearance techniques are indicated where atelectasis is suspected to

INDICATIONS FOR AIRWAY CLEARANCE

be caused by mucus plugging (Marini, 1979, Hammon, 1981).

Oxygen transport is the primary purpose of the car diopulmonary system (see Chapter 1). Ventilation of

4. Respiratory muscle weakness-Many patients

the alveoli is an important step in the oxygen trans

with neurological or metastatic diseases or gen

port chain that allows optimal delivery of oxygen to

eral debilitation, tend to hypoventilate or have an

the tissues. Several medical and surgical conditions

increased work of breathing. They are unable to


Physiological Basis for Airway Clearance Techniques

19

323

maintain adequate control of respiratory secre

tance of gravity (Figure 19-1). Positioning the patient

tions and often have a weak, ineffective cough

to enable gravity to assist the flow of bronchial secre standard treatment

(Massery, 1987). This is especially true in pa

tions from the airways has been

tients with diminished diaphragm innervation re

for some time in patients with retained secretions

sulting from spinal cord injuries (Wetzel, 1990).

(Zadai,1981).

a

5. Mechanical ventilation-Patients on ventilatory

Knowledge of the anatomy of the tracheobronchial

support for any reason, including obtunded or

tree is vital to an effective treatment. Each lobe to be

comatose patients, are at risk for atelectasis and

drained must be aligned so that gravity can mobilize

are unable to independently manage their secre

the secretions from the periphery to the larger, more

tions (Dickman, 1987).

central airways. The mechanism of postural drainage

6. Neonatal respiratory distress syndrome-These

is considered to be a direct effect of gravity on

infants are born lacking surfactant in the lungs,

bronchial secretions, although a study by Lannefors

which results in atelectasis. Airway clearance

(1992) observing that gravity influences regional

techniques may be useful in clearing secretions

lung ventilation and volume suggested these other

and preventing atelectasis but must be moni

mechanisms are also involved.

tored carefully in this population (Finer, 1978).

Postural drainage (also k n o w n as b r o n c h i a l

7. Asthma-This condition is characterized by the

drainage) has been shown t o b e effective i n mobiliz

presence of hyperreacti ve airways and mucus

ing secretions in patients with cystic fibrosis (Wong,

plugging. Airway clearance techniques may be

1977, Lorin, 1971), bronchiectasis (Mazzacco, 1985),

beneficial to assist with the mobilization of

and other pulmonary diseases (Bateman, 1981; Zaus

mucus plugs but are not helpful in treating un

mer, 1968). Other treatments such as percussion, vi

complicated acute exacerbations (Eid, 1991).

bration, and the active breathing cycle (ACB) tech

Chest physical therapy techniques appear not to be

nique may be used while the patient is in postural

beneficial in the treatment of patients with pneumo

drainage positions.

nia or chronic bronchitis without large amounts of se

There are many contraindications to optimal posi

cretion production. No differences were found with

tioning for PO, especially the head down or Trende

the inclusion of postural drainage and percussion in

lenberg positions required for the lower lobes.

these populations (Britton, 1985; Sutton, 1982; Rochester, 1980; Wollmer, 1985). Viral bronchiolitis is an asthma-like lung disease

Percussion

occurring in infants less than 2 years of age. These

Percussion, sometimes referred to as chest clapping,

patients do not appear to benefit from airway clear

is a traditional approach to secretion mobilization. A rhythmical force is applied with cupped hands to the

ance techniques (Webb, 1985). Also of little benefit, and possibly harmful, is the

patient's thorax over the involved lung segments with

inclusion of chest physical therapy in the routine care

the aim of dislodging or loosening bronchial secre

of postoperative patients without extensive secretions

tions. This technique is performed with the patient in

(Eid, 1991). Even in patients with a history of lung

postural drainage positions and requires a caregi ver

disease, the use of airway clearance techniques have

to administer. In the United States,percussion in con

failed to affect the incidence of atelectasis as a post

junction with postural drainage continues to be a

operative complication (Torrington, 1984).

mainstay of treatment of the person with pulmonary disease, especially in neonates or patients who are unresponsive.

Postural Drainage

The proposed mechanism of action of percussion

Postural drainage (PO) is a passive technique, in

is the transmission of a wave of energy through the

which the patient is placed in positions that allow the

chest wall into the l u n g . T h e resulting motion

bronchopulmonary tree to be drained with the assis

loosens secretions from the bronchial wall and


324

PART III


Normal

Phase: 1

2

3

FIGURE 19·1 Phases of autogenic drainage shown on a spirogram of a normal person. Phase 1: unstick phase 2: collect, phase 3: evacuate. volume,

FRC

=

(VT

=

ERV expiratory reserve volume. RV reserve IRV inspriatory reserve volume; fRV + VT + ERV

tidal volume,

Punctual residual capacity,

=

=

=

=

vital capacity)

moves them proximally where ciliary motion and cough (or suction) can remove them. The combina tion of postural drainage and percussion has been shown to be effective in secretion removal (Denton, 1962; May, 1979, Radford, 1982). A study by Ross man et al. (1982) is in disagreement, finding that me c h a n i c a l p e rcussion did n o t enhance postural drainage in secretion removal. A handheld mechanical percussor may be used by a caregiver to decrease fatigue or by the patient for self-administration of percussion. The effectiveness of mechanical versus manual percussion has been studied. Maxwell and Redmond (1979) found me chanical percussion equivalent to manual percussion in affecting removal of secretions. This is supported by Pryor et a1. (1979) in patients using the forced ex piration technique, although there was a significant increase in pulmonary function with manual tech niques (Pryor, Parker, and Webber, 1981). There are many contraindications to percussion. If the patient's pulmonary status is of greater concern than the relative contraindications, it may be decided to modify and administer the treatment.

Vibration Vibration is a sustained cocontraction of the upper extremities of a caregiver to produce a vibratory force that is transmitted to the thorax over the involved lung segment. Vibration is applied throughout exha lation concurrently with mild compression to the chest wall. Vibration is often applied in postural drainage positions following percussion to the area. A mechanical vibrator may be used by the patient or a caregiver in place of manual vibration. Vibration is proposed to enhance mucociliary transport from the periphery of the lung fields to the larger airways. Since vibration is used in conjunction with PD and percussion, many studies do not separate out the effects of vibration from the other compo nents. In fact in multiple studies, the techniques of PD, percussion, and vibration are described as a single entity and referred to as chest physical therapy (CPT), pulmonary therapy, or postural drainage therapy. Pavia (1976) demonstrated a higher, though not sta tistically significant, rate of secretion clearance and sputum production with vibration. However, this study was conducted with subjects in an upright position


19


325

only, not a replication of the use of vibration clinically.

applies shaking or vibration at the very beginning of

Mackenzie et al. (1980) used measurement of total

exhalation to mobilize secretions. The timing of this

lung/thorax compliance to assess the effect of secre

sequence is important to achieve the desired effect

tion clearance. Significant improvement in total

(Webber, 1988). It has been likened to simulation of a

lung/thorax compliance was demonstrated after treat

cough----deep inspiration, pause, and forceful exhala

ment with postural drainage, percussion, and vibra

tion. Saline may be instilled into the airway at the be

tion in mechanically ventilated patients. Feldman et

ginning of the cycle, with suctioning a component at

al. (1979) demonstrated improved ventilatory func

the end of treatment of each side. Manual hyperventi

tion by showing a significant improvement in expira

lation is peIt'ormed in postural drainage positions and

tory flows at lung volumes in patients receiving pos

requires two competent caregivers to peIt·orm.

tural drainage, percussion, vibration, and coughing.

The inspiration provided by the manual ventilation bag, which is deeper than the patient could generate, promotes aeration of the alveoli. The compression of

Shaking

the thorax augments the high expiratory flow rate

Shaking consists of a bouncing maneuver sometimes

from the bag, accelerating the movement of the secre

referred to as "rib splinging" against the thoracic wall

tions from the smaller airways to the larger bronchi

in a rhythmic fashion throughout exhalation. A concur

(Clement, 1968).

rent pressure is given to the chest wall, compressing

Clement (1968) reports this method of airway

the thorax. Shaking is similar in application to vibra

clearance enables patients to be maintained on ventila

tion, with shaking being on one end of the spectrum in

tors for long periods with normal lung function. It has

application of force, and vibration being on the oppo

been demonstrated that hyperinflation and suction in

site end, supplying a gentler amount of pressure. Many

the treatment of atelectasis was enhanced by the addi

variations exist throughout the spectrum between these

tion of positioning and vibrations (Stiller, 1990).

techniques. Shaking may be used in place of percus sion or intermittently with percussion and vibration. Shaking may be used in postural drainage positions

Active Cycle of Breathing Thompson (1973) in New Zealand described clearing

and requires the assistance of a caregiver. Shaking is proposed to work in the same manner

bronchial secretions in patients with asthma by a

as vibration, mobilizing secretions to the central,

technique of forced expirations and diaphragmatic

larger airways from the lung periphery. Since the

breathing. British physiotherapists have modified the

compressive force to the thorax is greater, producing

technique and further described it in the literature,

increased chest wall displacement, the stretch to the

first as the forced expiration technique (FET) (Pryor,

respiratory muscles may produce an increased inspi

1979) and later as the ACB technique (Webber and

ratory effort and lung volume (Levenson, 1992).

Pryor, 1993).

The same relative contraindications for percussion

As described by Webber and Pryor (1993), the

should be observed for shaking, since it does involve

ACB consists of repeated cycles of three ventilatory

application of force to the thorax.

phases: breathing control, thoracic expansion exer cises, and the FET. Breathing control is described as gentle tidal volume breathing with relaxation of the

Manual Hyperinflation

upper chest and shoulders. The thoracic expansion

This technique is used on patients with an endotra

phase consists of deep inspiration, and may be ac

cheal or tracheostomy tube that can be attached to a

companied by percussion or vibration peIt'ormed by a

manual ventilation bag. One caregiver uses the bag to

caregiver or the patient. This phase helps to loosen

hyperinflate the lungs with a slow, deep inspiration

secretions. The forced expiration technique involves

and after a short inspiratory pause, provides a quick

one or two huffs (forced expirations). Webber and

release to allow rapid exhalation. A second caregiver

Pryor (1993) report huffing from a mid-lung volume


326

PART III

Therapy Interventions

Cardiopulmonary

(a medium sized breath

and continued down to

the

hV[)OSi�Cn tlOn. This sug

low-lung volume will move secretions from the pe to the upper tions may be cleared ume (a

breath

a huff from

effective in gravity assisted

1990). The

bronchospasm o f thoracic expansion,

which increases

described the

in a relaxed state without use of

aohragmatic breathing to mobilize secre

airflow. It consists of three

at low-lung volumes to "unstick"

is the point in the airways

where the pressure is

nMtn ,,1

(Chevaillier,

of "equal

to the pleural pressure.

The forced expiratory maneuver

PD and cJap-

AD is an antidyspnea technique based on

pressure point," which is the basis for the FET. The pressure point

the day,

mucus was mobilized better than

Mead et at

I

1967 for treat

ment of asthmatic patients. He observed that during

behind secretions and

assist in their mobilization

was in

Chevaillier in Belgium in

sleep, as well as playing and laughing

collateral

ventilation, allowing air to

(1

(AD) or troduced

The period of breathing control is essential be (Lapin,

Autogenic Drainage

drainage) posi

1992).

tween the other phases to

retention of

little sputum.

lung vol

The ACB may be performed

in the sitting position, but has been shown to be more tions (Steven,

nJY'HmcrPfl

secre

peJ]DJ1eral secretions,

(2) breathing at low- to mid

volume (tidal volume) to collect the mucus in the

compres

(3) breathing at mid- to

sion of the airway peripherally to the EPP. A huff

middle

from high lung volume causes compression within

volumes to evacuate the mucus from the central air

the trachea and bronchi to move secretions from

ways

these

laxed position and exhales actively with the mouth and

airways. A huff continued to low lung

volume shifts the EPP more oeripherallv to move

and

1984). The patient is seated in a re open and listens for the movement of mucus

while

a wheeze. The phases in the AD techdelJ'ict<�d in

a patient

nhU ;AIA""

by pa

by Shoni

tients independently has been shown to clear more sputum in a shorter amount of time than PD with selfcombined with

and shaking by

a physical therapist (PT)

1986) and sputum

clearance (Sutton,

1983) have been demonstrated in

patients with cystic fibrosis who

the FET

ensure

of lung segments by collateral fill-

serve volume range. By lowering mid-tidal volume below functional residual capacity

lapsible bronchial wails, it increases the expiratory

tidal volume is lowered in the range of normal tory reserve volume. The second

air

of tidal volume

Another benefit of this

from

flow in patients with obstruction without

lies in its ability to maintain oxygen satura tion. The decrease in oxygen saturation that has been demonstrated with postural

secretions

from peripheral lun!:! regions are mobilized alveolar ducts.

Because huffing has been shown to stabilize col

(Hietpas,

re

and then a deep exhalation into the

into their postural drainage treatments.

way

has been ex

(1989). The first

starts with an inspiration, followed by a breath hold to

Improvement

in pulmonary function

19-1.

of AD's three

and percussion

has been prevented with the use of the ACB technique

1990). Hassani et al. (1994) has recently shown

of AD consists

so that

is

reserve volume into the in-

reserve volume range to mobilize secretions from the

of the lungs. The

of the so

airflow must be adjusted at each level of

that the maximal expiratory ailflow is reached without being high enough to cause collapse of the

that unproductive cough and FET resulted in the

Flow volume curves show that higher flows of

movement of secretions proximally from all regions of

duration can be achieved with AD (Dab.


1

19

demonstrating that mucus can be moved further and at a faster rate. The third phase consists of deeper inspira tion into the inspiratory reserve volume, with huffing often used to help in evacuating the mobilized secre tions. Control of ailflow during this final phase is es sential to avoid uncontrol led, unproductive coughing. The Belgian method has been modified by German practioners to use a combination of diaphragmatic and costosternal breathing in a treatment that is not delin eated into phases (David, 1991). The patient varies his or her mid-tidal volume in a passive exhalation followed by an active exhalation through pursed lips or through the nose. The German method includes other maneuvers in conjunction with autogenic drainage, including in halation therapy, FET, chest wall exercises, and sports. Autogenic drainage has been compared with posi tive expiratory pressure and PD with percussion/ vibration. More sputum was produced with AD in pa tients with hyperreactive airways (Davidson, 1988). In a 2-year crossover trial, AD was found to be as ef fective as conventional CPT among patients with cys tic fibrosis for improving pulmonary function (Davidson, 1992). However, patients exhibited a strong preference for AD, increasing the likelihood of compliance. Miller (1993) showed greater clearance of inhaled radioisotope with AD vs. the ACB tech nique, with no significant differences in sputum weight, spirometry, or transcutaneous oxygen satura tion. Giles (1993) also studied oxygen (02) saturation in AD and found an increase in O2 saturation with AD over PD with percussion and greater sputum re covery with AD. The learning of AD requires tactile and auditory feedback and continued modifications of the patient's technique is necessary, at least initially, to achieve a good result. AD takes considerable time to learn and requires a great deal of cooperation from the patient. Therefore it is not suitable for the very young or dis tractable patient.

Positive Expiratory Pressure The development and utilization of positive expira tory pressure (PEP) breathing came about in the 1980s in Denmark and is now widely used in Europe with increasing acceptance in the United States.


327

The application of PEP consists of a mask or mouthpiece connected to a one-way breathing valve to which expiratory resistors are attached. This re sults in positive pressure in the airways during exha lation. A manometer in the circuit determines and monitors the correct pressure generated by the pa tient. A patient uses PEP in a cycle of about 10 breaths at tidal volume with slightly active expiration followed by huffing or coughing to expectorate secre tions (Falk and Kelstrup, 1993). High- or low-pressure PEP may be prescribed. In low-pressure PEP, the resistance is regulated to achieve 10 to 20 cms of water pressure during expira tion. The pressure should be sustainable during only slightly active expiration. The prescription for high pressure PEP requires the patient to perform forced vital capacity maneuvers through the range of expira tory resistances with the mask connected to a spirome ter. The appropriate resistor is one that produces a flow volume curve demonstrating a maximal forced vital capacity, good plateau, and no curvilinearity (Prasad, 1993). In general, the range of pressure generated with high pressure PEP is 50 to 120 cms of water pressure. Low-pressure PEP is used more often, as it offers equal effectiveness at a lower risk of pneumothorax. It is theorized that PEP allows more air to enter through collateral channels, allowing reinflation of collapsed alveoli. Pressure is built up distal to an ob struction, promoting the movement of secretions to wards the larger airways (Anderson, 1979; Groth, 1985). Airway stability is maintained with PEP pro moting improved ventilation and gas exchange, as well as airway clearance (Hardy, 1994). Supplemen tal oxygen can be supplied during treatment with PEP and nebulized medication has been shown to be ef fectively delivered with this treatment as well (An derson, 1982). PEP has been shown to benefit patients at risk for postoperative atelectasis but has also gained wide practice in the area of airway clearance, especially for patients with cystic fibrosis (MaJhmeister, 1991). Nu merous studies have demonstrated PEP's effective ness. Tyrrell (1986) has shown the PEP mask to be as effective as conventional physiotherapy over a 1 month period with no difference in pulmonary func tion. Falk (i 984, 1993) demonstrated increased spu


328

PART III


tum production and clearance with the use of PEP

Recently approved by the FDA for use by patients

over FET alone. However. Hofmeyer (1986) found

with cystic fibrosis, the Flutter'M continues to be the

FET produced a greater quantity of sputum without

focus of study in the United States. Konstan et a!.

the addition of PEP. Oberwaldner (1986) evaluated

(1994) compared the amount of sputum expectorated

lung function during 10 months of regular treatments

with use of the Flutter'" vs. vigorous voluntary cough

with high-pressure PEP and found reduced pul

vs. PD, percussion and vibration. More than three

monary hyperinflation and airway instability and

times the amount of sputum was produced by subjects

conventional CPT.

with cystic fibrosis using the Flutter'" than with the

higher flow rates with PEP

VS.

These improvements in lung function deteriorated

other two methods and no adverse effects were re

only 2 months after a return to conventional CPT. A

pOited. Ambrosino (1991) has reported success in the

study by Plfeger et a!. (1992) compared PEP to AD

treatment of COPD patients with the device.

and found that PEP produced the highest amount of

Reports in the European literature advocate the

sputum and an increase in lung function when added

use of the Flutter'" for airway clearance (Althaus,

to both techniques. Finally, decreased duration of

1989). In comparison with AD, the Flutter'" was

hospitalization has been cited as a benefit of PEP for

found to be equal in amount of mucus expectoration

airway clearance (Simonova, 1992).

(Lindemann, 1992). When compared with the PEP

Increased independence for the patient and pre

m ask, the Flutter'" showed a small increase i n

sumably, better compliance have been cited as advan

spirometry, whereas the PEP-mask did not, but the

tages of this technique. However, frequent assess

two techniques were otherwise comparable (Schw.

ment of patient technique and appropriate level of

Med. Wschr. 1989).

resistance is recommended (Lapin, 1990). A PEP

The advantages of the Flutter'" device lie in its

mouthpiece (Resistex) has recently been FDA ap

pOltability and ease of learning. Young children can

proved, but the PEP mask has not yet been approved

be taught to use the device effectively, and because

by the FDA.

of its small size, it can easily be used for multiple

A form of PEP in combination with high fre

treatments throughout the day.

quency oscillation is available in a device developed in Switzerland. which is quickly gaining popularity in the United States. The Flutter™ VRP1 (VarioRaw SA,

High Frequency Chest Compression

Aubonne, Switzerland) is a handheld device that in

EffOits aimed at mucus clearance by creating a differ

terrupts the expiratory flow and decreases the col

ential air flow rate, that is, greater expiratory than in

lapsability of the airways. The pipe-like device con

spiratory flow rate, led to the development of a high

sists of a steel ball, a plastic cone, a pertorated cover,

frequency chest compression (HFCC) systcm.

and a mouthpiece. The patient completes about lO to

Hansen and Warwick (1990) designed a large-vol

15 deep breaths keeping the cheeks flat while the

ume variable frequency air-pulse delivery system to

Flutter'M is tilted to achieve the maximum effects of

be used by patients with obstructive lung disease to

the vibration in the chest. This is followed by huffing

promote mucus clearance. The ThAIRapy'" Vest (American Biosystems,

to eliminate the airway secretions. Exhalation through the Flutter'M device causes air

Inc.) system consists of an inflatable fitted vest con

way vibrations and oscillating endobronchial pres

nected to an air-pulse. generator by flexible tubing.

sures (Althaus, 1993) to ease the expectoration of

This device provides oscillation of the entire thoracic

mucus. The PEP maintained by the Flutter™ (5 to 35

cavity at varying frequencies (5 to 25 Hz) and is used

cms of water pressure) prevents dynamic airway

while sitting upright. The lung volume expired tends

compression and improves airflow acceleration.

to increase with lower frequencies (less than to to 12

Therefore the improvement in expectoration is based

Hz), whereas the flow rates tend to increase with

on the increase in airway diameter, as well as on the

higher frequencies (12 to 20 Hz). Three frequencies

improvement in airflow acceleration (Schibler, 1992).

are selected for large volume and three for high


19


329

flows. Each frequency is used for 3 to 5 minutes with

Hospitalized patients with acute exacerbation of

conti I1UOUS ul:J"osolized medication or saline to assist

their lung disease have been shown to tolerate HFCC

secretion Illohilil.ation (Warwick, 1992).

well (Burnett, 1993), and safety and tolerance of this

Two probahlc mechanisms of action have been of fered to explain the significant increase in sputum mo

method has been demonstrated in long-term mechani cally ventilated patients (Whitman, 1993).

bilizJlion (Kious, 1(94). The first mechanism pro

Expense of the apparatus may be a significant de

poses that oscillatory airflow· leads to changes in the

terrent to its use; it is more costly than other mechan

con.;islency of mucus, which result in increased spu

ical aids for airway clearance. However, in a study of

tum mobilil.ation. Significant decreases in mucus vis

HFCC users insured by Blue Cross and Blue Shield,

coelasticity were observed during administration of

a 49% reduction in health care costs was shown in

oscillatory aitflow (Tomkicwicz et aI, (994). The sec

the year following initial use of the vest as compared

ond mechanism proposes that the difference between

with the year prior to HFCC use (Ohnsorg, 1994).

the expiratory and inspiratory velocities produces

The impact of the llse of the HFCC device in a hospi

enough to move muclls. Chang et

tal department was analyzed with a substantial sav

al. (1988) lkmonstrated that nonsymmetrical airflow

ings resulting from therapy self-administration

(peak expiratory flow rates greater than inspiratory

(KIous, 1993).

shear forces

s lrong

flow ratt:s) could be a significant factor leading to en harlCed mllcus clearance during the administration of HFCC. Each chest compression produces a transient

Exercise

flow pulse similar to that observed during coughing

In addition to its many effects on health and well

and by using those flows with the greatest rates and

being, exercise has been shown to assist in secretion

volumes, sufficient force is obtained to move mucus

clearance. It has been suggested that exercise can re

in the airway (Warwick, 1991).

place all or pmt of a conventional chest physiotherapy

High frequency chest wall compression has been shown to inc re as e mucus clearance rates in dogs,

routine in some patients or at some stages of lung dis ease (Zach, 1982; Andreasson, 1987; Cerny, 1989).

with the most pronounced effect in the II to 15Hz

Exercise increases mucociliary transport in pa

frequency range (King, 1983). Radford et al. (1982)

tients with chronic bronchitis (Oldenberg, 1979).

used bronchoscopy to demonstrate a marked increase

Higher transpulmonary pressure with aerobic exer

in speed and flow of mucus by oscillations at even

cise may open closed bronchi as well as increase col

higher frequencies not attainable by manual percus

lateral ventilation to allow mucus to be movcd (An

sion. Results of short-term use of the ThAIRapy'"

dreasson, 1987). It has also been shown that exercise

vest have been mixed, but show HFCC to be at least

induced hyperventilation is more effecti ve than eu

as effective as conventional CPT. Robinson (1992)

capnic hyperventilation in mobilizing bronchial se

showed no significant i m pro vement or deterioration

cretions (Wolff, 1977). The contribution of expira

of lung function with its use. In two different studies,

tory ailflow and exercise-induced coughing are other

Kluft (1992) and Faverio (1994) demonst rated in

factors in more effective secretion removal.

creased wet and dry sputum weights using HFCC vs.

Some studies conclude that exercise alone is not

manual CPT, and Arens (1993) showed similar dry

sufficient and recommend its use to complement

sputum weight, but an increase in wet sputum weight

other forms of airway clearance. Airway clearance

and a significant improvement in pulmonary function

using PD and FET was shown to be more effective

with HFCC vs. conventional CPT. One 2-year study

than exercise with a cycle ergometer at inducing spu

showed improved lung function and greater sputum

tum expectoration (Sath, et ai, 1989). Results from

production in subjects with cystic fibrosis with the

Bilton et al (1992) demonstrated that any modality

use of HFCC vs. manual CPT (Warwick, 1991). No

which included the ACB technique in PD positions

adverse effects were ohsL rvcd with long-term use of

alone or in combination with exercise is better than

the ThAIRapy'" vest.

exercise alone at clearing sputum.


330

PART III


Other studies have suggested that some forms of

1990). However, if the patient develops atelectasis,

exercise may serve as a replacement for chest physio

the stress of respiratory embarrassment may also in

therapy, citing a lack of decrease in lung function fol

crease intracranial pressure. In this instance, the deci

lowing the cessation of CPT and continuing with an

sion may be made to tip the patient to clear the at

exercise program (Zach, 1984; Andreasson, 1987). In

electasis and then subsequently return to a modified

hospitalized patients with cystic fibrosis, no signifi

conservative regimen (Frownfelter, 1987).

cant change in pulmonary function was reported

A fall in arterial O2 saturation has been reported

when exercise was substituted for two treatments of

with the use of postural drainage from additional in

PD, percussion and vibration, and the weight of spu

chest physiotherapy, although the effects of PD were

tum produced was equivalent (Cerny, 1989).

not separated techniques (Selsby, 1990; Huseby,

When mucous clearance was studied, no signifi cant differences were found between exercise on a cycle ergometer, postural drainage, and PEP mask

Contraindications for Postural Drainage

breathing (Lannefors, 1992). Increases in sputum ex pectoration on exercise vs. nonexercise days have

All Positions Are Contraindicated

been reported (Zach, 1981; Baldwin, 1994). For pa

for the Following:

tients with cystic fibrosis who demonstrate compli

Intracranial pressure (ICP)

ance with an exercise program alone or in addition to

>

20 mm Hg

Head and neck injury until stabilized

another form of secretion mobilization, there is evi

Active hemorrhage with hemodynamic instability

dence of positive prognostic value (Nixon, 1992).

Recent spinal surgery (e.g

It is difficult to compare these studies across the board; however, because the mode and length of ex

spinal injury

ercise differs, as does the measurement of effective

Active hemoptysis

ness of airway clearance. Exercise as an airway clear

Empyema

ance technique is not suitable for the very young (less

Bronchopleural fistula

than 4 to 5 years of age), patients with neuromuscular

.•

laminectomy) or acute

Pulmonary edema associated with congestive heart

limitations, or patients with severely limited exercise

failllJ'e (CHF)

tolerance. Moreover, the potential need for supple

Large pleural effusions

mental oxygen during exercise should be monitored.

Pulmonary embolism

Nonetheless, evidence suggests that an exercise pro gram, in addition to clearing secretions, may decrease

Aged, confused, or anxious patients

morbidity and mortality t J improving exercise ca

Rib fracture. with or without flail chest

pacity (Lapin, 1993).

Surgical wound or healing tissue

Contraindications/Precautions to Airway Clearance

Trendelenburg Position is Contraindicated . for the Following:

General precautions and contraindications

Patients in whom increased ICP is to be avoided

to postural drainage positioning

Uncontrolled hype11ension

It is essential that the therapist and the health care

Distended abdomen

team discuss treatment priorities. A decision to use

Esophageal surgery

postural drainage might be made despite a contraindi

Recent gross hemoptysis related to recent l ung carcinoma

cation, if the benefits were thought to outweigh the risks in a particular case.

Uncontrolled airway at risk for aspiration

For example, it is known that use of the Trende lenburg (head down) position increases intracranial

AARC Clinical Practice Guideline.

pressure in neurosurgical patients (Humberstone,

apy.


(1991). Postural drainage ther RespiraIOI)' Care, 36 (12), 1418-1426.

19

Physiological Basis ror Airway Clearance Techniques

331

[976). Therefore O2 saturation levels should be mon

show an intolerance for percussion as part of chest

itored during treatment, most importantly in those pa

physiotherapy. Campbell et a1. (1975) demonstrated

tients with known [ow Pa02 values.

a fall in FEV I associated with percussion that was

Caution must also be used in treating the patient

not evident when percussion was omitted. Adminis

with end-stage lung disease in postural drainage posi

tration of a bronchodilator before treatment with per

tions because of the risk of hemoptysis (Hammon,

cussion abolished the fall in FEV I. Wheezing has

1979; Stern, [978).

also been associated with percussion and vibration in

Decreased cardiac output (Laws, 1969; Barrell, [978) has been associated with chest physiother

1975; Feldman, 1979).

patients with cystic fibrosis and COPD (Tecklin,

apy treatment; however, the effects of postural

The box below summarizes the precautions and

drainage were not separated from those of percus

contraindications for external manipulation of the thorax associated with percussion, shaking, and high

sion and vibration. In the pediatric population, some experts recom

frequency chest compression. Vibration involves less

mend caution with the position used to treat the ante

force to the thorax and may be better tolerated than

rior lower lobes because of the risk of gastroe

the aforementioned techniques. A nebulized bron

sophageal reflux. The box on p. 330 summarizes the

chodilator may be administered during a treatment of

precautions and contraindications for postural

high frequency chest compression to avoid the conse

drainage.

quences of hyperreactive airways.

General contraindications and precautions

to external manipulation of the thorax

Other precautions Manual hyperinflation has been shown to cause sig

In patients who are very young, who have limited

nificant depression of cardiac output in patients who

ability to cooperate, or who are not compliant with other airway clearance techniques, percussion, shak ing, and vibration offer a method to dislodge retained secretions. Because of the force transmitted to the thoracic cage with these techniques, there are many precautions and contraindications to consider. The therapist should not make this decision alone, but needs direction from the medical team. Chest physio therapy is not a completely benign procedure and should not be peliormed in the absence of good indi cations (McDonnell, 1986). Percussion has been shown to contribute to a fall

Contraindications to External Manipulation of the Thorax In Addition to Contraindications for Postural Drainage: Subcutaneous cmphysema Recent epidural spinal infusion or spinal anesthesia Recent skin grafts, or flaps, on the thorax Bums. open wounds. and skin infections of the thorax

in Pa02 in acutely ill patients (Connors, 1980), espe

Recently placed pacemaker

cially in patients with cardiovascular instability (Oor

Suspected pulmonary tuberculosis

menzano, 1972) and in neonates (Fox, 1978). The factor that seems most associated with or predictive of the effect is the baseline or before-therapy Pa02 (McDonneJl, 1986). Cardiac arrhythmias have been associated with

Lung contusion Bronchospasm Osteomyelitis of the ribs Osteoporosis

chest percussion for bronchial drainage (Hammon,

Coagulopathy

1981). Huseby (1976) hypothesizes that hypoxemia

Complaint of chest-wall pain

may be the underlying mechanism of CPT-caused cardiac arrhythmias.

AARC Clinical Pracli ce Guideli'ne. (1991). Postural drainage ther

Patients with hyperreactive airways (e.g., asthma)

apy. Respil'(l/ory Care,]6 (12),1418-1426.


332

PART III


are unable to compensate hemodynamically with lit

Factors to Be Considered When Selecting

tle cardiac reserve (Clement, 1968; Laws, 1969). Sig

an Airway Clearance Technique

nificant and deleterious increases in ICP have also been demonstrated (Garradd, 1986). Webber (1988)

Motivation

offers these additional contraindications to manual

Patient's goals

hyperinflation: severe hypoxemia with few bronchial

Physician/caregiver's goals

secretions as in ARDS, acute pulmonary edema, air

Effectiveness (of considered technique)

leak (e.g., pneumothorax), severe bronchospasm as in

Patielll's age

acute asthma, and hemoptysis.

Patient's abiliLY to concentratc

The use of PEP for airway clearance carries an in creased risk of pneumothorax (Oberwaldner, 1986).

Ease (of learning and of teaching)

Bronchodilator premedication should be considered

Skill of therapists/teachers

when applying PEP in patients who show clinical

Fatigue or work required

and/or physiological signs of airway hyperreactivity

Need for assisLants or equipmelll

(Pfleger, 1992).

LimiLations of technique based on disease type and

The increased aitilow produced by the huff cough,

severity

as in the ACB technique, may aggravate bron chospasm (Hietpas, 1979). Additionally, Hietpas cau

Costs (direct and indirect)

tions that spontaneous explosive coughing may be

Desirability of combining methods

precipitated by the movement of secretions into the Hardy, K.A. (1994). A review of airway clearance: new techniques,

larger airways by the huff cough. Several precautions must be observed when using

indications, and recommendations. Re.ljJimlorv Care, 39 (5), 440-452.

exercise as a form of airway clearance. Desaturation has been shown to occur with exercise in people with pulmonary disease (Lane, 1987; Henke, 1984), and

a prescribed treatment has a negative influence on pa

therefore it becomes prudent to monitor oxygen satu

tient adherence. It has been suggested that enhanced

ration, providing supplemental oxygen for the exer

compliance might be achieved if the treatment were

cise period when indicated. Exercise-induced bron

specifically tailored to the individual patient's needs

chospasm must also be considered when pulmonary

with regard to clinical status, family functioning, and

compromise is seen with exercise, especiall y with

family concerns. Negotiation between the patient and

higher intensity exercise (Godfrey, 1975). When indi

the caregiver to agree on follow-through with the pre

cated, it is recommended to provide an inhaled bron

scribed treatment regimen is also effective (Shultz,

chodilator 20 to 30 minutes before exercise to allevi

1980). For this reason, it is imperative to consider

ate this symptom (Orenstein, 1985). Andreasson

multiple factors in the recommendation of a specific

(1987) reports a risk of pneumothorax in conjunction

technique of airway clearance, especially in the pa

with exercise in those patients with extensive bullae.

tient with a chronic disease (see box above). The age of the patient will affect the usefulness of a particular technique. Infants and very young chil

Factors Affecting Selection of

dren are limited to conventional physical therapy

Airway Clearance Techniques

(postural drainage, perc'ussion,

In the pulmonary population, lack of compliance in

they are not able to cooperate with other methods of

performing airway clearance on a regular basis has

airway clearance. After the age of 3 or 4, a youngster

been well documented (Currie, 1986; Passero, 1981;

may be taught huffing and brcathing control, and as

Muszynski-Kwan, 1988; Litt, 1980). The problem is

sisted with the ACB technique. A vest for use with

worse in the adolescent group. Litt (1980) has also

HFCC is now available for children as young as 2 or

shown that the complexity and increased duration of

3 years of age. PEP, FlutterT' and exercise also are


19


333

suitable for this age group, depending on the child's

Accessibility of equipment or trained personnel

attention span and cooperation. Children 12 years of

limits the use of some airway clearance techniques.

age and older are capable of using any of the airway

Many of these techniques are new or not available to

clearance techniques, including AD, which requires

many health care centers, especially in the United

more concentration than a younger child is typically

States, since they were pioneered in Europe. Proper

able to exhibit.

instruction and review of a patient's technique is im

The lack of an assistant to provide airway clearance

perative to achieve optimal results, and in the case of

is a factor that prompts many patients to seek methods

PEP, the reassessment of resistance is recommended.

other than postural drainage and percussion. HFCC,

In the case of AD, the method is limited by the num

PEP, Flutter''", ACB, exercise and AD are techniques

ber of instructors available to teach the technique to

that provide independence from a caregiver. These

patients and requires a great deal of time on the part

methods have been chosen by adults living on their

of the health care team member to learn. The patient

own, students away at school, and adolescents eager

must possess motivation and the time to learn the

for independence. For optimal results, each tech

technique and be willing to "fine tune" the technique

nique's effectiveness must be regularly reevaluated by

with the therapist periodically.

a health care team member skilled in the area of air

In this area of cost containment, the financial re

way clearance after it has been agreed that a patient ex

quirements of a technique must also be taken into con

hibits independence in a given technique.

sideration, especially in the case of a chronic condi

The clinical status of the patient during each hos

tion. The availability of any given method then, could

pital admission must be evaluated to determine the

be determined by the insurance coverage or additional

appropriateness of an ACT. For example, airway hy

financial resources of the patient. If several methods

perreactivity might be worsened by PO and percus

prove to be equally effective, it would be prudent to

sion, and care must also be taken when using ACB in

select the methods requiring the least expense. Al

this case. HFCC, Flutter''", and exercise should be

though the most common form of airway clearance in

preceded with an inhaled bronchodilator in this case,

the United States continues to be postural drainage

and PEP can be performed concurrently with bron

and percussion by a caregiver, this often proves to be

chodilator administration. AD lends itself well to use

quite expensive, especially if a family member is not

by patients with airway hyperreactivity.

available for ongoing home treatments. The equip

Gastroesophageal reflux prohibits patients from

ment needed for ACTs varies. The generator required

performing airway clearance in conventional PO po

for HFCC is expensive to purchase or rent on a

sitions. In this instance, AD, Flutter''', PEP, HFCC,

monthly basis. Mechanical percussors or vibrators are

and exercise, or ACB in upright positions, are the

moderately priced, and PEP and the Flutter™ valve are

preferred treatments. In infants or neurologically im

the least expensive of those techniques requiring

paired patients where PO and percussion is the treat

equipment. A patient independently using ACB or AD

ment of choice, modified PO positions are used and

consumes the least financial resources.

sufficient time allowed between a feeding and a treat ment with PD.

Ultimately, the regular use of a particular ACT by a patient is governed by personal belief in the effec

The severity of a patient's lung disease will affect

tiveness of the method for his or her own disease

the choice of ACT. Specifically, a patient with end

process, the manner in which the method affects the

stage lung disease or an acute exacerbation might not

patient family's life habits, and the patient's willing

have the required energy level to carry out an active

ness to use the technique on a daily basis. Compli

airway clearance technique such as AD or PEP effec

ance is ultimately the best measure of any airway

tively. A more passive technique would be appropri

c1earancc technique's effectiveness.

ate, at least temporarily. Also a marked decrease in

Clinical outcome measures to assess the effective

PFT's limits the airflow control necessary for AD,

ness of an airway clearance technique can be fol

F1utter™, or PEP.

lowed during clinical appointments or periods of hos


334

PART III


pitalization. Radiographic changes, arterial blood gas

must consider many factors in recommending an

values, O2 saturation, and pulmonary function tests

alternate form of airway clearance. Age of the pa

may demonstrate adequate airway clearance or the

tient is a prime factor in the appropriateness of a

need to reassess the appropriateness of the technique

selected technique. For infants, PO, percussion,

or the application of it by the patient. Though it is

and vibration remain the mainstay of secretion

difficult to quantify, many patients subjectively rely

clearance. In older children, the active cycle of

on amount of sputum production to guide their choice

breathing may be initiated, positive expiratory

of secretion clearance method. This measure provides

pressure and Flutter'" may be taught, and high fre

immediate feedback to the patient without visiting the

quency chest compression is available for children after about age 3 or 4. Exercise should be included

hospital or clinic.

in treatment as well. Children 12 years of age or older and adults have the complete range of airway

SUMIVIARY

clearance techniques at their disposal, including

The goals of airway clearance are to decrease airway

autogenic drainage.

obstruction, improve secretion clearance, and im

Treatments aimed at secretion clearance require an

prove ventilation and gas exchange. Routine applica

individualized approach to tailor the treatment to the

tion of airway clearance techniques in many condi

patient's condition and lifestyle, to continuously

tions has not been shown to be effective in achieving

reevaluate the patient's status, and to monitor the re

these goals. ACTs are not without side effects or

sponse to treatment.

complications; routine use of these methods is not

Acceptance of the specific treatment technique by the patient and family is paramount; compliance is

recommended without clear indications. Indications for ACTs have been divided into those for acute illness and chronic disease states.

the key to achieving effective treatment, especialJy in chronic lung disease.

In acute illness, traditional chest physical therapy,

Further research in the area of airway clearance

that is, PO, percussion, and vibration, has been

is certainly needed. Studies with consistent applica

shown to be beneficial in patients with copious se

tion of techniques, similar outcome measures, and

cretions and in the treatment of atelectasis (Kir

consistent study design will assist practitioners in

iloff, 1985). For patients with cystic fibrosis, treat

evaluating and recommending a given technique of

ment with PEP and exercise in conjunction with

airway clearance.

PO, percussion, and vibration were also shown to be effective in an acute exacerbation (Boyd, 1994). Acute asthma, bronchitis, and pneumonia without copious secretions, bronchiolitis, and routine post

REVIEW QUESTIONS I. What kinds of pulmonary conditions would not be likely to benefit from ACTs?

operative conditions were not shown to benefit from PO, percussion, and vibration (Sutton, 1982;

2. Which ACTs would be the easiest (for the thera pist and the patient) to incorporate into a routine

Eid,1991).

of conventional PO and percussion?

In chronic disease states, patients with cystic fi brosis and bronchiectasis were found to benefit from

3. What possible factors could be considered a con

PO, percussion, and vibration (Kiriloff, 1985). Posi

traindication to chest percussion with PO in a

tive expiratory pressure and exercise were also shown

trauma or postoperative patient?

to be effective in the chronic management of patients

4. What factors might make it difficult for a patient to accept a new method of airway clearance?

with cystic fibrosis (Boyd, 1994). In those patients for whom traditional chest

5. Which ACTs would be most appropriate during

physical therapy is not effective, the caregiver


an acute exacerbation of a pulmonary disease?

19


335

Chang, H.K., Weber, M.E., King, M. (1988). Mucus transport by

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48, 586·591

Clinical Application of Airway Clearance Techniques Anne Mejia Downs

KEY TERMS

Active cycle of breathing technique (ACBT)

Manual hyperventilation

Airway clearance techniques (ACTs)

Percussion


Postive expiratory pressure (PEP)

Dynamic air therapy bed

Postural drainage (PD)

Flutter™

Shaking

Forced expiratory technique (FET)

Trendelenburg

High frequency chest compression (HFCC)

Vibration

INTRODUCTION

The previous chapter addressed the physiological

Oxygen transport from the lungs to body tissues can

basis of each technique, the history of its use, and re

be limited in patients that possess an ineffective

search to establish its effectiveness. This chapter pro

cough or an impairment of normal mechanisms of

vides an introduction to the application of these tech

mucociliary clearance. The caregiver must augment

niques to patients and addresses the benefits and

these mechanisms using the array of techniques avail

liabilities of each technique.

able for airway clearance. Each technique has a phys

Airway clearance techniques differ with respect to

iological basis for improving the mobilization of

equipment needs, the skill level required to perform

secretions. The caregiver must consider the patho

them, and their usefulness with various clinical prob

physiology and the symptoms of the disease, the

lems. Matching a patient with an appropriate method

availability of the technique to the patient, and the

or combination of methods may increase effective

patient's acceptance of the technique in prescribing

ness, reduce complications, and promote adherence

an optimal method of airway clearance.

to the long-term treatment. 339


340

PART III

Cardiopulmonary Physic.al Therapy Interventions

UTILIZATION OF AIRWAY CLEARANCE TECHNIQUES

of tube feedings or meals. The inhalation of bron

This section will deal with the application of airway

chodilator mcdications should take place before air

clearance techniques (ACTs) with specific instruc

way clearance maneuvers. Inhaled antibiotics are best

tions for patient treatment. Contraindications and pre

scheduled after airway clearance has taken place for

cautions for each ACT are addressed in Chapter 21.

optimal deposition of medication. Adequate pain con

This section will speak to practical concerns regard

trol is necessary to receive a patient's best effort and

ing patient care.

cooperation with a treatment. It is also impOitant to

Preparation for any secretion removal technique should include evaluation of the patient's pulmonary status (see Chapter

15)

have all necessary equipment and personnel available at the start of the treatment.

so that measures may be com

pared before and after a treatment is completed. A physical examination, including inspection, palpa

POSTURAL DRAINAGE

tion, measurement of vital signs, and chest ausculta

Postural drainage (PO) is accomplished by position

tion provides assessment of a treatment's effective

ing the patient so that the position of the lung seg

ness. Laboratory tests including chest x-ray, arterial

ment to be drained allows gravity to have its greatest

20- I

20-5).

blood gas measurements, and pulmonary function

effect (see Figures

studies should be reviewed, since these may be used

sitions are used when a precaution or relative con

as measures of treatment effectiveness.

through

Modified po

traindication to the ideal position exists. For example,

Scheduling an optimal time for patient treatment

if an increase in intracranial pressure is a concern, the

must take into account several factors. At least I half

head of the bed should remain flat instead of being

hour to I hour should be allowed for the completion

tipped into Trendelenburg (head down) position.

Both Upper Lobes Apical Segments

Right Upper Lobe Anterior Segment - hIps .:Ire in external rotiltJon, smilH pillow under knee:s for :support 0' JoInts and comfort.

1

----

KPS.

FIGURE 20-1 Upper lobes.


,;,1>(1,.,

20

Clinical Application of Airway Clearance Techniques

Right Upper Lobe Posterior Segment

Left Upper Lobe Lingula

Both Lower Lobes Superior Segments (Apicall

Right Middle Lobe

FIGURE 20-2 Upper, middle, and lower lobes.

Both Lower Lobes Anterior Segments

Right Lower Lobe Lateral Segment

Both Lower Lobes Posterior Segments

Left Lower Lobe Lateral Segment, RLL Cardiac (Mediall

FIGURE 20-3 Lower lobes.


341

342

PART III


FIGURE 20-4 A, right upper lobe-posterior segment (anterior view-patient positioned three-fourths prone). B, right upper lobe-posterior segment (posterior view).

NOTE:

Upper extremities toward prone,

underneath arm pulled free from under patient's body. This position may also be a modified position for right lower lobe posterior segment.

FIGURE 20-5 Both lower Jobes-posterior segments (shown using teJeJphone books or piJlows for home use). A beanbag chair is also helpful for home treatments.


20

Equipment Required For Postural Drainage


343

specific lobe. Extended times in a position may

I. For the hospitalized patient, there exists a vari

be used by coordinating the positioning with

ety of beds that employ manual or electric de

nursing care for skin pressure relief. If postural

vices to position the patient. Air therapy beds,

drainage is used in conjunction with another

most often used in the intensive care unit (lCU),

technique, the time in each position may be de

are valuable aids allowing ease of positioning,

creased. For example, if percussion and vibra

especially in large or unresponsive patients.

tion are performed while the patient is in each

2. Make use of pillows or bedrolls to support

PO position, 3 to 5 minutes is sufficient.

3. A patient who requires close monitoring should

body parts or relieve pressure areas.

3. For home treatmcnt, aids in positioning might

not be left unattended in a Trendelenberg posi

include pillows, a slant board (or ironing board

tion, but this may be appropriate if patients are

if the patient is small), a foam wedge, sofa

alert and able to reposition themselves.

4. It is not necessary to treat each affected lung

cushions, or a bean bag chair.

segment during each treatment; this may prove to be too fatiguigg for the patient. The most af

Preparation for Postural Drainage

fected lobes should be addressed with the first

l. Nebulized bronchodilators before PO may fa cilitate the mobilization of sputum.

treatment of the day, with the other affected areas addressed at a subsequent treatment.

2. An adequate intake of fluids (if allowed) de

5. The patient should be encouraged to take deep

creases the viscosity of the secretions, allowing

breaths and cough after the treatment and if

easier mobilization.

possible after each position. Having the patient

3. Become familiar with the workings of the model of bed the patient is occupying, espe cially the movement of the bed into the Trende

sit upright or lean forward optimizes this effort (Frownfelter, 1 987).

6. Secretions may not be mobilized immediately after the treatment but possibly 1 half hour to

lenberg position.

4. In the ICU, it is imperative to be familiar with

1 hour later. The patient should be thus in

the multiple lines, leads, and tubes attached to

formed and requested to clear secretions then.

the patient. Allow enough slack from each de

The nurse or family member should be in

vice to position

cluded in this aspect of treatment, especially

a

patient for postural drainage.

5. Make sure there are enough personnel to posi tion the patient with as little stress to both pa

with difficult patients who need such encour agement (Frownfelter, 1987).

tient and staff as possible (Frownfelter, 1987).

6. Have suctioning equipment ready to remove se cretions from an artificial airway or the pa tient's oral or nasal cavity after the treatment.

Advantages and Disadvantages of PO PO is relatively easy to learn; the patient and/or care giver must be familiar with the appropriate position ing for the affected lung fields. Treatment in the hos

Treatment with PO

p i t a l m a y be c o o r d i n a t e d w i t h o t h e r p a t i e n t

1 . After determining the lobe of the lung to be

activities-po sitioning for s k i n pressu r e relief,

treated, position the patient in the appropriate po

bathing, or positioning for a test or procedure. Home

sition, using pillows or bed rolls as needed to sup

treatment may be coordinated with activities such as

port the patient comfortably in the position indi

reading or watching television.

cated. See figures 20-1 through 20-5, p. 340-342.

2. If postural drainage is used exclusively, each

However, for many patients, optimal PO positions will be contraindicated for a variety of reasons (see

position should be maintained for 5 to 1 0 min

Chapter 21). Compliance with PO may be reduced

utes, if tolerated, or longer when focusing on a

because of the length of the treatment, especially in


344

PART III


FIGURE 20-6 A and B, If children are able to role play the treatment, they will better understand what is expected and be more cooperative with therapy.

the pediatric population, who will require consider

breathing. Percussion is used in postural drainage po

able distractions to maintain a desired position.

sitions for increased effectiveness (Sutton, 1985;

The cost of the equipment required for PD is mini mal; inexpensive items may be used for home treat

Bateman, 1979) and may also be used dUling the ac tive cycle of breathing (ACB) technique.

ment. However, the cost of a caregiver's time to pro vide the treatment, especially in the case of a chronic disease, may be substantial. A family member may

Equipment Required for Percussion

be willing to learn the procedure, which would pro

1. The only equipment required for manual per

vide a benefit in terms of expense, as well as flexibil

cussion is the caregiver's cupped hands to de

ity in scheduling (Figure 20-6).

liver the force to mobilize secretions.

2. For the adult and older pediatric population, electric or pneumatic percussors that mechani

PERCUSSION

cally simulate percussion are available. This

Percussion is performed with the aim of loosening re

enables a patient to apply self-percussion more

tained secretions from the airways so they may be re

effectively. Several models have variable fre

moved by suctioning or expectoration. A rhythmical

quencies of percussion, as well as different lev

force is provided by clapping the caregiver's cupped hands against the thorax over the affected lung seg

els of intensity. 3. Several devices may be used to provide percus

ment, trapping air between the patient's thorax and

sion to infants: padded rubber nipples, pediatric

the caregiver's hands (Figure 20-7). It is performed

anaesthesia masks, padded medicine cups, or

during both the inspiratory and expiratory phases of

the bell end of a stethoscope.


20


345

FIGURE 20-7 Chest percussion.

Preparation for Percussion

thema occurs with percussion, it is usually a re

1. Placing the patient in appropriate PD positions (as the patient's condition allows) enhances the effect of percussion.

sult of slapping or not trapping enough air be tween the hand and the chest wall (Imle, 1989). 3. An even, steady rhythm will best be tolerated

2. Place a thin towel or hospital gown over the pa

by the patient, and the rate of manual percus

tient's skin where the percussion is to be ap

sion is normally between 100 and 480 times per

plied. The force of percllssion over bare skin

minute (lmle, 1989).

may be uncomfortable; on the other hand,

4. The force applied to the chest wall from each

padding that is too thick absorbs the percussion

hand should be equal. If the nondominant hand

without benefit to the patient.

is not able to keep up with the dominant hand,

3. Adjust the level of the bed so that proper body

the rate should be slowed to match that of the

mechanics may be used during the treatment.

slower hand. It might also be helpful to start

Fatigue or injury of the caregiver may be the

with the nondominant hand and let the domi

result of lengthy or numerous treatments if

nant hand match the nondominant (Frownfelter,

1987). The force does not have to be excessive

proper body mechanics are ignored.

to be effective; the amount of force should be adapted to the patient's comfort.

Treatment With Percussion

5. If the size of an infant does not allow use of a

I. Position the hand in a cup with the fingers and

full hand, percussion may be done manually

thumb adducted. It is important to maintain this

with four fingers cupped, three fingers with the

cupped position with the hands throughout the

middle fi nger "tented," or the thenar and hy

treatment, while letting the wrists, arms, and

pothenar surfaces of the hand (Crane, 1990).

shoulders stay relaxed.

6. Hand position should be such that percussion

2. The sound of percussion should be a hollow

does not occur over bony prominences. The

sound as opposed to a slapping sound. If ery

spinous processes of the vertebrae, the spine of


346

PART III


the scapula, and the clavicle should all be

The expense of a mechanical device for percus

avoided. Percussion over t h e floating ribs

sion is minimal compared with the ongoing cost of a

should also be avoided, since these ribs have

caregiver to provide percussion and PD in the hospi

only a single attachment.

tal setting or a home care situation. In the case of

7. Percussion should not be performed over breast

young children or unresponsive patients, there are

tissue. This would produce discomfort and di

few choices for airway clearance. For other popula

minish the effectiveness of the treatment. In the

tions, however, a more independent method would

case of very large breasts, it may be necessary

also prove to be more cost-effective if adequate com

to move the breast out" of the way with one

pliance was achieved.

hand and percuss with the other hand.

8. A patient may be taught to perform one-handed self-percussion to those areas that can b e reached comfortably, either manually o r with a

VIBRAnON/SHAKING The techniques of vibration and shaking are on oppo

mechanical percussor. This does however, vir

site ends of a spectrum. Vibration involves a gentle,

tually preclude the treatment of the posterior

high frequency force, whereas shaking is more vigor

lung segments.

ous in nature. Vibration and shaking are performed with the aim of moving secretions from the lung pe

Advantages and Disadvantages of Percussion

riphery to the larger airways where they may be suc tioned or expectorated. Vibration is performed by co

The addition of percussion to a PD treatment may en

contracting all the muscles in the caregiver's upper

hance secretion clearance and shorten the treatment.

extremities to cause a vibration while applying pres

Patients often find the rhythm soothing and are re

sure to the chest wall with the hands. Shaking is a

laxed and sedated by percussion, especially young

stronger bouncing maneuver, which also supplies a

children and infants.

concurrent, compressive force to the chest wall.

Patients with chronic lung disease, who have used

Like percussion, vibration and shaking are lIsed in

PD and percussion for many years and have found it

conjunction with PD positioning. Unlike percussion,

effective, are reluctant to try an alternative method of

they are performed only during the expiratory phase

airway clearance. Compliance with this method is de

of breathing, starting with peak inspiration and con

pendent on the availability of a family member or

tinuing until the end of expiration. The compressive

other caregiver to provide the treatment. Mechanical

forces follow the movement of the chest wall.

percussors allow the patients more independence or decrease fatigue of a caregiver, and are especially use ful in patients requiring ongoing treatment at home.

Equipment Required for Vibration/Shaking I. For manual techniques, the only equipment re

Percussion is not well-tolerated by many patients postoperatively without adequate pain control. The

quired is the caregiver's hands.

2. Mechanical vibrators are available to administer

force of percussion is also a threat to patients with os teoporosis or coagulopathy. Other contraindications

the treatment and are useful for self-treatment

are listed in Chapter 21. Percussion has been associ

by a patient or to reduce fatigue in the caregiver.

ated with a fall in oxygen saturation, which can be

3. For infants, a padded electric toothbrush is an

eliminated with concurrent thoracic expansion exer

alternative (Crane, 1990).

cises and pauses for breathing control (Pryor, 1990). Delivering percussion for extended periods on an ongoing basis can result in injury to the caregiver,

Preparation for Vibration/Shaking

whether a family member or a health care provider.

I. Place the patient in the appropriate PD posi

Repetitive motion injuries of the upper extremities

tion or modified position as the patient's sta

may occur in long-term delivery of percussion for

tus allows.

airway clearance.

2. Place a thin towel or hospital gown over the


20

patient's skin. The material should not be thick enough to absorb the effect of the vibra


347

ment of chest deflation. 4. If the patient is mechanically ventilated, the previously described techniques must be timed

tion or shaking. 3. Proper body position of the caregiver is impor tant to deliver an effective treatment and to de crease caregiver fatigue.

with ventilator-controlled exhalation. 5. If the patient has a rapid respiratory rate, either voluntary or ventilator-controlled, it may be necessary to apply vibration or shaking only during every other exhalation.

Treatment with Vibration/Shaking

6. The frequency of manual vibration is between

I. Conventional chest physical therapy is often re ferred to as a combination of postural drainage

12 and 20 Hz; shaking is 2 Hz (Gormezano, 1972; Bateman, 1981). 7. A mobile chest wall is necessary to apply a com

and percussion, vibration, or shaking.

2. For shaking, with the patient in the appropriate

pressive force without causing discomfort. If a pa

PO position, place your hands over the lobe of

tient has limited chest wall movement, vibration

the lung to be treated and instruct the patient to

will probably be tolerated better than shaking.

take in a deep breath. At the peak of inspiration,

8. Mechanical vibrators may be used by patients

apply a slow (approximately 2 times per sec

themselves, realizing that limited attention can

ond), rhythmic bouncing pressure to the chest

be paid to the posterior portions of the lungs.

wall until the end of expiration. The hands fol low the movement of the chest as the air is ex haled. 3. For vibration, the hands may be placed side by

Advantages/Disadvantages of Vibration/Shaking The use of vibration or shaking with PO may enhance

side or on top of one another as shown in Fig

the mobilization of secretions. Shaking or vibration

ures 20-8 and 20-9. As with shaking, the pa

may be better tolerated than percussion, especially in

tient is instructed to take in a deep breath while

the postsurgical patient.

in a proper PO position. A gentle but steady co

Manual vibration and shaking allows the caregiver

contraction of the upper extremities is per

to assess the pattern and depth of respiration. The

. formed to vibrate the chest wall, beginning at

stretch on the muscles of respiration during expira

the peak of inspiration and following the move-

tion may encourage a deeper inspiration to follow. A

FIGURE 20-8

FIGURE 20-9

Vibration-hands positioned on both sides of the chest.

Vibration-hand p)acement one on top of the other.


348

PART III


mechanical vibrator, more commonly used with pedi

Equipment Required for Manual Hyperinflation I. A manual ventilation bag, such as the Ambu, at

atric patients, may be preferred by a caregiver to de

tached to an oxygen source is needed for lung

liver long-term airway clearance. The patient cannot apply these techniques her

inflation. A positive-end expiratory pressure

self, except in a limited manner with a mechanical

(PEEP) valve may be attached. This is recom mended when greater than 10 cm PEEP is being used for mechanical ventilation (Webber, 1993).

vibrator, so compliance and regular administration of vibration depends on caregiver availability. The same contraindications for percussion apply,

2. A second trained caregiver is necessary to pro

since compression to the thorax is involved with shak

vide shaking or vibration in an appropriate se quence with lung inflation.

ing and vibration. The technique of vibration is less

3. Normal saline should be available for installa

constrained by these contraindications than is shaking.

tion into the airways to assist with loosening secretions.

MANUAL HYPERINFLATION The technique of manual hyperinflation is used in pa tients with an artificial airway, who are mechanically

Preparation for Manual Hyperinflation

ventilated or who have a tracheostomy. This method of

1. It may be necessary to premedicate the patient

airway clearance promotes mobilization of secretions

with a sedative or analgesic so that airway

and reinflates collapsed areas of lung. Two caregivers

clearance may be better tolerated.

are necessary to provide this treatment and the coordina

2. The two caregivers providing the treatment

tion between these two people is key to achieving satis

should be positioned on opposite sides of the

20-10.

bed to allow greater freedom of movement and

factory results. This technique is shown in Figure

FIGURE 20-10 Simulated cough using self-inflating bag and chest compression with vibration.


20

improved observation of the patient's response


349

Advantages/Disadvantages of Manual Hyperinflation Manual hyperinflation may be helpful in managing air

to treatment.

3. Normal saline (2 to 3 mL) may be used before

way secretions in those patients requiring long-term me

hyperinflation to assist with loosening, thick se

chanical ventilation. In this patient population, the

cretions (Webber, 1993).

choice of airway clearance techniques is limited, espe

4. The positions for treatment will be primarily

cially when the patient is unresponsive. Manual hyperin

side-lying with the head of the bed flat or

flation simulates a cough by augmenting the inspiratory effort, momentarily maintaining a maximal inspiratory

slightly elevated to patient tolerance.

hold, and causing an increased expiratory flow. However, hyperinflation has the potential to cause

Treatment With Manual Hyperinflation

significant barotrauma. There are a number of con

1. One caregiver squeezes the manual ventilation

traindications to this technique including unstable he

bag slowly to inflate the lungs. A pause i s

modynamics, pulmonary edema, air leak, and severe

maintained momentarily at the peak o f inflation

bronchospasm (Webber, 1988). In addition, it is not

to allow collateral ventilation to fill underex

appropriate for infants with increased pulmonary resis

panded areas of the lung. Release of the bag

tance requiring high inflation pressures or in preterm

should be rapid, resulting in a high expiratory

infants at risk of pneumothorax (Webber, 1993). Other

flow rate (Clement, 1968).

contraindications are discussed in Chapter 21.

2. A second caregiver provides thoracic compres sion with shaking or vibration to assist with the

Thus manual hyperinflation requires two well-trained caregivers. This may be its biggest disadvantage.

mobilization of secretions. The compression phase should begin just before the inflation pressure has been released and continue until the end of the expiratory phase.

ACTIVE CYCLE OF BREATHING TECHNIQUE The active cycle of breathing (ACB) technique involves

3. In a patient who is breathing spontaneously,

three phases repeated in cycles: breathing control, tho

"bag squeezing" with the manual ventilation

racic expansion, and the forced expiratory technique

bag should be timed to augment the patient's

(FET). This method encourages active participation of

inspiratory effort, making vibration more effec

the patient and has been shown to be as effective when

tive (Imle, 1989).

perfonned by the patient alone as with the aid of a care

4. After about six cycles of inspiration/expiration,

giver (Pryor, 1979). Postural drainage positions may be

the patient's airway is suctioned using sterile

used in conjunction with ACB technique. This method

technique. The length of treatment is individu

of airway clearance may be used with some children as

alized and depends on the amount of secretions

young as 3 or 4 years of age. The sequence of ACB

present in the airways and the areas of the

technique is shown in the box on p. 350.

lungs affected.

5. Manual hyperint1ation may be performed with intubated infants or children using an appropri

Equipment Required for ACB Technique

ately sized ventilation bag. Care must be taken

1. The only equipment required for this manual

to apply slow inflation, so as to avoid a high

technique is the patient's or caregiver's hands

peak inspiratory pressure, which carries the risk

to percuss or shake/vibrate the chest wall dur

of barotrauma (Webber, 1993).

ing the thoracic expansion phase.

6. When manual hyperinflation is contraindicated,

2. Mechanical percussors or vibrators may be

shaking or vibration may be timed with the expi

used during the thoracic expansion phase, ei

ratory phase of the ventilator without additional

ther for self-percussion by the patient or for use

inflation during inspiration (Webber, 1988).

by the caregiver.


350

PART III


ACB Technique •

Breathing control Diaphragmatic breathing at no nnal tidal volume

•

3-4 Thoracic expansi on exercises Deep inhalation with relaxed exhalation at vital capacity

with or without chest percussion •

•

•

•

Breathing control

Three to four thoracic e xp an sion exe rcises Breathing control Forced exp iratory technique One to two huffs at mid to low lung volume Abdominal muscle contracti on to produce forced exhalation

•

Breathing control

J. (1993). Physiotherapy skills: B. Pryor, J. (eds.). (1993). Physiotherapy for respiralory and cardiac problems. Churchill

Adapted from Webber,

B.,

FIGURE 20-11 Peak flow meter mouthpiece.

Pryor,

techniques and adjuncts. In Webber,

ducti ve area of the lungs. The entire treatment

Livings\one: Edinburgh.

may also be done in the sitting position.

3. A minimum of 10 minutes in any productive position may be necessary to clear a patient

3. If PD positions are used, equipment for posi

with a moderate amount of secretions. Patients

tioning will be required.

after surgery or with minimal secretions may

4. To teach the huffing maneuver (part of the

not require as much time, and very ill patients

FET), it may be helpful to use a peak flow

may fatigue before optimal treatment is given

meter mouthpiece to keep the mouth and glottis

(Webber, 1993).

open (Figure 20-11). Young children may be taught games of huffing at cotton balls or tissue to improve the technique (Webber, 1993). To help them focus on the expiratory maneuver,

Treatment With the Active Cycle of Breathing Technique

small children may also be taught to flap their arms to their lateral chest as they perform the

I. Breathing

control-The

patient is instructed to

breathe in a relaxed manner using normal tidal

huff, a technique referred to as the "chicken

volume. The upper chest and shoulders should

breath" (Mahlmeister, 1991).

remain relaxed and the lower chest and ab domen should be active. The phase of breathing control should last as long as the patient re

Preparation for ACB Technique

quires to relax and to pr epare for the next

I. Treatment of two or three productive areas during one session may be tolerated by most patients.

phases, usually 5 to J a seconds.

2. Thoracic expansion

The emphasis during this

-

2. The patient is positioned or positions herself in

phase is on inspiration. The patient is instructed

a PD position to stimulate drainage of a pro-

to take in a deep breath to inspiratory reserve;



20

Ineffective Huffing

Effective Huffing

•

Mouth half or almost closed

•

Mouth open, O-shaped to keep glottis open

•

Expiratillfi always starting from high lung volume

•

Forced expiration

•

Abdominal muscles not used

•

•

From mid to low lung volume moves periph eral secretions

Sound more like hissing or blowing •

from high to mid lung volume moves proxi

Mouth shaped ;)s for "E" sound

mal secretions

Incorrect quality of expiration •

Too vigorous or long. producing paroxysmal

•

Muscles of the chest wall and abdomen contract.

•

Sound is like a sigh. but forced.

•

Rate of expiratory flow varies with the following:

coughing

•

•

Too gentle

•

Too short

351

The individual The disease

"Catching" or "grunting" at the back of the throat

The degree of airflow obsu'lIction •

Crackles heard if excess secretions are present

From Partridge, et ai, Physiotherapy, March 1989, Vol. 75, No.3 expiration is passive and relaxed. The caregiver or the patient may place a hand over the area of the thorax being treated to further encourage in creased chest wall movement.

breath in will be effective. This huff will be

3. Chest percussion, shaking, or vibration may be

longer and quieter. To clear secretions that

performed in combination with thoracic expan

have reached the larger, proximal airways, a

sion as the patient exhales. For surgical pa

huff after a deep breath in will be effective.

tients or those with lung collapse, a breath hold

This huff will be shorter and louder.

or a sniff at the end of inspiration encourages

6. The patient must pause for breathing control

collateral ventilation to assist with reexpansion

after one or two huffs. This will prevent any in

of the lung.

crease in airflow obstruction.

4. FET: This phase consists of huffing inter

7. The ACB technique may be adapted to the indi

spersed with breathing control. A huff is a

vidual patient's needs. If secretions are tena

rapid, forced exhalation but not with maximal

cious, two cycles of the thoracic expansion

effort. This maneuver can be compared with

phase may be necessary to loosen secretions

fogging a pair of eyeglasses with warm breath

before the FET can follow. In a patient with

so they may be cleaned. Unlike a cough in

bronchospasm or unstable airways, the period

which the glottis is closed, a huff requires the

of breathing control may be as long as 10 to 20

glottis to remain open. In an effective huff, the

seconds (Webber,

muscles of the abdomen should contract to pro

tient may be shown how to support the incision

1993). After surgery, the pa

vide greater expiratory force. Other characteris

with their hands during the FET to achieve suf

tics of effective vs ineffective huffing are

ficient expiratory force.

shown in the boxes above.

8. When a huff from a medium-sized inspiration

5. Two different levels of huffing are character

through complete expiration is nonproductive

ized in the FET. To mobilize secretions from

and dry sounding for two cycles in a row, the

peripheral airways, a huff after a medium-sized

treatment may be concluded (Pryor,


1991).

352


PART III

Advantages and Disadvantages of ACB Technique

quired for the patient in whom percussion or shaking during the thoracic expansion phase increases the ef

Incorporation of the ACB technique into a treatment

fectiveness of the treatment.

of PO and percussion allows the patient to participate

Care must be taken to adapt the ACB technique for

actively in a secretion mobilization treatment and of

patients with hyperreactive airways or after surgery.

fers the prospect of independently managing airway

This individual approach will be helpful with all pa

clearance. The ACB may be introduced at

3 or 4

tients using the technique to optimize effectiveness.

years of age, with a child becoming independent in the technique at 8 to 10 years of age. The technique may be adapted for patients with gastroesophageal reflux, bronchospasm, and an acute

AUTOGENIC DRAINAGE Autogenic drainage (AD) is a breathing technique

exacerbation of their pulmonary disease. A decrease

that uses expiratory airflow to mobilize bronchial se

in oxygen saturation caused by chest percussion may

cretions. It is a self-drainage method that is per

be avoided by using the ACB technique (Pryor,

formed independently by the patient in the sitting po

[990). When the technique is performed indepen

s i t i o n . AD c o n s i s t s of three phases:

dently, the cost of using ACB technique for the long

"unsticking" phase. which loosens secretions in the

term is minimal.

peripheral airways,

However, in young children and in extremely ill

(1) the

(2) the "collecting" phase, which

moves the secretions to the larger, more central air

(3) the "evacuating" phase, which results

adults, a caregiver wi/I be necessary to assist the pa

ways, and

tient with this technique. An assistant will also be re-

in the removal of the secretions. This technique of airway clearance requires much patience and concen tration to learn and is therefore not suitable for young children. It is ideal, however, for the adolescent or adult who prefers an independent method.

Equipment Required for AD 1. No equipment is needed for a patient to perform the technique of AD. The patient must possess good proprioceptive, tactile, and auditory per ception of the mucus moving; this feedback makes it possible to adjust the technique of AD.

2. To teach this method to a patient, a caregiver requires keen tactile and auditory senses to coach a patient to move between the phases by listening to and feeling the location and the quality of the secretions. FIGURE 20-12 Autogenic drainage: German method. Autogenic drainage

Preparation for AD

shown on a spirogram of a normal person. The method is not divided into separate phases. (Vt=tidal volume, ERV=expiratory reserve volume, RV=reserve volume, FRC=functional residual capacity, IRV=inspiratory reserve volume, IRV

+

Vt

+

ERV = vital capacity). (From David,

A. (1991). Autogenic drainage-the German approach. In

I. The patient should be seated upright in a chair with a back for support. The surroundings should be devoid of distractions, allowing the patient to concentrate on the breathing technique.

2. The upper airways (nose and throat) should be

Pryor, J. (Ed.), Re pir{/{orv Care, Edinburgh: Churchill

cleared of secretions by huffing or blowing

Livingstone.)

the nose.



20

3. The caregiver should be seated to the side and

353

5. The evacuating phase-In this phase, the pa

slightly behind the patient, close enough to hear

tient increases inspiration into the inspiratory

the patient's breathing. One hand should be

reserve volume range. This middle-to-high

placed to feel the work of the abdominal mus

lung volume breathing continues until the se

cles and the other hand placed on the upper

cretions are in the trachea and are ready to be

chest (see Figure 20-12).

expectorated. The collected mucus can be evacuated by a stronger expiration or a high volume huff.

Treatment With Autogenic Drainage

Nonproductive coughing should

be avoided, since it may result in collapse of

l. In all phases, inhalation should be done slowly,

airways.

though the n o s e if possible, using the di

6. Compression of the airways should be avoided.

aphragm or lower chest. A 2- to 3-second

If wheezing is heard, the expiratory t10w rate

breath hold should follow, allowing collateral

must be decreased. Beginners may have to use

ventilation to get air behind the secretions.

p u rs e d l i ps to a v o i d a i r w a y c o m p r e s s i o n

2. Exhalation should occur through the mouth

(Chevaillier, 1992). Instructing the patient t o

with the glottis open, causing the secretions to

roll the tongue (if possible) may assist i n con

be heard. The vibrations of the mucus may also be felt with the hand placed on the upper chest.

trolling the expiratory flow rate. 7. A German modification of AD resulted from

The frequency of these vibrations reveals their

the observation that many patients had diffi

location. High frequencies mean that the secre

culty breathing in the expiratory reserve vol

tions are located in the small airways; low fre

ume range. In the simplified procedure, the pa

quencies mean that the secretions have moved

tient begins by varying the mid-tidal volume

to the large airways (Chevaillier, 1992).

without excessive effort. After a passive but

3. The umticking phase-This phase mobilizes

rapid expiration, an actively performed expira

mucus from the periphery of the lungs by lower

tion follows, achieving exhalation to a low ex

ing the mid-tidal volume below the functional

piratory reserve volume (David, 199 1). See

residual capacity level (Schoni, 1989). In prac

Figure 9- 1, p. 155. for the difference between

tice, inspiration is followed by a deep expiration

the two methods of AD.

into the expiratory reserve volume. The patient

8. The duration of each phase of AD depends on

attempts to exhale as far into the expiratory re

the location of the secretions. The duration of

serve volume as possible, contracting the abdomi

a session depends on the amount and viscos

nal muscles to achieve this. This low lung volume

ity of the secretions. A patient who is experi

breathing continues until the mucus is loosened

enced in autogenic drainage will clear secre

and starts to move into the larger airways.

t i o n s in a s h o r t e r a m o u n t of t i m e t h a n a

4. The collecting phase: This phase collects the mucus in the middle airways by increasing the

beginner. An average treatment wiiJ be 30 to

45 minutes in length.

lung volume over the unsticking phase. Tidal volume breathing is then changed gradually from expiratory reserve volume toward the in

Advantages and Disadvantages of AD

spiratory reserve volume range (Schoni, 1989)

After instruction in the technique of AD has been

so that the lungs are expanded more with each

completed, it may be performed independently by pa

inspiration. The patient increases both inspira

tients over 12 years of age and requires no additional

tion and expiration to move a greater volume of

equipment. Since it does not require the use of pos

air. This low to middle lung volume breathing

tural drainage positions, it is appropriate for patients

continues until the sound of the mucus de

with gastroesophageal ret1ux. It is also recommended

creases, signaling its movement into the central

f o r use in patients with airway hyperreactivity

airways to be evacuated.

(Pfleger, 1992).


354

PART III


Although it is widely used in Europe, the use of

PEP is performed in the upright position and can

AD in the United States is limited by the lack of

be used during acute episodes, as well as chronic pul

trained caregivers but is growing in popularity.

monary conditions. Children over 4 years of age may

To learn this technique, patients must demonstrate

be instructed in the technique, and PEP may provide

good self-discipline and possess the ability to concen

an independent method of airway clearance in older

trate. This method takes more practice than others. A

children and adults.

patient must also be available for periodic reevalua tion and refinement of the technique. AD is not the treatment of choice for a patient who is unmotivated or uncooperative, and the study of

Equipment Required For Positive Expiratory Pressure

flow volume curves suggests that AD would not be

I. A PEP mask is manufactured by Astra Tech in

appropriate for small children even if they are coop

Denmark, but is not approved by the Federal

erative (Dab,

Department of Agriculture (FDA) and is not

1979).

The period of hospitalization for an acute pul

available in the United States. However, a self

monary exacerbation is a difficult time for a patient

made PEP mask system may be assembled

to learn AD. In fact, patients who are skilled in the

using a soft ventilation mask, a T-piece, a one

technique choose a more passive (less energy-con

way valve, and resistors of various sizes or an

suming) form of airway clearance at such a time until

adjustable resistor valve (Figure

they return to their baseline pulmonary status.

mask should fit tightly but comfortably over the

20-13). The

mouth and nose.

2. Another form of PEP delivery consists of a

POSITIVE EXPIRATORY PRESSURE

mou thpiece attached to a one way valve (for

Positive expiratory pressure (PEP) creates a back

use with noseclips) with adjustable expiratory

pressure to stent the airways open during exhalation

resistance. The Resistex

and promotes collateral ventilation, allowing pressure

Medical, Clearwater, Fla.) has recently been

to build up distal to the obstruction. This method of

™

valve (from Mercury

FDA-approved.

airway clearance prevents collapse of the airways,

3. A manometer is placed proximal to the resistor

which eases the mobilization of secretions from the

in the initial stages of instruction in the use of

periphery toward the central airways. A mask or

PEP. First, the manometer helps to determine

mouthpiece apparatus provides a controlled resis tance

(10 to 20 cm water pressure) to exhalation and

and monitor the appropriate level of resistance needed for the patient to achieve

10 to 20 cm of

requires a slightly active expiration; tidal volume in

water pressure throughout exhalation. Sec

spiration is unimpeded.

ondly, the visual display of the manometer

A variation of positive expiratory pressure, known as high-pressure PEP, uses the same mask apparatus but at much higher levels of pressure

serves as feedback to assist the patient in mas tering the technique (Mahlmeister,

1991).

(50 to 120 cm

4. Aerosol medication by nebulizer or metered

water pressure). Inspiration is performed to total lung

dose inhaler may be placed inline to be deliv

capacity; this is followed by a forced expiratory ma

ered simultaneously with PEP for airway clear ance. Deposition .of medication improves with

neuver against the PEP mask. A form of intermittent PEP is provided by a de vice called the FlutterT". This pipe like device pro

PEP (Andersen,

1982; Frischnecht-Christensen,

1991).

(I) positive expiratory pressure, (2) oscillation 6 to 20 Hz) and

5. Supplemental oxygen may also be placed inline

(3) accelerated expiratory flow rates to loosen secre

6. With high-pressure PEP mask therapy, spirom

vides

of the airways (at frequencies of

for patients who are hypoxic. etry is used to determine the appropriate resis

tions and move them centrally.


20


355

FIGURE 20-13 Self-made PEP mask system.

2. If aerosolized medication is to be used simulta

tance for each patient individually. 7. The Flutter'M VRPI valve (from VarioRaw,

neously, the patient should be instructed in how

Switzerl and), recently FDA - a p p roved, is

to stop the flow of the aerosol when the mask

marked in the United States (by Scandipharm

or mouthpiece is removed during the PEP treat

Pharmacy, Birmingham, Ala.). It is a pipe-like device consisting of a mouthpiece, a plastic cone, a steel ball, and a petforated plastic cover.

ment session.

3. To determine the correct level of resistance for low-pressure PEP, the patient inhales using

8. The PEP mask, mouthpiece, and the Flutter™

tidal volume and exhales actively into the

should be cleaned regularly with hot, soapy

mask/mouthpiece. Different resistors are tested

water. The one-way valve should be cleaned

(or the resistor valve is adjusted) while the

with hot water only; soap may cause it to stick

level of PEP is monitored on the manometer.

or become brittle. In the hospital, the equip

The resistance is gradually decreased until the

ment will need to be sterilized according to in

PEP level supplying 10 to 20 cm of water pres

fection control recommendations.

sure

has

been

identif i e d

(Falk

1993).

Mahlmeister (199 J) reports most patients achieve this pressure range with flow resistors

Preparation for PEP

of 2.5 to 4.0 mm in diameter. Selection of the

1. For PEP therapy, the patient should be seated

proper resistor produces the desired inspiratory

upright with elbows resting on a table. Use of a

to expiratory ratio of l:3 to 1:4 (Mahlmeister,

mask may require securing the device with both

1991). The use of too great a resistance will

hands for a tight seal (Figure 20-14).

create too Iow a pressure or an increased respi


356

PART III


FIGURE 20-15 Use of Flutrer (R) valve. pressure and frequency while movement of the device downward results in lower pressure and frequ e n c y (Al t h a us, 1993). The Flutter™ reaches frequencies of between 6 and 20 Hz. FIGURE 20-14

Treatment With PEP

Preparation for PEP therapy.

1. The patient should be instructed to breathe into ratory rate, whereas too small of a resistor will

the mask or mouthpiece to tidal volume using

create too high a pressure or a slow respiratory

the lower chest and abdomen. Exhalation into

rate (McIlwaine, 1993).

the mask or mouthpiece should be slightly ac

4. For high-pressure PEP, appropriate resistance is

tive but not forced.

determined by connecting the outlet of the PEP

2. The patient continues breathing into the mask

mask to a spirometer. Forced vital capacity ma

or mouthpiece for 10 to 15 breaths, using a nor

neuvers are peliormed through different expira

mal respiratory rate. Initially, the patient and

tory resistors. The resistor producing the highest

caregiver monitor the effort by means of the

forced vital capacity through the PEP mask is

manometer, ensuri'ng that a pressure of 10 to 20

selected for continued use (Oberwaldner, 1986).

cms of water pressure is achieved throughout

5. To use the Flutter'" valve, the patient should be

exhalation. After the technique is mastered with

seated upright (Figure 20-15). The full effects

the appropriate resistor, the manometer may be

of the vibration induced by the Flutter™ may be

removed from the system. The appropriate re

received by changing the angle of the device.

sistance should be rechecked periodically dur

Movement of the Flutter'M upward increases the

ing clinical visits or periods of hospitalization.


20

•

the mucus is mobilized (Mcllwaine, 1993).

6. The recommended procedure for use of the Flut

Inhale deeply and hold breath for 2 to ) seconds.

ter'''' is shown in the box at left. The device is

Place Flutter"" in mouth and, keeping cheeks as

held horizontally with the lips tightly around the

stiff as possible, exhale through Flutter'M adjust ing the degree of tilt to maximize vibrations. •

mouthpiece. After a deep inspiration through the nose, the breath is held for 2 to 3 seconds before

Exhalation need not be forced. Patient best deter

exhaling deeply through the Flutte r'''. The

mines "speed" of exhalation. •

cheeks must be kept flat and to use the abdomi

Perform multiple exhalations through the Flutter'"

nal muscles for effective exhalation. The vibra

(usually 5 to 15) with breath hold to maximize

tion of the chest may be palpated by the patient

mobilization of mucus. •

•

Ajier pelforminR

multipl e

" lo o s e ning "

357

against the PEP mask. This is repeated until all

Technique for Using FlutterT" •


and caregiver to provide feedback as to the opti

breaths,

mal angle of the device. A Flutte,:'''' session con

increase depth of breath and speed of exhalatioll '" Ihrough F/uller to Ilrecipilllle coughing and

sists of I 0 to 15 breaths followed by huffing

mucus expectoration,

(this may be done into the device), with a ses sion lasting about 15 to 20 minutes. To avoid

Repeat entire sequence until "clear,"

dizziness due to hyperventilation. a patient

For more information abollt Flutter"". contact' Sandipharl11; 22 In verness Center Parkway; Birmingham, AL 35242; (205) 991-8085.

should refrain from forced exhalation. It may be necessary to pause every 5 to to exhalations be fore resuming the session (Althaus, 1993).

Advantages and Disadvantages of PEP 3. After a series of 10 to 15 breaths, the mask is

PEP therapy does not possess some of the limitations

removed from the face and the patient performs

of conventional PD and percussion for secretion clear

a series of huffs (and coughing if necessary) to

ance and is therefore applicable to a wider patient pop

expectorate any mucus that has been mobilized.

ulation. It is relatively easy to learn in one or two ses

4. The series of PEP breaths followed by huffs

sions, and may be applied equally to the pediatric and

should be repeated about four to six times. The

adult populations. PEP is appropriate for use in hospi

total treatment lasts about 15 to 20 minutes and

talized patients, as well as long-term use at home.

should be repeated twice to three times during

The expense of the equipment is minimal and once

the day. The frequency and duration of the

the patient is competent in the technique. it provides

treatment must be individualized for each pa

independence (except for small children). All of the

tient. During periods of pulmonary exacerba

PEP devices (the Flutter'" in particular) are quite

tion, patients are encouraged to increase the

portable, making airway clearance easier to perform

frequency of PEP treatments, rather than ex

during travel or when away from home during the day.

tending the length of individual s e s s i o n s (Mahlmeister, 1991).

Although rare, pneumothorax has been reported with high-pressure PEP (Oberwaldner, 1986). A deci

5. The procedure for use of high-pressure PEP

sion to use PEP should be carefully evaluated in

differs from that of low-pressure PEP. The ex

cases of acute sinusitis, ear infection, epistaxis, recent

piratory pressure used in this method usually

oral or facial surgery or injury (Mahlmeister, 199/).

ranges between 50 and 120 cms of water pres

For PEP therapy to be effective, a patient should be

sure. The patient breathes in and out through

able to cooperate and actively participate with the

the mask at tidal volume for 6 to LO breaths,

treatment. Pfleger (1992) recommends that patients

then inspiration is done to total lung capacity

with airway hyperreactivity should take a bron

and a forced expiratory maneuver is performed

chodilator premedication before the use of PEP.


358

PART III


Low-pressure PEP is more commonly used i n North America, because it is felt t o be a s effective, easier, and safer to use and monitor than high-pressure PEP. In those patients in whom PEP is an appropriate airway clearance technique, a high degree of accep tance has been shown (Falk, 1984; Steen, 1991). This may translate into better adherence in the long term.

HIGH FREQUENCY CHEST COMPRESSION The ThAIRapy® (from American Biosystems, Inc., St. Paul, Minn.) system of high frequency chest com pression (HFCC) (also refelTed to as high frequency chest wall oscillation) consists of a vest linked to an air-pulse generator. Figure

20-16 shows a patient

using HFCC. Although the sensation of the device is somewhat akin to mechanical percussion, it differs significantly in its mechanism of action. HFCC works by differential airtlow, that is, the expiratory flow rate is higher than the inspiratory flow rate, al lowing the mucus to be transported from the periph ery to the central airways for expectoration. HFCC has also been shown to decrease the viscosity of mucus, making it easier to mobilize. FIGURE 20-16 Patient using high frequency chest compression.

Equipment Required for High Frequency Chest Compression I. The air-pulse generator, required for a treat ment of HFCC, weighs just over

100 Ibs, but

should not feel restricted while the vest is de

can be wheeled from one room to another.

flated. A single layer of clothing should be

2. The inflatable vest is constructed to fit over the

worn under the vest.

entire thorax and should extend to the top of the

2. The pressure control setting should be adjusted

thigh when the patient is sitting upright. Five

to either the high or the low setting according

different sizes are available (from child to large adult). For use in a hospital setting, adjustable

to patient comfort. 3. The foot/hand control may be placed on the

vests are available, which are fitted to subse

floor to be activated by stepping on it, or placed

quent patients with velcro straps.

under the thigh to be activated by leaning onto

3. Simultaneous use of an aerosolized medication

it, or pressed with the hand.

or saline is recommended throughout the treat ment. This humidifies the air to counteract the drying effect of the increased airflow.

Treatment With HFCC I . The treatment should progress through different frequencies, from low (7 to 10 Hz) to medium (10 to IS Hz) and then to high (IS to 25 Hz), to

Preparation for HFCC 1. The patient should be seated upright in a chair.

achieve both higher flow rates and increased

The vest should fit properly, but breathing

lung volume. Warwick (1991) reported that the


20


359

frequencies associated with the highest flow

successfully in reclining patients who are unable to

rates were usually greater than 13 Hz, whereas

tolerate the upright sitting position.

those associated with the largest volume were

Use of HFCC may result in time savings at home as well as in a hospital or long-term care facility.

usually less than 10Hz. 2. The recommended protocol (American Biosys

Nebulized medications are administered concurrently

tems, Inc., 1994) gives the option of intermit

with the airway clearance treatment, and all lobes of

tent or continuous us· e . For the intermittent

the lungs are treated simultaneously. The amount of

(only on exhalation) method, the patient should

time for patient contact required for a hospital care

inhale deeply and depress the foot/hand control

giver is much less with this method than with con

at peak inspiration. Exhalation should be pas

ventional PD and percussion.

sive and relaxed while the vest is pulsating. For

A disadvantage of this method of airway clearance

the continuous method, the foot/hand control

is the cost of the equipment. A monthly rental fee is

should be depressed while breathing normally.

reimbursed by most insurance companies. However,

At least once per minute, the patient should in

a study by Ohnsorg (1994) demonstrated a decline in

hale to total lung capacity.

t o ta l h e a l t h care costs for t h e y e a r a f t e r t h e

3. The average length of time spent at each fre quency is 3 to 5 minutes, but this will vary ac

ThAIRapy® Vest was put into use b y I I patients. A study of the impact of the device in a hospital setting

cording to patient tolerance, amount, and con

(KIous, 1993) showed a substantial savings as a result

sistency of secretions, and the phase of the

of therapy self-administration. A disadvantage of

patient's illness (acute or chronic).

HFCC is its lack of portability. Although the device

4. After treatment at each frequency for the pre

can be readily moved from room to room in the

scribed length of time, the foot/hand control

house, i t does not accommodate use away from

should be released and the patient instructed to

home.

huff or cough to clear loosened secretions. The

In those patients for whom it is appropriate (and

control is adjusted to the next prescribed fre

reimbursable), HFCC is an effective method of air way clearance. It provides independence for long

quency, and the procedure is repeated. 5. HFCC has been used on a smaller scale with patients requiring long-term mechanical venti

term use at home as well as for acute exacerbations in the hospital.

lation. Whitman et al. (1993) found use of the ThAIRapy'M vest to be safe and effective, and resulted in time savings over conventional PD

EXERCISE FOR AIRWAY CLEARANCE A regular program of exercise has been shown to im

and percussion. 6. Patients requiring central intravenous (IV) ac

prove many variables in patients with lung disease.

cess such as a Porta-cath or Hickman are able

Peak oxygen consumption, maximal work capacity,

to use the ThAIRapy"''' Vest with sufficient

respiratory muscle endurance, and exercise tolerance

padding (such as a foam doughnut pillow) to

all improve with an exercise program (Orenstein,

relieve pressure around the access site.

1981, Andreasson, 1987). Secretion clearance is also improved with exercise (Zach, 1981; Oldenburg, 1979). Based on improvement in pulmonary function,

Advantages and Disadvantages of HFCC

exercise has been recommended as a replacement,

This method of airway clearance allows indepen

partial or complete, for conventional chest physical

dence and is easy to learn in a short period. The

therapy (PD and percussion) (Zach, 1982; Cerny,

ThAIRapy® Vest is now designed to accommodate

1989; Andreasson, 1987).

children as young as 3 years of age, and a vest may

Exercise for secretion clearance has focused on

be custom-made for very large or obese adults.

aerobic or endurance exercise to increase ventilation.

HFCC is appropriate with those patients in whom PD

The many forms of exercise must be adapted to the

positions are contraindicated, and it has been used

individual patient's status and abilities.


360

PART III


Equipment Required For Exercise

5. Supplemental oxygcn and oxygen delivery sup

I. A walking program requires nothing more than

plies will be necessary for those patients who demonstrate oxygen desaturation during exercise.

a suitable pair of shoes and a safe location. 2. The following exercise equipment may be suit able for a patient who is beginning an exercise

Preparation for Exercise

program: treadmill, bicycle ergometer, mini I. Patients with hyperreactive airways should be

trampoline, or arm ergometer.

premedicated with a prescribed bronchodilator

3. For more accomplished exercisers or patients

before exercise.

with a higher exercise tolerance, equipment

2. Baseline vital signs should be recorded before

may include a stair climber, cross-country ski

beginning the exercise. In a home setting, pa

machine, or rowing machine. 4. Tools to monitor a patient's response to exer

tients should be knowledgeable in pulse taking

cise include a blood pressure monitor, heart

and estimating their level of perceived exel1ion.

rate monitor, pulse oximeter, and a scale to

For those patients who require closer monitor

measure patient's level of perceived exertion

ing, a pulse oximeter may be rented from an

(Figure 20-17).

oxygen supply company.

6 7 8 9 1 0 1 1 1 2 1 3 1 4 1

Treatment With Exercise

Very, very light

1. The principles of an excrcise prescription ad dressing intensity, duration, and frequency, as well as principles of warm up and cool down

Very light

are addressed in Chapter 24 and should be fol

Fairly light

for each patient is important.

lowed when using exercise as a form of airway clearance. Individualizing an exercise program

2. Patients in the hospital for an acute exacerba tion may not be able to perform endurance ex

Somewhat hard

ercise for the first couple of days. They should be started slowly and progressed as tolerated. Monitoring of heart rate, blood pressure, oxy gen saturation, respiratory rate, and level of

Hard

perceived exertion at periods before and during exercise, and during recovery, will allow titra tion of the workload and duration for optimal

Very hard

performance. 3. The patient should be instructed in huffing or

Very, very hard

coughing (productive, not prolonged) to expec torate secretions as they are loosened. 4. A regular, consistent program of exercise must be scheduled around the patient's daily activi

FIGURE 20-17

ties to achieve adherence (e.g., walking the

Perceived exertion scale. (From Borg, G., 1982.

dog, sports at school, stopping by the health

Psychophysical basis of perceived exertion, Med Sci Sports

club after work).

Exer,

14(5),377.)


20


361

TABLE 20·1 Airway Clearance Techniques Applied to Patients TYPE Traditional

INDEPENDENCE No

EQUIPMENT

REFLUX

REACTIVE

NEEDED

<4

>4

>12

PRESENT

SEVERE EXACERBATION

PD board

Yes

Yes

Yes

Modified

Modified

No

Yes

Yes

Yes

Yes

May include

No

Yes

Yes

Yes

Yes

May include

Yes

Yes

Modified

Modified

AGE

percussor

CPT"

AIRWAYS May cause bronchospasm

HFCC

Yes

Vest and

PEP

Yes

Mask or

ACB

Yes

PD board

No

Yes

None

No

No

Yes

Yes

No

Good results

Yes

Variety

No

Yes

Yes

Yes

No

Bronchodilator

generator

bronchodilator bronchodilator

mouthpiece

Needs care

Technique

AD Exercise

Premedication

*Includes pOSlural drainage, percussion, shaking, vibralion, and coughing.

Modified from Maggie Mcllwaine, 1993, unpublished.

Advantages and Disadvantages of

Andreasson (1987) observed that regular contact

Exercise For Airway Clearance

with a caregiver seems to be necessary for success

Exercise has the advantage of being the only airway

ful exercise training as does family support, espe

clearance technique that is peliormed regularly by

cially in young children. Compliance will also be

people without lung disease. This factor that makes it

affected by a patient's preference for a particular

appealing to those patients who do not want to call

activity, scheduling conflicts, and commitment by

attention to their differences from their peers. Exer

friends and family members.

cise may improve self-esteem, a sense of well-being, and quality of life. The level of exercise tolerance in patients with cystic fibrosis has been demonstrated to

SELECTION OF AIRWAY CLEARANCE TECHNIQUES The process of prescribing an appropriate technique

be of prognostic value (Nixon, 1992). Because the amount or frequency of exercise re

for secretion mobilization should be ongoing, with pe

quired to achieve its benefits would not be tolerated

riodic reevaluation of the method and its effects on the

by many patients, it is often recommended as an ad

patient. Because of the low compliance reported with

junct to other forms of airway clearance. This is par

conventional chest physical therapy (Passero, 1981), it

ticularly true during an acute exacerbation when ac

is necessary for caregivers to address the many factors

tivity tolerance is limited, or in infants or patients

that may alter a patient's adherence to a particular

with neurological or muscular limitations.

method. These factors include the availability of both

Care must be taken in prescribing exercise to pa

the caregiver to teach the technique and the patient to

tients with hyperreactive airways or with a tendency

learn it; the effectiveness of the technique (subjective

toward oxygen desaturation. Use of bronchodilator

and objective); support for the technique from family,

medication and supplemental oxygen delivery may

friends, and health care personnel; and the cost of the

be necessary to achieve exercise tolerance, but these

treatment. Table 20-1 summarizes factors that influ

patients require close monitoring as well.

ence the choice of an airway clearance technique.


362

PART III

Cardiopulmonar)' Physical Therapy Interventions

AVAILABILITY

A patient's subjective response to the treatment has implications for adherence to any technique. The

Many techniques of airway clearance are new to health

ease of sputum mobilization and the quantity of spu

care providers in the United States although they have

tum are useful feedback for a patient. How much ef

been used in Europe for some time. Use of a method

fort the treatment requires, or more importantly, how

may be limited by the lack of caregivers trained to in

much energy remai ns after completion of the treat

struct patients in a particular technique. This is espe

ment, will affect the patient's willingness to continue.

cially tllle for AD, which takes longer for a caregiver

Complications that occur as a result of a technique

to learn to teach than does ·use of the FlutterT" or

or precautions to be observed must guide a patient

ThAIRapyTM Vest. The ACB technique is easily incor

and caregiver to find an alternate technique in many

porated into conventional chest physical therapy by

instances. A patient hospitalized with an acute pul

learning the FET and modifying the use of percussion

monary exacerbation may need to be assisted with a

or shaking. Manual hyperinflation, on the other hand,

more passive method of secretion clearance until the

because of increased precautions for its use, requires

patient's condition allows a return to a more indepen

more study and observation before implementation.

dent technique. A patient with hyperreacti ve airways

Exercise for airway clearance may be out of the realm

may find that bronchospasm renders percussion inef

of a caregiver who is trained in respiratory care but not

fective. The presence of gastroesophageal reflux may

exercise therapy.

force the decision to use a technique which can be

The patient's availability must also be taken into

pelformed in an upright position. Sinus surgery may

consideration. An outpatient clinic visit does not lend

make use of a PEP mask intolerable. Placement of a

itself to instruction in AD, but instruction in PEP,

chest tube may necessitate a temporary replacement

ACB technique, HFCC, or Flutter"< can be initiated,

for HFCC.

with further training during return visits. On the other hand, if a patient is admitted for exacerbation of a pulmonary disease, the patient is a captive audience for instruction of AD or a home exercise program

SUPPORT When airway clearance must take place on a daily basis, it becomes necessary to accommodate a pa

once the acute stage has passed. Reevaluation of any airway clearance technique is

tient's schedule. A patient may have a preference for

key to its success. The patient and caregiver must be

the most effective treatment performed in the shortest

available to demonstrate and review the technique pe

amount of time. A patient may also be interested in

riodically so that modifications can be made. A

performing another activity during the airway clear

change in a patient's level of independence or motiva

ance treatment: AD or Flutter'M may be performed

tion, a decline or marked improvement in pulmonary

while riding in a car (as a passenger); HFCC can be

status, or a decrease in the effectiveness of a technique

conducted while studying for an examination; and

all necessitate reevaluation of the current method.

while running on a treadmill or during percussion by an assistant, a patient can be watching the news. Many patients adopt a multifaceted approach to

EFFECTIVENESS

secretion clearance, becoming adept at several meth

The prime consideration in selecting a technique is

ods and using them as conditions dictate. Patients

the effectiveness of the technique measured both sub

who use AD or exercise primarily will need to use an

jectively and objectively. Objective measures in

alternate form of airway clearance during an acute

clude: pulmonary function studies, chest x-rays,

exacerbation of an illness. Use of HFCC at home

blood gas values, changes in mechanical ventilator

may necessitate use of a more portable technique

settings, changes in auscultation, and quantity of spu

when away from home for long periods. Patients who

tum produced. A patient's response to treatment can

rely on an assistant to perform percussion may need

be evaluated by changes in heart rate, respiratory rate,

to learn a more independent method for occasions

oxygen saturation, and level of fatigue.

when the assistant is not available.


20


363

In a home where more than one family member re

The effectiveness of these newer techniques com

quires ongoing airway clearance, as can be the case for

pared with more established methods are just begin

parents of children with cystic fibrosis, spending the

ning to be studied. Health care providers have anec

least amount of time for the greatest benefit becomes of

dotally reported their effectiveness, but long term,

primary importance. For an infant or young child, per

well-designed studies are needed.

formance of secretion mobilization must be carried out by an adult. As the child grows older and the choices of a technique increase, close supervision remains neces sary. In the adolescent, even when physical assistance

INTRAPULMONARY PERCUSSIVE VENTILATOR (IPV) The intrapulmonary percussive ventilator (IPV) (from

is no longer required, emotional support from family

Percussionaire Corp., Sandpoint, Idaho) is an airway

and friends is paramount to continued success with a

c l e a r a n c e device t h a t s i m u l t a n e o u s l y delivers

technique. Finally, the support received from health

aerosolized solution and intrathoracic percussion

care providers is vital to the patient's motivation to con

(Homnick, 1994). The functional component in the IPY is an apparatus known as the phasitron. The pha

tinue with a technique, or to learn a new one.

sitron was originally developed by Bird in 1979 for the volumetric diffusive respiration (VDR) ventilator.

COST

It is used with thermally injured patients in place of

In this age of health reform, especially in long-term

conventional mechanical ventilation. The VDR venti

care or chronic disease, cost of a treatment must be

lator functions by accumulation of subtidal volume

considered. The initial cost of equipment, replace

breaths, which build to an oscillatory equilibrium that

ment costs, and the expense of assistance required, all

is followed by passive exhalation (Rodenberg, 1992).

figure into the total cost of treatment.

Figure 20-18 shows a YDR ventilator waveform.

The generator for HFCC is the most costly piece

In the IPV, the phasitron provides high-frequency

of equipment presented here, but replacement should

impulses during inspiration, and positive expiratory

not be necessary. The vest itself should not require

pressure maintained throughout passive exhalation.

replacement except for growth of a child. PEP masks

The pressure generated is 10 to 30 cms. of water

and mouthpieces, and the FlutterT" are relatively inex

pressure. Treatment with IPV is titrated for patient

pensive, with replacement of equipment expected to

comfort and visible thoracic movement.

occur occasionally during a lifetime of use (more

Homnick et a!. (1994) performed a 6-month study

often for a one-way valve in a self-made PEP). AD

using the IPV for airway clearance in patients with

and ACB require no equipment.

cystic fibrosis. No significant differences were

Payment of a trained assistant for home use of

demonstrated in pulmonary function studies, body

postural drainage and percussion when family sup

weight, use of antibiotics, or hospital days between

port is not available is at great expense. Depending

the IPV and conventional chest physical therapy

on the duration and frequency of treatment, this cost

group. Three fourths of the patients estimated in

may outweigh that for other airway clearance tech

creased sputum production with IPY and satisfaction

niques on a long-term basis.

was high for comfort and independence.

Often the choice of an airway clearance technique is limited by the reimbursement available for equip ment or assistance. Nonetheless, the caregiver must

DYNAMIC AIR THERAPY BED

strike a balance between economic and clinical con

The E FICA CC'" Dynamic Air Therapy® bed (from

siderations in choosing a mode of therapy.

HILLROM, Batesville, Indiana) is used in hospital ized patients, primarily in an intensive care setting. The modes available from the bed are continuous lat

FUTURE TRENDS IN AIRWAY CLEARANCE

eral rotation, percussion, vibration, and the ability to

A recent resurgence of interest in airway clearance

position the patient in postural drainage positions.

has led to the introduction of additional techniques.

Use of the bed demands less time of the caregivers


364

PART III


11111AlII 1 AI IUUIUU'IUV 'II I" I" \ I,

IIIIHulI, !nll,I"HUIVUU UU IlIUVIII' I" frI 11 I I

llIlHIIH UlnllIHVIIVUI UUM .JIII" I" II 'I AI fI I,

'VY 'VIII

till, IAIlAllA uAflJUVIIIUVIIVVIIUI m '" " AI I' I I 'YV

I

.11 AI " ,yv

FIGURE 20-18

VDR ventilator waveform. (From Rodeberg, D.A., (1992). Decreased pulmonary barotrauma with the use of volumetric diffusive respiration in pediatric patients with burns: The 1992 Moyer Award,

Journal of Burn Care Rehabilitation 13, 506-511.)

presented by patients and choose a technique or combi

for hands on airway clearance treatment. A smaJi pilot study by Samuelson et al.

(1994)

nation of techniques that best suits each patient's needs.

compared the bed to manual percussion and postural

An individualized approach to airway clearance re

drainage in adult patients with cystic fibrosis. Patients

quires consideration of the multitude of variables, both

were randomized to receive four treatments a day with

physiological, psychological, and practical that affect a

either the Dynamic Air Therapy® bed or manual chest

patient's response to treatment. Health care providers

physical therapy for I week and then switched to the

are challenged to keep abreast of techniques and their

other modality for an additional week. Outcome mea

modifications to best provide for the patient's needs.

sures included pulmonary function studies, 6-minute

The role of the caregiver involves more than tech

walk distance, dyspnea score, and a Quality of WeJl

nical expertise. The caregiver is uniquely positioned

Being Scale. Both therapies demonstrated a positive

to simplify medical language for a patient and en

effect from baseline, but a significant improvement

courage adherence to airway clearance. Support of a

was found only in the 6-minute walk distance of those

treatment by a health care provider can increase the

patients treated with the bed therapy first.

benefit derived from the treatment.

Studies on more appropriate patient populations,

Further study is needed to compare and standardize

especiaJly nonambulatory, critically ill patients, for

techniques, follow long-term outcomes, and establish

whom the Dynamic Air Therapy® beds are generally

optimal treatment guidelines. This information will

prescribed, are necessary to demonstrate the most ef

assist both patients and caregivers to maximize treat

fective use of this expensive equipment.

ment with airway clearance techniques.

SUMMARY

REVIEW QUESTIONS

Numerous airway clearance techniques have been

1. Which ACTs can be performed without acquir ing additional equipment?

shown to reduce obstruction, enhance mucociliary clearance, and improve ventilation, accomplishing the

2. Are there any ACTs that are not suitable for use in an intensive care unit?

goal of improved oxygen transport. Their effectiveness has been demonstrated in controlled situations and eval

3. What are the airway clearance methods most

uated with sophisticated equipment. Caregivers must in

suited for instructing a patient/family in during a

corporate this information into the real life situations

single outpatient clinic visit?


20

4. What outcome measures do you have at your dis posal for evaluating the effectiveness of airway clearance? 5.

How would you encourage adherence of a pre scribed method of airway clearance in: •


365

Gormenzano,J .• Branthwaite,M.A. (1972). Pulmonary physiother apy with assisted ventilation. Anaeslhesia, 27, 249-257. Homnick, D., SpiJlers, e., White,F. (1994). The intrapulmonary percussive ventilator compared to standard aerosol therapy and chest physiotherapy in the treatment of patients with cystic ti brosis. Abstracted in Pedialr Pulmonology, Suppl. 10,266.

a fiercely independent adolescent with a spinal

[mle, P.e., (1989). Percussion and vibration. In Mackenzie, (Ed.). CheSi Physical Therapy in the Inlensive Care Unil, 2nd Ed.

cord injury? •

a 3 year old newly diagnosed with cystic fibrosis?

•

an older patient with bronchiectasis?

(pp. 134-152). Baltimore: Williams

& Wilkins.

Kious,D.,et al. (1993). Chest vest and cystic fibrosis: Better care for patients. Advanced RespiralOry Care Management, 3,44-50. Kious, D.R. (1994) High-jrequency chest wall oscillation: Princi ples and appiicalions. Published by American Biosystems, Inc.. St. Paul. 626-630.

References

Mahlmeister,M.J.,et al. (1991). Positive-expiratory-pressure mask Althaus, P. (1993). Oscillating PEP. [n Bronchial Hypersecretion: Current Chest Physiotherapy in Cystic Fibrosis (CF), Published Andersen,1.B.,Klausen. N.O. (1982). A new mode of administra tion of nebulized bronchodilator in severe bronchospasm. Euro

63, 119,97-100.

Andreasson,B., et al. (1987). Long-term effects of physical exer cise on working capacity and pulmonary function in cystic fi

fresher Class. Presented at Seventh Annual North American Cystic Fibrosis Conference, DaJlas. Nixon, P.A. (1992). The prognostic value of exercise testing in pa tients with cystic fibrosis. New England Jo umal of Medicine,

327, 1785-1788. Oberwaldner,

brosis. ACIO Paedialr Seal/d, 76,70-75.21-38. Bateman, 1.,et al. (1979). Regional lung clearance of excessive bronchial secretions during chest physical therapy in patients

B., Evans, J.e.. Zach, M.S. (1986). Forced expira

tions against a variable resistance: A new chest physiotherapy method in cystic fibrosis. Pediatr Pulmol/ology, 2, 358-367. Ohnsorg, F. (1994). A cost analysis of high-frequency chest waH

with stable chronic airways obstruction. Lancel, I, 294-297. Bateman, J.• et al. (1981). [s cough as effective as chest physiother apy in the removal or excessive tracheobronchial secretions?

36. 683-687. FJ. (1989). Relative effects of bronchial drainage and exer

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Mcllwaine, M. (1993). Airway clearance techniques (ACT) Re

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osc illa t i o n in cystic fibrosis. A b s t r a c t presented a t t h e ALNATS International Conference, Boston. Oldenberg. FA.,et al. (1979). Effects of postural drainage,exer cise, and cough on mucus clearance in chronic bronchitis. American Review of Respiralory Diseases,

120, 739-745.

Orenstein, D.M., et al. (1981). Exercise conditioning and car

cal Therapv, 69,633-639. Chevaillier,1. (1992). Airway clearance techniques. Course Pre sented at Sixth Annual North American Cystic Fibrosis Confer

diopulmonary fitness in cystic fibrosis. Chest. 80 (4),392-398. Passero, M.A., Remor, B., Salomon,

J. (1981). Patient-reported

compliance with cystic fibrosis therapy. Clinical Pedialrics,

ence,Dallas. Clement,A.1., Hubsch. S.K. (1968). Chest physiotherapy by the 'bag squeezing' mcthod: A guide to technique. PhysiOlilerapy,

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autogenic drainage. Lung, 170, 323-330. Pryor, J.A., et al. (1979). Evaluation of the forced expiration tech nique as an adjunct to postural drainage in treatment of cystic

cal Therapy (pp. 409-410). St. Louis: Mosby. Dab,I., Alexander,F. (1979). The mechanism of autogenic drainage

tibrosis. Brilish Medical Joumal, 18,417-418. Pryor,J.A., Webber B.A., Hodson, M.E. (1990). Effect of chest

studied with flow volume curves. Mon Paed, 10,50-53. David, A. (1991). Autogenic drainage-the Gelman approach. In Pryor.

physiotherapy on oxygen saturation in patients with cystic fi

J (Ed.), Respiratory Care. Edinburgh: Churchill Livingstone. Falk,M.,el al. (1984). Improving the ketchup bottle method with

Pryor,1.A. (1991). The forced expiration technique. In Pryor,1.A.

PEP, PEP in cystic fibrosis. Euro pean 10/lmal of Respiralory

65, 423-32. Frownfelter D. (1987). Postural drainage. In Frownfelter, D. (Ed.). ClTesl Physical Thempy (lnd Pulmol/Qly Rehabilil{lIion (2 nd Ed.) (265-290). Chicago: Year Book Medical Publishers. Dise(lses,

Frischknecht-Christensen E., Norregaard,

0., Dahl, R. (1991).

Treatment of bronchial asthma with terbutaline inhaled by

brosis,45, 77. (Ed.), Respiralory Care (pp. 79- 100). Edinburgh: Churchill Livingstone. Rodeberg, D.A., et al. (1992). Decreased pulmonary barotrauma with the use of volumetric diffusive respiration in pediatric pa tients with burns: The 1992 Moyer Award. Joumal of Burn Care Rehabilitation, 13. 506-5 I Samuelson, W., Woodward.

I. F, Lowe,V. (1994). Utility of a dynamic

conespacer combined with positive expiratory pressure mask.

air therapy bed vs. conventional chest physiotherapy in adult CF

CITesI, 100 (2), 317-321.

patients. Absu'acted in Pediatr Pulmol/ology, Suppl.


10, 266.

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Therapy Interventions

SchonL M.H. (1989). Autogenic drainage: A modern approach to

Cystic Fibrosis (CF). Published by International Physiotherapy

physiotherapy in cystic fibrosis. Journal of the Royal Society of

Committee for Cystic Fibrosis (lPC/CF). Webber, BA, Pryor, JA (1993). Physiotherapy skills: techniques

Medicine, suppl. 16,82,32-37.

Steen, H.F., et aL (1991). Evaluation of the P E P mask in cystic fi

and adjuncts. In Physiotherapy for Respirator\' and Cardiac

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Problems. Edinburgh: Churchill Livingstone,

Sutton, P.P., et aL (1985), Assessment of percussion, vibratory

Whitman, J"

cally ventilated patients. RespiralOly Care, 38 (10),1081-1087.

pean Journal of Respirator'>' Diseases, 66, 147-152.

Warwick, WJ .. Hansen, LG (1991). The long-term effect of high

Zach, M.5" Purrer, B., Oberwaldner B. (198 l). Effect of swim ming on

frequency chest compression therapy on pulmonary complica tions of cystic fibrosis. Pediwr Pulmonol, 1 1,265-271 Webber, B,A, (1988). Physiotherapy for

receiving me

10

expiration and sputum clearance in

11,1201-1203. Zach, M" OberwaJdner, R, Hausler, F. (1982), Cystic

chanical ventilation. In Webber, B,A, (Ed,) The BromplOn Hos pilal Guide

et aL (1993). Preliminary evaluation of high-fre

quency chest compression for secretion clearance in mechani

shaking and breathing exercise in chest physical therapy. Euro

Chest Physiotherapy (Fifth Ed.). Oxford: Black

well Scientific Publications. Webber, S" Pryor, J. (1993), Active cycle of breathing techniques. In Bronchial Hypersecretion: Current Chest Physiotherapy in


phYSical eases of/he Child,

chest physiotherapy. Archives of Dis

57. 587-589,

Facilitating Airway Clearance With Coughing Techniques Mary Massery Donna Frownfelter

KEY TERMS

Airway clearance deficits

Mucous blanket

Assisted cough

Reflex cough

Complications with coughing

Smokers cough

Cough

Swallowing disturbance

Cough pump

Throat clearing

Cough stages

INTRODUCTION Cough truly serves many purposes: a therapeutic technique, a

diagnostic signpost, and a social necessity. If it didn't al

ready exist, we would have to invent it.

of food goes "down the wrong hole" or into the tra chea rather than the esophagus, a cough is not the usual mechanism to clear mucus.

Glen A. Lillington, MD

A nervous cough or throat clearing may also sig

The cough is an interesting phenomenon. A cough

nal that the airways are irritated, mucus is not clear

can either be a reflex or a voluntary action. Gener

ing normally, or the person is in an uncomfortable

ally, in healthy individuals a cough is rarely heard

situation. This is something to be aware of especialJy

unless the person has a cold or an irritant is inhaled

when treating asthmatics, patients with cystic fibro

and a sneeze or a cough ensues to evacuate the for

sis, or patients with psychological problems.

eign body. The mucociliary escalator functions to

In reality the mucous blanket and the cough

clear secretions and inhaled particulate matter. Unless

mechanism are the two ways the lungs have of pro

the mucus is very thick, such as in individuals with

viding airway clearance under normal everyday cir

dehydration, inhalation of a foreign body, or a bolus

cumstances. 367


368

PART III


It is interesting how many people are unaware of

Airway clea rance techniques, such as postural

their coughing. For example, when asked if they

drainage, autogenic drainage, or active cycles of

cough, smokers with typical morning and ongoing

breathing, need to be used to mobilize the secretions

smoker's coughs will deny that they do. Spouses will

to the area where the cough will be effective (see

chime in, "He coughs and hacks all the time." An in

Chapter 20).

dividual might constantly clear his or her throat and swallow mucus but will claim to be unproductive of mucus and free of coughing. It is important for thera

COUGH ASSOCIATED WITH EATING OR DRINKING

pists to be aware of both the reflex and voluntary na

If a cough is associated with eating or drinking or

ture of their patients' coughs.

taking medications, the patient should be evaluated

Frequent coughing or throat clearing may also in

for a swallowing disturbance. This usually consists of

dicate other problems than airway clearance deficits.

a "cookie swallow," a fluoroscopy study where the

For example, a patient may have postnasal drip from

patient is given barium or

a sinus infection or allergy. When the mucus drips

liquids and solids to swallow and observed to see if

a

variety of consistency

down into the back of the throat, it can cause a reflex

aspiration into the respiratory tract occurs. Patients

cough to clear it. Other causes include bronchogenic

may have dysfunction after a cerebrovascular acci

carcinoma, nervousness, and smoking. In a pediatric

dent (CY A) or prolonged intubation or because high

patient, a foreign body or object inserted or inspired

placement of a tracheostomy tube inhibits the proper

into the nose or airway should be ruled out.

function of the larynx during swaJlowing. Speech

Cigarette smoking paralyzes the cilia so airway

language pathologists working with patients with

clearance is altered. It has been noted that for every

dysphagia can help patients learn techniques to pre

cigarette an individual smokes the cilia are paralyzed

vent aspiration. They also help the patient and spouse

for approximately 20 minutes. Many individuals are

(significant other) to understand cognitively proper

chain smokers and light up one cigarette after the

positioning (usually sitting up in semi-Fowler's) and

other. Consequently, coughing is the only means of

proper head and neck position (usually chin tuck and

clearing the lungs. This is understandable when a

slight neck flexion) during swallowing. If a patient

smoker coughs up a large amount of mucus in the

has dysphagia and cannot or will not follow a safe

early morning on arising. After sleeping for hours the

swallowing retraining program and continues to

individual's cilia are able to clear secretions; a cough

choke and aspirate food and liquid, aspiration pneu

assists in airway clearance. During the day the

monia will occur and can lead to the patient's condi

smoker who chain smokes must cough regularly to

tion deteriorating and even to death. In a situation

clear secretions because the cilia are paralyzed by the

such as this, alternative feeding would need to be

smoke.

considered.

COUGH PUMP

COMPLICATIONS OF COUGHING

One must appreciate the complexity and intricacy of

The act of coughing can be hazardous to the patient.

the cough pump. Mucus is transported up against

A patient should never be asked to cough repeatedly

gravity by the mucous blanket and propelled cepha

as a routine part of treatment. The irritation and pos

lad by the action of the cough.

sible narrowing of the airways during the forced ex

In general the cough is most effective at high expi

halation may cause bronchospasm. If a patient is

ratory flow rates and at high volumes. The cough is

sounding dry and unproductive, do not encourage fre

of limited value beyond the sixth or seventh genera

quent coughing. This is especially true in patients

tion of airway branching. Consequently when a pa

with asthma.

tient has a lower lobe pneumonia or atelectasis,

If a patient demonstrates retained secretions on x

coughing alone will not clear the retained secretions.

ray, encourage hydration (drinking water), use airway


21

Facilitating Airway Clearance With Coughing Techniques

clearance mobilization techniques, and carefully eval

369

for a forceful cough. Generally, adequate inspiratory

uate the cough. Instruct the patient in controlled

volumes for a cough are noted to be at least 60% of

coughing when mucus is felt in the throat or upper

the predicted vital capacity for that individual. The

airways. The patient may try to cough in a controlled

second stage involves closing of the glottis (vocal

fashion after a postural drainage session or use the

folds) to prepare for the abdominal and intercostal

forced expiratory technique. The forced expiratory

muscles to produce positive intrathoracic pressure dis

technique uses midlong volume ventilation followed

tal to the glottis. The third stage is the active contrac

by one to two huffs, which can include chest com

tion of these muscles. The fourth and final stage in

pression with the arms. Forced coughing can also in

volves opening of the glottis and forcefully expelling

crease blood pressure and Jower cardiac output. Tus

the air. The patient should be able to cough three to

sive syncopy can occur when a patient goes into a

six times per expiratory effort. A minimal threshold of

series of coughs in which the intrathoracic pressure

a FEY) (forced expiratory volume in I second) of at

becomes so high that venous return to the heart is im

least 60% of the patient's actual vital capacity is a

paired. The cardiac output falls and the patient be

good indicator of adequate muscle strength necessary

comes very dizzy, progressing to unconsciousness.

for effective expUlsion (Figure 21-1). During a cough,

Care must be exercised, especially with patients with

alveolar, pleural, and subglottal pressures may rise as

primary lung disease; they must learn to control their

much as 200 cm H20 (Bach, 1993; Jaeger, 1993; Lin

coughing to prevent untoward side effects.

der, 1993).

Stages of Cough

COUGH EVALUATION

There are four stages involved in producing an effec

How do you assess whether a patient's cough is ef

tive cough (Linder, 1993). The first stage requires in

fective? The answer appears to be obvious: ask the

spiring enough air to provide the volume necessary

patient to cough. However, the obvious answer often

FIGURE 21-1 Cough mechanics. A, Stage I: adequate inspiration. B, Stage 2: glottal closure; Stage 3: b u i l ding up of intrathoracic and intraabdominal pressure. C, Stage 4: glottal opening and expUlsion.


370

PART In


does not adequately analyze the functional perfor

inspiration or expiration cycle? Did the patient sponta

mance of a cough, especially for a neurologically im

neously use trunk extension, an upward eye gaze, or

paired patient. The clinician must first take time to

the arms to augment the inspiratory effOlt? Did the pa

set up the patient for successful evaluation of their

tient take enough time to fully inspire before cough

cough. Guidelines for setting up the patient follow:

ing? If the patient inspires adequately, he or she should

I. Do not ask the patient to cough in whatever

be able to sustain two to six coughs per expiratory ef

posture you happen to find him or her in. Ask,

fort for a cascade effect. Neurologically impaired pa

"What position do you like to cough in when

tients who have inadequate inspiratory effol1s usually

you feel the need to cough?" Then ask the pa

present with only one or two coughs per breath and

tient to assume that posture, or assist him or her

generally produce a quieter cough (Hoffman, 1987).

in assuming a posture as close to the preferred posture as possible. Listen closely to his or her answers. A patient should s po n t a n e o u s l y

Stage 2: Glottal Closure

choose a posture that lends itself to trunk flex

Did the patient hold his or her breath at the peak of

ion, which is necessary for effective expulsion

inspiration before the expulsion phase or did the pa

and airway protection. A red flag or inappropri

tient go directly from inspiration to expiration? Did

ate choice would be a preference for coughing

you hear a cough or a huff? A huff (or a complete ab

while supine, which involves the opposite:

sence of a hold between inspiration and expiration),

trunk extension and poor mechanical alignment

when the patient intended to give you a cough, is an

for airway protection.

indication of insufficient glottal closure. This can re

2. Now the patient is ready to demonstrate cough

sult from a wide variety of situations including glottal

ing. Do not make the mistake of asking a pa

edema after prolonged intubation, partial or full

tient to "show me a cough" or he or she may

paralysis of the vocal folds, hemiparesis of the vocal

simply "show you" a cough. It may not be the

folds, or timing or sequencing difficulty secondary to

way the patient coughs to clear secretions. In

brain injuries to name a few. A complete lack of glot

stead continue to set the patient up for success

tal closure will not produce any cough sound because

by asking him or her to "show me how you

the vocal folds are not approximating.

would cough if you had secretions in your chest and you felt the need to cough them out." With these instructions you are asking the patient to show you something functional not theoretical.

Stage 3: Building up of Intrathoracic and Intraabdominal Pressure

Cough effectiveness can now be accurately as

Did you see active contraction of the intercostal

sessed. Guidelines for objective evaluation with pul

and abdominal muscles? D id the patient sponta

monary function tests have been indicted. This sec

neously move into trunk flexion during this phase?

tion focuses on analyzing the movement during all

Did the cough have a low resonant sound? Inade

four stages. An effective cough should maximize the

quate force is usually heard as a higher pitch cough,

function of each individual stage. Thus the clinician

often called a throaty cough. The sound is quieter

should see a deep inspiratory effort paired with trunk

overall and does not produce as many coughs per

extension, a momentary hold, and then a series of ex

expiratory effort. It is sometimes associated with

piratory coughs on a single breath while the patient

neck extension rather than flexion as the patient at tempts to clear the upper airway only. The air ap

moves into trunk flexion.

pears to leak out rather than being propelled out of the larynx during the cough. Like inadequate lung

Stage 1: Adequate Inspiration

volumes, inadequate pressure also prevents the pa

Did the patient spontaneously inspire a deep breath be

tient from coughing more than once or twice on one

fore coughing or did he or she cough regardless of the

expiratory effort.


21

371


Stage 4: Glottal Opening and Expulsion

tient to take a deep breath and cough because this can

Timing of the opening of the glottis and forcefully ex

cause more air trapping, which does not facilitate ex

pelling the air is directly tied into the function of the

pulsion of secretions. Patients will be more effective

third stage. During expulsion, does the patient appear

trying to take controlled small or medium breaths fol

to gag before successfully allowing the air to be ex

lowed by huffs or a small series of coughs.The active

pelled? Does the patient seem to get stuck holding his

cycles of breathing and forced expiratory pressure

or her breath? Deficiencies in this area are often re

technique is also a good choice for these patients.

lated to brain injuries and coordination difficulties. The

Several ideas are presented because the therapist

opposite can also occur. Some patients will get stuck at

needs a bag of tricks. Some techniques work well

the end of expulsion, especially those with severe neu

for some patients and not for others. Try several

rological impairments or bronchospasms and may

with each patient and let him or her determine what

have difficulty initiating the next inspiratory effort.

works best. Another variation that decreases stress on the pa tient is to use a series of coughs starting with a small

PATIENT INSTRUCTION

breath and a small cough, then a medium breath and a

When working with patients, especially those with

medium cough, then a larger breath and a large

primary pulmonary disease or primary disease super

cough. This is a good technique to use with postoper

imposed on secondary disease (i.e., a patient with a

ative patients, who get fatigued trying to maximally

CY A and asthma), there are some helpful techniques

cough each time. For patients with transient or permanent neuromus

to make secretion mobilization more effective. Patients with asthma tend to go into an expiratory

cular weakness or paralysis, further instructions may be

1993; Braun, 1984). These patients

wheeze when they force and prolong exhalation.This

necessary (Jaeger,

can lead to bronchospasm and respiratory distress.

must use every physical trait to maximize the function

The patient can be taught a pump cough, a variation

of each stage of the cough (see Figure

on a huff technique. A huff may be used when pa

the box on p.

tients have had an endotracheal tube in for an ex

during the expulsion stage of the cough only addresses

tended time. The vocal folds are swollen and irri

one aspect (Slack,

tated. Consequently, they will not close and form a

taken to look at all four stages to maximize the airway

21-1, p.369, and 372). Physically assisting these patients 1994; Fishburn, 1990). Care must be

tight seal to build up pressure and cough. The patient

clearance potential of any assistive cough technique.

is instructed to huff rather than cough to mobilize se

First, the patient must be positioned for success.The

cretions.It is done with more open vocal folds, a low

beginning of any cough requires trunk extension or in

sound, and less effort, yet it is quite effective in mo

spiratory movement to maximize inhalation, whereas the expulsion stage requires trunk flexion or expiratory

bilization of secretions. The pump cough extends the huff and is more ef

movement to maximize exhalation (Massery,

1994).

fective. The patient is instructed to take three short

Thus for any given posture, the clinician must assess

huffs and follow it with three short, easy coughs at

the following:

lower lung volume, not deep breaths or deep lung

trunk movements,

(1) whether the posture allows for both (2) whether flexion and extension

volumes. Three or four sequences are done ...huff,

are possible, which movement is more important for

huff, huff, cough, cough, cough, huff, huff, huff,

that particular patient, and whether that posture facili

(3) how gravity is effecting the

cough, cough, cough, huff, huff, huff, cough, cough,

tates this occunence,

cough.Usually if secretions are present a sponta

patient's muscle strength and function in this posture,

(4) whether the patient can still protect the airway

neous cough might occur or the secretions will mobi

and

lize with the small cough.

in this posture. When these questions are answered sat

Patients with emphysema have overdistel')ded lungs and difficulty with exhalation. Do not instruct the pa

isfactorily, the clinician is ready to instruct the patient in the act of coughing.


372

PART III


Positioning and Patiellt Instructioll to Improve Cough Effectiveness

scribed previously, these subtle motions may signifi cantly increase the patient's inspiratory effort and pro vide a more active means for the patient to participate

•

Position the patient for success, especially in

•

Maximize inspiratory phase through verbal cues,

•

Improve hold stage through verbal cues and

loud command to "hold it" at the peak of inspiration,

positioning.

may be sufficient to facilitate closure. Remember to

Maximize intrathoracic and intraabdominal

allow enough time for the patient to take in a deep

regard to trunk alignment. positioning, and active arm movement.

•

pressures with muscle contractions, physical assist, or trunk movement. •

Instruct the patient in appropriate timing and trunk movements for expulsion.

•

in his or her own coughing program. Stage two involves closing the glottis. For some patients with weakness or timing problems, a sharp

inspiratory effort before asking them to "hold." Some clinicians rush the first phase, by saying in quick succession: "take a deep breath and hold it,"

Make the procedure physically active on the

thus unintentionally limiting the time of the inspira

patient's part.

tory effort. A more appropriate verbal cue would be: "take a deep breath in . . . in .. .in. . .in ... , and now hold it," allowing adequate time for the patient to inhale. Stages three and four (building up pressure and ex pulsion) are discussed together because their timing is

An example may provide the best illustration of

interdependent. The patient now needs to move into

these instructions. A clinician may pick a modified

trunk flexion, with or without the clinician's assis

sitting position for a patient with generalized weak

tance, to maximize expulsion. For those patients who

ness (e.g., incomplete spinal cord injury, developmen

can assist, they can be asked to do the opposite of stage

tal delay, or temporary weakness or exhaustion after a

one:

medical or surgical procedure). The patient looks

of your arms down to your hips as you cough."

slumped, so the clinician places a lumbar support

(3) "Roll your shoulders forward while you cough." (4) "Bend your trunk forward while you cough." like

(e.g., a lumbar roll, a towel, or a pillow) behind the

(I) "look down while you cough." (2) "Pull both

lower back to increase trunk extension in that posi

wise, patients with more limited aim function can be

tion. The patient is asked if he or she is comfortable

asked to do the following:

and if he or she can swallow safely. Next the clinician

your chest while coughing." (2) "Roll your shoulders

(1) "Squeeze your arms to

tries to maximize the first cough stage by asking the

and arms inward while coughing."

patient to take in a deep breath. Observing that the pa

hands down while coughing."

(3) "Turn your

tient did not appear to take in as deep a breath as the

In this manner the clinician has used every con

clinician perceived capable, the clinician adds further

ceivable resource to maximize a voluntary cough.

(1) "look upward

Even the weakest cough can be made more effective

instructions such as the following:

(I) posi (3) ask

while you inhale." (2) "Raise both of your arms up

by applying the following simple concepts:

over your head as high as you can while you inhale,"

tion for success, (2) maximize inhalation first,

(3) "Squeeze your shoulders back while you inhale." (4) "Straighten or extend your back while you inhale."

racic and intraabdominal pressures,

for a breath hold,

(4) encourage maximal intratho (5) instruct the

For those with more limited arm function, apply ap

patient in appropriate timing and trunk movements

propriate ventilatory strategies detailed in Chapter 22.

for expulsion, and

Very subtle movements can then be requested, such as

as possible for the patient. However, even with excel

(6) make the procedure as active

(I) "Bring your arms up and out while

lent instructions, many neurological patients require

you inhale." (2) "Rotate your arms outward while you

the clinician's physical assistance to inhale deeper or

(3) "Turn your forearm up while you inhale."

to exhale more forcefully because of muscle weak

the following: inhale."

Although less dramatic than the larger movements de

ness or paralysis (Maclean,


1989).

21


ACTIVE ASSISTED COUGH TECHNIQUES

If after instruction and modification in the patient's cough as described previously, the patient still can not produce an effective cough, then one of the following assistive cough techniques may be appropliate. How ever, a patient who needs some assistance to improve a cough is not excused from ·an active role in cough ing. Keep the act of coughing as active as possible for each patient. whether that is accomplished by adding a few verbal cues to improve overall timing or posture while the patient independently performs the cough, or whether it is accomplished by adding eye gazes for a very weak patient who cannot move the upper ex tremities and breathes with the assistance of a ventila tor. Encourage the patient to be responsible for his or her own care by teaching the concepts involved in producing an effective cough (Estenne, 1990). In that manner, you will help the patient develop the problem solving skills necessary for modifications later. Mod ify and develop additional techniques on the princi ples presented thus far. See the box below for tech niques presented in this chapter. Manually Assisted Techniques Costophrenic assist

The first assistive cough technique, the costophrenic assist, can be used in any posture. After assessing the most appropriate position for the patient (most often sitting or sidelying) and giving the patient instruc tions to maximize all four coughing stages, the thera

373

pist places his or her hands on the costophrenic an gles of the rib cage (Figure 21-2). At the end of the patient's next exhalation, the therapist applies a quick manual stretch down and in toward the pa tient's navel to facilitate a stronger diaphragmatic and intercostal muscle contraction during the suc ceeding inhalation. The therapist can also apply a se ries of repeated contractions from proprioceptive neuromuscular facilitation (PNF approach (Sullivan, 1982). throughout inspiration to facilitate maximal inhalation. The patient may assist the maneuver by actively using his or her upper extremities, head and neck, eyes, trunk, or all of the above to maximize the inspiratory phase. The patient is then asked to "hold it." Just a moment before asking the patient to ac tively cough, the therapist applies strong pressure through his or her hands, again down and in toward the navel. In this manner the therapist is assisting both the build up of intrathoracic pressure and the force of expiration. Of course, the patient would also actively participate by using his or her arms, trunk, or other body parts throughout the entire procedure (see Chapter 22). This technique's obvious use would be for patients with weak or paralyzed intercostal or abdominal mus cles. The therapist must remember to evaluate the ef fect of gravity and posture in each position for the ap propriateness of this technique (Massery, 1987). It is

Assisted Cough Techniques Manually assisted lechniques

I. 2. 3. 4.

Costophrenic assist H ei m li ch-type or abdominal thrust assist Anterior chest compress i on assist Counlerrotation assist

Self-assisted techniques

I. 2. 3. 4. 5.

Prone on elbows head flexion sel f-assisted cough Long-silting self-assisted coughs Short-sitting self-assisted coughs Hands-knees rocking self-assisted cough

FIGURE 21-2

Standing self-assisted coughs

Assisted cough techniques in supine position; costophrenic assist.


374

PART III


helpful for lower airway clearance but does not di

the heel of his or her hand, as in a Heimlich choking

rectly assist in upper chest clearance unless the pa

maneuver. The patient is instructed to assist with ap

tient is able to move his or her upper body indepen

propriate trunk movements to the best of his or her

dently while the therapist assists the lower chest. This

ability. TechnicalJy, this procedure is very effective

technique is easy to learn and teach and can usually

at forcefully expelling the air (Braun, 1984), as in a

be used from the acute phase through the patient's re

cough, but it can be extremely uncomfortable for the

habilitation phase, thus accounting for its popularity.

patient because of (1) its concentrated area of contact,

Heimlich-type assist or abdominal thrust assist The second technique, the Heimlich-type assist or an

(2) the abrupt nature, which may elicit an undesired high neuromuscular tone response or worse when combined with the sensory input that the therapist's

abdominal thrust, requires the therapist to place the

manual contacts supply, (3) the force, which may

heel of his or her hand at about the level of the pa

cause an abdominal herniation. Because of its limited

tient's navel, taking care to avoid direct placement on

usefulness, the Heimlich type of assist or abdominal

the lower ribs (Figure 21-3). After appropriate posi

thrust should only be used when the patient does not

tioning, the patient is instructed to "take in a deep

respond to other techniques and the need to produce

breath and hold it." Unfortunately, manual facilita

an effective cough is imminent. Patients with low

tion of inhalation is not feasible with this technique.

neuromuscular tone or flaccid abdominal muscles

As the patient is instructed to cough, the therapist

fare best with this procedure.

quickly pushes up and in, under the diaphgram with

-

FIGURE 21-3 Hand position for Heimlich-type assist or abdominal thrust.


21


The therapist can simultaneously use both of the

375

enhance the first two cough stages. The therapist then

above techniques in sidelying. If the patient is hemi

applies a quick force through both arms to simulate

plegic or suffered from an unilateral lung or thorax

the force necessary during the expulsion phase. The

disease or trauma, emphasizing one side of the thorax

directions of the force are

over the other may be an appropriate focus during

upper chest, and

airway clearance treatments. One upper extremity is

or abdominal arm. Performed together the compres

used to perform the Heimlich"type of assist while the

sion force from both arms makes the letter V.

(l) down and back on the (2) up and back on the lower chest

other does an uni lateral costophrenic assist. In this

The anterior chest compression technique is more

manner the therapist can compress simultaneously all

effective than the costophrenic assist for patients with

three planes of ventilation in the lower chest. The

very weak chest wall muscles because of the added

possibilities of combining techniques and positions

compression of the upper anterior chest wall. These

are almost endless once the therapist understands the

authors have found sidelying or 3/4 supine position to be the most effective position for this technique.

principles on which they were developed.

However, the anterior chest compression technique is

Anterior chest compression assist

not appropriate for patients with a cavus condition of

The third assistive cough is called the anterior chest

the upper anterior chest because it promotes further

compression assist, since it compresses both the

collapsing of the anterior chest wall.

upper and lower anterior chest during the coughing maneuver. This is the first single technique thus far to

Counterrotation assist

address the compression needs of the upper and

The most effective assistive cough for the widest

lower chest in one maneuver. The therapist puts one

cross-section of neurological patients, in these au

arm across the patient's pectoralis region to compress

thors' clinical experience, is the fourth and final

the upper chest and the other arm is either placed par

method described in sidelying, the counterrotation as

21-4) or

sist. The positioning and procedures required for the

placed like in the Heimlich type of maneuver (Figure

counterrotation technique are described in detail in

allel on the lower chest or abdomen (Figure

22 and apply for both the patient and the ther 21-6). The therapist should recall that

21-5). The commands are the same as in the other

chapter

techniques. Because of the direct manual contact on

apist (Figure

the chest, inspiration can be easily facilitated first,

orthopedic precautions of the spine, rib cage, shoul

followed by a "hold." Thus the therapist can readily

der, and pelvis still persist for this technique.

FIGURE 21-4

FIGURE 21-5

Assistive cough techniques in supine position; variation of

Assistive cough techniques in supine position; variation of

the anterior chest compression assist.

the anterior chest compression assist.


376

PART III


FIGURE 21-6

Counterrotation assist; A, Hand placement during expulsion phase; B, Hand placement during

inspiration phase.


21


377

The therapist begins by following the patient's

tion before passively coughing in a comatose

breathing cycle with his or her hands positioned over

patient can reduce high tone and frequently re

21-6).

duce a high respiratory rate. Both of these re

The therapist then gently assists the patient in inhala

duce the possibility of the patient keeping his

the patient's shoulder and pelvis (see Figure

tion and exhalation to promote better overall ventila

or her glottis closed during the expulsion phase.

tion. This sequence is generally repeated for three to

2. Counterrotation is an excellent mobilizer for a

five cycles or until the patient appears to have

tight chest, which in itself can facilitate sponta

achieved good ventilation to all lung segments.

neous deeper breaths. Tidal volumes (TVs) can

At this point, the patient is ready to begin the coughing phase of the procedure. The patient is asked to take in as deep a breath as possible with the

therefore be increased for many patients by mo bilizing the chest walls. 3. Finally, rotation can be a vestibular stimulator

therapist assisting the patient in chest expansion

and may assist in arousing the patient cogni

21-6, 8). The patient is then instructed

tively, allowing him or her to take a more ac

(see Figure

to "hold it" at the end of maximal inspiration. The

tive role in the procedure.

patient is then commanded to cough out as hard as

The true beauty of the technique is the fact that no

possible while the therapist quickly and forcefully

active participation on the part of the patient is re

compresses the chest with his or her hands in their

quired for success. Incoherent or unresponsive pa

flexion phase positions (see Figure

21-6, A).

tients, such as those patients with low functioning

The importance of following a true diagonal plane

following a head trauma, CVA, or cerebral palsy, will

of facilitation during both the flexion and extension

still demonstrate good secretion clearance with this

phases of this technique cannot be overemphasized.

technique. The mechanics of the procedure dictate

Failure to do so will result in shifting of the air within

that the air within the lungs be rapidly and forcefully

the chest cavity rather than the desired forcing out.

expelled regardless of the patient's level of active

This air shifting can occur to varying degrees, when

participation. Obviously, patient participation is de

the upper and lower chest are not used together, as in

sirable to clear secretions even more effectively and

all the other assistive cough techniques. When done

for teaching the patient to eventually clear his or her

properly, the counterrotation assist is the only one to

own secretions, but it is not critical.

rapidly close off the chest cavity in all three planes of

Clinical experience has demonstrated with patients

ventilation in all areas of the chest. Unless the patient

who have extremely tenacious secretions, use of vi

voluntarily closes his or her glottis, it is impossible to

bration instead of quick chest compression during the

withhold the air from being forcefully expelled.

cough itself may be more effective. This prolongs the

However, a common mistake made by the therapist is

cough phase and gives the secretions time to be

pulling the patient back into trunk extension during

moved along the bronchi for successful expUlsion.

the expUlsion phase rather than into trunk flexion. A

These patients may also require a series of three or

good rule of thumb: if you can see your patient's face

four cough cycles before clearing most of their secre

when you are applying the compression force, you

tions. In general, patients from all the diagnostic

have pulled them into extension. The head and neck

groups discussed thus far with or without good cogni

should stay forward and flexed, thus only a facial

tive functioning are appropriate for this procedure.

profile should be seen.

The majority of them find it to be the most comfort

Other effects of countcrrotation make this proce dure particularly beneficial to patients with low levels

able and effective assistive means of expectorating secretions.

of cognitive functioning. I. The rotation component is

a

natural inhibitor of

high tone. Thus this is the least likely of all

Self-assisted Techniques

techniques discussed so far to elicit an increase

The coughing techniques d iscussed in this section

in abnormal tone during the coughing phase. In

are intended to be used as self-assisted procedures,

fact the opposite usually prevails. Gentle rota

thus usually taught later in a patient's rehabilitation


378

PART III


process. Five different techniques will be presented

capitalize on the functional increase in chest expan

in detail. Suggestions for variations are included.

sion and compression abilities. For the population of

All self-assisted cough techniques can start out as

patients who can assume a prone on elbows posture

physically assisted techniques; however, because

independently (i.e., some patients with tetraplegia),

they are more active and require greater gross motor

this t ec hniquc may be used functionally. Here, they

movement, they lend themselves to self-assisted

can assist their own coughs when the need arises,

techniques.

rather than wait for someone to assist them in a posi

Prone on elbows head flexion self-assisted cough

tion change. The head flexion assist requires good use of head

Prone is not frequently used as a posture for coughing

and neck musculature, scen in patients sustaining a

because the position itself inhibits fuJI use of the di

spinal level injury below C4 (e.g., spinal cord injuries

aphragm by preventing lower anterior chest and ab

(SCIs), spina bifida). It can be used either as a self

dominal excursion following a neurologic insull. This

assisted or therapist-assisted procedure, using the

forces the patient to use an alternate breathing pattern

principles of trunk extension to facilitate inspiration

that facilitates greater accessory muscle use. Because

and trunk flexion to facilitate expiration. With the pa

this change in breathing patterns often occurs sponta

tient prone on elbows, the therapist instructs him or

neously, prone on elbows can be an effective posture

her to bring the head and neck up and back as far as

for promoting spontaneous use of the accessory mus

possible, breathing in maximally (Figure 21-7). The

cles in a more difficult activity (coughing). However,

patient is then instructed to cough out as hard as pos

without the full use of the diaphragm, the resultant

sible while throwing the head forward and down

cough will be weaker than in other postures. Prone on

(Figure 21-8). This head-and-neck pattern can be ini

elbows should not be the exclusive posture for assist

tially assisted by the therapist to establish the desired

ing a cough. After mastering the timing of the proce

movement pattern, and gradually progressed to a re

dure, most patients move back to another posture,

sisted pattern to promote increased accessory muscle

usually sitting or sidelying, and to other techniques to

participation and to strengthen those muscle groups.

FIGURE 21-7 Head flexion assistive cough in prone on elbows; extension and inspiratory phase.


21


379

FIGURE 21-8 Head flexion assistive cough in pTone on elbows; flexion and coughing phase.

FIGURE 21-9

FIGURE 21-10

Tetraplegic-self-assisted cough in long sitting: maximizing

Tetraplegic-self-assisted cough in long sitting: maximizing

the inspiration phase.

the expiration or coughing phase.

inhalation, whereas the flexion aspect is used to max

Long-sitting self-assisted cough

imize expiration. The self-directed chest compression

For the first procedure, tetraplegic-Iong-sitting self

occurs mainly on the supetior-inferior plane of venti

assist, the patient is positioned on a mat in a long-sit

lation only.

ting posture (legs straight out in front of the patient)

The second procedure, the paraplegic-long-sit as

and with upper extremity support. The therapist in

sist, uses the same principles as the techniques de

structs the patient to extend his or her body backward

scribed for the tetraplegic-long-sit assist. These pa

while inhaling maximally (Figure 21-9). The thera

tients have active spinal extension musculature and

pist then tells the patient to cough as the patient

can achieve greater trunk extension and flexion

throws his or her upper body forward into a com

safely, achieving greater chest expansion before the

pletely flexed posture, using shoulder internal rota

cough and greater chest compression on a superior

tion if possible (Figure 21-10). Once again, the exten

inferior plane during the cough. The patient positions

si0n aspect of the procedure is used to maximize

his or her upper extremities in a butterfly position or


380

PART III


self-assist, is typically performed in a wheelchair or over the edge of a bed. The patient is instructed to place one hand over the other at the wrist and place them in his or her lap. As in the previous technique, the patient is then asked to extend his trunk backward while inhaling maximally, followed by a strong vol untary cough. During the cough, the patient pulls his or her hands up and under the diaphragm, resembling the motion of a Heimlich maneuver (Figure 21-13). The hands mimic the abdominal muscles, which would ordinarily contract to push the intestinal con tents up and under the diaphragm to aid its recoil ability. This short-sitting technique uses the di FIGURE 21-11

aphragm more substantially than the long-sitting pro

Paraplegic-self-assisted cough in long-sitting: inspiration.

cedure and is therefore generally more effective as an assistive cough. It is an effective self-assisted method for patients who have weak diaphragms or abdominal musculature. Most SCI or spina bifida patients, Cs or b e l ow , c a n s u c cessf u l l y l e a r n t h i s t e c h n i que. Tetraplegics usually require trunk support from their wheelchairs to perform it independently and safely, whereas most paraplegics can perform it from an un supported short-sitting position. Patients who lack good upper-extremity coordination. such as many Parkinson's and multiple sclerosis (MS) patients, cannot perform the procedure quickly or forcefully enough to make it effective and usually require assis tance from another person. Variations on all sitting techniques can be readily

FIGURE 21-12

made. Use the concepts explained in the introduction

Paraplegic-self-assisted cough in long-sitting: expiration.

to cough techniques to develop techniques that work

uses elbow retraction, depending on the level of in

your patient to lift his or her arms up while inhaling,

jury (Figure 21-11). During the flexion phase, pa

hold, and then cough while he or she throws the arms

tients throw themselves onto their legs, thereby com

down toward feet or lap using maximumlrunk flexion.

for your patients. For example, in a wheelchair, ask

pressing both the upper and lower chest (Figure

(Use a seat belt for safety.) Another idea is to have the

21-12). This can be taught very successfuJly to pa

patient hook one arm on a push handle of the wheel

tients with paraplegia, provided they do not have an

chair, move the other upper extremity up and back (as

interfering tone problems. If the patient lacks hip

in a PNF D2 pattern), watch the patient's moving hand

flexion or is worried about bony contact or skin in

to maximize trunk rotation, inhale during the move

jury, place a pillow (or two as needed) on the legs.

ment, hold, and again cough as he or she throws trunk

This will limit the hip flexion and minimize trauma

and upper extremity down toward opposite knee.

from the quick thrust onto the legs.

When devising the most appropriate self-assisted cough for your patient, remember to look for combina

Short-sitting self-assisted cough

tion of trunk, upper extremity, head, neck, and eye pat

The third assistive cough in sitting, the short-sitting

terns that will maximize all four phases of the cough.


21


381

FIGURE 21-13 Assisted cough in short sitting. A, Hand

position for patient with good hand function; B, Hand position for patients with only wrist function.

Hands-knees rocking self-assisted cough The last assistive cough to be discussed is performed most frequently as a multipurpose activity to increase the patient's balance, strength, coordination, and func tional use of breathing patterns (including quiet breath ing and coughing) simultaneously. The patient as sumes an all-fours position (hands-knees). He or she is then instructed to rock forward, looking up and breath ing in as he or she moves to a fully extended posture (Figure 21-14). After this, the patient is told to cough out as he or she quickly rocks backward to the heels with a flexed head and neck (Figure 21-15). Once again, the importance of flexion and extension compo nents of a cough are noted. The rocking can be done with or without a therapist's assistance. For patients with generalized or spotty weakness throughout (e.g., some SCI, head traumas, Parkinson's, MS, cerebral palsy, or spina bifida patients), this method is perfect for incorporating many functional goals into a single activity. It can help prepare them for more challenging respiratory activities that they will undoubtedly meet after their discharge from a rehabilitation center. For patients with limited lower-extremity range of movement or skin concerns associated with a quick force, a pillow can be placed on the lower legs, thus

FIGURE 21-14

restricting knee flexion and preventing direct contact

Assisted cough in hands-knees position; extension or

of bony prominences.

inspiratory phase.


PART III

382


5. What is a smoker's cough, and why does it L

I. . :: I .

.... . .!

'

't .

occur? 6. What are the stages of a cough?

_

7. What should the therapist interpret when a pa tient's cough is associated with eating or drink ing?

8. What effect does coughing have on the blood pressure and cardiac output? 9. What special techniques can be taught to asth matic patients to mobilize secreations?

10. What manual techniques are most effective in

FIGURE 21-15

spinal cord patients?

Assisted cough in hands-knees position; flexion or coughing phase.

References Standing self-assisted cough

Bach. J.R. (1993). Comparison of peak expiratory flows wilh man

Standing uses the same concepts and can be readily used for self-assisted coughs, provided the patient has adequate standing balance and/or upper extremity support. Use any technique previously described and modify for this higher developmental posture. Com binations of trunk, head, and extremity movements during the cough maneuver is almost endless, thus specific techniques are not itemized.

ually assisled and unassisled coughing techniques. Chest

104(5): I 553-{i2. Braun. S.R.. Giovannoni, R.,

& O'Connor, M. (1984). Improving

cough in patients with spinal cord injury. American Journal of

Physical Medicine 63( I): 1-10. Estenne, M .. Detroyer, A. (1990). Cough in letraplegic subjects: an active process. Annals of Internal Medicine 12(1):22-28. Fishburn,

M.J.. Marino, R.J., & Dittuno, J.F. (1990). Alelectasis

and pneumonia in acute spinal cord injulY Archives of Physical

Medicine and Rehabilitation 71: 197-200. Hoffman, L.A. (1987). Ineffeclive airway clerarance related

10

neuromuscula.r dysfunction. Nursing Clinics of North America

SUMMARY

22(1):151-66.

In all postures and in all techniques, both for assisted and self-assisted coughs, the importance of initial po sitioning and ventilatory strategies is of utmost im portance to the success of the airway clearance tech nique. There is an effective i dea waiting to be incorporated for all patients to improve their cough, from the tiniest postural change to full body move ments and physical assists. Be creative in applying the concepts to all patient populations.

Jaeger, R.J., Turba, R.M., Yarkony, G.M.,

& Roth, E.J. (1993).

Cough in spinal cord injured patients: comparison of three methods to prodoce cough. Archives of Physical Medicine and

Rehabilitation 74: I 358-{i1. Linder.

S.H. (J 993). Functional electrical slimulation

cough in quadriplegia. Chest 103( I): 166-9. MacLean, D., Drummond.

.

10

enhance

c., & Macpherson, C . et a!. (1989).

Maximum expiratory airflow during chest physiotherapy on ventilated patients before and after the application of an ab dominal binder. Intensive Care Medicine 5:396-399. Massery, M.P. (1987). An innovative approach to assistive cough techniques. Topics in Acute Care Trauma Rehabilitation

(3):73-85.

REVIEW QUESTIONS

Massery, M.P. (1994).. What's positioning got to do with it? Neu

rology Report 18(3):11- I 4'.

1. What is the purpose of a cough?

Slack, R.S., Shuca11.

2. W h a t a r e t h e two m e c h a n i s m s f o r a i rw a y

Medicine 15(4):739-49.

clearance? 3. Why would a therapist assist a patient to cough? 4.

What techniques are most effective to assist coughing?

W. (1994). Respiratory dysfunction wilh trau

malic injury to the central nervous system. Clinics in Chest Sullivan, R.E., Markos, P.D.,

& Minor. A.D. (1982). An integraled

approach to therapeutic exercise: Theory and clinical applica· tion. Reston, Va.: Reston Publishing.


Facilitating Ventilation Patterns and Breathing Strategies Mary Massery Donna Frownfelter

KEY TERMS

Controlled breathing

Ventilatory strategies

Diaphragmatic breathing pattern

Work of breathing

Jacobsen's progressive relaxation

INTRODUCTIOtJ

tient. No single technique is appropriate in all cases.

Attaining optimal ventilatory patterns requires the use

Sound clinical judgment and experience must be exer

of a variety of techniques. Some are passive in nature,

cised when applying these ideas with each patient. It

such as passive positioning of the patient or applica

is the hope of these authors that the techniques identi

tion of an abdominal binder for better diaphragmatic

fied in this chapter will stimulate the clinician's cre

positioning. Some require very active participation on

ative talents, and that they will extrapolate and im

the part of the therapist and/or patient, such as in as

prove on the techniques according to specific patient

sisted-cough techniques or in glossopharyngeal

population needs. See the box on next page for spe

breathing instruction. Other techniques are subtly in

cific areas covered in the chapter.

corporated into the patient's total physical rehabilita tion program, requiring little overt attention to the pa tient's respiratory performance, such as when using

POSITIONING CONCERNS

ventilatory strategies. All of these diverse aspects of

All patients spend some portion of the day in a hori

treatment play an important role in the total develop

zontal position for rest or sleep. Using this opportunity

ment of a successful respiratory rehabilitation pro

to assist the patient in passive drainage of lung secre

gram for the neuromuscular and musculoskeletal pa

tions is a natural beginning in the development of a pa 383


PART III

384


Just as passive positioning of the patient in bed

Categories of Therapeutic Interventions Presellted in this Chapter to Optimize Ventilation Patterns

helps to maintain bronchial hygiene and improve ventilation potential, passive positioning of the pa tient's skeletal frame in an upright posture (sitting, standing) helps to maximize the patient's mechanical

I. Positioning concerns

advantage of breathing. For example, patients with

2. Ventilatory and movement strategies

spinal cord injuries (SCIs) resulting in tetraplegia

3. Manual facilitation techniques •

Fac i l i tating contr olled breathing patterns (diaphragmatic)

expansion of the chest in all three planes of ventila

•

Mobilizing the thorax

•

Facilitating upper chest breathing patterns (accessory muscles)

•

Promoting symmetrical breath ing patterns (unilateral dysfunction)

•

will be unable to support their intestinal contents properly under the diaphragm to al]ow for maximal tion (see Chapter 37). Use of an abdominal support from the iliac crest to the base of the xiphoid process provides positive pressure support to restore intesti nal positioning in an upright position (Figure 22-1). Research has documented well the significant im

Reducing high respiratory rates

provements in vital capacity, inspiratory capacity,

4. Glossopharyngeal breathing

and tidal volume in sitting with use of a strong ab dominal support. These binders have also been used

S. Enhancing phonation skills

in nursing care to provide for better circulation and in the prevention of hypotension. The abdominal binder's value in cosmesis may be underrated. Many of these neurological patients were tient's long-term respiratory program. Specific pos

once normal, healthy individuals with high self-es

tural drainage positions are covered extensively in this

teem who took great pride in their appearances. They

book (see Chapter 21). Using a combination of these

now present with a protruding belly (the anterior and

positions in your patient's bed position rotation, in the

infelior shift of the intestines resulting from flaccid

hospital, or at home can help to achieve multiple goals.

abdominal muscles), which may be psychologically

First, they can assist the patients in clearing secretions

disturbing to them. Thus the use of a binder may

passively that they may have difficulty performing ac

greatly aid in the restoration of that person's self-es

tively. Second, these position changes provide for skin

teem, which should be a high-priority goal in any re

relief and better circulation. Finally, they assist in re

habilitation program.

tarding the development of joint contractures or other

A rigid type of abdominal support can be used

musculoskeletal abnormalities. A four-position rota

when the vertebral column and the abdominal viscera

tion (i.e., supine, prone, side-to-side) is usually an ef

need support. These are called body jackets or total

fective and reasonable means of incorporating these

contact thoracic lumbar sacral orthosis (TLSOs).

goals into a long-term prophylactic program.

(Figure 22-2). A TLSO is a rigid trunk support

Simple adaptations may make ventilation easier in

molded individually to the shape of the patient's en

each of these postures. For example, in supine, plac

tire trunk from the axilla down to the pubis. It is

ing the arms lip over the patient's head facilitates greater anterior upper chest expansion. Likewise, po

made up of two separate front and back pieces, with ' an anterior cutout in the abdomen to allow for normal

sitioning the pelvis in a slight posterior tilt facilitates

diaphragmatic displacement of the viscera. Many of

more diaphragmatic excursion. See Chapter 40 for

these jackets also use a strong elastic support across

more detailed explanations. Observation of all pre

the cutout to allow for diaphragmatic motion but to

cautions and contraindications to passive positioning

minimize excessive displacement of the abdominal

is still warranted.

contents. This is very appropriate for the growing


22

Facilitating Ventilation Patterns and Breathing Strategies

385

"

FIGURE 22-1 A, Abdominal binder-Velcro fastener. B, placement of abdominal binder.

child who needs more spinal stability or the com

as well as many other areas of rehabilitation, depends

pletely flaccid tetraplegic patient who may also re

on good alignment of the body against the forces of

quire the same support. Because head and neck posi

gravity. Symmetry must be strived for through the

tioning are so interdependent on trunk positioning, a

use of a body jacket, lateral trunk supports in the

body jacket may be the difference to these patients

wheelchair, abdominal binders, or some other means

between being dependent or independent in an up

(Figure 22-3). This is especiaJly important for pa

right posture. It may result in significantly better head

tients with hemiplegia where habitual asymmetrical

control, eye contact, longer phonation, and possibly

posturing leads to musculoskeletal problems later.

better articulation. However, because it limits trunk

Symmetrical breathing patterns and uniform aeration

movement, its usefulness for each patient must be as

of all lung segments are augmented by careful up

sessed carefuII y.

right positioning. Therefore everything from the type

Logically, the next consideration under passive

of neck support to the height and width of the arm

respiratory techniques is proper wheelchair position

rests to the length and type of the foot supports must

ing. Optimal performance in respiratory functioning,

be carefully analyzed for each patient.


386

PART III


FIGURE 22-2

A, patient with CS congenital tetraplegia independent long sitting. B, long sitting with body jacket

support. Note changes in head position and eye contact, hip alignment, and shoulder rotation.


22


VENTILATORY AND MOVEMENT STRATEGIES

387

ally, these simple concepts take no more than I to

FOR IMPROVING FUNCTIONAL OUTCOMES

2

additional minutes of therapy, with no additional

Once the patient is positioned for success, motor ac

equipment costs other than a few extra pillows or

tivities should be introduced that improve the pa

towels. Therefore time or money are not mitigating

tient's ventilatory support, or the therapist should

factors. However, these ideas do require the practi

capitalize on the patient's good ventilatory support to

tioner to look carefully at the patient before begin

improve the motor activity. Using ventilatory strate

ning any therapy, asking "Have J positioned my pa

gies to improve motor performance or movement

tient for respiratory success?" "Am J simply treating

strategies to improve ventilation performance enables

the patient in whatever position J found them in?"

patients to achieve their functional goals sooner than

and "Have I carefully chosen my verbal cues to in

other patients; patients also get sick less often. Gener

clude a respiratory response and a functional re sponse?" The practitioner must actively include res piration in every single activity to help the patient understand that breathing transcends all activities. See the box below for a summary of the most impor tant ventilatory-movement strategies.

Incorporating Simple Therapy Tasks

Inspiration After the patient has been carefully positioned for respiratory success, as described previously, begin the patient's therapy or daily-living activities. From an anatomical perspective, the pattern of inspiration

(1) trunk (2) shoulder flexion, abduction, and exter

is naturally associated with the following: extension,

nal rotation movements, and (3) an upward eye gaze. Expiration is logically associated with the opposite: (I) trunk flexion,

(2) shoulder extension, adduction,

and internal rotation movements, and (3) a downward

Significant Ventilatory-Movement Strategies J. Pair trunk extension activities with inspirati o n 2. Pair trunk flexion activities with exhalation 3. Pair shoulder flexion, abduction and/or external rotation activities with inspiration

4. Pair shoulder extension, adduction and/or inter nal rotation activities with exhalation

5. Pair upward eye gaze with inspiration FIGURE 22-3

6. Pair downward eye gaze with exhalation

Wheelchair alignment considerations.


388

PART III

Ca.-diopulmonary Physical Therapy Interventions

eye gaze. Accordingly then, the simple task of pas

nity to learn from the beginning of his or her rehabili

(ROM) can easily include

tation process that movement and breathing go hand

the active goal of increasing ventilation by asking the

in hand. C1inicaJly, incorporating appropriate breath

sive range of movement

patient to breathe in and look up every time his or her

ing pattems with movement early in the rehabilitation

arm is raised up into shoulder flexion. This encour

process discourages the development of Valsalva pat

ages the patient to breathe in when his or her chest

tems or shallow breathing pattems when the motor ac

wall muscles are being maximally stretched and the

tivities become more difficult and complex.

ribs are naturally opening up, causing both activities to be more successful. It also begins to teach the pa tient to use ventilatory strategies to optimize potential functional movement, such as in reaching up to a kitchen cabinet.

Dynamic Activities Inhalation promotes trunk extension and exhalation promotes trunk flexion and vice versa. This basic theme occurs naturally in all motor activities but

Expiration

may have ceased to become spontaneous after a

Likewise, active or passive exhalation should be co

neuromuscular or musculoskeletal insult. Valsalva

ROM pat

maneuvers during transitional movements, such as

ordinated with the reverse upper extremity

tern (i.e., the arm returning from flexion back to the

rolling or coming to sitting

patient's side). This can be done using all types of ex

noted with these patients. By teaching them strate

or

standing, are often

halation patterns, including the following:

(1) passive (2) forceful exhalation as in blow ing, coughing, or pursed-lips exhalation, or (3) vocal

gies that incorporate breathing into their motor

quiet exhalation,

plans for all motor activities, Valsalva patterns can

ization patterns. Thus the therapist may ask the pa

promoting beller cardiac function.

be eliminated or minimized while simultaneously

tient to slowly count out loud to 10 while the arm is

Every activity of daily living cannot be described

being returned to his or her side. Subconsciously, the

in this book, however, suggestions for typical gross

patient learns to correlate exhalation with shoulder

motor activities using ventilatory strategies as a

extension while simultaneously learning a much

means to improve these motor tasks are presented.

more complex idea-that of controlling his or her

Extrapolation of these concepts to all other motor ac

rate and volume of expiration by including deliberate

tivities should be carefully analyzed by each therapist

speech during exhalation maneuvers.

for each individual patient.

To improve exhalation potential, increase the pa tient's relative trunk flexion alignment. While sti II

Rolling

ROM, this

Ask patients to attempt to roll and assess whether

can be simply accomplished by asking the patient to

they tend to move with trunk extension or flexion to

supine and performing upper-extremity

lift his or her head and watch the hand as it returns to

begin the roll. If they roll with a trunk extension pat

his or her side, which increases abdominal and inter

tern ask them to breathe in while they roll and to look

costal activation, or by increasing knee flexion,

up. If they roll with trunk flexion as their primary

which increases posterior pelvic tilting and trunk

movement pattern, instruct them to roll while blow

flexion. Pairing trunk flexion with exhalation com

ing out and tucking their chin. In doing

pletes the ventilatory-trunk movement strategy.

work with, not against natural whole patterns of

Combining positioning with respiratory verbal

ROM activities, changes passive upper-extremity ROM exercises to dynamic upper-ex tremity ROM exercises. It encourages increased inspi

:\0,

patients

movements to increase the likelihood of success.

cues, as described in

Coming up to sitting Pushing up to sitting from sidelying should be evalu

ratory and expiratory capacities, develops early func

ated in much the same manner. If patients are more

tional motor planning strategies, and facilitates trunk

effective in coming upright when using trunk exten

mobility. In this manner the patient has the opportu

sion, have them inhale as they push up to sitting.


22


Asking them to "look up" as they move will reinforce

389

independent one. Returning to sitting should be ac

the upper chest movements through the use of the

companied with slow controlled exhalation, such as in

symmetrical tonic neck reflex (STNR). If they have

pursed-lips blowing or counting out loud, to maximize

more success pushing up with trunk flexion, have

the body's controlled descent into gravity's influence.

them blow out and tuck the chin while moving.

FACILITATING A CONTROLLED DIAPHRAGMATIC

Dressing Dressing activities can benefit from the same con

BREATHING PATTERN

cepts. While putting on lower-extremity items such

Why woul.d a therapist want to change a patient's

as pants, socks, and shoes in a long sitting position,

breathing pattern? The answer is simple-when the

have the patient first take in a deep breath while ex

pattern being used is ineffective. Patients generally use

tending his or her trunk. Then have the patient blow

a pattern of breathing that is the most efficient for them.

out, huff out, or cough while flexing the trunk to

A healthy person uses approximately 5% of the

reach his or her toes. This combines the functional

total oxygen consumption for the muscular work of

daily task of dressing with improving breath control,

breathing and 10% of their vital capacity. Conse quently, breathing at rest is generally perceived as ef

trunk control, and airway-clearance techniques. Upper-extremity dressing and upper-extremity ex

fortless under normal conditions.

ercising can incorporate the same ideas. All move

However, in patients that physical therapists evalu

ments should be coordinated with harmonious chest

ate and treat (often after surgery, respiratory disease, or

wall movements to maximize upper-extremity tasks.

dysfunction secondary to neurological insult or injury),

Thus every time the arm is moving up above 90 de

the vital capacity may be significantly decreased and

grees of shoulder flexion, the patient should be asked

the oxygen consumption may be greatly increased re

to breathe in, allowing for the normal shoulderlrib

sulting from the use of accessory muscles or the extra

cage rhythm to occur. Full shoulder flexion requires

effort needed to breath or cough. In the example of a

opening of the intercostal spacing and the separation

patient with tetraplegia the vital capacity may be re

of the individual ribs. Many neurological patients

duced to 1000 to 1500 m!. If the normal tidal volume

have lost the intrinsic mobility of the chest wall and

(normal volume of breathing) is 500 ml that would

thus may have lost some functional shoulder ROM as

mean that with each breath the patient would use 33%

well. Not pairing inspiration with shoulder flexion is

to 50% of his or her vital capacity (maximal inspiration

likely to limit the patient's shoulder ROM to approxi

followed by maximal exhalation). This would greatly

mately 140 to 150 degrees. It may also encourage

increase the oxygen consumption just for normal quiet

Valsalva maneuvers during the activity and may

breathing. The patient would have little pulmonary re

cause more shoulder pain.

serve. During exercise or stress, the patient would have an increased subjective feeling of shortness of breath

Coming up to standing

(dyspnea) and feel an increase in their work of breath

Coming up to standing requires both trunk move

ing. There are specific terms to describe breathing pat

ments, thus the patient should initiate the forward

terns, the most common are listed in the box on p. 390

trunk lean with exhalation and initiate the standing

at top. Also see the box on p. 390 at bottom for indica

phase with inhalation and neck extension. Active neck

tions for teaching controlled-breathing techniques.

extension during assumption of standing not only fa

It should be appreciated that breathing comfort

cilitates greater inhalation but, along with the influ

ably and in control is associated with wellness and a

ence of the tonic labyrinthine reflex (TLR), facilitates

sense of ease. Even in normal individuals who are

more significant contractions of the trunk and hip ex

under stress and have increased work levels we are

tensors. Clinically, this often results in a more notice

more cognizant of the increase in work of breathing.

able upright posture and may make the difference be

For a patient that is struggling with every breath and

tween an assisted standing pivot transfer and an

wonders how he or she will get through the day, ven


390

PART III


Breathillg Pattern Termillology Eupnea-Normal breathing, repeated rhythmic inspiratory-expiratory cycles Hyperpnea-Increased breathing. usually refers to increased tidal volume with or without increased frequency Polypnea, tachypnea-Increased frequency of breathing Hyperventilation-Increased alveolar ventilation in relation to metabolic rate (an increase in alveolar ventilation seen is a decrease in the arterial Peo2 Hypoventilation-Decreased alveolar ventilation in relation to metabolic rate (a decrease in alveolar ventilation) seen as an increase in Peo2 Apnea-Cessation of respiration in the resting expiratory position Dyspnea-The patient's subjective feeling of shortness of breath Apneusis-Cessation of respiration in the inspiratory position Apneustic breathing-Apneusis intelTupted periodically by exhalation Cheyne-Stokes respiration-Cycles of gradually increasing tidal volume followed by gradually decreasing tidal volume (usually followed by an apneic period) Biot's respiration-Sequences of uniformly deep gasps and apnea, followed by deep gasps

Adapted from Comroe. J. H .• Jr. (1974). Physiology 0/ respiration, (2nd ed). SI. Louis: Mosby.

Indications for Teaching Controlled-Breathing Techniques Patients with any or t.he following: •

Pulmonary dysfunction either pIimary or secondary causes

•

Pain from surgery, trauma, or disease

•

Apprehension or nervousness

•

Bronchospasm or impending bronchospasm in asthma

•

A irw ay clearance dysfunction

•

Restriction of inspiration resulting from musculoskeletal dysfunction such as scoliosis. kyphoscoliosis, pectus ex cavatum, obesity, pregnancy, pulmonary pathology such as fibrosis, scarring from radiation therapy. neurological weakness such as spinal cord injury. Parkinson's disease, or myasthenia gravis

•

Congestive heart failure, pulmonary edema, or pulmonary emboli

•

Rib fractures

•

Ventilated patients on assist control or intennittent mandatory ventilation (lMV)

•

Metabolic disturbances that have a compensatory respiratory response

•

Debilitated or bedridden patients that tend to have constant volume ventilation, retain sel:relions. and are prone to pneumonia and atelectasis from poor airway clearance


22


them to relax the neck and chest accessory muscles

Goals of Teaching Controlled-Breathing Techniques •

To decretlse the work of breathing

•

To improve alveolar ventilation

•

•

and use more diaphragmatic breathing to reduce the work of b r eath ing in co mbination with relaxed pursed-lip breathing on exhalation. Their treatment programs focus on energy conservation and pacing activity with breath control.

