Boards and Beyond: Cardiology A Companion Book to the Boards and Beyond Website Jason Ryan, MD, MPH Version Date: 9-20-2017
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Table of Contents Cardiac Anatomy Cardiac Physiology CV Response to Exercise Blood Flow Mechanics Mechanics Regulation of Blood Pressure PV Loops Wiggers’ Diagram Venous Pressure Tracings Starling Curve Cardiac Ischemia STEMI Unstable Angina/NSTEMI Stable angina EKG Basics High Yield EKGs Action Potentials AV and Bundle Branch Blocks Atrial Fibrillation AVNRT WPW Antiarrhythmic Drugs
1 3 7 9 15 19 23 25 27 30 37 41 43 49 54 58 62 67 73 75 77
Heart Sounds Heart Murmurs Heart Failure Basics Systolic and Diastolic Heart Failure Restrictive Restricti ve Cardiomyopathy Acute Heart Failure Chronic Heart Failure Cardiac Embryology Shunts Cyanotic Congenital Heart Disease Coarctation Coarctati on of the Aorta Hypertension Hypertensio n Secondary Hypertension Hypertension Hypertensio n drugs Valve Disease Shock Pericardial Pericardi al Disease Aortic dissection Cardiac Tumors Hypertrophic Cardiomyopathy Endocarditis Endocardit is
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88 92 97 103 106 109 114 118 121 125 130 133 136 141 149 155 159 165 169 171 175
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The Heart Chambers
PVs
SVC PA LA RA
Cardiac Anatomy
Aorta
LV
IVC
Jason Ryan , MD, MPH
RV
The Heart
Anterior-Posterior Structures
Valves
Right Ventricle Anterior PV
AV
Left atrium
Posterior
TV
MV
Coronary Arteries
Coronary Artery Territories
90% Right dominant 10% Left dominant
Heart drains to coronary sinus CS Right atrium
•
•
•
Left Main LCX
RCA
•
LAD
PDA
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Anterior wall, anterior septum, apex LAD Lateral wall LCX Inferior wall, inferior septum PDA •
RCA 90% of the time
•
10% of people “left dominant” - LCX supplies PDA
Occlusion occurs LAD>RCA>LCX
Mitral Valve
Cardiac Electrical System •
Twopapillarymuscles •
•
•
AL has dual blood supply
•
PM single blood supply
•
AL
•
PM
•
SA/AV node Usuallysupplied by RCA
Anterolateral (AL) Posteromedial (PM) LAD/LCX
SA
RCA (or LCX)
AV
Inferior infarction can lead to rupture of PM pap •
•
LBB His
Severe mitral regurgitation Acute heart failure
SA Node – Right atrial wall AV Node –Interatrial Septum HIS – Interventricular septum
2
Purkinje Fibers RBB
Heart Volumes ESV EDV
Cardiac Physiology Jason Ryan, MD, MPH End diastolic Volume Filling completed Contraction beginning
Important Terms •
•
•
Important Terms
Stroke Volume (SV) = EDV - ESV
•
Ejection Fraction (EF) = SV / EDV Cardiac Output (CO) = SV * HR •
Blood Pressure Terms •
•
•
•
•
Largely determined by TRP
Pulsepressure •
SBP – DBP
•
Proportional to SV
•
Blood returned to left ventricle
•
Should be equal to the cardiac output
Total peripheral resistance •
Resistance to blood flow from peripheral structures
•
Vasoconstriction
•
Vasodilation ↓ TRP
↑ TPR
Mean arterial pressure (MAP) • 2/3 DBP + 1/3 SBP
Largely determined by cardiac output
Diastolic Blood Pressure (DBP) •
Venous Return (VR)
Blood Pressure Terms
Systolic Blood Pressure (SBP) •
End systolic Volume Emptying completed Relaxation beginning
3
Example: SBP 120/80 • MAP = 80 + 1/3 (40) = 93.3
Cardiac Output
Cardiac Output •
•
•
Determinants
Very important physiology parameter
1. Preload
Must rise to meet demands More cardiac output = more work/O2
2. Afterload 3. Contractility
•
CO = HR x SV
•
More beats per minute = more work
•
More volume per beat = more work
4. Heart rate
Preload •
•
To INCREASE Preload
Amount of blood blood loaded loaded into left left ventricle ventricle
1. Add volume(blood, volume (blood, IVF)
Also how much stretch is on fibers prior to contraction
2. Slow heart rate more filling more volume 3. Constrict veins
•
Some books say “length” instead of “stretch”
•
More preload = more cardiac output
•
More preload = more work the heart must do •
↑O2 required
•
2. Raise heart rate (opposite mechanism above) 3. Pool blood in veins Mechanism of action of nitrates Relieve angina
•
Lower preload less work for heart
Veins hold LARGE blood volume
•
Response to blood loss venous constriction
•
Sympathetic stimulation α1 receptors in veins
Important Terms
1. Remove volume(bleeding, volume(bleeding, dehydration)
•
Veins force blood into heart
•
Preload
To DECREASE Preload
•
•
•
LVEDV • Volume of blood in the left ventricle when filled LVEDP
• Pressure in the left ventricle when filled
4
Afterload •
•
•
•
To INCREASE Afterload
Forces resisting flow out of left ventricle
1. Raise mean blood pressure
Heart must squeeze to increase pressure Needs to open aortic valve push blood into aorta This is harder to do if:
2. Obstruct outflow of left ventricle
•
Blood pressure is high
•
Aortic valve is stiff
•
Something in the way: HCM, sub-aortic membrane
•
To DECREASE Afterload
Contractility
1. Lower the mean blood pressure
•
2. Treat aortic valve disease, HCM More afterload = more work
•
•
•
•
More oxygen required
•
Sympathetic innervation to heart
•
Circulating catecholamines (epinephrine, norepinephrine)
•
↑ calcium release from sarcoplasmic reticulum
•
Triggers: stress, exercise
•
•
•
•
Dopamine, dobutamine, epinephrine, norepinephrine Inhibits Na-K pump ↑ calcium calcium in myocytes
5
Beta blockers
Calcium channel blockers •
Verapamil, diltiazem
•
Less calcium for muscle contraction
Heartfailure •
Digoxin •
Also increases heart rate
Sympathetic Sympathetic systemblocking drugs •
Sympathomimetic drugs •
Ejection fraction = index of contractility Major regulator:sympathetic regulator: sympathetic nervous system
To DECREASE Contractility
Sympathetic nervous system activity •
How hard the heart muscle squeezes
•
To INCREASE Contractility •
Aortic stenosis, HCM
Disease of myocytes
Heart Rate •
•
•
•
Heart Rate
Increases cardiac output under physiologic conditions
•
↑ HR = ↓ stroke volume (less filling time)
Mainly regulated by sympathetic nervous system Also increased by sympathomimetic drugs Decreased by beta blockers and calcium blockers e m ul o V e k or t S
Heart Rate
Heart Rate •
Heart Rate
↑HR = ↑ cardiac output
•
•
Sympatheticnervoussystem: ↑HR and ↑contractility Stroke volume rises with increased HR
CO = SV * HR t u
e m
tp lu u o O V c e ia k dr or t a S C
Heart Rate
Heart Rate
Work of the heart
Heart Rate •
•
Myocardial O2 demand •
At pathologic heart rates ↑ HR = ↓ CO High heart rate with arrhythmia can lead to ↓CO
•
•
•
CO = SV * HR t u
Preload (LVEDV/P) Afterload(MAP) Contractility (EF) Heart Rate
Hearts starved for O2 Reduce O2 demand Low output Need to increase work
tp u O c ia d r a C
Heart Rate
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Response to Exercise
Cardiovascular Response to Exercise
•
Body’s overall goal: •
Maximize perfusion skeletal muscles and heart
•
Minimize perfusion all other areas
•
Initiator: Muscle hypoxia
•
Mediator:Sympathetic Mediator:Sympathetic nervous system
Jason Ryan, MD, MPH
Response to Exercise •
•
•
•
•
Response to Exercise
Process begins with muscle contraction
•
ATP consumed oxygen consumed (need mor e ATP) Result: Local hypoxia in muscle tissue Vasodilation occurs •
Multiple mediators released released into plasma
•
Adenosine generated generated from ATP consumption
•
Lactate
•
Carbon dioxide, potassium
•
•
•
Sympathetic nervous system activated ↑contractility (stroke volume) ↑HR Net result: ↑ cardiac output
•
Results in ↑ systolic blood pressure (SBP)
•
Vasoconstriction in some areas (gut, skin) •
Redistributes blood to important areas (i.e. heart/muscles)
Lowers total peripheral resistance (TPR)
Response to Exercise
Response to Exercise
Blood Pressure Summary
Ejection Fraction
•
•
SBP rises
•
LVEF increases
•
More CO = more blood in arteries arteries = more pressure
•
More vigorous contraction
•
Primary determinant systolic BP = cardiac output
•
Major impact: ESV decreases decreases
DBP decreases slightly or stays normal •
Local dilation of skeletal skeletal muscles
•
Primary determinant diastolic diastolic BP = peripheral resistance
•
Pulse pressure increases
•
TPR goes down
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EF =
EDV - ESV
•
EDV effects minor/variable
•
More preload but less filling time at fast heart heart rates
EDV
Response to Exercise
Response to Exercise
Coronary Perfusion
Preload
•
•
•
Fast HR shortens diastole
•
LESS coronary filling time Coronary vasodilation increased blood flow •
Only way to get more oxygen
•
Cannot extract more O 2
•
Cardiac tissue extracts maximum oxygen from RBCs
•
Cannot extract more to meet increased demand
•
•
•
•
•
Contributes to rise in cardiac output Along with increased heart rate and contractility
Lusitropy
Lusitropy=myocardial =myocardialrelaxation •
Sympathetic stimulation venous contraction Increases preload/EDV •
Lusitropy •
Preload rises with exercise
•
Opposite of contractility
Increased with exercise Contributes to increased preload ↑ cardiac output
Key regulatory protein: Phospholamban •
Inhibitor: sarcoplasmic r eticulum Ca2+-ATPase (SERCA)
•
Phosphorylated via beta adrenergic stimulation
•
Stops inhibiting SERCA
•
Result: SERCA takes up calcium
SERCA
relaxation
Exercise Begins
Sarco/endoplasmic reticulum
Ca2+-ATPase
•
Sympathetic stimulation phosphorylates phosphorylates PLB
•
Inactivates PLB (relieves inhibitory effect)
•
Allows SERCA to uptake more calcium
Muscle Hypoxia
↓TPR (Afterload)
Vasodilation Sympathetic Activation
P SERCA
Sarcoplasmic Reticulum
PLB
Beta Adrenergic Stimulation
Heart
↑ Contractility
↑ HR
ESV
↑ CO
Ca++
↑EF
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↓/- DBP Peripheral Vessels
↑ Lusitropy
Venous Constriction
↑Preload ↑EDV ↑SBP
Arteriole Constriction
Flow Equations
Blood Flow Mechanics Jason Ryan, MD, MPH
Flow Equations
Resistance and Compliance Compliance
Velocity Area
Resistance = resistance to flow Compliance = distensability of vessels
Velocity * Area = Flow Stiff Vessels ↑ resistance ↓ compliance
(m/s) * (m2) = (m3/s)
Stretchy Vessels ↓ resistance ↑ compliance
High resistance = low compliance (vice versa)
Pulse Pressure •
Systolic BP – diastolic BP •
•
•
•
•
Pulse Pressure
Normal = 120 – 80 = 40mmHg
Older patients = ↑ pulse pressure Hypertensive patients = ↑ pulse pressure
•
Compliance = Δ volume / Δ pressure
•
Stiff vessel ↓ compliance ↑ pulse pressure
•
Stretchy vessel ↑ compliance ↓ pulse pressure
•
Related to vesselcompliance ↓ compliance = ↑ pulse pressure
•
Small change in volume for given pressure applied to walls Large change in volume for given pressure applied to walls
C = ΔV / ΔP
ΔP = ΔV / C
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Flow Equation
Pulse Pressure
Total Peripheral Resistance
•
Pulse pressure varies with vessel compliance
•
Stiff vessels ↓ compliance
ΔP = CO * TPR Distensible Vessel 120/80
Stiff Vessel 170/100
↑ resistance = ↑ pressure to maintain flow ↑ pressure = ↑ cardiac work
Total Peripheral Resistance •
•
•
Types of Vessels
Easy to push blood out of heart less O2 required Resistance to flow more work for heart What resists forward flow out of heart? 1.
Types of vessels (i.e. pipes/tubes)
2.
Thickness of blood (viscosity)
•
•
•
•
•
Types of Vessels •
Major determinant of total peripheral resistance
•
Large pressure drop
•
Vasoconstriction = ↑ TPR
•
Vasodilation = ↓ TPR
Large arteries: Falls few mmHg Small arteries: 10-20mmHg Arterioles: Arterioles: 35mmHg Capillaries: 25mmHg
Viscosity
Arterioles= “resistance vessels” •
Aorta: SBP 100mmHg
•
Thickness of blood
•
Low viscosity
•
High viscosity
•
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Anemia
•
Polycythemia
•
Multiple myeloma
•
Spherocytosis
Series and Parallel Circuits
Poiseuille's Law •
Δ P = Q X R Human organs arranged in parallel Resistances add up differently in series than in parallel
8 η (viscosity) L (length) Π r (radius) 4
ΔP Q
R =
1 1 = Rtotal R1
Changes in radius large change in resistance
1 + R2
Parallel
For two resistances (2 and 2), what is total R?
ΔP = Q * R
•
Used to calculate resistance, CO, or ΔP
•
Often applied to body and lungs •
1 = Rtotal R
Series
Flow Equation
Series and Parallel Parall el Circuits
1
Rtotal = R1 + R2
For both systems Q = Cardiac Output Output (CO)
1 + R2
1
Rtotal = R1 + R2 Rtotal = 2 + 2 = 4
1
1
= Rtotal 2
1 + 2
Rtotal = 1
Flow Equation •
Body •
•
Mean Arterial Pressure
ΔP = Q * R
ΔP = Arterial pressure – right atrial pressure
•
R = Total peripheral resistance resistance (TPR)
•
R = Systemic vascular vascular resistance (SVR)
Lungs •
ΔP = Pulmonary artery pressure – left atrial pressure
•
R = Pulmonary vascular resistance (PVR)
•
Diastolic plus 1/3 (Systolic – Diastolic)
•
Total body
•
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•
Arterial blood pressure = 120/80 mmHg
•
Mean arterial pressure = 80 + 1/3 (40) = 93 mmHg
Lungs •
Pulmonary artery pressure = 40/20 mmHg
•
Mean pulmonary artery pressure pressure = 20 + 1/3 (20) (20) = 27 mmHg
Total Body
Lungs ΔP = CO * TPR
ΔP = CO * TPR
•
R = TPR
•
R = PVR
•
ΔP = MAP – RAP
•
ΔP = PA – LAP
•
•
MAP = mean arterial pressure
•
PA = mean pulmonary artery pressure
•
RAP = right atrial pressure
•
LAP = left atrial pressure
CO of 5L/min; BP 155/80 (MAP 105), RA 5
TPR = ΔP = MAP – RAP = CO
5
105 – 5
•
CO of 5L/min; PA 40/10 (MAP 20), LA 5
PVR = ΔP =
= 20
PA – LAP
CO
5
Lung and Body Flow Variables
20 – 5
=
5
= 3
5
Velocity and Area •
Flow = Velocity * Area
•
Changes as blood moves through vessels •
Aorta arterioles capillaries veins
•
Cardiac output moves through system (same (same flow)
•
Different vessels different area, velocity
•
Area ↑↑, velocity ↓↓
Velocity Area
Flow = Velocity * Area (m3/s) = (m/s) * (m2)
Flow Properties of Blood Vessels
Law of Laplace •
•
•
Wall tension or wall stress Applies to vessels and cardiac chambers ↑ tension ↑ O2 demand ischemia/angina
P*r Tension α
2h Flow = Vel * Area ΔP=QXR
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Wall Tension •
Wall Tension
Afterload: Increases pressure in left v entricle
•
Preload: Increases radius of left ventricle
•
Hypertension, aortic stenosis
•
Chronic valvular disease disease (aortic/mitral regurgitation)
•
Will increase wall tension tension
•
Will increase wall tension tension
•
“Pressure overload”
•
“Volume overload”
P*r
P*r
Tension α
Tension α
2h
2h
Eccentric Hypertrophy Hypertrophy
Wall Tension •
Hypertrophy: Compensatory mechanism •
•
Will decrease wall tension
•
•
Force distributed over more mass
•
Occurs with chronic pressure/volume overload
•
•
Longer myocytes Sarcomeres added in series Left ventricular mass increased Wall thickness NOT increased
Normal LV Size
Dilated LV
P*r Tension α
Increased myocyte size Sarcomeres in series Normal wall thickness
2h
Eccentric Hypertrophy •
•
Concentric Hypertrophy Hypertrophy
Volume overload of left ventricle •
Aortic regurgitation
•
Mitral regurgitation
Cardiomyopathy •
•
Pressure overload
•
Chronic ↑↑ pressure in ventricle
•
Sarcomeres added in parallel
•
Ischemic and non-ischemic non-ischemic
•
Left ventricular mass increased Wall thickness increased
Normal LV Size
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↓ LV Size
Increased myocyte size Sarcomeres in parallel Increased wall thickness
Concentric Hypertrophy •
Classic causes: Hypertension, Aortic stenosis •
•
•
Both raise pressure in LV cavity
Decreased compliance (stiff ventricle) Often seen in diastolic heart failure
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Blood Pressure
Regulation of Blood Pressure
•
Required for perfusion of tissues
•
Varies with sodium/water intake
•
Regulatedbynervoussystem
Jason Ryan, MD, MPH
Baroreceptors •
•
•
Blood pressure sensors via stretch
•
Signal central nervous system (brain) Response viaautonomic via autonomic nervous system •
•
Baroreceptors
•
Sympathetic and parasympathetic parasympathetic
Quick response to changes changes in blood pressure
•
Rapid response via autonomic nervous system
Kidneys (renin release)
Heart rate/contractility
•
Arterial tone (vasoconstriction)
•
Venous tone (more tone = more preload to ventricle)
•
Renal renin release
Baroreceptors
•
•
Modify: •
•
Aortic arch and carotid sinus
Blood Pressure Control Sympathetic Parasympathetic
Aortic arch •
Senses elevated blood pressure
•
Poor sensing of low blood pressure
Aortic Arch CN X (Vagus)
Carotid Sinus
Carotid sinus •
Most important baroreceptor
•
Modifies signals over wider range of blood blood pressure
•
Senses low and high blood pressure
a
Blood Pressure
e
Brain a
Carotid sinus CN IX (GP)
e
Veins/Arteries Constrict/Dilate Heart ↑↓HR
Afferent = Arrive at the brain Efferent = Exit the brain Nucleus Solitarius
Aortic Arch
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Hemorrhage
High Blood Pressure Sympathetic Parasympathetic
Aortic Arch CN X (Vagus) a ↑ Blood Pressure
Aortic Arch CN X (Vagus)
Veins Dilate Arteries Dilate
e
Brain a
Sympathetic Parasympathetic
↓ Blood Pressure
Heart ↓ HR/Contractility
↑ Salt/Water Retention
Kidney
Carotid Occlusion Sympathetic Parasympathetic
Aortic Arch CN X (Vagus) a
e
Brain a
e
Carotid sinus CN IX (GP)
Sympathetic Parasympathetic
Aortic Arch CN X (Vagus)
Veins Dilate Arteries Dilate
a
Blood Pressure
Heart ↓ HR
e
Brain a
e
Carotid sinus CN IX (GP)
Tricks carotid sinus into thinking ↑ BP Result: ↓ HR, Vasodilation, ↓ BP
Veins Constrict Arteries Constrict Heart ↑HR
Tricks carotid sinus into thinking ↓ BP Result is ↑HR, Vasoconstriction, ↑BP
Severing CN IX
Severing CN X Sympathetic Parasympathetic
Aortic Arch CN X (Vagus) a
Blood Pressure
Heart ↑ HR/Contractility
Retention
Carotid Massage
Blood Pressure
e
Carotid sinus CN IX (GP)
↓ Salt/Water
Kidney
Veins Constrict Arteries Constrict
Brain a
e
Carotid sinus CN IX (GP)
Syncope while shaving or buttoning shirt
e
a
e
Brain a
Carotid sinus CN IX (GP)
e
Sympathetic Parasympathetic
Aortic Arch CN X (Vagus)
Veins Constrict Arteries Constrict
a
Blood Pressure
Heart ↑HR
e
Brain a
Carotid sinus CN IX (GP)
Tricks brain into thinking ↓ BP Result is ↑ HR, Vasoconstriction, ↑BP
e
Veins -Arteries -Heart ↑HR
Vagotomy Unopposed Sympathetic Cardiac Stimulation Result is ↑ HR
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Coronary Blood Flow
Summary of Techniques
120
Aortic Pressure
80
Coronary Flow
Time(s)
•
Regional Blood Flow
•
Epicardium site of coronary arteries
•
Subendocardium receives smallest amount blood flow
Organ Circulation
Autoregulation •
•
•
In tachycardia, less time in diastole less flow
Organ
Key Features
Lung
100% of Cardiac Output Output
Liver
Largest Systemic Blood Flow
Kidneys
Highest blood flow by weight
Heart
Largest Δ02 (80%) ↑ demand vasodilation
Autoregulation
Some tissue beds maintain constant blood flow ↑ BP ↑ flow vasoconstriction ↓ flow (normal) Use local metabolites to sense blood pressure
Kidney, brain, heart: Excellent autoregulation systems Skin: Poor autoregulatory capacity
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Capillary Fluid Exchange •
Two forces drive fluid into or out of capillaries
•
Hydrostatic pressure (P)
•
Capillary Fluid Exchange •
Hydrostaticpressure – fluid PUSHING against walls
•
Oncotic pressure –solutes PULLING fluid in
•
•
Molecules against capillaries walls walls
•
Pushes fluid out
•
High pressure drives fluid TOWARD TOWARD low pressure High pressure draws fluid AWAY AWAY from low pressure
Oncotic pressure (∏) •
Solutes (albumin) drawing fluid into capillaries
Pc ∏c Capillary
∏c
Pc
Pi ∏i Net Pressure (NP) = (Pc –Pi) + (∏i - ∏c)
Interstitial Space
Pi
∏i
Flow = (NP) Kf
Edema
Capillary Fluid Exchange •
Hydrostaticpressure – fluid PUSHING against walls
•
•
High pressure drives fluid TOWARD TOWARD low pressure pressure
•
Oncotic pressure –solutes PULLING fluid in
•
•
•
High pressure draws fluid AWAY from low pressure
•
Excess fluid movement out of capillaries Tissue swelling Lungs: Pulmonary edema Systemic capillaries: Lower extremity edema
Pc (100) ∏c (50)
Pi (50) ∏i (30) Net Pressure (NP) = 50 - 20 = 30 Flow = (NP) Kf
Edema
3rd Spacing
Net Pressure (NP) = (Pc –Pi) + (∏i - ∏c)
•
Capillary
•
∏c
Pc
Intracellularfluid – 1st space
•
Extracellularfluid – 2nd space •
Pi
Interstitial Space
•
∏i
•
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About 1/3 body fluid
Third spacing - fluid where it should NOT be •
↑ capillary pressure, ↑ Pc (heart failure) ↓ plasma proteins, ↓ ∏c (nephrotic syndrome, liver failure) ↑ capillary permeability, ↑Kf (toxins, infections, burns) ↑ interstitial osmotic pressure, ↑ ∏i (lymphatic blockage)
About 2/3 body fluid
Pleural effusions
•
Ascites
•
Cerebral edema
•
Low intravascular volume/High total volume
Occurs post-op, sepsis sepsis
PV Loops er u s s
er e
Pressure Volume Loops r
u s P s V
e r L P V L l o V V L
Jason Ryan, MD, MPH
LV Vol
Time
PV Loops
PV Loops ESPVR
er re u
u
s s
re V
e
s
e
s
r
e
re V
e
r u
u
s P
s P
s r L
s r L
P
P
V
V L
L
l
l V
V
o
o
EDPVR
V
V L
L
LV Vol
Time
LV Vol
Time
PV Loops Systole
S2 re u s s
A
e re r
re
A
u s
P u
s s
V e
re V
L
s L
P r
l
P o
M
V L
A
L
V
V A
Time
M
M
M
S1 LV Vol
EDP
Diastole LV Vol ESV
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EDV
PV Loop Parameters Afterload
•
•
•
•
•
Stroke Volume
Changes in preload Changes in afterload Changes in contractility Changes in compliance In reality, these are inter-related •
Example: ↑ preload
↑ contractility (Frank-Starling)
Preload
Preload Changes Increase
Preload Changes
↑ EDV ↑ SV ↑ EF (slightly)
Decrease
↓ EDV ↓ SV ↓ EF (slightly)
SV = EDV - ESV
SV = EDV - ESV
EF = EDV - ESV
EF = EDV - ESV
EDV
EDV
Afterload Changes
Afterload Changes
Increase
Decrease
↑ ESV ↓ SV ↓EF
↓ ESV ↑SV ↑EF
EF = EDV - ESV
EF = EDV - ESV
EDV
EDV
20
Contractility Changes
Contractility Changes
Decrease
Increase ESPVR
↑ ESV ↓ SV ↓ EF
↓ ESV ↑ SV ↑ EF
EF = EDV - ESV
EF = EDV - ESV
EDV
EDV
Compliance Changes
Work of the Heart
Decreased Compliance
More area = More work
↓EDV ↑ EDP
EDPVR
Commonly Tested PV Loops •
Aortic Stenosis
•
Mitral Regurgitation
•
Aortic Regurgitation
•
Mitral Stenosis
Aortic Stenosis
e r u s s e r P V L
LV Vol
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Mitral Regurgitation Regurgitation
Aortic Regurgitation Regurgitation
Isovolumic Contraction Disrupted
Isovolumic Relaxat ion Disrupted
e r
er s
s
u
u s
s re
re P
P V
V L
L
LV Vol
LV Vol
Mitral Stenosis Ventricle can’t fill properly
e r u s s e r P V L
LV Vol
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Wiggers’ Diagram Aorta LV LA
Wiggers’ Diagram
S1 Heart Sounds
Jason Ryan, MD, MPH
S2
VenousPressure EKG
Left Ventricular Volume
Aorta
LV LA
Normal Heart
Normal Heart
Diseased Heart
Diseased Heart
Mitral Stenosis
Aortic Stenosis
23
Normal Heart
Normal Heart
Diseased Heart
Diseased Heart
Aortic Regurgitation
Mitral Regurgitation
24
Venous Pressure a
Venous Pressure Tracings
v c
x
y
Jason Ryan, MD, MPH
Venous Pressure
Venous Pressure
Tricuspid valve
Atrial relaxation Atrial contraction Pressure goes up
TV opens Pressure Falls a
c
a
TV Closes
c
c
v
TV closes
Venous filling Pressure rises
No RV filling RV Contraction
Wiggers’ Diagram
Classic Findings •
Large a wave
•
Cannon a wave
•
Absent a waves
•
Large v waves
Aorta LV LA LV Volume S1 Heart Sounds
S2
c x
v
y
EKG
25
x
y
a wave = A = Atrial trial contraction v wave = Venous filling c wave = triC tri Cuspid valve x descent = atrial relaX rela Xation y descent = empt Y Y ing ing of the atrium atrium
a
a
v
x
VenousPressure
TV Closes
TV Opens
RV filling RV Relaxation
Left Atrial Pressure
High Yield Findings •
•
Large a wave (increased atrial contraction pressure) •
Tricuspid stenosis
•
Right heart failure/Pulmonary hypertension
a
Cannon a wave (atria against closed tricuspid valve) •
Complete heart block
•
PAC/PVC
•
Ventricular tachycardia
•
Absent a wave (no organized atrial contraction)
•
Giant V waves
•
•
v c
x
Atrial fibrillation
Tricuspid regurgitation
26
y
Frank-Starling Curve
Starling Curves Jason Ryan, MD, MPH
Frank-Starling Curve
Frank-Starling Curve
Left and Right Shifts
Left and Right Shifts •
↑ Contractility ↓ Peripheral Resistance (afterload) Normal
•
↓ Contractility ↑ Peripheral Resistance (afterload)
Stroke Volume
Contractility •
Increase: Exercise, inotropes
•
Decrease: Myocardial Myocardial infarction, heart failure
Peripheral resistance: •
Total peripheral resistance (TPR)
•
Systemic vascular resistance (SVR)
•
Increase: Vasopressors
•
Decrease: Vasodilators, sepsis sepsis
Preload (LVEDP, LVEDV)
Venous Return Curve
Right Atrial Pressure
Right Atrial Pressure
Venous Return or Cardiac Output
27
Venous Return Curve
Venous Return Curve
Left and Right Shifts
Volume Venous Tone
↑ Blood Volume Venous constriction (↑ tone)
Venous Return or Cardiac Output
Venous Return or Cardiac Output
Mean Systemic Filling Pressure (MSFP) Pressure if heart stops stops
Normal
↓ Blood Volume Venous dilation (↓ tone)
Right Atrial Pressure
Right Atrial Pressure
Venous Return Curve
Combined Curves
Changes in Slope
Starling and Venous Return ↓ Total peripheral resistance resistance
Venous Return or Cardiac Output
CO or VR
Normal
↑ Total peripheral resistance resistance
Right Atrial Pressure Right Atrial Pressure or Preload
TPR change shifts curve right/left No change in MSFP Result: change in slope of Venous Return curve
Heart Failure
Hemorrhage ↓contractility ↑ TPR ↑ Fluid volume
CO or VR
Blood loss ↑ TPR ↑ Contractility
CO or VR
Right Atrial Pressure or Preload
Right Atrial Pressure or Preload
* Black = normal
* Black = normal
28
Exercise
AV Fistulas
•
Decreased afterload (TPR)
•
Decreased afterload (TPR)
•
Venous contraction
•
Increased contractility
•
Increased contractility
•
Venous contraction
•
Net result = increased CO
•
Net result = increased increased CO
Combined Curves
Vasopressors •
•
•
Starling and Venous Return
Increased afterload (TPR) Alters VR and Starling Curves Net result = decreased CO
A 15
CO or VR
B 10
5
C
10
12 14
Right Atrial Pressure * Black = normal
29
For a patient on starling curve A with a MSFP of 10 what is the cardiac output?
