CARDIOLOGY CARDIOMYOPATHIES •
Cardiomyopathy refers specifically to problems within the heart muscle, and these problems usually result in heart failure.
Dilated Cardiomyopathy o
Dilated cardiomyopathy implies that the muscle damage has resulted in enlargement of the heart Generally Idiopathic Impaired Systolic Function ________________________
Etiologies •
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Most times – Idiopathic (50%) Myocarditis (in Children) Alcohol Abuse
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Cocaine Abuse Tachycardias – AFib / SVT Autoimmune Disease - Lupus and Rheumatoid Arthritis Pheochromocytoma- Excess Catecholamine release from a tumor Coronary Artery Disease - Ischemic Cardiomyopathy Deficiencies of certain vitamins and minerals - Thiamine, Calcium, Magnesium End-stage kidney disease _________________________
1. Dilated 2. Hypertrophic 3. Restrictive Ischemic cardiomyopathy implies that the cause of muscle damage iscoronary artery disease
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Most common Cardiomyopathy Dilated Cardiomyopathy is a condition in which the heart becomes weakened and enlarged, and it cannot pump blood efficiently The decreased heart function can affect the lungs, liver, and other body systems _________________________
Etiologies •
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Thyroid Infections - HIV / Viral Chagas Disease, and Lyme disease Inherited Disorders - Muscular Dystrophy Chemotherapy Meds / Toxic Medications – **Doxorubicin ** HTN Pregnancy - Peripartum Cardiomyopathy Stress-induced Cardiomyopathy Trace elements, such as Lead, Arsenic, or Mercury Family History _________________________
Dilated Cardiomyopathy
Dilated Cardiomyopathy Physical Exam
Signs & Symptoms •
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Crackles S3 Gallop Elevated JVD Cardiomegaly
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CHF Systemic Embolus Pulmonary Embolus Deadly Arrhythmias Sudden Death
Treatment ECHO • • • • •
Global Chamber Enlargement Mitral Regurgitation Tricuspid Regurgitation ↓ Ejection Fraction Thrombosis
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Treat Underlying Disease ETOH Abstinence Thyroid Management Treat CHF Anticoagulants Arrhythmia Prophylaxis Heart Transplant
EKG Medications • • •
BBB Poor R-wave Progression Arrhythmias
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CXR • • •
Global Cardiomegaly – “Global Heart” CHF
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ACE inhibitors Angiotensin Receptor Blockers (ARBs) Losartan Candesartan Beta-blockers, such as Carvedilol Metoprolol Diuretics, including thiazide, loop diuretics, and potassium-sparing diuretics Digitalis glycosides _________________________
Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy •
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Hypertrophic cardiomyopathyinvolves enlargement and thickening of the heart muscle. A leading cause of sudden cardiac death in young athletes A significant cause of sudden unexpected cardiac death in any age group. Younger people are likely to have a more severe form of hypertrophic cardiomyopathy _________________________
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Unexplained Ventricular Hypertrophy
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NOT due to HTN or Aortic Stenosis
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_________________________ ECHO •
Etiologies • • • •
Genetic Myocyte Disarray Myocyte Hypertrophy Interstitial Fibrosis
Signs & Symptoms
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Often Asymptomatic DOE Angina Pre-Syncope / Syncope CHF Deadly Arrhythmias Sudden Death
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Pulse – “Rapid Upstroke” Bifid Carotid Pulse Sustained “Strong” PMI LV Lift
LVH High Voltage Q Waves in 1 & aVF
CXR - is Normal Treatment •
Avoid Volume Depletion
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Avoid Strenuous Exercise
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Physical Exam •
*Asymmetric* Septal Hypertrophy
EKG
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Disease of the Myocardium - Cardiac Muscle is Hypertrophied - without any obvious cause.
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Beta-blockers If refractive, Surgery is indicated Surgical Myectomy Septal Alcohol Ablation Dual Chamber Pacing Arrhythmia Prophylaxis Amiodarone Implanted Defibrillator
Murmur: • • • •
Harsh, Systolic Diamond Shaped LLSB / Erbs Point Increased w/ Valsalva & Standing
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Restrictive Cardiomyopathy •
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A group of disorders in which the heart chambers are unable to properly fill with blood because of “stiffness in the heart”.
Restrictive Cardiomyopathy •
Systolic Function is preserved
The heart is of normal size or only slightly enlarged. However, it cannot relax normally during the time between heartbeats when the blood returns from the body to the heart (diastole) _________________________
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Physical Exam
Etiologies • •
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Infiltrative Amyloidosis Sarcoidosis Non-Infiltrative Scleroderma Idiopathic Myocardial Fibrosis Storage Disease Hemochromatosis Fabry’s Glycogen Storage Endomyocardial Diseases of the heart lining (endocardium) Endomyocardial Fibrosis Loeffler's Syndrome Radiation Carcinoid
Signs & Symptoms • • • • • • •
CHF (w/ preserved Systolic Function) Arrhythmias Elevated JVD + Kussmaul’s Sign S3, S4 Gallop Mitral Regurgitation Tricuspid Regurgitation _________________________
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Signs of Right Heart Failure S/S of underlying condition
ECHO • •
LVH, RVH, LAE, RAE Valve Thickening
EKG •
Low Voltage
CXR •
Normal to Mild Enlargement
Treatment •
Endo-myocardial Biopsy to determine etiology
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Exclude Constrictive Pericarditis
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Treat underlying disease
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Control HR / manage AFib Supportive Care Heart Transplant Poor Prognosis _________________________
Conduction Disorders
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NARROW QRS
NARROW QRS
Regular Rhythms
Irregular Rhythms
Sinus Tach – Atrial Flutter – SVT –
(100 – 140) (150) (160+)
Atrial Fibrillation •
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No P-waves
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Irregular Rhythm
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Atrial Fibrillation Multi-focal Atrial Tach
A. Fib –vs. –NSR
“Quivering” of the heart muscles of the atria Narrow QRS,
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Most common cardiac arrhythmia
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Asymptomatic and not generally lifethreatening May have palpitations, fainting, chest pain, or congestive heart failure Treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as Warfarin to protect them from stroke.