To improve airway clearance by improving cough

However, with secondary pulmonary dysfunction

To increase strength, coordination. and efficiency

patients, such as spinal cord injury, there is a more

of respil'lltory muscles •

restrictive component to inspiration. In this case, they

To teach the patient how to respond to and control

may have accessory muscles intact, but they are not

breathing •

To assist in relaxation

•

To mobilize and maintain mobility of the thorax

•

To enable patients to feel self-control and confi

391

using them to faciliate deep breathing or coughing. They may have a strong diaphragmatic breath but the upper chest collapses on inspiration (paradoxical breathing, see Chapter 37). In these cases the goal is

dence in managing disease or dysfunction

to teach them to use the accessory muscles to balance the upper and lower chest. This facilitates an increase in vital capacity to prevent atelectasis and pneumonia

tilatory strategies and breathing-control techniques

by increasing the volume of ventilation and improv

can be the key to maximizing potential. See the box

ing the cough mechanism. The choice of appropriate venti latory strategies

above for a list of goals in teaching controlled-breath

depends on the patient's individual problem. The fol

ing techniques. Breathing control has long been used in yoga to foclls and promote meditation. This is a key to maxi

lowing questions should be considered when evaluat ing patients:

mizing rehabilitation. If you can not breathe you can

Does the patient have more difficulty in inspira

not function! It is of primary importance to assess the patient's breathing at rest and during exercise. We

tion or exhalation? •

often hold our breath with exertion, especially with

Is there a normal sequence to inspiration (i.e., ab dominal wall rises, then mid chest, then upper

new activities. We must assess the cardiopulmonary

chest, with a full inspiration? Or does the chest

and neuromuscular response to each new activity.

sink and the abdomen rise on inspiration? •

CONSIDERATIONS FOR TEACHING BREATHING CONTROL TO PATIENT'S WITH PRIMARY VERSUS SECONDARY PULMONARY DYSFUNCTION

Does the patient appear to be working hard to breathe? Is the patient using the accessory muscles to an extreme?

•

ing a normal volume and for the normal length of

Patients with primary lung disease, such as emphy sema, asthma, bronchitis, or cystic fibrosis, present a much different picture than patients with spinal cord ' injury, Parkinson's disease, myasthenia gravis, or

Does the patient have trouble coughing or speak sentences?

•

Is ventilation the limiting factor in accomplishing an activity (i.e., transfer, gait, or bed mobility)?

Patients with primary pulmonary disease generally

Guillain-Barre syndrome. In general, patients with primary lung disease use

benefit from ventilatory strategies that relax the ac

their accessory muscles and greatly increase the work

cessory muscles and facilitate relaxed diaphrag

of breathing secondary to the shortness of breath or

matic breathing.

coughing. They often complain that they have more

On the other hand, patients with secondary pul

difficulty "getting air out," which demonstrates the

monary dysfunction usually benefit from the balanced

decreased expiratory flow rates noted on pulmonary

use of the diaphragm and accessory muscles to in

function tests. The goal with these patients is to teach

crease vital capacity and breath support for activities.


392

PART III

Car·diopulmonary Physical Therapy Interventions

obstructive pulmonary disease (COPD) patients.

Diaphragmatic Facilitation Techniques

Neurologically impaired patients need modifica tion with their activity levels and capabilities.

I. R elaxation technique 2. Re patterning techniques •

•

Relaxed pursed-lip breathing

POSITIONING CONCERNS

Exhalation, hold, and inhalation

Position of Pelvis

3. Sniffing

The first step in facilitating any breathing pattern is to

4. Diaphragmatic scoop technique

position the patient for respiratory success. The de

5. Lateral costal facilitation technique

tails are discussed in this chapter and Chapter 40.

6. Upper chest inhibiting technique

Often the patient's posture and pelvic position has a dramatic effect on breathing. In general, a slight, rela

7. Normal timing technique

tive posterior tilt of the pelvis facilitates diaphrag matic breathing and a relative anterior tilt facilitates

FACILITATING DIAPHRAGMATIC BREATHING This section is laid out starting with the easiest interven

opening of the anterior chest and upper chest breath ing. It is helpful to see what difference a slight, rela tive change in pelvic position will do to the patient's

tion to facilitate diaphragmatic breathing and progress

ability to ventilate. This is especially true with sec

ing to specific inhibition and facilitation techniques.

ondary pulmonary problems related to neurological

See the box above for a summary of methods to

and neuromuscular dysfunction.

facilitate diaphragmatic ventilation patterns.

RELAXATION OF UPPER CHEST AND SHOULDERS DIAPHRAGMATIC CONTROLLED BREATHING Diaphragmatic breathing is the normal mode of respi

Jacobsen's progressive relaxation exercises are famil iar to physical therapists. Jacohsen proposed that a

ration. The diaphragm and intercostals are the normal

maximal muscle contraction would yield a maximal

muscles of quiet inspiration. When evaluating a pa

muscle relaxation. This technique can be applied to

tient's breathing pattern, the use of accessory muscles

the upper chest and shoulders. The therapist places

during quiet breathing should be noted; the patient

his or her hands on the patient's shoulder girdle. The

with primary pulmonary disease should be instructed

patient is asked to shrug his or her shoulders up into

in relaxation of the accessory muscles to decrease the

the therapist's hands and hold it. "Don't let me push

work of breathing. In a patient with a spinal cord in

your shoulders down," is the therapist's command.

jury or other neuromuscular disorders, these muscles

Then, "Let your shoulders relax, let them go." The

may assist in balancing ventilation and may be useful

emphasis is on the relaxation phase. Verbal com

in increasing vital capacity, and improving the ability

mands can be very important with this procedure. A

to cough, improving breath support for speaking, and

strong command to, "Raise your shoulders into my

increasing potential for functional activities.

hands" is followed by a quiet, more relaxed, "Now

In general, controlled diaphragmatic breathing needs

relax and let them go," repeating quietly, "That's it,

to be emphasized in each posture and with all therapeu

let them go, feel them t:elax." Sometimes the relax

tic activities. CatTY-over is not necessarily present. If the

ation activity is all that it takes to resume a more nat

patient is only shown the pattern in supine, it may not

ural pattern of breathing and you can move on to

carry over to sitting or during a sliding-board transfer

other therapeutic activity. If the patient starts to use

when the activity becomes difficult. A helpful sequence

accessory muscles again the technique is repeated.

to use might be teaching the breathing pattern in sidely

The patient learns to feel the difference between ten

ing, supine, sitting, standing, walking, stairs climbing,

sion and relaxation of the shoulders and can self

and other functional activities, especially with chronic

monitor and perform the relaxation independently.


22


REPATTERNING TECHNIQUE

rotation), and

If a patient needs more support to gain control of breath

393

(4) choosing to use a pillow or pillows

under the head. (For details on positioning, see Chap

40.) For each patient, choices will be different (i.e.,

ing and is experiencing shortness of breath, a simple

ter

repatterning technique is very beneficial. An example

the amount of knee flexiol1 or the number of pillows).

might be an asthmatic patient with a high respiratory

Find the right combination of positioning characteris

rate who is feeling panicky. When the patient is asked

tics that best facilitates diaphragmatic movement for

why he or she is breathing so fast the reply will usually

that particular patient. In this manner the therapist sets

be, "I am n ot getting enough air, I can't catch my

up the patient for respiratory success before beginning

breath." The patient is asked to start with exhalation.

the manual or verbal techniques.

"Try to blow out easily with your lips pursed. Don't

Now, begin the techn ique. A s k the patient to

force it just let it come out." By doing this, the respira

place his or her hands on their stomach for increased

tory rate will automatically be decreased. When the pa

proprioceptive feedback and the relative extension,

tient feels some control of this step, then ask him or her

adduction, and internal rotation position of the shoul

to "hold the breath at the top of inspiration just for a sec

ders. In a quiet melodic voice, ask the patient to

ond or two." Make sure the patient does not hold his or

"sniff in 3 times." Note if the patient demonstrates

her breath and bear down as in a Valsalva maneuver.

more abdominal rise and/or lower chest expansion . If

Lastly, ask the patient to take a slow breath in, hold it,

so, draw attention to this fact. During exhalation, tell

and let it go through pursed lips. Patients often learn that

the patient to "let it out slow," which helps to inad

when they are short of breath, this technique will help

vertently slow the respiratory rate

them gain control, making them feel less panicky.

courages some relaxation. Progress the training by

(RR) and often en

asking the patient to "now sniff in twice." Do you still see greater diaphragmatic excursion and less

Sniffing

upper chest excursion? If so, continue by asking for

If working toward a generalized controlled-breathing

"one long slow sniff." If successful, the therapist

pattern does not improve the patient's ventilatory pat

should follow with: "now do it quieter," then "now

tern adequately, a technique that more specifically

do it slower," "even quieter," and so forth. By this

addresses the n eed to initiate breathing from the di

time, the patient should be demonstrating an easy

aphragm can be attempted. Sniffing is a simple and

onset, slow

effective means of teaching increased diaphragmatic

shoulders.

breathing. Sniffing is primarily diaphragmatic breath

RR, diaphragmatic pattern with relaxed

Clinical experience has shown this technique is

80% of patients who

ing by nature. Use this technique first when attempt

highly successful with about

ing more specific diaphragmatic training with all pa

have primary pulmonary pathologies or neurological

tients who are capable of attempting sniffing because

impairments. The key to success seems to stem from

of its simplicity.

the relaxed tones and words that the therapist uses,

As with all procedures, the most imp0l1ant step is

which decrease anxiety and imply relaxation and not

the first step: position the patient appropriately to in

"effort." Once the pattern has been established, the

crease the likelihood of increased diaphragmatic

patient can easily be instructed to go through the

breathing resulting from musculoskeletal alignmel1t.

training as needed indepen dently. The sequence (in

(I) choosing a gravity

whole or in part) may be appropriate for patients be

eliminated position, such as sidelying, or a gravity-as

fore getting out of bed if they become anxious and

sisted position, such as supported semi-Fowler's sit

demonstrate excessive upper chest breathing during

(2) choosing a relatively posteriorly tilted pelvis with flexed knees, (3) choos ing the arms to be down below 90 degrees of flexion

this activity. For other patients, it may be appropriate viously, the application of this technique will be indi

(in relative shoulder extension, adduction, and internal

vidualized for each patient, depending on the deficits.

This includes the following:

ting (supported spin e),

before or during eating or before climbing stairs. Ob


394

PART III


PROCEDURE FOR TEACHING CONTROLLED DIAPHRAGMATIC BREATHING (SCOOP TECHNIQUE)

j

Minimal patient instruction is necessary to facilitate allows the patient to feel the breathing pattern, then it is brought to the patient's cognitive awareness. The

.

breathing pattern. 1. Position the patient for success, generally in a s i d e l yi n g p o s i t i o n w i t h t h e b e d in s e m i Fowler's or supine in semi-Fowler's with a pelvic tilt and relax the abdominal muscles.

)'

r

The following is a suggested sequence:

bend in the knees to achieve a relative posterior

/

Y?.

C

"'.

""f f ! .. '

I! /, J ))

diaphragmatic breathing using the scoop technique. It

patient then learns to self-cue to incorporate the

/

-::0..

,,/ ,

"-

1

FIGURE 22-4 Therapist's hand placement for diaphragmatic breathing.

2. Place your hand on the patient's abdomen at the level of the umbilicus. Tell the patient you

perventilate and blow off too much CO2. The fact

want to feel his or her breathing. Follow the pa

that they are breathing more with their diaphragms is

tient's breathing pattern for a few cycles until

the important consideration. Note also the position of

you are in his or her rhythm. Do not invade the

the pelvis and trunk.

patient's breathing pattern rather, at first, fol low their movement.

When the patient has mastered the breathing pat tern in sidelying, try supine. Then progress to sitting

3. After the nonnal rate at the end of the patient's

(Figure

22-6), standing (Figure 22-7), walking (Fig 22-8), and finally stairs (Figure 22-9). Each de

exhalation, give a slow stretch and "scoop" your

ure

hand up and under the anterior thorax as shown

velopmental position increases the difficulty in per

in Figure

22-4. The command, "Breathe into my

forming diaphragmatic breathing. In sidelying or

hand," is given as the slow scoop stretch is done.

supine the patient is fully supported. The sidelying

4. As the "scoop stretch" is performed instruct the

position is especially good for initially teaching di

patient to, "breathe into my hand" during the

aphragmatic breathing because the diaphragm is in a

inspiration. Give a scoop at the end of exhala

gravity-eliminated position. In supine the patient

tion with each breath. The verbal command can

must breathe up against gravity. However, as we

be effectively replaced with audible breathing

progress to sitting, the patient must now provide

to facili tate the ventilatory pattern if verbal

trunk support and maintain stability up against grav

cues are ineffective or inappropriate.

ity, as well as relax the shoulders. In standing the en

5. After achieving some success, it is helpful to

tire body must be supported, and when walking or

call the patient's attention to the awareness of

stairs are added, the element of breathing coordina

the breathing pattern. For example, the thera

tion really comes into play.

pist can ask, "Can you feel how your abdomen rises as you breathe in?"

Coordination of breathing for walking involves being careful not to allow patients to breath hold. They

6. The patient's hand can be placed on the ab domen with the therapist's hand on top. Rein

need to keep inspiration and exhalation regular at least at a ratio of 1'1, preferably exhaling a little longer.

force the breathing pattern, then remove your

In general the preferred pattern for patients with pri

hand and allow the patient to independently

mary pulmonary dysfunction is as follows:

feel the ventilatory pattern (Figure

the base of the stairs to gain controL

22-5).

A few things should be taken into consideration. Try

(I) Pause at (2) Have the pa

tient take a breath in and move as he or she exhales up

not to have patients take too many deep breaths; they

one stair.

may begin to feel light-headed because they may hy

hales as he or she walks up one stair.


(3) The patient then pauses to inspire and ex (4) The patient


22

395

FIGURE 22-5

FIGURE 2-6

The patient is encouraged to continue practicing

The patient advances to the sitting position for breathing

diaphragmatic breathing to become aware of his breathing

retraining. Note the relaxed position of the patient's

pattern. this is usually the first position of the

shoulders and hands.

diaphragmatic breathing teaching sequence.

FIGURE 22-7

FIGURE 22-8

The third position in the sequence is standing. Full-length

Walking is the fourth stage of retraining. The patient is

min'ors are helpful at this point.

encouraged to relax, control his breathing, take long steps and slow down.


396

PART III


C1 0f

-- \y

FIGURE 22-9

FIGURE 22-10

Stairs are important, especially if the patient has them at

Bilateral lower lobe expansion (this also facilitates

home. He is instructed to pause slightly as he breathes in

diaphragmatic movement).

and to exhale as he climbs one to two stairs.

should be encouraged to use the handrail and pace his or her movement slowly and with breath controL In general neuromuscular patients with lower-ex

Upper Chest Inhibition If all other manual facilitation techniques cease to produce the desired increase in diaphragmatic breath

tremity weakness may benefit from inspiration

ing, then inhibiting the upper chest during inhalation

while ascending stairs and exhalation during de

may be effective.

scent. Going downstairs is an eccentric muscle pat

Again, position the patient appropriately. These

tern and exhalation is a relative eccentric contrac

authors usually choose sidelying or 3/4 supine.

tion of the diaphragm.

Begin by facilitating the diaphragm, usually with the

Refer to the section on ventilation and movement

diaphragm scoop. Slowly bring your other arm

strategies on p. 387 of this chapter to determine appro

across the upper chest at about the level of the ster

priate incorporation of breathing in functional tasks.

nal angle. Leave it there for a couple of respiratory cycles without applying any pressure to feel the upper chest's movement.

LATERAL COSTAL BREATHING

After assessing this movement, gently allow your

Lateral costal breathing also facilitates diaphragmatic

arm to follow the upper chest back to its resting posi

excusion. This may be done bilaterally as in Figures

tion when the patient exhales. Now on the patient's

22- I 0, 22-11, 22-12, 22-13, and 22-14 or unilaterally

next inspiratory effort, do not move your arm's posi

as in Figures 22-1S, 22-16, and 22-17. Lower chest

tion. Thus your arm position will apply pressure or

lateral costal expansion facilitates diaphragmatic and

resistance to the expansion of the upper chest. This

intercostal breathing where the mid chest will recruit

gentle pressure will cause postural inhibition to the

primarily intercostal activity.

anterior and superior movement of the upper chest.


22

RGURE22

1


RGURE22

Bilateral midchest expansion exercise.

2

Self-assisted bilateral chest expansion exercise. Keep the patient's shoulders relaxed.

l

j

397

1

----"

,-"I{

FIGURE22-13

FIGURE22-14

Bi lateral posterior chest expansion exercise.

Bilateral posterior chest expansion exercise.


398

PART III


FIGURE 22-16

FIGURE 22-15

Unilateral (segmental) breathing, left

field.

the left lower shoulder must remain down, with hands

on ulnar border or palm up in his lap.

FIGURE 22-17 The

either hand on the side of the by

chest to be


his hand up.

22


399

After each expiratory cycle, add more pressure until

the chest wall to the lower sternum and touches the

the patient subconsciously increases the lower chest

patient with the instructions again to "now breathe here." Finally, the therapist uses the first hand to

breathing out of necessity. When you note more diaphragmatic and/or lower

move up to the upper sternum (usually around the

intercostal muscle excursion, verbally note this to the

level of the sternal angle) and asks the patient to

patient. Ask the patient to try to reproduce this pat

"now breathe here." It is impol1ant that the therapist

tern. With your other arm continue to facilitate the

smoothly transitions from one hand to the next to as

desired response, such as with the diaphragm scoop.

sist the patient in developing a smooth motor transi

Slowly, during each of the next series of inhalation,

tion from one area of the chest to the other. The man

release your inhibition as the patient tries to maintain

ual cues provide tactile cuing rather than true motor

the improved lower chest breathing pattern. If the pa

facilitation. Because of this, the normal timing se

tient is only partially successful, the inhibition can be

quence is obviously a more-advanced technique in

partially reapplied to assist the patient. If the patient

tended for use after achieving initial diaphragmatic

becomes anxious because the therapist's inhibition is

training success.

preventing upper chest breathing, then decrease the inhibition to a comfortable level. This technique should never cause an increase in anxiety or it will

MOBILIZING THE THORAX

only encourage more upper chest breathing rather

For some patients, controlled breathing alone may

than less.

not alleviate the inefficient ventilatory patterns even with utilization of good positioning and appropriate ventilatory strategies. The thorax itself may be inca

Normal Timing

pable of moving freely enough to allow for adequate

During normal quiet inspiration (controlled breath

chest wall excursion necessary for that breathing pat

ing), the diaphragm contracts, which is seen out

tern. For example, a patient with a spinal cord inj ury

wardly as a gentle rise of the abdomen. The second

who is demonstrating an excessive diaphragmatic

movement is seen as lateral costal expansion of the

pattern that is unbalanced by the normal neuromuscu

lower chest and usually to a lesser extent, lower ante

lar support of the intercostal and abdominal muscles

rior chest expansion. Lastly, the upper chest rises

can breathe using minimal chest wall expansion. This

slightly in primarily a superior-anterior plane with

is often noted as belly breathing. It may be necessary

less lateral expansion noted. A normal timing tech

to mobilize individual rib segments to gain the poten

nique adapted from the physical therapy approach of

tial for chest walJ expansion in aIL three planes of

proprioceptive neuromuscular facilitation (PNF) can

ventilation before facilitating a specific breathing pat

help the patient work on this sequence. After the pa

tern. If the potential for movement is not there, then

tient has learned to initiate inspiration with his or her

the breathing pattern cannot change. Likewise, a pa

diaphragm and lower chest wall muscles more con

tient with primary pulmonary dysfunction undergoing

sistently, this technique can help to put the whole se

chest surgery, or a patient suffering from an acute

quence together. The diaphragm continues to be the

chest trauma, may also find the rib cage stiff or sore

primary mover, but the other accessory muscles are

and thus limited in its potential expansion. All three

encouraged to do what they should do, which is to as

of these patients may benefit from the inclusion of rib

sist the diaphragm for better overall ventilation.

cage mobilization in their therapy programs. The rib

Generally, the patient is positioned symmetrically

cage musculoskeletal limitation may be secondary to

in either supine or supported sitting with a neutral

muscular atrophy, spasticity, or pain. Thus patients

pelvic position. The therapist waits until the end of an

with either primary pulmonary dysfunction or sec

expiratory cycle and then, using the hand placement

ondary pulmonary dysfunction can benefit from the

of the diaphragm scoop, asks the patient to breathe in

concept of chest mobilization.

"here." With the other hand, the therapist moves up

It is beyond the scope of this textbook to detail all


400

PART III


her head (shoulder flexion), as far as possible while

Techniques to Mobilize the Thorax

watching his or her hands. Using the appropriate ven

I. Use of towel or pillow rolls to mechanically open up the anterior or lateral chest wall

2. Use of upper extremity pattern s to facilitate opening of individual rib segments

tilatory strategy, the patient is also instructed to in hale during this movement. Because fulJ shoulder flexion and inspiration both require opening of the in dividual rib segments, pairing them in this gravity-as sisted position wiII promote a greater passi ve chest

3. Counterrotation of the trunk 4. Use of ventilatory-movement strategies to facili tate opening of the entire thorax

5. Specific rib mobilization tu free up an individual segment

6. Myofascial release techniques to frec up restric tive connective tissue on and around the thorax

7. Soft tissue release techniques to lengthen indi vidual tight Illuscles

wall stretch then either technique alone. If straight flexion is not a viable option, use a buttelily position, raising the arms up in shoulder flexion, abduction, and external rotation with elbows bent (like butterfly wings), again pairing this with voluntary maximal in spiration and upward eye gaze. Pairing inspiration and shoulder flexion maximizes the stretch on the chest and encourages better ventilatory strategies. In sidelying, ask the patient to bring his or her arm up in straight flexion to maximize anterior chest ex

the numerous techniques involved in musculoskeletal

pansion or to move the arm into abduction to maxi

mobilization of the thorax, however, some simple

mize the lateral costal expansion. Pair either move

techniques and suggestions for further study are pre

ment with inspiration and upward eye gaze. If upper

sented. See the box above for a summary of mobi

extremity movement is not possible, the therapist can

lization techniques.

passively use countelTotation of the trunk to mobilize

Once again the therapist should note that the initial step in achieving success begins with positioning

the chest while in the sidelying over the towel or pil low roll. Continue to ask for active eye gazing.

considerations. Starting in supine, anterior chest wall

The same concepts can be used in upright postures,

mobility can be improved by placing a vertical towel

such as sitting or standing. Use a vertical towel roll

roll down the length of the thoracic spine and allow

again along the thoracic spine either along the back of

ing gravity to pull the shoulders back to the bed. In

a chair (wheelchair) or along the wall. Move the pa

this position, the anterior chest is opened up, placing

tient's arills passively or actively up into the most flex

the intercostal and pectoralis muscles on stretch for

ion or buttert1y ROM possible. The patient will get a

easier facilitation of upper chest expansion.

significantly greater stretch to the anterior chest wall

In sidelying, the lateral aspect of the chest can be

using the towel roll than without it. Precautions apply

passively mobilized with gravity'S assistance by plac

for patients with musculoskeletal problems along the

ing a towel roll(s) or pillow(s) under the lower chest

spine and for patients with impaired skin-tolerance.

(ribs 8 to 10) on the weight-bearing side. To determine

If these general mobilizing techniques do not pro

an appropriate amount of sidebending, make sure that

duce adequate chest wall mobility to allow for freer

the patient's shoulder and pelvis are still in direct con

breathing patterns to occur, then more specific tech

tact with the surface even with the towel roll(s) in

niques need to be considered including the following:

place. This maximizes the stretch on the chest without

(I) specific rib mobilization, (2) myofascial release to

placing the patient in a position that is too advanced

tight connective tissues (e.g., scar tissue secondary to

for his or her present chest wall mobility. Patients vary

surgical or traumatic areas), and/or (3) soft tissue re

from tolerating only a single thin towel roll up to toler

lease of tight muscle groups (neurological patients

ating three pillows under the lower ribs.

often present with tightness in the pectoralis, inter

In both postures, active or passive stretch ing can

costal, and quadratus lumborum muscles groups,

be added after positioning for success. In supine, ask

whereas orthopedic patients tend to have more tight

the patient to bring the arms directly up over his or

ness in the neck and back muscles). Use the position


22


ing and ventilatory strategies previously suggested (e.g., sidelying over a towel roll) during these spe

Accessory Muscle Facilitation Techniques

cific interventions to maximize the potential gains in

I. Pec to ral i s facilitation

chest wall mobility. It is beyond the scope of this

2. Sternocleidomastoid and scalenes facilitation

textbook to detail all the numerous techniques in volved in musculoskeletal mobilization and release of the thorax. These three interventions are intended as suggestions for further study in outside texts.

401

3. Trapezius facilitation 4. Diaphragm inhibiting technique •

Manual inhibition

•

Postural inhibition

5. Lateral costal facilitation

FACILITATING ACCESSORY MUSCLES IN VENTILATION

6. Serratus push-up

If the patient is still not demonstrating an optimal breathing pattern after f acilitating a preferred

muscle breathing, the patient would be put in an ad

breathing pattern through appropriate positioning,

vantageous posture by slightly anteriorly tilting the

appropriate ventilatory strategies, chest wall mobi

pelvis. In supine, this could be as simple as decreas

l ization, and diaphragmatic retraining, then specific

ing the amount of knee flexion that is present or

facilatory or inhibitory techniques should be initi

using a small towel roll under the lumbar spine.

ated to the accessory muscles of ventilation. Spe cific techniques are discussed here in detail. See the box above for a summary.

Pectoralis Facilitation

Because the diaphragm normally supplies the bulk

The pectoralis muscle group is a powerful anterior

of the inspired air during quiet breathing, diaphrag

and lateral expander of the upper chest and can sub

matic breathing is the preferred pattern of breathing.

stitute quite effectively for paralyzed intercostal mus

However, after some neurological insults, strictly di

cles in the upper chest when trained to do so. Train

aphragmatic breathing may not be possible or even

ing usually begins in either modified sidelying or

preferred. Unlike pulmonary rehabilitation programs

supine. To increase the use of this muscle during in

for chronic lung or asthmatic patients, where di

spiration, the therapist should place his or her hand in

aphragmatic breathing is almost always encouraged

the same direction as the contracting muscle fibers.

and use of accessory muscles discouraged, restoration

Specific proprioceptive input is very important when

of independent, efficient breathing patterns for the

facilitating a muscle, thus make sure the hand is diag

neurologically impaired patient may require the regu

onally placed on the upper thorax (Figure 22-18). The heel of the therapist's hand should be near the

lar use of accessory muscles. Positioning continues to be the single most impor

sternum and the fingers aligned up and out toward the

tant aspect of all ventilatory facilitation techniques. If

shoulder. The patient is then asked to breathe into the

your patient is positioned for success, the probability

therapist's hands while the therapist applies a quick

of a successful response is much more likely. By as

manual stretch (as in repeated contractions PNF) to

sessing the patient's head, upper-extremity, trunk,

the muscle fibers (down and in toward the sternum).

pelvic, and lower-extremity positioning before every

This elicits the quick stretch reflex of the muscle and

activity or technique, the therapist is empowered to

simultaneously provides added sensory input, which

use mechanical positioning and gravity to the pa

facilitates a stronger and more specific muscle con

tient's advantage rather than to a disadvantage. For

traction. To emphasize an increase in lateral expan

example, a slightly posteriorly tilted pelvis tends to

sion, facilitation should gradually be transferred from

facilitate diaphragmatic breathing, whereas a slightly

the sternal arca out toward the therapist's finger tips

anteriorly tilted pelvis tends to facilitate upper chest

by the patient's shoulder. Unlike in the case of facili

breathing. Thus when facilitating more accessory

tating a more diaphragmatic pattern, verbal cues


402

PART III


FIGURE 22-18 Hand placement for facilitation of the pectoralis muscles for upper chest breathing.

should be strong and demanding to elicit a stronger maximal voluntary effort.

Trapezius Facilitation The trapezius muscle assists in superior expansion of the chest. Facilitation can be initiated in supine

Sternocleidomastoid and Scalene Facilitation

or sidelying positions to decrease the resistance from gravity. It can be progressed to an upright

This same plinciple can be applied to the sternoclei

posture in which the patient would have to work

domastoid and scalene muscles. In supine, therapists

against gravity.

need only change the angle of their hand alignment to

Placing the hands over the tops of the patient's

more specifically facilitate the sternocleidomastoid

shoulders, the therapist quick stretches the trapezius

and scalene muscles. Turning the hands parallel to

in a downward direction to facilitate a stronger eleva

the trunk so that the fingers are pointing up toward

tion response. Repeated contractions e
the neck rather than pointing out toward the shoulder,

facilitate the contraction throughout the full ROM.

the therapist applies the same quick stretch and uses

Obviously, the shoulder shrug motion should be

the same verbal cues. The altered hand position now

paired with inhalation and upward eye gaze to maxi

specifically facilitates the sternocleidomastoid and

mize the facilitation response.

scalene muscles and secondarily influences the pec toralis muscles. The sternocleidomastoid and scalene muscles primarily expand the chest in a superior and anterior plane, whereas the pectoralis muscles expand

Inhibition of the Diaphragm Two techniques are described to inhibit the excessive

the chest in primarily a lateral and anterior plane,

use of the diaphragm during inspiration. Ideally, the

thus accounting for the slight difference in the facili

therapist is venturing to balance the use of accessory

tation positioning.

muscles, especially the intercostal, sternocleidomas


22


403

toid, scalenes, and trapezius muscles with the di

To perform the diaphragm-inhibiting technique,

aphragm's contraction. This is done to prevent para

the patient is positioned supine, semi-sitting or side

doxical movements of the chcst, or worse, to prevent

lying with the top arm positioned overhead or pulled

adverse musculoskeletal changes in the chest wall,

back at the waist to open up the upper chest. If toler

such as a pectus excuvatum that can result from mus

ated, remove pillows from under his or her head, an teriorly tilt the pelvis and assess patient's airway

cle imbalance. Inhibiting the diaphragm may be necessary during

safety by checking if he or she can still swallow

breathing retraining for somc patients with spinal

comfortably. The heel of the therapis t's hand is

cord injuries, polio, spina bifida, developmental de

placed lightly on the patient's abdomen at about the

lays, head traumas, and cerebral palsy. The di

level of the umbilicus. No instructions are given to

aphragm may be too weak to produce an adequate

the patient at this point. As the patient begins to ex

tidal volume or vital capacity without the assistance

hale a normal breath of air, the therapist gently al

of accessory muscles. In these cases the diaphragm

lows the heel of his or her hand to move up and in to

inhibiting technique is used to encourage the use of

ward the central tendon of the patient's diaphragm

the accessory muscles to assist in independent volun

(see Figure 22-4, p.

tary ventilation. Patients learn to use their weakened

breath is completed, the therapist strictly maintains

394). When expiration for that

diaphragm muscles in concert with intact accessory

the hand position in that shortened expiratory posi

muscles. Not only does this allow for an increased

tion. During the following inspiratory phase, the di

tidal volume and vital capacity, but it also provides

aphragm will experience some gentle resistance to its

better aeration of all lung segments and better mobi

inferior descent, causing inhibition to its full ROM.

lization of the entire thorax.

On the next expiration, the technique is repeated with

In contrast to the first reason that this technique

the therapist carefully pushing the heel of his or her

may be used, an unusually strong diaphragm, acting

hand further up and in, maintaining greater inhibition

without support from surrounding m u sculature,

during each inspiratory phase. After two or three

specifically the intercostals and abdominal muscles,

ventilatory cycles, a patient usually begins to subcon

may also need to be inhibited. For example, a para

sciously alter his or her breathing pattern to include

plegic or lower level tetraplegic patient with an intact

more upper chest expansion to reconcile the di

diaphragm but absent abdominal and intercostal mus

aphragm's transient inability to produce enough

cles may demonstrate a paradoxical breathing pattern

chest expansion to yield an adequate tidal volume.

(see compensatory breathing patterns, Chapter

The therapist should carefully observe which acces

37). In

this case the accessory muscles must be encouraged

sory muscles the patient spontaneously chooses. Are

to keep the diaphragm in check, attempting to avoid

they used symmetrically? What is the general quality

the development of a pectus excuvatum. The goal of

of the movement? Is the onset harsh or smooth? Does

this breathing retraining method is to stop the para

the patient appear fatigued or uncoordinated?

doxical movements of the upper chest during inspira

It is not until this point that the therapist should

tion by balancing the use of the upper and lower

verbally acknowledge any alteration of the patient's

chest. In some cases, spastic intercostal muscles, like

breathing pattern. Without changing his or her hand

in some spinal cord injury situations, may intercede

position, the therapist tells the patient what it is that

to prevent this paradoxical movement by maintaining

he or she likes about the new breathing pattern (e.g.,

the upper chest's position during inspiration in spite

balance between upper and lower chest expansion or

of the negative pressure within the chest and grav

less paradoxical motion of the sternum). Then the pa

ity's influence on top of the chest. Balancing the

tient is asked if he or she notices any difference from

chest's movements should produce an increase in

before, bringing this breathing pattern to a consciolls

tidal volume and vital capacity potential and mobilize

level. Only after some orientation to this pattern, usu

4 to 6 breathing cycles in the full

a greater portion of the chcst, just as the technique

ally no morc than

does in the first case presented.

inhibiting pattern, should the therapist begin to grad


404

PART III


FIGURE 22-1 9 Diaphragm inhibiting in prone on elbows position.

ually release the pressure being applied.

already been achieved. Extra care must be taken not to

While slowly releasing pressure with each cycle of

initiate any applied pressure quickly because of the

inspiration, the therapist asks the patient to attempt

likelihood of eliciting unwanted abdominal contrac

cognitively to reproduce the desired pattern. It should

tions or spasticity or eliciting a stronger diaphragmatic

take the same number of cycles to release the pres

contraction resulting from the quick stretch reflex. The

sure as it did to apply it. This technique easily allows

technique should never be painful. The therapist must

fo r gradations of i n h ibition, from full inhibition,

keep his or her hand on the abdomen, not the rib cage,

where the patient is forced to use upper accessory

to properly influence the diaphragm. This technique

muscles or risk becoming short of breath, to barely a

can be progressed by c hanging postures, which re

proprioceptive reminder to change his or her breath

quires greater tl1lnk control. Can the patient still main

ing pattern. It also allows for gradation of inhibition

tain the overall pattern? Can the patient breathe with

while the patient is learning to assume control over

out paradoxical movements against gravity?

the new breathing pattern. If during the releasing

The second technique is for the more advanced pa

phasc of this technique the patient begins to lose con

tient and simply presents a physical block to diaphrag

trol over the new pattern, the therapist can gently

matic excursion. The patient is positioned in a prone-on

reapply some pressure during the next expiratory

elbows position (Figure

phase to help the patient regain that control. At that

neurologically impaired patients, the lower chest will be

22-19). With most severely

point, the therapist can release or reapply pressure as

in direct contact with the surface, so lower anterior and

neccssary until the desired pattern is obtained and full

inferior expansion is inhibited and lateral costal expan

release of pressure is completed.

sion is limited. The upper chest is positioned in exten

This technique is particularly effective with patients

sion and the upper extremities are fixated, optimizing the

who are having difficulty cognitively altering their

length-tension relationsh.ip of the anterior and superior

own breathing pattern, such as with small children,

accessory muscles for easy facilitation. In addition, ante

brain-damaged patients, or slow motor learners, be

rior excursion of the upper chest is now in a gravity-as

cause it requires no cognitive effort until success has

sisted posture. Through the use of head and neck pat


22


405

FIGURE 22-20 Static-dynamic upper extremity activities in prone on elbows to encourage upper chest accessory muscle participalion.

terns, such as in PNF diagonals, or static-dynamic activi

now assisting anterior excursion of the chest and re

ties, such as in weight shifting to one supp0!1ing limb

sisting posterior excursion. To emphasize the serratus

while reaching out with the other extremity, the therapist

anterior muscle's role in posterior expansion, the pa

can readily facilitate greater upper chest breathing (Fig

tient is instructed to perform an upper body push-up

ure 22-20). These are the same patterns the therapist can

(with or without the therapist's assistance). The serra

use to achieve other goals, such as increased head and

tus anterior muscle causes lateral scapular movement

neck control, increased shoulder stability, or increased

thereby facilitating maximal posterior excursion of

upper body balance. Therefore, by helping the patients

the thorax. The patient is instructed to take a deep

to coordinate movement goals with ventilatory patterns,

breath in during the push-up and to exhale the air

it becomes more likely that the patients will incorporate

(passively or forcefully) when returning to the start

these patterns functionally into daily activities. This is

ing position. Forceful exhalation in this activity can

the ultimate goal of any ventilatol)' retraining procedure.

be used as a forerunner to effective cough retraining.

The manual diaphragm-inhibiting technique is

Gentle or controlled exhalation can be used to en

usually less threatening to the patient than the prone

courage greater breath support for vocalization or f6r

on-elbows-inhibition technique. Prone on elbows it

eccentric trunk muscle training.

self can inhibit the diaphragm so completely for neu

Emphasizing posterior chest expansion during in

rological patients lacking spinal extensors that they

halation is the only occasion where inspiration would

become extremely short of breath. Consequently, do

be paired with trunk flexion. In all other inspiratory

not position the patients in this more demanding pos

situations, inspiration is paired with trunk extension,

ture until success appears likely.

and exhalation is paired with trunk flexion.

Serratus Push-up

PATIENTS WITH ASYMMETRICAL DYSFUNCTION

Facilitating greater posterior chest expansion can be

Patients with asymmetrical weakness need a different

achieved in a prone-on-elbows position. Gravity is

approach from the controlled or upper chest breathing


PART III

406


Promoting Symmetrical Ventilatory Function for Patients With Asymmetrical DefICits

side with his or her arms positioned down below

90

degrees of shoulder flexion, lateral chest expansion into that side becomes inhibited because of the

I. Use of positioning to achieve more symmetrical

physical batTier. This forces the patient to find an

alignment of the chest and trunk in both reclin

other way to meet his or her ventilatory needs,

ing and upright postures

which indirectly facilitates chest expansion on the

2. Use of postural inhibition to the stronger or unin volved side to promote greater chest wall expan sion on the weaker or involved side

3. Timing for emp h asis technique to promote active symmetrical breathing anywhere in the thorax

opposite side (the uppermost side). The therapist can then supply sensory and motor input through his or her hands to the patient's upper, middle, or lower chest on the involved or weaker side to facilitate in creased ventilation on that side. Early in the rehabil itation process or soon after thoracic surgery, the patient may have difficulty performing lateral chest expansion against gravity in sidelying (gravity-re

patterns presented previously. These patients need

sisted movement). If so, position the patient in a

facilitation to the weaker side to promote symmetri

3/4-supine position to lessen the workload imposed

cal chest wall expansion in both the upper and lower

by gravity. Gradually, work the patient up to a full

chest. See the box above for a summary of tech

sidelying posture to achieve the greatest strengthen

niques.

ing benefits.

Symmetrical Positioning

Timing for Emphasis

Symmetrical ventilatory patterns may be effortlessly

Another technique to promote symmetrical chest wall

achieved by altering the patient's position in each

movements is performed in numerous postures, such

posture to maximize the chest wall's potential to

as supine, sitting, or standing. The therapist places his

move in a symmetrical pattern. This is especially true

or her hand symmetrically on the lower lateral chest

in an upright position in which asymmetry is gener

wall, on the mid chest, or on the upper anterior chest

ally more pronounced. For example, hemiplegic pa

wall. At the end of exhalation, the therapist gives a

tients may lean toward their involved side in sitting

quick stretch on the muscles being touched to facili

because of weakness or spasticity. Likewise, after

tate a deep inspiratory effort in that area of the chest.

thoracic surgery, a primary pulmonary patient may

Immediately after both sides begin to move into an

lean toward the surgical side to avoid pain caused by

inspiratory pattern, the therapist manually blocks (or

chest movement around the incision. Both situations

inhibits) expansion of the chest on the stronger side

cause asymmetrical breathing patterns and decrease

while giving continued quick stretches on the weaker

ventilation on the involved side. Improving chest

side. This facilitates greater expansion on the weak

wall alignment may alleviate the ventilatory deficit

side by use of an overflow response. This technique,

on the involved side.

adapted from the PNFs timing for emphasis tech nique, uses the strength of the stronger side to facili tate movement on the 'Yeaker side. It can be applied

Postural Inhibition

to any area of the chest where symmetrical move

For some patients, more aggressive positioning must

ments should be the norm.

be used to achieve greater chest wall excursion and ventilation on the involved side. This can be accom plished by inhibiting the chest wall movements on

REDUCING RESPIRATORY RATES

the uninvolved or stronger side. Usually, the best

In addition to altering breathing patterns through fa

posture in which to achieve this inhibition is sidely

cilitation and inhibition techniques, reducing respira

ing. When the patient lies on his or her uninvolved

tory rates


(RR) may also be necessary before arriving

22

Facilitating Ventilation Pattems and Breathing Strategies

at an efficient breathing pattern for some patients.

407

sisted cough technique. One medical contraindication

See the box below for a summary of techniques.

for this technique is bony instability of the spine be

Many neurological patients with high neuromuscular

cause of its rotary nature.

tone increase their RR to compensate for a decrease

In bed or on a mat, place the patient in sidelying

in their tidal volumes (TV) or because of brain-stem

with knees bent and arms resting comfortably out in

impairments to the respiratory centers. In addition,

front of the head or shoulders. In this technique the

many patients who are anxious, such as asthmatic, or

higher the upper extremities can be placed within a

thopedic, or surgical patients experiencing pain, may

comfort zone, the better the result. Relaxed position

also demonstrate an excessively high RR. Attempting

ing of the patient is essential to the success of this

to restore ventilatory efficiency may require increas

technique, thus position the patient in an open yet

ing TV while concurrently decreasing RR.

comfortable position. Normalizing neuromuscular tone is the first step in attempting to decrease a high RR. Patient discomfort is likely to elicit increased

Previous Facilitation Techniques

tone and an increased RR.

The techniques previously described in this chapter

The therapist's own position is also important be

promote an increase in TV by improving the overall

cause it directs the force that is applied to the pa

ventilatory patterns and often cause a secondary reduc

tient's chest. Initially, the therapist needs to stand

tion in RR. See sections on controlled breathing, mobi

behind the patient, perpendicular to his or her trunk.

lizing the thorax, and upper chest breathing facilitation.

If the patient is lying on the left side, the therapist places his or her left hand on the patient's shoulder and his or her right hand on the patient's hip. The

Counterrotation

therapist then leaves his or her hands in place and

The technique described next is specifically devel

simply follows the patient's respiratory cycle. This

oped to promote a lower RR. The counterrotation

allows the therapist to assess the patient's subjective

technique reduces high neuromuscular tone and in

rate and rhythm and the patient's overall neuromus

creases thoracic mobility, thus often resulting in an

cular tone. Only after this assessment should the

increase in TV and simultaneous reduction in RR.

clinician begin the active phase of the technique.

These authors have found this technique to be ex

Using a PNF technique called rhythmic initiation,

(I) patients with

the patient is gently log-rolled in a small ROM in

decreased cognitive functioning after a neurological

sidelying. The rolling is gradually increased achiev

tremely effective for the following:

insult or after surgery, (2) very young children be

ing more ROM from sidelying toward prone. This

(3) patients with

progression of movement generally reduces high

high neuromuscular tone. As described in Chapter 21,

tone, which usually makes the second phase of the

it can also be easily adapted as a very effective as-

technique more effective.

cause there are no verbal cues, or

During this phase, the therapist needs to audibly duplicate the patient's RR. As the patient moves into greater rolling ROM and begins to slow his or her Techniques to Reduce High Respiratory Rates

RR, the therapist needs to use the patient's audible cuing as a facilitator for establishing a slower RR.

I. Previous techniques that increased tidal volume

Thus the therapist begins by having the patient estab

2. Countenotation technique

lish the audible RR and then the therapist slowly

3. Butterfly technique in sitting •

Straight planes

•

Countenotation

takes over. Audible cues can be very strong facilita tors of ventilatory rhythms. Phase two requires the therapist to slowly change

4. Relaxed pursed lip breathing with inspiratory and expiratory pauses

his or her position. Transitioning to a diagonal pos ture, the therapist now stands or half kneels behind the patient near his or her hips, turning diagonal to


408

PART III


the patient until

the patient's head at roughly

Assume

more

that the patient is side-

lying on the left At the

removed should be the audible cues. As with the di-

to get

angle, The hand placement

at

biting tech

plying stronger manual input. If the

of the

left hand

cycle, the

patient's shoulder on the tips, and the

tation can be hand

to the patient's right

the patient or

back

fossa (the hollow of the

21-6, A, then

The

can

compress the rib cage in all three

planes of ventilation at the end of exhalation by gen

has an ex-

50 to 60 breaths/min), the facili every 2 to 3 breaths so as not to

RR

fast

care being taken not to unintentionally use the thumb or

the therapist can

reestablish control quickly if needed by simply reap

It should be apparent that this technique need not be used

for

goals but rather

can be

total rehabilita

tion program. It is a natural precursor to active rolling or it can be used as a vestibular stimulator.

tly pulling the shoulder back and down, while simul pushing the hip up and forward, This movement promotes more complete exhalation, When the patient

the next inspiration, the

therapist switches hand

to capitalize on the

for TV, The therapist's left hand

improved

Butterfly Technique version of this technique may be appropriate. In un supported

and the ther

slides back to the patient's

has greater motor control, an

If the

hand slides forward just anterior to the right iliac crest

21

Figure

stand behind or in front of the pa-

depending on his or her balance

B, p, 376).

or assist his or her arms up to this pos

As the patient inhales, the therapist slowly stretches volumes (TVs).

the chest to maximize left hand

The thorax if the

the scapula (or the

is unstable) up and away from

the spine and the

hand

back and

the

down to maximize all three planes of

re

in greater inspiration. The therapist should use

and ask

to bring his or her arms up into a butter from a comfortable that patient, tient's

ROM position for

to audibly breathe with the pa

RR. When the patient

raise the arms

up into slightly more shoulder flexion. When the pa tient

lower the arms slightly.

to move in greater and greater increments of range, all the while

out loud with your

the flat or heel of the hand whenever possible to

Through your audible breathing cues,

avoid unintentional patient discomfort and to maxi

your patient to slow down the

mize the facilitated area.

slower breaths. The use of the followi ng begins and ends the

Initially, the

cycle according to the patient's

RR.

deeper inhalations as

tone is relaxed and increased TVs are through the effects of counterrotation, the therapist

slows the rate of rotation down,

the

audible breathing cues to also facil

RR. The patient dates to a slower RR as the therapist

itate a slower

trol over the patient's

tension

more con

and

Thus it becomes

(2) shoulder ex

and

for the pa

tient to increase his or her TV and decrease

RR.

As in the previous technique, the therapist by

out loud at the audibly at a

pace, The

pace and transi more desirable

picks up on this subtle cuing and

subconsciously reduces his or her own

to assist in vol

RR even if

cannot follow verbal commands. This technique can be modified to encourage more

at the slower rate.

The therapist can progress the

with inspiration and

tension and trunk flexion paired with exhalation.

pattern. With many

cognitively follow commands, he or s h e can be untarily

and exhalations: ( l ) shoulder flexion and trunk ex

accommo

the results can be marked. If the patient can alerted to this

to "ask"

RR and take deeper

by de-

the manual input. The last facilitation to be

intercostal and oblique abdominal muscle contrac tions by using a diagonal rather than a straight


22

A


-

B

FIGURE 22-21

A, butterfly technique facilitating inspiration; B, butterfly technique facilitating exhaltation;

C, butterfly with twnk rotation facilitating inspiration. All threc planes of respiration are stretched

on the patients right side. D, butterfly with twnk rotation facilitating exhaltation. All planes

compressed on the right side.


409

410

PART III


of movement. Have the

look up and over one

and proceeds to force the air back and down the

shoulder as he or she breathes in and brings arms up

throat with a

and behind his or her head. Then have the

ynx, and larynx.

look down and away toward the opposite knee as he

Research has consistently shown that use of this

or she breathes out and brings arms down to the op knee (Fieure 22-21).

maneuver of the tongue,

with severely

pa

tients can increase pulmonary functions signifi especially for TV and Vc. If GPB is the only means of ventilation off of a ventilator or

Relaxed Pursed-lip Breathing

nerve stimulator, mastery of this technique is critical

Use of a relaxed

to a

survival in case of mechanical failure.

ously described under

All

should be made to successfullv teach

breathing pattern," is also a technique to reduce RR. By

the expiratory

through pursed

the patient secondarily decreases his or her RR.

GPB to this patient population.

SCI while

\"VllllJlilA\V

in front of a train. After he was

medically

GLOSSOPHARYNGEAL BREATHING

to illustrate its use

A clinical example may

fulness. A l4-year-old male sustained a C 1

two phrenic nerve stimulators were in his chest. The patient had no nonassisted

requires

means of ventilation.

the patient

more than just promoting the use of accessory muscles

had limited use of one

sternocleidomastoid,

A small population of neurological RR to meet basic

or

last decade, more

needs. In the

SCls (above C4) have sur

vived the initial trauma because of advances in med the rehabilitation

ical technology.

is then faced with the difficult task of

of life. For these patients, as well as many old polio breathing voluntary ventila

technique allows for tion, which many to

which was

lost as a result of high neurological

ily believed it could not bear the psychological bur went home to live.

den placed on them if the GPB instruction was

and

slowly be

stated that he learned motor skills the pa

tient learned to breathe without the use of his phrenic nerve stimulator for 3 to 5 minutes before this same patient learned to breathe for up to 2 hours

for a way to reduce their de

could actually

air to sustain life without mechanical

To the staff's

he even learned to talk and

mouth,

using the lips, soft

tongue, pharynx, and larynx, a

using GPB

off of his

pendence on the iron lung for ventilation. It was

inhale

wearing

immediate respiratory distress. The fam

and hypoventilating. Within the next I to 2

GPB is a polio patients found that

would

slowly. After a painstaking 2-month

some control over their Jives

control over their

and to

out,

cause the

state does improve the

ity of their Jives. This augmented breathing lows

home

be inevitable because of their fear of his nerve stimulator malfunctioning or a

quality

mastery of the

and intrinsic neck muscles. The patient and family feared that

his sip-

GPB. The patient to his home. This

was then successfully

does not imply that this was the only factor consid

ventilation. Only intact cranial nerves are

ered in his discharge olanning, but it was oerhaos the

This m e t h o d i s s o m e t i m e s referred t o as

most significant.

breathing because it uses the principles of tion common to the of cavity by

Instruction in GPB takes time and concentration. It

The

is best to statt off in small time blocks of 10 to 15 min However, it is

utes because it can be very

pressure that internal space,

causing the outside air to rush in. At that the patient closes off the entrance

lips)

to successful the patient gets

of the technique that preferably daily training.

Once the patient has mastered the


22


sessions can be lengthened considerably, and the pa

411

demonstrates to the patient what a stroking maneuver

tient can be taught self-monitoring techniques. Specific

looks like several times to give an idea of the motion

goals of GPB training must be explained to the patient

required. The therapist continues to mimic the pattern

before the beginning of treatment to gain his or her

as the patient attempts to duplicate it. This gives the

support and cooperation. In addition to providing the

patient an active model to mimic and decreases feel

ventilator-or stimulator-dependent patient with a TV

ings of uneasiness surrounding the necessary but

necessary for gaining independence from mechanical

somewhat silly facial grimaces. If the patient is able

assists, GPB has many other b e n e f i t s. F o r the

to breathe independently, his or her ability to breath

tetraplegic patient who has a partially intact diaphragm

hold and to close off the nasal passageway should be

(C3 to C4) or the loss of essential accessory muscles

checked because air leakage is a common cause of

(C5 to C8), GPB can accomplish the following: (1) in

failure. The patient is then instructed to take in a

(2) as

maximal inspiration before attempting the stroking

sist in a longer and stronger phonation effort, and

maneuvers to eliminate the possibility of using other

(3) act as an internal mobilizer of the chest wall.

accessory muscles during the technique.

crease VC to produce a more effective cough,

The muscles used in this technique do not have the

If possible, position the patient in an upright or at

same internal proprioceptive, sensory, or visual feed

least a symmetrical position. Specifically, the patients

back mechanisms as the trunk and limb muscles. Thus

are instructed to bring their jaws down and then for

necessary adjustments in the technique are sometimes

ward as if reaching their bottom lip up for a carrot

difficult to see or feel. The patient cannot see his or

dangling just in front and above the upper lip (Figure

her tongue pushing the air back or truly feel the phar

22-22, A). Slight cervical hyperextension is necessary

ynx swallowing the air into the lungs, so the thera

to allow for maximal temporal mandibular joint

pist's external feedback system is very influential.

(TMJ) excursion. (A contraindication for this tech

Use of a minor can greatly enhance the visual compo

nique is a TMJ disorder.) The lips should be shaped

nent of feedback. Small changes, like adjustments in

as if they were to make the sound "oop." The patient

posture or a suggestion of another sound to imitate,

is then told to close the mouth, reaching the bottom

may be all that is needed for the patient to learn tbe

lip up to the top lip (see Figure

stroking maneuver correctly. Success in GPB can be

and jaw are drawn back toward the throat, with the

22-22, B). The tongue

assessed objectively with a spirometer and a pulse

mouth and tongue formation of the word up or the

oximeter. For those patients incapable of breathing in

sound "ell" (see Figure

dependently, any TV reading will indicate successful

moving in roughly a rectangular pattern. Most pa

22-22, B). The lower jaw is

intake of air. For patients who are not ventilator de

tients learn the stroking maneuvers by making the

pendent, a VC reading that is greater than 5% over the

sounds at first, as they become more proficient, the

baseline indicates successful use of GPB. Lower-level

sounds and excessive head and neck motions dimin

tetraplegics, C5 to C8, have demonstrated increases in

ish. Often, the students (patients) outperform the

VC by as much as 70% to 100%.

teacher (therapist), because through consistent use,

Therapists can monitor their own successes with

they learn all of its finer subtleties.

this technique by taking VC readings with and with

Although this technique can be broken down into

out GPB or by subjective analyses. Maximal inhala

several stages as it has been here for the purpose of de

tion, followed by three or four successful GPB

scription, most of the literature cautions the therapist

strokes, will cause a feeling that the chest will burst if

against it. (Zumwalt, Adkins, Dail, and Affeldt, 1956).

an attempt is made to inhale more air. Likewise, a

Simple, minimal insuuctions seem to accomplish more,

sensation of "needing to cough" is another subjective

perhaps because the continuity of movement is so es

indication of successful GPB. However, a feeling of

sential to the success of the inhalation. Specific instruc

indigestion is usually indicative of swallowed air in

tions can be given later if necessary.

the stomach instead of the lungs.

Common problems encountered with GPB instruc

During the initial treatment session, the therapist

tion are as follows:


(I) an open nasal passage or glot

412

PART III


A

B

c

o

FIGURE 22-22 Glossopharyngeal breathing; A, mouth opened to draw in air; B, j aw closed to entrap the air; C, air pushed back with tongue into trachea; D, vocal folds closed to prevent passive air leaks. Entire maneuver is then repeated.

(2)

a feeling of indi

els begin to fall to the mid 90s and then the low 90s,

gestion indicating that the air is being swallowed into

you can anticipate when they will reach 90%. At that

tis that allows the air to escape,

the esophagus rather than the trachea,

(3)

incorrect

point, end the GPB training and put the patient back

shape of the mouth as the air is bein g drawn in, usu

on the previous ventilatory support system. Oximetery

ally not puckered enough, (4) uncoordinated back

not only allows for accurate monitoring but also pro

ward movement of the tongue, (5) inadequate jaw

vides a means for an objective means for monitoring

mobility, TMJ dysfunction, or decreased cervical

progress over time. In addition, a spirometer objec

ROM, or

(6) incorrect

sounds while performing the

tively measures improvements in VC using GPB. It

technique, such as the word gulp or an "em" sound.

gives the patients concrete indications of success or

A voiding any instruction for the tongue seems to pro

failure with the technique.

duce better results. Concentrate on assisting the pa tient in learning the external physical movements. Tolerance to GPB can be increased when mastery

ENHANCING VOCALIZATION SKILLS

of a single stroke becomes consistent. For patients

In contrast to procedures that assist the patient in in

using it as an assist to their own voluntary ventilation,

halation, procedures intended to improve a patient's

3

to 4 strokes on top of a maximal inspiration is usu

phonation skill must focus on elongating the expira

ally sufficient. Ventilator- or stimulator-dependent pa

tion phase. Coughing is a gross-motor skill that relies

tients may need to use as many as 10 to 14 strokes per

more on force than fine control of the ventilatory

breath. These figures should be used only as rough

muscles for its effectiveness. Conversely, phonation

guidelines. Each patient will use a slightly different

requires precise, fine-motor control of these muscles

technique with a different number of strokes, with the

and the vocal folds to provide a consistent air flow

only important factor being a method that works for

through the larynx. Both are expiration activities and

them. Fatigue with long trials of GPB can be moni

depend on the preceding inspiration for optimal per

tored effectively with an oximeter. The oxygen satura

formance; however, coughing uses concentric con

tion level should stay above 90% to maintain adequate

tractions of the expiratory muscles to force the air

Pa02 levels. For example, if the patient begins the

out, and quiet talking uses primarily eccentric con

GPB session with an oxygen saturation level in the

tractions of the inspiratory muscles to slowly release

upper 90s, fatigue can be monitored and anticipated

the air during expiration. Because of these differ

by watching if the oxygen levels decrease. If the lev

ences, procedures to improve coughing and phona


22


an open anterior chest wall will allow for the greatest

Ellhallcillg Vocalizatioll Skills through

potential for chest wall excursion and thus the largest

ill creased Breath Support

Vc. Use the previously described suggestions for po sitioning to determine if your particular patient needs

I. Position to achieve a neutral chin tuck and opti mal vocal fold alignment

positioning to encourage a more diaphragmatic, upper chest, or unilateral breathing pattern.

2. Manual techniques •

Vibration or shaking

•

Percussion or tapping

413

Manual Techniques

3. Eccentric resistance

Several simple techniques can be used to improve

•

Agonistic reversal technique

eccentric control of the diaphragm and intercostal

•

Functional resistance

muscles in preparation for speech. Vibration or shak ing to the lower chest during expiration assists in a

4. Verbal techniques to refine breath support •

Singing and whistling

•

Games

•

Wind or brass instruments

•

Stopping and starting vocalizations

slower, more controlled recoil of the diaphragm. Why this occurs is not fully understood. It may be that the sensory and proprioceptive stimulation that the vibration or shaking provides augments the pa tient's concentration on those muscles resulting in longer p h onation. The patient is instructed to phonate an "ah" or "oh" sound for as long as possi ble. The therapist simultaneously vibrates the pa

tion will be different in focus. See the box above for

tient's chest with an even and gentle force through

a summary of techniques. Coughing is covered in de

out and slightly beyond the full expiration phase,

tail in Chapter 21.

placing his or her hands on the lateral costal borders

Because the patient's TV and total inspiratory ca

of the thorax, the mid chest, or on the pectoral area,

pacity are the power source for phonation, they be

depending on which area of the chest needs the most

come important concerns in a phonation program.

help in controlling exhalation. This is very different

Generally, a normal TV is adequate for con versa

from the rapid, forceful pressure that is applied to the

tional speech. However, larger volumes of air, thus

patient's chest when promoting a deep cough. Be

greater inspiratory capacities, are required for

certain that the patients understand this important

singing, loud talking, or professional speaking.

difference. The therapist must stress to the patients

Therefore the breathing pattern facilitation techniques

that they should not let air escape before vocalization

described previously in this chapter are ideal before

and that they should try to keep the voice intensity

instructing the patient in better expiration control. For

consistent throughout the procedure. This will pro

example, facilitating diaphragmatic and/or accessory

mote slow eccentric release of the inspiratory mus

muscle breathing techniques, along with the use of

cles during the en tire course of the vocalization.

quick stretches or repeated contractions, can facilitate

Progress can be readily monitored by timing the pa

the desired deeper inhalation.

tient's vocalization, before, during, and after this technique. About 10 to 12 seconds of vocalization, or 8 to 10 syllables per breath, is generally consid

Positioning Concerns

ered adequate for functional use in speech.

Consistent with all previous techniques, the first as

For children, this technique can be modified. The

pect of improving breath support for vocalization is

child is asked to say "ah" or "oh" for as long as possi

to optimize the patient's position. The vocal folds

ble while the therapist percusses or taps lightly with his

have an ideal muscle length-tension relationship

or her hands on the child's upper or lower chest so as to

when the head is in a neutral chin tuck. In addition,

produce a series of staccato sounds. Most children


414

PART III


enjoy the new sound that this makes and will try repeat

the arm's descent. The activity can be progressed sev

edly to phonate longer and louder to accentuate the dif

eral ways. The activity can include lifting something

ferent intensities.

heavy off the shelf and controlling it along with the

Therapeutically, this requires them to take a

arm and trunk while lowering the object or weight to a

deeper inhalation before vocalizing, followed by an

table or to the patient's lap. Or the postural demands

elongated expiratory phase, both of which are neces

of the activity can be increased. The patient can still

sary for functional speech. As the child becomes

lift the heavy object or weight but he or she can now

more adept at it, the therapist can apply more pro

be required to do this in standing, which increases the

nounced clapping over the chest, accomplishing a

demands on the musculoskeletal system.

wider range of voice intensities and doubling as a means of percussion for postural drainage.

Verbal Techniques Speech activities that do not require a therapist's

Eccentric Resistance Techniques

physical assistance can be done in a group or individ

More specific facilitation can be used to increase

ual setting. Singing, for instance, promotes strong

breath support. Ideally, the patient is positioned sym

and prolonged vocalization with maximal inspiration,

metrically in supine or supported sitting, allowing for

which is a significant goal in a phonation program.

maximal chest wall expansion. The patient is in

Similarly, whistling promotes long, even exhalations

structed to visualize his or her chest being pulled up

but is nonverbal. Both are easily incorporated into a

toward the ceiling and held there. They are then told

group activity on the nursing floor, in therapy or in

to vocalize slowly trying not to let the chest "fall."

the community.

Meanwhile, the therapist is applying consistent pres

Along recreational lines, games that promote con

sure to the patient's chest to try to force a quicker ex

trolled blowing further the refinement of motor con

halation. The patient is told to resist this motion by

trol over the respiratory muscles. This can be accom

trying to control and prolong expiration. Like the an

plished by blowing bubbles, especially large ones,

tagonistic reversal technique described in PNF, the

blowing out candles, especially trick candles, blow

therapist is resisting the patient's attempt to eccentri

ing a ping-pong ball through a maze, or by blowing

cally contract and control the trunk muscles. This

air hockey discs across the table rather than pushing

strengthens the eccentric phase of exhalation and pro

them. Patients with musical inclinations should be

motes greater breath control for vocalization.

encouraged to learn to play wind or brass instruments

The same concept can be applied to functional

where refined breath control is mandatory for suc

tasks. Moving into gravity, that is, coming down to

cess. Obviously, the possibilities for recreational use

sitting from a standing posture, lying down from a sit

are endless, and simply require imagination on the

ting posture, and bringing an ann down from reaching

part of the therapist.

into a higher cabinet, all require eccentric control of

Further refinement of breath control for speech

the muscles involved in that activity to slow the

can be promoted by interrupting the outgoing air

body's descent into gravity's influence. Because quiet

flow. Functional speech is a series of vocal stops and

speech uses a similar muscular contraction, teaching

starts. This procedure is geared toward improving

the patient to count out loud or to otherwise vocalize

functional communication skills. The therapist tells

when performing an overall eccentric activity usually

the patient to take a deep breath and then to count out

improves both activities. For example, the patient can

loud to 100. After a few numbers, the patient is told

be instructed to reach up to a high shelf or cabinet

to "hold it." He or she is then told to start up where

while inhaling. Then, using gravity to provide the ec

he or she left off, with the therapist periodically inter

centric resistance, the patient is asked to bring his or

rupting. Because this activity requires the patient to

her arm back down to his or her lap or side while

stop and start the inhalation and exhalation phases at

slowly counting out loud and controlling the rate of

will in all aspects of the ventilatory cycle, it is more


22


415

advanced and should be used only after some control

more desirable. Some may benefit even more from

of exhalation has been mastered.

techniques to reduce the high RR or to mobilize the thorax. For a select patient population, instruction in GPB may be necessary to support breathing off

SUMMARY

of mechanical ventilatory support. Lastly, the ther

In summary, use of appropriate choices in positioning

apist can now choose to use techniques to improve

together with use of an appropriate ventilatory and

the patient in developing adequate breath support

movement strategy for any given task will make the

for vocalization and communication.

success of that task all the more likely. If these sim

It is these authors' hope that the therapist now un

ple, time-efficient methods of facilitation do not pro

derstands how widespread the influence of effective

duce adequate ventilatory changes by themselves, it

ventilation can be on a patient's recovery from dis

is then appropriate to add on the next layer of facilita

ease or trauma. Understanding that facilitating effec

tion-manual facilitation techniques. Specifically,

tive ventilation goes far beyond the old diaphrag

the techniques that are described in this chapter assist

matic exercises, therapists can be empowered to

(1) greater diaphrag

incorporate other techniques and strategies to get

matic breathing patterns (or controlled breathing),

their patients healthier quicker and to assist them in

(2) increased chest wall mobility, (3) greater acces

reaching their greatest rehabilitation potential.

in facilitating the following:

sory muscle breathing patterns (or primarily upper

(4) increased symmetrical breathing (5) reduction in high respiratory rates, (6) auxillary techniques GBP, and (7) improved phonation support. Obviously, not all

chest breathing),

patterns (unilateral disorders),

techniques would be appropriate for any single pa tient. It is up to the therapist to determine which tech niques would best address their patients' deficits.

REVIEW QUESTIONS 1. Why would a therapist want to try to change a patient's breathing pattern?

2. How can ventilatory strategies be incorporated into a treatment session?

3. When would a therapist not teach diaphragmatic

In conclusion, positioning has everything to do with increasing ventilation potential and functional skills. From the beginning of the patient's respira

breathing?

4. What is the role of relaxation in breathing control? 5. When would a therapist consider teaching the pa

tory program, optimizing ventilation and breath

tient to use his upper chest more in breathing?

control through passive and active positioning

6. When would a unilateral breathing pattern be

techniques should be used by all medical disci

taught?

plines, not just physical therapy. As the patients progress, the clinician can and should, assist them in developing better and more efficient movement strategies for higher level activities by coordinating

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&

Kornfralt,

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et al.

(1987).

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appropriate breathing patterns, such as trunk exten

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gies, into all activities. After these quick and easy suggestions are used, a therapist who is exposed to

dana via 76(1 ):70-75. Atrice, M. , Backus, D.A., Gonter, M.

numerous manual facilitation ideas and techniques

cord injury. Orthopedics

to promote more effective and efficient breathing

America 2(1 ):53-70.

patterns can now choose an appropriate interven tion. In some cases, i ncreasing diaphragmatic breathing may be the desired outcome. For other patients, increased upper chest breathing or in creased movements on one side of the chest may be

&

Morrison,

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Acute physical therapy management of individuals with spinal

Bach,

1.R. (1991).

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New approaches in the rehabilitation of the trau

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JounUlI of Physical

Medicine and Rehabililation 1 991;70( I): 13-9. Boughton, A.,

&

Ciesla, N.

(1986). PhySical therapy management the intensive care unit. Topics in

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Teamlalk 2(4):2-8. Braun, NT (1982). Force-length relati onship of the normal human diaphragm. Journal ofApplied Physiologl' 53:405-412. Brown, 1.e. Swank, S.M. Malla, J. & Farras, D.M. (1984). Late spinal deformity in quadriplegic children and adolescents. Journal of Pediatric Ort ho pedics 4(4) : 456-61 .

chest plJysiotlJ erapy on ventilated patient> before and after the application of an abdominal binder. intensive Care Medicine

15(6)'396-39 Mahler, D. A.,

Therapcutic S trat eg ie s in Mahler, D.A. (Ed.)

(199 0). Dyspnea New York: FulUra Publishing. 23 I - 263.

CaSh, J. (1977). NeurolagyJor physiotherapist;. (Ed. 2). London: JB Li ppincott.

Maloney, F.P. (1979). Pulmonary function in quadriplegia: effects of a co rs el . Archive,\" oj Physical Medicine Rehabililatilill 60:261-65.

Cheshire, D.J., Flack, W). (1979). The use o f operant conditioning

Martinez, FJ. (1991). Couser, J.I. ( 1 991). Celli BR: Respiratory re

techniques in the respiratory rehabilitation of the tctraplegic.

sponse to ann elevation in patients with chronic ai"now obstruc

Paraplegia 16:162-74.

tion. Arnerican Review of Respiraton' Diseases 143:476, 199 I.

Clough, P. ( 1983). Gl os s opharyng eal breathing: it's application with a traumatic quadriplegic p ati ent. Archives of Physical

Report 18(3): 11-14. Mazza, F.G., DiMarco, A.F" Allose, MD., & Strohl, K.P. ( 1 984).

Medicine Rehabilitation 64:384-85. Delgado, H.R. et al. Chest wall and abdominal motion during exer

cise in pat ient s with chronic obstructive pulmonary disease, !\mericon Repielv oj RespiratolY Disordel 'S, 126:200, 1982. DeTroyer,

Masscry, M.P. ( 1 994). What's positioning got to do with it? Neural

A. (1983 ) . Mechanical action of the abdominal muscles.

The flow-volume loop during glossopharyngeal breathing. Chest 85(5):638-40. Mellin, G., Hmj u l a , R. 1987). Lung function in relation

10

thoracic

spi nal mobility and kyphosis, Scallc/anavil/II JOl/mal 0/ Reha

bililalion Medicilll' 1987; 19(2):89-92.

Bull E.-III' Physiopathoi Respir 19:575.

DeTroyer, A., etr al. (1985). Mechanics of intercostal space and actions of external and internal intercostal muscles. 1. Clinics

Micheli, J. (1985). The use of the modified Boston orthosis sytem for back p ain: Clinical indications.'! Ol'lho Pros 3 9 : 41 46. Montero, J.e., Feldman, D.J., & Montero, D. (1967). Effects on

Invest 5.'85-87.

& Sharp, JT Electrical and Mechanical Activity of

glossopharyngeal breathing on respira tory function after cervi

the D i aphrag m A cco m pany i n g Body Position in Severe

cal cord transection. Archives of Physical Medicine and Reha

Druz, W.S.,

Chronic Obstructive Pulmonary Disease. A m er ic an Review

bilitation 48:650-53. Mueller, R.E., Petty. T .L., & filley, G.F. (1970). Ventilation and

Respiratory Disorders, 125:275, 1982. Esrenne, M., & DeTroy er, A. (1990). Cough in tctraplegic subjects:

an acti ve process. Annals of Interned Medicine 112( I ):22-28.

arterial blood gas changes induced by pursed lips bre'llhing. Journal o/Applied Physiology 28:784, 1970.

Fishburn, MJ., Marino, RJ., & Ditunno, J.F. (1990). Atelectasis

Roa, J., Epstein, S., Preslin, E., Shannon, T. & ('elli, kB. (1991).

and pneumonia in acute spinal cord injury. Archives oj Physi

Work of b re at hing and ventilatory mu sc l e recruitmcnt during

cal Medicine Rehabilitation 71:197-200.

pursed lips breathing in patients with chronic airway obstruc

Goldman, J.M., et al. (1986. Effect of abdominal binders on

breathing in tetrap legic patients. Thorax 41( 12):940-5. Gross, D., et al. (1980). The effec t of training on sU'ength and en

tion. American Re vi e w oj Resl'iralOry Disorders 143: pA 77. Rood, M.S. (1962 ) . The use of sen sory receptors to act ivate, facilitate and inhibit motor r esp onse. In Sa ttely , G. Approaches to the

durance of the diaphragm in quadriplegia. American Journol of

Trealmenl l
Medicine 68:27-35.

ternal Congress World Confederation of Occupational Therapists.

Hap y, MJ. (1992). Wheelchair seating and positioning: options

Saumarcz, R.e. (1986). An analysis of possible movements of human upper rib cage. Journal ofApplied Physiology (2):678-689.

and solutions. Physical Therapy FOrt/m issue:4-8. Hixon, TJ. (1991). Respiratory Junction in sp eech and song. San Diego: Singular Publ ishing Group.

Scheitzer, lA., (1994). Srccific breathing exercises for the patients with quadriplegia. Physiwl Them!'y Pmcticl' 1994;3(2): 10')122.

Hornstein, S. . & L edsome , 1. (1986). Venti lat or y muscle training in acute quadliplegia. Physiotherapy Canada 38(3): 145-49. Huss, D. (1987. Scating for spinal cord client". In Proceedings oj the

Shaffer, T. H. , Wolfson, M.R., & Bhut ani, V.K. Respiratory msucle functi on, assessment and training. Phys Ther 1981 ;61 : 1711-23. Sharp, JT, Drutz, W. S . , Moisan, T. , Foster, J., Machnach, W.

Third Ime rnatiollal Seating Symposium, Memphis , Tenn.: 209-22.

(1980). Postural Relief of D ysp ne a in Severe Chronic Obstruc

Imle, P .. Boughton, A . e. ( 1987). The physical therapist's role in

tive Pulmonary Disease. American Review of Respiratory Dis

the early managemenr of acute s p inal cord inj ury. Topics in Jasper, M., Kruger, M. Ectors, P., & Sergysels, R. (1986). Unilat eral chest wall paradoxical motion mimicking a nail chest in a

p ati ent with hemilateral C7 spinal injury. Intensive Care Medi

ment of respiratory failure in amyotrophic lateral sclerosi s. An nals of Neurology 1982; I 2: I 8-23. Sullivan, P.E., Markos, PD., & Minor, A.D. (1982) . An illtegraled approach to therapeulic exercise: Theory and clinical applica

cine 12(6):396-98. Johnson, E.W., Reynolds, HT, & Staugh, D. (1985). Duchenne muscular dystrophy: a case of prolonged s u rvi val. Archives of Physical Medicine and Rehabilitation 66(4):260-1.

o ders 122:201. Sivak, ED., Gipson, W.T., & Han s on, M.R. Long-term manage

Acute Care Trauma Rehabilitalion 1(3):32-47.

lion. Reston, Va.:Reston Publishing. Zumwalt, M., Adkins, H.V., Dail, e.W" & Affeldt, J.E. Glossopha ryngeal breathing. Physical Therapy Review 1956;36(7):455-459.


Exercise Testing and Training:

Primary Cardiopulmonary Dysfunction

Susan K. Ludwick

KEY TERMS

Arteriovenous-oxygen difference (a-v02 difference)

Forced vital capacity (FVC) Minute ventilation (YE)

Cardiac output (Q)

Oxygen consumption ('\102)

Forced expiratory volume in

Stroke volume (SV) Tidal volume (TV)

I second (FEV)

INTRODUCTION Shortness of breath, especially with activity, is very

and then be able to devise therapy programs that

common in patients who have cardiopulmonary dis

would keep these individuals active within the limits

eases. Shortness of breath can be quick in onset or

of their disease in order for them to maintain certain

of a chronic nature. One of the results of shortness

levels of independence.

of breath, especially when it is of a chronic nature, is the vicious cycle of deconditioning it causes in patients. Eventually, these individuals may become

LUNG DISEASE

deconditioned to the point that activities of daily liv

In individuals without lung disease the cardiovascular

ing usually taken for granted, such as washing up in

system normally limits maximal aerobic exercise.

the morning, may be overwhelmingly fatiguing.

Typically, maximal oxygen consumption (Vo2) may

Physical therapists need to understand the underly

be limited by the heart's inability to increase its cari.i

ing mechanisms of shortness of breath, evaluate

diac output (Q) either by an inability to increase heart

their patients appropriately given their limitations,

rate (HR) or stroke volume (SV) or by an inability to 417


418

PART III


provide adequate oxygen delivery to exerCISing

Impaired Gas Exchange

skeletal muscle represented by the arteriovenous

During exercise, there needs to be a balance of venti

oxygen difference (a-vo2difference). This relation

lation to perfusion (VIQ) in the lungs for adequate

ship of V02 to Q is represented by the Fick equation: V02

=

blood oxygenation to occur. In patients with airways disease, underventilation of the lungs could occur be

Q x a - V02 difference

cause of elastic tissue destruction. Underventilation

However, patients with lung disease may be lim ited in their exercise capacity for several reasons.

results in V/Q mismatches (low V/Q ratio). Hypox emia occurs as a result.

They may be limited by altered lung mechanics, im paired gas exchange, development of pulmonary hy pertension, or respiratory muscle fatigue. Each of

Pulmonary HypertenSion

these factors make traditional cardiovascular evalua

In normal individuals, there is typically an increase in

tion of exercise capacity inadequate, since these pa

the diameter and in the number of blood vessels with

tients are limited by their breathing and not by their

exercise. However, in patients with lung disease, there may be a decrease in the number and/or in the

cardiovascular systems.

distensibility of blood vessels. This results in the in crease of pulmonary vascular resistance. An increase

Altered Lung Mechanics

in the pulmonary vascular resistance contributes to a

One of the characteristics of obstructive lung dis

decrease in left ventricular filling. If there is a de

ease is the destruction of elastic tissue in the lung.

crease in left ventricular filling, then there will be a

The destruction of elastic tissue prevents normal

decrease in cardiac output, which would limit the

recoil of lung tissue on expiration. Therefore it is

ability to do work.

difficult for patients to empty their lungs. This coupled with the tendency for bronchial walls to collapse contributes to air trapping. This results in lung hyperinflation. With exercise, our bodies re

Respiratory Muscle Fatigue Respiratory muscles in a normal individual con

quire an increase in oxygen uptake to perform

sume little oxygen at rest or with moderately in

more work. Minute ventilation increases in order

creased ventilation during activity. With exercise,

for oxygen u ptake to improve. We know t h a t

oxygen consumption increases greatly. However, a

minute ventilation is t h e product o f tidal volume

patient with lung disease would have an increase in

VE. If respira

ventilatory muscle oxygen consumption up to 40%

tory rate increases as a natural response to an in

of the total body oxygen consumption. The respira

crease in exercise, it may not allow enough time

tory muscles may not be able to keep up with the

and respiratory rate (TV x RR

=

for lungs to adequately empty and fill again if elas

total demand and would start to fatigue (see Chap

tic tissue is destroyed. Therefore tidal volume can

ter

not adequately increase with increases in exercise

muscle fatigue is the musculoskeletal deformity

25). Another contributing factor in respiratory

intensity. The result is that minute ventilation will

that many of these individuals develop with the dis

not increase in proportion to exercise. If minute

ease processes. Muscle fibers need to be at an opti

ventilation does not increase as required, then oxy

mal length to work efficiently for adequate force

gen consumption and, therefore, amount of work

generation to perform work. However, with muscu

will be effected.

loskeletal deformity, these fibers may be placed at

Patients with restricture lung disease will have

lengths that make it difficult for efficient work to

stiffer lungs that are resistant to expansion on inspira

be done. Eventually, they fatigue because of inade

tion. The patient will have to work harder to maintain

quate force generation needed to support the work

pressures for adequate lung expansion and venti la

of breathing.

tion. Eventually all lung volumes and capacities be come decreased.

Clinically, patients with obstructive lung disease show breathing patterns that are slower and deeper at


23

Exercise Testing and Training: Primary Cardiopulmonary Dysfunction

419

rest and with exercise. Specifically, longer expiratory

consumption during exercise above which a sus

cycles are observed because of the extra effort these

tained lactic acidosis occurs, is useful in measuring

patients make to empty their lungs before inspiration.

exercise tolerance in normals. However, it is not par

Patients with restrictive lung disease have a pattern of

ticularly useful with patients, since peak exercise

rapid, shallow breathing in an effort to maintain ade

levels may be below the anaerobic threshold. Some

quate minute ventilation in the face of decreased lung

have looked at the measurements of FEV [ and FVC to predict exercise capacity. However, the literature

capacities.

has shown that there is no correlation between these measurements of lung mechanics and exercise ca

HEART DISEASE

pacity. It makes more sense to define exercise capac

Patients with acute or chronic cardiac failure or

ity by evaluating the patient's functional exercise ca

valvular heart disease have elevated pulmonary ve

pacity. This can be done by using timed walking

nous pressures. This develops into intersti tial

distances. The 12-minute walk as defined by Ken

edema. Therefore the lungs are said to be "wet,"

neth Cooper has been adapted by McGavin, Gupta,

their compliance is decreased, and the work of

and McHardy (1976) for use with patients that have chronic bronchitis. This test is also useful in deter

breathing is elevated. Clinically, these patients have pulmonary rales on

mining exercise capacity in other patient populations

auscultation. They adopt rapid, shallow breathing

as well. This evaluation is useful because it corre

patterns to minimize respiratory muscle work. These

lates with V02 as measured on the treadmill. How

patients, as with patients with chronic lung disease,

ever, results are reported in terms of distance walked

will have ventilatory responses to exercise, depend

and not in how much oxygen was consumed. There

ing on the severity of the disease.

fore it gives a more functional picture of exercise tolerance since it uses a familiar activity. If 12 min utes is too long for some patients, 3- and 6-minute

Assessment

walks are just as useful. These walking tests are sim

Before starting the actual exercise assessment, it is

ple to implement and use simple measurement de

important to get an idea of the patient's activity level

vices. Patients can also use them as methods to mon

and what activities cause shortness of breath. How

itor their own progress.

far can the patient walk before becoming short of

To assess patients using the 12-minute walk, one

breath? Can the patient tolerate walking outside? Is

must simply instruct the patient to walk as far as pos

he or she only able to walk comfortably to get about

sible in 12 minutes. It is not absolutely necessary to

inside a house or apartment? Can the patient walk up

walk without stopping. The patient may slow down

stairs? Does dressing, taking a bath or shower, or

or even stop to take a short rest if needed. The only

combing hair cause shortness of breath? Can the pa

required equipment is a stopwatch and a measured

tient do his or her own grocery shopping? Is the pa

corridor.

tient able to do any heavy housework, such as vacu uming or bed making? Is the patient able to make his or her own meals? If aerobic capacity is limited because of either

UPPER-EXTREMITY VERSUS lOWER-EXTREMITY ACTIVITY

cardiac or ventilatory limitations, how can we func

Up to this point, we have discussed exercise assess

tionally assess exercise capacity without the use of

ments in reference to lower-extremity activity. How

expensive testing equipment? Traditional methods of

ever, shortness of breath may be of even earlier onset

measuring maximal oxygen uptake, including tread

when perfomling routine activities of daily living in

mill testing, may have limited usefulness because

volving upper extremities (i.e., grooming, lifting, and

oxygen uptake for the pulmonary patient, as ex

carrying). This in fact may be the most frustrating

plained before, is limited by ventilation. Anaerobic

limitation to patients, since these are the types of ac

threshold, which is defined as the highest oxygen

tivities that we normally take for granted in our


420

PART III


everyday Ii ves. When patients begin to have diffi

ing expiration. There are no compressive forces

culty performing these activities, they feel a loss of

working to narrow the airways. However, in patients

control in their lives. It is important to note that the

with airflow limitation, the work of breathing is

exercise responses to these activities are different and

shifted to the muscles of expiration. Therefore expi ration becomes a more active process, resulting in the

should be assessed separately from walking. CeJli, Rassulo, and Make

(1986) have reported the

generation of more positive pleural pressures com

appearance of dyssynchronous thoracoabdominal

pressing the airways. Closing off of airways creates

movement when comparing arm activity with leg ac

the feeling of shortness of breath. An impOItant yet

tivity. Early fatigue was observed to occur despite

simple technique that can be taught to patients is the

lower heart rates, minute ventilation, and oxygen up

practice of purse-lipped breathing to control short

take when compared with leg work. It was hypothe

ness of breath. By having the patient expire through

sized that exercise limitation during arm activity was

pursed lips, a back pressure is created in the airways

probably because of a smaller contribution of acces

that helps to keep them from collapsing despite the

sory muscles to the work of breathing, since these

positive pleural pressures down on them. This is a

muscles must contribute to postural support of the

useful technique that can be used at rest and during

upper extremity during activity. Despite these limita

exercise to slow down respiratory rate, increase tidal

tions in upper-extremity exercise tolerance, improve

volume, and increase blood oxygenation.

ments have been demonstrated after an exercise train

When evaluating exercise tolerance with patients, it is impOItant to assess the work of breathing. Borg

ing program. Upper-extremity assessments may be considered

(1982) has developed two scales that can help to

two ways. They can be either supported or unsup

quantify dyspnea. In our facility, we have used a sim

ported (Criner and Celli,

1988). Supported assess

ments would be those that may involve the use of an

ple scale of I to

4 to describe shortness of breath (see 421). On our scale, a score of I

boxes below and on p.

upper-extremity ergometer. Unsupported assessments

would represent baseline (comfortable) breathing. A

would include those activities involving reaching.

score of

Since activities of daily living involve combing hair,

vere that one is not able to talk. Since exercise limita

washing, dressing, and reaching at various heights,

tion is more closely related to ventilatory rather than

4 would represent shortness of breath so se

assessments imitating these things would be most useful. One such test that could be used would in volve repetitive reaching at a height level to the head. Reaching up with a light object of approximately I pound may imitate reaching up to kitchen cupboards to put away groceries. Counting the number of repeti tions and timing the activity would give a functional

The 15 Point RPE Scale 6 7

VERY, VERY LIGHT

8 9

VERY LIGHT

10 II 12 13

picture of upper-body activity tolerance.

BREATHING

FAIRL Y LIGHT SOMEWHAT HARD

14

Patients who have pulmonary diseases have limited

15

ventilatory reserves, which manifests as shortness of

16

breath. The degree of the shortness of breath may de pend on the severity of the lung disease. Normally, during quiet breathing, average pleural pressures sur

HARD

17

VERY HARD

18 19

VERY, VERY HARD

20

rounding the large airways are typically negative, whereas intraluminal pressures are more positive.

Borg, G. (1982). PsychologicaJ Bases of Perceived Exertion, Medi

These positive pressures keep the airways open dur

cine and Science ill Spor/s and Exercise, 14,378.


23


reaching over the head, marching while sitting, knee

The 10 Point RPE Scale 0 0.5 I 2 3 4 5 6 7 8 9 10

421

extension, and stretching hamstrings with the leg

NOTHING AT ALL

being stretched propped on another chair in front. Ex

VERY, VERY WEAK

ercises should be timed with purse-lipped breathing

VERY WEAK

to pace the exercise comfortably and control short

WEAK

ness of breath. An example of this would be:

MODERATE SOMEWHAT STRONG

Start with your arms stretched forward at shoulder height.

STRONG

Breathe in through your nose while bringing your out stretched arms out to either side. Blow out through pursed

VERY STRONG

lips while bringing your arms back to the front and crossing them in a scissoring manner. Repeat 10 times.

VERY, VERY STRONG

Adding scapular retraction exercises to stretch out

MAXIMAL

pectorals (i.e., pinching scapulas together) is helpful

Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi cine a/ld Science ill SPOI'IS ond Exercise. i 4, 380.

since these patients spend many of their days in for ward flexion types of postures. These exercises help with posture and help to increase lung expansion with inspiration.

cardiovascular limitation, monitoring heart rate is not an accurate measure of exercise intensity. Asking pa tients to quantify their dyspnea is much more reliable.

Training Phase After completing the warm-up exercises, patients may now start their walks. The patients should prac tice their purse-lipped breathing during their walking.

EXERCISE GUIDELINES

Walking for 12 minutes at a comfOltable pace to keep

After evaluating your patient's exercise capacity, the

breathing at a level 3 should be the goa\. Rest periods

exercise program can be developed. Structuring the

are acceptable during the 12-minute time. Another

program with the warm-up, training and cool-down

goal could be to minimize rest periods to the points

phases shouId be done.

where a patient could walk for 12 minutes nonstop.

,

Before starting exercise, purse-lipped breathing

The upper-body exercise session could consist of

should be taught since this should be used throughout

low-resistance, high-repetition exercises combined

the exercise session to control shortness of breath. In

with purse-lipped breathing to help with shortness of

struction for teaching this technique could be as fol

breath. These exercises could consist of PNF patterns

lows: patients should be instructed to take a relaxed

or of ring shifting, for example, at a level just above

breath in through their noses. The breaths should be

the shoulder. Light weights could be added as a pro

relaxed. They should not be forced. Exhalation

gression in addition to adding repetitions.

should be through pursed lips as if to blow out a can dle. Again, expiration should not be forced.

Cool Down The cool-down period would consist of repeating the

Warm-up The exercise program should always start with warm up exercises. Chair exercises are desirable, since sit ting up to exercise can help conserve energy that the patient will need for the training portion. Mixing

warm-up exercises at a pace where breathing would be brought down to baseline.

Frequency

upper and lower body exercises should be done. Ex

Patients should exercise at least three to four times

amples of these exercises include arm scissoring,

per week.


422

PART III

Interventions

Cardiopulmonary Physical

Intensity

more commonly used because walking and running

Patients should exercise so that their breathing

are more natural activities. A

how hard

to reach his or her maximum oxygen consumption

are working. We advocate that

work no higher than a level 3. After the cool-down breathing should be at baseline.

is more likely

and heart rate. However, ECG recordings tend to have more artifact and blood pressure

are

more difficult to obtain at high intensities. If tread mill testing is the

Termination of Exercise Testing or Training Several

or symptoms will alert the therapist that This chapter focuses

the session should be

clinical situations not using electrocardio (ECG) or sophisticated monitoring systems. response must be watched closely, such as facial appearance of

in

in addition, blood

creased use of accessory

are

pressure, heart rate, and pulse oximeter

of choice, there are sev

eral different

protocols that use different

combinations of

elevation and belt

type of treadmill test used

The

on the fitness

level of the patient and the reason for doing the test. For example, certain

protocols may be used

to test initial aerobic fitness levels in individuals and athletes and then for fects of their training programs. Another type of treadmill test may be used to

diagnose cardiac

very important. Exercise should be terminated in any

disease. The two most

of the following situations:

the Bruce and Bakke exercise tests. They have nor

•

•

used protocols are

Patient

mative data from which functional aerobic

Chest pain occurs or increases from patient's

ment can be calculated.

normal •

•

Patient appears pale and skin is diaphoretic

Energy Conservation and Work Simplification

elevated or

Blood pressure is with exercise

•

•

•

•

with energy conservation and work

Patient complains of leg cramping

fication techniques is an important component of

Oxygen saturation drops below 90%

cardiopulmonary

Patient complains of dizziness

tient's work

Patient's coordination is affected by increased

tion with the goal of achieving increased functional

muscle weakness and

An

of the pa for modifica

life needs to be stressed. A brief

with prolonged ex

ercise rices to patients.

TESTING

TRADITIDNAl

Since most individuals have been accustomed to a

without shortness of breath from

For those

faster oaced life. oacing is a basic conceot worth dis-

lung disease or cardiac failure who could tolerate there are more traditional exercise

slow down when walking or climbing stairs. Patients

The primary modalities used

will not be as tired and out of breath when reaching

There

their destinations. Rest periods should be planned

are bicycle ergometry and treadmill are

and

to

it is

that are useful in assess-

to both. ECG

the

If wasting time is a concern while

monitoring and blood pressure readings may be more

taking a break, reading a book or doing some hand

easily obtained if a

work may make this time more worthwhile.

the

is tested on a to this modality is that

this is not as familiar an activity to some

a cart to carry items is quite helpful.

as

activity while

walking. Therefore maximal heart rates may not be

creases oxygen consumption when

achieved because of leg fatigue. Treadmill testing is

gen consumption is increased,


items in If oxy require

23


423

ments also will be increased as described previously.

3. Explain the physiological benefits of exercise

Shortness of breath will increase. If a shopping cart is

training with COPD and the perceived mecha

used, leaning on the cart to take a rest will help to

nisms of improvement. 4. Name the components of a pulmonary rehabilita

keep breathing under control. Sitting down to work is an energy saver because it saves the legs the work of standing. Standing in the bathroom to shave or wash at the sink can be elimi

tion program. 5. Name and discuss techniques of energy conser vation.

nated by placing a chair in front of the sink or by sit ting on the toilet-seat lid. Buying a shower chair helps make washing easier. After coming out of the

References

shower or bath, wrapping up in a terry-cloth robe and

American College of Sports Medicine. (1993). Resource manual

sitting on the toilet-seat lid can help the patient catch

for guidelines for exercise testing and prescription (2nd ed.).

his or her breath while drying off. An ironing board can be used as an adjustable table. Setting it at low levels can help with meal preparation while sitting.

Philadelphia: Lea

& Febiger.

Belman, M.1. (1989). Exercise in chronic obstructive pulmonary disease, in Franklin, B.A., Gordon, S.,

& Timmis,

G.e. (Eds.).

Exercise in modern medicine. Baltimore: Williams a n d

Organizing work areas can help eliminate unnec essary reaching. Items used most often should be kept at a level between the shoulders and the hips. Heavy appliances can be kept out on counter tops or on the stove so that bending, stooping, and lifting is elimi nated. Before cooking, filling the sink with soapy water and putting dirty dishes and utensils in immedi ately makes clean up easier. A dustpan with a long handle eliminates bending over when sweeping up. Understanding the development of shortness of

Wilkins. Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi· cine and science in sports and exercise, /4,378. Casey, L.e.,

diopulmonary exercise testing. Philadelphia: WB Saunders.

obstructive pulmonary disease, Chest, Celli, B.R., Rassulo, J.,

equipment for evaluating and training athletes. In ad dition to improvements in functional capacity, these patients may also show some desensitization to their shortness of breath with an overall improvement in their sense of well-being.

&

79,

393-398.

Make, B.1. (1986). Dyssynchronous

breathing during arm but not leg exercise in patients with icine,

testing to sophisticated use of metabolic carts and

Wilson, A.F.

chronic airflow obstruction, The New England Journal of Med· Criner, G.1.,

ing can range from simple, cost-effective in-home

&

(1981). Effects of breathing retraining in patients with chronic

and then evaluating them appropriately for exercise programs will help these patients improve their func

K.T. (1986) Chronic lung disease and chest

Casciari, R.1., Fairshter, R.D., Morrison, J.T.

breath in individuals with cardiopulmonary disease

tional capacity for activity. Exercise testing and train

& Weber,

wall deformities. In Weber, K.T., Janicki, J.S. (Eds.). Car

314, 1485-1490. & Celli, B.R.

(1988). Effect of unsupported arm exer

cise of ventilatory muscle recruitment in patients with severe chronic airflow obstruction, American Review of Respiratory Disease,

138.

856-861.

&

McGavin, e.R., Gupta, S.P.,

McHardy, G.J.R. (1976). Twelve

minute walking test for assessing disability in chronic bronchi tis, British Medical Journal, Reis, A.L., Ellis, B.,

&

I,

822-823.

Hawkins, R.W. (1988). Upper extremity

exercise training in chronic obstructive pulmonary disease, Chest, Tangri, S.,

93, 688-692. & Woolf, e.R.

(1973). The breathing pattern in chronic

obstructive lung disease during the performance of some com

63, 126-127. & Ross. J.e. (1966f

mon daily activities, Chest, Thoman, R.L Stroker, G.L.,

REVIEW QUESTIONS

The efficacy of

pursed-lips breathing in patients with chronic obstructive pul

1. Name and explain four limiting factors of exer cise in the patient with COPD.

monary disease, American Review of Respiratory Disease, Weber, K.T.,

2. Explain traditional measures of exercise capac ity. Which ones are useful for measuring exer

93.

100-106.

&

Szidon, J.P.

(J 986)

Exertional dyspnea. In Weber,

K.T., Janicki, J.S. (Eds.): Cardiopulmonary exercise testing. Philadelphia: WB Saunders.

cise capacity in COPD?


Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction Phyllis G. Krug

KEY TERMS

Exercise blood gases

Respiratory muscle endurance

Nocturnal ventilation

Respiratory muscle fatigue

Oxygen desaturation

Respiratory muscle strength

INTRODUCTION

every system in the body can develop a disorder that

When considering the sensation of shortness of

can have respiratory consequences. It is most effi

breath, one typically pictures someone afflicted with

cient to discuss the more common disorders that pre

a lung disease, such as asthma, bronchitis, emphy

sent themselves clinically. Case studies are presented

sema, or the like. A largely neglected area from the

at the end of the chapter to further elucidate and clar

perspective of physical therapy and rehabilitation is

ify the process clinically.

that population that develops rt:spiratory limitations secondary to other disease processes. Secondary respiratory problems are those restric

Psychological Factors

tions arising out of pathology other than primary lung

With respect to shortness of breath, studies related to

disease. Patients falling into this category present

those with the diagnosis of chronic obstructive lung

with a vast atTay of underlying pathologies. Virtually

diseases have shown that people tolerate shorlnt:ss of 425


426

PART III


breath up to 10 years before seeking medical
review presented here, notes arc included to encour

(Black, 1982). The patient usually attributes the symp

age critical analysis of diagnostic material.

toms to aging and lack of exercise before considering

Pulmonary function tests

a medical reason. It has even been documented that patients will curtail activities, social and recreational,

Pulmonary functions tests (PFTs) are used to evaluate

before seeking medical advice. By the time medical

flow rates and volume capacities of the lung. Detailed

attention is sought, a damaging cycle has been estab

descriptions of these are presented in Chapter 8. Un

lished (Figure 24-1). The results of inactivity con

derlying assumptions in these reports are that a patient

tribute to feelings of inadequacy and poor self image.

(1) has cooperated with the testing procedure, (2) has

The inactivity itself fosters and encourages atrophy,

understood the procedure and, (3) has normal respira

not only in the extremities where it is visibly apparent

tory muscle strength to accomplish the test. Let's try

but also in the respiratory muscles. This fUlther adds

and understand the factors that could blur optimal re

to the debilitating process, creating secondary weak

sults when taking a pulmonary function test. If a result

ness and disabilities that are not necessary and are

is produced that shows the patient has poor lung ca

avoidable. These issues are further addressed in the

pacity, you could walk away thinking. "Wow, that's a

approach to treatment and in the case studies.

really sick person there, most probably there isn't much I can do to help because he is so restricted in lung capacity." If you look further and investigate the

EVALUATION

possibilities, you begin to open windows or possibili

The evaluation begins before the patient arrives. It

ties for improvement. If there is weakness of the res

begins with the information collected from the diag

piratory muscles, then the results obtained reflect the

nostic data. Great benefits can be gained from under

patient's breathing capacity based on weak muscles.

standing the information, but it is equally essential to

This leaves open the option of improving the respira

recognize its limitations.

tory muscle strength to see how it may affect the ven tilatory capacity. Once you begin to think critically,

Critical Usage of Pulmonary Diagnostic Reports

many windows may become apparent that can provide options for improving the results. For example, if a

The diagnostic criteria for secondary cardiopul

patient with scoliosis has reduced volume capacity, it

monary dysfunction is similar to diagnosis criteria for

is unclear if it is a fixed piece of data or if there is

primary cardiopulmonary dysfunction. In the short

room for improvement from the perspective of posture and strength. The volume and flow measurements of a patient with a lot of secretions would be reduced be cause of the obstructive nature of the mucus. If that patient was on an aggressive program of postural

THE FOUR Ds

/ Progression

\

Depression

drainage, would those values improve? Address

Disease

whether the values obtained in the pulmonary function tests reflect a fixed, irreversible value. The author's

Dyspnea

J

clinical experience demonstrates that interventions ad dressing posture, strength, endurance, and optimal clearance of mucus work to improve values otherwise

Deconditioning

believed to be unchangeable.

X-ray

FIGURE 24-1 Flow of progression of respiratory disability. This

The use of x-ray testing is critical in identifying infil

demonstrates the chronic cyclic pattern that haastens

trates, pneumonias, tumors, and obstructions. Yet it

deterioration and death.

too has its limitations and should not be relied on


24

Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction

427

solely to assess a patient's capabilities. Mr. K had a

stood that patients will be more comfortable and

diagnosis of chronic obstructive lung disease with ex

probably perform better on equipment that mimic

tensive scarring from old tuberculosis. His x-ray was

their present life styles. Although the step test that

opaque. No viable ventilating lung tissue was seen on

has the patient going up and down a step at a given

the left side. Ausculation with a stethoscope revealed

rate is effective in identifying a change in the blood

no breath sounds. Yet after months of breathing re

gases, a patient may feel more comfortable and be

training, thoracolumbar mobilization and soft tissue

able to last longer on either a bicycle or treadmill.

mobilization, this patient established a most definite

Furthermore, during a step test, the patient may fa

improvement in breath sounds on the left side. No

tigue after only a few repetitions. There is more op

improvement was noted in his x-ray. So, our tools are

portunity to evaluate the following: (I) how quickly

helpful to a point, and we should always give our pa

the gases change, (2) if they improve over time, and

(3) the dynam ics of breath ing mechanics when

tient the benefit of the doubt and try.

choosing a modality that the patient may be able to

Auscultation

sustain over a longer period of time.

The stethoscope is effective in identifying many ab normalities within the lung, such as bronchospasm, mucous collection, consolidations, and infiltrates. Yet

Respiratory muscle strength and endurance The foundation of the respiratory system's ability to

it is not uncommon to hear perfectly normal breath

work is the strength and endurance of the respiratory

sounds, and the patient will still report tightness in the

muscles. Strength and endurance form the foundation

chest, wheezing, and even congestion. It is always im

because breathing is an ongoing activity from which

portant to have the patient cough or breathe deeply to

the body cannot take a vacation; it requires the en

increase the flow of air so as to pick up any of these

durance to continue without stopping. There are times

abnormalities. Yet even if this is done and the breath

when the respiratory system requires sudden bursts of

sounds seem normal, always defer to the patient.

increased strength, as is evidenced by the need to cough. Factors predisposing to fatigue are related to


muscular ability, ventilatory mechanics, reduction of

Arterial blood gases are designed to measure the

energy supply by hypoxemia, reduced cardiac output,

level of oxygen, carbon, dioxide, and pH in the arter

and malnutrition. The measure of respiratory muscle

ial blood (see Chapter 9). It reflects how effectively

strength is done via a gauge that measures inspiratory

the respiratory system is working in supplying the

muscle strength and expiratory muscle strength (PI

body with the fuel to carry on the task of living. It is

max and PE max). A patient unable to generate 60%

quite common to receive an order for physical ther

to 80% of these values reflects respiratory muscle

apy including exercise with the information that the

weakness (Edwards, 1978). A patient who is unable to

blood gases are within normal limits. It is critical to

maintain expected respiratory muscle force with con

identify if the blood gas values were taken at rest or

tinued or repeated contraction demonstrates the level

after exercise. If exercise blood gases are not i n

of respiratory muscle fatigue, which is the precursor

eluded in the report, there is no way of knowing how

of respiratory failure (see box below). A thorough

the patient's oxygenation will be affected by activity (desaturation). It is possible to have normal resting blood gases that drop precipitously with activity. This can be a result of limited ventilatory ability or venti lation-perfusion mismatch. It is the responsibility of the therapist of a patient with compromised ventila

Clinical Signs of Respiratory Muscle Fatigue Hypoventilation Rapid shallow breathing

tory ability to request exercise blood gases or use an

Paradoxical breathing

oximeter to determine if desaturation is occurring. In

Increased Paco2

discussing exercise blood gases, it should be under


428

PART III


background on a patient includes information on the

100

strength and endurance of the respiratory muscles so that an effective, practical intervention program can be planned. An aggressive exercise program cannot be initiated if a patient is unable to sustain ventilation to properly oxygenate the body. If a patient is in a state of respiratory muscle weakness and is then expected to perform aggressively on a bicycle or treadmill, one can inadvertently push the patient into respiratory fa

N

o

..0 ::c C

75

I

50

Qi

0...

tigue and possibly failure.

History-Critical Listening

o

In attaining a history from the patient, it is critical to

o

27 40

P02

work slowly, so that the patient feels comfortable, and to encourage what could be deemed as simple chatter. After discussing a patient's personal inter ests, family, and home life you will have the informa tion to recommend an intervention program that will

60

80 mm

100

150

Hg

FIGURE 24-2 Oxyhemoglobin dissociation curve. Demonstrates the point at which oxygen saturation drops precipitously to between

40 and 60111111 Hg

be beneficial for the patient and that the patient will actually do. If it is felt that the patient can improve

ally open the perspective of hope for improvement.

his or her endurance to be able to walk a mile and the

Because it is not just one system that becomes sud

patient is only interested in walking a few blocks, the

denly ineffective, physical therapists have the latitude

goals have to be set accordingly. Some therapeutic

to explore the full course of the history and look for

techniques require a quiet passive posture by the pa

the gaps where an intervention can be directed. Has

tient. A more tense individual who is pressed for time

posture changed over time? Has there been progres

will not tolerate that kind of intervention. It is there

sive weakness? Have activity levels diminished?

fore crucial to take the time to get the total picture. From the perspective of the history of respiratory

Were there frequent respiratory infections? Re sponses to each of these questions can greatly influ

symptomatology, it is common to hear, "I don't know

ence factors in a rehabilitation program. If a patient's

what happened, I was doing just great until r got that

posture deteriorated over the years, compromising

cold ... then it all fell apart." Pursue the investiga

respiratory ability, a program of stretching and

tion, because undoubtedly the history is much longer.

strengthening of the postural musculature may pro

The difference is that the patient was able to cope and

vide sufficient space in the thoracic wall for im

the presenting situation became excessive. The oxy

proved lung capacity and oxygenation. It takes a

hemoglobin dissociation curve in Figure 24-2 demon

small amount of objective improvement to make a

strates the underlying physiological process (Stoller,

big difference in the quality of life for the individual.

1988). Looking at the S curve, one can see that above

Regardless of the underlying cause, attaining a Pao2

60 mm Hg the curve is fairly flat, and Joss or deple

of at least 60 mm Hg is the primary concern.

tion of oxygen above the level can go undetected

Because the work of breathing becomes very diffi

clinically. However, as the curve demonstrates, there

cult in primary lung diseases or restrictions secondary

is a critical point around the Pao2 of 60 where the

to other disease processes, the symptomatic presenta

person will "suddenly" experience severe shortness

tions can be quite similar. It very closely simulates

of breath. In reality the oxygen level was dropping

the posture of the marathon runner at the end of a

progressively over time but was only critically felt at

run. The runner assumes a bent forward posture,

the drop of the curve. Understanding the progression

leaning on a wall or gaining support by leaning on

of the deterioration with shortness of breath can actu

the knees (Figure 24-3). This position is optimal for


24

Exercise Testing and Tmining: Secondary Cardiopulmonary Dysfunction

FIGURE 24-3

The flexed fOlward posture held when experiencing sho rtne ss of breath. Simi lari t ies between the healthy marathon runner and the person with chronic respiratory difficulty should be considered in reference to muscular, skeletal and pressure changes. (Courtesy of David Gorman, The Body Moveahle)


429

430

PART III


enhancing diaphragmatic excursion. After a few mO

baseline exercise test to identify exercise capability.

ments, the runner will get up and walk away. Unfor

It would be premature to begin an exercise training

tunately, the patient experiencing shortness of breath

program. The first step wou Id be to address improve

stays in that bent forward position. A patient may

ment of strength and posture. The goal is directed to

stay that way because it is easier to breath or because

ward improvement in height, lung capacity, and mus

he or she does not realize the precipitating event has

cle strength. The baseline data on the exercise test

passed. The point of emphasis is that any chronic dis

would likely improve. An exercise test subsequent to

ease resulting in shortness of breath will have pos

postural improvement would be a better baseline for

tural effects. Look for limitation in range of motion

an endurance training program.

of the hips and poor mobility of the thorax and the

For the patient with underlying neuromuscular

pelvis. This can be evident in a gait pattern that has

disease, an endurance training program may overfa

minimal rotation of the thorax on the pelvis. The

tigue muscle groups and cause damage. Therefore

stride length will be shortened, with minimal arm

the exercise test, again, is to get a baseline of exer

swing and an overall stiff, nonfluid gait pattern. The

cise ability. The therapeutic intervention would be

gait pattern of those suffering with chronic shortness

directed toward muscle re-education, postural exer

of breath and its associated postural changes can be

cises, and strengthening to help the patient move

described as walking cinder blocks, implying that the

more efficiently and reduce stress on the affected

muscles from the neck to the pelvis are fixed and do

m u s culature. The i m p r ovement in posture and strength provides a better baseline to sustain an exer

not allow for normal reciprocal movement.

cise test and subsequent training. A timed-walk test for a patient with severe limita

Exercise Testing

tion would be appropriate. Measure a walkway in

Exercise testing is performed for a variety of reasons. It is a means of

(1) gaining baseline information of (2) assessing functional

10-

foot increments and then time the distance walked for either 6 or

12 minutes. It may be necessary to further 2 minutes.

the patient's activity level,

modify this test into distance walked for

(3) prescribing graded-exercise programs, and (4) evaluating cardiovascular ability. The choice of

as possible for the timed segment. Record distance

ability,

Instruct the patient to walk as far as possible as fast

exercise testing should reflect the needs of the pa

walked. Monitor the blood pressure, heart rate, respi

tient, the cost-effectiveness of the procedure, and the

ratory rate, ventilatory muscle use, and O2 saturation.

consideration for the need of extensive diagnostic in

A patient at a higher level of function may benefit

formation and its practical application into the pa

from a more aggressive exercise test that allows for a

tient's life. The patient's addressed in this chapter are

more accurate level of cardiovascular response to ex

by and large severely limited in their physical abili

ercise as a basel ine for prescription for endurance

ties because of their underlying disease processes and

training. A baseline level is first obtained from the

their secondary respiratory effects. Typically the

timed-walk test or the patient can walk on the tread

overall presentation is one of atrophy, decondition

mill at 1 to 2 mph, 0% grade for 6 minutes.

ing, and poor mobility that greatly limits the distance

A patient whose exercise ability is limited by respi

walked. The severely limited patient would benefit

ratory factors before the healt rate or blood pressure is

with a simplified exercise test to identify exercise ca

even elevated does not rt;quire a full-graded exercise

pacity. When considering the patient with secondary

test with full ECG, metabolic gas analysis, heart rate,

cardiopulmonary restriction, treatment should be

and blood pressure measures. Interest should be more

aimed at improving the cardiopulmonary status con

directed toward the following:

current to the underlying primary process. A few ex

son walk,

amples can better illustrate this point. The scoliosis

(I) how far can this per (2) what happens to his breathing pattern and respiratory rate, and (3) does the oxygen saturation

patient who has progression of the spinal deformity

drop. Based on this, recommendations can be made for

and secondary pulmonary compromise requires a

use of supplemental oxygen and possibly more efficient


24


breathing patterns to allow the patient to persevere longer. For example, if a patient has a diffusion prob lem or a ventilation/perfusion mismatch, it would be helpful to evaluate whether a slower pace would allow the patient to walk longer. Consider enhancing the time allowed for diffusion of the oxygen. It may be found that a slower pace, with attention directed toward deep effective breathing, may yield different values in oxy gen saturation and the distance walked. The choice of testing modality should also take place or location into consideration. It seems inappropriate to demand that a severely limited patient being seen in the home undergo extensive graded-exercise testing before recommending an exercise program. The choice of exercise testing should reflect the goals of the patient. If the patient is ready for an aggressive exercise program, then more extensive testing is appropriate. Testing can then progress to stage II. A treadmill stess test begins with a speed that is comfortable for the patient-usually be tween 2 to 3 mph. Work is increased every 3 minutes by either increasing the speed or the incline. It is rec ommended to increase the speed by 0.5 mph incre ments, maintain it at a comfortable walking pace, and progress the incline by 2.5% increments after a com fortable pace has been established. Measurement of heart rate and blood pressure should be taken at the end of each 3-minute stage and Sa02 oxygen saturation should be monitored throughout and recorded at the be ginning and end of each stage. The test is terminated in the following situations: (I) when the patient reaches 65% to 75% of predicted maximal heart rate, (2) if oxygen saturation drops below 90%, (3) if the blood pressure drops with in creasing activity, or (4) the patient experiences symp toms of shortness of breath or muscular discomfort. If a patient is able to reach 65% of predicted maximum heart rate without cardiop u l monary symptoms, then the patient is capable of exercise conditioning. Oxygen saturation should be above 90%. Below this level requires supplemental oxy gen. If the carbon dioxide (C02) increases more that 10 torr of resting level, the patient will be limited in exercise potential. Individuals who reach their maxi mum volume ventilation (MVV) with minimum in tensity exercise may have difficulty with an en durance training program.

431

Exercise Training Design of an exercise prescription must be individu alized and must be prescribed within both useful and achievable levels. Exercise training should not be limited to a mode of exercise equipment, duration of time, or fre quency. A person with a chronic condition has chronic manifestations physically and psychologi cally. Therapy directed toward the chronic physical changes, that is, postural and overall movement, can result in improved endurance. This perspective should be seriously considered before using preciolls therapeutic time to put a patient on a treadmill three times per week to measure a heart rate that does not elevate because the patient is too short of breath. The severely limited patient may benefit from general body movement for a duration of 10 to 15 minutes. It could include standing and leaning on a chair and shifting the hips to the rhythm of music. The goal is initially just to move, create a challenge to the car diorespiratory system, focus on controlled hrcathing, and show the patient that he or she can sustai n move ment for prolonged periods. The therapeutic ball has proven to be beneficial. The 65-cm ball is a good size for a patient to sit on (Figure 24-4). It provides support yet allows for movement. Many severely limited patients have been able to sit on a ball shift ing their weight from side to side, working on leg strengthening, pelvic and spinal mobility, and chal lenging the cardiorespiratory system. Once a capahle patient becomes interested in a traditional endurance training program, the graded-exercise test can pro vide the necessary information to prescribe one. The prescription should include intensity, duration, fre quency, and modality as follows: (I) Intensity is based on 65% to 80% of the predicted heart rate or a level where the patient becomes symptomatic or the oxygen saturation drops to 90O/C . Consider, for exam ple, an exercise test that is terminated after walking at a speed of 3 mph, at a 5% elevation, 3 minutes into lhat level. If the limiting factor was shortness of breath with a drop in oxygenation, further testing should be conducted with the use of supplemental oxygen. If the limiting factor was shortness of breath without a drop in oxygen, 2.5 mph at 0% elevation can be used as a 5-minute warm-lip, followed by


432

PART III


training at 3 mph for up to 15 minutes with I minute

Caution is advised in understanding the underly

intervals at 2.5% elevation followed by a cool down

ing pathology that resulted in cardiopulmonary limi

of 2.5 mph, 0% elevation, for 5 minutes. (2) Dura

tations. Post polio syndrome is characterized by

tion of exercise is 15 to 30 minutes per session. Ini

muscles that were weakened during the initial onset

tially this can be broken down into interval training

of the disease and more recently report a recurrence

where short 1- to 2-minute rest periods can be used

of symptoms. Studies have shown that these patients

progressively, lengthening the intervals until the pa

benefit from strengthening and endurance exercise,

tient is able to maintain a c o ntinuous session.

but extreme caution must be directed toward avoid

(3) Frequency of e xercise is three to five times a

ing overuse (Dean, 1991 a; Owen, (985). The patient

week on alternate days. (4) Modality depends on pa

will benefit from a carefully considered, judicious

tient comfort. The target heart rate, or the level be

exercise program.

fore the patient developed symptoms, is used as the training level. Flexibility exercises or slow walking are recommended for warm-up before the endurance exercise program.

SYSTEMATIC APPROACH IN THE REHABILITATION PROCESS Nocturnal Ventilation-The Role of Rest and the Respiratory Muscles At this point the therapist is equipped with a vast array of information. The question is how to plan an effective intervention. Clinical experience has shown the importance of first directing attention toward the work of breathing. The literature is filled with discus sions about the role of resting the respiratory muscles (Braun, 1983). It is suggested that one of the factors leading to respiratory failure is the respiratory mus cles' inability to keep up with the demand of breath ing. If we consider the patient with severe scoliosis, the work of breathing is not shared equally by the respiratory muscles because of distol1ion of the chest wall. In addition, the curvature will add an additional load on the energy expenditure of breathing. Like any muscle in the muscular system, if a load is put on a muscle, it will train and get stronger. Yet, if this goes on for an extended period of time the muscle will be unable to maintain the added work load and the mus cle fibers themselves will begin to break down. This process is well understood in the fields of sports med icine and weight training. It is called overuse atrophy. This process also occurs in the respiratory system. In advising a patient in an exercise program, it is clitical to be aware of how much we are asking our patients to do. We walk a narrow path between (I) doing nothing and allowing the patient to accept life with

FIGURE 24-4 Therapeutic ball as part of a program of improving mobility

the shortness of breath and promote further atrophy

and endurance.

and (2) pushing too hard and risking breakdown of


24

Exercise Testing aod Training: Secondary Cardiopulmonary Dysfunction

433

the respiratory system. It is the responsibility of the

for good clinical judgement. Sometimes the patient

therapist to be aware of the diagnostic and clinical

has a bad day and just does not do well, other times

signs of respiratory muscle fatigue.

he or she may be in trouble.

Diagnostic criteria for respiratory muscle fatigue include the following: (I) increasing pulmonary arte rial carbon dioxide (Paco2). (2) reduction of high

Managing the patient with clinical

signs of respiratory fatigue

frequency signals (greatcr than 80 Hz) of muscular

If the patient has a prcscription for oxygen, make

activity on electromyography studies (EMG) despite

sure he or she is using it. Get the patient comfortable

continued contraction and dominance of the low

and use your hands to guide the body into shifting the

frequency signals (lcss than 80 Hz), (3) reduction of

work of breathing. This is a very critical factor. In

vital capacity with decrcascs in supine ye t o 50% of

dealing with acute shortncss of breath or muscle fa

sitting Ye, and (4) inspiratory muscle prcssure to

tigue the patient undoubtedly will be in a state of

below 66% of predicted mean.

panic. Panic complicates the situation by increasing

The clinical signs of rcspiratory muscle fatigue in

the respiratory rate and consequently reducing tidal

clude the following: (I) paradoxical breathing, (2) in

volume. The gentle placement of the therapist's

creased respiratory rate, and (3) shallow breathing

hands on the lower rib cage along with a calm, firm,

(see box below). First and foremost, we arc looking

soothing voice can hclp guide the patient into a more

at change from normal. This is where good baseline

calm, efficient breathing pattern. Studies have shown

information is critical. Baseline blood gases, the pa

that tension alone can reduce the expiratory flow rate,

tient's typical breathing patterns, and the baseline for

so the therapist's role in calming the patient is di

dyspnea should be considered. This is a critical area

rectly related to improving the breathing pattern (Kotses, 1981).

Resting the respiratory muscles There is increasing interest in the role of resting the respiratory muscles before it reaches the stage of res

Respiratory Muscle Function Assessment •

Pulmonary function test

•

Respiratory muscle strength

piratory fatigue and failure. This is accomplished through nocturnal ventilation using positive- or nega

Effort and strength dependent

tive-pressure ventilators (Figures 24-5 and 24-6). The focus is to increase muscle energy supplies and stores. Mechanical ventilation will assume the work

PI max-inspiratory pressure

of the respiratory muscles and allow them to rest.

PE max-expiratory pressure •

This may allow the time needed to reverse the factors

Respiratory muscle fatigue

that led to fatigue. It substantially reduces the oxygen

60% to 80% PI max •

consumption of the respiratory muscles, allowing for

Respiratory muscle enduram:e

more oxygen to reach the other tissues. Studies have

Maximum volume ventilation

shown that after a mean period of approximately 5

Maximum sustainable ventilation

months at home on daily 4- to IO-hour ventilatory support, there are significant increases in vital capac

80% MVV for 5 minutes or 60% MVV for 15 minutes

ity, PI max, and PE max (Marino, 1982). It also showed a reduction in Paco2 along with a reduction

Fatigue: when Ve
in hospitalizations and the number of days hospital ized. The topic of resting the respiratory system adds

NOTE:

Inability to reach

ness or fatigue.

a

predicted value reflects muscle weak

a different perspective in regard to traditional pul monary rehabi litation programs promoted. Before


434

PART III


FIGURE 24-5

Positive pressure ventilator used for nocturnal ventilation.

FIGURE 24-6

Negative pressure ventilator used for nocturnal ventilation.


24


435

initiating a progressive exercise program or for that

breath hold. Activities can be divided into two cate

matter, any sort of exercise program, it is important

gories. Static activities and rhythmic activities. Static

to assess the level of respiratory fatigue under which

activities are those that are done once. For instance,

the patient is living. Symptoms, clinical observations,

picking up a shoe. It is done once, until you are ready

or historical findings that are suggestive of further in

for the second shoe. The first rule of thumb is to take

vestigation into the benefit of nocturnal ventilation

a breath in before the activity to supply the body with

include sleep disorder, progressi ve dyspnea, hyper

the oxygen it needs, then exhale with the activity. It

capnia, and dyscoordinate breathing patterns. It has

is simple but it actually helps, and the patient is able

been recommended that a patient be allowed suffi

to perform an activity with less shortness of breath.

cient time to adjust to nocturnal ventilation before ad

The second rule of thumb is to maintain a rhythm

vancing into an active exercise program. This deci

with activity. If the activity is washing dishes, vacu

sion must be made with medical guidance. It is

uming the carpet, or climbing some stairs, the focus

sometimes recommended that a patient rest on this

is to maintain a rhythm. That rhythm will change as

system for a few months to allow the body to reach a

the activity continues, but the idea is to control it

stable level of metabolic rest.

through the purse-lip breathing. For example, climb

BREATHING TRAINING

ficult with each step. Breathe in on step one and ex

ing stairs may begin with ease and become more dif hale for step two, three, and four. As the activity

Paced Breathing

continues, modify according to the patient's need. It

These techniques are taught regardless of which mus

may progress to breathing in on one step and doing

cles patient uses to breathe. Because breathing is

the fu II exhalation on the second step. The patient

g

something we do all day lon , it is unfair to expect

may still experience shortness of breath but will have

patients to alter their breathing continuously. There

better control and get further.

fore it is helpful to break down breathing into various components. Foremost is coordinating breathing with activity. If a patient is short of breath, he or she needs to know how to get it back. Pursed-lip breathing is an

Signs of Improvement The direction toward improved posture and more effi

effective means of helping. Pursed-lip breathing

cient quality of movement is a slower process and

works as the center for controlling the respiratory rate

should be directed in the realm of kinesthetic aware

and maintains more efficient emptying of the lung.

ness. If you are working with a patient and find that in a

Paced breathing and the rule of thumb are handy

certain posture you observed a better breathing pattern

tools that help get through daily activities. Breathing

or that with a certain relaxation technique the patient

has a rhythm of inhale and exhale. Generally, the ex

found relief, you want to harness that sensation. Repeat

hale is longer than the inhale. At rest and with vari

it, use tactile input, have the patient close his or her

ous relaxation techniques, it is possible to greatly ex

eyes and imagine it. If the patient has just learned to

tend the length of the exhale. For example, if at rest

relax the upper thorax and get a good expansion in the

the person inhales for a count of two, the exhalation

lower thorax, he or she will not be able to walk out of

might be for a count of four or five. With deeper re

that session and breathe that way continuously. How is

laxation the length of the exhalation can be extended

this new skill incorporated into a new pattern of breath

to the count of five, six, or even longer. Patients are

ing? It is effective to stop 20 to 30 times per day, (1) pause, (2) relax the shoulders, (3) focus on the area to expand, (4) do the breathing technique for a few rep etitions, and (5) concentrate on it and put it away. The

encouraged to develop and heighten this sense of awareness and begin to coordinate it with activity. The concern is that frequently a person will perform an activity (i.e., bending down to get a shoe, reaching

focus of this exercise is not strength training but rather

to open a door, washing hair, or lifting a package)

kinesthetic awareness. About 2 weeks of this compul

and during the activity actually stop breathing or

sive stopping, sensing. and being aware is enough time


436

PART III


that it becomes the way the patient breathes, becoming

parted slowly, as opposed to thrust or high-velocity

incorporated into the patient's pattern of breathing. This

manipulation. The intent is to regain normal active

obviously will not be successful with someone who

range of motion, thus improving alignment and

mechanically, muscularly, or neurally is incapable of

stress distribution. The improvement in joint func

this parit cular

tion increases a joint's adaptive potential to mechan

panded using the tools of imagery. Too often a patient

ical stress and reduces the possibility of re-injury to

is taught how to brcathc and does so beautifully in the

that joint.

therapy session and then resumes the old pattern after leaving the office. It is a difficult task to incorporate a movement performed in a static stationary position and

Soft Tissue Therapies

maintain it during the dynamics of daily life. The

The purpose of soft tissue therapy is to normalize ac

power of suggestion and imagery can be used here.

tivity of the muscle fibers, restore extensibility, and

This scenario becomes a home exercise program of

reduce pain. Soft tissue mobilization includes mas

gaining control of the breathing system. Even if the pa

sage, accupressure, and soft tissue stretching. It uses

tient cannot maintain it through the whole process, it is

low-intensity pressure and should not cause pain. If

a crucial activity in self-control and minimizes the

applied properly, its techniques should result in local

sense of panic that goes along with activities that result

and general relaxation, and reduction in tone. Myofa

in shortness of breath. It is a very beneficial activity

cial release is a method to normalize myofacial activ

that can then be further advanced while working on a

ity, regain tissue extensibility, and reduce pain. It is

bicycle or treadmill. The underlying emphasis is opti

based on neuroreflexive responses that reduce tissue

mizing the patient's efficiency of movement and

tension. With the appropriate application of manual

breathing and reducing the work of breathing.

contact and the determination of the best point of entry into the musculoskeletal system, a relaxation of tissue tension and decrease in myofascial tightness

OVERVIEW OF THERAPEUTIC OPTIONS

can be attained.

A myriad of therapeutic techniques exist that are vi

able options in trying to maximize breathing oppor tunities. It is beyond the scope of this chapter to elaborate on the technique, rationale, and method of

Neuromuscular Therapy Proprioceptive neuromuscular facilitation is a method

all the options appropriate for the population. Once

of promoting the response of the neuromuscular

asked by a colleague the appropriate treatments for

mechanisms through stimulation of proprioceptors.

respiratory patients, I replied, "the same as with any

The application of a manual stimulus is used to elicit

disease process." Evaluate the total situation and

efficient neuromuscular responses. Its primary objec

plan an intervention that will reduce stress and in

tive is to develop trunk or proximal stability and con

crease opportunity. If the patient population has de

trol, as well as to coordinate mobility patterns. It can

veloped respiratory problems secondary to an under

be used to help stabilize vertebral motion and im

lying d i s e a s e, p o s ture, muscle l e n g t h , m u s c l e

prove spinal movement control.

strength, and endurance should be considered. The

Muscle energy works under the principle that

manual therapies are excellent vehicles in gaining

muscular activity can be used to restore physiologi cal joint motion. It uses active muscle contraction

access to improvement.

at varying intensitics from a precisely controlled position in a specific direction against a distinct

Mobilization: Thorax, Rib Cage, Pelvis,

counterforce. It is used to mobilize joint restric

Sacrum, Hip, Shoulders, and Neck

tions, strengthen weak musculature, stretch tight

Joint mobilization is a nonthrust manipulation. Pres

myofascia, reduce muscle tonus, and improve local

sures may vary from gentle to vigorous but are im

circulation.


24


Positional Release Therapies

437

through a treatment. Get comfortable hand contact

Strain/counterstrain is the passive placement of the

and feel the tissue soften in your hand, then wait.

body in a position of greatest comfort to reduce pain.

Watch what happens to the breathing. Hone in on any

Relief, if achieved by the reduction and arrest of con

changes and help the patient become aware of any

tinuing inappropriate proprioceptive activity, main

changes in the pattern of breathing. The diaphragm

tains the motion dysfunction. The underlying basis is

and thoracic release are also remarkably effective in

that every neuromuscular Clisorder has a palpable

encouraging greater thoracic expansion. These tech

point of tenderness and a position that can be ob

niques alone can be effective in relieving wheezing,

tained for comfort. It is a gentle, nontraumatic type of

improving aeration and even mobilizing secretions.

manipulation that is especially effective when irregu

Take the time to explore options. In reference to

lar neuromuscular activities have maintained and per

the cranial bones, restrictions in the movement of the

petuated abnormal mechanical stress to tissue. A re

temporal bones has been identified in those suffering

turn to normal length is achieved through positional

with shortness of breath, regardless of diagnosis. The

release of abnormal neuroreflexive activities.

temporal wobble therapy, ear pull, and finger in ear (craniosacral technique) have also becn effective in easing the work of breathing. The focus of the thera

Craniosacral Therapies

peutic intervention must be to find some relief from

Craniosacral therapy is a gentle hands-on method for

the work of breathing first and then begin a plan of

evaluating and treating problems affecting the cran

enhancement of relief followed by strengthening of

iosacral system. The craniosacral system provides the

those new found movements. Endurance activitics,

environment in which your brain and spinal cord de

that is, treadmills, bicycling or walking, are wonder

velop and function. The palpable parts of the cran

ful adjuncts after these important elements have been

iosacral system are the bones of the skull, sacrum,

addressed.

and coccyx, which attach to the membranes that en close the cerebrospinal fluid. Treatment involves the usage of fascial and soft tissue release techniques to detect subtle biological movements. A 10-step proto col is used for evaluating and treating the entire body.

CASE STUDIES Poliomyelitis with Secondary Severe Kyphoscoliosis Mr. L is a 65-year-old male with history of po liomyelitis onset at the age of 8 years old. He was left with a total paralysis of his left arm and a severe scol

Review

iosis secondary to muscle strength imbalance in the

In evaluating the disease process that results in respi

trunk. (Figure

ratory compromise, it is crucial to recognize the long

liomyelitis, his medical history was unremarkable. He

term chronic effects on the total body. It is short

lived independently in a fourth-floor walk-up apart

24-7). After recovery from the po

sighted to limit the focus to the thorax if there is a

ment and worked as a postal clerk until he was admit

respiratory problem. Take a step back and look at the

ted in respiratory failure. At that time his oxygen satu

total picture and look for those windows of improve

ration was 80%, his arterial carbon dioxide (Paco2)

ment. Some specific techniques have cdnsistently

was 61, and his arterial oxygen level (Pao2) was 53.

been helpful in helping ease the work of breathing.

His vital capacity was 1.8 liters-40% of predicted

Both myofacial release techniques and craniosacral

and his ECG showed right ventricular strain sec

therapies focus on the cranium and the sacrum. The

ondary to pulmonary hypertension. Additionally the

mobility of the sacrum and motion of the cranial

myocardium was situated in his right cavity secondary

bones have been shown clinically to be directly re

to pressure gradients that shifted it from its normal po

lated to the ease of breathing. The performance of

sition. His medical management required a tra

traction on the sacrum, a gentle hold, provides a re

cheostomy and respiratory support with a ventilator

lease on the thorax. The key is patience. Do not rush

and oxygen. He stabilized and was sent for an interim


438

PART III

Cal'diopulmonary Physical Therapy Interventions

The physical therapy program was problem oriented and was modified throughout as the patient's needs changed.

Problem 1: Shortness of breath at rest and with activity Mr. L was instructed in breathing techniques, includ ing paced breathing, pursed-lip breathing, and relax ation exercises to help relax the upper respiratory muscles and encourage deeper, more efficient expan sion of the thorax.

Problem 2: Paradoxical breathing pattern Because of the severity of the curve, the thorax moved in a rotation pattern to the right with the in hale and to the left with the exhale. It was unclear how much of this pattern was due to structural factors or secondary weakness that allowed such severe dis tortions. A path of exploration was initiated to find potential areas of movement and to further evaluate if there was potential to master those movements. Sub tle movements were evoked in the cervical area and initiated a treatment plan of soft tissue mobilization, craniosacral therapy, and strengthening exercises. The window found was that cervical traction allowed

FIGURE 24-7 Palil:nt with history of poliomyelitis and subsequent development of severe scoliosis secondary to muscle imbalances.

Mr. L to increase his head range of motion and he was able to better relax his sternum and allow for breathing from lower down. The terminology of lower down is used because it is mechanically impos sible for Mr. L to fully use his diaphragm. He was

of rehabilitation. At that facility he was accidentally ex

able to recruit other muscle groups, in addition to

tubated and the tracheal area was Iladly traumatized.

diaphragmatic, to allow for sufficient thoracic ex

The tracheal trauma left the patient comatose for 4 days. About 2 weeks before the patient's respiratory

pansion relieving the excessive work of his upper respiratory muscles.

failure, he was at a dinner with friends, and one of the

Aside from the primary paralysis of the left arm,

group videotaped the evening. The tape had invalu

the musculature of the left trunk was also weak and

able information in it. Firstly, in terms of posture, Mr.

kinesthetically deprived. The term kinesthetically de

L's head was totally sunk into the thoracic cavity

prived refers to the convex part of the curve that was

leaving him functionally without a neck. Around the

essentially folded inward in total paradoxical motion.

dinner table his friends were joking and remarking at

Mr. L was totally unaware of that part of his body and

how little he was eating. It is even more noteworthy

had no sense of movement. On soft issue mobilization

that he even dOI.cd during conversation at the table.

and tactile input on the left side, the patient began im

The labored breathing, the excessive use of the upper

mediately to expand on the left side of the thorax. Be

respiratory muscles, the sleepiness, loss of appetite,

cause of the severity of the curve, it would be impos

and lack of energy to eat his meal were all signs of

sible to have normal expansion on the left, but it was

pending respiratory fatigue and fail ure.

unclear if enough force and negative pressure could


24


439

be generated on the left to enable the patient to

with the patient reporting "Oh, I am getting more air!"

(I) shin the myocardium back into the left thoracic

This was easily confirmed; improved aeration was au

cavity, (2) increase his vital capacity enough to reduce

dible with the stethoscope.

his need for oxygen and possibly prevent future respi ratory complications. Mr. L began a home program using Theraband, which he looped around his left shoulder and held across his chest with his right hand (Figure 24-8). This position allowed him to grade re sistance to scapular adduction, elevation, and depres sion. He also used weights in trunk exercises. Therapy sessions focused on manual techniques to mobilize the rib cage, stretch the muscles, and release the connec tive tissue. The technique of the diaphragm and tho racic release were remarkably effective in opening the breathing. This method alone was frequently effective

Problem 3: Poor endurance Mr. L had become so deconditioned and anxious at the thought of movement that he was unable to walk even 20 feet. Outdoor ambulation created severe anx iety for which he was receiving psychological ther apy. He began a gradual program with walking in place at 2-minute intervals. It is important to note that he was extremely motivated and not only followed his exercise program, but expanded on it (Figure 249). He also used the P-FJex respiratory muscle trainer attached to his tracheotomy tube beginning on level I for IS-minute intervals, twice a day. After I year on the program, Mr. L grew in height I 114 inches and increased his vital capacity by 700

ml, he no longer required supplementary oxygen, and his myocardium shifted into the left thoracic cavity without any signs of right ventricular strain. His ejec tion fraction was 45%. He still demonstrated para doxical motion with respiration, but there was a sig nificant reduction in the amount of sucking in of the lower rib cage on the left with inhalation. Ausculta tion was remarkable with excellent breath sounds on the left and right and some reduced air movement near the lingula. Mr. L progressed up to walking in place for 25 minutes with 2-pound weights in both hands (he is able to clasp a weight with his paralyzed hand) and attached to both ankles. He gained enough motion in his neck to allow for full range of motion. Because the pull of gravity will continually work on Mr. L to pull him back into dysfunctional patterns, it is impOltant to keep Mr. L on a program. He is seen once every 2 months to modify and update his exer cises and work on his trunk to ensure optimal thoracic capability. Over this extended time other windows have been found working on his sacrum and pelvis. Manual traction, mobilization techniques, and soft tis sue releases in these areas all provide for improved thoracic expansion. Hand placement on the sacrum al lows for a slow release and relaxation of the upper chest. Manual techniques then followed, encouraging

FIGURE 24-8 Creative use of theraband in strengthening of the thoracic

progressively increasing diaphragmatic excursion. Mr.

musculature.

L is able to cue in to changes in his body and work on


440

PART III


Dystonia With Spasmodic Breathing Ms. B is a 36-year-old psychologist with the diagno sis of dystonia. She has a I O-ye ar history of torticollis that has been treated with Botox. IL is a treatment aimed at paralyzing selective muscle fibers to allow

for relief of severe spasms. She presented with recent onset of shortness of breath and inability to get air. On palpation over the lower rib cage and diaphragm, it became evident that there was discoordinate move ment of the thoracic musculature. It was unclear whether this was merely discoordinate movement or a function of the dystonia. The technique of diaphrag matic release as demonstrated in craniosacral therapy provided immediate release of the symptom of short ness of breath and reduced the amount of discoordi nate movement of the chest wall. Ms. B was taught how to perform the technique on herself and was suc cessful in the exercise. The P-Flcx was used to give added resistance to her breathing as a means of ex trasensory awareness. It gave her an added awareness of movement of the thoracic wall and a means of

controlling it. The final phase of her therapy was mild aerobic activity with the focus of coordinating breathing with movement and increasing overall en

FIGURE 24-9 Respiratory muscle training in p a t ien t with tracheotomy.

durance. She was on a program for 6 months and was followed once per week. Although her symptoms persist sporadicalJy, she is able to catch it in time and gain control of her brcathing. According to medical opinion, it is likely that she has the rare progression

gaining sensory awareness of the area and aim toward mastery and control of the movement.

of respiratory muscle dystonia. It is undear at this time how this situation

will progress, but in the

meantime, she has the means of controlling discoor

Summary of problems

dinate movement and breathing with ease.

Mr. L benefitted from a program that focused on im proving his total potential. He had the benefit of night ventilation so that his body was rested. His total en

Postpolio Syndrome

durance capability was based on finding those win

Dr. 0 is a dentist teaching in a dental school and

dows of improvement. The improvement in align

conducting research in a laboratory. He has a his

ment and strengthening of the trunk and respiratory

tory of poliomyelitis with a possible diagnosis of

muscles provided for maximizing his respiratory ca

postpolio syndrome (PPS). Diagnosis is difficult

pabilities, overall endurance, and quality of life. At

because PPS is characterized by progressive weak

this point Mr. L is totally independent. He walks 3

ness and pain in the musculature that survived the

miles per day and goes out with his wife and friends.

original poliovirus. The underlying mechanism is

He has even traveled abroad with a foreign medical

still unclear; it is suggested that the progression is

supply company providing for his ventilatory needs.

resultant to long-term overuse and deterioration of


24

441


surviving muscle fibers. Studies show that the di

primary foundation of rehabilitation potential. Im

rection of therapy is to unload or rest the overused

provement in breathing capacity and overall en

muscles and shift the work of the musculature. It is

durance can be accomplished through techniques to

difficult in the therapeutic setting to identify the

improve posture overall. Endurance training based on

weakness that may be from PPS or weakness from

graded-exercise tests is an important element in the

simple aging and inactivity. Great caution is needed

rehabilitation program but should be placed

in this situation because studies have shown that if

spective to other therapeutic options.

10

per

the PPS muscles are overworked, it can result in permanent irreversible damage. Dr. 0 presented with the complaint of cervical pain. On evaluation, it became evident that the pain was related to the

REVIEWaUESTIONS 1. What laboratory data are needed to determine if

cervical lordosis, resulting from the underlying

a patient is a candidate for endurance training?

muscle loss aggravated by the stooped posture nec

2. What types of treatment can be beneficial, if a

essary for his long hours of work in the laboratory. Dr. 0 primarily relied on his upper respiratory mus

patient is not a candidate for endurance training? 3. What types of interventions can best help a patient

cles for breathing because of diaphragmatic paraly

enter into a more aggressive exercise program?

sis and extensive intercostal muscle loss. Dr. 0 did

4. Is aerobic training limited to treadmi I I and bicy

not have much time available for home exercise or

cle? Think about the limitations of these modali

for physical therapy sessions. Exercise prescrip

ties and suggest alternatives.

tions that would isolate the weak muscles and then focus on repetitive exercises to strengthen them would be problematic because of the threat of tissue damage to muscles affected by PPS. Dr. 0 was given one e x ercise to perform twice per day, rolling, to roll from one end of the room to the

References Astrand, P.

& Rodahl, K. (1977).

Physical Training. Textbook of

work physiology. New York: McGraw Hill.

Austin, J. (1992). Enhanced respiratory muscular function in nor

adults after lessons

other and back. He was guided in maintaining con

mal

trol of the trunk musculature throughout the activ

cation without exercise. Che,'I, 102,486-490.

ity. This activity was performed semi regularly for a year with the goal of improving trunk strength and posture. Over the course of the year, endurance ex ercises were added using a home stationary bicycle. In I year, Dr. 0 grew I 1/4 inches. He continued to rely on the upper respiratory muscles for breathing, but his overall improved strength and posture left him pain free.

Basmajian, Willian,s

in proprioceptive musculoskeletal edu

J. (1993). Rational & Wilkins.

manu.al Iherapies. Baltimore:

Black, L. (1982), Early diagnosis of chronic obstructive pulmonary disease, Mayo Clinic Proceeds 57,765-772, Braun,

N, (1983), When should respiratory muscles be exercised?

Chest, 84,76.

Dean, E. (1991a), Clinical decision making in the management of the late sequelae of poliomyelitis. Physical Therapy, 71.' 757-761. Dean, E. (199Ib). Effect of modified aerobic training on move ment energetics in polio survivor. Orthopedics, 14,1243-1246, Edwards, R. (1978). Physiological analysis of skeletal muscle weakness and fatigue, Clinical Science and Molecular Medi

SUMMARY

cine, 54,463.

A multitude of therapeutic options exist for those suf fering with respiratory limitations. The presentation of symptomatology of dyspnea is similar in primary lung disease and in secondary cardiopulmonary symptoms. It is crucial to understand the underlying pathology so that the therapeutic intervention and ex ercise prescription reflect the potential of the patient. Focusing on issues of respiratory muscle fatigue is a

Feldman, R. (1985). The use of strengthening polio seq uelae :

methods and results.

exercises in

po s t

Orthopedics, 81.889-891.

Gorman, D. The body moveable. Guelph, Ontario, Canada:Amper sand Printing Co, Kotses, H, (1981), "Application of biofeedback to the treatment of asthma:

a

critical review, Biofeedback an d Self Regulation,

b,573-593. Lisboa, C. (1985), Inspiratory muscle function in patients with se vere kyphoscoliosis, American Review of Respiratory 132,48-51.


Disease,

442

PART III


Marino, W. (1982). Reversal of clinical sequelae of respiratory muscle fatigue by intermittent mechanical ventilation. Ameri can

Stoller. J. (1988). Oxygen therapy techniques-Current respiralol), care. Toronto: BC Della. Upledger, J. (1992). Craniosacral therapy. Washington: Eastland

Review ofRespiratOlY Disease, 125, 85.

Press.

Owen. R. (1985). Polio residuals clinic: conditioning exercise pro

Weiss, H. (1991). The effect of an exercise program on vital capac

gram. Orthopedics, 8,882-883. Shneerson, J. ( 1 97 8) . The Cardio respiratory response to exercise

ity and rib mobility in pa tients with idiopathic scoliosis. Spine.

in thoracic scol.iosis. Thorax, 33, 457-463.

16, 88-93.


Respiratory Muscle Weakness and Training Maureen Shekleton Jean K. Berry Margaret K. Covey

KEY TERMS

Inspiratory muscle trainin g

Respiratory muscle fatigu e

Muscle endurance

Respiratory muscle w eakness

Muscle s tre ngth

Wo rk of breathing

INTRODUCTION Roussos and Macklem

to ventilatory failure and death. Causes of respiratory

(1982) support the notion of a

pump failure can be grouped into the following two

(I) those in which the respiratory

two-part respiratory system made up of the lungs,

major categories:

which are the gas exchanging organs, and a pump,

drive is decreased or the sensitivity and function of

which ventilates the lungs. The pump is composed of

the respiratory center is altered (i.e., those that affect

the chest wall, the respiratory muscles, and the nerves

the central nervous system control), and

and centers in the nervous system that control the res

which the ventilatory response is decreased through

(2) those in

piratory muscles. The respiratory muscles are ex

impairment of the mechanics of respiration (i.e.,

pected to function continuously throughout life to

those that affect the chest wall or musculature) (Groer

p rovide the appropriate level of ventilation for meet

and Shekleton,

ing the body's metabolic needs.

1989).

The focus of this chapter is on the latter category,

Citing the analogy of the heart as the circulatory

and more specifically, on the role of weakness and fa

pump and the consequences of heart failure, Mack

tigue of the respira tory muscles as a pathophysiologi

(1982) maintains that the respiratory pump can

cal mechanism seen in many clinical conditions. The

fail, leading to a condition characterized by hypoven

view of respiratory muscle fatigue as a cause of venti

tilation and hypercapnia that may ultimately progress

latory failure is an idea becoming more widely ac

lem

443


444

PART III


cepted among pulmonary clinicians (Sharp, 1984).

of origin: central fatigue, transmission fatigue, or

Respiratory muscle fatigue is postulated to be the final

contractile fatigue. Central fatigue is due to a de

common pathway to respiratory failure in all condi

crease in neural drive, which reduces the number of

tions in which the respiratory musculature is affected

firing frequency of motor units. The resulting force

(Cohen, Zagelbaum, Gross, Roussos, and Macklem,

generated by voluntary effort is less than that which

1982; Grassino, Gross, Macklem, Roussos, and Zagel

can be achieved by electrical stimulation of the motor

baum, (1979); Derenne, Macklem, and Roussos,

nerves. If electrical stimulation can restore contractile

1978; Roussos and Macklem, 1982).

force or if stimulation and force decline in parallel,

Although both the inspiratory and expiratory res

central fatigue is present. Transmission fatigue results

piratory muscles are susceptible to fatigue, clinically,

from an impairment in the transmission of impulses

concern centers on the inspiratory muscles. The di

along the nerves or across the neuromuscular junc

aphragm is of particular interest. Under normal con

tions. Contractile fatigue results from impairment in

ditions, the inspiratory muscles including the di

the contractile response to neural impulses within an

aphragm, the external intercostals in the parasternal

overloaded muscle. Both transmission fatigue and

region, and the scalene muscles are responsible for

contractile fatigue are classified as peripheral fatigue.

the active process of breathing, and expiration is a

Peripheral fatigue is present if force is decreased but

passive process. An analysis of the phenomenon of

electrical stimulation is constant. All three types of

inspiratory muscle fatigue is presented initially in this

fatigue are reversible (Mador, 1991).

chapter. This is followed by a discussion of the iden

Peripheral fatigue can be further categorized ac

tification and management of inspiratory muscle fa

cording to the selective loss of contractile force that

tigue and its possible prevention through training of

occurs at varying stimulation frequencies. High-fre

the inspiratory muscles.

quency fatigue is a selective loss of contractile force at high-stimulation frequencies; low-frequency fa

THE CONCEPT Of INSPIRATORY MUSCLE fATIGUE

tigue is the selective loss of force at low-stimulation frequencies. High-frequency fatigue is thought to be

It is important to differentiate between muscle weak

the result of impaired neuromuscular transmission

ness and muscle fatigue, although both may lead to

and/or propagation of the muscle action potential.

hypoventilation (Bryant, Edwards, Faulkner, Hughes,

This type of fatigue is seen in myasthenia gravis, dur

and Roussos, 1979). Muscle weakness refers to a loss

ing ischemic exercise, with muscle cooling, and with

in the capacity of a rested muscle to generate force

partial curarization. It is reversible in minutes. The

that is chronic situation. Muscle fatigue refers to a

mechanism underlying low-frequency fatigue is

loss in the capacity of a muscle under load to develop

thought to be impaired excitation-contraction cou

force or velocity that is reversible by rest (NHLBI

pling. Recovery from this type of fatigue may take

Workshop Summary, 1990). Fatigue is an acute loss

hours to days and possibly longer. Intense dynamic

of contractile force wherein, despite constancy of

and static muscular activity can lead to low-fre

stimulation, force declines from the initial value. If

quency fatigue (Edwards, 1983; Moxham, 1990).

fatigue is the inability of a muscle to continue to gen erate a required force, then in the respiratory system, fatigue will be manifested by the inability of the in spiratory muscles to continue to generate the force re

Mechanisms and Etiology of fatigue The major mechanisms thought to be responsible for

quired to maintain the necessary level of alveolar

inspiratory muscle fatigue include an imbalance be

ventilation to meet the body's metabolic needs. Inspi

tween energy supply and demand and impaired exci

ratory muscle fatigue occurs when inspiratory effort

tation-activation. Edwards (1983) has proposed a

exceeds the capacity of the inspiratory muscles to

model that accounts for the interaction of both mech

sustain that effort (Rochester, 1982).

anisms in the development of muscle fatigue. He has

Physiologically, fatigue has been characterized as

also proposed the idea that fatigue serves a protective

one of the following three types, depending on its list

function in that serious irreparable damage may be


25

Respiratory Muscle Weakness and Training

Possible fatigue mechanism Psyche Brain Impaired motivation i.e. neural motor drive and motor unit recruitment SP'''' Co ,d

) p",p"r ""'"

I mpaired reAex drive

Impaired neuro muscular transmission

Muscle sarcolemma

j

Impaired action potential K*, Na*, H20

Transverse ,"bO',

'!

'y"eo"

imbalance

Impaired excitation

Ca**

1

Impaired activation Impaired energy supply

Actin-myosin interaction

CN" b'''g'

r1

"o"' + heat

Thermal damage

Sarcomere damage

Force power OUlput

FIGURE 25-1 Chain of command for muscular contraction and the possible mechanisms underlying fatigue.

(From Edwards, R.A.T. (1983). Biochemical basis of fatigue in exercise petformance: Catasptrophe theory of muscular fatigue. In Knuttgen, H., Vogel, J., Poortmans, 1. (Eds.). Biochemistry of

exercise. Champaign, Ill. Human Kinetics Publishers.).


445

446

PART III


prevented if the muscle is unable to continue per

pattern of fiber distribution is most pronounced in

forming beyond a critical point. The central nervous

the premature infant. This condition exists in infants

system may exert a protective mechanism to avoid

for up to a year after birth.

these adverse effects. This idea has persisted and the

The energy supply to the muscles depends on an

term central wisdom is used to describe the phenome

intact oxygen transport system, adequate oxygen-car

non (Moxham, 1990) (Figure 25- I, p. 445). The energy demands of the inspiratory muscles

rying capacity of the blood, blood tlow, substrate stores and availability, and the efficiency of oxygen

are determined by the work of breathing, the strength

uptake and uti lization by the muscles. The energy

and endurance of the respiratory muscles, and the ef

supply to the inspiratory muscles is compromised

ficiency of the muscles. The work of breathing is the

when cardiac output is reduced, the hemoglobin con

total amount of effort required to expand and contract

tent of the blood is low, blood flow to the muscles is

the lungs. It is determined by the degree of compli

decreased, or energy substrates are lacking.

ance of the lung tissue and the chest wall, the resis tance of the

Excitation-activation depends on intact, function

airways, the presence of active expira

ing, neuromuscular pathways. Impaired excitation-ac

tion (normally a passive process), and use of the

tivation is probably the primary mechanism underlying

accessory muscles of respiration. The work of breath

respiratory muscle weakness and fatigue in the patient

ing is increased by decreased pulmonary compliance,

with a neuromuscular disorder (Edwards, 1979). Dis

increased airway resistance, active expiration, and

ruption of excitation-activation can occur at any point

use of the accessory muscles.

along this pathway, which Edwards (1983) refers to as

Strength and endurance are the fundamental prop

a chain of command for muscular contraction. Pre

erties of muscle. Strength is defined as the maximal

sented in Figure 25-1 is a list of the possible mecha

force that a muscle can develop with maximal stimu

nisms that may lead to fatigue by disrupting the neuro

lation. Contractile force is governed by the force

muscular pathway. Impaired excitation of the muscle

length (length-tension), force-velocity, and force-fre

membrane is probably interrelated with energy metab

quency relationships. Contractile force diminishes in

olism. For example, if the ATP supply to the Na+ - K+

conditions characterized by increased lung volume

pump is compromised, an alteration in the Na+ and K+

(hyperinflation), since the muscles are stretched be

concentrations in the transverse tubular system may re

yond the optimal length to generate maximal force.

sult in impaired excitation-contraction coupling.

This stretching of the muscle fibers produces a less

Although it is difficult to demonstrate the precise

desirable length-tension relationship and causes a

mechanisms causing respiratory muscle fatigue in pa

loss of the zone of apposition, with resulting decrease

tients, support is found for the concept that central

in strength generation. Strength is also determined by

nervous system output is modified to avoid overt fa

the number and size of individual fibers in a muscle.

tigue. With extremely high loads imposed on respira

Strength is adversely affected in conditions in which

tory muscles, patients adopt a rapid shallow pattern

the size of the fibers is reduced (atrophy) or the num

of breathing that reduces the work of breathing and

ber of fibers is reduced (e.g., in malnutrition). Endurance is defined as the ability to maintain a contraction against a given load and is determined

can be sustained. Eventually, this pattern of rapid shallow breathing will lead to hypercapnia and acido sis (Moxham, 1990).

by muscle fiber type, blood supply, and the force

In summary, those patients who are at risk for the

and duration of the contraction. Normally, the inspi

development of inspiratory muscle fatigue are those

ratory muscles are fatigue resistant. Approximately

in whom energy demands are increased, energy sup

75% of the muscle fibers in the adult diaphragm are

plies are compromised, or whose neuromuscular

of the high oxidative, fatigue resistant type (type I

chain of command has been disrupted at some point.

and type IIA). In contrast the diaphragm of the

Patients at highest risk for the development of inspi

neonate contains a relative paucity of type I fibers

ratory muscle fatigue are those in whom the work of

that have the greatest endurance capacity, and this

breathing is increased, thus increasing the demands


25


447

for energy, and those who are experiencing hypox

power spectrum, which is indicative of muscle fa

emia, acidosis, low cardiac output, or any other con

tigue in normal subjects exercised to fatigue, in pa

dition in which the blood supply to the muscle is di

tients experiencing difficulty being weaned from me

minished, thus reducing oxygen supply. Patients

chanical ventilation, and in animals in whom fatigue

whose nutritional status is poor or who are experienc

was experimentally induced. When fatigue is present,

ing a catabolic state, such as stress or fever, will have

the ratio of high-to-low frequency power, which can

reduced energy stores and may experience muscle fa

be detected by EMG, shifts as low-frequency power

tigue during times of high need.

increases and high-frequency power decreases. The difficulty in obtaining an EMG at the bedside and in analyzing the results makes its use in most clinical

Assessment of Fatigue

situations unrealistic at this time.

The clinician will most often have to rely on physi

In summary, rapid shallow breathing is the initial

cal signs exhibited by the patient to recognize inspi

sign of inspiratory muscle fatigue (Yang and Tobin,

ratory muscle fatigue. Other laboratory methods that

1991). The physical signs previously described are

would yield more objective evidence of inspiratory

reliable and can be used in a clinical situation to de

muscle fatigue include power spectral analysis of the

termine whether the patient is experiencing inspira

electromyelogram (EMG), measurement of the max

tory muscle fatigue.

imal relaxation rate, and examination of twitch oc clusion pressure. The following signs are indicative of inspiratory

Treatment of Fatigue

muscle fatigue and are listed in their characteristic

The goals of treating inspiratory fatigue are as fol

order of appearance:

lows:

(I) restore the balance between energy supply (2) improve diaphragmatic contractility, and (3) increase the strength and endurance of the in

I. Tachypnea 2. Decreased tidal volume 3. Increased PC02 (which is a late sign)

and demand,

spiratory muscles. The last goal is obviously a more

4. Bradypnea and decreased minute ventilation

long-term preventive approach, whereas the first two

Formerly, development of a discoordinated respi

goals apply in the more acute situation when inspira

ratory pattern characterized by inward abdominal

tory muscle fatigue is present.

ab

Energy demands in the patient experiencing fa

dominal paradox) and alternating abdominal and tho racic respiratory patterns (a sign referred to as respi ratory alternans) were t h o u gh t to result f r o m

tigue can be decreased by reducing the work of breathing through activities intended to promote

respiratory muscle fatigue. Presently, these changes

wall and airways, and promote normal lung volumes

in breathing patterns are thought to result from in

and pressures. Energy supplies can be enhanced by

movement on inspiration (a sign referred to as

compliance, decrease resistance in the lung, chest

creases in respiratory load rather than muscle fatigue

ensuring maximal oxygen transpOit to the tissues and

(Mador,

1991; Tobin, Perez, Guenther, Lodato, and Dantzker, 1987). However, discoordinated respira

the availability of adequate amounts of oxygen and

tory patterns are important clinical signs of respira

hanced by promoting adequate cardiac output, blood

tory distress and, although they are not specific in

flow to the tissues, and oxygen-carrying capacity of

their etiology, they are sensitive indicators of impor

the blood. Various forms of respiratory therapy are

tant declining respiratory function.

other energy substrates. Oxygen transport is en

available to supplement oxygen supplies. Losses of

In animals in whom inspiratory muscle fatigue has

organic and inorganic energy in substrates must be

been experimentally induced the fall in respiratory

replenished and adequate levels maintained. Nutri

rate and minute ventilation immediately precedes res

tional supplementation and administration of elec

piratory arrest and death. This sequence of events has

trolytes and inorganic phosphate may be necessary to

been observed after an initial change in the EMG

augment energy supplies. Rest therapy with mechani


448

PART III


cal ventilation may be required to allow the fatigued

plished by training the inspiratory muscles in much

muscle to recover and to bring energy supplies and

the same way that athletes train and condition their

demand into balance.

muscles. Inspiratory muscle training may represent a

Much current research is being done in the area of

useful clinical approach to prevent the development

pharmacological interventions to improve diaphrag

of inspiratory muscle fatigue in those patients who

matic contractility. Aminophylline w as initially

are at risk.

thought to increase the contractile force of the di aphragm at any given level of activation, but further research indicates that this drug increases muscle en

INSPIRATORY MUSCLE TRAINING

ergy consumption and potentiates fatigue (Janssens,

Inspiratory muscle training (lMT) is currently used in

1988). Other drugs with

pulmonary rehabilitation to increase the strength and

Reid, Jiang, and Decrarner,

inotropic properties are the beta-agonists. Clinical in

endurance of the inspiratory muscles. Patients with

vestigation of the potential usefulness and application

chronic obstructive lung disease experience func

of these pharmacological agents in inspiratory muscle

tional weakness of the respiratory muscles, which can

fatigue is ongoing.

contribute to dyspnea and functional impairment.

The last goal, that of increasing the strength and

Theoretically, IMT should reduce dyspnea by im

endurance of the inspiratory muscles, can be accom

proving respiratory muscle function and exercise tOI-

RespiralOn' muslle Ir,lillillg

i Sirengill

I

,tlld cndurancc of respiralon' llluscies

I Delay lhe onsel of respiralory llluscle faligut'

IllllJrOl'e

I I

Prel'em/dcler I hc Ollsel of

Illlpn)IT lissuc o"ygemllio)l

1'espi1';lIOl} insuUiciell(Y allcl

•

faliguc

cog"niliol1 pcn:cplion pS)Tilo-lllOI01' hlllCiioll

ImpnJl'

1m p1'Ol'c

signs anc! "mplOms

\\ell-being.

Improl't'

IlllprOl'c

tlaih liling

life

FIGURE 25-2 Conceptual framework for respiratory muscle training. (From Kim M: Respiratory muscle training: Implications for patient care .

Hearl and Lung. 13(4):333-40).


25

erance. These effects have yet to be demonstrated in large, controlled studies (Smith, Cook, Guyatt, Mad havan, and Oxman, 1992). General principles of skeletal muscle training that must be considered when designing and evaluating an IMT program for respiratory patients include over load, specificity, and reversibility. To train a muscle to improve its functional ability, the muscle must be subjected to a stress greater than its usual load (over load), the training must be directed at developing spe cific functional attributes (e.g., strength or endurance) of the muscle (specificity), and the training must be maintained or function will revert back to pretraining levels (reversibility) (Kim, 1984; Sharp, 1985). The effects of strength training on the respiratory muscles may include an increase in the size (hypertro phy) and number of the muscle fibers by an increase in protein synthesis by the muscle fibers and a de crease in degradation. Endurance training of the inspi ratory muscles is thought to promote an increase in the proportion of fatigue-resistant fibers in the di aphragm, an increase in the metabolic capability of the muscle, and a reduction in the susceptibility of muscle fibers to the deleterious effects of exercise (Leith and Bradley, 1976). Newer evidence suggests an improvement in neuromuscular coordination and efficiency resulting from training (McComas, 1994). Strength training to increase the size and number of myofibrils requires a high load and a slow rate of rep etition. Endurance training to increase the metabolic capability of the muscle requires exercise of a suffi cient load, speed, and duration, such that cellular con centrations of energy producing substrates drop to minimal levels (Kim, 1984). Endurance training of skeletal muscle has been found to be most effective when brief periods of fatiguing exercise are alternated with periods of rest (Aldrich, 1985) and this concept may be applied to inspiratory muscle training regimes. Improvement in the strength and endurance of the inspiratory muscles through training has the twofold effect of enhancing the resistance to inspiratory mus cle fatigue and improving ventilatory function. The work of breathing is reduced and respiratory reserves are increased. Because the clinical signs and symp toms are diminished, the ultimate outcome for the pa tient is an improved quality of life. Kim (1984) has


449

developed a model that outlines the relationship be tween the effects of a respiratory muscle training and potential patient outcomes (Figure 25-2). Inspiratory muscle training has been used to suc cessfully increase muscle strength and endurance in healthy volunteers and in patients with chronic air flow limitation (Belman and Mittman, 1980; Larson, Kim, Sharp, and Larson, 1988), cystic fibrosis (Keens, Krastens, et ai, 1977). Early Duchenne mus cular dystrophy (Wanke et aI, 1994), and in those who are quadriplegic (Gross, et ai, 1980). Theoretically IMT in patients experiencing acute respiratory failure should promote improved function of the muscles, and fatigue resistance should facili tate the process of weaning these patients from me chanical ventilation. In conditions requiring full ven tilatory support, the respiratory muscles may contract at minimal levels for a period of time, possibly lead ing to the development of disuse atrophy. As their strength and endurance decrease, the inspiratory mus cles will be more prone to fatigue because of the in teraction of disuse, the underlying pathophysiological state, and catabolic effects of stress. The ultimate ef fect of these interacting processes will be difficulty in weaning the patient from the ventilator. An EMG pat tern of fatigue has been documented in the ventila tory muscles of neonates who experienced difficulty in weaning (Muller, Gulston, and G ade, 1979). Grassino et al. (1979) found an EMG fatigue pattern in a patient being weaned from mechanical ventila tion. Cohen et al. (1982) found an EMG pattern of fa tigue in 7 of 12 patients who experienced difficulty during discontinuation of mechanical ventilation. Resolution of the fatigue pattern was observed in those neonates who recovered and in adult patients who were successfully weaned (Andersen, Kann, Rasmussen, Howardy, Mitchell, 1978). There is some evidence that respiratory muscle training may prove to be an important adjunct therapy to facilitate wean ing in the patient who requires mechanical ventilation of acute respiratory failure (Aldrich and Karpel, 1985; Aldrich et ai, 1989; Shekleton, 1991). How ever, controlled studies have not been conducted in this patient population. Two techniques have been used for inspiratory muscle training: isocapnic hyperventilation (also


450

PART III


called isocapnic hyperpnea) and inspiratory resistive or resistance breathing. Isocapnic hyperventilation is dynamic and is used to increase the endurance of the inspiratory muscles. Expiratory muscles will benefit as well with this technique. Patients are asked to breathe at the highest rate they can manage for 15 to 30 minutes. A rebreathing circuit or the addition of CO2 to the inspired air must be used with this tech nique to prevent hypocapnia (Belman, 1981; Belman, and Mittman, 1980). Because of this requirement, the usefulness or this technique will be limited until portable, inexpensive, easy-to-use equipment for home use is developed. I nspi r a t o r y r e s i s t i v e b r e a t h i n g a l l o w s b o t h strength and endurance training, since i t incorporates both isometric and isotonic exercises. There are two devices available for this purpose, a nonlinear device and a threshold JMT device (Figure 25-3). The non linear device has been noted to produce unreliable training loads if the rate of inspiratory flow is not controlled (Guyatt, Keller, Singer, Halcrow, and Newhouse, 1992). With a controJI.ed rate of breath ing, patients inspire through a narrow tube that offers a nonlinear airway resistance for one to three daily periods of 15 to 30 minutes. The size of the orifice through which the patient inspires is adjusted to pro vide a level of resistance that the patient can tolerate without becoming immediately exhausted. In addi tion, this device is not well suited for stronger pa

FIGURE 25-3 Handheld resistive breathing training devices. A, Threshold; resistance level is altered by tightening screw to increase tension on the spring. B, P-Flcx; resistance level is altered by changing settings on dial.

tients, since they have difficulty achieving a satisfac tory tidal volume with the extremely small orifice at

Potential outcomes of a training program geared

higher loads. With the tllreshold device, a reliable in

toward increasing inspiratory muscle strength and

spiratory pressure load is provided regardless of air

endurance might include any of the following, de

flow rate. The load is adjusted by a nurse therapist,

pending on the individual patient's conditions and

or patient according to a desired percentage of the

goals of treatment: (I) prevention of acute deteriora

patient's maximal inspiratory pressure (PImax). Usu

tion of respiratory status and ventilatory failure,

ally, the patient begins training at a low load, equal

(2) improvement of ventilatory function and de

to about one third of the PImax and progresses slowly

crease in the work of breathing, which may lead to

in small increments adjusting a screw to alter the ten

an increase in general exercise tolerance and an im

sion until the training load reaches 60% of the cur

proved quality of life as tissue oxygenation improves

rent PImax. The threshold device delivers a reliable

and signs and symptoms are attenuated (Pardy,

tension because the poppet valve at the end of the de

Pardy, Rivington, Despas, and Macklem, 1981a;

vice will not open and allow inspiration unless the

1981b), (3) extension of time before onset of respira

patient generates the designated negative pressure.

tory muscle fatigue, and (4) facilitation of the wean

Both types of devices are hand held and pOltable and

ing process in acute respiratory failure patients who

are easily used and maintained by patients.

are being mechanically ventilated.


25


451

SUMMARY Edwards, RAT (1979). The diaphragm as a muscle: Mechanisms

Inspiratory muscle training and conditioning is a newer area of research and treatment for the respiratory pa tient. As such, further validation of its efficacy and tar geting of specific patient populations at greatest risk for loss of inspiratory muscl

strength will define its

use in pulmonary rehabilitation programs. At this time, inspiratory muscle training looks promising as a means of offering the respiratory patient one possible method of control over disease processes that are most often very debilitating and unrelenting in their course.

underlying fatigue. American Review of Respiratory [iseases.

fJ9, (2 pt 2),81-84. Edwards, RAT (19 83). Biochemislry of Exercise. Champaign, lL, Human Kinetics Publishers. Grassino,

A.,

Gross, D., Macklem, P., Roussos,

c., &

Zagelbaum, C.

(1979). Inspiratory muscle fatigue as a factor limiting ex.ercise. Bullelin European de Physiopalhogie Re.lpiraloire, 15, 105-111. Groer, M.,

&

Shekleton, M. (1989). Basic palhophysiology: A

holistic approach. (ed. 3).

Gross, D.,

St. Louis,

Mosby.

et al. (1 980) . The effect of training on strength and en

durance of the diaphragm in quadriplegia. American Journal of Medicine. 68, 27-35. Guyatt, G., Keller, J., Singer, J., Halcrow, S., Newhouse, M.

(1992). Controlled trial of respiratory muscle t raining in

REVIEW QUESTIONS

chronic airtlow limitation. Thorax, 47, 598-602.

I. What are three types of respiratory muscle fatigue? 2. Name two major mechanisms thought to be re sponsible for inspiratory muscle fatigue.

&

Decrame r. (1988).

Jardim, J., et al. (1982). Inspiratory muscle conditioning training in chronic obstructive pulmonary disease (COPD) patients. Amer ican Review ofRespiralory Diseases, 125. (pt 2 of 2), 132. Keens, T., et al. (1977). Ventilatory muscle endurance training in

3. What factors determine the work of breathing? 4.

Janssens, Reid Jiang,

What is the initial physical sign of inspiratory muscle fatigue?

S. What rehabilitation techniques should be used to increase the strength and endurance of the inspi

normal subjects and patients with cystic fibrosi s . American Re view ifRespiralory Diseas'es, 116, 853-860. Kim, M.J. (1984). Respiratory muscle training:

I mplic at io ns

for

patient care. Hearl and Lung, 13, (4),333-340. Larson, M., Kim, MJ. (1984). Respiratory muscle training with the incentive spirometer resistive breathing device. Hearl (lnd

ratory muscles?

Lung, 13. (4),341-345. Leith, D., Bradley, M. (1976). Ventilato ry muscle strength and en

References

traini ng. Journal of Applied Physiology, 41, 508-516. & Roussos, C. (1977). Respiratory muscle fatigue: A cause of respiratory failure1 Clin Sci Mol Med, 53, 419-422. Macklem, P.T (1982) The diaphragm in health and diseas e. Jour durance

Macklem, P. Aldrich, T (1985). The application of muscle endurance training teChniques to the respiratory muscles in COPD. Lung, 163, 15-22. Aldrich, T (1984). Inspiratory muscle resistive training in respira Aldrich, TK., Karpel, J.P., Uhrlass, R.M., Sparapani. M.A., Erami,

D.,

Fen·anti. R. (1989). Weaning from mechanical ventilation:

&

tern. Chesl, 100, 430-435. Martin,

L. (1984).

Respiratory

musc l e

function: A clinical study.

Hearl and Lung. /3,346-348.

Adjunctive use of inspiratory muscle resistive traini.ng.

J.,

ncd ojLaborolory and Clinical Medicine. 99. 601-610. Mador, JJ. (1991). Respiratory muscle fatigue and breathing pat

lory failure. CheSl. 86(2), 302.

Mitchell,

McComas, A. (1994). Human neuromuscular adaptations that ac

J. (1978). Respiratory thoracoabdominal coordination and mus

company changes in activity, Medicine and Science in Sporls

Andcrsen,

Kann, T, Rasmussen. J.P. , Howardy, P.

cle faligue in acute respiratory failure. American Review of

Respimlorv Dis('(I.I'es, 117 (2),89.

and Exercise, 26, 1498-1509. Muller, N., Gulston, G., Cade,

0.,

et al. (1979). Diaphragmatic

Belman, M. (1981). Respiratol)' failure treated by ventilatory mus

muscle fatigue in the newborn. Journal of Applied Physiology,

c a se s. European Journal of Respi 62, 391-395. Edwards, R., Faulkner, .I., Hughes, R.L., & Roussos, C.

Moxham, J. (1990). Respiratory muscle fatigue: mechanisms, eval

et al. (1986). Respiratory muscle failure: Fatigue or weakness.

National Heart Lung Blood Institute Workshop Summary (1990).

cle training: A report of two

ralorv Di.l'eoses, Bryant, S.,

Chesl, 89. (1),116-124. Cohen,

c.,

Zagei bau 111, G., Gross, D.,

Clinical mani

Medicine, 72, 308-316.

J.,

uation and therapy. Brilish Journal ofAnaeslhesia, 65, 43-53. Respiratory muscle fatigue: report of the respiratory muscle fa

et al. (1982).

festations or inspiratory muscle fatigue. American Journal of Derenne,

46, 688-695.

American Review ofResfliralOry Diseases. 118. 581-60 I.

ea se,

142,474-480.