Cardiac Ischemia •
•
•
Caused by coronary atherosclerosis O2 SUPPLY << O2 DEMAND = ISCHEMIA Typical symptoms •
Cardiac Ischemia
Chest pain (angina)
•
Dyspnea
•
Diaphoresis
Jason Ryan, MD, MPH
Stable Angina •
•
Acute Coronary Syndromes
Stable atherosclerotic plaque •
No plaque ulceration
•
No thrombus
•
•
Must occlude ~75% of lumen to cause symptoms •
Plaque rupture thrombus formation Subtotal occlusion •
Unstable angina
•
Non-ST elevation myocardial infarction
Total occlusion (100%) •
ST-elevation myocardial infarction (STEMI)
NO SYMPTOMS
SYMPTOMS WITH EXERTION (EXERTIONAL ANGINA) Subtotal Occlusion
Sudden Death
Total Occlusion
Risk Factors
•
Common complication of CAD
•
Major risk is prior coronary disease
•
Plaquerupture arrhythmias
•
Coronary risk equivalents
•
CAD is most common cause of sudden death adults •
Younger patients: Hypertrophic Hypertrophic cardiomyopathy (HCM)
30
•
Diabetes
•
Peripheral artery disease
•
Chronic kidney disease disease
Risk Factors •
•
•
•
•
Extent of Ischemia
Hypertension Hyperlipidemia Family History (1° relative, M<50, F<60) Smoking
•
Transmural ischemia
•
Subendocardial ischemia
•
Obesity, sedentary lifestyle
Occurs with complete 100% flow obstruction (STEMI)
•
Occurs with flow obstruction obstruction but some distal distal blood flow
•
Stable angina, unstable angina, angina, NSTEMI
Subendocardial Ischemia
Subendocardial Ischemia
Transmural Ischemia
Transmural Ischemia
Subendocardial Ischemia
Transmural Ischemia Complete Occlusion
Subtotal Occlusion
Limited distal flow
Ischemic EKG changes
Ischemic EKG changes
ST depressions
T wave inversions •
Many causes other than CAD
•
Raised ICP
•
Resolving pericarditis
•
•
•
Subendocardial Ischemia
31
Cerebral T waves
Bundle branch blocks Ventricular hypertrophy
Ischemic EKG changes
Ischemic EKG changes
T wave inversions
ST Elevations
Subendocardial Ischemia
Seen only with transmural ischemia
Evolution of EKG changes STEMI
Normal
Acute
Hours
1-2 Days
3-7 Days
Q wave
Hyperacute T waves
Poor R Wave Wave Progression Progression
•
Seen in transmural ischemia
•
•
Early sign of ischemia
•
•
Seen before ST elevations
•
R wave increases (progresses) in size V1-V6 Normally R>S waves seen by lead V3 Poor progression seen in anterior ischemia •
Acute or prior infarction
R
S
32
> 7 Days
Terminology •
•
•
•
Coronary Stents
Revascularization
•
Angioplasty Coronary stenting
•
•
Coronary bypass surgery surgery
•
•
Angioplasty: Reshape vessel Balloon angioplasty: Balloon inflation to open vessel Percutaneous Coronary Intervention (PCI) Stent placement About 600,000 stents/year implanted US
CABG
Revascularization
Coronary Artery Bypass Surgery
Major Indications
•
“Bypass Surgery”
•
Angina
•
Left Internal Mammary Artery (LIMA) Graft
•
Myocardial infarction
•
Saphenous (leg) Vein Vein Grafts
•
Systolic dysfunction
•
Radial (arm) Artery Grafts
•
33
Hibernating myocardium
Ischemic Pathologic Changes
Complications of Ischemia
Myocardium •
Zero to 4 hrs •
•
•
•
•
Gross: Mottled Micro: Necrosis, edema, hemorrhage
5 – 10 days
Gross: Hyperemia Micro: Surrounding tissue inflammation
5 – 10 days •
•
•
•
12-24 hrs •
•
First 4 days •
4 – 12 hrs •
•
No changes!
•
Gross: Central yellowing Micro: Granulation tissue
7 weeks •
•
Gross: Gray-white scar Micro: Scar
Arrhythmia
•
Free wall rupture
•
Tamponade
•
Papillary muscle rupture
•
VSD (septal rupture)
Weeks later •
Dressler’s syndrome
•
Aneurysm
•
LV Thrombus/CVA
Cause of Death
Cause of Death
0 – 4 days after MI
5-10 days after MI •
•
•
Ventricular Aneurysm
Free wall rupture •
Usually fatal – sudden death
•
May lead to tamponade
Papillarymuscle rupture •
Acute mitral regurgitation (holosystolic (holosystolic murmur)
•
Heart failure, respiratory distress
•
More common inferior MIs
Septal rupture – VSD •
Loud, holosystolic murmur (thrill)
•
Hypotension, right heart failure (↑ JVP, edema)
Ventricular Pseudoaneurysm
Weeks after MI •
More common anterior infarction
•
Rupture contained by pericardium/scar tissue
•
Risk of thrombus stroke, peripheral embolism
•
Not a true aneurysm •
•
•
•
•
Patrick J. Lynch, medical illustrator/Wikipedia
34
No endocardium or myocardium
Mayrupture Presents as chest pain or dyspnea Often seen in the inferior wall Occurs earlier (<2 weeks) than true aneurysm
Dressler’s Syndrome
Fibrinous Pericarditis
Weeks to months after MI •
•
•
Form of pericarditis
•
Occurs days after MI
•
Chest pain
•
Sometimes called “post -MI” pericarditis
•
Friction rub
•
Not autoimmune
•
Extension of myocardial inflammation
Immune-mediated (details not known) Treatment: NSAIDs or steroids
•
Dressler’s occurs weeks after MI
•
Rarely life-threatening
•
Secondary Prevention •
•
•
Secondary Prevention
Any CAD ↑ risk of recurrent events •
Sometimes called “post cardiac injury” pericarditis
•
STEMI, NSTEMI, stable stable angina
•
Preventative therapy used to lower risk Even in asymptomatic patients
•
Several proven therapies for risk reduction Aspirin Statins •
•
Atorvastatin, Rosuvastatin
Betablockers •
Used in patients with prior infarction (STEMI/NSTEMI)
Stent Complications
Stent Complications Complications
Restenosis
Thrombosis
•
•
•
•
•
•
Slow, steady growth of scar tissue over stent “Neo-intimal hyperplasia” Re-occlusion of vessel Rarely life-threatening
Polymer impregnated with drug to prevent tissue growth
•
Sirolimus
Same as STEMI: life-threatening event
•
Metal stent covered with polymer
•
Acute closure of stent
•
•
Slow, steady return of angina Most stents coated “drug eluting stents” •
•
35
Dual anti-platelet therapy for prevention Associatedwith missed medication doses
Stent Thrombosis Prevention •
antiplatelettherapy” “Dual antiplatelet
•
Typically one year of:
•
•
Aspirin
•
Clopidogrel, Prasugrel or Ticagrelor
After one year, stent metal no longer exposed to blood •
“Endothelialization”
•
Risk of thrombosis is lower (but not zero)
•
Most patients take aspirin only
36
STEMI
ST-Elevation Myocardial Infarction (STEMI)
•
Atherosclerotic Atherosclerotic plaquerupture
•
Thrombus formation
•
Ischemic chest pain
•
ST-elevations on ECG
Jason Ryan, MD, MPH
Leads go together t ogether
STEMI •
ST Elevations - Anterior
Transmural ischemia Transmural Ischemia Complete Occlusion
ST-elevation Myocardial Infarction Ulcerated Plaque – Thrombus Complete occlusion No distal blood flow
Leads go together
Leads go together t ogether
ST Elevations - Anterior
ST Elevations - Lateral
37
Leads go together
Leads go together t ogether
ST Elevations - Lateral
ST Elevations - Inferior
Leads go together
Coronary Artery Territories
ST Elevations - Inferior
•
Left anterior descending artery
•
Leftcircumflexartery
•
Posterior descending artery
•
•
Anterior
V1-V4
Lateral I, L, V5, V6
•
Inferior II, III, F
•
Branch of right coronary coronary artery 90 %
•
LCX 10%
Special Complications
Special Complications Complications
Inferior MI
Inferior MI
•
Right ventricular infarction
•
•
Loss of right ventricular contractility
•
Elevated jugular venous pressure
•
Decreased preload to left ventricle
•
Diagnosis: Right sided chest chest leads
Sinus bradycardia and heart block •
hypotension
38
Vagal stimulation from inferior wall ischemia
Left Main Occlusion
Posterior Myocardial Infarction
STEMI
Treatment of STEMI
Special Subtypes •
•
Left main •
ST-elevation aVR
•
Diffuse ST depressions
•
•
•
Posterior •
Anterior ST depressions with standard leads
•
ST-elevation in posterior leads (V7-V9)
•
•
Treatment of STEMI •
•
•
•
•
“Revascularization”
Option 1: Emergency angioplasty •
Mechanical opening of artery artery
•
Should be done <90min
•
Option 2: Thrombolysis •
Lysis of thrombus with drug
•
Should be done <30min
More likely the patient may die
•
More heart failure symptoms
•
More future hospitalization for heart disease
n=1791
Medical emergency
Treatment of STEMI
Main objective is to open the artery •
“Time ismuscle” is muscle” Coronary artery occluded by thrombus Longer occlusion more muscle dies
•
to needle” “Door to balloon” or “door to
39
Time matters •
Medical therapy is supportive supportive
•
Given while working to open artery
Remember: this is a thrombotic problem •
Aspirin to inhibit platelet aggregation
•
Heparin to inhibit clot formation
This is also an ischemic problem •
Beta blockers to reduce O2 demand
•
Nitrates to reduce O2 demand
Cautions •
•
Other STEMI Treatments
Beta blockers
•
Clopidogrel
•
Inferior MI stimulates vagal nerve
•
ADP receptor blocker
•
Bradycardia and AV AV block can develop
•
Inhibits platelets
Nitrates
•
•
Occlusion of RCA can cause cause RV infarct
•
RV infarction
•
Nitrates ↓ preload hypotension
↓ preload •
Typical STEMI Course
Eptifibatide •
IIB/IIIA receptor blocker
•
Inhibits platelets
Bivalirudin •
Direct thrombin inhibitor
•
Inhibits clot formation
Typical STEMI Course
•
Arrival in ER with chest pain 5:42pm
•
Arrival in ER with chest pain 5:42pm
•
EKG done 5:50pm
•
EKG done 5:54pm
•
Cardiac cath lab activated for emergent angioplasty
•
Meds given in ER
•
Meds given in ER
•
•
STEMI identified
•
STEMI identified
•
Aspirin
•
Aspirin
•
Metoprolol
•
Metoprolol
•
Nitro drip
•
Nitro drip
•
Heparin bolus
•
Heparin bolus
•
Transport to cath lab 6:15pm
•
Artery opened with balloon 6:42pm •
DTB time 60 minutes (i deal <90min)
40
tPA given based on weight 6:07pm •
IV push
•
Door to needle time 25min 25min (ideal <30)
NSTEMI Non-ST-Elevation Myocardial Infarction
NSTEMI and Unstable Angina
•
Atherosclerotic Atherosclerotic plaquerupture
•
Thrombus formation
•
Subtotal (<100%) vessel occlusion
•
Ischemic chest pain
Jason Ryan, MD, MPH
NSTEMI
Subendocardial Ischemia
ECGChanges
Subendocardial Ischemia
•
ST depressions
•
T-wave inversions
Subtotal Occlusion
Limited distal flow
Cardiac Biomarkers •
Biomarkers spill into blood with cardiac injury
•
Most common marker used: Troponin I or T
•
•
Increase 2-4 hours after MI
•
Stay elevated for weeks
Cardiac Biomarkers •
CK-MB also used •
Increase 4-6 hours after MI
•
Normalize within 2-3 days days
Several types of CK •
MM – Skeletal muscle
•
MB – Cardiac
•
BB – Brain
•
Most tissues have some of all three
•
Ratio of MB to total CK can be used in ischemia •
41
Helpful when total CK CK also up due to muscle damage
Cardiac Biomarkers •
Treatment of NSTEMI
Some AST found in cardiac cells •
Abdominal pain with isolated isolated ↑ AST could be MI
•
Thrombotic and ischemic syndrome (like STEMI)
•
Unlike STEMI: No “ticking clock”
•
•
Angioplasty (non-emergent)
Presents to ER with chest pain
•
•
•
Medical Therapy
•
•
Heparin drip
•
Admitted to cardiac floor
•
Hospital day 2 angiography
•
90% blockage of LAD Stent
•
•
Unstable Angina •
Diagnosis largely based on patient history •
Chest pain increasing in frequency/intensity
•
Chest pain at rest
•
ECG may show ST depressions or T wave inversions
•
Treatment is same as for NSTEMI
•
Condition often called “UA/NSTEMI”
No benefit to thrombolysis
Aspirin Beta blocker Heparin
Biomarkers elevated
Metoprolol
No emergency angioplasty
•
•
•
•
Some blood flow to distal distal myocardium
•
•
•
Aspirin
Subtotal occlusion
•
Unstable Angina
Typical NSTEMI Course
•
•
42
Atherosclerotic Atherosclerotic plaquerupture Thrombus formation Subtotal (<100%) vessel occlusion Ischemic chest pain Normal biomarkers
Stable Angina •
Ischemic chest pain with exertion
•
Relieved by rest
•
•
•
Stable Angina
Stable pattern over time Stablecoronary atherosclerotic atheroscleroticplaque No plaquerupture/thrombus
Jason Ryan, MD, MPH
Stable Angina
Stable Angina
•
Symptoms generally absent until ~75% occlusion
•
Diagnosis: cardiac stress test
•
Distal arteriolar dilation normal flow if <75%
•
Increases demand for O2
Stable Angina
Stable Angina: Typical Case
•
NOT a thrombotic problem
•
65-year old man with chest pain while walking
•
No role for heparin or antithrombotic drugs
•
Relieved with rest
•
In US usually treated with revascularization
•
Presents to ED
•
•
Most common indication indication PCI, CABG is stable angina Recent clinical trials suggest medical therapy may work just as well as PCI/CABG in some patients
•
EKG normal
•
Biomarkers normal
•
Stresstest
•
Cardiac catheterization performed
•
43
Walks on treadmill chest pain, EKG changes
•
90% LAD artery blockage
•
Stent placed angina resolved
Medical Therapy for Ischemia
Nitrates
O2 Demand
•
Converted to nitric oxide vasodilation
•
Predominant mechanism is venous dilation
O2 Supply
↑O2 Supply Dilate coronary arteries Increase diastole
↓O2 Demand ↓ Heart rate ↓ Contractility ↓ Afterload ↓ Preload
•
•
Bigger veins hold more blood
•
Takes blood away from left ventricle
•
Lowers preload (LVEDV) (LVEDV)
Also arterial vasodilation (art<< veins) •
Increase coronary perfusion
•
Some peripheral vasodilation
Nitroglycerine
Nitrates •
•
•
Nitrates
↓ preload ↓ cardiac output Sympathetic nervous system activation Increased heart rate/contractility •
Increases O2 demand demand
•
Opposite of what we want to do for angina
•
Rare patients with complex CAD angina
•
In most patients, preload reducing effects dominate
•
Co-administer Co-administer beta-blocker or Ca channel blocker
•
•
Nitrates alone often improve angina
Blunts “reflex” effect
Nitrates
Nitrates
Forms
Adverse Effects
•
Nitroglycer inTablets/Spray Tablets/Spray •
Rapid action ~5 minutes
•
Takeduring angina attack, before exercise
•
Isosorbide Dinitrate
•
Isosorbide Mononitrate
•
Topical Nitroglycer in
•
•
•
•
Headache (meningeal vasodilation)
•
Flushing
•
•
Effects last ~6hrs
Hypotension Angina •
Once daily drug drug Topical cream, patches
44
Reflex sympathetic activation
Nitrate Tolerance
Nitrate Withdrawal Withdrawal
•
Drug stops working after frequent use
•
Nitrate withdrawal (rebound) after discontinuation
•
Avoid continuous us for more than 24 hours
•
Occurs when using large doses of long-acting nitrates
•
Does not occur with daily isosorbide mononitrate
•
Angina frequency will increase
Monday Disease •
•
•
•
•
Beta Blockers
Workers in nitroglycerin manufacturing facilities Regular exposure to NTG in the workplace Leads to the development of tolerance Over the weekend workers lose the tolerance "Monday morning headache" phenomenon •
Prominent vasodilation
•
Tachycardia, dizziness, and a headache
•
•
Metoprolol, atenolol
Some beta blockers are partial agonists •
Pindolol, Acebutolol
•
Don’t use in angina
•
Slower heart rate = more filling time
•
Increase O2 demand demand
•
Blunts some beneficial effect
Reduced blood pressure (↓ afterload) Net effect = less O2 demand
Calcium Channel Blockers
For angina, generally use cardioselective (β1) drugs •
Increase preload (LVEDV) (LVEDV)
•
Beta Blockers •
Slow heart rate and decrease contractility
•
•
Re-exposed on Monday
•
•
•
45
Three major classes of calcium antagonists •
dihydropyridines dihydropyridines (nifedipine)
•
phenylalkylamines phenylalkylamines (verapamil)
•
benzothiazepines (diltiazem)
Vasodilators and negati ve inotropes
Antianginal Therapy
Calcium Channel Blockers •
•
Nitrates/Beta Blockers
Nifedipine: vasodilator •
Lower blood pressure
•
Reduce afterload
•
Dilate coronary arteries
•
May cause reflex tachycardia
Verapamil/diltiazem: negative inotropes •
Similar to beta blockers
•
Reduced heart rate/contractility
•
Can precipitate acute heart failu re if LVEFvery low
Antianginal Therapy
Ranolazine
Calcium Channel Blockers
•
•
•
Inhibitslate Inhibits late sodium current Reduces calciumoverload high wall tension Reduces wall tension and O2 demand Late Na influx
Na
•
Ca
Variant (Prinzmetal) Angina
Ranolazine •
Na
Constipation, dizziness, headache QT prolongation (blockade of K channels)
•
•
•
•
Prolong QT
46
Ischemia fromvasospasm from vasospasm •
Not caused by atherosclerotic narrowing
•
Often artery is “clean” with no stenosis
•
May also occur near sites of mild atherosclerosis
Spontaneous episodes of angina Transient myocardial ischemia ST-segment elevatio n on ECG
Variant (Prinzmetal) Angina
Variant (Prinzmetal) Angina •
•
•
•
Diagnosis
Episodesusually at rest Midnight to early morning Sometimes symptoms improve with exertion
•
Usually based on history
•
Intracoronary ergonovine •
Associated with smoking •
Variant (Prinzmetal) Angina •
Quit smoking
•
•
Calcium channel blockers, nitrates
•
•
Vasodilators
•
Dilate coronary arteries, oppose spasm
•
•
Avoid Avoid propranolol propranolol •
Non selective blocker
•
Can cause unopposed unopposed alpha stimulation
•
Symptoms may worsen worsen
•
Coronary Steal •
•
•
Significant (>75%) narrowing narrowing
•
Intracoronary acetylcholine •
Acts on endothelial muscarinic receptors
•
Healthy endothelium
•
Endothelial dysfunction
•
Vasospasm visualized on angiogram angiogram
vasodilation via nitric oxide vasoconstriction
Mechanism of angina Induced by drugs Blood flow increased to healthy vessels Blood flow decreased in stenotic vessels Blood “stolen” from diseased coronary vessels
•
Vasodilator administered
•
Stenoticvessels no response
•
Normal vessels vasodilation
•
Flow increases to normal vessels
•
Flow decreases to abnormal vessels
•
Results: ischemia due to coronary steal
Arterioles maximally maximally dilated to maintain flow
•
Normalvessels •
Vasospasm visualized on angiogram angiogram
Coronary Steal
Stenotic vessels •
Can be administered duri ng angiography angiography
•
Coronary Steal
Treatment
•
Acts on smooth muscle serotonergic (5-HT2) receptors receptors
•
No or minimal narrowing Arterioles NOT maximally maximally dilated
47
Arterioles already maximally dilated
Coronary Steal •
Rarely seen with nitrates, nifedipine
•
Key principle for chemical stress tests •
Adenosine, persantine, regadenoson
•
Potent, short-acting vasodilators
•
Brief ↓ in blood flow to stenotic vessels
•
Nuclear tracers can detect ↓ blood flow
ischemia
48
AV Node HIS Bundle Bundle Branches Purkinje Fibers
R A AV
EKG Basics
T
P
HIS Bundle
Jason Ryan, MD, MPH Q
Bundle Branches
S Atrial Depolarization
EKG
Ventricular Depolarization
Purkinje Fibers
EKG Electrical Activity
SA AV
LBB His Purkinje Fibers
RBB
EKG Electrical Activity
EKG Electrical Activity Activity
I AVR
V1 V2 V3 V4 V5 V6 AVL
II
49
III AVF
EKGs
EKG
Key Principles •
#1: Waves Waves represent repolarization/depolarizati on
•
#2: EKGs have 12 leads •
Pacemakers •
•
•
•
Other pacemakers exist but are slower If SA node fails, others takeover SA node (60-100 bpm) bpm)
•
AV node (40-60 bpm)
•
HIS (25-40 bpm)
•
Bundle branches (25-40 (25-40 bpm)
•
Purkinje fibers (25–40 bpm)
Electrical activity toward lead = upward deflection
•
Electrical activity away from lead = negative deflection
SLOWEST conduction is throu gh AV node •
•
•
Determining Heart Rate •
Each lead watches from different vantage point
•
Conduction Velocities
SA node is dominant pacemaker of the heart
•
Each lead watches the same same thing
•
Very important so ventricle has has time to fill
Purkinje fibers fastest conduction Purkinje > Atria > Vent > AV node
QRS Axis
3 – 5 big boxes between QRS complex
Left Axis Deviation LBBB Ventricular Rhythm
-90o Right Axis Deviation RBBB RVH +180 o
0o Normal QRS Axis -30 and +90 degrees
300 150 100 75 60 50
+90o
50
Determining Axis -)
Axis Quick Method •
-90o (
•
LAD ) (+
•
II
Lead I (-)
(+)
First, glance at aVr. It should be negative If upright, suspect limb lead reversal
d a e L
+180o
0o Normal Axis -30 to +90
RAD
+90o
Normal
Axis Quick Method •
If leads I and II are both positive, axis is normal
Axis Quick Method •
For left axis deviation: •
All you need is lead II
Lead I Lead I
Axis -30 to -90°
Axis 0 to 90° Lead II
Lead II Axis 0 to -30° Physiologic Left Axis
Lead II
Axis Quick Method •
For right axis deviation: •
All you need is lead I
•
Negative = RAD
Axis Quick Method •
Look at aVr: Make sure its negative
•
Look at I, II: If both positive, axis is normal
•
•
If II is negative: LAD If I is negative: RAD Normal
Lead I
Axis 90 to 180° Lead I
Lead II Lead II
51
Phys Left
Left
Right
PR Interval
QRS Interval Normal QRS <120ms
Normal PR 120-200ms
Right Bundle Branch Block
Prolonged PR 1° AV block
Left Bundle Branch Block
Short PR - WPW
Calcium
Qt Interval
MyocyteAction Potential
Normal Qt
Phase 1 IK+ (out)
ICa+
Phase 2 (in) & IK+ (out)
0mv Short Qt: Hypercalcemia
Phase 3 IK+ (out)
Phase 0 INa+ (in) -85mv
Phase 4
Prolonged Qt Hypocalcemia Drugs LQTS
Torsade de Pointes •
Feared outcome of Qt prolongation
•
Results in cardiac arrest
•
Congenital Long Qt Syndrome Syndrome •
Rare genetic disorder •
Abnormal K/Na channels channels
Antiarrhythmic Antiarrhythmic drugs
•
Hypokalemia, hypomagnesemia
•
Rarely from hypocalcemia
K
a
Prolonged QT
52
Congenital Long Qt Syndrome
Acquired Long Qt Syndrome
•
Family history of sudden death (torsades)
•
Antiarrhythmic drugs
•
Classic scenario: Young patient recurrent “seizures”
•
Levofloxacin (antibiotic)
•
•
EKG shows long Qt interval
•
Jervell and Lange-Nielsen Syndrome •
Norway and Sweden
•
Congenital deafness
•
•
T waves
Haldol (antipsychotic) Many other drugs Congenital LQTS: need to avoid these drugs
U waves Origin unclear
Peaked T waves ↑K Early ischemia (hyperacute)
U
May represent repolarization of Purkinje fibers Can be normal but also seen in hypokalemia
53
T
U
EKGs You Should Know 1. Sinus rhythm 2. Atrial Fibrillation/Flutter 3. Ischemia: ST elevations, ST depressions 4. Left bundle branch block 5. Right bundle branch block
High Yield EKGs
6. PAC/PVC 7. 1st , 2nd, 3rd degree AV block
Jason Ryan, MD, MPH
8. Ventricular tachycardia 9. Ventricular fibrillation/Torsades
Step 1: Find the p waves •
Sinus p waves
Are p waves present?
Originate in sinus node
•
Upright in leads II, III, F
Steps 1 & 2
Step 2: Regular or Irregular •
•
Distance between QRS complexes (R-R intervals)
•
Regular •
P waves present, regular rhythm •
Sinus rhythm
•
Rare: atrial tachycardia, atrial rhythm
No p waves, irregular rhythm •
•
Irregular
54
Atrial fibrillation – irregularly irregular Atrial flutter with variable variable block
Steps 1 & 2 •
Step 3: Wide or narrow
P waves present, irregular rhythm
•
•
His-Purkinje system works works
• Multifocal atrial tachycardia
•
No bundle branch blocks present
• Sinus with AV block •
Narrow QRS (<120ms; 3 small boxes)
PACs • Sinus rhythm with PACs
•
Wide QRS
No p waves, regular rhythm
•
Most likely a bundle branch block block
• Hidden p waves: retrograde
•
Ventricular rhythm (i.e. tachycardia)
• Supraventricular tachycardias (SVTs) (SVTs) • Ventricular tachycardia
QRS Interval
Step 4: Check the intervals
Normal QRS
•
•
Right Bundle Branch Block
PR (normal <210ms; ~5 small boxes; ~1 big box) •
Prolonged in AV block
•
Lengthens with vagal tone, drugs
•
Shortens with sympathetic tone
QT (normal <1/2 R-R interval) •
Prolonged with ↓ Ca (tetany; numbness; spasms)
•
Prolonged by antiarrhythmic drugs drugs
•
Shortened with ↑ Ca (confusion, (confusion, constipation)
Left Bundle Branch Block
Step 5: ST segments •
Normal Sinus Rhythm
T wave abnormalities •
Inverted: ischemia
•
Peaked: Early ischemia, ischemia, hyperkalemia (↑K)
•
Flat/U waves: Hypokalemia (↓K)
•
ST Depression
•
ST Elevation
•
•
Subendocardial ischemia Transmural ischemia
55
Right Bundle Branch Block
Left Bundle Branch Block
Atrial Fibrillation
Atrial Flutter
Ventricular Tachycardia Tachycardia
Ventricular Tachycardia Tachycardia
56
PAC and PVC
Torsades de pointes •
•
↑ risk with prolonged Qt interval •
Antiarrhythmic drugs
•
Congenital long Qt syndrome
•
Antibiotics (erythromycin, quiniolones) quiniolones)
Hypokalemia
•
Hypomagnesemia
•
Rarely hypocalcemia
57
Cardiac Action Potential
Cardiac Action Potentials
•
Changes in membrane voltage of cell
•
Transmit electrical signals through heart
•
Triggers contraction of myocytes
Jason Ryan, MD, MPH
Myocyte Action Potential
Phase 4
Atrial/ventricular Atrial/ventricular myocytes Phase 1 IK+ (out)
•
Phase 2 ICa+ (in) & IK+ (out)
•
•
0mv •
Phase 0 INa+ (in) -85mv
Resting potential: about −85mV Constant outward leak of K +
“Inward rectifier channels” Na+ and Ca2+ channels are closed
Phase 3 IK+ (out)
Phase 4
Phase 4
Phase 0
Phase 1
Phase 0
•
Nearby myocyte raise membrane potential
•
•
Gap junctions
•
•
•
•
Rising potential opens “Fast” Na+ channels Threshold potential reached (about -70mV) Large Na+ current rapid depolarization
•
Membrane potential overshoots (>0mV)
•
Fast Na+ channels close
•
Class I antiarrhythmic drugs: drugs: block Na channels
Phase 4
•
Membrane potential is positive K + channelsopen Outward flow of K+ returns membrane to ~0 mV Phase 1
58
Phase 2
Phase 3
•
L-type Ca2+ channels open inward Ca2+ current
•
•
Contraction trigger: excitation-contraction coupling
•
•
•
K+ leaks out (down concentration gradient) Delayed rectifier K+ channels
•
•
•
Balanced flow in/out= in/out = plateau of membrane charge
•
Verapamil/Diltiazem = block L-type Ca channels
Ca2+channels inactivated Persistent outflow of K + Resting potential back to −85 mV Class III antiarrhythmic drugs: drugs: block K channels
Phase 2 Phase 3
Refractory Period
Skeletal Muscle •
•
•
No plateau (phase 2)
•
No gap junctions Each cell has its own NMJ
•
•
Phase 0 until next possible depolarization Determines how fast myocyte can conduct Manyantiarrhythmic antiarrhythmicdrugs prolongrefractoryperiod Refractory Period
Na+
K+
Myocyte Action Potential
Pacemaker Action Potential Potential
Atrial/ventricular Atrial/ventricular myocytes
SA node, AV node
•
Similar AP in HIS, bundle branches, Purkinje fibers 0mv Phase 0 ICa -40mv
85mv
59
Threshold
Phase 4 If (Na)
Phase 3 IK
Pacemaker Action Potential
Pacemaker Action Potential
SA node, AV node
SA node, AV node
•
Funny current (pacemaker current) •
•
•
•
•
•
Spontaneous flow of Na+
About −40 mV: threshold potential L-type Ca2+ channels open depolarize depolarize cell Delayed rectifier K+ channels open
•
Automaticity •
Do not require stimulation to initiate actionpotential
•
Capable of self-initiated depolarization
No fast Na+ channel activity •
Return cell to −60 mV
Fewer inward rectifier K+ channels
•
Membrane potential never lower than −60 mV
•
Fast Na + channels need −85 mV to function
Pacemaker Action Potential
Pacemaker Action Potential Potential
SA node, AV node
SA node, AV node
•
Any drug that slows this AP may cause two effects:
•
Two key drug classes that affect pacemaker AP
•
Slower heart rate (sinus node)
•
Calcium channel blockers (Verapamil/Diltiazem)
•
Slower AV conduction (AV node)
•
Beta blockers
0mv
0mv Phase 0 ICa
-40mv
Phase 0 ICa
Threshold
-40mv
-85mv
-85mv
Pacemaker Action Potential Potential
Beta Blockers
SA node, AV node •
Threshold
Verapamil/Diltiazem = block L-type Ca channels •
Slow rate of sinus depolarization (slow heart rate)
•
Slow AV node conduction
•
•
Modify slope of phase 4 Less slope longer to reach threshold ↓ HR Beta Blocker Normal
0mv Phase 0 ICa -40mv
Threshold
Slower phase 4 (less slope)
-85mv
60
Slope of Phase 4
Beta Blockers
Sinus Node
•
Also prolong repolarization
•
Changes in slope modify heart rate
•
Slow AV node conduction
•
Decrease slope (slower rise)
•
Increased slope (faster rise)
•
Beta Blocker Normal
•
Parasympathetic NS, beta blockers, adenosine adenosine
Sympathetic NS, sympathomimetic drugs
Slower repolarization (slows conduction) Phase 4
Pacemakers •
Many cardiac cells capable of automaticity
•
SA node normally dominates
•
•
Fastest rise in phase 4
•
Controls other pacemaker pacemaker cells
Pacemakers: SA Node > AV Node > Bundle of HIS •
SA node (60-100 bpm) bpm)
•
AV node (40-60 bpm)
•
HIS (25-40 bpm)
61
AV Node HIS Bundle Bundle Branches Purkinje Fibers
R
AV and Bundle Branch Blocks
A AV
T
P
HIS Bundle
Jason Ryan, MD, MPH Q
Bundle Branches
S Atrial Depolarization
•
•
Purkinje Fibers
AV Blocks
AV Blocks •
Ventricular Depolarization
Symptoms
Slowed or blocked conduction atria ventricles Can cause prolonged PR interval
•
Often incidentally noted on EKG
•
Can cause bradycardia
•
Can cause non-conduc ted p wave
•
Especially milder forms with few/no few/no non-conducted p waves Occurs when many or all p waves not conducted
•
Fatigue, dizziness, syncope
•
Symptomatic AV block often treated with a pacemaker
Non-conducted P wave Prolonged PR Interval
AV Blocks
AV Blocks
Anatomy
Anatomy
•
Caused by disease in AV conduction system •
•
AV node HIS Bundle Branches
•
Purkinje fibers
Divided into two causes •
•
AV node disease
•
HIS-Purkinje disease
62
AV node disease •
Usually less dangerous dangerous
•
Conduction improves with exertion (sympathetic (sympathetic activity) activity)
HIS-Purkinje disease •
More dangerous
•
Usually does not i mprove with exertion
•
Often progresses to complete heart block
•
Often requires a pacemaker
AV Blocks
1st degree AV Block
Four Types •
•
•
Type 1 •
Prolongation of PR interval only
•
All p waves conducted
Type II •
Some p waves waves conducted
•
Some p waves waves NOT conducted
•
Two sub-types: Mobitz I and Mobitz II
Type III •
Prolonged PR (normal <200ms) Block usually in AV Node Beta blockers Calcium channel blockers blockers Well-trained athletes
No impulse conduction from atria to ventricles
2nd degree AVB
2nd degree AVB
Mobitz I/Wenckebach
Mobitz I/Wenckebach
Block usually in AV Node Progressive PR prolongation Grouped Beating RR intervals NOT regular Similar causes as 1 st degree AV block
Block usually in AV Node Progressive PR prolongation Grouped Beating RR intervals NOT regular Similar causes as 1 st degree AV block
2nd degree AVB
3rd degree AVB
Mobitz II
Block usually in the HIS-Purkinje System Regular RR intervals excludes Wenckebach Block usually in the HIS-Purkinje System Often seen with bundle branch block Usually symptomatic Dizziness, syncope
63
3rd degree AVB
Lyme Disease •
•
•
Spirochete infection with Borrelia burgdorferi Stage 2: Lyme carditis Varying degrees of AVblock •
•
1st , 2nd, 3 rd
AV block improves with antibiotics
Block usually in the HIS-Purkinje System Regular RR intervals excludes Wenckebach
Ventricular Tachycardia
Vocabulary •
Complete heart block •
•
Impulses cannot be transmitted from atria to ventricle
AV dissociation •
Atria and ventricular depolarization depolarization uncoupled (“dissociated”)
•
Can be cased by complete complete heart block
•
Also occurs if ventricular rate > sinus rate (no heart block)
•
Seen in ventricular tachycardia and other rhythms
Escape Rhythm
Ventricular Tachycardia
•
SA node: Dominant (fastest) pacemaker
•
Heart block: SA cannot send impulses to ventricles
•
Other pacemakers exist but are slower •
64
SA node (60-100 bpm)
•
AV node (40-60 bpm)
•
HIS (25-40 bpm)
•
Bundle branches (25-40 bpm)
•
Purkinje fibers (25–40 bpm)
Sites of AV Block
Escape Rhythm •
Heart block: lower pacemaker depolarizes ventricles
•
Rate of lower pacemaker determines symptoms
•
“Escape rhythm”
•
Very slow: dizziness, syncope, hypotension
•
Less slow: fatigue, exercise intolerance
Causes of Heart Block •
•
Drugs •
Beta blockers, calcium channel channel blockers
•
Digoxin
•
• Often in patients with symptoms (syncope, dizziness)
Athletes
Fibrosis and sclerosis of conduction system
Bundle Branch Blocks •
•
Treatment for “high grade” AV block
• Usually 3rd degree or Mobitz II
High vag al tone •
•
Pacemaker
Right Bundle Branch Block
Both bundle branches blocked •
Results in AV block
•
Form of HIS-Purkinje system disease
ONE bundle branch blocked •
Does not cause AV block
•
Normal PR interval
•
QRS will be prolonged
65
Bundle Branch Blocks
Left Bundle Branch Block
•
Symptoms: None
•
May progress to AV block (need for pacemaker)
•
Interfere with detection of ischemia
•
•
Bundle Branch Blocks Causes •
•
•
•
•
Often caused by slowly progressive fibrosis/sclerosis More common in older patients Can result from “structural heart disease” LBBB: Prior MI, cardiomyopathy RBBB: Right heart failure
66
Identified incidentally on ECG
ST elevations, T-wave inversions can be normal
Atrial Fibrillation
Atrial Fibrillation and Flutter Jason Ryan, MD, MPH
J. Heuser/Wikipedia
Atrial Fibrillation
Atrial Fibrillation
Atrial Fibrillation
Atrial Fibrillation
•
Cardiac arrhythmia
•
Results in an irregularly, irregularly, irregular pulse
•
Can cause palpitations, fatigue, dyspnea
•
Diagnosis: EKG
Terminology •
Paroxysmal •
•
Persistent •
•
67
Comes and goes; spontaneous conversion to sinus rhythm Lasts days/weeks; often requirescardioversion
Permanent
Atrial Fibrillation
Cardiomyopathy
Symptoms •
Wide spectrum of symptoms
•
•
Asymptomatic Asymptomatic Heart Rate <100bpm
•
•
•
•
AVnode refractory perioddetermines period determines heart rate
•
Systolicheartfailure
•
Young, healthy patients rapid heart rate Olderpatients slower heart rate Atrial rate in fibrillation: 300-500bpm
•
•
•
Ventricular rate: 70-180bpm
•
Atrial fibrillation eliminates ventricular pre-filling “Loss of atrial kick” Decreases preload Can lead to low cardiac output and hypotension Especially in “preloaddependent” “preload dependent” patients •
Aortic stenosis
•
LVH or diastolic heart failure (stiff ventricle)
Valvular Atrial Fibrillation
Cardiac Embolism
•
↓ LVEF
•
Preload
Atrial Fibrillation •
•
Palpitations, Dyspnea, Fatigue Heart Rate >100bpm
Heart Rate •
Caused by untreated, rapid atrial fibrillation “Tachycardia-induced cardiomyopathy”
Brain (stroke) Gut (mesenteric ischemia) Spleen
•
Associated with rheumatic heart disease
•
Usuallymitral Usually mitral stenosis
•
•
•
68
Often refractory to treatment VERY high risk of thrombus Non-valvular: not associated with rheumatic disease
Atrial Fibrillation
Hyperthyroidism
Risk Factors •
•
•
•
•
Age
•
•
~10% of patients >80
•
<1% of patients <55
•
•
More common in women Most common associated disorders: HTN, CAD Anything that dilates the atria atrial fibrillation •
Heart failure
•
Valvular disease
•
Commonly leads to atrial fibrillation Reversible with therapy for thyroid disease Atrialfibrillationtherapiesless effective Key diagnostic test:TSH test: TSH
Key diagnostic test: Echocardiogram
Atrial Fibrillation
Atrial Fibrillation
Triggers
Treatment
•
•
•
Often no trigger identified
•
(“holiday heart”) Binge drinking (“holidayheart”) Increased catecholamines •
Heart Rate •
“Rate control”
•
Ideally <110bpm
Heart Rhythm
•
Infection
•
Surgery
•
“Rhythm control”
Pain
•
Restoration of sinus rhythm
•
•
Anticoagulation
Rate Control
Rate Control
•
Use drugs that slow AV node conduction
•
Beta blockers •
Usually β1 selective agents
•
Metoprolol, Atenolol
•
Calcium channel blockers
•
Digoxin
•
•
Beta Blockers Calcium Channel Blockers Blockers Digoxin
69
Verapamil, Diltiazem Increases parasympathetic tone to heart
Rhythm Control •
Cardioversion
Goal: restore sinus rhythm
•
Electrical •
QRS Deliver “synchronized” shock at time of QRS
•
Administer anesthesia
•
Deliver electrical shock to chest
•
All myocytes depolarize
•
Usually sinus node node first to repolarize/depolarize
Cardioversion
Cardioversion •
Cardioversion
Chemical
•
•
Administration of antiarrhythmic medication medication
•
Often Ibutilide (class III antiarrhythmic)
•
Less commonly used due to drug toxicity
•
Cardioversion •
•
•
•
Chemical/electrical cardioversion may cause stroke
•
48hours required for thrombus formation Symptoms <48hours: cardioversion safe •
Anti-coagulation 3 weeks
•
Transesophageal echocardiogram echocardiogram to exclude thrombus
Administered before/after cardioversion
•
Class I drugs •
cardioversion
•
Emergent cardioversion performed
70
Flecainide, propafenone
Class III drugs •
Exception: Hypotension/shock •
Antiarrhyt Antiarrhythmic hmic medications medications
•
Symptoms>48hours(or unsure)
Often occurs after hours/days hours/days
Rhythm Control
Risk of Stroke •
Spontaneous
Amiodarone, sotalol, dofetilide
Anticoagulation •
•
Warfarin Requires regular INR monitoring
•
Goal INR usually 2-3
•
Rivaroxaban, Apixaban Factor X inhibitors Direct thrombin inhibitor
Aspirin •
Less effective
•
Only used if risk of stroke is very low
•
Less risk of bleeding bleeding
Stroke Risk •
Whether atrial fibrillation persists or sinus rhythm restored anticoagul ation MUST be administered Studies show similar stroke risk for rate control versus rhythm control control
Dabigatran •
•
•
•
•
•
Anticoagulation
Stroke Risk
CHADS Score
•
CHADS VASC VASC Score
•
CHF (1 point)
•
•
HTN (1 point)
•
HTN (1pont)
•
Age >75yrs (1 point)
•
Diabetes (1point)
•
Diabetes (1 point)
•
Stroke (2points)
•
Stroke (2 points)
•
Female (1point)
•
Age 65-75 (1point)
•
Age >75yrs (2points)
•
Vascular disease (1point)
•
Score >2 = Warfarin or other anticoagulant
•
Score 0 -1 = Aspirin •
•
Atrial Fibrillation New Onset Atrial Fibrillation
Echocardiogram TSH
Anticoagulation Aspirin Warfarin Other drugs
Score >2 = Warfarin or other anticoagulant Score 0 -1 = Aspirin
Atrial Flutter
Summary
Rate Control Beta Blockers Calcium Blockers Digoxin
CHF (1point)
Rhythm Control Cardioversion Antiarrhythmic drugs
71
Atrial Flutter
Atrial Flutter
Symptoms
Treatment
•
•
•
Generally the same as atrial fibrillation
•
May be asymptomatic Palpitations, dyspnea, fatigue
•
•
•
•
72
Generally the same as atrial fibrillation Rate or rhythm control Rate-slowing drugs Cardioversion Anticoagulation based on stroke risk
PSVT Paroxysmal Supraventricular Tachycardia •
Intermittent tachycard ia (HR >100bpm)
•
Sudden onset/offset
•
Electrical activity originates above ventricle
•
•
AVNRT
Contrast with sinus tachycardia
“Supraventricular”
•
Contrast with ventricular tachycardia
•
Produces narrow QRS complex (<120ms) (<120ms)
Jason Ryan, MD, MPH
PSVT
AVNRT
Paroxysmal Supraventricular Tachycardia
Atrioventricular nodal reentrant tachycardia
•
•
•
Often causes sudden-onset palpitations Chest discomfort
•
•
Rarely syncope
•
•
Most common cause of PSVT More common in young women Mean age onset: 32 years old Requires dual AV nodal pathways pathways
Dual Pathways
Normal Conduction
Sinus Rhythm
Slow Conduction Short RP
Fast Conduction Long RP
SA AV
LBB His RBB
Purkinje Fibers
HIS
73
Dual Pathways
Retrograde P Waves
PAC
Slow Conduction Short RP
Fast Conduction Long RP
HIS
AVNRT •
•
•
Recurrent episodes of palpitations
•
•
•
Many episodes spontaneously resolve ↓ conduction in AV node breaks arrhythmia •
•
Carotid Massage •
•
Will halt conduction is slow pathway
•
Carotid massage
•
•
•
•
•
•
Stretch of baroreceptors CNS response as if high blood pressure Increased vagal tone
↓ AV node conduction
Vagal Vagal maneuver s Adenosine
AVNRT
Vagal Maneuvers •
Examiner presses on neck near carotid sinus
Chronic Treatment
Valsalva •
Patient bears down as as if moving bowels
•
Increased thoracic pressure pressure
•
Blood forced from lungs to left atrium
•
Rise in stroke volume
•
CNS response via vagus nerve
•
Many patients need no therapy
•
Beta blockers, Verapamil/Diltiazem
•
Surgical ablat ion of slow pathway
•
rise in blood blood pressure
Breath holding Coughing Deep respirations Gagging Swallowing
74
Slow conduction in slow pathway pathway
WPW Syndrome Wolff-Parkinson White Syndrome •
•
Wolff-Parkinson White •
Jason Ryan, MD, MPH
EKG in WPW
Cardiac electrical disorder “Accessory atrioventricular pathway” •
Conducts impulses from atria to ventricles
•
Bypasses AV node
•
“Bundle of Kent” of Kent”
•
Ventricular depolarization before AV nodal impulse
May lead to arrhythmias
WPW EKG Short PR
Delta Wave
AVRT
Cardiac Electrical System
AV Re-entrant Tachycardia
SA AV
LBB His Purkinje Fibers
Orthodromic
RBB
75
Antidromic
Bypass Tract Consequences •
•
Atrial Fibrillation in WPW WPW
Most patientsasymptomatic patients asymptomatic •
EKG with delta wave only
•
Called WPW “pattern”
•
•
•
Some have tachycardias •
•
Presents as palpitations
•
Called WPW syndrome
•
AVRT (anti (anti or orthodromic)
•
Rarely causes syncope or sudden death
•
Treatment: Ablation of access ory pathway
•
•
•
Slowing AV node conduction is dangerous Allows more impulses over bypass tract Usual atrial fibrillation therapies contraindicated •
Beta blockers
•
Calcium channel blockers blockers
•
Digoxin
•
Adenosine
Acute treatment: Cardioversion or antiarrhythmics •
Ibutilide, procainamide
•
Slow conduction in bypass tract
Atrial depolarization rate 300-500/min AV node conducts <200/min Impulses may conduct rapidly over bypass tract
Wide complex, irregular, tachycardic
Atrial Fibrillation in WPW •
Atrial fibrillation can be life threatening
76
Vaughan Williams Class I Quinidine Procainamide
Antiarrhythmic Drugs Jason Ryan, MD, MPH
•
•
•
Drugs used to “suppress” arrhythmias
•
Prevent formation of aberrant impulses Most also cause arrhythmias Can lead to cardiac arrest and death
•
Used in dangerous arrhythmias
•
Also used in recurrent symptomatic arrhythmias
Ia Beta Blockers
Lidocaine Mexiletine
b
Flecainide Propafenone
c
Class III
Class IV
Amiodarone Sotalol Dofetilide Ibutilide
Ca-channel Blockers (Verapamil/Diltiazem
Use of Antiarrhythmic Antiarrhythmic Drugs
Use of Antiarrhythmic Drugs •
Class II
•
Persistent/recurrent ventricular tachycardia Recurrent atrial fibrillation
Ventricular Tachycardia
Rapid Atrial Fibrillation
Myocyte Action Potential
Mechanisms •
•
•
•
Atrial/ventricular Atrial/ventricular myocytes
All drugs slow cardiac electrical activity Class I drugs Block Na channel
Phase 1 IK+ (out)
Class III drugs Block K channels Class II, IV: Slow sinus and AV node conduction
ICa+
Phase 2 (in) & IK+ (out)
0mv Phase 3
Class I, III
Phase 0 INa+ (in)
BB, CCB (Class II, IV)
-85mv
77
IK+ (out)
Phase 4
Na Channel Blockade
K Channel Blockade Prolonged Repolarization
Slow Phase 0
R
Q
S
Prolong QRS
Prolong QT
Myocyte Action Potential
Class I drugs
Atrial/ventricular Atrial/ventricular myocytes
•
•
•
0mv •
Block sodium channels prolong QRS Some also affect K+ channels prolong Qt Can prolong action potential duration Can prolong effective refractory period
ERP -85mv
AP
Class I drugs
Class Ia Drugs
Effects on Resting Action Potential
Quinidine, procainamide
Ia
Ib
Ic
•
ProlongQRS
•
Can also prolong Qt (↓K+ outflow)
•
Quinidine
•
↑QRS ↑QT ↑AP ↑ERP
+/-QRS ↓ QT
↓AP ↓ ERP
↑ QRS +/-QT
•
Oral drug
•
Can decrease recurrence rate of atrial fibrillation
•
Associated with increased increased mortality
Procainamide •
+/-AP
78
Intravenous drug
•
Slows conduction in accessory pathways (WPW)
•
Used in arrhythmias associated with bypass tracts
Class Ib Drugs
Procainamide •
Associatedwith drug-induced lupus •
•
•
•
•
Lidocaine, Mexiletine
Classic drugs: INH, hydralazine, procainamide
Often rash, arthritis, anemia
•
Little/no effect on QRS at normal HR
•
Slight decrease in Qt interval (minimal)
•
Least effect on action potential of class 1 drugs
Antinuclear antibody (ANA) can be positive Key features: anti-histone antibodies Resolves on stopping the drug
Class Ib Drugs
Class Ib Drugs
Lidocaine, Mexiletine
Lidocaine, Mexiletine
•
•
•
Most Na channel binding in depolarized state
•
Ischemia more depolarized myocytes Effective drugs in ischemic arrhythmias
•
•
•
•
Most Na channel block here (depolarized state) 0mv