Pardy, R.L., Rivington, R.N., Oespas, PJ.,

Macklem, P., Roussos, C. (1978). The respiratory

muscles: Mechanics, control, and pathophysiology, Part

tigue workshop group. American Review of Respiralory Dis

III.

&

Macklem, P.T.

(l981a). The effects of inspiratory muscle training on exercise performance in chronic airtlow limitation. American Review of Respiralory Diseases, 123. 26-433.



Patient Education

Alexandra J. Sciaky

KEY TERMS

Education

Methods

Effectiveness

Needs assessment

Health behaviors

Resources

Learning theory

INTRODUCTION

in their care. Unless effective patient education is im

In cardiopulmonary physical therapy, sound treat

plemented this opportunity will be lost.

ment is based on the physiological assessment of the

The overall objective of this chapter* is to provide

patient. Similarly, effective patient education is based

the clinician with an understanding of the principles

on the learning needs assessment of the patient

and practice of effective patient education. To meet

(Rankin & Stallings, 1990). Cardiopulmonary patient

this objective, patient education is defined and perti

education poses a significant challenge because the

nent learning theories with examples of how they re

physical therapist's duties can range from teaching a

late to cardiopulmonary patient education are pre

hospitalized cardiac patient to do a self pulse check to

sented. The learning needs assessment of the patient

designing a series of community-based exercise

is explained, followed by a description of patient edu

classes for senior citizens with emphysema. Meeting

cation methods and materials. Because the effective

this challenge is important because the benefits of pa

ness of patient education efforts are important to

tient education include reduced health-care costs, re

evaluate, ways to determine this are addressed. Fi

duced patient anxiety, increased patient knowledge, satisfaction with care, and incrcased quality of life. In addition, physical therapists share the responsibility

thank Jennifer L. Wai ters, D. Min. and expertise in education and assistanc e man uscri pt

'The author wishes to

with other health-care providers of ensUling that pa

Patricia Wren, MPH for their

tients have the opportunity to make informed choices

in preparing this

.

453


454

PART III


nally, interdisciplinary considerations and educa tional resources are discussed.

Patient Education Objectives I. Enhanced patient-clinician rapport 2. I n creased

DEFINING PATIENT EDUCATION Physical therapists believe that patient education is an i m p o r t a n t part of

p a t i ent

knowledge

of

he alth

disorder/condition

t r e a t m e n t (C h a s e ,

3. Increased adherence to physical therapy treat-

E l k i ns,

ment plant

Readinger, and Shepard, 1993). The teaching role of

4. Decreased health-care costs

the physical therapist has been reported as highly val

5. Increased patient self-efficacy

ued by patients as well (Grannis, 1981). According to

6. Increased ability to make informed health-care

Bartlett (1985), patient education is "a planned learn

choices

ing experience using a combination of methods such as teaching, counseling, and behavior modification techniques which influence a patient's knowledge and health behavior."

patient education program, and finally evaluating its

Several factors make patient education unique when compared with other types of teaching. The pa

effectiveness. Specific examples of patient education learning objectives are listed in the box above.

tient may have limited or no access to the teaching

Achieving these objectives will lead to the enjoy

because of financial and/or geographical barriers to

ment of a host of documented benefits of patient edu

health care. The student may lack a sense of well

cation. These include reduced length of hospital stay

being because of signs and symptoms of an acute ill

(Devine & Cook, 1983), reduced patient anxiety

ness, making learning more difficult. The relationship

(O'Rourke, Lewin, Whitcross, and Pacey, 1990), im

between the teacher and the learner in patient educa

proved health-related knowledge (Rowland, Dickin

tion may be perceived as hierarchical-a medical au

son, Newman, and Ebrahim, 1994), increased quality

thority figure instructing a lay person. The student's

of life (Manzetti, Hoffman, Sereika, Sciurba, and Grif

emotional status may be fearful or anxious, depend

fith, 1994), and improved response to and adherence

ing on the medical situation. There may be superim

with medical treatment (Mazzuca, 1982). Patient edu

posed time constraints, such as length of hospital stay

cation has also been shown to empower patients to

or clinic appointment, which have a direct impact on

take more active roles in their health care (Smith,

patient education. All of these factors may pose barri

1987). Patients who are educated partners in their care

ers to learning. As in other types of teaching, how

are able to be smart consumers in the health-care sys

ever, patient education is information shared in the

tem and adapt more readily to changes in their life

hope that it will not only be understood but applied in

styles resulting from illness.

ways that produce the desired changes in health related behavior.

Learning Theory: Concepts Pertinent to Cardiopulmonary Patient Education

Objectives

The American Physical Therapy Association's Com

The overall objective of patient education is to affect a durable cognitive improvement that results in a pos

mission on Accreditation of Physical Therapy Educa ' tion (1990) requires that the graduate physical thera

itive change in an individual's or group's health be

pist be able to "... apply concepts of teaching and

havior. In many cases the physical therapist must em

learning theories in designing, implementing and

bark on a process to meet this objective in the course

evaluating learning experiences used in the education

of treatment. This process consists of assessing the

of patients." Twentieth century behavioral scientists

learning needs of the patient, identifying measurable,

have developed a variety of learning theories and

realistic objectives, planning and implementing the

models attempting to explain the complexities of


26

human behavior. Subsequent models have

455

Patient Education

pm,, r'(7pf1

address health behavior. Although a

that

discllssion of these models is a list of references for fur

the scope of this

on energy

receives

ther reading may be found at the end of this

conservation techniques from the staff (verbal persua

The discussion of the three theoretical

sion), and notes that oxygen saturation measured 95%

to

which follows is

the clinician

before

with a rationale for patient education practice in terms of its basis in learning

The concepts are

theory, the health-belief

and

the behavior-modification approach, The

theory as

by Ban

in the early are likely t o take a

1950s, theorizes that health action in the

Iieve

that human behavior can be ex-

dura (1986)

state).

The health-belief model, situations:

are at risk of illness;

the disease poses

be-

(I)

they believe that

serious threat to their lives should

they contract it;

they desire to avoid illncss and

believe that certain actions will prevent or reduce the of the a myocardial infarction value in following the exercise pro will attempt to exercise

This

gram

if he or she believes his or her current

life

and

believe that taking than the illness it

the health action is less

self (Roenstock, 1974). This model was originally de veloped in an attempt to understand why

num care or

bers of people failed to accept

poses a threat to health. The

tests for early disease detection. Subse

lieves exercise will reduce that threat (outcome ex

quent studies have used the model to

pectation) and that he or she

ance with

personally

of

betes

the exercise program Outcome and

compli asthma, and dia

for , 1985).

re

The health-belief model conveys that in the con

late to patients' beliefs about their capabilities and

text of health behavior some stimulus or "cue to ac

the

of their behaviors to successful out

comes, In essence

behavior is i nfluenced by

that create expectations for similar out comes over time. environment

a belief in one's ability to attain a certain level of

Bandura terms this

se(refficacy

He argues that percei ved sel f efficacy influences all aspects of behavior including new skills and inhibiting or behaviors,

current

has the

mary determinants:

(I)

cough) or external

structural, of

Once the behavior UUHV,",''''Ull

and social elements are the behavior. In may limit or

unpleasant side

barriers

prevent undertaking the recommended behavior. has its roots

The behavior-modification

four pri refers to

a productive

instructional video tape on

commences, it is understood that many

theory and consists of environmental rewards and

performance accomplish

ments, the strongest

ments in relationship to a specified behavior man, 1993). The theme of this approach

the desired behavior and mastery over the in increased

that an in

dividual's behavior can gradually be

involves learning comes;

necessary to initiate the

pulmonary hygiene

To function competently in a

others,

tion"

process. These cues can be internal

a set

Iy those with

(3) verbal

ical state as it relates to

rewarding out-

and (4) one's physiolog-

program increases a

(1

frequently follows a

plan: "identify the problem; describe the

ability to perform a

task. For example, a pulmonary rehabilitation

t o Becker

behavior-modification

in behavioral terms; select a that is

when he or


behavior

identify the antecedents and conset behavioral

456

PART III


Health Care Contract Date:

_ _ _ _ _ __ __

Contract Goal: (Specific outcome to be attained) I. (client's name), agree to (detailed descriptioll of required behaviors, time and frequency limitations) in retun! for (positive reinforcements contingent upon completion of required behaviors: timing and mode of delivery of reinforcements) I. (provider's name), agrees to (detailed description of required behaviors, time and frequency limitations) (Optional) I, (significant other's name), agree to (detailed description of required behaviors, time and frequency limitations) (Optional) Aversive consequences: (Negative reinforcements for failure to meet Illinium contract requirements). We will review the terms of this agreement, and will make my desired modifications. on (date). We hereby agree to abide by the terms of the contract describe above. Signed: (Client)

_ __ _ _ _ _ __ _ __ _ __ _ _ __ _ ___ _ _ _ _ _ __ _

Signed: (Significant other. if relevant). Signed: (provider)

____ ________ ______ ______ _

_ ___________________ ________ ____

Contract effective from (Date)

to (Date)

_ _______ ____

(From Janz NK, Becker MH, Harlman PE: Parienr Educ COUllS 5(4): 165-178, 1984).

devise and implemellt a behavior change program;

to facilitate the desired behaviors in the patient. Ide

and evaluate the program." This plan is very similar

ally, once the contract expires, the patient feels com

to the approach the physical therapist takes on being

petent and is able to continue the desired behaviors

referred to evaluate and treat a patient. The physical

without the external reinforcements.

therapist identifies the patient's deficits, describes the problem(s) in functional terms, sets short-term and long-term functional goals, designs a treatment plan to meet those goals, implements the treatment

NEEDS-BASED APPROACH TO PATIENT EDUCATION The most important aspect of planning for patient ed

plan and reevaluates the patient. These similarities

ucation is assessing the learners (Kopper, 1987). The

may facilitate the use of the behavioral-modification

process of patient education requires assessment of

approach by physical therapists.

the total patient, including an understanding of the

Health-care contracts can be useful in implement

psychosocial, socioeconomic, educational, vocational,

ing the behavior-modification approach. An example

and cultural qualities of the person (Verstraete and

of such a contract may be seen in the box above. The

Meier, 1973). Assessing educational needs of the pa

contract should be realistic, measurable, and renew

tient allows the physical therapist to determine what

able (Herje, 1980). Specific goals, time frames, be

the patient needs to know to meet the desired cogni

haviors, and contingencies are written in the contract.

tive and behavioral teaching objectives. This assess

The clinician and patient discuss, then sign the con

ment also increases patient-teacher rapport and pre

tract. Positive and negative reinforcements are used

vents needless repetition of already familiar material.


26

LEARNING NEEDS ASSESSMENT

Patient Education

457

Learning Needs Assessment Areas

Tools Perceptual

Learning needs can be assessed in a variety of ways. These include patient and family interviews, ques tionnaires and surveys, written tests, and observation of patient performance (Haggard,

1989). Interviews

allow the physical therapist to ask questions directed at determining the patient's view of the illness, in cluding associated beliefs and attitudes. Question naires and surveys can be used in conjunction with

Ability

to receive input (vision, hearing, and touch)

Comprehension of symbols (figures, numbers, words, and pictures) Cognitive Knowledge and analytical skills Memory Motor

the interview to document the patient's responses to

Fine- and gross-motor skills

specific questions about his or her condition. Open

Physical adaptations and responses to illness or

ended questions such as "What are the major prob lems your illness has caused for you and your fam ily?" elicit more information than a multiple-choice format. Written tests can be helpful in determining what patients already know when the tests are given before any teaching. These tests can also identify problems with reading and comprehension skills. Ob serving patients as they perform a skill, such as di aphragmatic breathing, reveals whether or not the pa tient can demonstrate the correct technique. The physical therapist can also pose questions to the pa tient during the demonstration to determine whether

stimuli Affective Attitudes Value-belief system Motivation (readiness to learn) Environmental Personal and societal resources Amount of instructor contact and setting Cultural influences (language. traditions, roles, religion. and life style)

or not the patient knows the rationale for the exercise. The cognitive area addresses the learner's knowl

Areas to Assess

edge and problem-solving skills. The instructor needs

The learning needs assessment encompasses the fol

to know how much the learner already knows and

(2) cognitive,

what needs to be learned. The instructor also needs to

(3) motor, (4) affective, and (5) environmental (see

know if the learner has any problems with memory.

the box at right). By addressing these five areas, the

Short- or long-term memory deficits may require that

lowing five major areas: (I) perceptual,

physical therapist will obtain an accurate picture of

the instructor integrate a prompting system into the

the patient's learning abilities, knowledge level, per

education plan. The patient's fine- and gross-motor skills and func

formance skills, attitudes, and cultural influences. The perceptual area encompasses the learner's

tional mobility are covered in the motor area. The in

ability to receive information via the senses. If the

structor needs to be aware of the physiological

learner's sight, hearing, or sensc of touch is impaired,

changes in the patient that affect abilities to perform

the instructor may need to makc modifications so that

activities necessary for a given education program.

the information can be received by the learner. The

For example, if a support group is being held in a

comprehension of symbols. such as numbers, words,

room that is not wheelchair accessible, patients who

or pictures. also needs to be assessed in the percep

are wheelchair users will not be able to readily attend.

tual area. The instructor nceds to know what meaning

The affective area comprises the learner's attitudes,

the learner attributes to the symbols that will be used

beliefs. and readiness to learn. Identifying the learner's

in the education program to ensure clarity.

value-belief system will assist the instructor in deter


458

PART III


Learning Needs Assessment Survey Your physical therapist would like to help you learn what you need to know to function as independently as possible and manage your illness/disability. Please answer the following questions to identify your own needs. Part I. Name: Your illness and/or disabi Iity is:

J.

Do you have any problems seeing

2.

Do yu have any body areas which are numb (can't feel)?

or

hearing?

3.

How long have you had this illness/disability?

4.

What problems has it caused you?

5.

Are you able to care for yourself at home?

6.

Are you responsible for the care of any others at home?

7.

Do you have someone at home to help you? If so, whom?

8.

What questions or concerns do you have?

9.

Do you practice a religion? If so, which?

10. The language you understand best is? I I. How much education/schooling have you had? Part II. There are many different ways to learn. Please read the list of ways to learn below and circle the ones which help you learn best. Group discussion

Reading materials Lectures (listening)

By myself

Demonstrations watching)

Games

Videos

Computer programs

Audiotapes (cassettes)

Seminars

Practice/Stimulation (doing)

Role playing

Written tests

Other

Part III I would like to know more about: (Check all that apply to you.) How to clear mucus from my lungs

What causes heart disease

How to avoid shortness of breath

What I should eat

Exercise

My medications

Monitoring myself

Planning my social life

What to do if I have chest pain

Planning for sexual intimacy

What causes lung disease

Coping with my feelings

Other things J would like to know: The three most important things I need to know are:


26

Patient Education

459

mining what is important to the learner and facilitate

learning activities. By identifying the patient's needs

motivation. What the instructor feels is important to

the physical therapist can then make informed

learn may not be what the patient feels is important to

choices in the course of planning and implementing

learn. Identifying what the patient values early will

each patient education experience.

prevent instructor (and patient) frustration later. Cultural influences and personal and societal re sources are included in the environmental area. Being aware of the patient's life style, religion, traditions,

Formulation and Prioritization of Goals As physical therapists set treatment goals for their pa

roles, and primary language are important for the in

tients, they should also set educational goals. Treat

structor to assess to individualize the patient's learn

ment goals usually describe functional outcomes

ing experience. Presence or absence of the patient's

(e.g., the patient will perform a stand and pivot trans

resources may affect consistency in and access to pa

fer from bed to chair, i ndependently) and they are

tient education.

written in behavioral terms. Educational goals should

All five of these areas can be addressed with the

also be written in behavioral terms. For example,

use of a learning needs assessment survey. See Figure

"Mr. J will safely perform percussion and postural

26-2 for an example. By using a survey in combina

drainage to Mrs. J's right lower lobe." The stated be

tion with the physical therapy patient evaluation, the

havior needs to be measurable in some way. Motor

therapist can gather all the necessary information to

skills can be observed, knowledge skills can be

create an optimal patient education experience. The

tested, and safety can be documented.

survey in the box on p. 458 consists of three parts,

Prioritizing the patient's educational goals in con

which can be adapted to any patient-care setting. In

junction with treatment goals enhances the therapist's

the pediatric setting, some of the questions could be

efficiency. Referring again to the learning needs as

asked of the parent(s) or rephrased to address elemen

sessment survey (see the box on p. 458) to determine

tary-school-aged children. Part I primarily assesses

what is important knowledge to the patient will guide

the patient's perception of the illness or disability and

the therapist in creating the most appropriate prioriti

its impact on the patient's life. Part II lists a wide va

zation of goals. Simplicity is usually best. Over

riety of teaching methods and asks the patient to indi

whelming patients with a huge list of items to be ac

cate which methods are most useful personally. Part

complished may discourage them before they even

III identifies specific topics about which the patient

start. If the patient's learning needs are very great,

would like to know more. This part is also helpful in

start by breaking down the list of goals into smaller

alerting the therapist that referrals to other members

groups. Choose the most important goals and try to

of the interdisciplinary health-care team may need to

accomplish them first. If you run into a series of fail

be made. For example, if the patient checked off

ures, tackle the next group. Build on each success the

"what I should eat," the therapist should make a re

patient experiences.

ferral to the dietician.

EDUCATIONAL METHODS Interpretation of Findings

.

Method Selection

The next important step after gathering information

Using the learning needs assessment survey (see the

with the learning needs assessment survey is to inter

box on p. 458) will allow the clinician to choose edu

pret the findings. The physical therapist must look at

cation methods that will facilitate optimal learning in

the answer to each item on the survey and use that in

a given patient or group. The patient(s) can self-select

formation in the process of designing the content and

the available learning methods that have the greatest

method for teaching that patient. Interpretation of the

learning potential. A combination of methods may be

survey findings means applying the patient's current

necessary to achieve the educational goals that have

health concerns and knowledge deficits to future

been set. If a patient is not sure which methods to in


460

PART III


dicate, the therapist can base the choice on the other

therapist in determining the settings and populations

information provided in the survey (e.g., sensory

in which the methods will be most useful. This is not

deficits, level of schooling, or type of information de

a comprehensive list. In fact, some health-education

sired). Surveys generally require regular updates to

challenges require truly innovative approaches.

ensure that all of the offered methods are listed and the discontinued methods are removed from the list.

In 1988, for example, community health-care providers in Boston were faced with a dilemma. The incidence of acquired immune deficiency syndrome (AIDS) among women of color was increasing and

Advantages and Disadvantages

Latino, African-American, and Haitian women were

Each education method has its own advantages and

not receiving vital information about how to prevent

disadvantages. Table 26-1 shows 13 education meth

the transmission of the human immunodeficiency

ods listed with their key advantages and disadvan

virus (HIV). These communities were largely dis

tages. The table is designed to assist the physical

trustful of the health-care establishment and were not

TABLE 26-1

Comparison Chart for Education Methods (Adult'i and children unless otherwise noted) TYPE

ADVANTAGES

DISADVANTAGES

Reading

Patient can refer back to material.

Requires instlUctor follow-up for comprehension.

Low effort for instructor. Lecture

Time-efficient for instructor. Cost-efficient.

Low interaction. May pacify rather than engage.

Demonstration

Adds sensory data to learning. Allows for

Instructor needs proficiency in skill to be

problem solving and modification. Video

Access to restricted areas. Portrays events that are infrequent, costly, and difficult to reproduce. Portable.

demonstrated. Noninteractive. May pacify rather than engage. Costly, requiring electronic equipment. Difficult to control quality.

Audiotape

Portable. Useful for sight-impaired learner.

Requires electronic equipment.

Group discussion

Effective use of instructor time. Enlarges pool

Not as much individual attention given. Group

Clubs, camps, and retreats Individual instlUction Games and directed activities

of real-life experiences. Nonthreatening to

may be hard to control (e.g., too talkative,

some learners. Mutual support possible.

shy,hostile). Strong facilitator skills needed.

Draws on community and individual resources. Needs less professional input and time. Instructor can tailor learning to student's needs and desires. More one-on-one time. Helpful for children. Reduccs anxiety. Uses

Same as above. Some risk of perpetuating myths and false information. Inefficient use of instructor time. Limited pool of experience on which to draw. Scheduling space. Finding participants.

repetition. Fun. Unexpected experiences can lead to new understandings or insights.

Computer programs

Interactive, self-paced. Large information capacity. Time-cfficient for instructor.

Seminars and workshops

Diversity of instructors and formats. Pool

Expensive. Special equipment and space needed. May require expert help. Expense, scheduling, and space.

of expel1s and community resources. Can tailor content broadly or narrowly.

Role-playing

Trial runs, problem-solving, simulated

Threatening to some. Can be time-consuming. Instructor needs to be skilled in techniques and

experiences.

dealing with effects on participants. Oral and written tests

Can provide instructor with evidence of what learner needs to be taught and what has been learned.


Literacy and supplies required, if written. May be time-consuming.

26

mobilized to stop the spread of HIV. How could they be reached? The Boston Women's AIDS Information Project (BWAIP) trained lay women to educate other women in the places where they congregate, such as beauty salons. Informational brochures, condoms, and posters were distributed in a number of beauty salons in communities where women were at highest risk for contracting HIV. Lay and professional educa

Patient Education

Cardiopulmonary Patient Education Content Smoking cessation

Risk-factor modification Benefits and effects of exercise Resumption of sexual activity Normal cardiopulmonary anatomy and physiology

tors would give presentations, show videos, and an

Cardiopulmonary disease process

swer questions of the staff and patrons of these estab

Airway clearance techniques and suctioning

lishments to empower them to disann myths about

Energy conservation and pacing techniques

AIDS, encourage other women to make appropriate behavior changes, and to make referrals to neighbor hood health centers for testing and evaluation. Teaching young children about their bodies and health may also require unique approaches. In 1993, members of the interdisciplinary team caring for chil

461

Stress management Cardiopulmonary resuscitation (CPR)-basic life support Hemt rate, blooo pressure, and dyspnea self-monitoring Nutrition

dren with cystic fibrosis (CF) at Texas Children's Hos

Medications (schedules. actions, and side effects)

pital, Houston, held a CF Education Day for the chil

Use of oxygen and other respiratory equipment

dren and their parents. The children ranged in age from

Medical procedures (e.g., cardiac catheterization or

7 to .1 I years old. To teach them about anatomy, a spe

cial anatomy apron was fabricated. The apron had life sized removable "organs" made of stuffed fabric. The children took turns wearing the apron and learned to

bronchoscopy) Community resources Emergency procedures

identify and locate the organs by removing and replac ing the apron's heart, lungs, intestines, and pancreas. By evaluating the advantages and disadvantages of available education methods, the physical therapist can choose the methods that are most effective and

education experience. Although the physical thera

use them to their best advantage. Consideration must

pist may not be responsible for teaching on all these

be given for cost, equipment, scheduling, labor, time,

topics, she or he should be familiar with them as

site, flexibility, and reusability. For example, video

they are taught by others on the health-care team.

taped presentations may be easy for the instructor to

Educational materials on all of these topics have al

schedule, present, and reuse but they can be costly to

ready been developed by a variety of health-care

purchase and require expensive equipment to view.

providers, educators, and organizations and may be available for physical therapists' use (see "Interdis ciplinary Considerations and Resources").

Content The specific content of patient education materials and programs should be determined by the needs of

DETERMINATION OF EFFECTIVENESS

the individual or group being taught. However, there

Determining the effectiveness of patient education ef

are topics common to many cardiopulmonary educa

forts involves evaluating not only what the patient

tion efforts. These topics are listed in the box above.

learned but also how the teacher taught. Sometimes

The physical therapist can use the topics listed in

patients learn in spite of educational efforts. As phys

the table as a checklist to explore the content cov

ical therapists, we need to examine how effective we

ered (or to be covered) in a given cardiopulmonary

are at teaching and strive to improve our teaching


462

PART III


skills just as we strive to improve our treatment

sition the woman without disturbing the many tubes

skills. Being able to communicate ideas and receive

and lines that were present. Later the woman ex

feedback from patients from diverse racial, ethnic,

pressed that she did not want to have two physical

vocational, religious, and generational backgrounds is

therapy clinicians working with her at the same time.

crucial for physical therapists. We develop rapport

She confided to the nurse that it was because she felt

with our patients by communicating to them that we

it was too much like the Jewish ritual washing of the

have an understanding of their illnesses or disabili

body after death, which is traditionally pelformed by

ties, as they perceive them, and that we plan to inte

two people. This interpretation of the therapy sur

grate their goals or priorities into the treatment plans.

prised the physical therapy staff members who treated the woman because they were also Jewish and the thought never occurred to them. The next time tl1e

Teacher-Learner Relationship

clinicians went to see the woman, they explained why

According to Locke (1986), the primary step to under

it was necessary for both of them to be present during

standing others, is an awareness of one's self. Ac

the treatment. They also encouraged the woman to

knowledging one's own personal values, interests, and

have other supportive people present and to play her

biases will significantly increase one's sensitivity to

favorite recorded music during the therapy session.

ward others. The skilled teacher is aware of her or his own communication style and its limitations and can convey the desire to help despite those limitations. The teacher-learner relationship that develops be

Patient Adherence The effectiveness of physical therapy treatment, or

tween physical therapist and patient largely is due to

of any medical treatment, depends on the patient

communication between the two in the context of

following the health-care provider's recommenda

culture. Communication is a two-way process con

tions (adherence.) Unfortunately there is often a gap

sisting of verbal and nonverbal messages. The inter

between what the patient is asked to do and what the

pretation of these messages depends on the cultural

patient actually does. This gap, or nonadherence,

cues operating in the educational setting. Fairchild

has an incidence rate estimated between 50% to

(1970) defines culture as all social behavior, such as

80% (Meichenbaum and Turk, 1987). Factors af

customs, techniques, beliefs, organizations, and re

fecting patient adherence include knowledge of and

gard for material objects, including behaviors trans

course of the illness, complexity of the recommen

mitted by way of symbols. "The primary mode of

dations, convenience, availability of support system,

transmission of culture is language, which enables

and the patient's beliefs.

people to learn, experience, and share their traditions

Patient education can improve adherence when the

and customs" (Locke, 1992). In addition, culture can

information given includes what behaviors are ex

be expressed or experienced via economic and politi

pected, when they should be performed and what to

cal practices, art, and religion. Health care and medi

do should problems mise. Plans for patient education

cine have their own cultures. To meet the needs of

sessions should strive to remove or avoid barriers to

culturally diverse populations and engage in positive,

patient adherence. These efforts include simplifying

productive relationships, physical therapists need to

and individualizing treatment regimens, fostering col

operate from a framework of cross-cultural under

laborative teacher-learner relationships, enlisting

standing. This understanding and knowledge can then

family support, making use of interdisciplinary and

be reflected in patient education efforts.

community resources, and providing continuity of

For example, in a large, urban, acute-care hospital

care (Meichenbaum and Turk, 1987). By using an ap

two physical therapy staff members were working to

proach that integrates these efforts, the physical ther

gether to treat an elderly Jewish woman who was

apist can optimize patient adherence to the prescribed

critically ill. The clinicians worked carefully to repo

physical therapy program.


26

INTERDISCIPLINARY CONSIDERATIONS AND RESOURCES

Patient Education

463

Health-related organizations can also be rich re sources for patient education information. The Amer

The interdisciplinary health-care team has evolved as

ican Heart Association and the American Lung Asso

the complexity and amount of available medical

ciation, for example, have many cardiopulmonary

treatments and information has grown. Physical ther

materials available to health-care providers for little

apists are trained to function as part of an interdisci

or no cost. State public health and local community

plinary team and are respohsible for learning the

service agencies may also be sources for printed or

areas of responsibility and expertise covered by each

audiovisual materials. The Health and Human Ser

member of their team. The team often consists of li

vices Department of the Federal government has nu

censed and nonlicensed health-care providers and

merous divisions addressing health education. Cata

may include any or all of the following:

logs listing these publications can be obtained from

Physician

the Federal Consumer Information Center, Pueblo,

Nurse

Colorado

Physical therapist

81009.

Community organizations such as YMCA, YWCA,

Occupational therapist

and the American Red Cross offer a wealth of health

Exercise physiologist

education materials and classes. Many of these agen

Dietician

cies also have catalogs of their educational offerings,

Laboratory technologist

which can be obtained by telephoning their local of

Pharmacist

fices. Local public, medical, and hospital libraries are

Social worker

also useful for seeking out available health-education

•

Chaplain or pastoral care associate

materials. Many Chambers of Commerce keep lists of

•

Clinical psychologist

local support groups or clubs, such as Breather's Club

•

•

Speech therapist

or Heartbeats. Regional state colleges or universities

•

Vocational rehabilitation counselor

have departments dedicated to health education and

Home-care personnel

may have cardiopulmonary materials to share.

•

All of the above providers may not be present on every team, but their services should be available for patients who need them. By understanding what ser

SUMMARY

vices and patient education material are provided by

This chapter defined patient education and described

each discipline, the physical therapist can reinforce

selected learning theories as they relate to cardiopul

previously presented concepts and avoid giving con

monary patient education. The evaluation of the pa

flicting information. This also allows the physical

tient's learning needs was emphasized and the advan

therapist to make referrals to the appropriate disci

tages and disadvantages of a variety of educational

pline when other knowledge deficits are identified.

methods were discussed. The role of the teacher-learner

Interdisciplinary team members can also provide

relationship and patient adherence were explained in

the physical therapist with important patient feedback

reference to the determination of patient education and

and information. Teaching methods found to be suc

treatment effectiveness. Finally, interdisciplinary

cessful with a given patient by the nurse, for exam

health-care team interactions and resources for patient

ple, could be communicated to the physical therapist.

education materials were considered.

The therapist can then use similar methods with that patient for physical therapy education objectives. Communication between team members is enhanced

REVIEW QUESTIONS

by regular team meetings or rounds and by having a

I. Discuss the benefits of patient education, includ

central location to document completed patient edu

ing impact on health care costs and patient's re

cation experiences (i.e., the medical record).

sponse to treatment.


464

PART III


2. Define the overall obj ective of patient education

Liedekerken, P.e., Jonkers,

ways to minimize them. 3. Explain the rationale for patient education using concepts of adult learning theories or models.

R.,

DcHaes. W.F., Kok, G.1., & Saan,

J. (Eds.) (1990). Effecti veness of healrh education: review alld

and discuss the potential barriers to learning and

analysis. Assen, Netherlands: Van GorcllJn. Locke, D.e. (1992). Increasing multicultural IJIlderstandillg: a comp rehensive lIIodel. Newberry Park: Sage Publications. Locke, D.C. (1986). Cross-cultural counseling issues. In A.J. Palmo & W.J. Weikel et al (Eds.), Foundations of Ille II ta I

4. Describe the most important aspect of planning

health counseling. Springfield, IL: Charles

for patient education. S. Discuss the components of a learning needs as

e.

Thomas.

Manzelli, J.D., Hoffman, L.A., Sereika, S.M., Sciurba, F.e., & Griffith, B.P. (1994). Exercise, education, and quality of life in

sessment survey and ways to modify it for spe

lung transplant candidates. Journal of Heart and Lung Trans

cific patient populations.

plantation. 13(2),297-305. Mazzuca, S. (1982). Does patient education in chronic disease have therapeutic value.

References Bandura. A. (1986). Foundations of thought and action: a social cognitive theOl)'. Englewood Cliffs, NJ: Prentice-Hall.

herence: a practitioner's guidebook. New York: Plenum Press. M. (1982). Health beliefs of and adherence to the medical regi men by patients with ischemic heart disease. Heart Lung,

havioral change. Psychological RevielV, 84(2), 191-215.

7. 323-324.

O'Rourke, A , Lewin, B., Whitcross, S., & Pacey, W. (1990). The effects of physical exercise training and cardiac education on

Becker, M.H. & Janz, N.K. (1985). The health belief model ap

levels of anxiety and depression in the rehabilitation of CABG

plied to understanding diabetes regimen compliance. Diabetes Education, 11,41-47. Becker, M.H. (1990). Theoretical models of adherence and strate gies of improving adherence. In S.A. Shumaker. Schron, E.R. & Ockene, J.K., (Eds.), The handbook af h ealth behavior change (pp. 26-27). New York: Springer Publishing. Chase, L., Elkins. J.A., Readinger, J., & Shepard, K.F. (1993). Per ceptions of physical therapists toward patient education. Physi cal Therapy.

73( 11),787-95.

Commission of Accreditation of Physical Therapy Education.

(1990). Evaluative criteria for accreditarion of educational

patients. Imernorional Disability SlUdie.\', 12(3),104-6. Pohl, M.L. (1968). Teaching function of the nl/rse practitioner. Dubuque, IA: Brown. Rankin, S.H., & Stallings, K.D. (1990). Patient education: issues, principles and pracrices. (2nd Mosby. model. Health Education Monogrophs.

Fairchild,

H.P.

exercise knowledge, attitudes and behavior of retired women in England. Joumal of Epidemiology and Comlllunity Health

H aggard,

Physical Therapy, 61. 479-86.

Smith, e.E. (1987). Nurses' increasing responsibility for patient education. In e.E.

Herj e, P.A.

5. 30-34.

Hoffman, S. (1987). Planning for patient teaching based on learn

FL:

Grune & Strarton. Verstaete, M., & Meier, M. (1973). Patient education in

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health

sciences center. Minnesora Medicine, 56(2), 31-35.

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cognitioll ro behavior (pp.

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(Ed.), Patient education: nurses ill

Publishers.

(1980). Hows and whys of patient contracting. Nursing

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A. (1989) Handbook of parient education. Rockville,

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Grannis, e.J. (1981). The ideal physical thera pist as perceived by

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Rowland, L. Dickinson, E.T., Newman. P., & Ebrahim, S.

Devine, E., & Cook, T. (1983). A meta-analysis of effects of psy

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Redman, B.K. (1993). The process of patient educatioll. SI. Louis:

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decade later. Health Educalion Quarlerly, II, 1-47, Leventhal, H., Meyer, 0, & Gutman, M, (1980), The role of theory in the study of compliance to high blood pressure regimens, In R,C, Haynes, ME Matlson, & T,O, Engebretson, Jr. (Eds),

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(1986), The role of self-efficacy in achieving health behavior change, Health Education Quarterly, 1373-92,

10


PART

IV

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions


Acute Medical Conditions

Elizabeth Dean Willy E. Hammon Lyn Hobson

KEY TERMS

Acute exacerbations of chronic

Cystic fibrosis

airflow limitation

Hypertension

Alveolar proteinosis


Alveolitis

Pneumonia

Asthma

Stable angina

Atelectasis

Stable myocardial infarction

Bronchiolitis

Tuberculosis

Bronchitis

INTRODUCTION

circulation to effect cardiac output and tissue perfu

The purpose of this chapter is to review the manage

sion (Dantzker, 1983; Dantzker, 1988; Scharf and

ment of primary cardiopulmonary dysfunction sec

Cassidy, 1989; Wasserman and Whipp, 1975). Thus

ondary to other medical conditions. Several types of

impairment of one organ inevitably has implications

medical conditions are presented to illustrate the prin

for the function of the other organ. In addition, threat

ciples and basis for cardiopulmonary physical therapy

to or impairment of oxygen transport has implications

in their management. These principles serve as a

for all other organ systems, thus a multisystem ap

guide to problem solving when the practitioner is con

proach is essential (see Chapters I and 5). The pri

fronted with pathologies that are not presented. Al

mary pulmonary conditions that are presented include

though conditions are usually classified as either pri

atelectasis, pneumonia, bronchitis, bronchiolitis, alve

mary lung disease or primary cardiovascular disease,

olitis, alveolar proteinosis, acute exacerbations of

the heart and lungs work synergistically to effect gas

chronic airflow limitation, asthma, cystic fibrosis, in

exchange and in series with the peripheral vascular

terstitial pulmonary fibrosis, and tuberculosis. For fur 469


470

PART IV

Guidelines for the Delivery or Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

ther epidemiological and pathophysiological detail on

have reduced lung volumes and are prone to breath

these conditions refer to Bates (1989), the Epidemio

ing at low lung volumes and microalelectasis, requir

logical Standardization Project of the American Tho

ing prophylactic measures to avoid significant effects

racic Society (1989), Luce (1986), Murray and Nadel

of atelectasis on oxygen transport and gas exchange.

(I 988a), Murray and Nadel (1988b), and West (1987).

When the conditions for normal lung inflation are re

The primary cardiovascular conditions presented in

moved, alveolar collapse occurs instantaneously.

clude hypertension, medically stable angina, and un

Microatelectasis is associated with reduced lung

complicated myocardial infarction. For further details

compliance because of reduced lung expansion. Me

on these condi tions refer to Goldberger (1990),

chanically ventilated patients are prone to microat

Sokolow, McIlroy, and Cheitlin (1990), and Under

electasis because the normal mechanics of breathing

hill, Woods, Froelicher, and Halpenny (1989).

are violated. In part, this may be explained by re

Treatment principles are presented that are not in

stricted mobility, recumbency, and reduced arousal,

tended to be a treatment prescription for a particular

in addition to reduced functional residual capacity

patient. The treatment priorities are presented based

(FRC). Positive end-expiratory pressure (PEEP) is

on the underlying pathology. However, without dis

routinely added to minimize these effects. High ven

cussion of a specific patient and knowledge of other

tilator system pressure is required to counter reduced

significant factors (i.e., the effects of restricted mobil

lung compliance, which indicates that atelectatic lung

ity, recumbency, and the effects of extrinsic and in

tissue it not readily reexpandible.

trinsic factors) (Chapter 16), the specific parameters

Microatelectasis is not detected readily with chest

of the treatment prescription cannot be established.

x-ray but is on the basis of clinical findings. Nonethe

Integration of this information is essential for treat

less, microatelectasis can be anticipated in every ill

ment to be specific and maximally efficacious. For

and hospitalized patient whose normal respiratory me

specific examples of patient treatment prescriptions

chanics are disrupted, and particularly, in recumbent,

refer to the companion text Clinical case studies in

relatively immobile patients. These effects are further

cardiopulmonary physical therapy.

exacerbated in older patients, patients who are over weight, have abdominal masses, spinal deformities, or chest wall asymmetry, smokers, and sedated patients.

Atelectasis Pathophysiology and medical management

Commensurate with its distribution, atelectasis presents with reduced chest wall movement and re

A t e l e c t a s i s refers to p a r tial collapse of lung

duced breath sounds over the involved area. A chest

parenchyma. The pathophysiological mechanisms

x-ray shows increased density over the involved areas

contributing to atelectasis are multiple (see box on

with a shift of the trachea and mediastinum toward

p. 471). These mechanisms include physical compres

the collapsed lung tissue. The patient may be tachyp

sion of the lung tissue (e.g., resulting from increased

neic and cyanotic because of shunting. Segmental at

pleural fluid, pus, pneumothorax, or adjacent areas of

electasis results from significant progression of mi

lung collapse) or from an obstructed airway (e.g., se

croatelectasis and by obstruction of airways with

cretions or tumor) with subsequent reabsorption of

resorption of gas in the distal lung units of a bron

oxygen from the trapped air by the pulmonary capil

chopulmonary segment or lobe.

laries resulting in a collapse of the lung tissue distal to the obstruction (i.e., reabsorption atelectasis).

The ventilator-dependent patient is predisposed to developing atelectasis because of an unnatural, mo

There are two primary forms of atelectasis-mi

notonous breathing pattern, restricted movement, and

croatelectasis and segmental and lobar atelectasis.

abnormal and prolonged recumbent body positions.

Microatelectasis is characterized by a diffuse area of

These factors contribute to reduced mucociliary trans

lung units that are perfused but not ventilated, hence,

port, abnormal distribution of pulmonary mucus, and

right-to-Ieft shunt. III and hospitalized patients who

the accumulation of mucus in the dependent lung

are deprived of being regularly upright and moving

fields. Furthermore, production of mucus may be in


Pathophysiological Mechanisms Contributing to Atelectasis Central Mechanisms Breathing at low lung volumes (e.g., when in pain or after certain medications) Inability to gcnerate adeljuate inspiratory pressure and volume Central disruption of breathing centers controlling normal periodic and rhythmic breathing pattern Extramural Mechanisms Chest wall deformity Asymmetry of intrathoracic ,tructures Respiratory muscle weakness (e.g., neuromuscular disease) Phrenic nerve inhibition (e.g., secondary to upper abdominal or cardiovascular thoracic surgery) Compression of lung parenchyma secondary to pleural tluid accumulation, blood, plasma. and pus

Compression of lung parenchyma during surgery Reduced lung expansion secondary to reduced movement Compression of lung parenchyma secondary to static body positioning Compression of lung parenchyma secondary to prolonged static body positioning Mechanical ventilation Increased alveolar surface tension Mural Mechanisms Airway narrowing seconuary to increased bronchial smooth muscle tone Calcification or altered anatomical integrity of airways Edema of the bronchial wall and epithelium Intramural Mechanisms Impaired mucocilial'Y transport Increased pulmonary secretions Inspissated pulmonary secretions Altereu distribution of pulmonary secretions

Mucolls plug Space.Occupying Lesions Exuuative and transudative tluid in the lung parenchyma Foreign-bouy aspiration Intlammation Other Factors Increased compliance and dynamic airway compression secondary to age-related changes to the lung Increaseu timc constants because of increased airway resistance. reduced compliance. or both Splinting or casting of chest wall restricting normal three-dimensional chest wall movement Pain anu altered breathing pattern Medications including narcotics, sedatives, and relaxants Oxygen


472

PART IV


creased due to tracheostomy or the presence of an

these interventions distributes ventilation more uni

endotracheal tube. Mucociliary clearance is further

formly rather than directing gas to already open alve

compromised by reduced ciliary activity resulting

oli, which will overdistend these units. The distribu

from high concentrations of oxygen, medication,

tion of ventilation is primarily altered by body

and loss of an effective cough because of an artifi

positioning and not by deep breathing (Roussos, Fix

cial airway.

ley, Geriest, Cosio, Kelly, Martin, and Engely, 1977).

The effect of atelectasis on oxygen transport re

Sustained maximal inspiratory efforts may augment

flects its type and distribution. Hypoxemia, right to

alveolar ventilation, however, the parameters for such

left shunt, reduced lung compliance, and increased

efforts to be maximally therapeutic have not been

work of breathing are common clinical manifesta

studied in detail.

tions. An increased temperature reflects an inflamma tory or infective process and not atelectasis per se.

Principles of physical therapy management Because it can develop instantaneously when respira tory mechanics are disrupted, microatelectasis should

If impaired mucociliary transport or excessive secre tions are obstl1lcting airways and contributing to atelec tasis, mobilization of pulmonary secretions is the goal that may be affected by mobilization and a "stir-up reg

1941; Ross and Dean, 1989). In addition, postural drainage coordinated with imen" (Dripps and Waters,

be anticipated and prevented. Those factors that con

breathing control and coughing maneuvers can facili

tribute to atelectasis for a given patient are countered

tate airway clearance. The addition of modified manual

accordingly with aggressive prophylactic manage

techniques may be indicated in some patients.

ment (see the box on p.

471).

Once developed, however, atelectasis is treated aggressively. Treatment is primarily directed at re versing the underlying contributing mechanisms whenever possible (Don, Craig, Wahba, and Couture,

1971; Glaister, 1967; Leblanc Ruff, and Milic-Emili, 1970; Lewis, 1980; Ray, Yost, Moallem, Sanoudos, Villamena, and Paredes, 1974; Remolina, Khan, San tiago, and Edelman, 1981). For example, atelectasis

Pneumonia Pathophysiology and medical management Pneumonia is a common cause of morbidity and mor tality in the hospitalized patient, particularly in very young and very old patients (Bartelett and Gorbach,

1976). Comparable wi th other systemic infections, pneumonia results when the normal defense mecha

resulting from restricted mobility is remediated with

nisms of the respiratory system fail to adequately

mobilization. Atelectasis resulting from prolonged

protect the lungs from infection.

static positioning and monotonous tidal ventilation is

Air inspired through the nasal passages is cleansed

managed with mobilization, manipulating body posi

of particulate matter by filtration (cilia sweep it to the

tion to increase alveolar volume of the atelectatic

nasopharynx); impaction (irregular contour of the

area, manipulating body position to optimize alveolar

chamber causes particles to rain out); swelling of hy

ventilation, or some combination of these interven

groscopic droplet nuclei, which are either filtered or

tions. Atelectasis arising from reduced arousal is

become impacted; and defense factors located in the

managed by reducing the causative factors contribut

mucous blanket, such as immunoglobulins (IgA),

ing to reduced arousal coupled with frequent sessions

Iysozymes, polymorphonuclear leukocytes, and spe

of mobilization and the upright position to increase

cific antibodies. Particles that escape one of these de

arousal, promote greater tidal volumes and alveolar

fense mechanisms in the nasopharynx may be pre

ventilation, increase zone 2 (area of optimal ventila

vented from entering the lower airways of the larynx.

tion and perfusion matching), increase FRC, and min

The mucosa of the larynx is sensitive to chemical irri

imize closing volume.

tation or mechanical deformation and responds to this

Breathing control and coughing maneuvers aug

stimuli by producing a cough. The high velocities

ment the cardiopulmonary physiological effects of

created by the cough are sufficient to clear several

mobilization and body positioning. Coordinating

branches of the tracheobronchial tree of particulate


27


473

matter. The cough reflex is frequently absent or de

common cold. The ciliated cells of the respiratory

pressed in hosts who are unconscious from drug

tract are the most frequent site of infection. They be

overdose, epilepsy, alcohol ingestion, or head injury.

come paralyzed and degenerate with areas of necrosis

Patients with artificial airways are more susceptible

and desquamation. The mucociliary blanket becomes

to infection because all the previously mentioned de

interrupted because destruction of the cilia leaves a

fense mechanisms are bypassed, causing organisms

thin layer of nonciliated basal replacement cells. In

to be deposited directly in the lower airways. In the

flammatory responses cause exudation of fluid and

lower airways the cough mechanism is rendered inef

erythrocytes in both the alveolar septae and airways.

fective by endotracheal tubes, which prevent approxi

Congestion and edema become predominant with the

mation of the vocal cords, and by tracheostomy

formation of intraalveolar hyaline membranes. These

tubes, which cause air to bypass the cords altogether. The trachea and the tracheobronchial tree to the

changes in the normal mucosal structure and cilia make involved areas of the lung susceptible to super

level of the respiratory bronchioles are protected by

imposed bacterial infections. This is the most com

the cough reflex, filtration (again by cilia which

mon complication seen in viral infections and is usu

transport particles to the pharynx), impaction, and

ally responsible for the fatalities that occur.

chemical factors (IgA). Below the level of the respi

The patient with viral pneumonia presents with

ratory bronchioles, the cough reflex is ineffective,

fever, dyspnea, loss of appetite, and a persistent non

and filtration and transportation of particles by cilia

productive cough. On auscultation, normal breath

cannot occur because cilia are absent. The alveolar

sounds are heard throughout both lung fields with

macrophages play an important role in protecting

scattered inspiratory crackles. X-ray changes range

these airways from particulate matter. Macrophages

from minor infiltrates to severe bilateral involvement.

ingest organisms and transport them to the lymphatic

Consolidation and pleural effusions occur less fre

system or higher in the tracheobronchial tree to

quently. Secondary bacterial infections occur fre

where cilia can sweep them to the pharynx. This

quently, causing patients to develop productive

process of phagocytosis can be slowed or stopped by

coughs.

hypoxia, alcohol ingestion, air pollutants, corticos

Influenza may lead to viral pneumonia in I % to

teroids, immunosuppressant agents, starvation, ciga

5% of cases. Influenza includes acute viral respira

rette smoke, and oxygen. Particulate matter may also

tory tract infection, characterized by a sudden onset

be removed from the airways below the level of the

of headache, myalgia, and fever. The route of infec

respiratory bronchioles by postural drainage.

tion is by inhalation of airborne particles from an in

Routes of Infection

hours.

A host who has impaired or ineffective defense

tory epithelium with necrosis and hemorrhage. At the

fected person. The incubation period is 24 to 72 Pulmonary lesions include edema of the respira

mechanisms of the respiratory tract becomes suscep

alveolar level, interstitial edema, proliferation of type

tible to a variety of organisms. The major routes of

I cells, hemorrhage, and an increased number of

infection include airborne organisms, circulation,

macrophages are seen. In patients with pneumonia,

contiguous infection, and aspiration.

secondary bacterial infections are frequent and are the cause of most fatalities. Medical treatment of viral infections is supportive

CLASSIFICATION OF PNEUMONIA Viral Pneumonias

and preventative. Patients should receive vaccines

Most respiratory viral infections are contracted by

cific viruses. Once the patient has contracted the or

droplets from the respiratory tracts of infected per

ganism, treatment becomes supportive, with rest, sali

whenever possible to buildup antibodies against spe

sons. These viruses are responsible for interstitial

c y lale s , and high f luid intake b e i n g the m a i n

pneumonias, tracheobronchitis, bronchiolitis, and the

treatment priorities. Patients w h o become more


474

PART IV


acutely ill with viral pneumonia should be on a vigor

illness characterized by fever, tachypnea, dyspnea, hy

ous preventative program to lessen the possibility of

poxemia, tachycardia, and a cough producing bloody

bacterial infection.

or purulent sputum. The clinical findings depend on

Recovery also depends on good nutrition, hydra

the organism involved and the extent of the pneumo nia in the lungs. The infective process may cease with

tion, sleep, rest, and reduced stress.

Principles of physical therapy management Patients may respond to mobilization coordinated

the use of chemotherapeutic agents, aerosols, and physical therapy, or it may spread to contiguous areas, causing pleural effusions and empyemas.

with breathing control exercises and positional rota

Bacterial pneumonias can occur as either primary

tion for enhancing alveolar ventilation, mucociliary

or secondary infections. Primary pneumonias arise in

transport, and gas exchange overall (Orlava, 1959).

otherwise healthy individuals and are usually pneumo

Extreme body positions may enhance alveolar volume

coccal in origin. Secondary pneumonias occur when

and ventilation and ventilation and perfusion match

the patient's defense system becomes ineffective.

ing (Dean, 1985; Douglas, Rehder, Beynen, Sessler,

Pneumococcal pneumonia is caused by pneumo

and Marsh, 1977; Grimby, 1974; Piehl and Brown,

coccal bacteria, a gram-positive organism. It occurs

1976). Vigorous treatment should be initiated at the

most frequently in the winter months among adults

first sign of a superimposed bacterial infection, which

between 15 and 40 years of age with a predilection for

is often accompanied by a productive cough. At this

males. Patients present clinically with an abrupt onset

time, the appropriate devices should be prescribed

of illness characterized by fever, cough, purulent or

(e.g., ultrasonic or medication nebulizers to loosen se

rust-colored sputum, and pleuritic chest pain over the

cretions). Postural drainage may be indicated in addi

affected lung field. Physical examination may reveal

tion to mobilization for airway clearance. Treatments,

decreased expansion of the chest over the affected

particularly mobilization, need to be paced to mini

area and muscle splinting. On auscultation, there may

mize unduly tiring the patient or increasing oxygen

be bronchial breath sounds (indicating consolidation),

demand beyond the patient's capacity to adequately

decreased or absent breath sounds, and wheezes or

deliver oxygen. Increasing oxygen demands exces

crackles over the affected lung. Chest x-rays may

sively may compromise the patient's gas exchange.

show infiltrates, consolidation, or atelectasis.

Patient education is also fundamental to the treatment

There are four stages associated with bacterial in

that is to be instituted between treatments (i.e., mobi

fection of lung tissue-engorgement, red hepatiza

lization and positional rotation coordinated with

tion, gray hepatization, and resolution. The engorge

breathing control and coughing maneuvers).

ment stage occurs within the first few days of

The focus of cardiopulmonary physical therapy in

infection and is characterized by vascular engorge

the management of viral pneumonia is to augment

ment, serous exudation, and evidence of bacteria col

alveolar ventilation, increase perfusion, increase dif

onization. Red hepatization occurs within 2 to 4 days

fusion, and improve ventilation and perfusion match

as a result of diapedesis of the red blood cells. The

ing, thereby reducing the threat to oxygen transport

alveoli are full of polymorphonuclear leukocytes, fib

and gas exchange. Treatments are prescribed to opti

rin, and red blood cells. The organism continues to

mize oxygen transport and gas exchange and to mini

mUltiply within the fluid exudate. Areas of consolida tion become evident. Gr
mize fatigue and lethargy.

4 to 8 days and is characterized by evidence of abun dant fibrin, decreased polymorphonuclear leukocytes,

Bacterial Pneumonia

and dead bacteria. Consolidation continues to be a

Bacterial pneumonia causes the largest number of

problem in this stage. Resolution occurs after 8 days

deaths per year by an infective agent and is the fifth

as areas of consolidation begin to resolve. Many

most common cause of all deaths in North America.

macrophages are seen and evidence of enzymatic di

The patient presents with an abrupt onset of a severe

gestion of exudate is present. The affected tissue be


27

comes softer with large amounts of grayish-red fluid


475

is the same as that for pneumococcal pneumonia.

present within the alveol i. This process continues for

Hemo philus inJluenzae pneumonia is caused by a

2 to 3 weeks with the lung gradually assuming a

gram-negative organism and occurs primarily in chil

more normal appearance.

dren as bronchiolitis and in adults who have chronic

Pleural involvement occurs frequently, with the

bronchitis. The clinical picture is the same as for the

pleural spaces filling with the same type of fluid

other bacterial pneumonias, with numerous areas of

seen within the alveoli. Resolution is much slower

infiltration evident on x-ray. On auscultation, breath

because there are few surfaces available for phago

sounds are generally good, with crackles heard at the

cytosis. Complications that may occur in patients

end of inspiration. Treatment of this pneumonia in

with pneumococcal involvement include empyema,

cludes chemotherapeutic agents (ampicill in), oxygen,

superinfections (occur when large numbers of new

ultrasonic nebulization, and physical therapy.

organisms invade the lung), abscesses, atelectasis,

Other gram-negative organisms causing pneumo

and delayed resolution (defined as taking more than

nia include Esch erichia co li and Pseudomo n as

aeruginosa. They are seen most frequently in patients

4 weeks to resolve). Treatment of pneumococcal pneumonia involves

with underlying disease, especially pulmonary dis

the use of chemotherapeutic agents, with penicillin

ease, or in those who are debilitated. They are fre

being the antibiotic of choice. If the patient is allergic

q uently the cause of superinfections in individuals

to penicillin, erythromycin or lincomycin is used.

who have received massive doses of broad-spectrum

Thoracentesis is performed when pleural fluid is pre

antibiotics. Clinically these patients present with

sent. The patient should also receive ultrasonic nebu

cough, fever, and dyspnea. On auscultation, crackles,

lization and physical therapy. Supplemental oxygen

bronchial breathing, and diminished

therapy may be indicated.

sounds can be noted. X-ray changes frequently show

Staphlococcal pneumonia is caused by a gram

or

absent breath

bibasilar infiltrates, with the amount of involvement

positive organism. It rarely occurs in the healthy

being widely variable. As for other bacterial pneumo

adult but is a frequent cause of pneumonia in chil

nias, treatment includes chemotherapeutic agents, ul

dren, infants, and patients with chronic lung diseases,

trasonic nebulization, and physical therapy.

especially carcinoma, tuberculosis, and cystic fibro sis. Clinically, the patient presents with the same pic ture as the patient with pneumococcal pneumonia.

Principles of physical therapy management The goals of management of bacterial pneumonia in

There are some differences in the chest x-ray (e.g.,

clude reversing alveolar hypoventilation, increasing

patchy areas of infiltrate). Consolidation occurs infre

perfusion, reducing right-to-Ieft shunt, increasing

quently in this type of pneumonia. Pleural effusions,

ventilation and perfusion matching, minimizing the

empyema, abscesses, bronchopleural fistulas, and

effects of increased mucous production, and optimiz

pneumatoceles (subpleural cyst-like structures) occur

ing lymphatic drainage. Bacterial pneumonia is fre

frequently. Treatment includes chemotherapeutic

quently associated with increased mucous produc

agents, rest, increased fluid intake, ultrasonic nebu

tion. With respect to airway clearance, management

lization or medication nebulizers, and aggressive

focuses on augmenting mucociliary clearance overall,

physical therapy.

reducing excess mucous accumulation, and reducing

Streptococcal pneumonia is caused by a gram-posi

mucous stasis. Patients are often mobile and should

tive organism, Streptococcus pyogenes. It occurs most

be encouraged to be so to promote mucociliary trans

frequently in very young, very old, and debilitated pa

port and enhance lymphatic drainage (Dean and

tients. The clinical picture is very similar to that of

Ross, I 992a; Orlava, 1959; Wolff, Dolovich, Obmin

staphlococcal pneumonia. Again consolidation is rare

ski, and Newhouse, 1977). However, the oxygen de

and chest x-rays usually show one or more areas of

mands of mobilization and exercise should be well

patchy infiltrates. Complications are rare but empyema

within the patient's capacity to delivery oxygen.

does occasionally occur. Treatment for this organism

These interventions should be prescribed to avoid


476

PART IV


jeopardizing this balance and unduly fatiguing the pa

term, the bone marrow produces more red blood

tient (Dean and Ross, I992b). Deep breathing and ef

cells, leading to polycythemia. The work of the heart

fective coughing are singularly important maneuvers

is increased due to increased blood viscosity. Long

for clearing airways with special attention to the avoid

term hypoxemia leads to increased pulmonary artery

ance of airway closure (Bennett et aI., 1990). Prescrip

pressure and right ventricular hypertrophy.

tive body positioning can be used to optimize ventila

Patients with chronic bronchitis have tenacious,

tion and perfusion matching (Clauss, Scalabrini, Ray

purulent sputum that is difficult to expectorate. In an

and Reed, 1968; Douglas et aI., 1977; Hietpas, Roth

exacerbation, usually because of inflammation, infec

and Jensen, 1974; Hasani, Pavia, Agnew, and Clarke,

tion, or both, they produce even more sputum, which

199 I; Ross and Dean, 1992; Ross, Dean, and Abboud,

tends to be retained and stagnate. Retained secretions

I992b; Zack, Pontoppidan, and Kazemi, 1974).

obstruct airways and thus air flow, and reduce alveo lar volume. The resulting venti lation and perfusion inequality increases hypoxemia, CO2 retention, ac

Acute Exacerbation of Chronic Bronchitis Pathophysiology and medical management

cessory muscle use, melabolic demand, and breathing rate. Pao2 is further reduced and Paco2 tends to in

Chronic bronchitis is a disease characterized by a

crease. Hypoxemia and acidemia increase pulmonary

cough producing sputum for at least 3 months and for

vasoconstriction, which increases pulmonary artery

2 consecutive years. Pathological changes include an

pressure and predisposes the patient to right heart

increase in the size of the tracheobronchial mucous

failure (cor pulmonale) over time.

glands (increased Reid index) and goblet cell hyper

A patient having an acute exacerbation of chronic

plasia. Mucous cell metaplasia of bronchial epithe

bronchitis tends to have the following characteristics:

lium results in a decreased number of cilia. Ciliary

(I) The patient is often stocky in build and dusky in

dysfunction and disruption of the continuity of the

color. (2) The patient exhibits significant use of acces

mucous blanket are common. In the peripheral air

sory muscles of respiration and has audible wheezing

ways, bronchiolitis, bronchiolar narrowing, and in

or wheezing that is audible on auscultation. (3) Inter

creased amounts of mucus are observed.

costal or sternal retraction of the chest wall may be

Chronic bronchitis results from long-term irrita

noted. (4) Edema in the extremities, particularly

tion of the tracheobronchial tree. The most common

around the ankles, and neck vein distention reflect de

cause of irritation is cigarette smoking. Inhaled

compensated right heart failure.

smoke stimulates the goblet cells and mucous glands

report that breathing difficulty began with increased

(5) The patient may

to secrete excessive mucus. Smoke also inhibits cil

amounts of secretions (with a change in their normal

iary action. The hypersecretion of mucus and ciliary

color), which is often difficult to expectorate, and in

damage and dyskinesis lead to impaired mucous

creased cough productivity. (6) Pao2 is reduced, Paco2

transport and a chronic productive cough. The fact

increased, and pH reduced.

that smokers secrete an abnormal amount of mucus

Pulmonary function tests indicate reduced vital

increases the risk of respiratory infections and in

capacity, FEY!, maximum voluntary ventilation,

creases the length of the recovery time from these in

and diffusing capacity and increased FRC and resid

fections. Although smoking is the most common

ual volume.

cause of chronic bronchitis, other factors that have been implicated are air pollution, certain occupational environments, and recurrent bronchial infections.

Principles of physical therapy management During an exacerbation requiring hospitalization,

Patients with chronic bronchitis have been referred

these patients are usually treated with intravenous

to as blue bloaters because of a tendency to have a

fluids, antibiotics, bronchodilators, and low-flow

dusky appearance and be stocky in build. Although

oxygen. Diuretics and digitalis are often given to treat

many patients have a high Pac02, the pH is normal

right heart failure. Airway clearance interventions are

ized by renal retention of bicarbonate. Over the long

selected (i.e., mobilization, body positioning, and


27


477

postural drainage). These interventions are coordi

thickened basement membrane. The obstruction as

nated with breathing control and coughing maneuvers

sociated with bronchiolitis leads to ventilation and

to facilitate secretion removal and optimize coughing

perfusion abnormalities and diffusion defect. Clini

and expectoration, while minimizing dynamic airway

cally, the patient presents with a productive cough.

compression and alveolar collapse. During recovery,

Obliterative bronchiolitis has been reported to be

exercise with supplemental oxygen may also benefit

the most significant long-term complication o f

the patient. It is important for these patients to avoid

heart-l u n g t r a n s p l a n t a t i o n (B u r k e , Gla n v i lle,

bronchial irritants (e.g., cigarette smoking, second

Theodore, and Robin, 1987).

hand smoke, and air pollutants), and to be adequately

Medical management is directed at inflammation

hydrated to thin secretions to facilitate mucociliary

control with pharmacological agents, fluid manage

transport and expectoration.

ment, and oxygen administration if necessary. Pre

Patients with chronic bronchitis can benefit from a comprehensive rehabilitation program designed specifically for patients with chronic pulmonary

vention of infection is a priority.

Principles of physical therapy management

disease (Murray, 1993; Oldenburg, Dolovich,

The principal pathophysiological defects include ven

Montgomery, and Newhouse, 1979). Specific de

tilation and pelfusion inequality and diffusion defect.

tails of exercise prescription in the management of

These defects result from secretions produced by in

chronic lung disease and of a comprehensive pul

flammation and increased mucous production and

monary rehabilitation program are described in

from atelectasis of adjacent alveoli. Physical therapy treatment should promote mucociliary transpol1 and

Chapter 23.

the removal of secretions and mucus to central air ways, promote alveolar expansion and ventilation,

Bronchiolitis

optimize ventilation and pelfusion matching and gas

Pathophysiology and medical management

exchange, and reduce the risk of infection.

Bronchiolitis results from peripheral airway inflam

Bronchiol i tis is primari Iy, al though not exclu

mation. In severe cases the exudate in the peripheral

sively, a childhood condition. The effects of inflam

airways becomes organized into a connective tissue

mation and obstruction in small children are always

plug extending into the peripheral airway. The in

serious because the anatomical and physiological

flammatory process resembles that in other tissues

components of the cardiopulmonary s ystem are

(i.e., an inflammatory stage followed by a prolifera

smaller, respiratory muscle tone is less well devel

tive healing stage). Such inflammation is associated

oped, the anatomical configuration of the chest wall

with vascular congestion, increased vascular perme

is cylindrical, breathing is less efficient until after the

ability, formation of exudate, mucous hypersecre

age of 2, spontaneous movement and body position

tion, and shedding of the epithelium. Fluid is exu

ing are more restricted (infants in particular spend

dated o u t of the circulation onto the alveola r

more time in nonupright positions), and children are

surfaces replacing the surfactant. This in turn in

at greater risk of infection (see Chapter 35).

creases the surface tension and promotes airway clo sure. The secretion production associated with air way irritants and inflammation results from the excess mucous production in combination with the inflammatory exudate consisting of fluid protein

Alveolitis Pathophysiology and medical management Bronchioalveolitis is another inflammatory disorder

and cells of the exudate. Airway obstruction results

of the peripheral airways that is often associated

if these substances are not removed. The airway ep

with an extrinsic allergic reaction. Comparable with

ithelium has the capacity to repair and reline the

bronchiolitis, alveolitis is prevalent in young chil

lumen. A rapid turnover of cells may contribute to

dren. In adults, chronic alveolitis may be a precursor

cell sloughing and further airway obstruction and a

to interstitial pulmonary fibrosis. Acute bouts of


478

PART

IV


alveolitis are reversible, however, chronic inflam

position with the lung to be lavaged downward. The

mation can produce airway narrowing secondary to

Carlen's tube enables the patient to be ventilated by

fibrosis in the alveolar wall and complete obstruc

the uppermost lung while the lower lung is care

tion of the airway by organization of the exudate.

fully filled with saline to FRC. Then an additional

Chronic inflammation can lead to permanent irre

300 to 500 ml of saline is alternately allowed to run

versible parenchymal changes and chronic restric

into and out of the lung by gravitational flow. As

tive lung disease.

the saline flows out, manual percussion over the af


fected lung being lavaged has been reported to in c r e a s e t h e a m o u n t of p r o t e i n a c e o u s m a t e r i a l

The principles of physical therapy management are

washed f r o m t h e lung (see Figure

comparable with that for the management of bronchi

(Hammon,

4-11, p . 86).

1987).

olitis. Principles of the management of cardiopul monary dysfunction in children are presented in Chapter

35. Because children and infants in particular

are physically immature, the principles of manage ment are different from those for adults.

Acute Exacerbation of Chronic Airflow limitation PathophYSiology and medical management Emphysema. There are two principal types of em physema-centrilobular and panlobular. BOlh types may coexist, however, centrilobular emphysema is

Alveolar Proteinosis Pathophysiology and medical management

20 times more common than panlobular emphy sema. Centrilobular is characterized by destruction

4-1, p. 73), as

Alveolar proteinosis is a condition of unknown etiol

of respiratory bronchioles (see Figure

ogy, characterized by alveoli filled with lipid-rich

well as edema, inflammation, and thickened bron

proteinaceous material and no abnormalities in the

chiolar walls. These changes are more common and

alveolar wall, interstitial spaces, conducting airways,

more marked in the upper portions of the lungs.

or pleural surfaces. Most often it is found in men be

This form of emphysema is found more often in

tween 30 and 50 years of age, although it has been re

men than in women, is rare in nonsmokers, and is

ported in both men and women of all ages.

common among patients with chronic bronchitis.

The most common symptoms are progressive dys

Panlobular emphysema is characterized by destruc

pnea and weight loss, with cough, hemoptysis, and

tive enlargement of the alveoli distal to the terminal

chest pain reported less frequently. Chest x-rays re

bronchioles (see Figure

veal diffuse bilateral (commonly perihilar) opacities

physema is also found in patients who have an antit

4-10, p. 86). Physical findings include

rypsin deficiency. Airway obstruction in these indi

fine inspiratory crackles, dullness to percussion and,

viduals is caused by loss of elastic recoil or radial

(see Figure

4-1, p. 73). This type of em

in the later stages, cyanosis and clubbing. Pulmonary

traction on the bronchioles. When individuals with

function studies usually show decreased vital capac

normal lungs inhale, the airways are stretched open

ity, FRC, and diffusing capacity. Arterial blood gases

by the enlarging elastic lung, and during exhalation

indicate a low P02, especially during exercise, with

the airways are narrowed due to the decreasing

often nonnal Pe02 and pH.

stretch of the lung. However, the lungs of patients


with panlobular emphysema have decreased elastic ity because of disruption and destruction of sur

One treatment for patients with moderate-to-severe

rounding alveolar walls. This in turn leaves the

dyspnea on exertion from alveolar proteinosis is

bronchioles unsupported and vulnerable to collapse

bronchopulmonary lavage. The patient is taken to

during exhalation. This form of emphysema can be

the operating room. After general anesthesia and

local or diffuse. Lesions are more common in the

placement of a Carlen's tube (which isolates each

bases than the apices and tend to be more prevalent

lung), the patient is turned in the lateral decubitus

in older people.


27

than I cm in

emphysematous spaces 4-2, p.

prolonged. On expiration, the neoLlsly

may be found in patients with It is thought that

develop

from an obstruction of the conducting airways that permits the flow of air into the alveoli


479

may sponta

a pursed-lip

pattern, which is

believed to augment alveolar

and

collateral ventilation and gas exchange in the by

positive back pressures

tion but does not allow air to flow out again

and

1970). In addition, the

expiration. This causes the alveoli to become

tively

to compensate for the loss of the passive

inflated and eventually leads to destruction of the

elastic recoil that normally

inspira

air space in

alveolar walls with a resultant

the lung parenchyma. These bullae can be more than 10 em in diameter

intervention to

4-3, p. 75). If this happens,

creased. As the rel-shaped and

bar

Loss of the normal

of the

chest and bucket and pump handle motions further mechanics and

efficient Dempsey, and

of

one of these bullae.

1976).

The emphysema patient's most common com

Both types of

can lead to chronic

chest wall

The loss of elastic recoil of the disturbs the balance between the

norma.!

become more chronically

the chest wall becomes

remove the buJla is often necessary. Pneumothorax, a serious complication, can result from the

the lungs at end

tidal volume. Overall the work of breathing is in

compression. can compro

mise the function of the remaining lung tissue (Figure

Petty, may ac

recoil pul

the chest wall in and the

is dyspnea.

these patients appear

thin and have an increased anteroposterior chest wall d iameter. breathe

on disease

, they

the accessory muscles of inspiration

natural tendency of the chest wall to spring out. This

(Chapter

These patients may be observed leaning

balance is essential in maintaining norma.! FRC

forward,

their forearms on their knees, or sit-

the air in the

at the end of normal end tidal ex

with their arms extended at their sides,

piration). Because the residual volume of the lungs is

down against the bed or chair to elevate their shoul

FRC is correspondingly increased. This in

ders and improve the effectiveness of the accessory

H"'vU

VU,

crease is not functional,

because it reflects are still prone to

muscles of

be-

have been referred to as pink puffers because of the increased respiratory work

cause of the loss of the normal elastic recoil of the

they must do to maintain relatively normal blood

(i,e., increased

gases. On auscultation, decreased breath sounds can

increased dead space, These dynamic airway lung

and airway closure

This

contributes to uneven distribution of ventilation and

be noted throughout most or all of the

decreased diffusing

diologically, the

The pressure volume

lungs, flattened hemidiaphragms, and a small, elon

curve is shifted and ventilation is less efficient.

gated heart

With loss of elastic recoil and the normal them patent, the chest wall to the

outward, thereby

tends to

fields. Ra

patient has overinflated Figure

p.

Pulmonary func

tion tests show a decreased vital capacity, FEY I, maximum voluntary

and a

hyperinflated chest associated with the patient with

duced diffusing

chronic airflow limitation. The alveolar units are

increased and the residual volume and FRC are even

less uniform and the distribution of venti

The total

is

more increased. Arterial blood gases reflect a mildly lowered

lation becomes even less homogeneous.

or

and expiratory times of the alveolar units also be

raised PaC02, and a normal pH. Emphysema pa

heterogeneous. The alveoli require

unlike patients with chronic bronchitis, tend to

filling times For this reason, the

long time conwith chronic air

flow limitation adopts a characteristic breathing tern in which

and expiration tend to be

a normal or slightly

with

cardiac

of the

condition,

to failure at the end stage of the

disease (see

4-5, p. 77). At this stage, cardiac

hypertrophy may be evident.


480

PART IV


Hypoxemia leads to hypoxic pulmonary vasocon

patients with a FEY1 less than 0.75 L. However, if

striction, which shunts blood from underventilated to

these flow rates are found in patients with complica

better-ventilated areas of the lung. The afterload

tions of resting tachycardia, chronic hypercapnia, and a

against which the right heart has to pump is in

severely impaired diffusing capacity, the survival rates

creased. This elevates the pulmonary artery blood

should be reduced by 25%. Other factors that have

pressure (i.e., pulmonary hypertension). Over the

been associated with a poor prognosis are cor pul

long term, the right heart hypertrophies to work

monale, weight loss, radiological evidence of emphy

against this increased resistance and eventually may

sema, a dyspneic onset, polycythemia, and Hoover's

fail (cor pulmonale). Heart enlargement secondary to

sign (inward movement of the ribs on inspiration).

any cause alters the electrical conduction pattern ef

The most frequent causes of death in patients with

fecting electromechanical coupling and cardiac out

airflow limitation are congestive heart failure (sec

put. The altered size and heart position within the

ondary to cor pulmonale), respiratory failure, pneu

chest wal.l can be detected by ECG changes.

monia, bronchiolitis, and pulmonary embolism.

Treatment of emphysema that requires hospitaliza

As emphysema becomes chronic, the hemidi

tion often includes intravenous fluids, antibiotics, and

aphragms become more horizontally positioned, plac

low-flow oxygen (Geddes, 1984; Make, 1983). Some

ing the muscle fibers at a less efficient position on

patients require bronchodilators, diuretics, and digi

their length tension curve (Druz and Sharp, 1982).

talis. Patients with chronic airflow limitation adapt to

Breathing when the muscle fibers of respiration are

high Paco2 levels, thus becoming dependent on their

mechanicall y disadvantaged increases the work of

hypoxic drives to breathe. Therefore, low flow oxy

breathing and therefore energy demands and oxygen

gen is administered to these patients to avoid abolish

cost. Respiratory muscle weakness and fatigue are se

ing their drive to breathe.

rious complications of chronic lung disease that pre

The etiology of emphysema is uncertain. The inci dence of emphysema increases with age. It is most

dispose the patient to respiratory muscle failure (Rochester and Arora, 1983) (Chapter 4 and 32).

often found in patients with chronic bronchitis and is

The net effect of these pathological changes on

significantly more prevalent in smokers than non

gas exchange is hypoxemia, hypercapnia, and re

smokers. There appears to be a hereditary factor. Se

duced pH consistent with respiratory acidosis. Long

vere panlobular emphysema can develop in patients

term respiratory insufficiency leads to chronically

with an alpha-antitrypsin deficiency relatively early

impaired oxygen transport and gas exchange. To

in life even though they never smoked. Repeated

compensate for hypercapnia, production of bicarbon

lower respiratory tract infections may also play a role

ate is increased to buffer retained CO2 (i.e., compen

in the pathology of emphysema. However, the inter

sated respiratory acidosis). Red blood cell production

relationship of these and other factors in producing

(i.e., polycythemia) is increased to increase the oxy

the condition is still not well understood.

gen-carrying capacity of the blood. The negative ef

Chronic bronchitis and emphysema are marked by a

fect of polycythemia, however, is increased viscosity

progressive loss of lung function and corresponding

of the blood, leading to increased risk of circulatory

cardiac dysfunction. At the end of 5 years, patients

stasis, thromboses, and increased work of the heart.

with chronic airflow limitation have a death rate four to five times greater than the normal expected value.


Death rates reported by various studies depend on the

The patient with emphysema is prone to pulmonary

methods of selection of patients, types of diagnostic

infections and respiratory insufficiency. The clinical

tests, and other criteria. In general the death rates 5

picture is hallmarked by alveolar collapse and de

years after diagnosis are 20% to 55%. The 5-year sur

struction, ventilation and perfusion mismatching, and

vival rates based on FEY I have been reported as fol

diffusion defect. These defects result in impaired or

lows: 80% in patients with a FEY I greater than 1.2 L,

threatened oxygen transport if the physiological com

60% in patients with a FEY L close to 1 L, and 40% for

pensations are unable to maintain adequate blood


27

gases. Shortness of breath is exacerbated and breath


481

the chest wall by the viscera falling against the un

ing is labored. Increased work of breathing reflects

derside of the diaphragm in this position (i.e., vis

airway obstruction and inefficiency of respiratory

cerodiaphragmatic breathing) (Barach, 1974). The

mechanics and the respiratory muscles. Because of

muscle fibers of the diaphragm are mechanically

long-term airway disease, mucociliary transport is

placed in a more favorable position with respect to

disrupted. Therefore, in the presence of a pulmonary

their length-tension characteristics. This effect may

infection and increased production of pulmonary se

further be augmented in the head-down position in

cretions, secretion removal can be a significant prob

some patients (Barach and Beck, 1954). Other pa

lem for the patient.

tients, however, cannot tolerate recumbent posi

Specific treatments are prescribed for the patient

tions; in fact, respiratory distress may be increased.

based on the specific clinical findings (i.e., the type

If optimal treatment outcome has not been achieved

and severity of the cardiopulmonary dysfunction

with mobilization and body positioning coordinated

and the presence of infection). Therefore treatments

with breathing control and coughing maneuvers,

include mobilization coordinated with breathing

conventional physical therapy procedures may offer

control and coughing maneuvers, which are effec

additional benefit in some patients (e.g., postural

tive in enhancing alveolar ventilation, mobilizing

drainage and manual techniques).

secretions, and in ventilation and perfusion match

Because of the tendency toward dynamic airway

ing. Body positioning can be prescribed to alter the

compression resulting from the highly compliant air

distribution of ventilation, to aid mucociliary trans

ways of emphysema patients, open-glottis coughing

port, and to remove pulmonary secretions. Although

maneuvers are indicated. Specific outcome measures

"pure" emphysema is t y p i c a l l y dry, p o s t u r a l

are recorded before, during, and after treatment to as

drainage positions can facilitate the removal o f pul

sess short- and long-term treatment effects. In addi

monary secretions from specific bronchopulmonary

tion, between-treatment treatments are central to

segments if indicated. In any given body position,

maximizing overall treatment efficacy. Thus convey

alveolar volume is augmented in the uppermost lung

ing information effectively and specifically to the pa

fields and alveolar ventilation is augmented in the

tient, nursing staff, and possibly family members is

lowermost lung fields. The type and extent of

crucial to achieve an optimal treatment outcome.

pathology will determine the degree of benefit these

Comparable with the chronic bronchitis patient, an

physiological effects will have on oxygen transport.

exercise program for these patients should be pre

In addition, body positioning is essential to optimize

scribed to maximize oxygen transport capacity. Such

respiratory mechanics and enhance pulmonary gas

conditioning may reduce the frequency and severity

exchange, thereby reducing the work of breathing

of subsequent acute exacerbations. In addition, the

and the work of the heart. The assessment will de

patient may benefit from other components of a com

fine the parameters of the treatment prescription that

prehensive pulmonary rehabilitation program.

will be effective in relieving the work of breathing and the work of the heart. This information is essen tial not only for prescribing beneficial positions but also for avoiding deleterious positions. A sitting

Acute Exacerbation of Asthma Pathophysiology and medical management

lean-forward position will assist ventilation sec

Asthma is a condition characterized by an increased

ondary to the gravitational effects of the upright po

responsiveness of bronchial smooth muscle to vari

sition on cardiopulmonary function. If the arms are

ous stimuli and is manifested by widespread narrow

supported, this position stabilizes the upper chest

ing of the airways that changes in severity either

wall and rib cage, thereby facilitating inspiration.

spontaneously or as a result of treatment (Hogg,

Some patients with horizontal diaphragms and sig

1984; Rees, 1984). During an asthma attack, the

nificant respiratory distress benefit from recumbent

lumen of the airways is narrowed or occluded by a

positions in which the diaphragm is elevated within

combination of bronchial smooth muscle spasm, in


482

PART

IV


flammation of the mucosa and an overproduction of

Factors That Precipitate Asthmatic Symptoms

viscous, tenacious mucus. Asthma is a widespread disorder affecting I % of the population. It is common in children under years of age; its prevalence is estimated to be

Allergic or Extrinsic Asthma

15

Pollen (especially ragweed)

5% to

Animals

15%. It is estimated that 80% of asthmatic children do not have symptoms after the age of 10 years. Asthma that begins in patients under the age of 35

Feathers Molds

is usually allergic or extrinsic. These asthma attacks

Household dust

are precipitated when an individual comes into con

Food

tact with a given substance to which he or she is sen

Nonallergic or Intrinsic Asthma

sitive, such as pollens or household dust (see the box at right). Often asthmatic patients can be allergic to a

Inhaled irrita1lts

number of substances rather than to one or two.

Cigarette smoke

lf a patient's first asthma attack occurs after the age of

35, often there is evidence of chronic airway

Dust

obstruction with intermittent episodes of acute bron

Pollution

chospasm. These individuals, whose attacks are not

Chemicals

triggered by specific substances, are referred to as having nonallergic or intrinsic asthma (see box at

Weather

right). Chronic bronchitis is commonly found in this

High humidity

group, and this is the type of asthma seen in the hos

Cold air

pital setting. The asthmatic patient presents wi th the follow

Respiratory i1lfectiOlls

ing picture during an attack. Lung volumes and ex

Common cold

piratory flow rates are reduced, and the distribution

Bacterial bronchitis

of ventilation is less homogeneous (Ross et aI., 1992a). The patient has a rapid rate of breathing

Drugs

and uses the accessory respiratory muscles (Figure

Aspirin

4-6, p.

78). The expiratory phase of breathing is Emotio1ls

prolonged with audible wheezing. The patient may cough frequently, although un prod ucti vely, and

Stress

may complain of tightness in the chest. Radiologi

Excitement

cally, the lungs may appear hyperinflated or show

Exercise

small atelectatic areas (reabsorption atelectasis). Early in the attack, arterial blood gases reflect slight hypoxemia and a low PaCo2 (from hyperven tilation). lf the attack progresses, the P02 continues to fall as the Peo2 increases above normal. As ob

tack more effectively, and also provides a means of

struction becomes severe, deterioration of the pa

helping to reduce subsequent attacks. Airway clear

tient is evidenced by a high CO2, a low Po2, and a

ance procedures may have a role should the cough

pH of less than

become productive. Patients should avoid bronchial

7.3.

Hospitalized asthmatic patients are treated with in travenous fluids, bronchodilators, supplemental oxy

irritants and substances that worsen or induce signifi cant bronchospasm or an attack.

gen, and corticosteroids. Breathing control in the

An asthmatic attack that persists for several hours

acute attack relaxes the patient, helps manage the at-

and is unresponsive to medical management is re


27


483

ferred to as status asthmaticus. This condition consti

bronchial lumen, further contributing to the stasis of

tutes a medical emergency, necessitating admission

secretions. Thus optimizing the mobilization of secre

to the intensive care unit (see Chapter

32).

tions and their removal is a priority even in tile pres ence of scant secretions. Interventions that optimize


mucociliary transport are selected to minimize exac

The hallmark of an acute exacerbation of asthma is

erbating bronchospasm and further increases in air

an increased responsiveness of airway smooth muscle

way resistance.

to various stimuli (bronchospasm) (i.e., reversible air

The primary goals in the management of asthma

way obstruction). Although bronchospasm can be a

include reducing airway narrowing, improving alveo

feature of chronic bronchitis and emphysema, the pri

lar ventilation, reducing the work and energy cost of

mary cause of airway obstruction in these conditions

breathing, reducing hypoxemia or minimizing its

results from anatomical and physiological changes

threat, and optimizing lung compliance. Treatment outcome is assessed with indices of

that are not usually reversible. Physical therapy is directed at improving gas ex

oxygen transport overall and of the function of the in

change without aggravating bronchospasm and other

dividual steps in the pathway (Epstein and Henning,

symptoms and reversing these when possible. Thus

1993). Bedside spirometry, including peak expiratory

promoting more effective and efficient breathing with

flow rate, is a sensitive indicator of ensuing compro

relaxed controlled breathing maneuvers and con

mise in oxygen transport. Some patients use a peak

trolled unforced coughing maneuvers in optimal body

expiratory flow rate meter at home to detect such

positions is a priority. Overall oxygen demand, in

changes and as an early indicator of the need for

cluding that associated with an increased work of

medical attention.

breathing, needs to be reduced during an exacerba tion of asthma. This may require reduced activity, body positioning that improves breathing efficiency, judicious rest and sleep periods, altered diet or re stricted diet, adequate hydration, maintaining a ther

Acute Exacerbation of Cystic Fibrosis Pathophysiology and medical management Cystic fibrosis (CF) is a complex multisystem disor

moneutral environment, rest, reduced arousal, re

der transmitted by an autosomal-recessive gene that

duced social interaction and excitement, and reduced

affects the exocrine glands (Landau,

environmental stimulation. Although general relax

volves all of the major organ systems in the body

1973). CF in

ation does not directly relax bronchial smooth mus

and is characterized by increased sweat electrolyte

cle, relaxation will assist breathing control, reduce

content, chronic airflow limitation, ventilation inho

arousal and metabolic demands, and promote more

mogeneity, and pancreatic insufficiency. Definitive

efficient breath ing.

diagnosis of CF includes positive family history,

Airway narrowing and obstruction is a hallmark of

clinical symptoms of poor digestion, growth or re

this condition secondary to increased bronchial

current pulmonary infection, and, most importantly,

smooth muscle tone and airway edema. Even small

a positive sweat chloride test. Survival has increased

amounts of pulmonary secretions can obstruct the

paired gas exchange, and reduced P aoz. Thus mu

1940 when survival was reported 1980, patients survival was estimated to be 20 years of age and in creasing (Hunt and Geddes, 1985). Thus although

cociliary transport is a priority. Mucous clearance can

CF is congenital and manifests in childhood, this

lumen of narrowed airways, which leads to reabsorp tion atelectasis distal to the site of obstruction, im

dramatically since

to be approximately 2 years of age. In

be further impclled by the addition of serous fluid to

condition has now become an adult disorder. Adult

pulmonary mucus, resulting from airway irritation

patients with CF often have an upper lobe infiltrate,

and inflammation. Cilia are less effective at clearing

with evidence of atelectasis and bronchiectasis, and

mucoserous fluid compared with mucus alone. In ad

chronic staphlococcal infections. The beat fre

dition, sheets of ciliated epithelium are shed into the

quency of the cilia is often slowed to approximately


484

PART IV

Guidelines for the Delivery of Cardiopulmonary Physical Thel'apy: Acute Cardiopulmonary Conditions

3 mm/min, compared w i t h 20 m m/min in age

The clinical deficits related to oxygen transport in

matched healthy control subjects (Wood, Wanner,

clude impaired mucociliary transport, increased mu

Hirsch, and Farrell, 1975). Patients can be catego

cous production, increased difficulty clearing mucus,

rized into three general groups-those with no sig

impaired ventilation and perfusion matching, right

nificant pulmonary signs, those with pulmonary

to-left shunt, a diffusion defect, respiratory muscle

signs and occasional cough and sputum, and those

weakness or fatigue, and reduced cardiopulmonary

with pulmonary signs and constant cough and spu

conditioning (Chatham, Berrow, Beeson, Griffiths,

tum. Those patients in the last group tend to have

Brough, and Musa, 1994). The incrcased production

significantly impaired pulmonary function test re

of mucus and the difficulty removing mucus in

sults, reduced diffusing capacity, and increased he

creases the risk of bacterial colonization and chronic

moptysis, particularly in the presence of an abnor

respiratory infections. These manifestations of CF are

m a l che s t x - r a y a n d h y p e r i n f la ti o n . A i r w a y

worsened with recumbency. Significant postural hy

hyperreactivity appears t o b e variable.

poxemia has been reported in CF patients when mov

The A-a gradient for nitrogen reflects lung regions

ing from sitting to a supine position (Stokes, Wohl,

with low ventilation and perfusion ratios. Peripheral

Khaw, and Strieder, 1985). Thus the object of treat

airways are often abnormal either anatomically or

ment is to optimize oxygen transport and pulmonary

functionally because of mucous plugging. The lungs

gas exchange. Given the pathophysiological deficits

of patients with CF may be excessively stiff at maxi

in an acute exacerbation of CF, the specific goals are

mal lung capacity, with a loss of elastic recoil at low

to enhance mucociliary transport, promote airway

lung volumes (Mansell, Dubrawsky, Levison, Bryan,

clearance, optimize alveolar ventilation and therefore

and Crozier, 1974). Regional ventilation is nonuni

gas exchange, maximize the efficiency of oxygen

form contributing to ventilation and perfusion mis

transport overall, and prevent and minimize infection.

match and hypoxemia (Cotton, Graham, Mink, and Habbick, 1985; Ross et aI., 1992a).

Although the degree to which patients with chronic lung conditions, and in palticular CF, can respond to

The chronic pulmonary limitation in CF is related

aerobic training may be limited, it is essential that

to increased secretion of abnormally viscous mucus,

their capacity to transport oxygen overall is optimized

impaired mucociliary transport resulting in airway ob

to compensate for deficits in specific steps of the oxy

struction, bronchiectasis, hyperint1ation, infection, and

gen transport pathway (Cystic Fibrosis and Physical

impaired regional ventilatory function, leading to im

Activity, International Journal of Sports Medicine,

paired ventilation and perfusion matching and gas ex

1988; Dean and Ross, 1989). Deconditioning severely

change. Radiologically, changes are most pronounced

impairs oxygen transport. Improved aerobic capacity

in the upper lobes, especially the right upper lobe.

Principles of physical therapy management Prophylactic cardiopulmonary physical therapy, in

and cardiopulmonary conditioning is central in the management of CF. Prescriptive aerobic exercise en hances the efficiency of oxygen transport overall by reducing airway resistance by mobilizing secretions,

cluding facilitation of mucociliary transport and max

improving the homogeneity of ventilation in the lungs

imizing alveolar ventilation, in conjunction with the

and therefore ventilation and perfusion matching, op

judicious use of antibiotics provides effective mea

timizing oxygen extraction at the tissue level, and in

sures for controlling or s l o w i n g the effects of

creasing respiratory muscle endurance (Keens,

bronchial and bronchiolar obstruction. Involvement

Krastins, Wannamaker, Levison, Crozier, and Bryan,

of the patient and caregivers in chronic care in the

1977; Zach et aI., 1992). If optimal conditioning is

long term is particularly important. Understanding of

maintained, oxygen transport is not as compromised

the pathology and course of CF is essential to modify

during acute exacerbations given the improved effi

treatment prescription during exacerbations and re

ciency of oxygen transport overall. These effects will

missions of the disease.

be lost, however, as the patient deconditions with re


27


465

stricted mobility and recumbency

the acute

sure, because of the concomitant increase in intratho

episode. Thus it is important that

is mlnl

racic pressure and strain on the heart and lungs. Pa

maJly restricted during an exacerbation (based on the

tients with CF have severe paroxysms of

clinical assessment and morbidity) and that exercise

This

conditioning is a

which in turn

of

between

clearance in these patients, the untoward

importance for CF Shepard,

1

cardiac effects need to be minimized.

1991). This may minimize

and

venous return and cardiac out

put. Although coughing is an essential mechanism for

exacerbations. An important additional effect of which has

increases intrathoracic pressure,

other interventions aimed at

Over the past

the risk of infection and perhaps minimize the

secretion clearance in the treatment of CF have in

of an infection once acquired.

cluded

the use of the positive ex-

In severe exacerbations the patient is has a

stressed oxygen

1993; Webber and Pryor, 1

increased and is prone to

is shifted along the airways

the selection of treatment

j.Jv,,,.-..tu'-"

at low lung volumes is believed to loosen

tions are selected based on the assessment and the pa to tolerate the treatment and derive body

enhance mu clearance and maxi

cociliary transport and

This is fol

secretions from the walls of the at mid

lowed

volumes, which

breathing at

lung volumes is believed to

centralize and facilitate the removal of the secretions Thus

with

may enhance manipulat

mize t he efficiency of t h e s t e p s i n t h e o x y gen transport pathway. Postural

can offer addi

tional benefit in these patients if further clearance i s The addition o f manual indicated, however,

ing

monitoring must be car

the

and Maz

Murray, 1979;

therapist

and deliber

the

who gauges

the patient's ventilatory effort and work with the chest. The patient is not

,,,,..; to breathe below

volume

"'''''An" ' ... ..

and expiratory techniques can

contribute to airway

whereas

and is encouraged to suppress coughing until the ex

and

other forms of modified

(i.e., the phase is breathing at high

tis minimize

which the patient

volumes), may be a useful adjunct for fa

tive in removing secretions that have accumulated

cilitating airway clearance in

centrally without compromising ventilation and gas

procedure that

1974; Nunn,

Sa

and Laws, 1965). Forceful closes, contributes to

with CF. It is a

may use independently and can

relatively unobtrusively. It

be

the patient's tial for

efforts and minimizes the poten airway closure in these

The PEP mask and flutter valve are believed to re

airway closure and thus should be avoided, lady in

is coached by

breathe

at the volumes set hands around the

1982). Forced

and wastc

of energy. The

ful

(Kirilloff,

volumes and flow rates and controlling

coughing to avoid unproductive

may be

ried out given their potential deleterious effects on gas

be

lieved to help localize and collect the secretions. Fi

benefit. Gradual, paced low-intensity mobi lization and

at low

volumes, then at mid and high lung volumes,

monitoring. These patients become and distressed readily, Treatment interven

tient's

and

tient initially breathes

interventions and their parameters in conjunction with

altering the

volume at which the patient breathes. The pa

arterial desaturation. Thus minimizing undue oxygen demand and

that the equal pres

is based on the

in part because of the increased

work of breathing and for the

mask, and the flutter valve

pressure

with elevated pulmonary artery pres

duce airway closure and thereby


alveolar

486

PART IV


ventilation and enhance mucociliary clearance in pa

als exposed to plastics being heated at high tempera

tients with CF.

tures are also exposed to gases that are toxic to the respiratory system. Chronic pathological changes and

Acute Exacerbation of Interstitial Pulmonary Fibrosis Pathophysiology and medical management Interstitial lung disease has been associated with var

impaired gas exchange can result. Medical management is directed at reducing in flammation, reducing pulmonary hypertension, and increasing arterial oxygenation. Pharmacological

ious occupations and the inhalation of inorganic and

management may include corticosteroids for inflam

organic dusts. Conditions associated with the inhala

mation, immunosuppressive agents, and oxygen

tion of inorganic dusts include silicosis, asbestosis,

therapy. Removing the patient from the work envi

talc coal dusts, and beryllium. These conditions are

ronment contributing to interstitial pulmonary fibro

most often seen in miners, welders, and construction

sis is essential in managing the disease and its long

workers. Workers exposed to organic material, such

term consequences.

as fungal spores and plant fibers, may develop a seri

PrinCiples of physical therapy management

ous pulmonary reaction known as extrinsic allergic alveolitis. Generally, interstitial lung disease is char

The primary clinical manifestations of an acute exac

acterized by inflammation of the lung parenchyma,

erbation of interstitial pulmonary fibrosis reflect an

which may resolve completely or progress to fibro

acute on chronic problem usually resulting from an

sis. Interstitial pulmonary fibrosis results from the

inflammatory episode, pulmonary infection, or both.

deposition of connective tissue after repeated bouts

The mechanisms responsible include reduced alveo lar ventilation, an inflammatory process and its mani

of infection. The pathophysiological deficits are commensu

festations, potential airway obstruction, and increased

rate with morphological changes of interstitial infil

work of breathing and of the heart in severe cases.

tration and fibrosis, intraalveolar exudate and alveo

These patients are prone to desaturation during exer

lar replacement (Chung and Dean, 1989) (see Figure

cise and thus need to be monitored closely.

4-12, p. 88). Lung compliance and lung volumes are

In mild cases, mobilization increases the homo

reduced, expiratory flow at mid lung volume is in

geneity of ventilation, and ventilation and perfusion

creased (stiff, inelastic lungs), diffusing capacity is

matching (Jernudd-Wilhelmsson et aI., 1986). Be

reduced, and hypoxemia can be present in the ab

tween treatments and in the management of the se

sence of hypercapnia (Chung and Dean; 1989; Jer

verely affected patient, body positioning is used to re

nudd-Wilhelmsson, Hornblad, and Hedenstierna,

duce the work of breathing and arousal, maximize

1986). The chest x-ray of a patient with interstitial

alveolar ventilation, maximize ventilation and perfu

pulmonary fibr osis secondary to sarcoidosis is

sion matching, and optimize coughing.

shown in Figure 4-12, p. 88. Other changes include

Patients with moderate-to-severe interstitial lung

increased resting heart rate, pulmonary hyperten

disease may desaturate during sleep (Perez-Padilla,

sion, impaired gas exchange, and shortness of breath

West, and Lertzman, 1985) and readily desaturate on

during exercise and, in some cases, at rest. Symp

physical exertion (Arita, Nishida, and Hiramoto,

toms can be reversed by removing the worker from

1981), thus warranting close monitoring during and

the exposure by a change of employment, by modi

between treatments. Increased pulmonary vascular re

fying the materials handling process, or by using

sistance secondary to hypoxic vasoconstriction con

protective clothing and masks. Repeated exposure to

tributes to increased work of the right heart and po

these organic dusts may result in irreversible inter

tential cardiac insufficiency. General debility and deconditioning warrant a

stitial fibrosis. Reaction to fumes and gases can also lead to

modified exercise program that can optimize the

chronic restrictive patterns of lung disease. Individu

function of all of the steps in the oxygen transport


27

pathway (Arita et aI., 1981; Chung and Dean, 1989).


487

in milder cases. If fibrosis has occurred, lung compli ance will be correspondingly reduced. Airflow resis tance may be increased from narrowing or distortion

Tuberculosis

of the bronchioles because of fibrosis. Pleural in


volvement may result in effusions, empyema, pleural

Although the incidence of tuberculosis, a life-long

fibrosis, and spontaneous pneumothorax. Unlike

disease, has declined significantly over the past sev

parenchymal damage, small amounts of pleural re

eral decades, this disease has been experiencing a

striction can produce significant changes in pul

resurgence in the industrialized world in recent

monary function. Clinically, patients with significant

decades. This may reflect declining sanitation and

pleural involvement have significant restrictive dis

health standards in some segments of the population

ease and correspondingly low lung volumes. The

and immigration patterns.

work and energy cost of breathing are markedly in

Most infections result from inhalation of airborne

creased. Shortness of breath is a common complaint.

tubercle bacilli, which triggers an inflammatory re

Comparable with an interstitial pulmonary fibrosis

sponse (luce, 1986). This response includes flooding

patient, the patient adopts a rapid shallow breathing

of the affected area with fluid leukocytes, and later

pattern to reduce the high cost of elastic work of

macrophages. The area becomes consolidated and

breathing. Thus the dead space tends to be hyperven

pathologically the condition is considered a tubercu

tilated and alveolar hypoventilation results.

lous pneumonia. The infiltrating macrophages be

In addition to alveolar hypoventilation, lung tissue

come localized and fused, resulting in the characteris

and pulmonary vascular damage impairs ventilation

tic tubercle. Within 2 to 4 weeks, the central part of

and perfUSion matching and diffusing capacity. In se

the lesion necroses. Tuberculosis is associated pri

vere cases, hypoxemia and hypercapnia are present.

marily with pulmonary infection that is comparable

Chronic adaptation includes polycythemia and hyper

with other infectious pneumonias. Tuberculosis, how

volemia. Right heart failure may ensue.

ever, is distinct in that it may affect other parts of the

The lungs become shrunken and geometrically

body. Symptoms include fatigue, fever, reduced ap

distorted because of fibrotic changes in the lungs.

petite, weight loss, night sweats, hemoptysis, and a

These changes can lead to kinking and obstruction of

cough with small amounts of nonpurulent sputum

the pulmonary blood vessels and maldistribution of

with pulmonary involvement. The course of the dis

pulmonary blood flow, which further compromises

ease is variable. Some lesions heal promptly, whereas

ventilation and perfusion matching.

other patients experience progression and ensui ng

Tuberculosis may be associated with an obstruc

death. Other systems that can be involved include

tive component. An increase in airflow resistance

brain and meninges, kidney, reproductive system, and

comparable with emphysema can be present. This ob

bone. In some individuals the disease appears to

struction results from chronic infection, mucosal

remit, whereas in others tuberculosis progresses to af

edema, retained secretions, and bronchospasm.

fect other organ systems or previously dormant foci can be reactivated.

Antibiotics can be effective in managing the dis ease such that hospitalization is avoided. If detected

The effects of tuberculosis on pulmonary function

early, the prognosis is favorable, provided the patient

are variable, depending on the extent and type of le

adheres to the medication schedule and the bacilli do

sions. lesions may involve the lung parenchyma, the

not become resistant to the medications. Surgery may

bronchi, the pleurae, and chest wall. Parenchymal i n

be indicated to resect lung segments that are chroni

volvement can reduce lung volumes, leading to hy

cally involved. The extent and seveJ;ty of the disease

poventilation of pelfused lung units. Significant dis

determines the course of recovery.

ease leads to impaired artcrial blood gases, whereas

The maintenance of good general health is particu

areas of unaffected lung may adequately compensate

larly important in the management, control, and pre


488

PART IV


vention of tuberculosis (e.g., sanitation, balanced diet, sleep, regular exercise, and stress control).


whether the patient is being treated for osteoarthritis, stroke, or cardiopulmonary dysfunction, treatment is modified accordingly. An exercise prescription in cludes generalized aerobic exercise at an intensity

Although the acute presentation of tuberculosis is com

that is optimally therapeutic and not associated with

parable with acute pneumonia (refer to pneumonia sec

any excessive or untoward hemodynamic responses

tion), there are some important differences with respect

(Blair, Painter, Pate, Smith, and Taylor, 1988).

to physical therapy management. First, tuberculosis is

Labile hypertensive patients are the most difficult

particularly infectious, thus special precautions should

patients to prescribe an exercise program for because

be taken by the physical therapist to prevent its spread

of the irregularity of their blood pressure responses.

during its infectious stage. Second, patients are prone to

The intensity is modified at each session to accom

excessive fatigue; treatments should be selected to pro

modate these variations. Because beta-blockers and

mote improved oxygen transport without exceeding the

other medications blunt heart rate responses to exer

patient's capacity to deliver oxygen and without con

cise, the exercise prescription parameters are defined

tributing to excessive fatigue. Stimulation of the oxy

on the basis of some other objective hemodynamic

gen transport system with exercise is necessary to avoid

response or on subjective responses (e.g., the Borg

the deleterious effects of deconditioning and further

scale of perceived exertion).

compromise of oxygen transport. The patient therefore warrants being monitored closely.

The benefits of a modified aerobic exercise pre scription include elimination of medication, reduction of medication, and improved pbarmacological control on the same dose of medication. In addition, the pa

Hypertension Pathophysiology and medical management Essential hypertension is the most common type of

tient derives all the other multisystem health benefits of exercise. A program of aerobic exercise should be carried out in conjunction with other life-style changes

hypeltension (90% of all reported cases) (i.e., of un

associated with blood pressure control (e.g., nutrition,

known etiology). Generally, hypertension is classified

weight control, stress reduction, and smoking cessation

as mild, moderate, or severe. Hypertension is man

program). Medications should be monitored by the

aged pharmacologically with vasodilators (i.e., after

physician during the training program. In addition to

load reducers), diuretics (i.e., volume reducers), and

exercise having a direct effect on controlling hyperten

beta-blocking agents (i.e., inotrophic agents). Hyper

sion, the effect of exercise on overall metabolism may

tension is a significant health-care concern in that this

alter the absorption and degradation of the medica

condition is frequently associated with heart disease

tions, which in turn can reduce the prescriptive re

and stroke. Thus its consequences can be dire.

quirements of that medication. Those types of exercise


that are associated with a disproportionate hemody namic challenge (e.g., static movements and stabilizing

Physical therapists treat patients with hypertension as

postures) are not usually indicated. Rather, aerobic ex

a primary or secondary condition. A prescription of

ercise that is rhythmic, involves the large muscles of

regular aerobic exercise may control hypertension

the legs and possibly the arms, and is performed fre

(Froelicher, 1987; Goldberger, 1990). The prescrip

quently is indicated (Blail: et aI., 1988).

tion is based on a consideration of the patient's coex istent problems and general health status. If obesity is a concurrent problem, an exercise program is pre scribed to address both concerns.

Angina Pathophysiology and medical management

More frequently, physical therapists treat patients

Angina refers to pain resulting from ischemia of the

whose hypertension is a secondary condition. Thus,

myocardium and often precedes myocardial infarction.


27


489

Coronary cutery disease is the primary cause of myocar

propriately? Is the prescription current? Are

dial infcu'ction and is among the leading causes of death

there other medications that may influence the

in the Western world. Life-style factors including rugh

patient's cardiopulmonary status and response to

fat diet, stress, and low activity levels contribute to ath

treatment? What are they? Does the patient have

erosclerosis and fat deposition within the coronary

the antianginaJ medication present at all times?

blood vessels. When these deposits narrow or totally occlude the vessel lumen, blood flow is restricted or to

5. What physiological parameters should be moni tored before, during, and after treatment?

tally obstl11cted. As the hecut continues to demand oxy

6. What is the patient's knowledge about his or

gen and nutrients to work, blood supply needs to be in

her condition? Can the patient clearly identify

creased. If one or more of the myocardial blood vessels

what triggers the angina and what makes it

is stenosed, insufficient blood reaches the working my

worse and better? What life-style changes have

ocardial fibers, and ischerrua and pain result. Although

been made? What should be reinforced and

the classic description of anginal pain is retrosternal vice-like, gripping pain radiating to the left side and down the

what education is needed? A key consideration in the management of any pa

and up into the neck, anginal pain may

tient with cardiovascular dysfunction is minimizing

occur bilaterally anywhere above the umbilicus. Fur

myocardial strain (Sokolow et aI., 1990). Thus mobi

arm

thermore, patients vary considerably with respect to the

lization and exercise prescription needs to incorpo

degree to which the severity of the pain correlates with

rate an appropriate warm-up, steady-rate, cool-down,

the degree of myocardial ischemia and infarction. Thus

and recovery phases, and the type of exercise should

even apparently minimal chest pain may be associated

be rhythmic and involve the legs (i.e., areas of large

with significant ischemia and should not be rrunirruzed

muscle mass) and possibly the arms as well. Initially,

with respect to its clinical significance.

low-intensity activity that restricts the heart rate to no more than 20 beats above resting heart rate may be


indicated to minimize the work of the heart without

The management of patients with healt disease who

immobilizing the patient completely. Ejection frac

are hemodynamically unstable and require intensive

tion is not necessarily a good indicator of exercise

monitoring to assess and to monitor physical therapy

tolerance because these vruiables are not well corre

treatment is described in Chapter 32. This chapter ad

lated (Dean, 1993). Upper-extremity work alone is

dresses the management of the cardiac medical patient

more hemodynamically demanding than lower ex

who is stable and uncomplicated. Physical therapists

tremity work and thus is prescribed cautiously if at

must be knowledgeable and proficient in the manage

all, at least in the early stage. Exercise or physical ac

ment of the cardiac patient because these patients are

tivity, involving sustained static postures and isomet

referred with cardiac disease as a primary or secondary

ric muscle contraction, are contraindicated. Breathing

problem. Because physical therapy invariably involves

should be coordinated with activity such that breath

physically stressing a patient either with therapeutic

holding and straining are avoided.

exercise or with the application of a therapeutic modal

A patient with a history of angina, regardless of

ity, the physical therapist must address the following

whether that individual is taking antianginal medica

questions when managing a patient with heart disease: I. Does the patient's cardiac status preclude treat ment? Why?

tions, must be hemodynamically monitored (i.e., heart rate, blood pressure, rate pressure product, and subjective responses).

2. Is additional information on the patient needed

Patients prone to angina may exhibit symptoms in

before physical therapy assessment and treat

certain body positions (L ange, Katz, McBrid e , Moore, a n d Hillis, 1988; Langou, Wolfson, Olson,

ment? What information? 3. How should treatment be modified? Why?

and Cohen, 1977; Prakash, Parmley, Dikshit, For

4. Is the patient using antianginal medication ap

rester, and Swan, 1973). Usually, this reflects an in


490

PART IV


creased workload and increased work of the heart. Recumbent positions increase the mechanical work of the heart by increasing central blood volume (Kaneko, Milic-Emili, Dolovich, Dawson, and Bates, 1966). These patients are not encouraged to lie flat, instead the head of bed is elevated 10 to 15 degrees. Sidelying positions, particularly left sidelying, in crease the work of the heart by compressing the heart and impeding ventricular filling and ejection. Patients with impaired oxygen transport and without prior car diac disease may exhibit myocardial stress and is chemia in these body positions. Thus patients with impaired or threatened oxygenation must be moni tored closely, particularly during turning and activi ties in which oxygen demand is increased and oxygen delivery needs to increase cOITespondingly. Uncompliicated Myocardial Infarction Pathophysiology and medical management

Myocardial infarction commonly referred to as a heart attack refers to insufficient myocardial pelfu

sion resulting in a macroscopic area of damage and necrosis of the heart. Infarction results most fre quently from narrowing and occlusion of the coro nary blood vessels secondary to atherosclerosis. Other causes include occlusion secondary to a throm bus or embolus, reduced blood pressure, or coronary vasospasm. Angina, or ischemic chest pai n, often precedes or accompanies a myocardial infarction. In farctions vary in severity from being silent (i.e., hav ing no characteristic signs and symptoms) and thus going undetected to being fatal. Most infarctions when detected require some hospitalization and mon itoring to ensure that the infarction is not evolving further and that the patient is medically stable and in no danger. Chapter 32 describes the management of patients with myocardial infarctions who are admit ted to a coronary care unit. This section focuses on the patient with mild heart disease, the medical car diac patient who is discharged from hospital, the pa tient who has a history of ischemic heart disease, and the patient who is hospitalized for a condition other than heart disease but develops and is being managed for myocardial ischemia. Judicious movement and body positioning are essential elements in the man

agement of the myocardial infarction patient (Harri son, 1944). Because these interventions can place sig nificant demands on cardiopulmonary function and oxygen transport, they must be prescribed specifi cally by physical therapists with considerable knowl edge and expertise in the area. Principles of physical therapy management

Physical therapy stresses patients hemodynamically (Dean, Murphy, Parrent, and Rousseau, 1995). Thus the adequacy of their cardiopulmonary system to ef fect oxygen transport during and between treatments is essential to establish. The optimal treatment pre scription is based on the patient's overall signs and symptoms of coronary insufficiency and hemody namic instability. The physical therapist must be knowledgeable in detecting inadequate myocardial tissue perfusion and in reducing and preventing my ocardial tissue damage. In addition, acute or chronic impaired heart pump function leads to reduced car diac output and systemic tissue perfusion. Clinical manifestations include reduced mentation, reduced renal function, fatigue, malaise, and moist, cool, and cyanotic skin. Regardless of whether the patient i s being treated in hospital, either on the ward or in the de partment, or in the private physical therapy clinic, the patient must be hemodynamically monitored. Minimall y, heart rate and blood pressure must be taken before, during, and after treatment, along with a subjective rating of anginal chest pain. ECG monitoring is usually continuous in the early stages of the infarction. The object of treatment is to have the patient remain below his or her anginal thresh old so that anginal pain is avoided. Breathlessness or rating of perceived exertion may also be used. The rate pressure product (RPP) (i.e., the product of heart rate and systolic blood pressure) is highly correlated with myocardial oxygen uptake and work. Previous stress tests will establish the RPP at which angina occurs and the intensity of the ex ercise dose should be set at 65% to 80% of this threshold. Patients on beta-blockers have a blunted hemodynamic response to exercise, particularly heart rate responses. Use of ratings of perceived exertion to define the upper and lower limits of an


27


491

acceptable mobilization stimulus may be indicated

they can undertake. Thus performing physical activ

in these patients.

ity and exercise while monitored and under the su

In some cases, patients have labile angina (i.e., the

pervision of a physical therapist is often reassuring

onset of angina does not occur reliably at a given

and gives the patient confidence for performing ac

RPP). This patient and the patient who reports angina

tivity when unsupervised.

at rest are at higher risk and appropriate precautions

The quality and quantity of the patient's sleep and

must be taken. First, the patient must be assessed to

a profile of sleep-wake periods should be reviewed to

establish that treatment is not precluded (see pertinent

ensure he or she is deriving maximal benefit. REM

questions to be answered before treating a patient

sleep with bursts of sympathetic activity during the

with angina). Second, monitoring is essential and

early hours of the morning may constitute a period of

may include ECG monitoring. Third, treatments are

increased risk for the cardiac patient.

prescribed below symptom threshold, which is usu

Appropriate safety precautions must be taken in

ally consistent with a low exercise intensity in these

all settings where physical therapists practice, given

patients. Comparable with any patient experiencing

that most physical therapy interventions physically

low functional work capacity, exercise prescribed on

stress patients and that coronary symptoms can occur

an interval schedule enables the patient to achieve a

regardless of whether the patient has a known under

greater volume of work.

lying heart disease. In addition, because the popula

Similar to the patient with angina, body positions

tion is aging, physical therapists are treating a grow

are selected for the patient with a myocardial infarc

ing number of older persons who are known to have a

tion that will minimize the work of breathing and of

higher prevalence of cardiovascular disease.

1968).

Good life-style habits are central to maximizing

Significant central fluid shifts are minimized by en

recovery and improving the long-term prognosis

the heart (Sonnenblick, Ross, and Bruanwald,

couraging the upright position as much as possible to

(e.g., good nutrition and hydration, good sleep habits,

reduce the work of the heart (Levine and Lown,

stress management, and regular physical exercise that

1952) and by maintaining the head of bed up to 10 to 15 degrees when the patient is recumbent. Patients

is prescribed by the physical therapist) (Underhill et aI.,

1989).

with elevated intracardiac pressures are less suscepti ble to orthostatism (Chapter

18).

Comparable with the management of the patient

SUMMARY

who has a history of angina, body positions, static

The primary acute cardiopulmonary medical condi

postures, activities, and respiratory maneuvers associ

tions that are treated by physical therapists include

ated with increased hemodynamic strain (e.g., breath

primary lung dysfunction (i.e., atelectasis, pneumo

holding) are avoided.

nia, bronchitis, bronchiolitis, alveolitis, alveolar pro

Relaxation is central in the management of the

teinosis, and acute exacerbations of chronic airflow

cardiac patient who is prone to being anxious and

limitation, asthma, cystic fibrosis, interstitial pul

apprehensive. Relaxation interventions include auto

monary fibrosis, and tuberculosis) and primary car

genic relaxation, progressive relaxation, Benson's

diac disease including hypenension, uncomplicated

relaxation response procedures. biofeedback, and

angina, and myocardial infarction. This chapter fo

1989). Also, the patient

cuses on the pathophysiology underlying these disor

meditation (Underhill et aI.,

needs to identify and minimize stress triggers and ef

ders and the mechanisms by which they threaten or

fective individual-specific nonpharmacological re

impair heart-lung interaction and oxygen transport.

laxants. Relaxation training with or without pharma

Thus the basis for the principles of cardiopulmonary

cological support can be integrated into treatment

physical therapy are described rather than specific

1989; Webber and Pryor, 1994).

treatment prescriptions. Treatment prescription is

(Underhill et aI.,

Patients with heart disease are often apprehensive

based on the effects of restricted mobility, recum

and anxious about the intensity of physical activity

bency, and extrinsic and intrinsic factors in addition


PART IV

492

Guidelines fOl" the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions

is directed

Bennett, W.o., Foster, W.M., & Chapman, W.E (1990). Cough

at the underlying pathophysiological mechanisms re

enhanced mucus clearance in the normal lung. Journal of Ap

to the underlying sulting from these four factors wherever

and

to symptom reduction. To prioritize treat

plie d Physiology,

(1988). Resource maaual for guidelines for exercise leslillg

interventions are ex

ments, the most

ploited foremost because these address multiple

and prescriplioll. Philadelphia: Lea

are instituted after the most physio

Lung immunogenicity, rejection, and obliterative bronchiolitis. Chesl, 92,547·549.

Chatham, K, Ben'ow, S .. Beeson. C, Griffiths, L., Brough. D" & Musa, L (1994). Inspiratory pressures in adult

interventions have been exploited or in con junction with these. The challenge of clinical lem

is

spect to oxygen transport with the least risk in the

fibrosis,

Physiorherap)" 80, 748-752,

Chung, F, & Dean, E. (1989). Pathophysiology and cardiorespira tory consequences of mterstitial lung diseasc:--review and clin

the optimal treatment

prescription that will effect the best results with re

& Febiger.

Burke, CM., Glanville. AR , Theodore, l, & Robin. E.D. (1987).

in the oxygen transport pathway. Less physiological , conventional

69, I 67()-1675,

Blair, S.N.. Painter, P., Pate, R,R., Smith, LX, & Taylor, CB.

ical implications. Phvsical Therap>", 69, 956-966 Clauss,R.H., Scalabrini, BY,Ray.R.F, & Reed, G.E. (1968), Ef fects of changing body posilion upon improved venliiation-per

shortest period of time.

fusion relationships. Circulalioll, 37 (SuppI4), 214-117. Cotton, D1.. Graham, BL. Mink. JT, & Habbick. B.t'. (1985). Reduction of the single breath diffusing capacity in cystic fibro

REVIEW QUESTIONS

sis. Europ ean Journal of Resp ira to ry Diseases, 66, 173-180.

I. Describe the primary cardiopulmonary patho

physiology of acute

pneumonia,

bronchitis, bronchiolitis,

alveolar pro-

acute exacerbations of chronic airflow

Cystic fibrosis and physical activity. (1988), illiemaliollul jouma! of SporlS Medicille,

xchange. Clinics in Chest Medicine,

lOry Care,

limitation, asthma, cystic fibrosis, interstitial and stable myocardial infarction.

2. Relate cardiopulmonary

ology of each of the above acute conditions and

Therapy,

Canada,

4/, 46-47.

Dean, E., &Ross, J. (1992a). Oxygen transport. The basis for con temporary cardiopulmonary physical therapy and

optimiza

tion with body positioning and mobilization. Physical Therapy

I, 34-44.

Dean, E. & Ross, 1. (I 992b). Mobilization and exercise condition

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Acute Surgical Conditions

Elizabeth Dean Maureen Fogel Perlstein Mary Mathews

KEY TERMS

Sedation

Anesthesia Cardiovascular surgery

Surgery

Risk factors

Thoracic surgery

INTRODUCTION

The four categories of factors contributing to or

The purpose of this chapter is to review the manage

threatening oxygen transport are described in Chapter

ment of cardiopulmonary dysfunction secondary to

16. Specifically, these factors include the underlying

acute surgical conditions. The cardiopulmonary ef

pathology, restricted mobility, and recumbency, ex

fects of surgery are described. The two types of

trinsic factors related to the patient's care and intrin

surgery that have the greatest impact on cardiopul

sic factors related to the patient. This chapter exam

monary function, namely, thoracic and cardiovascular

ines in detail the extrinsic factors related to surgery

surgery, are then presented. These surgeries are par

and anesthesia and the impact of underlying disease,

ticularly invasive and lengthy, require heavy and pro

restricted mobility, recumbency, and intrinsic factors

longed anesthesia and sedation, and are associated

on the effects of surgery and anesthesia.

with increased risk, thus warranting intensive periop erative physical therapy.

Treatment principles are presented. These are not intended to be a treatment prescription for a particular 495


496

PART IV


patient. The effects of surgery and anesthesia need to

Surgical Factors That Contribute to Perioperative Cardiopulmonary Dysfunction

be considered in addition to the underlying pathology, the effects of restricted mobility, body position, and intrinsic and extrinsic factors (see Chapter 28). All of

Type of surgery

these factors must be considered and integrated in the

Surgical procedures

treatment prescription and in defining the precise pa

Anesthetics (general, with or without intubation. or

rameters of the prescription. Such integration is es

regional) and sedation

sential for treatment to be specific and maximally ef

Muscle-relaxant agents and neuromuscular blockade

ficacious. For specific examples of patient treatment

Supplemental oxygen and humidification

prescriptions refer to the companion text Clinical

Static body position assumed

case studies in cardiopulmonary physical therapy.

Duration of surgery and static body positioning

PERIOPERATIVE COURSE

Incisions

Surgery and its Cardiopulmonary Consequences

Use of the cardiopulmonary bypass machine (CBM) Use of the extracorporeal membrane exchanger

Many factors contribute to perioperative cardiopul

(ECMO)

monary dysfunction (see the box at right). Anesthesia

Dressings and binders

and tissue dissection contribute to major changes in

Splints and fixation devices

lung volume, mechanics, and gas exchange. The ex

Lines and leads

tent and duration of these changes increase with the magnitude of the operative procedure and degree of

Monitoring devices

anesthesia required. Anesthesia results in depression

Chest tubes placement and number

of breathing. Thoracic respiratory excursion is signifi

Catheters

cantly reduced. The tone and pattern of contraction of

Perioperative pain

the respiratory muscles, particularly the diaphragm

Perioperative pain control management

and the intercostal muscles, change, which contributes

Peri operative fluid balance management

to many of the secondary cardiopulmonary effects ob

Perioperative blood and plasma transfusions

served after surgery (Muller, Volgyesi, B e cker, Bryan, and Bryan, 1979). The loss of end-expiratory diaphragmatic tone causes the diaphragm to ascend into the chest by 2 cm during anesthesia with or with out paralysis (Froese and Bryan, 1974). Reductions in

The consequences of reduced FRC with anesthesia

functional residual capacity (FRC) are correlated with

and surgery have significant implications for postop

this change and with altered chest wall configuration

erative complications and the course of recovery. Air

and increased thoracic blood volume (Hedenstierna et

way closure occurs with anesthesia and this likely

aI.,

1985; H e d e n s t i e r n a , Tokics, Strandberg, Lundquist, and Brismar, 1986). One of the most per

contributes to intrapulmonary shunting. Compression

vasive and predictable clinical effects observed in the

surgery. In addition, compression atelectasis occurs

atelectasis of the dependent lung fields occurs during

postoperative period is alveolar collapse. Total lung

when lung tissue and sur ounding structures are being

capacity, FRC, and residual volume are significantly

physically manipulated. Although reduced airway

decreased. The FRC is reduced by approximately I L

caliber in areas of low lung volume can be offset by

in supine compared with the erect sitting position

the airway-dilating effect of many inhaled anesthet

(Behrakis, Baydur, Jaeger, and Milic-Emili, 1983;

ics, airway resistance is increased by obstruction of

Nunn, 1989) and is further reduced with the induction

the breathing circuits, valves, and tracheal tubes. The

of anesthesia. Anesthesia, however, fails to reduce

airways may also be obstructed with foreign matter,

FRC in the sitting position (Nunn, 1989).

such as blood and secretions, or from bronchospasm


28


497

because of irritation of the airways. Because of the

fect is indicated. Patient controlled analgesia (PCA)

decrease in FRC, compliance is decreased and the

is an effective means of having the patient regulate

work of breathing is increased. Hypoxemia secondary

the amount of analgesia he or she is receiving. Intra

to transpulmonary shunting is usually maximal

venous administration prolongs the peak-effect time

within 72 hours after surgery and often is not com

of analgesics and therefore helps the patient tolerate

pletely resolved for several days. Persistent reduction

longer, more intense treatments. Transcutaneous elec

in FRC after surgery delays .the restoration of the nor

trical nerve stimulation (TENS) can be a useful ad

mal alveolar-arterial oxygen gradient (Alexander,

junct in the management of postoperative pain in

Spence, Parikh, and Stuart,

1973).

some patients. Pain control with TENS may enable

A complication of thoracic and upper abdominal

the patient to participate more fully in mobilization,

surgery, (e.g., cholecystectomy) is irritation or com

deep breathing, coughing, and bed mobility. Research

pression trauma of the phrenic nerve. This complica

is needed, however, to evaluate this technique in the

tion may be more common than expected. Inhibition

management of acute pain and define the prescription

of the phrenic nerve impairs the contraction of the af

parameters needed to produce an optimal therapeutic

fected hemidiaphragm, causing it to ascend into the

effect. A nonpharmacological, noninvasive means of

thorax and contribute to atelectasis on that side. This

managing acute pain would be of considerable bene

inhibition may last for several days (Dureuil, Viires, and Cantineau,

1986; Ford and Guenter, 1984).

fit to patients and would enable them to participate more fully in physical therapy treatments in the ab

The FIo2 depends on the mode of 100% oxygen administration. Low-flow nasal oxygen reduces hy

sence of untoward side effects often associated with drug administration.

poxemia in the absence of hypercapnia and marked

Although sedatives or tranquilizers are prescribed

transpulmonary shunting in the postoperative patient.

to make the patient more comfortable and to reduce

Low oxygen flows and low FI02S tend to be delivered

suffering, sedatives, in particular, reduce the patient's

via nasal cannulae, whereas higher flows can deliver

arousal and often the ability to cooperate actively

higher FIo2s via oxygen masks and masks with reser

with treatment. Thus these medications must be pre

voir bags. FIo2 and the body position of the patient at

scribed judiciously to ensure the patient is able to co

the time the blood sample was taken must always be

operate with physical therapy and other components

considered when interpreting arterial blood gases. The

of care. Oversedation must be avoided if the patient

FIo2 is selected to provide adequate oxygenation with

is to derive maximal benefit from cardiopulmonary

the lowest oxygen concentration possible.

physical therapy treatments.

After surgery the normal pattern of breathing is

Special attention in the postoperative period is

disrupted. Shallow, monotonous tidal ventilation

given to the prevention or management of cardiopul

without normal occasional, spontaneous deep breaths

monary complications associated with reduced arousal,

1989).

surgical pain, and restriction of lung capacity and sec

causes alveolar collapse within an hour (Nunn,

Unless resolved, atelectasis becomes increasingly re

ondary to dressings, binders, and diminished ability to

sistant to reinflation within a few hours. This compli

cooperate, move spontaneously, and hyperventilate the

cation is exacerbated in patients receiving narcotics.

lungs periodically. Patients are prone to aspiration in

Tachypnea and tachycardia are commonly ob

the immediate postoperative period, particularly while

served with gross atelectasis secondary to hypoventi

the sedation and anesthetic agents are wearing off.

lalion. Breath sounds are decreased at the bases, and

This risk is further increased if an airway is required or

the coarse wheezes associated with mucus obstruct

if an airway and mechanical ventilation is instituted.

ing airflow are heard on auscultation. Large areas of

Postextubation atelectasis must be anticipated and

atelectasis are present. Left lower lobe atelectasis is

avoided. To minimize this risk, patients are requested

common after cardiac surgery.

not to cat or drink fluids the day before surgery.

If narcotics impair the patient's ability to partici

Endotracheal intubation and mechanical ventila

pate in treatment, analgesia with a less systemic ef

tion are indicated if blood gases fail to improve with


498

PART IV


conservative management. See Chapter 32 for treat

tively, he or she will be better oriented and capable

ment priorities for a patient during ventilation and the

of cooperating when waking from anesthetic.

course of weaning from the mechanical ventilator.

The patient's position is changed frequently in the

The importance of a thorough preoperative as

initial postoperative period. The patient is usually en

sessment and teaching by the physical therapist can

couraged to change his or her body position fre

not be overstated. The components of preoperative

quently, transfer, sit in a chair, and ambulate as soon

teaching are summarized in the box below. In cases

as possible after surgery. The importance of frequent

of elective surgery, preoperative teaching includes a

postural changes and early ambulation in the initial

general description of the surgery to be performed,

postoperati ve period are stressed (Dull and Dull,

the effect of anesthesia and surgery on cardiopul

1983). Early ambulation is a priority in the manage

monary function, and the systemic effects of re

ment of all surgical patients unless contraindicated.

stricted mobility and recumbency. The lines, leads,

After surgery, the patient is detained in the recovery

and catheters usually associated with the surgery are

room until the vital signs have stabilized, there is no

explained. The patient i s instructed in breathing

apparent internal or external bleeding, and the patient

control maneuvers, supported coughing, chest wall

is responding to his or her name. Patients recovering

mobility exercises, mobility exercises for the limbs

from minor surgery are usually transferred to a ward

(e.g., hip and knee and foot and ankle exercises),

once discharged from the recovery room. A patient is

turning in bed, sitting up, transferring, chair sitting,

transferred to the ICU after surgery if complications

and walking erect postoperatively.

arise during surgery, if the patient cannot be readily

In addition, the

patient is taught methods of maximizing comfort

stabilized and requires close monitoring, or if the pa

with body positioning and supporting the surgical

tient has had more serious surgery such as cranial, car

incision. If the bed has controls the patient can ma

diovascular thoracic, or emergency surgery, such as

nipulate, she or he is taught how to make bed adjust

that resulting from mUltiple trauma (Chapter

34).

P a tients considered for elective surgery are

ments as required. The postoperative course is ex plained in general terms so the patient can anticipate

screened regarding their risks for postoperative

this period. If the patient is well informed preopera

complications. The physical therapist is often con-

Objectives of the Preoperative Physical Therapy Assessment and Teaching Develop rapport with patient Assess the patient and estimate degree of surgical risk (e.g .. age, smoking. previous cardiopulmonary dysfullction, neuromuscular dysfunction. musculoskeletal deformity, obesity. substance abuse, pregnancy. nutritional status, and hydration status) Describe the general preoperative, intraoperative, and postoperative course Review specific surgical procedures relevant to physical therapy (e.g., anesthesia. type of surgery. body position dur ing surgery, airway, mechanical ventilation, duration, incisions, infusions. drainage systems, chest tubes. and re covery room) Provide the rationale for, describe, demonstrate, and have the patient practice and provide feedback on the following breathing control maneuvers: maximal inspiratory hold, supported coughing maneuvers, relaxation, bed mobility and positioning, transfers, and mobilization For patients at risk of postoperative cardiopulmonary dysfunction and complications. review the use of the incelltive spirometer and conventional airway clearance interventions (e.g

.•

postural drainage and manual techniques if indicated)

Ask for any questions


28


499

su lted by the surgeon to help make a poor-risk pa

ing suboptimal, suprathreshold physiological states.

tient into a relatively better-risk patient. Patients

Suprathreshold states are associated with an inappro

wit h upper-respiratory tract infections before

priate balance between oxygen delivery and demand

surgery may have their surgeries postponed, de

such that the patient becomes compromised (e.g., he

pending on the type and extent of surgery to be per

modynamically unstable), cardiopulmonary distress

formed, levcl of anesthesia indicated, and other

is precipitated, or botb).

medical conditions, including cardiopulmonary dis ease, age, and smoking history. Patients with lower respiratory tract infections preoperatively constitute a greater operative risk, hence these patients often

Preparation for Surgery To minimize risk and reduce perioperative morbidity

have their surgeries postponed until the infection

and mortality, patients need to be in the best medical

has resolved. Patients with chronic cardiopulmonary

and physical condition before anesthesia and surgery.

diseases require a prolonged period of preoperative

In the case of elective surgery, some patients are pre

physical therapy in preparation for surgery. Elective

scribed modified aerobic training, smoking cessation,

surgery is not usually considered during an exacer

and weight control programs before surgery.

bation of chronic lung disease. Even minor surgery

Preoperative teaching is a central component of

may be potentially hazardous for the patient with

physical therapy management of the surgical patient.

previous lung disease. The adverse effects of total

Such teaching establishes rapport with the physical

anesthesia on these patients is magnified because of

therapist who informs the patient about what to ex

their reduced pulmonary reserve capacity. Smoking

pect before and after surgery. In addition to review

should be discontinued for as long as possible be

ing the surgical procedures, the physical therapist re

fore surgery. The patient is placed on an exercise

views, and has the patient perform, deep breathing

conditioning program, a regimen of bronchial hy

and supported coughing maneuvers, relaxation, bed

giene, oxygen if necessary, and prophylactic antibi

mobility, positioning, transfers, and mobilization.

otics. Even patients with extremely low functional

Preoperative teaching reduces the patient's anxiety

work capacity can enhance the efficiency of the

and encourages the patient to be as active as possible

steps in the oxygen transport pathway (Chapter 17)

in her or his recovery. Preoperative teaching reduces

with a modified aerobic exercise conditioning pro

postoperative complications and the length of the

gram. This preoperative preparation may take one to

hospital stay.

several weeks, depending on the patient and the in

There are no strict guidelines ahout which patients should receive peri operative physical therapy. Al

dications for surgery. Rest during the postoperative period is prescribed

though nonthoracic surgeries are generally associated

judiciously as treatment because rest is the time for

with fewer cardiopulmonary complications (e.g.,

healing, repair, and restoration. Sleep deprivation im

surgery of the extremities or lower abdomen), patients

pairs recovery and healing. Sleep at night is biologi

with preexisting cardiopulmonary, hematological or

cally more restorative than daytime sleep. Thus day

neuromuscular pathology, or musculoskeletal pathol

time and nighttime cues are given to restore the

ogy of the chest wall are at greater risk even in these

patient's circadian rhythms. Although injudicious and

relative low-risk types of surgeries. In addition, pa

excessive recumbency, bedrest, and prolonged peri

tients are at additional risk if they are older or

ods in any given body position are deleterious, spe

younger, smoke, or are overweight or pregnant. Thus

cial attention is given to maximizing the amount of

each surgical patient needs to be assessed individually

quality rest and sleep periods and minimizing disrup

to establish the degree of relative risk during surgery

tion of nighttime sleep. Rest needs to be prescribed

and the need for perioperative physical therapy. In this

both within and between treatments. Appropriate rest

way, perioperative complications can be anticipated

periods are interspersed witbin eacb treatment ses

and avoided or reduced, which is preferable to manag

sion, according to the patient's needs to avoid reacb

ing complications once they have developed.


500

PART IV

Guidelines for the Delivery of Cat'diopulmonary Physical Thet'apy: Acute Cardiopulmonary Conditions

MAJOR TYPES OF SURGERY

Factors Determining the Effect of Surgery A p atient's response to surgery and the cardiopul

Thoracic Surgery

monary complications that may develop depend on

Thoracic surgery refers to surgery necessitating

496). The type of

opening of the chest wall. By convention, this gen

many factors (see the box on p.

surgery determines the degree of invasiveness, the

eral term usually excludes specialized cardiovascular

type or types of anesthetics and sedatives, whether

surgery (i.e., surgery of the heart and great vessels).

the patient needs to be intubated, the static body posi

Thoracic surgery is commonly performed for lung

tion assumed during surgery, the approximate dura

resections secondary to cancer (e.g., pneumonec

tion of the surgery and period of anesthesia, the inci

tomy, lobectomy, segmentectomy, and wedge resec

sions that are required, the dressings, the lines, leads,

tion). In addition, thoracic surgery is performed to

catheters, and monitoring devices needed, the chest

remove an irreversibly damaged area of lung tissue

tubes, the type and degree of pain, and the need for

secondary to bronchiectasis, benign tumors, fungal

pain control after surgery.

infections, and tuberculosis. The most common incisions are posterolateral tho racotomy and median sternotomy. The posterolateral

Pathophysiology

thoracotomy procedure requires the patient to assume

The type and severity of underlying cardiopulmonary

the sidelying position with the involved side upper

dysfunction increases a patient's risk of compromised

most for the duration of the surgery. The uppermost

oxygen transport and gas exchange perioperatively.

arm is fully flexed anteriorly. The incision is made through an intercostal space, corresponding to the lo cation of the lesion to be excised. The muscles in

Restricted Mobility and Recumbency

cised include latissimus dorsi, serratus anterior, exter

Surgery imposes two nonphysiological states on the

nal and internal intercostals laterally, and trapezius

patient that impact significantly on oxygen transport.

and rhomboid posterioriy. At the conclusion of the surgery, chest tubes are

These conditions include the following: I. Restricted mobility

placed to evacuate air and fluid from the pleural space

2. Recumbency, specifically a prolonged period

by means of an underwater chest tube drainage sys

of static positioning with the patient breathing

tem. The chest tube and drainage system resolve the

at monotonous tidal volumes

pneumothorax created by reestablishing negative pres sure in the pleural space and help to reinflate the re maining atelectatic lung tissue. After thoracic surgery,

Extrinsic Factors

two chest tubes are usually inserted, one at the apex of

496 are

the lung to evacuate air and one at the base of the lung

the p rimary extrinsic factors contributing to cardiopul

Surgery including the factors in the box on p.

to drain serosanguinous fluid. The therapist should be

monary dysfunction in the perioperative period.

come familiar with the various drainage systems, how drainage can be facilitated with mobilization and body positioning coordinated with breathing control and

Intrinsic Factors

supported coughing malleuvers, and certain precau

Intrinsic factors that contribute to cardiopulmonary

tions that need to be observed to avoid impairing

dysfunction in the surgical patient include a patient's

drainage or disconnecting the tubing.

premorbid status (e.g., preexisting cardiopulmonary,

Provided the chest tubes are not kinked, there is

renal, endocrine, and hematologic pathology). In ad

no contraindication to lying on the side of the chest

dition, life-style factors are significant (i.e., preopera

tubes. Lying on this side, which is usually the side

tive conditioning level, nutrition, hydration, stress

of the surgery and incision, is typically avoided by

levels, weight, and smoking history).

the patient. Consistent with the adage, "down with


28

the good lung," a patient prefers to lie on the non surgical side. However, prolonged periods in any position, and particularly, lying on the unaffected side, places these lung fields at risk. To minimize the risk of positional complications and hypoxemia, the patient is encouraged to turn to both sides (Leaver, Conway, and Holgate, 1994; Seaton, Lapp, and Morgan, 1979; Sutton, Pavia, Bateman, and Clarke, 1982). The specific positions and the dura tion of time spent within each, however, is based on a comprehensive assessment of the patient's condi tion and the indications and contraindications for each body position. Patients may appear to splint themselves, thereby

restricting chest wall motion, to avoid including pain when moving and deep breathing. They also may re sist maximal inspiratory efforts when coughing. Al though pain likely contributes to breathing at low lung volumes and ineffective coughing, phrenic nerve inhibition in patients with thoracic and upper abdomi nal surgeries is likely a more important factor re stricting lung expansion than is fully appreciated in many patients (Ford and Guenter, 1984). Postoperative complaints of pain are both muscu loskeletal and pleural in origin. The large number of muscles incised, particularly in the posterolateral tho racotomy incision, combined with the operative posi tion, contributes to the patient's complaints of chest wall pain, shoulder soreness, and restricted move ment. Deep breathing and coughing maneuvers may be associated with considerable discomfort after surgery. Pain is accentuated by apprehension and anxiety. Therefore treatments are coordinated with relaxation, noninvasive pain control modalities, and

pain medication schedules to elicit the full coopera tion of the patient. Cardiovascular Surgery Cardiovascular surgery is specialized thoracic surgery involving the heart and great vessels. Be cause the flow of blood through the cardiopulmonary system is interrupted, the patient is placed on a car diopulmonary bypass machine or on a machine called an extracorporeal membrane oxygenator. Cardiovas cular surgery is most commonly performed for coro


501

nary artery bypass grafting, valve replacements, and aneurysm repairs. Bypass patients, in whom the saphenous vein is excised for graft material, have the added complication of surgery and wound healing in one leg. Mobility exercises on that leg are often re stricted until there is no risk of bleeding or interfer ence with healing. Comparable with the thoracic sur gical patient, a cardiovascular patient leaves the operating room with various monitoring Jines and leads, intravenous fluid infusions, possible blood or plasma infusions, a Swan-Ganz catheter (Chapter 15), a central venous pressure line, an arterial line, a Foley catheter, and oxygen cannulae. The preoperative preparation and teaching and the postoperative physical therapy management is intensive. Because of the invasiveness of cardiovas cular surgery, patients are usually treated postopera tively in a specialized intensive care unit (Chapter 31). The preoperati ve and postoperative physical therapy management of patients in the intensive care unit is a specialized area and is described in Chapter 34. Providing the patient with information about what to expect during the perioperative course re lieves fear and anxiety. In addition, relaxation pro cedures can be useful. Patients need to be reassured that their incisions and suture lines will not be dis rupted with movement and physical therapy and that supported coughing and supporting themselves when moving will maximize comfort. Until the pa tient has stabilized, the patient's mobility is re stricted to low-intensity mobilization to promote its benefits on gas exchange and reduce metabolic de mands and body positioning to optimize alveolar ventilation coordinated with deep breathing and supported coughing maneuvers. Conventional air way clearance interve n tio ns (e.g., postural drainage and manual techniques) may be prescribed in the presence of excessive secretions, difficulty in mobi lizing secretions, and in the event of productive hy drostatic pneumonia. Patients undergoing cardiovascular surgery are transferred from the cardiovascular intensive care unit to the ward as quickly as possible. From the ward, these patients should be referred to a physical therapist and a cardiac rehabilitation program in the community for continuity of care and to maximize


502

PART IV


the functional gains resulting from the surgery. Exer cise is prescribed progressively to maximize oxygen transport at each step of the rehabilitation period (i.e.,

Goals of Postoperative Physical Therapy Related to Oxygen Transport

acute, before and immediately after discharge, and

Maximize arousal

long term). The conditioning effects of exercise en

Maximize alveolar volume

able the patient to resume various activities of daily living commensurate with an increasing capacity of the patient's oxygen transport system to meet the de mands of these activities. Activities involving strain ing and isometric contractions are avoided. Weight lifting may be introduced in a long-term rehabilita

Optimize alveolar ventilation Optimize perfusion Maximize lung volumes and capacities, especially functional residual capacity Minimize closing volume

tion program, but the weights are not sufficient to

Minimize intrapulmonary shunting

cause strain. Patients with median sternotomy inci

Optimize lung compliance

sions are usually prohibited from using their anns to

Optimize mucociliary transport

support themselves when sitting or driving and dur ing activities that may strain the incision site for sev eral weeks or more.

Optimize mucous clearance Optimize ventilation and perfusion matching and gas exchange Maximize expiratory flow rates

PREOPERATIVE PHYSICAL THERAPY:

Maximize chest tube drainage

PRINCIPLES OF MANAGEMENT

Optimize fluid balance systemically (renal function)

Preoperative management includes assessment and

Optimize lung water balance and distribution

preoperative education; the primary components are

Promote optimal lymphatic draining

shown in the box on p. 498. During this time the phys ical therapist has an opportunity to develop rapport with the patient. The assessment establishes the risk of cardiopulmonary complications and prolonged hospi

Minimize third spacing and collection of fluid Minimize the risk of aspiration Minimize undue work of breathing

tal stay and the type and extent of perioperative physi

Minimize undue work of the heart

cal therapy required. The assessment establishes what

Maximize chest wall mobility and movement in

the postoperative priorities will be; however, these are modified based on the postoperative assessment. The surgical procedures are described and the effects of

three planes Optimize body and posture alignment when sitting, standing. walking, and recumbent

surgery and anesthesia and sedation on gas exchange

Optimize circulatory status and tissue perfusion

are reviewed so that the patient understands the im

Optimize peripheral blood flow and velocity

portance of being actively involved in physical ther apy, both dUling and between treatments after surgery.

Optimize muscle pump actioll Minimize effects of central fluid shifts with recum bency

POSTOPERATIVE PHYSICAL THERAPY:

Maintain t1uid-volume regulating mechanisms

PRINCIPLES OF MANAGEMENT

Minimize pain nonphal1nacologically and coordinate

The goals of postoperative physical therapy manage ment related to oxygen transport appear in the box at

with the patient's pain medications if indicated Maximize cardiopulmonary endurance

right. It is essential that these goals are addressed be

Optimize relaxation

tween and during treatments. Thus the patient is in

Provide instruction to patient on "between-treat

structed in mobilization and body positioning coordi nated with deep breathing and supported coughing


ment" treatment

28

maneuvers between treatment sessions, and these in


503

going thoracic or cardiovascular surgery, are usually

terventions should be performed hourly during wak

extubated before leaving the operating room or re

ing hours (Bennett, Foster, and Chapman, 1990;

covery area. Provided no complications develop,

Blomqvist and Stone, 1983; Bourn and Jenkins,

most other patients do not require an airway. Patients

1992; Hasani, Pavia, Agnew, and Clarke, 1991; Hiet

undergoing major thoracic surgery or cardiovascular

pas, Roth, and Jensen, 1974; Orlava, 1959). Pain

surgery remain intubated and mechanically ventilated

medications are coordinated as needed with treat

from several to 24 hours after surgery to minimize

ments to maximize treatment efficacy.

the work of breathing and hence the work of the heart

In addition to goals related to oxygen transport, other important postoperative goals include the following:

to meet the metabolical demands of respiration. These patients are informed that artificial airway and

I. Maximize joint range of motion

mechanical ventilation enables them to breathe more

2. Maximize muscle length and ligament integrity

efficiently initially. A patient is also informed that he

with range of motion exercises

or she will not be able to speak while the airway is in

3. Maximize patient's ability to perform activities of daily living

place and may have a sore throat after its removal. Patients are usually aroused and repositioned be

4. Maintain or increase general muscle strength and endurance

fore leaving the operating room, although this is sel dom remembered by patients. Not recalling the im

5. Maintain normal cognitive function to avoid

mediate postoperative course is common. Patients are

disorientation and hospital-related psychoses.

likely to be receiving some form of pharmacological

These goals are achieved with the prescription of

analgesia (e.g., morphine). If blood was required in

general mobility exercise, including hip and knee

traoperatively, whole blood, packed cells, or plasma

flexion and extension exercises and foot and ankle

may still be infused in the immediate postoperative

exercises. These exercises are performed hourly re

period or longer. Saline or other solutions are also in

gardless of whether the patient is sitting in the chair

fused for regulation of fluid balance until the patient

or resting in bed.

is able to drink and eat normally. Once vital signs

Finally, there are important preventative goals

have stabilized, wounds are stable and not draining,

(e.g., minimizing the effects of restricted mobility and

and the patient reasonably alert, the patient is trans

recumbency on all organ systems) (Chapters 17 and

ferred to the ward. The patient is retained in the re

l8). Of particular concern in the surgical patient is the

covery area should further monitoring be required. If

risk of thromboemboli and pulmonary emboli and the

complications develop and oxygen transport and gas

risk of pressure points and skin breakdown. Thus mo

exchange threatened, the patient may be transferred

bilization and regular activation of the muscle pumps

to the intensive care unit.

to minimize circulatory stasis and frequent body-posi

The physical therapist may be consulted to assess

tion changes are essential to reduce risks, which can

and treat the patient as soon as he or she leaves the

have serious consequences for the patient's recovery.

operating room or while in the recovery room. Most

Compression stockings are often put on the patient

frequently the physical therapist sees the patient once

after surgery. These are not removed other than for

he or she has been transferred to the ward and has

cleaning and redistributing pressure until the patient is

been settled. The first 24 hours are critical.

consistently up and about. These stockings facilitate

The risk of cardiopulmonary complications is

venous return and increase blood flow and velocity,

greatest during the perioperative period and dimin

thereby minimizing the risk of thrombus formation.

ishes as the patient becomes increasingly upright and

Should thrombus formation be suspected, an intermit

mobile. Atelectasis and aspiration after extubation are

tent compression device may need to be attached to

significant risks for the patient who has been intu

the legs to simulate muscle pump action.

bated. The goal immediately after extubation is to

Not all patients who have surgery are intubated.

promote optimal alveolar ventilation, maximize lung

Those that are, with the exception of patients under

volumes and capacities (especially FRC), minimize


504

PART IV


closing volumes, and maximize expiratory flow rates

There are several factors that are particulary im

and hence cough effectiveness. Areas most suscepti

portant in surgical patients that can affect their sensi

ble to atelectasis are those that may have been physi

tivity to narcotic analgesics, such as morphine

cally compressed during surgery (e.g., the left lower

(Gilman, Goodman, and Gilman, 1990: Malamed, 1989). First, there is considerable intersubject re

lobe of the cardiovascular surgical patient and areas adjacent to a lobectomy or segmentectomy). Surgery constitutes a significant insult to the body.

sponse variability to these agents. Second, older pa tients can be expected to be more sensitive to nar

After the trauma of surgery, anesthesia, sedation,

cotics. Three, diverse multisystem pathology has a

fluid loss, incisions, and the significant energy re

significant effect on the degradation, absorption, bio

quirements for healing and repair, patients can be ex

transformation, and excretion of morphine. Four, ex

pected to be lethargic and difficult to arouse. The re

aggerated effects of morphine have been reported

laxed state induced by anesthesia, sedation, and

when administered in conjunction with other agents,

narcotics increases the risk of aspiration. This risk is

such as other narcotic analgesics, phenothiazines,

exacerbated further in some patients by nausea and

tranquilizers, or sedative-hypnotics; in addition, such

vomiting associated with anesthesia and narcotics.

exaggerated effects have been reported in patients

Moving and positioning the patient upright whenever

with respiratory depression, hypotension, and seda

possible and interacting with the patient stimulates

tion and in patients who are unconscious. These situ

the reticular activating system making the patient

ations in which exaggerated drug effects have been

more responsi ve and aroused. The increased meta

reported are commonly encountered in the intensive

bolic demands that this requires, along with increased

care setting and can result in unpredictable responses.

catecholamine release, helps overcome the residual

Finally, the physical dependence and abuse potential

effects of anesthesia, sedation, and muscle relaxants

of these agents cannot be ignored.

and their threat to oxygen transport, provided the de

The physical therapist must be familiar with the

mands are not beyond the capacity of the oxygen

patient's medications and the medication's indica

transport system to deliver oxygen.

tions, side effects, and contraindications. The physi

Alternatively, some patients are restless and agi

cal therapist can determine to what extent oxygen

tated after the effects of anesthesia have worn off.

transport may be compromised by medication effects,

Hypoxemia can lead to restlessness and agitation.

whether some recommendation needs to be made to

Thus it is important that these patients are not inap

minimize untoward drug effects on arousal or some

propriately sedated. This compounds their need for

other factor that negatively affects oxygen transport

treatment while making them less able to cooperate

and gas exchange. For example, although narcotics

with treatment simultaneously (Dripps and Waters,

are excellent analgesics, they have widespread sys

1941; Ross and Dean, \989).

temic effects including cardiopulmonary depressant

At the outset of any treatment, the patient must be

effects, gastrointestinal depressant effects, and mus

aroused as much as possible to cooperate fully and

cle relaxant effects-all of which compromise oxy

derive the maximal benefit from treatment. The phys

gen transport. Thus consideration needs to be given

ical therapist interacts continuously with the patient

regarding whether other forms of analgesia can be

to arouse the patient fully, maintain arousal, stimulate

used. Have nonpharmacological means of analgesia

normal cognitive function and orientation, and elicit

been exploited? If pharmacological analgesia is indi

feedback from the patient to assess the response to

cated, can analgesics other than narcotics be used? Or

treatment. Narcotics depress respiratory status and

at least, can the dose of narcotic be reduced so that

arousal, and these effects are accentuated in patients

satisfactory pain control can be achieved in combina

whose metabolic states have been disrupted with ill

tion with nonpharmacological interventions?

ness and in older persons. Thus the physical therapist

Mobilization in the upright position coordinated

must be vigilant in detecting untoward residual ef

with breathing control and supported coughing ma

fects of narcotics in the surgical patient.

neuvers is encouraged immediately after the patient is


28


505

first aroused after surgery, unless contraindicated, to

cilitate frequent turning. Cycle pedals can be adapted

help reverse and mitigate reduced arousal, atelectasis,

to chairs and recumbent exercise in bed if necessary.

FRC, and impaired mucociliary transport associated

Patients whose positioning is restricted with fixation

with surgery. Mobilization augments cardiopul

and traction devices require hand, wrist, or ankle

monary function (see Chapter 1 7) particularly when

weights, and possibly pulleys and other devices, to

the patient is upright (Levine and Lown, 1952;

maintain muscle strength and power. Movements per

Lewis, J 980). These beneficial effects are enhanced

formed with moderately heavy weights for multiple

by improved three-dimensional chest wall motion,

sets (e.g., three sets of 10 repetitions) develop muscle

improved gut motility, and reduced intraabdominal

strength. Movements performed with lighter weight

pressure. Extremity movement during ambulation in

for multiple sets (e.g., 5 to 10 sets of 10 repetitions)

creases alveolar ventilation, enhances ventilation and

tend to develop endurance and aerobic capacity. Be

perfusion matching by increasing zone 2 of the lungs,

cause of the restrictions imposed by these devices,

and optimizes diffusing capacity. The upright posi

maintaining joint range is essential (i.e., of the neck,

tion is essential such that the spine is erect, upper

spinal column, and chest wall, as well as the extremi

body musculature relaxed, and the chest wall sym

ties). The rotation component of joint movement is

metrical. Slouching and leaning particularly to the af

readily compromised, thus this needs to be an integral

fected side reduces alveolar ventilation and con

component of joint range of motion exercises. Propri

tributes to uneven distribution of ventilation and

oceptive neuromuscular facilitation (PNF) move

areas of atelectasis (Bake, Dempsey, and Grimby,

ments of the extremities can be beneficial. PNF

1976; Don, Craig, Wahba, and Couture, 1971; Glais

movements of the chest wall can be coordinated with

ter, 1967). In addition, if this abnormal posture is

breathing control and supported coughing maneuvers.

maintained, mucociliary transport of the area is im

Upper body and trunk mobility and strengthening are

paired and mucus collects and stagnates, increasing

important goals particularly in the patient with chest

the risk of bacterial colonization and infection. Sym

wall incisions. The prescription is progressed gradu

metrical posture is monitored at a] I times (i.e., during

ally in the patient with a chest wall incision, particu

ambulation, sitting at bedside, bed mobility exercises,

larly in the patient with a median sternotomy who is

sitting up in bed, and lying in bed). Slouching and fa

usually restricted to unresisted, upper-extremity mo

voring the affected side will lead to cardiopulmonary

bility exercises in the first several weeks.

complications and possibly musculoskeletal compli cations in the short and long term.

Prescription of body positioning is essential in the management of the surgical patient for two reasons.

Mobilization and active exercise in upright pos

First, without direction, the patient will tend to as

tures whenever possible are prescribed based on the

sume a deleterious body position (i.e., maintaining a

need to enhance multiple steps in the oxygen trans

restricted number of body positions that favor the af

port pathway (Dean and Ross, 1992; Ray et aI.,

fected side for prolonged periods of time with mini

1974). The priority is to perform as much activity as

mal movement and "stirring up"). Thus once the ef

possible out of bed ancl upright (i.e., ambulation,

fects of mobilization have been exploited in a given

transferring, sitting upright in a chair, and chair exer

treatment session, body positions are prescribed for

cises with or without hand weights or exercise

"between-treatment" times that continue to enhance

bands). When in bed, similar devices can be used, in

oxygen transport for a given patient and discourage

cluding a monkey bar to facilitate moving in bed for

excessive time in deleterious body positions. When

patients other than cardiovascular thoracic patients

not ambulating, patients are encouraged to assume a

(e.g., the orthopedic patient with extremity fractures

wide range of body positions (e.g., semi-prone) be

and traction). In addition, the use of the monkey bar

tween treatments, as frequently as possible, (i.e., at

to perform repetitive bouts of exercise to maintain

least every I to 2 hours) (Dean, 1985; Douglas, Re

upper-extremity strength and some general endurance

hder, Beynen, Sessler, and Marsh, 1977; Piehl and

capacity, to relieve pressure and stiffness, and to fa

Brown, 1976; Remolina, Khan, Santiago, and Edel


506

PART IV


FIGURE 28-1

Incentive spirometers.


28

man, 19S I; Ross and Dean, 1992; Zack, Pontoppidan,


507

mizing FRC, reducing closing volume, maximizing expiratory flow rates, promoting mucociliary trans

and Kazemi, 1974). Alveoli are likely to remain patent for I hour after

port, promoting airway clearance, optimizing lym

reinflation. Thus to sustain alveolar inflation and nor

phatic drainage, minimizing the effects of increased

mal FRC, mobilization and body positioning coordi

thoracic blood volume, maintaining fluid-volume

nated with breathing control and supported coughing

regulating mechanisms, and minimizing the work of

must be carried out frequently (i.e., every I to 2

breathing and of the heart. Sustained maximal inspi

hours) to maintain optimal alveolar volume and dis

ration is one intervention that promotes alveolar ex

tribution of ventilation. Maximal inspiratory maneu

pansion. Each deep breath is performed to maximal

vers are coordinated with mobilization and body po

inspiration to total lung capacity with a 3- to 5-sec

sitioning at \east every hour as tolerated. Maximal

ond breath hold. This maneuver may reduce pul

inspiratory maneuvers alone, however, are unlikely to

monary complications by promoting alveolar infla

be effective because the inspiratory pressure may be

tion and gas exchange. The patient is encouraged to

insufficient to inflate atelectatic alveoli. Rather patent

repeat this maneuver several times hourly, and fre

alveol i will tend to be overexpanded. Mobilization

quently during mobilization, and before, during, and

and body positioning will directly alter the in

after body-position changes.

trapleural pressure gradient and thereby optimize alveolar expansion (Roussos et at. 1977).

Incentive spirometry can be useful in patients who are resistant or unable to cooperate fully with maxi

Normal passive expiratory efforts to end tidal

mal inspiratory efforts (Figure 2S-I ). Postoperative

volume are encouraged and maximal or forced expi

hypoxemia may be reduced with this technique,

ratory efforts are usually avoided to prevent airway

which uses the principle of sustained inspiration

closure and potential increase of atelectasis (Has ani

using a feedback device (either flow or volume feed

et aI., 1991; Hietpas et aI., 1974; Nunn, Coleman,

back) to achieve maximal inflating pressure in the

Sachithanandan, Bergman, and Laws, 1965). Huff

alveoli and maximal inhaled volume. The incentive

ing (glottis open) rather than coughing (glottis

spirometer can be used independently by the patient.

closed) also minimizes airway closure. There is less

This technique ensures that each inspiration is physi

risk of bronchospasm than with coughing in which

ologically optimal and is reproduced precisely from

the glottis is closed, transpulmonary pressure is in

one inspiration to the next. Patients who are surgical

creased, and a compressive phase is involved. If in

risks can benefit from being taught the use of the in

dicated, coughing maneuvers are most effective in

centive spirometer during preoperative teaching by

the sitting or slightly lean-forward position in which

the physical therapist to promote better inflation of

lung volumes and forced expiratory flow are maxi

the lungs with incentive spirometry postoperatively.

mized and the respiratory muscles are mechanically

The patient continues with a regimen of breathing

advantaged with respect to the length-tension char

control and coughing maneuvers until full mobility

acteristics of the muscle fibers. Airway closure is

and activities of daily living are resumed.

position-dependent (Chapter IS); therefore the de

The application of intermittent positive pressure

gree of expiration encouraged by the physical thera

breathing (IPPB) appears to be less effective for the

pist should be based on the patient's body position.

postoperative patient than previously believed. The

Airway closure is potentiated in patients who are

details of this modality are described in Chapter 41.

older, smoke, or are obese and in patients who are in horizontal as opposed to upright body positions. M obilization and body posi tioning coordinated

SUMMARY

with breathing control and supported coughing ma

This chapter reviews the management of cardiopul

neuvers offer the greatest benefit to oxygen transport

monary dysfunction secondary to acute surgical con

in the postoperative patient. Specific benefits are de

ditions. Surgery and its physiological effects are de

scribed in Chapters 17 and IS. They include maxi

scribed. Special reference is made to two specialized


508

PART IV


types of surgery that have the greatest impact on car diopulmonary function, namely, thoracic and cardio vascular surgery. The four categories of factors contributing to or threatening oxygen transport are described in Chapter 16. These factors include pathology, restricted mobil ity and recumbency, extrinsic factors related to the patient's care, and intrinsic factors related to the pa tient. This chapter examines in detail those extrinsic factors related to surgery and anesthesia, and the im pact of underlying disease, restricted mobility, re cumbency and intrinsic factors on the effects of surgery and anesthesia. In this chapter, treatment principles are pre sented rather than treatment prescriptions for partic ular patients. For specific examples of patient treat ment prescriptions refer

to

the companion

workbook Clinical case studies i n cardiopulmonary physical therapy.

Bennett, W.D., Foster, W.M.,

&

Chapman, W.F. (1990). Cough

enhanced mucus clearance in the normal lung. journal of Ap plied Physiology.

&

Blomqvist, e.G.,

69,

1670-1675.

Stone, H.L. (1983).

Cardiovascular adjust

ments /0 graviratiollal stress. Handbook ofphysi()lo y (Vol. 2). Washington, DC: American Physiological Society.

&

Bourn, J.,

Jenkins, S. (1992). Post-operative respiratory physio

78,

therapy. Indications for treatment. Physiotherapy, Dean, E.

(1985).

Physical Therapy, Dean, E.,

&

80-85.

Effect of body position on pulmonary function.

65,

613-618.

Ross, J. (1989). Integrating current literature in the

management of cystic fibrosis: a rejoinder. Physiotherapy Canad{1, Dean,

E., &

4/, 46-47. Ross, J. (1992).

Mobilization

and

exercise condition

ing. In e.e. Zadai (Ed.), Puhllo/1ary management in physical therapy. New York: Churchill Livingstone. Don. H.F., Craig, D.B., Wahba, W.M"

&

Couture, J.G. (1971). The

measurement of gas trapped in the lungs at functional residual capacity and the effects of posture. Anesthesiology,

K.,

Douglas, W.W., Rehder.

35,

582-590.

Beynen, F.M .. Sessler, A., D.,

&

Marsh, H.M. (1977). Improved oxygenation in patients with acute respiratory failure: the prone position. American Review oJ Respiratol), Dripps. RD.,

&

Disease,

//5,559-566.

Waters, R.M. (1941). Nursing care of the surgical

4/, 53-34. & Dull, W.L. (1983). Are maximal inspiratory breathing ex

patient. I. The "stir-up." American .lournal of Nursing,

REVIEW QUESTIONS

Dull,1. L.,

1. Describe the physiological effects of surgery in cluding the specific surgical procedure, the type, depth and duration of anesthesia, sedation, types of respiratory support, static body positioned as sumed during surgery, length of surgery, number and type of invasive periooperative procedures, and incisions.

ercises or incentive spiromeny betler than early mobilization after cardiopulmonary bypass surgely? Physical Therapy, Dureuil, B., (Viires, N.,

&

contractility after upper abdominal surgery. journal oJ Applied

6/, /775-1780. & Guenter. e.A. (1984).

Physiology, Ford, G.T.,

3. Relate cardiopulmonary physical therapy treat ment interventions to the underlying pathophysiol ogy associated with surgery and those factors listed in Question 1 and provide the rationale for your choice.

Toward

prevention of postop

erative complications. American Review of Respiratol)' Dis· eases,

/30,

4-5.

& Bryan, A.e. paralysis on diaphragmatic 4/,242-255.

Froese, A.B. ,

2. Describe surgical risk factors.

63, 655-659.

Cantineau, J.P. (1986). Diaphragmatic

(1974).

ErI'eCls

of anesthesia and

mechanics in man. Anesthesiology,

Glaister, D.H. (1967). The effect of posture on the distribution of ventilation and blood flow in the normal lung. Clinical Science,

33,

391-398

Gilman, A.G., Goodman, L.S., and

Gilnwn's th e

&

Gilman, A. (1990). Goodman

plwrmacological basis of therapeutics (8th

ed.). New York: Macmillan Publishing. Hasani, A., Pavia, D., Agnew, J.E.,

References

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Stuart, B. (1973).

The role of airway closure in postoperative hypoxaemia. British journal ofAnaeslhesiology, Bake, B., Dempsey, J.,

(1991). The ef

fect of unproductive coughinglFET on regional mucus move

&

59, 1070- 1 079.

85, 23-26.

Hedenstierna, G., Standberg, A.; Brismar, B., Lundquist, H., Sven son, L.,

&

Tokics, L. (1985). Functional residual capacity, Iho

racoabdominal dimensions and central blood volume during

Grimby, G. (1976). Effects of shape

on distribution of inspired gas. Amer icall Review of Respira/ory Disease, //4, 1113-/120. Behrakis, P.K., Baydur, A., Jaeger, M.J., & Milic-Emili, J. (1983). changes of the chest wall

general anesthesia with muscle paralysis and mechanical venti

lation.

Anesthesiology,

62, 247-254.

Hedenstierna, G., Tokics, L., Strandberg, A., Lundquist, H.,

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Brismar, B. (1986). Correlation of gas exchange impairment to

Lung mechanics in sitting and horizontal body positions. Ches/,

development of atelectasis during anaesthesia and muscle

83,

paralysis. Acta Anaesthesiologica Scal1dinavica,

643-646.


30, 183-191.


28

Hietpas, B,G" Roth, RD, & Jensen. W,M. (1974), Huff coughing and

patency, Respiratory Care, 24, The incidence

of post-operative hypoxaemia following a

and pneu

pilot study, PhysiOlherapy, 80.

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shunting, Archi ves

pulmonary Khan, A.U"

Santiago, T.V"

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(1981), Positional hypoxemia il) unilateral lung disease, New England Journal of Medicine.

Levine, S,A" & Lown, B, (1952), 'Armchair' treatment of acute

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537-54 L Remolina,

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Leaver, H" Conway. JR, & Holgate, S,T, ( monectomy:

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treatment of pneumonia. Physical Therapy Review, 39, 153-160,

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I/O, 149-153,

PAR T

V

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions


Chronic Primary Cardiopulmonary Dysfunction Elizabeth Dean Donna Frownfelter

KEY TERMS

Angina

Hypertension

Asthma


Bronchiectasis

Lung cancer

Chronic airflow limitation

Myocardial infarction

Cystic fibrosis


Diabetes

Val vula heart disease

INTRODUCTION

there is no clear line between obstructive and restric

The purpose of this chapter is to review the pathophys

tive patterns of lung disease, pathology can be gener

iology, medical management, and physical therapy

ally defined based on the primary underlying patho

management of chronic, primary, cardiopulmonary

physiological problems. Thus the primary conditions

pathology. Because the heart and lungs are interdepen

that are presented include obstructive lung disease

dent and function as a single unit, primary lung or

(i.e., chronic airflow limitation, asthma, bronchiecta

heart disease must be considered with respect to the

sis, and cystic fibrosis) and restrictive lung disease

other organ and in the context of oxygen transport

(i.e., interstitial pulmonary fibrosis). Lung cancer,

overall (Dantzker, 1983; Ross and Dean, 1989; Scharf

which has the characteristics of both obstructive and

and Cassidy, 1989; Wasserman and Whipp, 1975).

restrictive patterns of patho.logy, is also presented.

The long-term cardiopulmonary management of

The long-term cardiopulmonary management of

chronic lung diseases is presented first. Although

heart disease is then presented with special attention 513


514

PART V


to angina, myocardial infarction, and valvular heart

breathing re s ponse to vertilatioll-perfusion imbalance

disease. Chronic vascular diseases, including periph

and hypoxemia, and tissue defenses against elastase. Decline in pulmonary function and rate of devel

eral vascular disease, hypertension, and diabetes, are

opment of the syndrome depend on the combination

also presented. The principles of management of the various

of causative factors and individual responses to them.

chronic primary cardiopulmonary conditions are pre sented rather than treatment prescriptions, which can not be discussed without consideration of a specific

Chronic Bronchitis


patient. (For specific examples of patient treatment prescriptions refer to the companion test Clinical case

Chronic bronchitis is usually associated with a his

studies in cardiopulmonGl)1 physical therapy.) In this

tory of smoking and is defined as mucous hyper

context the goals of long-term management of each

secretion and cough producing sputum for three

condition are presented, followed by the essential

months or more over a two-year period (Murray and

monitoring required, and the primary interventions for

Nadel, 1988a). Over the first few years of smoking,

maximizing cardiopulmonary function and oxygen

reversible airways changes occur. Over 10 to 15

transport. The selection of interventions for any given

years of smoking, mucous hypersecretion and chronic

patient is based on the physiological hierarchy. The

bronchitis become apparent. After 25 to 35 years of

most physiological interventions are exploited first

smoking, irreversible airway damage and chronic dis

followed by less physiological interventions and those whose efficacy is less well documented (Chapter

16).

ability occur. Smoking is the major cause of lung cancer. The pathophysiology of chronic bronchitis is reviewed in detail in Chapter 29. The patient is prone to infection and repeated peri

PRIMARY PULMONARY DISEASE

ods of morbidity. Deterioration of aerobic capacity

OBSTRUCTIVE PATTERNS

and functional capacity is related to the severity of the condition. Nutrition and hydration may be im

Chronic Airflow Limitation

paired particularly in severe cases because of neglect

Chronic airflow limitation is a descriptive term that

and the excessive energy cost of activities of daily

refers to those disorders that previously have been

living. Sleep may be irregular, thus the patient's

termed chronic obstructive pulmonary disease (e.g.,

symptoms are worsened (e.g., reduced endurance, fa

chronic bronchitis, emphysema, bronchiectasis, and

tigue, and lethargy) because of lack of normal physi

cystic fibrosis). Although there may be a reversible

ological restoration from sleep.

component, airflow obstruction associated with these

The natural history of chronic bronchitis related to

disorders is largely irreversible. The pathophysiology

smoking includes mucous hypersecretion, reduction in

of these conditions is reviewed in detail in Chapter 29.

forced expiratory volume (FEV), and increased hetero

Bates (1989) described the syndrome of chroruc air

geneity of the distributions of ventilation, perfusion,

flow limitation as being caused by four external fac

ventilation-perfusion matching, and diffusion (West,

tors, mediated by four primary tissue responses, and

1987). General debility and deconditioning ensue.

modified by four physiological responses. The princi

Smoking contributes to increased mucous produc

pal external causative factors include inhaled irritants,

tion in the small airways, increased mucus in the large

allergens, infectious, and climate. The four principal

airways, respiratory bronchiolitis, reduced elastic re

tissue responses include large airway changes, small

coil, increased airway reactivity, and vascular changes

airway changes, airway hyperreactivity, bronchiolar

(Bates, 1989). These changes, lead to nonuniformity

damage, and alveolar destruction. The principal physi

of time constants in the lung, with consequent inho

ological responses include a reversible increased air

mogeneous distribution of inspired gas and premature

way reactivity component, pulmonary vascular re

small airway closure, and to nonuniformity of ventila

sponse to alveolar hypoventilation, control of

tion, perfusion, and diffusion distributions. Although


29

Chronic Primary Cardiopulmonary Dysfunction

515

vaJiable among smokers, pulmonary function changes

crease the demand on the left heart to maintain cardiac

generaHy corrcspond to the amount smoked and dura

output. Similar to right-sided failure, the left heart

tion of the smoking history. Over time, the pulmonary

may become hypertrophied, and over time, may fail.

function profile becomes increasingly consistent with

The significantly increased intrathoracic prcssures

chronic airflow limitation (i.e., reduced FEY, and re

generated during chronic coughing reduce venous re

duced FEY,IFYC), however, these are late indicators

turn, cardiac output, and coronary perfusion and in

of pulmonary changes. Signs of uneven distribution of

crease blood pressure. These effects exert additional

ventilation and increased closing volumes, indicative

myocardial strain, lead to arterial desaturation, and

of small airway involvement, are early pulmonary

increase the potential for cardiac dysrhythmias.

function changes in smokers. Exercise diffusing ca

The complications of chronic bronchitis are exacer

pacity is reduced which explains in part the reduced

bated by cardiopulmonary deconditioning. Despite the

maximal Y02 of smokers. Dynamic compliance with

pathology, the efficiency of oxygen transport along the

breathing frequency is also reduced. Residual volume

steps in the pathway is suboptimal. This reduced effi

is increased as a percent of total lung capacity. Tra

ciency increases the oxygen demands of the patient

cheal mucous velocity is reduced and secretion clear

overall who is unable to adequately supply oxygen.

ance is impaired. Any patient with a smoking history,

Pharmacological support in the tong-term manage

regardless of a diagnosis, has some degrcc of chronic

ment of chronic bronchitis includes bronchodilators

airflow limitation, which must be considered when

(e.g., oral, metered-dose inhalant, inhaled powdered, or

these patients are receiving medical or surgical care.

aerosol), corticosteroids (e.g., oral or inhaled), expecto

The cardiac manifestations of chronic bronchitis

rants, antibiotics, inotropic agents (e.g., digitalis), beta

stem from airway obstruction, secretion accumulation

blockers, antidysrhythmic agents, and diuretics. Patients

and reduced capacity to effectively expectorate, poly

with chronic lung disease must be monitored closely

cythemia, low arterial oxygen tensions, and cardiopul

during exercise given the potential cardiac effects of

monary deconditioning. Increased airway resistance

disease and medications (e.g., beta-blocker agents atten

secondary to obstruction increases oxygen demand

uate the normal hemodynamic responses to exercise and

and hence the work of breathing. This increased de

bronchodilators, such as ventolin, elicit tachycardia).

mand is superimposed on an oxygen transport system that is already compromised. The cardiovascular sys


tem attempts to compensate for chronically reduced

The goals of long-term management for the patient

arterial oxygen tension by increasing cardiac output

with chronic bronchitis include the following:

(i.e., stroke volume and heart rate). As blood gases de

•

(i.e., polycythcmia) to enhance the oxygen-carrying capacity of the blood. However, polycythemia in

Maximize the patient's quality of life, general health, and well-being and hence physiological

teriorate, the production of red blood cells increases

reserve capacity •

Educate about chronic bronchitis, self-manage

creases the viscosity of the blood, and in turn, the

ment, effects of smoking, nutrition, weight con

work of the heart to pump blood to the pulmonary and

trol, smoking reduction or cessation, other life

systemic circulations. Furthermore, viscous blood is

style factors, medications, infection control, and

prone to circulatory stasis and clotting.

role of a rehabilitation program

Low arterial oxygen tensions lead to hypoxic pul monary vasoconstriction and increased pulmonary vascular resistance (i.e., pulmonary hypertension).

•

Facilitate mucociliary transport

•

Optimize secretion clearance

•

Optimize alveolar ventilation

This also increases the work of the right heart in eject

Optimize lung volumes a n d capacities a n d

ing blood to the lungs. Chronic overwork of the right

flow rates

ventricle leads to hypertrophy, insufficiency, and

•

eventual failure of the right heart (cor pulmonale). Chronically reduced arterial oxygen levels can in

Optimize ventilation and perfusion matching and gas exchange

•

Reduce the work of breathing


516

PART V


•

Reduce the work of the heart

health practices (e.g., smoking reduction and cessation,

•

Maximize aerobic capacity and efficiency of

cold and flu prevention, flu shots, aerobic exercise,

•

•

oxygen transport

strengthening exercises, nutrition, weight control, hy

Optimize physical endurance and exercise ca

dration, pacing of activities, energy conservation, re

pacity

laxation, and stress management). Chronic bronchitis

Optimize general muscle strength and thereby

and emphysema are often associated with sleep distur bances. Obstructive sleep apnea is increasingly preva

peripheral oxygen extraction Patient monitoring includes dyspnea, respiratory

lent with disease severity. Thus activity and sleep pat

distress, breathing pattern (depth and frequency), ar

tems need to be assessed to ensure sleep is maximally

terial saturation, cyanosis (delayed sign of desatura

restorative and is not contributing to the patient's

tion), heart rate, blood pressure, and rate pressure

symptoms. Integral to an exercise prescription is the

product. Patients with cardiac dysfunction or low

time of day. Exercise is prescribed when the patient is

arteral oxygen tensions require ECG monitoring, par

least fatigued, most energetic, and when performing

ticularly during exercise. If supplemental oxygen is

such a program is most convenient.

used, the FIo2 administered is recorded. Subjectively,

Aerobic exercise is an essential component of the

breathlessness is assessed using a modified version of

long-term management of the patient with chronic bronchitis to optimize the efficiency of oxygen trans

the Borg scale of perceived exertion. Medication that is needed to maximize treatment

POit overall and mobilize and remove secretions (Old

response is administered before treatment (e.g., bron

enburg, Dolovich, Montgomery, and Newhouse, 1979).

chodilators). Knowledge of the type of medication, its administration route, and time to and duration of peak efficacy is essential if treatment is to be maxi mally efficacious.

Emphysema Pathophysiology and medical management

The primary interventions for maximizing car

Emphysema is associated with a prolonged history

diopulmonary function and oxygen transport in pa

of smoking and chronic bronchitis and indicates sig

tients with chronic bronchitis include some combina

nificant irreversible lung damage. A less common

tion of education, aerobic exercise, strengthening

type of emphysema not associated with smoking is

exercises, chest wall mobility exercises, range of mo

alpha-antitrypsin deficiency. Antitrypsin is essential

tion, body positioning, breathing control and coughing

in balancing elastin production and degradation and

maneuvers, airway clearance techniques, relaxation,

in preserving optimal lung parenchymal compliance.

activity pacing, and energy conservation. An er

A deficiency of antitrypsin reduces lung elasticity

gonomic assessment of the patient's work and home

and contributes to the characteristic increase in lung

environments may be indicated to minimize oxygen

compliance that is the hallmark of emphysema. The

demand and energy expenditure in these settings.

pathophysiology of emphysema is presented in detail

The use of supplemental oxygen depends on the

in Chapter 4. The principal pathophys iological

severity of the disease. Some patients have no need for

deficits include irreversible alveolar damage result

supplemental oxygen, some need it only during exer

ing from loss of elastic recoil and the normal tether

cise, and some patients require continuous oxygen with

i n g of

proportionately more delivered during activity and ex

parenchyma excessively compliant and floppy. Ex

ercise compared with rest. Supplemental oxygen is not

cessi ve distension and' dil atation of the termi nal

usually required until lung damage becomes extreme

bronchioles and destruction of alveoli reduces the

t h e a l v e o l i,

w h i c h renders t h e lung

(i.e., the morphological changes are consistent with the

surface area for gas exchange. Hence diffusing ca

irreversible changes associated with emphysema).

pacity is correspondingly reduced. The dead space in

Education is a principal focus of the long-term

the lungs and total lung capacity increase s ignifi

management of the patient with chronic bronchitis. Ed

cantly. Breathing at normal tidal volume, the pa

ucation includes the reinforcement of preventative

tient's airways close beyond that which normally oc


29


517

curs with aging, which contributes to ventilation and

poxic vasoconstriction in the lungs. Over time, the

perfusion mismatch and hypoxemia. Time constants

heart becomes enlarged and pumps even less effi

are altered such that alveolar units are not being

ciently. In the long-term management of the patient

evenly ventilated. In its nonacute, chronic stages the

with emphysema, alveolar ventilation, gas exchange,

primary problems include inadequate and inefficient

reduced oxygen transport efficiency, and the work of

gas exchange resulting from the structural damage to

breathing and of the heart are the primary pathophys

the lungs and altered respiratory mechanics of the

iological problems. Unlike chronic bronchitis, secre

lungs, chest wall, and their interaction. The lungs are -

tion accumulation may be less problematic in emphy

hyperinflated, the chest wall becomes rigidly fixed in

sema patients during nonacute periods. Nonetheless,

a hyperinflated position, the normal bucket handle

optimizing mucociliary transport is an ongoing con

and pump handle motions of the chest wall are im

cern in that the consequences of mucous retention

paired, the hemidiaphragms are flattened, the medi

and infection can be devastating.

astinal structures are shifted, and the heart is dis placed and rotated, making its function inefficient


(Bake, Dempsey, and Grimby, 1974; Geddes, 1984;

The goals for long-term management of the patient

Murray and Nadel, 1988a). The normal mucociliary

with emphysema include the following:

transport system is ineffective because years of

•

smoking destroy the cilia, reduce their number, and

reserve capacity

alter their configuration and orientation; thus their function is correspondingly obliterated or impaired.


•

In addition, these patients are unable to generate

Educate about emphysema, self-management, smoking reduction and cessation, medications,

high transpulmonary pressures and forced expiratory

nutrition, weight control, infection control, and

flow rates because of altered respiratory mechanics.

the role of a rehabilitation program

Consequently, coughing maneuvers are weak and in

•

effective. The administration of supplemental oxy

•

Optimize alveolar ventilation Optimize lung volumes and capacities and flow rates

gen is limited because these patients rely on their hy poxic drive to breathe. This life-preserving drive can

•

be attenuated with even moderate levels of oxygen.

•


Thus oxygen administration is limited to low flows.

•


The respiratory muscles are often weak, if not fa

•

•

•

transport system and the capacity of other steps in the pathway to compensate.

Optimize general muscle strength and thereby peripheral oxygen extraction

•

There are several physiological compensations

Optimize physical endurance and exercise ca pacity

sema, tend to be inactive and deconditioned, which further compromises the efficiency of the oxygen

Maximize aerobic capacity and efficiency of oxygen transport

tigued (Rochester, and Arora, 1983). Overall, pa tients with emphysema, particularly severe emphy

Optimize ventilation and perfusion matching

Optimize respiratory muscle strength and en durance and overall respiratory muscle efficiency

that occur in response to chronic hypoxemia. Stroke

Education focuses on teaching the patient about

volume and cardiac output are increased. The red

emphysema, self-management of the disease, the effect

blood cell count increases (polycythemia), however,

of smoking and smoking cessation. nutrition, weight

the blood becomes more viscous and requires more

control, hydration, relaxation, sleep and rest, stress

work to eject and distribute throughout the body.

management, activity pacing, energy conservation, and

Thus the stroke work of the heart is further increased.

prevention (e.g., cold and flu prevention, flu shots, aer

This load on the heart is additional to the increased

obic exercise, diet, sleep, and stress management).

afterload on the right ventricle because of an increase

Comparable with the patient with chronic bronchi

in pulmonary vascular resistance secondary to hy

tis, sleep disturbances are common in the emphysema


518

PART V


patient. Activity and sleep patterns are assessed to en

anaerobic capacity, improved ventilatory muscle

sure sleep is maximally restorative. If obstructive

strength and endurance, and increased motivation (Bel

sleep apnea is disturbing the patient's sleep, medical

man and Kengregan, 1981; Belman and Wasserman,

1981; Dean, 1993). Exercise intensity is prescribed

intervention is required. Patient monitoring includes dyspnea, respiratory

based on rating of breathlessness (mod ified Borg


scale) (Chapter 17), in conjunction with objective and

terial saturation, lightheadedness, discoordination,

other subjective responses from the exercise test.

heart rate, blood pressure, and rate pressure product.

Patients with chronic airflow limitation alter their

Patients with cardiac dysfunction or low arterial oxy

breathing patterns so that they are breathing on the

gen tensions require ECG monitoring particularly

most metabolically efficient portion of the pressure

during exercise. Subjectively, breathlessness is as

relaxation curve (Chapter 4 and 29). These patients

sessed using a modified version of the Borg scale of

tend to breathe with prolonged expiratory phases to

perceived exertion.

maximize gas transfer and mixing in the lungs to

Medication that is needed to maximize treatment

minimize the effects of altered ventilatory time con


stants. To facilitate such a breathing pattern, the pa

chodilator). Knowledge of the type of medication, its

tient tends to breathe through pursed lips, which may

administration route, and time to and duration of peak

create back pressure to maintain the patency of the

efficacy is essential if treatment is to be maximally

airways (Muller, Petty, and Filley, 1970). The meta

efficacious. When patients are on multiple medica

bolical efficiency of the patient's breathing pattern

tions, the interactions and implications on treatment

may be improved further by altering breathing me

response must be identified.

chanics rather than imposing a different breathing


pattern that may be suboptimal. Altering breathing


mechanics involves manipulating the patient's body

tients with emphysema include some combination of

position to promote alveolar ventilation, perfusion,

education, aerobic exercise, strengthening exercise,

and ventilation and perfusion matching.

ventilatory muscle training (strength and endurance)

The increased intrathoracic pressures generated

or ventilatory muscle rest, low flow oxygen, mechan

during chronic coughing limit venous return, cardiac

ical ventilatory support for home use, chest wall mo

output, and coronary perfusion. Blood pressure is

bility exercises, range of motion exercises, body posi

also increased. These effects exert additional myocar

tioning, breathing control and coughing maneuvers,

dial strain, lead to arterial desaturation, and increase

airway-clearance techniques, relaxation, activity pac

the potential for cardiac dysrhythmias. Breathing

ing, and energy conservation. An ergonomic assess

control and coughing maneuvers coupled with body

ment of work and home environments may be indi

positioning and exercise are instructed such that the

cated to minimize oxygen demands in these settings. The benefits of aerobic and strengthening exercise

work of breathing is minimized (i.e., alveolar ventila tion and gas transfer is as efficient as possible), and

in the long-term management of airflow limitation to

coughing is also as efficient as possible (i.e., maxi-

optimize oxygen transport in patients with compro

mally productive with the least energy expenditure).

mised oxygen delivery is well established (Dean,

Physical therapy is one component of a compre

1 9 9 3 ; Niederman et aI., 1 9 91 ; R i e s , Ellis, and

hensive rehabilitation program in the long-term man

Hawkins, 1988; ZuWallack, Patel, Reardon, Clark, and

agement of emphysema. Such a program also needs to

Normandin, 1991). Patients with severe limitations are

include information on health promotion and mainte

often unable to exercise at a sufficient intensity to ef

nance, ongoing review and log of medications, respi

fect aerobic adaptations to the exercise stimulus. Bene

ratory support (e.g., oxygen aerosol therapy, and me

fits of exercise in these patients may be explained by

chanical ventilatory support), occupational therapy,

desensitization of dyspnea, improved movement effi

sexual rehabilitation, psychosocial rehabilitation, and

ciency and hence movement economy, improved

vocational rehabilitation (Dean, 1993; Murray, 1993).


29

Asthma

Patients with cardiac dysfunction or low arterial oxy

Asthma is a common respiratory condition that is

gen tensions require ECG monitoring particularly dur

hypersensitivity of the airways to

various

and bronchial edema

struction (i.e.,

1984; M urray a n d Nadel, I (Chapter

exercise.

ob

in reversible

519

heart rate, blood pressure, and rate pressure product.

Pathophysiology and medical management characterized


breathlessness is assessed

a modified version of the Borg scale of per ceived exeltion. Medication that is needed to maximize treatment

In mild cases, no treatment


other than prophylaxis may be needed. In severe

chodilators and antiinflammatories). Knowledge of

cases, asthma can be life

the type of medication, its administration route, and

Once af

the

fected by the

narrow, increas

time to and duration of

efficacy is essential if

treatment is to be maximally efficacious. When panarrowed

Breathing

con-

tributes to wheezing, reduced alveolar ventilation, rapid shallow

shortness of breath, in

their interactions

tients are on multiple

must be known.

for

and the


c reased work of brea t h i n g , des a t u r a t i o n , a n d

diopulmonary function and oxygen

cyanosis. Increased inhomogeneity o f the distribu

tients with asthma include education, aerobic exer

tion of ventilation is present in some nonacute asthmatic patients boud, I

in pa

chest wall

Dean, and Ab

Although some

may

ing, and stress management.

mucous hypersecretion, even normal amounts of pulmonary secretions can obstruct narrowed air

E ducation is c e n t r a l to is

asthma. The

t of the basic pathophysiol Other central top

ways leading to atelectasis. Asthma that has welI

ogy of the disease and its

defined triggers is easier to manage than cases

ics including preventative health practices are also

where the triggers are less specific.

taught

cold and flu

t'f1J1CllJrt8S of physical therapy management

flu

control,

The goals of long-term management of the patient

reduction and

with asthma include the following:

agement, and the benefits of an

•

quality of

Maximize the

life-long

mention needs to be made regarding the

reserve capacity

•

relaxation and stress man rehabilitation program).

and hence

and

med

use of medications and inhalers. These are frequently

Educate about asthma, self-management, nutri

used

tion,

with the basic pharmacokinetics of the medications

control,

reduction and ces

sation, medications and their uses,

of

used and thus are not

and infection control

asthmatic •


•

Maximize aerobic

(i.e., the patient is unfamiliar ef

In addition, inhalers are often used improperly; therefore the patient does not derive the full benefit

and

of

oxygen transport

of the medication. The instructions provided

_

the

supplier of the inhalers should be strictly followed.

physical endurance and exercise ca

There are numerous types of ent applications.

pacity muscle

pe-

ripheral oxygen extraction

the

time and effort is wasted

haler ineffectively, the

Patient monitoring includes dyspnea,

all with differ

not adhering to the instructions, the in

does not derive the full

benefit of the medication, an excessive amount of in

,,,.,,,, ",,'", breathing pattern (depth and frequency), alter of desaturation),

haler may be used to

for ineffective ap

plication, there may be increased exposure of the pa


520

PART V


tient to the side effects of the

and there is

The patient with bronchiectasis has

considerable economic waste.

impaired respiratory

of the

A

of increased

sensitivity enables the

pattern, reduced

to exert control over

bronchospastic attacks, The patient is taught to record

cretions, reduced aerobic caDacitv. and is debilitated.

the freauencv of bronchospastic attacks and

The increased intrathoracic pressures

and what relieves them. In this way, the

bouts of chronic coughing limit venous return,

learns to avoid or minimize their frequency,

caridac output, and coronary perfusion, Blood pres

severity, and duration and minimizes the amount of medication

benefits.

These are

sure is also increased. These effects exert additional myocardial

The ex ercise prescription parameters are set

lead to arterial desaturation, and

increase the potential for cardiac dysrhythmias and

below the bronchospasm threshold, which is estab

17 and 23).

lished based on an exercise test

Principles of physical therapy manal,emrenl

tests are performed in a pul monary function laboratory with appropriate med to

ical support. Exercise training enables the

The goals of

management of the patient

with bronchiectasis include the

determine the balance between optimal aerobic ca

•

Maximize the patient's

and medication and the optimal physical en

and well-being and hence

vironment for exercise. Temperature and humidity

reserve capacity and function

can have significant effects on work outout in asth

•

matic n.,tipntc

Educate about nutrition,

control,

cessation, medications and their use, and infec tion control

Bronchiectasis •


Bronchiectasis is characterized by dilatation and

•


anatomical distortion of the airways and obliteration

•


of t h e

b r o n c h i a l t r e e (West,

Bronchiectasis is often the chronic

secretion clearance

1987).

of

ventilation and

infection. The associated inflammation

•

leads to occlusion of the airways, which results in

•

atelactasis of the tion of central

and

dilata •

In addition, •

to further dilatation. Fibrotic, connec

"'''''''!,'''::>

mechan

Optimize ohvsical endurance and exercise ca Optimize general muscle

and thereby

Patient monitoring includes dyspnea, breathing

distortion. These anatomical

adversely affect normal

of

oxygen extraction

tive tissue changes in the wall contribute further to dilatation and

Maximize aerobic

pacity

chronic inflammation weakens the walls of the air ways,

Reduce the work of oxygen

by increased traction on the

peribronchial sheath (Bates, I

and flow

Optimize lung volumes and rates

terial saturation,

(depth and (a delayed

ics and hence pressure volume characteristics of the

tion), heart rate,

lung. The chest wall becomes hyperinflated and as

product. Patients with cardiac dysfunction or low ar

sumes the barrel shape associated with chronic air

terial oxygen tensions

flow limitation. The overall

ticularly during exercise.

of bronchiectasis

on the number of lung segments involved. There is often some reversible airflow limitation as

pressure, and rate pressure ECG monitoring par breathlessness

is assessed using a modified version of the Borg scale of

exertion. Medication that is needed to maximize treatment

sociated with bronchiectasis.


29


521

response is administered before treatment. Knowl

Between exacerbations, the medical priorities are

edge of the type of medication, its administration

to reduce the risk of infection and morbidity and pro

route, and time to and duration of peak efficacy is es

mote optimal health, growth, and development.

sential if treatment is to be maximally efficacious. The primary interventions for maximizing car




tients with bronchiectasis include some combination

with cystic fibrosis include the following:

of education, aerobic exercise, strengthening exer

•

and physiological reserve capacity

exercises, body positioning, breathing control and coughing maneuvers, airway clearance interventions,

Maximize the patient's quality of life, general health and well-being, growth and development,

cise, chest wall mobility exercises, range of motion

•

Educate the patient and family about cystic fibro

optimizing rest and sleep, relaxation, pacing, and en

sis, self-management, nutrition, prevention of acute

ergy conservation. An ergonomic assessment of the

exacerbations of the disease, infection control, and

patient's work and home environments may be indi

medication's uses, modes of adi m nistration,

cated to maximize function in these settings.

macokinetics and times to peak efficacies.

Education is a central component of the patient's long-term self-management rehabilitation program. Preventative health practices are taught (e.g., cold and flu prevention, flu shots, smoking cessation, sleep,

•

•

•

•

benefits of an integrative, rehabilitation program).

•

•

•

•

Cystic Fibrosis

Optimize secretion clearance Optimize alveolar ventilation Optimize lung volumes and capacities and flow rates

aerobic exercise, nutrition, weight control, and hydra tion, relaxation, stress management, and the long-term


Optimize ventilation and perfusion matching Reduce the work of breathing Reduce the work of and strain on the heart Maximize aerobic capacity and efficiency of oxygen transp0l1


•

significant systemic effects (Landau and Phelan, 1973; Murray and Nadel, 1988b). The diesase is con


Cystic fibrosis is a complex exocrine disease that has •


genital and is hallmarked by nutritional deficits con

Patient monitoring includes dyspnea, respiratory

tributing to impaired growth and development. Pul


monary function shows progressive decline with

terial saturation, cyanosis (a delayed sign of desatura

commensurate reductions in homogeneity of ventila


tion and inspiratory pressures (Chatham et aI., 1994;

product. Patients with cardiac dysfunction or low ar

Cotton, Graham, Mink, and Habbick, 1985; Ross et

terial oxygen tensions require ECG monitoring, par

aI., 1989). Cardiopulmonary involvement can be clas

ticularly during exercise. Subjectively, breathlessness

sified into three groups, namely, no physical signs in

is assessed using a modified version of the Borg scale

the chest, occasional cough and sputum, and constant

of perceived exertion.

cough, sputum, and other signs. Patients in each clas


sification can benefit from physical therapy with re


spect to enhancing oxygen transport. Moderate and


severe disease is characterized by significant airflow


obstruction secondary to copious, tenacious secre

sential if treatment is to be maximally efficacious.

tions. In addition, pulmonary hypertension and right


heart insufficiency may be manifested and eventual

diopulmonary function and oxygen transport in

failure may ensue.

patients with cystic fibrosis include some combina


522

PART V


tion of education, aerobic exercise, strengthening ex

drainage can be integrated into breathing control.

ercise, ventilatory muscle training (strength and en

This procedure focuses on eliciting coughing when

durance), ventilatory muscle rest, supplemental oxy

it will be most productive, thereby minimizing less

gen, mechanical ventilation for home use, chest wall

productive, exhaustive coughing. Patients with cys

mobility exercises, range of motion exercises, body

tic fibrosis often cough so violently and uncontrol

positioning, breathing control and coughing maneu

lably that it leads to significant arterial desaturation,

vers, airway clearance interventions, relaxation, pac

vomi ting, and exhaustion and impedes venous re

ing, and energy conservation.

turn and cardiac output.

Education focuses on teaching preventative health

Ventilatory devices such as the positive expiratory

practices and infection control (e.g., cold and flu, flu

pressure (PEP) mask and the flutter valve have

shots, aerobic exercise, nutrition, hydration, relax

shown benefit in some patients with CF with respect

ation, stress management, activity pacing, and energy

to reducing airway closure, clearing secretions, and

conservation).

enhancing gas exchange (Pryor, 1993; Webber and

Physical activity and aerobic exercise need to be

Pryor, 1994). Such aids may be useful adjuncts in

integrated early into the life style of the child with

some patients, however, they do not replace the mul

cystic fibrosis (Cystic Fibrosis and Physical Activ

tiple benefits of physical activity and exercise on op

ity, International 10urnal of Sports Medicine, 1988;

timizing oxygen transport including mobilizing and

Keens, Krastins, Wannamaker, Levison, Crozier,

removing secretions.

and Bryan, 1977; Zach, Oberwaldner, and Hausler,

1992). As much as possible, the child is integrated into activities of his or her peer group. A prescribed aerobic exercise program is designed to optimize the efficiency of oxygen transport at all steps in the

RESTRICTIVE PATIERNS Interstitial Lung Disease Pathophysiology and medical management

pathway and thereby enhance functional capacity

The pathophysiology of restrictive lung disorders

overall. Physical activity and aerobic exercise en

and interstitial lung disease (ILD) in particular is

hances mucociliary transport and mucociliary clear

described in Chapter 4. This clasification of lung

ance, maximizes alveolar ventilation and ventila

disease is associated with various occupations and

tion and perfusion matching, increases ventilatory

the i n h a l a t i o n of i n o r g a n i c and organic dust

muscle strength and endurance and airway diame

(Chung and Dean, 1989). As the disease pro

ter, and stimulates a productive effective cough.

gresses, total lung capacity (TLC) and vital capac

Furthermore, physical activity and exercise have

ity (VC) are reduced. Residual volume often re

been associated with improved immunity and re

mains the same. Maximal flow rates tend to be

duced risks of infection (Pyne, 1994; Shephard,

increased as compliance is reduced. The drive to

Verde, Thomas, and Shek, 1991). These are signifi

breathe, breathing frequency, and the ratio of tidal

cant outcomes for patients with cystic fibrosis who

volume to total lung capacity are increased. Glan

have thick copious secretions.

dular hyperplasia may be present, leading to mu

In addition, breathing control and coughing ma

cous hypersecretion in some patients. Diffusing ca

neuvers are included as a component of a long-term

pacity may be reduced but may only be apparent

self-management rehabilitation program. Postural

during exercise (i.e., art.erial desaturation and dys

drainage and manual techniques have been the

pnea). Exercise-induced desaturation and reduction

mainstay of airway clearance in the past. Exercise,

in Pa02 may also reflect shunt and ventilation and

however, has a primary role in secretion mobiliza

perfusion mismatch (Jernudd-Wilhelmsson, Horn

tion and as an airway clearance intervention (Dean

blad, and Hedenstierna, 1986).

and Ross, 1989). Breathing control and coughing

Hemodynamic changes may be present (e.g., in

stategies are coupled with exercise to facilitate se

creased pulmonary artery pressure). Chronically in

cretion clearance. The principles of autogenic

creased pulmonary artery pressures and hence in


29

vascular

Chronic Primary Cardiopllinl10nal

Dysfunction

523

lead to in maneuvel'S, relax

hypertrophy,

and energy conservation. An er exercise

H

"Hv

assessment of work and home environ

ments may be indicated to maximize f u nction In these

Principles of physical therapy management management of the patient

of

The

with interstitial

-'.""'MC'

Education is a central component of a

disease include the following:

sive rehabilitation program for the management of in terstitiallung disease. Education includes information

quality of life, general and hence physiological

on preventative health

removal from

the causative vention shots, cessation, nutrition,

tion, medications and their uses, prevention, health promotion, and infection control

with interstitial

During aerobic

lung disease are prone to arterial desaturation (Arita,


•

ation, activity

volumes and capacities

Nishida, and

ventilation and perfusion matching

198

Patients who desatu

rate during

and oxygen

1985) require

The intensity of the exercise •

arterial

Reduce the work of the heart and efficiency of endurance and exercise ca and thereby

muscle oxygen extraction

heart, in

with other

Pathophysiology and 1lIt:UI(;,(l1 management incidence is

ar

responses.

lung Cancer

Lung cancer is a

includes

is defined by

breathlessness, and work of the

cause of death for men and for women. Once

80% of

cancer is

terial

heart rate, blood pressure, and rate

correlated with a

and exposure to

pressure

Patients with cardiac

coal tars, asbestos, and radioactive dusts. The

(depth and

low arterial oxygen tensions particularly

exercise,

ness is assessed scale of

or

ECG monitoring, breathless

a modified version of the Borg exertion,

Medication that is needed to maximize treatment of

its administration efficacy is es

sential if treatment is to be The

efficacious,

located and thus con

tribute to bronchial monia. Pathophysiologically,

response is administered before treatment. Knowl of the

ity of primary malignant tumors are bronchogenic carcinomas. They are

and pneu cancer has features

of both obstructive and restrictive lung disease. The patient presents with

obstruction, dyspnea,

cough, and hemoptysis (MlIITaY and

I

Treatment is limited to surgery, if metastasis has been mled out, or conservative management with radiation

interventions for maximizing car


and chemotherapy. Bronchogenic carcinomas metastasize

tients with interstitial lung disease include some

through the circulation and

c o m b i n a t i o n o f e d u c a t i o n, a e r o b i c e x e r c i s e,

other organs including

chest wall mobility exer

and adrenal glands.


channels to

524

PART V


If detected early, thoracic surgery may be per

diac dysfunction or low arterial oxygen tensions re

fonned to excise the cancerous tumor (Chapter 28). If

quire ECG monitoring. Subjectively, breathlessness

inoperable, or in the case of metastases, a patient may

is assessed using a modified version of the Borg scale

be managed at home or in a hospice. Patients are de

of perceived exertion.

bilitated, often undernourished, fatigued, short of


breath, lethargic, depressed, and in pain (Saunders

response is administered before treatment (e.g., anal

and McCorkle, 1985). Although these patients are

gesics or bronchodilators). Knowledge of the type of

often extremely ill, there is a growing trend to man

medication, its administration route, and time to and

age these patients in the community whenever possi

duration of peak efficacy is essential if treatment is to

ble. As the disease progresses, maintaining function

be maximally efficacious.

and reducing the rate of deterioration become pri

The primary interventions for maximizing car diopulmonary function and oxygen transport in pa

mary goals.


tients with lung cancer include some combination of education, mobilization, strengthening exercises,

The goals of long-term management of the medical

chest wall mobility exercises, body positioning, sup

patient with lung cancer include the following:

plemental oxygen, mechanical respiratory support,

•

Maximize the patient's quality of life, general health, and well-being and hence physiological reserve capacity

•

Educate the patient and family about the bene fits of a palliative program

•

Provide supportive care

•

Optimize pain control

•


•

Optimize scretion clearance

•


•

mobilization and physical activity (Calabrese, 1990). The prescriptive parameters are adjusted each session given the rapid changes in these patients' conditions. Patients with lung cancer often cough up and ex

Optimize lung volumes and capacities and flow

•

Optimize ventilation and pelfusion matching

•

Reduce the work of breathing Maximize aerobic capacity and efficiency of oxygen transpolt

•


•

tients' peak times during the day. logical effects, as well as oxygen transport effects of

rates

•

tivity pacing, and energy conservation. Treatments are timed whenever possible to coincide with the pa Patients with cancer may benefit frol11 the immuno

Promote self-determination

•

breathing control and coughing maneuvers, airway clearance interventions, sleep and rest, relaxation, ac

Otimize general muscle strength and thereby pe ripheral oxygen extraction

•

Optimize the benefits of sleep and rest

•

Minimize the effects of restricted mobility and recumbency

pectorate blood in their sputum. The airways need to be as clear as possible to avoid obstruction, atelecta sis, risk of infection, and pneumonia. Although air way clearance is an important goal, treatments should avoid contributing significantly to bleeding and blood loss if possible. This blood loss may contribute to anemia and fatigue. Manual airway clearance interventions may be in dicated in some patients. Postural drainage may be coupled with percussion and manual vibration. The impact of manual interventions, however, may con tribute to bleeding; thus the patient requires stringent monitoring. Metastases to the thoracic cavity and the ribs in particular may preclude percussion in favor of


manual vibration being petformed over nonaffected


areas. Treatment duration may be limited by the pa

terial saturation, cyanosis (a delayed sign of desatura

tient's tolerance. Tolerance may be improved by


modifying body position or by shortening treatments

product. Patients who can be mobilized but have car-

but increasing their frequency.



29

pist should examine the medication before treatment

PRIMARY CARDIOVASCULAR

and

to ensure that the expiratory date has not

Angina

to take responsibility for


the medication

near the patient for access to it should the patient de

from reduced

refers to pain

treatment.

blood flow to the myocardium. Even though elicited during

525

management of the patient include the following:

with

angina may be

stress or, in severe cases, may occur at rest. Atheroscle

•


rosis of one or more of the coronary arteries is the prin

health, and

cipal cause. Coronary vasospasm is a less common

serve

cause of

Educate about heart disease,

The pathophysiology of

is de

and hence

scribed in detail in Chapter 4. A history of cessitates further examination to establish the of the coronary

medica

occlusion. If severe, the patient is

scheduled for coronary

surgery

28) to

restore normal coronary blood flow. The acute and long-term management of the presented in

tions and their use, •

activity, and exercise

Maximize aerobic capacity and efficiency of oxy gen transport of all steps in the

cardiac

is

endurance and exercise

28. In less severe cases,

is

general muscle strength and thereby pe

with medications (e.g., sublin

managed

and physical has stabilized, a 2TElaea-E�xer

'J

H1

oxygen extraction Patient monitoring includes hemodynamic moni toring (i.e., heart rate, blood pressure, rate pressure

else tolerance test may be conducted under supervision

product, and

in a cardiac stress testing facility where l2-lead ECG

ment, particularly exercise, should also be recorded

monitoring can be performed. The exercise

(e.g.,

which the

chest

exhibits

(i.e., the and serve as the basis for

activity and exercise. is important in patients with heart disease. Positions to the central circulation. This in creases venous return and the work of the heart. Thus body positions are selected for these patients to minimize cardiac work during exercise and when resting after exercise Levine and

Wolfson,

and

Patients may be referred to lem. care and

or as a

need to be monitored.

(i.e., a is not an

symptom under any circurmstance. Should it occur, treatment is immediately

and

emergency measures instituted. Treatments will be safer and more EeG

prescribed with continous treat

Without ECG

ments need to be conservative. If there is any doubt at of a

any time about the

should be referred to a general practitioner or cardiologist for clearance before being treated.

therapy with a


prob


angina is managed with the same

of the

of medication, its administration

route, time to as well as duration of

given it can be a

condition. A patient for whom antianginal medication is prescribed must have the medication present. The medication must not have expired and must be within visible access during treatment. The

dizzi

and her or his ability to tolerate treatment safely, the

1952).

PrinCiples 01 physical therapy management history of angina as a

Signs of

n e s s, dis orientation, dis c oordination, cyanosis,

increase the volume of fluid shifted

Cohen,

rating of dyspnea,

coughing, and chest sound

The body position in which exercise is performed of

responses to treat

efficacy is

essential if treatment is to be maximally efficacious. For the long-term

of angina, interven

tions include some combination of education, aerobic

thera


chest wall

526

PART V


and energy con

activity

Injured myocar

jury and cell death

servation. Education includes information about heart

dial cells either recover or die

disease and risk factors

period. Thus minimizing further damage and maxi-

weight,

smoking, diet, stress,

and being

active in

hot environments) and

preventative strate

smoking reduction and

low-fat

reduced alcohol comsumption, exercise, relax ation, activity pacing, and stress management). are at risk of

Patients with

infarctions can range from

silent and unnoticed by the patient to threatening.

can occur

life in the my

ocardium but occur primarily in the ventricles. The the greater the risk of ventricu acute

monitor-

or frank myocardial

are needed to detect

during this 6-week period is crit

the ical.

an in-

and

the healing

edema, and left

ventricular failure. Because myocardial ischemia

infarction. These patients are potentially hemody

and infarction impair the pumping action of the

namically unstable; thus their

heart and thus cardiac output, patients tend to be

sponses

re

and in need of oxygen. Even after the oxy

during, and after treatment,

larly aerobic and

should be

has

gen has been discontinued and the

monitored and recorded. Minimally, heart rate,

healed, the patient may continue to be vulnerable

blood pressure, and rate pressure product should be

hemodynamically.

taken alonll with the

some

the myocardium will have

that will affect both the electrical ex

citability and the mechanical function of the heart. may continue to have low

the

In

normal arterial blood gases. Hypoxemia is lethal in that it

and predisposes tissues

to activity and aerobic exer

namic response.

must be avoided. Post

myocardial infarction

are usually dis-

home on several medications (e.g., nitro

heart rate or per

cise are prescribed at a

ceived exertion ranges that are below the anginal

glycerin, calcium antagonists, beta-blockers, and di

threshold based on a

uretics).

1

,f'V"""""'"

tolerance text Peak exercise tests in cardiac

of

on the

one or more of

usually continue to

that may elicit angina o r

these medications over the long term. The need for

are performed i n a cardiac stress

oxygen is usually short term and restricted to the

laboratory under the supervision of a

s hospital stay.

The body position in which aerobic exercise is IS

with heart disease.

Important in

Positions of

increase the volume of tluid

Principles of physical therapy management from hospital, many post myocardial

After

shifted from the periphery to the central circulation.

infarction patients see a physical therapist either pri

This increases venous return and the work of the

vately or through a cardiac rehabilitation program.

heart. Thus

positions are selected for exer

these patients to minimize cardiac work

cise and during rest after exercise (Lanllou et 1977; Levine and Lown, 1952).

The majority of

an exercise program

for 6 to 12 months. therapy in

Regardless of the setting, cludes education, for

vised

Myocardial Infarction Pathophysiology and medical management frequently

will remain on

rehabilitation program

frank myocardial is

confidence

support, and a super safely and physical exertion. In addition, an

exercise program is specifica!Jy prescribed for the pa tient to enhance oxygen transport

chemia and infarction. Myocardial ischemia is re whereas infarction denotes mvoeardial in


and utilization at the tissue level) the metabolic demand on the heart.

up-

29


527

A GXTT is conducted before leaving the hospital

Patient monitoring includes hemodynamic moni

or when the patient is enrolled in an exercise pro

toring (i.e., healt rate, blood pressure, and rate pres

gram. The time between the exercise test and the ex

sure product). Subjective responses to treatment, par

ercise prescription and implementation of the exer

ticularly exercise, should also be recorded (e.g.,

cise program should be minimal. Peak (formerly

Borg's rating of perceived exeI1ion). Angina is not an

referred to as maximal) exercise tests are conducted

acceptable symptom under any circumstance. Should

in the presence of a cardiologist and provide the opti

it occur, however, treatment is immediately discontin

mal basis for an exercise prescription. Submaximal

ued and emergency measures instituted. Treatments

exercise tests can be conducted by the physical thera

will be safer and more precisely presclibed with con

pist. These can provide the basis for an exercise pro

tinuous ECG monitoring. Without ECG monitoring,

gram, however, the prescription is conservative com

treatments need to be conservative. If there is any

pared with that based on a peak exercise test. The

doubt at any time about the hemodynamic stability of

principles and practice of exercise testing are de

a patient and her or his ability to tolerate treatment

scribed in Chapter 17, 23 and 24. Such testing is an

safely, the patient should be referred to a general prac

art and an exacting science and should be carried out

titioner for clearance before being treated.

in a rigidly standardized manner to ensure the test re

Medication that is needed to maximize treatment response is administered before treatment (e.g., an

sults are maximally valid, reliable, and useful. Comparable with the angina patient and not overt

tiarrhythic agents). Knowledge of the type of medica

infarction, the following caution must be adhered to

tion, its administration route, and time to and dura

with the patient who has a history of myocardial in

tion of peak efficacy is essential if treatment is to be

farction. A patient jar whom antianginal medication

maximally efficacious.

is prescribed must have the medication present. The


medication must not have expired and must be within


visible access during treatment. The physical thera

tients with myocardial infarction include some combi

pist should examine the medication before treatment

nation of education, aerobic exercise, strengthening

to ensure that the expiratory date has not passed and

exercises, chest wall mobility exercises, body position

to take responsibility for positioning the medication

ing, breathing control and coughing maneuvers, relax

near the patient for access to it should the patient de

ation, activity pacing, and energy conservation. An er gonomic assessment of b o th work a n d h ome

velop angina during treatment. The goals of long-term management of the patient

dial strain.

with myocardial infarction include the following: •

•

•

•

•

•

environments may be indicated to minimize myocar

Maximize the patient's quality of life, general

Education focuses on the teaching the basic patho

health, and well-being and hence physiological

physiology of heart disease, its risk factors, and pre

reserve capacity

vention. Health promotion practices are advocated

Educate about myocardial infarction, self-man

(e.g., smoking reduction and cessation, good nutrition,

agement, nutrition, weight control, smoking re

weight control, hydration, quality rest, and sleep peri

duction and cessation, risk factors, disease pre

ods). In addition, types of physical activity that im

vention, medications, life style, activities of

pose undue myocardial strain, increase intrathoracic

daily living, and avoiding static exercise, strain

pressure, and restrict venous return and cardiac out

ing, and the Valsalva maneuver

put, such as heaving lifting, straining, or the Val salva


maneuver, are avoided. The patient is taught to moni

oxygen transpOlt

tor and practice vigilance in monitoling his or her own


condition (e.g., new signs of infarction). These pa


tients are potentially hemodynamically unstable and

pacity

thus their hemodynamic responses before, dUling, and


after treatments, particularly exercise, should be mon

peripheral oxygen extraction

itored and recorded (i.e., heart rate, blood pressure,


528

PART V


and rate pressure product should be taken, along with their subjective responses to treatment).

Prophylactic antibiotics against endocarditis are administered to most patients with significant valvu

Peak exercise tests in cardiac patients that may elicit angina or ST -segment changes are performed in a cardiac stress testing laboratory under the supervi sion of a cardiologist. The parameters of the exercise

lar involvement and in mild disease before proce dures such as dental work.


prescription are set based on a peak exercise test. In


tensity is set within a heart rate, oxygen consumption,

with valvular heart disease include the following:

and exertion range (e.g., 70% to 85%, of the anginal

•

threshold) (Chapter 17).


Aerobic exercise of large muscle groups rather

reserve capacity

than small muscle groups (e.g., arm ergometry) is se

•

Educate about cardiac valvular disease, self

lected to minimize the increased hemodynamic de

management, nutrition, weight control, smoking

mand and strain and the increased work of the heart

reduction and cessation, cardiac risk factors, dis

associated with this type of work. Hot and humid con

ease prevention, medications, life style, activities

ditions also place additional stress on the heart, thus

of daily living, and avoiding static exercise, strain

exercising under these conditions should be avoided.

ing, and the Valsalva maneuver

The body position in which aerobic exercise is

•

performed is important in patients with heart disease. Positions of recumbency increase the volume of tliud

Maximize aerobic capacity and efficiency of oxygen transport

•




•

heart. Thus upright body positions are selected for

•

these patients to minimize cardiac work during exer

Reduce the work of the heart Optimize general muscle strength and thereby peripheral oxygen extraction

cise and during rest after exercise (Langou et aI.,

Physical therapists are involved with the manage

1977; Levine and Lown, 1952; Prakash, Parmley, Dik

ment of patients with valve defects medically, either

shit, Forrester, and Swan, 1 973).

as a primary or secondary problem, and surgically. After surgery, these patients progress well; the princi ples of their management are presented in Chapter

Valvular Disease Pathophysiology and medical management

28. With respect to the medical management of valve defects, the goal is to optimize oxygen transport in

Valve dysfunction is either congential or acquired and

the patient for whom surgery is not indicated either

may require treatment as a primary condition or is pre

because the defect is not sufficiently severe or be

sent as a secondary condition. Any of the heart and

cause the patient cannot or refuses to undergo

pulmonary valves may be affected. Rheumatic fever

surgery. Although the mechanical defect cannot be

was a common cause of rheumatic heatt disease and in

improved, oxygen transport may be improved with

particular mitral valve insufficiency (Goldberger,

judicious exercise prescription in some patients. The

1990). Interconnecting lymphatic vessels between the

parameters of the exercise prescription are usually

tonsils and the heart are thought to be responsible. Cal

moderate in that inapprop'riate exercise doses can fur

cification of valves that impairs opening and closing is

ther disrupt the inappropriate balance between oxy

another example of an acquired valve dysfunction.

gen demand and supply and thus further exacerbate

Clinically, patients may present with exertional

symptoms. In addition, there is the potential for fur

dyspnea, excessive fatigue, palpitations, fluid reten

ther valvular dysfunction if the myocardium is me

tion, and orthopnea (Sokolow, McIlroy, and CheitJin,

chanically strained.

1990). These sypmtoms are often relieved when exer tion is discontinued.

The goal of the aerobic exercise prescription is to identify the exercise dose that will optimize the effi


29


529

ciency of other steps in the oxygen transport pathway

pain, lightheadedness, dizziness, disorientation, dis

such that the available oxygen delivered to the pe

c o o r d i n a tion, c y a n o s i s , c ou g h i n g , chest s o u n d

ripheral tissues is maximally used without constitut

changes (i.e., a gallop) need t o b e monitored. Treat

ing a significant mechanical strain on the heart. Max

ments will be safer and more precisely prescribed

imizing work output over time is the goal. Thus the

with continuous ECG monitoring. Without ECG

severely compromised patient will perform a signifi

monitoring, treatments need to be conservative. If

cantly greater volume of functional work over time

there is any doubt about the hemodynamic stability of

with short, frequent sessions of exercise rather than

a patient and her or his ability to tolerate treatment

longer, less-frequent sessions.

safely, the patient should be referred to their general

If the valve defect is a secondary problem, the

practitioner for clearance before being treated.

physical therapist must assess the severity of the de


fect and its functional consequences. The following


questions must be addressed:

tients with cardiac defects include some combination

I. Does the defect preclude treatment?

of education, aerobic exercise, strengthening exercises,

2. Does the defect require that treatment be modi

chest wall mobility exercises, body p ositioning, breathing control, coughing maneuvers, relaxation, ac

fied, if so, how? 3. What special precautions should be taken?

tivity pacing, and energy conservation. An ergonomic

4. What signs and symptoms would indicate the

assessment of both work and home environments may be indicated to minimize myocardial strain.

patient is distressed?

Exercise prescription for patients with valvular heat1

5. What parameters should be monitored? 6. Is the patient taking medications as prescribed?

disease is modified to ensure that the energy demand is

How might these medications alter the patient's

commensurate with oxygen supply. Otherwise, exces

response to treatment?

sive oxygen demand will worsen the patient's response

7. Is there any evidence of heart failure? If so, what will the effects of exercise be?

to physical activity, lead to further distress, and possi bly reduced functional capacity. Aerobic exercise of

8. If there is no evidence of heart failure at rest,

large muscle groups rather than small muscle groups

what is the chance that insufficiency will de

(e.g., arm ergometry) is selected to minimize the in

velop with exercise?

creased hemodynamic demand and strain and the in

Comparable with the management of the patient with

creased work of the heat1 associated with this type of

a history of angina with or without a history of my

work. As for other types of cardiac conditions, exercis

ocardial infarction, body positions, activities, and res

ing in hot and humid conditions shoud be avoided.

piratory maneuvers that are associated with increased hemodynamic strain are avoided.

The body position in which aerobic exercise is performed is important in patients with heart disease.


Positions of recumbency increase the volume of fluid






heart. Thus upright body positions are selected for


these patients to minimize cardiac work during exer

These patients are potentially hemodynamically unstable; thus their hemodynamic responses before,

cise and during rest after exercise (Langou et aI.,

1977; Levine and Lown, 1952).

during, and after treatments, particularly exercise, should be monitored and recorded. Monitoring in cludes hemodynamic monitoring (i.e., heart rate, blood pressure, and rate prcssure product). Subjective

Peripheral Vascular Disease Patholphysiology and medical management

responses to treatment (e.g., rating of perceived exer

Peripheral vascular disease results primarily from ather

tion) should also be recorded. Signs of dyspnea, chest

osclerosis and occlusion of the peripheral arteries (e.g.,


530

PART V


thoracic aorta, femoral artery, and popliteal artery)

•

Educate about atherosclerosis, self-management,

1980). Diabetes mel

nutrition, weight control, smoking reduction and

litus, which can result in microangiopathy and auto

cessation, risk factors, disease prevention, medica

nomic polyneuropathy, is another contributing factor to

tions, life style, activities of daily living, and

(Juergens, Spittell, and Fairbairn,

peripheral vascular disease in the lower extremjties.

avoiding static exercise, straining, and the Valsalva

Al1erial occlusion results in reduced blood flow to the extremities and hence reduced segmental blood

maneuver •

pressure distal to the occlusion. In mild cases of arter ial stenosis the patient may be asymptomatic because considerable stenosis has to occur before significant

•

•

reduction in peripheral blood flow. Furthermore, if atheroslerosis develops gradually, collateral circula

Maximize arobic capacity and efficiency of oxy gen transport Optimize the work of the heart Optimize physical endurance and exercise ca pacity

•


tion may develop sufficiently to offset progressive vessel narrowing. Clinically, the patient presents with


complaints of limb pain on exercise, coldness in the

with peripheral vascular disease secondary to dia

1987).

betes mellitus must incorporate both the principles

The characteristic limb pain results from ischemia and

for the managment of the patient with peripheral vas

affected leg, and possibly numbness (Dean,

is referred to as intermittent claudication. Mild to

cular disease secondary to atherosclerosis and sec

moderately severe cases are managed conservatively.

ondary to diabetes mellitus.

Pain at rest is suggestive of severe stenosis and signif


icant reduction of blood flow to the limb. Signifi

toring (i.e., heart rate, blood pressure, and rate pres

cantly reduced blood flow leads to ischemia color

sure product). Subjective responses to treatment,

changes, skin breakdown, ulceration, and eventually

particularly exercise, should also be recorded (e.g.,

gangrene. Bypass surgery is carried to revascularize a

pain scale and Borg's rating of perceived exertion).

threatened limb or in severe cases where gangrene has

These patients have an increased risk of angina.

developed, amputation of the limb is indicated.

Angina is not an acceptable symptom under any cir

Intermittent claudication secondary to mild-to

cumstance. Thus patients should be cleared by their

moderate arterial stenosis can benefit from aerobic

physicians or cardiologists before undertaking a

exercise, which may stimulate the development of

therapeutic exercise program. Diabetic patients are

collateral blood vessels around the stenosed vessel.

potentially hemodynamically unstable; thus their he

This condition can severely restrict mobility, which

modynamic responses before, during, and after

reduces function in addition to aerobic capacity and

treatment, particularly exercise, should be moni

efficient oxygen transport overall.

tored and recorded (i.e., heart rate, blood pressure,

Patients with pelipheral vascular disease from dif

and rate pressure product should be taken) along

fuse systemic atherosclerosis can be expected to have

with their subjective responses to exercise (e.g.,

stenosis of the coronary arteries even though they

pain and perceived exertion). If there is any doubt at

may be asymptomatic. These patients are monitored

any time about the hemodynamic stability of a pa

as stringently as cardiac patients.

tient and her or his ability to tolerate treatment

Principles of physical therapy management The goals of long-term management of the patient with peripheral vascular disease secondary to athero sclerosis include the following: •

safely, the patient shou. l d be referred to a general practitioner for clearance before being treated or continuation of treatment. Medication that is needed to maximize treatment response is administered before treatment. Knowl





reserve capacity



29


531


The body position in which aerobic exercise is per

diopulmonary function and oxygen transport in patients

formed is important in patients with peripheral vascu

with pe[ipheral vascular di:;ease secondary to athero

lar disease. Positions of recumbency eliminate the

sclerosis include some combination of education, aero

vertical gravitational gradient. This gradient increases

bic exercise, strengthenjng exercises, relaxation, activ

blood pressure significantly to the lower extremeites.

ity pacing, and energy conservation. An ergonomic

Therefore the claudication threshold is lowered in re

assessment of both work and home environments may

cumbent positions. Recumbent positions also increase

be indicated to minimize myocardial strain.

venous return and the work of the heart. Thus upright

Education focuses on teaching the basic patho

body positions are selected for these patients to maxi

physiology of atherosclerosis, its risk factors, and

mize blood pressure in the lower extremities and to

prevention. Health promotion practices are advocated

minimize cardiac work during exercise and during rest

(e.g., smoking reduction and cessation, nutrition,

after exercise (Langou et aI., 1977).

weight control, hydration, quality rest, and sleep peri ods). In addition, types of physical activity that im pose undue myocardial strain, increase intrathoracic pressure, and restict venous return and cardiac output,

Hypertension Pathophysiology and medical management

such as heaving lifting, straining, or the Valsalva ma

Hypertension or high blood pressure is a serious

neuver, are avoided. The patient is taught to monitor

condition. Most patients experience no symptoms;

and practice vigilance in monitoring signs and symp

thus adherence to medication regimens is often

toms of vascular insufficiency in the affected limb

poor. Approximately 90% of hypertension is termed

and intermittent claudication. Any sign of skin red

essential hypertension (i.e., no known etiology).

ness in the feet should be monitored closely. In the

Hypertension predisposes a patient to stroke, my

diabetic patient, any threat of skin breakdown re

ocardial infarction, hemorrhage, and infarction of

quires medical attention and discontinuation of exer

other vital organs (Sokolow, McIlroy, and Cheitlin,

cise until medical clearance has been obtained. Pa

1990). Blood pressure tends to increase with age.

tients with peripheral artery disease are taught to take

With the aging of the population, the incidence of

care of their feet particularly before and after exer

hypertension is increasing. Increased blood pressure

cise. The feet and footwear should be kept clean. The

results from increased peripheral vascular resis

inner surfaces of shoes and socks should be smooth. During peak exercise tests, patients with periph eral vascular disease secondary to atherosclerosis

tance; therefore medications are prescribed that re duce myocardial afterload and peripheral vascular resistance (Goldberger, 1990).

have an increased risk of angina or ST-segment

Patients with existing cardiovascular disease (i.e.,

changes. Such tests therefore should be performed in

hypertension) are at risk for other manifestations. In

a peripheral vascular laboratory or cardiac stress test

addition, this population tends to be older and older

ing laboratory under the supervision of a peripheral

populations are known to have a higher prevalence of

vascular specialist or cardiologist. The parameters of

cardiac dysrhythmias. Thus knowledge of cardiac sta

the exercise prescription are based on a peak exercise

tus, including ECG history, should be obtained.

test. Walking is the activity/exercise of choice be cause this activity is most severely limited by inter


mittent claudication, which has significant implica

Physical therapy contributes to increased metabolical

tions for function. Intensity of the training stimulus is

demands and therefore imposes a hemodynamic load

based on pain rating in conjunction wi th hemody

resulting in increased heart rate and blood pressure.

namic and other subjective responses. The patient

The assessment should document the history of hy

walks at a comfortable, even cadence within her or

pertension, its medical management, and the patient's

his pain tolerance (objectively defined on the pain

response. Regardless of the condition being treated,

scale) so that limping and gait deviation is avoided.

the hypertensive patient's blood pressure must be


532

PART V

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chl"Onic Cardiopulmonary Conditions

monitored and treatment modified accordingly. How

sure product). Subjective responses to treatment, par

ever, blood pressure medications are known to atten

ticularly exercise, should also be recorded. Signs of

uate hemodynamic responses to exercise (Chapter

dyspnea, headache, lighheadedness, dizziness, disori

; thus the limitations of blood pressure measure

entation, discoordi nation, cyanosis, coughing, and

43)

ment must be considered.

chest sound changes (i.e., a gallop) need to be moni

A program of aerobic exercise can effectively re

tored. Blood pressure responses that fail to increase

duce high blood pressure in some patients (Blair,

with increasing work load and power output may be

Painter, Pate, Smith, and Taylor,

1988; Sannerstedt, 1987). The parameters of the exercise prescription

indicative of congestive healt failure.

needed to control hypertension include an aerobic

scribed with contiuous ECG monitoring. Without ECG

type of exercise that is rhythmic and involves large

monitoring, treatments need to be conservative. If there

muscle groups, an intensity of

Treatments will be safer and more precisely pre

is any doubt about the hemodynamic stability of a pa

60% to 75% of the pa tient's age predicted maximal heart rate, 60 to 90 min utes in duration, performed 5 to 7 times weekly, for 3

the patient should be referred to a general practitioner

months to achieve an optimal effect. The exercise in

or cardiologist for clearance before being treated.

tensity should be equivalent to a perceived exertion rating of

tient and her or his ability to tolerate treatment safely,


3 to 5 on the Borg scale (the patient is able to

response is administered before treatment (i.e., hyper

speak while exercising without gasping) provided that

tension medications). Knowledge of the type of med

blood pressure has not increased excessively. Only

ication, its administration route, and time to and dura

modest exercise intensities are prescribed if the pa

tion of peak efficacy is essential if treatment is to be

tient has extremely high resting blood pressure to en

maximally efficacious.

sure that the blood pressure does not rise excessively

The primary interventions in the long-term man

and is not maintained at a high pressure for a pro

agement of hypertension include education, aerobic

longed period. If the patient's hypertension responds

exercise, general body strengthening, range of motion,

to the exercise regimen, exercise needs to be included

body mechanics, relaxation, stress management, pac

into the patient's life style in order for the effects to be

ing, and energy conservation. The patient is instructed

maintained. In addition to exercise, many patients lose

in self-monitoring blood pressure, recording her or his

weight, adopt healthier life-style habits, and learn

blood pressure and those factors that associated with

stress management and coping skills concurrently.

both high and low pressures, and blood pressure

The goals of long-term management of the patient •

•

•

•

•

changes after having had medication. Such monitoring enables the patient to self-manage his or her hyperten

with hypertension include the following: Maximize the patient's quality of life, general

sion and thereby reduces the need for medication, if

health, and well-being and hence physiological re

not, eliminate it entirely. Patients, however, should

serve capacity

only alter their medications with their physicians' ap

Educate about hypertension, self-management, nu

proval. Physical therapists work closely with both hy

trition, weight control, smoking reduction and ces

pertensive patients and physicians.

sation, risk factors, life-style factors, disease pre

Systemic blood pressure responses to dynamic ex

vention, medications and their applications and

ercise are greater for upper-extremity than for lower

side effects

extremity work (Dean and Ross,

Maximize aerobic capacity and efficiency of oxy

cise prescription includes aerobic exercise of the

1992). Thus exer

gen transport

large muscle groups to avoid small muscle group

Optimize physical endurance and exercise capacity

work and increasing peripheral vascular resistance

Optimize general muscle strength and thereby pe

and hence hemodynamic work, and the increased ex


ertion, strain, and work of the heart experienced with


upper-extremity work. Exercise is also performed in

toring (i.e., heart rate, blood pressure, and rate pres

erect and upright rather than recumbent positions to


29

minimize the increased work of the heart secondary


533

can be tolerated over the short term. However, these

to central fluid shifts when the patient is Lying in re

factors may result in a critical situation for the dia

cumbent positions.

betic patient.

Principles of physical therapy management Diabetes Mellitus

Diabetic patients may be referred to a physical thera


pist for several reasons. First, a newly diagnosed dia

Diabetes mellitus is a condition associated with im

betic patient may be referred so that the physical ther

paired insulin metabolism that can result in serious

apist can expose the patient to a quantified exercise

long-term multisystem consequences (Guyton, L991).

stimulus under supervised conditions and thereby

The disease. is classified as insulin-d ependent

help refine the prescription of insulin. Second a pa

(100M) and non-insuLin-dependent diabetes mellitus

tient may be referred for an exercise prescription to

(NIODM). Insulin is the carrier responsible for trans

help minimize the insulin dose or avoid insulin ad

porting glucose into the cells to undergo oxidation.

ministration entirely, depending the disease type and

Juvenile-onset diabetes is frequently the insulin

severity and the patient's response. Third but most

dependent type, whereas adult onset diabetes often is

frequently, patients are seen by a physical therapist

non-insulin-dependent. The underlying pathophysiol

for the treatment of some other condition and also re

ogy of juvenile and adult-onset diabetes, however, is

port diabetes in their histories. A history of diabetes

distinct. Juvenile-onset diabetes results from an inad

must be considered in the treatment of a patient who

equate number of islets of Langerhan in the pancreas,

is referred for any reason to either improve or at least

which are responsible for insulin production. Adult

not contribute to abnormal blood glucose levels and

onset diabetes, on the other hand, results from re

late complications.

duced insulin sensitivity. In Western industrialized

Diabetic patients are treated cautiously. Exercise

countries, adult-onset diabetes is associated with obe

increases metabolical demand commensurate with

sity, inactivity, diet, and stress. In addition, medica

intensity and hence cellular demand for glucose

tions can contribute to blood sugar disturbances. The

(Amercan College of Sports Medicine, 1995; Blair

sequelae of diabetes mellitus that frequently result

et aI., 1988). Usually, insulin administration is in

from poor regulation and management of the disease

creased in preparation for exercise. Many acti ve di

include angiopathy, peripheral neuropathy, autonomi

abetic patients are closely attuned to their dietary

caL neuropathy, gastrointestinal paresis, visual distur

and insulin needs, which permits them to be as

bance, and renal dysfunction (Bannister, L988; Ewing

physically active as nondiabetic individuals. How

and Clarke, L986).

ever, the diabetic patients seen by physical thera

Patients with diabetes mellitus have an accelerated

pists are often labile and less well managed. Thus a

rate of atherosclerotic changes in the vasculature

readily available sugar source must be nearby for

compared with age- and gender-matched nondiabet

insulin reguLation when a diabetic patient exercises

ics. These patients are also prone to peripheral vascu

or when exercising a diabetic patient on a ergome

lar disease secondary to microangiopathy, macroan

ter after anterior cruciate ligament repair in a pri

giopathy, and autonomical neuropathy. Diabetic

vate clinic.

patients constitute a significant proportion of patients

In addition, diabetic patients may have hemody

with peripheral vascular disease who require surgical

namic disturbances because of a autonomic neuropa

amputation of affected limbs.

thy and may exhibit impaired fluid-volume regulation

Abnormalities of blood sugar metabolism may be

during exercise (Bannister, 1988). Patients may expe

observed also in nondiabetic patients. Diabetogenic

rience postural hypotension and become dizzy and

factors, such as restricted mobility and stress, lead to

Iightheaded. In addition, diabetic patients may re

glucose intolerance and insulin oversecretion (Lip

quire a longer cool-down period to adjust hemody

man, 1972). In the nondiabetic patient, these effects

namically after exercise.


534

PART V


Hypoglycemia or low blood sugar is one of the

lant in monitoring signs and symptoms of vascular in

most common complications of diabetes mellitus.

sufficiency in the affected limb. Any sign of skin red

This condition results from excess administration of

ness in the feet should be monitored closely. In dia

insulin or oral hypoglycemic agent, insufficient food

betic patients, any threat of skin breakdown requires

in relation to insulin dose, or an abnormal increase in

medical attention and discontinuation of exercise until

physical activity or exercise. Hyperglycemia is com

medical clearance has been obtained. Healing is con

mon in obese patients with adult-onset diabetes. High

siderably delayed in the diabetic foot. Without appro

insulin levels are associated with a higher risk of

priate attention, infection and potential necrosis can

coronary artery disease. Myocardial infarction and

ensue. Patients with peripheral neuropathy are taught

stroke are common causes of death. Another compli

to monitor their footwear and socks diligently, to en

cation is cardiac hypertrophy secondary to hyperten

sure the inner surfaces are clean and smooth before

sion and cardiomyopathy, which predisposes the pa

each exercise session, and to check for areas of red

tient to congesti ve heart failure. The incidence of

ness or abrasion of their feet after exercise.

peripheral vascular disease is also increased in dia betic patients. The goals of the long-term management of dia betes mellitus include the following: •

Medication that is needed to maximize treatment response is administered before treatment (e.g., in sulin or oral hypoglycemic agents). Knowledge of the type of medication, its administration route, and time


to and duration of peak efficacy is essential if treat

health and well-being, and hence physiological re

ment is to be maximally efficacious.

serve capacity •

The primary interventions in the long-term man

Educate about diabetes mellitus, self-management,

agement of diabetes mellitus include education,

nutrition, weight control, blood sugar regulation

maintainance of a log of diet and insulin regimens,

and its managment (i.e., the balance between nu

activity and exercise, aerobic exercise, strengthening

trition, diet, exercise, stress and insulin require

exercises, relaxation, stress management, activity

ments), medications, smoking reduction or cessa

pacing, and energy conservation.

tion, relaxation, stress management, foot care,

Generally, there are no contraindications to patients

hygiene, and infection control

with diabetes mellitus being physically active and par

Maximize aerobic capacity and efficiency of oxy

ticipating in an exercise program. Daily exercise is ad

gen transport

vocated for insulin-dependent and non-insulin-depen

•


dent diabetic patients to optimize glucose control. The

•

Optimize general muscle strength and thereby pe

exercise prescription parameters are set at 40% to 85%


of peak functional work capacity (American College

Patient monitoring includes signs and symptoms of

of Sports Medicine, 1991). If the patient is exercising

•

hypoglycemia (e.g., lightheadedness, weakness, fa

daily, the exercise parameters are set at the lower end

tigue, disorientation, and glucose tolerance test) or hy

of this range. If the exercise sessions are less frequent

perglycemia (e.g., glucose tolerance test). Hemody

(e.g., in the case of a non-insulin-dependent diabetic

namic responses (i.e., heart rate, blood pressure, and

patient whose blood glucose is well maintained and

rate pressure product) provide an index of the inten

whose weight is acceptable) the exercise intensity is

sity of an exercise stimulus, however, these responses

set at the higher end of this range.

may be attentuated in the diabetic patient because of

The risk of hypoglycemia can be reduced by observ

the autonomic neuropathy; both parasympathetic and

ing the following precautions: frequently monitor blood

sympathetic neuropathies.

glucose, decrease the insulin dose (in consulting with

Subjective responses to exercise, including the rat

the physician) or increase carbohydrate intake before

ing of perceived exertion, may be more valid indica

exercise, avoid injecting insulin into areas that are ac

tors of exercise intensity than hemodynamic responses

tive during exercise, avoid exercise during peak insulin

in the diabetic patient. The patient is taught to be vigi

activity, consume carbohydrates before, during, and


29

2, Relate

aerobic and symptoms of ican

Chronic Primary

of Sports Medicine,

un'l'u"mu",,,, J Dysfunction

535

physical therapy treat

ment interventions to the underlying pathophysi

1991).

ology of

each of the above chronic conditions rationale for your choice.

and provide the

SUMMARY

References reviews the

This

medical

management, and physical

management of

primary, cardiopulmonary tion as a

IJU'UV"V"

p",p.nliP,lt

that the heart and Iungs are

Given

and func

unit, primary

considered with respect to the other organ and in the context of oxygen transport overall. The

management of

chronic lung diseases is

first Although

there is no clear line between obstructive and restric tive

physiological problems, Thus the included obstructive chronic airtlow limitation, asthma, fibrosis) and restrictive

interstitial pulmonary fibrosis).

cancer, which

has the characteristics of both obstructive and restric of pathology, is also

The

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defined based on the primary

tive

changes of the

Bates. D,V, (1989), Respiratory jimclioll in diseases, (3rd ed}

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and

American College of Sports Medicine, (1991). ACSM's guidelines for exercise testing and prescription (4th ed,), Philadelphia: Williams & Wilkins, Arita, K,L, Nishida, 0" & Hiramolo, T, (1981), Physical exercise in "pulmonary fibrosis," Hiroshima Journal (If Medical Sci ence, 30, Bake, B" Dempsey, J" Grimby, G (1976), Effects of shape

nrf' pntp'li

'AnfT_"'rrn

atten

heart disease was then

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and diabetes

In C. Bouchard, R.I, Shepard, T. Stephens, l,R. Sutton, & B,D, McPherson, (Eds.). iitness, and health, A con sen su s of currenl knowledge, Champaign, IL: Human Kinet ics Books.

The principles of management of the various

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tion to

myocardial

heart disease. Chronic vascular diseases vascular disease,

h\fnp,rtpnc.

and val vular pe

were also presented, chronic primary cardiopulmonary conditions are pre sented rather than treatment

which

cannot be discussed without consideration of a spe

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cific

ical implications, PhYSical Therapy, 69, 956-966, Cotton, OJ" Graham. B.L, Mink, IT. & Habbick, BF (1985). Reduction of the single breath diffusing capacity in cystic fibro,

REVIEW QUESTIONS

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in

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Chronic Secondary Cardiopulmonary Dysfunction Elizabeth Dean Donna Frownfelter

KEY TERMS

Ankylosing spondylitis

Muscular dystrophy

Cerebral palsy

Osteoporosis

Chronic renal insufficiency

Parkinson's disease

Hemiplegia

Rheumatoid arthritis

Kyphoscoliosis

Scleroderma

Late sequelae of poliomyelitis

Spinal cord injury

Multiple sclerosis

Systemic lupus erythematosus

INTRODUCTION

injury, and the late sequelae of poliomyelitis. The

The purpose of this chapter is to review the patho

musculoskeletal conditions that are presented include

physiology, medical management, and physical ther

kyphoscoliosis and osteoporosis. The collagen vascu

apy management of chronic, secondary cardiopul

lar/connective tissue conditions that are presented in

monary pathology. Specif ically, this chapter

clude systemic lupus erythematosus, scleroderma,

addresses chronic cardiopulmonary dysfunction sec

ankylosing spondylitis, and rheumatoid arthritis. Fi

ondary to neuromuscular, musculoskeletal, collagen

nally, management of the patient with chronic renal

vascular/connective tissue, and renal dysfunction.

insufficiency is presented. The principle.<> of manage

The neuromuscular conditions that are presented in

ment are presented rather than treatment prescrip

clude muscular dystrophy, hemiplegia, Parkinson's

tions, which cannot be given without consideration of

disease, multiple sclerosis, cerebral palsy, spinal cord

a specific patient. (For specific examples of patient 537


538

PART V


treatment prescriptions refer to the companion text

abnormal ventricular wall motion. Fatty and fibrous

Clinical case studies in cardiopulmonary physical

tissue infiltrate the myocardium and conduction sys

therapy.) In this context the goals of long-term man

tem and electrical conduction is slowed. Thus sub

agement of each condition are presented, followed by

clinical cardiac involvement is prevalent in patients

the essential monitoring required and the primary in

with muscular dystrophy and may explain sudden

terventions for maximizing cardiopulmonary function

death in this patient population.

and oxygen transport. The selection of interventions

Chronic respiratory muscle weakness is character

for any given patient is based on the physiological hi

istic of muscular dystrophy and other neuromuscular

erarchy. The most physiological interventions are ex

disorders. Because the cardiopulmonary system is sel

ploited followed by less physiological interventions

dom stressed due to musculoskeletal dysfunction in

and those whose efficacy is less well documented

these patients, respiratory muscle weakness is seldom

(Chapter 16).

detected. Such weakness is significant, however, in that it contributes to several other serious problems, including thoracic mechanical abnormalities, diffuse

NEUROMUSCULAR CONDITIONS

microatelectasis, reduced lung compliance, a weak

Muscular Dystrophy Pathophysiology and medical management Degenerative neurological and muscular diseases, in

cough with impaired mucociliary transport and secre tion accumulation, ventilation and perfusion imbal ance, and noctural hypoxemia (Smith, Calverley, Ed

cluding Duchenne's muscular dystrophy, lead to res

wards, Evans, and Campbell, 1987; Smith, Edwards,

piratory muscle weakness and alveolar hypoventila

and Calverley, 1989). Progressive respiratory muscle

tion (Black and Hyatt, 1971; Braun, Arora, and

weakness increases the risk of respiratory muscle fa

Rochester, 1983; Inkley, Alderberg, and Vignos,

tigue and failure (Macklem and Roussos, 1977).

1974). Vital capacity, forced expiratory volume, air

The severity of disease is not consistently corre

flow rates, and maximum inspiratory and expiratory

lated with compromised pulmonary function; thus

pressures are reduced. These patients are at risk for

cardiopulmonary function must be assessed individu

the development of atelectasis, impaired mucociliary

ally in each patient (Hapke, Meek, and Jacobs, 1972).

transport, and pneumonia. In addition, long-term gen

Patients with mild-to-moderate involvement of pe

eralized muscular weakness, particularly of the tho

ripheral muscles may exhibit disproportionate respi

racic cavity and abdomen, as well as restricted mobil

ratory compromise (Kilbull1, Eagan, Sieker, and Hey

ity and confinement to a wheelchair, predispose the

man, 1959). This may be explained by differential

patient to thoracic deformities (e.g., scoliosis and

changes in the degree of involvement of the di

dropping of the ribs, and further muscle disuse). Pa

aphragm and the abdominal and intercostal muscles

tients with Duchenne' s muscular dystrophy are sus

(Nakano, Bass, Tyler, and Carmel, 1976). Over time,

ceptible to dysphagia and upper airway obstruction

musculoskeletal changes of the chest wall lead to

secondary to gag reflex depression and hypotonia of

spinal deformity and stiffness with loss of its elastic

the pharyngeal structures (Murray and Nadel, 1988a).

recoil. Chronic alveolar hypoventilation leads to res

These factors further compromise or threaten car

piratory insufficiency and the need for ventilatory as

diopulmonary function and oxygen transport.

sistance. With progressive respiratory insufficiency,

Cardiac dysfunction has also been reported in pro

noctural hypoventilation with hypercapnia and hy

gressive muscular dystrophy (Moorman et aI., 1985;

poxemia develop (Bach, O'Brien, Krotenberg, and

Perioff, de Leon, and O'Doherty, 1966). Although

Alba, 1987). Nocturnal respiratory support should be

the majority of patients have no clinical evidence of

considered early to postpone the need for intubation

cardiac dysfunction, a high proportion have abnormal

and mechanical ventilation, which is associated with

E CGs at rest or during exercise and a b n o r m a l

a poor prognostic outcome in patients who have

echocardiography and radionuclide ventriculography

chronically reduced vital capacities and weak cough.

showing reduced left ventricular ejection fraction and


Clinically, patients with muscular dystrophy pre

30

sent with low functional

commensurate

Chronic Secondary Cardiopulmonary Dysfunction

•


with the extent of muscle weakness and

•


cardiopulmonary function, including alveolar

•

Facilitate mucociliary

on re-

•


transport, difficulty

•

orthopnea (shortness of impaired


and increased work of breath-

clearing

provides an index

Abdominal muscle

539

oxygen transport Optimize physical endurance and exercise ca

•

of pulmonary function in that it is correlated with and expiratory flow rates

vital aI., 1

The

general muscle strength and thereby

et


progressive functional with Duchenne's muscular dystro

loss

susceptibility to the se-

phy increases the

and reduced

oxygen transport, circulatory

of desatura-

Lion), heart rate, blood pressure, and rate pressure

muscular weak

product. Patients with cardiac dysfunction need to be cleared

ness, and bone loss. of the complica

medical

(depth and frequency), ar

breathing

terial

of restricted mobility, including monary

respiratory

Patient monitoring includes LI,,,'""''''',

a

before

a rehabilita

when it involves a mobi

tion program,

tions of myopathies has significantly increased the

lization or exercise program, to refine the prescriptive

life expectancy of p atients, such as those with

of the program. If supplemental oxygen is

Duchenne's muscular

20

over the

age, further complications will

years. With

administered is recorded. breathlessness is assessed

arise from

the

function (Dean, 1994;

nighttime and

Thus in the years ahead an

needed because

of patients with myopathies will be

car

of long-term management for the patient

p at i e n t s with

of the

of medication, its administration

route, and time to and duration of


efficacy is es

sential if treatment is to be maximally efficacious .

health, and well-being and hence

•

in


with muscular dystrophy include the

reserve

rPt'r'lII'"tl,nl

n o c turnal h y p o x e m i a



•

with

Duchenne's muscular dystrophy,

diopulmonary management and prophylaxis.

The

a modified version of

scale of

The

interventions for

diopulmonary function and oxygen

--t"--" J

car in pa

Educate about cardiopulmonary manifestations

tients with muscular

of muscle

nation of education, mobilization, primarily in the

medica reduc

tion and cessation,

protection, infection

include some combi

form of functional activities, primarily in the form of functional activities ventila

control, the role of a rehabilitation program, and

maintain strength or reduce rate of

the eventual need for mechanical

tory muscle training, postural correction exercises,

support

chest wall mobility


cises,

volumes and rates

control and coughing maneuvers, ance

ventilation and perfusion

range of motion exer

prevention, body positioning, breath-

conservation. An

activity

clearand energy

assessment of the pa

tient's work and home environments may be indi from aspiration

cated to minimize oxygen demand and energy expen


540

PART V


diture in these settings. Such an assessment includes

impaired, leading to secretion accumulation, postural

review of aids and devices (e.g., wheelchair type,

drainage may need to be instituted, coupled with deep

weight, and size and noninvasive mechanical ventila

breathing and coughing maneuvers.

tion). Aids and devices are selected to minimize en

Although the primary factor contributing to respi

ergy demand such that energy is conserved for other

ratory compromise is respiratory muscle weakness,

activities and undue fatigue is reduced.

the capacity of the respiratory muscles to respond to

The use of supplemental oxygen depends on the

resistive loading is limited. However, ventilatory

severity of the disease. Some patients have no need

muscle training may have some role in selected pa

for supplemental oxygen, some need it only during

tients, particularly children (Adams and Chandler,

exercise, and some patients require continuous oxy

1974; Pardy and Leith, 1984). Improved respiratory

gen with proportionately more delivered during activ

muscle endurance and strength may have a general

ity and exercise compared with rest.

ized effect on functional capacity (Reid and Warren,


1984). Patients with signs of ventilatory muscle fa

management of the patient with muscular dystrophy.

tigue, as opposed to weakness, benefit from ventila

Education includes the reinforcement of preventative

tory support at night. Rest of the respiratory muscles

health practices (e.g., infection control, cold and flu

at night optimizes their function during the daytime.

prevention, flu shots, aerobic exercise, strengthening

Methods of facilitating effecti ve coughing in pa

exercises, nutrition, weight contrOl, hydration, pacing

tients with neuromuscular diseases are extremely im

of activities, and energy conservation). Weight control

portant because they constitute life-preserving mea

is an important goal in patients with chronic neuro

sures. Supported and unsupported coughing methods

muscular diseases because they have the least capacity

are described in detail in Chapters 20 and 21. Patients

to compensate for the cardiopulmonary sequelae of

on noninvasive ventilatory support who are unable to

obesity (Alexander, 1985). Obstructive sleep apnea is

generate adequate peak cough expiratory flow rates

related to hypotonia of the upper airway musculature

can benefit from manual assisted coughing and me

and obesity. Thus activity and sleep patterns need to

chanical insufflation-exsufflation, thereby minimiz

be assessed to ensure sleep is maximally restorative

ing the need for endotracheal suctioning (Bach, 1993;

and not contributing to the patient's symptoms. Mobilization is an essential component of the long

Barrach, Beck, Bickerman, and Seanor, 1952). Tra cheostomy is delayed as long as possible. Signifi

term management of the patient with muscular dystro

cantly reduced maximal insufflation capacity, how

phy to optimize the efficiency of oxygen transport

ever, is an indication for tracheostomy.

overall and minimize the sequelae of restricted mobil

Whenever possible, deep breathing and coughing

ity, including circulatory stasis. Maximizing ventila

are coupled with chest wall movement to facilitate

tion with mobilization is limited if the patient has se

maximal inflation of the lungs before coughing by in

vere generalized muscular weakness and increased

creasing pulmonary compliance (Ferris and Pollard,

fatigue. Functional activities provide the basis for the

1960) and maximal exhalation of the lungs during

mobilization prescription. Although heavy resistive

coughing. Body positions are varied and changed fre

strengthening exercise has been advocated for these

quently to simulate shifts in alveolar volume and ven

patients (Vignos and Watkins, 1966), a conservative

tilation and perfusion that occur with normal move

approach, including an exercise program based on

ment and body position changes. Glossopharyngeal

functional goals and energy conservation, is more jus

breathing is a nonmechanical method of assisting

tifiable physiologically. Chest wall mObility exercises

ventilation. The patient is taught to use the tongue

include all planes of movement combined with a rota

and pharyngeal muscles to swallow boluses of air

tional component. Body positioning to optimize lung

past the vocal cords and into the trachea (Bach, Alba,

volumes and airflow rates is a priority. Breathing con

Bodofsky, Curran, and Schultheiss, ) 987). The effi

trol and coughing maneuvers are coupled with body

ciency of training is monitored with spirometry to en

movement and positioning. If mucociliary transport is

sure the patient is able to achieve acceptable vital ca


30


541

pacities. Some patients are able to support their venti

can affect cardiopulmonary function. Such infarc

lation, ventilator-free, for several hours in a day.

tions, however, are I ikely to be lethal. More com

One intervention that is prolonging the life of pa

monly, after a stroke, chest wall movement and elec

tients with muscular dystrophy, as well as of patients

trical activity on the ipsilateral side are reduced

with other progressive neuromuscular diseases, is the

(DeTroyer, DeBeyl, and Thirion,

use of mechanical ventilatory support (Bach,

1992;

1981; Fluck, 1966). Facial and pharyngeal weakness contributes

1981). Home mechariical ventilation provides

to an inability to control oral secretions, swallow ef

a noninvasive method of providing positive airway

fectively, and protect the upper airway. Altered res

pressure through an oral or nasal mask. This provides

piratory mechanics and efficiency reflect impaired

Curran,

considerable advantage over invasive, full body or

chest wall movement, asymmetry, and the degree of

tracheostomy. ventilatory support. Used in conjunc

muscle paresis and spasm.

tion with an insufftation-exsufflation device, pul

Patients with hemiplegia have associated problems

monary complications can be minimized and life ex

that contribute to cardiopulmonary dysfunction.

pectancy increased. Other forms of noninvasive

These patients tend to be older, hypertensive, and

mechanical ventilation include intermittent abdomi

have a high incidence of cardiac dysfunction. Muscle

nal pressure ventilation, rocking bed, negative pres

disuse and restricted mobility secondary to hemiple

sure tank ventilator, and chest shell ventilator. The

gia lead to reduced cardiopulmonary conditioning

type of ventilation is determined individually based

and inefficient oxygen transport. Spasticity increases

on the indications for ventilation and the patient's

metabolical and oxygen demand. Hemiparesis results

status. The use of ventilatory aids as a component of

in gait deviations, which reduce movement efficiency

a comprehensive rehabilitation program maintains

and movement economy. Reduced movement econ

pulmonary compliance and cough efficacy. Introduc

omy results in an increased energy cost associated

tion of these devices early will facilitate increased use

with ambulation, which may reduce exercise toler

as the respiratory muscles progressively weaken.

ance because of fatigue (Dean and Ross,

1993). In

Patients with generalized neuromuscular weakness

addition, ambulating with a walking aid is associated

require prophylactic management given their high

with a significantly increased energy cost compared

risk of developing life-threatening respiratory infec

with normal walking. This increased energy cost re

tions and complications. Prophylaxis should include

duces the patient's exercise tolerance further and in

flu shots, avoiding polluted, smoky environments,

creases fatigue.

smoking reduction and cessation, controlling the types of food eaten and chewing well to avoid chok


ing, and regular deep breathing, frequent movement,


and change in body positions (even just shifting and

with hemiplegia include the following:

taking some deeper breaths while seated in a wheel

•


chair) to promote mucociliary transport. An optimal


time to take deep breaths and to cough is during

reserve capacity

transfers, which usually are physically exerting and

•

Educate about cardiopulmonary manifestations of hemiplegia, self-management, medications, smok

stimulate hyperpnea.

ing reduction and cessation, nutrition, weight con trol, and the role of a rehabilitation program

Hemiplegia •


•

Grimby,

•

1984; Griggs and Donohoe, 1982). A cere

bral infarct involving the vital centers of the brain

Optimize lung volumes and capacities and flow rates

Hemiplegia or stroke affects cardiopulmonary func tion either directly or indirectly (Fugl-Meyer and



•



542

PART V


•


sleep apnea). Thus activity and sleep patterns need to

•

Protect the airways from aspiration

be assessed to ensure sleep is maximally restorative

•


and not contributing to the patient's symptoms.

•


•


•

•

Aerobic excrcise is an essential component of the long-term management of the patient with hemiplegia

oxygen transport

to optimize the efficiency of oxygen transport overall.

Optimize physical endurance and exercise

Maximizing ventilation with mobilization is limited if

capacity

the patient has severe generalized muscular weakness


and increased fatigue. Although aggressive mobiliza


tion can be supported in these patients (Malouin,


Potvin, Prevost, Richards, and Wood-Dauphinee,

distress, breathing pattern (depth, symmetry, and fre

1992), appropriate selection of patients for such a reg

quency), arterial saturation, cyanosis (delayed sign of

imen, judicious exercise prescription, and monitoring

desaturation), heart rate, blood pressure, and rate pres

must be instituted to ensure the treatment is optimally

sure product. Patients with cardiac dysfunction require

therapeutic and poses no risk to a patient in this high

clearance from a cardiologist before participating in a

risk group. Chest wall exercises include movement in

rehabilitation program and may require ECG monitor

all planes combined with rotation. Body positioning to

ing, particularly during exercise. Subjectively, per

optimize lung volumes and aitflow rates is a priority.

ceived exertion is rated using the Borg scale.

Breathing control and coughing maneuvers are essen


tial and should be coupled with body movement and

response is administered before treatment (e.g., anti

positioning. Exercise is conducted in the upright posi

hypertensive and cardiac medications). Knowledge of

tions to minimize the work of the heart and of breath

the type of medication, its administration route, and

ing during physical exertion. Recumbent positions re

time to and duration of peak efficacy is essential if

duce lung volumes and expiratory flow rates, impair

treatment is to be maximally efficacious.

respiratory mechanics, increase closing volumes, in


crease thoracic blood volume, and increase compres


sive forces on both the lungs and the heart (Dean and

tients with hemiplegia include some combination of

Ross, 1992; Ross and Dean, 1992). Thus significant

education, aerobic exercise, strengthening exercises,

periods and intensities of aerobic exercise should be

spasticity control, postural correction exercises, gait

petformed standing or sitting. Lower-extremity work

reeducation, chest wall mobility exercises, range of

is preferable to upper-extremity work in that the latter

motion exercises, body positioning, breathing control

is associated with increased hemodynamic stress.

and coughing maneuvers, airway clearance interven

Rhythmic exercise of large muscle groups is prefer

tions, activity pacing, and energy conservation. An er

able to static exercise and exercise of small muscle


groups, such as the arms, in that it produces smaller


hemodynamic effects.


Ambulation or wheelchair locomotion should be


as efficient as possible so that the metabolical de

management of the patient with hemiplegia. Educa

mand of these functional activities is reduced. Per

tion includes the reinforcement of preventative health

forming these activities inefficiently on a frequent

practices (e.g., infection control, smoking reduction

basis contributes to an excessive oxygen demand.

and cessation, cold and flu prevention, flu shots, aero

The patient expends considerable energy in perform

bic exercise, strengthening exercises, gait reeducation,

ing these activities uneconomically, which impairs

nutrition, weight control, hydration, pacing of activi

the patient's tolerance and contributes to excessive

ties, and energy conservation). Hemiplegia is often as

fatigue. Conserving energy by performing these ac

sociated with sleep disturbances (e.g., obstructive

tivities more economically from an energetic per


30

spective will

more energy to "PIc-fArm more of

these or other activities.


which has been associated with the disease. The de gree to which these cardiopulmonary manifestations

neuromuscular weakness

of the disease are offset with used to treat rest tremor and reverse

their infec Prophylaxis should include

been reported. The upper extremities are rigid and held abducted from the chest wall during locomotion. The

polluted, smoky smoking reduction and cessation,

the

rigidity and dyskinesia associated with Parkinson's

types of food eaten and chewing well to avoid chok

disease leads to restricted movement and body

ing, and

tioning. The

deep breathing,

and

movement,

positions (even just

and

breaths while seated in a wheel nrr,rYI.c>'p

543

use. The

becomes deconditioned from dis immobile chest, coupled with reduced

body position

contributes to

monary

mucociliary transport. An breaths and to

Principles

are

nmrSIt:,al therapy management

The goals of

management for the

with Parkinson's disease include the following: •

Parkinson's Disease Pathophysiology and medical management

normal

•

resulting in the loss of

inhibitory and

199

et

Educate about cardiopulmonary manifestations self-

of Parkinson's d

neuronal

smoking reduction a n d

input in the execution of smooth coordinated move ment

quality of life, and hence physiological

reserve

Parkinson's disease i s associated w i t h reduced dopamine in the basal

Maximize the health, and

weight

The clinical manifesta

infection program

tions of the disease include stooped posture, stiffness and

•


tremor of the limbs. Patients with Parkinson's disease

•

Optimize

and inflexible. Movement initi

•

Optimize ventilation and perfusion

and slowed

fixed masklike

and gas

once initiated, movement is not walks with a quick,

volumes and capacities

•


These factors contribute to an increased energy cost

•


of movement.

•

Protect the

tion is

activity is restricted and func contributing to

aerobic

reduced movement efficiency, and hence re

Facilitate

•

Although chest wall rigidity and respiratory mus

•

cle weakness are associated with a restrictive

tory

and efficiency of

Optimize

endurance and exercise

capacity

of lung disease in the Parkinsonian patient (Mehta, Wright, and

Maximize aerobic oxygen

duced movement economy.

1978), obstructive type of

•


has been reported (e.g., reduced

Patient monitoring includes

respiratory

mid-tidal flow rates, increase airway resistance, im

distress, breathing

paired distribution of ventilation, and an increase in

arterial saturation, heart rate, blood pressure, and

functional residual

(depth and frequency),

Patients with cardiac dys

and

particularly dur

tive defect may reflect parasympathetic

breathlessness is as


544

PART V


sessed using a modified version of the Borg scale

Multiple Sclerosis Pathophysiology and medical management

of perceived exertion. Medication that is needed to maximize treatment

Multiple sclerosis is a demyelinating disease of the

response is administered before treatment (e.g., L

central nervous system. The focal or patchy destruc

dopa). Knowledge of the type of medication, its ad

tion of myelin sheaths is accompanied by an inflam

ministration route, and time to and duration of peak

matory response (McFarlin and McFarland, 1982).

efficacy is essential if treatment is to be maximally

The course of the disease consists of a variable num

efficacious. In addition, patients with Parkinson's

ber of exacerbations and remissions over the years

may be on a beta-blocker to suppress action tremor.

from early adulthood. Exacerbations are also vari

Because such medication reduces the heart rate and

able with respect to severity. The neurological

blood pressure, these patients are prone to orthosta

deficits include visual disturbance, paresis of one or

tic intolerance. In addition, heart rate and blood

more limbs, spasticity, discoordination, ataxia,

pressure responses to treatment and exercises will

dysarthria, weak, ineffective cough, reduced percep

be less valid.

tion of vibration and position sense, bowel and blad


der dysfunction, and sexual dysfunction (Wilson,


Braunwald, Isselbacher, Martin, Fauci, and Root,

tients with Parkinson's disease include some combi

1991). Breathing disturbances, including diaphrag

nation of education, aerobic exercise, strengthening

matic paresis, may occur (Cooper, Trend, and Wiles,

exercises, postural correction exercises, gait reeduca

1985). Autonomic disturbance in the form of im

tion, chest wall mobility exercises, range of motion

paired cardiovascular reflex function at rest and at

exercises, body positioning, breathing control and

tenuated heart rate and blood pressure responses dur

coughing maneuvers, activity pacing, and energy

ing exercise are relatively common in patients with

conservation. An ergonomic assessment of the pa

mUltiple sclerosis (Neubauer and Gundersen, 1978;

tient's work and home environments may be indi

Pentland and Ewing, 1987; Senaratne, Carroll, War


ren,and Kappagoda, 1984).

diture in these settings.


Education is a principal focus of the long-term management of the patient with Parkinson's disease.



with mUltiple sclerosis include the following:

health practices (e.g., infection control, airway pro

•

reserve capacity

prevention, flu shots, aerobic exercise, strengthening exercise, nutrition, weight control, hydration, pacing


tection, smoking reduction or cessation, cold and flu

•

Educate about cardiopulmonary manifestations of mUltiple sclerosis, self-management, medica

of activities, and energy conservation). Aerobic exercise is an essential component of the

tions, smoking reduction and cessation, nutri

long-term management of the patient with Parkinson's

tion, weight control, infection control, and the role of a rehabilitation program

disease to optimize the efficiency of oxygen transport overall, including maximizing alveolar ventilation and mobilizing secretions, as weJl as its musculoskeletal

•

•


benefits. Maximizing ventilation with mobilization is limited by the degree of hypertonicity and rigidity.


•


Chest wall exercises include all planes of movement with a rotational component. Breathing control and

•


coughing maneuvers are essential and should be cou

•


•


pled with body movement and positioning.


30

•

•

•

•

•


545


management, modified aerobic exercise, modified


strengthening exercises, pacing of activities, and en


ergy conservation). Multiple sclel'Osis is associated

oxygen transport

with significant fatigue. Thus activity and sleep pat


terns need to be assessed to ensure sleep is maximally

pacity

restorative and not contributing to the patient's symp


toms. By maintaining a log of activity and rest, the


patient can observe relationships between these fac


tors and identify when is the optimal time to rest.




long-term management of the patient with multiple


sclerosis to optimize the efficiency of oxygen trans

product. Patients with cardiac dysfunction require

port overall. In mild-to-moderate cases the goals of

ECG monitoring, particularly during exercise. Sub

aerobic exercise are to optimize cardiopulmonary

jectively, fatigue can be assessed using a modified

conditioning and enhance movement economy. Opti

version of the Borg scale. Perceived exertion is as

mizing cadence of walking or cycling is important to minimize discoordination, energy expenditure, and

sessed using the Borg scale. Medication that is needed to maximize treatment

fatigue and maximize safety. In more severe cases the


goal is to maximize ventilation and gas exchange in

spasticity medications). Knowledge of the type of

the patient who has severe generalized muscular


weakness, spasm, and excessive fatigue. Subjective


parameters (i.e., fatigue and exertion) provide the

be maximally efficacious. In addition, knowledge of

basis for the intensity of the exercise program in con

the cardiopulmonary side effects of other medications

junction with objective measures. Parameters, such as

is needed.

intensity and duration, may vary from session to ses


sion depending on the patient's general status, which

diopul monary function and oxygen transport in pa

tends to be variable. Aquatic exercise may be an al

tients with multiple sclerosis include some combina

ternative for patients whose discoordination pre

tion of education, aerobic exercise, strengthening

cludes ambulation and cycling or who are troubled by

exercises (to maintain or reduce rate of decline), re

heat. The use of a fan may also enhance the palient's

duce abnormal muscle tone, postural correction exer

work output.

cises, gait reeducation, chest wall mobility exercises,

Chest wall exercises include all planes of move

range of motion exercises, body positioning, breath

ment with a l'Otational component. Body positioning to

ing control and coughing maneuvers, airway clear

optimize lung volumes and airflow rates is a priority.

ance interventions, fatigue management, activity pac

Breathing control and coughing maneuvers are cou

i n g a nd e nergy conservation. An ergonomic

pled with body movement and positioning. If mucocil

assessment of the patient's work and home environ

iary clearance is impaired leading to secretion reten

ments may be indicated to minimize oxygen demand

tion, postural drainage may need to be instituted

and energy expenditure in these settings.

coupled with deep breathing and coughing maneuvers.


Methods of facilitating effective coughing in pa

management of the patient with multiple sclerosis.

tients with neuromuscular diseases are extremely im


portant because they constitute life-preserving mea


sures. Supported and unsuppolted coughing methods

prevention, flu shots, smoking reduction and cessa

are described in detail in Chapters 20 and 21. When

tion, nutrition, weight control, hydration, fatigue

ever possible, deep breathing and coughing are coor


546

PART V


dinated with chest wall movement to facilitate maxi

ipate actively in a long-term rehabilitation pro

mal inflation of the lungs before coughing and maxi

gram. Patients with cerebral palsy who are able to

mal exhalation of the lungs during coughing. Body

ambulate do so at exceptional energy expenditure

positions are varied and changed frequently to simu

both with and without walking aids (Campbell and

late as much as possible shifts in alveolar volume and

Ball, 1978; Mossberg, Linton, and Friske, 1990).

ventilation and perfusion that occur with normal

Central neurological deficits, generalized hyper

movement and body position changes (Ray et aI.,

tonicity, and musculoskeletal deformity contribute

1974). In addition, body positioning is used to maxi

to increased metabolical demand for oxygen and

mize the patient's coughing efforts.

oxygen transport.

Patients with generalized neuromuscular weakness

Principles of phYSical therapy management

require prophylactic management given their high risk of developing life-threatening respiratory infec



with cerebral palsy include the following:


•

smoking reduction and cessation, controlling the


types of food eaten and chewing well to avoid chok

reserve capacity

ing, and regular deep breathing, frequent movement,

•

Educate patient and/or family about cardiopul

and change in body positions (even just shifting and

monary manifestations of cerebral palsy, self

taking some deeper breaths while seated in a wheel

management, medications, nutrition, weight

chair) to promote mucociliary transport. An optimal

control, airway protection, infection control, and

time to take deep breaths and to cough is during

the role of a rehabilitation program

transfers, which usually are physically exerting and

•

stimulate hyperpnea.

•


•

Cerebral Palsy



•


Cerebral palsy results from insult to the central ner

•


vous system usually before birth (e.g., substance

•


abuse and underoxygenation perinatally) (Wilson et

•


aI., 1991). The clinical presentation includes spas

•


ticity and residual deformity from severe muscle

•


imbalance, hyperreflexia, and mental retardation.

oxygen transport

Although there are varying degrees of cerebral

•

palsy severity, patients most frequently seen by


physical therapy have significant functional deficits

•


and require long-term care. The loss of motor con trol and hypertonicity of peripheral muscles often

Maximizing aerobic capacity and efficiency of

restrict the mobility of patients such that they are

oxygen transport and optimizing general muscle

wheelchair dependent. Loss of motor function lim

strength pertain to the patient with cerebral palsy that

its p hysical activity and the exercise stimulus

is mild in severity. Unfortunately, many patients seen

needed to maintain an aerobic stimulus and optimal

by physical therapists have poorly controlled spastic

aerobic capacity. Often coupled with motor deficits

ity and extreme cognitive deficits, which preclude

are cognitive deficits and mental retardation. These

full participation in aerobic and strengthening exer

afflictions limit the degree to which the patient can

cise programs. These patients are at risk for the se

follow instructions, perform treatments, and partic

quelae of restricted mobility and recumbency.


30



547

patients often have poor swallowing and saliva con


trol and thus are prone to aspiration and microat


electasis, particularly when recumbent at night. In


ability to reposition themselves at night further

product. Unless mildly affected and not mentally in

increases the risk of aspiration and its sequelae.

capacitated, patients with cerebral palsy are less able

Mobilization is an essential component of the

to provide subjective ratings of treatment response;

long-term management of the patient with cerebral

thus the physical therapist relies particularly on clini

palsy to stimulate aerobic metabolism and optimize

cal judgment in conjunction with the patient's objec

the efficiency of oxygen transport overall, including

tive responses to treatment.

maximizing alveolar ventilation and mobilizing and


removing secretions (Wolff, Dolovich, and Obmin


ski, 1977). Maximizing ventilation with mobilization

spasticity medications). Knowledge of the type of

is limited if the patient has generalized spasticity.


Furthermore, mobilization stimuli are selected specif


ically to minimize eliciting further muscle spasm. Prescriptive hydrotherapy and equinotherapy (horse

be maximally efficacious. The primary interventions for maximizing car

back riding) can provide effective stimulation to the


cardiopulmonary system in the multiply handicapped

tients with cerebral palsy include some combination

individual and minimize the effects of spasticity.

of education, mobilization and coordinated activity

With training, coordination of ambulatory patients

(aerobic stimulation), strengthening e xercises

can be improved and aerobic energy expenditure re

(strength is often difficult to assess and treat because

duced (Dresen, de Groot, and Bouman, 1985). In ad

of overwhelming spasticity), chest wall mobility ex

dition, energy is conserved for performing more ac

ercises, range of motion exercises, body positioning,

tivity. Chest wall exercises includes all planes of

breathing control and coughing maneuvers, and air

movement with rotation. Body positioning to opti

way clearance interventions.

mize lung volumes and airflow rates is a priority.


Breathing control and coughing maneuvers are essen

management of the patient with cerebral palsy.

tial and should be coupled with body movement and

Whenever possible, education is directed at the pa

positioning. If mucociliary transport is impaired lead

tient, but it more likely is directed at the parents and

ing to secretion retention, postural drainage and man

care providers. Education includes the reinforce

ual techniques may need to be instituted with appro

ment of preventative health practices (e.g., infection

priate monitoring to ensure they do not have a

control, cold and flu prevention, flu shots, mobiliza

detrimental effect (Kirilloff, Owens, Rogers, and

tion, coordinated activity, strengthening exercise,

Mazzacco, 1985).

nutrition, weight control, and hydration). Patients

In this patient population, clearing oral secretions

with cerebral palsy can be expected to have abnor

and coughing maneuvers, require special attention.

mal sleep patterns. First, central cerebral involve

Methods of facilitating effective coughing in patients

ment may affect the periodicity of breathing. During

with neuromuscular diseases are extremely important

sleep, the effects of such dysfunction are accentu

because they constitute life-preserving measures. Sup

ated. Loss of normal periodic breathing and inter

ported and unsupported coughing methods are de

spersed sighs impairs mucociliary transport. Secre

scribed in detail in Chapters 20 and 21. Whenever

tions may accumulate and contribute to airway

possible, deep breathing and coughing is coupled with

obstruction and areas of atelectasis. Second, patients

chest wall movement to facilitate maximal inflation of

with cerebral palsy are unable to reposition them

the lungs before coughing and maximal exhalation of

selves during the night in response to both car

the lungs during coughing. Body positions are varied

diopulmonary and musculoskeletal stimuli. Third,

and changed frequently to simulate as much as possi


PART V

548


ble shifts in alveolar volume and ventilation and per fusion that occur with nomlal movement and smon

Chronic Cardiopulmonary Conditions

Guidelines for the Delivery of Cardiopulmonary Physical

po

Microaspiratiolls are likely a common

occurrence in this

population,

The

of long-term management for the patient

with spinal cord injury include the following:

at

•

Maximize the patient's quality of

and well-being and hence

night. Nighttime oositioning must be prescribed for

reserve


•

require

of spinal cord injury,

ri sk of rlpvpIon.

tions,

medica

reduction and cessation, nutri

tion, weight

infection

and the

role of a rehabilitation program alveolar ventilation Optimize lung volumes and caoacities and flow

•

rates ventilation and

and gas exchange

transport.

Spinal Cord Injury Pathophysiology and medical management The


•


•

Protect the

•

Facilitate

secretion clearance

manifestations and complica

tions of spinal cord

•

•

related to the

are

oxygen transport

Car

level of the lesion (Murray and

and efficiency of

Maximize aerobic

•


•

Optimize

diopulmonary impairment results from the loss of muscles and the

control of the heart below the

cord lesion. Loss of

Patient

matic innervation results in Loss of abdominal and intercostal innervation re duces the

muscle strength and thereby


to

transport, and

the ability to clear the airways. Denervation of the

includes pattern (depth and frequency), ar

terial

sign of desatura


in that the

product. Patients with high spinal cord injuries are

heart's autonomous function and increased respon

somewhat more hemodynamically unstable and have

siveness of the heart and blood vessels to circulati

more ECO

cathecholamines

dividuals; thus their cardiopulmonary status should

heart and orthostatism are less

The cough

mechanism of quadriplegic patients is ineffective in the airways

and Oorino, 1992).

than

control in

be monitored during treatment. ceived exertion is monitored

are

prone to the


effects of restricted mobility

the extent of their


functional motor loss and sensory

spasticity

on cardiopulmonary function (Bach, 1991). Mo bilization and cord injured

are essential for the to maintain

car

of the type of medica

tion, its administration route, and time to and dura tion of peak

is essential if treatment is to be

maximally efficaciolls.

diopulmonary function and oxygen transport effi


ciency and the optimal strength and endurance of the


respiratory muscles.

tients with soinet! cord iniurY include some combina


30

tion of education, aerobic exercise, strengthening ex


549

the strength and endurance of the respiratory muscles

ercises (to maintain or reduce rate of decline), pos

(Gross, 1980) and may improve the functional capac

tural correction exercises, chest wall mobility exer

ity of some patients. A stronger endurance-trained di

cises, range of motion exercises, body positioning,

aphragm wit! not fatigue as readily as an untrained di

breathing control and coughing maneuvers, airway

aphragm. Standardizing the resistance of the training

clearance interventions, activity pacing, and energy

stimulus alone, however, is not sufficient to produce


training effect. It is essential that flow rate is con


trolled using a gauge.

cated to minimize oxygen demand and energy expen diture in these settings.

a

Methods of facilitating effective coughing in patients with neuromuscular diseases are extremely important


because they constitute life-preserving measures. Sup

management of the patient with spinal cord injury.

ported and unsupported coughing methods are de


scribed in detail in Chapters 20 and 21. Whenever pos


sible, deep breathing and coughing is coupled with

prevention, flu shots, aerobic exercise, strengthening

chest wall movement to facilitate maximal inflation of

exercise, nutrition, weight control, hydration, pacing

the lungs before coughing and maximal exhalation of

of activities, and energy conservation).

the lungs during coughing. Body positions are v3lied


and changed frequently to simulate as much as possible

long-term management of the patient with spinal cord

shifts in alveolar volume and ventilation and perfusion

injury to optimize the efficiency of oxygen transport

that occur with normal movement and body position

overall, including maximizing alveolar ventilation

changes (Braun, Giovannoni, and O'Connor, 1984).

and mobilizing and removing secretions. With higher

A comprehensive program includes stretching of

lesions, exercise is usually confined to upper-extrem

the chest wall and passive range of motion exercises

ity work in the form of wheelchair ambulation.

of the shoulder girdle. Maximal insufflations are en

Preservation of upper-extremity muscle function and

couraged in optimal body positions. Glossopharyn

minimization of overuse are primary goals from the

geal breathing can enable high quadriplegic patients

outset. Patients can maintain adequate cardiopul

to be freed from mechanical ventilation for hours at a

monary conditioning with wheelchair exercise, how

time. Assisted or unassisted coughing is coordinated

ever, exercise prescription should be conservative to

with deep breathing and rhythmic rocking motion.

maximize the benefit-to-risk ratio of cardiopul

Manual assisted coughing and mechanical coughing

monary conditioning relying of upper-extremity

aids, including functional electrical stimulation and

work. Patients who are able to walk with leg braces

insufflation-exsufflation devices, can be useful

and crutches expend considerable energy doing so. A

(Bach, 1991; Linder, 1993). The pneumobelt is a de

decision needs to be made regarding the benefits of

vice that can facilitate ventilation without a tra

walking at high energy demand vs conserving energy

cheostomy (Miller, Thomas, and Wilmot, 1988). This

for other activities. Chest wall exercises can be used

device counters loss of abdominal tone and helps pre

and should include all planes of movement with a ro

serve normal thoracoabdominal interaction during

tational component. Body positioning to optimize

respiration, which is lost because of reduced rib cage

lung volumes and airflow rates is a priority. Breath

compliance and increased abdominal compliance.

ing control and coughing maneuvers are essential and

Patients with spinal cord injuries, particularly

should be coupled with body movement and position

those with high lesions, require prophylactic man

ing. Coordination of respiration with aerobic activity

agement, given their risk of developing life-threat

and wheeling is taught to maximize work output.

ening respiratory infections and complications. Pro

Ventilatory muscle training has a role in the long

p h y l a x i s s ho uld i n c l u d e flu s h o t s, a v o i d i n g

term rehabilitation of some patients with high spinal

polluted, smoky environments, smoking reduction

cord lesions. Ventilatory muscle training can increase

and cessation, controlling the types of food eaten


550

PART V


and chewing well to avoid choking, regular deep

•


breathing, airway clearance, and frequent move

of the late sequelae of poliomyelitis, self-man

ment and change in body positions (even just shift

agement, medications, smoking reduction or

ing and taking some deeper breaths while seated in

cessation, nutrition, weight control, infection

a wheelchair is beneficial). An optimal time to take

control, orthoses, mobility and ADL aids and

deep breaths a n d to c o u g h is during transfers,

devices, and the role of a rehabilitation program

which usually are physically exerting and stimulate

•

hyperpnea.

•


•

late Sequelae of Poliomyelitis



•

The late sequelae of poliomyelitis are reaching epi

•

demic proportions as poliomyelitis survivors from the

•

late epidemic in the 1940s and 1950s reach 35 to 40

•

years after onset. Three types of poliomyelitis were

Reduce the work of breathing Reduce the work of the heart Protect the airways from aspiration Maximize aerobic capacity and efficiency of oxygen transport

prevalent during the epidemic in the middle of this

•

century, namely, spinal (the majority of cases), bul

Opti mize physical endurance and exercise ca pacity

bar, and encephalitic. Many survivors are now pre

•

senting with disproportionate fatigue, increased


weakness, deformity, pain, reduced endurance, and


breathing and swallowing problems (Dean, 1991;


Howard, Wiles, and Spencer, 1988), and respiratory


insufficiency (Lane, Hazleman, and Nichols, 1974).


Although cardiopulmonary complications were not

product. Subjectively, pain, a feature of the late se

associated with the spinal form of poliomyelitis at

quelae of poliomyelitis, can be assessed using an ana

onset, late-onset breathing and swallowing complica

log scale, perceived exertion is assessed using the

tions can appear as a late effect of the disease (Dean,

Borg scale, and fatigue and breathlessness can also be

Ross, Road, Courtenay, and Madill, 1991). In addi

assessed using a modified versions of this scale.

tion, these patients may be deconditioned and have


poor movement economy (i.e., expend excessive en

response is administered before treatment (e.g.,

ergy because of postural deformities) (Dean and

analgesia). Knowledge of the type of medication, its

Ross, 1993). Thus delayed-onset cardiopulmonary

administration route, and time to and duration of

complications, coupled with the effects of overuse

peak efficacy is essential if treatment is to be maxi

and general deconditioning, increases the risk of car

mally efficacious.

diopulmonary compromise, reduces the ability to re


cover from these, and increases surgical and anes

diopUlmonary function and oxygen transport in patients

thetic risk.

with the late sequelae of poliomyelitis include some

PrinCiples of physical therapy management The goals of long-term management for the patient

combination of education, aerobic exercise, strengthen ing exercises, postural correction exercises, chest wall mobility exercises, range of motion exercises, body po

with the late sequelae of poliomyelitis include the

sitioning, breathing control and coughing maneuvers,

following:


•




environments may be indicated to minimize oxygen de

reserve capacity

mand and energy expenditure in these settings. Aids


30


551

and devices are reviewed to optimize energy expendi

ported and unsupported coughing methods are described

ture (e.g., electric wheelchair or scooter vs manual

in detail in Chapters 20 and 21. Whenever possible,

wheelchair) and to reduce cardiopulmonary distress

deep breathing and coughing is coupled with chest wall

(e.g., home mechanical ventilation).

movement to facilitate maximal inflation of the lungs


before coughing and maximal exhalation of the lungs

management of the patient with the late sequelae of

dUling coughing. Body positions are varied and changed

poliomyelitis. Education includes the reinforcement of

frequently to simulate as much as possible shifts in alve

preventative health practices (e.g., infection control,

olar volume and ventilation and perfusion that occur

cold and flu prevention, flu shots, aerobic exercise,

with nonnal movement and body position changes.

strengthening exercises, nutIition, weight control, hy

Progressive loss of pulmonary function in patients

dration, pacing of activities, and energy conservation).

with ventilatory compromise at onset can lead to res

Activity and sleep patterns need to be assessed to en

piratory insufficiency. Comparable with other neuro

sure sleep is maximally restorative and not contribut

muscular conditions, invasive mechanical ventilation

ing to the patient's symptoms. Functional work capac

is avoided. Promising alternatives are nasal and oral

ity and activity tolerance may be increased b y

methods of noninvasive assisted mechanical ventila

balancing activity t o rest, and maintaining fatigue

tion (Bach, Alba, and Shin, 1989). [n addition, airway

below the patient's critical fatigue threshold, i.e.,

clearance can be fUlther assisted with manual assisted

threshold requiring prolonged recovery time.

coughing, glossopharyngeal breathing, mechanical

Aerobic exercise is an essential component of the 10ng-tenTI management of the patient with the late se

exsufflation, and mechanical insufflation-exsufflation (Bach et aI., 1993).

quelae of poliomyelitis to optimize the efficiency of

Poliomyelitis survivors with ventilatory compro

oxygen transport overall. The two principal goals of ex

mise are comparable with other patients with general

ercise are to optimize cardiopulmonary conditioning

ized muscle weakness. Of particular concern in this

and movement economy. Maximizing ventilation with

population, however, is the need to establish the role

exercise is limited if the patient has severe generalized

of mobilization and exercise as a first line of defense

muscular weakness and increased fatigue. Dispropor

in the management and prevention of cardiopul

tionate fatigue and other symptoms experienced by pa

monary dysfunction. However, for those patients

tients with the late sequelae of poliomyelitis have been

whose late effects are due to overuse, additional exer

attributed to overwork of affected and unaffected mus

cise may be detrimental. Modified mobilization and

cles, terminal axon degeneration, and impaired impulse

exercise, however, may be prescribed in an interval

transmission (Dean, 1991). Exercise is therefore pre

schedule (McArdle, Katch, and Katch, 1991) (Chap

scribed judiciously to provide an optimal aerobic train

ter 17). The patient exercises for a period of time and

ing effect without contributing to further otheruse abuse

then rests or reduces to a lower intensity of exercise

(i.e., prescriptive parameters based on subjective re

to aJlow the muscles to rest. In addition to the multi

sponses using semi-quantitative scales in conjunction

tude of benefits of mobilization and exercise on oxy

with objective responses). Walking is the most func

gen transport overall, these interventions also opti

tional type of aerobic exercise, however, aquatic exer

mize respiratory muscle strength and endurance. If

cise provides a useful medium for patients with lower

the patient does not recover within a few hours, the

extremity paresis who require crutches to walk or are

mobilization or exercise stimuli was excessive and

confined to a wheelchair. Reducing physical activity

should be modified. Chest waH mobility exercises to

and exercise is indicated in some patients to optimize

facilitate breathing and coughing may have a role.

aerobic and muscle power. The effect of resting affected and unaffected muscles enhances functional capacity.

Patients with generalized neuromuscular weakness require prophylactic management, given their high

Methods of facilitating effective coughing in patients

risk of developing life-threatening respiratory infec

with neuromuscular diseases are extremely important


because they constitute a life-preserving measme. Sup



PART V

552

Guidelines for the Delivery of Larruopuunonal

controlling the

Physical Therapy: Chronic Cardiopulmonary Conditions

of food eaten and chewing well

and hypercapnia. With severe chest deof

to avoid choking, regular deep breathing, airway in

movement and

and

situation.

(even just shifting and taking some breaths while seated in a wheelchair is benefi


cial). An optimal time to take deep breaths and to

The goals of

cough is during transfers, which usually are and stimulate hyperpnea.

cally

pulmonary

and right heart failure can result in a

management for the

with thoracic rjptt>rrni

include the quality of and hence physiological

MUSCULOSKElETAL CONDITIONS Thoracic Deformities Pathophysiology and medical management

of thoracic ications, nutrition, weight control, infection con

can result from abnonnalities to congenital deformity,

trol, smoking reduction and cessation, and the

. and

acquired disease, and trauma

1988b ).


of the chest wall

alveolar ventilation

reduces the mobility of the bony thorax, thereby in-

VUUlIlILC

Shallow, rapid breath

the work of

ing often results. Minute ventilation is increased at the

•

Optimize ventilation and perfusion and gas

expense of alveolar ventilation. Severe deformity leads to

lung volumes and caDacities and flow

rates

of the mediastinal stmctures. The heart

•

Reduce the work of

and rotated, impeding its mechanical

•


•


can be

function. Examples of chronic deformities that im on pulmonary function are kyphoscoliosis sec ondary to poliomyelitis, tuberculous

and Other exam-

other causes and

•

Faci litate

•


•

Maximize aerobic

and

of

oxygen transport

of deformity include traumatic injury of the verte


bral column, ribs, and sternum. Routine cardiopul monary assessment should include a musculoskeletal examination of the spinal column and thoracic cavity.

•

Normal pulmonary function and gas function. Asymmetry of the chest

wall interferes with normal lung

re

of ventilation and

in the

gional

and the distribution of inspired gas (Bake, and Grimby, 1976; Sinha and

tance of the lung are characteristic of kyphoscolio

distress,

(depth and frequency), ar (delayed

may con

tribute to altered lung water balance and impaired lymphatic

The effects of

of desatura

lion), heart rate, blood pressure, and rate pressure product. Patients with cardiac tively,

exertion is assessed

the

and breathlessness is assessed usin!l: a modified version of this scale.

sis. Altered pressure gradients and uneven lung the

includes dyspnea,

ECG monitoring particularly during exercise. Subjec

compliance and

movement

and thereby

terial saturation,

the elastic resis

increase in work

muscle

Patient

depend on symmetry of cardiopulmonary anatomy and

Optimize


The primary interventions for maximizing car diopulmonary function and oxygen

in pa

tients with thoracic deformity include some combina tion of

dead space and shunt may be

aerobic postural correction


30


553

tion, chest wall mobility exercises, range of motion

Patients with chest wall deformities secondary to

exercises, body positioning, breathing control and

neuromuscular conditions require prophylactic man

coughing maneuvers, airway clearance interventions,

agement given their high risk of developing life


threatening respiratory infections and complications.


Prophylaxis should include flu shots, avoiding pol


luted, smoky environments, smoking reduction and cessation, controlling the types of food eaten and

demand and energy expenditure in these settings. Education is a principal focus of the long-term

chewing well to avoid choking, regular deep breath

management of the patient with thoracic deformity.

ing, airway clearance, and frequent movement and


change in body positions (even just shifting and tak


ing some deeper breaths while seated in a wheelchair

prevention, flu shots, smoking reduction or cessation,

is beneficial). An optimal time to take deep breaths

aerobic exercise, strengthening exercises, nutrition,

and to cough is during transfers, which usually are

weight control, and hydration).

physically exerting and stimulate hyperpnea.

Aerobic exercise is an csscntial component of the long-term management of the patient with thoracic de formity to optimize the efficiency of oxygen transport overall. Maximizing ventilation with exercise in pa

Osteoporosis Pathophysiology and medical management

tients with severe deformity may be limited. OptimiZ

Osteoporosis is a condition associated with reduced

ing alignment to minimize the cardiopulmonary limita

bone mass per unit volume (Smith, Smith, and Gilli

tions of the deformity during physical acti vity,

gan,

exercise, and rest is a priority. Chest wall exercises in

accelerates f a s t e r in w o m e n , p ar t i c u larly after

1991). Age-related bone loss begins earlier and

clude all planes of movement with a rotational compo

menopause, than men. Life-style factors, such as diet,

nent. Body positioning to optimize lung volumes and

exercise, and smoking, have a significant role in re

ailtlow rates is a priority. Breathing control and cough

ducing bone mass. Caffeine has also been implicated

ing maneuvers are essential and should be coupled

as a contributing factor to bone loss secondary to in

with body movement and positioning. If mucociliary

creasing urinary calcium loss.

transport is impaired leading to secretion retention,

Osteoporosis is classified as idiopathic osteoporosis

postural drainage may need to be instituted, coupled

unassociated with other conditions, osteoporosis asso

with deep breathing and coughing maneuvers.

ciated with other conditions (e.g., malabsorption, cal

Ventilatory muscle training may have a role in the

cium deficiency, immobilization, or metabolic bone

management of patients with reduced inspiratory

disease), osteoporosis as a feature of an inherited con

pressures and associated decreases in total lung ca

dition (e.g., osteogenica imperfecta or Marfan's syn

pacity and hypoxemia.

drome), and osteoporosis associated with other condi

Methods of facilitating effective coughing in pa

tions but the pathogenesis is not understood (e.g.,

tients with musculoskeletal deformity are extremely

rheumatoid arthritis, alcoholism, diabetes mellitus, or

important because they constitute life-preserving mea

chronic airflow limitation) (Wilson et aI., 1991).

sures. Supported and unsupported coughing methods

The most common clinical features are vertebral

are described in detail in Chapters 20 and 2l. When

pain and spinal deformity resulting from vertebral

ever possible, deep breathing and coughing is coupled

compression and collapse. Vertebral bodies tend to

with chest wall movement to facilitate maximal infla

collapse anteriorly, contributing to cervical lordosis,

tion of the lungs before and maximal exhalation during

thoracic kyphosis, postural slumping, and loss of

coughing. Body positions are varied and changed fre

height. Acute episodes may be relieved by restricted

quently to simulate as much as possible shifts in alveo

mobility. Straining and sudden changes in position

lar volume and ventilation and perfusion that occur

can exacerbate an acute episode. C ardiopulmonary

with normal movement and body position changes.

complications of osteoporosis are secondary to spinal


554

PART V


deformity, chest wall rigidity, and cardiopulmonary deconditioning resulting from restricted mobility.

Patient monitoring includes heart rate, blood pres sure, and rate pressure product. Patients with cardiac

Osteoporosis is a condition associated with aging

dysfunction require ECG monitoring particularly dur

and older age groups. The pain of acute episodes

ing exercise. Subjectively, pain and discomfort are as

leads to periods of restricted mobility and significant

sessed with an analog scale or modified Borg scale, and

cardiopulmonary dysfunction in older persons (Dean,

perceived exertion is assessed using the Borg scale.

1993). Exercise that is weight bearing and loads the


muscles around bone maintains bone density and de

response is administered before treatment (e.g.,

celerates bone loss thus has a central role in preserv

analgesics). Knowledge of the type of medication,

ing bone health. Generally, the growth and remodel

its administration route, and time to and duration of

lin g of b o n e d e p e n d s h i ghly on t h e e x e r c i s e

peak efficacy is essential if treatment is to be maxi

prescription parameters (e.g., type o f exercise, inten

mally efficacious.

sity, duration, and frequency). Bone mineral content


is more closely related to cardiopulmonary condition

diopulmonary function and oxygen transport in patients

ing than physical activity level. Furthermore, any

with osteoporosis include some combination of educa

detrimental effect of exercise on osteoporosis appears

tion, aerobic weight-bearing exercise, strengthening ex

to relate more to malalignment and injury rather than

ercises, chest wall mobility exercises, range of motion

activity itself.

exercises, activity pacing, and energy conservation. An

Principles of physical therapy management The etiology of osteoporosis is diverse; thus manage ment needs to consider the underlying pathophysiol

ergonomic assessment of the patient's work and home environments may be indicated to minimize oxygen de mand and energy expenditure in these settings. Education is a principal focus of the long-term man

ogy and that several factors may be contributing to

agement of the patient with osteoporosis. Education in

the presentation of osteoporosis in the same patient.

cludes the reinforcement of preventative health prac

The goals of long-term management for the pa tient with osteoporosis include the following: •

•

•

•

/"

•

•

•


aerobic exercise, strengthening exercises, range of mo


tion exercises, nutrition, weight control, hydration, pac

reserve capacity

ing of activities, and energy conservation).



of osteoporosis, self-management, medications,

long-term management of the patient with osteoporo

nutrition, weight control, smoking reduction and

sis to optimize the efficiency of oxygen transport

cessation, infection control, and the role of a re

overall. Upright, weight-bearing aerobic exercise is

habilitation program

essential to maintain bone density or reduce the rate


of bone loss. Maximizing ventilation with exercise is


limited if the patient has severe generalized muscular

rates

weakness and increased fatigue. Chest wall exercises


can be used and should include all planes of move

and gas exchange

ment with a rotational component. Breathing control


and coughing maneuvers are essential and should be


coupled with body movement and positioning. Strain

oxygen transport

ing, Valsalva maneuvers, and jarring activity and ex

Opt imize physical endurance and exercise

ercise are contraindicated. Methods of facilitating effective coughing in pa

capacity •

tices (e.g., infection control, cold and flu prevention, flu shots, smoking reduction and cessation, weight-bearing


tients with osteoporosis are extremely important be


cause they constitute life-preserving measures. Some


30


555

patients fracture ribs and vertebrae during coughing.

of SLE, self-management, nutrition, weight con

Patients at risk should rely on huffing maneuvers that

trol, smoking reduction and cessation, medica

do not require closing the glottis and do not generate

tions, infection control, and the role of a rehabil

high intrathoracic pressures (Hietpas, Roth, and

itation program

Jensen, 1979).

•


•


COLLAGEN VASCULAR/CONNECTIVE TISSUE DISEASES

•


Systemic Lupus Erythematosus Pathophysiology and medical management

•


•

Reduce the work of the hem1

Systemic lupus erythemat osus (SLE) is a disease

•


characterized by the presence of multiple antibodies

•


that contribute to immunologically mediated tissue

•


inflammation and damage (Segal, Calabrese, Ahmad,

•


Tubbs, and White, 1985). The disease affects the major organ systems, including the central nervous,

oxygen transport •

tems. Symptoms include arthralgic and myalgic stiff ness, pain, and fatigue.


musculoskeletal, pulmonary, vascular, and renal sys •


The cardiopulmonary manifestations of SLE in


clude atelectasis, resulting from inflammation of the


alveolar walls, and perivascular and peribronchial


connective tissue, effusions secondary to lung infarc


tion, reduced surface tension, and splinting secondary

product. Patients with cardiac dysfunction should be

to pleuritic pain. Other manifestations include pleuri

cleared by a cardiologist before being prescribed an

tis with or without effusion, pneumonitis, interstitial

exercise program. Subjectively, discomfort, pain, fa

fibrosis, pulmonary hypertension, diaphragmatic dys

tigue, and breathlessness are assessed using analog

function, pulmonary hemorrhage, systemic hyperten

scales or modified versions of the Borg scale, and

sion, myocarditis, constrictive pericarditis, dysrhyth

perceived exertion is assessed using the Borg scale.

mias, tamponade, pericardial pain, arteritis, and

Medication. that is needed to maximize treatment re

defects of the mitral and aortic valves (Dickey and

sponse is administered before treatment (e.g., analgesic

Myers, 1988). Other manifestations that affect car

and antiinflammatory agents). Knowledge of the type

diopulmonary function include anemia, leukopenia,

of medication, its administration route, and time to and

thrombocytopenia, thrombosis, splenomegaly, ascitis,


gastrointestinal bleeding, nephritis, and renal insuffi

be maximally efficacious.

ciency (Wilson et aI., 1991).

The primary interventions for maximizing car diopulmonary function and oxygen transport in pa


tients with SLE include some combination of educa


tion, aerob ic exerc i se, strengthen i ng exerc i scs,

with systemic lupus erythematosus (SLE) include the

postural correction exercises, chest wall mobility ex

following:

ercises, range of motion exercises, body positioning,

•

•


breathing control and coughing maneuvers, airway


clearance interventions, activity pacing, and energy

reserve capacity





556

PART V



deficit. Pulmonary hypertension may be a complicat

diture in these settings.

ing factor. Broncoal veolar lavage is consistent with


an acute inflammatory process. Cardiomyopathy is

management of the patient with SLE. Education in

associated with ischemia, areas of infarction, and my

cludes the reinforcement of preventative health prac

ocardial fibrosis (Gray, 1989). Fibrosis of the con

tices (e.g., infection control, cold and flu prevention,

duction system predisposes the patient to conduction

flu shots, smoking reduction or cessation, aerobic ex

defects and dysrhythmias. Other cardiopulmonary

ercise, strengthening exercises, nutrition, weight con

manifestations include pericarditis with

trol, hydration, pacing of activities, and energy con

fusion and pulmonary and systemic hypertension

or

without ef

servation). An ergonomic assessment of the patient's

from renal involvement. Half of patients with sclero

work and home environments may be indicated to

derma have renal involvement including intimal hy

minimize oxygen demand and energy expenditure in

perphasia, fibrinous necrosis of the afferent arterioles, and thickening of the glomerular basement mem

these settings. Aerobic exercise is an essential component of the

brane. Fibrotic changes and stenoses occur in the

long-term management of the patient with SLE to op

small arteries and arterioles systemically. Similar

timize the efficiency of oxygen transport overall, in

changes in the lymphatic vessels may obliterate

cluding maximizing alveolar ventilation and mobiliz

lymph flow.

ing and removing secretions. Parameters of the

Esophageal involvement contributes to regurgita

exercise prescription are based on subjective re

tion of gastric contents. which is exacerbated when

sponses, (e.g., discomfort, pain, breathlessness, and

the patient is recumbent or bends over. Bloating and

perceived exertion in conjunction with objective re

abdominal discomfort may reflect paralytic ileus and

sponses). Optimal types of aerobic exercise include

intestinal obstruction. Ascites and fluid accumulation

walking and cycling. Aquatic exercise may be prefer

in the gut increases abdominal pressure and en

able for patients with musculoskeletal involvement

croaches on diaphragmatic motion.

that precludes walking and cycling. Chest wall exer cises can be used and should include all planes of


movement with a rotational component. Body posi


tioning to optimize lung volumes and airflow rates is

with scleroderma include the following:

a priority. Breathing control and coughing maneuvers

•

are essential and should be coupled with body move ment and positioning. If mucociliary transport is im paired, leading to secretion r e te ntion, p o s tural

Maximize the patient's quality of life, general health, and well-being and hence physiological reserve capacity

•

Educate about cardiopulmonary manifestations of scleroderma, self-management, nutrition,

drainage may need to be instituted, coupled with deep breathing and coughing maneuvers.

weight control, smoking reduction or cessation, medications, infection control, and the role of a rehabilitation program

Scleroderma Pathophysiology and medical management

•


•


Scleroderma is characterized by the overproduction of collagen and progressive fibrosis of cutaneous and

rates •

subcutaneous tissues (Gray, 1989). The cardiopul monary manifestations of this condition result in in terstitial pulmonary fibrosis with significantly re

and gas exchange •


•


duced vital capacity, diffusing capacity, and arterial

•

oxygen tension (Bates, 1989; Wilson et aI., 1991).

•

Reduced static compliance is the primary mechanical


•


Protect the airways from aspiration Facilitate mucociliary transport Optimize secretion clearance

30

•

and

Maximize aerobic

Chronic Secondary Cardiopulmonary

557

cold and influenza

of

oxygen transport •


•

Optimize

nutrition, muscle strength and thereby oxygen extraction

tion). An ergonomic assessment of the patient's work and home environments may be indicated to

includes dyspnea, distress,

pattern

and frequency), ar

terial saturation, cyanosis (delayed

of desatura

during exercise. If sup-

oxygen is used, the FIo2 administered is recorded. Subjectively, breathlessness is assessed using a modified version of the ceived exertion and


require

Patients with cardiac

scale of per


of the patient with scleroderma to

of oxygen

overall.

Chest wall exercises can be used and should include all planes of movement with a rotational Body

to

flow rates is a

volumes and air Breathing control and

maneuvers are essential and should be coupled with

the Borg scale. Medication that i s needed to maximize treat ment response i s administered before treatment

movement and positioning. If mucociliary trans port is impaired leading to secretion

postural

may need to be instituted coupled with

(e.g., immunosuppressive agents and therapy).

in

minimize oxygen demand and energy these

heart rate, blood pressure, and rate pressure ECG monitoring,

of activities, and energy conserva

hydration,

of the type of medication, its

breathing and coughing maneuvers,

administration route, and time to and duration of efficacy is essential if treatment is to be max efficacious. The primary interventions for

car

Ankylosing Spondylitis Pathophysiology and medical management


Ankylosing spondylitis results in reduced total lung

tients with scleroderma include some combination of

capacity, vital capacity, and inspiratory muscle func and

tion (Lisboa, Moreno, Fava,

I

Muhm, and Ventilatory capacity is preserved maneuvers, clearance

that the respi

ratory muscles are not involved. The disease results

and energy

in spinal and chest wall

, thus there

conservation, An ergonomic assessment of the pa tient's work and home environments may be indi cated to minimize oxygen demand and energy expen

The pa spondylitis has an increased de

diture in these

function and therefore is at risk if administered respiratory depressant medica patients have

antacids between

meals, and do not lie down for a few hours after eat When recumbent, these patients have the head of bed elevated to minimize the risk of

of gas

tions or if he or she strand, I During

patients with ankylosing spondyli

tis show minimal chest wall

tric contents. Education is a principal focus of the

thoracic or upper ab

dominal surgery (Grim by, FugJ-Meyer, and Blom

compared with

persons (Elliott et aI., 1985). Although

management of the patient with scleroderma. Educa

workload

tion includes the reinforcement of preventive health


reduced, capacity, ventilation-perfusion

rather than

558

PART V


or abnormal blood gases is more

to be the limit

(e.g., infection

ing factor.

reduction and

Principles of physical therapy management with •

Aerobic exercise is an e sential component of the long-term management of the patient with

of life, and hence physiological

•

spondylitis to

transport overall. Maximizing ventilation with mobi

Educate about

lization is limited if the

weight control, infection reduction and

smok

and the role of

re

habilitation program

include all planes of movement with component. Body

to

vol control

and coughing maneuvers are essential and should be

Optimize lung volumes and

and flow

rates

Venti

with body movement and

latory muscle training in conjunction with exercise ventilation and perfusion

may have some additional benefit in maximizing aer obic

and gas

•

has extreme

Chest wall exercises can be used and should

umes and airflow rates is a priority.


•

of oxygen

ize the

reserve of ankylosing spondylitIS, selt-management, nu-

•

nutrition, weight con-

and hydration),

spondylitis include the Maximize the patient'

aerobic exer

strengthening

management for the

The goals of

reduction or ces

cold and flu prevention, flu

Facilitate Maximize aerobic capacity and efficiency of oxygen transport

•


•

Optimize

Rheumatoid Arthritis Pathophysiology and medical management Rheumatoid arthritis (RA) is

muscle strength and

disease

that is associated with weI I-documented cardiopul monary and cardiovascular with or without

Patient breathing pattern

including interstitial fibrosis, pul

monary vasculitis, an increased incidence of bronchi endo

arterial saturation,

tis and pneumonia

mation), heart rate, blood pressure, and rate pres

c a r d i t is, dysrhythmias, n e ur i t i s a n d v a s c ul itis

1987; S co t t, Wise,

b l o m a n d Nor de mar, _

interventions for maxlmlzll1g car

diopulmonary function and oxygen transport in pa tients with ankylosing

include some com

b i n at i o n of e d u cation, e x e r c is e. s t r e nl!th e n i n g

I Functional

is limited

pain and stiffness

in the affected muscles and joints, ber of

affected,

the num

and whether the patient

is having an acute episode. Self-limited

ac

tivity and exercise contributes to cardiopulmonary deexercises, range o f motion

Movement such as

control and cougnmg maneuvers,

tioning,

and energy conservation. An ergonomic as sessment of the ments may

work and home environ

indicated to minimize oxygen demand

and energy Education is a

in these

is often in

efficient because of limited by musculoskeletal

thus submaxi

mal tests are more functional in this popUlation, Tests of cardiovascular status must be to enable the

focus of the

without

management of the patient with ankylosing tis. Education includes the reinforcement of preventa

pain.

Graded low -intensity aerobic exercise for pa tients with RA from IS to 35 lllinutes three times a


30

Banwell, and

distress,

aerobic capacity, such an

fatigue. Should a


Subjectively,

and general

tlare-up occur while the pa

ar

(delayed sign of desatura

heart rate, blood pressure, and rate pressure

reduced affected joint count, improved activi reduced joint

pattern (depth and

terial saturation,

exercise prescription results in increased exercise ties of

559

Patient monitoring includes

week can be sufficient to enhance aerobic (Harkcom,

Chronic Secondary CardioPIJllJlonary Dysfunction

the Borg scale. Medication that is needed to maximize treatment

tient is on an exercise program, a few days or

response i s administered before treatment

weeks of restricted mobility and abstinence from

steroids, nonsteroidal antiinflammatory

exercise frequently ameliorate the symptoms. Gen

analgesics).

cou

tl.e mobilization (preferably

is essential if treatment is to be maximally

this pe

pled with range of motion exercises

its

of the type of

administration route, and time to and duration of

riod, will minimize the negative effects of reduced

efficacious. Gentle rhythmic,

activity.

prescribed, particularly for patients at risk of loss of

Prolonged use of steroids contributes to bone Thus physical

and exercise

bone mass

exercise is

to long-term steroid use. car

The primary interventions for

lions are modified accordingly.

diopUlmonary function and oxygen transport in pa tients with RA include some combination of educa

Principles of physicallherapy management

tion, aerobic exercise,

exercises,

postural correction exercises, chest wall mobility exbody

range of motion

breathing control and coughing maneuvers, airway •

•

Maximize the

activity pacing, and energy

clearance

quality of life,


conservation. An

reserve


'J

H.7


cated to minimize oxygen demand and energy expen diture in these

tion, weight

devices is carried out to maximize the


focus of the

management of the patient with RA. Education in

volumes and

and flow

health prac

cludes the reinforcement of

rates

infection control, cold and flu prevention, reduction or

Optimize ventilation and perfusion and gas exchange

aerobic ex-

strengthening nutrition,

Reduce the work of •


•

Protect the

•

Facilitate

•


•

Maximize aerobic

and energy

from aspiration


transport

long-term management of the patient with RA to op timize the

and

of

oxygen transport

both with

of oxygen

overall

to cardiopulmonary conditioning

and improving movement economy. Mild-to-moder

physical endurance and exercise capacity Optimize

func

tion and exercise tolerance. Education is a


•

A review of mobility aids and

of rheumatoid medications, infection control, and the

•

assessment of the pa

muscle


and

ate exercise during subacute periods can be benefi cial.

efficiency of RA

with

persons. The

l..Iall"'"l

however, is less in RA patients because of limping


560

PART V

Guidelines ror the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions


and associated deformity and pain. Non-weight bearing exercise is beneficial in patients with severe


deformity and pain (e.g., aquatic exercise or water

with chronic renal insufficiency include the following:

walking). Given the fluctuations in the patient's con

•


dition from day to day, exercise prescription is modi fied frequently to consider the patient's changing

reserve capacity

condition. Chest wall exercises include all planes of

•


movement with a rotational component. Body posi

of renal insufficiency, self-management, med

tioning to optimize lung volumes and airflow rates is

ications, nutrition, weight control, infection con

a priority. Breathing control and coughing maneu

trol, and the role of a rehabilitation program

vers are essential and should be coupled with body

•

movement and positioning.

•

Optimize alveolar ventilation Optimize lung volumes, capacities, and flow rates

•

Chronic Renal Insufficiency



•

Patients with chronic renal disease have significant

•

systemic complications. Cardiopulmonary manifes

•

tations include left ventricular hypertrophy and

•

congestive heart failure secondary to chronic vol

•

ume and pressure overload (American College of

•

Sports Medicine, 1991). Patients have a high inci

Reduce the work of breathing Reduce the work of the heart Protect the airways from aspiration Facilitate mucociliary transport Optimize secretion clearance Maximize aerobic capacity and efficiency of oxygen transport

dence of atherosclerosis, coronary artery disease,

•


glucose intolerance, and diabetes. Also, generalized muscle weakness and fatigue compromises func

•

tional work capacity.


Chronically increased fluid volume, although reg


ulated with dialysis, contributes to increased stroke


work of the heart and cardiomegaly and hyperten


sion. With respect to pulmonary function, increased


fluid volume increases peribronchial fluid and airway

product. Subjectively, perceived exertion is assessed

closure. After dialysis, the reduction in body weight

using the Borg scale. Medication that is needed to maximize treatment

is related to a reduction in closing volume, increased vital capacity, and forced expiratory flow rates.


The pulmonary-renal syndromes reflect the close


relationship between the lungs and kidneys. These


syndromes are characterized by altered immunologi


cal status, alveolar hemorrhage, interstitial and alveo


lar inflammation, and pulmonary vascular involve


ment (Matthay, Bromberg, and Putman, 1980). The kidneys have a primary role in the production

tients with chronic renal insufficiency include some combination of education, aerobic exercise, strength

and regulation of certain humoral regulators of me

ening exercise, chest wall mobility exercises, range of

tabolism, hemodynamics, fluid balance, and oxygen

motion exercise, body positioning, breathing control

transport (Rankin and Matthay, 1982) Thus pathol

and coughing maneuvers, airway clearance interven

ogy of the kidneys significantly affects those life-sus

tions, activity pacing, and energy conservation. An er

taining processes.



30


561


ditions presented include muscular dystrophy, hemi


plegia, Parkinson's disease, multiple sclerosis, cere

Education is a principal foclls of the long-term

bral palsy, spinal cord injury, and the late sequelae

management of the patient with chronic renal insuffi

of poliomyelitis. The musculoskeletal conditions

ciency. Education includes the reinforcement of pre

presented included kyphoscoliosis and osteoporosis.

ventative health practices (e.g., infection control, cold

The collagen vascular/connective tissue conditions

and flu prevention, flu shots, aerobic exercise,

presented include systemic lupus erythematosus,

strengthening exercises, range of motion exercises,

scleroderma, ankylosing spondylitis, and rheuma

nutrition, weight control, hydration, pacing of activi

toid arthritis. Finally, management of the patient

ties, and energy conservation.

with chronic renal insufficiency is presented. The


principles of management are presented rather than

long-term management of the patient with chronic

treatment prescriptions, which cannot be given with

renal insufficiency to optimize the efficiency of oxy

out consideration of a specific patient. In this con

gen transport overall. Maximizing ventilation with

text the goals of long-term management of each

exercise is limited if the patient has severe general

condition were presented, followed by the essential

ized muscular weakness and increased fatigue. Maxi

monitoring required, and the primary interventions

mal oxygen uptake increases in hemodialysis patients

for maximizing cardiopulmonary function and oxy

along with improvement in other indices of car

gen transport. The selection of interventions for any

diopulmonary conditioning (Painter et aI., 1986). Pa

given patient is based on the physiological hierar

tients may decrease or eliminate the need for antihy

chy. The most physiological interventions are ex

pertension medications. Exercise carried out during

ploited followed by less physiological interventions

hemodialysis treatment sessions is feasible and safe

and those whose efficacy is less well documented.

for appropriate patients. Because hemodialysis treat ments require sessions of several hours multiple times weekly, aerobic training (e.g., cycle ergometry)

REVIEW QUESTIONS

can be effectively incorporated into treatment time

I. Describe the chronic cardiopulmonary patho

(Shallom, Blumenthal, Williams, Murray, and Den

physiology secondary to muscular dystrophy,

nis, 1984; Zabetakis et aI., 1982). The exercise pre

hemiplegia, parkinson's disease, multiple sclero

scription of patients with blood glucose abnormalities

sis, cerebral palsy, spinal cord injury, late seque

and coronary artery disease is modified accordingly.

lae of poliomyelitis, kyphoscoliosis, osteoporo

Chest wall exercises can be used and should in

sis, systemic lupus erythematosus, scleroderma,

clude all planes of movement with a rotational com

ankylosing spondylitis, rheumatoid arthritis, and

ponent. Body positioning to optimize lung volumes

chronic renal insufficiency.

and ailflow rates is a priority. Breathing control and

2. Relate cardiopulmonary physical therapy treat

coughing maneuvers are essential and should be cou

ment interventions to the underlying pathophysi ology of each of the above chronic conditions

pled with body movement and positioning.

and provide the rationale for your choice.

SUMMARY This chapter reviews the pathophysiology, medical management, and physical therapy management of chronic, secondary cardiopulmonary pathology. Specifically, this chapter presents chronic cardiopul monary dysfunction secondary to neuromuscular,

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Guidelines for the Delivery of Cardiopulmonary Physical Therapy; Chronic Cardiopulmonary Conditions

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PART

VI

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care


Comprehensive Patient Management in the Intensive Care Unit Elizabeth Dean

KEY TERMS

Evidence-based practice

Quality care

Function optimization

Scientific evidence

Physiological evidence

Treatment goals

Prevention

Treatment selection and prioritization

INTRODUCTION

(Bar low, Hayes, and Nelson, 1984; Dean, 1985;

Because cardiopulmonary physical therapy in the in

Dean, 1994a; Hislop, 1975; Ross and Dean, 1989;

tensive care unit (lCU) is a specialty in itself, this

Schon, 1983; Worthingham, 1960; Zadai, 1986). A

chapter presents some general aspects of clinical and

superior knowledge of cardiopulmonary physiology,

nonclinical management in this setting. An overview

pathophysiology, pharmacology, and mu ltisystem

of the general goals of treatment and the rationale for

disease and its medical management is essential.

prioritizing treatments according to a physiological

Clinical decision making in the lCU and ration

hierarchy is described. Both clinical and nonclinical

al management of patients is based on a t r i pod

aspects of patient management are presented. Finally,

approach: (1) a knowledge of the underlying patho

issues related to the management of the dying patient

physiology and basis for general care, (2) the physio

are addressed.

logical and scientific evidence for treatment interven

The thrust toward evidence-based p ractice in

tions, and (3) clinical e xp e rie n ce (Figur e 31-1).

health care and the development of conceptual bases

Quality care is a function of these three areas of

for practice have had major implications for car

knowledge and expertise. Evidence-based practice

diopulmonary physical therapy practice in the ICU

and excellent problem solving ability will maximize 567


568

PART VI


therapist must work within narrow windows of opportu

Knowledge of underlying pathophysiology

nity to effect an optimal treatment response. Trc
GOALS AND GENERAL BASIS OF MANAGEMENT Clinical experience

Physiologic and scientific evidence for treatment interventions

The ultimate goals of cardiopulmonary physical ther apy treatment in the lCU include the following: 1. To have the patient alert and oriented to person, time, and place

FIGURE 31-1

2. To have the patient return to premorbid func

Tripod approach to patient management.

tional level to the greatest extent possible 3. To reduce morbidity. mortality, and length of

the benefit-to-risk ratio of cardiopulmonary physical therapy interventions (Riegelman, 1991).

hospital stay. As a precursor to achieving these three overriding goals, the immediate goals initially relate to the attain ment of optimal oxygen transport and hence car

SPECIALIZED EXPERTISE OF THE

diopulmonary function and secondly relate to the at

leu PHYSICAL THERAPIST

tainment of optimal musculoskeletal and neurological

Effective clinical decision making and practice in the

function. In the lCU the physical therapist must recog

ICU demands specialized expertise and skill including

nize the implications of cardiopulmonary insuffi

advanced, current knowledge in cardiopulmonary and

ciency on neuromuscular status and that apparent im

multisystem physiology and pathophysiology, and in

pairment of neuromuscular status in not necessarily

medical, surgical, nursing, and pharmacological man

indicative of neurological dysfunction. Rather, re

agement (see the box on p. 569). Physical therapists in

duced cardiac output and blood pressure, hypoxemia,

the lCU need to be first-rate diagnosticians. Given the

hypercapnia, and increased intracranial pressure (lCP)

multitude of factors that contribute to impaired oxygen

may be indirectly responsible for these changes.

transport (Dean, 1983; Dean, I 994b; Dean, 1994c), the physical therapist must be able to analyze these to de fine the patient's specific oxygen transport deficits and

Restricted Mobility and Recumbency

problems. Therefore the lCU physical therapist must be

Hospitalization particularly in the ICU is associated

capable of integrating large amounts of objective infor

with a considerable reduction in mobility (i.e., loss of

mation quickly, interpreting this information, and inte

exercise stimulus), and recumbency (i.e., loss of grav

grating it to provide the basis for a treatment prescrip

itational stimulus) (see Chapters 17 and 18). These

tion (i.e., the specific selection, prioritization, and

two factors are essential for normal oxygen transport;

implementation of treatment interventions) (Cutler,

thus their removal has dire consequences for the pa

1985). The integration and interpretation of the vast

tient with or without cardiopulmonary dysfunction.

amount of multiorgan system data is perhaps the single

In terms of a physiological hierarchy of treatment

most important skill in ICU practice and treatment pre

interventions (see Chapter 16), exploiting the physio-.

scription. With this database, the physical therapist

logical effects of acute mobilization, upright position

must identify the indications for treatment, contraindi

ing, and their combination, are the most physiologi

cations, and optimal timing of interventions. The condi

cally justifiable primary interventions to maximize

tion of the ICU patient can change rapidly. The physical

oxygen transport and prevent its impairment.


31

Comprehensive Patient Management in the Intensive Care Unit

569

Specialized Expertise and Skill of the lCU Physical Therapist Detailed, c omprehensive knowledge of cardiopulmonary physiology and pathophysiology, and phar macology . Thorough working knowledge of the monitoring systems routinely used in the ICU and an understanding of the inter pretation of the output of these mon itoring systems ( e. g. ,

ECG,

arterial blood gases, fluid and e lectrolyte balance,

hemodynamic monitoring, chest-tube drainage systems, intracranial pressure m onitoring ). This information is an integra l component of the physical therapy assessment of the und erlying problems, and for selecting, prioritizing. and progressing or modifying treatment.

E xte nsive expertise in c ardiopulmonary assessment and treatment presc ription : preferably a minimum of 2 to 3 years experience in ge ne ral medicine and surgery. Detailed understanding of multisystem physiology and pathophysiology and the cardiopulm onary manifestations of systemic disease. An ability to practice effectively under pressure and in often apparently congested, suboptimal working conditions. Knowledgeabh:: regarding all emergency procedures including those for respiratory and cardiac aITest, equipment. or power failure.

K nowledge abl e rega rding the paging system used in the unit for contacting the physical therapist when she or he is out of the unit and out of the hospital . On-call service, 24 hours a day. 7 days a week is a co mmon practice and should be considered in units without this service. Sensiti vity toward each patient's psychosocial situation, culture , and values, and active involvement of the patient and family in clinical decision making whenever feasible. Superior communication skills (e.g., ability to work coop era tively with other members of the

lCU team ( see Figure

31-2) and give ve rba l prescntations and discuss patients at rounds).

Recumbency is nonphysiological; it is a position

Specificity of Cardiopulmonary Physical Therapy

that all too often is to what most patients are injudi

Physical therapy interventions must be specifically

ciously confined. Changing the position of the body

geared toward the management of each organ sys

from erect to supine positions results in significant

tem, taking into consideration the pathophysiologi

physiol ogica l changes, which may jeopardize the pa

cal basic for the patient's signs and symptoms and

tient's already compromised or threatened oxygen

rational for each intervention and the physiological

transport system (sec the box on p. 570, at top left)

and scientific evidence supporting t h e efficacy of

the intervention (Dean and Ross, 1992). Physical

(see Chapter 18). The culmination of these deleterious effects off

therapy provides both therapeutic and prophylactic

sets the increased homogeneity of ventilation and

interventions for the ICU patient. The use of con

perfusion and their matching in the supine position.

servative, noninvasive measures is the initial treat

These effects compound the sU[lerimposed factors of

ment of choice to avert or delay the need for addi

immobility, recumbency-induced central fluid shifts,

ti onal

prolonged lying without the normal stimulation or

supplemental oxygen, pharmacological agents, and

invasive

mo n i t o r i n g

and

t r e a t m e nt,

will to turn the body, and underlying pathophysiol

the need for intubation and mechanical ventilation.

ogy or trauma that may contribute to impaired car

The physical therapist aims toward avoiding, post

diopulmonary function and oxygen transport. Theo

poning, or reducing the need for respiratory support

retically, the more compromised the patient, the

for as long as possible. In addition, the physical

greater the priority is to maximize time spent in the

therapist h e lp s to prevent the multitude of side ef

upright position in conjunction with exploiting the

fects of immobility and prolonged confinement to

benefits of acute mobilization.

bed. A su mm a ry of general information required


570

PART VI


Generallnformatioll Required Before Treating Normal Physiological Changes When Changing

the ICU Patient

from the Upright to the Supine Position

Medical and surgical histories

Cephalad displacement of the visceral contents and

Gender and age

diaphragm

Premorbid status (e.g., life style. ethnicity. culture, work situation. stress, cardiopulmonary condi

Compression on the posterior dependent lung

tioning, and oxygen transport reserve capacity)

fields

Smoking history

Cephalad tluid shift to the central circulation

Hydration and nutritional status: deficiencies. obe

Stroke volume and cardiac output

sity, or asthenia

Total lung capacity

Recency of onset and course of present condition

Vital capacity

Existing or potential medical instability

Functional residual capacity

Indications or necessity for intubation and mechani

Residual volume

cal ventilation

Forced expiratory volumes

Invasive monitoring, lincs. leads. anel catheters

Airway resistance

Existencc of or potential for complications and mul tiorgan system failure

Closing volumes of small airways Restriction of chest wall and diaphragmatic excursions

Coma Elevated intracranial pressure (lCP) and the need for

Arterial oxygen levels

ICP monitoring

Cough effectiveness Preload and afterload and myocardial work

Risk or presence and site(s) of infection Quality of sleep and rest periods

Myocardial efficiency Sympathetic stimulation and decreased peripheral

Nutritional support during ICU stay Pain control regimen

vascular resistance

General Physical Therapy Goals Toward Function Optimization in the ICU Patient Maintain or restore adequate alveolar ventilation and perfusion and their matching in nonaffected and affected lung fields and thereby optimize oxygen transport overall Prolong spontaneous breathing (to the extent that is therapeutically indicated) and thereby avoid, postpone, or mini mize need for mechanical ventilation Minimize the work of breathing Minimize the work of the heart Design a positioning schedule to maintain comfort and postural alignment (distinct from therapeutic body positioning to optimize oxygen transport) Maintain or restore general mobility, strength. endurance, and coordination, within the limitations of the patient's condition and consistent with the patient's anticipated rehabilitation prognosis (distinct from therapeutic mobiliza tion to optimize oxygen transport) Maximally involve the patient in a daily routine including self-care, changing body position, standing, transferring, sitting in a chair, and ambulating in patients for whom these activities are indicated Optimize treatment outcome by interfacing physical therapy with the goals and patient-related activities of other team members, coordinating treatments with medication schedules. and treating the patient specifically. based on results of objective monitoring available in the ICU and subjective findings


31


571

before treating the ICU patient is presented in the

scribed in Chapter 17 and relate primarily to the sta

box on p. 570, at top right.

tus of the cardiopulmonary, neuromuscular, and mus culoskeletal systems. In the ICU the negative physio logical effects of immobility are amplified in severely

Function Optimization

ill and older patients. A primary objective of the

Function optimization refers to promoting optimal

physical therapist, therefore, is to avoid or reduce

physiological functioning at an organ system level, as

these untoward effects on the patient's recovery and

well as promoting optimal functioning of the patient

length of stay in the ICU. Specifically, these goals in

as a whole. In critical care, primary goals related to

clude reducing the deleterious effects of immobility

function optimization are initially focused on car

and pathology on cardiopulmonary and neuromuscu

diorespiratory function. With improvement in oxygen

lar function and reducing the risk of deformity and

transport, increased attention is given to optimal

decubiti. The negative sequelae of relative confine

functioning of the patient with respect to self-care,

ment are largely preventable. Particular care must be

self-positioning, sitting up, and walking. General

taken to avoid pressure sores because these signifi

physical therapy goals related to function optimiza

cantly increase the risk of infection and deterioration.

tion are shown in the box on p. 570, at bottom.

Physical therapists and nurses need to examine rou tinely for sites of redness, pressure, and potential skin lesions in every patient, regardless of expected length

Prophylaxis

of stay in the ICU (Stillwell, 1992). The texture of

General aspects of patient care related to physical

bed coverings, their smoothness, bunching of the bed

therapy practice include the role of prophylaxis or

gown, or irritation from lines and catheters to the pa

prevention. The complications of immobility are de

tient need to be routinely monitored.

Specific Patient Information Required Before Treating the ICU Patient Detailed knowledge of the patient's history, including the differential diagnosis on admission to the rcu, and rele vant past medical. surgical, and social histories Detailed understanding and knowledge of the medications administered to the patient, their indications. and side ef fects, especially those affecting response to physical therapy Knowledgeable about the stability of vital signs since admission, including heart rate and rhythm, respiration rate and rhythm. blood pressure, skin color, core temperature, and hemodynamic stability Detailed knowledge of relevant findings of laboratory tests, procedures, and biopsies, including arterial blood gases, blood analysis, fluid and electrolyte balance, ECG, x-ray, thoracentesis, central venous pressure (CVP), left arttial pressure (LAP), pulmonary artery wedge pressure (PAWP), microbiology and biochemistry reports, and urinalysis If the patient is ventilated, detailed understanding of the rationale for the ventilatory mode and parameters used With respect to establishing a patient database, do the following: (I) Conduct a thorough, detailed clinical assessment specific to the patient's condition(s), including inspection, palpation, percussion, and auscultation of the chest, as well as a neuromusculoskeletal assessment to rule out any secondary effects of cardiopulmonary dysfunction and to establish rehabilitation prognosis. (2) Establish a physical diagnosis and problem list and prioritize the treatment goals and overall treatment plan. (3) Determine the optimal assessment and treatment outcome measures and be knowledgeable about their interpretation. (4) Conduct serial trend measurements to predict the patient's oxygen transport reserve capacity before treatment and stressing the oxygen transport system As treatment progresses, record objective and relevant subjective treatmenl outcome measures and revise treatment goals as indicated by the patient's progress


572

PART VI


Preparation for Treating the ICU Patient

Physical Therapy Uses of Monitoring Systems in the leU

Patients in the rcu are generally characterized by some degree of life-threatening medical instability. Be

Establish the indications for and contraindications of

fore treating a give:1 patient in the rcu, the physical

cardiopulmonary physical therapy

therapist should be thoroughly familiar with the spe

Define treatment intensity, duration, and frequency

cific information shown in the box on p. 571.

for optimal treatment outcome Determine the appropriateness of response to a spe cific intervention

GENERAL CLINICAL ASPECTS OF THE

Assess the need for supplemental oxygen before,

MANAGEMENT OF THE ICU PATIENT

during, and after treatmcnt

Assessment

Determine appropriate patient positioning between.

The fundamental assessment procedures for the car

during. and after treatments

diorespiratory system are described in detail in Part

Establish whether the patient is responding nega

Two. Laboratory reports, procedures, sputum culture,

tively to treatment and whether treatment should

and x-rays supplement the findings of inspection, pal

be discontinued or modified

pation, percussion, and auscultation of the chest. Of particular importance are the blood work, arterial blood gases, ECG, fluid and electrolyte balance, hemody

pulmonary artery pressure and wedge pressure, which

namic Ilionitoring, and intracranial pressure monitoring.

provide an index of myocardial sufficiency and

These are the most commonly monitored parameters in

specifically left heart function. Central venous pres

the ICU in addition to vital signs-respiration rate,

sure gives an indication of fluid loading and the abil

heart rate, temperature, and blood pressure.

ity of the right side of the heart to cope with changes in circulating body fluids. Pressures related to heart function give the physical therapist an indication of

Monitoring

pulmonary status and help to determine whether heart

Optimal physical therapy treatment depends on opti

dysfunction is affecting lung function, lung dysfunc

mal use of the monitoring systems available in the

tion is affecting heart function, or both. Existing car

rcu. Monitoring systems can be used to establish

diopulmonary stress alerts the physical therapist to

the indications and contraindications for treatment,

appropriately modify workloads or the physical de

parameters of the treatment prescription and pro

mands of treatment to keep the patient medically sta

gression. in addition to assessing the patient. These

ble, avoid undue fatigue, and deterioration.

are summarized in the box above. Physical thera

Changes in ECG may reflect heart disease, lung

pists need to exploit the considerable amount of ob

disease, altered acid base, and electrolyte and fluid bal

jective data available to them in patient manage

ance. The physical therapist is responsible for identify

ment. A thorough knowledge and routine use of

ing the patient's heart rhythm and ECG changes that

monitoring systems for each patient in the lCU can

might be expected with improvement or deterioration

not be overemphasized in terms of contributing to

in oxygen transport, and secondary to medical man

improved quality of care with less potential risk to

agement, drug intervention and changes in the course

the patient.

of the disease and response to treatment generally.

The monitoring systems described in Chapter 15 provide essential information with respect to the management of the ICU patient. Information regard

Pharmacological Agents

ing acid-base imbalance and fluid and electrolyte bal

The physical therapist needs a thorough knowledge

ance helps to establish specific treatment goals. The

of the common pharmacological agents used in inten

Swan-Ganz catheter in situ gives the pressures for

sive care (Chapter 43). With this knowledge, the


31


physical therapist can augment the effects of these

573

In addition, narcotics tend to have significant multi

agents and optimize physical therapy treatment re

system effects rather than localized effects. Because

sponse when treatments are coordinated with medica

physical therapy is the most physiological and nonin

tion schedules. Most medications have optimal

vasive intervention available to the ICU patient, it be

dosages for any given patient, optimal sensitivity, and

hooves the physical therapist to ensure that all other

peak-response time. Most medications have side ef

pharmacological agents that are effective and more

fects. Side effects may cause deterioration in the pa

selective than narcotics in achieving the desired ef

tient's condition, create apparent signs and symptoms

fect have been considered.

suggestive of other disorders, or alter response to treatment. The physical therapist therefore needs to identify the medications each patient is taking and

TREATMENT PRESCRIPTION IN THE ICU Physical therapy treatments in the ICU are judiciously

their side effects. Certain medications, such as bronchodilators,

selected in a goal-specific manner. As a general

sedatives, mucolytic agents, antianginal medications,

guideline, treatments descend in a physiological hier

and analgesics, help the patient to be able to cooper

archy. Mobilization, exercise, and body positioning

ate during treatments. Special consideration must al

should be exploited first with respect to their direct

ways be given to the different peak-response times of

and potent effects on oxygen transport overall. At the

medications used in the ICU. The patient is willing to

other end of the hierarchy (i.e., least physiological in

cooperate more actively in the treatment if pain is re

terventions that have a more limited effect on the

duced, breathing is easier, and mucus is easier to

steps in the oxygen transport pathway) are conven

clear. A better treatment effect is therefore more

tional interventions, such as manual techniques.

likely. These advantages result in more effective use

Mobilization and exercise can be prescribed to ef

of the physical therapist's time, and often a shorter,

fect three physiologically distinct outcomes based on

more cost-effective, efficacious treatment.

their acute effects, their long-term effects, and their

Certain other medications may prevent close moni

preventative effects (see Chapter 17). The treatment

toring of patients during exercise and activity. Patients

prescription needs to focus on which specific effects

on beta-blocking agents, for example, will not show

of mobilization and exercise are required to reverse

the normal changes in heart rate and blood pressure in

or mitigate deficits in the oxygen transport pathway

response to exercise. In addition, beta-blockers con

or prevent impaired oxygen transport. The treatment

tribute to fatigue. Caution must therefore be observed

prescription is different in each case.

when prescribing exercise for these patients. Another

Unlike other patient care areas, the frequency of

classification of drugs called vasopressor agents help

treatments may range from one to several treatments

regulate blood pressure and heart rate. Patients on

daily. The frequency depends on the patient's spe

these agents may also exhibit abnormal exercise re

cific treatment goals, the aggressiveness of treatment

sponses. Hence monitoring vital signs to assess treat

indicated, interfering related problems and their man

ment response may be of limited value for patients on

agement, patient cooperation, and tolerance for the

drugs acting on the cardiovascular system.

physical therapy treatments prescribed. The patient's

Narcotics is a commonly used classification of

oxygen reserve capacity needs to be assessed to en

drug used in the ICU and are often administered

sure that the patient can meet the demands of exercise

jointly with sedatives and tranquilizers. Despite their

stress. The physical therapist needs to assess the pa

beneficial effects on pain relief, narcotics of any clas

tient's tolerance with respect to duration, intensity,

sification of pharmacological agents and particularly

and frequency of treatments, as well as prescribed ex

in combination with other sedative type drugs antago

ercise. Objective and subjective measures of the pa

nize and often prohibit physical therapy treatments

tient's tolerance to the initial assessment and the ob

because of the patient's reduced arousal, monotonous

servations of other members of the team help to

ventilation, and inability to cooperate with treatment.

establish this baseline.


574

PART VI

Guidelines for the Delivery of Cardiopulmonary Physical Thel'3py: Intensive Care

Treatment goals and interventions are described in

progress notes during the ICU stay in order that the team

Part III. Interventions frequently used in the ICU in

responsible for the patient after discharge is able to con

clude those related to mobilization and exercise, body

tinue management with reduced risk of disruption of

positioning, breathing control and coughing, mucocil

care or regression of the patient's condition. The patient

iary transport and mucous clearance interventions,

should be consulted, if possible, and informed at all

such as deep breathing and coughing maneuvers,

times of his or her progress and plans made by the team

chest wall mobilization, postural drainage, percussion,

and family. The patient should be given as many

vibration, shaking, rib springing, relaxation, body

choices as possible about his or her care and be actively

alignment, and general strengthening exercises. These

involved in long-term planning.

interventions are the mainstay of cardiopulmonary physical therapy. Intensive care physical therapy de mands particular skill in selecting, prioritizing, and applying the particular interventions that can effect the optimal treatment outcome in the shortest time in a

NONCLINICAL ASPECTS OF THE MANAGEMENT OF THE ICU PATIENT Team Work

given critically ill patient. For example, a common

Comprehensive patient care in the ICU includes some

scenario in the ICU is the physical therapist's attempt

nonclinical activities. Team work is the cssence of

ing to reduce or reverse the adverse changes observed

optimal patient care, particularly in the ICU. The

in blood gases; that is, falling Pao2 levels and increas

physical therapist interacts frequently with other team

ing Paco2 levels in the patient for whom intubation is

members regarding observations and changes in the

being seriously considered if improvement is not ob

patient's condition, treatment goals, and treatment re

served soon. The focus of treatment for such a patient

sponse (Figure 31-2). In addition to providing therapy

is delineated into two parts. The physical therapist

for patients, the physical therapist is often consulted

first focuses on optimizing oxygen transpOit and car

regarding ambulation, body positioning, lifting, trans

diopulmonary function of the involved lung fields and

ferring, chair sitting, and self-care.

second on maintaining optimal cardiopulmonary func tion of the uninvolved lung fields. Contraindications and the awareness of potential ad

Infection Control

verse effects of cardiopulmonary physical therapy are

Personal hygiene and good hygienic practice on the

particular concems in the ICU. The physical therapist

part of the physical therapist cannot be overempha

needs to be well-versed about these. Treatments need to

sized. Patients in the ICU are usually prone to infec

be modified to achieve an optimal treatment effect with

tion. Meticulous hand washing with an antiseptic de

out posing a hazard to the patient. Herein lies one of the

tergent between patients is essential. Soaping for 30

many challenges of intensive care physical therapy.

seconds or more with a thorough scrubbing motion and followed by thorough rinsing should be carried out. After contact with infected wounds, saliva, wounds,

Discharge from the ICU

blood, pus, vomitus, urine, or stool, the physical thera

To be recommended for discharge from the ICU, the

pist must be particularly conscientious about washing

patient should not require cardiopulmonary physical

immediately. Given the concerns regarding HIV infec

therapy more than every 4 to 6 hours. The patient

tion and AIDS, physical protection, including gown

should be breathing spontaneously and independently

ing, gloving, capping, and masking, should be routine.

and elicit a cough with or without assistance, prefer ably one that is effective in clearing secretions. If alert, the patient should be moving purposefully in bed before transfer.

Recognition of the Patient as a Person Although constraints do exist in the high technology

The physical therapist is responsible for documenting

atmosphere of the ICU, the patient's dignity is ob

the physical therapy treatment priorities and frequent

served as much as possible regardless of the reason


31


FIGURE 31-2

Team work in the intensive care unit is essential to facilitate communication and patient

treatment. A, Physical ther
positioning for dependent, heavy patients prior to portable chest x-ray. C, Respiratory care

practitioners. D, Radiologist. E, Nursing staff.


575

576

PART VI


for admission, the level of consciousness, or belliger ent and objectionable behavior directed toward the

THE DYING PATIENT Anticipation of dying and death are traumatic for the

ICU staff. Gestures, such as using the patient's pre

patient, family and friends, and the health-care team.

ferred name, explaining aspects of the patient's care,

The phases of dying (Andreoli, Fowkes, Zipes, and

continually orienting the patient to person, place,

Wallace, 1991; Warner, 1978) that can be anticipated

time, and day, and having an interpreter available if

when caring for the dying patient are presented in the

necessary are widely practiced. A supportive caring

box on p. 577.

atmosphere is created in which the patient is free to

Principles 01 physical therapy management

make choices and ask questions as much as possible.

The dying patient and his or her family and friends have special needs that must be included in and in

leu as a Healing Environment

fact constitute an integral parl of the patient's over

The physical environment of the IC U has a profound

all care. In general the physical comfort and per

effect on the patient's recovery independent of the

sonal hygiene of the patient, as well as the quality of

level of care received. Windows with pleasant views,

the immediate psychosocial environment, are para

for example, help to orient the patient, and provide a

mount concerns. Compassion, understanding, and

sense of day and night and the passage of time (Fig

respect for the patient and the family must be forth

ure 31-3). Other benefits incl\lde reduced number and

coming from the ICU team. The ability to be atten

types of complications and reduced length of stay in

tive, comforting, and compassionate are invaluable

the ICU and in hospital overall. Physical therapists

personal qualities that need to be developed to a

who are involved in the designing of rcus should

high degree in the critical care area. The tcam needs

consider psychosocial, environmental, technological,

to attend to how the patient, if sufficiently alert, is

and clinical factors.

dealing with the possibility of dying and take their

FIGURE 31-3 An overview of an rcu room. Note large window area and openness of room. Windows help patients orient to day and night.


31


to the fatigue induced by treatment and by coughing.

Characteristics of the Dying Patient

Facilitated and supported coughing may help reduce

Loss of strength. motion, and reflexes in the legs and then in the

577

the effort required to cough productively.

anm,

The use of human touch may be the single most

Failure of the peripheral circulation and profuse

important means of communicating with and provid

sweating, causing body cooling

ing support to the dying patient who may be unable

The dying patient tends to turn toward the light

or disinterested in communicating. Supportive touch

Decreased sensitivity to touch and deep pressure

ing and handholding may be even more important to

and pain tends to remain

the patient on life support systems where these may

Often conscious until death

be experienced as a physical barrier between the pa

May experience pain. acute loneliness. and fear

tient and those around him or her.

May increase spiritual neeus, particularly at night

SUMMARY

an interval of 4uiescence just before death

From Andreoli KG, Fo\V cs VK. Zipl!s DP, Wallace AG: COl11pre hel1.live cardiac care, ed 7, St. Louis. 1991. Mosby.

Cardiopulmonary physical therapy in the ICU is a specialty in itself. The overriding goals pertain to returning the patient to a premorbid level of func tion and in the process minimize morbidity, mortal ity, and length of hospital stay. The general goals of critical care are function optimization and prophy

cues from the patient with respect to the role they

laxis. Specific primary goals are defined by the un

need to play. If requested by the patient or family,

derlying cardiopulmonary pathophysiology and

pastoral care services are summoned, preferably be

multisystem dysfunction and its sequelae. Specific

fore death is imminent.

secondary goals are defined by the presence of or

If life support systems are being continued, the

the potential for musculoskeletal and neuromuscll

physical therapist may provide treatment to keep

lar dysfunction. This chapter elaborates on some

the patient as comfortable as possible. Conservative

general a s p e c t s of treating ICU p a tients. The

prophylactic cardiopulmonary physical therapy

knowledge base and experience of physical thera

may be provided to reduce the work of breathing.

pists working in the area are presented. A broad

Treatments are kept to a minimum in terms of num

overview of the objectives of treatment and the ra

ber and duration if death is inevitable. Range of

tionale for prioritizing treatments according to a

motion exercises may help to reduce the discomfort

physiological hierarchy is described. General clini

of immobility and facilitate nursing management

cal and nonclinical aspects of patient management

and the basic care of the patient. Analgesics may be

are discussed. Finally, issues related to the manage

continued along with other medications to reduce

ment of the dying patient are addressed.

pain and sufl'ering and maximize comfort. If so, these are prudently timed with treatments if appro priate. In the presence of life supports the patient's needs may have to be anticipated somewhat more than without life supports because they severely limit communication. The dignity and modesty of

REVIEW QUESTIONS I. Describe the elements of evidence-based practice

in cardiopulmonary physical therapy. 2. Describe the general goals and principles of car

the patient continue to be observed even after death

diopulmonary physical therapy in the intensive

has occurred.

care unit.