Drugrapidly Drug rapidly unbinds Slow heart rates: little drug effect by next heart beat More effective in fast heart rates Less time to unbind before Na channels open again Main use: ischemic ventricular tachycardia •
Fast heart rates
•
Depolarized Na channels
ERP -85mv Phase 4
Class Ib Drugs
Re-entry •
•
Lidocaine, Mexiletine
Mechanism of arrhythmia in myocyte injury Lidocaine: Unidirectional block bidirectional block
•
•
•
•
A
Lidocaine also a local anesthetic
B
79
Na channel nerve block
May cause CNS stimulation •
Tremor, agitation
•
Tremor in patient on Mexiletine = toxicity
Cardiovascular side effects •
From excessive block of Na channels
•
Bradycardia, heart block, hypotension
Class Ic Drugs
CAST Trial
Flecainide, Propafenone
The Cardiac Arrhythmia Suppression Trial
•
Block open Na channels
•
Landmark clinical trial of antiarrhythmic drugs
•
Very slow unbinding
•
Tested the suppression hypothesis
•
•
•
Result:QRS Result:QRS can markedly prolong Limited use due to concern of toxicity Especially proarrhythmic effects
•
•
•
•
•
Class Ic Drugs •
•
•
Patients taking drugs had less arrhythmias Also: 3.6-fold increased risk of arrhythmic death
•
Result:Major ↓ antiarrhythmic drugs
•
Now used only with compelling indication
Use Dependence
Flecainide, Propafenone •
Suppression of arrhythmias with drugs is a good thing
Patients with asymptomatic arrhythmias after MI Encainide and flecainide administered
Only used in patients with structurally normal hearts
•
Effective in reducing recurrence of atrial fibrillation Must monitor forQRS for QRS prolongation prolongation
•
•
Prolonged QRS Risk of cardiac arrest
•
Na channels fluctuate between 3 different states Resting, Open and Inactivated Drugs bind more in certain states Class I drugs bind best in open/inactivate states •
•
States when Na channel is in “use”
These drug exhibit “use dependence” Inactive
Open
Resting
Use Dependence
Use Dependence 3 Seconds
Bradycardia Na Channels Open/Inactive
3 Seconds
•
Use dependent drugs: more binding fast heart rates
•
All class I drugs have some use dependence
•
Seen most frequently IC drugs
•
Practical implication: •
Na Channels Resting
Tachycardia
80
Flecainide and propafenone (IC drugs)
•
Marked use dependence
•
Toxicity Toxicity (QRS prolongation) at high heart rates
•
Stress testing often done to screen screen for toxicity
Class III drugs
Torsade de Pointes
Amiodarone, Sotalol, Dofetilide, Ibutilide
•
•
Delayed Repolarization K+ Channel Blockade
•
IA
Feared outcome of Qt prolongation Results in cardiac arrest Class IA, III drugs prolong Qt
III
+/-QRS ↑QT
↑AP ↑ERP
Amiodarone •
•
•
•
•
Amiodarone
Class III drug •
K channel blocker: Prolongs Q t interval
•
Lowest incidence incidence TDP of all class IIIs
•
•
•
Also has has class I, II, and IV effects •
Class I: Prolongs QRS
•
Class II, IV: Slow HR, delay AV conduction
•
•
Many potential side effects related to accumulation
•
Less likely at lower dosages
•
Safe in renal disease (biliary excretion)
Suppresses ventricular tachycardia
•
•
Accumulates in liver, lungs, skin, other tissues Half-life about 58 days Once steady state reached, very long washout
Very effective drug Suppressesatrial fibrillation
Amiodarone
Amiodarone
•
Highly lipid soluble
Side Effects •
Hyper and hypothyroidism •
Risk accumulates over time Young patients on indefinite therapy at greatest risk
•
Often used in older patients
•
Increased LFTs •
Usually asymptomatic and mild
•
Drug stopped if elevation is marked marked
Skin sensitivity to sun •
81
Contains iodine
Patients easily sunburn
Amiodarone
Amiodarone
Side Effects
Side Effects
•
•
Blue-gray discoloration •
Less common skin reaction
•
“Blue man syndrome”
•
Most prominent on face face
•
•
•
•
Corneal deposits •
•
Secretion of amiodarone by lacrimal glands
•
Accumulation on corneal surface
•
Appearance of “cat whiskers” on cornea
•
Does not usually cause vision problems
•
See in many patients on chronic therapy
Amiodarone When starting amiodarone •
Chest X-ray
•
Pulmonary function tests (PFTs)
•
Thyroid function tests (TFTs)
•
Liver function tests (LFTs)
Most common cause of death from amiodarone Foamy macrophages seen in air spaces Filled with amiodarone and phospholipids
“Honeycombing” pattern on chest x-ray
Sotalol and Dofetilide
Side Effects •
Pulmonaryfibrosis
•
•
•
•
•
•
Reverse Use Dependence
Both drugs block K channels (class III) Can prolong Qt interval torsade de pointes Practical consideration: •
Patients often admitted to hospital hospital to start therapy
•
Rhythm monitored on telemetry telemetry
•
Qt segment checked by EKG EKG each day
Sotalol: Also has beta blocking properties Can be used in patients with cardiomyopathy “Reverse use dependence”
Reverse Reverse Use Dependence 3 Seconds
•
K channels also fluctuate between 3 different states
•
Class III drugs bind best in resting state
•
These drug exhibit “reverse use dependence” Bradycardia K Channels Resting
3 Seconds
Tachycardia
82
K Channels Open/Inactive
Sotalol and Dofetilide
Sotalol and Dofetilide
•
Reverse use dependence: more binding slow rates
•
Commonly used in patients with atrialf ibrillation
•
Practical implication:
•
Typical case
•
Bradycardia in patient on sotalol/dofetilide sotalol/dofetilide
•
•
Qt interval may prolong
•
Sotalol/Dofetilide started
•
Increased risk of torsade de pointes
•
Cardioversion to restore sinus rhythm rhythm
•
Sinus rhythm persists on therapy
•
Other antiarrhythmic also used in this manner •
•
•
Amiodarone
•
Propafenone
•
Flecainide
Cardioversion
Ibutilide •
Recurrent episodes symptomatic atrial fibrillation
Intravenous drug
•
Half life of 2 to 12 hours “chemicalcardioversion” Used for “chemicalcardioversion”
•
Termination of arrhythmias Often atrial fibrillation or flutter
Ibutilide
Electrical Cardioversion Cardioversion Requires sedation
Beta Blockers
Beta Blockers
Class II Antiarrhythmics Antiarrhythmics
Class II Antiarrhythmics Antiarrhythmics
•
Main effect: Pacemaker cells (SA and AV node)
•
Decrease slope of phase 4
•
Prolong repolarizati on (phase 3)
↓HR ↓Cond Velocity ↑PR Interval
0mv
-40mv
-85mv
Threshold
Phase 0 ICa
Chemical Cardioversion No sedation May cause Torsade
Phase 3 IK
Phase 4 If (Na)
83
Calcium Channel Blockers
Calcium Channel Blockers
Verapamil and Diltiazem
Verapamil and Diltiazem
•
•
•
Block calciumchannels Slow hea rt rate Slow AV node conduction
Normal
Decreased Slope Slower Rise
0mv Phase 0 ICa -40mv
-85mv
Threshold
Phase 3 IK
Phase 4 If (Na)
AV Block •
Atrial Fibrillation
Beta blockers/Ca channel blockers ↓ AV conduction
•
•
Beta blockers and CCBs commonly used Controlventricularrate
Atrial Fibrillation with rapid ventricular response
Type 1 AV block
Wenckebach (Mobitz I)
Rate controlled with beta blocker or CCB
Sudden Cardiac Death •
•
•
↓HR ↓Cond Velocity ↑PR Interval
Ca Blocker
Adenosine
Increased risk among systolic heart failure patients Lower rates among patients on beta blockers
•
•
Improved mortality
•
Nucleoside base Used t o make ATP Receptors in many locations (purinergic receptors) •
•
AV nodal tissue Vascular smooth muscle
Ventricular Tachycardia
Adenosine Triphosphate
Ventricular Fibrillation
84
Adenosine •
AV nodal cells: •
•
Adenosine •
Activates K+ channels
•
•
Drives K+ out of cells
•
Hyperpolarizes cells: Takes Takes longer to depolarize
•
Also blocks Ca influx
•
Result: Slowing of conduction
Short half life Given IV for acute therapy of SVT Slows AV node conduction
through AV node
Narrow Complex Originates above HIS bundle
Adenosine •
Most common SVT: AV SVT: AVNRT NRT •
•
•
•
Adenosine •
AV node reentrant reentrant tachycardia
•
Effects blocked by theophylline and caffeine Block adenosine receptors
Slow and fast circuits in AV node arrhythmia Adenosine slows AV node conduction Arrhythmia with terminate
Adenosine
Adenosine
Adenosine
Magnesium
•
Also a vasodilator
•
•
Causes skin flushing, hypotension
•
•
•
•
Caffeine
Some patients also develop dyspnea, chest pain Effects quickly resolve
•
Acute management of torsade de pointes Mg blocks influx of Ca into cells Ca influx leads to early afterdepolarizations Phase 1 IK+ (out)
Must warn patients before administration for SVT 0mv
ICa+
Phase 2 (in) & IK+ (out)
0mv Phase 3
Phase 0 INa+ (out) -85mv
85
IK+ (out)
ERP Phase 4
Theophylline
Atropine
Atropine •
Muscarinic receptor antagonist
•
Used in bradycardia ↑ heart rate
•
Also speeds conduction through AV node
•
Useful for bradycardia especially from AV block
•
Parasympathetic block ↑ HR and AV conduction
Before Atropine
After Atropine
Atropine
Digoxin
•
May side effects related to muscarinic block
•
Two cardiac effects
•
Toxicity:
•
#1: Increases contractility
•
Dry mouth
•
Constipation
•
Urinary retention
•
Confusion (elderly)
•
•
Used in systolic heart failure with ↓ LVEF
#2: Slows AV node conduction •
Used in atrial fibrillation to slow ventricular ventricular rate
Digoxin
Digoxin
Increased Contractility
AV Nodal Slowing
•
Inhibits Na-K-ATPase
•
DIGOXIN X
K+ •
2 Ca+
1 Na+
•
ATP
Digoxin Na trapped inside of cell Less Na exchange for Ca (pump 2) Result: More Ca inside of cell
86
Suppresses AV Suppresses AVnode conduction •
Increased vagal (parasympathetic) tone
•
Separate effect from blockade of Na-K-ATPase
Can be used to ↓ heart rate in rapid atrial fibrillation •
Continued atrial fibrillation
•
Fewer impulses to ventricle
slower heart rate
Effects similar to BB and CCB in AV node
Digoxin Toxicity •
Renalclearance Renalclearance •
•
•
Digoxin Toxicity •
Gastrointestinal
•
Neurologic
Risk of toxicity in patients with chronic kidney disease
•
Hypokalemia promotes toxicity •
Caused by many diuretics, especially loop diuretics
•
Digoxin patient on furosemide
•
toxicity
Levels often need to be monitored
Anorexia, nausea, vomiting, abdominal pain Lethargy, fatigue
•
Delirium, confusion, disorientation
•
Weakness
•
Visual changes
•
Cardiac arrhythmias
•
Alterations in color vision, scotomas, blindness
Digoxin Toxicity
Digoxin Toxicity
Cardiac Toxicity
Treatment
•
•
More Na inside of cell atrial/ventricularcells ↑ restingpotentialatrial/ventricular
•
Increased automaticity
•
Dig toxic rhythms: rhythms: •
Extra beats: beats: atrial, junctional, ventricular
•
Evidence of AV of AV node block
•
•
87
Digibind •
Digoxin antigen binding fragments (Fab)
•
Produced in animals (sheep)
•
Dig bound to albumin (hapten)
•
Antibody converted to fragments
antibodies
Corrects hyperkalemia, symptoms
The Cardiac Cycle Aorta LV LA
Heart Sounds
LV Volume S1 Heart Sounds
Jason Ryan, MD, MPH
S2
VenousPressure EKG
S1 and S2
S1 and S2 •
Normal heart sounds
•
Each has two components
•
•
•
S1
•
S2
•
•
One from left sided valves (aortic, (aortic, mitral)
•
One from right sided valves (tricuspid, (tricuspid, pulmonic)
•
Mitral and tricuspid valves close
Aortic and pulmonary valves close
S1 usually “single” •
Two components components close together
•
Cannot distinguish separate sounds
S2 can be “split” •
Two components far enough apart to be audible MV TV S1
S2
S1
S1
MV TV
S2
AV
PeRsistent = Right Right sided delay MV TV
AV PV
S1
S2
S2
Exhalation
MV TV
AV PV
RBBB or Pulmonary Hypertension
S2
Exhalation
Inspiration
MV TV
Persistent S2 splitting
Physiologic S2 splitting S1
AV PV
Inspiration
PV
AV PV
S2
S1
MV TV
AV
PV
Delayed PV closure even during exhalation
Increased venous return delays P2 by 40-60ms Single to split with inspiration
88
Fixed S2 splitting
Paradoxical S2 splitting
Atrial septal defect
Delayed closure of aortic valve
S1
Atrial Septal Defect Fixed split S2 Systolic Ejection Murmur LSB
S2
Exhalation
S1
S2
Exhalation MV TV
AV
PV MV TV
S1
Inspiration
Inspiration
MV TV
PV
AV
S2
AV
S2
S1
PV MV TV
PV AV
Flow across ASD increased right sided flow
Paradoxical Splitting •
•
Summary of S2 Splitting
Electrical causes delayed LV activation •
LBBB
•
RV pacing
•
•
•
Mechanical causes delayed LV outflow •
LV systolic failure
•
Aortic stenosis
•
Hypertrophic Hypertrophic cardiomyopathy
•
Physiologic= normalrespiratoryvariation PeRsistent = RBBB, pulmonary HTN Fixed = Atrial septal defect ParadoxicaL = LBBB,cardiomyopathy
ParodoxicaL ParodoxicaL = Left sided delay
Loud P2
Cardiac Phonography
1, S2
•
Loud pulmonic component of S2
•
Pulmonary hypertension
•
•
Forceful closure of pulmonary valve Normally P2 not heard at apex •
Fixed Split S2
89
If you hear it here, it’s “loud”
S3 and S4 •
•
•
•
•
S3
Pathologic/a bnormal heartsounds
•
Occur in diastole during filling of left ventricle Low-pitched sounds heard best with bell S3: Early filling filling sound S4: Late filling sound sound
S1
S4
S1
•
S2
S2
•
•
•
High LA pressure rapid early filling of LV S3
•
Associated with ↑ LAP LAP & ↑LVEDP
•
“Pushers” push blood into LV
•
Very specific sign of high left atrial pressure
May be heard in normal hearts •
Young patients (<30), pregnant women
•
These patients are “suckers”
•
Vigorous LV relaxation lowers pressure rapidly
S3
S3 •
Commonly seen in acute heart failure
S4
Low frequency best heard with bell
•
Louder in left lateral decubitus position Loudest atapex at apex •
•
Heard in patients with stiff left ventricle •
Long-standing hypertension
•
Hypertrophic Hypertrophic cardiomyopathy
•
Diastolic heart failure
Rapid late filling of LV due to atrial kick Not heard in atrialfibrillation
Atrial Fibrillation
Right Sided S3 & S4 •
Systolic Clicks
Both sounds can occur in right ventricle
•
Same mechanisms as left sounds
•
Right heart failure right sided S3
•
Rightventricular hypertrophy right sided S4
S1
Click S2
Ejection Click Early in systole BEFORE carotid pulse Bicuspid Aortic Valve
90
S1
Click S2
Non-Ejection Click Late in systole AFTER carotid pulse Mitral Valve Prolapse
Mitral Valve Prolapse
Mitral Valve Prolapse •
•
•
Systole
Billowingof Billowing of mitral valve leaflets above annulus Common cause of mitral regurgitation Causes a systolic click •
Don’t confuse with opening snap of mitral stenosis
Mitral Valve Disorders Proclick Stenosnap
Click S1
Normal
MVP
91
Murmur S2
Diastole
Heart Murmurs •
Cardiac sound heard with stethoscope
•
Caused by turbulent blood flow
•
May be normal or pathologic
Heart Murmurs Jason Ryan, MD, MPH
Murmurs
Laminar vs. Turbulent Flow
Grading •
•
•
•
Laminar Flow = Quiet(er) Quiet(er)
I - barely audible on listening carefully II - faint but easily audible III - loud and easily audible, no thrill IV - loud murmur with a thrill
•
V –heard with scope barely touching chest
•
VI - audible with scope not touching the chest
Turbulent Flow = Loud High Flow Rates Narrow Flow Areas
Murmurs
Murmurs
Other Descriptors
Location
S1
Systole
Diastole
Systole
S2
S1
LUSB Pulmonic Murmurs PDA
RUSB Aortic Stenosis A
S2
LSB Aortic Regurg HCM Holosystolic Pansystolic
Crescendo
Decrescendo
Crescendodecrescendo
T
LLSB Tricuspid Murmurs VSD
92
P
M
Apex Mitral Murmurs
Murmurs
Innocent/Functional Murmurs
Location •
•
•
Point of maximal impulse (apical impulse) •
Left 5th intercostal space
•
Mid-clavicular line
•
•
•
Lateral shift = Enlarged heart heart Hyperdynamic
•
•
•
•
Base
•
Caused by normal flow of blood Common in children Also young, thin patients Generally soft murmurs No signs/symptoms of heart disease Stillsmurmur Pulmonic flow murmur Venous hum
Apex
Systolic Murmurs •
•
•
•
Diastolic Murmurs
Occur when heart contracts/squeez es
•
Between S1-S2 Aortic stenosis Mitral regurgitation
•
•
•
Occur when heart relaxes/fills Between S2-S1 Aortic regurgitation Mitral stenosis
•
Pulmonic stenosis
•
Pulmonic regurgitation
•
Tricuspid regurgitation
•
Tricuspid stenosis
•
Hypertrophic cardiomyopathy
•
Ventricular septal defect (VSD)
Aortic Stenosis
Aortic Stenosis
Murmur
Severe Disease Findings
•
•
Systolic crescendo-decrescendo murmur Also called an “ejection murmur”
•
Late-peaking murmur •
•
Soft/quiet S2 •
•
S1
S2
93
Slow flow across stenotic stenotic valve Stiff valve can’t slam shut
Pulsus parvus et tardus •
Weak and small carotid pulses
•
Delayed carotid upstroke
HCM
Aortic Regurgitation Regurgitation
Hypertrophic Cardiomyopathy Cardiomyopathy
Murmur
•
Same murmur as aortic stenosis
•
Differentiate d bymaneuvers
•
Valsalva •
Decreases venous return/preload
•
Increase HCM murmur
•
Decrease AS murmur
•
Decrescendo, blowingdiastolic blowing diastolic murmur
S1
S2
HCM
Mitral Regurgitation Regurgitation •
Mitral Stenosis
Holosystoli c murmur heard best at the apex •
•
5th intercostal space, mid-clavicular mid-clavicular line
•
Diastolic rumbling murmur Preceded by opening snap Systole
S1
Diastole
Systole
Diastole
S2
Holosystolic (Pansystolic)
S1
Mitral Stenosis
S2 OS
Diastolic Rumble (Murmur)
Tricuspid/Pulmonic Disease
•
No left sided S3, S4 in mitral stenosis
•
•
Time to opening snap associated with severity
•
Heard in different locations
•
Left upper sternal border
•
Left lower sternal border
•
High left atrial pressure in severe disease
•
Higher left atrial pressure
•
Short time to opening snap seen in severe disease
↓ time to opening snap
Valve lesions sound like left sided-counterparts
•
•
94
Pulmonic stenosis/regurgitation Tricuspid stenosis/regurgitation
VSD
Carvallo’s Sign •
•
•
•
Ventricular Septal Defect
Most right sided murmurs louder with inspiration
•
Inspiration draws blood volume to lungs Louder right sided murmurs Softer left sided murmurs
•
rIght sided murmurs increase with Inspiration
•
lEft sided murmurs increase with Exhalation
•
Holosystolic murmur similar to MR Small VSD more turbulence loud murmur
3 Causes Holosytolic Murmurs
S1
S2
Mitral Regurgitation Tricuspid Regurgitation VSD
Holosystolic (Pansystolic)
PDA
Maneuvers
Patent Ductus Arteriosus •
Continuous, “machine -like” murmur
•
•
•
S1
S2
S1
Valsalva Maneuver
Preload/Venous Return
•
•
May increase or decrease murmur Used to make diagnosis
S2
Maneuvers •
Performed at bedside with patient
Increase preload/venous return •
Leg raise – blood falls back toward heart
•
Squatting – blood in legs forced back toward heart
•
Bear down as if moving bowels
•
Phase I (few seconds)
Decrease preload/venous return •
ValsalvaValsalva- ↑ intra-thoracic pressure vein compression
•
Standing – Blood falls toward feet, feet, away from heart
↓ VR VR
Most murmurs INCREASE with more preload except:
•
•
↑ thoracic pressure
•
↓ venous return (compression of veins
•
Transient rise in aortic pressure (compression)
•
↓ heart rate and AV node conduction (baroreceptors)
↑RA pressure)
Phase II
•
HCM
•
↓ preload ↓ cardiac output
•
MVP
•
↑ heart rate and AV node conduction (baroreceptors)
95
Maneuvers
Maneuvers
Afterload
Afterload
•
Increase Afterload •
•
•
Backward Valve Valve Disorder s
Hand grip - clench fist
Decrease Afterload •
Amyl Nitrate - vasodilator •
•
•
AR, MR, VSD
•
Louder with more afterload
•
More force pushing blood backward
Forward Valve Valve Disorder s •
MS, AS
•
Softer with more afterload
•
Less pressure difference moving blood forward
MVP, HCM •
Softer
•
Increased LVcavity size
Amyl Nitrate
Summary
Clues to Diagnosis •
•
•
•
•
•
Commonly Tested Murmurs S1
Young female, otherwise healthy MVP Healthy, young athlete, syncope HCM Immigrant or pregnant Mitral stenosis IV drug abuser Tricuspid regurgitation
AS/HCM MR/VSD
Turner Syndrome or Aortic Coarctation •
Bicuspid AV
•
Early stenosis
•
Aortic regurgitation
AR MS
Marfan MVP
PDA
96
S2
S1
S2
Heart Failure •
Impaired ability of the heart to pump blood
•
Hallmark: Low cardiac output
↓ CO
Heart Failure Basics Jason Ryan, MD, MPH
Heart Failure
Heart Failure
H20 H20 Tank
Tank
Pump
Pump
Heart Failure
Heart Failure
H20
H20
Tank
Tank
Pump
Heart
97
Heart Failure
Heart Failure
Blood
Blood
ank
Tank
Heart
Heart
Heart Failure
Heart Failure
Pathophysiology •
“Failing” chambers Increased pressures
•
Pressures rise in cardiac chambers
Lungs & Veins
Heart
Heart Failure
Heart Failure
Pathophysiology
Pathophysiology
•
Left ventricular failure ↑ LV pressure •
LV systolic pressure: depends depends on contractility (can be low)
•
LVEDP = always high in left heart failure
•
Hallmark of left heart failure
•
Less blood pumped pumped out more left behind more pressure
•
Stiff ventricle (diastolic HF) high pressure
•
•
↑ LVEDP ↑ LA pressure ↑ pulmonary capillary pressure •
Dyspnea
•
Pulmonary edema Aorta
LV LA
98
Heart Failure
Heart Failure
Pathophysiology
Pathophysiology •
•
•
↑Pc
↑ pulmonary capillary pressure ↑ PA pressure ↑ PA pressure ↑ RV pressure ↑ RV pressure ↑ RA pressure •
Right atrial pressure = central venous pressure
•
High pressure in venous system
•
↑ jugular venous pressure (neck veins)
•
Capillary leak
pitting edema
Heart Failure
Heart Failure
Signs/Symptoms
Signs/Symptoms
•
•
•
•
Physiologic effects of lying flat (supine)
•
Left heart failure
•
Increased venous return
•
•
Redistribution of blood volume volume
•
Paroxysmal nocturnal dyspnea (wake up SOB)
•
From lower extremities and splanchnic beds to lungs lungs
•
Orthopnea (can’t (can’t breathe lying flat)
Little effect in normal individuals Impaired ventricle cannot tolerate changes
•
Right heart failure •
Worsens pulmonary congestion and breathing •
Dyspnea especially on on exertion
Increased jugular venous pressure pressure
•
Lower extremity edema
•
Liver congestion (r arely can causecirrhosis)
“Backward failure”
Heart Failure
Heart Failure
Right Heart Failure
Signs/Symptoms
•
Most common cause R heart failure: Left heart failure
•
Occasionally right heart failure occurs in isolation
.