The patient who has had life supports removed re

3. Describe the role of monitoring in cardiopul

ceives the same level of palliative care as the patient

monary physical therapy care of the critically-ill

with supports. Weakness and wasting may contribute

patient.


578

PART VI

Guidelines for the Delivery of Cardiopulmonary Physical The.-apy: Intensive Care

References

Dean. E" & Ross, J. (1992). Discordance between cardiopulmonary

Andreoli, K.G .. I·owke,. V.K., Zipes , D.P.. & Wallace. A.G. (1991). COlllprehensi!'e cardiac care, (7th ed.). St Louis: Mosby.

phy iology and physical therapy. Chest. 101. 1694-1698.

Hi slop. J.H. (1975). Tenth Mary Mc M illain lecture. The not-50-im

Barluw, D.H .. H ayes. S.c., & Nelson . R.O. (1 984). the scientist practitioner. research and accountability in clinical (lI1d educa

possible dream. Physical Thi'rapy. 55. 1069-1080. Riegelm an . R.K. (1991). Millillli illg lII e dico l lIliswkes. The art

tion "ettillgs. New York: Pennagon Press .

of lIledical decision II/akillg. Boston: Little_ Brown and

Cutler. P. (1985). Problem soil'ing in clinical medicine. from data to diagnoSis. (2nd

cd.). B altimore : Williams & Wilkins.

Company.

Ross. J

Dean, E. (1983). Research. The right way. Clinical Mal1af'emcnr,

.•

& D ean . E. (1989). Integrating physiological princi ples

into the comprehensive management or cardiopulmonary dys

3. 29-33.

function. Physica l Tlltrop),. 69. 255-259.

Dean. E. (1985). Psychobiolugical adaptation model fur physical

Schon. D.A. (1983). Til" rejleClil'e practitiollel'. HOlV IJruje.uilllwls

therapy practice. Physical Therapy. 65. 1061-1 06R. Dean. E. (1994a). Oxygen tran sport : A physiologically-based con

thillk ill act io ll. New York: Basic Books.

Stillwell. S. ( 1 992 ) . Mosby's critical care lIursill!; referellce, St

ceptual I'ramework for the practice of ca rdiopulmonary physio ther apy. Physiotherapy. 80, 347-355.

Louis: Mosby. Wo rth i ng ham. C. (1960). The de velopment of physical therapy as

Dean. E. (1994b). Physiotherapy skills: Positioning and mobili/.a

a profession through research and publica tion . Physical Ther

tion of the patient. In B.A. Webber & J.A. Pryor. (Eds.). Phys iother(l!I.1' lor Respimtorr and Cardiac Prnhlellls. Edinburgh:

apy.40.

573-577.

Zadai. C.C. (19 86) . Pathokinesiology: The clinical implications from a cardiopulmonary perspective. Physica l Therapy. 66

Churchill Livingstone. Dean. E. (1994c). Invited cOlllmental), to "Are incentive spirometry. intermittent positive pressure breathing. and deep breathing exer cises effectivc in the prevention of pos toperative pull11on ry complications after upper abdominal surgery? A systematic ovcrvi w and meta-analysis." Physica l Therapy. 74. 10-15.


368-371.

CHAPTER

32

Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction Elizabeth Dean

KEY TERMS

Cardiopulmonary failure

Primary cardiopulmonary dysfunction

Coronary artery disease

Restrictive lung disease

Obstructive lung disease

Status asthmaticLls

INTRODUCTION

not treatment prescriptions. Rather, each patient must

This chapter presents the principles of cardiopul

be assessed and treated individually taking into con

monary physical therapy in the management of criti

sideration all factors that contribute to impaired oxy

cally ill patients with primary cardiopulmonary dys

gen transport (i.e., immobility, recumbency, extrinsic

function that can lead to cardiopulmonary failure. The

factors related to the patient's care, intrinsic factors

categories of conditions presented are obstmctive lung

related to the patient, and the underlying pathophysi

disease, status asthmaticus, restrictive lung disease,

ology) (Chapter 1). For examples of treatment pre

and coronary art ry disease (medical and surgical con

scriptions for specific patients refer to the companion

ditions). Each category of condition is presented in

volume to this book entitled Clinical case studies in

two parts. First, the related pathophysiology and perti

cardiopulmon(/ry phY.licaltherapy.

nent aspects of the medical management of each con dition are pres nted. Second, the principles of physi cal therapy management are discussed. These are not mutually exclusive for each category because consid erable overlap may exist when conditions coexist.

CARDIOPULMONARY FAILURE Pathophysiology The heart and lungs work interdependently; thus fail

It should be emphasized that these principles are

ure of one organ has significant imp] ications for the 579


580

PART VI


TABLE 32-1 Classification of'Respiratory Failure by Cause and Mechanisms Origin

Drugs

Metabolic

Neoplasms

Injections

Trauma

Other

BRAIN

Narcotics Barbiturates

Hyponatremia Hypocalcemia

Plimary Metastatic

Meningitis Encephalitis

Direct injury Increased

Central alveolar hypovcntilation

Sedatives

Hypercapnia

Abscess

Poisons

Alkalosis

Bulbar polio

Anesthetics

Hyperglycemia

pressure

Obstructive sleep apnea

Myxedema

NERVES AND MUSCLES

Curariform drugs Arsenic Aminoglycosides

Hypophosphatemia Primary Hypomagnesemia Metastatic

Polio Tetanus

Direct injury

Motor neuron disease Myasthenia gravis Multiple sclerosis Muscular dystrophy GuilJain-Barre syndrome

UPPER AIRWAY

Tonsillar adenoid

Epiglottitis Vocal cord LaryngotraCheitis paralysis

hyperplasia

Tracheoma

Goiter

lacia

Polyps

Cricoarytenoid

Malignant

arthritis

tumors

Laryngeal edema

CHEST BELLOWS

Flail chest Burn with keloids

Sclerodenl1a Pleural inter position (fibrosis, fluid, tumor, air) Spondylitis Scoliosis Kyphosis

CONTRIBUTING FACTORS

Massive obesity A cites lleus Pain Recumbency

LOWER AIRWAY AND PARENCHYMA

Malignant Benign

Viral (bronchiolitis, broncho pneumonia) Bacterial (bronchitis, pneumonia, abscess, bronchiectasis) Fungal Mycoplasma

From Civelliu JM, Taylor RW, Kirby RR: Crilical care, Philadelphia, 1988, JB Lippincolt.


Contused lung

Bronchospasm Hea11 failure congestive restric tive OilSlIlJctive COPD Rcspiratory distress syndrome Interstitial lung disease Atelectasis Cystic fibrosis Pulmonary emboli

32

Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction

function of the other organ (Vincent and Suter, 1987; Weber, Janicki, Shroff, and Likoff, 1983). Insuffi ciency or failure of the cardiopulmonary system refers to the inability of this system to maintain ade quate oxygen and carbon dioxide homeostasis. Pulmonary failure reflects a gas exchange defect or defect of the ventilatory pump. Table 32-1 shows the classification of pulmonary failure by specific causes and the mechanisms involved. Some common predis posing conditions include primary cardiopulmonary conditions, (e.g., chronic lung disease, overwhelming pneumonia, and myocardial infarction) and secondary cardiopulmonary conditions (e.g., motor neuron dis eases, spinal cord injury, stroke, and muscular dystro phy) (Chapter 30). The oxygen and carbon dioxide tensions that have been used to define failure are vari able because they depend on factors such as premor bid status, general health, age, prior blood gas profile,

581

PATIENT WITH OBSTRUCTIVE LUNG DISEASE Pathophysiology and medical management Obstructive lung disease can result in ventilatory fail ure and admission of the patient to the intensive care unit (ICU), or this disease can complicate manage ment if the patient is admitted for other reasons (Boggs and Wooldridge-King, 1993; Un derhill, Woods, Froelicher, and Halpenny, 1989). If conserv ative management fails or is unlikely to improve crit ically impaired oxygen transport and gas exchange and to adequately remove copious and tenacious se cretions, intubation and mechanical ventilation are in dicated (Chapter 41). Complicating factors include impaired oxygen delivery, polycythemia, impaired respiratory mechanics secondary to lung damage and increased time constants impairing optimal inhalation and exhalation, flattened hemidiaphragms, rigid

and the time frame for the development of failure. Ar terial blood gases and pH are essential in the assess ment of cardiopulmonary failure, which is usually di agnosed when the Pa02 falls below 50 to 60 mm Hg and the PaC02 rises above 50 mm Hg (Shoemaker, Thompson, and Holbrook, 1984). Primary cardiac failure reflects failure of the my ocardium to pump blood to the pulmonary and sys temic circulations and maintain adequate tissue per fusion (Austin and Greenfield, 1980). Significant dysfunction of the left ventricle can lead to pul monary vascular congestion and cardiogenic pul monary edema ( i . e . , c o n g e s t i v e h e a r t f a i l u r e ) (Matthay, 1985). Diseases o f the heart that can lead to failure include significant myocardial damage as a result of infarction or myopathy, valvular heart dis ease, and congenital defects. Both primary pulmonary and cardiac failure can be classified into acute and chronic stages. The compen sation mechanisms that occur in the two stages are distinct. With adequate physiological comp:nsation, patients can tolerate some degree of chronic failure. Patients with a mild degree of failure can live I'eason ably independent lives. Moderate failure is signifi cantly more limiting, thus these patients may require home ventilatory support (e.g., supplemental oxygen and nighttime ventilation), and severe failure requires

FIGURE 32-1

hospitalization and mechanical ventilatory support.

Patient receiving mechanical ventilation.


582

PART VI


banel-shaped chest wall, increased accessory muscle

tion from the oropharyngeal cavity can be reduced by

use and work of breathing, reduced diffusing capac

suctioning through the airway with the cuff of the air

ity, impaired mucociJiary transport, secretion accu

way inflated, in addition to suctioning the oropharynx'

mulation, ineffective cough mechanism, increased

after suctioning via the airway. Suctioning can be performed frequently in a pa

oxygen consumption, increased work of the heart, and general debility and weakness.

tient with an artificial airway and is less traumatic.

The goal of intubation and mechanical ventilation

Patients should be suctioned only as indicated be

is to provide an airway and adequate alveolar ventila

cause this procedure can produce significant desatu

tion, which is based on arterial blood gas analysis. A

ration (up to 60%), particularly in the ventilated pa

tidal volume and a respiratory rate that provide satis

tient (Walsh, Vanderwarf, Hoscheit, and Fahey,

factory blood gas and pH values are established and

1989). Administration of 100% oxygen for 3 minutes

maintained unless the clinical condition changes. The

before and after suctioning (i.e., hyperoxygenation)

precise regulation of mechanical ventilation helps to

minimizes this desaturation effect. This can be ac

restore adequate blood gases and cardiopulmonary

complished by manually bagging the patient before

function, reduce the work of breathing, rest fatigued

treatment (i.e., manual hyperventilation) or by preset

ventilatory muscles, and provide an optimal fraction

ting the mechanical ventilator (Fell and Cheney,

of inspired oxygen (FIo2) and humidification (Figure

1971). Risk of aspiration of gastric contents is re

32-1) (Wilson, 1992).

duced by the use of a nasogastric tube.

Minute ventilation can be seriously impaired with a

A common cause of acute rcspiratory failure is ad

leak in the mechanical ventilator circuitry. The tube

vanced chronic airflow limitation (Civetti, Taylor, and

connecting sites are often the sites of air leakage. Com

Kirby, 1988). The pathophysiological deficits include

plete disconnection at the endotracheal or tracheostomy

significant loss of alveolar tissue, increased compli

connection may occur in those patients with high pul

ance of alveolar tissue, hyperintlated chest wall, im

monary resistance. Close monitoring of the exhaled

paired respiratory mechanics, flattened hemidi

tidal volume and end tidal carbon dioxide will ensure

aphragms, impaired breathing efficiency, and reduced

the patient is receiving sufficient ventilation.

diffusing capacity. Proportional changes in lung vol

Positive end expiratory pressure (PEEP) is useful

umes and capacities in patients with chronic airway

in promoting greater opportunity for gas exchange at

limitation compared with healthy persons are pre

end-cxpiration in mechanically ventilated patients.

sented in Figure 8-5, p. I SO. The primary abnormality

However, venous return, myocardial perfusion, and

is a significantly increased residual volume and inspi

cardiac output may be impaired during positive pres

ratory reserve volume and hence total lung capacity.

sure ventilation with PEEP administration (Jardin, et

Failure of oxygen transport ensues secondary to venti

aI., 1981; Kumar, Pontoppian, Falke, Wilson, and

lation and perfusion mismatch, ventilatory muscle fa

Laver, 1973). Excessive stimulation to cough in these

tigue, reactive pulmonary hypertension, and right ven

ventilated patients shOUld be avoided because this ac

tricular failure. Correcting the complications of

centuates the cardiovascular side effects of PEEP.

respiratory failure, however, is often more problem

Continuous positive airway pressure (CPAP) can

atic than treating the specific cause. Hypoxemia and

maintain airway patency during spontaneous ventila

hypercapnia are often present. Hypoxemia is usually

tion. This mode of ventilation, however, seems to be

improved with supplemental oxygen in the absence of

prcferred in children, whereas PEEP is used more

significant diffusion defect or shunt. Cardiovascular complications are among the most

commonly in adults. Interfcrence with the gag reflex in the patient with

prevalent observed in ventilatory failure. Marked hy

an endotracheal tube increases the risk of aspiration

percapnia (increased arterial P(02) with acidemia (re

of the oropharyngeal and gastric contents and can re

duced pH) can produce extreme vasodilatation and

sult in pneumonitis and pneumonia. Risk of aspira

hypotension resulting from the local action on blood


32


vessels (Boggs and Wooldridge-King, 1993). Mild

583

Nutrition

hypercapnia can produce reflex vasoconstriction and

Critically ill patients are hypermetabolical. Metaboli

hypertension. Occasionally systemic hypertension is

cal demand and oxygen consumption are increased

observed during weaning from the ventilator with the

secondary to healing and repair, increased tempera

presence of a moderate degree of hypercapnia.

ture, altered thermoregulation and after surgery. Pa

Right heart failure, cor pulmonale, is a well

tients with chronic cardiopulmonary limitation are

known complication of chronic lung disease and con

often undernourished because of the effort required to

gestive heart failure. Both hypoxia and reduced pH

purchase food, prepare, and consume it. Furthermore,

cause pulmonary vasoconstriction and an increase in

these patients have an increased oxygen consumption

pulmonary artery prcssure. Consequently, reversing

and energy expenditure secondary to the increased

bronchospa sm, hypoxemia, hypercapnia, a n d

work of breathing (Petty, 1985; Rochester and Esau,

acidemia can often reduce pulmonary vasoconstric

1984). Without adequate nutrition, patients incur the

tion, lower pulmonary artery pressure, and thereby

effects of deconditioning faster, are debilitated, are

improve hemodynamics.

less capable of responding optimally to therapy, and

The end stage of respiratory failure results in a pro

are more susceptible to infection. Intravenous hyper

gressive increase in airway resistance, work of breath

alimentation, or external hyperalimentation, is typi

ing, oxygen consumption, and carbon dioxide produc

cally instituted early to maintain optimal nutritional

tion. In areas of bronchial obstruction, marked

status and to avoid excessive physical wasting and

alveolar hypoventilation results and ventilation and

deterioration. If a tracheostomy has been pelformed,

pelfusion are severely mismatched. Hypoxemia and

the patient is able to eat normally.

respiratory acidosis produce reactive pulmonary hy pertension and further ventilatory failure. Profound


carbon dioxide retention, refractory hypoxemia, and

The principles of management of acute respiratory

respiratory acidemia may terminate in a fatal dys

failure are based on interventions that will enhance

rhythmia (Gibson, Pride, Davis, and Loh, 1977;

oxygen transport (i.e., oxygen delivery, oxygen

Macklem and Roussos, 1977; Rochester and Arora,

consumption, and oxygen extraction), and facilitate

1983; Vincent and Suter, 1987; Weinstein and Skill man, 1980; Wcissman, Kemper, Elwyn, Askanazi, Hyman, and Kinney, 1989).

carbon dioxide removal (Gallagher and Civetta,

1980). Thus the steps of the oxygen transport path way that have been identified as impaired or threat

Acidemia from respiratory causes with a pH of

ened by the patient's condition (i.e., immobility, re

less than 7.25 is often harmful with respect to dys

cumbency, and extrinsic and intrinsic factors in

rhythmia production. Conversely, hypoventilation is

addition to the underlying pathophysiology) (Chap

equally harmful, and pH elevations greater than 7.5

ter I) are the focus of treatment. Based on a de

may cause neurological and cardiovascular complica

tailed analysis of these factors, treatments are se

tions. In acute respiratory failure with profound

lected, prioritized, and applied to optimize the steps

acidemia, intravenous use of bicarbonate is used to

in the pathway that are affected. These may include

buffer the hydrogen ion concentration until the under

treatments to maximize the patency of the airways,

lying disorder is corrected. Bicarbonate infusion is

increase alveolar ventilation, facilitate mucuciliary

guided by frequent pH measurements.

transport, facilitate airway clearance, optimize the

Transport of oxygen and carbon dioxide to and

mechanical position of the diaphragm, optimize

. from the tissues depends on adequate pulmonary and

ventilation and perfusion matching, optimize pH,

systemic circulation. Frequently, blood volume has to

eliminate carbon dioxide, optimize peripheral circu

be restored by fluids or blood replacement or both.

lation and tissue perfusion, and reduce the work of

Inotropic agents are used to maintain adequate circu

breathing and of the heart. To optimize oxygen

lation by augmenting myocardial contractility.

transport, the primary goals of physical therapy


584

PART VI

include the following:

treatments with medications so the

l. To improve or maintain arterial oxygen tension (Pao2) or prevent its deterioration its deterioration

or

and pH or prevent its detedoration

levels

around rest Mobilization and exercise are at the top of the hi

3, To improve or maintain arterial carbon dioxide The means by which these

erarchy of physiological treatments; thus the potent and direct effects of these interventions are ex

are fulfilled de-

first (see Chapter I

on each patient's clinical presentation and the

control, and coor

maximal effect is

dinating treatments with peak energy periods and

2, To improve or maintain arterial oxygen satura tion

Intensive Care


factors that contribute t o cardiopul

monary dysfunction.

the upright

into

cardiopulmonary function and

promotes

gas exchange. Chairs should be available at the side of every ICU bed to provide greater opportunity for

Mobilization

the Datien! to be upright. The benefits of the upright

Mobilization and ambulation are

for normal

IUIU glCtll functioning of the human body (i.e., to stress and

stimulate exercise stress and

(Dean and

thereby optimize oxygen

propped up in during

the physical labor of lifting

transfers. These devices are designed to be

1992b). Although oatients in the ICU are to move,

are different to

bed. Stretcher chairs are particularly useful in reduc

tioned under the patient while recumbent in bed and

sit up, stand, sit in chairs, take a

then mechanically configured into a chair. One po

and in some circumstances, ambulate

tential danger, however, is overreliance on these de

across the unit even if they are ventilated (Macken

vices, Even minimal ability of the patient to assist

few

and Ciesla,

mobilization

is prescribed to exploit its long-term cumulative

(I) acute effects, (2) the and (3) the

These effects are

effects

cally distinct and need to be

with his or her bed minutes and

in the ICU, critically ill patients can move limits. is

among those activities that are the most metaboli cally

for ICU patients

Parrent and per, 1

Askanazi, and Kinney,

outcome that can be

the patient'S

with passive interventions. The

expected

fundamental goal is enhanced recovery, reduced

Murphy,

Weissman and Kem

tolerance to be

which also reduces the mobilized. What cost is the greater

Given that cardiopulmonary physical

so, the pa

tient's oxygen transport system deconditions fur-

address each patient's problems. With the monitoring and be moved within safe

assistants. These minimal ef

forts must be exploited. Without

specifically to

must

and

be exploited, even i f the maneuver takes several

reduced morbidity and mortalitv. and re duced ICU and hospital stay. Significant benefit can be gained from the ventilated

provided there are no absolute

to meet a given increase in oxygen demand must be

contraindications to being upright i n terms of car

determined before treatment. Even

diopulmonary

car

therapy stresses the oxygen as a means of

the func

ventilated patient is the and Jones,

tion and efficiency of this system, unnecessary or excessive energy

neuromuscular and muscu

loskeletal status, and skin

Ambulating the whenever 1972). The potential

i s undesirable and

Mobilization and

thus should be minimized. Interventions that can

exercise must be

minimize oxygen demand include relaxation,

the exercise stimulus is therapeutic

cious body

provides an

stressor to the oxygen transport pathway,

to facilitate oxygen trans

is not hazardous),

port, coordination of treatments with other interscheduling treatments at appropriate

specifically to ensure that

Standing and


even a few steps can be ex

32


tremely strenuous for the ICU patient with respect to oxygen demand, considering that this patient is hy permetabolical. Such activities need to be introduced gradually and with continuous monitoring to ensure the patient does not exceed the prescribed therapeutic intensity needcd to maximize oxygen transport. Standing and walking are coordinated with other as pects of the patient's care and should be carried out in several stages. Monitoring of the ECG and arterial saturation of the critically ill patient performing ac tivities such as standing or walking cannot be overemphasized. By disconnecting these monitors, the physical therapist is working blindly and poten tially dangerously because the leads do not reach or

585

Body positioning Body positioning is a potent therapeutic intervention that promotes optimal oxygen transport and gas ex change in two ways; one, from the physiological benefits accrued from the specific positions them selves, and two, from the physiological hcndits ac crued from physically changing from one position to another (see Chapter 18). Body position can be used preferentially to augment alveolar volume, alveolar ventilation, ventilation and perfusion matching, res piratory mechanics, cough effectiveness, eentral and peripheral hemodynamics and fluid shifts, mucocil iary transport, and secretion clearance (see Chapter

18). Both ventilation and perfusion are enhanced in

becausc of movement artifact. In anticipation of an

the inferior lung fields. Thus in postural drainage po

increased workload, ventilatory parameters for the

sitions the superior lung being treated is neither pref

ventilated patients may require adjusting. A greater concentration of oxygen should be delivered for at least 3 to 5 minutes before the activity and continued afterward for 10 minutes or so until the patient has recovered from the increased exertion and the heart

erentially ventilated nor perfused. The less affected lung fields therefore may be contributing more sub stantially to improving arterial gases. Hence the physical therapist must consider the goals of treat ment with respect to pulrnona:-y function in both the

rate and blood pre. sure have returned to within 5% to

involved and less-involved lung fields. During pos

10% of baseline values.

tural drainage, the length of time in a given position

Active movement has greater therapeutic effect on oxygen transport than assisted or passive move ments; thus the benefits of active movements are ex ploited first. Movement recruiting large muscle groups minimizes the disproportionate hemodynamic stress associated with movement of small muscle groups or movements requiring excessive dynamic stabilization (Hanson and Nagel, 1987). If active

needs to be monitored to avoid drainage of secre tions into the less involved, functional, inferior lung fields and to avoid the possibility of compression at electasis in the inferior lung (Dcan, 1985; Leblanc, Ruff, and Milic-Emili, 1970). Although positions can be predicted that will opti mize ventilation and pert'usion matching, each patient will respond differently, depending on such factors as

movements cannot be performed or excessively

pathology, age, weight, depth of breathing, and me

stress the oxygen transport system, then active as

chanical ventilation (Clauss, Scalabrini, Ray, and

sisted movements arc indicated. Passive movements

Reed, 1968; Ray et aI., 1974), Thcrefore the patient's

have a role primarily when the patient is paralyzed

response to specific positioning must be observed,

or' so hemodynamically unstable that the patient de

documented, and objectively monitored with respect

teriorates with active movement. With respect to car

to the effect on oxygen transport variables.

diopulmonary benefits, passive movement stimulates changes in ventilatory and circulatory patterns (West, 1995). These can be particularly beneficial in patients who have significant mobility restriction, however, they should not substitute for active and active-assisted movements, which are associated with even greater benefit because they are higher order activities on the physiologically based treat ment hierarchy (see Chapter 16).

Another important goal of body positioning is to potentiate position-dependent fluid shifts to optimize cardiovascular function. For this reason the patient should be positioned upright as often as possible. In addition, there are other beneficial effects of the up right position on pulmonary function (e.g., maximizc lung volumcs and capacities, minimize alveolar col lapse, decrcase airway resistance, increase lung eom pliancc and, therchy, reduce ventilator system pres


586

PART VI


sure). To maximize the effect of gravity on promot

increased before postural drainage and treatment to

ing fluid shifts, the legs should be positioned depen

help compensate for any physical stress imposed

dently at frequent intervals. In a patient who is not

by treatment. Oxygen, however, should always be

100% and inspired for at least 3 min

self-supporting with or without assistance, fluid

increased to

shifts can be stimulated with a high Fowler's posi

utes before and after suctioning. Should arterial de

tion coupled with the use of the bed knee-break. Be

saturation be apparent during treatment, oxygen

tween sessions of therapeutic body positioning, a

may need to be increased. If the patient is sponta

schedule of four-point turning (supine, left side,

neously breathing without oxygen, supplemental

prone, right side) is ideal and should be attempted

oxygen may also be indicated during treatment to

even in the ventilated patient if not strictly con traindicated (Dean,

1994).

avoid desaturation in some patients. Oxygen ad ministration must be knowledgeably regulated by

Extreme body positions have been reported to

the ICU team based on arterial blood gas results.

have beneficial effects on oxygen transport in pa

Severe hypoxemia is known to result in irreversible

tients with acute respiratory failure. The head-down

tissue damage within minutes, but hyperoxia can

position has been shown to reduce respiratory distress

also produce harmful effects within hours. By max

in some patients with obstructive lung disease

imizing alveolar ventilation, gas exchange, and

1954). The abdominal viscera are

ventilation and perfusion matching, supplemental

(Barach and Beck,

displaced cephalad, thereby elevating the typically

oxygen can be opti mally used and the effects of

flattened hemidiaphragms and placing them in a me

acidemia minimized.

chanically advantageous position. This effect may be

Treatment for respiratory acidosis is aimed at in

mimicked in other body positions by manual abdomi

creasing alveolar ventilation to improve the ex

nal compression and abdominal binders. In some pa

change of carbon dioxide and oxygen. Because the

tients, however, the additional load imposed by the

r e s p i r a t o r y c e n t e r is d e p ressed by i n creased

increased intraabdominal pressure on the underside

amounts of carbon dioxide (carbon dioxide narco

of the diaphragm may inadvertently increase the

sis), the lowered oxygen tension of the blood be

work of breathing and increase respiratory distress.

comes the stimulus for respiration. If the patient in

The prone position has been reported to be beneficial

hales

in patients with acute respiratory fai I ure (Douglas,

stimulation for respiration may be removed. For

Rehder, Beynen, Sessler, and Marsh,

1977; Piehl and 1976). A variant of the prone position, semi

this reason, oxygen is never given to patients with

Brown,

carbon dioxide narcosis.

prone, may be more beneficial in some patients by re

high

c o n c e n t r a t i on s

Low flow oxygen

of

oxygen,

the

(I to 3 Llmin) is given to a pa

ducing intraabdominal pressure. In addition, the

tient with chronic pulmonary disease who maintains a

semi-prone position may be safer and more comfort

chronically elevated arterial Pe02 in the presence of

able for the mechanically ventilated patient. The pre

arterial hypoxemia. If intermittent positive pressure

scription of any body positioning must be based on

breathing is indicated, compressed or room air is used

its anticipated benefits on oxygen transport. The

instead of oxygen in this situation.

more extreme positions should be introduced in pro

Severe hypoxemia usually suppresses cardiac out

gressive stages and the patient's response monitored

put to some degree. Cardiac output may be further

to ensure the response is favorable.

compromised immediately after a patient is placed on a mechanical ventilator because of impaired venous return by the elevated transpulmonary pressure

Supplemental oxygen

(Jardin et aI.,

1981). An attempt is made to carefully

Supplemental oxygen is usually administered con

balance ventilation with an optimal or adequate car

tinuously, whether the patient is ventilated or not,

diac output by shortening inspiratory time and by

to maintain Pa02 level within an optimal range (Dantzker,

1991). Oxygen concentrations can be

minimizing transpulmonary pressures by using lower tidal volumes.


32

Intensh'e Care Unit Management of Primary Cardiopulmonary Dysfunction

Bagging

Dean and Dr�lctl:ce in some ICUs is bagging, A self

manual

is temporarily connected to the

is to pro

I 992a), Thus these less

less physiological conventional proce

are manually inflated for a few breaths, The purpose of

587

and

should be considered after other more supported and

physiological treatments have been

Fur-

breaths during treatment, to

because of their documented adverse ef

maintain some degree of

end-expiratory

fects, it is essential that the patient be continuously

pressure, to assess lung

and to facilitate

monitored for safety reasons and to establish a favor

the effect of instillation of a small volume of saline

able treatment outcome, For the unconscious or para-

vide some

solution into the tracheobronchial tree to loosen se cretions, Bagging must be performed

Ag

can

The use is contro

in conjunction with versial. Some clinicians

needed to examine the role of of this

and the effect

on mucous removal.

to bag the patient after

suctioning to a void the

of the

pressure pushing the mucus distally, Others maintain that because of the adherent quality of the mucus to the walls of the

patient, the ventilator or self-inflating bag can be used to increase inflation volumes, Research is

Instillation Instillation is another procedure that should be used

and the dilatation of the air does

ways in response to positive pressure,

not propel the mucus distally, Rather, it is believed

in

A mucolytic effect of saline

has not been well established, Beneficial however, may be more apparent in neonates,

before suctioning promotes air entry dis

that

tal to the mucous

and movement of

cen

on expiration, Certain body ventilator is

lem when a

prob

The patient in

used,

tion to fluid balance to carefully

of the ventilator is greatly reduced

The

head is

when the

below the hips

because of an increase in total pulmonary resistance caused

the pressure of the abdominal contents,

tural

fluid, Normally the

of the tracheobronchial tree is therefore larly important in the

tidal volume can

an assistant while the pllysical ther

aids the patient with bronchial

With

the physical therapist

needs to ensure the

is adequately ventilated

than tidal breath every minute or

so, As soon

cant additional source of

alveolar gas is saturated with water vapor. The

tioning, The effect of humidification can be assessed

the use of the and takes a

and fluid volume, Inhaled humidified air is a

10 another and during some pos

positions,

be maintained

hydration

from erosion and potential infection, This is partiCLI

to maintain pressure when

from one

atten

failure needs

bag

Therefore the use of a may be

Mucociliary transport and secretion clearance

secretions, Thick

secretions suggest humidification may be and the patient may be systemically If the effects of mobilization on port and secretion accumulation have been and further secretion clearance is

breathing is en

possible,

of the

by the

suc

requmng

may be indicated, Postural

may be

couraged in conjunction with postural drainage, The

contraindicated in patients with unstable vital

small airways dilate

and is usually contraindicated immediately after feed-

on

and cause

mucus to peel away from the walls; thus, during expi mucous

are moved toward the trachea,

to which chest wall percussion, shaking, and vibration facilitate this movement is the literature (KiriJloff,

l!l

and meals, In some tients on continuous 24-hour tube after


are

has been discontinued for 15 minutes.

The cuff in the artificial

and Maz-

however, pa

A sequence

588

PART VI


and vibration may be indicated in conjunction with

clearance. Patients should not breathe below the end

postural drainage. Manual techniques have been asso

of normal tidal ventilation to avoid airway closure.

ciated with desaturation, atelectasis, musculoskeletal trauma, discomfort, cardiac dysrhythmias, and arrest (Kirilloff, et aL, 1985); therefore these techniques

Weaning from the mechanical ventilator

must be applied rationally and with attention to all

The physical therapist and the respiratory therapist

monitoring systems and changes in signs and symp

are primarily responsible for weaning the patient off

toms. The precise sequence, the duration, intensity,

mechanical ventilation. Thus coordinating their goals

and frequency of treatment is based on treatment out

and working together to ensure the weaning process

come rather than ti me. The application of manual

is carried out expediently and with the least risk of

techniques in the head-down position is contraindi

weaning complications (e.g., postextubation atelecta

cated in patients with acute myocardial infarction and

sis, aspiration and hypoxemia) is a priority (Marini,

increased intracranial pressure. Relative contraindica

1984; Shoemaker et aI., 1984). Blood gas analysis

tions include hemorrhage, bronchopulmonary fistula,

and pulmonary function provide the indications for

acute chest trauma, lung abscess, and gastric reflux

weaning. Ideally, the patient's spontaneous tidal vol

(Boggs and Wooldridge-King, 1993).

ume should approximate that delivered by the venti

The specific postural drainage positions to be used

lator. Forced vital capacity should be two to three

are determined based on the pathology, x-ray, and

times the patient's required tidal volume (Figure

clinical examination. The recommended positions for

32-2). Weaning is not usually indicated if the patient

the bronchopulmonary segments involved should be

requires PEEP greater than 5 cm H20 or FIo2 greater

approximated as closely as possible (Chapter 19) and

than 0.4. In addition, patients who are unable to gen

only modified if there are clear indications to do so.

erate a negative inspiratory pressure of -20 mm Hg

Frequently, specific positioning in the ICU is com

or greater are unlikely to be able to generate suffi

promised as a result of the patient's status, intoler

cient intrathoracic pressures for deep breathing and . airway clearance and thus are poor candidates for

ance to lying flat or being tipped, or limitations im posed by the monitoring apparatus or ventilator.

weaning. Minute ventilation and maximum voluntary ventilation can be measured at bedside and contribute to the decision whether to wean. Although weaning

Breathing and cOl)ghing maneuvers

protocols differ depending on the patient and the ven-

If the patient is nonventilated or recently extubated, body positioning and breathing and coughing maneu vers are emphasized to promote mucociliary transport and secretion clearance (Bennett, Foster, and Chap man, 1990), decrease minute ventilation and respira tory. rate, increase tidal volume, and improve arterial blood gases (Barach, 1974; Casciari, Fairshter, Harri son, M o r r is o n, Blackhurn, a n d Wi l s o n, 1981). Breathing exercises are believed to be most effective if pursed-lips breathing is performed in conjunction with mechanical pressure applied over the abdomen (Irwin and Tecklin, 1985; Mueller, Petty, and Filley,

1970). To derive the maximal benefits, breathing and coughing maneuvers should be performed in body positions that are most mechanically and physiologi

FIGURE 32·2

cally optimal. In addition, they are performed in the

Spirometer for bedside measurement of TV, ve, and

postural drainage positions to augment mucociliary

minute volume.


32


589

tilatory mode used, general guidelines for this com

include tachypnea, dyspnea, labored breathing, audi

mon ICU procedure are outlined in the box below.

ble wheezing, tachycardia, cyanosis, anxiety, and panic. If the patient is able to cooperate wilh spiro metric testing, the degree of reduced vital capacity,

PATIENT WITH STATUS ASTHMATICUS

peak flow, and forced expiratory volume provide in


dices of the severity of airway obstruction (Brunner

Status asthmaticus is a potentially life-threatening sit

and Wolff, 1988).

uation (Petty, 1982; Gaskell and Webber, 1988). The

Medical management is aimed at administering

pathophysiological features include marked airway re

drugs and fluids to reduce hypoxemia with oxygen,

sistance secondary to bronchospasm, edema, and mu

decrease airway inflammation and resistance, and

cous secretion and retention. The work of breathing is

hence reduce the work of breathing and anxiety. In

markedly increased, resulting in respiratory distress.

travenous sodium bicarbonate helps to reverse respi

A cycle results in which the patient becomes more hy

ratory acidosis and possibly m e tabolic acidosis

poxemic and hypercapnic secondary to alveolar hy

(Civetta, et aI., 1988).

poventilation, 'bronchospasm increases, and reactive


pulmonary hypertension may ensue along with a fur ther incrcase in the work of breathing and anxiety.

The prime objective of physical therapy is to optimize

The classical signs and symptoms of a severe asth

oxygen transpolt and possibly avoid or delay the need

matic attack that may progress to status asthmaticus

for mechanical ventilation. If ventilation becomes

General Steps in Weaning a Patient From the Mechanical Ventilator 1. An individualized weaning schedule is designed for each patient in which periods of time are spent off the venti lator and on a T tube thaI delivers appropriate oxygen and humidity 2. The initial time period off the venti lator is carefully selected; mornings are often good times 3. (a) Physical activity should be at a minimum d uring this period (e. g. , not during or after physical therapy. not after meals. rests,

4.

or

procedures, and not during family visits) (b) Supplemental oxygen and humidity are given

The physical therapist offers support and reassurance

5. Vital signs. and signs and symptoms of respiratory distress are monitored continuously during weaning 6. The patient is not left unattended in the initial weaning sessions until periods off the ventilator are reliably toler ated well for several successive minutes

7. (a) Deterioration of vital signs, blood gases. and evidence of distress indicate that the patient will have to return \0

ventilatory assistance imminently (b) Rest periods of at least an hour are strategi cally interspersed in the

weaning schedule

8. B lood gases are performed at regular intervals (e.g .. 15, 30. 60, 90, and 120 minutes or more or less frequently as indicated)

9. If blood gases stabilize within acceptable limits during the weaning period and the patient is generally tolerating the procedure well. the time off the ventilator is increased

10. Patients with underlying cardiopulmonary disease who are older, malnourished, obese, or smoke can be expected to take longer to be completely weaned from the ventilator

II. Weaning is generally faster in patients who have required a shorter period of mechanical ventilation 12. To hasten the weaning process, intermillent mandatory ventilation (lMV) has been reported to be useful in some patients. Others, however. have observed that the use of IMV tends to fatigue the patient and delay the patient's progress in wcaning. Thus IMV must be used cautiously. and individual variability must be considered in terms of its effectiveness.


PART VI

590


necessary, prognosis for recovery is poorer (Petty, Physical

I

can augment the medical

management of the

with status asthmaticus. In

expiration and to maintain the patency of the and relaxed

small airways. emphasized

with periodic

an attempt to avert intubation and mechanical ventila

huffing and avoidance of forced

tion the physical therapist coordinates treatment with

vers

medications

the

bronchodilators, mus control, en matching, promotes

mucociiiary

and secretion

reduces

and teaches the patient CO coordinate rewith general

movement. Cau

Despite

Nunn, Cole

J

and Laws,

man, Sachithanandan,

cle relaxants. steroids. and supolemental oxygen).

maneu

Roth, and

1965).

ve noninvasive management,

blood gases may deteriorate and mechanical ventila tion may be inevitable, Relaxation,

alveo

lar ventilation, and reducing airway

and ob

struction continue to be the primary means of achieving these

however.

differ when the patient

ventilated. Optimal prescriptive body

tion needs to be observed to avoid stimuli that poten

is

tiate bronchospasm and deterioration of the

positioning is the intervention of choice. Secretion

condition

clearance is achieved by judicious suctioning. Suc

that increase

tory distress rather than relieve it, chest wall percus forced

maneuvers,

bag

and possibly instillation). Attention to relaxation

tioning is

as required because it can con

tribute to reduced oxygenation,

collapse, and

atelect asis, increased arousal, increased work o f and generallv increased respiratory distress,

and reduction of excessive oxygen demands is a as was described for the patient with chronic air flow limitation. Certain be avoided, for

positions may have to in

because of the

colerance and exacerbation of symptoms in those positions. Because of the relationship of altered pul positioning

' PATIENT WITH RESTRICTIVE LUNG DISEASE Pathophysiology and medical management Acute

failure can be associated with

mary restnctlve

monary fibrosis). This is distinct from restrictive de

cautiously within the patient's tolerance.

fects secondary to neuromuscular and musculoskeletal

Those body positions that reduce respiratory distress and the work of

Guillain-Barn

diseases

and neuromuscular

and maximize alveolar ven

tilation, oxygen saturation and blood gases, are the

neuromuscular disorders that can

respira

tory failure in the absence of underlying primary

of choice.

problems in status asthmaticus are alveolar

airway obstruction secondary t o

(Chapter likely be

33). If on

bronchospasm, mucosal edema, and secretions. Thus maximizing alveolar ventilation and transport are priorities

mu-

1989). Other

dysfunction may,

the chest

or both may be involved.

and an ineffective cough. The physical therapist coor

fore reflect ventilatory

dinates treatment with the

failure, or both. The

and clear

the

sons other than cardiopulmonary disease. The lung The underlying cause of

medications to fa

will

admitted to the ICU for rea

because of an inefficient breathing pattern

mucociliary

the assistance.

management of

include significantly increased work of

cilitate

interstitial

disease

distress) must be

in patients in

failure may there failure, gas restrictions ro

monary function need to be identified and treated in treatment. Obstructive and re

a n c e of s e c r e t i o n s w i t h b r e a t hi n g c o n t r o l and

dividually t o

modified chest wall percussion.

stricti ve patterns of cardiopulmonary frequently

and huff

Obtaining a productive cough is a

thus the contribution of both types of defects to a patient's oxygen

should be determined.

Typically, in restrictive lung disease, all lung volumes


and

591

Intensive Cafe Unit Management of Primary Cardiopulmonary Dysfunction

32

are

tidal volume can

be relatively normal

considerations.

condition and

the

150). Patients

Movements may be totally assisted but more oftcn

with severe interstitial pulmonary fibrosis have in

are likely to be active-assisted and active. No mat

creased pulmonary artery pressures with an associated

ter how weak the patient may be, active-assisted

increase in

p.

ventricular work

and active movements a r e the mainstay of the

and

1989). These patients desaturate very

movement interventions performed by the physical

Restrictive ventilatory

near-upright positions. Assisted or passive move

is commonly as

sociated with both medical and

conditions.

The principles of management of acute respiratory with these differ in that medical

failure

unless

ments should not be indicated

the

is unable to execute these alone). Even modest at

movements

tempts at active-assisted movements, with perhaps only a minimal number of repetitions, benefit the

conditions are associated with underly versible

in

particularly if these can be


whereas in the

pa

considerably more both in terms of treat

tient the pulmonary restriction is reversible. The

ment

natural course of disease in the medical patient will

loskeletal function than assisted movements that do

sta

be determined in part by the patient's

related to cardiopulmonary and muscu endurance, and

not contribute to muscle

tus. The majority of surgical patients, however, will

coordination.

have had normal

sisted movements will contribute to the

function before surgery and

application of totaUy as s

the development of cardiopulmonary complications

deconditioning and physical deterioration. Regard

of whether mechanical

less of the type of mobilization, the patient is ob

Chapter

34).

tissue

carbon

for arterial

served

discomfort,

regulation of blood pH, and an ef

and extent of

output are priofltles.

fective

oxygen is often effective in

if ass isted-acti ve and acti v e move tissue oxy

ments are

in conditions associated with restrictive disease in the absence of a right to left shunt. In the presence of

supplemental oxygen does

performed.

Assisted movements are indicated to promote oxy gen

via their effects on ventilatory and cir Additionally, the

culatory patterns

is to maintain joint range of motion and tive

can also be if the

function, is

ventilated), reduce risks of

cardiopulmonary compl

of

soft tissue in particu

lar. Care must therefore be taken to movements

these

the complete range of movement

reduce muscu

for each joint, with special attention to rotatory com

loskeletal deformities and skin breakdown, and pro

ponents of joint movement. Lax joints can maintain

for

mote comfort. It is essential with body

any purpose that the patient is not confined unneces

range of motion daily. Lax

range with one joints are

and vulnerable to excessive

sarily and does not assume any position for too

strain. Protection may best be effected in these joints

Although lines, leads, monitoring dev

by

these are anchored as se

catheters may be as

with sufficient length to allow the

patient to move spontaneously, be mobilized as much IJV'''HL!lv,

..

.

as many positioning

as

range. In the presence of

the ICU, as much and as often as

that may be particularly beneficial in

One

given

or limb splinting

from two or more excursions through full range the distribution of ventilation and blood flow

body movement, par

ticularly in upright positions, is always a priority in

the ex

because of discomfort the involved joints will benefit

and facilitate routine patient care. Mobilization and

the joint more slowly

tremes of joint range and just short of complete

is

body and range of motion

particu

larly of the upper limbs. If the patient is able to


592

PART VI


however, greater cardiopulmonary stress occurs with

Optimizing oxygen transport using body positioning

upper limb exercise; thus heart rate, ECG, and blood

and then nonphysiological interventions may then

pressure need monitoring. Lower-extremity move

need to be considered. Furthermore, extreme caution

ments, such as hip and knee flexion, may help to posi

needs to be observed in positioning these patients and

tion the diaphragm for improved excursion. Lower-ex

moving their limbs because they are at risk of sublux

tremity movements will also increase venous return,

ations, pressure sores, bruising, and strains.

which may or may not be desirable, depending on the

Interventions to promote mucociliary transport and

patient. The goals of upper- or lower-extremity work

secretion clearance are applicable to all situations in

must therefore be clearly defined. Possible benefits

which secretions, mucosal edema, bronchospasm, or a

and untoward effects must be identified to ensure the

combination of these factors occur. If postural drainage

patient benefits optimally from the prescribed exercise.

is indicated to further facilitate mucociliary transport

The treatment of choice in all patients is to stimu

and secretion clearance, caution needs to be exercised

late those conditions that maintain optimal oxygen

to avoid inducing bronchospasm and hypoxemia; thus

transport in health or approximate those conditions as

the use of percussion should be considered carefully.

closely as possible. That is, the most physiological interventions are exploited first and the least physio logical interventions are exploited last or when more

PATIENT WITH RESTRICTIVE LUNG DISEASE Pathophysiology and medical management

physiological interventions are not possible. Physio logical interventions such as mobilization may be

The initial priority of management in the acute phase

contraindicated in patients whose oxygen delivery is

of myocardial infarction (MI) is the correction of the

too low. Without some reserve capacity in oxygen

immediate problems including dysrhythmias, my

transport, the patient cannot sustain the additional

ocardial insufficiency, reduced cardiac output, hy

metabolical load that mobilization imposes. Patients

poxemia, chest pain, and anxiety followed by imple

who are this critical are often put on neuromuscular

mentation of a progressive rehabilitation program

blocking agents to reduce muscle tone and thereby

ranging from the acute medically stable phase to post

reduce oxygen demand. Because these patients are in

discharge rehabilitation phase (Andreoli, Fowkes,

induced paralytic states, mobilization is not possible.

Zipes, and Wallace, 1991; Froelicher, 1987; Irwin

Means of Reducing Myocardial Work Load in Patients With Cardiopulmollary Disease 1. A quiet environment without excessive noise and stimulation. 2. Low-intensity activity until medical stability has been maintained and patient shows signs of physical improvement. 3. Progressive mobilization begun in conj unction with patient's medical status, ECG stability, and unchanging or re solving enzyme levels.

4. Reduce patient's anxiety about his or her condition, self-care activities, and family and work responsibilities. 5. Gentle mobilization exercises, deep breathing, and coughing are usually begun immediately as a prophylactic measure, although crepitations are frequently audible in the bases of the lungs of coronary patients; treatments need to minimize pulmonary congestion and cardiac stress.

6. Relaxation is often promoted with low-intensity activity. All levels of activity, including breathing exercises, are ped'ormed in a coordinated, rhythmic manner. Breath holding. Valsalva maneuvers, and isometric muscle contrac tions, (i.e., isometric exercise and exercise involving significant muscle or postural stabilization) are absolutely contraindicated during all activities in patients with coronary artery disease and should not be performed in any stage of a rehabilitation program.


32


593

and Tecklin, 1985). Before admission to the coronary

cluding generalized or localized pain anywhere over

care unit, continuous monitoring of the heart rate and

the thorax, upper limbs, and neck, palpitations, dysp

rhythm is established. An intravenous line is rou

nea, lightheadedness, syncope, sensation of indiges

tinely started for the administration of medications

tion, hiccups, and nausea.

and fluids. An arterial line may be started for serial

Depending on the degree of myocardial infarction

blood sampling for blood gases and enzyme mea

and damage, varying lengths of modified mobility

sures. Initially, pain medications, coronary vasodila

may be recommended (Andreoli, Fowkes, Zipes, and

tors, and diuretics are frequently used to minimize the

Wallace, 1991). During this period, the physical ther

work of the heart, anginal pain, and discomfort.

apist concentrates on rhythmic breathing exercises,

Drugs such as morphine serve to depress the respira

gentle coughing exercises or huffing, modified posi

tory drive; thus the physical therapist must be aware

tioning with the bedhead elevated at least 15 degrees

of corresponding changes in vital signs. Less potent

to facilitate the gravity-dependent mechanical action

sedatives and tranquilizers are more routinely pre

of the heart and thereby reduce myocardial oxygen

scribed. Increascd pain and anxiety potentially

demand. The patient is encouraged to perform deep

worsen the patient's cardiac status by increasing my

breathing and coughing every hour during the day.

ocardial oxygen demand and altering normal breath

Bed exercises including rhythmic, unresisted, hip and

ing pattern and gas exchange.

knee and foot and ankle exercises are usually per

The primary purpose of oxygen administration to

formed every 4 hours or so, or when the patient turns

the cardiac patient is to reduce hypoxemia, myocar

in bed. The patient is cautioned to exercise one leg at

dial work, and angina. Dyspnea, however, is com

a time, sliding one heel up and down the bed, guard

monly observed in the initial phases of myocardial

ing against lifting the leg off the bed. These exer

infarction and can be effectively controlled by sup

cises; when performed correctly and coordinated with

plemental oxygen administered by nasal cannulae or

inspiration and expiration require relatively little ef

mask. Oxygen may also correct potential ventilation

fort or additional physical stress to the MI patient.

perfusion mismatching and hypoxemia. Oxygen is

Comparable with the management of the postopera

always administered with humidity to avoid drying

tive patient, these exercises are performed prophylac

the airways.

tically to reduce the risk of venous stasis and forma

Blood gas analysis is performed within an hour of

tion of thromboemboli. In addition, they may help to

initiating oxygen therapy to establish a baseline of ar

regulate more coordinated breathing, encouragc deep

terial saturation. In this way, oxygen dose can be al

breaths and mucociliary transport, and rcduce atelec

tered to regulate blood gases and acid base balance.

tasis. The patient is cautioned against performing the VaJsalva maneuver and straining because these activ ities increase intrathoracic pressure and reduce car

MEDICAL CARDIAC PATIENT

diac output.


Electrocardiographic (ECG) monitoring of the car

A primary principle of the management of the patient

diac patient is the responsibility of all members of the

after myocardial infarction is to reduce myocardial

health-care team involved in the patient's care. The

oxygen demand and workload. The myocardium

physical therapist has a special responsibility to be

needs rest to promote optimal healing. Judicious rest

proficient in ECG interpretation in the coronary care

of the myocardium is a priority that can often be bal

unit because physical therapy is one of the most

anced with gentle rhythmic, non static movements.

metabolically demanding interventions for patients

The box on p. 592 illustrates several ways of reduc

(Dean et aI., 1995; Weissman et aI., 1984). The phys

ing myocardial workload in patients with cardiopul

ical therapist often has the responsibility of initiating new activities with the cardiac patient, which might

monary disease. The physical therapist should be watchful at all

include sitting over the edge of the bed, engaging in

times for signs of impending or silent infarction, in

self-care (particularly involving the arms being main


594

PART VI


tained in a raised position), getting in and out of bed,

duration, and frequency of these activities (Bjore,

sitting in a chair, going to the bathroom, walking

1972; Froelicher, 1987). The patient's tolerance and

around the room or in the hallways, and eventually

changes in ECG and vital signs are used as indicators

exercising on the treadmill or ergometer. Changes in

for establishing and modifying the treatment program.

the ECG must be watched for, particularly when in

These physiological parameters must be observed

troducing new activities and increasing the intensity

carefully as the patient progresses to optimize the po

of workload in activities. Careful attention to ECG

tential benefits of the therapeutic regimens as early as

changes and serum enzyme levels will contribute to

possible without endangering the patient.

enhanced physical therapy care of the acute MI pa

Patient education and prevention of infarction are

tient by optimizing the treatments prescribed and the

particularly important for the cardiac patient. As

margin of safety with which activities are performed. Congestive heart failure may be unavoidable in

soon as the patient is alert and able to cooperate, in formation about his or her condition with guidelines

cases of severe infarction or even milder infarction

about activity, diet, and stress management is rein

coupled with lung disease. Fluid intake and output

forced. The more involved and informed the patient

and daily weight measurements promote early detec tion of congestive heart fai lure. Routine fluid intake by an intravenous line should not exceed 20 to 30 ml per hour. Signs of imminent and established conges tive heart failure appear in the box below. The work of the heart can be significantly reduced in the up right position (Levine and Lown, 1952). All cardiac patients are prone to anxiety about their conditions and prognoses. The patient is given realis tic guidelines at each stage of recovery with respect to the level of activity that can be safely performed, which can potentially avert deterioration and promote recovery. Involving the patient in rehabilitation plan ning from the onset facilitates the patient's planning realistically for the future and may help to reduce the depression often experienced by the acute MI patient. The initial rehabilitation program is planned with the long-range rehabilitation goals in mind. The pro gram designed for the cardiac patient is progressive in terms of types of activities, usually beginning with ac tivities of daily living and with respect to the intensity,

Signs of Imminent Congestive Heart Failure Development of tachydysrhythmias Development of a ventricular gallop Pulmonary crackles and other persistent advenlitiae Development of dyspnea Development of increased jugular venous pressure and distention

FIGURE 32-3

Patient following open heart surgery (4 hours

postoperative).

NOTE:

patient on mechanical ventilator,

mediastinal drains, receiving blood, IV's, on EKG, CVP,

Swan Ganz, Arterial Blood Gas lines.


32

595


Guidelines to Stages of Physical Therapy in the Open Heart Surgical Patient Stage I Patient may be seen in the postanesthesia and recovery room for a physical therapy assessment; the patient is usually extubated within 24 hours after surgery. Although the patient must be permilled to rest as much as possible in the initial 24-hour period, judicious body positioning is instituted to stimulate physiologic "stir-up." Usually once ex tubated, the patient is positioned side to side for deep breathing and coughing at least four times in the first 24 hours and low-intensity mobilization is initiated. Medications are administered before lreatment to ensure optimal effect during treatment. Depending on the findings of x-ray, physical examination, and arterial blood gases, the pa tient may require vibrations and possibly percussion. Postural drainage positions are modi lied to avoid tipping the patient head-down and causing increased myocardial strain. A sputum sample for culture and sensitivity testing may be taken at this time. The patient can usually tolerate being dangled over the edge of the bed for a few min utes. Special care is taken for all hem1 patients to avoid the Valsalva maneuver, forced coughing, and huffing and ,

to maintain a semirccumbent or upright position for treatment. Blood pressure is checked before, during, and after treatment. Mobilization is progressed.

Stage 2 Deep breathing and coughing maneuvers coupled with mobilization are continued. Positioning for enhanced alveolar ventilation and ventilation and pelfusion matching may be indicated. If secretion accumulation is a problem and the patient too unstable to be optimally mobilized or positioned, postural drainage and possibly percussion and/or vibration may be indicated. Upper limb and neck exercises are introduced. Neck exercises are withheld if central venous pressure lines are still in place in the neck veins. The patient can sit in a chair at bedside as tolerated. The patient is encouraged to stand erect for a minute or so on transferring back and forth to the chair.

Stage 3 The patient can take ShOl1 walks as tolerated. Ambulation is not begun until arterial lines and the Swan-Ganz catheter have been capped or removed. Vital signs are monitored before and after standing and walking. Deep breathing and coughing maneuvers are continued even if the chest is clear, until the patient is up and about within reasonable limits as tolerated. The patient is encouraged in grooming and self-care.

Stage 4 Deep breathing and coughing should be done by the patient without supervision. The presence of atelectasis on x-ray or from assessment findings. however, would indicate the need for continuation of mobilization and body position ing with breathing exercises. Ambulation is increased as tolerated.

Stage 5 Palient can participate in individual or class activities, concentrating on trunk mobility, upper-extremity range of mo tion, coordinated breathing activities, posture. biomechanics, and increasing the patient's endurance gradually.

Stage 6 The palient can attempt six to eight stairs if progress has been satisfactory and as indicated. Aortic repairs in the first week or so are prone to rupture. Elevation of the blood pressure is therefore avoided to reduce the risk of break down of the aortic suture line.

Stage 7 The patient depends primarily on ambulation for maintaining optimal alveolar ventilation and mucociliary transport rather than brealhing and coughing exercises. The patient is cautioned to balance a period of exertion with a period of rest. The pat ient may be discharged. The physical therapi st ensures the patient fully understands the specific de tails of the home exe rci se progrdm. The emphasis of exercise for cardiac patients conlinues to be -

011

rhythmic, co

ordinated dynamic movements on discharge, avoiding isomelric, static exercise. If possible, the patient is invited to participate in a reconditioning and health promotion program as an oUlpatient in a physical therapy department.

NOTE: The physical therapist must guard againsl excessively intense treatmenl of open heart surgical palienLs or other patients who are on a prophylactic course of anticoagulants.


596

PART VI


is in self-management, the greater the likelihood of

cate different practices, depending on their facilities,

receptivity and adherence to a rehabilitation regimen

experience of the surgical and ICU team, and the in

after discharge.

cidence of postoperative complications and survival for that institution. The physical therapist must guard against exces

PATIENT AFTER OPEN HEART SURGERY Principles of physical therapy management

sively intense treatment of open heart surgical pa tients or other patients for whom periods of relatively

Patients scheduled for open heart surgery are treated

restricted mobility (4 to 5 days) are anticipated. Tn ad

as high-risk surgical candidates because of the nature

dition to the fact these patients may be hemodynami

and invasiveness of this type of surgery (Figure

cally unstable initially, these patients may be suscep

32-3), regardless of their general level of health be

t i b l e to s o f t t i s s u e bruising f r o m being on a

fore surgery (Trekova, Dementyeva, Dzemeshke

prophylactic course of anticoagulants.

vich, and Asmangulyan, 1994). Whenever possible,

Physical therapy follow-up should continue sev

patients prepare for surgery in advance by decreasing

eral months beyond discharge at which point the pa

or stopping smoking, by avoiding exposure to respi

tient should be well integrated into a cardiac rehabili

ratory tract infections, by avoiding stress, by eating a

tation program. Continuity and continuation of

balanced diet, and by getting adequate sleep. In addi

physical therapy throughout the entire rehabilitation

tion, patients can benefit from a modified, prescrip

period, from acute- to long-term, cannot be overem

tive exercise program before surgery to maximize

phasized given that achieving a maximal recovery

their aerobic capacity and thereby improve their peri

from surgery is the priority.

operative course. In the preoperative period the physical therapist may spend additional time with patients scheduled

SUMMARY

for open heart surgery to provide teaching of the

This chapter describes the principles of cardiopul

basic anatomy and physiology related to surgery to be

monary physical therapy in the management of criti

performed, the effect of anesthesia, the role of intuba

cally ill patients with primary cardiopulmonary dys

tion and mechanical ventilation, the incision lines to

function. Cardiopulmonary failure secondary to

be expected over the chest and the legs if veins are to

chronic lung disease and heart disease are described.

be removed for bypass surgery, the lines, leads, chest

Cardiopulmonary physical therapy management is

tubes, and catheters that will be in place after surgery,

based on the specific underlying pathophysiological

and the course of recovery the patient might expect

mechanisms of these various disorders. Tbese princi

barring complications (Chapter 26). The emphasis on

ples, however, cannot be interpreted to be guidelines

patient education in most open heart surgery units

for specific treatment in that each patient is an indi

may contribute to the generally low incidence of

vidual whose condition reflects mUltiple factors con

complications and mortality.

tributing to impaired cardiopulmonary function or

Some guidelines for physical therapy management

threatening it (i.e., the effects of restricted mobility,

of the open heart surgical patient appear in the box on

recumbency, extrinsic factors related to the patient's

p. 595. These guidelines are to be applied thought

care, and intrinsic factors related to the patient in ad

fully and cautiously with regard to each specific pa

dition to the underlying pathophysiology).

tient's condition and observed recovery. These guide lines suggest the upper limit of intensity of physical therapy if all is progressing well initially and sh0uld

REVIEW QUESTIONS

be reduced if warranted by the patient's condition.

1. With respect to critically ill patients with the fol

Progression from one stage to the next is based on an

lowing conditions, describe the pathophysiology

optimal and reliable treatment response at each level

of primary cardiopulmonary dysfunction, car

before proceeding. Different institutions may advo

diopulmonary failure, obstructive lung disease,


32


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Mueller, R.E., Petty, T.L.,

& Asman

gulyan, Y.T. (1994). Blood oxygen transport function in car diopulmonary bypass surgery for acquired valvular diseases.

& Roussos, e.S. (1977). Respiratory muscle fa

tigue: A cause of respiratory failure? Clinical Science

Care,

Trekova, N.A., Dementyeva, 11, Dzemeshkevich, S.L.,

& Clauss, R.H. (1974). Immobility, hypox

emia, and pulmonary arteriovenous shunting. Archives of

acute increase in oxygen consumption. fournal oj Critical Care,

8, 100-108.

Weissman, C.. Kemper, M., Damask, M.e., Askanazi, 1., Hyman, A.I.,

& Kinney, J.M. (1984). Etlcct of routine intensive care in

teractions on metabolic rate. Chest, 86, 815-818.

Surgery, f09, 537-541.

Weissman, e., Kemper, M., Elwyn, D.H., Askanazi, 1., Hyman,

& Arora, N.S. (1983). Respiratory muscle failure. Medical Clinics oj Norlh America, 67, 573-597. & Esau, S.A. (1984). Malnutrition and the respira 85, 411-415.

& Kinney, 1.M. (1989). The energy expenditure of the 2, 254-259. West, J.B. (1995). Respiralory physiology-Ihe essen/ials (51h ed.). Baltimore: Williams & Wilkins.

& Holbrook, P.R. (Eds.)

Wilson, R.F. (1992). Critical care manual (2nd ed.). Philadelphia:

Rochester, D.F., Rochester, D.F.,

tory system. Chest,

Shoemaker, W.e., Thompson, W.L.,

(1984). Texlbook oj crilical care. Philadelphia: W.B. Saunders.

A.I.,

mechanically ventilated critically ill patient. Chesl,

F.A. Davis.


Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction Elizabeth Dean

KEY TERMS

Burns

Musculoskeletal trauma

Head injury

Neuromuscular dysfunction

Morbid obesity

Spinal cord injury

INTRODUCTION

management are not mutually exclusive for each cat

This chapter describes the principles and practice of

egory. Rather, considerable overlap may exist when

cardiopulmonary physical therapy in the manage

conditions coexist. The principles presented are not

ment of secondary cardiopulmonary dysfunction that

treatment prescriptions. Each patient must be as

can lead to cardiopulmonary failure. Some common

sessed and treated individually taking into considera

categories of conditions described include neuro

tion the contribution of immobility, recumbency, ex

muscular disease, morbid obesity, musculoskeletal

trinsic factors related to the patient's care, and

trauma, head injury, spinal cord injury, and burns.

intrinsic factors related to the individual patient (see

Each category of condition is presented in two parts.

Chapter 16), in addition to the underlying pathophys

First, the related pathophysiology and pertinent as

iology. For examples of specific treatment prescrip

pects of the medical management of the condition

tions refer to the companion volume to this book en

are presented. Second, the principles of physical

titled Clinical case studies in cardiopulmonary

therapy management are discussed. Guidelines to

physical therapy. 599


600

PART VI


PATIENT WITH NEUROMUSCULAR DISEASE Pathophysiology and medical management

mobility and recumbency, in addition to the patho physiological consequences of respiratory failure.

GuiUain-Barre syndrome, myasthenia gravis, muscu

Provided the patient has some residual muscle

lar d y s t r o p h y , mUl tiple scl e r o s i s, s t r o k e , p o

power, the balance between oxygen demand and

liomyelitis, and neuromuscular poisonings are com

supply will determine the degree to which mobiliza

mon neuromuscular disorders that can precipitate

tion can be exploited to maximize oxygen transport.

respiratory failure in the absence of underlying pri

The treatment goals for these patients are to maxi

mary lung disease (Cooper, Trend, and Wiles, 1985;

mize oxygen delivery, enhance the efficiency of

Cu rran and Col b e rt , 1 9 8 9; Dean, Ross, Ro ad,

oxygen uptake and utilization, and thereby reduce

Courtenay, and Madill, 1991; Fug l-Me yer and

the work of breathing. In these patients, minimizing

Grimby, 1984; Griggs and Donohoe, 1982; Lane,

oxygen demand overall (i.e., during mobilization as

Hazleman, and Nichols, 1974). If paralyzed, the pa

well as at rest) is a priority. Mobilization needs to

tient will likely be dependent on ventilatory assis

be prescribed in body positions that enhance oxygen

tance. Cardiopulmonary physical therapy has a cen

transport and its efficiency so that the benefits of

tral role in minimizing the need for mechanical

mobilization can be exploited more fully without

ventilation in these patients because their prognosis

worsening arterial oxygenation (Dean, 1985). The

for weaning is poor. Progressive respiratory insuffi

patient requires continuous monitoring of oxygen

ciency is best addressed early with the institution of

transport and hemodynamic monitoring to ensure

nighttime ventilation at home (Curran, 1981) before

the exercise stimulus is optimally therapeutic and

the development of failure and necessity for hospi

not excessive.

talization. Patients with progressive neuromuscular

Although the mechanisms are different, patients

diseases (e.g., muscular dystrophy) are living longer;

with neuromuscular dysfunction can benefit from

thus cardiopulmonary insufficiency wil I be com

body positioning to reduce respiratory distress much

pounded by age-related changes of the cardiopul

like a patient with chronic airflow limitation (Barach,

monary system (Dean, 1994a; Leblanc, Ruff, and

1974). Upright and lean-forward positions will re

Milic-Emili, 1970).

duce distress to the greatest extent.

Neuromuscular conditions contribute to cardiopul

The patient's body position and length of time in

monary dysfunction in numerous ways (Chapters 21

any one position must be carefully monitored and

and 22). With progressive deterioration of inspiratory

recorded to minimize the risks of positions that are

and expiratory muscle strength and endurance, respi

deleterious to oxygenation and to ensure that a bene

ratory insufficiency and failure can ensue (Black and

ficial position is not assumed for too long because of

Hyatt, 1971). Depending on the specific pathology,

the diminishing benefits over time. This is particu

such deficits include reduced lung volumes and flow

larly important for the patient who is incapable of po

rates, reduced alveolar ventilation, increased airway

sitioning him or herself, who is incapable of commu

resistance, ventilation and perfusion mismatch, im

nicating a need to turn, and in whom muscle wasting,

paired mucociliary transport, mucous accumulation,

bony prominences, and thinning of the skin may pre

reduced cough and gag reflexes, relatively unpro

dispose the patient to skin breakdown.

tected airway secondary to impaired glottic closure

Patients who are hypotonic and generally weak

and weakness of the pharyngeal and laryngeal struc

and debilitated fail to adapt normally to position-de

tures, and increased work of breathing.

pendent fluid shifts and thus are Illore prone to ortho static intolerance (Marini and Wheeler, 1989). Gravi

Principles of physical therapy management A patient with restrictive pulmonary disease sec

tational stimulation is essential to maintain the volume regulating mechanisms. Tilt tables should be used judiciously given the potential risks in these pa

ondary to neuromuscular conditions is at consider

tients, which is compounded by the loss of the lower

able risk of succumbing to the negative cardiopul

extremity muscle pump mechanislll. Because of po

monary and cardiovascular sequelae of reduced

tential adverse reactions to fluid shifts and the


33

Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction

601

potential for desaturation. falling Pao2 levels and dys

sential that these attempts are maximized (i.e., the

rhythmias. the patient's hemodynamic status must be

patient optimally rested and medicated le.g., bron

monitored closely during gravitational challenges.

chodilators, analgesia, reduced sedation and nar

The importance of chest waH mobility to optimize

cotics] is physically positioned to optimize length

three-dimensional chest wall excursion in chronic

tension relationship of the diaphragm and abdominal

neurological patients is emphasized in Chapters 2 I

muscles, positioned vertically to optimize inspiratory

and 22. This goal is particularly challenging in the

lung volumes. and expiratory flows and avoid of as

neurological patient with acute respiratory insuffi

piration, and is provided thoracic and abdominal

ciency. The goal is to promote alveolar ventilation,

support during expiration to maximize intrathoracic

reduce areas of atelectasis. and optimize ventilation

and intraabdominal pressures) (see Chapter 21).

and perfusion matching and breathing efficiency to

These supportive measures will ensure that the bene

augment and minimize reliance on respiratory sup

fits of the normal physiological cough mechanism,

port (i.e., supplemental oxygen and mechanical venti

which is the single best secretion clearance tech

lation) while minimizing respiratory distress. This is

nique, is maximized (i.e., the most productive cough

especially important because patients with neuromus

with the least energy expenditure) (Bennett, Foster,

cular conditions are poor candidates for being

and Chapman, 1990; Hasani et aI., 1991; Kirilloff,

weaned off mechanical ventilation (Petty, 1982). In

Owens, Rogers, and Mazzocco. 1985; Zinman,

addition these patient are prone to microaspirations.

1984). Forced chest wall compression or forced ex

Promotion of mucociliary transport is therefore es

piratory maneuvers are contraindicated (Nunn, Cole

sential to facilitate clearing of aspirate and minimize

man, Sachithanandan, Bergman, and Laws, 1965). Impaired mobility, inability to cough effectively,

bacterial colonization and risk of infection. Another major problem for patients with restric

decreased airway diameter, and bronchospasm con

tive lung disease secondary to generalized weakness

tribute to impaired mucociliary transport and secre

and neuromuscular disease is an ineffective cough.

tion accumulation. In addition, impaired glottic clo

Cough facilitation techniques (e.g., body positioning,

sure and increased risk of reflux in this patient

abdominal counter pressure, and tracheal tickle can

population exposes the airway to risk of aspiration.

be used to increase intraabdominal and intrathoracic

Prophylactically, multiple body positions and fre

pressures and cough effectiveness. A natural cough,

quent position changes will minimize the risk of se

even when facilitated, is preferable and more effec

cretion accumulation and stasis. If mechanically

tive in dislodging mucus from the sixth or seventh

ventilated. these patients are suctioned as indicated.

generation of bronchi than repeated suctioning. Even

If pulmonary secretions become a significant prob

a weak, facilitated cough may be effective in dis

lem despite these preventative measures, postural

lodging secretions to the central airways for removal

drainage positions are selected to achieve the opti

by suctioning or for redistributing peripheral secre

mal effect (i.e., secretion mobilization and optimal

tions (Hasani, Pavia, Agnew. and Clarke, 1991).

gas exchange). Given the treatment response. man

Huffing, a modified cough peJformed with the glottis

ual techniques of which manual vibration would

open and with abdominal support. may help to mobi

have the greatest physiological justification, may

Jize secretions in patients with generalized weakness

yield some benefit.

(Hietpas, Roth, and Jensen. 1979). In some cases,

Patients with chronic neuromuscular dysfunction

suctioning may be the only means of eliciting a

and residual musculoskeletal deformity pose an ad

cough and clearing secretions simultaneously.

ditional challenge to the cardiopulmonary physical

Coughing attempts are usually exhausting for these

therapist in that cardiopulmonary function is less

patients. Thus ample rest periods must be inter

predictable because of altered lung mechanics

spersed during treatment, particularly for the venti

(Bake, Dempsey, and Grimby, 1976) and possibly

lated patient. Coughing maneuvers need to be strate

cardiac dynamics. Thus clinical decision making is

gically planned. Even though the patient may be

more experiential in these patients who require

only to effect a series of a few weak coughs, it is es

close monitoring.


602

PART Vl


OBESITY



The obese patient can be treated aggressively pro

Restriction of cardiopulmonary function secondary to

vided there are no contraindications and he or she is

morbid obesity is called the alveolar hypovenlilalion

being fully monitored. Treatments need to be intense,

syndrome or Pickwickian syndrome. In this syndrome

to the limits of the patient's tolerance, provided this

the weight of excess adipose tissue over the thoracic

is not contraindicated. An aggressive approach is es

cage and abdominal cavity restricts chest wall move

sential given that the obese patient is at greater risk of

ment and movement of the diaphragm and abdominal

deteriorati ng between treatments than a nonobese

contents, respectively, during respiration. In very

counterpart. Recumbency is tolerated poorly by an

heavy individuals, cardiopulmonary function can be

obese patient. Positional decrements in Pa02 and

significantly impaired, resulting in hypoxemia and

Sa02 can induce dysrhythmias. The weight of the ab

cardiopulmonary failure. The major pathophysiologi

dominal viscera limit diaphragmatic descent and ele

cal mechanisms include significant alveolar hypoven

vate the resting position of the diaphragm, impeding

tilation, reactive hypoxic pulmonary vasoconstriction,

its mechanical efficiency.

increased pulmonary vascular resistance, myocardial

These patients need to be aggressively mobilized;

hypertrophy, increased right ventricular work, altered

both whole body exercise stress and range of motion

position of the thoracic structures, abnormal compres

exercises between mobilization sessions. Active and ac

sion of the heart, lungs, and mediastinal structures, ab

tive assisted upper-extremity range-of-motion exercises

normal position of the heart, cardiomegaly, increased

are associated with increased hemodynamic stress; thus

intraabdominal pressure, elevated hemidiaphragms

the patient must be monitored closely. Lower-extremity

with resulting pressure on the underside of the di

exercise, such as pedaling and hip and knee flexion and

aphragm, impaired cough effectiveness, impaired mu

extension exercises, may help position and improve the

cociliary transport, mucous obstruction of airways,

excursion of the diaphragm. Lower-extremity move

airway narrowing, bronchospasm, impaired mechani

ment will augment venous return. Depending on the pa

cal efficiency of diaphragmatic excursion, and im

tient and the work of the heal1, the effect of lower-ex

paired respiratory mechanics and breathing efficiency

tremity movement will need monitoring to ensure that

(Bates, 1989). In addition, such patients are likely to

myocardial work is not increased excessively.

have poor cardiopulmonary reserve capacity sec

The erect upright position is optimal to augment

ondary to increased metabolical rate and minute venti

ventilation and reduce the work of the mechanical

lation at submaximal work rates, increased metabolic

ventilator and the risk of barotrauma. The upright po

cost of breathi ng, and increased work of breathing.

sition, coupled with leaning forward, displaces the

Moderately heavy patients whose pulmonary function

abdominal contents forward, thereby reducing in

is normally not compromised may exhibit cardiopul

traabdominal pressure and facilitating diaphragmatic

monary dysfunction when their oxygen transport sys

descent. The posterior lung fields, particularly of the

tems are stressed because of illness.

bases, are at risk for dynamic airway closure and at

Mechanical ventilation can be a challenge in that

electasis. Numerous positions and position changes

the system pressure required to inflate the lungs may

ensure that the dependent alveoli remain open. The

predispose the patient to barotrauma. Furthermore,

time spent in the supif!e position should be mini

high system pressures contribute to reduced stroke

mized. In fact, greater emphasis should be placed on

volume and cardiac output. Adequate circulation is

nursing these patients in the upright position (i.e., the

essential to fulfill the goals of medical management

position of least risk and its variants). In addition to

(i.e., to optimize tissue oxygenation and carbon diox

its pulmonary benefits, the upright position can re

ide removal). Thus a delicate balance between ade

duce compression of the heart and mediastinal struc

quate alveolar ventilation, cardiac output, and periph

tures and there is a potential decrease in stroke vol

eral circulation is maintained.

ume and cardiac output. The weight of the chest wall,


33

Intensiye Care Unit Management of Secondary Cardiopulmonary Dysfunction

in addition to the weight of internal fat deposits in

603

are taught comparable with those described for the

and around the cardiopulmonary unit, can compro

patient with neuromuscular disease. Body positioning

mise cardiac output and contribute to dysrhythmias.

to facilitate coughing and supported coughing need to

Thus during all body position changes the patient

be instituted to maximize cough effectiveness. These

should be monitored hemodynamically to ensure the

maneuvers should be carried out in conjunction with

position is being tolerated well. Obese patients often

hourly extreme position shifts.

slump after being positioned in the upright position.

Morbidly obese patients have a high incidence of

It is crucial that the position of these patients is

upper airway obstruction and sleep apnea secondary

checked frequently and corrected. The slumped posi

to floppy compliant pharyngeal tissue. Thus the qual

tion can be counterproductive in that the benefits of

ity of their sleep and rest is suboptimal, and they are

the upright position are significantly reduced and can

apt to desaturate significantly while sleeping. These

lead to deterioration.

patients are also at high risk for esophageal reflux

Although obese patients do not tolerate the prone position well, the semi-prone position can be benefi

and aspiration. The optimal resting position is with the head of bed up.

cial by simulating the benefits of the upright lean-for ward position on the displacement of the abdominal viscera (Ross and Dean,

1992). This position also

PATIENT WITH MUSCULOSKELETAL TRAUMA Pathophysiology and medical management

simulates the prone abdomen-free position, which is associated with even greater benefit than the prone abdomen-restricted position (Dean,

1985). The bene

fits of the prone position for the obese individual in

Crush and penetrating injuries of the chest are com monly seen in the ICU (Moylan,

1988). Damage to

the chest wall, lung parenchyma, and heart contribute

clude increased lung compliance and enhanced gas

to the risk of cardiopulmonary failure (see box on

exchange and oxygenation. The full prone abdomen

p.

restricted position is contraindicated in the obese in

and abdomen may also contribute. Fractures of long

dividual with cardiopulmonary failure, however, be

bones and pelvis are associated with fat emboli,

cause this position can compromise diaphragmatic

which pose the threat of pulmonary embolism. In ad

604). Associated injuries of the head, spinal cord,

descent and contribute to further cardiopulmonary

dition, fluid loss in multiple trauma contributes to

distress and failure and possibly cardiac arrest.

loss of blood volume, hypovolemia, and hcmody

Mucociliary transport is slowed and ineffective in

namic instability. The more extensive the injuries, the

obese patients with cardiopulmonary failure. Fre

greater the pain and need for analgesia. Pain con

quent body positioning will facilitate mucociliary

tributes significantly to reduced alveolar ventilation,

transport and lymphatic drainage. The postural

airway closure, and inefficient breathing patterns.

drainage positions can be effective in mobilizing se

Paradoxical motion of the chest wall associated

cretions should accumulation become a problem.

with flail chest and rib fractures results from instabil

Manual techniques are not likely to add much benefit

ity of portions of the rib cage after trauma to the

particularly in the morbidly obese patient. Suctioning

chest. If severe, patients may require surgical stabi

is essential to clear pulmonary secretions from the

lization of the ribs or stabilization by continuous ven tilatory management. Chest wall injuries and rib frac

central airways. The obese individual is at risk for postextubation

tures are particularly painful.

atelectasis. Thus aggressive mobilization and numer

The presence of blood or air in the chest cavity

ous positions and frequent position changes need to

and in the potential spaces of the pericardiai sac and

be continued.

intrapleural cavity impairs cardiac distension and

The spontaneously breathing obese patient has a

contraction, impairs venti lation, promotes retention

weak ineffective cough, which will be even less ef

of secretions, interferes with effective clearance, and

fective after a period of intubation and mechanical

impairs lymphatic drainage (Marini and Wheeler,

ventilation. Deep breathing and coughing maneuvers

1989). Resolution of effusions can be facilitated with


604

PART VI


sion. A tension pneumothorax results when air col

Factors COlltributillg to Cardiopulmonary Failure After Trauma and Their Diagnostic Signs

lects under tension in the pleural cavity. The tension pneumothorax promotes lung collapse on both the ip silateral and contralateral sides, which furlher threat

Airway Obstruction

ens respiratory failure. Phrenic nerve injuries inhibit

Respiratory insufficiency

diaphragmatic function (Dureuil, Viires, and Canti

Respiratory distress

neau, 1986). The position of the affected hemidi

Impaired blood gases

aphragm rests higher in the thoracic cavity, which may restrict ventilation to the lung base and con

Inadequate Ventilation

tribute to airway closure and basal atelectasis. Di

Reduced thoracic movement

aphragmatic injuries directly affect ventilation in two

Paradoxical thoracoabdominal movement

ways. First, the bellows action of the lungs is com

Tension Pneumothorax

promised. Second, the lung is displaced by herniation

Cyanosis

of the abdominal contents into the thoracic cavity. Analysis of blood gases in the patient with post

Unilaterally absent breath sounds

traumatic injuries of the chest often shows severe hy

Distended neck veins

poxemia and moderate elevations of arterial PC02.

Subcutaneous emphysema

The presence of acidemia is common, which may

Cardiac Tamponade

have both respiratory and metabolical components.

Distended neck veins Muffled heart sounds


Narrowed pulse pressure

Severe restlessness and dysp nea in a patient with

Paradoxical pulse

chest injury are classic indications of respiratory fail

Open Pneumothorax

ure. Auscultation and percussion can usually reveal

Decreased breath sounds

an underlying pneumothorax or hemothorax. Tension

Penetration of thoracic wall

pneumothorax is confirmed by chest x-ray or aspira tion of the chest with a needle and syringe.

Myocardial Contusion

Flail chest refers to fractures involving the chest

Dysrhythmia

cage where there are two or more fractured ribs at

Flail Chest

two or more sites. This results in instability of the

Loose segment

chest wall. The so-called flail segment is usually ap parent on physical examination. Paradoxical move

Multiple palpable fractured ribs

ment of the flail segment can often be observed. The

Decreased or moist breath sounds

chest is depressed rather than elevated over the site

Modified from Moylan, J. A. (Ed.). (1988). Trauma surgery. Philadelphia: .IB LippincOl1.

during inspiration. Rib fractures are indicated by ten derness and crepitations on physical examination and from x-ray findings. Nonventilatory management of chest injuries in the absence of severe hypoxemia is preferred in these patients.

mobilization and body positioning. These interven tions reexpand underlying atelectasis and help restore fluid balance by their effects on lymphatic drainage.

Rib Fractures

Furthermore, by shifting the effusion fluid, atelectatic

Simple uncomplicated rib fractures often receive no

areas can reexpand. The presence of a pneumothorax

specific treatment. Pain from complicated fractures

or hemothorax can severely compromise lung expan

may be treated with intercostal nerve blocks and tran


33


scutaneous electrical nerve stimulation and analgesia.

605

ventilator. Small leaks can be tolerated and are usu

Optimizing alveolar ventilation and mucociliary trans

ally compensated for by a n increase in tidal or

port and avoiding pulmonary complications are pri

minute ventilation.

mary goals. Strapping the chest is avoided because this further restricts and compromises chest wall expansion. The CUITent method of therapy for flail chest is in ternal stabilization of the chest and use of a mechani

Multiple Trauma The management of multiple trauma is a major chal

cal ventilator. Slight hyperventilation will usually re

lenge for the rcu team. Multisystem involvement

duce the respiratory drive of most patients to allow

and complications often present a precarious situation

the ventilator to take over the full work of breathing.

in which priorities have to be defined for each indi

The flail segment is then stabilized by internal expan

vidual situation. Multiple trauma can include head in

sion of the lungs. The treatment ensures adequate

jury, chest wall injuries, fractures, lung contusions,

ventilation with the least pain possible. After 2

diaphragm injury, pleural space disorders, internal in

weeks, the flail segment is usually stable.

juries, thromboemboli, fat emboli, and cardiac contu

When the patient can maintain a reasonable tidal

sions. Shock and adult respiratory distress syndrome

volume and normal blood gases, weaning is begun.

may ensue (see Chapter 34). The clinical picture of

As soon as tidal volume and forced vital capacity are

the patient with mulliple trauma is compounded by

within acceptable limits, oxygen can be administered

the mobilization and positioning restrictions imposed

through an endotracheal tube with a T tube assembly.

(Ray et aI., 1974). Positive end-expiratory pressure

Arterial blood gases are monitored closely after the

(PEEP) is frequently used to reduce the effects of

ventilator has been discontinued. Once the blood

lung congestion secondary to shock or adult respira

gases are in acceptable ranges over a reasonable pe

tory distress syndrome (ARDS) (McAslan and Cow

riod of time (i.e., 12 to 24 hours) the endotracheal

ley, 1979). Arterial blood gases are assessed to evalu

tube is removed.

ate the effectiveness of PEEP in effecting improved oxygen transfer.

Pneumothorax and Hemothorax Air or blood in the pleural cavity after chest trauma

Multiple Fractures

must be removed through a chest tube. For a pneu

Multiple trauma patients are assumed to have spinal

mothorax the chest tube is positioned in the second or

involvement, particularly of the cervical spine, until

third intercostal space in the midclavicular line. For a

ruled out with appropriate scans and x-rays. Mean

hemothorax the chcsl tube is positioned in the sixth

while the physical therapist performs repeated assess

intercostal space in the posterior axillary line. Usually

ments to establish a baseline and recommend posi

the chest tubes are sutured and taped into position and

tions for the patient that will ma ximize oxygen

therefore are not easily dislodged. If the tubes are

transport. Treatment to enhance oxygen transport and

pulled out, subcutaneous emphyscma or a pneumotho

mucociliary lransport is primarily restricted to body

rax results. A pneumothorax will also result if the tube

positioning using log rolling maneuvers and a se

is disconnected from the underwater seal. This is the

lected range of motion exercises (i.e., not of the head

reason for securing the collecting reservoirs of a chest

and neck, and possibly shoulders).

tube drainage system with tape to the floor. Mobiliz

Fixation, traction. and casting of fractures and dis

ing and frequency repositioning the patient facilitates

locations of the limbs complicate the management of

chest tube drainage and reexpansion of collapsed alve

the trauma patient. Restrictions to mobilization and

oli. Care is taken to avoid kinking or straining chest

body positioning arc primary concerns of the physical

tubes during patient treatment.

therapist (Mackenzic, 1989). Mobilization in the up

A bronchopulmonary fistula can be responsible

right position provides both a gravitational stimulus

for a major loss of the tidal volume delivered by the

and an exercisc stimulus, both of which are essential


606

PART VI


to optimize oxygen transport. This is preferable to

the trauma patient to reduce excessive oxygen con

mobilization exercises in the recumbent position. In

sumption and promote comfort (Malamed, 1989).

some cases, traction can be transferred from over the

Active relaxation refers to relaxing the patient

end of the bed to over a chair. A strict routine of body

through participation of the patient in relaxation pro

positioning is maintained, although severe limitations

cedures. Passive relaxation refers to relaxing the pa

often exist with respect to the specific positions and

tient using passive procedures (e.g., body positioning,

the degree of turning permitted. Lower limb traction

physical supports, talking slowly and calmly, and tak

can be maintained when the patient is positioned in a

ing adequate time for conducting treatments). Taking

modified sidelying position. Coordinating treatments

time to implement mobilization is essential. First,

with analgesia schedules reduces the patient's pain

mechanically moving and having patients who have

and fatigue, thereby improving tolerance to and pro

mUltiple injuries move requires a prolonged period of

longing the treatment. These patients usually tolerate

time. In addition, however, the cardiovascular and

the head-down position well provided head injury

cardiopulmonary systems of critically ill need time to

does not complicate the clinical picture.

adapt to new positions physiologically and to control

The acute effects of mobilization that will benefit

concommitant discomfort. Prolonged periods of time

the patient with musculoskeletal trauma include aug

may be required to turn a patient, dangle him or her

mentation of ventilation, perfusion, ventilation and

over the bed, or transfer him or her to chair with con

perfusion matching, and promotion of mucociliary

tinuous monitoring. Every effort is made to maintain

transport and cough effectiveness. General mobiliza

the patient's spirits, reduce stress, and encourage a

tion exercises and propriocepti ve neuromuscular fa

positive attitude toward active participation early in

cilitation (PNF) can be used to promote a mobiliza

the rehabilitation program that begins in the ICU.

tion stimulus. Cycle pedals can be attached to a chair

Care must be taken to avoid undertreating or

or the end of the bed to provide a low-intensity exer

overtreating trauma patients. A clear chest can

cise challenge for some patients. Maximal work out

rapidly regress because of general immobility and

put can be achieved within the patient's capacity

limitations to body positioning imposed by traction

using an interval training type schedule (i.e., schedule

and pain. Treatments should always be coordinated

of work to rest periods). A mobilization program that

with the patient's analgesics to optimize treatment re

promotes the long-term effects of exercise can be pre

sponse and for the patient's comfort. Whenever pos

scribed that involves as many large muscle groups as

sible, the patient should be equipped with slings and

possible in rhythmic, dynamic exercise.

pulleys and weights at bedside and a monkey bar

Frequent deep breathing and coughing is continued

overhead for bed mobility and upper-extremity exer

during and between treatments, depending on whether

cise. In addition to their cardiopulmonary benefits,

the patient requires mechanical ventilation. Body posi

PNF patterns are useful in preparation for slings and

tioning is carried out within the limits of the patient's

pulleys. The use of PNF patterns for trauma and post

traction and casts. Impaired mucocil iary transport is

operative patients can be well tolerated by these pa

treated with body positioning and frequent position

tients. All activities are taught in conjunction with

changes. Secretion accumulation may require postural

breathing control exercises and coordination with the

drainage. Modified positions may be indicated because

respiratory cycle.

of the positioning restrictions imposed by the fractures, traction, and fixation devices. If indicated manual tech n i q u e s may be c o u p l e d with postu ral drainage (Mackenzie, Shin, Hadi, and Ilnle, 1980). Care must

PATIENT WITH HEAD INJURY Pathophysiology and medical management

be taken to ensure the addition of manual techniques is

Hypoxemia is observed in many patients with injury

beneficial and is tolerated by the patient.

to the central nervous system (Demling, 1980). This

Relaxation interventions, both active and passive,

may reflect primary damage to the cardiopulmonary

should be integrated into the treatment regimen for

centers of the brain or secondary effects of associated


33


trauma. Arterial blood gases are therefore closely monitored in these patients. Acute cerebral edema with sudden increase in in tracranial pressure (ICP) and reduction in cerebral pelfusion pressure, rapidly affects central control of respiration (Borozny, 1987). Advancing cerebral edema is evidenced by deterioration in level of con sciousness, pupillary reflexes, ocular reflexes, pattern of respiration, and exaggerated muscle tone and pos ture. The sequence of these clinical signs corresponds to progressively increasing ICP from the cortex to ward the medullopontine region. With involvement of the brain stem, respiration becomes variable and inco ordinate. With loss of central control and imminent cessation of breathing, respiration is shallow and ataxic. The appearance of the jaw and laryngeal jerk with each inspiratory effort suggests a poor prognosis. Physical therapy and the patient's normal routine may have a dramatic effect on the ICP. ICP can be el evated indirectly by an increase in intrathoracic pres sure as a result of physical therapy or suctioning. Turning and positioning may produce obstruction to cerebral venous outflow. Noxious stimuli, such as ar terial and venous punctures or cleansing wounds, can elevate ICP and relatively innocuous stimuli, such as noise or pupil checks. Wbether these factors elevate

607

ICP depend on cerebral blood volume and intracranial compliance. On cerebral stimulation, a chain reaction is initiated. Cerebral activity is increased, which in turn elevates metabolical rate, blood flow, and hence volume and ICP. Alternatively, increased cerebral blood volume secondary to gravitational effects, in creased ICP, and reduced cerebral perfusion pressure. The head of the bed is usually maintained between 30 and 40 degrees to promote venous drainage and thereby reduce ICP. The patient's head and neck can be fixed in a neutral position by halo traction or by sand bags positioned on either side (Figure 33-1). Mechani cal hyperventilation is used to maintain PC02 below normal limits but above 20 mm Hg. Arterial blood gases are checked during or immediately after hyper ventilation. Prolonged hyperventilation is avoided. Barbiturate coma may be induced to decrease the cerebral metabolical rate for oxygen and hence cere bral blood flow. The reduction in cerebral metaboli cal rate exceeds the reduction in blood flow and thus oxygen supply exceeds demand, which is a desirable treatment outcome. Invasive hemodynamic monitor ing is instituted in conjunction with barbiturate coma because barbiturates contribute to hemody namic instability. A complication of head injuries is acute lung in

' ......... IIIft,-

--

. ' .

. . .

FIGURE 33-1 Patient following neurosurgical procedure; head of bed elevated 20 degrees to help reduce ICP.


608

PART VI


jury, specifically, neurogenic pulmonary edema (see

may be acceptable provided the pressure returns to

Chapter 34). Antonomical nervous system dysfunc

normal immediately after the removal of the pres

tion contributes to hypertension and neurogenic pul

sure-potentiating stimulus. Prolonged elevation of

monary edema. The endothelial tight junctions in the

ICP suggests low cerebral compliance and the possi

pulmonary capillaries leak protein into the intersti

bility of potential brain damage unless pressure is re

tium along with fluid. Constriction of the lymphatic

duced. Thus all interventions must be performed

vessels may also contribute to fluid accumulation by

guardedly with due consideration being given to cor

impeding the removal of lung water. Increased fluid

responding changes in ICP. Typically, management

accumulation in the interstitium may progress to the

of patients with central nervous system trauma in

alveoli contributing further to impaired gas exchange

cludes judicious tracheal suctioning, a stringent turn

and reduced lung compliance.

ing regimen, lung hyperinflation with the manual breathing bag in the nonventilated patient, or deep


breathing with occasionally increased tidal volumes or sighs in the ventilated patients.

Physical therapy priorities in the management of the

If the ICP is unstable and a risk of brain damage

patient with cardiopulmonary dysfunction secondary

exists, physical therapy should follow sedation. Ide

to head injury appear in the box below.

ally, treatments should be peIformed when the ICP is

In cases of abnormally elevated ICP, mechanical

low and intracranial compliance is satisfactory. The

hyperventilation and maintenance of Pe02 around 25

head-down position is contraindicated. Noise and

mm Hg are effective measures to reduce cerebral

noxious stimulation that increases rcp should be kept

edema by reducing blood flow. Intracranial pressure

to a minimum.

may increase with treatment and in particular with

If the ICP is elevated, all noxious stimuli should

turning or suctioning. An ICP of up to 30 mm Hg

be removed. In severe conditions a decision may

Physical Therapy Priorities in the Management of the Patient with Cardiopulmonary Dysfunction Secondary to Head Injury

I. Prevention of cerebral hypoxia by maintaining a patent airway 2. Reduction of intracranial pressure and optimal cerebml perfusion pressure 3. Position the patient within the limits of fracture stabilization and elevated intracranial pressure to promote alveo lar ventilation and ventilation and pert'usion matching

4. Position the patient to reduce pathological patterns of muscle synergy and thereby promote ventilation and re duce oxygen consumption

5. Position the patient to reduce myocard ial stress 6. Avoid a ctivities and stimuli that increase ICP 7. Reduce atelectasis 8. Shift lung fluid accumulations and areas of atelectasis 9. Promote lymphatic dr ainage 10. Promote m ucocil i ary transport and reduce pooling of secretions. and risk of chest infection II. Reduce the work of breathing and improve the efficiency of the muscles of respiration, particularl y if long-term disability is a risk

12. Perform active, active-assisted, or passive movements as soon as possible to enhance cardiopulmonary function and secondarily to preserve musculoskeletal and neuromuscular function and reduce the risk of thromboemboli


33


609

have to be made by the team to limit or withdraw in

sions, is cardiopulmonary complications. Lung vol

terventions that lead to an excessive ICP increase that

umes are reduced with the exception of residual vol

does not remit instantly (e.g., physical therapy, posi

ume that increases. Interestingly, vital capacity in

tioning, suctioning, or neurologic assessment).

creases in the supine compared with the sitting

Movement of the limbs is performed gently and in a

position in quadriplegic patients. However, this does

relaxed manner. Patients in a comatose state may expe

not counter the negative effects of reduced functional

rience passive limb movement noxiously. Intracranial

residual capacity (FRC) and increased airway closure

pressure may be elevated as a result. Passive move

in this position and reduced flow rates.

ments, however, may have the added benefit of pro

Spinal cord injuries above C3 result in loss of

moting improved tidal ventilation in the nonventilated

phrenic nerve i n n e r vati on, necessitating a t ra

patient by providing afferent stimulation to the respira

cheostomy and mechanical ventilation. The lower the

tory center via peripheral muscle and joint receptors.

level of the spinal cord lesion, the lower the car

Severe head injury may produce flexor or extensor

diopulmonary risk. All patients with spinal cord in

posturing. These synergies may be inhibited by ap

juries are at risk for developing atelectasis and pneu

propriately positioning the patient. Judicious body

monia. The coughing mechanics of quadriplegic

positioning, in turn, reduces oxygen consumption and

patients are abnormal and contribute to ineffective air

the patient's overall energy requirements.

way clearance (Estenne and Gorino, 1992). In addi

Neurophysiological facilitation of respiration has

tion the quadriplegic patient is at risk for developing

been proposed as a treatment intervention to improve

pulmonary emboli. Prophylactic low-dose heparin is

ventilation, coughing, and breathing pattern in the un

used routinely unless the presence of pulmonary em

conscious patient (Bethune, 1975). Neurophysiologi

boli is suspected and higher dosages are indicated.

cal facilitation techniques include cocontraction of

Patients with suspected spinal cord injuries usually

the abdominal muscles, vertebral pressure, intercostal

undergo immediate spinal fixation on admission. De

stretch, lifting the posterior basal areas of the lungs,

pending on the level of injury detennined by clinical

and perioral stimulation. Although these techniques

signs and x-rays, traction, and fixation may be local

are believed to stimulate reflex involuntary respira

ized to the head and neck or spinal support and cast

tory movements, there is no evidence to support their

ing may be required in the thoracic or lumbar regions.

efficacy in the management of the unconscious pa tient. Comparable with conventional chest physical therapy procedures, reported benefits associated with


neurofacilitation cannot be discriminated from the

Because of the need to maintain relative immobility

potent and direct physiological effects of increased

in the acute stabilization period of suspected spinal

arousal, body positioning, and mobilization on oxy

cord injury, therapeutic body positioning rather than

gen transport (Dean, 1994b). These latter effects have

mobilization is a primary intervention for optimizing

been well documented.

oxygen transport. Although modified body position

Although arousing the patient and increasing oxy

ing can be achieved, the provision of optimal care

gen consumption occurs with cardiopulmonary physi

under these restricted conditions is a singularly im

cal therapy, arousal and oxygen consumption are

pOl'tant challenge to the physical therapist, particu

generally minimized to reduce hemodynamic and

larly with respect to the management of adequate

metabolical demands in head-injured patients.

oxygen transport while the patient is in the ICU. Pa tients with high spinal cord lesions can be positioned in all positions within the limits of the cervical trac

PATIENT WITH SPINAL CORD INJURY

tion device being used, barring head injury. Both


head and foot-tipped positions, however, are intro

The principal cause of death in the early stages of

duced cautiously and with hemodynamic monitoring

acute spinal cord injury, particularly for the high le

because both positions can have significant car


610

PART VI


diopulmonary and hemodynamic consequences sec

respiratory muscles. In some centers, patients are

ondary to spinal nerve loss and hence sympathetic

started in the weaning period on respiratory muscle

nerve loss to the peripheral blood vessels. Turning

training. The physical therapist must be well versed

frames such as the Stryker frame facilitate turning

and practiced in this procedure before using it in con

and tipping these hemodynamically labile patients in

junction with weaning the quadriplegic patient off the

the supine and prone positions (Douglas, Rehder,

ventilator. Because of the potential risk of inappropri

Beynen, Sessler, and Marsh, 1977).

ate application and of danger to the patient, respira

Effective body positioning, despite the need in some cases for extensive modification, may be suffi

tory muscle training must be effected knowledgeably to optimize its benefits for each individual patient.

cient to optimize oxygen transport secondary to im proved regional ventilation and perfusion to all lung fields. In the spontaneously breathing patient, deep

Respiratory Muscle Training

breathing and coughing maneuvers need to be cou

Respiratory muscle weakness and fatigue, two physio

pled with position changes to optimize mucociliary

logically distinct entities, are probably much more

transport (Alverez, Peterson, and Lunsford, 1981;

common in the ICU than appreciated. These states

Braun, Giovannoni, and O'Connor, 1984). Some pa

need to be recognized and detected early because both

tients may not tolerate numerous positions and posi

can cause respiratory muscle failure (Macklem and

tion changes and thus have impaired mucociliary

Roussos, 1977). The distinction between the two con

transport. If secretion accumulation and stasis de

ditions is that weakened muscles respond to resistive

velop, postural drainage can be instituted; however,

muscle training, whereas fatigued muscles do not. Ex

tipping must be attempted very cautiously. Patients

posing fatigued respiratory muscles to resistive loads

should be monitored closely during and after treat

can accentuate respiratory failure. The indication for

ment. Because of their well-documented side effects

respiratory muscle training, therefore, is weak rather

(Kirilloff et aI., 1985) and the hemodynamic lability

than fatigued respiratory muscles. Rest is indicated for

of acute quadriplegic patients, percussion and vibra

fatigued respiratory muscles. Whether the respiratory

tion are applied cautiously, should they be indicated,

muscles are weak or fatigued must be established be

depending on the severity of any complicating frac

fore prescribing respiratory muscle training.

ture-dislocation(s), the stability of fixation, the condi

The combination of immobilization and cardiopul

tion of the lungs, the presence of chest wall injuries,

monary involvement secondary to multiple trauma

and hemodynamic lability.

may result in similar disuse atrophy and weakness of

The high-frequency oscillating ventilator may

the diaphragm as observed in other skeletal muscles.

have some benefit in the management of mUltiple

Respiratory muscle weakness and fatigue can be a

trauma patients with spinal injuries who require ven

component of both obstructive and restrictive pat

tilation. The advantages of the high-frequency oscil

terns of lung disease. Patients with spinal cord in

lating ventilator include improved spontaneous mu

juries do not have the same advantage of performing

c o c i l i a r y clearance and r e d u c e d i n c i d e n c e of

coordinated general body activity and relaxation ma

atelectasis (Gross and King, 1984). Weaning quadri

neuvers to help reduce the work of breathing. This

plegic patients off the ventilator requires special skill

contributes to a marked decrease in respiratory mus

because of the lost function of the respiratory mus

cle strength and endurance resulting in reduced vital

cles. For these patients, weaning can be particularly

capacity, rib cage mobility, and the ability to cough.

fatiguing, frightening, and frustrating. Patients are

For these reasons, patients with paralysis and demon

weaned lying supine when they are alert and able to

strated respiratory muscle weakness are particularly

cooperate. Short periods off the ventilator on the T

well suited for respiratory muscle training. The quad

piece are used initially. Use of the accessory muscles

riplegic patient has lost the function of the intercostal

of respiration and any other muscular reserves are en

muscles which are important muscles of inspiration

couraged to compensate for the loss of function of the

and are responsible for thoracic cage expansion. In


33


611

addition, the absence of the abdominal muscles,

fatiguing factors as eating a meal, talking, exposure to

which are the primary expiratory muscles, drastically

heat and humidity, sitting upright, overcoming a respi

reduces the ability to cough effectively and to per

ratory tract infection, and so on.

form a forced expiration. The diaphragm and the ac

A candidate for respiratory muscle training is

cessory muscles of inspiration, namely the scaleni

equipped with an individual resistive breathing pack

and sternocleidomastoid muscles, then become the

age containing the valve, mouthpiece, noseclip, flow

quadriplegic patient's respiratory muscles.

regulator, and a series of resistors that attach to the

These factors as well as the effects of heat, humid ity, and the vertical position, all predispose the quad

inspiratory side of the valve (Figure

33-2). It is es

sential that flow rate is controlled in that patients can

riplegic individual to the development of respiratory

negate the training effect of a set resistor by chang

muscle weakness and failure. The physical therapist

ing flow rate.

can help avert the effects of respiratory muscle weak ness with respiratory muscle training.

An initial pretraining assessment is performed to determine the appropriate resistor with which to com

Respiratory muscle training with a regimen of pro

mence training. The progression to the next level of

gressive resistive breathing has been demonstrated to

resistance is based on specific criteria of endurance

improve the strength and endurance of respiratory

on the current resistor. Once the resistor has been

1980; Loveridge and Dubo, 1990; Pardy and Leith, 1984) and improve functional capacity in some patients (Reid and Warren, 1984).

shown in the box on p.

Resistive breathing exercise is aimed at the prevention

pacity can be measured routinely to monitor change

of respiratory failure by increasing the strength and

in diaphragmatic function. The level of inspiratory

muscles (Gross and King,

chosen, a typical training session includes the steps

612.

Maximum inspiratory mouth pressure and vital ca

particularly endurance of the key muscle of inspira

resistance and the duration for which the patient can

tion, the diaphragm. Because the diaphragm is skeletal

use each resistor are indications of the endurance of

muscle, it can be reconditioned using a series of inspi

the inspiratory muscles. Measurement of vital capac

ratory resistance maneuvers. A stronger, endurance

ity and maximum inspiratory and expiratory mouth

trained diaphragm will not fatigue as quickly as an un

pressures provide an index of the strength of the in

trained diaphragm when exposed to such potentially

spiratory muscles.

FIGURE 33-2 Handheld resistive breathing training devices. Left, P-Flex; resistance level is altered by changing settings on dial. Right, DHD device; resistance level is altered by inserting stopper with different size orifice into inspiratory port.


612

PART VI


General Steps Involved in Respiratory Muscle Training and Its Prescription I. The patient is usua lly in the sitting or upright position for training initial l y unless sitting is not yet indicated 2. The noseclip is attached snugly 3. The mouth pi e ce is p l aced securel y in the individual's mouth and a l l ows him or her to select an indi v i dual rate and pattem of breathing

4. The patient adjusts flow rate to that designated and maintains it with feedback from the flow regulator 5. Breathing is performed comfortably without force 6. The patient is instructed to stop the exercise by letting go of the valve if the resistance becomes too difticu lt

or

if

lightheadedness or dizziness occur

7. When the individual has adjusted to the resistance in the initial training position. an attempt can then be made to train at the same load in other positions

8. The parameters of the respiratory muscle training is determined by thc patient" s baseline: specific paramcters of the prescription include initial resistance, the flow rate, the number of repetitions, the number of sets. the fre quency of sessions. and progression

Modified from Hornstein S: Ventilatol), muscle training. jury Unit, Shaughnessy Hospital,

J 984,

Vancouver.

A

clinical guide for physiotherapis/s, Unpublished

manual

of the Spinal Cord

In

Be.

Celtain precautions must be observed with respira

plicate the clinical picture further and seriously

tory muscle training. Each time a new resistance is

threaten tissue oxygenation (Cahalane and Deming,

tried, the physical therapist should be with the patient.

1984; Cane, Shapiro, and Davison, 1990). Hemoglo

The patient selects his or her own rate and pattern of

bin has a higher affinity for binding with carbon

breathing. The inspiratory rate is usually constant.

monoxide than oxygen. A carboxyhemoglobin level

Too shallow breathing is inefficient, and too slow,

greater than 20% denotes carbon monoxide poison

deep breathing may result in accumulation of carbon

ing. Levels in excess of 50% may produce irre

dioxide. The patient is cautioned about avoiding hy

versible neurological damage. The principal danger

perventilation. The physical therapist, or the patient

of carbon monoxide poisoning is that arterial Paoz

when he or she is capable, should check the valving

can be adequate and tissue oxygen tension inade

system on the respiratory muscle trainer before each

quate. Administration of high levels of oxygen is an

training session to ensure it is functioning properly.

initial priority to reduce the half-life of carbon monoxide to 1 hour from several hours. Depending on the severity and extent of the burns,

PATIENT WITH BURNS Pathophysiology and medical management

treatment ranges from conservative medical interven tions to multiple surgeries related to progressive de

Cardiopulmonary complications are common in pa

bridement and skin grafting. Both second and third

tients with smoke inhalation with or without severe

degree burns can result in severe disfigurement and

burns and are a major cause of death (Marini and

disability. Second-dcgree burns are partial thickness

Wheeler, 1989). Smoke and chemical inhalation pro

burns and tend to be painful. Third-degree burns are

duce edema, bronchospasm, cough, mucosal slough

full thickness burns; these tend to be anesthetic in that

ing, hemorrhage, hoarseness, stridor, and profuse

the nerves themselves have been destroyed. Body po

carbonaceous secretions. Irritation of the alveoli and

sitioning to optimize oxygen transport is life-preserv

acute pulmonary edema can result in a condition re

ing; however, positioning and limb splinting must also

sembling adult respiratory distress syndrome (see

be considered from the outset to minimize defonnity

Chapter 34). Carbon monoxide poisoning may com

and restore optimal neuromuscular and musculoskele


taJ statllS.

and preventing infec

is effectively treated with the ad

tion.

ministration of oxy g e n a n d m a in t a i n i n g c l e a r airways. I f the oxygen is

is breathing spontaneously, via nasal cannulae or mask at tlows on the arterial oxygen sat

of I to 5 L/min,

di

pulmonary edema consists typically of

Treatment is directed at improving arterial satura fluid

Treatment of

monary circulation in these

in the burn

must address both these aspects of management. tion,

613


33

uretics, and mechanical ventilation. Positive end ex piratory pressure is usually indicated in the ventilated Mist or aerosol inhalation is also used to

burn

reduce the thickness of pUlmonary secretions.

halation

In

are common in burn heat trauma, and chemical

uration. Moisture can be administered through a face

ing from smoke

tent with a heated nebulizer. Fluid balance is

and gas inhalation.

larly

usually administered

in the burn patient because of the

to hospital, the

On admission of the burn patency of the airway is assessed

Heat may cause

and bronchial edema. If

which is essential to the retention and

occlusion

compartmentalization of body fluids and in the regu

from

lation of fluid and electrolyte loss from the body. In

formed. If indicated early, intubation may avoid res

edema threatens, intubation is per

these patients may lose blood because of in

distress within the critical 24-hour period after admission. Particular care

at the time of the accident. There is also a

given to children

to

and older adults with inhalation injury because these

the time medical attention is available and IV tluid

have a higher risk of developing secondary

without tluid replacement from before the

complications.

resuscitation commenced. Because of the nature of even when tluid resuscitation has

fluid

balance remains a challenge until con

and

siderable healing and

has occurred. Fluid and

imbalances have considerable implica tions for hemodynamics and cardiopulmonary func

15) and contribute to

tion

management.

An the

in anticipation of progres

which would make the insertion of air

sive

impaired thermoregulation, hypermetabolism and in creased energy expenditure, ileus and

disten

sion, pain, and infection. Eschar formation associated cally restricts chest wall movement and can lead to respiratory failure. Tissue edema that can continue for

may be inserted initially with burns to airway, and

nrp'\iPI1fP

with circumferential burns of the chest wall mechani

instability, which necessitates modification of the physical

must be tient and

a few

after the bum contributes to increased tis

sue pressure and

tissue

potentiat

tissue ischemia and necrosis. Late complications

way considerably more difficult hours or days later.

include gastrointestinal bleeding

Ventilatory assistance is indicated with evidence of

ulceration and the continued high risk of infection.

to stress

to smoke inhala throat, airway,

and burns of the nose,

lungs, and chest wall. A nasotracheal tube i s pre ferred to


tracheostomy tube because complications

with a tracheostomy tube are greater in burn patients. Cardiopulmonary lated to

are

re

or tluid overload in the initial stage.

Acute pulmonary edema and preventable with careful fluid nous pressure can be

pressure more

Central ve

verely i

to

prevent atelecta and improve or main

Pulmonary function may be se r e d as t h e n e t result of i n halation burns and trauma to the chest wall,

and

tluid imbalance.

artery

reflects the status of the

with inhalation of the

sis and retention of tain gas

in the burn patient

pulmonary edema.

maintain the

are largely

because of severe fluid loss and may remain at low values

physical therapy is often required immediately for the

physical modified in the burn


often has to be 1984). Mobi

614

PART VI


lization to enhance oxygen transport is exploited as

traindicated over freshly grafted skin; however, man

much as possible, however, because of blood volume

ual vibration may be transmitted from a more distal

and hemodynamic problems, orthostatic intolerance

site to a lung field that cannot be vibrated directly.

may limit mobilization and positioning alternatives.

Risk of aspiration is increased if tube feedings are

With more severe burns and more extensive burn dis

not discontinued for at least I hour before treatment.

tribution, body positioning is the primary interven

A nasogastric tube is often used and should be cor

tion. Positioning to effect an optimal therapeutic ef

rectly positioned particularly during treatment.

fect on oxygen transport is challenging because of the

Stimulating exercise and gravitational stress may

significant physical limitations that may exist. Given

initially consist of being in the upright position prefer

that body positioning profoundly influences ventila

ably with the legs dependent, performing selected

tion and perfusion matching (Clauss, Scalabrini, Ray,

limb movements and dangling over the edge of the

and Reed, 1968), the reduced number of positioning

bed for a few minutes if this can be tolerated. how

alternatives will contribute to shunt, ventilation and

ever, in patients with severe burns and significant

perfusion mismatch, and hypoxemia. This effect will

fluid imbalance, active and active-assisted movements

be accentuated if the patient is mechanically venti

in an upright position that can be tolerated, may sub

lated (see Chapter 32).

stitute. As the patient's tolerance increases, free un

Patients who have skin grafts require particular

supported sitting can progress to standing and walk

care when moving or positioning because of the dan

ing. Ambulation during ventilator-assisted breathing

ger of sheering forces of the graft, which can disrupt

should always be considered for any patient for whom

the circulation, nutrition, and healing of the new skin.

this activity is not contraindicated. The upright posi

Sterile procedures must be observed at all times. The

tion and physical activity in the upright position are

physical therapist is usually required to cap, gown,

likely to enhance markedly the patient's cardiopul

mask, and glove before treating the patient with ex

monary and neuromuscular function, and improve the

tensive exposed areas and to cover the chest with a

patient's strength and endurance in preparation for

sterile drape. Facilitating mucociliary transport is a

long-term rehabilitation. If sitting up and ambulation

priority if the patient has significant mobility and po

are not imminent, appropriate limb movements,

sitioning restrictions because of the burn severity.

preferably active, can help provide an exercise stimu

Wherever possible, mobilization in conjunction with

lus that can enhance oxygen transport. Passive full

multiple body positions and position changes is at

range of motion exercises, in addition, are required to

tempted to maximize mucociliary clearance (Wolff,

maximize joint range (a distinct goal from that to en

Dolovich, Obminski, and Newhouse, 1977). If secre

hance oxygen transport), wherever possible.

tions have accumulated, positioning for postural

Positioning to minimize deformity is a priority

drainage requires the same consideration as position

given the potential consequences for cardiopul

ing for improved alveolar ventilation and ventilation

monary function and oxygen transport, as well as

and perfusion matching. In the spontaneously breath

musculoskeletal and biomechanical reasons. Position

ing patient, postural drainage positions can be used

ing a burn patient regardless of the goal should con

selectively to increase alveolar volume in the superior

sider alignment, pressure points, muscle balance, and

lung fields and alveolar ventilation to inferior lung

effect on healing and grafted skin.

fields, in addition to purposes of drainage of the su

Certain precautions have to be observed in the

perior bronchopulmonary segments. However, if the

management of the burn' patient. First, skin loss con

patient is mechanically ventilated, the superior lung

tributes to substantial fluid loss, often resulting in la

fields are preferentially ventilated (see Chapter 32).

bile fluid and electrolyte imbalance. This situation

Should the addition of manual techniques be indi

enhances myocardial irritability and the risk of dys

cated, percussion may not be comfortably tolerated in

rhythmia. Hemodynamic and ECG monitoring is per

the presence of first and second degree burns. Manual

formed routinely during physical therapy treatment.

vibration may substitute. Manual techniques are con

Second, large areas of skin loss increase the risk of


33 infection; therefore the

Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction therapist must be fa

miliar with sterile technique.

Barach, A.L. (1974). Chronic obstructive lung disease: Postural re of dyspnea. Archives oj Physical Medicine & Rehabilila

lion,

495-504,

SUMMARY

Bates, D.V. (1989). Respiralory JU i leli on

This chapter describes the principles and practice of

Bennett, W.D., Foster, WM,

secondary to neuromuscular and

monary

musculoskeletal conditions that can lead to cardiopul monary failure.

of conditions included are

neuromuscular conditions_ musculoskeletal condi tions, morbid obesity, head

spinal cord injury,

and burns. A detailed

of the underly

pathophysiology of these conditions and their medical management provides a basis for defining and

the physical

treatment.

The principles described in this chapter cannot be in terpreted as treatment

in that each pa

tient is an individual whose condition reflects multifactors contributing to

oxygen transport

care, and intrinsic factors related to the dition to the

in ad

pathophysiology).

plied Physiology,

69, 1670-1675.

Bethune. D.o, (1975). NeurophysiOlogical facilitation of respira tion in

unconscious adull patient. Physiotherapy Canada,

27(5), Black, L.F.,

& Hyatt, R.E. (1971). Maximal static respiratory pres

sures in generalized neuromuscular disease. American Review oJRespiralOJ), Diseases, 103,641-650. M.L. (1987). Intracranial hypertension: Implications for the physiotherapist. Physiotherapy Canada, 39, 360-366. Braun, S.R., Giovannoni, R.,

& O'Connor, M. (1984). Improving

the cough in patients with spinal cord injury. American Journal oj P ilfl ical Medicine, 63, 1-10.

& Deming, R.H. (1984). Early respiratory abnor

Cahalane, M.,

malities from smoke inhalation. .Iournal oj the A m eri can Med ical Associalion, 25, Cane, R.D., Shapiro, B.A., care

Davison, R. (1990). Case silidies in

me d ic ine (2nd cd.). St. Louis: Mosby.

Clauss, R.H., Scalabnni, BY, Ray, J.F., Ill,

Reed, G.E. (1968).

Effects of changing body position upon improved vemilatio!l

Circulalion, 37(SuppL 4), 214-217. & Wiles, C.M. (1985). Severe di aphragm weakness in multiple sclerosis. Thorax, 40, 631-632.

perfusion relationships.

Cooper, C.B., Trend, P.S.,

Curran, FJ. (1981). Night vent.ilation

REVIEW QUESTIONS

body respirators for pa

tients in chronic respiratory failure due to late stage muscular

Curran, F.J.,

& Colbcr!, A.P. (1989). Ventilator management in

Duchenne muscular dystrophy and postpoliomyelilis syn

\P{''''IfU/f

drome: twelve years' experience. Archives of Physi cal

morbid

musculoskeletal trauma, head

spinal cord

injury, and burns.

Dean, E, (1985). Effect of body position on pulmonary function.

65, 613-618.

Dean, E.

ment interventions to the underlying

Cardiopulmonary development. In B.R. Bonder

&M.B.

ology of each of the above conditions in the criti the rationale for

your choice.

Medi

cine and Rehabilila/ion, 70, 180-185. Physical

2. Relate cardiopulmonary

cally ill patient and

Gnd Rehabilitation,

62.

describe the

of cardiopulmonary dysfunction neuromuscular

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dystrophy.

1. With respect to critically ill lowing

& Chapman, WF (1990). Cough

enhnnced mucus clearance in the normal lung. Journal

the effects of restricted mobility,

recumbency, extrinsic factors related to the patient's

(Eds.). Philadelphia: FA Davis.

Dean, E. (l994b). Invited commentary on "Are incentive spirom etry, intermittent positive pressure breathing, and deep breathing exercises effective in the prevention of postopera p ul m o n a r y c o m p l i c a t i o n s a f t e r u p p e r a b d o mi n a l P

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& Lunsford, RR, (1981). Respiratory

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Madill,

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Mackenzie, D.F. (Ed.). (1989). Chest physiolhempv in the in ten

Marsh, H.M. (1977). Improved oxygenation in patients with acute respiratory failure: The prone position. American Review

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of Respi ralOl y Disease, 115(4),559-566.

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Dureuil, B., Viires, N., & Cantineau, J.P. (1986). Diaphragmatic contractility after upper abdominal surgl'l'y . Joumal ofl\pplied PhysioioRY.

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Gross, D. (1980). The efleet of training on strength ancl endurance

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Pardy, R.L., & Leith, DE (1984). Ventilatory muscle training.

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I.

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Review of ReSI) i ralOr y Diseases, 129. 1 82-184.


Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure Elizabeth Dean

KEY TERMS

Acute lung injury

Respiratory failure

Adult respiratory distress syndrome

Sepsis

Multiorgan system failure

Shock

Perioperative complications

INTRODUCTION

physiological deficits in these complex conditions is

The purpose of this chapter is to describe some com

the basis for efficacious management in addition to re

mon complications seen in critically ill patients. Com

ducing the risk of an untoward treatment response and

plications arising from the following conditions are

preventing worsening the patient's condition.

included: respiratory failure, surgery, acute lung in jury and adult respiratory distress syndrome, shock, sepsis, and multiorgan system failure. Second, the im plications for cardiopulmonary physical therapy are presented. Complications add further complexity to

RESPIRATORY FAilURE Metabolical Dysfunction

the diagnosis of the multiple factors contributing to

The range of complications associated with respira

impaired oxygen transport and to the challenge of pre

tory failure that can further impair tissue oxygenation

scribing effective treatment. Understanding the patho

are described in the box on p. 619. The metabolical 617


618

PART VI


consequences of these complications and impairment

(Fenwick, Dodek, Ronco, Phang, Wiggs, and Russell,

of oxygen transport are lifc threatening for the pa

1990). This so-called pathological dependence of

tient. Thus prevention of their development is a prior

oxygen consumption on oxygen delivery occurs

ity. Should complications develop, however, early

when the cells are inadequately extracting and using

detection and definitive management becomes the

oxygen even in the presence of supranormal oxygen

priority if the patient is to survive.

delivery levels. This phenomenon is observed in pa

A hallmark of these complications is the impair ment of multiple steps in the oxygen transport path

tient with adult respiratory distress syndrome and shock (discussed later this chapter).

way, which adds to the complexity of management

Given physical therapy is one of the most meta

(Dantzker, 1991). The three major components of

bolically demanding rcu interventions (Dean, Mur

oxygen transport can be affected individually or in

phy, Parrent, and Rousseau, 1995; Weissman and

combination (i.e., oxygen delivery, consumption, and

Kemper, 1993), the physical therapist needs to be

extraction) (Pallares and Evans, 1992; Wysocki, Bes

able to calculate this safety margin to prescribe the

bes, Roupie, and Brun-Buisson, 1992).

type of treatment and its parameters (i.e., intensity,

In health the ratio of oxygen consumption to deliv

duration and frequency) such that treatment is maxi

ery is low (i.e., 23%, which ensures an over supply of

mally beneficial and associated with the least risk to

oxygen as a safety margin) (see Chapter I). This

the patient.

safety margin also ensures that most patients are able

The ultimate treatment outcome measures are

to recover from insults to the oxygen transport sys

markers of oxygen tissue metabolism (Dantzker,

tem. However, if the insult is extreme, such as that

1993; Nightingale, 1993; Pallares and Evans, 1992).

resulting from complications of respiratory failure,

In addition, hourly assessment of oxygen delivery,

surgery, acute lung injury and adult respiratory dis

consumption, and extraction provide the basis for di

tress syndrome, shock, sepsis, and multiorgan system

recting management of oxygen transport deficits.

failure, significant metabolical dysfunction secondary to tissue hypoxia can result (Guiterrez, 1991). The relationship between oxygen consumption

Pulmonary Dysfunction

and delivery has elucidated our understanding of he

Complications of the cardiopulmonary system can

modynamic and metabolical changes observed in

lead to respiratory failure (see box on p. 619) (Boggs

critical illness (Vincent, 1991). The phenomenon of

and Wooldridge-King, 1993; Civetta, Taylor, and

oxygen-delivery dependence of oxygen consumption

Kirby, 1988). Some of these relate to being mechani

occllrs when a patient's oxygen transport system is

cally ventilated. Certain technical problems related to

unable to supply sufficient oxygen to meet basal oxy

the cuffs used in conjunction with artificial airways

gen demand (Phang and Russell, 1993). Oxygen de

may occur (e.g., overinflation, distortion, and hernia

livery below 300 ml 02/min/M2 limits the oxygen

tion of the orifice of the tube). Mucous plugs can oc

diffusion gradient and reduces oxygen extraction and

clude the endotracheal tube or tracheostomy and im

utilization at the ceLlular level. This is termed the

pede ventilation. The common complications can be

critical/evel of oxygen delivery. When oxygen deliv

reduced if the tube is changed frequently and if mini

ery exceeds 300 ml/min/M2, oxygen consumption

mal amounts of air are used for cuff inflation.

does not depend on delivery. Thus the greater the de

Prolonged endotrach al intubation can result in la

livery in relation to consumption the greater the

ryngeal edema, ulceration, and fibrosis. Mechanical

safety margin. When oxygen transport is so severely

ventilation may also rupture a bleb on the surface of

compromised that oxygen delivery falls below the

the lung and produce a pneumothorax with rapid ten

critical level, anaerobic metabolism is triggered.

sion development. Chest tubes are inserted immedi

However, anaerobic metabolism may also be trig

ately to relieve the tension. Blebs occur when alveoli

gered at levels of oxygen delivery that exceed the

rupture, causing air to track to subpleural sites.

normal critical threshold for anaerobic metabolism


Mechanical ventilators can be a source of infection.

34

Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure

ated with some complications (see Chapter

Complications of Respiratory Failure

619

15). In

fection may lead to bacteremia and septicemia. Judi cious selection and application of any invasive proce

Life-threatening impairment of oxygen transport and tissue oxygenation

dure is warranted to minimize undue hazard. The presence of these catheters limits head and neck posi

Fluid ,md electrolyte imbalances

tions and requires mobilization be carried out cau

Cardiac dysrhythmias and hemodyn,lmic instability

tiously within the patient's hemodynamic tolerance.

Myocardial dysfunction Metabolical dysfunction

Acid-Base Abnormalities

Thromboembolism Neurological dysfunction

Any combination of acid-base imbalance may occur

Gastrointestinal dysfunction

either acutely or chronically during respiratory fail

Renal dysfunction

ure. Severe alkalemia associated with potassium and chloride losses may occur after mechanical ventila

Metabolical and blood sligar irregularities

tion and can precipitate serious cardiovascular and

Infection

15) (Petty, 1982). Significantly impaired oxygen delivery to pe

neurological complications (see Chapter

Nutritional deficits Complications of intubation and mechanical ventila

ripheral tissue may contribute to increased anaerobic

tion, including increased risk of infection

metabolism and metabolic acidosis (Fenwick, Dodek,

Complications of oxygcn therapy

Ronco, Phang, Wiggs, and Russell,

1990).

Fluid and Electrolyte Abnormalities T':L: physical therapist can help minimize this risk by

Fluid retention can occur with prolonged mechanical

not directly handling the ventilator attachments that

ventilation in a patient with no evidence of cardiac

communicate with the air flow channels. Condensation

failure. Pulmonary edema, weight gain, decreased pul

from the hose should not be drained toward the venti

monary compliance, and reduced oxygen transport are

lator or toward the patient. The physical therapist

common signs. Fluid overload is a common cause of

should be maskcd and gloved when connecting and

this fluid retention. Mechanically ventilated patients

disconnecting the patient to and from the ventilator.

are therefore usually maintained underhydrated. Be

Oxygen toxicity is a significant clinical complica

cause of a tendency for sodium retention and hence

tion of mechanical ventilation. Mechanical ventila

fluid retention, intravenous saline solution is kept to a

tors have precise oxygen controls to deliver the low

minimum. Humidifiers attached to mechanical venti

est possible inspired oxygen concentration needed to

lators are responsible for adding a considerable

maintain arterial oxygen tensions. Because of the ia

amount of water by absorption through the lungs.

trogenic complications of high FIo2 levels (i.e., deni trogen atelectasis and oxygen toxicity) excess oxygen above the patient's needs is never indicated other than short periods of hyperoxygenation before suc

Cardiac Dysrhythmias Cardiac dysrhythmias are a common complication of

tioning or in preparation for, during, and immediately

respiratory failure. In addition, patients in respiratory

1971; Shoe

failure tend to be older adults who as a group have a

after mobilization (Fell and Cheney, maker,

1984).

greater incidnce of dysrhythmias secondary to cardiac

Flow-directed pulmonary artery catheters (i.e.,

disease. Electrocardiographic monitoring is therefore

Swan-Ganz catheters), commonly used in the inten

essential for all patients requiring ventilatory assis

sive care unit (lCU) for monitoring patients who de

tance in addition to patients with overt or suspected

velop hemodynamic complications, are also associ

heart disease. Both atrial and ventricular tachydys


620

PART VI


rhythmias are seen in acute respiratory failure. Sinus

over the lower legs to minimize venous pooling and

tachycardia and premature ventricular contractions,

assist venous return (see Chapter 32). JOBST® and

however, are particularly common. With rapid lower

TED® stockings also may be applied over the feet

ing of arterial Pe02, ventricular fibrillation, or even

and legs to increase circulatory transit time in the de

death may occur.

pendent areas and reduce circulatory stasis.

In the presence of respiratory failure and in the ab sence of cardiac disease the management of cardiac dysrhythmias lies predominantly in the correction of

Myocardial Dysfunction

blood-gas abnormalities. Effective supportive man

As in any clinical situation, acute myocardial infarc

agement can usually be achieved with pharmaceutical

tion can occur during the management of acute respi

agents. Intravenous injection of lidocaine followed by

ratory failure. The risks are increased because pa

continuous infusion is useful in managing premature

tients in respiratory failure tend to be older and more

ventricular contractions, which may be the precursor

susceptible to positional hypoxemia. The probability

of potentially fatal tachydysrhythmias and cardiac ar

of heart failure and associated dysrhythmias is in

rest. Electrolyte replacement may also be required.

creased and significantly compounds the problems of

A thorough understanding of the clinical presenta

the patient in respiratory failure.

tion, electrocardiographic diagnosis, and correct man agement of cardiac dysrhythmias is fundamental to the optimization of physical therapy treatments in the

Gastrointestinal Dysfunction

ICU and minimizing any risk to the patient. Cardiac

Peptic ulcer is commonly associated with chronic

dysrhythmias resulting from any cause necessarily re

airway obstruction. The stress of respiratory failure

quire ongoing evaluation and therapy.

predisposes the patient to peptic ulceration. Pro

The physical therapist must be able to treat the patient optimally and safely within the restrictions of

found hemorrhage may occur and blood replace ment is necessitated.

any dysrhythmia in addition to other medical or sur

Gastric dilation may occur in patients who are re

gical conditions. The implications of the dysrhyth

ceiving mechanical ventilation. Gastric dilation is

mia on the patient's clinical presentation and for

best managed by means of a nasogastric tube and in

treatment selection and response must be recognized

termittent suction. Care must be exercised to avoid

by the physical therapist and considered in designing

hypokalemia and hypochloremia caused by excessive

the treatment plan.

gastric suctioning. Special care is also taken to avoid fecal impaction, particularly in the paralyzed patient. This risk can be reduced with suitable fluid balance,

Thromboembolism

mobilization, frequent turning in conjunction with ap

A high incidence of pulmonary thrombosis or em

propriate trunk and lower limb movements.

bolism exists in patients in acute respiratory failure. Early diagnosis and management of pulmonary thromboembolism have been greatly facilitated by the

Neurological Dysfunction

use of serial ultrasound procedures and scans. Physi

A close correlation exists between the state of con

cal therapy has a key role in preventing the develop

sciousness and the arteri 1 P02 and Pe02. In addition,

ment of t hromboemboli by p r o moting f r equent

changes occur in alertness, personality, memory, and

changes in position, specific bed exercises, particu

orientation with altered blood gases. Motor changes

larly of the lower limbs, and passive range of motion

also occur, including generalized or localized weak

exercises if indicated. It is essential that movement

ness, tremors, twitching, myoclonic jerks, gross

and repositioning are performed regularly to maxi

clonic movements, convulsions, and flaccidity. Neu

mize their cardiopulmonary protective benefits. Pneu

rological complications of respiratory failure must be

matic extremity cuffs apply pressure intermittently

differentiated from those of nonpulmonary origin.


34


The physical therapist must be aware of the spectrum

621

teredo The presence or absence of cyanosis may be an

of neurological complications that can result from

unreliable sign because peripheral cyanosis can occur

respiratory failure and recognize that apparent im

despite adequate arterial P02. Morbidity and mortality

provement of neurological signs may reflect im

has been reported to be reduced in patients with se vere respiratory failure and system involvement when

proved cardiopulmonary status.

Sllpranormal levels of oxygen delivery was achieved (Hayes, Yau, Timmins, Hinds, and Watson, 1993;

Renal Dysfunction

Waxman and Shoemaker, 1980; Yu, Levy, Smith,

The development of renal failure greatly compro

Takiguchi, Miyasaki, and Myers, 1993).

mises the chances of the patient's survival. Renal failure can result from gastrointestinal bleeding, sep sis associated with shock, drug-induced nephrotoxic ity, and hypotension, Urinary outputs are maintained with adequate fluid and diuretics, with care not to in duce pulmonary edema. Dialysis may need to be in

Common Postoperative Complications Hypoxemia

stituted if more conservative management fails

Hypercapnia

(Phipps, Long, and Woods, 1991). If dialysis is antic

Increased work of breathing

ipated, the physical therapist should review existing

Increased work of thc heart

treatment goals to mOdify treatment accordingly,

Fluid shifts and third spacing Fluid and electrolyte imbalances

POSTOPERATIVE COMPLICATIONS

Metabolic and blood sugar abnormalities Reduced blood volume



Respiratory failure in the postoperative patient is usu ally associated with a low Pao2 and a high Paco2. This situation is likely to be more common than generally appreciated. If the patient is in good general health and is free from underlying cardiopulmonary disease,

Reduced cardiac OUlput Reduced tissue perfusion and oxygenation Anemia Pain

recovery is usually rapid. Otherwise, more severe

Alveolar hypoventilation

complications and cardiopulmonary failure may result

Airway collapse

and progress to a life-threatening situation. The effects

Atelectasis

of surgery on oxygen transport and on the varioLls organ systems are described in Chapter 28. Common postoperative complications and their causes appear in the box at right and the box on p. 622.

Physiological shunting Ventilation and ped'usion mismatching Impaired mucociliary t ransport Mucus accumulation and stasis

Pneumonia

Hypoxemia

Thromboemboli

The most common postoperative complication is hy poxemia secondary to alveolar hypoventilation, re duced functional residual capacity (FRC), airway clo sure, and postsurgical atelectasis (Leblanc, Ruff, and

Pulmonary embolus Coaglliopathies Sepsis

Milic-Emili, 1970; Marini, 1984; Ray et aI., 1974).

Shock

Adequate oxygenation, however, can be present de

MlIltiorgan system failure

spite hypoventilation when oxygen is being adminis


622

PART VI


Factors Contributing to Postoperative Complications That Affect Oxygen Transport Pre morbid cardiopulmonary status Premorbid oxygen transp0l1 (aerobic) capacity Premorbid systemic disease Premorbid general health and immune status Smoking history Age and gender Lifestyle factors-nutlitional status. stress, work situation. family situation, psychosocial support system. and substance abuse Obesity Pregnancy Perioperative pain and anxiety Perioperative reduced arousal Perioperative reduced mobility Perioperative recumbency Perioperative medications (e.g .. narcotics) Perioperative nutritional deprivation Perioperative reduction in normal sleep quality and quantity Type of surgery Extent of physical manipulation and compression of lung parenchyma, phrenic nerves, diaphragm. and the heart Perioperative fever and increased oxygen consumptions Duration of surgery Position assumed during surgery Duration of static positioning during surgery Type. depth, and duration of anesthesia and sedation Use of an airway Use of mechanical ventilation Oxygen therapy Neuromuscular blockade Fluid loss and chest tube drainage Fluid accumulation and third spacing Infusion of blood products Site. number. and extent of incisions Dressings and binders Traction and splinting devices Placement of lines, leads, catheters. and monitoring devices Invasive monitoring equipment (e.g., Swan-Ganz catheter, Foley catheter, intracranial pressure monitor. central venous line, arterial lines, intravenous lines, and intraaortic balloon counter pulsation pump) Need for cardiopulmonary bypass machine Duration on cardiopulmonary bypass machine Infection


34

Comp,lic:�ti(ms, Adult Respiratory Distress Syndrome, Shock, Sepsis, and

Pain

these in addition to the effects of anesthesia, fre contributes to alveolar hypoventilation and

atelectasis after abdominal or thoracic surgery.

.....'''r
increase with the magnitude of the op

erative procedure and and the

of anesthesia required

premorbid risk factors. These abnor

malities observed in the

period are and

Rapid, shallow, and monotonous breathing may be spontaneously adopted by the patient to avoid pain and

623

System Failure

alveolar

FRC, and residual vol decreased in

minute ventilation is fa-

Because of the

alveolar ventilation is compromised by the in creased ratio of dead space to tidal volume. Further

crease in FRC (30% o r m o r e), c o m p liance is

more, in the absence of

vv"",-,a,,,"u,

breaths, coughs, and

atelectasis may develop in the underventilated portions of the

The ventilation-perfusion ratio

and therefore the work of

is in

creased, Hypoxemia secondary to transpulmonary shunting usually becomes maximal within 72 hours

is disturbed because blood flow to underventilated

after surgery, and often is completely resolved with

physiological shunting

conservative management within seven days. The

tends to may be

although Peo2

on the mode of 100% oxygen ad-

will

An abnormally

Low oxygen flows and low amounts of

monary pressure is then needed to reinflate these at

tend to be delivered via nasal cannulae. flows can deliver higher amounts of

electatic alveoli.

masks and masks with reservoir bags.

Pulmonary Embolism and Deep Vein Thrombosis

ial blood gases. The

embolism is a potentially life-threatening complication. Pulmonary embolism usually results from a thrombus forming in the veins of the lower limbs,

in the

atrium, or in the

tricle. Patients may be at risk if chronic heart failure or if nant, or

oral

ven

have varicose are

arter

always be taken into account when

preg

is selected to provide ade

quate oxygenation with

lowest oxygen concentra

tion possible. Based on the

assessment, arterial blood

gases, fluid and

balance, hemodynamic

status, and x-ray, a decision is made as to which hierarchy will opti

treatments on the

mize oxygen transport and what

rr""tr"""nh

The patient with a pulmonary thromboembolism

will be

used for each treatment.

usually has a sudden onset of

and mobilizing them wherever possible will

chest pain, and apparent

Occasionally,

maximize FRC and reduce closing volumes and

heart failure follows.

are often elevated.

hence enhance gas

P waves, and inverted T

bundle branch

waves may be seen. No abnormality may be noted on

to treatment because of this can b e discussed at

for and cir

Treatment consists of primary with

oxygenation of pe

ripheral tissues. Anticoagulants, such as

are

rounds and other medications should be considered so that the

is able to

.. nl",n'·r

f'"

more. Thus

even extreme body positioning will achieve more fa

infused intravenously to minimize further formation

vorable results

of thromboembolic substrates.

(1973;

and Geraghty Ray, and Reed, 1968; Oou-

Beynen,

and

1977;

Piehl and Brown, 1976).


Endoctracheal intubation and mechanical ventila

of lung volume, and gas

What even minimally

their lack of alertness which must be explained. If the patient is unable to

chest x-ray. culatory

and these

heart strain may be evidenced on ECG. Right

tion may be indicated if blood gases fail to

uniformly occur after anesthesia

and tissue dissection. The extent and duration of

with conservative management. The treatment ties for the ventilated patient before and during


624

PART VI


weaning are presented in Chapter 32. Special atten tion in the postoperative patient is given to the pul monary complications associated with diminished ability to move spontaneously, surgical pain, restric tions imposed by dressings and binders, diminished ability to cooperate, and to periodically hyperventi late the lungs. Facilitating mucociliary transport is a primary goal in these patients. Impaired mucociliary transport can be precipitated by alveolar hypoventilation, perhaps the most common cause of postoperative complica tions. Sufficient impairment can lead to mucous sta sis, airway obstruction, atelectasis, and infection. Multiple positions, including upright positions and 360-degree axial turns, and multiple position changes facilitates mucociliary transport. In the event of mu cous accumulation and difficulty in removing pul monary secretions, specific body positions are se lected to optimize postural drainage of the affected bronchopulmonary segments and to maximize alveo lar volume and ventilation. The addition of manual techniques can be detrimental in severely ill patients (Mackenzie, 1989; Poelaert, Lannoy, Vogelaers, Everaert, D ecruyenaere, Capiau, and Colar dyn, 1991), thus their use needs to be considered carefully. Suctioning may be most effective immediately be fore and after position changes. The appropliate oxy gen transport variables are monitored to assess treat ment outcome and minimally to ensure the patient who may be unstable is not deteriorating. If the pa tient begins to deteriorate, treatment is discontinued until the patient stabilizes. Why the patient deterio rated is determined so that a decision can be made as to whether treatment can be reintroduced, and if so, what modifications are indicated. Pain management is integral to the management of the surgical patient. Noninvasive and nonphannacologi cal pain control strategies need to be exploited for all surgical patients to augment or reduce the need for po tent analgesics especially narcotics. Chapter 28 de scribed some physical therapy pain control strategies for surgical patients that can be applied with modification to the patient with surgical complications. Of these, use of electrotherapy modalities, such as transcutaneous elec trical nerve stimulation, may be limited in the ICU be cause of electrical interference with monitoring devices.

Rest is prescribed as judiciously as treatment inter ventions to enable the patient to physiologically restore between and within treatments. This is particularly im portant for ICU patients who are hypermetabolical and have increased oxygen demands. Particular care must be observed in prescribing treatment threshold parame ters for these patients. Suprathreshold states can be as sociated with an inappropriate balance between oxy gen delivery and oxygen consumption such that the patient becomes compromised (e.g., hemodynamically unstable, cardiopulmonary distress is precipitated, or both). A greater volume of a mobilization stimulus, however, may be delivered to these patients with an in termittent mobilization regimen than with a single pro longed course of mobilization. Thus the benefits that would be accrued would be correspondingly increased. Prevention of thromboemboli is a major treatment objective and is best achieved with mobilization, body positioning, passive movements, and physical devices, such as pneumatic cuff devices and stockings, to aug ment low-dose anticoagulants in patients at risk. Pa tients who develop pulmonary emboli are treated medically and physical therapy needs to be corre spondingly modified to minimize oxygen consump tion until the embolus resolves and the patient is in no imminent danger. ACUTE LUNG INJURY ANI) ADULT RESPIRATORY DISTRESS SYNDROME

Acute lung injury results from damage to the alveolar epithelium (Gattinoni et aI., 1994). The extent of the damage reflects damage to the type I and type II alve olar cells. Damage to the type I cells results in alveo lar edema, atelectasis, and loss of lung compliance secondary to loss of structuraJ integrity of the alveoli provided by the type I alveolar cells. Damage to the type II cells also contributes to atelectasis and loss of lung compliance, but the mechanism relates to im pairment of the production of surfactant and pul monary fluid that covers the alveolar epithelium. Pulmonary edema refers to the accumulation of vascular fluid in the interstitial spaces and alveoli. In acute lung injury the mechanism of pulmonary edema involves increased water movement across the pul monary endothelial cells and increased permeability


34

Complications, Adult Re5ioirato:rv

and Multiorgan System Failure

625

of the endothelium to protein. This type of pulmonary

Acute lung injury is characterized as a clinical spec

edema is referred to as noncardiogenic pulmonary

trum of parenchymal cell dysfunction. Mild injury re

in ori

edema. Pulmonary edema that is

results from left ventricular failure. An increase

flects predominantly endothelial cell

and

noncardiogenic edema. Severe injury reflects a progres

in hydrostatic pressure damages the interstitial

sion to both endothelial and

spaces, which normally provide an effective barrier

and adult respiratory distress syndrome

between the pulmonary circulation and alveoli. The

clinical spectrum of acute lung injury and the clinical

critical distinction between the two

manifestations of mild and severe

of pul

pulmonary edema

monary edema is that

primarily involves the movement of water across the

alveolar or

of the edema

and

MILD AU

HYPOXEMIA

MILD

MILD O2 responsive

causes of ARDS include shock, severe trauma or in fection, overwhelming

and inhaled tox

ins. Increased vascular

that

response is a common feature.

MODERATE All

SEVERE All

Late ARDS

SIGNIFICANT

SEVERE

PEEP resp onsive

HH

non·PEEP responsive

SIGNIFICANT

SEVERE

PEEP responsive

02 or

to

ENDOTHELIAL CELLS INTERSTITIUM EPTHELIAl CELLS TYPE 1

PERMEABILITY tt

EDEMA

TYPE 2

METABOLIC DYSFUNCTION 1 +

METABOLIC DYSFUNCTION 4+

EDEMA ttt

EDEMA ttt

SLOUGHING

ttt

HYPERMITOSIS

SLOUGHING

tttt

METABOLIC

CONSOLIDATION

tttt

FIGURE 34-1 manifestations

and in

to the alveolar-capillary membrane. Some of the

ARDS

LUNG COMPLIANCE

insult to the

ARDS results from

of the

the amount of fluid accumulation.

of moderate in

jury falls between these two extremes.

pulmonary edema involves the movement of and water into the interstitial and alveolar

The are shown in

34-1. The clinical

alveolar capillary membrane, whereas noncardio

spaces. The clinical consequences reflect the location

cell dysfunction

the spectrum of acute

severe disease. (From Shapiro BA, Peruzzi WT: Changing review of the literature and suggest clinical correlates,


injury from mild to

inventilatator management: a

117:121-133,1991.)

626

PART VI

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Cm'e

Fluid seeps into the interstitial spaces and over

alveoli open and thereby optimizes gas transfer at

whelms the alveoli, leading to p u lmonary edema.

end e xpiration. Arterial oxygenation is usually im

Lung compliance and gas exchange are severely

proved with PEEP because the effect of shunting is

compromised. Thus the patient presents with severe

reduced and a given Fl02 tends to be more effective.

-

trates appear on x-ray. Arterial hypoxemia results pri

Although the Fl0 2 may be reduced, which reduces the possibility of oxygen toxicity, supranonnal oxygen

marily from underventilated but pelfused lung units

delivery can be beneficial in these patients (Bishop et

dyspnea and hypoxemia. Diffuse pulmonary infil

1993).

and right to left shunt. In this situation, hypoxemia is

aI.,

relatively refractory to increases in Fl0 . 2 Fibrinogen in the fluids leaking into the alveoli

of multiorgan system failure reduced.

contributes to fibrosis and reduction of lung compli

junction with arterial blood gases is essential for fol

Survival may be improved and frequency

Further monitoring of respiratory status in con

ance associated with ARDS. Increased lung surface

lowing the progress of the syndrome. In addition to

tension and alveolar collapse tend to result from an

the oxygen transport variables the principal parame

inactivation of surfactant with the accumulation of

ters monitored in ARDS are reduced lung compli

fluid in the alveolar spaces. Thus reduced lung com

ance, tachypnea, and the concentration of inspired

pliance produces

oxygen needed to maintain acceptable levels of the

a

significant decrease in FRC in the

arterial blood gases.

patient with ARDS.

48

The signs and symptoms of ARDS may take up to

ARDS is characterized by a major pathophysio

hours to be fully manifested. The prognosis for

logical restrictive component. Hence the principles of

survival of patients is

40%

to

60%.

Hypoxemia is a

principal feature of the syndrome, and results from a right to left shunt, whereby fluid-filled alveoli are in

management of restrictive lung disease can be effec tively applied. Changes in lung compliance and Fl0

2 requirements provide guidelines to treatment re

effectively ventilated. Hyperventilation and labored

quired, treatment response, and course of the syn

respiration can be expected in conjunction with hy

drome. Patients with ARDS require close monitoring

poxemia. Oxygen therapy has little effect in the pres

and often frequent treatments aimed at promoting op

ence of shunting. Hypercapnia is not usually a major

timal gas exchange because of the severity of the syn

problem in the ARDS patient.

drome and high incidence of mortality associated

The metabolical perturbations that can result in clude problems with oxygen delivery, consumption

,

with it. Special attention is given to body positioning to promote ventilation and perfusion matching and

and extraction as discussed previously. When oxy

mucociliary transport and to minimize the effect of

gen delivery falls below the critical level, anaerobic

restriction of diaphragmatic and chest wall excursion.

metabolism is triggered resulting in increased lactate

Some patients, for example, benefit from side lying

production. Elevated serum lactates are associated

in which excursion of the inferior hemidiaphragm is

with a poor prognosis.

favored. Other patients, however, seem to detel;orate from apparent restriction of the inferior lung in side

Principles of physical therapy management Intubation and ventilatory support are implemented if

lying. Each patient's condition and specific areas of lung involvement must be taken into consideration when prescribing a turning regimen. The effect of the

arterial blood gases are severely affected and rerspi

patient's body position on blood gases helps to estab

ratory distress worsened. An endotracheal tube can

lish a suitable regimen on a rational basis.

be placed t h r o u g h t h e n o s e o r mouth or a tra

The sitting position optimizes lung capacity. The

cheostomy can be performed. The tidal volume is set

use of a reclining chair at the bedside perhaps should

10

mUkg of the patient's body weight. The

be considered more often in the management of pa

patient usually establishes the respiratory rate, al

tients with acute lung inj u ry. Theoretically, the poten

though it may be rapid. A positive end expiratory

tial function of all lung fields will be benefited with

pressure (PEEP) of around 12 cm H20 maintains the

the lungs in a more upright position. Patients who are

at about


34


too unstable to tolerate upright positions may respond

627

tribute to intracellular digestion and calcium deposi

favorably to extreme body positions and the prone

tion. Once the lysosomes have ruptured and intracel

position (Albert, Leasa, Sanderson, Robertson, and

lular digestion is triggered, irreversible cell damage

Hlastala, 1987; Langer, Mascheroni, Marcolin, and

ensues, impairing oxygen extraction and uptake

Gattinoni, ] 988).

(Wysocki, Besbes, Roupie, and Brun-Buisson, 1992).

Severely affected patients may require neuromus

The pathology of shock and the effect on the res

cular blockade to reduce their oxygen demand and

piratory membranes of the mitochondria follow a

enable them to respond to ventilatory assistance more

similar course regardless of cause. Swelling of the in

effectively. Handling and positioning patients on neu

terstitial tissue disrupts the perfusion of the pul

romuscular blockade requires particular care because

monary capillaries. Congestive atelectasis and pul

these patients lack muscle tone to protect their mus

monary edema ensue. In the advanced stages, hyaline

cles and joints. Rotating beds can be extremely bene

membrane changes and pneumonitis may occur.

ficial for these patients who are either too hemody namically unstable or difficult to turn manually. These mechanical beds slow ly rotate side to side


through an arc, thus changing the patient's body posi

Foremost, the physical therapist must be knowledge

tion continuously (Gentilello et aI., 1988; Pape,

able about the relationship of oxygen delivery and

Regel, Borgman, Sturm, and Tacherne, 1994).

consumption in these patients, as well as the implica tions of the pathophysiological processes on oxygen extraction. The type of treatments and their pat'ame

SHOCK

ters are based on a careful analysis of oxygen trans

Common causes of shock include hypovolemia, sep

port variables. Treatments are prescribed within the

ticemia, heart failure, and direct insult to the central

patient's safety margin. Physical therapists in the

nervous system. Some of the classical features of

ICU must also be knowledgeable about the signs and

shock are hypotension, reduced cardiac output, tachy

symptoms associated with impending and frank

cardia, hyperventilation, diaphoresis, pallor, confu

shock. By recognizing and understanding the compo

sion, nausea, and incontinence. Inadequate tissue per

nents of the different types of shock and the effect on

fusion results in extracellular acidemia and loss of

the cardiopulmonary system, the physical therapist

potassium ions from the cells. The pulmonary blood

can better prescribe a rational treatment plan for the

vessels constrict in response to hypoxemia, which

short- and long-term management of the patient.

tends to increase pulmonary artery pressures.

Although physical therapy may be limited in re

Failure of cellular function secondary to shock can

versing the signs and symptoms of shock, physical

result from a deficiency of substrate for energy pro

therapy can help to restore and maintain optimal car

duction, a reduced ability to use the nutrients for en

diopulmonary function, reduce the risk of complica

ergy production, or both. The pathophysiological

tions associated with immobility and with recum

mechanisms responsible include hypoperfusion of the

bency, and maintain physical status at the best

tissues, hormonal and metabolical cellular changes,

possible optimal level during the episode and in an

and the toxic effects of the metabolical changes. Col

ticipation of the patient's recovery. The primary ob

lectively, these produce cellular damage. With hy

jective, however, is to minimize oxygen demand. A

poperfusion and decreased oxygen delivery and other

minimal objective is not to worsen the patient's con

nutrients, the production of adenosine triphosphate is

dition by imposing excessive metabolical demand.

reduced. The maintenance and repair of cell mem

This is the case in patients whose oxygen delivery is

branes is disrupted, resulting in swelling of the endo

approaching the critical level with respect to oxygen

plasmic reticular and eventually the mitochondria.

consumption dependence. Excessive demands in

Persisting cellular hypoxia contributes to rupture of

these patients can be life threatening.

the lysosomes, which releases enzymes that con

Patients in shock are usually unresponsive. The


PART VI

628


course of the shock episode is often complicated with

The fluid is drained after about 30 minutes. Car

the sequelae of immobility and recumbency. The spe

diopulmonary physical therapy is most effective if

cific goals related to optimization of cardiopul

performed after the fluid has been completely drained

monary and musculoskeletal function and prevention

from the peritoneum. After drainage of the fluid the

of further complications associated with cardiopul

diaphragm is at a more optimal functional length for

monary function in particular are priorities.

respiration, which potentially can improve treatment

Specific concerns for the patient in shock include

response. If hemodialysis is indicated, the patient is

the need for short, efficacious treatments and avoid

connected to a unit that dialyzes the blood externally.

ance of unnecessary fatiguing of the patient. Treat

This process takes several hours and is usually re

ment goals are therefore critically appraised and pri

peated every few days.

oritized throughout each day to target physical

In the end stages of shock, as for other severely ill

therapy treatment only to the very immediate and es

medically unstable patients, physical therapy may

sential needs of the patients. Prudent patient position

constitute primarily supportive care and comprehen

ing is a priority because of the relative immobility

sive monitoring.

and reduced spontaneous movement observed in these patients and recumbency. Approximations to the upright position (i.e., head of bed up and foot of

SEPSIS AND MULTIORGAN SYSTEM FAILURE

bed down) can augment sympathetic stimulation and

Sepsis is the response to bacteremia or other by prod

improve hemodynamic status and reduce sympath

ucts of bacteria in the blood. The clinical features of

omimetic medications. In addition, this position sim

sepsis include fever, tachycardia, tachypnea, and res

ulates the upright sitting position (although not per

piratory alkalemia. Metabolical abnormalities are

fectly) with re spect to i t s beneficial effects on

also a common feature of sepsis. Sepsis is the most

pulmonary and cardiac function.

common predisposing factor contributing to multior

Late stages of refractory shock leading to renal

gan system failure (MOSF), which typically involves

failure may necessitate dialysis. In peritoneal dialysis

failure of more than two organ systems (Carrico,

a liter of fluid with a high osmotic fluid content is in

Meakins, and Marshall,

jected into the patient's abdomen to draw fluid out.

34-1 shows the major organs affected and their clini-

1993; Vincent, \993). Table

TABLE 34-1 Presentation of Multiorgan System Failure CLIN[CAL PRESENTAnON

SYNDROME

Lungs

Hypoxemia, lung compliance, diffuse infiltrates

Acute lung injury/AROS

Kidneys

Creatine> 2 mg/dl

ORGAN

Urine output Liver

<

Oliguric ARF

500 m1l24 hr

Urine output> 500 m1l24 hI'

Nonoliguric ARF

Bilirubin 2 mg/dl, SGOT and LOH

Jaundice

Intractible hyperglycemia or hypoglycemia

Hepatocyte failure

Cholecystitis

Acalculous cholecystitis

Gut

Upper gastrointestinal bleed

Stress ulceration

Coagu lation

Thrombocytopenia, prolonged PT and PTT

Hypofibrinogenemia DIC

Heart

Hypotension, Cl

Heat1 failure

CNS

Response only to painful stimuli

Obtundation

Modified from Civetta.

J.M., Taylor, R.W., &

ARF.

SCOT.

acute renal failure;

coagulalion;

PT.

Kirby,

R.R. (1988).

Critical care. Philadelphia:

serum glutamic oxaloacetic transaminase;

prothrombin time;

PIT.

partial prothrombin time;

LDH.

C/, c ardiac

index


JB Li ppi ncott

lactate, dehydrogenase;

DIC,

.

disseminaling intravascular

34


cal manifestations (i.e., pulmonary, gastrointestinal,

629

fective Floz. Even though the patient wi II likely bene

hepatic, renal, cardiovascular, hematological, and

fit more from some positions than others, frequent

central nervous systems). The cascade of pathophysi

body position changes, preferably 360-degree turning

ological features of this MOSF is believed to be pre

regimen, are still necessary to avoid the sequelae of

cipitated by mUltiple mediator systems. The release

static body positioning. Semi-prone positions can

of these mediators impairs oxygen delivery and uti

substitute well for full prone positions if the patient is

lization of oxygen by the cells. Thus the supply of the

too hemodynamically unstable. Semi-prone positions

major energy source to the cell, adenosine triphos

may be tolerated better by the patient and may be

phate, is reduced which leads to structural and func

safer. Even though hourly position changes may not

tional damage of the various organ systems. The mor

be feasible in these severely ill patients, prolonged periods in a static position (more than 2 hours) is

tality rate ranges from 60% to 80%. Conditions that predispose a patient to MOSF in clude sepsis, overwhelming infection, multiple

deleterious to the patient. Thus a balance between these two concerns must be achieved.

trauma and tissue injury, inflammation, and tissue

Promoting optimal mucociJiary transport remains a

perfusion deficits. Patients who are older, have

priority even in the absence of secretion accumula

chronic diseases, are immunosuppressed or have a se

tion. Frequent position changes and numerous posi

vere initial presentation have an increased risk of fail

tions ensure pulmonary secretions are continually being redistributed to prevent accumulation and en

ure and mortality.

hance removal. Should postural drainage be indicated, these positions may need to be modified. Head-down


positions in particular may not be tolerated well.

The patient with sepsis and MOSF, like the patient in

Based on a careful assessment, the relative benefits of

shock, is gravely ill and unlikely to be able to cooper

superimposing manual techniques must be established

ate with treatment. The principles for management

in that these procedures are associated with increased

are comparable with those for managing the patient

metabolical demand to which the patient is not readily

in shock, however, oxygen delivery is likely to be

able to adapt. Increasing the oxygen demand of these

consistently compromised in these patients. If oxygen

patients may worsen their condition.

delivery is critically low, oxygen consumption de pends on oxygen delivery and the patient is in of metabolical acidosis (see Chapter

a

state

I). In this situa

SUMMARY

tion, where oxygen delivery is compromised to the

This chapter presents several major complications

point of not meeting tissue oxygen demands, the goal

that occur secondary to various conditions in the in

of treatment is to maximize oxygen delivery (Bishop

tensive care unit. Complications add significantly to

et aI., 1993; Yu, Levy, Smith, Takiguchi, Miyasaki,

the complexity of the physical therapy diagnoses of

and Myers, 1993) and minimize oxygen demand so

the patient'S underlying problems with respect to

that oxygenation of vital organs is threatened to the

oxygen transport and cardiopulmonary management.

least extent. Thus the physical therapist must estimate

The complications highlighted in the chapter include

the oxygen reserve capacity (i.e., the balance between

those that impair multiple steps in the oxygen trans

oxygen demand and oxygen) in every assessment to

port pathway and hence jeopardize metabolism at the

select optimal treatment, which is associated with the

cellular level. This sequence of events is most fre

least risk. Treatments are selected to improve the effi

quently associated with the complications of respira

ciency of oxygen transport and utilization a n d

tory failure, surgery, adult respiratory distress syn

thereby reduce the work of the heart and o f breathing.

drome, shock, sepsis, and multiorgan system failure.

Above all, treatment should not worsen the patient's

Physical therapy treatments in critical care areas

oxygen transport status. Selective body positioning

are typically short, frequent, and should always be ef

can augment oxygen transport and maximize the ef

ficacious. Patients with the complications, however,


630

PART VI


are usually severely compromised and often unable to cooperate with treatment necessitating particularly short and frequent sessions. Because of the severity of illness, patients with the complications described often require treatments that are more passive (i.e., stress the oxygen transport system minimally, thus are lower on the physiological treatment hierarchy). These patients require frequent and comprehensive monitoring (often several times daily) of their oxygen transport capacity (i.e., the relationship between oxy gen delivery and consumption, and oxygen extrac tion, to establish if and when treatment is indicated, and the specific parameters of treatment. If a patient is thought to be too unstable for treatment at a given time, continued monitoring of her or his status is es sential so that small windows of opportunity can be exploited during stable periods. During periods of monitoring rather than active treatment intervention, the physical therapist continues to have an impoltant role in recommending body positions and frequency of body position changes so that these can yield the

manual for Cane, R.D.,

critical care medicine ( 2nd ed.), St. Louis: Mosby. Carrico, C.J. , Meakins, 1 ,L.,

&

J.e. (1993),

Marshall,

Multiple

organ failure syndrome, The gastrointestinal tract: the motor of MOF. Archives of Surge/y, 121, 197-208. Civetta, 1.M., Taylor, R,W.,

&

Kirby, R.R. (1988), CrilicaL care.

Philadelphia: 18 Lippincott. Clauss, R.H., Scalabrini, BY. Ray,

1.F, III, & Reed,

G.E. (1968).

Effects of changing body position upon improved ventilation perfusion relationships. Circulatioll, 37(Suppl. 4), 214-217. Dean, E" Murphy, S., Parrent, L.,

&

Rousseau, M. (1995), Meta

bolic consequences of physical therapy in critically-ill patients. Proceedings of the World Confederation of Physical Therapy Cogress, Washington, De. Dantzker, D.R. (1991). Cardiopulmonary critical care (2nd ed.). Philadelphia: WB Saunders. Dantzker, D.R. (1993). Adequacy of tissue oxygenation, Critical Care Medicinc, 21, S40-S43. Douglas, W.W., Rehder, K., Beynen, FM., Sessler, A.D.,

&

Marsh, H,M, (1977), Improved oxygenation in patients with acute respiratory failure: the prone position, American Review of Respirato/y Disease, 115, 559-566. Fell,

greatest benefit to oxygen transport.

& Wooldridge-King, M. (1993). AACN procedure critical care (3 rd ed.). Philadelphia: WB Saunders. Shapiro, B.A., & Davison, R. (\990). Case sludies ill

Boggs, R.L.,

T, & Cheney, F W. (J 971),

Prevention of hypoxia during en

dotracheal suction. Annals of Surgery, 174, 24-28. Fenwick,

l,e.,

D odek, P.M., Ronco, 1.1., Phang, P.T" Wiggs, B"

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Russell, 1 , A. (1990), Increased concentrations of plasma lactate

REVIEW QUESTIONS

predict pathologic dependence of oxygen consumption on oxy

1. Describe the complications associated with respi

gen delivery in patients with adult respiratory distress syn drome, loumal of Crilical Care, 5, 81-86,

ratory failure. 2. Describe the implications for cardio ulmonary physical therapy of respiratory failure, surgical complications, acute lung injury, adult respira tory distress syndrome, shock, sepsis, and multi

Gattinoni, L., Bombino, M., Pelosi, P., Lissoni, A., Pensenti. A.,

R., &

Fumagalli,

Tagliabue,

M,

Lung structure and function in

different stages of severe adult respiratory distress syndrome, loumal of the American MedicaL Association, 2 71 , 1772-1779, Gentilello,

L,

Thompson, D.A., Tonnesen, A,S" Hernandez, D" Ka

padia, A,S., Allen, S.1., Houtchens, B.A.,

organ system failure.

Effect of a rotating

bed

& Miner, M.E. (1988),

on t he incidence of pu I monary complica

tions in critically ill patients. Crilica! Care Medicine, 16,783-786. Gutierrez, G. (1991). Cellular e nergy metabolism during hypoxia.

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Phipps, W.J., Long, B.e., & Woods, N.F. (Eds.). (1991). Medical surgical nurs ing : conce"ls and clinical practice (4th ed.). St.

Louis: Mosby.

100-108 Wolff, R,K., Dolovich, M.B., Obminski, G., & Newhouse, MT (1977). Effects of exercise and eucapnic hyperventilation on

Piehl, M.A., & Bcown, R.S. (1976). Use of extreme position changes in acute respiratory failure. Critical Care Medicine, 4(1),13-14

bronchial clearance in man, Journal oj Applied Physi olo gy 43, ,

46-50. Wysocki, M., Besbes, M., Roupie, E" & Brun-Buisson, e. (1992),

Poelaert, 1., Lannoy, B., Vogelaers,D., Everaert, 1., Decruyenaere, J., Capiau, P., & Colardyn, F. (1991). Influence of chest phys iotherapy on arterial oxygen saturation. Acta Anaesthesiologica Be/gica, 42, 165-170.

Modification of oxygen extraction ratio by change in oxygen transport in septic shock. Chest, 102,221-226. Yu, M., Levy, M.M., Smith, p" Takiguchi, SA, Miyasaki, A" & Myers, S.A. (1993). Effect of maximizing oxygen delivery on

Ray, J.F., [[[, Yost, L., Moallem, S., Sanoudos, G.M., Villamena,

morbidity and mortality rates in critically ill patients: A

P., Paredes, R.M., & Clauss, R.H. (1974). Immobility, hypox

prospective, randomized, controlled study. Crilica/ Care Medi

emia, and pulmonary arteriovenous shunting. Archives oj

cine, 21,830-838.

Surgery, 109, 537-541.


Care oJth

PART

VII

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases


The Neonatal and Pediatric Patient

Victoria A. Moerchen Linda D. Crane

KEY TERMS

Bronchopulmonary dysplasia

Hyaline membrane disease

Chest physical therapy with

Patent ductus arteriosus Pediatric cardiac rehabilitation

infants/children Childhood asthma

Pediatric pulmonary rehabilitation

Cystic fibrosis

Pulmonary development

Endocardial cushion defect

Transitional circulation

Handling for ventilation

Trunk-ventilation interaction

INTRODUCTION

(3) present principles and precautions of direct respi

Pediatrics entails a "special" application of cardiopul

ratory care; and (4) incorporate these principles into

monary physical therapy. This chapter stresses that

suggestions for practice.

cardiopulmonary development and its related vulner

This chapter begins with a brief description of crit

abilities form the basis for cardiopulmonary practice

ical events and important characteristics of cardiac

with neonatal and pediatric patients.

and pulmonary development. Relevant diagnoses are

The objectives of this chapter include to: (l) re

then presented to build onto this developmental per

view cardiopulmonary development and related vul

spective and to stress that cardiopulmonary pathology

nerabilities; (2) relate developmental pathologies to

and ventilatory compromise are often related to de

issues of adequate ventilation and oxygen transport;

velopmental vulnerabilities. Finally, treatment ap 635


636

PART VII


proaches are described, including pediatric cardiac

men ovale allows right-to-left blood flow through the

rehabilitation, pulmonary care for neonatal and pedi

atria, bypassing the lungs (Yao, 19H3). Left ventricular

atric patients, pediatric pulmonary rehabilitation, and

output (LVO) is well-oxygenated blood that then enters

developmental motor approaches for trunk and venti

the ascending aorta and flows to the brain and upper body. The ductus arteJiosus similarly allows the lungs

latory muscle function. A knowledge of cardiopulmonary development,

to be bypassed, as most of the right ventricular output

congenital and d evelopmental cardiopulmonary

(less well-oxygenated than the LVO) flows to the de

pathology, and pediatric cardiopulmonary treatment is

scending aorta and from there to the lower body.

essential for any therapist serving children. Most pedi

Fetal blood flow to the lungs is minimal, secondary

atric patients require ongoing attention to respiratory

to high pulmonary vascular resistance during fetal cir

function, whether as a primary focus of physical ther

culation. Only 10% to 12% of evo goes to the lungs

apy or as an inherent aspect of motor development.

(Koff, 1993; Phelan, Olinsky, and Robertson, 1994),

This chapter is relevant to therapists who perform di

with the function of nourishing the developing lung

rect cardiopulmonary care and to therapists who incor

tissue rather than providing gas exchange.

porate a cardiopulmonary awareness into developmen tal motor therapy.

Neonatal circulation Adult-like circulation occurs at or shortly after birth, with separation from the placenta and ventilation of

CARDIOPULMONARY DEVELOPMENT

the lungs resulting in closure of the ductus venosus,

The application of cardiopulmonary physical therapy

foramen ovale, and ductus arteriosus. This process,

to infants and children requires a special understand

referred to as transitional circulation, occurs early in

ing of developmental cardiopulmonary anatomy and

neonatal life and increases the efficiency of oxygen

physiology. Knowledge of normal development and

uptake and transport (Heyman and Hanley, 1994;

its inherent points of vulnerability will help the

Rudolph, 1970).

reader understand some of what is known about car diopulmonary pathology in pediatric patients.

The initiation of breathing and the removal of lung fluid increases pulmonary blood flow. Whereas fetal circulation was characterized by high pulmonary vas cular resistance and low systemic resistance, separa

Cardiac Development

tion from the placenta causes a rise in systemic resis

Differences in fetal and neonatal gas exchange ac

tance and a decrease in pulmonary vascular resistance.

count for differences in the anatomy and physiology

As this shift in relative pulmonary and systemic resis

of fetal and neonatal circulation. A basic review of

tances occurs, sites of intercommunication (shunts)

developmental circulation is essential for discussion

close, and the ventricles shift from working in parallel

of congenital heart defects and the role of pediatric

to working in series (Heyman and Hanley, 1994).

Closure of Foramen Ovale. The increased left atrial

cardiopulmonary physical therapy.

pressure that occurs during transitional circulation re

Fetal circulation

sults in apposition of the valve of foramen ovale

Placental oxygenation is a major characteristic of

against the interatrial septum, functionally closing this

fetal circulation. Additionally, in fetal circulation

site of fetal circulatory shunting (Rudolph, 1970). In

blood flow through the right and left sides of the

most infants, anatomical closure occurs 2 to 3 months

heart occurs in parallel, such that cardiac output is ac

later (Emmanouilides and Baylen, 1988; Yao, 1983).

tually combined ventricular output (eVO) (Heyman

Closure of Ductus Arterioslls. Functional closure or

and Hanley, 1994). This is possible as a result of

constriction of the ductus arteriosus occurs postnatally

shunts in fetal circulation (Parks, 1988).

within the first IS to 72 hours in response to increased

Two points of shunting during fetal circulation are at

arterial oxygen saturation (Daniels, Hopman, Stoelinger,

the foramen ovale and the ductus arteriosus. The fora

Busch, and Peer, 1982). Anatomical closure of ductus


35


637

arteriosus occurs by 2 to 3 weeks in most term neonates

diaphragm of a newborn has fewer type I (high oxida

(Rudolph, 1970). It is important to note that the respon

tive) muscle fibers (25% compared with 50% in adult)

siveness of the ductal smooth muscle to arterial oxygen

(Muller and Bryan, 1979). This difference predisposes

tension and to endogenous prostaglandins is impacted

an infant to earlier diaphragmatic fatigue when stressed.

by gestational age (Pack, 1988; Yao, 1983).

A biomechanical difference between the infant and child is the circular and horizontal alignment of the ribs and the concomitant horizontal angle at

Pulmonary Development

which the diaphragm inserts on the ribs during new

Structural and functional characteristics of pulmonary

born and early infant chest development (Massery,

development in infants and children are significant

1991; Muller and Bryan, 1979). This, along with the

because they may contribute to aspects of respiratory

more cartilaginous nature of the rib cage, results in

vulnerability (Muller and Bryan, 1979).

less efficient chest wall mechanics. The result, again, is increased work to breathe. (See Chapter 37 for a

Newborn respiration

more complete discllssion of chest development).

The pulmonary anatomy of t h e term i n f a n t i s markedly different from the adult but also different

Respiration in the child

from the child. An infant's airways are narrower from

Two residual strllctural differences exist beyond the

the nares to the terminal bronchioles. This presents a

newborn period and have potential implications for

point of pulmonary vulnerability because a smaller

pulmonary vulne rabili ty in the child. First, the some

diameter airway is more easily obstrllcted by mucus,

what horizontal angulation of the ribs persists unti I

edema, foreign objects, and enlarged lymphatic tis

approximately 7 years of age and results in less effi

sue. The infant also has a high larynx (Laitman and

cient chest wall mechanics (Muller and Bryan, 1979).

Crelin, 1980). Although this position of the larynx

Secondly, lymphatic tissue (especially adenoids)

enables the newborn to breathe and swallow simulta

grows rapidly until about 6 years of age (Sinclair,

neously, it may also contribute to predominant pat

1978) and can continue to be a potential source of

terns of infant nasal breathing, which can result in in

upper airway obstruction.

creased work to breathe during any compromise of

As infants and children grow and develop, how ever, most structural and functional disadvantages

the nasal airway. Even without airway compromise, the work of

disappear. An aspect of growth and development that

breathing is increased during the neonatal period.

can be protective for infants and younger ch i ld re n is

The initial low compliance of the newborn's lungs

alveolar multiplication. This begins in the rirst year

requires increased effort for ventilation, which re

of lire and continues until approximately 8 years of

sults in a high rate of respiration and increased oxy

age (Blackburn, 1992; Thurlbeck, 1975).

gen consumption. Although the process of transitional circulation al lows more efficient O2 transport in the neonate than in the fetus, gas exchange in the newborn is still

Cardiopulmonary Considerations in the Preterm Infant

somewhat inefficient because of immature alveolar

All of the cardiopulmonary structural and functional·

structure and function. The surface area for gas ex

characteristics of neonates that have been previously

change is 1120 that of an adult (Johnson, Moore, and

discussed apply to the premature infant. Additionally,

Jefferies, 1980), and the diffusion distance across the

there arc signi["jeant gestationa l characteristics and as

alveoli-capillary membrane is increa sed as a result of

pects or cardiopulmonary vulnerability that are more

thick alveolar walls (Blackburn, 1992).

pronounced and create more problems in premature

Functional characteristics of infant pulmonary de

infants Cfable 35- I).

velopment are also significant to understanding possi

Recall that the transitional circulation of a term

ble contributions to pulmonary distress in infants. The

newborn includes a decrease in pulmonary vascular


638

PART VII


TABLE 35-1 Factors Contributing to Cardiopulmonary Dysfunction in the Premature Infant* ANATOMICAL

PHYSIOLOGICAL

Capillary beds not well developed before 26 weeks' gestation

Increased pulmonary vascular resistance leading 10

Type II alveolar cells and surfactant production not mature

right-to-Ieft shunting

Decreased lung compliance

until 35 weeks' gestation; elastic properties of lung not well developed; lung space decreased by relative size of the heart and abdominal distention Decreased responsiveness of the ductus arteriosus to oxygen

Left-to-right shunting

tensions; delayed ductal closure Type I, high-oxidative fibers compose only 10% to 20% of

Diaphragmatic fatigue: respiratory failure

diaphragm muscle Highly vascular subependymal germinal matrix not resorbed

Decreased or absent cough and gag reflexes; apnea

until 35 weeks' gestation, increasing the vulnerability of the infant to hemorrhage Lack of fatty insulation and high surface area to body-weight ratio

Hypothermia and increased oxygen consumption

*Modified from Crane, L.D. (J 995). Physical Therapy for the Neonate with Respiratory Disease. In S. Irwin & lS. TeckJin (Eds.).

Cardiopulmonary physica/therapy. St. Louis, Mosby.

resistance over the first day. In preterm infants, how

Most significantly, the immature status of car

ever, lung immaturity and abnormal surfactant func

diopulmonary anatomy in preterm infants predisposes

tion (Jobe, 1988) may result in retained high pul

them to h ypoxia under any conditions that require in

complia nce),

creased oxygen (Blackburn, 1992). Cardiopulmonary

hypoperfusion, and respiratory distress syndrome

pathophysiology and/or the stressors inherent to med

(Walther, Benders, and Leighton, 1992). Persistent

ical care often present challenges beyond the adaptive

pulmonary hypertension will reinforce persistent

capacities of these fragile little systems.

m o na r y

resistance

(p o o r

lung

right-to-Ieft shunting through the ductus arteriosus (Nude! and Gootman, 1983; Rudolph, 1980). In fact, respiratory distress syndrome (RDS) has been identi fied as the best predictor of prolonged patency of duc tus arteriosus (Milne, Sung, Fok, and Crozier, 1989). As the respiratory distress of the premature infant

COMMON PEDIATRIC DIAGNOSES The sections that follow present and discuss specific cardiac and pulmonary diagnoses. Common neuro muscular or developmental diagnoses that have in

improves with neonatal intensive care, cardiopulmonary

herent to them the risk of compromised respiration or

vulnerabilities can then occur in the opposite circulatory

associated cardiopulmonary disease are also dis

direction. Given the gestationally related responsiveness

cussed. The diagnoses presented are not all inclusive

of ductus arteriosus to oxygen, some preterm infants re

but merely represent an attempt to give the reader a

tain patency of the ductus even when pulmonary vascu

preliminary knowledge of underlying pathologies and

lar resistance falls (Archer, 1993). The result is Ieft-to

medical management of diagnoses commonly en

right shunting that may lead to congestive heart failure

countered in the practice of pediatric cardiopul

(Nudel and Grootman, 1983; Parks, 1988).

monary physical therapy.


3S


639

TABLE 35-2 Common Pediatric Diagnoses and Associated Heart Defects DlAGNOSIS

HEART DEFECTS

Duchenne's muscular dystrophy

Cardiomyopathy (adolescence)

Fetal alcohol syndrome

Ventricular septal defect Tetralogy of Fallot Pulmonary value stenosis Patent ductus arteriosus

Friedreich's ataxia

Ventricular hypertrophy Congestive heart failure

HIV-l infection

Myocarditis Ventricular dysfunction

Juvenile rheumatoid arthritis

Pericarditis

Marfan syndrome

Aortic aneurysm AorticlMitral insufficiency

Noonan's syndrome

Dystrophic pulmonary valve (Pulmonary stenosis)

Prematurity

Patent ductus arteriosus

Trisomy 13 (Patau's syndrome)

Ventricular septal defect Atrial septal defect Patent ductus arteriosus

Trisomy 18 (Edwards' syndrome)

Ventricular septal defect Patent ductus arteriosus (large)

Trisomy 21 (Down syndrome)

Endocardial cushion defect Ventricular septal defect Atrial septal defect Tetralogy of Fallot

Turner's syndrome Williams syndrome

Coarctation of the aorta Supravalvular aortic stenosis Supravalvular pulmonary stenosis

Cardiac Diagnoses

the most common heart defect during the neonatal

Patent ductus arteriosus, endocardial cushion defects,

period (Musewe and Olley, 1992). In term newborns,

and tetralogy of Fallot are the cardiac defects dis

however, PDA accounts for 10% of congenital heart

cussed within the limits of this chapter. Additionally,

disease (Mitchell, Korones, and Berendes, 197 I).

Table 35-2 provides a summary of common develop

Gestational age, the presence of lung disease, the

mental diagnoses and their associated cardiac defects.

size of the ductus, and the direction of the shunt me d i a t e the clini c a l f e a t u r e s of P D A (Gr e e n e ,

Patent ductus arteriosus

Mavroudis, and Backer, 1994; Musewe and O lley,

Patent ductus arteriosus (PDA), already introduced as

1992). The preterm infant with very low birth-weight

a cardiopulmonary complication in preterm infants, is

will have the most extreme clinical picture. An infant


640

PART VII

Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases

obvious

of mitral valve regurgitation (Merrill et ai., 1994).

clinical presentation. Tachycardia, an ejection sys

For infants with complete ECD, early surgical repairs

or child with a large ductus will also have

an

tolic murmur, bounding peripheral pulses, increased

are indicated (Bender, Hammon, Hubbard, Muirhead,

respiratory distress, and poor feeding or poor weight

and Graham, 1982; Graham and Bender, 1980).

gain are the classical signs of PDA (Archer, 1993;

Tetralogy of Fallot

Greene et ai., 1994; Musewe and Olley, 1992). In the

(TOF) is named for its "tetrad" of

term infant, PDA may be more clinically silent, espe

Tetralogy of Fallot

cially when the ductus is small (Parks, 1988).

defects: ventricular septal defects, right ventricular

Medical management of PDA includes nonsurgi

outflow obstruction, right ventricular hypertrophy,

cal use of indomethacin or direct surgical closure of

and aortic override (Bove and Lupinetti, 1994; Pin

the PDA (Musewe and Olley, 1992).

sky and Arciniegas, 1990). A neonate with TOF will have symptoms dependent on the extent of right ven

Endocardial cushion defects and

tricular tract obstruction, which results in decreased

artrioventricular defects

pulmonary blood flow and the presence of right-to

Endocardial cushion defects (ECD) represent a spec

left shunting (Bove and Luppinetti, 1994). The clas

trum of defects characterized by malformation of the

sic picture is one of cyanosis, especially with crying

atrial septum, the mitral and tricuspid valves, and/or

(EmmanouiIides and Baylen, 1988; Pinsky and

the ventricular septum (Emmanouilides and Baylen,

Arciniegas, 1990).

1988). Combinations of these defects are categorized

In neonates, initial medical management may in

as complete, transitionaVintermediate, and partial, de

clude treatment of hypoxemia by pharmacologically

pending on degree of ventricular septal deficiency

maintaining patency or reopening the ductus arterio

(Merrill, Hoff, and Bender, 1994; Spicer, 1984). In

sus for additional pulmonary blood flow (Driscoll,

the complete fOlm of ECD, all of the structures are

1990; Freedom and Benson, 1992). The elimination of

deficient. In the partial form, only an atrial septal de

conditions that produce hypoxemia may also include

f e c t w i t h a cleft mit ral valve is present ( E m

pharmacological agents to increase systemic vascular

manouilides and Baylen, 1988; Merrill e t ai., 1994;

resistance and decrease myocardial contractility (Bove

Parks, 1988).

and Lupinetti, 1994). Surgical repairs are generally

T h e r e is marked variation in the underlying anatomy of this class of cardiac defects, such that

performed within the first year (Bove and Lupinetti,

1994; Starnes, Luciani, Latter, and Griffin, 1994).

clinical features are equally varied and difficult to in clusively summarize. In neonates with a complete de fect, heart failure may manifest in infancy. However, neonates with milder forms of this defect may not be

Pulmonary Diagnoses The section that follows provides a brief discussion

symptomatic until much later in development (Parks,

of common pulmonary disorders for which chest

1988). Additionally, endocardial cushion defects are

physical therapy is indicated. Additional physical

frequently associated with other cardiac defects (Em

therapy treatment is described later in this chapter.

manouilides and Baylen, 1988).

Hyaline membrane disease

Although the total incidence of endocardial cush ion defects in infancy is 1 % to 4%, the incidence in

The most common respiratory disorder in premature

infants and children with Down syndrome is 40%

infants is hyaline membrane disease (HMD) or infant

(Freedom and Smallhorn, 1992). In fact, in these chil

respiratory distress syndrome (IRDS or RDS). Occur

dren a complete ECD is the most common cardiac

ring almost exclusively in preterm infants younger

malformation (Spicer, 1984).

than 37 weeks' gestation, HMD results from lung im

Operative management of infants and children

maturity and an inadequate amount and regeneration

with ECD depends on the morphology of the defect,

of surfactant (Phelan et ai., 1994). Surfactant func

the degree of pulmonary hypertension, and the extent

tions to decrease alveolar surface tension and thus en


35


641

abies the neonate to stabilize terminal air spaces (Wal

with severe BPD (Berman, Katz, Yabek, Dillon,

lis and Harvey, 1979). Surfactant deficiency results in

Fripp, and Papile, 1986; Gerhardt, Hehre, Feller, Re

alveolar collapse and increased effort to breathe.

infenberg, and Bancalari, 1987). Right-sided heart

Clinical signs of respiratory distress resulting from

failure (cor pulmonale) is a common sequelae of this

HMO occur early (usually within I to 2 hours) and

disease, especially in the first few years. Addition

persist for at least 48 to 72 hours (Farrell and Avery,

ally, BPD survivors demonstrate an increased inci

1975). Respiratory failure is 'common in these infants,

dence of neurodevelopmental sequelae, including

necessitating oxygen therapy and assisted ventilation. Chest physical therapy (CPT) is commonly indi

cerebral palsy and general development delay (North way, 1979; Vohr, Bell, and Oh, 1982).

cated in the management of infants with HMO. There

Chest physical therapy is an important component

is usually a marked increase in airway secretions in

of the management of an infant with BPD. Airway

the "recovery" state of the syndrome (after approxi

clearance problems are common due to submucosal

mately 2 to 3 days), which is exacerbated by oxygen

and peribronchial smooth muscle hyperplasia, in

therapy and endotracheal intubation (Crane, 1981;

creased mucous secretions, oxygen therapy, and fre quent lower respiratory tract infections. Infants with

Finer and Boyd, 1978).

BPD also frequently have poor growth, which may be

Bronchopulmonary dysplaSia

a consequence of a higher resting V02, such that

As more preterm newborns survive neonatal respira tory distress, the prevalence of chronic lung disease or bronchopulmonary dysplasia (BPD) has increased

caloric needs are greater (Weinstein and Oh, 1981).

Transient tachypnea of the newborn

(Parker, Lindstrom, and Cotton, 1992). Although

Transient tachypnea (TTNB) is another neonatal

controversial, the etiology of BPD is usually linked

problem considered in the differential diagnosis of

with positive pressure ventilation and oxygen therapy

HMD/RDS. It is associated with delayed clearance of

in the treatment of respiratory distress during the

amniotic fluid from the lungs, results in early presen

neonatal period. The risk of BPD is highest in

tation of respiratory distress, and is most common in

younger, low-birth-weight premature infants (Abman

full-term and postterm neonates (especially if deliv ered by cesarean) (Avery, Garewood, and Brumley,

and Groothius, 1994). Northway, Rosan, and Porter's (1967) classic de

1966; Emmanouilides and Baylen, 1988). Chest

scription of BPD includes four pathological stages.

physical therapy is occasionally indicated for infants

The f irst stage invo lves s ymptoms si milar t o

with this problem, but TINB is uSllally self-limited.

HMD/RDS, but b y the fourth stage, BPD has pro gressed to include characteristics of chronic lung dis ease (Voyles, 1981).

Meconium aspiration syndrome Meconium is the content of fetal and newborn bow

Clinically, infants with BPD often present with

els. Although the cause of meconium passage is

rales, wheezing, cyanosis, hypoxemia, increased inci

highly debated (Bacsik, 1977), once meconium is

dence of lower respiratory tract infections, and abnor

present in the uterine environment the risk for aspira

mal chest radiographs by I month postnatally

tion is significant. It is generally accepted that meco

(Abman and Groothius, 1994). Medical management

nium aspiration most frequently occurs with the first

of BPD is primarily supportive. Long-term oxygen

postnatal breaths of term or postterm infants (Gre

therapy is often necessary for infants who exhibit

gory, 1977), but it may also occur with gasping in

persistent severe hypoxemia.

utero just before delivery (Katz and Bowes, 1992;

The cardiopulmonary outcome of BPD is variable,

Wiswell and Bent, 1993). Research has supported tile

ranging from near normal pulmonary function by age

contention that meconium aspiration syndrome

3 to 5 in children who had milder forms of BPD, to

(MAS) is often preventable if the upper and lower

continued poor cardiopulmonary function, chronic

a i r w a ys a r e s u c t i o n e d immedi atel y after b i r t h

distress, and ongoing oxygen dependence in children

(Wiswell, Tuggle, and Turner, 1990). The lower air


642

PART VII


ways especially should be suctioned in infants deliv

i n g c a u s e of s y m p t o ms in ch ildren with HIV

ered through thick, particulate ("pea soup") meco

(Marold a, Pace, Bonforte, Kotin, Rabinowitz, and

nium in amniotic material (Gregory, 1977). Aspiration of meconium can result in serious and

Katlan, 1991). In infants with perinatally acquired HIV, pneumocyctis carnii pneumonia (PCP) fre

devastating pathophysiology. Most commonly, the

quently occurs within the first 15 months of life

meconium will partially or completely block the

(Connor et aI., 1991). The risk of mortality during

peripheral airways (Wiswell and Bent, 1993). At

the infant's first episode of PCP is high (Bagarazzi,

electasis is the classic finding, but with partial ob

Connor, McSherry, and Oleske, 1990; Bernstein,

struction, hyperexpanded areas will also be ob

Bye, and Rubinstein, 1989; Scott et aI., 1989).

served as a result of air that was inspired but then

The clinical presentation of PCP includes failure

trapped in distal, small airways. Common compli

to thrive, cough, dyspnea, tachypnea, fever, hypox

cations of MAS include tension pneumothorax, per

emia, and chest radiograph evidence of prominent air

sistent pulmonary hypertension, and bronchiolitis

b r onchograms

and pneumonitis secondary to chemical irritation

(Bagarazzi et aI., 1990; Berdon, Mellins, Abramson,

and mUltiple

cysts

or

bullae

from the components of the meconium (Wiswell

and Ruzal-Shapiro, 1993; Bernstein et aI., 1989).

and Bent, J 993). A d d itionally, long-term pul

PCP is most often diagnosed after bronchoalveolar

monary sequelae have been reported (MacFarlane

lavage studies (Phelan et aI., 1994).

and Heaf, 1988; Swaminathan, Quinn, Stabile, Bader, Platzker, and Keens, 1989).

Treatment is supportive and includes antibiotic therapy, antiretroviral therapy, nutritional support,

Medical management of MAS is supportive, with supplemental oxygen and, if necessary, mechanical

and mechanical ventilation as needed (Bagarazzi et aI., 1990; Phelen et aI., 1994).

ventilation. Chest physical therapy is especially advo

Asthma

cated during the first 8 hours of life, although it may be necessary for a longer period of time if the infant

Although asthma is discussed in detail in Chapter 4, a discussion of pediatric pulmonary problems would

requires assisted ventilation.

not be complete without some discussion of this com

Pneumonia

mon cause of childhood lung disease. An estimated

Neonatal Pneumonia. The most common organisms

8% to 10% of children in the United States have

producing neonatal septicemia associated with pneu

asthma, with asthma accounting for the most lost

monia in neonates are group B streptococcus and He

time from school and 33% of pediatrician visits per

mophilis inJluenzae (Emmanouilides and Baylen,

year (Magee, 1991).

1988). Neonatal pneumonia mimics HMD/RDS in clinical presentation and chest radiographs.

Childhood asthma can begin at any age, and its clinical etiology and clinical course are variable.

Aspiration Pneumonia. Aspiration is an unfortunate

Children with early medical histories including very

result of small children's "indiscreet curiosity" (War

low birth weight, bronchopulmonary dysplasia, and

ing, 1975) in exploring their environment and relying

respiratory syncytial virus infection may be at in

on their mouths for sensory learning. Aspiration can

creased risk for developing asthma (Pullen and Hey,

also result from gastroesophageal reflux and de

1982; Rickards, Ford, Kitchen, Doyle, Lisseden, and

creased upper airway neuromuscular control (Oren

Keith, 1987; Smyth, Tabachnik, Duncan, Reilly, and

stein and Orenstein, 1988).

Levison, 1981).

Bronchial drainage techniques are often indicated

Medical management usually includes avoidance

as part of the medical management of infants and

of known precipitants, adrenergic drugs, and corti

children after aspiration to aid with airway clearance

costeroids (in chronic, severe cases). Chest physical

and reduce the possibility of bacterial superinfection.

therapy for this disease includes patient and family

Pneumocystis Carnii PneumonialHIV-lnJected

education in breathing control, relaxation, effective

Children. Pulmonary involvement is often the lead

coughing, and exercise. Older children, in paJticular,


35


643

may benefit from CPT especially when they are re

breathing (ACB) technique, use of a positive expira

sponding slowly to pharmacological treatment alone

tory pressure (PEP) mask, autogenic drainage (AD),

(Asher, Douglas, Airy, Andrews, and Trenholme,

and use of the flutter device, have been shown to be

1990). Exercise, also highly effective in the treatment

effective in assisting sputum expectoration, often in

and management of asthma, is discussed in a later

greater amounts and in less time per treatment

section on pulmonary rehabilitation.

(Konstan, Stern, and Doershuk, 1994; Mahlmeister, Fink, Hoffman, and Fifer, 1991; Pryor, 1991; Pryor

Cystic fibrosis

and Webber, 1979; Schoni, 1989).

Cystic fibrosis (CF) is a complex autosomal-reces

Although postural drainage, percussion, and vibra

sive disorder that affects the exocrine glands. Defini

tion remain the treatment of choice for infants and

tive diagnosis of CF includes positive family history,

children who are unable to be instructed in tech

obstructive pulmonary disease, recurrent pulmonary

niques that use patterns of voluntary breathing, other

infection, intestinal malabsorption and poor growth,

techniques are available for children who can follow

the

specific breathing instructions and who can perform a

presence

of

Slaphylococcus

aur eus

or

Pseudomonas aeruginosa i n the respiratory tract,

reliable pulmonary function test. Children as young

and, most importantly, a positive sweat chloride test

as 2 to 3 years can be taught to "huff' as part of FET

(Cystic Fibrosis Foundation, 1990).

(Pryor, 1991), the PEP mask has been used with chil

The chronic pulmonary disease in CF is related

dren as young as 3Y2 years (Mahlmeister et aI., 1991),

to increased secretion of a b n o rm a lly v i s c o u s

and AD can reportedly be taught to children as carly

mucus, impaired mucociliary transport, airway ob

as 4 to 6 years of age (DeCesare and Graybill, 1990;

struction, bronchiectasis, overinflation, and infec

Sci1oni, 1989). The benefits of each technique should

tion. Radiographic changes are most pronounced in

be carefully considered relative to each child's cogni

the upper lobes, especially the right (Wood, Boat,

tive, respiratory, and motor planning abilities when

and Doershuk, 1976).

choosing or modifying the child's program for airway

The early institution of prophylactic pulmonary

clearance.

physical therapy, including postural drainage and the

Ventilatory muscle training is an important aspect

judicious use of antibiotics, provides effective mea

of pulmonary treatment in older children with CF.

sures for controll ing or slowing the effects of bron

Studies have demonstrated that training to improve the

chiolar and bronchial obstruction. Involvement of the

endurance of ventilatory muscles decreases dyspnea

child and family in pulmonary care is particularly im

and increases general exercise tolerance in patients

portant. Family understanding of the nature of the

with CF (Keens, Krastins, Wannamaker, Levison,

disease and the purpose of each therapeutic measure

Crozier, and Bryan, 1977; Reid and Loveridge, 1983).

promotes successful management of the child. A

The role of general exercise in the cardiopul

home program of CPT should be established for each

monary management of children with CF is specifi

child, taking into consideration the child's ongoing

cally discussed within the context of pulmonary reha

pulmonary needs and the family's unique contribu

bilitation. However, it is important to realize that

tions and constraints.

some debate exists as to whether exercise can replace

Bronchial drainage is an aspect of conventional

more traditional airway clearance techniques. Pryor

treatment for CF that in recent years has gained sev

(1991) has suggested that exercise should be an addi

eral options that allow both efficacy and patient in

tional component rather than a substitute for breath

dependence (Davis, 19(4). Airway clearance tech

ing techniques. Cerney (1989) in contrast, reported

niques are described in detail in Chapter 20, but

that some children with mild disease may be able to

alternatives to traditional percussion and postural

use regular exercise in place of bronchial drainage

drainage warrant mention within the context of CPT

treatments. The severity of the disease process and

for children with CF. Specifically, the forced-expi

the child's condition at any one point in time, will

ration technique (FET) as part of the active cycle of

clearly mediate the appropriateness and effectiveness


644

PART VII


of exercise as either a component or as a primary

These deviations and other aspects of ventilatory

means of airway clearance.

compromise are discussed with regard to motor diag

Special respiratory problems associated with intubation and tracheostomy Once an infant or child develops respiratory failure,

noses common to pediatric practice.

Cerebral palsy Children with cerebral palsy generally have weak trunk

intubation and mechanical ventilation are usually re

and postural muscles, which, when combined with atyp

quired. The goals of medical management are then to

ical neural mechanisms, produce atypical movement

treat the cause of the respiratory failure as aggres

pattems and functional alignment deviations. The trunk

sively as possible and to wean the child from me

and respiration relationshi[ls described in Table

chanical ventilation as quickly as possible.

consistent with the clinical picture of external pul

If a child's condition necessitates long-term me

35-3 are

monary development in children with cerebral palsy.

chanical ventilation, or if an artificial airway is needed

Although the extent of mobility impair ment is

to bypass an upper airway obstruction, a tracheostomy

variable between children, hypoventilation, increased

is usually petformed (Scott and Koff,

1993).

Infants and children who have a tracheostomy and

work to breathe, inefficient cough, increased risk for aspiration, and poor breath support for vocalization

1993). Limited active mobility

are intubated for long periods of time require vigorous

can occur (Alexander,

prophylactic airway management, such as bronchial

and the use of habitual patterns with little deviation

drainage and airway suctioning. Chest PT, including postural drainage and vibration emphasizing right upper lobe segments, has been shown to significantly decrease the incidence of postextubation atelectasis in infants intubated for more than 24 hours (Finer, Mori artey, Boyd, Phillips, Stewart, and Ulan,

1979).

Pulmonary Considerations in Neuromuscular and Motor Diagnoses Although cardiopulmonary symptoms may not be the primary reason for referral to physical therapy in children with neuromuscular and general motor de velopmental diagnoses, these children do have motor involvement that can result in respiratory and pos tural muscle weakness, immobile chests, and hy p oventilation. Furthermore, many of these children have had medical histories remarkable for cardiopul monary complications or have diagnoses that entail progressive processes that will result in cardiopul monary compromise. Table

35-3 provides an extensive summary of the

interactions between trunk musculature and ventila tion in children with atypical development. Although the biomechanical deviations noted are frequently seen in children with atypical tonal presentations,

FIGURE 35-1

they are also common in children with scoliosis, ster

Flattened anterior chest with marked rib flaring in a child

nal deformity, or general immobility of the thorax.

with cerebral palsy.


35


645

TABLE 35-3 Functional Relationships of Trunk Control and Respiration BIOMECHANICAL

POSTURAUfRUNK CONTROL

RESPIRATORY

COMPONENT

CONSEQUENCES

CONSEQUENCES

Passive lumbar lordosis

Ineffective cough

Weak abdominal obliques

Protruding tummy

High chest

Lower rib flaring

Retained horizontal rib alignment

Decreased trunk rotation Unable to weight shift

Tight rectus abdominis may lead to

Dependence on rectus abdominis

pectus excavatum Child may use diapl1ragm for trunk control, limiting its function as a primary muscle of respiration Decreased support of abdominal contents under diapmagm Anterior upper chest cannot adequately

Forward shoulders

Tight pectoralis minor

Scapula pulled laterally and anteriorly,

expand

away from the thoracic wall Upper thoracic flexion Weak serratus anterior

Wcak upper fibers-medial edge of scapula Icaves the thoracic wall

Decreased structural reinforcement of the posterior chest wall Interdigitation of the lower fibers of serratus anterior with the external abdominal oblique will interact to affect the dynamic stability of the rib cage

Decreased active upper

Approximation of upper ribs

Kyphotic upper trunk

thoracic extension

scapular retractors

-7

decreased oxygenation of the upper lobe

Decreased rib cage stability

-7

decreased upper chest mobility

Passive overlengthening of the

Serratus anterior will elevate the ribs rather than stabilize the scapula

-7

abdominal breathing

Decreased structural support for the respiratory muscles to work from

against the thoracic wall

Modified from Moerchen the

Neurology Report

V A:

Respiration and motor development: a systems perspective,

with the permission of the Neurology Section,

Neural Rep 18 (3): 8-10, 1994.

Reprinted from

APTA.

of the center of gravity beyond the base of support

chest excursion and should be incorporated into a

contribute to thoracic stiffness. A high chest, flat

home program. Mobilization of the ribs and thoracic

tened anteriorly, with excessive rib flaring, is com

spine are important precursors to improving chest ex

mon in these children (Figure 35-l).

cursion during ventilation.

Therapeutic attention to respiration should first

Chest PT may be indicated if the child develops a

identify possible aspiration and suggest modifications

primary pulmonary complication. Prophylactic pos

for positioning during feeding. Additionally, certain

tural drainage can also be integrated into many sen

postures for sleep and play may be less restrictive for

sory stimulation programs for more severely involved


646

PART VII


children. Additional "handling" to address ventilatory function will be discussed in

a

subsequent section on

motor approaches to respiratory treatment.

Myelomeningocele Myelomeningocele or spina bifida are diagnoses that physical therapists generally equate with issues of am bulation and mobility. However, central ventilatory dysfunction is prevalent in infants, children, and ado lescents who also have an associated Arnold-Chiari type II malformation (Hays, Jordan, McLaughlin, Nickel, and Fisher, 1989; Swaminathan et aI., 1989; Ward, Jacobs, Gates, Hart, and Keens, 1986). The Arnold-Chiari type II malformation, which oc curs in 90% of infants with myelomeningocele, is a hindbrain malformation consisting of a caudal helllia tion of the cerebellum and brain stem into the cervical canal (Charney, R orke, Sutton, and Schut, 1987). Ventilatory problems associated with a symptomatic Arnold-Chiari type II malformation include inspira tory stridor (vocal cord paralysis), central apnea, and respiratory distress (Hays et aI., 1989; Hesz and Wol raich, 1985; Oren, Kelly, Todres, and Shannon, 1986). However, abnormal ventilatory patterns have also been observed in asymptomatic infants (Ward et aI.,

1987) and adolescents (Swaminathan et aI., 1989). Ventriculoperitoneal shunting (management of hy

FIGURE 35-2 An 8nterior cut-out and elastic support in a body jackel/spinal orthosis aids diaphragm function.

drocephalus) and, if necessary, cervical decompres sion are the surgical approaches to treatment of life

Down syndrome

threatening ventilatory complications in this population. Other

p u lmonary

issues

in

c h ildren

with

Impaired pulmonary function in children with Down

myelomeningocele warrant discussion. TtUnk weakness

syndrome is clearly related to generalized weakness of

and hypotonia are observed early in the motor develop

trunk musculature (Dichter, Dm·bee, Effgen, and Pal

ment of infants and toddlers who have shunted hydro

isano, 1993). The postural deviations common in these

cephalus. Additionally, in children with thoracic and

children reflect (Figure 35-3) inefficient muscle func

high lumbar level lesions, abdominal muscle SUpp0l1 for

tion for both ventilation and movement

diaphragm function may be insufficient. The use of ab

1994). Again the ttUnk-ventilation relationships delin eated in Table 35-3 summarize the subtle but significant

dominal binders, and spinal othoses/body jackets with

(Moerchen,

(anterior) diaphragm cut-outs and an elastic inse11 are

clinical presentation of external pulmonary develop

indicated to aid in diaphragm function (Figure 35-2).

ment in these children. Too often only motor develop

Although progressive scoliosis is not the natural history

ment is addressed by physical therapists who are treat

of children with spina bifida, it is a symptom of unstable

ing children with Down syndrome. Respiration needs to

neurology (tethered cord), and attention to ventilatory

be considered if therapy goals include increased vocal

ability is necessary both for general monitoring and for

izations or improved tolerance for exercise.

possible preoperative evaluation.

Pulmonary hypoplasia may also challenge the res


35


647

FIGURE 35·3 A, Characteristic posture of a child with Down syndrome/hypotonia. Note the abdominal protrusion and sternal retraction. B, Rib flaring with upper extremity movement; the abdominal obliques are not stabilizing the lower ribs.

(1994). Respiration and Motor Development: a Systems Perspective. 18(3), 8-10. Reprinted with the permission of the Neurology Section, APTA.

Photos from Moerchen, V.A. Neurology Report,

piratory function of these children. Cooney and Thurl

Muscular dystrophy

beck (1982) observed a consistent combination of de

Duchenne's muscular dystrophy involves end-stage

creased numbers of alveoli and larger alveolar ducts

respiratory failure that results from progressive respi

in individuals with Down syndrome, not related to age

ratory muscle weakness, thoracic deformity, reduced

or incidence of heart disease. Although these re

lung compliance, retained secretions, ventilation

searchers had a small sample size, their results do sug

peIi'usion imbalance, and hypoxemia (Bach, O'Brien,

gest that trisomy 21 may result in lung vulnerability.

Krotenberg, an d Alba, 1987; Smith, C alverley,


648

PART VII


Edwards, Evans, and Campbell, 1987). In 70% to

niIe rheumatoid arthritis (JRA) may have inflamma

90(;1(:

tion of thoracic joints or may splint through their

strictive respiratory complications (Bach et aI., 1987;

trunks when they try to move painful extrcmities.

Smith et aI., 1987).

With thcsc children, brcathing exercises will have a

Physical therapists are typically involved in treat

role both in pulmonary carc and in pain management.

ment of these paticnts for preservation of motor func

Put simply, children who make cumpensatiuns in

tion. Early attention to ventilation, however, is war

their movement patterns to accomlllodate pain, weak

r a n t ed. P r o phyla c t i c spi n a l f u s i o n to pre v e n t

ness, or deformity, may limit the mechanics of their

scoliosis-related compromise o f ventilation i n these

thoraces. Con versel y. chi I dren who cannot ade

patients considers both the progrcssion of the spinal

quately oxygenate may make compensations in their

curvature and vital capacity (YC) (Rideau, Glorion,

movement patterns to SUpp0l1 ventilation. Clearly, at

Delauber, Tarle, and Bach, 1984).

tention to ventilation should be an inherent aspect of

Chest physical therapy should be a component of the overall rhysical therapy management of children

observing motor development and quality of move ment in all children.

with muscular dystrophy. Deep breathing, coughing, and activitics to addrcss cndurance arc recommended but will require ongoing modification as the disease progresses. Inspiratory muscle training in these chil dren remains controversial. Although some researchers

PHYSICAL THERAPY TREATMENT APPROACHES Postoperative Pediatric Cardiac Rehabilitation

havc del11on. trated improved endurance of ventilatory

Postopcrative physical therapy consists largely of

muscles (DiMarco, Kelling, DiMarco, Jacobs, Shields,

techniques to increase respiration, mobilize secretions,

and Altose, 1985; Martin, Stern, Yeates, Lepp, and Lit

and progress physical mobility. Positional rotation for

tle, 1986; Stern, Martin, Jones, Garrett, and Yeates,

pulmonary care is pussible if the child has a stabilized

1991), other researchers have suggested that inspira

sternum. Breathing exercises and coughing will need

tory resistance may over-tax respiratory muscles that

to be modified based on the child"s age and cognitive

are all'eady near fatigue due to working against incom

level. Huckabay and Daderian (1990) reported im

pliant structures (lungs, thorax) (Smith, Coakley, and

proved postoperative cooperation in children 3 to 10 years of age when choice making was incorporated

Edwards, 1988). Respiratory dependence does occur as the disease

into a breathing program.

progresses. Protocols for point of initiation and type

Immobilization after cardiac surgery is to be

of mechanical ventilation are being studied. There is,

avoided as much as medically possible. Passive range

however, agreement that close monitoring of YC and

of motion may be initiated immediately, with care to

of nocturnal hypoventilation can allow respi ratory

avoid compromising arterial lines. Ambulation is

support to be implemented before the onset of acute

generally initiated once the child is extubated and has

respiratory failure (Bach, Alba, Pilkington, and Lee,

had atrial and groin lines removed (Johnson, 199 I).

1981; Bach et aI., 1987; Curran, 198 I).

Child and family education as part of pediatric cardiac rehabilitation has been observed to reduce

Miscellaneous conditions

parent and child anxiety related to safe levels of

Multiple other pediatric diagnoses and musculoskele

pllysical activity (Balfour, Drimmer, Nouri, Penning

tal conditions include clinical presentations (strength,

ton, Hemkens, and Harvey, 1991; Calzolar et ai,

alignment, and limited mobility) that should cue the

1990; Mathews et ai, 1983). Although studies of pe

therapist'S attention to pulmonary function. Syn

diatric cardiac rehabilitation have been focused on

dromes that involve sternal deformity such as Marfan

children older than 6 years, monitored exercise has

syndrome or Poland's syndrome will clearly entail

been shown to safely produce an increase in peak

possible ventilatory compromise. Children with juve

oxygen consumption and a decrease in resting heart


35


649

Nouri, P e n n i n g t o n,

of lymph nodes, making it vulnerable to extrinsic

Hemkins, and Harvey, 1991; Calzolari et aI., 1990;

compression. Important considerations and essentials

Mathews et aI., 1983).

of a positional rotation program for infants are out

r a t e (B a l f o u r, Dri m m e r,

Exercise prescription for cardiopulmonary rehabili

lined in the box below.

tation of older children who have undergone cardiac re

It is important to note that premature infants do

pairs at an early age will require careful monitoring.

tolerate and benefit from prone positioning. Studies

Lower exercise V02 values, lower cardiac output, and

have demonstrated improved oxygenation, tidal vol

lower values of diffusion capacity of the lung for car

ume, dynamic lung compliance, and synchrony of

bon monoxide have been observed in response to exer

chest wall movement when preterm infants are put in

cise in children who have undergone cardiac surgery as

prone positions (Hutchinson, Ross, and Russell,

compared with the responses of age-matched controls

1979; Lioy and Manginello, 1988; Martin, Harrell,

(Gildein, Mocellin, and Kaufmehl, 1994; Tomassoni,

Rubin, and Fanaroff, 1979).

Galioto, and Vaccaro, 1991). Exercise recommenda

Positional rotation is generally performed manu

tions include submaximal performance (Tommassoni et

ally every 2 hours, and, although this provides pul

aI., 1991) and technique training to increase the biome chanical efficiency of movement while decreasing the associated metabolical costs (Gildein et aI., 1994).

Essentials of a Positional ROUl/ion Program Chest Physical Therapy for Neonates and Infants

I.

The plimary goal of chest physical therapy for neonates and infants is to improve airway clearance. If tech niques of bronchial drainage can increase the diameter of the airways through secretion mobilization, then ventilation may also be improved and the work of breathing reduced. These techniques should be judi ciously applied for prophylaxis and treatment in infants who have or are at risk for developing airway clearance problems. Applying bronchial drainage techniques to infants requires a thorough understanding of each in

Care should be taken to coordinate any change in the infant's position with other nursing proce dures to avoid unnecessary stimulation.

2.

Infants should never be left unattended when in a head-down position.

3. Vital signs should be monitored closely by res piration and heart rate monitors. The alarms should be turned on.

4. The infant's chest should be auscultated for ad ventitious breath sounds after positioning.

5. While the infant is in a drainage position, secre tions will be more easily mobilized. The infant's

fant's condition and the precautions and considerations

trachea or endotracheal tube should be suctioned

inherent to any technique or combination of techniques.

as needed.

6. Avoid placing the infant in a head-down posi tion for approximately I hour after eating to

Positional rotation Frequent changing of position will prevent prolonged dependency of any one portion of the lung, so that pooling of secretions can be limited/avoided and im proved ventilation can be achieved (Menkes and Britt, 1980; Ross and Dean, 1989). Whereas posi tional rotation programs for adults emphasize the lower lobes, positional programs for infants must em phasize all lung areas (Figures 35-4 to 35-6). The upper lobes and right middle lobe are common sites of airway collapse and atelectasis in infants, and the

avoid aspiration of regurgitated food.

7. Any change in the infant's position should be done slowly to minimize stress on the cardiovas cular system.

8. Infants with umbilical arterial lines can be placed on their abdomens. However, one should

always check that the line has not been kinked. 9. Some infants might require modified drainage positions. Infants with severe cardiovascular in stability or suspected intracranial bleeding should not be placed in a head-down position.

right middle lobe bronchus is surrounded by a collar


650

PART VII


2

��

J. FIGURE 35-4 Sequence for positional rotation.

Position I.-Segments that come off the left lower bronchus posteriorly are drained by positioning the infant on his right side, three-foUl1hs prone with a head-down angle. Position 2.-The posterior segment of the right upper lobe is drained by positioning on the left side, three-fourths prone with the bed flat. Position 3.-The anterior segments of the upper lobes are drained by positioning supine with the head of the bed elevated or flat. Position 4.-Segments that come off the right lower lobe bronchus posteriorly are drained by positioning on the left side, three-fourths prone with a head down angle.


35


4.

5.

FIGURE 35-4-cont'd Position 5.-The posterior segment of the left upper lobe is drained by positioning on the right side, three-fourths prone with the head of the bed elevated. Position 6.-Segments that come off the tracheobronchial tree anteriorly are drained by positioning supine with a head-down angle.

Positu)1Is 7 and 8.-Segments such as the right middle lobe or lingula that come off the tracheobronchial tree anterolaterally will be drained in a three-fourths spine position, slightly head dow (see Figure 35-5, p. 652). NOTE:

Babies on ventilators may also be positioned prone. This is usually done by the therapist

rather than in a routine positional rotation (see Figure 35-6, p. 652).


651

652

PART VII


FIGURE 35-5

FIGURE 35-6

Three-fourths supine position for right middle lobe. Lingula

Premies (even those on ventilalOrs with numerous

is the same three-fourths supine position with the patient

catheters) may be placed prone when care is taken.

lying on his right side.

monary benefit, it may also contribute to the disrup

ing less than 800 grams) usually require and benefit

tion of homeostasis that has been documented to

from modification of the head-down position. Hori

occur in the course of neonatal intensive care (Long,

zontal to slightly elevated positioning of the head may

Philip, and Lucey, 1980; Yeh, Lilien, Leu, and

be best (Thoresan, Cowan, and Whitelaw, 1988). This

Pildes, 1984). Use of nursery beds that provide con

modification primarily is due to the high incidence of

tinuous positional oscillation (from right side to

intraventricular hemorrhage in premature infants

supine to left side, and so forth) might provide an op

(Crane, Zombek, Krauss, and Auld, 1978; Emery and

tion that allows the benefits of position change while

Peabody, 1983). Other precautions for Trendelenburg

also minimizing the homeostatic disruption. Murai

positioning of infants include but are not limited to

and Grant (1994) demonstrated that continuous posi

abdominal distention, congestive heart failure, dys

tional oscillation as part of a total chest physical ther

rhythmias, hydrocephalus, frequent episodes of apnea

apy program decreased the duration of oxygen sup

and bradycardia, and acute respiratory distress.

p l e m e n t a ti o n w i t h o u t a d v e r s e ly e f f e c t i n g t h e cardiopulmonary status o f the neonates.

Chest percussion and vibration Percussion and vibration are used in conjunction with

Postural drainage

postural drainage to augment the effect of gravity in

Postural drainage (PD) positions to promote gravity

the removal of secretions. There are several ways to

assisted drainage of specific segmental airways can be

perform percussion on infants. For a larger infant, it

safely applied to infants and children. In the acute care

is possible to use a cupped hand, similarly to per

setting, however, many of the head-down positions

cussing an adult's chest. For a smaller infant, some

are modified according to tolerance and precautions or

modification of this technique is needed. Chest per

contraindications (Table 35-4). The rule for modifica

cussion for a smaller infant is accomplished by the

tion of any position for PD is that the position used

use of tenting three fingers, four fingers, or using any

should be as close to the classical (anatomically cor

of the commercially available percussion devices

rect) position for that segment as safely possible. Ex

made for neonates (Figure 35-8). A small anesthesia

amples of the classical PD positions for each bron

mask or "palm cup" can also be used effectively.

chopulmonary segment are pictured in Figure 35-7. Tiny infants (especially premature infants weigh-

Precautions for chest percussion in the infant in clude but are not limited to unstable cardiovascular or


3S


653

TABLE 35-4 Precautions and Contraindications for Postural Drainage in a Neonate* POSITION

PRECAUTION

CONTRAINDICA TlON

Prone

Umbilical arterial catheter

Untreated tension pneumothorax

Continuous positive airway pressure ·in nose Excessive abdominal distention Abdominal incision Anterior chest tube Tendelenburg position

Distended abdomen

(head down)

Untreated tension pneumothorax

SEHlIVH* (grades I ancllI)

Recent tracheoesophageal fistula repair

Chronic congestive heart failure or

Recent eye or intracranial surgery

cor pulmonale

Intraventricular hemorrhage (grades III

Persistent fetal circulation

and IV)


Acute congestive heart failure or cor pulmonale

Apnea and bradycardia Infant exhibiting signs of acute respiratory distress Hydrocephalus Less than 28 weeks' gestational age

'Subependymal hemorrhage/intraventricular hemorrhage. From Crane LD: Physical therapy for the neonate with respiratory disease. ln [rwin S, Tecklin JS, editors:

therapy,

SI. Loui"

1995,

Cardiopulmonary physical

Mosby.

oxygenation status (although percussion may be pro

bration will depend on the day-to-day medical status of

vided safely if continuous transcutaneous monitoring

the infant and the infant's response to treatment.

is available), coagulopathy, subcutaneous emphy sema, or intraventricular hemorrhage. Additionally,

Airway suctioning

percussion is generally contraindicated over a healing

Sterile airway suctioning is discussed in detail in

thoracotomy incision or if the child displays ilTitabil

Chapter 42. However, some special considerations

ity and signs of rcspiratory distress with the treatment.

for suctioning the a i rway of an infant need to be

Vibration is accomplishcd either through manual vi

highlighted (Durand, Sangha, Cabal, Hoppenbrowers,

bratory motion of the therapist's fingers on the infant's

and Hodgman,

chest wall (Figure 35 -9) or through the use of a me

Volpe,

1989; McFadden, 1981; Perlman and

1983).

chanical vibrator. An electric toothbmsh can be adapted

1. If possible, suction with a transcutaneous oxy

by padding the bristle portion with foam (Cun'an and

gen monitor in place. These monitors give con

Kachoyeanos, ) 979). Vibration has been observed to

tinuous feedback regarding the infant's oxy

occasionally increase irritability and may be less well

genation status.

tolerated than percussion. The most common precau

2. Bagging should be done only with a bag at

tion for vibration is increased irritability with the devel

tached to a pressure manometer to ensure that

opment of bradycardia alld respiratory distress.

sufficient prcssures are being used without ex

The decision to use chest percussion and vibration will depend on the reviewed principles and precautions, the medical condition of the infant, and the infant's tol erance to handling. Continuation of percussion and vi

ceeding the maximum safe le v els (these l imits should be similar to the ventilator settings).

3. Suction for no more than 5 seconds with each catheter withdrawal.


654

PART VII

Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cllses

A

- --:---

'-

:.-

C

B

D

FIGURE 35-7 Postural drainage with an infant. A, Both upper lobes-apical segments. B, Left upper lobe- anterior segment. C, Right upper lobe-anterior segment. D, Lingula.


35

E

F

G

H


FIGURE 35-7-cont'd E, Right middle lobe. F, Right upper lobe-posterior segment. G, Left Lipper lobe-posterior segment. H, Both lower lobes-apical (superior) segments.


655

656

PART VII


K

FIGURE 35-7-cont'd I, Both lower lobes-anterior basal segments. J, Left lower lobe-lateral basal segment; Right lower lobe

arduac (medial) segment. K, Both lower lobes-posterior basal segments. L, Right

lower lobe-lateral basal segment.


35


657

FIGURE 36-8 'Tenting" of the finger for percussion of premies or small children.

FIGURE 36-9 Manual chest wall vibration of a premie.

4. Infants should be carefully hyperoxygenated

tions and imitating a therapist's demonstration of deep

when hyperventilated so as to minimize hyper

breathing, coughing, and active exercise. Chest physi

oxia and hypoxia. Bagging usually does not

cal therapy in children is focused on improving venti

10 seconds

lation, improving the efficiency of breathing, increas

5. Monitor the blood pressure of preterm infants be

on muscles of respiration, improving posture, and ad

need to continue for more than 5 to to maintain adequate oxygen levels.

ing general strength and endurance with an emphasis

fore, during, and after suctioning. Change in

dressing relaxation, breathing control, and pacing.

blood pressure may indicate increased intracra

The application of chest PT with children often re

nial pressure and risk for intracranial hemOtThage.

quires patience and creative adaptation (Figure 35-

10). The challenge is to make it seem less like a treat ment and more like a game. It is important, however,

Chest Physical Therapy for Children

to be honest in your explanations and to speak to the

The goals for chest physical therapy with children

(2

years and older) include more than improving airway clearance. Children are capable of following direc

child with respect and at a level appropriate to the child's age and development. Involving the family in PT treatment of a child can


658

PART VII


FIGURE 36-10 A, B, C, Few areas of health care delivery require creative adaptation and problem solving to the extent that pediatrics does.

be invaluable. In some cases the parent may do most

tant to have his position changed, changing the loca

of the "hands-on" and repeat instructions to the child

tion of the television may be helpful. Be creative!

under the direct guidance of the therapist. This

Young Children. In younger children (18 months to 3

arrangement will also help reinforce parent and fam

years) deep breathing is usually encouraged by blow

ily education for carry-over of home therapy.

ing bubbles, tissue paper, mobiles. or simple horns. To achieve maximal chest expansion, the child should be

Positional rotation

positioned on each side while playing blowing games

The goal of positional rotation and postural drainage

or singing. The theory behind the side lying position is

is to prevent the accumulation of secretions and to aid

that the downside lung ventilates more effectively (see

in their removal. Any child who is immobile, receiv

Chapter 18). Additionally, if the poorly ventilated

ing artificial ventilation, or not expanding his chest

lung is uppermost, stretch techniques can facilitate

adequately should have his position changed at least

deeper breathing (see Chapter 22).

every 2 hours. Recall that positional changes will en

Spontaneous coughing in younger children often

hance oxygen transport and promote pulmonary

occurs with a change in position or with crying. For

drainage (Ross and Dean, 1989). If the child is reluc

the child who does not cough spontaneously or whose


35


659

FIGURE 35-11 Whistles such as these encourage increased inspiration and controlled, sustained expiration to make the whistle components move

(left:

a fish with a wheel that moves at its back fin;

middle:

a race car

that drives around a track making whirling sounds; right: a ball that moves up and down in a train).

cough is inadequate to clear secretions, nasopharyn

treat ment by therapists helps to decrease the inci

geal suctioning may be necessary.

dence of postoperative complications.

Older Children. School-age children can be more

Preoperative teaching is extremely important for

specifically instmcted in various breathing exercises,

both the child and the family. Parents can often be

such as diaphragmatic breathing, pursed-lip breathing,

more anxious than the child, so patient and family ed

and segmental lateral costal breathing. They may also

ucation is important. The level of preoperative train

be candidates for using relaxed deep breathing for

ing with the child will depend on the child's age.

control and pacing of activity. Cooperation with this

If the child is very young (under 2 years), the thera

age group, however, still remains higher if some as

pist will meet with the parents and explain the purpose

pect of therapy is fun. Elaborate whistles are available

of bronchial drainage treatments, potential airway clear

that encourage deep breathing as a fun means to an

ance problems, and possible complications. The pre

end of making the whistle components move (Figure

ventative nature of these treatments should be stressed,

35-11). Additionally, pediatric incentive spiro meters

and procedures that might be done with the child after

are available with cheerfull"cool" pictures to make

surgery should be demonstrated and discussed. These

respiration exercises more like a game (Figure 35-12).

might include: (I) positioning, (2) chest percussion,

Older children (not infants) can be stimulated to cough by applying a firm pressure over the trachea in

(3) vibration, and (4) airway suctioning. In addition, al ways allow time for the parents to ask questions.

the suprasternal notch. Beware t h a t coughi ng,

If the child is able to understand simple concepts,

whether spontaneous or stimulated, may elicit gag

the therapist can, in addition to parent orientation, in

ging and vomiting, especially if airway clearance is

stmct the child in various breathing games, use of an incentive spirometer, coughing, and general upper

scheduled too soon after a child has eaten.

and lower extremity exercises.

Preoperative and postoperative care

In older children (8 years or older), postoperative

The efficacy of postoperative chest PT is highly re

procedures can be explained and demonstrated. The

lated to preoperative care. The appropriate applica

importance of bronchial hygiene should be stressed

tion of preoperative assessment, instruction, and

during demonstration of deep breathing and cough


660

PART VII


are atelectasis, infection secondary to pooling of se cretions, and airway obstruction. Infants and children with the following characteristics will be at risk for developing postoperative pulmonary complications:

(I) preexisting lung disease, (2) thoracic or upper ab (3) prolonged post operative bedrest or restricted mobility, and (4) neu

dominal location of the incision,

romuscular involvement that affects the ability to be mobile and to cough and deep breathe. Postoperative treatments generally focus on in creasing ventilation, coughing, and active mobility. Specific bronchial drainage is used only if the child is unable to clear his or her airways or is at risk due to chronic lung disease. After high abdominal or thoracic surgery, there may be a tendency for the child to splint on the side of his or her incision. Arm, shoulder, and trunk movement should be encouraged to prevent any post operative complications. For the younger child, chest mobility can be encouraged by clapping the hands overhead or by dramatizing songs such as The Itsy Bitsy Spider. More conventional exercises may be taught to the older child. Children tend to mobilize very quickly (unless their movement is limited secondary to motor in volvement or to a specific surgical procedure). Once the child is out of bed and moving about, with clear lungs and an effective cough, postoperative CPT treatments can generally be discontinued. FIGURE 35-12 A pediatric incentive spirometer. (Photo provided courtesy of DHD Medical Products. Used by permission.)

Pediatric Pulmonary Rehabilitation Rehabilitation programs for pediatric patients with chronic lung disease include the same components and have essentially the same goals as adult pul

ing. The child can be shown how to splint the inci

monary rehabilitation. The major difference is related

sion using a pillow or stuffed animal to assist with

to different diagnoses being most prevalent in the

comfort while coughing. Do not tell the child that

children versus adult age groups. Asthma and CF are

coughing will not hurt; be honest but reinforce that

the most common diagnoses of children who are can

splinting will help. Teach the child diaphragmatic

didates for pulmonary rehabilitation.

and pursed-lip breathing with an inspiratory-hold ma

Exercise and asthma

neuver, and, if appropriate, teach the child how to use an incentive spirometer.

Exercise and conditioning are very important compo

Postoperative pulmonary complications may not

nents of the treatment of the child with asthma. Im

be as prevalent in the pediatric age group as in adults,

proved chest and trunk mobility, control of breathing,

but they still occur. The most common complications

strength, posture, and an increased tolerance to exer


35

cise are all goals that can be addressed in the design


661

oxygen desaturation during exercise in children with

of exercise programs for these children (Magee,

CF (Coates, 1992). Loutzenhiser and Clark (1993),

1991; Seligman, Randel, and Stevens, 1970).

however, suggested that severity of CF is not the pri

Part of a pulmonary rehabilitation program may

mary limiting factor in the exercise capacity of these

involve providing recommendations for the child's

children. Clearly, any aerobic exercise program de

participation in physical education (PE). Certain as

signed for older children with CF will require careful

pects of exercise relative to pul monary function in

monitoring of pulmonary support during exercise.

children with asthma need to be communicated to the PE teacher. Running is the form of exercise most likely to aggravate exercise-induced asthma, espe cially if performed in a cool, dry environment. Swim

Motor Approaches to Maximize Trunk and Ventilatory Function

ming, by contrast, is an excellent activity. Continuous

Attention to pulmonary function is easily accom

or high burst exercise might induce bronchospasm,

plished within any "handling" approach to motor

whereas short periods of exercise (less than 6 contin

therapy for children with trunk weakness, tightness,

uous minutes) may be beneficial for conditioning

alterations in tone, or general immobility. Most "han

wi thout bronchial aggravation (Magee, 1991). PE

dling" consistent with a neurodevelopmental tech

teachers should also be aware that the child may need

nique (NDT) approach lends itself readily to a dual

to use a preexercise aerosol to participate in PE with

focus on movement quality and ventilation. Extrinsic

out pulmonary consequence (Magee, 1991).

pulmonary development is clearly interrelated with musculoskeletal and motor development of the trunk.

Exercise and cystic fibrosis

Treatment should begin with assessment and ini

Physical activity designed to improve exercise toler

tial handling for functional range of motion through

ance helps children with CF to mobilize secretions

the trunk. This will typically require elongation of the

and to improve body image. The development of an

pectoral, sternocleidomastoid, upper trapezius, and

exercise program for children with CF should be done

rectus abdominis muscles. Manual lowering of the rib

on a individualized basis and a preexercise assessment

cage will also be necessary to work toward maximiz

should include but not be limited to the following:

ing chest mobility (Figure 35-13).

I. Assessment of range of motion, strength, and

Passive elongation of muscles must always be followed by active elongation. Controlled prone

posture.

2. Complete chest evaluation.

extension off the ball is both fun for the child and

3. Evaluation of ADL tolerance and limitations.

effective for the therapist (Figure 35-14). Manual

4. Inspiratory muscle strength (maximal inspira

guidance for upper extremity abduction and exter

tory ncgativc pressure at the mouth) and en

nal rotation will facilitate active elongation of the

durance testing. This inspiratory endurance

pectoral muscles via active firing of the scapular

testing can be done with an inspiratory muscle

retractors. The ball can be used to impart move

training device by having the child breathe for

ment and support the lower rib cage. This elon

a predetermined length of time at progressively

gates the anterior trunk (rectus abdominis), length

increased resistances until tolerance is reached.

5. Exercise tolerance testing, performed with ECG, blood pressure, and oxygen monitoring. A basic exercise program for children with CF

ens intercostal muscles, and facilitates increased upper chest expansion. Handling to achieve proprioceptive input of the scapulae on the posterior thorax, will help reinforce

should include activities to strengthen the back and

active thoracic extension and anterior chest expan

shoulder extensors, to elongate the trunk t1exors, and

sion. The therapist's hands can stabilize the rib cage

to address overall endurance. The role of more vigor

to reinforce abdominal oblique function during

ous exercise and fitness training in these children is a

movement (Figurc 35-15).

issue of debate, based on inconsistent incidence of

Activities requiring alternating extension-rotation


662

PART VII


FIGURE 35-13

Manual lowering of the rib cage. NOTE:

Arrows indicate direction of therapist's hand movement (caudal and medial).

FIGURE 35-15

FIGURE 35-14 Handling to facilitate active upper thoracic extension, as a

Handling to reinforce upper chest expansion and abdominal

means of actively opening the anterior chest and

oblique stabilization of the lower ribs.

lengthening rectus abdominis while supporting the lower

rib cage on the ball.


35


663

and flexion-rotation will recruit control of the abdom

4. Compare the goals of chest physical therapy for

inal obliques and maintain active upper trunk exten

infants and older children. What are the similari ties and differences?

sion. Bubble blowing, whistle toys, and singing are excellent means o f monitoring the ventilatory

5. When treating infants to improve airway clear

changes that occur with active use of increased upper

ance, what are the precautions/considerations of:

chest expansion. As tidal volume increases, vocaliza

•

positional rotation?

tions should increase in frequency, sound higher, and

•

postural drainage?

become louder.

•

percussion?

•

vibration?

•

airway suctioning?

The concept of functional carry-over is central to the treatment approach presented here. Addressing ventilation and trunk control simultaneously has intu itive appeal based not only on shared musculoskeletal relationships but also on the necessity of pulmonary ,

6.

How might neuromotor (neuromuscular) dys function affect pulmonary development and con tribute to possible postoperative complications?

7. Describe goals, precautions, and suggested monitor

tolerance for motor activity.

ing for exercise in children who have the following:

SUMMARY Cardiopulmonary physical therapy with infants and

•

a history of cardiac surgery

•

asthma

•

cystic fibrosis?

children is presented starting with issues related to development and developmental vulnerabilities. Spe cific cardiopulmonary diagnoses in pediatrics are de scribed and treatment recommendations are provided. Cardiopulmonary development and function are pre sented as the basis for indications and precautions for treatment of neonatal and pediatric patients. The link between pulmonary and motor function

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The Aging Patient

Elizabeth J. Protas

KEY TERMS

Aging

Exercise changes

Autonomic

Pulmonary changes

Cardiovascular changes

INTRODUCTION

linear but curvilinear, with changes accelerating after

Cardiopulmonary and autonomic nervous system

age 65. Thus many of the physiological studies that

functions are dynamic and undergo changes as people

have been done with 60 year olds may not apply to in

age. It is important for physical therapists to be aware

dividuals who are 80, 90, or 100 years old. Most of the

of changes that are to be expected with normal aging

studies that

to better understand the impact of disease and impair

als have been conducted with subjects who are under

ment on these functions. In addition, a clear under

age 65. A vast majority of these studies only used men

are

available on exercise in older individu

standing of how these systems respond to exercise

as subjects or had a small number of women in the

training will assist the clinician in prescribing and

sample. Gender may be an important variable in rela

evaluating exercise interventions in elders.

tion to exercise and aging, but there is limited data

Unfortunately, aging is a bit more complicated to

available on this issue. Another consideration is the

understand than just the issue of chronological age. As

composition of study populations. With increasing age,

people age, greater variability occurs between individu

there is a greater incidence of disease. Latent cardiovas

als, making predications about any one individual more

cular disease and histories of chronic illnesses are com

difficult. The trends of some changes are probably not

mon in older populations. Comorbidities are frequently 669


670

PART VII


encountered in elders. It may be more uncommon to have a person over age 75 without any problems than to have a healthy older individual. As a physical therapist, I may be more interested in the responses of a frail 85 or 90-year-old woman who has a history of hyperten sion, coronary artery disease, and diabetes than some one who is healthy at this age because this reflects the population who is referred to physical therapy. The oc currence of disease states in study populations may im pact the cardiopulmonary responses to exercise. Fi nally, the study of the physiological aspects of exercise and aging is still evolving. The literature can be confus ing and contradictory, making conclusions and general izations difficult. An attempt is made to provide some direction in this confusing maze of infonnation. An additional issue is a model of aging that might sort out some of the determinants of aging. (Figure 36-1) The model identifies biological factors, disuse, disease, and psychosocial concerns as determinants of aging. Biological factors address genetics, gender, cel lular mechanisms, and metabolical, and physiological responses that influence aging. Disuse is implicated in more sedentary life styles led by many elders, which results in loss of exercise capacity (Bortz, 1993). Ca pacities that decline as a result of disuse should be re versible or attenuated with exercise training. The em phasis in this chapter is on the biological and disuse

characteristics of aging. The impact of various dis eases is discussed in other chapters. Psychosocial is sues related to exercise and aging are not discussed. CARDIAC CHANGES WITH AGING Aerobic Capacity

The aerobic capacity is the maximum ability to per form exercise with large muscle groups. This ability is produced by the interaction of the lungs, heart, and peripheral tissues. The most common indirect mea sure of the aerobic capacity is the maximum oxygen consumption (Vo2ma,), or the maximum oxygen used during exercise. The Vo2max is directly related to the cardiac output (the amount of blood pumped by the heart) and the arteriovenous oxygen difference (the amount of oxygen extracted in the periphery). The cardiac output is the product of the heart rate times the stroke volume. The aerobic capacity reflects the central cardiac function and the efficiency of the pe ripheral tissues to extract and use oxygen. The Vo2max declines with age between 0.40 to 0.50 ml/kg/min per year in men and between 0.20 to 0.35 mllkg/min per year in women (Figure 36-2) (Buskirk and Hodgson, 1987). The reduction is ap proximately 10% per decade. The decline is larger in

V02max (ml/kg/min)

Disuse

Biological factors

--

I L:J

--

Psychosocial factors

50 1 45 40 35 30 25 20 15 10 5 o

20-29

30-39

40-49

50- 59

Age (years)

60- 75

FIGURE 36-2 Decline in maximum oxygen consumption

Disease FIGURE 36-1

from

permission Hossack KF, Bruce RA: Maximal cardiac

A model of aging which identifies the major determinants underlying the aging process.

(Vo2max)

age 20 to 75 in both men and women. (Redrawn with

function in sedentary normal men and women: comparison

of age-related changes, J App/ Physio/53:799-804, 1982.)


36

The Aging Patient

671

men than women; however, the capacity of the males

ation of the myocardial fibers, sufficient venous re

is larger than the females (Hossack and Bruce,

turn to rapidly fill the heart, and the timing of the

1982). Vo2max is related to body size, which tends to

atrial contraction to contribute to the end diastolic

be smaller in women than men. Increases in body

volume. Relaxation is hampered possibly by an in

weight as people age results in reduced V02max even

crease in ventricular stiffness, although there is lim

if the aerobic capacity remains the same, since rela

ited evidence of this in humans (Lakatta, 1993). The

tive oxygen consumption is related to body weight.

period of the isovolumic myocardial relaxation (be

Reduced physical activity with aging also con

tween aortic valve closing and mitral valve opening)

tributes to a loss of Vo2ma".

is prolonged. Likewise the peak rate of left ventricu

Considerable disagreement exists about the mecha

lar filling during early diastole is reduced in older,

nisms that contribute to the decline in V02max with

healthy men and women compared with younger in

age. Both cardiac and peripheral changes contribute to

dividuals. Despite the changes in early diastole, the

the loss. A reduction in maximum cardiac output ac

resting left ventricular end-diastolic volume remains

counts for 50% to 100% of the total reduction in

the same because of an enhanced left atrial contribu

V02max (Dempsey and Seals; Ogawa et aI., 1992;

tion to ventricular filling. This is accompanied by an

Saltin, 1986). Decreased maximum arteriovenous

enlarged left atrium and an audible fourth heart sound

oxygen consumption accounts for whatever is not due

in most older adults (Lakatta, 1993; Fleg, Gersten

to decreased maximal cardiac output. A major compo

blech and Lakatta, 1988).

nent to the decline in maximal cardiac output is a de

Considerable disagreement exists about what hap

creased maximal heart rate (Ogawa et aI., 1992; Hag

pens to diastolic function during exercise. Some re

berg, 1987). The decline in heart rate is linearly

cent studies suggest that end-diastolic volume during

related to age and occurs in both sedentary and active

exhaustive exercise increases in older men but not it

elders (Sidney and Shephard, 1977). Reduced maxi

women (Lakatta, 1993). Filling pressures during ex

mal stroke volume has also been observed as people

ercise in men increase with age (Ehrsam, Perruchoud,

age (Ogawa et aI., 1992) Recent studies suggest de

Oberholzer, Burkhart, and Herzog, 1983). In addi

creased stroke volume is associated with a decrease in

tion, peak left ventricular diastolic filling rate during

total blood volume in healthy older men and women

submaximal and maximal exercise decreases with

(Dempsey and Seals, 1995; Davy and Seals, 1994;

aging (Levy, Cerqueria, Abrass, Schwartz, and Strat

Stevenson, Davy, Reiling, and Seals, 1995). Most evi

ton, 1993; Schulman, Lakatta, Fleg et al. 1992) De

dence suggests that decreased V02max with aging is re

creased filling rate is associated with increased ven

lated to decreased maximal heart rate, stroke volume,

tricular stiffness and prolonged relaxation times

and arteriovenous oxygen difference, although each

(Ehsani, 1987).

component's contribution varies (Dempsey and Seals,

1995; Lakatta, 1993),

Resting measures of systolic and cardiac pump function do not change with aging. The resting end systolic volume and stroke volume do not change with age. Likewise, the ejection fraction at rest (end

Cardiac Mechanics

diastolic volume - end-systolic volume/end-diastolic

The most consistent cardiac structural change is a

volume) is similar in healthy older and younger indi

modest increase in left ventricular wall thickness in

viduals (Lakatta, 1993).

80 year olds compared with 20 year olds (Lakatta,

Unlike resting systolic function, the pumping func

1993), attributed to an increase in size of cardiac my

tion of the heart changes considerably in response to

ocytes and is exaggerated by hypertension and/or

exercise. Myocardial contractility as measured by the

coronary artery disease (Lakatta, 1993). After age 80,

ratio of end-systolic volume to systolic arterial pres

the left ventricular wall thickness again decreases.

sure declines during exercise as people age (Lakatta,

The cardiac filling or diastolic properties of the

1993). The end-systolic volume increases, whereas

heart are altered with age. Diastole requires a relax

the ejection fraction decreases during exercise. These


672

PART VII


changes reduce stroke volume

exercise. Re

duced contractile performance is related to a decrease

Special Cases

catecholamines is most often cited as the reason for "'

"<"vu

in maximal heart rate with

(Rodehef

in the response to beta-adrenergic stimulation,

f e r, Gerste nbl

changes in the myocardium, increased

Lakatta, 1984). Relatively intense endurance training

blood

pressure, a n d v e n t r i c u l a r w a l l abnorma l i t i e s

W e i sfeld, and

for a year or more can increase

1995).

(Dempsey and

Beck er,

stroke volume in

Ogawa, Miller,

and Jilka, 1991;

Spina,

Impact of

Training on Aerobic Capacity

older women have been attributed

and Cardiac Mechanics Older persons who continue to be active reduce the decline of 10% per decade in

1987). A recent metaanaly

sedentary adults

sis of 29 studies including 1030 men and 466 women between the ages of 61 and 78 and endurance trainconcluded that endurance increases functional

(Spina,

Kohrt, Martin, Holloszy, and Ehsani,

1993). This apparently occurs desoite intensive en durance

over a year-long

The diastolic changes thal occur with

endurance trained 13 rigor-

screened older men low

and short duration of exercise

sessions. The analysis suggests that a

68-

can be

et al., 1993).

reversed by exercise training Levy et al.

increasing age, a shorter length of Vo2rnax before

ence rather than central changes in cardiac function

in young elders

Less improvement was seen with

and

to

in arteriovenous oxygen differ

rate of decline in Vo2max to 5% per decade compare with an

and

Adaptations to exercise training in

age

60 to 82

68) and II younger men in their twenties for 6 months. The training increased and

submaximal,

rates for the older group comparable seen in the younger group (Levy et

with the

year-old individual who exercises for 30 minutes

aI., 1993). End-diastolic peak volume at rest and ex

three times per week for 4 to 6 months can improve

ercise also increase after lengthy endurance training

14%

and

1

Similar

occur in both men and women (Kohn,

Vo2max i n the

with endurance

in

which pro

in cardiac relaxation

1

This implies that

c oxidase levels and Stratton, I

1992; in the

in elders. The

on maximal cardiac (Ehsani, 1

Taffet,

McBride, and Michael, 1990;

skeletal muscles account for some of the increase in

decreases

reduces the decline of left ventricular

pressure, enhances fatty acid oxidation, and increases

duces a wider arteriovenous oxygen difference in both older men and women

reduces the age

have shown that exercise training increases calcium

are not

clear. One consistent finding is greater extraction of oxygen in the exercising skeletal

1991). Thus

response are uncertain in humans. Studies in rats

1991; Warren et The mechanisms underlying

(Ehsani et

associated diastolic changes. The mechanisms of this

and Edington, 1

All of these

have been associated with reduced diastolic

of exercise i s uncertain can either

Exercise

can also

remain the same or increase after exercise training,

mance in older men as reflected by the increase in the

depending on the effect of training on maximal stroke

exercise stroke volume. Increased

volume and maximal heart rate. Maximal heart rate

ume occurs with an increased exercise

remains the same in older men

of activity

that the decline in maximal heart on factors other than exercise and physiHagberg,

and Hol-

A decrease in response to circulating

stroke vol frac

tion, a decrease in end-systolic volume, and greater left ventricular wall mass (Ehsani et

Seals et al.,

1994). These changes apparently do not occur in older,

women

Table 36-1 contains a summary of these


et

1993).

36

TABLE 36-1

160

Cardiac Changes With Aging* BECAUSE OF AGING

Blood pressure (mm/Hg)

120 100

Oxygen consumption Heart rate Stroke volume

J, J, J,

i H i,H

J, J,

i i, H

Arteriovenous oxygen difference Cardiac output

80 60

--+-Systolic -D-Diastolic

40

Cardiac function

20

Diastolic

o �--�----�--� 35 40 45 50 55 60 65 70 75

Left ventricular wall

i, J, after 80

i

J, H

i i

J, i J,

i ,Hi J" Ht i,Ht

Left ventricular filling rate End-diastolic volume

Age FIGURE

36-3

Changes in systolic and diastolic bl.ood

Systolic

age. (Redrawn with permission from Timiras PS:

Myocardial contractility End-systolic volume Ejection fraction

Cardiovascular alterations with age: atherosclerosis, coronary heart disease and hypertension. In Timiras, PS:

basis of aging and geriatrics.

°i increase; J, decr as : H no change; =

673

140 AFTER EXERCISE TRAINING

Maximum Exercise

thickness

The Aging Patient

=

over the age of

=

tin women

Physiological

Boca Raton, Fla., 1988, CRe.)

70 (Lipsitz, 1989). Orthostatic intoler

ance is associated with decreased resting diastolic function, decreased stroke volume, extreme inactiv ity, and, in individuals with hypertension, high levels

Vascular and Autonomic Changes with Aging

of systolic blood pressure (Harris, Lipsitz, Kleinman,

Aging results in an increase in arterial stiffness be cause of a loss of elastin and an increase in collagen (Lakatta,

1993; Roach and Burton, 1959). Arterial

wall thickness and diameter and resting systolic pres

and Cornoni-Huntley,

1991).

There are decreases in baroreceptor and cardiopul

1993; Cleroux, 1989) Arterial and venous dilation are reduced,

monary reflexes with aging (Lakatta, et a\.,

36-3) (Lakatta, 1993). It is

but vasoconstriction is relatively spared. The heart

unclear whether peripheral vascular resistance in

demonstrates an overall decrease in responsiveness to

creases in normotensive older adults. Changes in the

autonomic stimulation. Older individuals experience

sure also increase (Figure

structure, size, and reactivity of the arteries increase

higher central venous and mean arterial pressures, but

the work of the left ventricle and have been directly

lower forearm blood flow and forearm vascular resis

implicated in the increase in cardiac myocyte size.

tance in response to passive leg raising (Cleroux et aI.,

Complaints of dizziness when an older patient

1989). During submaximal and maximal exercise, ar

moves from supine to standing are frequently en

terial blood pressure is either unchanged or increased

countered by the physical therapist. Postural hypoten

when comparing younger and older subjects (Seals,

sion, or orthostatic intolerance, generally does not

1993). There also appears to be impaired peripheral

occur in healthy community dwelling elders but is

vasodilation in skeletal muscle in response to exercise

common in debilitated, institutionalized individuals

(Ogawa et a\.,


1992). Redistribution of blood flow

674

PART VII


during exercise normally involves the shunting of

chest wall (Dempsey and Seals, 1995). The lung's

blood from inactive limbs and viscera. There seems to

elastic recoil depends on the composition of the con

be an enhanced vasoconstriction in inactive muscles

nective tissue, the structure of the connective tissue,

during dynamic exercise in healthy older men (Taylor,

and alveolar surface tension produced by surfactant (Dempsey and Seals, 1995). Very limited evidence

Hand, Johnson, and Seals, 1992).

suggests that the structure of the connective tissue may be the primary mechanism for age-associated

Effect of Exercise Training on Vascular

change in elastic recoil. Chest wall stiffness is ac

and Autonomic Function in Aging

companied by an increase in chest anterioposterior

Exercise training improves peripheral bloodflow in

diameter, coastal cartilage calcification, nan'owing of

skeletal muscle in 60-year-old men and women (Mar

the intervertebral disks, and changes in the rib to ver

tin, Ogawa, Kohrt, Malley, Korte, and Stoltz, 1991).

tebrae articulations (Crapo, 1993).

Systolic and mean arterial blood pressure responses

Decreases occur with the alveolar-capillary sur

to submaximal exercise are lower in physically active

face area, the alveolar septal surface area, and the

adults compared with sedentary individuals (Martin

total surface area of lung parenchyma (Brody and

et aI., 1991). Endurance training also increases mus

Thurlbeck, 1985). This reduces the surface area avail

cle sympathetic nerve activity and plasma norepi

able for gas exchange.

nephrine concentrations at rest and during a moderate

Loss of elastic recoil with aging is directly associ

isometric handgrip, indicating elevated sympathetic

ated with reduced forced expiratory flow. Limitations

nerve activity in response to exercise (Table 36-2)

in exhalation are caused by airway narrowing and

(Ng, Callister, Johnson, and Seals, 1994).

closure at all lung volumes; thus reducing forced ex piratory volume in I second (FEV1) (Dempsey and Seals, 1995) Early airway closure also produces an

PULMONARY FUNCTION

early closing volume and a relati ve increase in the

Structural and Functional Changes With Aging

total residual volume. The combination of reduced elastic recoil and increased chest wall stiffness leads

Two major changes with aging of the pulmonary sys

to a decrease in the forced vital capacity in older indi

tem are decreased elastic recoil and stiffening of the

viduals. Flow rates are also significantly lower in women and African-Americans than in Caucasian men at any age (Dempsey and Seals, 1995). Respiratory muscle strength, as reflected by the abil ity to create pressure over a range of lung volumes and

TABLE 36-2

flow rates, is similar when comparing healthy 30 and 70

Vascular and Autonomic Changes With Aging* BECAUSE OF AGING

i i

Arterial wall thickness Systolic blood pressure

i

Diastolic blood pressure Orthostatic tolerance

and

H

Vasoconstriction

pressures have been reported to decrease 15% between

?

the sixth and eighth decades (Figure 36-4) (Enright,

t t

these observed differences are similar to the differences

? ?

H

H

i

Central venous pressure

AFTER EXERCISE TRAINING

t

H

Arterial and venous dilation

year olds (Johnson and Dempsey, 1991) This suggests that respiratory muscle strength does not change with aging; however, maximal inspiratory and expiratory

Kronmal, Manolio, Shanker, and Hyatt, 1994). Perhaps observed with submaximal and maximal cardiac re sponses with the dynamic pressure measures over dif ferent volumes and flows considered submaximal. Changes in the surface area result in a decrease in

"i ?

=

=

increases;

t

=

decreases;

H =

unchanged;

insufficient data on older adult subjects

the diffusion capacity of the lung (Murray, 1986). Both the loss of surface area and a decrease in pul


36

The Aging Patient

675

monary capillary blood volume contribute to reduced

mains unchanged as people age, although the vital ca

and uneven ventilation to perfusion matching in el

pacity for elders is reduced. Likewise, as exercise and

ders. The resting partial arterial pressure of oxygen

the tidal volume increase there is a slight drop in the

declines 5 to 10 mm Hg between ages 25 and 75

ratio of dead space to tidal volume. This drop is not

(Dempsey and Sea Is, 1995). These changes do not af

effected by aging, although the older person will

fect the arterial oxymyoglobin saturation or oxygen

breathe more (have a higher minute ventilation) in re

content. Paralleling changes in the peripheral vascu

sponse to submaximal exercise.

lature, pulmonary vascular resistance and pulmonary arterial pressure at rest increase (Table 36-3).

The work of breathing is increased during exercise as people age as a result of a number of factors. Higher ventilation during exercise requires the devel opment of higher pleural pressures; thus increasing

Changes in Pulmonary Responses to

the work required. In addition, an increase in the end

Exercise With Aging

expiratory lung volume with increasing exercise re

In addition to the structural and functional changes at

sults in breathing that occurs at a stiffer point in the

rest, a number of significant changes occur in breath

lung-volume relationship. The increased stiffness im-

ing during acute exercise. Expiratory flow limitations occur at lower exercise intensities as people age. A normal, healthy 69 year old will begin to experience

TABLE 36-3

flow limitations even in response to moderate exercise

Pulmonary Function Changes With Aging*

(Dempsey and Seals, 1995). Practically, this may be

BECAUSE OF AGING

experienced by the individual as having greater diffi culty "catching his or her breath" during exercise. Normally as people exercise, the tidal volume in creases directly with increasing exercise intensity up to about 50% to 60% of the vital capacity. This re

Structure and Function Elastic recoil Chest wall stiffness Alveolar-capillary surface area

200 180 160 140 120 100 80 60 40 20

Forced expiratory flow

MEP(cmHpl ,--

Total residual volume

,-r--

Men lD.Women -

Forced vital capacity Maximum inspiratory and

J, i J, J, i J, J,

expiratory pressure Ventilation-perfusion matching Partial arterial pressure oxygen Oxygen saturation Pulmonary vascular resistance

J, J, H i

Exercise response

i i i i

Expiratory flow limitation

o f--�

65-69

Minute ventilation

70 - 74

75-79

80-84

Work of breathing

Age

Respiratory muscle oxygen consumption

FIGURE 36-4

Arterial hypoxemia

Decrease in maximum expiratory pressures between ages

Pulmonary artery pressure

65 to 84 for both men and women. This is a measure of

H,i i i

Pulmonary wedge pressure

respiratory muscle strength. (Redrawn with permission from Enright PL, Kronmal RA, Monlio TA, Schenker MB, Hyatt RE: Respiratory muscle strength in the elderly, Am J

Respir Cril Care Med 149:430-438, 1994.)

'i

increases; J, Tsubmaximal t maximal =


=

decreases; H

=

unchanged

AFTER EXERCISE TRAINING

PART VII

676

Guidelines for the Delivery of Cardiopulmonary Physical Therapy:

Cases

elastic recoil on the ventilatory mus

diffusion and may contribute to ventilation

greater pressure development by the

maldistribution ( Dempsey and

1995)

inspiratory muscles. The increase in expiratory flow resistance likewise requires greater pressure muscles. Both the inspiratory

ment by the

changes increase the work of breath

and

Effects of ExerCise Training on Pulmonary Function Aerobic training in elders can reduce some of the

ing. The increase in the work of breathing increases

that have been described. There are limited or

the respiratory muscle oxygen consumption so that

no studies that address some of the changes, such as

the

chest wall

muscles alone can

12% of the total

10% to

oxygen

during

maximal exercise in a sedentary 70-year-old man )""W.N'"

(995).

and

young

What is also apparent is that the reserves used to

artery pressure.

who are 60 to 70 years

which does

insights into what exercise might do for

not

respond to exercise represent a greater percent of the

or

The studies that are available deal with relatively

the those in their

or beyond.

Aerobic training can significantly decrease sub-

available capacity. An older individual can exceed 50% of inspiratory muscle capacity even during mod

Jones, program with

erate exercise. This is in contrast to the younger indi vidual who

exceeds 50% of the capacity with

exercise

and

Thus the reserve

maximal minute ventilation

36-5)

et

pleural pressure is reduced in eI

al., 1993). Decreased minute ventilation is accompa

v irtue of the fact that greater caoacitv is

nied by a decrease in carbon dioxide production, the

capacity to ders

1

women over a 12

and demonstrated a 7.7% drop in the sub

needed even for moderate exercise.

respiratory exchange ratio (carbon dioxide produc

The variability characteristic of exercise r e

tion/oxygen consumption), and the blood lactate level

sponses in older individuals is particularly evident

for any

when

et aI., 1986; Warren et aI., 1993). Thus the improved

and

gas

cular hemodynamics. I n demonstrate only slight

most individuals in arterial blood-gas

ventilatory than an

d e m on s t r a t e a r t e r i a l h y p o x e m i a w i t h e x e r c i s e

proved

1995). Some studies suggest

after

may have more to in the

do with improved

but a small number of individuals and

level of submaximal exercise (Makrides

rather Im

on the pulmonary system

metabolical efficiency results in the

production of less carbon dioxide; therefore the

that this response may be a factor of fitness level.

do not have to work as hard to eliminate the carbon

More fit older individuals showed progressive arter

dioxide. The important functional results of these

and carbon dioxide retention during

ial

changes are that the older adults will

laud, and Masse-Biron, 1994;

et aI., 1994).

The pulmonary artery pressure is increased with at any oxygen consumption or cardiac output during exercise (Reeves,

and

less

experience a lower perceived exertion,

mild-to-moderate exercise (Prefaut, Anselme, Cail

and use a lower

of their maximal ventila

tory capacity during exercise (Jones, Exercise training also increases maximal ventila-

\989).

maximal exercise 12-week

In addition, the maximal pulmonary artery pressure at

et pro

maximal exercise is reached at substantially lower oxy

gram referred to above increased maximum minute

gen consumption and cardiac output in older individu

ventilation

als

36-5) (Jo n e s, I

with younger persons. The pulmonary pressure also increases with age and can exceed

25 mm Hg Seals, I

peak supine exercise (Dempsey and Limited data suggest that these

pres

14% in

s/week at an

women .

Figure

These w o me n walked 5 of 78% of the maximal

treadmill heart rate or 118 beats/minute on average, so the program was not very strenuous but

IJH;'UWc.C'u

sures may in tum induce pulmonary edema during in

substantial

tense exercise in elders. Pulmonary edema would limit

training can improve submaximal ventilatorv effi


in maximum ventilation. Exercise

70

Ventilation (L/min)

677

The Aging Patient

36

REVIEW QUESTIONS which occur

What are the

1.

with

in the cardiovascular

What outcomes will exercise

2.

pro

duce in an older adult's cardiovascular sys tem?

3.

What are the major

that occur with

in the autonomic nervous and which of these

sponse to

can be influenced by execise What are the major

4.

that occur in the

pulmonary system with

and in reo

to exercise?

5.

Describe the possible impact of exercise on the

system.

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FIGURE 36·5 Submaximal and maximal minute ventilation pre- and postwith a 12-week

exercise

program in women

whose mean age was 72.5 years. (Redrawn with

aging of the lung. In Fishman, A.P. (Ed.). Handbook oj physi

14:60-65. 1993).

ciency and increase maximum ventilation in elders.

36-3 on p. 675 summarizes the pulmonary willi

41, 1004-1008,

ology. (Vo! 3).

in

Buskirk, E.R., & Hodgson, l.L. (1987). Age and aerobic power: the rate of changes in men and women. Federation Proceed ings,

Table

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Brody, 1.S., & Thurlbeck, W.M. (1985). Development, growth, and

O'Donnell KA, Haddock BL, Butterworth DE: septua,genansiO wonnen, Inl J Sports Med

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Bortz, W.M. (1993). The physics of frailty, Journal American Ger ia/ric Society,

from Warren BJ, Nieman DC, Dotson RO, Adkins CH, responses to exercise

exercise-induced hypoxemia in highly trained athletes. Juurnal

and exereise.

46, 1824-1829.

Cleroux, 1. et a!. (1989). Decreased cardiorespiratory reflexes with aging. American Journal oj Physiology 257, H961-H968. Crapo, R.O. (1993). The aging lung. In Mahler, DA (Ed.). Pul monalY disease in Ihe elderly, New York: Marcel Dekker.

Davy, K.P., & Seals, D.R. (1994). Total blood volume in healthy young and older men. Journal o f Applied Phy siology, 76,

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2059-2062.

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submaximal and maximal exercise as

age.

Many of these changes are reduced or reversed as a result of exercise training. The many of these use than

Dempsey, J.A., & Seals, D.R. (1995). Aging, exercise, and car diopulmonary function. In Holloszy, 1. (Ed.), Perspectives in exercise science. New York: Williams & Wilkins.

Ehrsam, R. E., Perruchoud. A., Oberholzer, M., Burkhart, F.&

is that

Herzog, H. (1983). Influence of age on pulmonary hemody

may have more to do with dis

namics at rest and during supine exercise. Clinical Science,

individuals tend to

65, 653-660, Ehsani, A.A. (1989), Cardiovascular adaptations to exercise training in the elderly. Federation Pro ceedings, 46 1840 ,

1843.

at any age can derive benefits from exercise training. Even very modest, short· term interventions have efficacious. Older individuals should be en· couraged to engage in regular physical activity to im· prove their exercise

Ehsani, A.A, Ogawa, T, Miller, T.R., Spira, R.J., & liIka, S,M. (1991). Exercise training improves left ventricul3( systolic function in older men. Circulation, 83, 96-103. Enright, PL, Kronmal, R.A., Manolio, T.A. Shenker, M.B., & Hyatt, RE (1994). Respiratory muscle strength in the elderly. American Journal Respiratory Critical Care Medicine, 149,430-438.


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Fleg, J.L., GerstenbIeth, G" & Lakatta, E.G. (1988). Pathophysiology

Roach, M.R" & Burton, A.e. (1959). The effect of aging on the

of the aging heart and circulation. In Messerli, FH. (Ed.). Cardio

elasticity of human iliac arteries. Canadian Journal Biochem

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Green, J.S., & Crouse, S.F. (1995). The effects of endurance train

Rodeheffer. R.1., Gerstenhlith, G., Becker, J.L., Fleg, J.L., Weis

ing on functional capacity in the elderly: a meta-analysis. Med

field, M.L., & Lakatta, E.G. (1984). Exercise cardiac output is

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maintained with advancing ages in healthy human subjects: car

Hagberg, J.M. (1987). Effect of training on the decline of V02max with aging. Federation Proceedings, 46, 1830-1833.

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Harris, T., Lipsitz, L.A., Kleinman, J.e., & Cornoni-Huntley, J.

Saltin, B. (1986). The aging endurance athlete. In Sutton, J.R., &

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Brock, R.M. (Eds.). Sports medicine for the nU:IIure athlete. In

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Hossack K.F, & Blllce, R.A. (1982). Maximal cardiac function in

L.e., & Gerslenhlith, G. (1992). Age-related decline in left

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ventricular filling at rest and exercise. American Journal of

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Johnson,B.D., & Dempsey, J.A. (1991). Demand vs capacity in the

Seals, D.R. (1993). lnflucnce of aging on autonomic-circulatory

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control in humans at rest and during exercise. In Gisolfi, e.V.,

sport sciences review. (Vol 19). Baltimore: Williams & Wilkins.

Lamb, D.R., & Nadel, E.R. (Eds.). Perspectives in exercise sci

Jones, N.L. (1986). The lung of the Master's athlete. In Sutton, J.R., & Beck, R.M. (Eds.). Sports medicine for the mature ath lete. Indianapolis Benchmark Press.

ence and sports medicine. (Vol 6) Exerci.l'e, heat, and ther moregulation. Dubuque: Brown & Benchmark. Seals, D.R., Hagberg, J.M., Hurley, B.F., Ehsani, A.A., Holloszy,

Kohrt,W.M., et al. (1991). Effects of gender,age, and fitness level

J.O. (1985) Endurance training in older men and women. l.

on response of V02max to training in 60-71 yr olds. Journal of

Cardiovascular response to exercise: Journal of Applied Physi ology, 57, 1024-1029.

Applied Physiology, 71,2004-2011. Lakatta, E.G. (1993). Cardiovascular regulatory mechanisms in ad

Seals, D.R .. Hagberg, J.M., Spina, R.J., Rogers, M.A., Schechtman, K.B

vanced age. Physiology Review, 73,413-467.

..

& Ehsani, A.A. (1994). Enhanced left ventricular perfor

Levy, W.e., et al. (1993). Endurance exercise training augments

mance in endurance trained older men. Circulation, 89, 198-205.

diastolic filling at rest and during exercise in healthy young and

Sidney, K.H., & Shephard, R.1. (1977). Maximum and submaximum

older men. Circulation 88, 116-126.

exercise tests and men and women in the seventh, eighth, and

Lipsitz, L.A. (1989). Orthostatic hypotension in the elderly. New England Journal Medicil1e 3 2 1, 952-957.

ninth decades of life. Joumal of Applied Physiology 43,280-287. Spina, R.J., Ogawa, T, Kohn, W.M., Martin 1lI, W.H., Holloszy,

Makrides, L., Heigenhauser, G.1., Jones, N.L. (1986). Physical training in young and older healthy subjects. In Sutton, J.R., Brock, R.M. (Eds.). Sports medicine for the mature athiete. In

J.O., & Ehsani, A.A. (1993). Differences in cardiovascular adaptations to endurance exercise training between older men and women. Journal of Applied Physiology, 75:849-855. Starnes, J.W., Beyer, R.E., & Edington, D.W. (1983). Myocardial

dianapolis: Benchmark Press. Martin,Ill, W.H., Ogawa,T,Kohrt, W.M , Malley,M.T, Korte,E.,

& Stolz, S. (1991). Effects of aging, gender, and physical train ing on peripheral vascular function. Circulation, 84, 654-664. Murray, J.F (1986) Aging in the normal lung. (2nd ed.). Philadel phia: WB Saunders.

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Ng, A.V" Callister, R., Johnson, D.G., & Seals, D.R. (1994) En durance exercise training is associated with elevated basal sym

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old rats. American Journal of Physiology, 27, H431-H435.

Ogawa, T, el al. (1992). Effects of aging, sex, and physical train ing on cardiovascular responses

10

exercise. Circulation, 86,

Taylor, J.A., Hand, G.A., Johnson, D.G., & Seals, D.R. (1992). Augmented forearm vasoconstriction during dynamic exercise in healthy older men. Circul{ltion, 86, 1789-1799.

494-503. Prefaut, e., Anselme, F, Caillaud, e., & Masse-Biron, J. (1994). Exercise-induced hypoxemia in older athletes. Journal of Ap plied Physiology 76, 120-126.

Timiras, P.S. (1988). Cardiovascular alterations with age: athero sclerosis, coronary heart disease and hypertension. In Timiras, P.S. (1988). Physiological basis of aging and geriatrics. Boca

Reeves, J.T, Dempsey, J.A., & Grover, R.F. (1989). Pulmonary

Raton, FL: CRe.

circulation during exercise. In Weir, E.K., & Reeves, J.T.

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Sports Medicine, 14, 60-65.


The Patient with Neuromuscular or Musculoskeletal Dysfunction Mary Massery

KEY TERMS

Adverse musculoskeletal changes

Paradoxical breathing

Chest development

Planes of ventilation

Effects of gravity

Pulmonary function tests

Gravity

Respiratory impairments

Impaired phonation support

Respiratory muscles

Musculoskeletal deficits

Sleep disorders

Neuromuscular deficits

Triad of ventilation

Nighttime hypoxemia

INTRODUCTION

muscular and/or musculoskeletal deficits and what

It is often observed in a rehabilitation setting that

clinicians can do to minimize or eliminate these

patients with neurological deficits continue to ac

complications. The focus of this treatment approach

quire respiratory problems long after their acute

is primarily aimed at the physical therapist (PT).

phases have subsided. Research has repeatedly doc

Every effort is made to explain specific physical

umented a decrease in pulmonary function for the

therapy concepts so that all clinicians, occupational

chronic neurologically impaired patient, yet many

therapists (OTs), speech language pathologists

therapists do not appear to fully comprehend why

(SLPs), respiratory therapists (RTs), and nurses

this occurs. This section tries to elaborate the causes

(RNs), family members, and others can benefit from

of respiratory complications secondary to neuro

the ideas presented in this chapter. 679


680

PART VII


DIAGNOSES ADDRESSED

ing may respond better to techniques that act primarily

The following treatment ideas are applicable for all

on the subconscious and require little cognitive partici

neurological and orthopedic diagnoses including the

pation. Finally, the differcnce between rehabilitation

following: spinal cord injuries (SCI), head traumas,

and habilitation must be understood. Rehabilitation in

cerebral vascular accidents (CV A), multiple sclerosis

volves restoring function, and habilitation teaches

(MS), amyotrophic lateral sclerosis (ALS), Parkinson's

functioning for the first time. Children with acquired

disease, cerebral palsy (CP), muscular dystrophy (MD),

deficits in utero or shortly after birth have never expe

polio myelitis (polio), spina bifida, and neuropathies as

rienced normal movement patterns. Therefore they

well as back, neck, and shoulder injuries or dysfunc

cannot depend on the memory of past motor experi

tion. However, it is by no means an exhaustive list. The

ences to help con'ect abnormal motor patterns the way

primary consideration for application of these treatment

adults going through rehabilitation can. This important

techniques is the residual physical deficits left by a neu

difference must be accounted for when developing

rological or musculoskeletal insult. Therefore a patient

their treatment programs.

presenting with hemiplegia will be treated with tech niques geared toward promoting increased function on the involved side, regardless of how the original deficit

PLANES OF VENTILATION

was acquired (e.g., from a CVA, head trauma, or CP).

This neuromuscular/musculoskeletal treatment ap

Likewise, tetraplegia or paraplegia not only refers to

proach is based on the premise that ventilation does

patients that have suffered from SCls but any patient

not take place in a one-dimensional plane but rather as

that presents with tetraplegic or paraplegic deficits. However, three aspects of neurological/muscu

a three-dimensional activity. The chest expands in an anterior-posterior plane, an inferior-superior plane, and

loskeletal disorders must be clarified here to assist the

a lateral plane (Figure 37-1). Too often, therapists treat

therapist in discerning which techniques, described

patients with neuromuscular and/or musculoskeletal

later, are appropriate for his or her particular patient.

dysfunctions with apparent disregard for this ex

(1) progressive vs. nonpro

tremely important fact. This one-dimensional fallacy

(2) cerebral vs. noncerebral injuries,

has been perpetrated by techniques taught to new ther

and (3) rehabilitation vs. habilitation. Single-insult in

apists that describe the patient's breathing program in

The three aspects follows: gressive injuries,

juries, such as SCTs, traumatic brain injuries, CVAs,

only one or two postures, most often supine and sit

CPs, or cervical whiplash, are nonprogressive. The

ting. To be effective, we must acknowledge this three

damage was only inflicted once and does not repeat it

dimensional movement of the thorax and use this con

self. Progressive diseases, on the other hand, such as

cept when determining treatment protocol.

MS, ALS, Parkinson's disease, MD, or scoliosis, show increasing physical deficits over time. Goals for these groups will be different, with maximal respiratory functioning stressed for the single-insult diagnoses and

EFFECTS OF GRAVITY If chest expansion takes place in three planes, the ef

comfort and ease of ventilation stressed for progres

fect of gravity on these planes must be considered.

sive diagnoses. Similar treatment consideration is

Physical therapists would not exercise a weak muscle

given for patients with detrimentally affected cerebral

without taking into account the effect of gravitational

functioning, such as with traumatic brain injuries,

pull on that muscle, tbereby making the positioning

CVAs, and Parkinson's disease, versus those whose

of the limb in space an important consideration in

deficits are at the spinal level, such as with SCIs, neu

treatment planning. This same consideration must be

ropathies, myopathies, and polio. Patients with only

given for the weakened ventilatory muscles. Gravity

spinal involvement may respond favorably to complex

can assist, resist, or have no effect on the movement

techniques and demonstrate better conscious carry

of the chest wall, according to the chest's position in

over, whereas those with impaired cerebral function

space. Consider weakened intercostal muscles. Plac


37

TIle Patient with Neuromuscular or MuscuJoskeletal Dysfunction

681

in abdominal tone (many SCIs, Guillian-Barre syn drome, or spina bifida), intestinal positioning be comes an important factor in respiratory functioning. The abdominal wall acts as the anterior support for the intestines, causing the intestines to sit high in the abdominal cavity (see Chapter

2). This forces the

diaphragm to rest high, at approximately the level of the fifth rib in an erect posture (Figure

37-2). The di

aphragm contracts, drawing its origins toward its in sertion (concentric contraction). These muscle fibers, which originate down as low as the tenth rib, must rise up superiorly and then medially toward the cen tral tendon (see Chapter

2). This movement pattern

causes primarily superior and lateral expansion of the lower chest. Without abdominal wall support, the intestines shift inferiorly and anteriorly, the "beer belly" effect, allowing gravity to position the di aphragm lower in the abdominal cavity (Figure

373). This p u t s t h e d i a p h r a g m at an e x t r e m e

mechanical disadvantage. Instead o f having t o rise

••

up and over the intestines, the lateral fibers of the di aphragm can now move more horizontally to reach the central tendon, thereby significantly reducing ex cursion in all three planes of expansion. This adverse positioning may be so significant as to cause a nega

FIGURE 37-1

tive lower chest expansion on inspiration for patients

Planes of respiration (anterior-posterior, inferior-superior,

with tetraplegia. Quantitatively, this may be seen as

and lateral).

much as

Y2- to I-inch decrease rather than increase in

overall lower chest expansion, measured at the ing a patient with this deficit in a supine position for

xiphoid process, when the patient proceeds from

initial treatment in his or her rehabilitation program

maximal expiration to maximal inspiration.

and then asking the patient to "breathe up into your

Since gravity causes the intestines to shift, the ef

hands" is asking the patient to attempt the most diffi

fect on the diaphragm will be most dramatic in a

cult gravitational posture first (breathing into the an

gravity-dependent position, such as sitting or stand

terior plane with gravity resisting the movement). It

ing, rather than in a gravity-eliminated position, such

would seem more appropriate to start retraining tech

as supine. Thus the imponance of providing the pa

. niques in a gravity-eliminated posture for anterior

tient with an external abdominal wall support in these

chest expansion, such as side lying, or a gravity

upright postures should be undeniably clear. Al

assisted posture, such as hands-knees, and then

though not as effective as the abdominal muscles

progress to gravity-resisted postures, such as supine. Gravity also affects the positioning of the in testines under the diaphragm. In the normal, neuro

themselves, abdominal supports help restore the nat ural mechanical advantage of the diaphragm (see Chapter 22).

logically intact person, this seems to have a minor ef

In addition to changing muscle effectiveness,

fect on respiratory functioning. However, for many

gravity also affects bony structures. Obviously, this

neurologically impaired persons with a marked loss

affects a growing child more so than a fully devel


682

PART VII


FIGURE 37-2 Proper mechanical positioning of the diaphragm relative to the abdominal viscera. Note the high dome shape of the diaphragm.

oped adult, but both will be affected. Bones grow ac

plays an extremely crucial role in the skeletal devel

cording to stress laid on them, thus abnormal stresses

opment of the chest in the newborn. Normal, neuro

produce abnormal bony developments. For persons

logically intact infants move freely in and out of pos

with severe neurological deficits, gravity becomes the

tures, such as prone, hands-knees, and standing, as

main force acting on the bones and joints, unopposed

they progress developmentally, allowing gravity to

by normal muscle action. This can result in many

alternately assist or resist the movements. Through

skeletal deformities, such as flattening or flaring o f

this, the infant begins to strengthen and develop mus

the lower anterior rib cage, narrowing of the upper

cle groups and learn to interact with the gravitational

chest, loss of normal spinal curves, and chest cavus

force in his or her environment.

deformities. Prevention of these deformities, rather

This combination of normal movement patterns in

than their cure, must be the aim of a good long-term

a gravitational field, along with genetic predisposi

ventilatory program for the neurologically impaired.

tion, accounts for the normal development of the bones, muscles, and joints that comprise the chest

GRAVITY: EFFECTS ON CHEST DEVELOPMENT

wall. Conversely, infants with severe neurological impairments do not have that same freedom of move

Thus far the effects of gravity on the planes of venti

ment within their environments. This applies to chil

lation, muscle function, and bony changes in the

dren with congenital deficits, such as CP or spina bi

adult have been discussed. This same force, gravity,

fida, or for children who acquire deficits at an early


37

The Patient with Neuromuscular or Musculoskeletal Dysfunction

683

FIGURE 37-3 Independent upright posturing in a patient with congenital quadriplegia. Note relationship of rib cage and abdominal viscera.

developmental age, such as some CY As, head trau

neck renders the upper accessory muscles nonfunc

mas, or SCIs. These children become subjugated to

tional as a ventilatory muscle. The infant's arms are

the effects of gravity on their growing and develop

held in flexion and adduction across the chest, signif

ing bodies because they are unable to independently

icantly hampering lateral or anterior movement of the

counteract its constant presence. A variety of reasons

chest wall. This all points to underdevelopment of the

may account for their inability to change their own

upper chest region in the newborn. The infant, forced

(I) muscle weakness, (2) tonal problems (e.g., spasticity or flaCCidity), (3) reflex dominance, (4) incoordination, or (5) a combination

to be a diaphragmatic breather, shows greater devel

positions in space:

of the above. Typically, these children spend signifi cantly more time in supine than in any other posture, which can lead to undesirable changes in the thorax.

opment of the lower chest and hence leads to the tri angular shaping of the rib cage. From

3 to 6 months of age, the infant begins to de

velop more trun k extension tone, they spend more time in a prone on elbows position, and they begin to

Understanding the basic steps and principles in

reach out into the environmenr with the upper extrem

normal chest development is essential for accurately

ities. This facilitates development of the anterior

assessing abnormal chest deformities often seen in

upper chest. Constant stretching helps to expand the

this physically challenged population. Initially, the

anterior upper chest both anteriorly and laterally. An

newborn's chest is triangular in shape, narrow and

increase in intercostal and pectoralis muscle strength

flat in the upper portion, and wider and more rounded

improves the infant's ability to counteract the force of

37-4). The infant's short

gravity on the anterior upper chest in supine, leading

in the lower portion (Figure


684

PART VII


FIGURE 37-4 Newborn chest configuration. Note triangular shape.

FIGURE 37-5 A and B, I O-month old infant chest configuration. Note shape of chest changes and angle of ribs.


37

The Patient with Neuromuscular or Mu culoskeletal Dysfunction

685

to the development of a slight convex configuration of

Children with severe neurological deficits often

the area and a more rectangular shaping of the thorax

show a very different picture of chest development.

from a frontal plane.

Frequently, they do not develop adequate upper

The next significant development occurs when

extremity and neck muscle control (e.g., weak mus

the child begins to independently assume erect pos

cles, tone problems, reflex dominance, or incoordina

tures (e.g., sitting, kneeling, or standing). Until this

tion), causing their upper chests to retain the more

time, the ribs are aligned 'fairly horizontally, with

primitive triangular, flattened shape. Inadequate mus

narrow intercostal spacing (see Figure 37-4). In fact

cle control or chronically shortened neck muscles

the newborn's chest only comprises approximately

also renders the accessory muscles less able to assist

one tbird of the total trunk cavity. As the child be

if needed in ventilation. In some cases the child's di

gins to move up against the pull of gravity, the ribs

aphragm remains so strong and unbalanced by the ab

rotate downward (more so in the lower ribs), creat

dominal and intercostal muscles that it creates a

ing the sharper angle of the ribs as seen in the adult

cavus deformity (pectus excuvatum) at the sternum

(Figures 37-5 and 37-6). This markedly elongates

(Figure 37-7). This occurs when the intercostal mus

the rib cage until it eventually occupies more than

cles are incapable of maintaining the anterior chest

half of the trunk cavity. A comparison of chest x

wall's position against gravity and the abdominal

rays of newborns and adults, as well as pictures of

muscles are weak or flaccid, thus not stabilizing the

infants, clearly shows these developmental trends

lower borders of the thorax. This may also eventually

(see Figure 37-4 to 37-6). Development trends are

cause an anterior flaring of the lower ribs.

summarized in Table 37-1.

Most of these children with severe neuromuscular

FIGURE 37-6 Normal adult chest x-ray. Chest shape is rectangular, ribs angled downward, upper and lower chest equally developed.


686

PART VII


impairments require significant assistance to maintain

rectus abdominus, as seen in many children with spastic

an upright posture, therefore they spend more time in a

tetraplegia CP, the chest will become flattened anteri

recumbent position. Thus the rib cage tends to show

orly, yet flared laterally in the lower ribs (Figure

less downward rotation and elongation than that of the

These children are unable to stabilize the lower lateral

37-8).

normally developing child. In some cases of prolonged

borders of their rib cage and are unable to counteract

supine posturing combined with hyperactivity of the

gravity's influence on the anterior chest wall move-

TABLE 37-1 Chest Development Table

Chest

Infant

Ad ul t

Size

Occupies one third of the trunk cav ity

Occupies greater than one half trunk cavity

Shape

Triangular frontal plane

Rectangular frontal plane

Circular anterior-posterior plane

Elliptical anterior-posterior plane

Upper chest

Narrow

Wide

Flat apex

Convex apex

Circular

Elliptical

Flared lower ribs

Integrated with abdominals

Ribs

Evenly horizontal

Rotated downward; especially inferiorly

Intercostal spacing

Narrow

Wide

Limits movement of ribs

Allows for individual movement of ribs

Lower chest

Diaphragm Accessory muscles

Adequate

Adequate

Minimal dome shape

Large dome shape, greater excursion

Nonfunctional

Functional

FIGURE 37-7 Pectus excavation deform i t y (secondary to spinal cord injury and resultant muscle imbalance).


37


687

ments. Thus we see these adverse musculoskeletal

occurs because of pressure gradients between the air

changes, which limits the breathing patterns options.

outside the lungs and the air inside. These gradients

As long as the neurological deficits are present,

are achieved through movements in the chest wall.

these children will never develop normally. However,

Muscle contractions provide the power to move the

frequent position changes, inhibition of undesired

chest wall. If these muscles do not overcome the ef

tone, facilitation of weakened chest muscles, promo

fect of gravity because of weakness, paralysis, abnor

tion of preferred breathing patterns, and incorporation

mal tone, or inadequate muscle control, the chest will

of ventilatory strategies with movement will stimu

be unable to expand in all three planes of ventilation,

late normal chest development. Optimum respiratory

thus limiting pulmonary function. Because of this im

function cannot be expected from a severely underde

portant fact, all muscles originating or inserting into

veloped chest.

the chest wall become "ventilatory muscler" The box on p. 688 lists these muscles and how they affect chest expansion and other specific respiratory function.

MUSCULAR AND TONAL INFLUENCES

They are listed in the following two distinct groups:

ON CHEST DEVELOPMENT

the primary muscles needed for normal ventilation

Adverse effects of gravity are counteracted by func tioning musculature. Recall that inspiration/expiration

(the triad of normal ventilation) and all other acces sory muscles of ventilation. Impairment to any of these muscles may result in respiratory deficits. Another factor that determines a muscle's effec tiveness as a chest wall mover is neurological tone in the muscle. Rigidity of movement, as seen in some patients with head traumas and Parkinson's disease will render the chest immobile, severely limiting its ability to expand in any plane. Spasticity, more often to a lesser degree than rigidity, can render the chest immobile. Spasticity (i.e., SCI, CP, some head trauma), is frequently activated by quick movement of the affected muscle either actively or passively. A quick activity like coughing may activate this abnor mal tone and work against the patient as he or she tries to produce an effective cough. The other extreme of abnormal muscle tone is flaccidity or lack of any muscular tone, as seen with some SCIs, CY As, and MD. In this case the muscle is entirely unable to move the chest wall or to counteract the effects of gravity. Of the three types of abnormal tone, flaccidity is the most adversely influenced by the effects of gravity. At the same time, postural reflexes and their effect on muscle tone must be considered. For instance, the tonic labrinthyne reflex (TLR) increases extensor tone when the person is supine and increases flexor tone when that person is prone. For patients with CP, for example, this reflex may stay a dominant force in

FIGURE 37-8

their motor control, interfering with their ability to

Musculoskdetal changes secondary to static positioning

move freely in supine and prone positions. Because

and neurological deficit.

of this, a child with CP with increased extensor tone


688

PART VII


Trunk Muscles and Their Function in Ventilation Muscles of Velltilatioll-Three-Dimensional Movements Triad of lIormal velltilatioll Diaphragm •

Major muscle of passive ventilation

•

Innervation-phrenic nerve-C3 to C5

•

Primary movement-all three planes

•

Dependency on intercostal and abdominal muscles

•

Concentric contractions--quiet and forceful inhalation

•

Eccentric contractions---controlled exhalation and speech

Intercostals •

Primary function-stabilizes rib cage

•

Innervation-Tl to T2

•

Primary movement-concentric contractions •

Lateral and superior expansion in lower chest during both quiet and forceful inhalation. Anterior expan sion occurs to a lesser degree.

•

•

Anterior and superior expansion in upper chest, lateral expansion occurs to a lesser degree. Forceful exhalation-primarily medial and inferior compression in lower chest, posterior and inferior compression in upper chest

•

Eccentric contractions-needed for controlled exhalation and speech

Abdominals •

Stabilizes inferior border of rib cage-provides mid trunk control

•

Innervation T6 to L I

•

Provides visceral support

•

Provides positive pressure support for the diaphragm

•

Provides necessary intrathoracic pressure for an effective cough

Accessory muscles Erector spinae •

Stabilizes thorax posteriorly to allow for normal anterior chest wall movement to occur

•

Innervated at TI to S3

Pectoralis muscles •

Provides upper chest anterior and lateral expansion

•

Innervated C5 to TI

•

Can be a substitute rib cage stabilizer after paralysis of the intercostal muscles

Serratus anterior •

Provides posterior expansion of rib cage when upper extremities are fixated

•

Innervated C5 to C7

•

Only inspiratory muscle that is paired with trunk flexion movements rather than tnlllk extension mo.ements


37

The Patient with Neuromuscular or Musculoskeletal Dysfullction

689

Trunk Muscles and Their Function in Ventilation-cont'd Scalenes •

Provides superior and anterior expansion of the upper chest

•

Innervated C3 to C8

Sternocleidomastoid •

Provides sup e ri or and anterior exp ansi on of upper chest

•

Innervated C2 to C3 and accessory cranial nerve

Trape zi us •

•

Provides superior expansion of the upper chest Innervated C2 to C4 and accessory crani al ne rve

will see an even greater increase in that abnormal

DECREASED CHEST EXPANSION

tone if placed supine. That will make it more difficult

Muscle weakness or abnormal tone, combined with

for the child to attempt any flexion phase of a breath

the effects of gravity that were previously discussed,

ing pattern in supine (coughing or exhalation). Chil

serve to decrease the ability of the chest to expand in

dren should not be left supine as the therapist teaches

one or all three planes of ventilation. Quantitatively,

them altered breathing patterns. If the goal of that

chest expansion can be measured via lung volumes

treatment session is to promote controlled exhalation

by taking vital capacity readings and comparing them

maneuvers, the child would have been positioned for

with the norms, and it can be measured by taking

failure rather than success. Therefore positioning of

chest excursion measurements during inhalation with

the patient and tonal inhibitory or facilatory tech

a tape measure in three places: under the axilla, just

niques become of vital importance when developing

beneath the nipple line, and on the lowest most ribs

a treatment plan for maximizing respiratory function.

(8,9, and 10). Although both methods give an objec tive measurement, neither technique can assess which

SPECIFIC RESPIRATORY IMPAIRMENTS

planes of ventilation are being compromjsed. Subjec

The first half of this chapter discusses the forces that

ing factors. The box on p. 690 gives detailed sum

influence the functioning of the neurologically im

maries of such assessments for persons with aU levels

paired chest. Understanding these forces allows one

of SCls. These characteristics can be extrapolated to

to discern the impairments that will appear as a di

subjective chest assessments of other neurological

tive assessment skills are needed to dctermine limit

rect or indirect result of those neurological deficits.

and/or musculoskeletal disorders, especially where

Decreased chest expansion, abnormal or inefficient

weakness is present.

breathing patterns, abnormal bony changes, de creased cough effectiveness, decreased coordination of breathing with functional activities, decreased

COMPENSATORY BREATHING PATTERNS

ability to phonate, and decreased ability to self-main

Limitations in chest expansion inevitably lead to

tain bronchial hygiene can all be direct results of se

changes in breathing patterns. Severely involved

vere neurological deficits. These specific impair

CV As or head trauma patients may show severe ab

ments are addresseu now in detail.

normalities in their breathing patterns in response to


PART VII

690


Neuromuscular Effects

Oil

Respiratory FU1lction in Spi1lal Cord Injuries

Paraplegia: Primarily Tl to T5 I.

Weakened and/or absent •

2.

•

Intercostal

•

Erector spinae

Planes of ventilation limited •

3.

Abdominal

Slight decrease in anterior and lateral expansion

Resulting in •

Slight to moderate decrease in chest expansion and vital capacity (YC)

•

Decreased ability to build up intrathoracic and intraabdominal pressures

•

Decreased cough effectiveness

•

Possible paradoxical breathing

Tetraplegia: C5 to C8 I.

2.

3.

Missing aforementioned muscles and weakened •

Pectoralis

•

Sen-atus anterior

•

Scale·nes


Marked decrease in anterior and lateral expansion

•

Slight decrease in posterior expansion

Resulting in •

Significant decrease in chest expansion and VC

•

Significant decrease in forced expiratory volume (FEY)

•

Significant decrease in cough effectiveness

•

Paradoxical breathing in acute phase and perhaps longer

Tetraplegia: C4 I.

2.

3.

Missing aforementioned muscles and weakened •

SClllenes

•

Di aphragl1l


Marked decrease in anterior and lateral expansion

•

Slight decrease in inferior and superior expansion

Resulting in •

More pronounced limitations in all three planes of ventilation

•

Possible decrease in tidal volume (TY)

•

Possible need for mechanical ventilation


37


691

Neuromuscular Effects on Respiratory Function in Spinal Cord Injuries-cont'd Tetraplegia: Cl to C3 I.

2.

Missing aforementioned muscles and weakened and/or absent, the last of the remaining accessory muscles •

Sternocleidomastoid (SCM)

•

Trapezius


3.

All severely limited including superior expansion

Resulting in •

Significant decrease in TV

•

The need for full-time mechanical ventilation (at least in acute phase)

impairments to their respiratory centers in the brain stem. This chapter focuses on compensatory breathing patterns that develop as a result of muscular weakness or paralysis, high tone, or pain. Details of breathing

Possible Compensatory Breathing Patterns after a NeurologicallnjurylDisease •

pattern changes secondary to brain stem lesions can

Paradoxical breathing (see-saw breathing) •

be found in Chapter 22. The compensatory patterns discussed here are itemized in the box at right. There are two types of paradoxical, or "see-saw," breathing. The first is caused by a strong diaphragm

•

in the absence of the two other triad muscles, inter costal muscles and abdominal muscles (e.g., polio, tetraplegia, or paraplegia). Normal diaphragmatic ex

•

cUl'sion requires the muscular support and function of the intercostal and abdominal muscles to optimize the

•

•

paradoxical breathing.

abdomen rises excessively

Paralyzed diaphragm •

lower chest collapses

•

upper chest rises excessively

Diaphragm and upper accessory muscles only Upper accessory muscles only (all three "triad"

Asymmetrical breathers (hemiplegia, unilateral disorders)

•

of the stabilizing contraction of the intercostal mus cles (Figure 37-9). This is the more common form of

•

muscles paralyzed)

excessively because of flaccid abdominal muscle tone, and the upper chest collapses because of a lack

upper chest collapses

(paralyzed intercostals)

diaphragm's contractions. In this type of paradoxical breathing the diaphragm contracts, the abdomen rises

Paralyzed intercostals and/or abdomina Is •

Lateral or "gravity eliminated" breathers (weak ness not paralysis)

•

Shallow breathers (typically associated with high tone)

The second type of paradoxical breathing occurs when there is diaphragm paralysis while the upper accessory muscles are still intact. The abdominal muscles may or may not be functional. The see-saw

primarily in a superior plane. Anterior and lateral ex

action here is the opposite motion of that described

pansion may also occur if the intercostal and pec

previously (Figure 37-10). With this type of paradox

toralis muscles are functioning. Generally, this com

ical breathing, the abdomen draws inward during in

pensatory breathing pattern requires some kind of

spiration and the upper chest rises. The upper acces

assisted ventilation, at least part time, because the di

sory muscles c o n t r a c t , exp a n d i n g the r i b c a g e

aphragm normally supplies most of the expansion


692

PART VII


FIGURE 37-9 Paradoxical breathing, strong diaphragm, absent accessory muscles and abdominal muscles.

W((I' FIGURE 37-10 Paradoxical breathing, diaphragm paralysis.

necessary to maintain adequate oxygenation levels.

Another type of compensatory breathing pattern oc

Total accessory muscle breathing is generally inca

curs when the intercostal and abdominal muscles are

pable of providing adequate independent long-term

paralyzed but the diaphragm and upper accessory mus

ventilation because of the likelihood of respiratory

cles still function (i.e., tetraplegia, Cs to Cs; and para

muscle fatigue.

plegia, T I to T5). These patients learn to counterbal


37


693

FIGURE 37-11 Shortened neck musculature secondary to accessory muscle breathing pattern.

ance the strength of the diaphragmatic pull by using

Neurological insults that affect the chest asymmet

their sternocleidomastoid muscles and possibly their

rically, such as with CV As and some head traumas,

scalene, trapezius, and pectoralis muscles. Allowing

show another type of compensatory breathing pattern.

for superior and possibly some anterior and lateral ex

These patients can still acti vely ex pand their unaf

pansion of the chest, this compensatory breathing pat

fected side in all three planes of ventilation. Often,

tern prevents the collapse of the upper chest seen in

they accentuate this asymmetry to achieve more ex

paradoxical breathing. This must be cognitively coor

pansion on their unaffected sides. This may be seen

dinated with the inspiratory phase and is generally a

as increased sidebending toward their involved side

more effective breathing pattern. On subjective breath

(Figure 37-13). This leads to inadequate venti lation

ing assessment, these patients often present with short

on the affected side, which puts these patients at a

ened neck muscles (Figure 37-11). Intercostal retrac

higher risk of developing respiratory complications

tions, or the collapsing of the intercostal spaces on

secondary to inadequate ventilation. In addition, the

inspiration, may be seen here. The paralyzed inter

adverse effects on their posture can lead to undesired

costal muscle tissue will be sucked in toward the lungs

musculoskeletal changes over a prolonged period of

during the creation of negative pressure within the

time especially for the pediatric patient. Prevention of

chest, thus the observance of the retractions (Figure

these secondary changes is of utmost importance.

37-12). This may be the most accurate way of assess

Patients with generalized weakness, such as with Guillain-Barre syndrome, some myopathies, neu

ing intercostal paralysis without an EMG test. If the patient lacks all "triad ventilatory muscles,"

ropathies, or incomplete SCls, may show a tendency to

they may be able to breathe using their upper acces

ward lateral breathing, or breathing that takes place pri

sory muscles only. Generally they will need mechani

marily in gravity-eliminated planes. For example, in

cal ventilation to augment their independent effort.

supine, patients with weakened chest muscles could not


694

PART VII


FIGURE 37-12

Intercostal retractions noted during inspiration.

FIGURE 37-13

A and B, patients with hemiplegia. Note asymmetry of trunk.


37


695

effectively oppose the force of gravity in the anterior

disorder with oximeter)' during sleep. Patients show

plane, thus they alter their breathing pattern to cause ex

ing deficiencies may need repositioning of their sleep

pansion in the lateral plane where gravity is eliminated.

postures, nighttime ventilation, oxygen support, or a

In sitting, these same patients would tend to breathe in

combination of these. Rigorous exercising or activities

feriorly where gravity would assist the movement.

of daily living (ADL) training may be more appropri

Likewise, in side lying, they would tend to breathe in

ately scheduled later in the day for these patients until

an anterior plane. Overall, these patients have the best

their sleep problems have been rectified.

prognosis for effective breathing retraining methods be cause they have weakness, not complete paralysis. The last breathing pattern to be discussed involves

CHANGES IN PULMONARY FUNCTIONS

patients with central nervous system deficits resulting

The abnormal breathing patterns discussed previously

in high tone, such as MS, Parkinson's disease, and

develop secondary to the patient's neurological

some head traumas. Their breathing patterns are altered

deficits. However, those new patterns then change the

not so much by muscle weakness as by the following:

patient's pulmonary function, which in turn affects

(1) chest immobility because of abnolmally high neuro

functional respiratory status. Specifically, changes in

muscular tone (spasticity, rigidity, tremors), which se verely limits chest expansion in any plane,

(2) cerebel

respiratory rates (RR), tidal volume (TV), and vital capacity (VC) are addressed here.

(3) improper sequencing because

Alveolar minute ventilation is the product of TV

of lesions in the brain, most commonly seen with

times RR. The optimal relationship between these

lar incoordination, or

medullary lesions. Breathing is usually symmetrical,

two parameters is those values that result in minimiz

shallow, sometimes asynchronous, and frequently

ing the mechanical work that the lungs must perform

25 breaths/minute).

with a particular breathing pattern. In other words, it

Initiation and follow-through of a volitional maximal

is the combination of RR and TV that requires the

tachypneic (respiratory rates over

inspiration is difficult or impossible for these patients.

body to put out the least muscular effort per breath.

This will markedly curtail the ability to produce an ef

Because most of the compensatory breathing patterns that have been discussed thus far reduce the patient's

fective cough and to maintain bronchial hygiene.

TV, the only recourse this patient has is to increase RR. Normal RR is between

SLEEP DISORDERS

12 to 20 breaths/minute;

however, for this neurological population, it is not

The patients described in this chapter frequently

uncommon to see RRs at least twice that figure.

need to use their accessory muscles cognitively, to ar

Although adjusting RR does bring the patient's res

rive at a work-efficient, ventilation-efficient, breathing

piratory system back to a state of equilibrium, it may

pattern. Because of this, they should be evaJuated for

not produce the most efficient pattern in the long run.

nighttime ventilatory assistance. Muscle weakness or

The idea of the oxygen cost of breathing in that pat

breathing inefficiency may cause a state of chronic

tern must be considered in its long-term functional

hypoventilation and/or sleep apnea episodes during

use. Ideally, TV at rest should be about

sleep. Drowsiness, lack of concentration, disturbed

actual Vc. At this level, the able-bodied person needs

sleep, and/or irritability are common complaints of

less than

this s t ate. In the c l i n i c a l setting, we see m a n y

to operate the respiratory mechanisms. When per

10% of one's

5% of the total oxygen available to the body

tetraplegic patients and other severely involved neuro

forming a normaJ physical task or low-level exercise,

logical patients who are lethargic after awakening.

this oxygen consumption rate increases slowly, never

Hospital staff may incorrectly label these patients as

quite reaching a point where the oxygen cost of oper

lazy or uncooperative. It should be assessed whether

ating the respirator), system outweighs the cost of per

this behavior is volitional or whether it is due to a

forming the activity. However, for patients with im

state of chronic nighttime hypoxemia. Assessments

paired chest functions, such as in this popUlation, the

can be made by screening high-risk patients for this

total oxygen consumption level of the respiratory


696

PART VII


muscles at rest can be as much as 4 to 10 times that

the work of breathing. If VC remains less than 60% of

amount. These patients may have TVIYC ratios that

the predicted value, most research indicates that these

are already in the 33% to 67% range at rest, indicating

patients will demonstrate inadequate coughs. Similarly,

inefficient breathing patterns, reduced VCs, inade

a FEV 1 less than 60% indicates lack of sufficient power

quate respiratory reserves, or both. When they attempt

behind the cough. When VC remains or decreases to

a mild exercise, they become quickly short of breath.

only 25% to 30% of the predicted nonn, then ventila

They do not have adequate oxygen reserves to supply

tion assistance usually becomes necessary.

the respiratory and the nonrespiratory muscles simul taneously, thus severely limiting exercise tolerance. Therefore although these patients may show adequate

ADVERSE MUSCULOSKELETAL CHANGES

maintenance of alveolar minute ventilation at rest, a

Neuromuscular wea kness and the compensatory

mild increase in activity level may magnify respira

breathing patterns may cause adverse musculoskele

tory insufficiencies.

tal changes over a prolonged period of time. Previous

An adequate VC is imperative in restoring a pa

discussion in this chapter revolved around the ad

tient's functional status. Without the ability to expand

verse effects that gravity can play on the skeleton if

the chest maximally under his or her own muscle

the body is unable to counteract its force. Pronounced

power, VC will decrease after a neurological insult. For

deformities are more prevalent in children, of course;

example, studies show that tetraplegia resulting from

however, both children and adults are effected. Sev

SCIs may reduce the patient's VC to 33% of the pre

eral examples of specific changes are presented.

dicted value, increasing the TVIYC ratio to 30%. For

A common musculoskeletal deformity secondary

SCIs, an adequate VC is generally considered to be

to muscle weakness is seen as a flattened anterior

66% of the expected value. This would restore the

c h e s t w all, as s e e n w i t h m a n y p a r a p legic and

TVIYC ratio to approximately 15%, thus decreasing

tetraplegic patients. (Figure 37-14) For the patient

FIGURE 37-14 Musculoskeletal changes in adult chest secondary to spinal cord injury anterior chest wall and narrowing of the upper chest.


(SCi). Note

flattening of the

37

The Patient ith Neuromuscular or Musculoskeletal Dysfunction

697

with weak or paralyzed intercostal muscles, this t1at

Anterior or lateral t1aring of the lower rib cage

tening often occurs because of prolonged supine posi

may also be noted. This is usually a result of insuffi

tioning along with the significant resistance that ante

cient abdominal strength, thus the lower ribs are not

rior chest expansion meets from gravity.

stabilized and integrated into the abdominal area (see

Another common deformity is a pectus excuva

Figure 37-8, p. 687). In upright, this is seen as a

tum at the base of the xiphoid process. Patients who

marked delineation between the rib cage and abdom

have a strong diaphragm but no muscular support

inal area in the mid-trunk region (see Figures 37-3,

from the intercostals and abdominal muscles may

p. 683 and 37 -15).

develop this type of musculoskeletal deformity (see

Upper chest ad verse m uscu loskeletal changes

Figure 37-7, p. 686). It can result from the di

occur when the intercostal and/or other upper acces

aphragm pulling inward so hard that the sternum,

sory muscles are impaired. The diaphragm is not po

without intercostal muscle support, cannot maintain

sitioned to assist in expansion of this area. Therefore,

its neutral position. Over time, it caves in, resulting

without those accessory muscles, the anterior wall of

in a permanent deformity.

the upper chest wiII become flattened and appear

FIGURE 37-15 Independent upright posturing. Adult with tetraplegia. Kyphosis restricts chest movement for respiration. Note folding at mid-trunk line.


698

PART VII


more narrow than that of the normal upper chest (see Figure 37-14, p. 696), resembling the more primitive triangular shaping of the chest seen in the newborn (see Figure 37-4, p. 684). Spinal curves are not spared deformities. In a weakened, low-tone patient, scoliosis is common be cause the patient cannot adequately maintain himself or herself upright against gravity. Slowly, the spine collapses on itself, seeking stability; therefore scolio sis is developed. All types of patients with the neuro logical diagnoses discussed in this chapter are at risk for developing scoliosis. The second possible spinal change, a lumbar and thoracic kyphosis, can occur as well because of the force of gravity on a mobile spine and lack of paraspinal muscle support. Secondary to these kyphoses, many patients develop an excessive cervical lordosis to maintain eye contact. In sitting the patient hunches over his or her trunk, making eye contact and head righting difficult (see Figures 37-3, p. 683 and 37-15, p. 697). These spinal changes affect the functioning of the respiratory system adversely. With a kyphotic thorax in an upright posture, expansion of the chest in all three planes of ventilation will be impaired. The ribs require a stable base from which to become properly mobilized. A kyphotic, weak posterior support does not provide the necessary stability for optimal rib mobility and function. Therefore proper elevation and angulation of the ribs becomes impossible. This lim its overall chest expansion and vital capacity. Musculoskeletal changes in children must be ad dressed. They are in a state of habilitation rather than rehabilitation. Because of this, the neurological deficit affects their developing chests more severely. Their rib cages remain more triangular in shape, since the muscles of the upper chest never develop fully or normally. The ribs also remain more horizontal than in the normal adult, probably because of less upright posturing and lack of intercostal and abdominal mus cle contractions on the rib frames. Their necks and shoulders do not mature developmentally, often be cause of overuse of the neck accessory muscles. This leads to a permanent shortening of the neck strap muscles, making the child appear to lack a cervical area (see Figures 37-7, p. 686, and 37-8, p. 687).

Proper elongation of the cervical spine cannot occur, resulting in skeletal changes to that area. Scoliosis, along with thoracic kyphosis, tends to be more pro nounced than in the adult. DECREASED COUGH EFFECTIVENESS With decreased chest expansion, the presence of compensatory breathing patterns, and the adverse musculoskeletal changes, the patient's ability to cough will be drastically reduced. Vital capacity will be impaired as will the ability to build up sufficient intraabdominal pressure, especially for patients with weakened, flaccid, or uncoordinated abdominal mus culature. For many patients with traumatic brain in juries, Parkinson's disease, CP, and CVA, the inabil ity to coordinate an effective cough will be significantly impaired. This inability may be due to cerebellar damage or to high neuromuscular tone (spasticity, rigidity, tremors). Frequently, the quick action required to produce an effective cough will be the same action that will trigger a sudden increase in the abnormal neuromuscular tone. Objectively, when the patient can not expel at .Ieast 60% of his or her ac tual vital capacity in 1 second (FEV d, he or she will often be incapable of producing an effective cough without some assistance or retraining. MAINTAINING BRONCHIAL HYGIENE All these changes in respiratory functioning lead to a decreased ability of the neurologically impaired pa tient to independently maintain bronchial hygiene. Complete expansion of the chest in all three planes of ventilation and in all postures is impaired, so the ability to properly aerate all lung segments is im paired. Thus the ability to perform independent bronchial drainage will I ikewise be impaired. Ineffi cient breathing patterns rl)ay cause them to remain in a state of chronic hypoventilation. Inability to pro duce an effective cough impairs the ability to clear the lungs of secretions. Therefore most of these pa tients will require some assistance, either physically or through verbal instruction, to achieve adequate bronchial hygiene.


37

TIle Patient with Neuromuscular or Musculoskeletal DysfWlction

IMPAIRED PHONATION

699

provided by the muscles of ventilation (Figure 37-16).

Aphasia, as a secondary impairment to neurological

When the respiratory muscles are malfunctioning, as

deficits, is generally recognized by all members of the

in the neurological diseases discussed, the patient's

medical team as a problem that necessitates speech

ability to regulate the flow of air out of the lungs may

therapy. However, many persons with neurological

be impaired. Good eccentric control of the inspiratory

impairments display serious deficits in communica

muscles (the ability to slowly release these muscle

tion that remain untreated and the deficits remain un

during exhalat ion) is needed to p r oduce normal

acknowledged. Primarily, that deficit is inadequate

lengths of phonation. Otherwise, the air may be ex

breath support for phonation; in other words the pa

pelled from the lungs too quickly because of the nat

tient's inability to control the force and duration of ex

ural elastic recoil of the diaphragm, rendering that

halation for the purpose of phonation. Duration of

volume of air useless for phonation. Therefore both a

phonation and voice intensity are regulated by a deli

decrease in tidal volume and a decrease in eccentric

cate balance between airway resistance, provided by

control of the respiratory muscles will lead to impair

the laryngeal muscles, and the force of exhalation,

ments in functional speech.

FIGURE 37-16 Relationship of air flow and vocal folds.


700

PART VII


The average adult breathes at a ratio of 1:1 or 1:2

Airtlow out of the lungs should be as impOitant to

(inhalation time: e x h alation time) d u ring quiet

clinicians as airflow into the lungs. An evaluation of

breathing. The average ratio during phonation be

expiratory eccentric control is nccessary for all neu

comes I :5, with 8 to 10 syllables per breath being a

rological patients regardless of diagnoses. All disci

comfortable speaking length. Clinically, many pa

plines should incorporate a phonation facilitation pro

tients are seen to struggle with two- to thee-syllable

gram into their rehabilitation program, especially for

phrases because of inadequate breath support. Often

those patients who would otherwise not receive any

these same patients are not referred to speech therapy

speech training.

for training because they are not diagnosed as having a "speech" problem (e.g., many patients with SCIs, MDs, polio, or spina bifida). Optimally, these pa ticnts should be able to phonate (an "ah" or "oh"

GOALS OF A NEUROMUSCULAR OR MUSCULOSKELETAL RESPIRATORY PROGRAM

sound) for at least I 0 to 12 seconds during a con

In conclusion, the combination of secondary cfJ'ects

trolled expired vital capacity. Many of their voices

that follow a neurological and/or musculoskeletal in

fade away after 3 to 4 seconds. Without the ability to

sult are responsible for leaving the person with residual

communicate with normal speaking lengths and nor

musculoskeletal or neuromuscular deficits at greater

mal voice intensities, these patients' successful reen

risk for developing respiratory complications long

try into society's mainstream becomes significantly

after their acute phases have subsided. The long-term

more difficult.

goal of any respiratory rehabilitation program for these

Another misconception about these patients is that

patients is obvious; reduce their risk for developing

they are mentally slow or retarded because they do

these complications. First and foremost is the need to

not use all the proper figures of speech. In reality,

increase or maintain chest expansion in all three planes

these patients may exclude figures of speech because

of ventilation. Second, educating the patient and/or

of the extended time it takes them to communicate

family in methods to maintain good bronchial hygiene

something. For them, it is more expedient to forego

must be emphasized to prevent infections. Logically,

their inclusion.

improving cough effectiveness will improve airway

A marked example of this was seen in our clinic.

clearance. Next, increasing the patient's vital capacity

A 3-year-old girl who sustained a complete C4 to C5 spinal cord lesion at birth and had not received prior rehabilitation was seen. On initial examination, her speech was choppy, brief, and grammatically incor rect. She rarely initiated conversation and her voice

Respiratory Rehabilitation Goals •

intensity was very low. It was suspected that she per haps suffered some anoxic brain damage to account

•

with a physical rehabilitation program, her speech

•

•

changed drastically. She spoke fluently, with 8 to 10 syllables/breath, correct inclusion of grammar, and louder and more varied voice intensities. Instead of being quiet and more reserved as she had been before treatment, the mother reported that the child was a

became understood that her cognitive skills were well

maintain chest expansion in all three

Educate the patient and/or family in methods for Improve cough effectiveness Inc r e a s e the patient's vital capacity and t idal volume

•

Reduce high respiratory rates

•

Modify inadequate breathing pattern s

•

Improve eccentric control of the diaphragm and other ventilatory muscles for improved phonation

regular chatterbox. Her new communication skills ap peared to improve her self-esteem. At that point, it

or

maintaining good bronchial hygiene

for her developmentally delayed speech. After an in tense breathing retraining program in conjunction

lncrease

pl anes of ventilation

skills •

underestimated on initial screening.


Incorporate effective ventilatory strategies with all

motor tasks

37


and tidal volume, where indicated, will help to im prove aeration of the lungs. If necessary, reducing high respiratory rates to improve pulmonary functions will be a goal. Other goals include modifying inadequate breathing patterns, which could mean increasing or de creasing the use of accessory muscles to achieve maxi mal breathing efficiency, and improving eccentric con trol of the diaphragm and other ventilatory muscles for improved phonation skills. These concepts lead us to realize the need for incorporating effective ventilatory strategies with all motor tasks. These goals are summa rized in the box on p. 700. When implementing this program, it is necessary to recall that the patient's res

Aronson, A. (1985). Clinical voice disorders: An

701

interdisciplinary

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Ashw0l1h, B. & Hunter, A.R. (1971). Respiratory failure in myas

London (Bioi) 64:489-90. J.R. (1991). New approaches in the rehabilitation of the trau matic high level quadriplegic. Americal JOllm,,1 of Physical Medicine and Rehabilitation 70( I):1]-9. thenia gravis. Proc R Soc

Bach,

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Borden, G.,

H a r ris, K. Speech Science Primer: Physiology,

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able to apply what they learn from this program into

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all phases of their lives. Thus incorporation of these goals into ADL or mUltipurpose activities will yield the most successful results.

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Braun,

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pulmonary alveolar development i n late gestation and the peri

shortly after birth?

natal period. In Hudson, W.A. (Ed). Development and grm4'lh

can be associated with cardiopulmonary dys function? 3.

i n heallh and disease. (Second Edition). Philadelphia: PA

Saunders.

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Cherniak, N.S. and clinical

A bnormal breathing pal/ems: Their mech(lI1isms

significance.

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Clough, P., Lindenauer. D., Hayes, M., & Zekany, B. (1986). Guidelines for routine respiratory care of patients with spinal

66(9): 1395-402. e.B., Trend, P.S. & Wiles, e.M. (1985). Severe di aphragm weakness in multiple sclerosis. Thorax 40:631-32. cord injury. Physical Therapy

Why should a therapist be concerned about phonation in patients with neurological dys function?

7.

7(2): 110-14.

How should the effect of gravity on ventilation

What symptoms would be noted in patients

6.

severity. Sleep

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offhe airways. New York: Marcel Dekker. 399-418.

Cartwright, R.D. (1984) Effect of sleep position on sleep apnea Cherniak, R.M. Cherniak, L., Naimark, A. (1972). Respiration

What factors contribute to normal chest de

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A.e. Mansell, A.I.. & Levison, H. (1977). Regulation of

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2.

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Bymn,

What are the goals of a neuromuscular/mus culoskeletal cardiopulmonary program?

Cooper,

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15( 1):84-88.

E., Ross, J. Road, J.D., et al. Pulmonary function in individ

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J.M., Ackermann, D., & Kresslring. J. (1990). Respiratory Inl Disabil Studies. May:78-80.

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DeReuck, A.V, &

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Ciba foundation

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30:6 I 7-630.


Para

The Transplant Patient

Susan Scherer

KEY TERMS

Cardiac rehabilitation

Organ rejection

Denervation of the heart

Psychosocial

Immunosuppression

Pulmonary rehabilitation

Organ donation

Secretion management

HISTORY

BACKGROUND

The ability to transplant an organ from one individual

Early transplant experiments were carried out on ani

to another is a relatively new phenomenon. Early at

mals in the early 1900s, with success at maintaining

tempts at transplant were barely successful. New ad

life for 90 minutes to 8 days (Hosenpud, Cobanoglo

vances in surgical techniques and immunosuppres

Norman, Starr, 1 991). Medical advances in car

sive drugs, however, have made transplantation of

diopulmonary bypass and immunosuppressive med

solid organs a viable treatment option. The increased

ications provided the opportunity for successful

life expectancy of transplant patients means that

transplants. After many trials and failures, the first

physical therapists have many opportunities to treat

successful orthotopic heart transplant was performed

patients after transplant in various settings. Trends in

in 1967 by Barnard; the first successful lung trans

patient demographics indicate that a physical thera

plant was performed in 1963 by Hardy and Webb.

pist may see a transplant patient not only in a re

Improvements in surgical technique, detection of

gional medical center setting but also in outpatient

rejection, and immunosuppressive drugs means trans

and rural clinics. This chapter contains guidelines for

plants are increasing in number. Virtually every solid

treating patients with heart or lung transplants.

organ can be transplanted from one individual to an 703


704

PART VII


other of the same species if there are similarities in

National I-year survival rates are as follows:*

immune system markers. Kidney transplants are the simplest and most common, whereas heart-lung block

Kidney

93 8%

transplants are uncommon.

Liver

76.7'k 82.6% 57% 68%

Heart Heart-lung Lung

Purpose of Transplants Although transplants are considered an acceptable treatment option, a solid organ transplant is usually

.

Organ Donation

considered a last-resort therapeutic intervention.

The major limitation of organ transplantation is a

Medical intervention for diseases, such as cardiomy

supply and demand issue. The number of patients

opathy and interstitial pUlmonary fibrosis, is limited.

who could benefit from transplant significantly ex

When conventional medical therapy has failed, a

ceeds the number of organs available. Media cover

transplant may be considered. Although a transplant

age assists with identifying the issues and may play a

offers a patient a second chance at life, the medical

role in increasing the number of donors. To become

management of a transplant causes a patient to re

an organ donor, check with your state about specific

quire medical intervention on a long-term basis.

requirements; often a driver's license has a space to identify you as an organ donor. Make sure that you discuss your wishes with your family. If you are hos

Availability of Transplants

pitalized, family members or close personal friends

The number of medical centers who perform trans

wil I often be approached about donating your organs.

plants has grown to approximately 175 worldwide

If your family is confident that you wished your or

in 1989 (Hosenpud et aI., 1990). Because of the suc

gans to be donated, they will more likely say "yes" to

cess rates, many types of transplants are no longer

organ donation.

considered experimental but are considered appro priate treatment for organ failure. In 1994 approxi mately 10,000 kidney transplants were performed

CURRENT TRANSPLANT ISSUES

and 2500 heart transplants were completed (Col

Transplant trends include early detection of rejection,

orado Organ Recovery Systems [CORS], Denver,

development of new immunosuppressive medica

Colorado 1994).

tions, and donor management. For donor organs to be viable, the donor must be managed in a way that pre serves organs. In the past, fluids were pushed to pre

Rejection Issues

serve kidney function for transplant. This extra fluid,

Although transplants are successful, some health pro

however, made the lungs unusable. New donor man

fessionals believe that patients are merely exchanging

agement techniques are increasing the viability of

one set of problems for another. For a transplant to be

multiple organs from the same donor.

successful, a patient must remain on powelful immuno suppressive drugs for the remainder of his or her life. Some of these medications have crippling side effects. The effects of long-tenn prednisone are well known:

Ethical Considerations Should a p e rson who h a s developed end-stage

osteoporosis, muscle weakness, and glucose intoler

chronic obstructive pulmonary disease (COPD) from

ance, whereas the long-term effects of cyclosporine and

smoking be allowed to receive a lung transplant?

azathioprine impact on the patient's ability to fight in

Should a heart transplant be given to someone who

fection. Patients also need to manage medication side

developed alcoholic cardiomyopathy? Should a pa

effects on a day to day basis. It is these medications, however, that make for impressive survival rates.

'Source: CORSo Denver. 1994.


38

tient with cystic fibrosis receive a double-lung trans


705

transplant program. Because of these needs, most

plant even though the donor lungs could go to two

transplants are performed at large, regional medical

different individuals with pulmonary fibrosis? These

centers, often those associated with a medical school.

are some of the ethical issues with which transplant

Because donor organs are viable for only hours after

teams struggle. There are no easy answers nor is there

removal from the donor, patients waiting for trans

unanimous agreement on each case. Despite the diffi

plant are required to live within a several-hour radius

culty of making wise choices, each team carefully

of the transplant center. Some patients may arrange

considers each candidate for transplant. Criteria are

air transportation to the medical center, others may

used so that individual preferences of team members

relocate themselves and family to temporary housing

are not given priority. When and if health-care re

within the metropolitan area. Most patients are given

sources become more limited, the decisions may be

a beeper to maintain contact in a timely manner.

come more difficult. If transplant success improves and donor organs increase in number, transplants could become

a

mainstream of treatment.

Psychosocial Implications A strong support system is considered an essential

Criteria for Being listed on a Transplant Waiting list

component of a successful transplant. Demands of waiting and relocation to the transplant city put con

Virtually every medical center with a transplant

siderable stresses on the patient and significant others.

program has developed criteria for patient selec

The patient is torn between wanting to remain hopeful

tion. Although each center may set its own criteria,

that a transplant will provide new life and the reality

there are similarities among the medical centers

of knowing that death may come before the transplant.

(see box below).

Patients feel these oppositional forces continuously and struggle to keep a balance between hope and real ity. Therapists can assist patients by listening to feel

Waiting Time

ings, being supportive, and encouraging participation

The time spent waiting for a transplant can vary con

in support groups. Because most patients experience

siderably. Some patients wait less than a week; others

these feelings, support groups offer invaluable inter

wait up to 18 months. During the waiting period, pa

vention. Groups which include patients both before

tients struggle with the need to carry on their lives, all

and after transplant probably have the most to offcr in

the while knowing that at any moment they may be

terms of psychosocial support. Those patients who re

called to the hospital for transplant.

locate to transplant centers may have the most diffi

The number of transplant centers in the United

cult time psychologically, especially as they leave

States is limited. State of the art hospital facilities and

family and significant others behind. Feelings of

surgeons are neccssary components of a successful

being useless are common because patients waiting in a foreign city must find something to do. Spouses and significant others also benefit from group support. The psychological stresses are some what different on spouses. Spouses speak of the

Criteria for Transplant Waiting List

struggle to remain hopeful, yet plan for a future that may not include their loved one. If the patient and

Age: under 65 (60 in some centers) Terminal illness (expected life span less than I year Nonsmoker

spouse move to a new city to wait for transplant, they may find themselves with more time together than they have ever spent before. ]n this forced retirement,

Adequate social support system

new stresses are added to relationships. Transplant

Disease free in other systems

teams usually include a psychologist or social worker to whom patients may be referred for individual or


706

PART VII


family counseling if the stresses limit function or par

fort and function after surgery. The physical therapist

ticipation in pretransplant programs.

should be familiar with the surgical incisions and im

After transplant, patients struggle with conflicting

pact on rehabilitation.

feelings. Patients are often emotionally overwhelmed

Heart transplants are usually performed through a

with a feeling of gratefulness that they are alive and

median sternotomy incision and cardiopulmonary by

feel guilty that someone else's glief has given them a

pass is used. A midline incision from sternal notch

chance to rejoice. Psychological or spiritual support

distally allows the sternum to be accessed and split.

may be requested or s u g gested after transplant (Craven, Bright, and Dear,

1990).

Although the native heart is excised, a portion of the right atrium and the SA node is preserved. The donor heart is sutured to the atrial cuff and the major ves sels reattached. After surgery, the two halves of the

Patient Education

sternum are wired together, the new heart defibril

The waiting period time provides an ideal opportu

lated, bypass reversed, and the patient awakened.

nity for patient education. Nursing generally provides

Lung transplantation surgical incisions depend on

much of the education regarding preoperative proce

whether a single or double-lung transplant is to be

dures, postoperative course, and medication. Rehabil

performed. Single lung transplants are performed

itation teaching includes breathing training, airway

through a posterolateral thoracotomy incision, with

clearance techniques, and activity progression.

the patient side lying on the opposite side. To allow visual access for the surgeon, the latissimus dorsi and lower trapezius muscles are cut. The incision through

TRENDS IN TRANSPLANT CARE

the fourth or fifth intercostal space also means the in

Transplants are being made available to a broader

tercostal muscles at this level may be incised. If the

group of patients. Although transplants are only per

rib at the surgical level fractures, it is resected so that

formed in certain centers, patients from rural areas

the bone ends do not rub or puncture the lung. The

are being evaluated at regional centers. Because

serratus anterior muscle is preserved if at all possible,

transplant criteria differ slightly from center to center,

but the lateral portion of the rhomboid may be cut to

some patients may be evaluated at several centers.

allow more access for the surgeon. Postoperative pain

The increased availability of transplants and the relia

and impaired upper quarter movement patterns may

bility of air transportation means that even patients

present significant problems for patients.

from outlying geographical areas may be considered

Double-lung transplants are performed through an

for transplant. After transplant, improved medical

anterior incision sometimes described as a clamshell

care has led to shorter hospital stays. For the patient

approach. A horizontal incision above the level of the

who has relocated to the transplant city this means

diaphragm is performed, but the distance needed for

that he may be discharged to an apartment and return

adequate visualization means that the pectoralis

to the hospital several times a week for physician fol

major and minor may be incised bilaterally.

low-up and rehabilitation. Once medically stable, pa tients may be allowed to return to their homes as early as 2 to 3 months after transplant, if medical sup

PHYSICAL THERAPY CONSIDERATIONS As important members of the transplant team, physi

port and rehabilitation needs can be met.

cal therapists need an understanding of the physiolog ical components of both the pretranspJant disease and

SURGICAL PROCEDURES

posttransplant state, the influence of surgery or physi

The surgical approach for transplant is chosen to pro

ology on musculoskeletal structure and function, and

vide the surgeon the optimal working area and visual

how medical management may necessitate modifica

field. The choice of incision may affect patient com

tion of therapeutic interventions.


38

Physiology


707

c1es of respiration is reduced. The physical therapist

The cardiovascular and respiratory systems are criti

needs to optimize breathing in the preoperative pe

cal elements of functional ability, in areas of en

riod, yet prepare the chest and shoulder muscu

durance and movement. Adequate oxygenation and

loskeletal system for normal function.

circulation are needed to provide fuel to perform daily activities. In the patient awaiting heart trans plant, cardiac output is significantly compromised,

Medical Management

and hemodynamics may be unstable. Because of

Knowledge of medical management including med

these limitations, pretransplant exercise is inappropri

ications, ventilatory support, and hemodynamic mon

ate. Posttransplant. however. the main interventions

itoring assists the therapist in determining whether

will be to restore normal cardiac output. Knowledge

modifications are needed during rehabilitation. Table

of physiology allows the therapist to choose appropri

38-1 lists suggested areas to monitor during both be

ate interventions.

fore and after transplant rehabilitation. For example,

In patients with terminal lung disease. the primary

patients often complain of tremors during rest and ac

limitation is ventilation. Pulmonary rehabilitation has

tivities. Therapists should be knowledgeable enough

been beneficial in improving daily function (Toronto

to question other health professionals as to whether

Lung Transplant Group, 1988; Petty, 1980; Moser,

the tremors are a result of medications, such as cy

Bokinsky. Savage, Archibald, Hansen, 1980) and

c1osporine, a metabolic abnormality, a seizure disor

may be used in the pretransplant period. Supplemen

der, or muscle weakness.

tal oxygen can be lIsed during exercise to maintain adequate oxygenation. The waiting period before transplant is an ideal time to optimize muscle func

PHYSICAL THERAPY ASSESSMENT The purpose of physical therapy before transplant is

tion and flexibility.

to identify baseline function and to screen for impair ments that may limit rehabilitation goals. In some in

Musculoskeletal Considerations

stances, physical therapists will provide treatment in

The musculoskeletal problems of patients with pul

the pretransplant period; in other cases, the informa

monary disease are well documented (see Chapter 4).

tion gained from early assessment allows the thera

Patients undergoing lung transplants are unique in

pist to identify areas needing attention or modifica

that after transplant the musculoskeletal system re

tion after transplant. Physical therapy assessment in

turns to normal structure. The chest wall adapts in

the postoperative period addresses specific impair

size to the new lung. The need to use accessory mus-

ments and functional limitations of the individual.

TABLE 38-1 Recommended Monitoring "

=

heart

x =

lung BLOOD PRESSURE

Before exercise

-.J

x

HEART RATE x

-.J

Sa02

RA TING OF PERCEIVED EXERTION

x

During exercise

-.J

x

-.J

x

After exercise

-.J

x

-.J

x


x

-.J

708

PART V[[

Guidelines for the Delivery of Cardiopulmonary Physical Therapy; Special Cases

PRETRANSPLANT REHABILITATION

Cardiac Patients Pretransplant assessment of the cardiac patient in cludes functional ambulation (6-minute walk) and

Heart Transplant

screening for deficits in muscle strength or range of

Because the patient awaiting heart transplant has sig

motion. Exercise training is not generally recom

nificantly compromised cardiac output and may be

mended pretransplant. Range of motion may be in

hemodynamically unstable, preoperative rehabilita

creased or specific muscle strengthening may be ac

tion is generally not recommended. Some patients

complished, however, if the need is determined to be

with moderate congestive heart failure may be able to

significant. All patients will be limited in functional

tolerate a mild level of exercise (Roubin, Anderson,

endurance, therefore the results of the 6-minute walk

et aI., 1990; Hillegass and Sadowsky, 1994). Most

is compared with posttransplant functional status.

patients, however, are unable to tolerate endurance training. Some patients may need musculoskeletal interven

Pulmonary Patients

tion for decreased range of motion, muscle weakness, or

Because rehabilitation in the pretransplant period is

general discomfort. If physical intervention is needed,

often indicated in patients waiting for lung transplant,

heart rate, blood pressure, and ECG monitoring is used

the physical therapy assessment information may be

to guide treatment. If heart rate or blood pressure de

used to design a more effective rehabilitation pro

creases during exercise, exercise should be stopped.

gram. Upper and lower extremity muscle strength

The main goal in the preoperative period is to pre

and range of motion is assessed, as well as posture,

vent losses of function. Maintenance of range of mo

shoulder and trunk mobility, breathing pattern, breath

tion, soft tissue extensibility, and muscle strength are

sounds, and functional mobility.

suggested goals.

Posttransplant Assessment

Lung Transplant

(Heart and Lung)

Although each patient is treated individually, there

After transplant, physical therapy assessment ad

are similarities among patients, resulting in a stan

dresses all areas of functional limitations and the cor

dard program for pretransplant rehabilitation (Figure

responding impairments. Patients should be evaluated

38-1). Pretransplant rehabiIi tation resembles pul

in the immediate postoperative phase, and reevalu

monary rehabilitation programs in existence for pa

ated on admission to the outpatient treatment phase.

tients with COPD, CF, and restrictive d i seases

Because of the surgical intervention, bed mobility,

(Toronto Lung Transplant Group, 1988; Conners and

ventilation, secretion management, range of motion,

Hilling, 1993; Malen and Boychuck, 1989).

and pain control are important areas to address.

General Considerations for Rehabilitation REHABILITATION OF THE TRANSPLANT

Since the primary limitation in pulmonary disease is

PATIENT

ventilatory, oxygen needs are essential to monitor. A

To assist in treatment planning, rehabilitation is cate

pulse oximeter with finger or ear probe is mandatory

gorized into the following four phases: pretransplant,

in a pretransplant pulmonary rehabilitation program.

postoperative acute phase, postoperative outpatient

Oxygen saturation should be maintained above 88%

phase, and community- or home-based phase. Al

at all times. A source of supplemental oxygen is nec

though the ultimate goal of transplant rehabilitation is

essary, whether the patients bring their own oxygen

to improve the patient's function and quality of life,

or it is supplied by the center. In patients with severe

each phase of rehabilitation has its own emphasis.

disease, oxygen-conserving devices may need to be


38


709

loskeletal impairments to function. Using the waiting time to maximize muscle strength and range of mo tion means that less time is needed posttransplant to return to functional activities. Pretransplant rehabilita tion programs have been shown to decrease posttrans plant hospital stay (Scherer, 1995). It is reasonable to set goals to achieve normal muscle strength in lower extremity musculature, increase upper extremity mus cle strength, increase shoulder and chest wall range of motion to normal or within functional limits, demon strate coordinated diaphragmatic breathing with exer cise and activities, and improve cardiovascular en durance. An example of a preoperative pulmonary rehabilitation program is in the box on p. 710.

Interventions Deficits which are found in any of the above areas may be addressed in the pulmonary rehabilitation program, except in patients with primary pulmonary hypertension or Eisenmenger's syndrome. In those patients, exercise which increases cardiac workload is contraindicated. However, if cardiac output is monitored and the physician agrees, range of motion exercises may be taught and light strengthening ex ercises may be performed. For example, a 22-year old female with primary pulmonary hypertension was found to have injured her shoulder 4 weeks pre

FIGURE 38-1

viously, resulting in decreased range of motion in a

Pre-lung transplant rehabilitation.

capsular pattern. She has been on the lung transplant waiting list for 3 months. The physician wants her

used. Patients with COPD should have blood gases monitored for carbon dioxide retention, since increas ing exercise often requires an increase in supplemen tal oxygen. Several of our patients has carbon dioxide levels in the 88 to 100 range. Although heart rate is not a good measure of exercise intensity, patients with lung disease may demonstrate signs of right heart failure and should have heart rate and blood pressure monitoring on a regular basis.

only to walk as necessary for her daily activities. With consultation with the physician, joint mobi lization, range of motion activities, and modalities may be used with few precautions. Strengthening exercises may be used cautiously, avoiding breath holding and Valsalva maneuvers.

Other Transplants Patients awaiting other organ transplants may also be referred to physical therapy for treatment of muscu loskeletal problems. Because of the level of meta

Goals

bolic abnormality in patients awaiting liver and kid

The overall goal of pretransplant pulmonary rehabili

ney transplants, endurance training is difficult to

tation is to maximize function and reduce all muscu

perform. Other physical therapy interventions, how


710

PART VII


Preoperative Pulmonary Rehabilitation 10 minute

Warm-up (group) Active range of motion Upper body Lower body Trunk Light resistance (5 to 10 reps)

Individualized Endurance Program Bike (Airdyne)

25 to 30 watts

Treadmill

0.8 to 1.5 mph 0% to 5% grade

10 to 30 minutes

Arm ergometer

0 to 25 watts

10 to 15 minutes forward and backward

10 to 20-minute intervals

15 to 20 minutes

Individualized Strength Program Pulleys

Theraband

Latissimus pull-downs

Rhomboids

Diagonal arms

Shoulder extension rotation

Pectoral

Shoulder flexion

Latissimus Triceps Subscapularis Lower Extremity Quadriceps Hip extensors Hip abductors

10 minutes

Cool-down (group) Stretching (full-body) B reathing Relaxation

ever, m a y be u s e d as appropriate (i.e., muscle

and increasing functional abilities in self-care and

strengthening, range of motion).

ambulation.

ACUTE PHASE REHABILITATION

Heart Transplant (Acute)

The acute phase of rehabilitation begins in the inten

Considerations

sive care unit and continues throughout the patient's

In the immediate postoperative period after heart

hospital stay. Interventions are focllsed on facilitat

transplant, cardiac output is compromised and hemo

ing normal cardiovascular and pulmonary function

dynamic responses slowed. A transplanted heart is



38

711

University Hospital Cardiovascular Rehabilitation Supervised Exercise/Activity Plan/Surgical Patients DX

Physician

MEDS

Step/Date

Exercise

Activity

I ICU

-Active/Passive ROM, in bed

x

5 reps

-Partial self care -Feed self

1/5 METS

-Use of bedside commode

I

I

/

/

-Teach hourly ROM exercise

-UP in chair for meals as -Turn, cough, deep breathe & use incentive spriometer, q2-4° -Sitting bed bath

21CU

-Active ROM, sit on edge of bed

1.5-2.0 METS

-Teach Rating Perceived Exertion

x

5 reps

-Sit in chair as tol -Partial/complete self care -Up in chair for meals -Turn, cough, deep breathe and use incentive spriometer, q2-4° -Sitting bed bath

3 FLOOR

-Active ROM/warmups, standing

2.0 METS

-Walk 100 ft. slow pace

x

IO reps

-Sit in chair 2-3x/day (20 min) -Complete self care -Sitting bed bath -Incentive spriometer indep, TID

4FLOOR

-Warmups, standing

2.5 METS

-Walk 150 ft, average pace

-Use of bathroom w/assist

-Teach pulse counting

-Walk around room

x

10 reps

-Complete self care

-May take warm shower after pacer wire removed -Incentive spriometer indep, TID

IO reps

5 FLOOR

-Warmups, standing

3METS

-Walk 300 ft, average pace

6 FLOOR

-Warmups. standing

3.5 METS

-Walk 500 ft. average pace

x

x

-Dressing indep -May stand at sink for ADLs

10 reps

-As above -Introduce to phase II

-Walk down flight of stairs -Instruct in home exercise

7 FLOOR

-Warmups, standing

4METS

-Walk up flight stairs

x

-All self care indep

10 reps

-As above

-Walk 500 ft average pace -Schedule sub max ETI -Enroll in Phase II

Guidelines for Exercise -Pt HR to be 50-120 bpm

-no significant anhythmias

-Exercise HR not more than 20 beats above rest

-SBP

-No worsening ST changes

-<

-RPE of IO or less

-no angina or other symptoms

<

200, DBP

<

120 during exercise

10-15 DBP drop during exercise


712

PART VII


stiff for several days, and the sympathetic nervous

the heart is denervated. Because of the lack of sym

system input to the heart is destroyed in the transplant

pathetic input, heart rate cannot increasc quickly and

process. To maintain cardiac output (HR x SV) in a

contracti I ity is not under sympathetic control. The

heart with decreased stroke volume a fixed rate pace

only mechanism by which heart rate can be increased

m a k e r is u s e d at a r a t e of a p p r o x i m a t e l y 120

is by circulating catecholamines, which take 10 to 15

beats/minute for several days. ECG readings may be

minutes to influence a response. Therapists working

normal because the donor heal1 has an intact conduc

with heart transplant patients should allow time for

tion system, although the atrial cuff left from the na

patients to adapt to changes in position and may want

tive heart may cause the ECG to have two P waves.

to use light active bed exercises as a warm-up activity

The therapist working with heart transplant patients

(Irwin and Tecklin, 1995 ).

in the ICU should be aware that heart rate cannot in crease significantly, therefore blood pressure and pa tient response should be monitored. Surgical cardiac rehabilitation guidelines can be used to guide treat

Lung Transplant Considerations

ment, with increases of 0.5 to I metabolic equivalent

After lung transplantation, patients are generally me

(MET) per day (see box on p. 711). Complications of

chanically ventilated for 24 to 72 hours. Often, para

heart transplant include sternum instability, infection

lytic agents are lIsed in this period so that ventilation

or pain, and potential nerve or circulatory damage to

can be optimized. Patients who received double-lung

the femoral area because of intraaortic balloon pump

transplants may be more hemodynamically compro

(lABP) cardiac assist. Acute rejection episodes are

mised if they were on bypass during surgery. Chest

characterized by flu-like symptoms including low

tubes are likely in place, and patients are medicated

grade fever and muscle achiness and is often accom

for pain. Infection control is imperative; isolation

panied by dysrhythmias. Rejection episodes can only

rooms with negative-pressure ventilation are used

be confirmed by tissue biopsy.

and medical personnel at minimum are required to wash their hands and wear masks when in the pa

Goals

tient's room. Isolation or reverse-isolation procedures

Goals of the acute phase of rehabilitation include the

are followed (the patient wears the mask when leav

following: (I) regain normal postural cardiovascular

ing the room). The primary monitoring is oxygen sat

responses (no postural hypotension) and (2) increase

uration, followed by heart rate and blood pressure. A

functional activities. The former is primarily focused

common complication in the immediate postoperative

on the patient being able to tolerate changes in posi

period is pneumothorax.

tion, increase time in upright sitting, and transfer in dependently. Upper and lower extremity range of

Goals

motion and strength need to be adequate to perform

In the immediate postoperative period the major goals

activities of daily living.

are to increase time out of bed, optimize ventilation perfusion ratio, and increase active range of motion on

Exercise Guidelines

the surgical side (Malen and Boychuck, 1989). Major

Deconditioning and lack of sympathetic input to in crease heart rate response contribute to the possibility of hypotension. Because of the high incidence of pos tural hypotension, patients need to change positions

problems and goals are listed in Table 38-2.

Interventions The range of therapeutic interventions are many. In

slowly and be given time to adapt to the new posi

general an intervention may continue until an abnor

tion. Exercise may be continued during mild-to-mod

m a l exercise response is reached. Abnormal re

erate rejection episodes but is not performed during

sponses include a decrease in heart rate or blood pres

periods of severe rejection. The main consideration

sure with an increase in exercise, a decrease in

for exercise in patients with heart transplants is that

oxygen saturation below recommended levels (88%


38


713

TABLE 38-2 Problems and Goals for Acute Posttransplant Rehabilitation: Lung Transplant PROBLEM

GOAL

Decreased secretion clearance

Independent secretion management

Because the lungs are denervated, there is decreased sensation of secret ions. Incisional pain

Pain management

Postoperative pain is related to the surgical incision

Pain medication

and decreased movement of muscles Abnormal postural hemodynamic responses

Normalize hemodynamic response

(i.e., postural hypotension and fatigue)

(i. e. , no postural hypotension, normal heart rate, respiratory

Increased oxygen/venWatory requirements

Adequate oxygenation without supplemental (Sa02 94%

rate, and blood pressure response to exercise) to 96% on room air) Diaphragmatic breathing Normal vital capacity Decreased runctional mobility

Independent activities of daily living (dressing, hygiene,

Decreased shoulder range of motion

Need adequate shoulder range of motion to perform these

Decreased exercise tolerance

Independent transfers

shower, toilet) activities Out of bed most of day Independent ambulation SOO ft Bicycle 10 minutes, no resistance Compromised nutrition

No supplemental feedings

to 90%), or symptoms of dizziness and diaphoresis. Suggested treatments are shown in Table 38-3.

(IV)

Considerations As mentioned before, transplanted hearts lack auto nomic innervation. Implications for exercise response are that heart rate increases can only be accom

POSTOPERATIVE OUTPATIENT REHABILITATION

plished, using circulating catecholamines. For the phase II cardiac rehabilitation patient, this means that

Heart Transplant

the warm-up and cool-down portions of exercise

Once the patient leaves the hospital, rehabi litation

should be increased to 10 t o 15 minutes and pro

looks much like phase II cardiac rehabilitation. The

gressed slowly. Resting heart rates are close to the in

overall objective is to increase functional activity to

trinsic heart rate of 100, and heart rate should not be

within normal limits.

used as an indication of fitness nor to establish exer

Duration of this phase of rehabilitation generally

cise intensity. Rating of perceived exertion is a more

continues for 8 to 12 weeks, at which time the patient

appropriate indication of exercise intensity. Recom

is encouraged to continue exercise on his or her own

mended guidelines are 11 to 13 on the 20-point Borg

or at a fitness facility. Many heart transplant patients

scale (Irwin and Tecklin, 1995; Hosenpud et aI.,

return to predisease levels at this stage.

1990). Both endurance and strength exercise can be


714

PART VII


TABLE 38-3 Acute Rehabilitation Interventions GOALS

INTERVENTIONS

Independent secretion management

Incentive spirometer

I I

Secretion removal (positioning, percussion, and vibration) Assisted cough or instruction Active range of motion shoulder girdle

Pain management Pain medication

Positioning Mild heat Massage/soft tissue techniques

Normalize hemodynamic response

Sitting on edge of bed

(i.e., no postural hypotension, normal heart rate,

Out of bed to chair day 1 or 2

respiratory rate, or blood pressure response to

Ambulation to bathroom day 2 or 3

exercise) Adequate oxygenation without supplemental oxygen

Instruction of diaphragmatic breathing

Diaphragmatic breathing with activity

Facilitation of diaphragmatic breathing

Normal vital capacity

Lateral costa l expansion techniques (surgery side)

Independent activities of daily living (dressing,

Encourage and assist with activities of daily living

Incentive spirometry

hygiene, shower, toilet)

Active and active-assisted range of motion All motions shoulder girdle

Need adequate shoulder range of motion to

Wand exercises

perform these activities

Side lying shoulder abduction Independent transfers

Daily schedule

Out of bed most of day

Assisted ambulation in room initially, to hallway within

Independent ambulation 500 ft

2 to 3 days Bicycle in room, 2 minutes initially, progress to 10 minutes

Bicycle 10 minutes, no resistance

Schedule rehabilitation around meals

No supplemental feedings (IV)

Medical management of nausea

performed in this rehabilitation stage, although upper

should be reported to the physician immediately. Re

extremity strengthening should only be started after

jection episodes are monitored by biopsy. Exercise

the sternum has healed. To protect the sternum, lift

can continue if the rejection episode is mild or mod

ing should be limited to Jess than 10 lbs for 6 to 8

erate as determined by biopsy. Summary guidelines

weeks. Treadmill, bike, arm ergometry, and indoor

for postoperative rehabilitation for heart transplant

cross-country ski equipment are all appropriate

are outlined in the box below.

choices.

Signs of Rejection

Lung Transplant

The primary signs and symptoms of rejection include

Because patients are discharged from the hospital as

flu-like symptoms including low-grade fever and

early as 8 days after transplant, much of their medical

muscle aches. Dysrhythmias and bradycardia below

management and rehabilitation occurs on an outpatient

60 or relative bradycardia (decreased compared with

basis. In the early stages of this postoperative outpa

patient's normal resting heart rate) are significant and

tient phase, patients are medically labile and need


38


715

portable oximeter at home and may report episodes

Summary Cardiac Guidelines

of desaturation. Rejection should be suspected and reported if a decrease in Sa02 of 4% to 5% for the

Cardiac phase II protocols

same amount of activity is seen (Malen and Boy

Heart rate is not intens ity regulator

chuck, 1989).