•
Lowflow signs/symptoms signs/symptoms (“forwardfailure”) (“forward failure”) •
Loss of appetite Weight loss (cachexia) Confusion
•
Normal left atrial pressure
•
•
High pulmonary artery, artery, right ventricular, right atrial pressure
•
•
Usually secondary to a lung process
•
Cool extremities
•
Pulmonary hypertension
•
“Narrow pulse pressure”
•
COPD
•
This is often called “cor pulmonale”
99
•
Seen only with very low cardiac output (systolic HF)
•
Not seen in diastolic heart failure
Heart Failure
Heart Failure
Lung Findings
Lung Findings
•
Classic finding israles is rales •
•
•
•
Fluid filled alveoli “pop” open with inspiration
•
Chest X-ray shows congestion Lungs/CXR can be clear in chronic heart failure •
•
Heart failure cells Hemosiderin (iron) laden macrophages Brown pigment in macrophages
↑lymphatic drainage
Heart Failure
Heart Failure
Signs/Symptoms
Hepatojugular Hepatojugular Reflux
•
Elevatedjugular Elevated jugular venous pressure (normal 6-8cmH2O)
•
Pressure on abdomen raises JVP 1-3cm normally
•
Look for height of double bounce (cause by a and v waves)
•
With failing RV, increase is greater
Heart Failure
Heart Failure
Signs/Symptoms
Abnormal Heart Sounds
•
Lower extremity pitting edema
•
S3 (associated (associated with high left atrial pressure)
•
Increased capillary hydrostatic pressure
•
S4 (associated with stiff left ventricle)
•
Fluid leak from capillaries tissues
•
Displaced apical impulse – enlarged heart
•
Gravity pulls fluid to lower extremities
S1
↑Pc S4
100
S1
S2
S2
S3
Heart Failure
Heart Failure
Pathophysiology
Total Peripheral Resistance
•
All forms of heart failure lead to ↓ cardiac output
•
Cardiac output falls vasoconstriction
•
Activates two physiologic systems
•
Angiotensin II, sympathetic nervous system
•
•
Activation of sympathetic nervous system
•
Activation of renin-angiotensin-aldostero renin-angiotensin-aldosterone ne system
•
All RAAS hormone levels will rise
•
•
•
Both systems lead to two key effects: •
Increased peripheral vascular resistance resistance (vasoconstriction)
•
Retention of sodium/water (kidneys)
TPR alwayshigh Blood pressure often high but may be low Depends on combined changes CO and TPR
BP = CO X TPR
Heart Failure
Heart Failure
Sodium/Water Retention
Other Hormones
↓ cardiac output
•
•
•
↓ Effective Circulating Volume
•
•
↑ RAAS
↑ SNS ↑ ADH
•
ANP (Atrial natriuretic natriuretic peptide) peptide) Atrialstretch (pressure/volume) (pressure/volume) ANP release Vasodilator (↓TPR) Constricts renal efferents/dilates afferents ↑ diuresis Opposite effects of RAAS system
↑ Na/H2O Afferent
Efferent
↑ Total Body Water
Heart Failure
Nesiritide
Other Hormones •
•
•
•
•
ANP released by atrial myocytes BNP (brain natriuretic peptide): Ventricles Both rise with volume/pressure overload
High levels suggest heart heart failure
•
Low levels suggest other causes of dyspnea
Recombinant BNP
•
Vasodilation
•
Both counter effects of RAAS system BNP sometimes used for diagnosis in dyspnea •
•
•
ANP/BNP RAAS
101
↓ afterload,↑CO afterload, ↑CO Failed to show benefit in clinical trials
Heart Failure Diagnosis •
•
•
Most common: typical signs/symptoms Elevated BNP level Heart catheterization •
Increased LVEDP = left heart congestion/failure
•
Increased RA, RVEDP = right heart congestion/failure
102
Heart Failure Systolic and Diastolic •
Systolic and Diastolic Heart Failure
•
Same congestive signs/symptoms •
Dyspnea, orthopnea, paroxysmal paroxysmal nocturnal dyspnea
•
Rales, ↑ JVP,pitting edema
Exception: Low flow symptoms symptomsin in systolic only •
Cool extremities
•
Cachexia
•
Confusion
Jason Ryan, MD, MPH
Dilated Cardiomyopathy Cardiomyopathy
Concentric Hypertrophy
•
Systolic heart failure with LV cavity dilation
•
Pressure overload
•
“Eccentric” hypertrophy
•
Chronic ↑↑ pressure in ventricle: HTN, Aortic stenosis
•
Volume overload (chronic retention of fluid in cavity)
•
Longer myocytes
•
Sarcomeres added in series
Normal LV Size
•
•
Dilated LV
Decreased compliance (stiff ventricle) Often seen in diastolic heart failure
Normal LV Size
Increased myocyte size Sarcomeres in series Normal wall thickness
↓ LV Size
Increased myocyte size Sarcomeres in parallel Increased wall thickness
Systolic Heart Failure •
e
re
•
s s
•
r u u s s e e r
r V L
P P
•
V L
LV Vol Systolic Heart Failure ↓ Contractility
LV Vol
↓ Cardiac output Problem in SYSTOLE Can’t get get blood out ↓ Stroke volume •
SV = EDV – ESV
•
↑ ↑ ESV (↓ contractility)
•
↑ EDV (↑ESV + VR)
•
↑ LVEDP
er u s s e r P V L
LV Vol
Diastolic Heart Failure ↓ LV Compliance ↓ Lusitropy
Systolic Heart Failure ↓ Contractility
103
Frank-Starling Curve
Diastolic Heart Failure •
•
•
Normal
•
•
↓ Contractility
Stroke Volume
↓ Cardiac output Problem in DIASTOLE Can’t get get blood in Small ↓ stroke volume
•
er u s s e r P
↓ EDV (↓ filling)
↑↑ LVEDP (stiff ventricle)
V L
LV Vol
Preload (LVEDV)
Diastolic Heart Failure ↓ LV Compliance ↓ Lusitropy
Systolic Heart Failure •
•
Most common cause: Myocardial infarction •
Myocytes replaced by scar tissue
•
“Ischemic” cardiomyopathy
Many causes of “non-ischemic” cardiomyopathy •
•
Diastolic Heart Failure •
Exact cause unknown
•
Many cases have concentric hypertrophy
•
Many associated conditions •
About 50% idiopathic Many other causes: viral, familial, peri-partum, chemotherapy toxicity, toxicity, HIV, alcoholic, alcoholic, sarcoidosis, tachycardia-mediated
•
Age, diabetes, hypertension
Terms: •
Heart failure preserved preserved EF
•
HFpEF
•
Diastolic dysfunction
Nonischemic Cardiomyopathy
Nonischemic Cardiomyopathy
Viral
Peri-partum
•
May follow upper respiratory infection
•
•
Many associated viruses
•
•
•
•
•
•
Coxsackie
•
Influenza, adenovirus, others
•
Virus enters myocytes Causes myocarditis cardiomyopathy Myocarditis phase may go undiagnosed No specific therapy for virus
104
Late in pregnancy or early post-pregnancy Exact cause unknown (likely multifactorial ) Women often advised to avoid future pregnancy
Nonischemic Cardiomyopathy
Nonischemic Cardiomyopathy
Chemotherapy
Familial
•
Usually after treatment with anthracyclines
•
Mutations
•
Antitumor antibiotics
•
Often sarcomere proteins
•
Doxorubicin and daunorubicin daunorubicin
•
Beta myosin heavy chain chain
•
Alpha myosin heavy chain
•
Troponin
Daunorubicin
•
Many autosomal dominant
•
X-linked, autosomal recessive also described
Doxorubicin (Adriamycin)
Nonischemic Cardiomyopathy
Nonischemic Cardiomyopathy
Tachycardia-mediated
Takotsubo/Apical ballooning
•
•
•
Constant, rapid heart rate for weeks/months Leads to depression of LV systolic function
•
•
Reversiblewith Reversible with slower heart rate
•
•
Alcohol •
Chronic consumption can cause cardiomyopathy
•
Believed to be due to toxic metabolites
•
Stress-induced cardiomyopathy
Occurs after severe emotional distress Markedly reduced LVEF Increase CK, MB, Tro Troponin; ponin; EKG changes
•
Looks like anterior MI (but no coronary disease)
•
Usually recovers 4-6 weeks
High Output Heart Failure •
Can recover with cessation of alcohol
•
Heart in overdrive •
Severe anemia
•
Thyroid disease
•
Thiamine (B1) vitamin deficiency (beriberi)
•
A-V fistulas (post-surgical)
Exact mechanism unclear •
•
105
Decreased LV filling time
Defining characteristic: HIGH cardiac output •
Heart failure symptoms in absence of low output
•
↑JVP, pulmonary edema
Restrictive Restricti ve Heart Disease •
Restrictive Cardiomyopathy
Something “infiltrates” the myocardium •
Granulomas (Sarcoid)
•
Amyloid protein (Amyloidosis)
•
Heart cannot relax and fill
•
SEVERE diastolic dysfunction
Jason Ryan, MD, MPH
Restrictive Restricti ve Heart Disease
Restrictive Heart Disease •
•
•
•
•
Clinical Features
LVEF = normal Left ventricular volume = normal (not dilated) Restricted filling = ↑ atrial pressure Dilated left and right atria
•
Dyspnea
•
Prominent right heart failure •
Classic imaging findings: •
Normal left ventricular function/size
•
Bi-atrial enlargement
Markedly elevated jugular venous pressure
•
Lower extremity edema
•
Liver congestion
•
May lead to cirrhosis (“nutmeg liver”)
Restrictive Restricti ve Heart Disease
Restrictive Restricti ve Heart Disease
Classic signs
Rhythm Disturbances
•
Kussmaul’s sign •
•
Inspiration causes rise in JVP
Myocardialinfiltrationmaydisruptelectricalactivity
•
Arrhythmias (sudden death)
•
AV block
Ventricular Tachycardia
106
3rd Degree Heart Block
Restrictive Heart Disease
Restrictive Restricti ve Heart Disease
Major Causes
Classic signs
•
Amyloidosis •
Amyloid protein deposits in heart
•
Various forms (primary, secondary, etc.)
•
Can see thickened myocardium
•
Low voltage on EKG
•
Classic finding in amyloidosis and Fabry’s disease
Restrictive Heart Disease
Restrictive Restricti ve Heart Disease
Major Causes
Major Causes
•
Sarcoidosis
•
Fabry disease
•
Granuloma formation
•
Lysosomal storage disease disease
•
Usually involves lungs
•
Deficiency of α-galactosidase A
•
Extra-pulmonary or gans include heart heart
•
Accumulation of ceramide trihexoside
Restrictive Heart Disease
Restrictive Restricti ve Heart Disease
Major Causes
Major Causes
•
Hemochromatosis •
Iron excess
•
Commonly causes dilated cardiomyopathy cardiomyopathy
•
Rarely may cause restrictive
•
•
•
107
Post-radiation Acutely: May cause inflammation Fibroblast recruitment
•
Extra-cella r matrix deposition
•
Collagens and fibronectin
Restrictive Heart Disease
Restrictive Restricti ve Heart Disease
Major Causes
Major Causes
•
Pericarditis may occur acutely after therapy
•
Long term effects
•
•
Loeffler’s syndrome •
Hypereosinophilic syndrome
•
Pericardial disease
•
High eosinophil count
•
Coronary artery disease disease
•
Eosinophilic infiltration of organs
•
Valvular disease
•
Conduction abnormalities
•
Skin (eczema)
•
Lungs (fibrosis)
Restrictive cardiomyopathy •
Fibrous tissue accumulation
•
Diastolic dysfunction
Restrictive Heart Disease
Restrictive Restricti ve Heart Disease
Major Causes
Major Causes
•
•
•
Primary HES •
Neoplastic disorder
•
Stem cell, myeloid, or eosinophilic neoplasm
•
Acute phase
•
Chronic phase
Secondary HES •
Reactive process
•
Eosinophilic overproduction overproduction due to cytokines
•
Occurs in parasitic infections (ascaris lumbri coides)
•
Some tumors/lymphomas
•
Idiopathic HES
Major Causes Endocardial fibroelastosis •
•
Eosinophilic infiltration of myocardium •
Restrictive Heart Disease •
•
Endocardial thickening (innermost myocardium)
•
Infants in first year of life
•
Thick myocardium
•
Proliferation of fibrous (collagen) and elastic fibers
Restrictive cardiomyopathy
108
Common mode of death death Myocarditis (often asymptomatic)
•
Endomyocardial f ibrosis and myocyte death
•
Can see restrictive restrictive heart disease
•
Thrombus formation common (embolic stroke) stroke)
Heart Failure Acute vs. Chronic Acute •
•
•
•
Acute Heart Failure
Chronic
Congested/Swollen Pulmonary Edema Pitting Edema ↑JVP
•
•
•
•
Euvolemic Clear lungs No pitting edema JVP flat
Jason Ryan, MD, MPH
Acute Exacerbations Exacerbations
Dietary Indiscretion Indiscretion
Causes •
•
•
↑Na Intake
#1: Dietary indiscretion
Plasma Na = 140meq/L
High salt intake
↑Plasma Osmolarity
#2: Poor medication compliance
↑ADH ↑Free Water
↑Volume
Normal Plasma [Na]
↓RAAS ↓ADH ↑Urine Output
Acute Exacerbations Exacerbations
Acute Heart Failure Therapy
Causes •
Infection/trauma/surgery • Activation of sympathetic nervous system
•
•
Ischemia (rare) • Decreased cardiac output Inhibit cyclooxygenase (COX) ↓ prostaglandins
• Prostaglandins maintain renal perfusion •
Often treated in the hospital
•
Goal: Symptom relief
•
Often same therapies for diastolic versus systolic
•
NSAIDs •
•
Result: Less renal perfusion salt/water retention
109
Contrast with chronic HF: reducemortality/hospitalizations
Loop Diuretics
Loop Diuretics
Furosemide, Bumetanide, Torsemide, Ethacrynic Acid •
Result in salt-water excretion
•
Relieve congestion
•
Na •
K
Inhibit Na-K-Cl pump in ascending loop of Henle
•
2Cl
•
IV better than PO (gut is swollen) Key side effects •
Hypokalemia
•
Volume depletion (Renal (Renal failure; hypotension)
Sulfonamide drugs: allergy (except ethacrynic acid)
Ascending Limb Loop Diuretics
Metolazone •
•
•
•
•
Nitrates
Thiazide-like diuretic
•
Inhibits Na-Cl reabsorption distal tubule Gives loop diuretics a “kick” Vigorousdiuresis Side effects: additional fluid, K+ loss
Predominant mechanism is venous dilation •
Bigger veins hold more blood
•
Takes blood away from left ventricle
•
Lowers LVEDV LVEDV (preload), LA pressure pressure
•
Less pulmonary edema improved dyspnea
Vasodilators
Nitrates
“Afterload reduction” •
Side effects •
Headache (meningeal vasodilation)
•
Flushing
•
Hypotension
•
•
•
•
110
ACE inhibitors Hydralazine Cause peripheral vasodilation Reduced afterload increased cardiac output
Nitrates plus Hydralazine •
Inotropes • Increase contractility • Only for systolic heart failure
Combination therapy for acute and chronic HF •
Studied in systolic heart failure
•
Reduction in preload (nitrates) and afterload afterload (hydralazine)
•
Acute therapy: Improves symptoms
•
Chronic therapy: Lowers Lowers mortality in some studies
•
Largely replaced by ACE inhibitors
•
Some studies suggested benefit in black patients
•
No role in diastolic heart failure (normal contractility)
•
All activate β1 pathways in myocytes
•
Can also active β2 pathway β2 pathways s in smooth muscle
•
•
Increased HR and contractility contractility Vasodilation
hypotension
Inotropes
Inotropes
Milrinone
Dobutamine
•
•
•
•
Phosphodiesterase 3 inhibitor •
PD3 breaks down cAMP in myocyctes
•
Inhibition ↑cAMP contraction
•
Vascular smooth muscle ↑cAMP (β2)
•
Mostlybeta-1agonist
•
Weak beta-2 agonist
•
dilation
•
↑Inotropy ↑Vasodilation
•
•
Hypotension
Increases heart rate and contractility Vasodilation
↑Inotropy ↑Vasodilation
•
Hypotension
•
Similar effects to milrin one
Inotropes
Inotropes
Dopamine
Epinephrine
•
•
•
Does not cross blood brain barrier (no CNS effects) Peripheral effects highly dependent on dose Low dose: dopamine agonist •
•
•
Low dose: beta-1 and beta-2 agonist
•
High dose: alpha agonist •
Increased heart rate and contractility
High dose: alpha agonist •
Also dose dependent effects
•
•
Vasodilation in kidneys
Medium dose: beta-1 agonist •
•
Vasoconstriction
111
Increased heart rate & contractility, vasodilation
Vasoconstriction
A Typical Acute Heart Failure Course
Inotrope Risks •
•
Numerous registries and clinical trials demonstrate increased mortality with routine use of inotropes Dangerous drugs used in very sick patients under monitored conditions
•
ER presentation:
•
Admitted to hospital
•
•
•
A More Complex Heart Failure Course •
•
•
•
Nitro drip to relieve dyspnea
•
IV Furosemide to remove fluid
Hospital Day 2 •
Weight down 4kg, feels better
•
Nitro drip stopped
•
Changed to oral furosemide
Hospital Day 3: Discharge Discharge
A More Complex Heart Failure Course
ER presentation:
•
Hospital Day 3-5
•
Dyspnea, edema, sleeping in chair
•
Good urine output output
•
Known LVEF 10%
•
Weight loss 4kg
•
Breathing improves
Admitted to hospital •
Nitro drip to relieve dyspnea
•
IV Furosemide to remove fluid
•
Hospital Day 2 •
Poor urine output, Cool extremities, Cr rises 1.1 1.4
•
Dobutamine drip started
Hospital Day 6 •
Dobutamine stopped
•
Furosemide drip stopped
•
Hospital Day 7
•
Hospital Day 8: Discharge Discharge
•
Heart Failure Readmission •
Dyspnea, edema, sleeping in chair
Oral furosemide given
Acute Heart Failure
Recurrence of HF after discharge common
•
Most patients require chronic, daily diuretic
•
Post-discharge follow-up VERY important
•
Helps to maintain euvolemic euvolemic status
•
“Readmissions” a focus of public health policy
•
Often oral furosemide or other loop diuretic
•
High risk of readmission within 30 days
•
Highest risk category among Medicare population
•
Some patients require daily long acting nitrate •
112
Often oral isosorbide mononitrate
Acute Heart Failure •
Digoxin
Rare patients: continued treatment for low output •
Systolic heart failure only
•
Chronic, IV infusion inotrope inotrope (i.e. “home dobutamine”)
•
Left ventricular assist device (LVAD) (LVAD)
•
Heart transplant
•
•
•
Only available oral inotrope
“Dig and diuretic” once the mainstay of HF treatment What changed? •
Digoxin shown to have no mortality benefit
•
Digoxin not effective for diastolic heart heart failure
•
Digoxin carries significant risk of side effects
•
About 50% of all cases cases
Digoxin Mechanism
Digoxin
Two important cardiac effects
Benefits in Heart Failure
•
•
#1: Inhibits Na-K-ATPase pump
•
More Na in cell more Ca++ in cell cell
•
Symptoms despite maximal therapy on other drugs drugs
•
More Ca++ more contractility
•
i.e. persistent dyspnea dyspnea despite good volume volume status
#2 Suppresses AV node conduction (parasympathetic) •
Can be used to slow heart rate in rapid atrial fibrillation
Digoxin Benefits in Heart Failure •
•
•
Useful for systolic HF patients
•
Increased cardiac output Improved symptoms and quality of life No established mortality benefit
113
•
Can be administered for acute heart failure
•
Can be administered long ter m to maintain CO
Heart Failure Treatment Pathway Acute Heart Failure
Chronic Heart Failure
Rx Chronic Heart Failure Diastolic Heart Failure
Jason Ryan, MD, MPH
Chronic Heart Failure •
•
Drugs: ACE-inhibitors, beta blockers, aldosterone antagonists
•
Defibrillators
•
Bi-ventricular Bi-ventricular pacemakers
NO direct therapies for diastolic heart failure •
Guidelines recommendations: recommendations: treat HTN, diabetes, A. fib
•
Mainstay of therapy: monitor for symptoms, diuretics
ARBs
•
Chronic over-activation of two physiologic systems
•
Renin-angiotensin-aldosterone system
•
Sympathetic nervous system (β1 stimulation)
•
Blockade ↓ mortality and disease progression
RAAS Drugs
Renin-Angiotensin System Angiotensinogen
Sympathetic System
•
+ Renin AI
ACE Inhibitors Inhibitors •
Renal Na/Cl resorption + ACE
•
A2
•
Arteriolar vasoconstriction
•
•
Adrenal aldosterone secretion
•
Net Result
•
114
Candesartan, Ir besartan, Valsartan Valsartan Directly block AII receptor
Both classes: ↓ morality, ↓ hospitalizations Side effects •
Pituitary ADH secretion
↑Salt/Water Retention ↑Preload ↑TPR ↑Afterload
Captopril, Enalapril, Lisinopril, Ramipril Block conversion AI AII
Angiotensin Angiotensin ReceptorBlockers (ARBs) •
ACE Inhibitors
Systolic Heart Failure
Systolic Heart Failure
LOTS of therapies for systolic heart failure •
Symptom Relief Loop diuretics Nitroglycerine Inotropes
Hyperkalemia (↓aldosterone) Renal failure (↓GFR)
ACE Inhibitors
Bradykinin
Unique Side Effects •
Due to increased bradykinin
•
Dry Cough •
•
Bradykinin X
Angioedema •
Swelling of face, tongue
•
Can be life-threatening
•
•
Negative inotropes
May worsen cardiac output and symptoms •
Three agents beneficial in chronic systolic HF failure •
Metoprolol (β1)
•
Carvedilol (β1β2α1)
•
Bisoproplol (β1)
↓ morality, ↓ hospitalizations
Spironolactone, Eplerenone
Aldosterone Antagonists
Potassium-sparing diuretics •
Sympathetic System
•
Renal Na/Cl resorption
↑Na/H2O excretion (diuretics) “Spare” potassium •
A2 Arteriolar vasoconstriction
A2
Beta Blockers
Not used in acute heart failure •
ACE Inhibitors
X
Inactive Metabolites
Once contraindicated in systolic heart failure •
AI
Occurs in ~10% of patients patients
Beta Blockers •
Cough Vasodilation
X
Spironolactone Eplerenone
Adrenal aldosterone secretion
Pituitary ADH secretion
115
Unlike other diuretics, do not not increase K + excretion
•
HYPERkalemia is side effect
•
Reduced mortality
•
Reduced hospitalization rate
Spironolactone, Eplerenone
Neprilysin Inhibitors Inhibitors
Potassium-sparing diuretics
Sacubitril
•
•
Similarstructureto testosterone testosterone •
Blocks testosterone effects
•
Gynecomastia in men
•
Eplerenone: No gynecomastia gynecomastia
•
Neprilys in: Degrades atrial/brain natriuretic peptide
•
Inhibition ↑ANP/BNP
Derivativ e ofprogesterone •
•
Activates progesterone receptors
Eplerenone
Amenorrhea in women
•
Antagonists to RAAS system
•
Vasodilatation
•
Natriuresis (sodium excretion) excretion)
•
Diuresis (water excretion) excretion)
•
Reduced sympathetic tone ANP/BNP RAAS
Spironolactone
estosterone
Progesterone
Neprilysin Inhibitors
Neprilysin Inhibitors Inhibitors
Sacubitril
Side Effects
•
Entresto: oral combination sacubitril/valsartan •
•
•
•
Valsartan: angiotensin receptor blocker (ARB)
•
↓ morality ↓ hospitalizations
•
•
•
Studied in combination with valsartan Many side effects similar to ARBs Hypotension Hyperkalemia Angioedema •
ANP/BNP
Rare, feared adverse effect
•
Neprilysin also degrades bradykinin (like ACE)
•
Angioedema may occur occur
•
Cannot be given together together with ACE inhibitors
RAAS
Chronic Systolic Heart Failure Failure
Ivabradine
Drug Therapy
•