Increase warm-up and cool-down to 10 to 15 minutes

RPE II to 13 (20-point Borg scale)

Goals

No exercise in severe rej ection ( b iops y )

Patients are generally excited about the improvement

Continue exercise in mild rejection

in shortness of breath and surprised at the level of muscle weakness seen especially in the lower extrem ities. Once ventilation is no longer a limiting factor in function, other deficits emerge. In the initial stages of

Once- or twice-a-week monitoring of medical status.

outpatient rehabilitation, patients may have multiple

Rehabilitation should progrcss in this phase, but close

complaints about the side effects of medications and

communication with medical personnel is recom

often generally do not feel well. Rehabilitation

mended because of thc many medication changes.

should continue through these periods of malaise.

Blood levels of immunosuppressive drugs are moni

The overall objective of outpatient rehabilitation is to

tored and metabolic function (fluid and electrolyte lev

improve function to levels appropriate for the pa

els, kidney and liver function) are followed.

tient's age and interests. Generally, patients are closely followed by the medical staff for 2 to 3

General Considerations

months after transplant, and rehabilitation 2 to 3

Patients in the outpatient phase of rehabilitation begin

times per week continues throughout this period.

at low levels of function and progress to having few

The most common impairments that limit func

functional limitations. Therapists need to adapt and

tion are decreased cardiopulmonary endurance, de

progress the rehabilitation program appropriately. If

creased muscle strength and endurance, range of mo

rehabilitation is not aggressive, patients may succumb

tion limitations, and abnormal movement patterns of

to the effects of prednisone and cyclosporine. Because

the shoulder or trunk. Impairments may be caused by

of the debilitating side effects of immunosuppressive

the surgical procedure itself or as a result of years of

medications, rehabilitation needs to be aggressive and

abnormal muscle mechanics, posture, and decreased

preventive in nature. Rehabilitation can occur in a

activity. Cardiopulmonary endurance training is em

group setting and/or on an individual basis.

phasized at this stage of rehabilitation, as is posture reeducation, range of motion, and upper extremity

Monitoring

movement patterns. Lower extremity strengthening

The areas of emphasis in the lung transplant patient

can begin early, but upper extremity resistive train

follow from the physiology and surgery performed.

ing should be delayed until wound and tissue healing

The primary limitation pretransplant is ventilatory,

is complete, generally about 6 weeks because of the

with the surgery intended to improve ventilation.

delays in wound healing caused by prednisone.

Monitoring of ventilatory status should be the pri

Goals which specifically address impairments may

mary consideration of the therapist. Respiratory rate

include normal shoulder range of motion, normal

and oxygen saturation should be followed closely

muscle strength in all major muscle groups of upper

during exercise sessions.

and lower extremities, and normal thoracic mobility (Figure 38-2).

Rejection The primary symptoms of acute rejection are short

Interventions

ness of breath, exercise intolerance, and desaturation

To achieve the goals of rehabilitation and address im

at rest or with exercise. Patients generally have a

pairments, a pulmonary rehabilitation protocol may be


716

PART VII


Lung Transplant Guidelines Keep S a0 2 above 90% Add supplemental oxygen if necessary during treated acute rejection episodes Patient should wear mask when with people Increase strength program during prednisone bursts

Return to home can occur at this point in time, whether or not rehabilitation goals have been met. The major goal of community-based rehabilitation is return to normal function with minimal limitations. Many pa tients feel so good after transplant that return to prior FIGURE 38-2

level of function, including employment, is a natural

Post-single lung transplant inp atient.

phenomenon. Formal rehabilitation may only be neces sary in complicated cases or after rejection episodes or illness. Patients may also seek physical therapy advice

used, or the therapist may creatively design a rehabili

for musculoskeletal problems unrelated to the trans

tation program. Except for delaying upper extremity

plant. Therapists should be comfortable treating pa

strengthening for 6 weeks after surgery, no therapeutic

tients in many settings, addressing the common com

interventions are contraindicated. For endurance train

plications, and watching for signs of rejection.

ing, stationary bicycles, treadmills, arm ergo meters, indoor nordic ski machines, rowers, and stair climbers may be used. Pulleys, weight equipment, free weights,

Heart Transplant

resistive elastic bands, or gymnastic balls all may be

Ironically, the medications used to prevent rejection

appropriate for strengthening and facilitation of nor

in transplant patients may increase the incidence of

mal movement patterns. Because of the effects of

coronary artery disease. It is recommended that pa

prednisone, proximal muscle function must be ad

tients partici pate in a regular exercise program to

dressed, and strengthening programs should be ag

manage the effects of the medications and to prevent

gressive, keeping the repetitions to 10 or less. Once a

coronary artery disease complications. Hospital

patient has achieved a satisfactory level of function

based phase III cardiac rehabilitation programs are

(determined by the therapist and patient), formal reha

appropriate, or patients may elect to independently

bilitation may be discontinued.

exercise in a fitness facility. Some follow-up by the

The general considerations for lung transplant pa tients are to monitor oxygen saturation and prevent

center is important to encourage compliance in exer cise programs.

the patient from contracting respiratory infections. A summary of lung transplant treatment guidelines are listed in the box below.

lung Transplant For patients who have left their home community to

COMMUNITY OR HOME-BASED REHABILITATION

wait for lung transplant, the transition to home fre quently occurs at 3 months after transplant. Ideally,

Patients are generally followed at the transplant center

rehabilitation goals from the outpatient phase will

until the medical staff is satisfied with patient progress.

have been accomplished, and the patient will be able


38


717

and needed long-term therapy. A 55-year-old male had a bowel obstruction after surgery, which length ened his recovery time. If the patient is medically sta ble but has rehabilitation needs, the patient may be referred for physical therapy in his or her home town, possibly away from the transplant center. Other pa tients may have multiple episodes of rejection, which are treated with high-dose steroids, and develop steroid myopathy, requiring intensive and progressive strength training. Goals Physical therapy assessment is critical to identify problem areas and evaluate progress toward goals. Goals at this stage should be primarily guided by spe cific patient quality of life issues. Common long-term impairments are chest wall soreness, abnormal upper quarter movement patterns, and low back and knee pain from overuse. Influence of Medications on Treatment

FIGURE 38-3 Post-douhle lung transplant outpatient at approximately 3

months pust-surgery.

Patients are on a multitude of medications after trans plant, and additional medications may be added to decrease the side effects of the primary immunosup pressive drugs (Miller, 1995). Prednisone, cy closporine, and azathioprine (lmuran) are the main stay of immunosuppression, with OKT 3 and FK 506 being additional options. Prednisone

to return home to pursue his or her own interests. Success stories are many. One patient returned home and progressed to walking 5 miles a day, fishing 4 to 5 times/week, and bow hunting with a 50-lb bow. One gentleman reported at a 6-month follow-up visit that he was pleased to be riding around his ranch and checking up on things. The therapist asked if he was riding in the truck, and he replied, "no, on my horse." A 21-year-old male (130 Ib) with cystic fibrosis re sumed weight lifting and bench pressed 1 JO Ibs, 8 months after a double-lung transplant (Figure 38-3). Other patients have more rehabilitation needs. For example, a 40-year-old single-lung transplant patient sustained a brachial plexus injury from the surgery

Because organ rejection is primarily an inflammatory response, corticosteroids are usually used in trans plant patients. Steroid therapy may be delayed until primary wound closure is certain (1 to 2 weeks) at which time the patient is begun on low-dose oral steroids. Acute rejection episodes are treated with oral or intravenous steroid pulses. Corticosteroids work by immobilizing macrophages and decreasing B and T lymphocytes. Cyclosporine Cyclosporine is a very powelful immunosuppressive agent that works by inhibiting T lymphocyte growth factor and T helper cells. Side effects are common and annoying to patients. It is considered a peripheral


718

PART VII


Side Effects of Immunosuppressive Medications Prednisone

Cyc1osporine

Hypertension

Tremors

Glucose intolerance

Hypertension

Osteoporosis

Increased cholesterol

Muscle weakness

Nephrotoxicity

ability to analyze movement and function allow reha bilitation professionals to maximize a patient's qual ity of life. The field of organ transplant is exciting and growing. New advances in long-term manage ment of transplant recipients means that rehabilitation professionals need to continue to develop and evalu

Delayed wound healing

ate approaches to care.

REVIEW QUESTIONS I.

What feelings do patients and family com monly experience before and after an organ

nerve irritant. Therapists should watch for muscle tremors and peripheral neuropathy.

transplant? What is the role of pretransplant pulmonary

2.

rehabilitation?

Azathioprine Azathioprine ({muran) is a powerful drug that inhibits

How does the surgical incision affect the

3.

musculoskeletal function of a posttransplant

RNA and DNA synthesis of most immune system cells. Bone marrow suppression (leukopenia, anemia) is common as are gastrointestinal symptoms of nau

patient? 4.

What are the signs of organ rejection in the cardiac transplant patient? the lung trans

sea, vomiting, and anorexia.

plant patient? How is the rehabilitation of the heart trans

5.

New Drugs

plant patient similar and different than tradi

Research has added drugs such as OKT 3 and FK 506 to the immunosuppression regimen. OKT 3 is a mon oclonal antibody that is used for management of

tional cardiac rehabilitation') How is the rehabilitation of the lung trans

6.

plant patient different than other forms of

acute rej ection and is not used on a daily basis. OKT 3 blocks all T lymphocyte functions for a short time after administration and can help remove T cell

pulmonary rehabilitation? How do immunosuppressive drugs affect a

7.

patient's neuromuscular function? Muscle

byproducts from the graft site. Because of its dra

strength? Cardiopulmonary endurance?

matic and potentially dangerous side effects, this medication is given in a controlled setting where the patient can be carefully monitored at 15 or 30 minute intervals. Pulmonary edema, bronchospasm, fever, chills, and hypokalemia are common reactions. Rehabilitation should not be given during ad ministration of these medications. The box above summarizes the effects of common immunosup pressive medications.

References Conners,

G., &

Hilling, L. (1993). AACVPR guidelines for pul

rnon{/l)' re/wiJililalion programs. Champaign.

111.:

Human

Ki

netics Publishers. Craven, J.L., Bright,

J., &

Dear. C.L.

(J991).

Psychiatric, psy

chosocial, and rehabilitative aspects of lung transplantation. Clinics Chesl Medicine,

E., &

Hillegass,

1/(2),247-57.

Sadowsky. S.A. (1994). Essenlials of cardiopul

monary rei1.aiJilirarion. Philadelphia: WB Saunders.

Hosenpud,

SUMMARY

.I .D.,

Cobanoglll,

A., et al. (199 I).

Cardiac rral/splanra

liol1. New York: Springer-Verlag.

Physical therapy has an important role in maintaining and improving functional levels of patients both be fore and after organ transplant. Knowledge of cardio vascular and pulmonary physiology along with the

Irwin, S.,

&

Tecklin, 1.S. (1995). Cardiopulmol/ary physical rher

apy. St. Louis: Mosby.

Malen,

J.F., &

Boychllck. J.E. (1989). Nursing perspectives on

lung transplantation. Crilical Care Nursing Clinics of Norlh America,


1(4),707-722.

38

Moser, K.M., Bokinsky, G.E., et al. (1990). Results of a compre hensive rehabilitation program: physiologic and functional ef fects on patients with chronic obstructive pulmonary disease.

Archives of Intemal Medicine 140( 12): 1596-1601.


719

Toronto Lung Transplant Group. (1988). Experience with Singlc

lung transplantation for pulmonary fibrosis. lAMA, 259(15),

2258-2262

Urliversill' Hospital surgical cardiac rehab ilitation proto col.

Scherer, S.A. (1995). Preoperative pulmonary rehabilitation re

(1994). Denver.

duces pot-operative length of hospita l stay after lung trans plant. Denver: International Conference on Pulmonary Reha bilitation and Home Ventilation; abstract.


The Patient in the Community

Donna Frownfelter

KEY TERMS

Assisted living

Outpatient

Continuity of care

Skilled nursing and rehabiliatation facilities

Home care

Subacute hospitals

Managed care

Transitional care units

INTRODUCTION

This chapter focuses on patients in the skilled

Physical therapy in the community may take on a

nursing home, home care, and alternative long-term

wide variety of forms. The practice has certainly

care settings. These concepts and ideas could easily

changed dramatically over the last few years. Diag

be used in an adult day care or outpatient setting,

nostic related groupings (DRGs) began the trend of

senior housing, or a transitional or an assisted liv

patients leaving the hospital earlier and often in a

ing facility. The settings described in this chapter

more acute stage of recovery. Subacute hospitals,

will be used only as examples on which to focus the

Medicare skilled nursing, and rehabilitation facili

discussion.

ties with transitional care units provide therapy and

Continuity of care is an essential component of qual

facilitate patient progression so that he or she will

ity health care in light of the trend toward earlier hospi

be back home within a short (perhaps a month) pe

tal discharge either to a skilled nursing/rehabilitation fa

riod of time. Managed care has had a significant

cility or to home with nursing and therapy support. A

impact on diagnoses and treatment authorization,

colleague in hospital practice recently commented that

which affects the type of diagnosis given to patients

she feels more like a triage therapist than a physical

and the number of therapy sessions authorized for

therapist. At times the absolute basics of therapy (i.e.,

given diagnoses or symptoms.

transfers and gait with an assistive device) are all that a 721


722

PART VII

Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases

patient is able to receive before leaving the hospital set

live fuller and more salisfying lives even if they are

ting. An exercise sheet may accompany the patient

unable to return home aCLcr rehabilitation. Many

home but, in general, after discharge from the hospital,

nursing home chains have developed beautiful, hotel

most patients do not know their exercise programs. In

like atmospheres with a range of services. The resi

addition, they have poor endurance because they are

dents may live in independent apartments and, if a

generally still healing from the insults or injuries for

disease or trauma occurs, may return to the skilled

which they were hospitalized. In the geriatric popula

nursing area to receive rehabilitation services. When

tion the caregiver is often an elderly spouse who also

they are able, they transfer to an assisted living area

has medical problems and is limited in the ability to as

and continue to live there or will transfer back to

sist the patient.

their apartments when they are sufficiently recovered.

The types and diagnoses of patients seen in the com

Even after an acute incident (e.g., a cerebrovascu

munity may vary; often they are the very young and the

lar accident [eV AD, a patient may not be able to re

very old. With the medical community's ability to save

turn home in a month but may continue to make

premature, low-birth-weight infants we have had an in

gains up to a year or more as strength, balance, and

flux of ventilator-assisted, oxygen-dependent infants

endurance improve. Therapists can screen residents

with bronchopulmonary dysplasia (BPD). They may be

and continue to try to improve their physical status

slow to develop and need intervention to prevent pul

and to enable them to live to their fullest capacity.

monary infections and to improve in the natural devel opmental sequence. Often they may have difficulty swallowing, and nutritional issues may delay their

MANAGED CARE

physical gains, as well as their speech and language,

Managed care groups are having a significant impact

secondary to poor breath SUppOit.

on placement and case management of individuals

Specialty hospitals have been developed to care for

who are able to return home. We are seeing many pa

the medically fragile, ventilator-assisted (dependent)

tients in home care 5 days a week with caregivers pre

patient who is not stable enough to be at home or

sent around the clock. Significant cost savings may be

lacks the resources to be at home. Many patients, es

noted compared with an extended hospitalization or

pecially children on ventilators whose parents can

stay in a skilled nursing facility. Most managed care

provide some care and are assisted by nursing staff,

companies are willing to listen to suggestions that

are coming home successfully on ventilators. They in

save money and improve customer satisfaction.

tegrate into the community in school and recreation, function well, and perceive a high quality of life.

When we think of these practice settings, it be comes obvious that cardiopulmonary concerns are

Elderly patients will often try valiantly to remain

highlighted. From the very young to the very old, pri

at home and independent, amazing the most seasoned

mary and secondary cardiopulmonary issues are often

clinician with their inventiveness and family/friend

the limiting factor in a patient's rehabilitation progress.

supports. Others will recognize that they no longer

Before considering some specific differences in

are able to care for themselves and that the caregiver,

community settings, we will look at the commonalities

who is often also elderly (often a frail spouse), cannot

in the principles of exercise training and prescription.

continue in that role. Nursing homes, long thought of as a place "to go to die," have become centers of skilled nursing and rehabilitation. The trend is moving toward "transi tional care units" where a patient will go for approxi mately I month to gain strength and practice activi

GENERAL PRINCIPLES OF EXERCISE TRAINING AND PRESCRIPTION Specificity of Training

ties of daily living, transfers, and gait and develop

Exercise programs are ind i viduall y developed to

endurance that will allow them to return home.

meet specific goals. To develop muscle strength, a

The focus of long-term care is to help residents

high-resistance, low-repetition program (i.e., weight


39


723

lifting) is prescribed. To develop muscle endurance, a

of resting. Even more troublesome were the results

low-resistance, high-repetition program (i.e., walk

that it took 10 to 50 days for the values to return to

ing, treadmill) is prescribed. The benefits of exercise

the level before resting (Saltin et aI., 1968).

depend on the targeted exercise. Strength training in

In normal individuals who received ventilatory

creases muscle fibers (white) and endurance training

muscle training followed by a month without train

increases the number of capillaries and mitochondrial

ing, the subjects lost the achieved training effect

content (Celli, 1994).

(Keens et aI., 1977).

It is noted that a weight lifter is usually not a long term runner, and few runners are able to lift heavy arm weights. In developing exercise programs, we must keep in mind the goals for the individual. Gen

SPECIFIC CARDIOPULMONARY CONCERNS IN THE COMMUNITY

erally, some form of both strength and endurance is

Patients in nursing homes, alternative long-term care

desired. However, programs often focus on one or the

and independent living facilities, and the home after disease or trauma often have several problems in

other, not both.

common. They may have decreased independence, mobility level, strength, and endurance, as well as

Intensity and Duration of Training

poor posture, and are at risk for falls 'if:condary to

Both intensity and duration have significant conse

poor balance and weakness. Often they are poorly

quences on the amount of training effect. Olympians

nourished, either from lack of appetite or dysphagia

often train at maximal or near maximal levels to

or as a result of depression brought on by their physi

achieve their "superstar" level of fitness. However, it

cal limitations and feelings of being overwhelmed

has been noted that middle-aged, nonathletic individ

with their situations. At times there is a sense of

uals benefit from lesser levels of exercise. Siegel et

hopelessness and a feeling that things will not be the

a!. (1970) demonstrated that training sessions of

30

same again. This depression is especially common

minutes about three times a week significantly im

when patients are placed in nursing homes when they

proved V021l1a, when the heart rate was raised over

wanted to go home but realized they could not take

80% of predicted maximal heart rate. Casaburi et al. (1991) studied 19 COPD patients who could achieve either 50% or 80% of maximal

care of themselves or their families insisted on the placement.

exercise (anaerobic threshold). They found that pa

disease, such as asthma, emphysema, bronchitis,

tients who participated in the higher intensity training

coronary artery disease, prior myocardial infarction,

program benefited more than the lower intensity

hypertension, dysrhythmias, or congestive heart fail

training patients. However, significant training did

ure. In addition to those diagnoses, they often have

occur in the lower intensity group (Casaburi, 1991). The number and length of treatments have a sig

Many patients have a preexisting cardiopulmonary

fractured hips, knee replacements, or CV A. The car diopulmonary factors may in fact be the limiting con

nificant effect on endurance training. An intense pe

sideration to the progress with therapy. These con

riod of care followed by a maintenance or managed

cerns need to be dealt with so that the patient reaches

care period prevents the effects of stopping exercise

his or her full rehabilitation potential.

training. Carry-over and maintenance is extremely important (Make, 1991).

IF YOU CANNOT BREATHE YOU CANNOT FUNCTION Functioning depends on the ability to breathe. An ex

Deconditioning Effect

ample of this was seen in a patient that fell in the

Training effect can be lost after the exercise has

parking lot of a hospital while going to a pulmonary

stopped. Bed rest in normal individuals was shown to

rehabilitation program. She was in a long leg cast at

result in a significant decrease in Vo2max with 21 days

home and became very short of breath with sit-to


724

PART VII


stand transfers. Limited by severe shortness of breath,

dentures fit or is he or she not eating or chewing

she could barely ambulate across the room with her

food because of poor dentition or denture fit? Is he

pick-up walker. When observed using her bron chodilator metered-dose inhaler (MDI), she was

or she aspirating? Does he or she have dysphagia? •

Is the patient sleeping? Many patients after

found to be using it improperly. After she was in

surgery, trauma, or a CVA are left supine or in a

structed on how to use it properly, she used the bron

side-lying position to sleep. They may not have

chodilator before transfer and gait and was like a dif

ever slept in that position before. However, they

f e r e n t patient. She was able to coordinate h e r

do not recognize that may be the reason they are

breathing pattern with control t o match her activity

not sleeping. If the patient states he or she cannot

and her endurance was remarkably improved.

sleep ask him or her about previous sleep posi

With these principles in mind, we can look at

tions and try to work with the nursing aide staff

some of the considerations in nursing home and home health settings.

on positioning for sleep. •

Follow-through of methods of working with the patient should be consistent so as not to confuse the patient. For example, breathing ex

lONG-TERM CARE FACILITIES

ercises in conjunction with activities should be

AND NURSING HOMES

consistent. If the patient is taught in therapy to

As mentioned previously, with the changes in health

inspire when extending the trunk, that should

care, much rehabilitation is now taking place in transi

be communicated to other caregivers and con

tional care units, Medicare skilled nursing homes, and

sistently encouraged. If the goal is for the pa

assisted living facilities.

tient to walk to meals, a coordinated effort

The following are special considerations when

should be made to try to have the patient ac

working in a long-term care setting. •

complish this as a transition plan. For example,

There are several layers of care from geriatric

when the therapist talks with the aide and a

specialist nurse consultants to head nurses to

care plan is established, the patient can start

general floor nurses to aides.

walking to one meal or as far as he or she can

•

Most patient care is given by aides.

toward the dining room. When that is accom

•

Communication and cooperation are the keys to

plished, the goal will be to walk to two meals,

achieving patient goals and success.

and so on. Then additional goals can be added

•

•

Input and involvement of the patient and family or

to walk to activities, social settings, out to the

significant others is essential in developing goals.

car to meet the family, and other functional,

Clear and achievable goals need to be devel oped and revisited as the patient progresses or

•

•

appropriate goals. •

In-services to reinforce the therapy techniques and

regresses in therapy. Is the goal to transition to

goals should be done individually and in formal

home, to assisted living, or to living at the

classes. Classes are helpful, on a one time basis, to

nursing home?

discuss and instruct on a particular topic. How

Quality of life issues need to be taken into con

ever, an ongoing one-on-one therapist/aide pa

sideration. How mobile is the patient? Is he or

tient-specific mini-in-service is essential. The

she independent? Is he or she a morning person?

classes need to be repeated on a regular basis for

When is therapy going to be most efficient time

new staff and as a refresher for some aides who

wise? Will it conflict with his or her other inter

have not used or practiced the techniques. The

ests and activities, which may give him or her

aides may at first feel they are "too busy and un

moral support or act as a distractor and provide

able to do the job," but you can convince them

real recreation?

that it will be of benefit to dle aide, as well as the

Nutritional concerns need to be taken seriously. Is

patients. The patient will be able to do more and

the patient losing or gaining weight? Do his or her

in the long run, the aide will have less work. In ad


39

dition, the family members will be pleased and re

markable in their patient care follow-through for therapy goals. Be on the look out for ways to

also benefit the nursing home because it will be

praise and thank them in a sincere manner. They

care, which will make the director of nursing and

will be more willing to help in the future. •

the administrator pleased. Most aides would like

Sponsor open house times in the therapy depart ment so that the staff come in and can see the ther

to do the best for their. patients and provide the

apists. You can provide educational material for

best care they can render.

the staff (and food). Welcome their input and sug

Try to get other programs and nursing home ac

gestions for patients who may benefit from ther

tivity groups to follow-through with therapeutic goals. Talk with the activity department if pa

•

725

gard the work of the aide more highly. This will known for its individualized, excellent patient

•


apy but are not on the physical therapy caseload. •

Prepare a bulletin board to show the accom

tients need extra encouragement or help with

plishments of patients in pictures and descrip

oxygen to participate. If patients need to drink

tion. We all love success stories and being part

more water for increased hydration, ask them to

of the success. Show pictures of aides, as well as

remind the patient and provide water.

therapists, helping the patients.

As a therapist, be willing to pitch in and help whenever you are able, even if it "isn't in your

•

In addition to chart reviews and talking about pa tients with the nurses, screen patients in the din

job description." Your willingness to be a

ing rooms and activity sessions and walking in

team player will be noticed. If an aide is off

the hall. The aides will be a terrific source of pa

sick and you are available at lunch and see

tient referrals; they are with the patients more

there is a problem passing out trays, offer to

than anyone else.

help. The next time you ask an aide for help there will probably be more willingness. If there is a patient that is difficult to transfer, offer to help in getting the patient up for phys ical therapy. This will serve as both a teaching

•

MONITORING CARDIOPULMONARY STATUS IN THE LONG-TERM CARE FACILITY With the increase in patient acuity, it is more impor

opportunity and as a help to the aide. Look for

tant than ever to monitor the patient's response to

ways of blending your therapy with the needs

mobilization and exercise. Many long-lerm care and

of the nursing staff.

subacute facilities are purchasing pulse oximctcrs and

Give recognition to aides who have been re

portable ECG monitors because they have more

FIGURE 39-1 Pulse oximeter.


726

PART VII


unstable patients (Figure 39-1). In addition, all thera

oxygen in the arterial blood) or to relieve the myocar

pists should be competent in blood pressure monitor

dial work, such as in a patient with a severe myocardial

ing and taking pulse rates; auscultation training is

infarction or other cardiac dysfunction (see Chapters 4

highly recommended (see Chapter 14).

and 27).

During the initial evaluation the vital signs and

It is important to note that the arterial blood gas

oximetry should be taken. The readings should be

is drawn at rest with no patient activity unless

taken at rest in a supine or semi-Fowler's position for

specifically noted otherwise (such as an exercise

a baseline. Readings should then be taken in sitting

test blood gas). Generally the Medicare guidelines

and standing positions. It is helpful to take the blood

require that the patient has a P02 of 55 mm Hg

pressure on both arms to see if there is a difference in

(Torr) to be placed on oxygen. This is on the steep

the readings.

part of the oxyhemoglobin dissociation curve (see

When the patient begins treatment, vital signs and

Chapter 3).

oximetry should be performed before and after the

When the patient exercises he or she consumes

mobilization or gait activity. A normal exercise re

more oxygen than at rest. Consequently if a patient

sponse would be that the blood pressure and pulse

is on oxygen at rest and the P02 is 55 or 60 mm Hg

would increase in relation to the activity. An increase

he or she may desaturate during exercise. This

of 20% to 30% might be expected and would be

means that the red blood cell Hg will give up more

within normal limits. The time the vital signs take to

oxygen to supply the exercising muscle. However,

return to normal (recovery time) should be within 5

it is enough oxygen for exercise and the patient will

to 10 minutes.

experience i n c reased s h o r tness of b r eath, the

Many patients who are not considered cardiopul

oximeter will note a drop below 90%, and the blood

monary patients have an abnormal response to exer

pressure and heart rate may initially increase be

cise. If we are not observing and measuring objec

cause of the stress and later drop as the heart cannot

tively, we will not know the cardiopulmonary response

compensate for the decrease in oxygen level.

is abnormal, and deleterious effects may occur.

The pulse oximetry reading of normals is 97.5%

An example of this was seen in a patient one

oxygen saturation. It is clinically acceptable to main

month after a CV A. The patient was very fatigued

tain oxygen saturation at 90% or above. This satura

and complained that his knees felt like they were

tion corresponds with keeping the P02 generally at

going to buckle. This patient had been doing quite

above 55 mm Hg. When the P02 drops below 55 mm

well and was not being monitored. However, after the

Hg, a dramatic drop in oxygen saturation will occur

patient ex pressed the feeling of weakness the thera

for a small drop in P02.

pist took the vital signs after the patient rested and

If the nursing home does not have an oximeter, the

walked again. The blood pressure and heart rate

durable medical equipment company that supplies the

dropped during the exercise. The doctor was in

oxygen may be called and will bring an oximeter

formed and ordered a blood test that revealed the pa

when they check the oxygen. However, any patient

tient did not have an appropriate blood level of digi

on oxygen at rest should be tested for desaturation.

talis. The medication was increased and the patient

Another option is to call the patient's doctor to re

improved. Had the therapist not checked the vital

quest an increase in oxygen during exercise. For ex

signs and continued to push the patient, there could

ample, a patient on I Llmin at rest can have a pre

have been serious consequences.

scription written for I Llmin at rest and 2 or 3 I/min during exercise. The increase in oxygen is no prob lem as long as the oxygen is decreased back to the

SPECIAL MONITORING CONSIDERATIONS FOR PATIENTS ON OXYGEN

resting amount as soon as the patient recovers back to

Patients receiving oxygen therapy have usually been

ers whose oxygen is carefully titrated to prevent tak

placed on oxygen because of hypoxemia (low levels of

ing away the hypoxic drive to breathe.

baseline. This is even true for carbon dioxide retain


39


727

DOCUMENTATION

CARDIOPULMONARY CONCERNS IN HOME CARE

Functional outcomes are key to documentation. As

Home care takes the practice setting one step further

we evaluate patients and write care plans, we set

from the hospital. Managed care is having major im

goals that are both short and long tenn. Each goal

pacts on changes in this area of therapy and nursing

should be linked to functional outcomes that enable

care. Cost effective yet excellent therapy is the goal

the patient to be more mobile, safe, as independent as

of managed care. There is a great deal of creativity;

possible, and functional in. the care setting in which

deals can be made if a provider group can demon

he or she lives.

strate that the patient will benefit and a cost savings

Documentation needs to show progress toward

to the managed care group will occur. We are seeing

the functional outcomes the therapist has developed

coalitions form between' contract service therapy

with the patient. Goals should be attainable and real

agencies, durable medical equipment companies,

istic. If there is poor or slow progress to a goal, there

nursing agencies, and enteral feeding companies to

needs to be documentation and explanation in the

provide "one-stop shopping" groups. The managed

notes of what has occurred and how the treatment

care companies prefer to make one call that will pro

program will be modified or how the goals need to

vide them with nursing service, therapists, and home

be changed.

medical equipment, such as walkers, canes, tub seats,

When the functional outcomes have been met, the patient is reasscssed to see if they can accomplish more

raised toilet seats, oxygen, IVs, and enteral feeding. Home care involves not only seeing more acutely ill patients but also seeing some interesting cardiopul

or if the patient should . a maintenance program. A screening date should be set

monary situations. For example, in working with

to check back and monitor the patient to ensure mainte

major medical centers who perform transplant surgery

nance, improvement, or decline in condition. At times

the therapist works with patients before and after heart

patients who have "plateaued" will improve and may

and lung and other transplant surgeries. It has been

be picked up on a screening to request a doctor's order

demonstrated that patients, even as seriously ill as pre

to have additional therapy with specific increased goals

transplant patients, can improve their functional abili

defined. If a patient's condition has declined, the pa

ties, strength, and endurance to be better candidates

tient can be reevaluated to see if the patient's former

for surgery. Postoperative care is also improved when

status can be resumed or maintained.

the patient is in better physical condition before

It shou ld be remembered that third party payors

surgery. Other diagnoses are also being treated effec

are reading the notes to understand what the evalua

tively before and after surgery. It makes sense to

tion and treatment plan for the patient is and how

begin preoperative orthopedic consults to evaluate pa

the patient has progressed in meeting functional out

tients and teach them the exercises they will be doing

comes. Because the patient is receiving long-term

after surgery. In addition, any patient facing abdomi

therapy, the more therapy the patient needs, the

nal or thoracic surgery could benefit from a preopera

more documentation is necessary to tell the story to

tive visit if coming to the hospital presents difficulty.

the third party payor or the managed care group. A

Consequently, therapists who never thought they

good quote to remember is, "If it wasn't written, it

would be required to work with cardiopulmonary pa

wasn't done!"

tients are needing to increase their knowledge bases to

In summary, every patient in a long-term facility

treat these patients appropriately.

is a patient with cardiopulmonary concerns. The car

In the home-care setting the therapist is alone with

diopulmonary system needs to be optimized for full

supports through the nursing and home-care agencies.

rehabilitation to occur. Cooperation with the nurses

However, in the home they usually must be prepared to

and aides, as well as special activities staff, is essen

evaluate patients and their progress with very little su

tial for follow-through of treatment programs and pa

pervision or consultation. In addition, they must be able

tient success. Teamwork is the key, and communica

to handle emergencies and crisis situations. AU home

tion and documentation are vital.

care therapists must have a basic CPR certification


728

PART VII


renewed annually. Policies and procedures dealing with

friends, or a caretakers smokers? Signs need to be

how to handle emergencies, infection control, and

posted to warn of danger of smoking and flames

safety are essential for any therapist in the home. Therapists need to know how to obtain necessary

around oxygen. Patients who are smokers need to have this reinforced very clearly.

information and equipment for the patient. They need

Does the patient have stairs? I s the bedroom up

to be creative in adapting equipment and be innova

stairs? Is there a first floor bathroom? If the bathroom

tive if the patient cannot afford to purchase medical

is on the second floor can the patient get up the stairs

equipment. This is not the setting for new graduates,

safely and in a timely manner, or does a commode on

but rather for the experienced therapists.

the lower level seem more appropriate? Is the bed the proper height? Are there handrails? I s i t difficult for the patient to transfer into bed? Is a de

HOME SETTING

vice needed to help the patient transfer independently?

In the hospital or outpatient center the patient comes to

The question of the bed arose with one home-care

your place of business. They come where you work.

patients who had a fractured pelvis. When I first vis

With long-term care and home care, you go to work

ited her, I asked how she had broken her pelvis and

where they live. A certain etiquette is required when

she replied, "Hopping into bed." I questioned what

going into a patient's residence. Pennission needs to be

she meant and she said, "I' JI show you." I followed

requested to enter the residence, alter their living space,

her to her bedroom watching her gait with her walker.

put in grab bars, remove scatter rugs and telephone

When we got to her bedroom, it was quickly noted

cords that are seen as a safety hazard, or rearrange

that this very short patient had

rooms that you may consider too cluttered and unsafe.

mattress was between her iliac Crest and waist when

a

very tall bed. The

The therapist must remember that this is the patient's

she backed up to the bed. She stated, "I used to have a

home and must be tactful in the way recommendations

stool that I climbed into bed on, but my son thought it

are made. The cluttered room may hold treasures that

wasn't safe and took it away. Now I have to hop up

have been accumulated over a lifetime. They may sur

into bed!" She had returned home to do the same ac

round themselves with items that are all they have left to

tivity that had put her in the hospital with a fractured

remember. It may be true that a path needs to be made

pelvis. Looking at the bed, I noted that there were 3-

for safe walker ambulation, but how this is communi

inch rolling casters and a caster pad under the hed.

cated may make all the difference in developing good

The son was called and the casters and pads removed.

rapport between a home-care therapist and the patient. I nitially, an evaluation of the patient's home needs

The patient was quite pleased that the bed was 4 inches lower and she could transfer in quite easily.

to be made. What equipment do they have, is it in

Is there family support or a caretaker if the patient

working order, do they know how to use it? Often a

is not independent? If the spouse needs to work or go

patient borrows "grandpa's cane" and does not real

out, how long can the patient be safely left alone?

ize that he or she is eight inches shorter than grandpa.

Does the patient know how to obtain a caretaker? Are

Modifications may need to be made so that existing

they able to financially afford the support?

equipment fits properly and is functional.

Most home-care agencies have social worker sup

Safety is a primary consideration. Are there cords

port to help patients discover resources available to

across the floor? Are scatter rugs loose or tacked down

them. A physician's referral is needed and the service

with carpet tape? Can the patient pick up his or her foot

is generally covered under Medicare.

sufficiently to walk over the scatter rug without trip ping? Are there pieces of kitchen linoleum that have come up and might trip the patient? Are the kitchen chairs on rollers and the patient's balance poor?

COMMUNICATION AND CROSS REFERRALS TO OTHER DISCIPLINES

Is the patient on oxygen and you discover that he

It is essential that communication take place between

or she h a s a gas stove? Are the close relatives,

the members of the home-care team. Communication


39


729

is difficult because everyone is on the road and travel

and is having difficulty swallowing may benefit from

ing to patients' homes. Generally, pager numbers of

speech and occupational therapists working on seating

therapists and nurses are exchanged and compliance

systems and feeding. The interaction and communica

with answering pages is good. However, considera

tion between therapists facilitates ideas for both thera

tion needs to be given to the realization that we do not

pists, provides continuity and follow-through, and

like to be interrupted frequently when seeing patients.

helps to optimize patient care.

Generally a system of timing the calls or pages is wel comed. A 91 I can be placed after the page number to identify an urgent call if the call is very impOltant or information needs to be given immediately. Physical therapy is the most common therapy. How

MONITORING CARDIOPULMONARY STATUS AT HOME Cardiopulmonary status at home is similar to that in a

ever, at times another therapy will be indicated but not

long-term care facility. However, at home there is not

made when the patient is discharged. When a patient

usually an oximeter available. This is unfortunate, since

expresses a problem that could be handled better or

many more patients are coming home on oxygen and

could provide increased service to a patient, a cross re

ventilators. This trend should change and home-care

ferral should be made by calling the home-care agency

therapists should have oximeters available for evaluation

or the patient's nurse case manager. Identify the prob

of patient status and exercise desaturation. The durable

lem and why you feel the additional therapy is indi

medical equipment company has oximeters and the ther

cated. The physician will be called and the order gener

apist may reqnest an oximetry study done with a physi

ally obtained. It would then be helpful for the refelTing

cian referral. It is helpful to make an appointment and

therapist to call the new therapist and update rum or her

meet the therapist to see the results and to try to reenact

on the patient and reason for the referral. This commu

the therapy to see if the patient de saturates with exercise.

nication should be documented to show the necessary communication between the therapists and nurses. An example of this was seen in

a

The same blood pressure and pulse monitoring should be done at rest on both arms and in sitting,

patient that I re

ceived a refelTal on for home care that had been on a

standing, and before and after exercise as mentioned previously in this chapter.

ventilator for a month in the hospital. She had been intu bated, was very hoarse, and complained that she was having trouble swallowing and eating. Liquids espe

HOME OXYGEN

cially were going down the wrong way. The home-care

Home oxygen may be supplied by an oxygen concen

referral said that the patient had a swallowing study in

trator, by tanks or as a liquid oxygen system (Figure

the hospital that demonstrated she was aspirating. A

39-2) (Chapter 41). One consistent problem that must

speech language pathologist had been working with her

be dealt with in exercise with patients at home on oxy

on swallowing in the hospital. However, speech therapy

gen is the incredibly long oxygen tubing needed to

had not been ordered at home. Nothing had changed on

allow patients t o go to the bathroom, out to the

the day the patient had been discharged. Since the pa

kitchen, and to the living room (Figure 39-3). Often 60

tient was still aspirating, a speech consult was requested.

to 90 feet of tubing must be used. The question often

At times it is helpful to do a joint treatment session

arises, "Does the patient get the right amount of oxy

with another discipline. This can be done to coordinate

gen with such long tubing?" The answer is yes because

therapy and provide focus and continuity of goals. It

the flow meter is a compensated one, which means it

will also lead to success for the patient. For example, a

reads what really is occurring. If more tubing is added

physical therapist and a speech language therapist may

and a lesser flow was occurring, the flow meter would

meet to focus on a patient with poor posture who lacks

drop to indicate that had happened. Then it would be

breath support for phonation. Another patient who is

readjusted to the proper liter flow as ordered.

having difficulty feeding because of trunk weakness

It has been found that the portable oxygen systems,

and is sitting in flexion with a forward head and neck

in particular the demand oxygen system, do not always


730

PART VII


·"1 ••

jf

r-;- . --

-f .

,

FIGURE 39-2

FIGURE 39-3

Oxygen concentrator.

Oxygen tubing presents a significant safely hazard.

deliver the exact amount expected (Figure

39-4). It is

•

Be compliant with medications and health

•

Learn preventative care (i.e., prevent pulmonary

precautions.

necessary to use oximetry to determine whether the pa tient has an appropriate oxygen saturation reading. Patients need to be taught either to coil the tubing or

infections and not increase salt/water intake if

to develop a means to make sure that they do not trip over the tubing because it creates a safety hazard.

on cardiac precautions or taking steroids). •

Some patients have more than one tank or concentrator in the home to prevent having long lengths of tubing.

Learn ventilatory strategies to increase comfort and function (see Chapter

•

pending trouble

change in mucus, decreased urine Olltput, or rapid weight gain) (Figure •

monary dysfunction need to: •

(i.e., increased shortness of

breath, swelling in ankles, productive cough,

THERAPEUTIC GOALS FOR HOME-CARE PATIENTS WITH CARDIOPULMONARY DYSFUNCTION To be independent at home, patients with cardiopul

00).

Learn to monitor themselves for signs of im

39-5).

Train to pace activity and use energy conserva tion techniques and rest periods to accomplish more with less stress.

Understand the dysfunction or disease.


39


731

FIGURE 39-4

Portable demand oxygen system.

FIGURE 39-5

Patient monitoring oximeter

with exercise.


732

PART VII


FIGURE 39-6 Nasal CPAP unit.

•

Maintain proper nutrition and hydration.

•

Develop a support network to help when needed

patients at home. As health-care practitioners, we

and to check on the patient occasionally.

offer helpful suggestions for modification of the pa

Maintain walking program and general exercise

tient's home environment and life style. However, we

•

tion are essential in the progress and maintenance of

to continue functional gains.

cannot force a patient to comply or accept what we

Some patients may need noctural nasal continu

have proposed. The patient in the home setting is in

39-6).

dependent in his or her judgments and activities. We

ous positive airway pressure (CPAP) (Fig.

This may be ordered to treat sleep apnea or to rest

need to respect that and at the same time provide our

the patient and assist with ventilation. A Bt-PAP

experience and therapeutic judgment and expertise.

unit allows the patient to rest and let the machine as

This setting is often the most rewarding a therapist

sist ventilation by providing pressure support on in

can have, although at times it also may be the most

spiration and exhalation. Often at first, the patient

frustrating. One thing is certain, if you ask a patient

may have difficulty adjusting to the nasal CPAP, but

where they want to be, the answer sounds like,

in time, the patient will adapt to the assistance and

"There's no place like home'"

feel it is beneficial.

REVIEW QUESTIONS SUMMARY

I. What are some common problems patients in the

Education, self-monitoring, compliance to medica tion, reduction of risk factors, nutrition, and hydra

community have in common? 2. What role does a preexisting cardiopulmonary


39

condition play in a new diagnosis or trauma (e.g.,

Jackson,

D.E., &


Wilhoire, M.J. (1985). Home health physical

therapy, considerations for the provision of care.

CV A, hip fracture)? 3. What are some uniques situations or concerns about patient care being delivered in a nursing home, assisted living center, home care?

agement in

Physical Therapy,

Clinical Mun

5: I O.

May, B.1., ( 1 993 ) . Home health and rehabilitation,

Ca re,

733

Conce pis of

Philadelphia. F.A. Davis.

May, B.J. (1990). Principles of exercise for the elderly, In Ba5ma

4. What role can a physical therapist play in opti mizing the patient's care in the above settings? 5. How can cardiopulmonary function be monitored outside the hospital?

jian, J.V.

&

Wolf, S.L. (Eds.). (1990). Therapeutic exercise,

& Wilkins. 1990. exe rc ise inslrllClion sheets: Home exercise fo r rehabili/{llion therapy skill b uilders. Tucson. (5th ed.). Baltimore: Williams

Pfau, J. (1989). Adull

Polich, C. (1990). The provision of home health care services

6. What special considerations should be taken with

through health maintenance organizations: Conflicting roles for

Home He alth Care Quarterly, II: 17. J. & Adam, L. (1986). Geriatric exercise booklet, Cli nical Manageme nt in Physical Therapy. 6:32, 1986. Schaefer, K. & Lewis, C. Marketing geriatric programs-A home care example, Clinit'al Management in Physical The rap y , HMOs.

a patient on oxygen')

Sallade,

References Emlet,

c.,

Cragtree, J., Condon,

V., &

Tremel, L. (1995).

In - ho me

aHessmenl of older aduil.\', an inlerdisciplinary approach.

G ithersburg, Md.: Aspen Publishers. Harrington, J. (1983). The case for home heallh

6: \1-17,1986. Vassif, J.A. (1985). Harper

specialization.

Clillical Mallagemenl in Physical Therapy, 3: 17.

&

The

Home Health Care Solution, New York:

Row.

Zola. I.K. (1990). Aging, disability and the home care revolution, Archives of Physical Med icine and Rehabilitation, 71:93.

Jackson. B.N. (1984). Home health care and the elderly in the

1980's. Am erican Journal of OccupalirJII(l1 Therapy. 38:717.


PART

VIII

Related Aspects of Cardiopulmonary Physical Therapy


Body Mechanics-The Art of Positioning and Moving Patients Mary Massery Donna Frownfelter

KEY TERMS

Body mechanics

Ventilation related to:

Dependent patients

Supine

Lifting and moving

Sidelying

Upright

Upright

Neutral alignment of trunk, head and shoulders

INTRODUCTION

who can move independently and assume any given

Body mechanics may be defined as the efficient use of

position with ease. In this chapter, the principles of

one's body as a machine and a locomotive entity. In

body positioning and moving dependent patients are

working with critically ill or chronically dependent pa

discussed.

tients, it is essential that optimal body positioning is ac complished to facilitate maximal ventilatory potential. Therapists and nurses attempting to position or move

POSITIONING FOR OPTIMAL VENTILATION

dependent patients must understand and use proper

Because of the three-dimensional nature of breathing,

body mechanics (Neil, 1959; Fuerst and Wolff, 1969).

the therapist's goal is to facilitate chest excursion in

This is necessary to reduce stress and trauma and to

all three planes of ventilation-anterior-posterior, su

promote success for both the patient and the nurse or

perior-inferior, and lateral (Massery, 1994). This can

therapist. Positioning and moving dependent patients is

be accomplished by improving the length-tension re

an art that is quite different than working with a patient

lationships of the muscles used in inspiration (Crosbie 737


738

PART VIII


1985; Kendall, 1993). Massery reasons

Upper chest expansion can be increased by remov

that the success of proper positioning to enhance in

ing pillows under the patient's head to increase tho

and Myles;

spiratory muscles will do the following:

racic extension. This will increase the length-tension

I. Improve the length-tension relationship of the

relationship of the neck accessory muscles (scalene

accessory ventilatory muscles involved in that

and sternocleidomastoid muscles). Increased move

posture

ment will be noted in the upper chest in a superior

2. Incorporate a passive stretch of the chest wall 3. Use the natural coordination of the trunk-chest

and anterior plane. Further anterior expansion can be achieved by using a towel roll placed longitudinally

wall movement with inspiration and exhalation

at the vertebral spine to open the anterior chest of a

patterns to maximize movement

patient who tends toward excessive flexion of the

The following are some common improvements that can be incorporated into normal positioning.

trunk (Figure

40-1).

If the patient needs some support under his or her head to achieve a neutral chin tuck to protect his or her swallowing ability, then

Supine Position

a

thin pillow or horizontal

towel roll under the occiput, may be used (Figure 40-2).

37, all activity is performed

External rotation of the shoulders with the scapula

in the field of gravity. Patients in a supine position

in a neutral or retracted position will place the pec

As mentioned in Chapter

may find breathing difficult because they must over

toral is and intercostal muscles on stretch. This will

come gravity to move the chest wall with each

improve lateral and anterior chest wall movement

1993). If a patient has full range of motion

breath. Using towel rolls or pillows to facilitate a bet

(Kendall

ter position may significantly improve the patient's

(ROM) and is comfortable with the arms placed over

opportunity for improved respiration.

head or in full flexion/abduction/external rotation for

"

// ,'\

\ '.t

FIGURE 40-1 Placement of vertical towel roll.


40

Body Mechanics-The Art of Positioning and Moving Patients

FIGURE 40-2

Increased openness of anterior chest wall with the vertical thoracic towel roll and the occipital towel roll combined.

FIGURE 40-3

Buttertly position with thoracic towel rolllO open anterior chest.


739

740

PART VIII


maximal stretch, this is the optimal po ition for full excursion of the anterior chest wall (Figure 40-3). If there are significant shoulder limitations, moderate shoulder abduction with forearm supination lUay be the best position available to facilitate chest excur sion. Whenever significant limitations are found, the therapist should try to modify the position to accom modate the patient and achieve optimal ventilation.

Sidelying Position Side lying is an optimal position for improving breath ing pattell1s. Gravity is elimi. nated sion and the diaphragm moves freely. In addition side lying is a reflex-inhibiting posture, and some high-tone patients will be able to relax and breathe more freely. It is impoltant to consider the shunt effects if a patient has lung pathology. For example, if a patient has right lower lobe pneumonia or atelectasis, sidelying on the good side will improve oxygenation. Conversely, side lying with the affected side down will cause a decrease in oxygenation (differential shunt) because a poorly ventilated patient receives more perfusion to the down lung and more shunting will occur. The patient's hip and knee joints should be flexed and supported for comfOlt. The upper extremities can be moved up and away from the body to allow for

free movement of the

upper chest wall. A pillow can be used to support the upper arm anteriorly, or the patient can be placed in a three-quarter supine position and

a

back to support the uppermost arm.

pillow behind the

If the patient has

full range of motion and is comfortable,

a

FIGURE 40-4 Unsupported upright position of patient with Tl paraplegia.

NOTE: Posterior plevic tilt and excessive thoracic khyphosis with resulting collapse of anterior chest wall.

butterfly po

sition of the anns can be used. This will automatically open up the rib cage and facilitate inspiration. (Woodhall-McNeal, and Gee,

Upright Postures

1992; Borello-France, Burdett, 1988). The anterior tilt of the pelvis will im

prove upper-extremity ROM and ventilation poten

Upright postures create new challenges to breathing

tial. Attending to this one consideration may be all

by adding the component of balance and an unsup

that is necessary to improve the breathing capacity in

ported spinal column. Pelvic alignment is a key com

some patients, allowing them to continue to advance

ponent. An anteriorly tilted pelvis in healthy flexible

in their exercise programs or rehabilitation courses.

adults will tend to do the following: kyphotic curve in the thoracic spine,

(I) reduce the (2) adduct the

tilt in sitting is to have the patient lean forward over

One simple means of attaining an anterior pelvic

scapula toward a neutral position, (3) produce a more

his or her legs, then slide a towel roll horizontally just

neutral or externally rotated upper-extremity position,

behind the ischial tuberosities, which will prevent the

and (4) pull the head back into a neutral chin tuck

pelvis from rolling back into a posterior tilt (Johnson,


40


741

and head back into a more neutral alignment. The an terior chest wall will also be more open with this technique. A neutral head and neck position is important for patients with impaired speech volume or endurance and for patients with swallowing or aspiration dys function. A neutral chin tuck will optimize the length-tension relationship of the vocal folds, mini mize vocal strain, and improve protective airway re flexes (Massery, 1994). It is also vital to evaluate the patient's shoulder positioning. Internal rotation of the shoulders and scapular protraction tends to block the upper chest from reaching its full expansion potential. Alter n a tely, external rotation of the s h o u l ders will markedly increase upper chest wall movements and thoracic extension. Clinically, improved lung vol umes will be noted when these positioning considera tions are taken into consideration. Often these smail, seemingly insignificant changes will position the pa tient for success with other therapeutic activities. If unattended, these small factors can impede patient progress. Positioning has everything to do with in creasing ventilation and functional skills.

LIFTING AND MOVING DEPENDENT PATIENTS There has been a change from earlier concepts and

FIGURE 40-5 Ischial towel roll to support pelvis in anterior tilt in patient

principles of lifting. As discussed, the body has

with Tl parapkgiJ. NmL: ch enges in the thoracic spine and

been thought of as a machine. It was believed that

open anterior chest wall as well as improved head and neck

improper mechanics of lifting would result in tremendous loads on the disks. The key components

alignment..

of lifting were to "keep it close," "bend knees," "lift with the legs." Later the spinal posture was the cen ter of attention during lifting (Physical Therapy 1989) (Figures 40-4 and 40-5). This is well tolerated

Forum, 1985).

for many patients with intact sensation and a pelvis

During observation, lifting seemed to occur "natu

that is at least minimally mobile. For neurological pa

rally" from slightly bent knees and then, during the

tients with impaired sensation or less pelvic mobility,

raise lift butt-end first, with the patient rearing back

a wedge may be substituted; however, caution must

ward at the start as the therapist started to extend the

be used because some sliding may occur.

knees before lifting. The predominance of injuries seems to occur with the back in flexion. There is a ra tionale for strengthening abdominal muscles to pro

Neutral Alignment of the Head and Shoulders

mote safer lifting. Abdominal strength is necessary to

A vertical or horizontal towel roll may also be used

support a pelvic tilt during lifting. Many commer

with wheelchair positioning to bring the shoulders

cially available lumbar and abdominal elastic velcro


742

PART VIII


supports are now available and widely accepted.

factors, such as limited space (i.e., small hospital

They provide additional abdominal wall support.

rooms), clothing, or degenerative knee joints.

Another current school of thought advocates lift

The first consideration in body mechanics is the

ing with the lordotic lumbar curve intact. This is the

need for maintenance of proper posture and balance

technique used by weight lifters. When these individ

(body stability). Consideration should he paid to the

uals are questioned about backaches, they usually

relationship between gravity, posture, and body sta

deny any problems.

bility (Figure 40-6). It is commonly known that grav

The lifting technique may be modified by other

itational force is always exerted in a vertical direction toward the center of the emth. In addition, that point in a patient or object at which all of its mass is cen tered is called the (·crller or gravity (the point at whieh the patient's maximum weight is concen

;�"

trated). In the standing position the human body's center of gravity is approximately SSG;!., of the body's e

0'

gm"",

total height and in the pelvic cavity, slightly anterior to the upper part of the sacrum. The lower the center of gravity, the greater the hody stability. Conse quently, when the human body is used as a machine to lift an object, muscular cffort great enough to maintain stability and to lift against the force of grav ity is necessary, especially when the patient's center of gravity is fUlthcr removed from your own. There fore one way to conserve energy and maintain stabil

I

Center of gravity

4

ity is to carry the weight of the patient (or object) as close to one's own centcr of gravity as possible. This allows maximal conccntration of onc's own energy toward movement of the patient, with minimal stress or injury to oneself. To help accomplish this, the bed

I ) I.

should be adjusted so the therapist or nurse can reach the patient comfortably. Usually adjusting the bed to one's hip level is adequate. This makes the patient close to the therapist's center of gravity. The majority of lifting should be done with the legs (knees) and not by straining to lift with the arms and back (Figure 40-7). Whenever there is a question about one's ability to lift a patient alone, generally it should not be done, and assistance should be obtained (Rantz & Courtial, 1977). Another point to consider is the base of support while lifting. The base of support is defined as the

- Base of support

area between the feet that provides the body's stabil ity. It is easily appreciated that the wider the base of support, the greater the body's stability. To enlarge on this concept, one also needs to define the line of grav

FIGURE 40-6

The line of gravity passes through the center of gravity and

ity and its relationship to body stability. The line of

the base of support to maintain body stability.

gravity is an imaginary line passing through the center


40


of gravity of an object and perpendicular to the sur

743

places the center of gravity in the direction of

face on which the object (body) rests (see Figure 40-

the weight being lifted. To conserve energy and

6). The closer the line of gravity passes to the center

maintain stability, carry the weight as close to

of the base of support, the greater the body's (ob

your own center of gravity as possible. Lower

ject's) stability. Increased muscular effort needs to be

your hips to the level of the surface supporting

exerted in proportion to the distance the line of gravity

the weight you plan to lift by flexing your hips

shifts away from the base of support (Rauch, 1971).

and knees. Adjust the bed up as high or down

To summarize and apply these concepts, one can

as low as you need for comfortable and effi cient work.

list the following guidelines: 1. The lower the center of gravity, the wider the

3. The effort to petform a given activity depends on

base of support, and the nearer the line of grav

the weight of the object to be lifted. Know your

ity falls to the center of the base of support, the

limits. Do not attempt to lift alone if YOLl have

greater the body's (object's) stability. When

any doubts about your ability to do so. Don't be a

lifting, stand with feet well apart, knees slightly

hero in a back brace. Obtain assistance for the

tlexed, and one foot forward. Keep head and

sake of both the patient and yourself.

trunk in proper alignment. 2. When our bodies are used as machines, the ex ternal weight on which we are working dis-

4. Other general tips for lifting are as follows (Figure 40-7): •

Lift with your legs. Keep legs in a position that permits them to supply most of the force for shifting your trunk.

•

•

Do not attempt to lift with your arms and back. W hen lifting, avoid rotation of the spine. Shift feet into position for weight shift when moving or lifting patient.

•

Stabilize your body against a stationary ob

•

For best efficiency, coordinate the move by a

ject whenever possible. synchronized verbal expression understood by therapists and patient, such as "1-2-3 lift." One additional consideration mLlst be noted moving against the resistance of friction. Friction is defined as a force that opposes the movement of one object over the SUlface of another. Friction is reduced as the amount of surface area contact between two objects is reduced. W hen moving a patient side to side or up and down in bed, the therapist or nurse attempts to reduce the contact of the patient's body sutface with the bed. This can be accomplished by several maneuvers use a turning sheet (placed just above the patient's shoulders to just below the patient's hips), cross the patient's arms over the chest or abdomen, flex the pa

FIGURE 40-7 Reach work level by bending the knees and hips rather than

tient's knees and hips, and ask the patient to flex his

the back. Lift with the legs! This can also be done with a

or her neck and raise the head as he or she is lifted (if

full double knee squat similar to techniques by

the patient is unable to do this, the therapist or nurse

weightl ifters.

will assist) (Figure 40-8).


744

PART VIII

Related Aspects of Cardiopulmonary Physical Thel'apy

MOVING DEPENDENT PATIENTS r.

Moving the patient up or down (Roper, 1973; Lewis, 1976; Neil, J 976). A. Using a turning sheet (Figures 40-9 to 40-11).

\

I. Sheet should cover from shoulders to hips. 2. Gather material as close to the patient's body as possible.

3. Hold at shoulders and hips, with a flexion pattern (see Figure 40-10).

4. Cross patient's arms over chest, flex knees and hips. 5. Ask patient to raise head if possibl e.

6. Synchronize action by counting"1 2 3 lift." -

-

7. Shift weight from one leg to the other rather than lifting up and pulling on back. B. Without turning sheet (up or down), two people. I. Follow basic procedurc-cross arms, lift head, tlex knees and hips. 2. The therapist places his or her hands and forearms under the patient's shoulders and hips.

-0.

3. If patient is extremely hea vy or tall, an other person can bend knees and assist.

FIGURE 40-8 The patient should be prepared for a position chenge: knees bent, arms crossed over chest and head lefted up to reduce friction between the patient's body and the bed.

GIfJ "\ FIGURE 40-9 To insert the drawsheet, the patient is tumed to his side and the half-rolled drawsheet is tucked under him (from just above the shoulders to just below the hips). He rolls over the drawsheet and it is pulled out behind him.


40


745

FIGURE 40-10 The drawsheet should be rolled close to the patient's body.

A flexion hand grip at the patient's shoulders and hip is most efficient.

FIGURE 40-11 Moving the patient toward the head of the bed. The patient is prepared. The therapist is positioned to move toward the

II. Moving the patient to the side of the bed.

head of the bed in order to shift his body weight to move

A. With turning sheet.

the patient.

I. Cross arms, and other body parts, toward the side to w hich the patient is to be moved. 2. Therapist's hands at patient's hips and shoulder on material close to patient's body.

2. Bring right arm to the side at a 90-degree

3. One therapist pushes, the other pulls.

angle up and away from body. 3. Place left arm across chest.

B. Without turning sheet. I. Both persons stand on the desired side.

4. Place left leg over right leg.

2. One therapist's forearms under patient's shoulder, the others under patient's hips. 3. Synchronize action by counting "1-2-3

5. Pull sheet at patient's back to turn. B. Without turning sheet (to right side). I. Move to opposite side (therapist's hands

pull."

and forearms under patient's shoulders

III. Turning the patient to his side.

and hips).

A. With turning sheet (to right side) (Figures 40-

2. Same steps as 2, 3, and 4 above. 3. Roll to right side using left shoulder and

12 and 40-13). l. Move patient supine to opposite side of turn (e.g., if turning to right side, move patient to left side of bed).

left hip to push or pull. IV. Turning the patient prone (e.g., roll to right side) (Figure 40-14).


746

PART VIII


'� ------ J

FIGURE 40-12 Preparation for the patient to turn to his left side: move patient to the right side of the bed, position his left arm up to the side at a 90-degree angle, cross the right leg and arm over his body and turn the patient's head to the left.

) FIGURE 40-13 A one-person turn to the right side using a drawsheet. The patient's body position is the same as for the turn to the side. The therapist is positioned with one foot forward, the other back. He pulls the sheet with his hands positioned at the hips and shoulders of the patient.


k!-

"@::

-

40


747

physical therapy. It is so often taken for granted and pelformed with little thought or planning. Therapists and nurses need to analyze beforehand their physi cal activities in relation to the principles of efficient movement and the proper application of body me chanics. A "tube index", counting and identifying each technical attachment, (e.g., IV, Foley cather, arterial blood gas stint, or chest tubes) should be done before moving a patient. Extra care needs to be taken to prevent dislodging important medical equipment. This could prove life threatening if ven tilator tubing was pulled and a patient was extu bated. The practical application of body mechanics will not only conserve energy and preserve muscles and joints but will also allow the patient to be moved with a minimum amount of pain and discom fort, with greater safety.

REVIEW QUESTIONS I. Why is it important to utilize efficient body me chanics when positioning and moving dependent patients? 2. FIGURE 40-14 Positioning pa tient prone

How can changing a patient's position affect ventilation?

3. How can therapist use towel rolls and easily ac

(EXM"IPLE: Rolling to the right

side). The patient's right arm is tucked in at his side with

cessible equipment to improve a patient's posi

the left arm and leg crossed ove r.

tion and potential for improved ventilation? 4. What ventilation/perfusion changes occur when a patient is turned from the "bad" side down to the "good" side down? S. Can positioning alone be considered therapeutic when it accomplishes the plan of treatment goal?

A. With or without turning sheet. l . Move patient to opposite side of bed from side toward which he or she is turning.

References

2. Cross left arm and left leg over body. 3. Right hand and arm at body side tucked in

B orello-France, D.P., Burdett, R.G.,

&

(1988). Modifi using seat 68(l), 68-7l.

Gee, Z.L.,

cation of silting posture of patients with hemiplegia

as close as possible.

boards and backboards, Physical Therapy,

4. Use hips and shoulders to turn. S. Free both arms, do not allow patient to lie on arm or hand.

6. May want pillow under hips and lower legs to bend knee and relieve back strain at lumbar spine. To summarize, we find patient positioning and movement is a necessary and integral function of

(1985). An investigation into the effect on some aspects of normal pulmonary function. Physiolherap)" 7,(7),311-314. Fuerst, E., & Wolff, L. (J 959). Fundamel1lals of nursing (4th ed) Philadelphia: 18 Lippincott. [s there a right way to lift') ([985). Physical Therapy Forum, 4, 23. Johnson, G. (1989). Functional Orlhopedics I. San Ansellmo, Crosbie, W.J.,

&

Myles, S.

of postural modification

Calif: Institute of Physical Art. Chicago: Course presentation June

8-11,1989.


748

PART VIII


Kendall, FP., McCreary, E.K., & Provance. P.G. (1993). Muscles lesling am/ flUlellOll. Baltimore: Williams & Wilkins.

Lewis. L (1976). FUlldamellfai skills in patient care Philadelphia: .

Lijiing, moving and

ferring

Irans

paliellls: a manual, S . . Louis, Mosby.

Rauch, B. (J 971 L Kinesiology alld app/red allatomy, Philadelphia: Lea & Febiger.

JB LippincotL

Masscry. M. (1994). What's positioning got to do with it? Neuml Report, /8 (3). 11-14.

Roper, N. (1973). Principles of

(2nd ed). New

Churchill Livingstone.

Neil, C. (1959). Body management in nursing. Nursing Times, 55,163.

Rantz. M. & Comiial, D.

Woodhall-McNeal, A. P. (19')2). Changes with age, Aging, 4 (3), 219-225.


1I1

posture and balance

Respiratory Care Practice Review

Michael Wade Baskin

KEY

TERMS

Aerosol

Mechanical ventilation

Humidity

Oxygen Oxygen delivery

rntermittent positive pressure breathing

(IPPB)

INTRODUCTION

OXYGEN THERAPY

Proper care of the pulmonary patient involves a multi

The atmosphere around us contains 20.95°/'1 oxygen,

disciplinary approach, and all professionals involved

one of the most essential elements needed to sustain

should have a working knowledge of each individual

human life. Oxygen exerts

profession's scope of care. As respiratory therapists,

mm Hg at sea level (dry air) and approximately 97

a

partial pressure of 159.6

physical therapists, occupational therapists, and nurses

mm Hg in arterial blood. The normal range as mea

apply their expertise in providing care for pulmonary

sured by arterial blood gas analysis is

patienls, it becomes ev ident that coordi nated team

Hg. Under normal circumstances, this molecule trav

80

to 100 mm

work is essential 10 ensure errective treatment pro

els from the atmosphere to the mitochondria at the

gramming. The purpose of this chapter is to provide

cellular level where it is used to produce ATP in a

nonrespiratory therapist health-care professionals with

process called aerobic metabolism. The pathway in

an overview of respiratory care principles and modali

volves the lungs, blood, circulation, and the muscle

ties frequently encountered in the various settings. It

tissue where the mitochondria reside. Any process

is also the intention of this chapter to eliminate the

that inhibits the transport of oxygen from the atmos

anxiety experienced by professionals because of the

phere to the cellular level can cause tissue hypoxia

plethora of attachments to the cardiopulmonary pa

and ultimately death.

tient. Interaction with the various modalities and pieces of equipment is also discussed.

One of the most common drugs that a respiratory therapist uses is oxygen. Patients with cardiopul 749


750

PART VIII


monary problems frequently need oxygen supple

The nasal cannula, also called nasal hi-prongs, is

mentation. Respiratory therapists and the nursing

one of the most common low now devices encoun

staff are generally responsible for administration of

tered because of its low expense and high patient

this drug under a physician's order. There are several

compliance (Figure 4 1-]). This device supplies be

different methods a therapist may choose to deliver

tween 24% and 40% oxygen with flow rates from I

oxygen in the most effective way.

Llmin to 6 Llmin. Flow rates above 6 Llmin can

The purpose of oxygen therapy is to treat and to

cause nasal mucosa irritation and drying. The approx

prevent hypoxemia, excessive work of breathing, and

imate liter flow and resultant Flo2 values are shown

excessive myocardial work (Kacmarek, Mack, and

in Table 41-1.

Dimas, 1 990). Although individual oxygen appli

Nasal canulas deliver 100% oxygen, however, this

ances offer suggested guidelines regarding oxygen

percentage significantly lessens as the oxygen mixes

administration, the only way to ensure effective de

with inspired air from the room. The amount of oxy

livery from a given device is blood gas monitoring of

gen delivered depends on the now rate and the venti

Pao2, partial pressure of oxygen in the arterial blood

latory pattern of the patient. A larger minute volume

or by monitoring hemoglobin saturation by oximetry.

(TV

Oxygen therapy can be administered by one of two

rate causing a greater decrease in the percentage de

methods-low-flow and high-flow systems.

livered to the lungs. In other words, the faster and

x

RR) would dilute the oxygen at any given flow

deeper a patient breathes, the more diluted the oxy gen will become. On the other hand, if a patient has a

Low-Flow Systems

low minute volume, the oxygen percentage delivered

A low-flow oxygen system is that which does not in

will increase (Kacmarek et aI., 1990). If precise con

tend to meet the total inspiratory requirements of the

trol of Flo2 is needed, the nasal cannula should not be

patient. This method of oxygen delivery is not used

used (Bazuaye, Stone, Corris, and Gibson, 1992).

when a specific concentration of oxygen is needed (Burton, Hodgkin, and Ward, 1991).

Mouth breathing by patients on a nasal cannula typically causes the attending health-care provider to switch the patient to a mask; however, this may be un necessary. If the nasal passages are unobstructed, then oxygen is able to collect in the oral and nasal cavity (anatomical reservoir). On inspiration, the oxygen col lected in this area is drawn into the airway system. If a patient with a nasal cannula is mouth breathing, the practitioner should ensure the nasal passages are un obstructed. If there is concern that the patient is not

TABLE 41-1 Approximate liter flow Hod resultant Fl02 values.

FIGURE 41-1 Oxygen cannula.


FLOW (Llmin)

Flo2(%)

I 2 3 4 5 6

24 28 32 36 40 44

41


751

receiving adequate oxygen, an oxygen saturation mea

cheal oxygen catheters are more efficient than nasal

surement should be obtained. If this is not feasible, or

cannulas, and they have a high patient acceptance

if the patient is unable to breathe through the nose, it

rate with low complications (Kent, et a!., 1987). Be

would be appropriate to switch the patient to a mask.

cause the oxygen is administered directly into the tra

Breathing through the nosc should be encouraged

chea, 50% less oxygen is needed (Kacmarek et a!.,

to receive maximum benefil from the nasal cannula;

(990). For people who use portable oxygen systems,

however, mouth breathing does not mean the patient

and for those who require high oxygen flow rates,

is not receiving oxygen (Dunlevy & Tyl, 1992).

tracheal oxygen catheters may be beneficial (Jackson,

The simple mask, or open-face mask, is another

King, Wells, and Shneerson, 1992). The catheter can

low-flow oxygen delivery device commonly used. It

be covered by the patient's clothing, therefore, it is

can deliver from 40% to 60('>(; oxygen, depending on

cosmetically appealing.

the flow rate and the patient's ventilatory pattern. This device requires a flow rate of 5 to 6 Llmin to prevent rebreathing and excessive respiratory work (Jensen, Johnson, and Sandstedt, 1991). As with the

HIGH-FLOW SYSTEMS A high-flow oxygen delivery system is that which de

nasal cannula, this type of oxygen delivery method

livers a specific oxygen concentration despite the pa

should not be used if precise control of oxygen con

tient's ventilatory pattern. If it is found that a patient requires oxygen delivered at an FIo2 of 50% to keep

centration (FI02) is required. The partial rebreathing mask is basically a mask with a reservoir bag attached. The oxygen source

the oxygen saturation at a safe level, then a high-flow system would be the method of choice.

supplics the bag with 100% oxygen where it mixes

This type of system is also used when there is fear

with exhaled anatomical dead-space-air that has not

of administering too much oxygen to a hypercapneic

taken place in gas exchange. This exhaled air is rich

patient. The respiratory drive to breath could be re

in oxygen. The exhaled air that has taken place in gas

duced and possibly result in apnea. Precise control of

exchange and contains CO2 is vented through the

low-concentration oxygen is warranted in such cases.

open ports on each side of the mask. This mask can deliver oxygen concentrations from 70% to more than 80%, and it requires flows between 7 and 10 Llmin to keep the bag from fully collapsing during inspiration (Kacmarek et a!., (990). The nonrebreathing mask is another low-flow de livery device that also contains a bag reservoir, but it can deliver up to 100% oxygen. This mask contains valves at the reservoir bag and the side vents to pre vent ambient air mixing on inspiration and exhaled air mixing on expiration. In order for this mask to operate effectively, a good seal between the patient's face and the mask should be achieved. The bag should partially deflate during inspiration (Figure 41-2). Another interesting form of low-flow oxygen de livery is the transtracheal oxygen calheter. This method has gradually gained wider acceptance as a long-term oxygen delivery device. It is surgically

FIGURE 41-2

placed into the trachea via a small incision between

Left to right,

the second and third tracheal rings. Generally, these

nonbreathing bag.

devices are seen in home-oxygen patients. Transtra

junction between the mask and bag.


mask without bag, partial rebreathing bag, NOTE:

the valves on the mask and at the

752

PART VIH


The Venturi mask is a common method of deliver ing high-flow oxygen concentrations from 24% to

50%. This mask operates via the Venturi principle, which provides for a mixing of 100% oxygen and en trained ambient air. The oxygen flows though a nar row orifice at a high velocity causing a subatmos pheric pressure. This drop in pressure is what causes the ambient air to be entrained through a port. The size of the port determines the amount of air to be en trained and thus the percentage of oxygen delivered. The Venturi mask has a rotating air entrainment port that allows the health-care provider to "dial in" the desired FI02 (Figure 4 1-3).

Mechanical aerosol systems also operate via air en trai nment, but the mask is connected to the aerosol unit by large-bore tubing to allow a specific FI02 to be

FIGURE 41-3

delivered with high humidity (Figure 41 -4). Although

Venturi mask.

drainage bags are usually attached to the tubing to col lect condensation, the tubing must be monitored for possible pooling of water causing flow obstruction to the patient. If pattial obstruction occurs, a mild back pressure results in the tubing, causing less air entrain ment. This means that a higher concentration of oxy gen will result and possibly deliver a higher dosage of oxygen to the patient than desired.

FIGURE 41-4 A, Heated aerosol. B, Nebulizers.


41

HOME AND PORTABLE OXYGEN


753

Smaller tanks are used for portability and can provide

As health care continues to move out of the hospital set

up to 3 hours of use. They can be refilled by transfer

ting and into the home, more health-care practitioners

ring gas from the larger reservoir tank.

will be providing care to oxygen patients in their homes.

Liquid oxygen is a low-pressure oxygen delivery

Oxygen is most commonly delivered in the home for

method, and it tends to be more convenient than

those needing long-term oxygen, usually chronic ob

using the high-pressure tanks, especially for the ac

stl1lctive pulmonary disease (COP D) patients. Generally

tive oxygen patient. The canisters are lightweight and

I to 2 Llmin is prescribed via nasal cannula, but the

allow patients to be away from the home reservoir for

flow rate will depend on the patient's need.

up to 8 hours. The down side is that liquid oxygen

Home oxygen-delivery systems can be divided

costs more, and the reservoirs need to be filled up to

into three categories: high-pressure oxygen cylinders,

twice a week with continuous use. If high flows are

low-pressure liquid oxygen, and oxygen concentra

needed, these units are not recommended.

tors (Burton et aI., 1991).

Oxygen concentrators are commonly seen in the

High-pressure oxygen tanks come in various sizes.

home health setting, especially since Medicare offers

The larger ones such as the H and K sizes are used as

coverage for these devices (Figure 4 I -5). Generally,

a base unit or reservoir. Long oxygen tubing con

they tend to be expensive initially but are actually

nected to these tanks allows for patient mobility.

less expensive for long-term use. They are electri cally powered and create oxygen by drawing ambient air across a semipermeable membrane, separating oxygen from nitrogen. They generally operate at 2 Llmin and provide 90% oxygen. Long oxygen tubing, up to 50 ft, allows patients extra mobility. Patients using concentrators should have a back-up device, such as a pOJ1abie tank, in case of a power outage.

RESPIRATORY MODALITIES Intermittent Positive Pressure Breathing Intermittent positive pressure breathing (lPPB) is mentioned here not to educate the reader about its use but to inform the reader about its declining use. Al though this particular modality continues to be used in some hospital settings, there is little evidence to supports its efficacy. This particular technology was developed during World War II to assist pilots breathing in unpressur ized cabins at high altitudes. IPPB subsequently be came a very popular respiratory therapy device in the 1960s and I970s (Figure 41 -6). However, its use began to decline in the 1980s. In 1983 the National Heart, Lung, and Blood Institute reported that IPPB has limited therapeutic benefit. This clinical trial is only one of several studies that show IPPB is an out moded medical technology. In fact, research dating FIGURE 41-5

back to the 19 50s questions the efficacy of this de

Oxygen concentrator.

vice (Duffy and Farley, 1992).


754

PART VIII

Related Aspects of Cal'diopulmonary Physical Therapy

FIGURE 41-6

Left, Bird Mark and righI, Bennett AP-S IPPB machines.

FIGURE 41-7

Incentive spirometry device in use,


41

The purpose of the IPPB machine is to increase


755

rina. This humidification process is important to mu

alveolar ventilation, to improve the ventilation-pelfu

COlIS

sion ratio, to mobilize and facilitate expectoration of

ratory tract. When this normal humidification process

thick secretions, to decrease the work of breathing,

is interferred with, other methods of adding moisture

and to deliver aerosolized medications. It is a pres

to the respiratory system must be employed.

sure-cycled ventilator that, when triggered by a pa

production, ciliary activity, and a healthy respi

Humidification is the addition of water vapor in its

tient's inhalation, delivers ambient air or oxygen to

molecular form to a gas. When a dry gas is being ad

the patient until a preset pressure is rcached. It is ba

ministered to a patient (e.g., via a nasal cannula),

sically a lung expansion device that helps deliver an

some type of humidification appliance would be used

increased tidal volume. IPPB is used for a variety of

to prevent unneccssary complications. Flows of 2

pulmonary conditions, and treatment scssions usually last

Llmin or less may not require humidification when using a nasal cannula. Humidification therapy is also

10 to 15 minutes.

This modality comes into question in the clinical

indicated in the presence of thick tenacious secretions

setting because it has not shown to provide benefits

and when an artificial airway is in place. Artificial

over that of other simpler respiratory treatment meth

airways, such as endotracheal and tracheostomy

ods. It also introduces potential complications and

tubes, bypass the normal humidification system (the

hazards that the other treatments do not. Typically,

upper airway); therefore, supplementation is essential

IPPB has been used to treat asthma, COPO, and post

(Frownfelter,

operative atelectasis; however, other therapies, such

1987).

There are basically two types of humidifiers. Bub

as incentive spirometry (IS), postural drainage, and

ble-through humidifiers are those which are generally

aerosol therapy, tend to prevai I as the treatment of

used with simple oxygen appliances. The pass-over

choice over IPPB.

type of humidifier is usually found in conjuction with

Although IPPB is questionable regarding its clini

a mechanical ventilator. Both bubble-through and

cal efficacy, it may be a beneficial form of treatment

pass-over humidifiers are available for ventilators,

in acute asthma or COPO that is refractory to stan

and they are usually heated to warm the humidified

dard therapy, atelectasis that has not responded to

air to body temperature before entering the airway

simpler therapy, and the prevention of respiratory

(Kacmarek et ai., 1991).

failure in patients with kyphoscoliosis and neuromus cular disorders (Handelsman,

199 I).

Aerosol Therapy An aerosol is created when a suspension of liquid or

INCENTIVE SPIROMETRY

solid particles exists in a gas. Today, the two most

Incentive spirometry (IS), also called sustained maxi

common forms of medication aerosol delivery in the

mum inspiration (SMI), is simply a visual and/or

clinical setting are the small.

audio feedback device that encourages slow, deep in

and the metered dose inhaler (MOl). A bland aerosol

spiration (Figure

41-7). Generally, this treatment is

performed frequently, up to every hour, and its pur pose is to treat and prevent atelectasis, especially in postoperative thoracic and abdominal patients.

is administration of water or saline solution to the pa tient's lungs. In general the goals of aerosol therapy are to hy drate dried retained secretions, to improve cough effi ciency, to restore and maintain function of the mu cociliary elevator, to deliver medications, and to

HUMIDITY AND AEROSOL THERAPY

humidify gases delivered through artificial airways.

Humidity Therapy

The MOl is strictly used for medication delivery.

Under normal circumstances, when inhalation takes

Other forms of aerosol delivery are the spinning

100(;'(; saturated with water vapor

disk, such as in a room humidifier or mist tent, and

before entering the lower airway tracts below the ca

the ultrasonic nebulizer. Both of these are electri

place, air becomes


756

PART VIII


ble while taking slow, deep breaths with a short 3- to 4-second inspiratory hold. Mouth breathing is en couraged if aerosol therapy is delivered by mask. Nasal breathing may filter out particles of optimal size. Of course, not all patients will be able to achieve this position and ventilatory pattern, and the therapist must modify accordingly. In comparing SVN with MOl's ability to deliver medications, it is found that the MOl is either equal in efficacy or outperforms nebulizers. Significant cost savings are also realized by those institutions who recog nize M O l usage as an effec tive means of aerosol medication delivery over SVN (Orens, Kester, Fergus, and Stoller, 1991). To further enhance the efficacy of the MOl treat ment, a spacer or holding chamber may be attached to trap the aerosol particles before inhalation. This device allows greater drug particle deposition to the

FIGURE 41-8

airways and reduces oropharyngeal deposition (Ash

Commonly used spacer device.

worth, Wilson, Sims, Wotton, and Hardy, 1991). Ventilator patients that are receiving drug aerosol therapy also receive greater benefit from an in-line MOl with a holding chamber as compared with a jet nebulizer (Fuller, Oolvich, Posmituck, Pack, and

cally powered as opposed to the SVN, which is

Newhouse, 1990).

pneumatically powered (Figure 41-8) (Branson and Seger, 1988). A key element in aerosol delivery is particle size.

Aerosol-Therapy Precautions

The size of the aerosol particle will determine its abil

It should be mentioned that there are hazards associ

ity to penetrate into the airway before depositing or

ated with aerosol therapy. Bronchospasm may occur

raining out. The therapeutic range is considered I 11

as the smooth muscle of the bronchial passages

with the smaller range of paJticles having the greatest

react to foreign particles entering the lung. Short

penetrating ability. The larger particles deposit sooner.

ness of breath and respiratory distress may also

If they are greater than 5 11 then the chances of entry

o c c u r as a r e s u l t of d r i e d retained secretions

into the airway are less. The particles may deposit in

swelling and occluding portions of the lung. Cross

the nose and proximal airway. The greatest amount of

contamination is a concern in that aerosol devices

alveolar deposition (95% to 100%) occurs in the I to

may harbor organisms that can be transmitted to pa

2 11 range. On the other hand, aerosol particles smaller

tients. Frequent equipment changes and proper ster

than I 11 are so stable that they may not deposit at all

ilization and cleaning techniques are key in prevent

(Kacmarek et aI., 1991).

ing this occurrence.

Although particle size is important in determining appropriate deposition, a patient's ventilatory pattern is probably more important in that it is the more vari

MECHANICAL VENTILATION

able and controllable of the two. Gravity also plays a

The subject of mechanical ventilation is vast and

factor, and it too can be used to benefit particle depo

highly technical. The purpose of this section is to give

sition. Patients should be sitting up as much as possi

the reader a concise overview of mechanical venti la


41


757

FIGURE 41-9 A, Puritan Bennett 7200a microprocessor driven ventilator. B, Bennett MA-I ventilator-bellows system driven by an electric compressor.

tion and provide a foundation from which to make ap

tive pressure breaths to a patient. Positive pressure

propriate decisions when working in this environment.

ventilation is opposite of normal physiological venti

Many disease states that lead to cardiac and/or res

lation in that normal ventilation occurs when negative

piratory failure will require mechanical ventilation to

pressure, created by contraction of the diaphragm,

support the patient's effort to ventilate and oxygenate

causes air to enter the lungs. Whereas normal inspira

41-9). Today, patients receiving mechanical

tion occurs by "pulling" air into the lungs, ventilators

(Figure

ventilator support can be found in both the hospital

"push" air into the lungs. This is important in that the

and the home. Acute exacerbations of disorders such

thoracic cavity becomes an area of higher pressure,

as emphysema, COPD, and chronic hronchitis com

which may create adverse cardiovascular and hemo

monly require mechanical ventilation and are gener

dynamic events.

ally seen in hospital rcus. Disorders requiring long term ventilation, such as spinal cord injury, brain injury, and certain neuromusculoskeletal diseases,

Modes of Mechanical Ventilation

may be found receiving mechanical ventilation in the

The physician and respiratory therapist have a nev

home or long-term care facility.

erending sea of choices in which to choose the most

Today, mechanical ventilator assistance is pro

appropriate method of ventilation. This area some

vided primarily by machines that deliver preset posi

times presents confusing terminology and a lack of


758

PART VIII


consistency. In fact, choosing the appropriate mode

breaths with the patient's spontaneous breaths. In

of ventilation may be considered more of an art than

IMV the machine may cycle a breath before the

a science. Before describing the modes of ventilation,

patient can completely exhale a spontaneous

the following terms should be defined:

breath. If no inspiratory effort is present, the ma

1. Trigger-Variable that causes a breath to be delivered by the ventilator. A patient may inhale

chine delivers the mandatory breaths. •

causing the ventilator circuit pressure to drop to

Continuous positive airway pressure (CPAP). The patient spontaneously breathes and a preset

a preset number (i.e., less than 1 or 2 em H20).

level of pressure is constantly maintained. This

This is called a pressure trigger. Some ventila

method of ventilation can also be achieved

tors are volume and flow triggered.

through use of commercially available pneumati

2. Flowrate-The speed at which the ventilator

cally powered units that hook directly into the

breath is deli vered. This parameter is usually

oxygen wall outlet. A tight fitting mask is secured

measured in liters per minute.

around the patient's mouth and nose, and a preset

3. Frequency-R e fers to the number of breaths delivered over time (e.g., 10 breaths per minute).

pressure and oxygen percentage is delivered. •

4. Spontaneous breath-Breathing through the

Airway pressure release ventilation (APRV). The patient is allowed to spontaneously breathe

ventilator circuit without assistance.

with a set amount of CP AP. If additional ventila

The following is a descri ption of common current

tion is required, the CPAP will be dropped period

ventilator modes:

ically, releasing the pressure, causing the patient

•

Controlled mechanical ventilation (CMV). The

to exhale. When the exhalation is complete, CPAP

control mode is a lesser used method of ventilation

is restored. Proponents of this mode claim that by

and generally requires the patient be sedated and

allowing the patient control, patient comfort and

paralyzed. The ventilator delivers all breaths at a

compliance are high.

p r e s e t f re q uency, volume or p r e s sure, a n d

•

•

•

Pressure support ventilation (PSV). In using pressure support the patient is allowed to breathe

breaths or trigger the machine.

spontaneously and receives a preset amount of

Assist control (AC). The patient receives a preset

inspiratory support until the fIowrate reaches a

pressure or volume, f requency or number of

minimal level. The patient controls the fre

breaths, and fIowrate. In between machine-cycled

quency, tidal volume, inspiratory time. This

breaths, the patient can trigger the machine to de

mode is often used in conjuntion with SIMV.

li ver another breath at the preset parameters. All

This mode is also popular due to high patient

breaths are machine delivered. No spontaneous

compliance.

breathing can occur. •

•

flowrate. T h e patient cannot take spontaneous

•

Mandatory minute ventilation (MMV). The pa

Assisted mechanical ventilation. This mode is

tient is allowed to breathe spontaneously; how

similar to AC, however, there is no set frequency.

ever, a minimal level of minute ventilation will be

The patient triggers the machine at will to deli ver

achieved through ventilator-assisted breaths. This

a set pressure or volume at a set fIowrate.

is usually accomplished by using PSV.

Intermittent mandatory ventilation (lMV). As

•

Volume-assured pressure support (V APS).

the ventilator delivers a set mandatory frequency

This is one of the newest modes of ventilation. It

and volume or pressure, the patient is allowed to

allows the patient to breathe spontaneously in the

take spontaneous breaths between cycles. This is a

PSV mode and monitors each breath's tidal vol

former popular mode.

ume. If the breath is not going to reach the set

Synchronized intermittent mandatory ventila

volume, the ventilator will hold the fIowrate con

tion (SIMV). This mode improves on that of IMV

stant and increase the pressure until the desired

in that it synchronizes the machine delivered

volume is reached (Branson and Chatburn, 1992).


41

Alarm Management and Precautions


759

or excessive water buildup (Figure 41-10). Low

When working around ventilators, it is inevitable that

pressure may signify a leak in the ventilator circuitry

alarms will sound. Alarms are important indicators of a

or a bad patient connection.

patient's condition or machine malfunction. All alarms

If you are unfamiliar with a particular ventilator

should be recognized and valued as excellent sources

and an alarm sounds that you are unable to identify

of information. If alarms are silenced or ignored with

and/or remedy, first ensure the patient is not in any

out interpretation, patient fatalities may result.

extra distress. Assess the overall appearance and,

The most common alarms are those which moni

most of all, rise and fall of the chest as the ventilator

tor high and low pressurc. FI02, apnea, disconnec

cycles. If the patient does not appear to be receiving

tion, and volume. Generally, if the high-pressure

breaths, immediate action should be taken to remove

alarm continucs to sound, the patient should be

the ventilator from the patient and to begin manual

checked for secretion buildup. Suctioning can rem

ventilation with a self-inflating bag. The respiratory

edy this problem. The ventilator tubing should also

care practioner should be called to rectify the situa

be checked for possibJe occlusion from compression

tion. When the problem is resolved, the patient should be returned to the mechanical ventilator. One primary precaution to keep in mind when working with a ventilator patient is to watch for con densation in the tubing that could accidentally be poured directly into the patients lungs. When moving a ventilator patient, plan ahead by securing aJl lines, wires, and tubing. Follow the appropriate procedure for emptying any water from the ventilator tubing be fore moving the patient. Aspiration of water from ventilator tubing can be fatal.

SUMMARY Physical therapists need to understand the basic equipment and principles of respiratory care in order to optimize functional outcomes of their patients.

REVIEW QUESTIONS I. If precise control of oxygen percentage to a pa tient is wananted, what type of delivery system is indicated? 2. Does mouth breathing by a patient on a nasal cannula indicate that he is receiving no oxygen? 3. Why do low-flow oxygen masks require a certain minimum liter flow, that is,S to 6 Llmin for a simple mask?

4. Why is IPPB come into question as an effective FIGURE 41-10 Condensation build-up in ventilator tubing-a potential hazard.

modality? 5. What are two concerns regarding condensation collecting in mechanical ventilator tubing?


760


PART VIII

References Fuller, H.D., Dolovich, M.B., Posmituck, G., Pack, W.W., Ashworth, HL, Wilson, CG., Sims, E.E., Wotton, P.K.,

& Hlirdy,

& New

house, M.T. (1990). Pressuril.ed aerosol versus jet aerosol de

lG. (1991). Delivery of propellant soluble drug from a metered

livery to mechanically ventilated patients. Comparison of dose

dose inhaler. Thorax, 46(4),245-247.

to the lungs. American

Barharash, R.A., Smith, L.A., GOdwin, J .E.,

& Sahn, SA (1990).

Mechanical ventilation. DICP, The Annals of Pharmacother apy.

24, 959-970.

of Respiratory Disease. 141(2),

>f' Handelsman, H. (1991). Intermittent positive pressure breathing (IPPB) therapy. Health Technology Assessment Reports.

Bazuaye, E.A . , Stone, T.N , Corris, P.A.,

& Gibson, GJ. (1992)

Variability of inspired oxygen concentration with nasal cannu

4 7(8 ) , 609-611. ranson, R.D., & Seger, S.M. (1988). Bronchial hygiene tech niques. In R.M. Kacmarek, & 1.K. Stoller. C urren l respiralory las. Thorax,

care (pp. 24-28). Philadelphia: B.e. Decker.

Branson, R.D.,

Rel'iew

440-444.

1. 1-9.

-J Hodgkin, J.E., Connors, G.L., & Bell, e.w. (1993). Pulmonary re habilitation guidlines to success (2nd ed.). Philadelphia: JB

Lippincotl. Jackson, M., King, M.A., Wells, F.e.,

& Shneerson, J.M. (1992).

Clnical experience and physiologic resulls with an implantable intratracheal oxygen catheter. Chest, 102(5), 1413-8.

& Chatburn, R.L. (1992). Technical description and

Jensen, A.G., Johnson, A.,

& Sandstedt, S. (1991). Rebreathing

classification of modes of ventilator operation. Respiralory

during oxygen treatment with face mask. The effect of oxygen

Care, 37(9),1026-1044.

flow rates on ventilation. Acta Anaesthesiologica Scandinal'

-*' Burns, S.M. (1990). Advances in ventilatory therapy: high-fre quency, pressure support, and nocturnal nasal positive pressure ventilation. Focus on Critical Care. 17(3),227-237.

f Burton, G.G., Hodgkin, J . E., & Ward, J.J. (1991). Respiratory care a

guide to

clinical

practice (3rd ed.) (pp. 524-525). Philadel

phia: J.B. Lippincott. Duffy S.Q.,

& Farley, D.E. (1992). The protracted demise of med

ica, 35(4),289-292. Kacmarek, R.M., Mack, e.W.,

& Dimas, S. (1990).

The essentials

o{respiratory care (3rd ed.). SI. Louis: Mosby.

Kent, e., et a!. (1987). A program for transtracheal oxygen deliv ery: Assessment of safety and efficacy. Annals of Internal

Medicine, 107,802-808. Orens, K.D., Kester, L., Fergus L.e., & Stoller, J.K. (1991). Cost

ical technology: the case of intermittent positive pressure

impact of metered dose inhalers vs small volume m:huli/.crs in

breathing. Medical Care, 30(8),718-734.

hospitalized patients: the cleveland clinic experience. Resp ira

..( Dunlevy, e.L., & Tyl, S.E. (1992). The effect of oral versus nasal breathing on oxygen concentrations received from nasal cannu las. Respiratory Care, 37(4),357-60.

tory Care, 36( I 0), 1099-1104.

Pilbeam, S.P. (1992). Mechanical ventilatioll physiological alld clinical applirllliol1s. St. Louis: Mosby.

Frownfelter, D.L. (1987). Chest physical therapy and pulmanary rehabilitation an interdisciplinary approach (2nd ed.). St

",*, .zadai, e.e. (1992). Pulmonary manogclllcnt in phvsical therapy. New York: Churchill Livingstone.

Louis: Mosby.


Care of the Patient With an Artificial Airway Lisa Sigg Mendelson

KEY TERMS

Airway clearance

Tracheostomy

Artificial airway

Tracheostomy tube/cuff

Suctioning

HISTORICAL PERSPECTIVE

purposes:

An artificial airway is a tube inserted in the trachea

(I) to bypass upper airway obstruction,

(2) to assist or control respirations over prolonged pe

(3) to facilitate the care of chronic respiratory (4) to prevent aspiration of oral

either through the mouth or nose or by a surgical in

riods,

cision. Artificial airways have been known to med

tract infections, and

ical science for

3000 years. George Washington ulti

and gastric secretions. Multiple disease processes and

mately died of upper airway obstruction because his

traumatic problems can require an artificial airway,

p h ysicians could not agree on t h e use of tra

but each situation, simple or complex, can fit into one

cheostomy. It was not until

1909, when Chevalier

or several of these categories (see box on p. 762).

Jackson published his classical paper on tracheotomy, that this procedure gained some acceptance. The pro

cedure did not become a highly specialized technique in patient care until the invention of modern tra

INDICATIONS OF NEED-OBSERVATION The respiratory care team can play a vital role in rec

cheostomy tubes and the development of intermittent

ognizing patient need for a tracheostomy from physi

positive-pressure ventilators. In today's clinical prac

ological changes that indicate respiratory distress.

tice, artificial airways have the following four basic

Cardinal signs of dangerous airway obstruction are 761


762

PART VIII


Disease Processes that CouLd Require all ArtificiaL Airway because of Respiratory Illsufficiency I. Primary lung disease (e.g.. emphysema. chronic bronchitis, pulmonary fibrosis. cystic fibrosis,

severe

pneumonia,

burned lung, and toxic inhalation).

2. Systemic disease with secondary lung involvement (e.g.. cardiac failure, renal failure (fluid overload), and Illulti organ system failure).

3. Neuromuscular disease (e.g., polio, Guillain-Barre syndrome, my asthenia gravis usc of muscle relaxants. and ,

tetanus).

4. Central nervous system depression (e.g.. drugs, postanesthesia, metabolical coma. cerebrovascular accident, meningitis. and central nervous system tumors).

5. Trauma (e.g.. head/necklchest surgery or injuries). 6. Diseases complicated by extremes of age (e.g., premature infant or elderly). 7. Mechanical obstmction (e.g., upper airway infection. laryngeal paralysis, tumor. edema. bleeding. foreign body, and thyroid malignancy).

8. Recurrent aspiration (e.g .. glottic incompetence, occlusive diseases of the esophagus, and swallowing disorders of various causes).

From Selecky PA: Tracheostomy-a review of present day i ndicat ions complications and ,

care,

!-Iellrt Lung 3: 272-283, 1974.

stridor and chest wall retractions. Early clinical signs

long-term intubation. The nasal tube is more efficient

may include restlessness, agitation, tachycardia, con

in that it is better secured, the patient may eat, it is

fusion, motor dysfunction, and decreased oxygen sat

easier to suction, and it is generally more comfortable

uration on pulse oximetry. These signs may be ac

for the patient.

c o m p a n i e d by h e a d a ch e , f l a p p i n g t r e m o r, a n d

There are certain complications with nasotracheal

diaphoresis. Cyanosis from impaired oxygenation of

tubes. Among these are sinus blockage and pain,

the blood is a late, ominous sign.

vocal cord damage, or pressure necrosis to the carti

In children, restlessness must be due to lack of

laginous structure of the nose. To reduce these com

oxygen unless another factor (e.g., thirst) is clearly

plications, the airway should be evaluated daily. The

evident. Extreme fatigue and an inability to sleep in

tube should be removed as quickly as possible when

dicate impending danger. Apprehension, restlessness,

the indication for intubation is reversed. However, if

and mental confusion at any age may be taken as

there appears to be a need for a more long-term air way, a tracheostomy should be considered. The pro

early signs of hypoxia.

cedure should not be taken lightly because many ad ditional complications may occur.

Complications of Tracheostomy

Complications of tracheostomy can be surgical,

The selection of the appropriate airway is made by

postoperative, or physiological. Complications that

the following factors:

(I) What is the best means of (2) Is it an emergency or a controlled, determined situation? (3) Will the airway

occur at the time of the operation are more frequently

accomplishing the goal?

direct results of the surgical procedure itself. Delayed

be needed for long-term care? In general, oral endo

surgery, from postoperative care, or from the abrupt

tracheal tubes are inserted in emergencies. They are

physiological changes resulting from tracheostomy.

complications may result directly or indirectly from

the quickest and easiest tubes to insert even for rela

Nursing objectives in caring for the patient after a tra

tively untrained personnel. A nasotracheal tube will

cheostomy are to maintain patency of the tube, clean

generally replace the oral endotracheal tube for a

liness of the wound site, and good aeration and to ob


42

serve any changes in the patient's vital signs and oxy

Care or the Patient With an Artificial Airway

763

A patient with an artificial airway is understand

ably apprehensive and has special communication

genation by pulse oximetry. In patients with artificial airways the normal phys

needs. He or she should also be reminded that the in

iological mechanism for adding moisture to the air

ability to phonate is only temporary. The patient must

via the nasal mucosa obviously is bypassed. There

be reassured that he or she will be attended to con

fore supplemental humidification is extremely impor

stantly and will be able to trust and depend fully on

tant to protect the mucosa from drying and crusting,

the nursing staff to attend to his or her needs. If alert,

which results in obstruction.

the patient must be equipped with a signal light or

The dressing under the tracheostomy tube and tra cheostomy ties should be changed when they become

bell, paper and pencil, magic slate, or picture board for communication.

soiled because dried blood and other secretions near

Airway obstruction is the foremost complication that

the incision can encourage bacterial growth. The inci

exists for the postoperative tracheostomy patient. Tra

sion should be checked frequently for bleeding. The

cheal secretions are the major source of obstruction,

skin may be cleaned with half-strength hydrogen per

particularly if they are excessive or viscous. When

oxide and sterile saline when a new dressing is ap

using cuffed tube, acute obstruction might occur from

plied. The dressing should be folded into place

overinflating the cuff, which would allow it to balloon

never cut. This eliminates the possibility of lint or

over the end of the tube. Other causes of obstruction are

frayed threads being aspirated. Commercially pre

dislodgement of the tube into a false tract anterior to the

pared dressings best meet these criteria.

tube tracheal opening, occlusion by an overinflated

When changing the tapes that hold the tube in

cuff, and kinking of softened plastic cannula.

place, it is best to have one nurse hold the tube in

Tracheobronchitis, inflammation of the trachea and

place while another replaces the old tapes. An angle

bronchus, is a complication resulting primarily from ir

is cut at the end of the tape to facilitate its placement

ritation resulting from incorrect suctioning technique.

through the flange of one side of the tube. The tape is

Crusting is a common and complex problem that

then threaded through the back of the tracheostomy

may result from inadequate humidification of inspired

tube and through the other flanged opening and tied

air or may result from dehydration. In many instances,

securely with a square knot placed on one side of the

ulceration of the tracheal mucosa results from irrita

patient's neck. One finger should be placed under the

tion by the airway or incorrect suctioning. This ulcer

twill tape while tying to prevent the tape from being

ated area becomes infected with various organisms

tied too tight.

and is virtually covered by crust. Further suctioning

Pneumothorax can occur immediately after tra

removes the crust, causing discharge of serum and

cheostomy because of laceration of the mediastinal

bleeding. The discharge produces a wet eschar that is

24 hours (arises

covered with mucus. Because of the drying effect of

often in children and patients with chronic obstructive

air passing over this mass, a hard crust can form. This

pleura at the time of surgery or within

lung disease). Other problems include air embolism,

process can compound the difficulty because the de

aspiration, and subcutaneous and mediastinal emphy

velopment of this crust in the trachea might eventually

sema. Recurrent laryngeal nerve damage or posterior

produce a mass large enough to completely plug the

tracheal penetration may occur but is uncommon.

tracheal cannula and almost completely obstruct the trachea. Cases have been cited where an entire cast of the tracheobronchial tree has been removed.

Postoperative Physiological Complications

Other physiological complications may be related

(1) hypoxia developing before or

Attentive nursing care is the single most essential

to the following:

factor in postoperative management. A ratio of one

during the procedure and resulting in an uncontrol

nurse for each patient is the ideal; however, since this

lable patient, cardiac arrest, and increased myocardial

is not often possible, increased vigilance by the entire

sensitivity to adrenalin;

respiratory care team is of vital importance.

rapid carbon dioxide wash-out after establishment of


(2) alkalosis developing from

764

PART VIII


the airway, resulting in myocardial fibrillation and

tube can be replaced by the nurse on written order of

apnea; (3) cardiac fa i lure resulting in profuse bron

the physician.

,

chorrhea caused by pulmonary edema and shock. Other chronjc complications cited by Dailey, Simon, Young, and Stewalt (1992) include the following:

(1) in

fection at the surgical site, (2) aspiration, (3) aerophagia, (4) persistent stoma, and (5) tracheal stenosis.

TRACHEOSTOMY TUBES Metal Tubes Tracheostomy tubes are of two basic types-metal and polyvinyl chloride (hard and soft). Metal tubes

Postoperative Mechanical Complications

can be made of either stainless steel or sterling silver

Dislocation of the tube may result from unsatisfactory

and composed of the following three parts: (I) an

nursing care, poor attention to the airway during posi

outer cannula that fits into the tracheal incision,

tioning, or ventilator tubing pulling on the airway. If

(2) an inner cannula that fits into the outer cannula,

the tracheostomy tube tapes are not kept tight and tied

and (3) an obturator. Before the outer cannula is in

with a square knot or if they become loose as a result

serted into the tracheal incision, the obturator is

of cervical emphysema or edema, the tube may be

placed inside. The lower end of the obturator pro

coughed out of the trachea and become lodged in the

trudes from the end of the outer cannula and facili

tissues of the neck and obstruct the airway.

tates its insertion into the trachea. This is the only

Stay sutures are useful in tracheostomy patients

purpose of the obturator. The protruding end of the

when there is the possibility of tube displacement.

obturator obstructs the lumen of the outer cannula.

These sutures are valuable during recannulization of

When the obturator is removed, immediately replace

the tube if it comes dislodged before a tract has been

it with the inner cannula. When dealing with metal

well established. Stay sutures will prevent entry into

tubes, the parts of each set are not interchangeable

a false tract. Advantages of this technique include the

and fit only one particular set. If one part is lost or

following:

(I) blockage or displaced tubes can be

damaged, the entire set is useless. Therefore each

rapidly replaced, (2) exposure of the trachea at surgi

part, including obturator, is accounted for carefully.

cal intervention is improved, (3) firm anchoring of

Plastic tubes generally have interchangeable parts.

the trachea at the moment of incision, (4) decreased

Care should be exercised in handling sterling silver

trauma associated with extubation, and (5) uniform

tubes, since silver is easily dented.

tracheostomy technique for aJJ ages.

Mucus that has dried inside the inner cannula can

Dislodgement of the outer cannula or required re

not be cleaned by merely rinsing in water. The can

moval before a tract has been well established (usu

nula should be soaked in hydrogen peroxide and

ally 5 to 10 days) again requires diligence and quick

scrubbed with a tracheostomy brush and rinsed with

action by the nurse. No attempt at reinsertion should

saline to be sure aJJ secretions have been removed. If

be made without adequate light, satisfactory tissue re

a silver inner cannula becomes discolored, it may be

traction, tracheal hook, and a Trousseau's dilator. A

cleaned with silver polish.

Trousseau's dilator and tracheal hook should be read

The inner cannula should always be inspected to

ily available. A spare tracheostomy tube of the cor

be sure it is clean and clear of secretions before it is

rect size should be kept at the patient's bedside at all times. Then, should the tube be coughed out, the

reinserted. Be sure to lock the inner cannula in posi .

tion after reinsertion.

nurse uses the Trousseau's dilator to hold the wound apart while summoning the physician. Tragedies have occurred from inserting the tube into the soft tissues of the neck or mediastinum because of a dislodged

Polyvinyl Chloride (Plastic) Disposable Tubes and Cuff Inflation

cannula and the frantic efforts to replace it. Once the

The development of plastic tracheostomy tubes came

tracheostomy tract has been firmly established, the

about for the following three important reasons:


42

Care or the Patient With an Artificial Airway

765

(1) application of silicone to the inner sUliace of the

fore insertion of the tube into the trachea to be certain

plastic tube minimizes crusting and adherence of se

that there are no leaks. The Luer valve inflation port

cretions; (2) there is greater ease in attaching a safe,

to the pilot balloon is self-sealing. Some Luer valves

dependable, permanent inflatable cuff to the plastic

have a relief valve when pressure exceeds 25 mm Hg.

tube that cannot slip off and occlude the tracheal opening; and (3) lower costs allow the tube to be dis posable. Plastic tubes come with and without cuffs. The cuffed tracheostomy tube is primarily used in

Cuff Inflation There are two commonly used methods of cuff infla

conjunction with a positive-pressure ventilator to

tion. These are the minimal air leak, in which a small

form a closed system (Figure 42-1). It is also used to

amount of air escapes on inspiration, and minimal oc

reduce the possibility of aspiration because of absent,

clusive volume, in which just enough air is placed in

protective laryngeal, and pharyngeal reflexes. The in

the cuff to stop air from escaping on inspiration. Ac

flatable cuff is located around the lower portion of

cording to Crabtree Goodnough (1988), the minimal

the tube and, when inflated, seals the trachea from

leak cuff technique may produce less injury than the

most airtlow except through the tube itself (see Fig

minimal occlusive volume inflation technique. Re

ure 42-1). The cuff, usually made of pliable plastic, is

gardless of which technique is used, the pressure of

inflated by injecting air into the fine-bore tubing. A

the cuff should be checked every 4 to 8 hours and the

small pilot balloon is located proximally in the tubing

pressures documented. With continued research and

and indicates that the cuff is inflated. The nurse must

monitoring of tracheal cuff pressures, potential tra

check the inflation end of the cuff and the balloon be

cheal injury can be prevented.

FIGURE 42-1 A, Cuffed adult tracheostomy tubes, uncuffed pediatric tracheostomy tube (far left). B, Cuffed adult endotracheal tubes, uncuffed pediatric endotracheal tube (far left).


766

PART VIII


Once the cuff is inflated, the only route for air ex

ideall y every 8 hours but at least once every

24

hours.

change is through the patient's tracheostomy tube;

The Communitrache I is a tracheostomy tube that

therefore careful observation of the patient by the

permits the removal of secretions above the inflation

nurse is essential. If the patient is on mechanical ven

cuff without nasotracheal suctioning. The other plus

tilation, observation is essential if there is ventilator

factor to this tracheostomy tube is the patient's ability

failure because asphyxiation may occur. Alarms are

to communicate, especially while on a ventilator.

always in the "on" position when a patient is being

When the patient is weaned from the ventilator, a

mechanically ventilated. Some means of resuscita

fenestrated tube may be used. Fenestrated comes

jenesfre,

tion, such as a manual resuscitating bag with mask,

from the French word

must be available at the bedside to ventilate the pa

There is a window (fenestration) in the outer cannula.

meaning window.

is

tient in case the tracheostomy tube comes out or is

When the tube is used for speaking the cuff

dislodged.

the inner cannula removed, and an external plug is in

down,

Considerable emphasis has been given to the inci

serted to cap the tracheostomy tube to allow the pa

dence of tracheal ischemia and resulting stenosis

tient to speak. The cuff must be deflated when the

from the use of a cuffed tube. This ischemia results

cap is in place. If the cuff was inflated, the patient

from the pressure of the cuffed tube against the tra

would be unable to breathe air into the lungs. The pa

cheal wall, which heals with scar formation, resulting

tient exhibits immediate distress if this mistake is

in subsequent stenosis. This complication can be re

made. If a patient with fenestrated tube needs to be

duced or eliminated by minimal air leak or minimal

suctioned, the inner cannula must be placed so that

occlusive volume. For the minimal occlusive volume,

the suction catheter does not enter the fenestration

the cuff must be inflated to eliminate any air leak on

and cause injury to the tracheal wal.l mucosa.

inspiration. Cuff pressures should be monitored and documented every

4

to 8 hours to prevent tracheal in

jury. The recommended cuff pressure is I S to

2S

mm

Other Airway Devices

Hg. Inflate the cuff until there is no air leak between

The Olympic tracheostomy button is used as an in

the wall of the trachea and the cuff, and then release a

terim airway after tracheostomy tube removal (Figure

small amount of air to allow only a slight air leak be

42-2).

tween the walls of the trachea and the cuff. This re

patient from tracheostomy tube but still maintaining

duces the pressure of the cuff, still allows the ventila

the stoma should a tracheostomy be again needed.

This method is another example of weaning a

tor to function properly, and reduces the likelihood of

The patient that benefited most from the procedure

tracheal ischemia. Any difficullY in properly inflating

was the COPD patient. This was one method used to

the cuffed tracheostomy tube should be immediately

facilitate secretion removal after hospitalization when

reported to the physician.

it became necessary because of the disease proces?

If the tracheotomized patient is conscious, he or

The Olympic tracheostomy button allowed the tra

she may attempt to speak. If the cuff is properly in

cheostomy patient the opportunity to reestablish an

flated, he or she will be aphonic, since no air can pass

unobstructed airway and at the same time allowed the

over the vocal cords. If he or she needs to speak, the

patient to speak.

cuff can be deflated, and the patient may be given a

The Passy-Muir valve is used for patients with

sterile dressing to hold over the tube. This will allow

upper airway obstruclion, and with difficult decannu

him or her to speak and also simulate a cough by

lation (Figure

rapid exhalation to clear secretions.

valve, allowing inspiration only and forcing exhala

Inspired air must be continuously and adequately

42-3).

The Passy-Muir is a one-way

tion through the upper airway. By using the valve the

humidified by means of nebulizing equipment to pre

upper airway muscles gradually recover, allowing for

vent the formation of crusts. The equipment used for

transition to a fenestrated tube or a smaller size tra

this purpose can be a possible source of infection.

cheostomy tube and preparing the patient for eventual

Therefore the nebulizer and tubing should be changed

decannulation (Pierson and Kacmarek,


1992).

42

Basic length 27-40

Care of the Patient With an Artificial Airway

mm

-I

FIGURE 42-2 Dimensions and actual positiorung of an Olympic tracheostomy button. (From Pierson OJ and Kacmarek

RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh © David 1. Pierson.)

A

B

FIGURE 42-3 The Passy Muir Valve. This valve attaches to a standard lS-mm tracheostomy adapter. It allows inspriation A, via the valve, but exhilation 8, must occur via the upper airway. (From Pierson OJ and Kacmarek RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh

© David J. Pierson.)


767

768

PART VIII


Airway Care Normally, the mucociliary escalator and the cough reflex provide ajrway clearance. When these mecha nisms fail, suctioning of the airways is indicated. Suctioning does have potential hazards, but it should be a safe procedure with proper guidance and care.

\

I

Suclioning Proper explanation of the suctioning technique to the patient helps allay apprehension and enhance cooper ation. Medicate your postoperative patient before suctioning to decrease the pain of coughing. Always maintain a calm and reassuring manner. Maintain aseptic technique throughout the entire procedure. Use sterile gloves and a sterile disposable catheter for each suctioning. Position the patient properly unless contraindi cated. Nasotracheal and/or pharyngeal suctioning should be done with the patient in Fowler, 60 to 70 degrees, or semi-Fowler position, approximately 45 degrees, with the neck hyperextended (Figure 42-5).

FIGURE 42-4 The Montgomery T-tube. (Reprinted with permission from Montgomery WW: Manual care of the Montgovery silicone tracheal T-tube. The annals of olOlogy rhinology &

lQ/yngology (supplement 73) 89(4): 3,1980.)

The supine position is best for the patient with tra cheostomy or endotracheal tubes (Figure 42-6). Pharyngeal suctioning may be necessary before de flating the cuffed tracheostomy tube. The nurse should not suction the pharynx and then the trachea with the same catheter, but the trachea may be suctioned first and then the pharynx with the same catheter. Duration of suctioning is of extreme importance. Each suctioning procedure should last no longer than

The management of major airway obstruction

5 to 10 seconds to avoid hypoxia.

by tracheal tumor, external compression, or tra

Prolonged suctioning may result in precipitating a

cheal disease below the thoracic inlet still present

dysrhythmia or cardiac arrest. A good way to judge

difficult problems. The Montgomery T tube is a bi

the elapsed time is to hold one's

furcated silicone rubber stent designed to preserve

guided by the development of discomfort. This is

patency of the airways in a patient with injury to

most important for the patient who depends on venti

the trachea or main bronchi (Figure 42-4). When

latory assistance.

OWIl

breath and be

the T tube is in place, the patient breathes normally

The lowest possible vacuum settings are to be llsed

through nose and mouth and can speak. The T tube

(below 120 mm Hg) that will still support suctioning

is a method in which secretions can be removed if

the tracheostomy tube. The higher the setting is

necessary and is helpful in long-term therapy to al

raised, the greater the risk of trauma to the tracheal

l e v i a t e o b s t r u c t i o n or d u r i n g r e c o n s t r uctive

mucosa. Caution should be exercised to avoid kinking

surgery. This device does not cause any adverse

the suction tubing or catheter. When negative pressure

tissue reaction on a long-term basis, according to

is excessive and released suddenly, inadvertent re

Montgomery.

moval of portions of tracheal mucosa may occur.


42

. t With . an Artificial Airway Care 0 f the Pahen

Fowler 60-70 degrees

Seml-Fowler 10- 12" .

FIGURE 42-5 A, Fowler ' s an , dB, Semi-Fowler's positions.

FIGURE 42 6 Supine posillon,


769

770

PART VIII


(

)( FIGURE 42-7 The catheter will simulate coughing when it contacts the carina (in a patient with cough reflex).

FIGURE 42-8 The catheter is withdrawn I cm after it reaches the carina, before applying suction.


42


771

Insertion of the suction catheter should be done

Right main-stem bronchus aspiration is the usual

gently, using aseptic technique and sterile gloves.

case because of the more direct alignment of this

Goggles are used as part of universal precautions if

bronchus with the trachea. This can be carried out al

there is any danger of coughed-ollt secretions. The

most always with a straight tracheal catheter.

catheter should first be moistened in sterile saline or

Excessive suctioning can be harmful. Use judg

with a water-soluble gel. Suction is not applied while

ment to determine just how often a patient requires

the catheter is passed down into the trachea. Proper

suctioning. Auscultation by stethoscope should be

insertion of the catheter will stimulate coughing when

used to determine the thoroughness of suctioning.

it contacts the carina (Figure 42-7). It is then immedi

Suction only when it is needed (Carroll, 1994). Allow

ately withdrawn I cm before suction is applied (Fig

the patient to rest and breathe between each insertion

lire 42-8). Do not force the catheter lip and down

of the suction catheter and, if necessary, ventilate him

while suctioning. Suction is applied only while the

or her for few minutes before further suctioning. Re

catheter is being wi thdrawn. Rotating the catheter

member each suctioning attempt removes air as well

during withdrawal results in suctioning a larger area

as secretions. Hyperoxygenation and hyperinflation

and increases the surface contact of the trachea and

with 100% oxygen has been suggested with better re

tracheostomy tube (Figure 42-9).

sults and fewer complications. Complications from

Left main-stem bronchus aspiration is more diffi

tracheal suctioning include the following: (l) hypox

cult because of the anatomical arrangement of the

emia, (2) cardiac dysrhythmia, (3) bronchospasm,

bronchus. It was formerly thought that left bronchial

and (4) infection. Suctioning can lead to hypoxemia

aspiration was facilitated by turning the patient's

because oxygen is removed from the airways, and

head to the right. Studies by Kirimli et al. (1970) and

this could lead to tissue hypoxia. To minimize this

Panacek et £II. (1989) indicate that left bronchial aspi

problem, preoxygenation is recommended. This can

ration is best accomplished by using a Coude tip

be done by hyperinflating the patient with Ilf2 times

catheter. After its insertion into the trachea. the

their normal tidal volume on a ventilator and hy

curved tip should be positioned to point toward the

perox-genating with 100% oxygen for 3 to 5 breaths.

left main-stem bronchus. Even so, insertion is diffi

Cardiac dysrhythmias, such as premature ventricular

cult, and auscultation by stethoscope is necessary to

contractures, bradycardia, and tachycardia, can be di

thoroughly access the suctioning.

minished by hyperinflating and hyperoxygenating the

To suction unit

(

Connection Detall Air vent I Catheter

FIGURE 42-9 The catheter is rotated during withdrawal in order to suction a larger surface area.


772

PART VIII


patient with 100% oxygen. If any dysrhythmias occur

18. Discard used equipment and remove gloves.

on the monitor, the suctioning procedure should be

19. Wash your hands.

discontinued. Bronchospasm may be effectively pre vented by a few puffs of a bronchodilator, such as al buterol, to the tracheostomy tube before suctioning.

Nasopharyngeal Airways

Infection can be decreased by maintaining sterile

When frequent, aggressive nasopharyngeal suction

technique with sterile gloves and sterile catheters

ing is indicated in a semicomatose patient, a nasopha

when suctioning.

ryngeal airway (NPA) will lessen the trauma of fre quent passage of the catheter. The NPA is a soft latex material that provides easy access to the trachea for

Suctioning Artificial Airway Nasotracheal, Endotracheal, and Tracheostomy I. Check equipment, be sure you have all necessary equipment and maintain sterile field.

nasopharyngeal suctioning. The nasal and pharyngeal mucosa are protected and the procedure thus becomes more co mfortable to the patient. In addition, a fiberoptic bronchoscope may be passed through the

2. Check monitors.

airway if the procedure is indicated.

3. Wash your hands. 4. Inform patient of the procedure. 5. Hyperoxygenate with 100% oxygen for three to five breaths with manual resuscitation bag.

Endotracheal or Tracheostomy Suctioning The procedures are the same except sterile technique

6. Place patient's neck in extension.

is followed and no lubrication is usually necessary,

7. Put on sterile gloves.

although it may be used if there is difficulty passing

8. Lubricate catheter with sterile saline or water

the catheter.

soluble gel. 9. Place catheter (without suction) upward and backward in short increments. Continue until an obstruction (the carina) is reached.

Sterile Suctioning The technique for correct sterile suctioning of artifi

10. When the carina is stimulated, the patient will

cial airways is perhaps the most important and vital

generally cough un less his or her reflexes are

segment of care for the patient because it removes se

obtunded.

cretions that would otherwise obstruct the airway. If

11. The catheter should be pulled back slightly, from the carina, then suction applied with no more than 120 mm Hg pressure as catheter is with drawn in a rotating motion.

suctioning is not performed properly, it can cause physiological or psychological trauma to the patient. The equipment necessary for proper sterile suc tioning includes proper mechanical apparatus, con

12. The aspiration time should be within 10 to 15 sec

necting tubing, sterile gloves, sterile saline, suction

onds total. (A good guideline is for the therapist to

catheters, dressings, and goggles as indicated with

hold his or her breath during suctioning as the pa

universal precautions. While suctioning the patient, it

tient is also not breathing. This gives the therapist a

should be remembered that the patient's only air pas

better sensitivity for what the patient experiences.) 13. The patient should be allowed to rest for several seconds and again be preoxygenated.

sage is being partially occluded. Thus the suction catheter should never be larger than one half the di ameter of the tube opening; if it is larger, it may com

14. Check the patient's breath sounds and repeat the procedure if necessary to remove more secretions. 15. Suction pharynx.

pletely occlude the patient's air passage. One method of determining the size of the catheter used for suctioning is to double the size of the tra

16. The monitor is to be watched for any dysrhytlunias.

cheostomy tube in place and add two. For example, if

17. Pulse oximetry is to be used for indications of

the patient has a #6 tube, the calculation would be as

desaturation.

follows: 6 + 6


=

12 + 2

=

14. Therefore a 14-fr catheter

42


773

the trachea or large bronchi is usually indicated by

TABLE 42-1

coarse rattling sounds. Fine bubbling sounds usually

The Pediatric Trach Card TRACHEOSTOMY SIZE

suggest fluid located more peripherally (i.e., in the alveolar spaces). If accumulated secretions are not

RECOMMENDED CATHETER SIZE

cleared, they can cause respiratory and cardiac rates to increase; effective oxygen and carbon dioxide

Pediatric Tubes

transfer is impaired causing cyanosis to appear and

6.S FR 6.S FR

8FR

8FR

10 FR

IOFR

OOPT OPT I PT 2 PT 3 PT 4 PT

low-grade fever to develop.

Extubalion/Decannulalion Extubation or decannulation is the removal of the ar

Neonatal Tubes

tificial airway. The patient is helped to gradually re

00 NT ONT I NT

learn normal breathing through his or her upper respi

6.S FR 6.S FR 6.S FR

ratory tract before the tube is removed. This can be a time of considerable fear and anxiety for patients be cause they have learned they can breathe safely

SCT-Single Cannula Tracheostomy Tubes

S seT 6 seT 7 seT 8 seT

through their tracheostomy, and they may become

10 FR 12 FR 14 FR 14 FR

apprehensive when asked to breathe in a normal man ner. The relearning process can be accomplished under the physician's direction by reducing the lumen of the tube for a day or two or by partially obstructing

Reprinted with permission of Janetti Publications, Inc., publisher

Pediatric Nursing,

Volume

20,

Number

2,

(March-April,

1994).

the tube's outer opening for increasing lengths of time. Eventually, the patient is able to tolerate the complete occlusion of the tracheostomy opening. This is sometimes difficult and similar to breathing through a straw.

would be the largest catheter that could be used to suc

When occluding the tracheostomy opening with a

tion the #6 tracheostomy. See Table 42-1 for a correla

cuffed tube, the cuff must be deflated first. Failure to

tion of tracheostomy sizes to catheter sizes.

do this will result in total obstruction of the patient's

The catheter used for pharyngeal suctioning

airway as the tube opening is occluded.

should never be used for subsequent suctioning of the

Fenestrated tubes have also been excellent for

artificial airway, but using an artificial airway suction

weaning the patient from the tracheostomy tube. Ac

catheter for pharyngeal suction is acceptable. Aseptic

tually, they do not increase the airway resistance as in

technique is absolutely necessary to minimize the risk

the above method and are probably more effective.

of infection and, ideally, only disposable catheters

They also allow the patient to talk and attempt to cough to mobilize secretions. Other methods used in

should be used. Suctioning may be necessary every few minutes

decannulation include the Olympic tracheostomy but

when the patient initially returns from surgery be

ton and the Passy-Muir valve. The Olympic tra

cause there is an increase in secretions, which usually

cheostomy button allows the airway to remain patent

results from irritation of the endotracheal tube plus a

for suctioning and reinsertion of a tracheostomy tube

reflex mechanism initiated by the surgical trauma.

should it become necessary. The Passy-Muir valve

Usually by paying attention to the patient's color, res

allows for normal recovery of the upper airway mus

piratory rate, lung sounds, and oxygen saturation on

cle, making it possible to reduce the size of tra

pulse oximetry, the nurse or therapist can determine

cheostomy tube leading to eventually plugging and

the amount of secretions present. Excessive mucus in

decannulating. Careful observation and documenta


774

PART VIII


tion of the patient's ability to ventilate must be done when either of these devices are used in the decannu lating process.

Goodwell, EW. (1':)34). The story of

trach"ostolll)'.

Srilish .Iour

l1al of ('hildren '.\' iJi.l'l'{/se.l', 31(367-36')),167-176. Goodwell, E.W. (1934). The story of tracheostomy. Srilish Jour nal of Children's Diseases, 31(370-372),253-27 I.

Close supervision should continue after extuba

Jackson,

tion. After a tracheostomy tube is removed, the skin

Jackson,

C (1909). Tracheostomy. Laryngoscope, 18,285-290. C (1921). High tracheostomy and other errors. The chief

edges are usually taped together with butterfly strips

causes of chronic laryngeal atenosis. Surgery, CynecoIOfi.Y, Ob

for a few days until the wound heals. While healing,

slelrics, 32, 392-395

air will escape through the wound and reduce the ef fectiveness of the patient's cough. The patient should be instructed that the noise from the partially closed trachea is normal and small secretions should be re moved from this area. The patient should be taught to hold a sterile dressing firmly over the incision when coughing until the opening healed.

&

Jackson, D.,

Albamonte, S. (1994). Enhancing communication

with the Passy-Muir valve. Pedialric Nursing, 20,(2),149-153.

J .A. (1980).

Kirchner,

Tracheostomy and its problems. Surgical

Clinics ofNorih America, 60,(5), 1093-1104.

lE., &

Kirimli, B., King,

Pfaeffle, H.H. (1970). Evaluation of tra

cheobronchial suction technique. Journal of Thoracic and Car

59, 340-344. OJ., & Tyler, ML (1993).

diovascular Surge!)" Lull,

J.M,

Pierson,

Methods of Air

way Maintenance. In Inlellsive respiralOry care. Philadelphia: WB Saunders.

S., &

Mocaluso,

REVIEW QUESTIONS I. What physiological changes occur with surgical placement of tracheostomy tube? with a tracheostomy. List information that you would include in a teaching plan for the tracheostomized patient. 4.

How does the patient care team prepare the tra

silicone tracheal T-tube. Annals of OlOlof!)" Rhinology and Montanari,

1., &

Spearing,

C (1986).

Of measuring tracheal curf

pressure. Nursing, 86(7),46-49. Noll, M.L., Hix, CD"

&

Scott, G. (1990). Closed tracheal suction

systems: effectiveness and nursing implications. In ArlCN clin ical issues in crilical care nursing. Philadelphia: JB Lippincott. Panacek, E.A., Albertson, T.E., Rutherford, W.F., Fisher,

C.J., &

Foulke, G.E. (1989). Selections left endobronchial suctioning

cheostomized patient for self care? Compare emergency care, acute care, and long

5.

Montgomery, W.W. (1989). Manual of care or the Montgomery La!)'ngology (Supp. 73),89(4),3.

2. Discuss possible psycosocial concerns of patients 3.

Roman, M. (1994). Managing post-intubation in

juries. Medsurg Nursing, 3(3),192-202.

term care for a patient with upper airway ob struction and tracheostomy placement.

of the intubated patient. Chesl, 95,885-87.

C (1991).

Patton,

Reviews for Ihe Pierson,

OJ., &

The critical airway classic problems. CurrenI

p(1S! Aneslhesia Care NI/rses, 13(5),33-40.

Kacmarek, R.M. (1992). In Foundalions of respi

ralory care. New York: Churchill Livingstone. Roberts,

References

J.T. (1994).

In Clinical Management of the Airway,

Philadelphia: WB Saunders. Selecky, P. (1974). TraCheostomy-a review of present day indica

Carroll, P. (1994). Safe suctioning PRN. RN, May. 32-37. Class, P. (1992). Nursing considerations for airway management in the PAC U . Currenl Reviews for POSI Aneslhesia Care Nurses.

14(1),1-8.

tion, complications and care. Hearl Lung, 3. 272. Tr acheoslomy lUbe a d u l l homecare guide. (1993). Irvine: MaLlinckrodt Medical TPT. Traver,

Crabtree Goodnough, S.K. (1988). Reducing tracheal injury and aspiration. Dimension of Crilical Care Nursing, 7(6),324-331. Dailey, R.H., Simon. B., Young, G.P.,

&

Stewart, R.D. (1992).

l.A.,

Mitchell, IT.,

&

Flodquist-Priestly,

Gaithersberg, Md.: Aspen Publishers. Traver,

J.A.,

Mitchell,

IT, &

Flodquist-Priestly, G. (1991). Suc

Airway maneuvers. In The airway emergency management. St.

lioning. In RespiraIO!), care: a

Louis: Mosby.

Md.: Aspen Publishers.

Frost,

E.A. (1976). Tracing 85, 618-624.

the tracheostomy. Annals of OlOlaryn

Warnoch,

C, &

clinical approach.

Gaithersberg,

Porpora, K. (1994). A pediatric tmche card: trans

fonning research into practice. Pediatric Nursing, 20(2), 186-188.

gology,

Funllll, N.D, Dutcher, P.O.,

d. (1991). Artifi

cial airway care. In RespiralOry care: a clinical approach.

&

Roberts,

J.K. (1993).

The safety and

Weilitz, P.B.,

&

Dertenrneier,

P.A. (1994).

Back to basics test your

efficacy of bedside tracheostomy. OlOlaryngology-Head alld

knowledge of tracheostomy tubes. American Journal of Nurs

Neck Surgery, (109),707-711.

ing, 94(2),46-50.


Respiratory and Cardiovascular Drug Actions Arthur V. Prancan

KEY TERMS

Adrenergic drugs

Corticosteroids

Antihistamines

Functional reflex

Cardiovascular reflex

Metered dose inhalers

Carotid baroreceptors

Mucolytics and expectorants

Cholinergic blocking drugs

Sympathomimetic drugs

Cholinergic drugs

Xanthines

INTRODUCTION

Before a drug can be used effectively, the system

The respiratory and cardiovascular systems have

it is to modify must be understood. How the mecha

many built-in mechanisms for controlling their func

nism of the drug action relates to the biological sys

tions during health and disease. In healthy individu

tem must be clear before an effect can be predicted.

als, both systems act quickly and positively to main

This chapter describes much of the basic respira

tain proper functioning under the most complicated

tory and cardiovascular physiology that underlies the

conditions. Even during trauma or disease, these sys

action of the drugs presented. Hopefully, the relation

tems often overcome distress and regain normal func

ship between basic physiology and the drug mecha

tion. The physiology of respiration or circulation is

nism of action is also evident.

sometimes altered by a disease so that the homeosta

All pharmacological interventions for the respi

tic mechanisms are no longer effective. In such a

ratory and cardiovascular systems are not covered.

case, a drug with the appropriate action becomes nec

Certainly no attempt has been made to describe the

essary to restore normal physiological function.

pharmacology of other systems or disease states. 775


776

PART VIII


For further study, one of the books listed in the ref

tagonistic action of the two components of the auto

erence section at the end of the chapter is highly

nomic nervous systcm. Some organs, however, have only one innervation.

recommended.

Much of the arterial blood vessel network is con trolled only by sympathetic nerves. Also, gastric se

AUTONOMIC PHARMACOLOGY

cretion and gastric motility are primarily regulated by

This section introduces the basic aspects of drug action

one system-the parasympathetic.

related to both components of the autonomic nervous system-the sympathetic and parasympathetic nervous systems. For both systems, synthesis, storage, and re lease of the chemical neurotransmitter are described to

SYMPATHETIC NEUROTRANSMISSION Sympathetic nerves transport impulses from the vaso

emphasize the places in the metabolical scheme where

motor center in the medulla of the brain through the

drugs can intervene. The sites of action for the adrener

spinal cord and out to the smooth muscle, heart mus

gic (sympathetic) and cholinergic (parasympathetic)

cle, and secretory cells. These tissues have receptor

transmitters and blockers is also described.

sites that will accept the norepinephrine released

The autonomic nervous system controls all of the

from the nerve ending. Norepinephrine, also called

bodily functions over which you have no voluntary

noradrenalin. is synthesized in the nerve ending only

control, and perhaps which you might not control as

in the sympathetic neurons. It is stored in the terminal

well if you had the opportunity. The functions in

until an electric impulse reaches the terminal, then it

clude regulation of respiratory airway diameter, res

is released into the synapse.

piratory secretions, blood vessel diameter, heart rate,

The norepinephrine molecule attaches to a recep

intestinal motility, pupil size, and many others. It is

tor molecule on a cell sUlface in the immediate vicin

easy to see that it might take more than the talents of

ity of its release. This drug-receptor combination

a well-trained expert to keep an active person func

causes a biological change, such as stimulation of the

tioning day and night.

pacemaker cells in the heart to fire more frequently

The sympathetic nervous system is the half of the

(increased heart rate). The effect is terminated when

autonomic system that takes a dominant role in the

the norepinephrine is reabsorbed into the nerve termi

cardiovascular and respiratory systems when some

nal. About 90% of the released norepinephrine is

sort of bodily activity is necessary. This includes ac

taken back into the neuron. There, it is either restored

tions such as increasing ventilation capacity, elevat

into granules for future release or it is destroyed by

ing blood pressure, and shunting blood flow to the

the enzyme monoamine oxidase (MAO).

skeletal muscles. Classically, the sympathetic compo

There are two types of sympathetic receptors

nent of the autonomic nervous system has been called

alpha and beta. The alpha-receptor is found in the

the fight-or-t1ight system. The other half of the auto

arterioles, and the beta-receptor is found in the arte

nomic system is called the parasympathetic nervous

rioles, heart, and bronchioles. Stimulation of the

system. It is most important in maintaining the less

alpha-receptor in the arteriole causes vasoconstric

exciting functions of the body like digestion, saliva

tion that results in increased blood pressure. The

tion, and urination. In some organs the two systems

beta-receptor in the arterioles causes vasodilation

work against each other to provide very fast and very

and a lowered blood pressure. Some drugs stimu

fine control. For example, the size of the pupil re

late both receptors, and in those cases the effect

sponds quickly to a change in light intensity. The

will be determined by the degree of alpha or beta

parasympathetic system actively functions to de

activity of the drug. An example is norepinephrine.

crease the size of the opening while the sympathetic

It has 90% alpha activity and 10% beta activity, and

system relaxes, thereby causing a quick decrease in

it always causes vasoconstriction. Epinephrine is

pupil size. If the light is turned down, the opposite

50% alpha and 50% beta and may cause a rise or

occurs just as fast. This is a good example of the an

drop in blood pressure.


43

Stimulation of the beta-receptor in the heart results in increased heart rate (beats per minute) and in

Respiratory and Cardiovascular Drug Actions

777

Epinephrine (Adrenalin) Epinephrine (Adrenalin) is also a mixed activity drug

creascd stroke volume (number of milliliters of blood

(50% alpha, 50% beta). It is naturally produced in the

the left ventricle pumps out into the aorta every time

adrenal medulla and can be released during sympa

it contracts). Incidentally, the combination of these

thetic nervous system activation. When this occurs, it

two changes (heart rate [HR] x stroke volume [SV])

acts as a circulating hormone, stimulating both alpha

is another way of saying cardiac output (CO) (milli

and beta-receptors. This drug wi II increase heart rate

liter of blood pumped per minute):

and stroke volume and may slightly increase or de

beats/min(HR) x mllbeat(SV)

=

crease total peripheral resistance at the arterioles. In

mllmin(CO)

any case, cardiac output always goes up; blood pres

This expression, cardiac output, is a common one and it constitutes half of the blood pressure regulation equation: CO x TPR

=

BP, where CO is cardiac out

sure may go up or down slightly. In the bronchioles, epinephrine exerts a dramatic dilating effect that is mediated by the beta-receptor.

put, TPR is total peripheral resistance, and BP is

Epinephrine can be administered by inhalant aerosol

blood pressure. Total peripheral resistance is deter

to reverse a bronchoconstrictive episode. It is also

mined by vasoconstriction or vasodilation in the arte

administered intramuscularly and subcutaneously to

rioles. Vasoconstriction increases resistance so TPR

treat asthma, anaphylactic reactions to an allcrgic re

and BP goes up.

sponse, cardiac arrest, heart block, and as a mild

Stimulation of smooth muscle beta-receptors will relax these tissues wherever they are found. Respiratory airway smooth muscle will decrease tension when the beta-receptor is activated by beta-acting drugs like epi

vasoconstriction to keep local anesthetics at the in jection siteo

Isoproterenol (Isuprel)

nephrine or isoproterenol. The functional result will be

Isoproterenol (lsuprel) is a synthetic compound that

an increase in air flow because of a larger airway diam

has 100% beta activity. This means that it can in

eter. Likewisc, blood vessels respond to beta-acting

crease heart rate and stroke volume to produce a great

drugs by increasing in diameter, allowing a greater rate

rise in cardiac output, and it stimulates the beta-recep

of flow. In this case, TPR has decreased and blood

tor on the arterioles to effect a profound vasodilation.

pressure will drop.

The final result can be a high cardiac output with low blood pressure. This drug improves blood circulation in shock patients by increasing local blood flow (va

Adrenergic Drugs

sodilation) and elevating cardiac output. Isoproterenol is considered very useful for treating acute asthmatic

Norepinephrine (Levarterenol, Levophed) As

mentioned

previously,

conditions because of its bronchodilating action.

n o repinephrine

(Levarterenol, Levophed) is a mixed-activity drug

(90% alpha, 10% beta). It stimulates beta-receptors in the heart, which results in an increase of heart rate

Phenylephrine (Isophrin, Neo-Synephrine) and Metaraminol Both phenylephrine (lsophrin, Neo-Synephrine) and

and stroke volume (increased cardiac output). In the

metaraminol are powerful and prolonged stimulators

arterioles, norepinephrine causes vasoconstriction via

of alpha-receptors. The action is directly on the re

the alpha-receptor, resulting in increased total periph

ceptor site itself. The response to the administration

eral resistance. The total effect, of course, is an in

of either of these drugs is a rise in blood pressure be

crease in blood pressure. Norepinephrine has little ef

cause of vasoconstriction accompanied by a reflex

fect on the bronchioles. This drug is given only

bradycardia, which causes a decrease in cardiac out

intravenously, and it can be used clinically to raise

put. Reflex alterations of cardiovascular function are

blood pressure. The natural sympathetic compounds

explained later in this chapter. The primary useful

are known as catecholamines.

ness of these drugs is in various hypotensive states.


778

PART VIII


Phenyle phrine is used as a nasal decongestant and

asthma. The drugs are metaproterenol (Alupent,

mydriatic and for the relief of paroxysmal atrial

Metaprel), terbutaline (Brethine, Bricanyl), albuterol

tachycardia. Phenylephrine affords relief from the

(P r o v e n t il, Ven t o l i n ), i s o e t h ar ine ( B r on kosol,

tachycardia because it increases blood pressure and

Bronkometer), and salmeterol (Servant).

evokes the cardiovascular reflex that is marked by high vagal tone and bradycardia.

Alpha-Adrenergic Blocking Drugs

Ephedrine

Phentolamine (Regitine)

Ephedrine has both alpha and beta activity as direct

Phentolamine (Regitine) is a competitive alpha-receptor

effects and it also causes release of epinephrine and

blocker. Its action is reversible. This drug prevents the

norepinephrine. Its pharmacological actions are simi

hypertensive effect of norepinephrine, and it reverses

lar to epinephrine, with the main exception that dura

the blood pressure elevating effect of epinephrine (epi

tion of action of ephedrine is longer. Ephedrine in

nephrine reversal). Epinephrine reversal looks like an

creases cardiac o utput and vascular resistance,

isoproterenol effect with high cardiac output and low

resulting in increased blood pressure. Ephedrine also

blood pressure. Phentolamine may be used clinically as

causes bronchial muscle relaxation, which is less po

a vasodilator. It is also useful as a clinical diagnostic

tent than that of epinephrine but has a longer duration.

agent in evaluating hypertensive patients who may

This drug is useful in controlling milder cases of bron

have pheochromocytoma, which is a tumor that grows

choconstriction that require long-term drug therapy.

in the gastrointestinal chromaffin tissue. The tumor pro

Amphetamine (Dextroamphetamine, Dexedrine) Amphetamine (Dextroamphetamine, Dexedrine) drug has pharmacological properties related to the cate cholamines because it causes release of norepinephrine

duces epinepJu'ine and norepinephrine and may be re sponsible for one aspect of a clinical hypeltension.

Phenoxybenzamine (Dibenzyline) Phenoxybenzamine (Dibenzyline) is also an alpha

from the nerve terminal. Amphetamine has both alpha

adrenergic blocki ng agent. It has effects similar to

and beta-receptor activity, although indirectly, through

phentolamine in the cardiovascular system but it is

its release of norepinephrine. The usual cardiovascular

less reversible. This drug is gaining some usefulness

response is an increase in blood pressure often accom

in the treatment of shock syndromes characterized by

panied by a reflex bradycardia. Amphetamine also has

high vascular tone.

potent central nervous system (CNS) activity. It is a stimulant of the medullary respiratory center, and it can antagonize drug-related central nervous system de

Prazosin (Minipress), Doxazosin (Cardura), and Terazosin (Hytrin)

pression. Respiratory depression often accompanies

Prazosin (Minipress), doxazosin (Cardura), and tera

overdoses of CNS depressant drugs and this effect may

zosin (Hytrin) are selective for arterioles and venules

be overcome by amphetamine. This drug is usually

and are the most useful against hypertension of the

used for its central nervous system effects and not for

drugs in this class. Although they act by vasodilation,

peripheral cardiovascular or respiratory effects.

these drugs exert minimal reflex tachycardia because they do not potentiate the vasomotor center and the

BetarReceptors Stimulants

increased venous capacitance reduces venous return

There are several drugs that act primarily at the beta2

and cardiac output.

smooth muscle receptor site, causing selective actions in the bronchioles and arterioles but not in the heart. Thcse drugs will produce a bronchodilation without increasing cardiac output. This particular lack of car

Beta-Adrenergic Blocking Drugs

Propranolol (/nderal)

diovascular effect makes them safer than isopro

Propranolol (Inderal) is a beta-adrenergic blocker. This

terenol or epinephrine in treatment of bronchial

drug occupies the beta-receptor sites of the heart, the


43

blood vessels, and the bronchioles. It prevents the beta


779

crease in catecholamine response to sympathetic stim

adrenergic effect usually seen with drugs like epineph

ulation. Blood pressure in humans does not drop dra

rine, norepinephrine, and isoproterenol. In the arteri

matically with therapeutic doses of reserpine, but when

oles, when epinephrine is given after propranolol, the

reserpine is used in combination with diuretics or other

usual mixed alpha and beta effect is eliminated, leav

antihypertensive agents, a significant antihypertensive

ing only an alpha-adrenergic action. This causes pro

effect is obtained. Reserpine is used in this way to treat

found vasoconstriction, allowing greater increase in

essential hypertension. One serious side effect related

blood pressure than is normally seen with epinephrine

to reserpine use is the behavioral modification that can

alone. In the heart the beta-receptors are blocked and,

result in severe depression and suicide.

since there are no alpha-adrenergic receptors in this organ, all effects of catecholamine drugs on the heart

Guanethidine (Ismelin)

are effectively eliminated, allowing the vagal influence

Guanethidine (Ismelin) is an adrenergic neuron

on the heaJ1 to predominate. Propranolol decreases the

blocking agent that works by replacing norepineph

heart's requirement for oxygen because it blocks the

rine in the nerve terminal. Norepinephrine is usually

cardiac stimulant action of norepinephrine. In the res

taken up by the nerve terminal after its discharge and

piratory system the administration of propranolol re

i s r e u s e d to m a i n t ain g r a n u l e c o n c e n t r a t i o n s .

sults in bronchoconstriction. This effect is increased

Guanethidine takes the place o f norepinephrine i n the

dramatically in patients who are susceptible to asthma.

granules and prevents the reuptake of norepinephrine,

The main use for propranolol is in conditions related to

thereby causing its metabolism outside of the neuron

hypertension and tachycardia, where a decrease in car

and its eventual depletion. The result on the cardio

diac output is beneficial.

vascular system of this action is postural hypoten

Metoprolol (Lopressor) and Atenolol (Tenormin)

sion. The patient is unable to control blood pressure by sympathetic activity. This drug is used in treat

Metopolol (Lopressor) and atenolol (Tenormin) are

ment of severe hypertension, usually after diuretics

beta-adrenergic antagonists that have been designed

and reserpine are shown to be ineffective.

to be cardioselcctive. This offers an advantage in safety when a beta-blocker must be used in asthmatic patients, in whom this disease would be aggravated if

Methyldopa (Aldomet) and Clonidine (Catapress) Methyldopa (Aldomet) and c10nidine (Catapress) de

respiratory beta-receptors were blocked. The natural

crease the activity of the sympathetic nervous system

beta-adrenergic agonist, epinephrine, is bronchodilat

at its control center in the brain. The consequence is a

ing, and an important class of bronchodilating drugs

total decrease in sympathetic activity in the heart and

acts at bronchiolar beta-adrenergic receptors.

blood vessels leading to a reduction in blood pressure.

SympatholytiC Drugs

PARASYMPATHETIC NEUROTRANSMISSION

Reserpine

The center for parasympathetic control is the vagal

Reserpine is an alkaloid of Rauwolfia serpentina, also

nucleus in the medull a . T h e vagus nerves p a s s

known as the Indian snake root plant. There are many

through t h e spinal c o r d a n d out to t h e heart, the

commercial preparations of this compound, but it is

smooth m u s c l e , and e x o c r i n e g l a n d s ( s a l i v a r y

widely sold as the simple plant extract. This compound

glands and pancreas). In all of these tissues, acetyl

depletes norepinephrine from the nerve endings in the

choline is released from the nerve terminals and

various tissues of the body that produce and store nor

combines with receptor sites to cause an effect such

epinephrine, including the brain. The depletion takes

as bradycardia (slowing of the heart) or an increas

several days to accomplish, and it may take several

ing gastric motility. Acetylcholine is found in many

weeks to restore catecholamine levels to normal after

parts of the central and peri pheral nervous system.

therapy is discontinued. During this time, there is a de

Acetylcholine is the only transmitter used in the


780

PART VIII

Related Aspects or Cardiopulmonary Physical Therapy

parasympathetic system. It is used to transmit im

acid and choline. The acetic acid is washed away for

pulses from the nerve that comes out of the spinal

further metabolism, and the choline is reabsorbed into

cord to the nerve that finally reaches the cells in the

the nerve terminal for resynthesis to acetylcholine.

organ being affected. This connection is called a gan glion and exists in both sympathetic and parasympa thetic systems. Acetylcholine is also the neurotrans m i t t e r t h a t m a k e s t h e c o n n e c t i o n b e t w e e n the voluntary (somatic) nerves and the skeletal muscle. There are two types of receptors in these systems.

Cholinergic Drugs AcetylchOline Acetylcholine is the endogenous cholinergic trans mitter that accounts for nicotinic and muscarinic ac

Acetylcholine affects both, but some drugs affect only

tions within the autonomic nervous system. It is

one and not the other. The two types of receptors are

rapidly hydrolyzed by acetylcholinesterase and the

called nicotinic and muscarinic. They are named after

nonspecific cholinesterase and therefore has a short

the drugs that selectively stimulate them. Nicotine

duration of action if administered parenterally. This

stimulates only those receptors in the ganglia and at

makes acetylcholine (ACh) a poor drug. Nicotinic ef

(I) stimulation of parasym

the neuromuscular junction. The muscarinic receptor

fects of acetylcholine are

site is found everywhere a parasympathetic nerve ter

pathetic ganglia, causing occurrence of all muscarinic

(2) stimulation of sympathetic ganglia, caus

mjnal synapses at a tissue. The biological effects usu

effects,

ally attributed to the parasympathetic nervous system,

ing increase in vascular resistance and cardiac output

such as bradycardia, salivation, and bronchoconstric

to produce hypertension, and (3) stimulation of the

tion, for example, are produced when the muscarinic

neuromuscular junction (NMJ) at the skeletal muscle

receptors are stimulated. Of course, it is also possible

(muscle contraction and movement). Muscarinic ef

to stimulate muscarinic receptors indirectly with a

fects of acetylcholine are bradycardia, salivation, pin

nicotinic drug by activating the parasympathetic gan

point pupils, bronchial constriction, gastric and in

glia. In fact, in a sirilliar way, it is possible to stimulate

testinal hypermotility, increased gastric acid and

the entire sympathetic nervous system. The neuro

mucous secretion, and facilitated urination. Toxic ef

transmitter at the sympathetic ganglia is acetylcholine

fects of cholinergic stimulation include diarrhea, uri

and it affects nicotinic receptor sites there. One of the

nary incontinence, bradycardia, bronchoconstriction,

toxic effects of acetylcholine and drugs that act like it

excessive salivation, CNS excitement, and respiratory

is hypertension with tachycardia because of stimula

collapse. In all of these toxic effects, atropine, a com

tion of the sympathetic postganglionic fibers.

petitive muscarinic blocker, is the antidote of choice.

To better understand the action of acetylcholine and related drugs, let us consider the synthesis, re lease, and inactivation of this transmitter. Acetyl

Bethanecol (Urecholine) Bethanecol (Urecholine) is a synthetic choline ester

choline is synthesized inside the nerve terminal from

that is not destroyed as easily as acetylcholine by

acetyl-CoA and choline. The acetylcholine is then

cholinesterase enzymes. It is useful in treating patients

stored in granules and is released out into the synapse

with urinary retention and paralytic ileus, and it is ad

when an action potential reaches the terminal. The

ministered orally or subcutaneously. The side effects

acetylcholine molecule attaches to a receptor site,

and toxicities for this drug are exactly those for ACh.

muscarinic or nicotinic, or to the enzyme that breaks it

However, since the drug is not given intravenously,

apart. Combination with the receptor site results in bi

cardiac and respiratory effects are minimized.

ological action, and coupling with the enzyme ends in destruction. The enzyme, acetylcholinesterase, is

Carbachol (Carcholin)

found at all cholinergic synaptic sites. A nonspecific

Carbachol (Carcholin) is a mixed nicotinic and mus

variety of the enzyme is also prevalent in many other

carinic drug because it releases acetylcholine from the

tissues. It too will break down acetylcholine. The final

nerve ending, producing the expected cholinergic ef

action of either enzyme is the production of acetic

fects at all receptor sites. The drug is useful for treat


43


781

ment of glaucoma (applied topically), paralytic ileus,

cholinesterase, such as diisopropy lfluorophosphate

and urinary retention (orally and subcutaneously).

(DFP) or sarin, is ingested, inhaled, or absorbed across the skin, a great variety of toxic cholinergic ef

Pilocarpine

fects are seen. The first effects seen after exposure to

Pilocarpine is a cholinomimetic that is useful in oph

an anticholinesterase are often ocular and respiratory

thalmology as an antiglaucoma agent. Cholinergic

effects. In the eyes, marked miosis is produced

compounds decrease intraocular pressure by relieving

quickly. In the respiratory system, bronchoconstric

the obstruction to the canal of Schlemm, a drainage

tion and bronchial secretions combine to produce

circuit for the eye. Miosis (pinpoint pupils) is one

tightness in the chest and wheezing. Gastrointestinal

feature of cholinergic therapy and may be beneficial

symptoms include nausea, vomiting, cramps, and di

to glaucoma treatment because the muscular base of

an·hea. Other muscarinic effects are severe salivation,

the relaxed iris may contribute to the drainage block.

involuntary defecation and uri nation, swea ting,

Another use of pilocarpine is to promote salivary

lacrimation, bradycardia, and hypotension.

flow in patients with a ganglionic blockade.

Further effects are related to nicotinic functions of acetylcholine. These include skeletal muscle twitch ing, weakness, and paralysis. CNS effects include de

Anticholinesterases Before proceeding to sp

pression of the respiratory and cardiovascular control ific anticholinesterase drugs,

centers, leading to respiratory collapse. At the time of

it is important to understand the basic mechanism of

death, respiratory paralysis is evident and it is because

action for these compounds. Acetylcholinesterase is

of a combination of bronchoconstriction, bronchose

the enzyme responsible for destroying acetylcholine at

cretions, respiratory muscle paralysis from overstimu

the various nerve junctions where it is released. The

lation, and CNS and control depression. The treatment

class of drugs that intetfere with this function is called

of this toxicity is closely related to preserving respira

anticholinesterascs. These drugs attach to the enzyme

tory function. Administration of atropine, a mus

and thereby block the enzymatic hydrolysis of ACh,

carinic blocker, will effectively decrease bronchocon

causing ACh to accumulate outside of the nerve end

striction and secretion. Another drug, pralidoxime

ing. This results in a greater response than normal to

(Pr o t o p am), is u s e d to re a c t i v a t e the a c e t y l

any cholinergic nerve stimulation. Some of these anti

cholinesterase. I t i s most effective shortly after expo

cholinesterases are relatively short-acting compounds

sure to the toxic agent because it breaks down the an

and are therapeutically impot1ant, whereas others are

ticholinesterase so it can be removed from the enzyme

ext.remely long-lasting and potent compounds that are

site. Additional measures are related to physiological

important only as poisons. The long-acting compounds

suppOt1 of the patient. Maintenance of an airway, arti

have been used as insecticides and as nerve gases in

ficial respiration, and oxygen administration are im

chemical warfare. The therapeutically useful anti

portant therapeutic applications for these patients.

cholinesterases are beneficial in problems related to the eye, intestine, and the skeletal neuromuscular junc

Physostigmine (Eserine)

tion (NMJ). In these applications, these drugs increase

Physostigmine (Eserine) is useful in glaucoma and in

the amount of ACh available for activity, an effect that

selected therapeutic measures where a cholinergic ef

is es

ially impOt1ant in cascs where the synthesis or

release of acetylcholine is lower than normal, as in myasthenia gravis. There is also great medical interest in the toxicol ogy of the anticholinesterases, especially the ex

fect is beneficial. It functions as an indirect choli nomimetic by blocking the acetylcholinesterase.

Neostigmine (Prostigmine) Neostigmine (Prostigmine) is useful in patients with

tremely potent irreversible anticholinesterases. Toxic

nonobstructive paralytic ileus to increase tone and

ity because of these compounds is not uncommon

motility of the small and large intestines. It is also

and is often severe. When a toxic irreversible anti

useful for stimulating skeletal NMJ. Neostigmine is


782


PART VIII

used for treating

gravis because it indi

increases acetylcholine at the NMJ and it acts directly at the nicotinic receptor site itself. The dis

and does not counteract the nicotinic 2:aufllionic ef fects or the nicotinic effects at the NMJ. Because heart rate is controlled

resulting i n skeletal muscle weakness.

parasympathetic effect on the heart,

temporarily restores muscle Nrpncrth

the sym

system to increase heart rate and stroke vol ume to cause an increase in cardiac output. In

Edrophonium (Tensilson) This a very

both sympathetic

and parasympathetic tone, atropine will eliminate the

ease is marked by subnormal response t o

may occur after atropine administration. In

anticholinesterase. It is pri

marily useful as a diagnostic agent in

cases where

exists because of high vagal

tone, atropine can be used to reverse this depression.

to reveal, for a few minutes, if the dose of w o u ld risk a serious c holinergic

In the

tract,

is a bronchodila

tor. It is also possible to

is appropriate. A longer-acting if t h e

neostigmine dose was alreadv at the therapeutic limit.

respiratory depression

associated with

tranquilizing, and anti

cholinesterase drugs

atropine, either as a

agent or as an antidote tion to

is a transmitter. There are for each type of acetylcholine blocks all cholinergic action right

at the muscarinic receptor site on smooth muscle, ex and myocardium. Another cholinergic curare, works only at the neuromuscular

the antidote of choice for all cholinergic toxicities. One of the most important clinical uses for at

type of nicotinic blocker is the

blocker,

which blocks both sympathetic and occupvinfl the

acts to de

in the OI tract so that other antiulcer

crease

and it is possible that it also decreases acid se cretion, Other

related to hypermotility of

the OJ tract are treated with atropine,

to de

muscle activity during treatment of

conditions such as cramping and diarrhea. tone needs to be

In ophthalmology,

decreased. It is possible to selectively inhibit cholin effects in the body to produce a desired effect or to eliminate an undesirable effect. Because of this se

is useful for dilation. It is contraindi

which is cated in glaucoma an acute attack.

Atropine itself is also capable of producing toxic

have

use in many areas of medicine.

dry

effects. These are mydriasis,

and urinary retention, Effects related to

Atropine

the central nervous

ladonna, also known as the deadly

An

and hallucinations,

other plant extract, scopolamine, has action similar to works by establishing a

atropine,

at the muscarinic receptor

the effector at all tissues innervated nervous

are also apparent, and

these include sedation initially, followed by delirium

Atropine is an extract from the

tive

agent. This

cer and

crease

choline receptor there. These

lectiveness,

(Ol) tract as an antiul

ropine is in the

in paralysis of skeletal muscle. Still another

ever sympathetic or

A more general med

ical use for atropine exists as an emergency tool. It is

agents can remain in contact with the OI mucosa

to block the nicotinic effect of

parasympathetic ganglia

bronchiolar secretions and laryngeal

spasm, as well as

antagonists block the various

receptor.

medica

Atropine is used widely as

Cholinergic Blocking Drugs

respiratory which is

lead to a coma, In severe convulses and

severe

which may be the final course. and

Anticholinesterase drugs, such as

the parasym

are effective antidotes for atropine be

This blockade is selective

cause they increase the amount of acetylcholine that

for the tissue effect of the parasympathetic system

will compete with atropine for the


rl

43 --------� -----

Homatropine (Novatrin) and

783

.----

some way this reflex is i

Cyelopentolate (Cyelogyf)

a condition

known as orthostatic hypotension will exist. A com mon manifestation of this condition is fainting on

( Novatrin) and cyclopentolate gyl) are anticholinergic ropine.


------

because of inadequate blood flow to the

related in action to at

brain. This section is devoted to the functional as

are useful in ophthalmology to

of the retlex after a change in blood pressure.

mydriasis.

Dicyelomine (Bentyl) Dicyclomine (Bentyl) is considered very useful in the gastrointestinal tract to decrease secretions and motU

that fire electrical im

These are stretch

rr;hexyphenidyl HCL (Artane) and

pulses at a rate

Benztropine Mesylate (CogenUn)

related to the blood pressure,

As the pressure in the

and

me

sylate (Cogentin) are antiparkinson

that enter

the CNS to reverse the imbalance between the cholin and

Neuronal elements, known as baroreceptors, exist in the sinus of the carotid arteries supplying the brain.

It is sometimes called a chemical vagotomy,

Trihexyphenidyl HCL

The Carotid Baroreceptors

systems in this disease, They

(and

the receptor firing rate. Conversely, a decrease in blood pressure results in a decrease in stretch receptor is sent directly to

firing rate. This firing rate the

have some of the same side effects as

the ves:-;el wall

stretches, causing an increase in

where the vasomotor center and

nu

cleus respond to it.

Penlolinium (Ansolysen) and Hexamethonium (Methium) Pentolinium (Ansolysen) and hexamethonium (Me block the

thium) are nicotinic

acetylcholine receptor site in the ganglia in both the

The Functional Reflex To create an

experienced a loss of

blood pressure. The carotid

sympathetic and are used to control to a

slow their

hypotension. They will also decrease

cholinergic effects at the parasympathetic effector sites because

block the

of mouth, and

by in

sympathetic nerve activity, This control al ways

to information If the pressure had would have increased their

as well. This means blurred vision, dryness as well as other atropine

blood pres of the

sure in the carotid artery by doing the

for the entire

nervous that a patient may

shorten and

This message is then delivered to

the brain, and the vasomotor center

tonc, Because of their

action at the sympathetic ganglion, these drugs pro duce a

this

let us assume we have

the barore rate and the

vasomotor center would have responded by slowing the sympathetic nerve

rate. Since the blood

pressure in this example is

like peripheral effects.

increases

nerve

in in

creased release of norepinephrine from the nerves

THE CARDIOVASCULAR REflEX

that reach the heart and arterioles. Norepinephrine in

The cardiovascular reflex involves many of the com

creases the heart rate and stroke volume, thereby pro

ponents of the autonomic nervous system to maintain

ducing an increase in cardiac output. In the

a normal blood pressure. This mechanism is impor tant for

blood pressure within certain of physical from a

Even the position

stimulates the ducing

"rt"rlrllp

pro

which results in increased

resistance result in raised blood pressure. A third component of the sympathetic nervous system can be

by this reflex system, If in

involved


activation.

784

PART VIII


released from the adrenal medulla also increases car

creasing release of histamine, and in a broader ap proach, the general stabilization of cells that can re

diac output. Meanwhile, the vagal nucleus is responding to the decreased baroreceptor firing by decreasing its own ac

lease mediators of the disease, thereby lowering the severity of the disease.

tivity. The vagus nerve to the heart will release less acetylcholine, allowing the sympathetic effect to pre dominate. The total effect becomes an increase in blood pressure, which is the response required to re turn the systemic pressure to normal. If the original pressure alteration had been an increase above normal,

Sympathomimetic Drugs Isoproterenol (Isuprel) and Epinephrine (Adrenalin) The muscle relaxant bronchodilator effect attributed to

the opposite reflexive actions would have occurred to

the beta-adrenergic sympathomimetic compounds is

return pressure to a normal range. In this case the pre

most commonly required for asthmatic or allergic

dominant effect would have been an increase in vagal

emergencies. Isoproterenol (Isuprel) is often self-ad

nerve tone, releasing high amounts of acetylcholine at

ministered by inhalation to reverse mild-to-moderate

the heart, causing a dramatic slowing of heaJ1 rate, ac

obstructive episodes. However, during a severe acute

companied by a decrease in stroke volume. This com

obstruction, the airway is unable to pass the drug to the

bination produces a decrease in cardiac output. The

alveoli, and the intramuscular or subcutaneous routes

sympathetic system would have responded to the in

for epinephrine (adrenaline) and isoproterenol are

creased baroreceptor firing by decreasing firing in all

used. Isoproterenol is a purely beta compound. Epi

sympathetic nerves, thereby decreasing norepinephrine

nephrine has 50% beta-adrenergic activity and also ex

and epinephrine release. All of these factors combine

erts a great bronchodilating effect. Both of these agents

to decrease blood pressure to normal.

are useful when given parenterally or by inhalation. The most common side effects of isoproterenol are

DRUGS USED IN AIRWAY OBSTRUCTIVE DISEASE

flushing of the skin, headache, palpitation, and tachy cardia. Epinephrine may cause an anxiety reaction in a

Patients suffering from asthma, emphysema, and

patient along with headache, palpitations, and respira

chronic bronchitis may have an obstructed airway for

tory difficulty. Both drugs can cause serious cardiac

several reasons. Acute asthmatic obstruction and

reactions (dysrhythmias), which have resulted in death.

some chronic airway obstruction are due to bronchial smooth muscle contraction, resulting in a smaller di ameter airway. Inflamed passageways, wh ich are swollen because of edema, may also constitute an air

Metaproterenol (Alupent), Isoetharine (with Phenylephrine, Bronkosol-2), and Salmeterol (Servant)

way obstruction. A further complication seen in

Metaproterenol (Alupent), isoetharine (with Phenyle

many respiratory diseases is the thickening and col

phrine, Bronkosol-2), and salmeterol (Servant) are

lection of secretions that cannot be eliminated from

isoproterenol analogs that exert most of their action

the respiratory tree and subsequently block the air

on respiratory or vascular smooth muscle but have lit

way. In this section the various drugs that can reverse

tle effect on the heart. They are useful compounds for

smooth muscle contraction, inflammatory edema, and

selectively relaxing bronchial smooth muscles without

collection of secretions are presented.

directly affecting the heart. The major advantage of

A variety of therapeutic mechanisms are useful

these drugs is that their action on the heart is minimal

against this collection of obstructive conditions. The

or absent, and their potential for inducing cardiac toxi

single most effective mechanism for relief of smooth

cities is correspondingly reduced. However, because

muscle spasm is the beta2 activity that is available in

vascular smooth muscle responds much like respira

some of the adrenergic agents. Other useful mecha

tory smooth muscle to these drugs, arterial resistance

nisms aim at potentiating the beta activity of adrener

can be decreased, leading to a drop in blood pressure

gic agents, decongesting the inflamed airway, de

and a reflexive tachycardia. The beta agonists are


43 -... --.---


785

--�----------------.-----

inhalation, which minimizes their sys

often

temic absorption and potential for side effects, variety of antiinflammatory pOltenCle:s.

Ephedrine

of corticosteroids in from

and

the symp

on the ability of these

is a sympathomimetic that acts by liberat

toms of inflamed tissue. The mechanism of action for

sites in addition to having a possible direct effect on

the drugs, however, has not clearly been defined. Some

receptors. Its usefulness and side effects

specific effects of corticosteroids that relate to the anti

<>,""··c> ,,,'
are similar to those of epinephrine. One beneficial

dilation

inflammatory action are decreased and stabilization of

factor in ephedrine use is that it can be administered

and

orally for convenient

branes in white blood cells, In

I"Q.-'Q(";,
that can

pounds decrease the synthesis of nr"
Xanthines

broncho-obstl11ctive disease- prostaglandins use of the corticos

and ieukotrienes. The

XanthineI' have effects similar to the catecholamines in

teroids is recommended

the respiratory and cardiovascular systems. This simi

The reason for this caution is that they produce serious side effects and permanent

in effect may be due to the elevation of AMP. Both the catecholamines and xanthines are elevated

known to

AMP levels in the tis

if used for 2 weeks

After I week of corticosteroid therapy, be

or havioral

ulcers may be ob

and acute

is instituted and

sues they stimulate. The catecholamines activate

served. However, when

ate cyclase, the enzyme that converts A TP to

adrenal suppression occurs, the patient requires supple

AMP. The

formed cyclic AMP exelts its effects

on the local tissue (e.g., bronchial muscle relaxation)

until normal adrenal cor

mental corticosteroid

tex function is restored. This state of

and is inactivated by the enzyme

last for as long as several months after

The xanthines inhibit

Most promoting its effects. Addi

AMP and

tional actions of xanthines may be direct smooth muscle

who receive corticosteroids for long-term syn

therapy develop a condition called

of muscles be

drome. It is characterized by

relaxation that cou Id increase

cause of the breakdown of

tagonism of adenosine, which is brC)fIctlo(;on

of fat from the extremities to the face and the trunk, Eventually these patients develop osteoporosis and dia

Theophylline and Aminophylline

betes. Other serious complications are

Theophylline and aminophylline are structurally very similar to caffeine. They are llsed to control asthma when given

or

is

intercranial

aminophylline is the treatment of acute asthmatic air to epinephrine alone. Intravenous administration of this

and

retardation. The time to onset of side effects can applying dosing

antiin

benefit in the

at low systemic doses.

m!m"t",I"V

COiticosteroids can be administration or

in cases that do not

ulcers,

be prolonged and the

often used orally for long-term maintenance of mild-to moderate disease. One of the most common uses for way obstruction,

redistribution

at low doses in alternate

can be

inhalation in

a form that is not systemically absorbed.

drug increases the opportunity for serious side which are hypotension and cardiac dysrhythmias,

Antihistamine

Cromolyn Sodium (intal) and

Nedocromil Sodium (Ti/ade)

Corticosteroids The antiinflammatory steroids are related to the natu glucocorticoid, cortisol (Prednisone,

Cromolyn sodium (Intal) and nedocromil sodium have limited usefulness


with the

786

PART VIII


other drugs presented here-they can only prevent an

torants that are usually used in mixtures or adminis

asthmatic episode. The mechanism of action is proba

tered as cough syrups are ammonium chloride, syrup

bly the stabilization of the mast cell that synthesizes,

of ipecac, and glyceryl guaiacolate. These are useful

stores, and releases histamine. Since histamine can

for patients who cannot tolerate the iodide salts.

precipitate broncho-obstructive reactions, these drugs are useful by preventing its release. They are admin istered by inhalation.

DRUG INHALATION DEVICES Most drugs given by inhalation in respiratory disease are deli vered by pressurized metered-dose inhalers

Mucolytics and Expectorants

(MDI). These devices rely on pressurized chlo

Acetylcysteine (Mucomyst) and

roflurocarbon propellants to deliver very small drug

Pancreatic Dornase (Dornavac)

particles (less than

Acetylcysteine (Mucomyst) and pancreatic dornase

5 micron diameter) into the air

way. Each activation of the metered valve allows an

(Dornavac) act by breaking the chemical bonds that

accurately determined volume (dose) of propellant

hold together the large protein structure that con

and drug mixture to be released at a high velocity.

tributes to the viscosity of mucus. Mucolytics are in

The delivery of drugs to the site of action in the

haled to liquify mucus so that it can be moved out of

airway by any type of inhalation is inefficient, and

the bronchial tract to prevent airway obstruction. Side

therefore, correct technique in use of the MDI is an

effects associated with these drugs are bronchospasm,

important concern. The MDI will allow delivery of

nausea, and vomiting. Acetylcysteine also inactivates

20% of the metered drug to the airway if the pa

the penicillin antibiotics and is contraindicated in

tient correctly coordinates the proper rate of inhala

their presence.

tion with activation of the device and then ade quately holds the breath before exhalation. It is

Trypsin (Tryptar)

estimated that

50% or fewer patients manage the

Trypsin (Tryptar) is a proteolytic enzyme that may

drug delivery correctly. In response, patient educa

also be useful for liquefying respiratory secretions. It

tion on correct MDI technique is an important part

can be administered by inhalation, although it can

of therapy, and additional devices, called spacers,

cause irritation to the eyes, nose, and throat. An addi

have been developed to allow success with varia

tional problem with this drug is a possible anaphylac

tions in technique. The spacers come in various

tic reaction in sensitized patients. There is a variety

configurations, but they all provide a chamber be

of other enzymes with specific actions on protein that

tween the patient and the MDI, which can be

may be useful in liquefying secretions.

charged with the drug-propellant mixture that is then inhaled without concern for critical timing.

Sodium Iodide and Potassium Iodide

Patients with poor MDI technique should benefit

Sodium iodide and potassium iodide are expectorants

from the addition of a spacer.

that act by increasing the amount of respiratory secre

An alternative to the MDI, in patients who have

tion so that is relatively less viscous and can be more

difficulty with inhalation technique, is the single-dose

easily removed. The iodide salts are often used in late

or multi-dose powder inhaler. This device offers a

bronchitis, bronchiectasis, and asthma, and they break

drug compounded into a fine powder, which is deliv

up especially tough bronchial secretions by attracting

ered from a container on simple inhalation by the pa

fluid to the respiratory tract. Characteristic side effects

tient. Coordination of drug delivery is simple and not

with these compounds are gastric irritation, nausea,

a pl'Oblem, because only inspiration by the patient

and vomiting. More serious complications occasion

drives powder delivery to the airway. The method of

ally involve the respiratory tract. These patients

fers the same or lower efficacy of drug delivery

wheeze and experience bronchial spasm. Other expec

to

20%), compared with MDI.


(69'c

43

787

References

REVIEW QUESTIONS 1. Why is it important to have an understanding of

Clark, TJ.H., Godfrey,

S., & Lee, T.H., (Eds.). (1992). Asthm({.

London: Chapman and Hall.

the system a drug is to modify? 2. What are the primary and secondary effects of

the commonly used bronchodilators, Ventolin and Alupent?

Hardman,

J., Gilman, A.G., Limbird, L., & Rail, T.W., (Eds.).

(1995). The pharmacological basis of therapeutics. New York: McGraw-HilI. Kaliner, M.A. (1993). How the current understanding of the patho

3. What is the cardiovascular reflex and why is it

physiology of asthma influences our approach to therapy. .lour1101 afAllergy and Clinical Immunology,

important to physical therapists? 4. What is the pharmacologic rationale for treat

ment of patients with chronic obstructive airways disease. (COPD)?

92( I pI. 2), 144-147.

Katzung, B.G., (Ed.). (1995). Basic and clinical pharmacology. East Norwalk, CT: Appleton

& Lange.

O'Brien-Ladner, A. (1994). Asthma: new insights in the manage ment of older patients. Geriatrics,

5. Why is patient compliance with their medica

tions a concern of the physical therapist?


Powell,

C.Y. (1993).

49( 11),20-25,30-32.

Management

of ac ute

asthma

in

ch ildhood.British .lournal ( fHospil{/1 Medicine, 50(5),272-275. Whelan, A.M.,

& Hahn, N.W. (1991). Optimizing drug delivery

from metered-dose inhalers. Drug Intelligence and Clinical Pharmacology,


25, 638-645.

GLOSSARY

Acid-base balance:

a condition existing when the net

rate at which the body produces acids or bases equals the net rate at which acids or bases are excreted. The

surgery, gram-negative sepsis, multiple blood transfusions, oxygen toxicity, trauma, pneumonia, or other respiratory infection.

result of acid-base balance is a stable concentration

Aerosol:

of hydrogen ions in body fluids. The amount of acid

Airway clearance:

or base in the arterial blood is measured by pH.

Acidosis:

the removal of mucus and foreign

material from the airways.

Airway-clearance deficits:

a process causing acidemia, which is a

blood pH of less than 7.38.

deficits in the ability to

remove mucus and foreign material from the airways.

Acute exacerbation of chronic airflow limitation:

nebulized particles suspended in a gas or air.

Alveolar proteinosis:

an increase in the severity of the signs

a disorder marked by the

accumulation of plasma proteins, lipoproteins, and

and symptoms of chronic airflow limitation usually

other blood components in the alveoli of the lungs.

triggered by infection, inflammation, or increased

The cause is unknown and clinical symptoms vary,

sputum production.

although only the lungs are affected. Some patients

Acute lung injury:

injury to the lung characterized by

a clinical spectrum of parenchymal lung dysfunction

are asymptomatic, whereas others show dyspnea and an unproductive cough.

Alveolar ventilation:

resulting from multiple etiologies and leading to alveolar capillary membrane leaking (high protein

the volume of inspired air that

reaches the alveolar level and participates in gas exchange, measured by Peo2.

content). Mild-to-moderate lung injury results in noncardiogenic edema and severe injury results in adult respiratory distress syndrome. The hallmarks of

Alveolitis:

an allergic pulmonary reaction to the

inhalation of antigenic substances characterized by

worsening lung injury include refractory hypoxemia,

acute episodes of dyspnea, cough, sweating, fever,

right-to-left shunt, and reduced lung compliance.

weakness, and pain in the joints and mnscles

Adult respiratory distress syndrome (ARDS):

a

lasting from 12 to 18 hours. Recurrent episodes

respiratory syndrome characterized by respiratory

may lead to chronic obstructive lung disease with

insufficiency and hypoxemia. Triggers include

weight loss, increasing exertional dyspnea, and

aspiration of a foreign body, cardiopulmonary bypass

interstitial fibrosis.

G-1


G-2

Glossary

Anesthesia:

the absence of normal sensation, especially

sensitivity to pain, as induced by an anesthetic substance or by hypnosis or as occurs with traumatic or pathophysiological damage to nerve tissue. Angina:

angina pectoris, the paroxysmal chest pain

an abnormal condition characterized by

Atelectasis:

the collapse of lung tissue, preventing the respiratory exchange of carbon dioxide and oxygen. Symptoms may include diminished breath sounds, a mediastinal

caused by anoxia of the myocardium. a paroxysmal thoracic pain caused

Angina pectoris:

bronchodilators, beta-adrenergic drugs, methylxanthines, and sh0l1-term use of corticosteroids.

most often by myocardial anoxia as a result of atherosclerosis of the coronary arteries. The pain

shift toward the side of the collapse, fever, and increasing dyspnea. a common arterial disorder

Atherosclerosis:

usuall.y radiates down the inner aspect of the left arm

characterized by yellowish plaques of cholesterol,

and is frequently accompanied by a feeling of

lipids, and cellular debris in the inner layers of the

suffocation and impending death. Attacks of angina

walls of large and medium-sized arteries. The vessel

pectoris are often related to exertion, emotional

walls become thick, fibrotic, and calcified, and the

stress, and exposure to intense cold.

lumen narrows, resulting in reduced blood flow to

Ankylosing spondylitis:

a chronic inflammatory

organs normally supplied by the artery.

disease of unknown origin, first affecting the spine

Antilipidemic agents do not reverse atherosclerosis,

and adjacent structures and commonly progressing to

but a diet low in cholesterol, calories, and saturated

eventual fusion (ankylosis) of the involved joints. In

fats, adequate exercise, and the avoidance of

addition to the spine the joints of the hip, shoulder,

smoking and stress may help prevent the disorder.

neck, ribs, and jaw are often involved. Physical therapy aids in keeping the spine as erect as possible to prevent flexion contractures. In advanced cases,

Blood:

the liquid pumped by the heart through all the

arteries, veins, and capillaries. The blood is

surgery may be performed to straighten a badly

composed of a clear yellow tluid, called plasma, and

deformed spine.

the formed elements, and a series of cell types with

Arrhythmia:

an abnormal heart rhythm represented

different functions. The major function of the blood

by an irregularity of the timing or the appearance of

is to transport oxygen and nutrients to the cells and to

the ECG tracing. This term is often used

remove from the cells carbon dioxide and other waste products for detoxification and elimination.

synonymously with dysrhythmia. Arterial blood gas:

a test to evaluate the acid-base

balance and panial pressures of oxygen and carbon

the difference between the oxygen

breaths per minute. Bronchiectasis:

an abnormal condition of the

bronchial tree, characterized by irreversible dilatation

blood. Artifact:

an abnormally slow heart rate. a decreased respiratory rate under 10

Bradypnea:

content of arterial blood and the amount in venous

using one's body effectively to

prevent injury. Bradycardia:

dioxide in the anerial blood. Arteriovenous-oxygen difference (a-vo2 difference):

Body mechanics:

extraneous detlection of the ECG waveform

and destruction of the bronchial walls. Symptoms of

caused by movement or electrical interference.

bronchiectasis include a constant cough productive

Artifact may be mistaken for a dysrhythmia.

of copious purulent sputum, hemoptysis, chronic

Artificial airway:

a plastic or rubber device that can

sinusitis, clubbing of fingers, and persistent moist,

be inserted into the upper or lower respiratory tract to

coarse rales. Treatment includes mobilization,

facilitate ventilation or the removal of secretions.

frequent postural drainage, antibiotics, and, rarely,

Assessment:

an evaluation or appraisal of a condition.

Assisted cough:

the physical assistance of a cough,

an acute viral infection of the lower

respiratory tract that occurs primarily in infants under

either by the patient or an assistant. Asthma:

surgical resection of the affected part of the lungs. Bronchiolitis:

a respiratory disorder characterized by

recurring episodes of paroxysmal dyspnea, wheezing on expiration/inspiration because of constriction of the bronchi, coughing, and viscous mucoid bronchial

18 months of age, characterized by expiratory wheezing, respiratory distres , inflammation, and obstruction at the level of the bronchioles. Bronchitis:

an acute or chronic inflammation of the

secretions. Treatment may include elimination of the

mucous membranes of the tracheobronchial tree.

causative agent, hyposensitization, aerosol or oral

Acute bronchitis is characterized by a productive


Glossary

G-3

cough, fever, hypertrophy of mucous-secreting

present at birth or shortly thereafter. Early

structures, and back pain. Most common in adults, it

identification of the disorder facilitates the handling

is uften a complication of cystic fibrosis in children.

of infants with cerebral palsy and the initiation of an

Treatment includes the cessation of cigarette

exercise and training program. Treatment is

smoking, avoidance of airway irritants, the use of

individualized and may include the use of braces,

expectorants, and postural drainage. Currently,

surgical correction of deformities, speech therapy,

prophylactic antibiotics, steroids, and desensitization

and various indicated drugs, such as muscle rel. À

therapy are not recummended.

Bronchopulmonary dysplasia:

and anticonvulsants.

an iatrogenic condition

Childhood asthma:

reversible airway hyperreactivity

observed in neonates that resembles chronic airflow

and edema affecting children that is often triggered

limitation and is associated with positive pressure

by dust or animals; hallmarked by narrowing of the

mechanical ventilation and oxygen therapy.

airways, wheezing, shortness of breath, accessory

Burns:

an injury to tissues of the body caused by heat,

electricity, chemicals, radiation, or gases in which the extent of the injury is determined by the amount of exposure of the cell to the agent and to the nature of the agent. The treatment of burns includes pain relief,

muscle use, and impaired oxygenation. a lung condition characterized

Chronic bronchitis:

by the presence of a chronic productive cough for at least 3 months in each of 2 successive years. impaired function of the

Chronic renal insufficiency:

careful asepsis, prevention of infection, maintenance

kidneys manifested by impaired blood urea nitrogen,

of the balance in the body of fluids and electrolytes,

creatinine clearance, and reduced urinary output.

and good nutrition. Severe bUllls of any origin may cause shock, which is treated before the wound.

Renal insufficiency may precipitate renal failure.

Chronic airflow limitation:

a more precise term for

chronic obstructive pulmonary disease (e.g., chronic

Cardiac output (Q):

bronchitis and emphysema).

the amount of blood ejected

from the heart into the aona each minute.

Clinical decision making:

the process of making

decisions based on a thorough history, assessment,

a supervised program of

Cardiac rehabilitation:

integration of the results of laboratory tests and

progressive exercise, psychological support, and education or training to enable a myocardial

investigations, and the patient's needs and wants.

infarction patient to resume the activities of daily

Complications with coughing:

living on an independent basis. Special training may

Complications

associated with an impaired cough (e.g., impaired

be needed to adapt the patient to a new occupation

mucociliary transport, mucous accumulation,

and lifestyle.

pulmonary aspiration, and increased risk of infection).

Cardiopulmonary failure:

progressive insufficiency

Congestive heart failure (CHF):

an abnormal

of cardiopulmonary function resulting in significant

condition that reflects impaired cardiac pumping,

impairment of cardiac output and/or ventilation that

caused by myocardial infarction, ischemic heart

cannot be adequately compensated without

disease, or cardiomyopathy. Failure of the ventricle to

ventilatory support.

eject blood efficiently results in volume overload,

Cardiopulmonary function:

the integrated function

of the heart and lungs.

Retrograde transmission of increased hydrostatic

Cardiopulmonary physical therapy: see p. ix. Cardiopulmonary unit: the heart and lungs, which function interdependently as a unit.

Catabolic:

congestion; elevated right heart pressure causes

Connective tissue dysfunction:

relating to catabolism, which is the

impaired function of

connective tissue observed in connective tissue and

compounds into simpler ones, often accompanied by the liberation uf energy.

vascular collagen conditions.

Continuity of care:

the processes involved with

the provision of continuous care

from one setting to another (e.g., inpatient to

cellular metabolism, including energy transfer,

outpatient facilities).

oxygen utilization, and carbon dioxide production.

Cerebral palsy:

pressure from the left heart causes pulmonary systemic venous congestion and peripheral edema.

breaking down in the body of complex chemical

Cellular respiration:

chamber dilatation, and elevated intracardiac pressure.

a motor function disorder caused by

a permanent, nonprogrcssive brain defect or lesion

Controlled breathing:

teaching a patient ventilatory

strategies to exert cognitive control over ineffective breathing patterns.


G-4

Glossary

Control of breathing:

the central and peripheral

regulation and control mechanisms of breathing.

Control of the heart:

the central and peripheral

regulation and control mechanisms of the heart.

Coronary artery disease:

any one of the abnonual

conditions that may affect the arteries of the heart

constituents of saliva, and overactivity of the autonomic nervous system. The glands most affected are those in the pancreas, the respiratory system, and the sweat glands. Because there is no known cure, treatment is directed at the prevention of respiratory infections, which are the most frequent cause of

and produce various pathological effects, especially

death. Mucolytic agents and bronchodilators are used

the reduced flow of oxygen and nutrients to the

to help liquefy the thick, tenacious mucus. Physical

myocardium. Any of the coronary artery diseases,

therapy measures, such

such as coronary atherosclerosis, coronary arteritis,

drainage, and breathing exercises, can also dislodge

or fibromuscular hyperplasia of the coronary arteries,

secretions. Life expectancy in cystic fibrosis has

as

exercise, postural

may produce the common characteristic symptom of

improved markedly over the past several decades,

angina pectoris. Studies over the last 30 years

and with early diagnosis and treatment, most patients

confirm that coronary atherosclerosis occurs most

can be expected to reach adulthood.

frequently in populations with regular diets high in calories, total fat, saturated fat, cholesterol, and refined carbohydrates. Other risk factors include

Dead space:

the amount of lung in contact with

ventilating gases but not in contact with pulmonary

cigarette smoking, hypertension, serum cholesterol

blood tlow. Alveolar dead space refers to alveoli

levels, coffee intake, alcohol intake, deficiencies of

that are ventilated by the pulmonary circulation but

vitamins C and E, water hardness, hypoxia, carbon

are not perfused. The condition may exist when

monoxide, social overcrowding, heredity, climate,

pulmonary circulation is obstructed, as by a

and viruses.

thromboembol.us. Anatomical dead space is an area

Cough:

a sudden, audible expulsion of air from the

in the trachea, bronchi, and air passages containing

lungs. Coughing is preceded by inspiration, the

air that does not reach the alveoli during respiration.

glottis is partially closed, and the accessory muscles

As a general rule the volume of air in the

of expiration contract to expel the air forcibly from

anatomical dead space in millimeters is

the respiratory passages. Coughing is an essential

approximately equal to the weight in pounds of the

protective response that serves to clear the lungs,

involved individual. Certain lung disorders, such as

bronchi, or trachea of irritants and secretions or to

emphysema, increase the amount of anatomical

prevent aspiration of foreign material into the lungs.

dead space. Physiological dead space is an area in

It is a common symptom of diseases of the chest and

the respiratory system that includes the anatomical

larynx. Because the function of coughing is to clear

dead space together with the space in the alveoli

the respiratory tract of secretions, it is important that

occupied by air that does not contribute to the

the cough bring out accumulated debris. Where it

oxygen-carbon dioxide exchange.

does not, because of weakness or inhibition of the

Denervation of heart:

the transplanted heart initially

force of the cough caused by pain, instruction and

loses its innervation (i.e., it is deriervated and relies

assistance in effective coughing and deep-breathing

on exogenous catecholamines for cardiac

exercises are required.

Cough pump:

acceleration and deceleration).

the integrated thoracic and abdominal

mechanisms involved in cough resulting in forced expiration and evacuation and clearance of the airways.

Cough stages:

the stages of cough include maximal

inspiration, closure of the glottis, increased intraabdominal pressure, opening of the glottis, and forced expiration.

Cystic fibrosis:

Dependent patients:

patients unable to help

themselves.

Depolarization:

the changes in ionic concentrations

across muscle cell membranes leading to contraction of the cell.

Diabetes:

a clinical condition characterized by the

excessive excretion of urine. The excess may be

an inherited disorder of the exocrine

caused by a deficiency of antidiuretic hormone

glands, causing those glands to produce abnormally

(ADH), as in diabetes insipidus, or it may be the

thick secretions of mucus, elevation of sweat

polyuria resulting from the hyperglycemia OCCUlTing

electrolytes, increased organic and enzymatic

in diabetes mellitus.


Glossary

Diaphragmatic breathing pattern:

involves teaching

the function of the endocrine

Endocrine function:

glands responsible for normal physiological function.

patients with CO PO how to relax the accessory muscles and to pelform controlled diaphragmatic

Evidence-based practice:

practice based on evidence

from the physiologic and scientific literature.

breathing. the process in which solid, particulate

Diflusion:

G-5

Exercise:

(I) The petformance of any physical

activity for the purpose of conditioning the body,

matter in a t1uid moves from an area of higher concentration to an area of lower concentration,

improving health, or maintaining fitness or as a

resulting in an even distribution of the particles in the

means of therapy for correcting a deformity or

fluid. No energy is required.

restoring the organs and bodily functions to a state of

Documentation:

written material associated with the

history, the compilation of laboratory reports and

health. (2) Any action, skill, or maneuver that exerts the muscles and is performed repeatedly in order to

investigations, and the results of the clinical

develop or strengthen the body or any of its parts.

assessment.

(3) To use a muscle or part of the body in a repetitive

Dyspnea:

way to maintain or develop its strength. The physical

the sensation of difficulty in breathing.

therapist constantly assesses the patient's needs and ECG monitoring:

electrocardiographic monitoring

involving electrode placement on the chest wall and

provides the proper type and amount of exercise, taking into account the patient's physical or mental

on the limbs for a 12-lead ECG; such monitoring

limitations. Exercise has a beneficial effect on each

provides a tracing of the electrical activity of the

of the body systems, although in excess it can lead to the breakdown of tissue and cause injury.

heart. evaluation of cardiac structure

Echocardiography:

Quantitative and qualitative measurements can be dimensional, Doppler, and transesophageal echoes. a measure of myocardial function,

it is the amount of ventricular volume ejected with each heart beat. Expressed as a percent, the ejection volume)

=

Expiratory reserve volume (ERV):

the maximum

volume of gas that can be expired from the resting expiratory level. factors related to the patient's care

that contribute to cardiopulmonary dysfunction and

100 end-diastolic volume.

Electrocardiogram (ECG):

the physical stress imposed by

movement (i.e., mobilization and exercise.)

Extrinsic factors:

(end-diastolic volume - end-systolic

x

exercise on oxygen transport. Exercise stress:

derived. The most common types include two

fraction

blood gases taken before,

during, and after exercise to determine the effect of

and function by using the properties of sound.

Ejection fraction:

Exercise blood gases:

the tracing produced by

impaired gas exchange.

the sequential depolarization and repolarization of myocardial cells as detected by sutface electrodes Electromechanical coupling: cardiac output.

effect on electrolytes. Forced expiratory volume in one second (FEV I):

the

amount of air expired in I second during a forced

electromyography is the

process of recording the electrical activity of muscle

exhalation after a maximal inhalation. Forced vital capacity (FVC):

on a cathode-ray oscilloscope. The electromyographic (EMG) power spectrum is the full

the total amount of air

exhaled during a forced exhalation after a maximal inhalation.

range of electrical activity of the muscle. Emphysema:

the status of blood

balance in the body; fluid balance often has a direct

the coupling of

electrical and mechanical events of the heart to effect EMG power spectrum:

Fluid and electrolyte status:

volume and distribution, and the status of electrolyte

placed on the skin.

a lung condition characterized by an

Functional residual capacity:

the volume of gas in

abnormal permanent enlargement of the air spaces

the lungs at the end of a normal expiration. The

distal to the terminal bronchioles, accompanied by

functional residual capacity is equal to the residual

destruction of their walls. Endocardial cushion defect:

volume plus the expiratory reserve volume. any cardiac defect

Function optimization:

optimal functioning of the

resulting from the failure of the endocardial cushions in

patient as a whole person based on optimal

the embryonic heart to fuse and form the atrial septum.

physiological functioning at an organ system level.


G-6

Glossary

Gas exchange:

the movement of oxygen and carbon

temperature. The percentage is usually represented in

dioxide between the pulmonary capillary blood and

terms of relative humidity, with 100% being the

the alveolar tissue and between the systemic capillary

point of air saturation or the level at which the air can absorb no additional water.

blood and peripheral tissue cells.

Gastrointestinal dysfunction:

abnormal function of

the gastrointestinal system.

Gravitational stress:

disease of the newborn,

characterized by airless alveoli, inelastic lungs, more

stress imposed on the human

body by gravity and its physiological effects.

Gravity:

Hyaline membrane disease:

the heaviness or weight of an object resulting

from the universal effect of the attraction between any

than 60 respirations a minute, nasal flaring, intercostal and subcostal retractions, grunting on expiration, and peripheral edema. The condition occurs most often in premature babies. The disease is

body of matter and any planetary body. The force of

self-limited; the infant dies in 3 to 5 days or

the attraction depends on the relative masses of the

completely recovers with no after-effects. Treatment

bodies and on the distance between them.

includes measures to corTect shock, acidosis, and hypoxemia and use of positive airway pressure to

Head injury:

any traumatic damage to the head

resulting from blunt or penetrating trauma of the skull. Blood vessels, nerves, and meninges can be torn; bleeding, edema, and ischemia may result.

Health behavior:

an action taken by a person to

maintain, attain, or regain good health and to prevent

prevent alveolar collapse. This is also called

respiratory distress syndrome (RDS) olthe newborn. Hypercapnia:

the presence of an abnormally large

amount of carbon dioxide in the circulating blood.

Hyperpnea: Hypertension:

rapid shallow breathing. a common, often asymptomatic

illness. Health behavior reflects a person's health

disorder characterized by elevated blood pressure

beliefs. Some common health behaviors are

persistently exceeding 140/90 mm Hg. Patients with

exercising regularly, eating a balanced diet, and

high blood pressure are advised to follow a low

obtaining necessary inoculations.

sodium, low-saturated-fat diet, to reduce calories to

Heart:

the muscular, cone-shaped organ, about the

size of a clenched fist, that pumps blood throughout the body and beats normally about 70 times per minute by coordinated nerve impulses and muscular

control obesity, to exercise, to avoid stress, and to take adequate rest.

Hypoxemia:

a low level of oxygen in the blood, often

characterized by a Pa02 of less than 80 mm Hg.

contractions. Enclosed in pericardium, the heart rests on the diaphragm between the lower borders of the lungs, occupying the middle of the mediastinum. The sinoatrial node of the heartbeat sets the rate. Other factors affecting the heartbeat are emotion, exercise, hormones, temperature, pain, and stress.

Heart-lung interdependence:

the heart and lung are

paralysis of one side of the body. status of the heart and its

capacity to effect blood movement to perfuse the tissues of the body.

Hibernating myocardium:

abnormal function of

Immunosuppression:

of or peI1.aining to a suhstance or

procedure that lessens or prevents an immune response. the maximum volume of

gas that can be inhaled from the resting expiratory level. Equal to the sum of the tidal volume and the inspiratory reserve volume, it is measured with a spirometer.

contractile dysfunction of

the myocardium as a result of prolonged ischemia, appearing as a regional wall motion abnormality.

Home care:

immunological protection.

Immunological dysfunction:

Inspiratory capacity (Ie):

a cardiopulmonary unit.

Hemodynamic status:

function of the immunological

system and its components in effecting optimal

the immunological system.

structurally and functionally interdependent and form

Hemiplegia:

Immune function:

a health service provided in the patient's

place of residence for the purposes of promoting,

Inspiratory muscle training:

resistance ventilatory

training designed to increase the strength and endurance of the inspiratory muscles.

Inspiratory resistance breathing:

a method of

respiratory muscle training that includes normal

maintaining, or restoring health or minimizing the

ventilation with added external threshold loading

effects of illness and disability.

on inspiration consisting of 15 to 30 minutes of

Humidity:

pertaining to the level of moisture in the

atmosphere, the amount varying with the

training 5 days per week. External loading is increased from 30% of maximal inspiratory pressure


Glossary

G-7

to 60% of maximal inspiratory pressure as patient's

nephrons. All the blood in the body passes through

tolerance increases.

the kidneys about 20 times every hour but only about

Inspiratory reserve volume:

The maximum volume

one fifth of the plasma is filtered by the nephrons

of gas that can be inspired from the end-tidal

during that period. The kidneys remove water as

inspiratory level.

urine and return water that has been filtered to the

Intermittent positive pressure breathing (IPPB):

a

form of assistive or controll.ed respiration produced

blood plasma, thus helping to maintain the water baJance of the body. Hormone, especially the

by a ventilatory apparatus in which compressed gas

antidiuretic hormone (ADH), produced by the

is delivered under positive pressure into the person's

pituitary gland, control the function of the kidneys in

airways unti I a preset pressure is reached. Passi ve exhalation is allowed through a valve, and the cycle

regulating the water content of the body. an abnormal condition characterized

Kyphoscoliosis:

begins again as the flow of gas is triggered by

by an anteroposterior curvature and a lateral

inhalation. This is also called i11lermillent positive

curvature of the spine. It occurs in children and

pressure ventilation (IPPV).

adults and can be associated with cor pulmonale.

Interstitial pulmonary fibrosis:

a classification of

restrictive lung disease including conditions that result in a final common pathway of bouts of chronic

the late effects of

poliomyelitis that may occur in poliomyelitis survivors 30 to 35 years after onset. These effects

lung infection and irreversible fibrosis.

Intraaortic balloon counter pulsation:

Late sequelae of poliomyelitis:

procedure for

include disproportionate fatigue, weakness, pain,

assisting left ventricular function and coronary

reduced endurance, choking and swallowing

petfusion involving the insertion of a balloon in the

problems, altered temperature sensitivity, and

femoral artery. The inflation and deflation of the balloon is synchronized with the ECG such that it inflates during diastole and deflates during systole. pressures within the

Intracardiac pressures:

psychological problems.

Learning theory:

a group of concepts and principles

that attempts to explain the learning process. One concept, Guthrie's contiguous conditioning premise,

chambers of the heart. Optimal movement of blood

postulates that each response becomes permanently

through the heart depends on pressure gradients

linked with stimuli present at the time so that

throughoLlt the heart. Normal pressures within each

contiguity rather than reinforcement is a part of the

heart chamber are within a restricted range.

Intracranial pressure monitoring:

learning process.

invasive

Liver:

monitoring instituted to measure changes in cranial

the largest gland of the body and one of its

most complex organs. More than 500 of its functions

pressure usually resulting from increased volume of

have been identified. It is divided into four lobes,

the brain because of injury. bleeding, fluid

contains as many as 100,000 lobules, and is served

accumulation, or an intracranial mass.

Isocapnic hyperpnea:

by two distinct blood supplies. Some of the major

a method of respiratory muscle

training that includes high ventilation with low

functions performed by the liver are the production of bile by hepatic cells, the secretion of glucose,

external loading consisting of sustained periods of

proteins, vitamins, fats, and most of the other

hyperpnea lasting 15 to 30 minutes daily for several

compounds used by the body, the processing of

weeks with the addition of carbon dioxide to

hemoglobin for vital use of its iron content, and the

maintain a normal level.

conversion of poisonous ammonia to area.

Lung cancer: Jacobsen's progressive relaxation exercise:

a

a pulmonary malignancy attributable to

cigarette smoking in 50% of cases. Lung cancer

technique involving contraction followed by

develops most often in scalTed or chronically diseased

relaxation to progressively relax muscle groups.

lungs and is usual. because metastases may precede the detection of the

Kidneys:

a pair of bean-shaped urinary organs in the

dorsal part of the abdomen, one on each side of the

primary lesion in the lung. Symptoms of lung cancer include persistent cough, dyspnea, purulent or blood

vertebral column. The kidneys produce and eliminate

streaked sputum, chest pain, and repeated attacks of

urine through a complex filtration network and

bronchitis or pneumonia. Surgery is the most

reabsorption system comprising more than 2 million

effective treatment, but only one half of cases are


G-8

Glossary

operahle at the time of diagnosis and of these 50% are

Metabolical demand fluctuates depending on the

not resectable. Thoracotomy is contraindicated if

activity level of the individual, the presence of illness

metastases are found in contralateral or scalene lymph

and increascd temperature, and the requirements of

nodes. In"adiation is used to treat localized lesions and unresectable intrathoracic tumors and as palliative therapy for metastatic lesions. Radiotherapy may also be administered after surgery to destroy remaining tumor cells and may be combined with chemotherapy.

Lung capacities:

lung volumes that consist of two or

more of the four primary nonoveriapping volumes. Functional residual capacity is the sum of residual volume and expiratory reserve volume. Inspiratory capacity is the sum of the tidal volume and

healing and repair.

Method:

a technique or procedure for producing a

desired effect, such as a surgical procedure, a laboratory test, or a diagnostic technique.

Minute ventilation (VE):

the amount of air inspired

in I minute. It is the product of tidal volume and respiratory rate. the total expired volume of air

Minute ventilation: per minute.

Mobilization:

the therapeutic and prescriptive

inspiratory reserve volume. Vital capacity is the sum

application of low-intensity exercise in the

of the expiratory reserve volume, the tidal volume,

management of cardiopulmonary dysfunction usually

and the inspiratory reserve volume. Total lung

in acutely ill patients. The primary goal of

capacity, at the end of maximal inspiration, is the

mobilization is to exploit the acute eflects or exercise

sum of the functional residual capacity and the inspiratory capacity.

Lung compliance:

the volume change per unit of

pressure change in the lungs.

Lungs:

to optimize oxygen transport.

Morbid obesity:

an excess of body fat that threatens

normal body functions, such as respiration.

Mucous blanket:

a pair of light, spongy organs in the thorax,

the normal layer of mucous lining

the bronchopulmonary tree. This blanket provides a

constituting the main component of the respiratory

medium through which foreign material and bacteria

system. The two highly elastic lungs are the main

can be wafted centrally by the cilia for eventual

mechanisms in the body for inspiring air from which oxygen is extracted for the arterial blood system and

removal by coughing or swallowing.

Multiple sclerosis (MS):

a progressi ve discase

for exhaling carbon dioxide dispersed from the

characterized by disscminated demyelination of

venous system.

nerve fibers of the brain and spinal cord. It begins

Lung volume:

the volume of the lungs that may be

slowly, usually in young adulthood, and continues

compartmentalized into component volumes and

throughout life with periods of exacerbation and

capacities.

remission. As the disease progresses, the intervals between exacerbations grow shorter and disabil ity

Malnutrition:

any disorder of nutrition. It may result

from an unbalanced, insufficient, or excessive diet or

becomes greater. There is no specific treatment for the diseasc; corticosteroids and other drugs are

from the impaired absorption, assimilation, or use of

used to treat the symptoms accompanying acute

foods.

episodes. Physical therapy may help to postpone

Managed care:

a health care system in which there is

or prevent specific disabilities. The patient is

administrative control over primary health care

encouraged to live as normal and active a life

services in a medical group practice. Redundant

as possible.

facilities and services are eliminated and costs are reduced. Health education and preventive medicine

Multisystem assessment: the assessment of multiple organ systems based on clinical examination

are emphasized. Patients may pay a flat fee for basic

and investigative laboratory reports. Such assessment

family care but may be charged additional fees for

helps identify all factors that contribute to deficits in

secondary care services of specialists.

Measurement:

oxygen transport.

the determination, expressed

numerically, of the extent or quantity of a substance, the use of artificial

the maximum force that a muscle

can develop with maximal stimulation.

mechanical means to support ventilation.

Metabolical demand:

the ability to sustain repetitive

contraction against a given load.

Muscle strength:

energy, or time.

Mechanical ventilation:

Muscle endurance:

Muscular dystrophy (MD):

the energy and oxygen

demands of the body required to support metabolism.

a group of genetically

transmitted diseases characterized by progressive atrophy of symmetrical groups of skeletal muscles


Glossary

without evidence of involvement or degeneration of neural tissue. [n all forms of muscular dystrophy, there is an insidious loss of strength with increasing disability and deformity, although each type differs

Oxygen (02):

G-9

a tasteless, odorless, colorless gas

essential for human respiration.

Oxygen consumption (Vo2):

the difference between

oxygen that is inspired and the amount of oxygen

in the groups of muscles affected, the age of onset,

exhaJed. The difference between inspired and expired

the rate of progression, and the mode of genetic

oxygen is a primary measure of aerobic fitness.

inheritance. The basic cause is unknown but appears to be an inborn error of metabolism. Treatment of the muscular dystrophies consists primarily of supportive measures, such as physical therapy and orthopedic procedures to minimize deformity.

Myocardial infarction:

Oxygen delivery (Do2):

the delivery of oxygen to the

tissues of the body. an essential component of oxygen transport.

Oxygen desaturation:

the desaturation of oxygen

from the hemoglobin molecule in the blood in

necrosis of a portion of

response to a reduction of tissue oxygen levels.

cardiac muscle caused by obstruction in a coronary

Oxygen transport:

the process by which oxygen is

artery from either atherosclerosis or an embolus.

absorbed in the lungs by the hemoglobin in

Also called a heart attack.

circulating deoxygenated red cells and carried to the peripheral tissues. The process is made possible

Needs assessment:

assessment of the patient's specific

physical, functional, and psychological needs.

Nocturnal ventilation:

because hemoglobin has the ability to combine with oxygen present at a high concentration, such as in the

the selective use of

lungs, and to release this oxygen when the

mcchanical ventilation during the night. Patients with cardiopulmonary dysfunction are at greater risk

concentration is low, such as in the peripheral tissues.

Oxygen transport pathway:

during the night when they are recumbent and the respiratory drive is depressed.

the pathway for oxygcn

delivery to the tissues from the ambient air, through the airways and lungs, across the alveolar capillary membrane, into the pulmonary circulation through

Obesity:

an abnormal increase in the proportion of fat

cells. mainly in the viscera and subcutaneous tissues

the chambers of the heart, via the peripheral and regional circulation to the tissues and the

of the body. Obesity may be exogenous or

mitochondria where oxygen is used in cellular

endogenous. Hyperplastic obesity is caused by an

respiration.

incrcase in the number of fat cells in the increased adipose tissue mass. Hypertrophic obesity results from an increase in the size of the fat cells in the

(I) A goal. (2) Of or pertaining to a

phenomenon

or

a measurement of the amount of

oxygen attached to a hemoglobin molecule.

Oxyhemoglobin dissociation:

the dissociation of

oxygen from the hemoglobin molecule in peripheral

increase adipose tissue mass.

Objective:

Oxygen saturation:

tissues when the concentration of oxygen is low.

clinical finding that is observed; not

subjective. An objective finding is often described in health care as a sign, as distinguished from a

the tissue of an organ as distinguished

from supporting or connective tissue.

symptom, which is a subjcctive finding.

Obstructive lung disease:

Parenchyma:

Parkinson's disease:

a classification of lung

a slowly progressive,

degenerative, neurological disorder characterized by

disease referring to airflow limitation secondary to

resting tremor, pill rolling of the fingers, a masklike

obstruction and increased airway resistance (e.g.,

expression, shuffling gait, forward flexion of the

chronic bronchitis and emphysema).

trunk, loss of postural reflexes, and muscle rigidity

Osteoporosis:

a disorder characterized by abnormal

and weakness. It is usually an idiopathic disease of

rarefaction of bone, occurring most frequently in

people over 60 years of age, although it may occur in

postmenopausal women, in sedentary or immobilized

younger people, especially after acute encephalitis or

individuals, and in patients on long-term steroid

carbon monoxide or metallic poisoning, particularly

therapy. The disorder may cause pain, especially in the lower back, pathological fractures, loss of stature, and various deformities.

Outpatient:

a

facility.

the pressure exerted by an

individual gas, a percent of the total pressure of gases.

patient, not hospitalized, who is being

treated in an olTiec, clinic,

by reserpine or phenothiazine drugs.

Partial pressure of gases:

or

other ambulatory care

Patent ductus arteriosus (PDA):

an abnormal

opening between the pulmonary artery and the aorta caused by failure of the fetal ductus arteriosus to


G-10

Glossary

close after birth. The defect, which is seen primarily in premature infants, allows blood from the aorta to flow into the pulmonary artery and to recirculate through the lungs, where it is reoxygenated and returned to the left atrium and left ventricle, causing an increased workload on the left side of the heart and increased pulmonary vascular congestion and resistance.

Prevention:

any action directed toward preventing

illness and promoting health to avoid the need for secondary or tertiary health care. Primary cardiopulmonary dysfunction: cardiopulmonary dysfunction resulting from a primary condition of the heart, lungs, or both. Pulmonary rehabilitation:

rehabilitation of

cardiopulmonary dysfunction including the acute,

Pediatric cardiac rehabilitation:

specialized cardiac

subacute, and chronic phases of the disease or after

rehabilitation for children instituted in the chronic

thoracic surgery. The long-term management

stage of heart disease or after cardiovascular surgery

includes a comprehensive program of exercise, ventilatory support, additional airway clearance

when the patient is through the acute phase. Pediatric pulmonary rehabilitation:

specialized

pulmonary rehabilitation for children instituted in the

interventions as needed, nutrition, stress reduction, smoking cessation, pacing and energy

subacute or chronic stages of lung disease or after

conservation, vocational rehabilitation, sexual

thoracic surgery when the patient is through the acute

rehabilitation, and education.

phase. Perfusion:

Pulmonary development: the passage of a fluid through a specific

organ or an area of the body. Perioperative complications:

system during nom1al growth and development. complications before,

during, and after surgery. Peripheral circulation:

the anatomical and

physiological development of the cardiopulmonary Pulmonary circulation:

the blood flow through a

network of vessels between the heart and the lungs

the systemic circulation,

which excludes the circulation to the heart and lungs

for the oxygenation of blood and removal of carbon dioxide.

(the central circulation). Peripheral vascular disease:

any abnormal condition

that affects the blood vessels outside the heart and

Quality care:

the provision of holistic care in which

the needs and wants of the patient are considered.

the lymphatic vessels. Pneumonia:

an acute inflammation of the lungs,

usually caused by inhaled pneumococci of the

Recumbency:

species Streptococcus pneumoniae. The alveoli and

Reflex cough:

bronchioles of the lungs become plugged with a

Reliability:

fibrous exudate. Pneumonia may be caused by

the state of lying down or leaning

against something. a cough stimulated reflexively.

the extent to which a test measurement or

a device produces the same results with different

other bacteria, as well as by viruses, rickettsiae,

investigators, observers, or administration of the test

and fungi.

over time. If repeated use of the same measurement

Positron emission scans:

tomographic scans using

positron emitting radionuclides. The tracers used are often taken up in the metabolical pathways of the tissues being studied (e.g., oxygen metabolism or gluclose metabolism). Prescription:

tool on the same sample produces the same consistent results, the measurement is considered reliable. Residual volume: Resources:

an order for medication, therapy, or a

therapeutic device given by a properly authorized person to a person properly authorized to dispense or perform the order. A prescription is usually in written form and includes the name and address of the patient, the date, the [4]+ symbol (superscription),

the volume of air remaining in the

lung after a maximal expiration. services, personnel, and treatment options

that can be drawn on to maximize treatment delivery and effectiveness. Respiratory muscle fatigue:

a loss in the capacity of

a muscle underload to develop force or velocity that is reversible by rest. Respiratory muscles:

the muscles that produce

the medication prescribed (inscription), directions to

volume changes of the thorax during breathing. The

the pharmacist or other dispenser (subscription),

inspiratory muscles include the hemidiaphragms,

directions to the patient that must appear on the label,

external intercostals, scaleni, sternomastoids,

the prescriber's signature, and, in some instances, an

trapezius, pectoralis major, pectoralis minor,

identifying number.

subclavius, latissimus dorsi, serratus anterior, and


Glossary

muscles that extend the back. The expiratory muscles

Sclerodenna:

G-11

a relatively rare autoiuunune disease

are the external intercostals, abdominals, and the

affecting the blood vessels and connective tissue. The

muscles that flex the back.

disease is chaJ'acterized by fibrous degeneration of lhe

Respirator), muscle weakness:

a chronic loss in the

Respiratory mechanics:

the physical properties of

the lung including resistance and compliance

Scleroderma is most common in middle-aged women. Secretion management:

management of airway

secretions.

characteristics. Respiratory failure:

connective tissue of the skin, lungs, and intemal organs, especially the esophagus, digestive tract, and kidneys.

capacity of a rested muscle to generate force.

the inability of the cardiac and

Sedation:

an induced state of quiet, calmness, or sleep,

as by means of a sedative or hypnotic medication.

pulmonary systems to maintain an adequate exchange of oxygen and carbon dioxide in the lungs.

Sepsis and multiorgan system failure:

overwhelming

systemic infection and pathogens leading to failure

Respiratory failure may be oxygenation or

within multiple organ systems.

hypcrcapniac. Treatment of respiratory fai lure includes maximizing ventilation, clearing the airways by suction, bronchodilators, or tracheostomy,

Shock:

an abnormal condition of inadequate blood

flow to the body s peripheral tissues, with life

antibiotics for infections usually present,

threatening cellular dysfunction, hypotension, and

anticoagulants for pulmonary thromboemboli, and

oliguria. The condition is usually associated with

electrolyte replacement in fluid imbalance. Oxygen

inadequate cardiac output, changes in peripheral

may be administered in some cases; in others it may

blood flow resistance and distribution, and tissue

further decrease the respiratory reflex by removing

damage. Causal factors include hemorrhage,

the stimulus of a decreased elevated level of oxygen. Restrictive lung disease:

a category of lung disease

involving restriction of the lung parenchyma and

vomiting, diarrhea, inadequate fluid intake, or excessive renal loss, resulting in hypovolemia. Skilled nursing and rehabilitation facilities:

an

characterized by stiffness (reduced compliance) and

institution or part of an institution that meets criteria

reduced lung volume.

for accreditation established by the sections of the

Rheumatoid arthritis:

a chronic, destructive, sometimes

Social Security Act that determine the basis for

deforming collagen disease that has an autoimmune

Medicaid and Medicare reimbursement for skilled

component. Rheumatoid aJthritis is characterized by

nursing care, including rehabilitation and various

symmetric inflammation of the synovium and increased synovial exudate, leading to thickening of the synovium and swelling of the joint. Rheumatoid arthritis usually

medical and nursing procedures. Spinal cord injury:

any one of the traumatic

disruptions of the spinal cord, often associated with

first appears in early middle age, between 36 and 50

extensive musculoskeletal involvement. Common

years of age, and most commonly in women. The

spinal cord injuries are vertebral fractures and

course of the disease is variable but is frequently

dislocations, such as those commonly suffered by

marked by remissions and exacerbation.

individuals involved in car accidents, airplane

Risk factors:

factors that cause a person or a group of

crashes, or other violent impacts. Such trauma may

people to be particularly vulnerable to an unwanted,

cause varying degrees of paraplegia and

unpleasant, or unhealthful event, such as

quadriplegia. Treatment of spinal cord injuries varies

immunosuppression, which increases the incidence

considerably and involves numerous approaches,

and severity of infection, or cigarette smoking, which

such as exercise, ambulatory techniques, and special

increases the risk of developing a respiratory or

physical and psychological therapy.

cardiovascular disease. Routine body positioning:

Stable angina:

the routine use of body

positioning in the management of patients to

anginal pain that is well-controlled,

medically stable, and has a predictable activity/exercise threshold.

minimize the negative effects of static positioning

Status asthmaticus:

an acute, severe, and prolonged

and maximize comfort. The purposes of routine body

asthma attack. Hypoxia, cyanosis, and

positioning are distinct from the specific goals of

unconsciousness may follow. Treatment includes

prescriptive body positioning, which are related to

bronchodilators given intravenously or by aerosol

optimizing particular components of

inhalation, corticosteroids, controlled positive

cardiopulmonary function and gas exchange.

pressure ventilation, sedation, frequent therapy,


G-12

Glossary

and emotional support. A bronchodilator may be

myocardium based on perfusion of the area. This

given by aerosol inhalation from a ventilator.

agent can be used for rest studies, exercise stress

Stroke volume (SV):

the amount of blood ejected

Stunned myocardium:

contractile dysfunction of the

myocardium as a result of an acute episode of ischemia that persists even after perfusion has hospitals that specialize in the

the diaphragm, and associated muscles.

Thoracic surgery:

the branch of medicine that deals

manipulative and operative methods.

Throat clearing:

management of nonacute conditions.

Subjective:

the cavity enclosed by the ribs, the

thoracic portion of the vertebral column, the sternum,

with disease and injuries of the thoracic area by

returned to normal.

Subacute hospitals:

studies, and pharmacological stress studies.

Thoracic cavity:

from the ventricles during systole.

the spontaneous elicitation of a

(I) Pertaining to the essential nature of an

coughlike maneuver to clear secretions or an

object as perceived in the mind rather than to a thing

obstruction from the oropharynx that may be

(2) Existing only in the mind. (3) That

in itself.

which arises within or is perceived by the individual,

threatening the upper airway.

Tidal volume (TV):

the amount of air inhaled and

as contrasted with something that is modified by

exhaled during normal ventilation. Inspiratory

external circumstances or something that may be

reserve volume, expiratory reserve volume, and tidal

evaluated by objective standards.

Suctioning:

volume make up vital capacity.

the use of mechanical airway suctioning

that uses a catheter and negative pressure to remove oropharyngeal or airway secretions when the patient is unable to spontaneously or voluntarily take deep breaths and cough effectively.

Supraventricular:

pertaining to a feature or event

the branch of medicine concerned with

diseases and trauma requiring operative procedures.

Syncytium:

the volume of gas in the

lungs at the end of a maximum inspiration. It equals the vital capacity plus the residual capacity.

Tracheobronchial tree (TBT):

an anatomic complex

that includes the trachea, the bronchi, and the

occurring superior to the ventricles of the heart.

Surgery:

Total lung capacity (TLC):

the arrangement of cells, as in the

myocardium, such that stimulation of one cell causes

bronchial tubes. It conveys air to and from the lungs.

Tracheostomy:

an opening through the neck into the

trachea through which an indwelling tube may be inserted.

Tracheostomy tube/cuff:

a tube/cuff that is

positioned directly through the trachea in the neck to

stimulation of adjacent cells, thus causing an action

provide a functioning airway that bypasses the nares

potential to spread from the initial focus.

and oropharynx.

Systemic disease:

dysfunction or condition affecting

one or more systems.

Systemic lupus erythematosus (SLE):

Transitional care units:

settings that specialize in

providing care between the acute, subacute, and a chronic

inflammatory disease affecting many systems of the body. The pathophysiology of the disease includes severe vasculitis, renal involvement, and lesions of the skin and nervous system. The primary cause of

long-term stages of a patient's illness.

Transitional circulation:

a transition from one type

of blood vessel to another on moving peripherally through the circulation.

Treatment selection and prioritization:

the process

the disease has not been determined; viral infection

of selecting treatments and then prioriti7.ing the order

or dysfunction of the immune system has been

in which these treatments are administered. This

suggested. Adverse reaction to certain drugs also

process is based on the relati ve contribution of the

may cause a lupus like syndrome. SLE occurs four

pathogenesis that each treatment addresses with

times more often in women than in men.

respect to oxygen transport deficiencies.

Trunk-ventilation interaction: Tachycardia: an abnormally rapid heart rate. Tachypnea: an increased respiratory rate over 20 breaths per minute.

Thallium-20l scan:

the interrelationship of

the shape and movement of the trunk or chest wall on alveolar ventilation. Trunk and ventilation interaction depends on body positioning and movement.

a radionuclide scan that evaluates

myocardial perfusion. The tracer is taken up in the

Tuberculosis: callsed by


an

a chromic granulomatous infection acid-fast baci Ilus, mycobacterium

Glossary

tuberculosis, generally transmilled by the inhalation or ingestion or infected droplets and usually affecting the lungs, although infection of multiple organ systems occurs Type I fibers: a type of skeletal muscle fiber that is also called slow-twitch and is suitable for sustained .

tonic activity (e.g., the maintenance of posture or breathing, which require resistance to fatigue). Type IlA fibers: a type of skeletal muscle fiber that is also called fast-twitch; this type of fiber is used for short-term, fast, powerful activity in which endurance to fatigue is not required. Validity:

the extent to which a test measurement or

other kind of device measures what il is intended to measure.

G-13

with high, intermediate, or low probability of pulmonary embolus. Ventilation and perfusion matching: the matching of ventilation and perfusion in the lungs. Optimal ventilation and perfusion matching occurs in the mid zones of the upright lung where the ratio is 0.8 to 1.0.

a measurement of the amount of air that can be expelled at the normal rate of exhalation after a maximum inspiration, representing the greatest possible breathing capacity. The vital capacity equals the inspiratory reserve volume plus the tidal volume plus the expiratory reserve volume.

Vital capacity (Ve):

The average normal values of 4000 to 5000 ml are affected by age, physical dimensions of the chest cage, posture, and gender. The vital capacity may be

an acquired or congenital disorder of a cardiac valve, characterized by stenosis

reduced by a decrease in functioning lung tissue,

and obstructed blood flow or by valvular

pneumonia, pulmonary resection, or tumors; by limited chest expansion, resulting from ascites, chest deformity neuromuscular disease, pneumothorax, or pregnancy; or by airway obstruction.

Valvular heart disease:

degeneration and regurgitation of blood. the process by which gases are moved into and out of the lungs. Ventilatory strategies: teaching patients to control breathing with the utilization of ventilatory patterns (e.g., combining inspiration with trunk extension and

Ventilation:

exhalation with trunk l1exion). two scans which are used to assess patients for the presence of pulmonary emboli. Criteria (BIELLO or PIOPED) are used to determine if matched defects present

Ventilation-perfusion scan:

resulting from atelectasis, edema, fibrosis,

the total amount of effort required to expand and contract the lungs; the physiological "cost" of breathing. Generally, quiet

Work of breathing:

breathing consumes 2% to 3% of the oxygen consumption and requires 10% of the vital capacity. If a greater amount is used, one would say the work of breathing is increased.


I N D E X

bronchiOlitis, 477

A

bronchitis, 476--477

Abscesses

chronic airflow limitation, 478--481

radiography of, 164, 164

chronic bronchitis, 476--477

respiratory failure and, 579,580t, 581

cystic fibrosis, 483--486

AC; see Assisted control (AC)

ACB;

see

emphysema, 478--481

Active cycle of breathing (ACB)

hypertension, 488

Acetylcholine, pharmacology of, 780

Acetylcysteine (Mucomyst), pharmacology of, 786

Acid base balance

in arterial blood

gases, 153,154

tuberculosis, 487--488

Acute surgical conditions, primary dysfunction secondruy to, 495-508

respiratory failure and, 619

cardiovascular surgery, 501-502

symptoms of, 236t

extrinsic factors, 500

Acidosis, anaerobic metabolism and, 6

Acquired immunodeficiency syndrome (AIDS); see AIDS sec

Airway clearance

techniques (ACT)

Acute dyspnea, patient history and, 130

Acute heart failure, pathophysiology of, 93

Acute medical conditions, primary dysfunction secondary to,

469-492

alveolitis, 477-478

angina, 488-490

asthma, 481-483

atelectasis, 470--472,471

pathophysiology, 500

postoperative management, 502,502-505, 506, 507

in airway clearance, 325-326

clinical applications of, :149-352, 350, 35 I

intrinsic factors, 500

mobility/recumbency, 500

perioperative course, 496, 496-500, 498

Active cycle of breathing (ACB)

alveolar proteinosis, 478

myocardial infarction, 490-491

pneumonias, 472--476

ICU, and, 236, 2361

Active assistivc cough techniques;

interstitial pulmonary fibrosis, 486

preoperative management, 502

surgical effects, 500

surgical prep, 499

thoracic, 500--502 AD; see Autogenic drainage (AD)

Adenosine, for stress testing, 199

Adenosine triphosphate (ATP)

nuclear imaging and, 203

in oxygen transport, 4, 6-11,13,18

i

Adenosinetriphosphatase pump, tha lium 20 I'and, "200--20 I

1-1


1-2

Index

Adolescents, myelomeningocele in, 646, 646

anterior chest compression, 375, 375

Adrenal runetion

co stoph renic, 373, 373-374

cardiopulmonary effects of, 109-110, 110

counter rotation, 375, 376,377

laboratory tests in,193t, 194

hands-knees rocking,38 I -382

Adrenergic drugs, pharmacology of,777-778

Heimlich, 374, 374-375

Adult respiratory distress syndrome (ARDS); see also Respiratory

long silting self, 379, 379-380, 380

distress syndrome (RDS)

prone on elbows, 378, 378-379

management of, 625, 625--627

self, 377-382

Adventitious breath sounds, patient assessments and,219-220

associated with eating/drinking, 368

Aerobic capacity, cardiac aging changes and, 671,671--674,673,673t

complications, 368-369

Aerobic metabolism, in oxygen transport, 6-8, 10-11

evaluations, 369-371

Aerosol therapy

infants, 653, 657

defined, 755-756, 756

patient instruction, 371-372

for oxygen transport treatment, 259-260,260

pumps, 368

precautions in, 756

stages of, 369-371

Afterload

physiology and, 321-334

cardiopulmonary physiology of. 65

active cycle of breathing, 325-326

oxygen transport and, 13

assessments,334

Aging changes

autogenic drainage,326-327

cardiac, 670, 670-671

contraindications. 330, 330-334

aerobic capacity, 671,671--674,673, 673t

exercise, 329-330

vascular/autonomic, 673, 673-675, 674t

factors affecting, 332, 332-334

pulmonary, 674--677, 675, 675t

The Flutter"", 328

high frequency chest compression. 328-329

exercise, 675-677, 677, 677t

AIDS; see also HIV

indications, 322-323

cardiopu Imonary effects of, 110

manual hyperventilation, 325

galliu III scintigraphy for, 206

percussion, 323-324

Air, ambient; see Ambient air

positive expiratory pressure,327-328

Air-conditioned environments, oxygen transport and, 16

postural drainage, 323, 324

Air flow measurements

shaking, 325

airway closure volume, 149,149-150

vibration, 324-325

flow volume curve, 147, 148,149

Airway closure volume tests, 149, 149-150

forced expiration, 147

Airway obstructive diseases,drugs for, 784-785

Airway p re s sure release v e ntila t i o n (APR V), defined, 758

Airway clearance techniques (ACT) clinical applications of, 339-365,365t

Airway resistance,physiology of,58-59, 59

active cycle breathing,349-352, 350, 35 I

Airways, al1ificial; see Artificial airways

assessments, 364

Akinesia, nuclear imaging of, 200

autogenic drainage, 352-354, 355

Albumin

costs,363

laboratory tests of, 190, 191t

dynamic air therapy bed,363-364

in oxygen transport, 15

effectiveness, 362

for plasma volume, 234

exercise,359-361, 361t

Albulerol (Proventil, Ventolin), pharmacology of, 778

future trends, 363

Alkaline phosphatase, laboratory teSls and, 194, 194t

high frequency chest compression, 358. 358-359

Alkalosis, intensive care of, 579, 580t, 581

intrapulmonary percussive ventilator, 363,364

Allergies, treatment of, 784

manual hyperinflation, 348, 348-349

Alpha-adrenergic blocking drugs, pharmacology of, 778-779

percussion, 344-346,345

Alternative long-term care facilities; see Long-term care facilities

positive expiratory pressure, 354-358,355

Alveolar diseases,radiography of, 162, 162

postural drainage, 340, 340-344, 341,342

Alveolar ducts, anatomy of, 42t, 44

selection of,361,361

Alveolar proteinosis

support, 362-363

management of, 478

utilization of,340

pathophysiology of,86, 86-87,478

vibration/shaking,346-349, 347, 348

cough/suction for, 367-382

active assistive, 373-382

Alveolitis

management of,478

pathophysiology of, 477-478


Index

chronic secondary dysfunction and

Ambient air, oxygen transport and, 15-16

management of, 558

threats/treatment, 261


Aminoglycusides, intensive care and, 579,580t,581 Aminophylline, pharmacology of, 785

Anorexia nervosa, cardiopulmonary effects

Amphctnminc (Dextroilmphetamine, Dexedrine), pharmacology

ANS; see Automatic nervous system (ANS)

0 1',

1 10-11 1 , II I

Anterior chest compression, 375, 375

uL 77R Amylase, lahoratory tcsts of, 193t, 193-194, 194t

Antianginal agents, for reus, 572-573

Anaerobic Illcwh"lism. in oxygen transport, 6-8, 10-11. 13

Anticholinesterases, pharmacology of, 781

Analgesic

Antihistamines, corticosteroids and, 785-786

for leUs, 572-573 fur oxygen transport treatment 259-260, 260 Anaphylactic rc·actions. trcatment of.777 Anatomy

Antiinflammatory agents for oxygen transport treatment, 259-260, 260 treatment with, 784 Anxiety, oxygen transport threats and, 255

bronchopulmonary segment, 4 I, 42t, 43. 44

Aortic volume, cardiopulmonary physiology of, 66, 66

canliupulmonary.2-'-50

Apnea

circulation. 48--50 heart. 44-4R,45,46,47,48 fetal,6Je)

cardiopulmonary effects of, 109 patient asseSSlnents for, 216 respiratory failure and, 579, 580t, 581

lungs.40-A4. 41. 42t, 43

Appearance, patient assessments and, 212-213

lymphatic circulation, 50

APRY; see Airway pressure release ventilation CAPRY)

muscle" 26--40

Arrhythmias

diaphragm, 26, 2li28. 27, 28 erector spi nac 30. 3 I ,

expiration, 27. 31-32 inspiration, 26 intercostal>. 2R, 29

electrocardiograms and, 177, 178, [79-184,179-184 supraventricular. 177, 178, 179,179,180,181 ventricular, 180-184, 182, [83, 184 intensive care of, 236, 236t, 239 pathophysiology of, 91-92

larynx. 35. 1536

Arsenic, respiratory failure and, 579, 580t,581

lower airways. 36--40, 37,39t

Arterial blood gase s 153-157 ,

nose, 32-34, 33, 34

acid base balance and, 153- [54

pectoralis major, 29, 30

assessment purpose in, 153, 157

pe<:toralis minor, 30

chemoreceptorslhypoxemia response and, [55

pharynx, 33, 34-35

excess/deficit in, 154

ribs. 24-25, 25y

factors affecting, 156-157

scalenes, 29, 29

hemoglobin and, 155

serratus antcrior. 29-30

interpretation of, 155-156

sternocleidomastoid, 28-29.29

normal values in, 154

trapezius. 30. 30

partial pressure of, 154-155

nerve system, 47,47--48. 48

renal buffering and, 154

patient assessments and, 210-211, 21 I, 212, 213


pediatric, 1,36-637 thorax, 23-25. 24, 25 Anesthetics

in secondary dysfunction, 427 Arteritis, cardiopulmonary effects of, 102-103, 103 Artificial airways,761-774

cpinephrine and, 777

care of, 768

respiratory failurc and, 579. 580t, 581

endotracheal,772 extubationldecannulation and, 773-774

Angina chronic primary

history of, 76 I

management of, 525-526

Montgomery T tubes and, 768

pathophysiolugy of, 525

nasopharyngeal,772

management of, 489--490 pathophysiology of. 90-91. 488--489 Angiography cardiovascular, 20 [t, 205 respiratory, 206 Ankylosing spondylitis cardiopu lmonary effects of. 102-103, [03

Olympic tracheostomy buttons and, 766, 767,768, 768 Passy-Muir valves and, 766, 767,768, 768 postoperative complications of, 763-764 mechanical, 764 suctioning of, 768,769-771,77 1 ,772, 773, 773t tracheostomy tubes and,764-766, 765,767-771, 768, 77 [-774, 773t


1-3

1-4

Index

use of, 761-764, 762

B

Aspiration

Bacterial pneumonias

GI dysfunction and, 107


infant aspiration pneumonia in, 642

meonium aspiration syndrome (MAS), management of,

641-642

Aspiration pneumonia, pediatric, 642

Assessments;

see also

specific value being tested, e.g., Blood

gases, arterial multisystem laboratory,

Barbiturates, respiratory failure and, 579, 580t,581

Baroreceptors, defined, 783

Barrel chest, patient assessments for, 214-2 I 6,216

J 89-195

Basal metabolic rate (BMR), in oxygen transport, 19

Assisted control (AC), defined, 758

Beclomethasone, pharmacology of, 785

Assisted mechanical ventilation, defined, 758

Bed rest

Asthma

alternatives to, 293-294

chronic primary

hazards of, 293

management of, 5 I 9-520

pathophysiology of,S I 9

indications for, 294

as therapy, 291-292

pathophysiology of, 77-80, 78, 79, 80,481-483

Benztropine mesylate (Cogent in), pharmacology of, 783

pediatric, 642-M3

exercise for, 660--66 I

Beta-adrenergic blocking drugs, pharmacology of, 778-779

Beta-blocking agents, for ICUs, 572-573

primary, management of, 483

primary/ICU, 589-59 I


Bagging, obstructive lung disease and, primary/lCU, 587

Beta2-receptor stimulants, pharmacology of, 778

Bethanechol (Urccholine), pharmacology of, 780


Blood

pathophysiology of, 589

complete count, 190--192, 191t

treatment of, 777,784

desaturated, 19

beta2-receptors stimulants for, 778

laboratory tests of, 190-- I 92, 191t

Asymmetrical dysfunction, facilitation and, 405-406

oxygen transport and,

Atelectasis

differential diagnosis of, 227t

flow, 12, IS

management of, 472

hematocrit, 14

pathophysiology of, 470-472,471

hemoglobin, 11-12,14-15,155

radiography of, 164-165, 165,166

respiratory failure and, 579, 580t, 58 I

plasma, 11-12,15


Atenolol (Tenormin), pharmacology of, 779

viscosity, 14

Atherosclerosis, pathophysiology of, 89-90

volume, 13-15

Atmospheric air content, oxygen transpol1 and, 15-16

Blood gases, arterial, 153-157

ATP; see Adenosine triphosphate (ATP)

acid/base balance of, 153-154

ATPase pump, thallium 201 and, 200--201

assessments of, 153, 157

Atrial pressure, left, ICU measurement of, 24 I -243

Atrioventricular (A V) conduction, electrocardiograms and, 170-172

Atropa belladonna, extract of, 782

hemoglobin in, 155

Auscultation, 217,217-221, 2J8, 219

ICUs and, 236-237

breath sounds, 218-220, 219

interpretation of, 155-156

chest sounds, 217-218

normal values in, 154

heart sounds, 221-222

partial pressure of, 154-155

secondary dysfunction and, 427

renal buffering and, 154

stethoscope use in, 2 I 7,217


techniques for, 217, 218

Blood loss, dextran for, 234


Blood pressure, oxygen transport threats and, 254


Blood urea nitrogen (BUN), laboratory tests of, 192, 192t

clinical applications and, 352-354, 355

Automatic nervous system (ANS), oxygen transport and, 19

Autonomic nervous system, systemic disease effects on, 106-107

A V conduction; see Atrioventricular (AV) conduction

base excess/deficit of, 154

chellloreceptors/hypoxemia responses in, 155

factors affecting, 156-157

AU'opine, pharmacology of, 782

Azathioprine, for organ transplants, 718

I 1-15

cardiopulmonary physiology of, 67-68,68

BMR; see Basal metabolic rate (BMR) Body mechanics; see Positioning, body mechanics Body positioning; see Positioning BPD; see Bronchopulmonary dysplasia (BPD) Bradydysrhythmias, intensive care of, 239, 240t-241 t


Index

Bradypnea, patient assessments for, 216

future trends in, 363

Breath sounds, patient assessments and, 218-220, 219

high frequency chest compression, 358, 358-359

abnormal, 219

intrapulmonary percussive venti lators, 363, 364

adventitious. 219-220

manual hyperinflation, 348,348-349

bronchial, 218

percussion, 344-346, 345

bronchovesitular,218

positive expiratory pressure,354-358, 355

extrapulmonary,220

postural drainage, 340, 340-344, 341, 342

vesicular, 218-219

selection of,361, 361

voice. 220

support, 362-363

Breathing

utiliwtion of, 340

control in, 53-55,54

vibration/shaking, 346-349. 347,348 cough/suction, 367-382

exercise testing/training in primary dysfunction, 420, 420-421


seconoary dysfunction,435-436

complications of, 368-369

glossopharyngeal, 410-412,412

costophrenic, 373,373-374

laterRI costal facilitation of, 396, 397, 399, 399

counter rotation,375, 376, 377

mechanical function 01',56-59,57,58,59

eating/drinking type, 368

oxygen transport treatment and, 261

evaluation of, 369-371

patient assessments and, 216

hands-knees rocking,381-382

patterns

Heimlich, 374, 374-375

musculoSKeletal/neuromuscular disorders,689, 691-693, 692,693,694,695

long sitting, 379, 379-380, 380 patient instruction and, 371-372

paced,435-436


paradoxical. 438-439

pumps, 368

physiology of, 321-334 active cycle of breathing,325-326 assessments in, 334

self, 377-382 stages of, 369-371 Bronchi, radiography of, 162, 162

autogenic drainage, 326-327

Bronchial breath sounds, patient assessments and,218

contraindications for,330,330-334

Bronchial muscle relaxants

exercise, 329-330 factors affecting, 332,332-334 The F1utterT", 328 high frequency chest compression, 328-329 indications for, 322-323 manual hyperventilation and, 325 percussion and, 323-324 positive expiralOry pressure, 327-328 postural drainage and, 323, 324

ephedrine as, 778 inhaler treatment and,784, 785 Bronchiectasis chronic primary management of, 520-521 pathophysiology of, 520 pathophysiology of, 80, 80-83, 81 mdiography of, 162, 163, 164 Bronchiolitis

shaking and, 325

acute medical conditions, primary secondary to, 477

vibration and, 324-325


repattcrning in, 393

management of, 477

secondary dysfunction

pathophysiology of,477

exercise testing/training and, 435-436 paced,435-436 systemic disease effects on, 104 Breathing clearance techniques active assistive, 373-382 airway (ACT), 339-365, 365t active cycle breathing, 349-352, 350,351 assessments of, 364 autogenic drainage, 352-354, 355

Bronchitis chronic differential diagnosis of,227t management of, 515-516 pathophysiology of, 72-73,76-77, 514-515 chronic primary management of, 476-477 pathophysiology of, 476-477 Bronchodilators

costs, 363

betarreceptors stimulants as, 778, 779

dynamic air therapy bcd, 363-364

for leUs, 572-573

effectiveness of, 362

metered-dose inhalers, 723-724

exercise, 359-361, 361t

for oxygen transport treatment, 259-260, 260


1-5

Index

1-6

Bronchograms,radiography of,162, 162

arrhythmias,91-92

Bronchopulmonary dysplasia (BPD),preterm infants and,641

chronic hean failure,93-94

Bronchopulmonary segments, anatomy of,41,42t, 43,44

compensated/decompensated heart failure, 94

Bronchovesicular bn:ath sounds, patient assessments and,218

congestive heart failure, 93

Buildings,health issues and,16

coronary artery disease, 89-90, 91-94

Burns


respiratory failure and, 579,580t,581

patient classification and,133

secondary dysfunction and

patient history and, 133

pediatric,639t,639-640

management of,613-615

pathophysiology of, 612--{)13

respiratory failure and,620

BUlleLfly techniques,ventilation facilitation and,408,409,410

systemic, 100-101

fluid balancc effects of,101

c

ischemic, 109

II C acetate,for cardiovascular testing,201t,203

Cardiac function

CAD; see Coronary artery disease (CAD)

afterload in,13

Cameras, for nuclear imaging,198-202

aortic volume and,66, 66

Capillary function,in oxygen transport,18

cardiopulmonary physiology of, 65,65-67,66, 67t

Carbachol (Carcholin),pharmacology of,780-781

electrocardiograms and, 169-187

Carbohydrates,laboratory tests of,194, 194t

arrhythmias, 177,178,179-184,179-184

Carbon dioxide

conduction, 170-172,171

blocks, 184--186, 185, 186

ambient air/oxygen transport and,15-16

transport physiology of,68-69

evaluation of, 174, 174--177,175,176,177

Carbonic anhydrase,in C02/H02 reactions, 14

myocardial infarction, 186-187, 187

Cardiac aging changes

rate, 174, 174-176, 175, 176

aerobic capacity,671, 671-674, 673,673t

recording, 172, 172-174,17,1

defined,670, 670-671

rhythms, 176- 177, 177

use of, 169-170

vascular/autonomic, 673, 673-675, 674t

heartbeat physiology and, 66

Cardiac arrest, treatment of, 777

left atrial pressure, 241-243

Cardiac aLThythmias

electrocardiograms and, 177, 178, 179-184, 179-184

supraventricular, 177,178, 179, 179, 180, 181

myocardial contractility in, 13

myocardial viability and, 202-203

myocardial workload reduction and,592, 59l-594, 596

ventricular, 180-184, 182, 183, 184

intensive care of, 236, 236t,219

nuclear imaging of,200


output in, 11,12,14,17,636

patient assessments in,220-221

respiratory failure and,619-620

preload, Il

Cardiac development anatomy of,44-48,45,46,47,48

septal defects/ICU and,245

fetal, 636

ventricular

diastole/systole,66

neonatal,636

left assist devices/lCU,245

Cardiac disorders

dyspnea/patient history and,134

left ejection fraction, 200

exercise testing/training in, primary dysfunction,419

left end diastolic volume, 13

fluid balance effects of,101

left fetal anatomy of,636

functional/therapeutic classification of, 133

left output,636

ischemic,109

left pressure/ICU, 241-243, 245

left ventricular assist devLces,245

right ejection fraction, 200

right pressure/1CU,241-243


chronic primary dysfunction and,526-528

Cardiac sounds,patient assessments and,221-222


Cardiac surgery

pathophysiology of,91-93,490

myocardial ischemia,245

oxygen transport threats and,254

treatment,261

pathophysiology of

acute heart failure, 93

ICUs and, 245

open heart, 595,596

CaJdiac transplants

acute phase care in,710-7 I 1,714

assessments in,708

considerations jn


Index

availability. 704

lCUs and

ethical. 704-705

monitoring systems, 229-246

organ donation, 704

patient management, 565-577

organ preservation, 704

primary dysfunction, 579-596

patient education, 706

incentive spirometry and, 754, 755

p ychosocial impl icat ions, 705-706

intermittent positive pressure breathing and, 753-755

purpose of. 704

laboratory assessment and, 189-195

trcnds in. 706

lung injury and, 625, 626

waiting list criteria. 705. 705

measurements and, I 17-123

waiting time. 705

mechanical ventilation and, 756-759

when to

musculoskeletal/neuromuscular disorders and. 679-701

lise,

704

equipmcnt/monitoring in, 708-709

neonatal, 635--{i63

cxercise guidelines in. 712

nuclear imaging/radiopharmaceuticals and. 197-207

facility vs. home based rehabilitation in, 716-718

organ failure and, 628t, 628--{i29

goals in. 712

oxygen thera py and, 749-753

history of. 704

oxygen transport in, 3-20

interventions in. 710-711, 714

pathophysiology of, 71-95, 251-263

medication in. 716-718

patient assessments in. 209-228

other tr lI1splants and, 709-710

patient education and, 453-463

outpatient care in, 713-714, 714

patient history in, 127-142

pos t-transplant care in , 70S

pediatric, 635-663

pre-transplant care in. 70H

physical therapy role in, 3-20

rej ec tion signs in, 714, 715, 716

physiology in, 53--{i9

surgery and, 706

positioning and, 299-318, 737-747

therapy in

postoperative complications and, 621, 621-624, 622

assessments, 707-708

primary dysfunction and

tlefined, 708-709, 710. 710-713

acute medical conditions and, 469-492

medical management. 707, 707t

acute surgical conditions and. 495-508

musculoskeletal considerations, 707, 709-710

chronic, 513-535

physiology and, 707

ex e rcise testing/training in,417-423 rcus and, 579-596

therapist rt' quiremcnts, 706 Cardiogenic shock. ICUs and, 245

pulmonary aging changes and, 674-677

Cardiopulmonary failure, primary. intensive care of, 579, 580t, 581

pulmonary function tests and, 145-151

Cardiopulmonary function

respiratory failure and, 617--{i30

acute medical conditions and, 469-492

respiratory muscle fatigue and, exercise training,443-451

acute surgical conditions and, 495-508

secondary dysfunction in

aerosol therapy and, 755-756, 756

chronic, 537-561

airway clearance techniques and, 339-365, 365t

exercise testing/training in, 425-441

cough/suction, 367-382 physiology,321-334

lCUs, 599-615 sepsi:; and, 628t, 628-629

anatomy in. 23-50

shock and, 627--{i28

arterial blood gases in, 153-157

systemic diseases and, 99-112

artificial airways and, 761-774

transplant patients and, 703-718

cardiac aging changes and. 671--{i74

treatment in, 256-263, 257,258-259,260,261,262

chronic primary dysfunction and. 513-535

ventilation facilitation and, 383-415, 756-759

chronic secondary dy sfunction and, 537-561

x-ray interpretation, 159-167

documentation and, 12:1-126

Cardiovascular disease, chronic primary

drug and,775-7R6


exercise/mobility and. 265-296


exercise testing/training in

pri mary dysfunction. 417-423 secondary dysfunction,425-441

Cardiovascular reflex, defined, 783-784 Cardio va:;cular su rgery , p rimary dysfunction secondary to, 501-502

horne-based/facility care and, 721-732

Carotid barorece ptors, defined. 783

humidity therapy and, 755

Carrying, primary dysfunction and, 4 I 9-420


1-7

1-8

Index

Cascade oxygen, defined, 12, 12

ventilation facilitation and,392

Case studies

Chest tubes, in ICUs, 235, 235-236

exercise testing/training in, secondary dysfunction, 437--440.

438,439

Chest walls

oxygen transport and, 16-17

patient assessments and, 225-228

patient assessments and, 214-216, 216

Catecholamines, laboratory tests of,194

restriction effects on, 102-103, 103

Catheters,in (CUs

Chloroflurocarbon propellants, for metered-dose inhalers, 786

Swan Ganz,233,241-243, 243

Cholesterol,laboratory tests of, 191, 191 t

two-lumen, 241-242

Cholinergic blocking drugs,pharmacology of, 782

CBC; see Complete blood count (CBC)

Cholinergic drugs,pharmacology of,780-781

Cellular respiration

Chronic airflow limitation

oxygen transport and, 3, 4-8, 10

management of, 481

oxyhemoglobin dissociation and, 15

pathophysiology of, 478--480.514

Cellular responses, exercise and. 269-270

Chronic airway obstruction disease (COA), pathophysiology of,

Central chemoreceptors, cardiopulmonary physiology of,54

71-72

Chronic bronchitis

Central nervous system (CNS)

amphetamines and,778




treatment of, 261

pathophysiology of, 72-73,76-77,514-515

systemic disease effects on, 103,105-106

primary

Central venous pressure (CYP), ICUs and,243-244

management of, 476--477

Cerebral palsy

pathophysiology of,476--47 7

cardiopulmonary effects of, 104

Chronic heart failure (CHF),pathophysiology of, 93-94


Chronic obstructive airway di se a se (COAO), pathophysiology of,


71-72


Chronic obstructive lung disease (COLD), 71-72

Cerebrospinal fluid (CSF), cardiopulmonary physiology of, 54

CF; see Cystic fLbrosis (CF)

patient assessments in, 214-2 J 5,222,224

Chemical vagotomy, defined, 783

Chemoreceptors

respiratory failure and, 579, 580t.581

cardiopulmonary physiology of

Chronic primary dysfunction

central, 54

angina,525-526

peripheral, 54-55

asthma,519-520

response to hypoxemia and, 155

bronchiectasis, 520-521

Chest development, in musculoskeletaVneuromuscular disorders,

682-689,684-689,686t

Chest pain, patient history and, 137-138

esophageal, 139


Chronic obstructive pulmonary disease (COPO)

chronic airflow limitation, 514

chronic bronchitis, 514-516

cystic fibrosis, 521-522

diabetes mellitus, 533-535

pericardial,139

emphysema, 516-518

pleuritic,138

hypertension, 531-533

pulmonary hypertension, 139

interstitial lung disease, 522-523

Chest radiographs, lateral, 159-160

lung cancer,523-524

Chest sounds, patient asse ssments and, 217-218

myocardial infarction,526-528

Chest therapy

obstructive patterns in, 514-522

child, 657-660, 658

peripheral vascular disease,529-531

positional rotation, 658-659,659, 660

primary cardiovascular disease, 525-535

pre/postoperative, 659-660

restrictive patterns in, 522-523

compression

anterior, 375, 375

valvular disease, 528-529

Chronic renal insufficiency, chronic secondary dysfunction and

high freq uenc y, 358, 358-359

infant

airway suctioning, 653, 657



Chronic secondary dysfunction

percussion, 652---{i53, 657

ankylosing spondylitis and, 557-558

positional rotation, 649,649,650-651

cerebral pal sy and, 546-547

postural drainage, 652,653t, 654---{i56

chronic renal insufficiency and, 560-561


Index

L ollagen v
ischemic heart disease and, 109

hemiplegia and. 541-543


Intc sequelae or poliomyd itis and. 550-552

pleural effusions and, 101

lllltitirk sL'icrosis and, 544-546

primary/lCU, 594, 594, 596

l11usL'lIlar dystrophy and, 5]8-5]9

radiography of, 164 165, 166,167 ,

osteoporosis and, 553-555

Connective tissue disorders chronic secondary dysfunction and

P

scleroderma

spinal L'Ilrd injury and. 54t\-550

systemic, cardiopulmonary effects of, 103, 103

systemic lupus erythematosus ancl. 555-556

Consumption, oxygen; see Oxygen, consumption

thoracic JdUllllitics and, 552-553

Content, oxygen; see Oxygen,content Continuous positive airway pressure (CPAP)

Circul'ltion anatomy in. 40-49

defined, 758

fetal. 636


neo nata l, 636-6]7

Controlled mechanical ventilation (CMV), defined, 758

peripheral

Contused lung, respiratory failure, 579, 580t, 581

anatomy in. 4R-49

COPD; see Chronic obstructive pulmonary disease (COPD)

in oxygen tJ'ansrort, 18

Coronary artery disease (CAD)

physiology of, fl7, 67t

associated conditions of, 90-94

threats/trealment,262

cholesterol and, 191, 191 t

pulmonary. threats/treatment, 261

pathophysiology of, 71,89-90,91-94

Clol1idine (Catarrcss), pharmacology of, 779

primary/lCU management of, 593-596

Closing volumL'fairway closure, pulmonary function tests and, 149, 1 49 150


Closure of ductus arterimus, pediatric anatomy and, 636---63 7 Closure or' foramen ovale, pediatric anatomy and,636---637

single photon emission tomography (SPECT) for, 199 transplant medication and, 716

Clubbing

Corticosteroids

Crohn's disease and, 214, 214

Cushing's syndrome and, 785

hepatic fibrosis and. 214, 214

pharmacology of, 785 Costophrenic assist techniques, 373, 373-374

patient assessments for, 214, 214 CMY; see Controlled mechanical ventilation (CMY)

Costs, airway clearance techniques and, 363

CNS; see Central nervous system (CNS)

Cough

COA; see Chronic airway obstruction disease (COA)


COAD; see Chronic obstructive airway disease (COAD)


Co gulation, laboratory tests and, 190, 191t

costophrenic, 373, 373-374

Cognition, oxygen trans port threats and, 255

counter rotation, 375, 376, 377

COLD; see Chronic obstructive lung disease (COLD)

hands-knees rocking, 381-382

Collagen vascular/connective tissue diseases. chronic secondary dysfunction and

Heimlich, 374, 374-375 long sitting self, 379, 379-380, 380



pathorhysiology of, 555

self, 377-382

Collimatol.s. Jcfined, 19R

complications of, 368-369

Combined ventriL'ular output (CVO), fetal anatomy of, 636

eating/drinking and, 368

Community concerns. home-based/facility care, 721-7]2

evaluation of,369-371

Complete blood count (CBC), laboratory tests and, 190-192 191t ,

in museuloskeletalfneuromuscular disorders, 698

Comrliance, cardiopulmonary physiology or. 56-57, 57

obstructive lung disease and, primary/lCU, 588

Computerized tomography (CT), for respiratory use, 206-207

patient history and, 135, 136t, 137

Conduction, ck troeardiograrns and, 1 70- 172 171 ,

blocks, 184-186, 1 5, 186 CongenitaJ. IKart disC'asc neonate s and, 6.\9-640 patent ductus arterio>lIs and, 639-640 Congestive hemt failure (CHF) intensive carc or. 2]5, 245

patient instruction and, 371-372 pumps and, 368 reflex physiology of, 55 stages of,369-371 suction and, 367-382 Counter rotation assist techniques,375, 376, 377


1-9

Index

1-10

chronic primary dysfullction and

for ventilation, 407-408. 409


CP; see Creatine phosphate (CP) CPAP;

see


Continuous positive airway pressure (CPAP)

Diaphragm

Crackles,defined, 219-220

Craniosacral therapies, secondary dysfunction and, 437

anatomy of. 26,26-28, 27, 28

Creatine phosphate (CP), in energy transfer, 8

contractilit y and, 444-448

Creatinine, laboratory tests of,

1 92t.

movement and, 222, 223

192-193

ventilation facilitation and

Crepitus, defined, 223

Cricoarytenoid arthritis. respiratory failure and, 579. 580t, 581

breathing, 389, 390, 391,392.394,394, .105, 396, 396

Critically ill patients

inhibition, 402-405, 404. 405

Diastole, ventricular physiology of. 66

acidosis/anaerobic metabolism in, 6

arterial blood gases in, 156

Dicyc10mine (Bentyl), pharmacology or, 783

oxygen consumption in, 13

Di fferential diagnosis, patient assessments and. 227t

oxygen transport in, 3

Diffuse interstitial pneUillonitis, cardiopulmonary effects of,


102-103, 103

Crohn's disease, clubbing and, 214, 214

Diffuse interstitial pulmonary fibrosis, pathophysiology of, 83-85

Cromolyn sodium (Intal), pharmacology of, 785-786

Diffusion cardiopulmonary physiology of, 60, 60-61

Cross-referrals, in home-based care, 728-729

oxygen transport and,5. 12, 17

Crystal cameras, for Duclear imaging, 198

Diphosphoglycerate (DPG), in oxygen transport, 15

CSF; see Ccr\!brospinal fluid (CSF) CT; sec Computerized tomography (CT)

Dipyridamole, for pharmacologic stress testing. 199

Curariform drugs,respiratory failure and, 579, 580t, 581

Discharge, from ICUs, 574

Cushing's syndrome, corticosteroids and, 785

Disseminated intravascular coagulation, pulmonary hemorrhage

and, 108

Cyanosis intensive care of, 240

Disseminated intravascular coagulation (DIC), laboratory tcsts of, 190,191t

patient assessments and, 214

Cyclopentolate (Cyclogyl), pharmacology of, 783

D02; see Oxygen, delivery

Cyclosporin, for organ transplants, 717-7 J 8

Documentation, 123-126

side effects of. 718

Cystic fibrosis (CF)

assessments and. 1 25- J 26

content for, 124

management of, 484-486. 521-522

exercise testing/training and, secondary dysfunction,426-432

pathophysiology of, 483-484, 521

in homellong-term care facilities, 727

patient assessments and. 225. 227

objective. 125

pediatric

plans and. 126

exercise for. 661

pur'pose of, 123


recording electrocardiograms and. 172, 172-174, 173

Pseudomonas aeruginosa and, 643--&14

subjective, '124-125

respiratory failure and. 579, 580t, 581

types of, 123-124

Doppler echocardiography, defined, 20 It, 204

D

Down syndrome

2D echocardiography, defined, 201t. 203-204. 205

cardiology of, 639t

Dead space. defined,145-146

managcment of. 645t, 646--647. 647

Death

Doxazosin (Cardura), pharmacology of, 778

exercise and dying patients, 576-577, 577

DPG; see Diphosphoglycerate (DPG)

ICUs and, 576-577, 577

Dressing techniques, ventilation Lrcilitation and, 389

patient fear in, 577, 577

Drinking, coughs associated with, 368

Debt. oxygen; see Oxygen, debt

Drugs, 775-786

Deep vein thrombosis, management of, 623-624

for airway obstructive disease,784-785

Delivery, oxygen; see Oxygen,delivery

autonomic pharmacology of, 776

Demand, oxygen; see Oxygen. demand

rcus and, 572-573

Desaturated blood/C02, oxygen transport and, 19

immunosuppressive,717-718, 718

Dextran, for blood loss, 234

in intensive care, 572-573

Diabetes mellitus

pharmacology of


adrenergic agents,777-778


Index

anticholineSterascs.781

E

antihistamines, 785-786

Eating. coughs associated with, 368

antiinflammatory agents, 784

Eccentric resistance techniques. ventilation facilitation and. 414

beta- Ad rene rg ic blocking dru!!s. 778-779

ECD; sec Endocardial cushion defects (ECD)

8

bet32-receptors stimul ants, 77

ECG; see Electrocardiograms; Elect r ocardiograms (ECG)

bronchial muscle re l a x ants. 778

Echocardiography

bronchodilators. 778, 779

defined, 20 I t, 203-205

cholinerg i c blockin g drugs, 782

M -mode, 20 I t, 203-204, 205

d rugs. 78{}-78 I

cort icos tcroi C\s . 785

cholinergic

Edem a

patient assessments and. 223

cxpeetor'lnts. 785, 786

patient history and, 14{}-141

inhalers. 777, 786

r adiogra phy of, 165, 166

mucolytics, 786

Edrophonium (Tensilson), pharmacology of, 782

sympaiholytic drugs. 779

Education, patient, 453-463

sympathomimctic drugs, 7R4-7X5

defined, 454-456

vasa Iilators, 777. 778

Down syndrome, 645t, 646-647, 647

xanthines. 785

effectiveness in, 461-462

rcspiratorylcardiovascular systems and. 775-776

fundamentals of, 454-456

sympathetic ncurotransmission of, 776

interdisciplinary care and, 463

for trans plant pa tients

leaming needs assessments and, 457, 459

cardiac, 716-- 718

,Ireas, 457,457.459

pulmonary . 717-718

findings, 459

Dry environments. oxygen transport and, 16

goals, 459

DTPA (Tel; see Tcchnetium-99M-diethylcne triamine penta-acetic (DTPA) aerosol

needs-based, 456

patient adherence and, 462

management oj', 647--648

teacher-learner relationship and, 462

Dynamic activitics, ventilation facilitation and, 388·-389

Edward's syndr o m e, cardiology of, 639t

Dynamic a ir therapy bed. clinical applications of, 363-364

beLl. clinical a p p l ications and. 363-364

Dys func tion; see speci fic typcs, e.g . . Primary dysfun ction.

Secondary dysfunction

patient history and. 128-·130. 129. 134-135

acute, UO

in cardiac patient s . 134

in

lCUs, 238. 239-241, 240t-241t

myocardial int'arction and, 186-187. 187

recording of, 172, 172- I 74, 173

use

exercise limiting, 1 31t on exertion. 13{}-131. 131t. 132, 132t. 133.133, 134

fu nc tio n al, 135

of, 169-170

Electroencephalo grams (EEG), in IC U s, 246

Electrolyte abnormalities, respiratory failure and, 6 I 9

El ect rolyte balance

onhopnea. 134

ICUs and, 23{}-231, 234t, 234-235

paroxysmal noctumal. 134-135

laborato r y tests and, 191t, 191-192

platypnea. 135


trcpoplH:a. 135

Elevations, high; see High elevation environments

Dysrhyt h mias

Embolism. pulmonary, differential diagnosis of, 227t

ca rd iopulmona r y effects or. 101

electrocardiograms and. 177, 17X. 179-184. 179-184

pathophysiology oc. 91-92

arrhythmias and. 177, 178, 179-184, 179-184

evaluation of, 174. 174-177, 175, 176, 177

pat ient assessments and. 216

ventricular. 180-184. 182, 183. 184

Elect r oc ardiograms (ECG), 169-187

blocks, 184--186, 185, 186

Dyspnea

i nte n si vc care or. 236, 236t. 239

EEG; see Electroenc e phalograms (EEG)

conduction and, 170-172, 171

Dyskinesia. nucie,lr imaging of. 200

supraventricular . 177. 178. 179. 179,

tools. 457

methods in, 459-461, 460t, 461

D uchcn ne ' s musc ular dystrop hy card io logy of. 639t

Dynamic ail ther a py l "

1-11

ISO, 181

Emotional stress

fight/f1ighUfright and, 20


Emphyse ma chronic primary management of. 517-518


1-12

Index

dyspnea and

pathophysiology of, 5 16-5 17


on exertion, 130- 13 1. 13lt. 132. 132t,133. 133, 134


limiting, J3 l t intensity/duration of, 723

pathophysiology of, 73,73-77,74. 75,76,77,478-48 1


long term respons s of. 278-280,279

radiography of. 162, 163

monitoring and, 275, 285-286, 288, 289, 290. 29 1-292

Endocardial cushion defects

(ECD), management of, 640

multisystem effects of. 278-280, 279

oxygen transport and. 8. 10- 12, 13. 19

Endocrine disorders

cardiopulmonary effects of, 109- 1 10, 110

oxygen transporUmetabolic demand and. 267-268,268. 270

pathophysiological conditions and. 270-271. 27 I

laboratory tests and, 193, 193t

for pediatric asthma. 660-661

Endotracheal artificial airways, 772

Energy transfer, oxygen transport and, 4. 6--8,8, II

prescription for, 266--267. 268, 270-276. 273. 274t. 276. 278t

Enhancement ratio, oxygen; see Oxygen, enhancement ratio

preventive effects of. 291-292. 295

Environment

pulmonary aging changes and, 675-677,677. 677t

ICU, 576, 576y

stimulus in. 277-278, 278

oxygen transport and. 15- 16

stress and. 20

testing/training and

Eosinophilia, pulmonary, pathophysiology of, 85

Eosinophilic granulomas, pathophysiology of, 85-86

prescriptions in, 274,274. 276--277,280-285,281. 282t,

283t. 284--286, 290,290-29 1

Ephedrine, pharmacology of, 778, 785

Epiglottitis, respiratory failure and, 579,580t,58 1


breathing, 420,420-421

Epinephrine

laboratory tests and. 194

guidelines, 42 1-422

pharmacology of, 777. 778, 784

heart disease. 419

reversal of. 778

lung disease, 4 17-4 18

Eq uipment for active cycle breathing

traditional, 422-423

(ACB), 349-352. 350, 351

upper/lower extremity, 4 19-420

for autogenic drainage, 352

secondary dysfunction, 425-441

for exercise airway clearance, 359-361, 36 1 t

breathing training, 435-436

for high frequency chest compression, 358,358-359

case studies, 437-440. 438. 439

for manual hyperinflation, 348. 348-349

evaluation, 426-432

for percussion, 344

patient history. 428,428. 429, 430

for positive expiratory pressure, 354--355

patient management. 432-433. 435

for postural drainage, 340,340-344,34 1,342

psychological factors. 425-426,426

for shaking, 346--349. 347, 348

testing guidelines, 430-43 I

for transplant patients

therapeutic options, 436-437

training guidelines. 43 1-432,432

cardiac, 708-709

training and prescription for, 722-723

pulmonary, 708-709, 7 15

for transplant patients,cardiac, 7 I 2

for vibration. 346--349, 347, 348

Erector spinae. anatomy of, 30, 3 1

Exercise stress testing, nuclear/cardiovascular. 199

Ergometers, for oxygen transport treatment. 259-260. 260

Expectorants, pharmacology of. 785. 786

Erythrocyte disorders. cardiopulmonary effects of, 108

Expiration

Escherichia coli, in bacterial pneumonias, 474-475

forced. 147

Esophageal chest pain, patient history and. 139

muscle anatomy in. 27, 31-32

Ethical considerations. transplant patients and. 704-705

ventilation facilitation and, 388

Eupnea. patient assessments and. 2 1 6

External thorax manipUlation, contraindications for,331, 331-332

Exercise. 8 , 10- 12. 1 3 , 1 9

Extrapulmonary breath sounds, patient assessments and, 220

acute responses to. 270-271. 27 1. 272. 273, 274. 274t

airway clearance teChniques and. 329-330. 359-36 1. 361 t

F

assessment of. 295-296

18F-f1uoro-deoxyglucose (FOG), for cardiovascular testing. 20 1t. 203

bed rest and. 291. 29 1-295

Facility-based care

cardiac aging changes and. 671, 67 I -674,673. 673t

concerns in, 723

cellular responses to. 269-270

documentation in, 727

deconditioning effects and, 723

monitoring in

defined. 265-266

cardiopulmonary, 725. 725-726

dying patients and, 576--577. 577

oxygen, 726--727


Index


1-13

Friedreich's ataxia, cardiology of. 639t

cardiac, 716--718

Fright/flight/fight reactions; see Fight or flight syslCms

pulmonary, 716--718

Function optimization, defined, 570, 571

work consideratIons in, 724-725

Functional reflex, defined. 783-784

FAD; see Flavin adenine dll1uclcotide (FAD)

G

Family history, patients and, 142

Gallium scintigraphy, for respiratory testing,206

Fatigue. patient history and, 140

FDG; sec 18F-fluoro-deoxyglucose (FDG)

Gallops, patient assessments and, 221

Fear

Gamma cameras,defmed, 198

dying patients and, 577, 577

Ganglionic blockade,defined,781

oxygen transport threats and, 255

Gas exchange

FET; see Forced expiratory techniques (FET)

cardiopulmonary physiology of

Fetal alcohol syndrome (FAS), cardiology of, 639t

diffusion, 60, 6

Fetal development, circulatory, 636

perfusion, 6 J -65,62, 63,64

61

exercise testing/training in,primary dysfunction, 418

Fetal disorders

in oxygen transport, 5,16

fetal alcohol syndrome, 639t

diffusion,5,12, 17

meconium aspiration syndrome,641-642

perfusion, 17

Fibrinogen, oxygen transport and, 15

ox ygen transport threats and, 254

Fibrobullous disease, cardiopulmonary effects of, 102-103, 103

Gaseous vapors, environmental effects of, 16

Fibrosis


Gases, arterial blood; see Arterial blood gases

diffuse interstitial pulmonary, pathophysiology of, 83-85

Gastrointestinal disorders


Fight or flight systems


systemic effects and, 107, 107

Glaucoma,treatment of, 78

parasympathetic system and, 776

781

Glossopharyngeal breathing, ventilation facilitation and,

First pass radionuclide testing, cardiovascular, 199, 20 It

410--412,412

Fixed position radiographs. interpretation of, 159-160

FK 506, for organ transplants, 718

Goals

Flail chest, patient assessments and, 214-216, 216

for home-based care,73

Flavin adenine dinucleotide (FAD), in energy transfer, 8

for lCU patient management, 568-572,570

732, 731, 732

for musculoskeletal/neuromuscular disorders, 70

Flight or fight systems

70 I

for transplant care, 709,712, 713t, 715

ox ygen transport and, 2 0

parasympathetic system and. 776

Gravitational flow, physiology of, 61-65, 62, 63, 64

Flow

Gravitational stress, oxygen transport and, 19-20

Gravity

blood in oxygen transport,12, 15

gravitational, 61-65, 62,63, 64

body positioning and,300-301, 301

volume curve, 147, 148, 149

in musculoskeletal/neuromuscular disorders, 68

Fluid balance

687,

682-687,686t

cardiac effects on, 101

Guanethidine (lsmelin), phalmacology of, 779

cardiopulmonary physiology of, 67,67t

Guillain-Barre syndrome, respiratory failure and,579, 580t, 581

hematologic conditions and, 108

H

ICUs and, 230-231, 234t, 234-235

oxygen transpol1 and, 13-14, 17

Hands-knees rocking assist techniques, 381-382

plasma protein disorders and, 109

Hct; see Hematocrit (Hct)


HDL; see High-density lipoproteins (HDL)

systemic disease effects on, 101-102

Head down body positioning,312

Head injuries, secondary dysfunctionlICU

Fluid collection, in ICUs, 235, 235-236

Fluid volume, oxygen transport threats and, 255

management of, 606-609, 608

FluLlerrM, for airway clearance, 328

pathophysiology of, 606--609, 607

Flutter valves, for oxygen transport treatment, 259-260, 260

Health issues, oxygen transport and, 16

Forced expiration, pulmonary function tests and, 147

Heart anatomy, 44--48, 45,46, 47,48

Forced expiratory techniques (FET), active cycle breathing and, 349-352,350,351

Heart block, treatment for, 777

Heart disorders

Fractures, secondary dysfunctionllCU and, 605-606

exercise testing/training in, primary dysfunction,419

Friction rub, defined, 220

fluid balance effects of, 101


1-14

Index

ischemic. 109

left ejection fraction,200

myocardial dysfunctionlrespiratory failure and, 620

left end diastolic volume, 13


left output, 636

chronic primary dysfunction and,526-528

left pressure, 241-243

management of,490-49 j

Heart sounds,patient assessments and, 221-222

pathophysiology of, 91-93,490,526

Heart surgery

myocardial ischemia,245

ICUs and,245

myocardial perfusion, 202-203

open,595,596

oxygen transport threats and. 254

Heart transplants

treatment,261

acute phase care in. 7 J07 ll, 714

pathophysiology of

assessments in, 708

acute heart failure,93

considerations in

arrhythmias. 91-92

availability, 704

chronic heart failure, 93-94

ethical, 704-705

compensated/decompensated heart failure, 94

organ donation,704

congestive heart failure, 93

organ preservation, 704



patient classifIcation and, 133

psychosocial implications,70S-706

patient history and,1:l3

purpose of,704

Heart failure

trends in, 70G

acute,pathophysiology of,93

waiting list criteria, 70S,70S

compensated/decompensated. pathophysiology of, 94

waiting time,705

congestive

when to use,704

intensive care of,235,245

equipment/monitoring in,70S-709

ischemic heart disease and,109

exercise guidelines in, 712


facility vs. home based rehabilitation in,716-718

pleural effusions and,101

goals in. 712

primary/lCU, 594,594,596

history of, 704

radiography of,164, 165, 166, 167

interventions in, 7 J0 711, 7 I 4

respiratory failure and,579, 580t,58 I

Heart function

medication in,716-718

other transplants and,709-710

afterload in,13


anatomy and, 44-48, 45, 46, 47, 48

post-transplant care in,708

aortic volume and,66,66

pre-transplant care in, 70S

cardiopulmonary physiology of, 65,65-67, 66, 67t

rejection signs in,714, 715, 716


surgery and, 70G

arrhythmias, J 77,178, 179-184,179-184

therapy in

conduction,170-172, 171

assessments,707 -70S

blocks,184-186,185, 186

defined,70S-709, 710,710--713

evaluation of. 174, 174-177. 175, 176,177

medical management, 707,707t

myocardial infarction, 186-187. 187

musculoskeletal considerations,707,709-710

rate, 174,174-176, 175, 176

physiology and,707

recording,172, 172- t 74,173

rhythms, 176-177, 177

use of, 169-170

heartbeat physiology and,66

left atrial pressure,241-243

myocardial contractility and,13

myocardial viability and, 202-203

therapist requirements, 706

Heartbeat, cardiopulmonary physiology and, 66

Heimlich assist techniques,374. 374-375

Hematocrit (Hct)

laboratory tests of,190-192, J 9 J t


Hematologic disorders,cardiopulmonary effects of

myocardial workload reduction, 592, 593-594, 596

malignant. 109

output in, I I, 12, 14,17,636

systemic, !O8-109, J09

preload,13

Hematology,oxygen transport and,S

ventricular

Hemiplegia,chronic secondary dysfunction and

diastole physiology,66


fetal anatomy of, 636



Index

Hemoglobin (Hgb)

1-15

respiratolY failure and, 579, 580t,581

ancri 1 blood gases and,155

Hyperglycemia, respiratory failure and,579, 580t, 581

laboratory tests of,190-192,191 t

Hyperinflation, manual, 348,348-349

in oxygen transport, 11-12, 14-15

Hyperoxia, ICUs and, 238

Hemophilia,pulmonary hemorrhage and, 108

Hypertension

chronic primary dysfunction and management of, 531-533

Henull,hilis il(/ll/enlOe, pneumonia in neonates, 642


Hemophilus inj7uelllOe, in bactcrial pneumonias, 474--475

management of,488

Hemoptysis, patient history and, 140

Hemorrhages


preterm infants and, 637-638, 638t

anticoagulants and, 108

disseminated intravascular coagulation. 108

treatment of,777, 778, 779

electrolyte balance and,230

Hyperrhyroidism, cardiopulmon8lY effects of, 109-1 10, I 10

hepatic failure and,108

Hyperventilation, manual airway clearance and, 325

Hcmosiderosis. pathophysiology of, 87

Hypocalcemia, respiratory failure and, 579, 5801., 581

Hemostasis, laboratory tests in, 190,191t

Hypocapnia, ICUs and, 238-239

Hemothorax, secondary dysfunctionllCU and, 605

Hypokinesia, nuclear imaging of, 200

Hepatic fibrosis,clubbing and, 214, 214

Hypomagncsemia, respiratory failure and, 579,580t, 581

Hering-Breuer reflex, cardiopulmonary physiology of, 55

Hyponatremia, respiratory failure and, 579, 5801, 581

Hexamethonium (Methium), pharmacology of,783

Hypophosphatemia, respiratory failure and, 579, 580t, 581

HFCC; sec High frequency chest compression (HFCC)

Hypothyroidism, cardiopulmonary effects of, 109-110, 110

Hgb; see Hemoglobin (Hgb)

Hypoxemia

High-dcnsity lipoproteins (HOL), cholesterol and, 191, 191t

cardiopulmonary cl'fects of,

High elevation environments, oxygen transport and, 16

ICUs and,237t, 237-238

High frcljuency chest comprcssion (HFCC), 328-329, 358, 358-359

management of,621

High-resolution computerized tomography (HRCT), for respiratory

101

symptoms of, 236t Hypoxia, critical facts relating to, 252

tcsting, 206-- 207

Hip mobilization, secondary dysfullction and, 436

I

History

IABP; see Intraaortic balloon counter pulsation (IABP)

of artificial airways. 761

of organ transplants, 704

[CP; see Intracranial pressure (ICP)

of patients/family, 142

ICS; see Intercostal space (ICS) ICUs; see Intensive care units (ICUs)

HIY; see also AIDS associated cardiology of,639t

Idiopathic pulmonary hemosiderosis, pathophysiology of, 87


Immobility/recumbency,intensive care units and, 568

HMO; see Hyaline membrane disease (HMO)

Immunological disorders, systemic,cardiopulmonary effects of, I 10

Hoarseness, patient history and, 141

Immunological function, laboratOIY tests in, [94t, 194-195

Hodgkin's disease, cardiopulmonary effects of, 109

Immunosuppressive drugs

Homatropine (Novatrin),pharmacology of, 783

for organ transplants, 717-718

Home-based care

side effects of, 7J 8

concerns in, 727-728

IMT; see Inspiratory muscle training

goals for, 730-732, 731, 732

IMY; see Intermittent mandatory ventilation (IMY)

management of,722

Incentive spirometry (IS), defined, 754, 755

monitoring in, 729

Indices/measures, oxygen transport and, 5

oxygen, 729-730, 730

Indirect percussion; see Mediate percussion

III antimyosin, for cardiovascular testing,201t, 203

setting requirements in, 728

Indium

team communication in,728-729

Individualized education plan (lEP), Oowo syndrome and, 645t,


646--647,647

cardiac, 716--718

Indoor environments,oxygen transport and, 16

pulmonary, 716--718

Infants

airway clearance techniques (ACT) for, 653, 657

Home environments, oxygen transport and, 16

Human immunodeficiency virus (HIY); see

HIY

aspiration pneumonia in, 642

Humidity therapy, defined, 755

chest therapy for

Hyaline membrane disease (HMO), preterm infants and, 640-641

airway suctioning, 653,657

Hypercapnia

percussion/vibration,652---653, 657

ICUs and,239

pOsitional rotation, 649, 649, 650-651


Index

1-16

Swan Ganz catheter. 233, 241-243, 243

postural drainage,652, 653t, 654-656

patient management in. 565-577

intubation tracheostomy and, 644

assessments,572

myelomeningocele in,646, 646

Infarct avid scans,defined. 20 I t. 202

death, 576-577,577

Infection

discharge, 574

ICUs and,574

environment, 576. 576y


function optimization,570,571

Inflammatory bowel disease,cardiopulmonary effects of. 107

goals, 568-572,570

Information, ICU patients and, 571-572,572

immobility/recumbency, 568

Inhaled materials, toxic. 16

infection, 574

Inhalers

monitoring,572,572

patient information,571-572,572

metered-dose. 777,778

bronchodilators,723-724

personal recognition,574--575

defined,755-756,756

pharmacological agents,572-573

for oxygen transport treatment,259-260,260

preventive care,571-572

pharmacology of,777. 786

team work,574, 575

precautions in. 756

therapist expertise, 568,569

spacers for, 786

treatment in. 569-571, 570, 572-574

powder,pharmacology of,786

upright to supine position,570

Injuries

primary dysfunction and,579-596

head, secondary dysfunctionllCU and

asthma, 589-591

management of,606-609, 608

cardiopulmonary failure,579,580t, 581

pathophysiology of,606-609. 607

congestive heart failure,594,594,596

respiratory failure and,579,580t. 58 I

coronary artery disease,592-596

Inspiration

myocardial workload reduction, 592, 593-594,596

exercise for fatigue in. 444--448, 448-450, 450

obstructive lung disease, 581-589, 589

muscle anatomy in,26

open heart surgery,595,596

positioning and. 387-388

restrictive lung disease, 590-592

secondary dysfunction and,599--615

sustained maximum, 754, 755

Inspiratory muscle training (lMT), fatigue and, 444-448,

burns, 612--615

448-450.450

fractures, 604--606

lnspired air

head injuries, 606-609, 607,608

in ambient air, 15-16

hemothorax.605

in oxygen transport,5, 15-16

musculoskeletal trauma,603-604,694

Instillation therapy, obstructive lung disease and,primary

neuromuscular disease,600--602

dysfunction/lCU,587

obesity, 602--603

Insulin production,laboratory tests of. 193,193t

pneumothorax,605

Intensive care units (ICUs)

respiratory muscle training,610--612,6 I 1,612

monitoring systems for. 229-246, 572. 572t

rib fractures, 604--605

acid base balance. 236.236t

spinal cord injuries, 609--612

blood gases, 236-237

trauma, 605

central venous pressure. 243-244

Intercostal muscles, anatomy of, 28,29

chest tubeslfluid collection, 235.235-236

Intercostal space (lCS). defined, 220

description of,229-230, 230,231,232.233

Intermittent mandatory ventilation (IMY), defined, 758

ECG, 238, 239-24 I, 240t-24 I t

Intermittent positive pressure breathing (IPPB),defined.753, 754,755

EEG,246

Interstitial lung disease

fluid/electrolyte balance, 230-231, 234t, 234-235

gallium scintigraphy for, 206 .

hypercapnia. 239

management of, 486-487, 523

hyperoxia.238

pathophysiology of, 486, 522-523

hypocapnia, 238-239

radiography of, 162,163

hypoxemia,237t, 237-238

respiratory failure and,579, 580t. 581

intra-arterial I ines,24 I. 242

Interviews

intraaortic balloon counter pulsation, 244, 244-245

intracranial pressure, 245-246

intravenous lines. 243

patient assessments and,209-210

for patient history, 127-128

Intra-arterial lines, in ICUs, 241,242


Index

Intraaortic balloon counter pulsation (IABP), in ICUs, 244, 244-245

liver, 194, 194t

Intracranial pressure (ICP), ICU monitoring of,245-246

multisystem, 190- I 95

Intrapulmonary percllssive ventilators (IPV), 363, 364

pancreatic, 193,193t

Intravascular echocardiography, 204

peripheral vascular, 192, 192t

Intravenous lines. in ICUs, 243

thyroid,193t, 194

1-17

Lactic aci d. laboratory tests of, 190, 19 I t

Invasive cardiac testing. 205-207

Iodine, laboratory tests of. 194

Laryngeal edema, respiratory failure and, 579, 580t. 581

IPPB; see Inte.rmiltent positive pressure breathing (JPPB)

Larynx, anatomy of, 35, 35-36

IPV; see Intrapulmonary percussive ventilators (IPV)

Late sequelae of poliomyelitis, chronic secondary dysfunction and

IS; see Incentive spirometry (IS)


Ischemia, myocardial; see Myocardial infarction


Isocapnic hyperpnea, for respiratory muscle fatigue. 450-451

Lateral chest radiographs, interpretation of, 159-160

Isocapnic hyperventilation, for respiratory muscle fatigue, 449-450

Lateral costal breathing, ventilation facilitation and, 396, 397, 399

lsoetharine (Bronkosol, Bronkometer, Servant), pharmacology of,

LOL; see Low-density lipoproteins (LOL)

Left atrial pressure (LAP), ICU measurement of, 241-243

778,784-785 Isoproterenol (Isuprel), pharmacology of,777,784

Left ventricular assist devices, ICUs and, 245

J

Left ventricular end diastolic volume (LVEOV), oxygen transport

Left ventricular ejection fraction (LVEF), nuclear imaging of, 200

and, 13

.IRA; see Juvenile rheumatoid arthritis (JRA) Jugular venous distension (1VO), patient assessments and,214

Left ventri cu l ar output (LVO), fetal anatomy of, 636

Jugular venous pressure,electrolyte balance and. 231

Left ventricular pressure (LVP), intensive care units measurement

Jugular venous pulse, patient assessments and, 214

of,241-243 Leukemia, cardiopulmonary effects of, 109

Juvenile rheumatoid arthritis (1RA) cardiology of, 639t

Lifting, primary dysfunction and, 419-420

management of. 648

Lipoprotei ns, cholesterol and, 191, 191 t

JVO; see Jugular venous distension (1VO)

Listening skills, secondary dysfunction and,428,429, 430 428

Liver disorders, systemic, cardiopulmonary effects of, 107-108, 108

K

Liver function, laboratory tests in, 194, 194t

Kidney disorders

Long sitting self assist techniques. 379, 379-380, 380

Long-term care facilities

acid base imbalances and, 154

concerns in, 723

cardiopulmonary effects of, 108, 108

chronic secondary dysfunction and, 560-561

documentation in, 727

effects of systemic types of, 108, 108

monitoring in

organ damage and, 108

cardiopulmonary, 725, 725-726


oxygen, 726-727


work considerations in, 724-725

Low-density lipoproteins (LOL), cholesterol and, 191, 19 I t

Kidney function arterial blood gases and, 154

Low elevation environments, oxygen transport and,16

laboratory tests in, 192t,192- I 93

Lower airways, anatomy of, 36-40, 37, 39t

Knees-hands rocking assist techniques, 381-382

Lower/upper extremity exercise. testing/training in, primary

Krebs cycle, in aerobic transport, 8-9, 18

dysfunction, 419-420

Kyphoscoliosis

Lung anatomy,40-44, 41, 42t, 43

patient asscssments and, 216, 216

Lung cancer,chronic primary dysfunction and management of, 524

poliomyelitis and, exercise training for, 437-440, 438, 439

radiography of, 167, 167

Kyphosis, respiratory failure and, 579, 580t, 581


Lung disorders contused, respiratory failure and, 579, 580t, 581

exercise testing/training in, primary dysfunction, 417-418

L


Laboratory assessments, 189-195

adrenal,193t,194

treatment, 261

Lung function

blood, 190-192, 191t


endocrine, 193, 193t

pulmonary function tests and, 146, 146-147

immunological, 194t,194-195

Lung injury, management of, 625. 626

insulin production, 193, 193t

Lung transplants

kidney,192t, 192-193


1-18

Index

cardiology of, 639t

assessments in, 708

pediatric management of, 648

considerations in

availability, 704

MAS; see Meconium aspiration syndrome (MAS)

ethical, 704--705

Maximal voluntary ventilation, pulmonary function tests and, 149,

149-150

organ donation,704

organ preservation, 704--706

MOl; see Metered-dose inhalers (MOl)

patient education,706

Mean oxygen pressure, defined,12

psychosocial implications,705-706

Mean oxygen tension, defined, 12

rejection,704

Measurements, I 17-123

trends, 706

characteristics of, I 18-122

waiting list criteria, 705, 705

documentation and, 123-126

waiting time, 705


when to, 704

interpreting, 122-123

I 19

equipment/monitoring in, 708-709, 715

interval,

facility vs. home based rehabilitation in, 716--718

nominal, 118

goals in, 709, 712, 713t, 715

nuclear-derived,199-200

history of, 704

objective/subjective, 121, 121-122

interventions in, 709,712-713, 713t, 7 I 5-716,716

ordinal, 118-119

medication for, 7 I 7-718

performing, 122

other transplants and,709-710

ratio,119

outpatient care in, 714--7 I 6, 716

reliability and, I 19-120

post-transplant care and, 708, 7 I 2-7 I 3, 7 I 3t

selecting, 122

validity and, 120-121

pre-transplant care and, 708-709, 710

rejection signs in, 7 I 5

Measures/indices, oxygen transport and, 5

surgery and,706

Mechanical body positioning, 316

therapy in

Mechanical breathing function, cardiopulmonary physiology in, 56--59,57,58,59

assGssments,707-708 defined, 708-709, 710, 710-7 I 3

Mechanical ventilation

medical management,707, 7071

assisted, 758

musculoskeletal considerations, 707, 709-7 I 0

controlled, 758

physiology, 707

Meconium aspiration syndrome (MAS), management of, 641-642

pre/post assessments, 707-708

Mediate percussion, patient assessments and, 222

therapist req uirement s , 706

diaphragmatic movement,222, 223

techniq ues, 222

Lupus erythematosus,systemic (SLE)

Medical conditions


chronic primary dysfunction and


LVEOV;

sec

angina,525-526

Left ventricular end diastolic volume (LYEOV)

LYEF; see Left ventricular ejection fraction (L YEF)

asthma,5 I 9-520

Lymphatic circulation

bronchiectasis,520-521

chronic airflow I imitation,5 I 4

anatomy of, 50

in oxygen transport,16-17

chronic bronchitis,514--5 I 6

systemic disorders and, fluid imbalance,101

cystic fibrosis, 521 -522 diabetes mellitus, 533-535

M

emphysema, 516-518

M-mode echocardiography, defined, 201t, 203-204,205

hypertension, 531-533

MAB scans, defined, 20 I 1,206

interstitial lung disease, 522-523

Magnetic resonance imaging (MRI),defined, 207

I ung

Malignancies


cancer, 523-524

hematologic, cardiopulmonary effects of,109

obstructive pallerns in, 514--522

lung, chronic primary dysfunction and, management of,524

peripheral vascular disease, 529-531

radiography of,163, 165,166

primary cardiovascular disease, 525-535


restrictive pallerns in, 522-523

Managed ca re , defined, 722

Mandatory minute ventilation (MMY), defined, 758

valvular disease,528-529

chronic secondary dysfunction in

Marfan syndrome

ankylosing spondylitis, 557-558


Index

cer ebral palsy , 546--547

bronchodi lators, 723-724

chronic renal insufficil'llcy, 560--561

defined, 755-756, 756

collagen vascular/connective tissue diseases, 555-556


hemiplegia, 541-54

pharmacology of, 777, 786

latc sC4udae of poliomyditis, 550--552

precautions in, 756

multiple sclerosis, 544-546

1-19

spacers for, 786

muscular dystrophy, 538-539

Methyldopa ( Aldome t) , pharmac ology of, 779

os teoporos is, 551-555

Methylprednisolone, pharmacology of, 785

Parkinson's disease, 543-544

Metoprolol (Lopressor), pharmacology of, 779

rheumatoid "rthritis, 558-560

MI; see Myocardial infarction

scleroderma, 556-557

M ic rocircu lation

spinal cord inj ury, 548-550

cardiopulmonary physiology and, 67, 67t

systemi c lu pus erythematosus, 555-556


thoracic deformities, 552-553

MMV; see Mandatory minute ventilation (MMV)

primary dysfu nction secondary to, 469-492

Mobility

alveolar protcinosis, 478

acute responses to, 270-- 271, 271, 272, 273, 274, 274t

alvcolitis, 477-478

assessment of, 295-296

angina, 488-490

bed rest and, 291, 291-295

asthma, 481-483

cellular response to, 269-270

atelectasis, 470-472, 471

defined, 265-266

bronchiolitis, 477

long term responses of, 278-280, 279

chronic airflow limitation, 478-481

monitoring of, 275,285-286,288,289,290, 291-292


motor t h erapy, pediatric, 661-663, 662

cy stic fihrosis, 48 -4R6

mu ltisystem effects of, 278-280, 279

emphysema, 478-481

obstructive lun g disease and, primary dysfunction/ICU, 584-585

hypertension, 488

intcrstitial pulmonary fibrosis, 486

oxygen transportfmetabol ic demand and, 267-268, 268, 270


oxygen transport threats and, 256, 256

pneu monias, 472-476

pathophysiological conditions and, 270--271, 271

tuberculosis, 487-488

prescription for, 266-- 267, 270--276, 273, 274t, 278t

Medical su rgical con d itions, primary dysfunction secondary to,

preventive effects of, 291-292, 295

secon dary dysfunction and, 436

495-508


stimulus in, 277-278, 278

extrinsic factors , 500

surgery and, 500


testing/training and, 274, 274, 276--277, 280-285, 281, 282t,

mObilitylrecumbency,500

283t, 284, 285, 286,290, 290-291


Monitoring of body positioning, 317-3 I 8

perio[Xrative course, 496, 496--500, 498

postoperative management, 502, 502-505, 506, 507

exercise and, 275, 285-286, 288, 289, 290, 291-292


in fa cility-based care

su rgical effects, 500

cardiopu lmonary, 725, 725-726

oxygen, 726-727

surgical prep, 499

in home-based care

thoracic, 500--502

cardiopulmonary, 729

Medication; see Drugs Med ullary respiratory center, cardiopulmonary physiology of, 54

oxygen, 729-730, 730

Men ingitis, re spirato ry failure and, 579, 580t, 581

in ICUs, 572, 572

Metabolic acidosis, intensive care of, 236, 236t

in transplant patients

Metabolic alkalosis, intensive care of, 236, 236t

cardiac, 708-709

Metabolic disorders

pulmonary, 708-709, 715


Monoamine oxidase (MAO), 776

respiratory failure and, 580t, 617-618

Montgomery T tubes, 768

Metabolism, muscle, 10--11

Motion radiographs, interpretation of, 159-160

Metaproterenol (Alupent), pharmacol ogy of, 778, 784-785

Motor neuron disease, respiratory failure and, 579, 580t, 581

Metaraminol, pharmacology of, 777-778

Motor therapy, pedi atric, 661-663, 662

Metered-dose inhalers (MOl)

MS; see M u ltiple sclerosis (MS)


Index

1-20

99mTcOTPA; see Technetium-99M-diethylene triamine penta

chest development in,682-689, 684---{i89,686t

acetic COTPA) aerosol

compensatory breathing patterns in,689,691---{i93,692, 693,694,695

Mucolytic agents

for intensive care units, 572-573

di agno sis in, 680

for oxygen transpOlt treatment, 259-260, 260

gravity in, 680---{i87,682---{i87,686t

pharmacology of,786

impaired

MUGA; see Multiple uptake gated scans (MUGA)

chest expansion, 689

Multicrystal cameras,for nuclear imaging, 198

cough effectiveness, 698

Multiple fractures,secondary dysfunctionllCU, 605-606

function,689

Multiple sclerosis (MS)

phonation, 699-700

cardiopulmonary effects of,104

muscle/tonal effects in, 687-689,688, 689


planes of ventilation and, 680


program goals for, 700--701


pulmonary changes in,695-696 systemic,cardiopulmonary effects of,102,102-103


transplant patients and,707,709-710

Multiple trauma,secondary dysfunction/ICU and, 605 Multiple uptake gated scans (MUGA), defined, 199,20 I t

Musculoskeletal trauma, secondary dysfunction/ICU and, 603-606,604

Muhisystem assessment, laboratory,189-195

management of,604

Murmurs,patient assessments and,221 Muscarinic blockers, defined, 779-781

pathophysiology of, 603-604,604 Myasthenia gravis

Muscarinic receptors, defined, 780 Muscle contraction

respiratory failure and,579,5801,581

emotional stress and,20

treatment of, 781-782

oxygen lranspolt and, 9,10, 10--1 2

Myelomeningocele, pediatric management of, 646,646

Muscle fatigue, exercise test i ng/traini ng in, primar y dysfunction, 418-419 Muscles

Myocardial contractility, oxygen transport and, 13

Myocardial dysfunction,respiratory failure and,620 Myocardial infarction chronic primary dysfunction and



in respiration anatomy diaphragms,26,26-28, 27, 28


erector spinae, 30, 3 I

electrocardiograms and,186-187, 187

expiration,27,31-32

management of,490-491 pathophysiology of,91-93, 490

inspiration,26 intercostals,28,29

Myocardial ischemia,ICUs and,245

pectoralis major, 29, 30

Myocardial perfusion

pectoralis minor, 30

nuclear imaging for,202-203

scalenes, 29, 29


serratus anterior, 29-30

Myocardial viability, testing for,202-203

sternocleidomastoid, 28-29, 29

Myocardial workload reduction, primary dysfunctionllCU and,

trapezius, 30,30

592,593-594,596

in secondary dysfunction, 427-428,432-433, 435

Myoglobin, in oxygen transport, 18

ventilation facilitation and, 401-405,402, 404,405

Myxedema,respiratory failure and, 579, 580t, 581

Muscular dystrophy cardiology of, 639t chronic secondary dysfunction and management of,538-539

pathophysiology of, 538 management of,647-648

N NAO; see Nicotinamide adenine dinucleotide Narcotics for ICUs, 572-573 respiratory failure and,579,580t,581

pediatric management of,647-648

Nasopharyngeal suctioning,772

respiratory failure and,579,580t, 581

NOT; see Neurodevelopmental (NOT) treatment

Musculoskeletal conditions chronic secondary dysfunction and,552-555 neuromuscular disorders and, 679-701

adverse changes in, 696,696-698, 697 bronchial hygiene and,698

Nebulizers,for oxygen transport treatment, 259-260,260 Neck mobilization in secondary dysfunction and,436 patient assessments and,214,215 Nedocromil sodium (Tilade),pharmacology of,785-786


Index

Neonates

1-21

phonation, 699-700

chest therapy fo r

muscle/tonal effects in, 687-689, 688,689

airway suctioning, 653, 657

planes of vemilation and, 680

chest percussion/vibration,652-653,657

program goals for, 700-701

positional rotation, 649, 649, 650-651

pulmonary changes in,695-696

secondary dysfunction and,436

postural drainage, 652,653t, 654--656

chronic,538-543

development in

ca rd iac, 636-637

ICU,600-602

prelenn respiration,637, 1i38, 6381

management of. 600-60 I

pulmonary, 637-63tl


endocardial cushion defects in,640

Neuromuscular ju ncti on (NMJ), defined, 780-781

intubation tracheostomy in,644

Neurotransmission, drugs and, 776-777,778, 779-784

meconium aspiration syndrome in, 641-642

Nicotinamide adenine dinucleotide (NAO), in energy transfer, 8

myelomeningocele in, 646, 646

Nicotinic receptors, defined, 780

patent ductus arteriosus in, 639--640

Nitrogen, ambient air co ntent of, 15-16

pneumonia in, 642

NMJ;

preterm

Nocturnal ventilation, secondary dysfunction and,432-433, 435

sce

Neuromuscular junction (NMJ)

associated cardiology of, 639t

Noncardiogenic pulmonary edema, management of,625, 625

bronchopulmonary dysplasia in, 641

N onsmoking, environments, 16

Noonan's syndromc, cardiology or. 6391

chest therapy for

Noradrenalin, in neurotransmission, 776

airway suctioning,653, 657

Norepinephrine,laboratory tests of,194

postural drainage, 652,6531, 654-656

dysfunction factors in, 638t

Norepinephrine (Leval1erenol, Levophed),pharmacology of', 777

hyaline membrane disease in,640--641

Normal blood gas values, 154

patent ductus arteriosus in,639-640

Nose,anatomy of,32-34, 33, 34

respiration in, 637-638, 638t

Nuclear imaging for cardiovascular t"sting, 199-204,20 I t

tetmlogy of fallot in, 640

angiography, 205

transient tachypnea of the new born in, 641

echocardiography, 197, 203-205

Neoplasms,respiratory failure and, 579, 580t, 581

Neostigmine (Prostigminc),pharmacology of,781-782

with exercise stress,199

Nervous systems

18F-fluoro-deoxyglucose (FOG), 203

gatedlungnted,199

drug interaction and,776-777

in heart anatomy, 47,47-48, 48

Indium II I antimyosin, 203

systemic, 103-107,104

in vasi ve, 205-207

Neurodevclopmental (NOT) treatment, pediatric motor therapy

myocardial viability, 202-203

noninvasive, 199-205

and, 661-663,662

nuclear-derived measurements,199-200

Neurological disorders respiratory failure and,620-621

perfusion, 199-200

with pharmacologic stress, 199

systemic,103-107, 104

autonomic nervous system, 106-107

Technetium-99M-pyrophosphate, 203

central nervous system,103,105-106

Technetium-99M-sestamibi,202

peripheral nervous system,106

Technetium-99M-teboroxime,202

Thallium 201, 200-202, 20lt

Neuromuscular disorders musculoskeletal,679-70 I

planar, 198-199

respiratory,205-207

advcrse changes in, 696,696-698,697

angiography,206

bronchial hygiene and,698

chest development in, 682-689,684-689,686t

computerized tomography,206-207

compensatory breathing patterns in,689,691-693, 692,

gallium scintigraphy,206

693,694,695

diagnosis in,680

gravity in,680-687, 682-687,686t

impaired

magnetic resonance imaging, 207

ventilation-perfusion lung scan,206

tomographic/SPECT,198-199

Nursing homes

chest expansion, 689

concerns in,723

cough effectiveness, 698

documentation in,727

function,689

monitoring in


Index

1-22

cardiopulmonary, 725, 725-726

content,11-12

oxygen, 726-727

debt,13

delivery, 4, 6, II, 12. 13,14, 14. 19

work considerations in,724-725

demand,4, 13

Nutrition

obstructive lung disease and, primary dysfunctionflCU, 583

enhancement ratio,4, 6, 13


gravitational stress. 19-20

Nutritional disorders, systemic, cardiopulmonary effects of.

hyperoxia and, 238

110-111,111

mean pre.,sure defined, 12

mean tension defined, 12

o

myocardial function, 17-18


Obesity cardiopulmonary effects of. 110-111,III

tissue extraction, 18-19

respiratory failure and, 579, 580t,581

transport, 3-20,4,5, 6

airways, 16

secondary dysfunction/ICU,602-603


desaturated blood/C02, 19


diffusion,S, 12,17

inspired/ambient,S, 15-16

Obstructive lung diseases COPO patient assessments and, 214-215, 222, 224

lungs/chest walls,16-17

pathophysiology of,71-72

measures/indices. 5

primary/le U

perfusion, 17

bagging,587

peripheral circulation, 18

body positioning, 585-586

Oxygen therapy

breathing,588

basics of, 749,750, 750t, 751,752

coughing, 588

high-flow systems in, 750, 751-752


home/portab le,751, 753

mobilization, 584-585

low-flow systems in,750. 750. 750t,751

nutrition,583

obstructive lung disease and. primary dysfullctionlICU, 5g6

oxygen, 586

Oxygen transport


airways, 16

secretion ckarance,587-588

threats,253

selective instillation, 587

treatment, 261

analysis schematic of. 129

ventilator withdrawal, 588, 588-589, 589

pulmonary function tests and, diagnosis, 150, 150-151

cardiopulmonary physiology or. blood, 67-68, 68

Obstructive sleep apnea, respiratory failure and,579,580t, 581

exercise/metabolic demand and, 267-268. 268. 270

Occupational history,patient,141

mobilization and,270

OER; sec Oxygen, enhancement ratio


OKT 3, for organ transplants, 718

critical problem-solving Sleps, 252,252

Olympic tracheostomy buttons, 766, 767, 768, 768

deficits/threats, 253-255,256

Open heart surgery, primary dysfunction/ICU and, 595. 596

extrinsic, 256

Organ damage, renal conditions and, 108

fundamental knowledge, 252, 252

Organ donation, 704-706

indirect dclicits,255,256

Organ failure, management of,628t, 628-629

problem list, 252, 253, 254, 255

Orthopnea,dyspnea/patient history and,134

restricted mobilitylrecumbency,256

Orthostatic hypotension,defined,783

treatment,256-263,257, 258-259, 260,261.

Osteoporosis, chronic secondary dysfunction and management of, 553-555

Oxyhemoglobin dissociation, cellular respiration and, 15


p

Outdoor environments, oxygen transport and, 16

Outpatient care; see Home-based care, Facility-based care

Oxygen

Pain management of, 623

cascade, 12, 12

consumption,4,6,

262

Oxyhemoglobin,cardiopulmonary physiology and. 67-68,68

oxygen transport

II, 13

IABP and, 244, 244-245

threats
respiratory failure and,579, 5801, 581

Palpation, patient asscssments and, 222-225

supply-dependent, 13, 14

chest wall, 224, 224

vs. delivery , 14, 14, 19

edema, 223


Index

tactile fremitus, 225, 225, 226

intcrdisciplinary care and, 46J

tenderness, 223

learning needs asse.SSlllcnts, 457. 459 areas, 457, 45 7, 459

tracheal d viation, 225, 226 Pancreatic disorders, cardiopulmonary ef fe ct s of, 107, 109

findings, 45 9

Pancreatic dornase (Dornavac),pharmacology of, 786

goals, 459

Pancreatic function. laboratory tests in, 193, 193t

tools, 457

Paradoxical breathing patterns, poliomyelitis and, exercise training for, 438--439 Parasympathctic neurotransmission

methods in, 459--461, 460t, 461 needs-based,456 patient adherence and, 462

defined,779-783

secretion mobilization, 371-372,372

fight

teacher-learner relationship and, 462

or

fl ig ht system and,776

Parkinson" disease cardiopulmonary <:Ffeets of, 104 chronic secondary dysfunction and management of, 543-544

pathophysiology of, 543 treatment of, 783 Paroxysmal nocturnal dyspnca . patient hi s tory and, 134-135

for transpl a nt patients, 706 Patient history, 127-142 c h es t pain , 137-138 cardiac, 138-139 c hest wall, 139 esop hageal , 139 pericardial, 139

Partial thromboplastin (PTT), laboratory tests of, 190, 191t

pleuritic, 138

Particulate matter, in ambient air, 16

pulmonary hyper tension, 139

Passy - Muir valves, 766,767, 768, 768

cough, 135,136(,137

Pa tau ' s sy nd ro me , card iology of. 639t

dyspnea,128-130,129

Patient assessments,209-228

acute, 130

anatomic features in,210-211, 211, 212, 213

in cardiac pa l ients, 134

auscultation and, 217, 217-221, 218,219

exercise limiting,131t

breath sounds, 218-220,219

on exerlion, 130--131, 131.

chest sou n ds,217-218

functional, 135

heart sounds, 221-222

orth opnea, 134

techniques in, 217, 218 for barrel chest, 214-216, 216 breathing patterns and, 216 case studies and, 225-228

paroxysmal nocturnal, 134-135 platypnea, 135 trepopnea, J 35 exerc ise testing/training in, secondary dy sfullction , 428, 428,

429,430

chart review/interview in, 209-210 chest wall cunfi gura lion in. 214-216, 216

family, 142

differential diagnosis in,227t

fatigue/weakness, 140

general appearance in, 212-213

heart discasc classification, 133

jugular venous distension and, 214, 215

hemoptysis, 140

medi a te percussion in, 222, 222 diaphragmatic movement, 222, 223 techniques in, 222, 222

hoarseness, 141 interview, 127-128 occupational, 141

neck and, 214, 215

pedal edema, 140--141

palpation

prior treatment,142

chest wall, 224, 224

questionnaires, 128

edema. 223

smoking,141-142

tactile fremitus, 2 5. 22<;, 2:!6 tcnde rn e s s,

22]

tracheal de v i ation, 225, 226 palpation and, 222-225

wheezing, 135 Patient management exercise testing/training in, secondary dysfunction, 432--433,435 in leUs, 565-577

physical cxams in, 210

assessments, 572

skin in, 214,214

death,576-577,577

vi " ual inspl!ction in,211-214, 214

discharge,574

Patient education, 453--463

1-23

environment, 576, 576y

defined,454--456

function optimization, 570,571

effectivenl!SS in, 461--462

goals, 568-572, 570

fundamentals of, 454--456

immobility/recumbency, 568


1-24

Index

Perfusion

infection, 574

cardiopulmonary physiology of, 61-65,62,63,64

monitoring,572, 572

ventilation matching,61-65,62. 63. 64

patient information, 571-572, 572

personal recognition, 574-575

myocardial,199-200,201t


pharmacological agents,572-573

preventive care, 571-572

Pericardial chest pain, patient history and. 139

team work, 574,575

Perioperative management,primary dysfunction/acute surgical

conditions and, 496, 496-500, 498

therapist expertise,568, 569

Peri phera I chemoreceptors

treatment in,569-571,570,572-574

arterial blood gases and,response to hypoxemia,155

upright to supine position, 570

cardiopulmonary physiolugy of,54-55

transplant,703-718


PD; see Postural drainage (PD)

anatomy 01',48-49

Pectoralis facilitation,ventilation and, 401-402,402

Pectoralis major, anatomy of, 29. 30

in dying patients, 577,577

Pectoralis minor, anatomy of, 30

laboratory tests in, 192,192t

Pectus carinatum,patient assessments and. 214-216, 216



Pectus excavatum,patient assessments and,214-216,216

Pedal edema,patient history and,140--141

Peripheral nervous system, systemic disease effects on, 106

Pediatrics

Peripheral vascular disease, chronic primary

asthma in,642

management of,530--531

43, 660--661

bronchopulmonary dysplasia in,64 I


cardiac development in, 636-638

Peritoneal cavity,oxygen transport and,17-18

cerebral palsy in,644,644-646, 645t

PET imaging; see Positron emission tOl1lography (PET)

chest physical therapy in

for children,657

PFT; see Pulmonary function tests (I'I'T)

Pharmacologic stn.:ss testing,cardiovascular,199

60,658

positional rotation,658-659, 659,660

Pharmacological agents; see Dl1Jgs

pre/postoperative,659-660

Pharynx,anatomy of, 33,34-35

Phenoxybenzamine (Dibenzyline), pharmacology of, 778

for infants,649,649,650--651, 652

Phentolamine (Regitine)

airway suctioning,653,657

chest percussion/vibration,652

for epinephrine reversal, 778

53,657

pharmacology of,778

positional rotation,649,649,650--651

postural drainage,652,653r,654 common diagnoses in, 638t,638 cardiac,639t, 639 pulmonary,64 cystic fibrosis in,643

Phenylephrine (lsophrin,Neo-Synephrine), pharmacology of,

56

777-778

48

Pheochromocytoma, phentolamine and,778

40

Phonation, musculoskeletal/neuromuscular disorders and,699-700

48

44, 661

Physical exams,patient assessments and,210

Down syndrome in,645t,646-647, 647

Physical therapist requirements, in ICUs,568, 569

endocardial cushion/artrioventricular defects in,640

Physical therapy

hyaline membrane discase in, 64

41

body positioning,299-318

intubation tracheostomy in, 644

motor therapy in, 661

considerations in,316-317

gravity/physiology and, 300-301,30 I

63,662

muscular dystrophy in,647

head down,312

8

mechanical, 316

myelomeningocele in,646,646

patent ductus arteriosus in, 639

0

monitoring of,317-318

pneumonia in,642

physiological effects of,301-313, 302

pulmonary development in,637,638,638t

frequent changes,313,315

prescription for,313-316.314

rehabilitation in, 660--661

vs. routine,301

tetralogy of fallot in, 640

prone,312-313

transient tachypnea in, 641

Pelvis mobilization, secondary dysfunction and,436

side-lying positions, 311,311-312

Pentolinium (Ansolysen),pharmacology of,783

supine,308-309,309, 310

PEP; see Positive expiratory pressure (PEP)

Percussion

upright, 302-308, 303, 304,305, 306,307, 308

exercise/mobility,265-296

in airway clearance,323-324

acute responses to, 270--271,271,272,273,274, 274t

clinical applications of,344-346,345

assessment of, 295-296


1-25

Index

bed rest and, 291, 291-295

Pneumotaxic centers, cardiopul monary physiology of. 54

cellular responses to 269 -270

Pneumothorax

.

de fined 265-266

different ial diagnosis of, 227t

long term responses of, 278-280,279

radiography of. 164. 165

,

monitoring and. 275, 285-286,288, 289,290, 291-292 multi syst em effects of. 278-280,279

secondary dysfunctiun/ICU and. 605 Point of maximum impulse (PM!), defined, 220

oxyge.n transport/metabolic d em and and, 267-268,268,270

Poisons, respiratory failure and, 579, 580t,581

pathophysiological c on d iti ons. 270--271,271

Poland's syndrome, pediatric management of, 648

prescription for. 266-267. 268. 270--276. 273, 274t,276,278t

Polio, respiratory failure and,579,580t,581

preventivc crfc(,ts or. 291 292 . 295

Poliomyelitis

-

stimulus in, 277-27R. 278


impact of sy temic diseases on, 99-100


oxygen ll'llnsport and, 3-20


pediatric, 648--663

with s econdary kyphoscoliosis, exercise training for 437-440,

,

cardiac,648 - 649

438,439

positional release therapies,secondary dysfunction and 437

Pontine respiratory center, c ardiopulmonary physiology of, 54

shock,627-628

Positional release therapies. secondary dys function and. 437

.

Positioning, 299-318

Physiology cardiopulmonary, 53-69

b ody mechanics. 737-747

blood transport of oxygen,67--68,68

lifting, 741-743. 742, 743, 744

breathing control, 53-55. 54

moving, 744, 744-745. 745, 746. 747, 747

carbon diuxide transport. 68--69

uptimal ventilation, 737-738. 740-741

cardiac. 65,65--67,66. 67t

side lying. 740

diffusion, 60,60--61

supine, 738. 739, 740

mechanical, 56-59, 57,58,59

upright, 740,740--741,741

perfusion,61--65. 62. 63, 64

considerations in, 316--317

reflexes, 55, 55-56

cough/suction,367-382


ventilation, 59--60 in tra n splant patients,707

anterior chest compression, 375,375

Physostigmine (Eserine), pharmacology of, 781

costophrenic, 373,373-374

Pilocarpine,pharmacology of, 781

counter rotation, 375, 376, 377

Planar imaging. defincd, 198-199, 201t

hands knees rocking,381-382

Plasma, in oxygen transport, 11-12,15

long sitting self, 379, 379-380, 3S0

-

Plasma volume. albumin for,234


Platelet count. laboratory tests of, 190, 191 t

self, 377-382

Platelet inhibitors, pulmonary hemorrhage and, 108

gravity/physiology and, 300--30 I, 30 I

Platypnea, patient history and, 135

head down, 312

Pleural effusions

mechanical 316

,

cardiopulmonary effects uf, f02-I03, 103, 109

moni toring of,317-318

congestive heart failure and, 101

obstructive lung disease, primary/ICU, 585-586


physiological effects of, 301-313,302

patient a"",,ments and,2 27·- 228 radiography of, 164, 165, 166

Pleural tluids, imbalance dkcts of, 101

Pleuritic chest pain, paticnt history and. 138

frequent changes, 3 I 3,315

prescripti on for, 313-316,314 vs. routine, 30 I

prone, 312-313

PMI; sec Point uf maximum impulse (PMI)

rotation for infants,649,649, 650--651

Pneumonias

side-lying positions, 311, 311-312

di f ferential diagno sis of, 227t

supine, 308-309,309,310

management of, 472476

upright,302-308,303,304,305,306,307,308


ventilation facilitation and, 383-415

patient assessments and 227

asymmetrical dysfunction and,405-406

pediatric, 642

butterfly techniques and, 408,409, 410

.

radiograph s of, 162,162,163, 164, 164,167

chest/shoulders and, 392


counter rota tion 407-408, 409

,


1-26

Index

Preoperative management

diaphragm inhibition and, 402-405,404,405 diaphragmatic breathing and,389,3'10,391,392,394

pediatric chest physical thelapy,659-660 primary dysfunction/acute .surgical conditions anu, 502

395,396

Pressure gradients (P)

dressing techniques and, 389

in blood now, 15

dynamic activities and,388-389 eccentric resistance techniques and,414

Pressure support ventilation (PSY),ucfJllcd, 7. X

expiration and,388

Pressure/volume, cardiopulmonary physiology and,57-58, 58,66

glossopharyngeal breathing and, 410-4 I 2,4 I 2

Preterm infants associated cardiology of, 639t

inspiration and,387-388 lateral costal breathing and,396, 397,399

bronchopulmonary dysplasia and,641

manual. 413-414

chest therapy for

mobilizing the thorax in,399-401,400

airway suctioning,653, 657

muscles and,401-405,402,404,405

postural drainage, 652, 653t,654-656 dysfunction factors in, 638t

normal timing and,399 postural inhibition, 406

hyaline membrane disease in,640-641

primary vs. secondary dysfunction and, 390,391

patent ductus arteriosus in,63lJ-MO respiration in,637-638, 638t

pursed-lip breathing,410 repatterning, 393

Preventive care, ICUs and, 571-572

rolling,388

Primary cardiovascu.lar disease. chronic primmy dysfunction and management of,525-535

sitting, 388


snifli ng, 392

Primary dysfunction

standing,389

chronic

strategies for,387-389 symmetrical,405-406

angina, 525-526

verbal,414-415

asthma, 519-520 bronchiectasis, 520-521

vocalization enhancement, 412-41.5

chronic airnow limitation, 514

Positive expiratory pressure (PEP) in airway clearance,327-328

chronic bronchitis,514-516

clinical applications and,354--358,355

cystic fibrosis,521-522

Positron emission tomography (PET), defined,199,20 I t

diabetes mellitus,533-535

Posteroanterior (PA) radiographs,interpretation of, 159-160

emphysema,516-518

Postoperative complications,621,621--624, 622

hypertension,531-533 interstitial lung disease,522-523

in artificial airways,763-764

lung cancer, 523·- 524

mcchanical, 764


hypoxemia and, 621 management of, 621, 621-624

obstructive patterns in,514-522

pain and, 623

peripheral vascular disease,529-531

pulmonary embolism and,623-624

primary cardiovascular disea,,:, 525-535 restrictive patterns in, 522-523

Postoperative manngcment pediatric,659--660

valvular diseasc, 528-529

primary/acute surgical conditions and,502, 502-505,506,507 Postural drainage (PD)

exercise testingitraining in, 417-423 intensive calC of,579-596 asthma,589-591

clinical applications and,343-344,345 contraindications for,330-331

caruiopulll1onary failule,579,580l, 581

for infants. 652, 653t,654-656

congestive heart failure, 594, 594,596 coronary artery disease,592-596

Postural inhibition, ventilation facilitation and,406 Potassium iodide, pharmacology of,786

myocardial workload redLtction,592, 593-594, 596

Powder u inhalers, spacers for,786

obstructive lung disease, 581--589,589

Prazosin (Miniprcss),pharmacology of, 778

open heart surgery, 595,596 restrictive lung uiseasc, 590-592

Precapillary arteriole function,in oxygen transport,18 Prednisone for organ transplants,717

primary vs . secondary,390,39 I secondary to acute medical conditions,469-492

side effects,7 I 8

alveolar proleinosis,478

pharmacology of, 785

alveolitis,477-478

Preload, cardiopulmonary physiology of,65

angina,488-490

Preload function, in oxygen transport, 13

asthma, 481-483


Index

atelectasis, 470-472, 471

Pulmonary deVelopment

bronchiolitis, 477

in rmr cllloskclctal/neuromuscul"r disorders, 695-696

chronic airl10w limitation, 478-41:1 I

pediatric, 637--638, 63 t


cardiac, 636-637

cy stic fibrosis, 483-486 em phy se ma , 478-481

Pulmonary disorders

respiratory failure and, 618-619, 619

hypL'rlellsion, 488

sy:;temie, cardiac diseases and, 10 I-I 02

intL'rstitial pulmonary fibrosi" 486

Pulmonary edema, noncardiogenic, defined. 625, 625

myocardial inrarction, 490-491

Pulmonary embolism

pn ulllonias, 472-47/i

differential d i agnosis of, 227t

tuherculosis, 4 7-4gS


sectlillidry to a utc surgical conditions, 495-508

respiratory failure and, 579, 580t, 581

c'ardiovascu idr sur»cry. 501-502

Pulmonary eosinophilia, palhorhysiology of, 85

extrinsic' ractors. SOO

Pulmonary functio n tests (PFf), 145-151

intnnsiL' ract,llS. SOli

air flow measurements, 147, J 48, 149

11\(,bility!rclulllhency. SOO

flow volume cu rve , 147, 148, 149

pathophysiology, SOli

forced expira tion . 147

c lo sing volume/airway closure, 149, 149-150

peri<>pcrativc course, 4l)(,. 4Sl6-501l, 4t)K postoperative manageillent, 502, 5()2-, ()5. 5116,507

maximal voluntary ventilation, 149, 149-1 SO

prL()p r;Jliyc 1ll00Ilagl:IllL'llt, 50'2

ckad space. 145-140

surgical errects ..'iOO

clel'ineel, 145

surgical prcp, 499

diagnosis and

obstructive lung disease. 150, 150-ISI

thoracic, 500-502 Progressive systemic s clerosis (sclerodcrma), pathophysiology oL 89

restrictive lung disease. 150, 15(),-151 lung capacities, 14 6. 147

Pronc positioning, 312-31

lung volumes. 146, 1 46 - 1 47

on elbows assist techniqucs, 371:\, 378-379 infant positional rotation. 64Sl, 649, 650-651

Puirllonary hemorrhages anticoagulant.s and. 108

Propranolol (Inderal), pharmacology of. 778-779 Proteins, laboratory tests or, 190, 19 1 t, 194, 194t

hematologic conditions and, lOS ' Pulmonary hemosiderosis, idiopathic, p athophy si 'log y 01.

Pseudomonas acruginosa

Pulmonary hypertension

in bacterial pneumonias, 474-475

exercise testing/training for, primary dysfunction, 41 X

pediatric cystic fibrosis and, 643-644

patient history and, 139

PSV: see Pressurc support vcntilation (PSV)

Pulmonary scans, defined. 20 I t, 205-207

Psychological considerations, exercise testing/training and,

Pulmonary thrombocmboli, hematologic conditions and, lOS

secondary elysfunction, 425-426, 426

Pulmonary Lransplants

Psychosocial considerations oxygen transrorr thrcats and, 255

assessments in, 708

transplant paticnts "nel, 705-706

considerations in

PTT: see Panial thromboplastin (PIT)

availability, 704

Pulleys, for oxygen transport treatment. 259-260, 260

ethical,704-705

Pulmonary aging c hanges

organ donation. 704

exercise and, 675-677, 677, 677t

organ preservation, 704-706 patieot education, 706

structural/functional, 674-677,675, 675t Pulmonary alveolar proteinosis. pathophysiology of, 86, 86--87

psychosocial implications, 705-706

Pulmonary aneritis, cardiopulmonary ef fects of, 102-103, 103

rejection, 704

Pulmonary ,u1cry balloon Ilotation catheters: see Swan Ganz catheters

trends, 706

Pulmonary artery occlusion prcssure (PAOP). intensive care units

wai ting list criteria, 705, 705

w a it ing time, 70S

measurement of, 241-243 Pulmomuy artery pressure (PAP), intensive care units measurement of. 241-241

equipment/monitoring in, 708-709, 715

Pulmonary artcry wedge pressure (PA WP), intensive c
when to, 704 facility vs. horne based rehabilitation in, 716-718 goals in, 709, 7J2, 713t, 7J5 h istor y of, 704

anatomy of. 4Sl-50

interventions in, 709, 712-713,713t, 715-716, 716

oxygen transport threats and, treatment, 261

medication in, 717-718


1-27

1-28

Index

other transplants and, 709-710

metabolic demand and, 267


RBC; see Red blood count (RBC)

post-transplant care in, 708. 712-713, 713t

Recording, electrocardiograms and, 172, 172-174. 173

pre-transplant care in. 708-709. 710

Recumbency

rejection signs in, 715

intensive care units and, 568

surgery and. 706

respiratory failure and. 579, 580t, 581

Red blood count (RBC), laboratory tests of, 190-192, 191t

therapy in assessments. 707-708

Ret1exes, cardiopulmonary physiology of, 55, 55-56

defined. 708-709. 710, 710-713

Rejection

medical management, 707, 707t

cardiac signs of. 714. 715, 716

musculoskeletal considerations. 707, 709-710

of organ transplants. 704

physiology, 707

pulmonary signs of, 715

Renal disorders

therapist requirements, 706

Pumps, cough, 368

acid base imbalances and, 154

Pursed-lip breathing


for primary dysfunction, 420-421

chronic secondary dysfunction and, 560-561

management of. 560-561

ventilation facilitation and. 410


Push-ups. serratus, 405

effects of, 108, 108

Q

organ damage and, 108

Quadriplegic patients, chronic secondary dysfunction and.


Questionnaires. for patient histOlY, 128


respiratory failure and. 620

systemic, J08, 108

Repatteming techniques, ventilation facilitation and, 393

R

Reserpine, pharmacology of. 779

RA; see Rheumatoid arthritis (RA)

Respiratory centers, cardiopulmonary physiology of, 54-55

Radiography

Respiratory distress syndrome (RDS); see also Adult respiratory

distress syndrome (ARDS)

abscesses. 164, 164

alveolar disease, 162, 162

atelectasis, 164-165, 165, 166

basic structures/shapes, 160

preterm infants and. 637-638, 638t


Respiratory fai lure, 617-630

bronchi, 162, 162

acid-based abnormalities and, 6 I 9

bronchiectasis, 162, 163, 164

arterial blood gases and. 156

bronchograms in, 162. 162

cardiac dysrhythmias and. 619--Q20

congestive heart failure,164. 165, 166, 167

complications of, 618--Q19, 619

description of, 159-161,160

fluid/electrolyte abnormalities and, 6 I 9

edema, 165,166

gastrointestinal dysfunction and, 620

emphysema, 162, 163

metabolic dysfunction and, 617--Q I 8

fixed position, 159-160

myocardial dysfunction and, 620

interstitial pulmonary disease, 162, 163

neurological dysfunction and. 62O--Q2 I

kyphoscoliosis, 167, 167

primary dysfunction and. 579, 580t, 58 I

lateral chest, 159-160

pulmonary dysfunction and, 618--Q19, 619

malignancies. 163, 165, 166

renal dysfunction and, 620

motion, 159-160

pleural effusions. 164, 165, 166

thromboembolism. 620

Respiratory muscles

pneumonias. 162, 162, 163. 164,167

defined, 26--40

pneumothorax. 164, 165

exercise training for fatigue, 443-451

assessments in, 447

posteroanterior (PA), 159-160

requirements for. 159-160. 161-162

etiology of, 444-447

routine exams, 160-161

inspiration. 444-448, 448-450. 450

suspended motion, 159-160

isocapnic hyperpnea, 450-451

uremia. 165, 166

isocapnic hyperventilation, 449-450

Radiopharmaceuticals, nuclear imaging and. 197-207


Rales, defined, 219-220

treatment for, 447-448

Range of motion (ROM) exercises

dying patients and, 577, 577

oxygen transport thn;ats and, 254

secondary dysfunction and, 427-428, 432-433, 435


Index

secondary dysfunctionllCU,training for, 610-- 612, 61 I, 612 Rest, bed

1-29

Sclerosis (scleroderma) pathophysiology of, 89

alternatives to,293-294

progressive systemic,pathophysiology of,89

hazards of, 293

SCM; see Sternocleidomastoid (SCM)

indications for, 294

Scoliosis, respiratory failure and, 579, 580t,581

as therapy, 291-292

Secondary dysfunction chronic

Restrictive lung diseases

ankylosing spondylitis and, 557-558

pathophysiology of, 83-89 diffuse interstitial pulmonary fibrosis, 83-85

cerebral palsy and,546--547

eosinophilic granuloma, 85-86

chronic renal insufficiency and,560--561

idiopathic pulmonary hemosiderosis,87

collagen vascular/connective tissue diseases and, 555-556

progressive systemic sclerosis (scleroderma),89

hemiplegia and, 541-543

pulmonary alveolar proteinosis, 86,86--87

late sequelae of poliomyelitis and, 550--552

pulmonary eosinophilia,85

multiple sclerosis and, 544-546

pulmonary infiltrates, 85

muscular dystrophy and,538-539

rheumatoid arthritis,88

osteoporosis and, 553-555

sarcoidosis, 87-88, 88

Parkinson's disease and, 543-544

systemic lupus erythematosus (SLE), 88-89

rheumatoid arthritis and,558-560 scleroderma and. 556--557

primary/ICU,590--592 management of, 591--592

spinal cord injury and,548-550

pathophysiology of, 590--591

systemic lupus erythematosus and, 555-556 thoracic deformities and,552-553

pulmonary function tests and, diagnosis, 150,150-151

ICUs, 599-615

Rheumatoid arthritis (RA)

burns, 612-615


fractures,605-606

management of,558-560 pathophysiology of,558-560

head injuries, 606--609, 607, 608 hemothorax, 605

pathophysiology of, 88 Rhonchi, defined, 219-220

musculoskeletal trauma, 603-604, 694

Rhythms, electrocardiograms and, 176--177, 177

neuromuscular disease, 600--602

Ribs

obesity,602-603

anatomy of,24-25, 25y

pneumothorax, 605

secondary dysfunction and. cage mobilization,436

respiratory muscle training, 610-- 612,611, 612

secondary dysfunctionfICU,fractures,604-605

rib fractures, 604-605 spinal cord injuries, 609-612

Right ventricular ejection fraction (RVEF'), nuclear imaging of, 200

trauma, 605

Right ventricular pressure (RVP),intensive care units measurement of,241-243

vs. primary, 390, 391

Rocking assist techniques, knees-hands, 381-382

Secretions

Rolling techniques, ventilation facilitation and,388

obstructive lung disease and,primary dysfunctionfICU,587-588 treatment of, 782,783, 786

ROM exercises, metabolic demand and, 267 Rowing machines, for oxygen transport treatment, 259-260,260 Rural environments,oxygen transport and, 16 RVEF; see Right ventricular ejection fraction (RVEF)

Sedatives for ICUs, 572-573 respiratory failure and, 579, 580t,581 Self assist techniques, 377-382

s

Sepsis, management of, 628t,628-629

SA; see Sinoatrial node (SA)

Serratus

Sacrum mobilization,secondary dysfunction and, 436

anterior anatomy of, 29-30

Salmeterol (Servant), pharmacology of,778

push-ups for, 405

Sarcoidosis, pathophysiology of,87-88,88 Scalenes anatomy of,29, 29 ventilation and, 402

Shaking in airway clearance, 325 clinical applications of,346--349, 347, 348 Shock

Scintillation detectors,defined, 198

cardiogenicfICU and, 245

Scleroderma

management of, 627-628,777,778

chronic secondary dysfunction and,556--557

Shoulders

progressi ve systemic, 89

mobilization, 436

respiratory failure and, 579,580t, 581

ventilation facilitation and,392


1·30

Index

Sickle SIMV;

of, 108

anemia, cardiopulmonary

Side-lying body positioning, 311, 31 ,ce

Stretch reflex, cardiopulmonary physiology of,

12

Synchronized intermittent mandatory ventilation (SIMV)

Single crystal cameras, for nuclear imaging, 198

Suctioning, of artificial airways, 768, 769-77 I, 77!, 772, 773, 773t

Supine positioning. 308-309, 309, 310

Single photon emission tomography (SPECT), defined, 198-199,

201 t, 202-203

ICUs and, 570

Supraventricular arrhythmias,

In

electrocardiograms, 177, I

179,179,180,181

Sinoatrial node (SA)


Surfactants, for

oxygen transpOl1 and, 18

Surgery

Sitting techniques, 379,379-380, 380

transport treatment, 259-260, 260

open heal1, primary dysfunction/ICU, 595, 596

for primary dysfunction, 421

organ transplant, 706


primary dysfunction secondary to, 495-508

Skin, patient assessments and, 214, 214


SLE; see Systemic lupus erythematosus (SLE)

extrinsic factors, 500

Sleep apnea



mobilnylrecumbency, 500

respiratory failure and, 579, 580t. 581


Sleep di:;turbance, oxygen transport threats and, 255

perioperative course, 496, 496-500, 498

SI\1I;

postoperative management,

Sustained maximum inspiration (SMI)

502-505,506, 507


Smoking

oxygen transport

16

;,urgical effects, 500

patient history and, .141-142

surgical prep, 499

Sniffing techniques, ventilation facilitation and, 392

thoracic, 50( 502

Sodium iodide, pharmacology of, 786

Suspended motion nldiographs, interpretation of. 159-160

Soft tissue therapies, secondary dysfunction and,

Sustained maximum im:piration (SMI), defined,

Spacers, for metered-dose inhalers (MDI), 786

Swan Ganz catheters, in ICUs, 233, 241-243, 243

SPECT imaging;

Single photon emission tomography (SPECT)

Spinal cord injuries

Symmetrical positioning, ventilation facilitation and, 405-406

Sympathomimetic drugs, pharmacology of. 784-785


Synchronized intermittent mandatory ventilation (SI\1V), defined,

pathophysiology of,

Systemic circulation, anatomy of, 48-49

secondary dysfunction/ICU, 609-612

Systemic diseases. cardiopulmonary effects of. 99-112


cardiac, 100-10 I


connective tissue, !O3,103

Spirometers, f1uner, for oxygen transport treatment, 259-260. 260

endocrine. J 09····110. I 10

Spondylitis, respiratory failure and, 579, 580t, 581

gastrointestinal, 107, 107

Standing techniques, ventilation facilitation and, 389

hematologic, 108-109, 109

Glireus,

755

Sympatholytic drugs, pharmacology of, 779


S/aph)loCliccus

55-56

Stroke, cardiopulmonary effects of, 104

pediatric cystic fibrosis and, 643

Starling effect

immunological, J 10

liver, 107-108, 108

cardiac effects on, 101

musculoskeletal, 102,102-1 m

cardiopulmonary physiology of, 65

neurological, 103-107, 104

nutritional, 110- I I I, I J I

plasma protein disorders and, 109

Sternocleidomastoid faciliwtion, ve-lltilalion and, 402

phy:;ical

Sternocleidomastoid (SCM), anatomy of, 28-29, 29

pulmonary, 101-102

Sternum, anatomy of, 24

impact, 99-100

rellal, 108, 108

Stethoscopes, auscultation and, 217, 217

Systemic lupus erythematosus (SLE)

Sirepiococcus B, pneumonia in neonates, 642


StreplOcoccUS pyogenes, in bacterial pneumonias, 474-475

chronic semndary dysfunction and

Stress


emotional, 3


Stress testing, nuclear/cardiovascular

exercise, 199



Systemic sclerosis (sclerode!ma), progressive, pathophysiology of, 89

Systole, ventricular. cardiopulmonary physiology of, 66

pharmacologic, 199


Index

Thorax

T

anatomy of, 23-25, 24. 25

T3; sec Triiodothyronine (T3) T4;

1-31

mobilization of, 399-401,400

Thyroxine (T4)

ec

secondary dysfullcl"ion and. 436

Tachycardia, trc.
Thromboembolism

Tachyuysrhythmias. intensive care of, 239, 240t-241t

cardiopulmonary

Tachypnea. patient assessments and, 216 Tactile fremitlls. patient assessments and, 225, 225,226

Thrombosis, deep vein, management of, 623--624

Tc-99M-macroaggregated albumin; see Technetium-99M-

Thyroid function, laboratory tests of,193t,194

Illacroaggregatcc\ albumin

Thyroid stimulating hormone (TSH), laboratory tests of. 194

Tc-99M-Pyp; scc Technctiulll-99M-pyrophosphate (TcPyp)

Thyroxine (T4), laboratory tests of, 194

Tc-99M-sl)stamibi; sec Ted1l1etium-99M-sestamibi

TI A; see Transient ischemic attack (TI A)

Tc-99M-teboroximc, Technctium-99M-tcboroxime Tc-99mDTPA; see Technetium-99M-diethylene triamine penta-

acetic (DTPA) aerosol


home-based care communication in, 728-729

Tissue assessments, in oxygen transport treatment, 262

in ICUs, 574, 575

Tissue extraction, oxygen transport and, 18-19

Tec hnct ium-99M-die t hy l ene triamine pe nta-ac etic (DTPA)

Tissue perfusion

aerosol,for ventilation-perfusion scans,20 It, 206

in oxygen transport,S

Technetium-99M-mncroaggregated albumin, for ventilation-

oxygen transpOIt threat.s

perfusion scans, 20 It, 206

TLC; see Total lung capacity (TLC)

Technetiull1-99M-pyrophosphate (TcPyp),defined, 20 I t,203

TLSO; see Total contact thoracic lumbar sacral orthosis (TLSOs)

Technetium-99M-sestamibi, defined,20 I t, 202

TOF;

Technetium-99M-teboroxime, defined,20 I t, 202

see Tetralogy of fallot (TOF)

Total contact thoracic lumbar sacral orthosis (TLSOs), defined,

TEE; see Transesophagcal echocardiography (TEE)

384-385

Tenderness. patient assessments and, 223

Total lung capacity (TLC)

Tcrazosin (Hytrin), pharmacology of,778

sickle cell anemia and, 109

Terbutaline (Brethine, Bricanyl), pharmacology of,778

systemic disease effects on, 106

Testing

Toxic-inhaled materials,oxygen transport and, 16

arterial blood gases and, 153-157

Tracheas

documentation and, 123-126

anatomy of, 36-40, 37, 39t

electrocardiograms, 169-187

deviation assessments and,225, 226

exercise pre scriptions and,274, 274, 276-277, 280--285, 281, 282t, 283t, 284-286,290, 290--291

TracheomaJacia, respiratory failure and,579, 580t, 581 Tracheostomy tubes, artificial airways, 764-766, 765,767-771, 768,771-774,773t

training and, secondary dysfunction, 426-432

cuff inhalation, 765-766

ICU unit monitoring systems,229-246

metal,764

measurements and, 117-123

plastic, 764-765, 765

multisystem laboratory assessments and, 189-195

Training,exercise and, 274,274, 276-277, 280--285, 281,282t,

nuclear imaging/radiopharmaceuticals, 197-207

283t,284, 285, 286. 290, 290-291


Tranquilizers, for I CUs, 572-573

pulmonary function, 145-15 I

Transesophageal echocardiography (TEE), defined, 197, 20 It,

routine radiographs, 16(}-161

204, 205

x-ray interpretation, 159-167

Transient ischemic attack (TI A), transesophogeal

Tetanus, respiratory failure and, 579, 580t, 581

echocardiography (TEE) for, 205

Tetralogy of fallot (TOF), pediatric management of,640

Transient l
ThAIRapy (TM), clinical applications and, 358, 358-359

management of, 641

Thallium 20 I, for cardiovascular testing, 200-202, 20 It

Transplant patients, 703-718

The Flutter (TM), for airway clearance, 328

cardiac, 708

Theophylline,phannacology of, 785

acute phase care, 710--711,714

Thempist requirements

assessment, 708

in I CUs, 568, 569

equipment/monitoring, 708-709

for transplant patients, 706 see

Tidal volume (TV),systemic disease effects on, 106 Timing asymmetrical dysfunction and, 406

Teams

Therapy, physical;

effects of, 108


exercise guidelines, 712

Physical therapy

Thoracic disorders, primary dysfunction secondary to, 500--502

facility vs. home based rehabilitation, 716-718 goals, 7 J 2


1-32

Index

interventions, 710-711,714

Tumors,respiratory failure and,579, 580t, 581

medication, 716-718

Turner's syndrome, associated cardiology of,639t

outpatient care, 713-714, 714

TV; see Tidal volume (TV)

post-transplant,708

Two-lumen catheters, in ICUs, 241-242

pre-transplant, 708

u

rejection signs, 714, 715,716

considerations for

Upper airways, anatomy of,32-36,33, 34, 35

Upper/lower extremity exercise,testing/training and,primary

availability,704

ethical, 704-705

dysfunction,419-420

Upright body positioning,302-308,303,304,305,306, 307,308

organ donation,704

organ preservation, 704-706

to supine positions, lCUs and, 570


Urban environments, oxygen transport and, 16

psychosocial implications, 705-706

Uremia, radiography of, 165,166

rejection,704

Urinary retention, treatment of,780-781

trends, 706

v

waiting list criteria,705, 705

Valves

waiting time,705

when to,704

flutter,259-260,260

history of, 704

in heart anatomy, 45,45-47, 46

Valvular disease

other transplants and,709-7.10 pulmonary

chronic primary dysfunction and

assessments in, 708


equipment/monitoring in, 708-709,715


facility vs. home based rehabilitation in,716-718


goals in,709, 712, 713t, 715


interventions in,709, 712-713,713t,715-716,716


medication in, 717-718

VAPS; see Volume-assured pressure support (VAPS)

outpatient in,714-716, 716

Vascular resistance

post-t.ransplant in,708,712-713,713t

Vascular systems

(R), in blood flow,15

pre-transplant in,708-709, 710

aging changes in,673,673-675, 674t

rejection signs in, 715

peripheral laboratory tests and,192, 192t

surgery and,706

Vasodilators, treatment with, 777, 778

therapy in

Vasopressor agents, for lCUs,572-573

Ventilation facilitation,3 3-415

assessments, 707-708

defined, 708-709, 710, 710-7!3

asymmetrical dysfunction and,405-406

medical management,707,707t

buttertly techniques and,408, 409,410

musculoskeletal considerations, 707, 709-710

cardiopulmonary physiology of,59-60

physiology, 707

chest/shoulders and, 392

diaphragm inhibition and,402-405, 404, 405

therapist requirements,706

diaphragmatic breathing and,389,390,391, 392,394,394,

Trapezius

anatomy of, 30,30

395,396,396

ventilation and, 402

dressing techniques and,389

Trauma, secondary dysfunctionllCU and, 605

dynamic activities and, 388-389

Treadmill, for oxygen transport treatment, 259-260, 260

eccentric resistance techniques and,414

Trepopnea, patient history and,135

expiration and,388

Trihexyphenidyl HCL (Artane), pharmacology of, 783

glossophMyngeal breathing and,410-412,412

Triiodothyronine (T3),laboratory tests of, 194

inspiration and,387-388

Trisomy 13, associated cardiology of, 639t

intrapulmonary percussive, 363, 364

Trisomy 18, associated cardiology of,639t

lateral costal breathing and, 396, 397, 399,399

Trisomy 21, associated cardiology of,639t

manual, 413-414

Trypsin (Tryptar), pharmacology of, 786

mobilizing the thorax in,399-40 1,400

TSH,Thyroide stimulating hormone (TSH)

muscles and,401-4D5, 402, 404, 405

TINB; see Transient tachypnea of the new born (TINB)

musculoskeletal/neuromuscular disorders and, 680

Tuberculosis

normal timing and, 399

management of,488

oxygen rransport and,5,16


to perfusion ratio, 17


Glossary

Vital capacity (VC), Duchenne's muscular dystrophy and, MH

positioning in, 383-385,385, 386, 392,413

primary vs. secondary dysfunction and, 390,39 J

G-33

Vitamin-K deficiency, pulmonary hem orrh age and, lOR

pursed-lip breathing and,410

Vo,: see Oxygen, consumption

repalterning and, 393

Vocalization enhancement, ventilation facilitation and, 412-415

rolling,388

Voice breath sounds,patient

sitting, 388

Volume-assured pressure support (YAPS), defined, 758

assessments and, 220

sniffing, 392

Volume/pressure, cardiopulmonary physiology and 57-58, 58, ,

standing, 389

w

strategies for, 387-389

Waiting lists,for transplant patients, 705, 705

verbal, 414-415

time of,705

voc liz tion enhancement,412-415

Ventilation-perfusion lung scans, defined,201t, 206

Walking,primary dysfunction and, 421

V.:ntilator withdrawal, obstructive lung discas.: and, primary

Wall motion,nuclear imaging of,200

dysfunction/ICU, 588,5RH-589,589

WBC; see White blood count (WBC)

Weights, for oxygen transport treatment, 259-260, 260

Ventricular function

Wheezing

al'tcrload in, 13

defined,219-220

cardiopulmonary physiology of, 65, 65--67, 66,67t

patient history and,135

diastol.: physiology of,66

electrocardiograms and, 180-184, 182, 183,184

White blood count (WBC),laboratory tests of, 190-192,1911

alThythmias, 177, 178, 179-184,179-184

Williams syndrome, associated cardiology of, 639t

conduction, 170--172, 171

Work environments

facility-based

blocks, 184-186,185,186

myocardial infarction, 186-187, 187

ratc,174, 174-176, 175, 176

recording, 172, 172-174, 173

177

use of,169-170

care and,724-725


evaluation of,174, 174-177, 175, 176, 177

rhythms,176-177,

x

X-ray testing abscesses. 164,164

alveolar disease, 162, 162

atelectasis, 164-165, 165,166

left

assist devices/ICU,245

basic structures/shapes, 160

ejection fraction,200

bronchi, 162, 162

end diastolic volume, 13

bronchiectasis, 162,163, 164

output,636

bronchograms in,162, 162

pressurenCU, 241-243,245

left atrial pressure, 241-243

output and,

II,

66

12, 14,17,636

patient assessments and,220--221

congestive heart failure,164, 165,166,167

description of, 159-161, 160

edema, 165,166

emphysema, 162,163

preload, 13

fixed position, 159-160

right

interstitial pulmonary disease, 162, 163

ejection fraction, 200

kyphoscoliosis, 167,167

prcssurenCU,241-243

lateral chest, 159-160

septal defects/ICU and,245

Venue function, oxygen transport and, 18

malignancies,163, 165,166

motion,159-160

Verbal techniques, ventilation facilitation and, 414-415

pleural effusions, 164,165, 166

Vesicular breath sounds, patient assessments and,218-219

pneumonias, 162, 162, 163, 164, 164, 167

Vibration th.:rapy

pneumothorax, 164,165


posteroanterior (PA), 159-160

clinical applications and, 346-349,347, 348

requirements for, 159-160, 161-162

for infants, 652--653,657

routine exams, 160-- 16 J

Viral p ncumo nias management of, 474


in secondary

dysfunction, 426-427

suspended motion, 159-160

uremia, 165,166

Viscosity,of blood, 14

Xanthines, pharmacology of,785

Visual inspection, pntient assessments and,211-214,214

133Xe gas, for perfusion testing,20 It, 206


Principles_and_Practice_of_Cardiopulmonary_Physical_Therapy__3rd_Edition.pdf

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