Selective sinus node inhibitor
•
•
Elevated HR worse prognosis
•
•
Slows heart rate without ↓ contractility
•
Aldosterone antagonists
•
Neprilysin inhibitors
•
Ivabradine
•
•
•
Inhibits SA pacemaker “funny current” (If ) Used in patients on max-dose beta blocker with ↑HR Limited evidence of ↓ morality and ↓hospitalizations
116
ACE inhibitors/ARB Beta Blockers
ICD
ICD
Implantable Cardiac Defibrillator
Implantable Cardiac Defibrillator
•
Annual risk SCD >20% some studies
•
Improve mortality in appropriate patients
•
Most due to ventricular tachycardia
•
Implantation carries some risk: •
Bleeding, infection
•
Inappropriate shocks
Heart Failure Treatment Pathway
Biventricular Pacemakers Cardiac Resynchronization Resynchronization Therapy (CRT), BiV pacer
Acute Heart Failure Out of Synch
After Pacemaker
Rx
Lasix Nitroglycerine Inotropes
Chronic Heart Failure Diastolic Heart Failure No specific therapy
117
Systolic Heart Failure Drugs ICD Bi-V Pacer
Primitive Heart 22 days
Cardiac Embryology Jason Ryan, MD, MPH Sinus Venosus
OpenStax Colleg/Wikipedia
Primitive Heart
Sinus Venosus
22 days
Left Horn
Right Horn
Aorta Pulmonary Artery Smooth LV/RV
Smooth Right Atrium (sinus venarum)
Trabeculated LV/RV
Coronary Sinus
Trabeculated Atria Sinus Venosus Right Atrium Coronary Sinus OpenStax Colleg/Wikipedia
OpenStax Colleg/Wikipedia
Cardinal Veins
Primitive Heart
•
Form SVC/IVC (not from heart tube)
•
Connect to right atrium
•
Superior vena cava cava
•
Inferior vena cava
•
•
R common cardinal vein and R anterior cardinal vein Posterior veins
OpenStax Colleg/Wikipedia
118
Ventricular Ventricular Septum Formation Formation
Cardiac Looping •
•
•
•
Heart tube “loops” at about 4 weeks gestation
•
Seen in in Kartagener Kartagener syndrome
•
Part of primary primary ciliary dyskinesia
Muscular Ventricular Septum
Ventricular Septum Pathology •
Membranous VSD (most common type)
•
Muscular VSD
AP Twist
Aorticopulmonary Septum
Establishes left-right orientation in chest Requires cilia and dynein Dextrocardia (heart on the right side of body)
Membranous Septum Forms
AP Fuses Muscular Septum
Endocardial Cushions Separate R/L atria R/L ventricle
Endocardial Cushions •
•
Contribute to several cardiac structures •
Atrial septum
•
Ventricular septum
•
AV valves (mitral/tricuspid)
•
Semilunar valves (aortic/pulmonic)
Endocardial cushion defects •
Atrioventricular canal defects defects
•
Atrioventricular septal defects defects
•
ASD, VSD, Valvular malformations
•
Common in Down syndrome
Endocardial Cushions Separate R/L atria R/L ventricle
Aorticopulmonary septum
Aorticopulmonary Aorticopulmonary septum
Spiral Septum
Spiral Septum
•
Formed from neural crest cells
•
Abnormal formation congenital pathology
•
Migrate to truncal and bulbar ridges
•
Transposition of great vessels
•
Separates aorta and pulmonary arteries
•
Fuses with interventricular septum
•
TetralogyofFallot
•
Persistent truncus arteriosus
•
OpenStax Colleg/Wikipedia
•
•
Wikipedia/Public Domain
119
Failure to spiral
Skewed septum development development
Partial/incomplete septum development
Atrial Septum Septum Primum
Atrial Septum Septum Primum
Septum primum fuses Endocardial cushion
Foramen Secundum
Septum secundum grows
RA RA
LA Foramen Secundum
LA
Foramen Primum Future Ventricles
Endocardial Cushion
Future Ventricles
Future Ventricles
PFO
Fetal Circulation
Patent Foramen Ovale •
•
•
Future Ventricles
Found in ~25% adults Failure of foramen ovale to close after birth
•
High resistance to flow in lungs
•
Oxygenated blood umbilical veins
•
Travels directly to right atrium
Septum primum/secundum fail to fuse
•
•
•
•
RA
About 80% saturated saturated (30mmHg O2) Bypasses liver via ductus venosus venosus
Bypasses lungs via foramen ovale Some blood gets to RV (SVC) •
Bypasses lungs via ductus arteriosus
•
Left pulmonary artery to aorta
LA
Changes at Birth
Changes at Birth
•
Pulmonaryresistancefalls
•
•
More blood to left atrium
•
•
•
•
LA pressure > RA pressure Foramen ovale closes (fossa ovalis)
•
•
Ductus arteriosus closes closes •
In utero: ↓ O2, ↑ prostaglandins prostaglandins maintain patency
•
Birth: ↑ O2, ↓ prostaglandins (loss of placenta)
120
Placenta has low resistance to flow In utero: helps keep LA pressure low At birth: increase in peripheral resistance Rise in systemic blood pressure
•
Rise in left ventricular pressure
•
Contributes to rise in LA pressure
Remaining Opening Foramen Ovale
Shunts RA
LA
RV
LV
PA
Ao
Shunts Jason Ryan, MD, MPH
Shunts •
•
Shunts
Left side pressures >> Right side pressures
•
At birth:
•
LA ~10mmHg >> RA ~6mmHg
•
Left to right flow volume overload of right heart
•
LV ~120/10 >> RV ~24/6
•
Blood flow to lungs unimpaired
•
Ao ~ 120/80 > > PA ~24/12
•
•
Pulmonary vessels become stiff/thick
•
VSD (LVRV)
•
Right ventricle hypertrophies
•
ASD (LARA)
•
Right sided pressures rise rise
•
PDA (Aorta Left pulm artery)
•
Shunt reverses (now R L)
•
Cyanosis occurs (Eisenmenger syndrome)
“Blue kids” not “blue babies”
VSD
VSD
Ventricular Septal Defect
Ventricular Septal Defect
•
•
Most common congenital anomaly
•
Communication LV/RV LV/RV Harsh, holosystolic murmur •
no cyanosis
YEARS later (untreated)
Left to right connection Left to right flow
•
•
Tricuspid area (LLSB)
121
Characterized i n many ways •
Size
•
Location
•
Associated defects
VSD
ASD
Ventricular Septal Defect
Atrial Septal Defect
•
•
Small VSD
•
•
Tiny hole resists flow across defect (“restrictive”)
•
Lots of turbulence
•
Small shunt (small volume of flow across defect)
•
loud murmur
•
•
Large VSD •
Large hole (“non-restrictive”)
•
Significant shunting
•
Often closed surgically
•
•
•
Communication between left/right atrium Adds volume to RA/RV Delays closure of pulmonic valve Wide, fixed splitting of S2 Increased flow across PV/TV Systolic ejection murmur Rarely a mid-diastolic murmur
ASD
ASD
Atrial Septal Defect
Atrial Septal Defect
•
•
•
Oxygenated blood LA RA ↑ O2 saturation in RA, RV, PA PA “Shunt run” run” •
•
Series of blood samples
•
SVC = 65%
•
IVC = 65%
•
RA = 75%
•
RV = 75%
•
PA = 75%
Secundum type is most common •
Defects at site of foramen ov ale/ostium secundum
•
Poor growth of secundum septum
•
Or excessive absorption of primum septum
•
Located mid-septum
•
Often isolated defect Foramen Ovale
“Stepup” “Step up” R
Septum secundum Septum primum L
ASD
ASD
Atrial Septal Defect
Atrial Septal Defect •
Septum Secundum Too Short
Foramen Ovale
L
•
Defect at site of ostium pri mum
•
Failure of primum septum to fuse with endocardial cushions
•
Located near AV valves; valves; often occurs with other defects
•
Seen in endocardial endocardial cushion defects (Down syndrome) Primitive Atria
Primitive Atria
R
R
R
Septum Primum Excessive Reabsorption
Primum type
L
L
fusion
Septum secundum Septum primum
entricle
122
Septum primum Endocardial cushion
Ventricle
PDA
PDA
Patent Ductus Arteriosus
Patent Ductus Arteriosus
•
Ductus arteriosus shunts blood in utero •
•
•
Left pulmonary artery aorta
•
Rarely remains patent (3 to 8 per 10,000 births)
•
Associatedwith congenitalrubella syndrome
Closes close after birth
•
ToRCHeS infection
•
“Functional” closure 18 to 24 hours (smooth muscle)
•
Mother: Rash, fever, fever, lymphad enopathy
•
“Anatomic” occlusion over next few days/weeks
•
Baby: Deafness, cataracts, cardiac disease
•
Becomes ligamentumarteriosum
•
PDA common
•
Rare in developed countries (vaccination) (vaccination)
•
Consider in infants whose mothers are immigrants
Patency maintained by prostaglandin E2 •
Major source in utero is placenta placenta
PDA
Alprostadil
Patent Ductus Arteriosus •
Continuous, Continuous , machine-like murmur
•
•
Widened pulse pressure
•
•
•
Loss of volume in arterial tree through PDA
•
Low diastolic pressure Increased pulse pressure
•
•
Differential cyanosis •
Occurs when shunt reverses reverses R L
•
Blue toes, normal fingers
Indomethacin
Prostaglandin E1
Maintains patency of ductus arteriosus Key effect: delivers blood to lungs Useful when poor RV PA blood flow •
Tetralogy Tetralogy of Fallot
•
Pulmonary atresia
Qp:Qs
•
NSAID
•
•
Inhibits cyclooxygenase
•
•
Decreases prostaglandin formation
•
•
Can be used to close PDA
•
Qp = Pulmonary blood flow Qs = Systemic blood flow Qp:Qs should be 1:1 In shunts, Qp:Qs may be > 1:1 •
123
1.5:1, 2:1, 3:1, etc.
Eisenmenger’s Syndrome
Fetal Alcohol Syndrome
•
Uncorrected ASD/VSD/PDA
•
•
Right heart chronically overloaded
•
•
•
RV Hypertrophy
•
Pulmonary hypertension
•
•
Shunt reverses right left •
Cyanosis
•
Clubbing
•
Polycythemia (very high Hct)
Patent Foramen Ovale
•
•
Characteristic facial features Impaired neurologic function Congenitalheartdefects •
PFO •
Caused by prenatal exposure to alcohol (teratogen)
Found in ~25% adults Failure of foramen ovale to close after birth Can lead to strokein stroke in patients with DVT/PE
124
Atrial septal defect
•
Ventricular septal defect
•
Tetralogy of Fallot
Cyanosis
Cyanotic Congenital Heart Disease
•
Central cyanosis
•
Peripheral cyanosis
•
Cardiac output normal normal
•
Low blood flow
•
Blood is flowing flowing
•
Severe heart failure
•
Not enough O2
•
Cold extremities
•
Lips
•
Nail beds
•
Conjunctivae
•
Warm extremities
Jason Ryan, MD, MPH
Blue Babies •
Centralcyanosis early in life
•
Blood not going through lungs after birth
Tetralogy of Fallot •
Constellation of four abnormalities •
Ventricular septal defect defect (VSD)
Tetralogy Tetralogy of Fallot
•
Rightward deviation of aortic valve (“overriding aorta”)
•
Transposition of great vessels
•
Subpulmonary stenosis
•
Truncus arteriosus
•
Right ventricular hypertrophy
•
Tricuspid atresia
•
Total anomalous pulmonary venous return return
•
Infundibulum
Infundibulum
Conus Arteriosus
Conus Arteriosus
•
•
•
“Funnel” leading to pulmonic valve Developsfrombulbus from bulbuscordis Smooth, muscular structure at RV outflow to PA
•
Septum displac ed (moves toward RV) in TOF
•
Causes “overridingaorta” “overridingaorta”
•
Causes VSD
•
•
125
5-95% of aorta may lie over RV
Usually large (“non-restrictive”)
Infundibulum
Tetralogy of Fallot
Conus Arteriosus
Physiology
•
•
“Infundibular stenosis” •
Subpulmonary stenosis
•
RV outflow tract obstruction
High resistance resistance to flow RV pulmonary artery •
•
Abnormal pulmonary valve •
•
•
•
Rarely main cause of obstruction
•
Flow obstruction RVH
•
RV outflow pulmonic stenosis
Diverts blood across VSD to left ventricle Severity of flow obstruction determines symptoms Severe obstruction: severe cyanosis Mild obstruction: less shunting (“pink” tets)
Tetralogy of Fallot
Tetralogy of Fallot
Physiology
Murmur
•
Poor blood flow RV lungs
•
Left to right shunts beneficial •
Bring back to pulmonary artery
•
Diverts blood to lungs
•
Improves oxygenation
•
•
Systolic ejection murmur •
Crescendo-decrescendo
•
RV outflow and pulmonic stenosis
•
Heard best at left sternal border
Single S2
•
Patent ductus arteriosus
•
S2 = closure of aortic and and pulmonic valves
•
Aortopulmonary collateral arteries
•
TOF: Diseased pulmonic valve
•
Surgical shunt
•
no sound
VSD murmur (holosystolic) not typically heard •
Large VSD no murmur
Tetralogy of Fallot
Tetralogy of Fallot
Other Features
Other Features
•
Squatting improves symptoms
S1
•
“Tet spells” spells”
•
Increased afterload/TPR (resists flow out of LV)
•
Sudden cyanosis often when agitated agitated
•
Pressure rises in the aorta/left ventricle
•
Severe/complete Severe/complete RVOT obstruction obstruction
•
Less blood shunted RV LV via VSD
•
O2, knees to chest, chest, beta blockers (propranolol)
•
More blood to lungs
126
S2
Truncus Arteriosus Common arterial trunk Mixing of blood
•
•
Failure of neural crest cells to drive formation ofaorticopulmonary of aorticopulmonary septum
•
•
Transposition of Great Great Vessels Vessels Normal heart: •
Aorta is posterior and to right of pulmonary artery
Almost always always has VSD
Transposition of Great Vessels Vessels
Transposition of Great Great Vessels •
D-transpos ition (most commontype): •
•
Aorta forms anterior and rightward of pulmonary pulmonary artery
•
Aorta arises from right ventricle
•
Pulmonary artery from left ventricle
•
•
•
RV Aorta body RA RV LV Pulmonary artery LA LV Two completely separate circuits NOT compatible with life unless shunt present •
Usually PDA or VSD
No Lungs
L-TGA
Maternal Diabetes
L-Transposition -Transposition of the Great Arteries •
•
•
•
•
•
•
No Body
“Double switch”: Aorta/PA and LA/RA “Congenitally corrected TGA” Venous blood RA LV PA Lungs Lungs PV LA RV Aorta Two circuits not separated Wrong connections (RV-Aorta, LV-PA) Eventuallyrightventriclefails
127
•
Infants at increased risk congenital anomalies
•
Common congenital heart defects •
Transposition of great vessels
•
Truncus arteriosus
•
Tricuspid atresia
•
VSD
•
PDA
Tricuspid Atresia •
•
•
Tricuspid Atresia
Abnormal AV valves from endocardial cushions
•
All cases have RL shunt • Always seen with ASD
No tricuspid valve No blood RA RV
• Allows blood flow to LA •
LA
All cases have LR shunt • Allows blood flow to lungs
ASD RA
LV RV
•
LV RV via VSD
•
Ao PA via PDA
VSD
LA ASD RA
LV RV
TAPVR
TAPVR
Total Anomalous Pulmonary Venous Return
Total Anomalous Pulmonary Venous Return
•
Normal: pulmonary veins drain to left atrium
•
•
TAPVR: pulmonary veins drain to venous system
•
•
Innominate (brachiocephalic) (brachiocephalic) veins SVC
•
Coronary sinus
•
Portal vein
RV Lungs Pulm Veins RA RV RA and RV dilate Must have a right to left shunt
•
•
•
•
•
•
•
PDA
Mixed (low O2) blood to body
•
Ebstein’s Anomaly
ASD (most common)
Ebstein’s Anomaly
Apical displacement of TV small RV “Atrialization” of RV tissue Severe tricuspid regurgitation Can lead to right heart failure
•
Right to left shunting and cyanosis if ASD •
•
128
High RA pressure
Associated withWPW withWPW •
Electrical bypass tract often present
•
Delta wave on EKG
VSD
Maternal Lithium •
•
•
•
Pulmonary Atresia
Teratogen
•
Completely equilibrates across the placenta Teratogenic effects primarily involve heart
•
•
Ebstein’s anomaly most common
•
Failure of pulmonic valve orifice to develop No flow from RV to lungs In utero blood bypasses lungs (normal development) At birth: No blood flow to lungs through PV •
Often co-exists with VSD for outflow of RV
•
Survival depends on ductus arteriosus
•
•
Alprostadil •
•
•
•
•
Maintains patency of ductus arteriosus Key effect: delivers blood to lungs Useful when poor RV PA blood flow Tetralogy of Fallot
•
Pulmonary atresia
Similar to a severe form of Tetralogy of Fallot
Alprostadilgiven Alprostadil given to keep DA open
Conotruncal Heart Defects
Prostaglandin E1
•
PVR should fall but does does not
•
129
Outflow tract anomalies •
Trunk = Truncus arteriosus
•
Conus = Conus arteriosus
•
TetralogyofFallot
•
Truncus arteriosus
•
Transposition of the great arteries
•
22q deletion syndromes •
DiGeorge syndrome (Thymic Aplasia) Aplasia)
•
Immunodeficiency, Immunodeficiency, hypocalcemia
•
Conotruncal anomalies
Coarctation of the Aorta BC Artery
Left Carotid
Subclavian
Coarctation of the Aorta Jason Ryan, MD, MPH
Coarctation of the Aorta •
•
•
•
Coarctation of the Aorta
Congenital disorder Usually involves thoracic aorta distal to subclavian Near insertion of ductus arteriosus “Juxtaductal” aorta
•
Subtypes based on location of ductus arteriosus
•
High resistance resistance to flow in aorta
Ductus Arteriosus Ductus Arteriosus
Pre-ductal Coarctation
Ductus Arteriosus
Post-ductal Coarctation
Coarctation of the Aorta Preductal or Infantile
•
Shunts blood in utero
•
Ductusarteriosussupplies lowerextremities
•
Left pulmonary artery aorta
•
Poor development of collateralvessels
•
•
•
Patency maintained by ↓O2 and ↑ prostaglandins At birth: ↑O2 and ↓ prostaglandins
“Functional” closure 18 to 24 hours after birth •
Smooth muscle constriction constriction
•
“Anatomic” occlusion over next few days/weeks
•
Becomes ligamentum arteriosum
130
Coarctation of the Aorta
Coarctation of the Aorta
Preductal or Infantile
Preductal or Infantile
•
At birth ductus arteriosus open (not closed yet)
•
•
Deoxygenated blood to lower extremity
•
•
Lowerextremitycyanosis may occur
•
•
•
•
•
Ductus closure symptoms may develop All flow through aorta with severe narrowing Abrupt increase afterload Rise in LVEDP Acute heart failure LV can dilate fail shock All caused by closure of DA
Coarctation of the Aorta
Coarctation of the Aorta
Preductal or Infantile
Postductal or Adult type
•
•
•
Key associations: Turner syndrome (45, XO) Short stature, webbed neck 5-10% have coarctation of the aorta
Coarctation of the Aorta •
↑ Renin release
•
Salt/water retention
•
Vasoconstriction (AII)
•
Weak pulses (“brachio -femoral delay”)
•
Upper extremities and head high blood pressure
•
Secondary hypertension
Ductus arteriosus does not supply lower extremities
•
Collaterals develop
•
May go undetected until adulthood
Coarctation of the Aorta
Lower extremities low blood pressure •
•
131
•
Key association: bicuspid aortic valve
•
Found in up to 60% of coarctation cases
Coarctation of the Aorta
Coarctation of the Aorta
Signs/Symptoms
•
Key association:intracranial association: intracranial aneurysms
•
•
Occur in about 10% of patients with coarctation
•
•
•
Only sign may be hypertension in arms Murmur over back between scapula Weak femoral pulses Pain with walking (claudication)
Coarctation of the Aorta
Coarctation of the Aorta
Signs/Symptoms
Signs/Symptoms
•
Rib notching
•
•
High pressure above coarctation coarctation
•
Intercostals enlarge to carry blood around obstruction
•
Bulge into ribs
•
x-ray “Rib notching” seen on chest x-ray
3-sign •
Bulge before and after coarctation
•
“3 sign” on chest x-ray
Coarctation of the Aorta
Coarctation of the Aorta
Physiology
Complications
•
Autoregulation Autoregulationmaintains maintains regional blood flow •
•
•
•
•
Normal upper/lower perfusion despite high/low pressures
•
Upper extremities
•
High blood pressure
•
Arterioles constrict to limit flow to normal level level
•
Local effect – not mediated by sympathetic/parasympathe sympathetic/parasympathetic tic
•
Resistance to flow is high (Q = Δ P / R )
high flow
Lower extremities •
Low blood pressure
•
Arterioles dilate to increase flow to normal level (Q = Δ P / R )
Heartfailure
Result is normal (“compensated”) flow
132
Pressure overload of left ventricle ventricle
•
Aortic rupture/dissection
•
Endocarditis/endarteritis •
High-low pressure across narrowing
•
Endothelial injury
•
Low pressure distal to narrowing
•
Bacteria may attach more easily
Hypertension •
Bloodpressure>140/90
•
Need more than one measurement
Hypertension Jason Ryan, MD, MPH
Hypertension
Etiology •
Most (90%) is primary (“essential”) HTN •
•
Risk Factors •
Cause not clear clear
•
Remainder (10%) secondary
•
•
•
Obesity
•
Physical inactivity inactivity
Associations
↑ Na
•
Stroke
•
Heart disease
↑ Posm ↑ ADH ↑ ECV
African-American race
High salt intake Alcohol
Hypertension
Sodium Intake
↑ H2O
Family history
↑ BP
[Na] = 140meq/L
133
•
MI
•
Heart failure
•
Renal failure
•
Aortic aneurysm
•
Aortic dissection
Hypertension Effects
Hypertension Effects
•
Atherosclerosis– lipid/fibrous plaques in vessels
•
Arteriosclerosis– thickening of artery wall •
•
Response to chronic hypertension
Hyperplastic arteriosclerosis •
Arteries look like “onion skin”
•
Occurs when hypertension is severe (usually DBP>120)
•
“Malignant” hypertension
•
Thickening of small arteries arteries
•
Seen with aging
•
Also common with diabetes
•
Loss of arterioles
•
Arterioles close off and get resorbed
Retinal hemorrhages, exudates, or papilledema
Hypertension Effects •
•
Arteriolar Rarefaction
Hypertension Effects •
Hyaline arteriosclerosis
Pulse pressure may increase •
Example: Normal 120/80; HTN 170/100 170/100
•
Stiff arteries ↓compliance
Distensible Vessel 120/80
Hypertension Effects
C = ΔV / ΔP
ΔP = ΔV / C
Stiff Vessel 170/100
134
•
Afterload on heart is increased
•
Left ventricle: concentric hypertrophy •
Large voltage on EKG
•
Displaced apical impulse
•
S4
Hypertensive Urgency
Hypertensive Emergency
•
Severe hypertension without end-organ damage
•
•
No agreed upon BP value
•
•
Usually>180/120
•
•
Also no definite value BP usually >180/120 Patient longstanding HTN, stops meds Neurologic impairment •
•
•
Hypertensive Emergency •
•
•
Retinal hemorrhages, encephalopathy encephalopathy
Renal impairment •
Acute renal failure
•
Hematuria, proteinuria
Cardiac ischemia
Malignant Hypertension Hypertension • Historicalterm Mostcases hypertension: hypertension: “benign”
Associated with MAHA Endothelial injury thrombus formation Improved with BP control
•
•
•
Modestly elevated blood pressure
•
Stable over years
“Malignant hypertension” •
135
Rare form, often fatal
•
Severe elevation of blood pressure (diastolic >120mmHg)
•
Rapidly progressive over 1 to 2 years years
•
Renal failure, retinal hemorrhages, ischemia
Etiology •
Most (90%) is primary (“essential”) HTN
•
Remainder (10%) secondary
•
Secondary Hypertension
Cause not clear
Jason Ryan, MD, MPH
Blood Pressure
Chronic Kidney Disease
Determinants •
Cardiac output •
•
Increased with renal salt/water retention
•
Over 80% of patients have hypertension
•
Multiple causes:
Total peripheral resistance
•
Sodium retention
•
Key vessels: arterioles
•
Increased renin-angiotensin-aldosterone activity activity
•
Increased by vasoconstrictors (i .e. catecholamines)
•
Increased sympathetic nervous system activity
•
Increased by sympathetic nervous nervous system
BP = CO X TPR
NSAIDs
Obstructive Sleep Apnea
Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
•
Sleep-related breathing disorder
•
•
Apnea during sleep
•
•
Often associated with hypertension
•
•
Treatment may reduce BP
•
136
Nonsteroidalanti-inflammatory anti-inflammatory drugs Inhibit cyclooxygenas e inkidneys Decrease synthesis of prostaglandins PGE-2: Renal vasodilator
NSAIDs
Oral Contraceptive Pills
Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
OCPs
•
•
•
Na/Water excre tion ↓ Na/Water May cause hypertension May exacerbate heart failure
Pseudoephedrine
•
Estrogen and progesterone analogs
•
Cause mild increase in blood pressure
Cyclosporine Cyclospori ne & Tacrolimus
•
Nasal decongestant
•
•
Alpha-1 agonist
•
•
Vasoconstriction ↓ nasal blood flow
•
•
Epinephrine
Immunosuppressants Calcineurin inhibitors Renal vasoconstriction vasoconstriction salt/water retention Diltiazem: Diltiazem: drug of choice •
Impairs metabolism (↑ drug levels)
•
Treats HTN and allows lower lower dose cyclosporine to be used
Pseudoephedrine
Primary Aldosteronism
Primary Aldosteronism
•
Excessive levels of aldosterone secretion
•
•
Not due to increased activity of RAAS system
•
•
Adrenal adenoma (Conn’s syndrome)
•
•
Bilateral idiopathic adrenal hyperplasia
137
↑Na reabsorption distal nephron ↑ECV ↑CO Hypertension ↑K excretion hypokalemia
Aldosterone Escape •
•
•
•
Excess aldosterone does not lead to volume overload
•
•
Usually no pitting edema, rales, increased JVP Na/Fluid retention hypertension Compensatory mechanisms activated •
•
Primary Aldosteronism
•
Increased ANP
Increased sodium and free water excretion Result:diuresis normal volume status •
Clinical features •
Resistant hypertension
•
Hypokalemia
•
Normal volume status on physical exam
Diagnosis •
Renin-independent aldosterone section
•
Low plasma renin activity
•
High aldosterone levels
Drugs of choice:Spironolactone/Eplerenone choice: Spironolactone/Eplerenone •
Liddle’s Syndrome
Aldosterone antagonists
Collecting Duct
•
•
•
•
Genetic disorder
Hypertension
•
Hypokalemia
Na+
Na+
Increased activity of ENaC Similar clinical syndrome to hyperaldosteronism •
Interstitium/Blood
Principal Cell
Lumen (Urine)
Aldosterone
ATP K+
K+ H2O
Aldosterone Aldosterone levels low Intercalated Cell
Aldosterone H+
Cushing’s Syndrome
Pheochromocytoma •
Catecholamine-secreting tumor •
•
•
•
•
•
Epinephrine, norepinephrine, dopamine
Usually arises from adrenal gland Triad: Palpitations, headache, episodic sweating •
Often from steroid administration
•
Other causes •
Most patient have hypertension Diagnosis: Catecholamines breakdown products Metanephrines
•
Vanillylmandelic acid (VMA) (VMA)
Excesscortisol Excess cortisol
•
PHEochromocytoma
•
Cl-
•
Tumors (i.e. small cell lung cancer cancer secretes ACTH)
•
Adrenal tumor secretes cortisol cortisol
Cortisol hypertension •
138
Cushing’s Disease (pituitary oversecretes ACTH)
•
Increased vascular sensitivity to adrenergic adrenergic agonists
Aldosterone
Renal Artery Stenosis •
•
•
Renal Artery Stenosis
Vascular disease of renal arteries
•
Decreased blood flow to kidneys Key exam finding: renal bruit
•
•
•
Increased renin, salt-water retention HTN Often unilateral stenosis Normal kidney compensates Results:No Results: No signs of volume overload
Kidney
Renal Artery Stenosis
Renal Artery Stenosis
Angiotensin II •
↑RAAS ↑ BP Euvolemia •
↑Renin ↑ Na
•
•
•
•
•
•
AII efferent arteriole vasoconstriction vasoconstriction
•
Maintains GFR
ACE inhibitors can precipitate renal failure
Normal
Fibromuscular Dysplasia •
•
↓Renin ↓Na
Stenotic
•
Normal GFR depends on angiotensin II
Coarctation of the Aorta
Vascular disease obstruction to flow
BC Artery
Common among women Often occurs in 40s-50s Non-atherosclerotic, non-inflammatory Often involves medial layer fibroplasia Stenosis and aneurysms of vessels (“string of beads”) Most common in renal and carotid arteries Can lead to renal artery stenosis
139
Left Carotid
Subclavian
ADPKD Autosomal dominant polycystic kidney disease •
•
•
•
Genetic disorder Mutations of PKD1 or PKD2 Presents in adulthood with HTN and renal cysts Increased RAAS activity
140
BP = CO X TPR
Antihypertensives
Heart Rate Contractility
Jason Ryan, MD, MPH
Beta Blockers
Beta Receptors •
•
Circulating Volume
β1-selective antagonists
β1 receptors in heart, kidneys •
Increase heart rate and contractility contractility
•
Stimulate renin release release
•
Blockade ↓ CO, ↓ ECV ↓ BP
•
Atenolol, Metoprolol, Esmolol
•
Used for hypertension
•
Metoprolol: Systolic heart failure
•
β2 receptors •
Dilate blood vessels vessels (muscle, li ver)
•
Bronchodilate
•
Blockade does not lead to lower blood pressure
Blockade ↓ CO, ↓ ECV
•
Blocks sympathetic stimulation of heart
•
Reduces mortality
Beta Blockers
Beta Blockers
β1β2 (nonselective) antagonists
β1β2α1
•
•
•
•
Propranolol,Timolol,Nadolol Can be used for hypertension Nadolol, Propranolol: Used in portal hypertension
•
Beta 1 blockade: ↓ CO, ↓ ECV
•
Beta 2 blockade: ↓ portal blood flow
Timolol: Used in glaucoma •
Beta 1 and Beta 2
•
Carvedilol,Labetalol
•
Labetalol: Hypertensive Emergency
•
Carvedilol:Systolicheart failure
•
↓ BP
aqueous humor humor production
141
↓ B P
Rapid reduction in blood pressure
•
Blocks sympathetic stimulation of heart
•
Reduces mortality
Vascular Tone
Beta Blockers
Beta Blockers
Partial Agonists
Side effects
•
Pindolol: β1β2 (nonselective)
•
Acebutolol: β1-selective
•
“Intrinsic sympathomimetic activity”
•
Fatigue, erectile dysfunction, depression
•
Hyperlipidemia
•
More common with older beta blockers (propranolol)
•
Beta agonist when sympathetic activity is low
•
Mild increase i n triglycerides
•
Beta blocker when sympathetic sympathetic activity is high
•
Mild decrease in HDL
•
Can cause angina through beta 1 activation
•
Effect varies with different beta blockers
•
Special pharmacologic properties
Beta Blockers
Beta Blockers
Side effects
Side effects
•
Caution indiabetes in diabetes
•
Blockade of epinephrine effects •
•
•
•
Epinephrine raises glucose levels Blockade
hypoglycemia
Blockade of hypoglycemia symptoms
•
Caution in asthma/COPD •
β2 receptors: bronchodilators
•
β2 blockade may cause a flare
•
β1 blockers (“cardioselective”) (“cardioselective”) often used
Decompensated heart failure
•
↓ glucose sweating/tachycardia
•
β1 blockers lower cardiac ou tput worsening of symptoms
•
Symptoms “masked” by beta blockers
•
Commonly used in compensated compensated heart failure
•
Mortality benefit
Beta Blockers
Beta Blockers
Overdose
Overdose
•
Depression of myocardial contractility shock
•
Bradycardia/AV block
•
Treatment: Glucagon •
Activates adenyl cyclase at different site from beta receptors
•
↑ cAMP ↑ intracellular Ca
•
Increased contraction and heart rate
Glucagon
β1 AMP
142
AC cAMP
α1 Blockers
Alpha 2 Receptors
Tamsulosin, Alfuzosin, Doxazosin, Terazosin •
α1 receptors in periphery: vasoconstrict
•
Blockade vasodilation ↓ TPR ↓ BP
•
Used in benign prostatic hyperplasia
•
•
•
Relax smooth muscle of bladder/prostate
•
Increase urine flow
α2 receptors in CNS Presynaptic receptor Feedback to nerve when NE released Activation leads to ↓NE release
Common side effect: Postural hypotension Tamsulosin: “Uroselective” •
Neuron
α2
Less hypotension effect
Norepinephrine
NE
Vascular Smooth Muscle
Clonidine
Methyldopa
α2 agonist
α2 agonist
•
Old, rarely used hypertension hypertension drug
•
•
Key side effect: Rebound hypertension
•
•
•
Abrupt cessation of drug (usually at high dose)
•
Severe hypertension (SBP>200; DBP>120)
•
Symptoms of high BP and and sympathetic over-activity
•
Nervousness, sweating, headache, headache, chest pain
•
Drug of choice in pregnancy Also causes sedation sedation Key side effect (rare): Hemolytic anemia
Also causessedation causes sedation
RBC
Calcium Channel Blockers •
•
Calcium Channel Blockers
Three major classes of calcium antagonists •
dihydropyridines (nifedipine)
•
phenylalkylamines phenylalkylamines (verapamil)
•
benzothiazepines (diltiazem)
•
Vascular smooth muscle effects •
•
Heart rate/contractility effects •
Vasodilators and negative chronotropes/inotropes
143
Nifedipine>Diltiazem>Verapamil Verapamil>Diltiazem>Nifedipine
Calcium Channel Blockers
Calcium Channel Blockers •
Dihydropyridines (nifedipine) vasodilators •
•
Dihydropyridines (nifedipine)
Main effect: ↓TPR
•
Used for hypertension
•
Flushing, headache, hypotension
•
Key side effect: edema
Non-dihydropyridines (Verapamil, diltiazem) •
Similar to β1 blockers
•
Main effects: ↓HR; ↓ contractility
•
Peripheral vasodilation
•
Increased capillary hydrostatic pressure
•
Pre-capillary arteriolar vasodilation vasodilation
Calcium Channel Blockers
Calcium Channel Blockers
Dihydropyridines (nifedipine)
Verapamil, diltiazem
Pre- Capillary Arteriole
100
Capillary
50
Systemic
•
Used for hypertension
•
Also used in heart disease
50 •
•
Arrhythmias (atrial fibrillation)
•
Stable angina (lower oxygen demand) demand)
Potential side effect: Negative inotropes •
Pre-Capillary Arteriole
80
Can precipitate heart failure
Capillary
60
60
Systemic
Calcium Channel Blockers
Calcium Channel Blockers
Other Side Effects
Other Side Effects
•
Constipation •
•
Most commonly with verapamil
144
Hyperprolactinemia •
Seen with verapamil
•
Blocks calcium channels CNS
•
Causes hypogonadism
•
Men: ↓ libido, impotence
•
Pre-menopausal women: irregular menses,galactorrhea
↓ dopamine release
Calcium Channel Blockers
Angiotensin II
Other Side Effects •
Angiotensinogen
Gingival hyperplasia
Sympathetic System
+ Renin
•
Seen in all types CCB
•
Also with phenytoin, cyclosporine
AI
Renal Na/Cl reabsorption + ACE
A2 Arteriolar vasoconstriction
Adrenal aldosterone secretion
Net Result
Pituitary ADH secretion
↑Salt/Water Retention ↑Preload ↑Afterload ↑BP
AII Drugs
Angiotensin II Inhibition Angiotensinogen
ARBs
•
ACE Inhibitors
Renal Na/Cl reabsorption
•
Angiotensin Receptor Blockers (ARBs)
Arteriolar vasoconstriction
•
Side effects
Sympathetic System
+ Renin
Aliskiren
•
AI
+ ACE
A2
•
X
•
ACE Inhibitors
•
Adrenal aldosterone secretion
Captopril, Enalapril, Lisinopril, Ramipril Candesartan, Ir besartan, Valsartan Valsartan Hyperkalemia (↓aldosterone) Renal failure (↓GFR)
Pituitary ADH secretion
Net Result ↑Salt/Water Retention ↑Preload ↑Afterload ↑BP
ACE Inhibitors
Bradykinin Bradykinin
Unique Side Effects Cough asodilation
AI
•
Due to increased bradykinin
•
Dry Cough
•
Angioedema
•
X
Inactive Metabolites
ACE Inhibitors
X
A2
145
Occurs in ~10% of patients
•
Swelling of face, tongue
•
Can be life-threatening
Aliskiren
Diuretics
•
Direct renin inhibitor
•
Reduces angiotensin I levels (unique effect)
•
Loopdiuretics
•
Thiazide diuretics
•
Potassium sparing diuretics
•
•
Angiotensinogen
•
Furosemide, bumetanide, bumetanide, torsemide, ethacrynic acid Hydrochlorothiazide;; chlorthalidone; metolazone Hydrochlorothiazide Spironolactone, Eplerenone, Triamterene, Amiloride
+ Renin AI
+ ACE
A2
Hydralazine •
•
•
•
•
Drug-induced Lupus
Direct arteriolar vasodilator
•
Rarely used for hypertension Combined with nitrates for heart failure Safe in pregnancy •
Causes drug-induced lupus
•
Hypertensive Emergency •
•
•
Intravenous, rapid acting
Lowering BP too fast can cause ischemia •
Autoregulation of vascular beds
•
Often rash, arthritis, low blood cell counts
•
Milder than SLE
•
Usually no associated associated renal failure/CNS disease
Key finding: anti-histone antibodies Three drugs •
Hydralazine
•
Procainamide
•
Isoniazid
Hypertensive Emergency
Unique drugs used for therapy •
Syndrome similar to lupus
vasoconstriction
•
Nitroprusside •
Short acting drug
•
↑ intracellular cGMP
•
↑ nitric oxide release
•
Venous and arteriolar vasodilation
•
↓ preload (VR); ↓ afterload
Cyanide toxicity with prolonged use •
146
Multiple cyanide groups per molecule
•
Inhibits electron transport
•
Toxic Toxic levels with prolonged infusions
Sodium Nitroprusside
Hypertensive Emergency •
Hypertensive Emergency
Fenoldopam •
D1 agonist
•
Arteriolar vasodilation
•
Increased urinary sodium/water excretion excretion
•
Maintains renal perfusion while vasodilating
•
Labetalol
•
Esmolol
•
Nicardipine, Clevidipine
•
•
•
β1 and α1 Blocker Rapid acting intravenous intravenous β1 blocker Intravenous dihydropyridine calcium channel blocker
Orthostatic Hypotension Hypotension
Orthostatic Hypotension Hypotension
Postural Hypotension; Orthostasis
Postural Hypotension; Orthostasis
•
↓blood pressure due to gravity with standing
•
Alpha-1blockers
•
Compensation from sympathetic nervous system
•
ACE-inhibitors
•
Increased VR, CO, HR, TPR
•
Especially in patients on diuretics
•
Impaired with low volume, low TPR, blunted ANS
•
Volume depletion
•
“First dose hypotension”
•
Severe ↓BP (>20mmHg) = orthostatic hypotension
•
Common etiologies:
•
•
Hypovolemia
•
Hypertensive medications
•
Vasodilation ↓BP ↑SNS
•
Reflex response: ↑ HR
Choosing Drugs •
Can be caused by vasodilators •
↑RAAS
Dizziness, syncope
Reflex Tachycardia
•
Hydralazine •
Diabetes •
ACE inhibitors: Protective of kidneys
•
Beta blockers can lower lower glucose and mask hypoglycemia
•
HCTZ can increase glucose
Systolic Heart Failure
•
Alpha-1 blockers
•
Dihydropyridine calcium channel channel blockers
•
ACEi, beta blockers, aldosterone aldosterone blockers: mortality benefit
•
Nitroglycerine
•
Calcium channel blockers
•
May exacerbate chronic stable angina
•
Drugs may be co-administered with β blocker
147
↓ contractility
Choosing Drugs •
Hypertension in Pregnancy •
•
Methyldopa
•
Beta blockers, nifedipine, hydralazine
•
Avoid: ACE Avoid: ACE inhibitors, ARBs, direct renin renin inhibitors
•
Associated with congenital malformations
Significant renal failure or ↑K •
Avoid: ACE- inhibitors, ARBs (↓AII, ↓aldsoterone) ↓aldsoterone)
•
Avoid: Potassium sparing diuretics diuretics (↑ K)
•
Avoid: Other diuretics diuretics (↓ECV ↓GFR)
•
Calcium blockers, beta beta blockers usually ok
148
Heart Valves
Pulmonic
Valve Disease
Aortic
Tricuspid Mitral
Jason Ryan, MD, MPH
Valve Disease •
•
Valve Lesions - Systole Systole
Stenosis •
Stiffening/thickening of valve leaflets
•
Obstruction to forward blood flow
•
•
•
Regurgitation •
Malcoaptation of valve leaflets
•
Leakage of blood flow backwards backwards across valve
•
•
Occur when heart relaxes/fills
•
•
Aortic regurgitation
•
•
Tricuspid regurgitation
Treatments
•
•
Aortic stenosis Mitral regurgitation Pulmonic stenosis
Valve Disorders
Valve Lesions - Diastole
•
Occur when heart contracts/s queezes
Mitral stenosis Pulmonic regurgitation
•
Onlysevere Only severe valvularlesions treated Mostlysurgical Mostly surgicaldiseases Surgical repair •
Tricuspid stenosis
•
•
149
Often done for mitral valve prolapse mitral regurgitation
Valve replacement •
Bioprosthetic (pig or cow)
•
Mechanical (requires life-long anticoagulation)
Valvuloplasty (stenotic lesions)
Stenotic Valve Disorders •
•
•
•
Rheumatic Fever
Stiffvalve “Gradient” across valve Highpressureupstream Lower pressure downstream
•
•
•
•
Rheumatic Fever •
Joints: Polyarthritis (>5 joints)
•
♥:
•
Nodules (subcutaneous)
•
Erythema marginatum (rash on trunk)
•
Sydenham chorea (jerking movement movement disorder)
•
•
Carditis (valvulitis, myocarditis, myocarditis, pericarditis)
•
•
•
Caused by carcinoid tumors of intestines
•
•
Secrete serotonin
•
Fibrousdepositstricuspid/pulmonic deposits tricuspid/pulmonic valves Leads to stenosis and regurgitation
•
Serotonin inactivated by lungs
•
Left sided lesions rare
Damage to heart valves by rheumatic fever Mitral valvemost valvemostcommonlyinvolved Often presents years after acute rheumatic fever Many patients do not recall acute symptoms Common in developing countries •
Limited access to medical medical care for pharyngitis
•
Often seen in immigrants to US
Pathophysiology
•
•
Antibodies to bacterial M proteins cross-react
Aortic Stenosis
Carcinoid Heart Disease
•
Common inchildren in children Autoimmune: type II hypersensitivity reaction
Rheumatic Heart Disease
Jones criteria •
Occursweeksafter streptococcal pharyngitis
•
150
Stiff aortic valve Systolicproblem Increased afterload
Aortic Stenosis
Aortic Stenosis
Hemodynamics
Clinical features
•
LV pressure systolic >> aortic pressure •
•
•
LVSP = 160mmHg (normal = 120)
•
SBP = 120mmHg (normal = 120)
•
Gradient = 40mmHg 40mmHg
•
•
•
↑ LVEDP due to ↑ afterload
Normal
Supravalvular Aortic Stenosis
Causes Senile aortic stenosis •
•
•
•
“Wear and tear”
•
Collagen breakdown
•
Calcium deposition
Left heart failure: failure: ↑ LVEDP
Aortic Stenosis
Aortic Stenosis •
Systolic crescendo-decrescendo murmur
Syncope:failure Syncope: failure to ↑CO due to ↑ afterload Angina: Angina: ↑ LVEDP ↓ coronary blood flow
•
•
Narrowing of ascending aorta above aortic valve Seen in Williams syndrome Genetic deletion syndrome
Bicuspid aortic valve Rarely rheumatic heart disease
Mitral Stenosis
Mitral Stenosis
Pathophysiology
Clinical features
•
•
•
•
Stiff mitral valve Diastolic problem LA pressure >> LV diastolic pressure •
Left atrial pressure pressure 20mmHg (normal = 10) 10)
•
LVEDP 5mmHg (normal = 10)
•
Gradient = 15mmHg 15mmHg
•
Caused by rheumatic fever
•
Most common symptom: dyspnea
•
Murmur: diastolic rumble with opening snap
•
Decreased preload
151
↑ LA pressure
pulmonary congestion
Tricuspid Stenosis •
•
•
Very rare valve disorder Diastolic murmur at left lower sternal border Caused by rheumatic fever (with mitral disease) •
•
Pulmonic Stenosis •
Congenitaldefect in children
•
Carcinoid heart disease
•
Tricuspid regurgitation more common common
Carcinoid heart disease
Aortic Regurgitation Regurgitation
Regurgitant Regurgitant Lesions
Pathophysiology
•
Acute and chronic forms
•
•
Acute regurgitation (often from endocarditis)
•
•
Fused commissures with thickened leaflets
•
May cause shock
•
Activation of sympathetic sympathetic nervous system
•
Increased contractility
•
Increased afterload
•
•
•
•
Chronic regurgitation •
Blood leaks across aortic valve Diastolic problem Increased preload, stroke volume Increased afterload More stroke volume
aorta ↓ compliance (stiffening)
Blowing diastolic murmur
No shock
•
Leads to chronic heart failure
•
Sympathetic activation only if severe heart heart failure
Aortic Regurgitation Regurgitation
Aortic Regurgitation Regurgitation
Causes
Clinical features
•
•
•
•
Dilated aortic root leaflets pull apart
•
Leaking blood back int o LV causes low diastolic BP
•
Often from HTN or other aortic aneurysm
•
120/80 (normal)
•
Rarely from tertiary syphilis (aortitis)
•
Low diastolic pressure
Bicuspid aortic valve •
Turner syndrome
•
Coarctation of the aorta aorta
•
Almost always with mitral disease
152
120/40
•
Wide pulse pressure
•
Wide pulse pressure symptoms
•
Endocarditis Rheumatic heart disease
High cardiac output with low diastolic pressure
•
“Water hammer” pulses
•
Head bobbing
•
Many, many others (mostly historical)
Mitral Regurgitation Regurgitation
Mitral Regurgitation Regurgitation
Pathophysiology
Causes
•
•
•
•
•
Blood leaks across mitral valve Increased LA volume Starling mechanism
•
Primary MR caused bymitral by mitral valve prolapse •
Increased left ventricular filling from LA Increasedpreload,stroke volume
•
Reduced afterload
•
•
Also called degenerative degenerative or myxomatous
Billowing of mitral valve leaflets above annulus Common cause of mitral regurgitation Causes a systolic click •
Don’t confuse with opening snap of mitral stenosis
Mitral Regurgitation Regurgitation
Mitral Regurgitation Regurgitation
Secondary causes
Causes
•
Ischemia damage to papillary muscle
•
•
Left ventricular dilation
•
•
•
Dilated cardiomyopathy
•
Leaflets pulled apart
•
“Functional” MR
•
Endocarditis Rheumatic heart disease Congenital •
Hypertrophic cardiomyopathy
Cleft mitral valve
•
Endocardial cushion defect defect
•
Down syndrome
Mitral Regurgitation
Afterload Reduction
Clinical Features
Aortic and Mitral Regurgitation
•
Holosystolic murmur at apex
•
•
•
S1
S2
153
In theory, ↓ afterload can improve forward flow For severe, acute regurgitation this helps For chronic disease, clinical trials with mixed results
•
In general, these are surgical diseases
•
Common test scenario “Best medical medical option?”
Tricuspid Regurgitation •
•
•
Pulmonic Regurgitation Regurgitation
Small amount of TR normal (“physiologicTR”) (“physiologic TR”) Holosystolic murmur at left sternal border Pathologic causes •
Functional TR from RV enlargement
•
Endocarditis - classically IV drug drug users
•
Carcinoid
•
Ebstein’s anomaly
•
Most common cause: repaired Tetralogy of Fallot
•
Endocarditis (rare)
•
Rheumatic heart disease (rare)
•
Repair of RVOT RVOT obstruction damages valve
Tetralogy of Fallot
154
Shock •
•
•
Shock
•
Life-threatening fall in blood pressure Poor tissue perfusion Lowcardiac output •
Loss of contractility
•
Low intravascular volume
Peripheral validation
Jason Ryan, MD, MPH
BP = CO X TPR
Types of Shock •
Cardiogenic •
•
•
•
Types of Shock
Cardiac disorder
fall in cardiac output
•
Different treatments for different types of shock
•
Often can determine type from history
Hypovolemic •
Fall in intravascular volume fall in cardiac output
•
Hemorrhage
•
•
Myocardial infarction
•
Massive bleeding hypovolemic shock
cardiogenic shock
Shock of unclear etiology: Swan-Ganz catheter
Distributive •
Peripheral vasodilation
•
Septic, anaphylactic
Obstructive
Swan-Ganz Catheter
Swan-Ganz Data
Pulmonary artery catheter
•
RA Pressure (Normal ~ 5mmHg)
•
RV Pressure (20/5)
•
•
Pulmonary Capillary Wedge Pressure PCWP “Wedge Pressure” Equal to LA pressure
•
PA Pressure (20/10) PCWP Pressure (10) Mixed venous O2 sat •
155
Oxygen concentration after all veins mix
Fick Equation
Flow Equation
Oxygen Consumed = O2 Out Lungs – O2 In Lungs
•
Used to determine systemic vascular resistance
= CO (Art O2 – Ven O2)
ΔP = CO * SVR MAP – RAP = CO * SVR
Cardiac Output = O2 Consumption (Art O2 – Ven O2)
SVR = MAP – RAP CO
O2 Consumption α body size Arterial O2 Content = O2 sat on finger probe Venous O2 Content = O2 from Swan-Ganz
Swan-Ganz Catheter gives SVR
Swan-Ganz catheter gives cardiac output
Swan-Ganz Data •
Direct •
RA Pressure (Normal ~ 5mmHg)
•
RV Pr essure (20/5)
•
PA Pressure (20/10)
•
PCWP Pressure (10) (10)
•
•
Hemodynamic of Shock •
•
•
Calculated Cardiac output
•
Systemic Vascular Resistance
Cardiogenic Shock Hallmark is low cardiac output
•
•
High cardiac pressures
•
•
•
Cardiogenic
•
Hypovolemic
•
Distributive
•
Obstructive
Hypovolemic Shock
•
•
All have different hemodynamics fr om Swan Swan can be used to determine etiology of shock •
Mixed venous O2 sat
•
Four major classes of shock
High SVR (sympathetic response) Classic cause: large myocardial infarction
•
•
Also seen in advanced heart failure (depressed LVEF)
156
Poor fluid intake High fever, insensible losses Hemorrhage Lowcardiac output
•
Low cardiac pressures
•
High SVR (sympathetic response)
Type of Shock
Distributive Shock •
•
•
•
Hallmark is low SVR Diffuse vasodilation and/or endothelial dysfunction Sepsis (most common) Anaphylaxis
•
Neurogenic
•
Cardiac output classically high (variable)
•
Cardiac pressures variable
Physical Exam
Major Shock Types
•
SVR Low
High
•
Distributive
Cardiogenic
•
•
Low
•
Obstruction to blood flow from heart
•
Low cardiac output despite normal contractility
•
•
•
•
Cardiogenic
•
Hypovolemic
Warm skin low SVR and high CO Distributive
Jugular venous pressure high RA pressure Pulmonaryrales high LA pressure
Hypovolemic
Obstructive Shock
•
•
•
Pressures High
Cold skin high SVR and low CO
Treatment of Shock •
Cardiogenic: inotropes •
•
Tamponade Tension pneumothorax
Hypovolemic: volume •
Massive pulmonary embolism Low cardiac output
Distributive: vasopressors
•
Obstructive: resolve obstruction •
157
Blood transfusions, IV fluids
•
•
High SVR
Milrinone, Dobutamine
Phenylephrine, epinephrine, norepinephrine Treat tamponade, embolism, tension pneumothorax
Swan in Valve Disease
Swan in Valve Disease
Mitral Stenosis
Aortic Stenosi Stenosiss
Swan in Valve Disease
Left Atrial Pressure
a
v c
x
Aortic Regurgitation Regurgitation
Giant V waves •
•
Seen in mitral regurgitation in PCPW tracing Similar to giant V waves in tricuspid regurgitation •
Seen in venous pressure tracing
a
v c
158
y
Pericardium
Pericardial Disease
•
Fibrous pericardium
•
Serous pericardium
•
•
Pericardial Diseases •
Three layers
•
•
Jason Ryan MD, MPH
•
•
•
Parietal layer
•
Visceral layer
Pericardial cavity between serous layers Innervatedbyphrenic by phrenic nerve Pericarditis referred pain to the shoulder
Pericarditis
Pericarditis
•
Tamponade Constrictive pericarditis
•
•
•
Most common pericardial disorder Inflammation of the pericardium Immune-mediated (details not known) May recur after treatment
Pericarditis
Pericarditis
Clinical Features
EKG Findings
•
Chest pain •
Sharp
•
Worse with deep breath breath (pleuritic)
•
Worse lying flat (supine)
•
Better sitting up/leaning forward
•
Fever
•
Leukocytosis
•
Elevated ESR
159
Pericarditis
Pericarditis
EKG Findings
EKG •
•
ST Elevation
•
•
•
Technically, Technically, 4 stages of EKG changes Stage 1: diffuse ST elevations, PR depressions Stage 2 (~1 week later): Normal Stage 3: T wave inversions Stage 4: Normal
PR Depression
Pericarditis Diffuse ST elevation PR depression
Pericarditis
Pericarditis
Physical Exam
Etiology
•
Pericardial friction rub
•
Usually idiopathic
•
Scratchy sound
•
Viral
•
Systole and diastole
• Classic cause is Coxsackievirus upper respiratory infection (URI) • Often follows viral upper •
Bacterial • Spread of pneumonia • Complication of surgery • Tuberculosis
•
Fungal
Pericarditis
Pericarditis
Etiology
Treatment
•
Uremic (renal failure)
•
•
Post-myocardial infarction
•
•
•
Fibrinous (days after MI)
•
Dressler’s syndrome (weeks after MI)
•
Autoimmune disease (RA, Lupus)
160
NSAIDs Steroids Colchicine •
Inhibits WBCs via complex mechanism
•
Useful in gout and familial Mediterranean Mediterranean fever
•
Added to NSAIDs to lower lower risk of recurrence
Myopericarditis
Tamponade
•
Myocarditis = inflammation of myocardium
•
•
Similar presentation to ischemia
•
•
Chest pain
•
EKG changes
•
Increased CK-MB, Troponin Troponin
•
•
Accumulation of pericardial fluid High pericardial pressure Filling restriction of cardiac chambers Amount of fluid variable •
Acute accumulation (bleeding): small amount of fluid
•
Chronic accumulation (cancer): large amount of fluid
Tamponade
Tamponade
Causes
Clinical features
•
•
•
•
•
Cancer metastases metastases to pericardium Uremia Pericarditis Trauma
Tamponade
•
•
•
Distant heart sounds sounds
•
Elevated JVP
•
Hypotension
Dyspnea •
High left atrial pressure
•
Pulmonary edema
Elevatedjugularvenous pressure
Pulsus Paradoxus
Beck’s Triad •
Distant heart sounds
•
•
Treatment: Drainage of effusion
Clinical features •
•
Seen in rapidly-developing traumatic effusions Severe impairment LV function low cardiac output Slower effusions: Pericardium stretches/dilates
161
•
Classic finding in tamponade
•
Systolic BP always falls slightly on inspiration
•
Exaggerated fall (>10mmHg) = pulsus paradoxus
•
Severe fall = pulse disappears
Pulsus Paradoxus
Pulsus Paradoxus
Inspiration
•
•
↑ VR
•
•
↑ RV Size Septum bulges
•
Also seen in asthma and COPD Inspiration: ↓ left sided flow Caused by pulmonary pressure fluctuation Exaggerated in lung disease •
Normal lungs: 0 to -5mmHg
•
Lung disease: Change Change up to 40mmHg
Large drop in left sided flow pulsus paradoxus
↓ LV Size ↓ CO
Pulsus Paradoxus
Tamponade
Measurement Technique
EKG
•
Raise cuff pressure until no sounds heard
•
Sinus tachycardia
•
NORMAL respirations
•
Low voltage – EKG sees less electricity due to effusion
•
•
Slowly lower cuff pressure First point (P1): intermittent sounds
•
Second point (P2): constant sounds
•
Pulsus = P1 – P2
lectrical Alternans
Tamponade
Equalization of Pressures
Prominent x descent, Blunted y descent a
a
Prominent x descent ↓ RA pressure during RV contraction a in systole
c
v
v Blunted y descent Poor RV filling in diastole
v
162
•
Occurs when cardiac chambers cannot relax
•
Pressure in RA, RV, LA, LV falls but then abruptly stops
•
Seen in tamponade and pericardial constriction
Constrictive Pericarditis Pericarditis
Constrictive Pericarditis •
•
•
Clinical Features
Fibrous, calcified scar in pericardium Loss of elasticity: stiff, thickened, sticky Can result from many pericardial disease processes
•
•
Prominent right heart failure •
•
Lower extremity edema
•
Radiation to chest
•
Liver congestion
•
Heart surgery
•
May lead to cirrhosis (“nutmeg liver”)
Kussmaul’s Sign
Pulsus paradoxus uncommon (~20%)
ac
•
Pericardial knock
Inspiration ↑ VR slight fall in mean JVP Kussmaul’s sign = ↑ JVP with inspiration •
S1
S2 Pericardial Knock
•
Ventricle cannot accept ↑VR
•
Constrictive pericarditis
•
Restrictive cardiomyopathy cardiomyopathy
•
RV myocardial infarction
Not seen in tamponade
Constrictive Pericarditis
Pulsus and Kussmaul’s
Rapid/prominent y descent
Pulsus paradoxus: classic sign of tamponade •
•
v
High RA, RVEDP, RVEDP, PCPW pressures Equalization of pressures •
•
Markedly elevated jugular venous pressure
Pericarditis
Constrictive Pericarditis •
Dyspnea
•
•
Other Features •
•
v
Pulsus in tamPonade
Kussmaul’s sign: classic sign of constriction •
Also seen in restrictive heart disease
•
Kussmaul’s in Konstriction/Restriction
a
c
v
Rapid y descent Rapid filling of RV Abrupt stop in filling
Myocardium adherent to pericardium In diastole: rapid relaxation and suction of RA volume
163
Dip and Plateau
Venous Pressure Findings
Square Root Sign Right Ventricular Pressure Rapid filling, abrupt stop
Normal
Constriction and Restriction •
•
•
•
Constrictive pericarditis/Restrictive heart disease Many common features Prominent right heart failure Kussmaul’s sign
•
Rapid y descent
•
Dip and plateau
164
Constrictive Pericarditis
Dip & Plateau
Aortic Dissection •
Three layers to aorta •
Aortic Dissection
Adventicia
Intima
•
Media
•
Adventicia
•
Dissection tear in intima
•
Blood “dissects” intima and media
Jason Ryan, MD, MPH
Com Carotid
Propagation •
•
•
Brachiocephalic
Types
Subclavian
Blood enters dissection plane Spreadsproximal,distal
•
Can disrupt flow to v essels Diaphragm
•
Type A •
Involves ascending aorta and/or arch
•
Treated surgically
Type B •
Descending aorta
•
Can be treated medically
•
Control hypertension/symptoms
•
Surgical mortality high
Illiacs
Symptoms •
Other symptoms
“Tearing” chest pain radiating to back
•
•
Propagation to aortic root •
Aortic regurgitation
•
Pericardial effusion/tamponade
•
Myocardial ischemia (obstruction RCA origin)
Propagation to aortic arch •
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Stroke (carotids)
•
Horner’s syndrome
•
Vocal cord paralysis
Media Intima
Recurrent Laryngeal Nerve •
•
•
Other findings
Branch of vagus nerve Supplies larynx and voice box Compression: •
Aortic dissection
•
Massive left atrial enlargement
Suggested by history, exam, chest x-ray
•
Definitive diagnosis
Widened mediastinum on chest x-ray
General Principles •
Medial layer of aorta •
Tensile strength and elasticity elasticity
CT scan
•
Key proteins: collagen and elastin
•
MRI
•
Weakness of medial layer dissection/aneurysms
•
Transesophageal echocardiogram (TEE) (TEE)
•
Common aneurysm feature: medialdamage/destruction
•
•
Blood pressure differential between arms
•
Risk Factors
Diagnosis •
•
•
D-dimer
Vasa vasorum Network of small vessels vessels primarily in adventitial layer
•
Sensitive but not specific
•
•
Normal value makes aortic dissection unlikely
•
Supplies blood to medial medial layer in thick vessels (i.e. aorta)
•
Thickening (HTN) weakening of medial layer
Risk Factors
Risk Factors
General Principles
General Principles
•
•
Requires tension on wall •
Common in proximal aorta aorta (near aortic valve)
•
High tension from blood moving moving out of heart
•
Worsened by hypertension hypertension
•
•
•
•
Requiresweakness Requires weakness of media layer •
Also caused by hypertension
•
Seen in collagen collagen disorders (genetic)
Cystic medial necrosis
•
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Development of cysts and necrosis in medial layer
Occurs to mild degree with aging More rapid with: •
Bicuspid aortic valve
•
Marfan syndrome
Common in ascendingthoracic aneurysms
Risk Factors
Aortic Aneurysms
Aortic Dissection
• Aortic damage •
HTN - #1 risk factor
•
Atherosclerosis
•
Thoracic aneurysm
•
•
•
•
• Abnormal collagen •
Marfan Syndrome
•
Ehlers-Danlos
•
Dilation/bulge of aorta More than 1.5x normal Involves all three 3 layers Thoracic (TAAs) Abdominal (AAAs)
• Others •
Bicuspid aortic valve
•
Turner Syndrome (bicuspid, coarctation)
•
Tertiary syphilis: Aortitis
Thoracic Aortic Aneurysms
Thoracic Aortic Aneurysms •
•
•
Symptoms
Important risk factor for dissection
•
Usually occur in proximal/ascending aorta Usually seen in association with another disorder •
•
•
Marfan, Turner, Turner, Bicuspid aortic valve,Syphilis valve,Syphilis
•
Family history of aneurysm important
•
May be associated with atherosclerosis •
More common in descending aorta
•
Occur in association with atherosclerosis atherosclerosis risk factors
•
HTN, smoking, high cholesterol
Abdominal Aortic Aneurysms
Abdominal Aortic Aneurysms
Risk Factors
•
More common than thoracic aneurysms
•
•
Classically taught as a disease of atherosclerosis
•
•
•
•
Infrarenalaorta most affected by atherosclerosis Also most common site of AAA
•
Current research suggests many factors •
Most are asymptomatic Can cause aortic regurgitation Surgery if size >5.0cm
•
Genetic, environmental, hemodynamic, immunologic
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Smoking:strongest Smoking: strongest association with AAA Males: 10x more common men vs. women Age •
Rare before 55
•
As high as 5% in men men >65
HTN, hyperlipidemia
Abdominal Aortic Aneurysms •
•
•
•
Aortic Rupture
Most are asymptomatic
•
Some detected on physical exam Pulsatile mass from xiphoid to umbilicus Natural history is enlargement rupture
•
Followed with ultrasound or CT scan
•
Surgery if >5.0cm
•
Usually from trauma Most common site is isthmus
Isthmus
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Cardiac Tumors •
Myxoma
•
Rhabdomyomas
•
Metastatic tumors
•
•
Cardiac Tumors
•
Most common 1° cardiac cardiac tumor Most common 1° cardiac cardiac tumor children Most common cardiac tumor overall
Jason Ryan, MD, MPH
Myxoma •
•
Myxoma
Common in the left atrium (80%) •
Usually attached to to atrial septum
•
Often at the border of fossa ovalis
•
•
•
Benign (do not metastasize)
•
Myxoma •
•
Mesenchymal cells (undifferentiated cells) Endothelial cells Thrombus/clot Mucopolysaccharides
Myxoma
Often cause systemic symptoms
•
May disrupt mitral valve function
•
“B symptoms”
•
Regurgitation
•
Fevers, chills, sweats
•
Heart failure
Can embolize stroke
•
•
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Can sit in mitral valve •
“Ball in valve”
•
Mitral stenosis symptoms
•
Syncope or sudden death
Auscultation: Auscultation: Diastolic“tumor plop”
Cardiac Rhabdomyomas •
•
•
•
Cardiac Rhabdomyomas
Tumors of muscle cells
•
Benign (do not metastasize) Usually children (most <1year) Sometimes detected prenatal
•
•
•
Associated with tuberous sclerosis (90%) Autosomal dominant genetic syndrome Mutation in TSC1 or TSC2 gene TSC1: Hamartin
•
Tumor embedded in ventricular wall
•
TSC2: Tuberin
•
Most regress spontaneously
•
Mutations widespread tumor formation
•
Rare symptoms from obstruction of blood flow
Tuberous Sclerosis •
•
•
•
Involves MULTIPLE organ systems Numerous hamartomas and other neoplasms Seizures – most common presenting feature “Ash leaf spots”: Pale, hypopigmented skin lesions
•
Facial skin spots (angiofibromas)
•
Mental retardation
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Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy Jason Ryan, MD, MPH
Hypertrophic Cardiomyopathy
HCM
Names •
•
•
Hypertrophic cardiomyopathy (HCM)
•
Hypertrophic obstructive cardiomyopathy (HOCM) Idiopathic hypertrophic subaortic stenosis (IHSS)
•
•
•
•
Point mutation altered amino acid in protein
•
15+ genes with 1500+ 1500+ mutations identified
Often involve genes for cardiac sarcomere proteins •
Beta-myosin heavy chain chain (40% cases)
•
Myosin binding protein (40% cases) cases)
Variable expression •
Significant variation in severity severity of symptoms
•
Many variations in location/severity of hypertrophy
Histology
Often single-point missense mutations •
About 50% cases familial (50% sporadic) Autosomal Autosomal dominant dominant
HCM
HCM •
Genetic disorder caused by gene mutations
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•
Myocyte disarray (excessive branching)
•
Hypertrophy
•
Interstitial fibrosis
HCM
HCM
Clinical Features
Clinical Features
•
Many patients asymptomatic
•
Heartfailure
•
•
•
Abnormal myocytes ventricular arrhythmias
• Most common cause SCD in young patients
•
Diastolic dysfunction
•
Impaired emptying due to LVOT LVOT obstruction
•
Chest pain (angina) •
Sudden cardiac death
Syncope • Arrhythmias may lead to syncope
Increased O2 demand demand
•
•
Thickened myocardium
HCM
HCM
Clinical Features
Clinical Features
•
Problem #1: Arrhythmia problem
•
LVOT obstruction
Problem #2: Outflow obstruction problem •
Thickened myocardium obstructs blood leaving LV
•
Same physics and symptoms as aortic stenosis
•
Thick myocardium vulnerable to arrhythmias
•
Most serious is ventricular tachycardia
•
Exercise (catecholamines) (catecholamines) increase risk SCD
•
Heart failure, chest pain, exercise-induced syncope
•
Sudden death in athletes
•
Treated with surgery
•
Defibrillators for high risk patients patients
•
Beta blockers (↓ contractility)
•
Avoidance of exercise
•
Ca blockers (verapamil)
suddendeath
HCM
HCM
Clinical Features
Clinical Features
•
Mitral regurgitation
#3: Mitral valve problem •
High velocity in LVOT LVOT tugs mitral valve chords and leaflets
•
Causes systolic anterior anterior motion (SAM) of mitral valve
•
Over time this leads to mitral regurgitation
•
Systolic ejection murmur
•
Caused by outflow tract obstruction
•
Sounds just like AS unless you do maneuvers
•
Lots of associated abnormal heart sounds •
S4
•
Holosystolic murmur of MR
•
Paradoxical split S2
S1
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S2
HCM
HCM
Maneuvers
Maneuvers
•
For any HCM maneuver, maneuver, think about size of LV
•
↑ LV size ↓ murmur
•
•
Valsalva •
↓ LV size ↑ murmur
Patient bears down as if having a bowel movement
•
Or blows out against closed closed glottis
•
Increase thoracic pressure compression of veins ↓ VR
•
Less VR Less preload Smaller LV cavity
•
Obstructing septum moves further into the the outflow tract
•
Murmur INCREASES in intensity
HCM
HCM
Maneuvers
Other maneuvers
•
Squatting
•
Forces blood volume stored in legs to return to heart
•
Increases venous return
•
Preload rises size of LV increases
•
More VR More preload
•
Murmur DECREASES in intensity
•
This moves the obstructing septum out of the way
•
Murmur DECREASES in intensity
less obstruction
•
•
•
Less effect of maneuvers on aortic stenosis •
•
•
•
Fixed obstruction
Opposite effects of maneuvers in aortic stenosis •
•
Less preload less flow quieter AS murmur
173
Bigger LV cavity
•
Opposite mechanism of leg raise
•
Murmur INCREASES in intensity
Maneuver Summary
Both HCM and AS cause a systolic ejection murmur
Standing
HCM
Aortic Stenosis •
Raising th elegs
•
Valsalva INCREASE Standing INCREASE Squatting DECREASE Leg Raise DECREASE
HCM
HCM
Associations
Associations
•
Maternal diabetes
•
Friedreich Ataxia
•
Infants: transient hypertrophic cardiomyopathy
•
Autosomal recessive CNS disease disease
•
Usually thickening of interventricular septum
•
Trinucleotide repeat disorder
•
May have small LV chamber
•
Spinocerebellar symptoms
•
Resolves by a few months of age
obstruction in newborn
•
Often have concentric left ventricular hypertrophy
•
Also septal hypertrophy
Cardiac Hypertrophy
Cardiac Hypertrophy
Other Causes
Rare Pathologic Causes
•
•
•
Hypertension
•
Valve disease Athlete’s heart
Cardiac Hypertrophy Rare Pathologic Causes •
Pompe Disease •
Glycogen storage disease disease (develops in infancy)
•
Acid alpha-glucosidase deficiency
•
Enlarged muscles, hypotonia
•
Cardiac enlargement
174
Fabry Disease •
Lysosomal storage disease disease
•
Deficiency of α-galactosidase A
•
Neuropathy, skin lesions, lack lack of sweat
•
Left ventricular hypertrophy
Endocarditis •
•
•
•
Inflammation of endocardium of heart Usuallyinvolves cardiac valves Often causes new regurgitation murmur Consequence of bacteremia
Endocarditis Jason Ryan, MD, MPH
Regurgitant Valve Disease
General Symptoms •
•
•
•
Fever
•
Chills Sweats Petechiae •
Small vessel inflammation
•
Leakage of blood
•
•
Embolic Symptoms
Aortic regurgitation Mitral regurgitation Tricuspid regurgitation
Endocarditis Stigmata
•
Brain (stroke)
•
Physicalexamfindings in endocarditis
•
Spinalcord (paralysis)
•
Caused by septic emboli and immune complexes
•
Very rare in modern era
•
•
•
•
•
Eye (blindness) Legs (ischemia) Splenic or renal infarction Pulmonary embolism (tricuspid) Coronary artery (acute myocardial infarction)
175
Endocarditis Stigmata •
•
Roth spots
•
Positive blood cultures
•
Red with pale center
•
Vegetation on echocardiogram echocardiogram
Oslernodes
•
Nontender red macules on palms palms and soles
Splinter hemorrhages
•
Fever
•
Risk factors
•
Roth spots, Osler nodes, Janeway Janeway lesions, splinters splinters
2 major, 1 major 3 minor, or 5 minor
Staph Aureus
•
Staphylococcus aureus
•
•
Viridans streptococcus
•
•
Streptococcus Bovis
•
•
Enterococcus
•
•
Staphylococcus epidermidis
•
Culture negative endocarditis
•
Libman-Sacks
Staph Aureus •
Causes acute endocarditis
•
Rapid, severe infection
Gram positive cocci Catalase positive Coagulase positive May infect tricuspid valve in IV drug users
Viridans Streptococcus •
Group of gram positive cocci •
Symptoms occur over days Can occur in patients with normal heart valves •
•
Reddish-brown l ines under fingernails
Microbiology
•
Minor Criteria
Painful bumps on pads of fingers and and toes
Janeway lesions
•
•
Major Duke Criteria
Retinal lesions
•
•
•
•
•
•
Diagnosis
No pre-disposing valvular heart condition
176
S. mitis, S. mutans, S. sanguinis
•
Catalase negative
•
Mouth flora
•
Endocarditis may occur afterdental after dental procedure
Viridans Streptococcus
Viridans Streptococcus
•
Low virulence bacteria
•
Causes subacuteendocarditis subacute endocarditis
•
Often affect damaged valves
•
Less severe symptoms symptoms
•
Symptoms occur over days to weeks
•
•
Bacteria synthesize dextran
•
Dextran adheres to fibrin
•
Fibrin found with endothelial endothelial damage
Classic predisposing condition: mitral valve prolapse
Streptococcus Bovis •
•
•
•
Enterococcus Endocarditis
Gram positive cocci
•
Lancefield group D Normal gut bacteria Associatedwith colon cancer •
All subtypes associated associated with cancer
•
Strongest association: S. gallolyticus (S. bovis type 1)
•
•
•
•
•
Prosthetic Valve Endocarditis Endocarditis
Gram positive cocci Lancefield group D Normal gut bacteria Usually a subacute endocarditis course Commonly Commonly occurs in older men Associated with manipulation manipulation of GI/GU tract •
Abdominal surgery
•
Urinary catheter
•
TURP for treatment of BPH
Staphylococcus Epidermidis
•
Occurs with mechanical or biologic valves
•
Catalase positive
•
Rarely cured with antibiotics
•
Coagulase negative (unlike S. Aureus)
•
•
•
Usually requires repeat valve surgery Similar bacteria to native valve endocarditis
•
•
Staphylococcus epidermidis •
•
Rarely cause endocarditis endocarditis except in prosthetic valves
•
Most common coagulase negative staphylococcus Normal skin flora Low virulence Commonly cause infection of prosthetic material •
177
Cardiac valves
•
Intravascular catheters
•
Prosthetic joints
Culture Negative Endocarditis •
•
•
•
Coxiella Burnetii
Evidence of endocarditis with sterile blood cultures
animals) • Zoonotic bacteria (transferred from animals) • Obligate intracellular bacteria
Caused by rare bacteria difficult to culture Coxiella burnetii
• Found in farm animals
Bartonella
• Cattle, sheep and goats •
Abortions in farm animals: Coxiella placenta infection
• Humans inhale aerosolized bacteriafrom bacteria from animals • Causes Q fever
Coxiella Burnetii
Bartonella
• Acute Q fever
•
Bartonella quintana
•
Flu-like illness
•
Small, gram-negative rod
•
May present as pneumonia pneumonia
•
Transmitted by lice
•
More than half half of cases: no symptoms
•
Patients with poor hygiene
• Chronic Q fever •
•
Most common manifestation is endocarditis
Bartonella henselae •
Found in cats
•
Causes cat scratch fever
NBTE
NBTE
Non-bacterial, thrombotic endocarditis
Non-bacterial, thrombotic endocarditis
•
•
•
•
•
•
Libman-Sacks Endocarditis or Marantic endocarditis
•
Lesions on valves that look like endocarditis Found on both sides of valve
•
•
Mitral valve most common Formed by thrombus, immune complexes Seen in hypercoagulable states •
•
•
•
•
Advanced Advanced malignancy
•
Systemic lupus erythematosus erythematosus
178
Often asymptomatic identified at autopsy Rarely cause regurgitation or murmurs Thrombus easily dislodges embolization Most patients asymptomatic until embolism occurs May embolize to sp leen, kidney, kidney, skin, extremities May cause stroke Can cause myocardial infarction
Bacterial Endocarditis
Bacterial Endocarditis
Treatment
Complications
•
•
•
•
Several weeks appropriate antibiotics Broad spectrum antibiotics initially Drug therapy changes when bacteria identified Valve surgery sometimes required •
Large vegetation
•
Severe valve disease heart failure
•
•
•
May form abscess beneath valve annulus
•
Persistent fever, bacteremia often indicates abscess
•
Aortic valve abscess can lead to heart block •
AV node dysfunction
Prophylaxis
Prophylaxis •
•
Primary prevention for bacterial endocarditis Done before high-risk medical procedures Antibiotics given to some high-risk patients New guidelines restrict to highest risk circumstances
Amoxicillin Clindamycin
179