1. Narrow QRS 2. No P’s, 3. Irregular Rhythm
Wolff – Parkinson – White (SVT) •
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Wolff-Parkinson-White syndrome is a heart condition in which there is an extra electrical pathway (circuit) in the heart. Leads to episodes tachycardia “Pre-excitation” Syndrome
WPW is the most common tachycardia in infants and children Death from WPW occurs secondary to associated dysrhythmias or from mistreatment of these dysrhythmias with inappropriate medications. S/Sx 1. 2. 3. 4. 5.
Chest pain or chest tightness Dizziness Light-headedness Syncope / Near Syncope Shortness of breath
HR commonly presents @ 250 bpm Often with associated hypotension. Many patients are not aware of their underlying condition
Treatment Medication used to control or prevent tachycardia. 1. Adenosine 2. Antiarrhythmics 3. Amiodarone. Cardioversion Radiofrequency Catheter ablation RCA is curative •
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Wolff – Parkinson – White (SVT)
Atrial fibrillation in a patient with Wolff-ParkinsonWhite syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.
Atrial Flutter •
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Atrial Flutter
Electrical impulses take an abnormal path through the atria, typically circulating around the tricuspid valve in the right atrium. The abnormal path of the impulses makes the atria contract very rapidly, typically about 250-350 beats per minute. “Sawtooth Pattern”
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These rapid contractions are slowed when they reach the AV node often with every second ventricle.or third contraction reaching the
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Regular Rhythm, but Tachycardic AF comes from the atria – “Supraventricular tachycardia” - (above the ventricles) May cause decreased vital organ perfusion May be transient - known as Paroxysmal Atrial Flutter. More often, AF lasts for days to weeks and is known as Persistent Atrial Flutter. With proper treatment, Atrial F is rarely lifethreatening.
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Complications of Atrial Flutter – Stroke, but can be prevented with Anti-Thrombolytic Warfarin
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Calcium channel blockers
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Beta-blockers
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Adenosine
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Radio-Ablation to restore Rhythm
1st Degree AV Block • • •
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P for every QRS PR > 0.20 sec Seen in Lyme Disease
No Intervention Required Do Not Add Digoxin
2nd Degree AV Block (Mobitz II) • • •
Note a P with no QRS after Check PR Interval PR Interval is equal, then Mobitz II
Treatment: As with type I block, AV nodal agents should be avoided, and an anti-ischemic regimen should be instituted if ischemia is suspected. •
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1st Degree AV Block
Transcutaneous pacing pads should be applied to all patients, including asymptomatic patients, as patients with Mobitz II second-degree AV block have a propensity to progress to complete heart block.
2nd Degree AV Block (Mobitz II)
2nd Degree AV Block (Mobitz I) (Wenckebach) “Longer, Longer, Longest…
– Dropped QRS” •
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No specific therapy is required unless the patient is symptomatic
Patients with suspected myocardial ischemia should be treated with an appropriate anti-ischemic regimen. AV nodal blocking agents (including betablockade) should be avoided Symptomatic patients should be treated with atropine and transcutaneous pacing. However, atropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur in this situation.
3rd Degree AV Block (Complete) • • •
P followed by P Slow HR P waves everywhere
Treatment: •
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For any symptomatic patient, transcutaneous pacing. Valsalva should be avoided Atropine cautiously - likely to be ineffective in a wide complex QRS rhythm and can be dangerous if the patient is having a concurrent MI.
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Urgent placement of Pacemaker
2nd Degree AV Block (Mobitz I) (Wenckebach)
LBBB
LBBB
A cardiac conduction abnormality where activation of the Left Ventricle is delayed, which results in the left ventricle contracting later than the Rght Ventricle. Among the causes of LBBB are: Aortic stenosis Dilated cardiomyopathy Acute myocardial infarction Extensive cases of coronary artery • • • •
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disease disease of the cardiac electrical Primary conduction system Long standing hypertension leading to aortic root dilation and subsequent aortic regurgitation
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Treatment Medical Care: Patients with LBBB require complete cardiac evaluation, and those with LBBB and syncope or near-syncope may require a pacemaker. Surgical Care: Some patients with LBBB, a markedly prolonged QRS, and congestive heart failure may benefit from a pacemaker, which provides rapid left •
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ventricular contractions.
RBBB During a right bundle branch block, the right ventricle is not directly activated by impulses travelling through the right bundle branch. The left ventricle however, is still normally activated by the left bundle branch. These impulses are then able to travel through the myocardium of the left ventricle to the right ventricle and depolarise the right ventricle this way. As conduction through myocardium is slower than conduction through theBundle of His-Purkinje fibres the QRS complex is seen to be widened.
The QRS complex often shows an extra deflection which reflects the rapid depolarisation of the left ventricle followed by the slower depolarisation of the right ventricle. Otherwise healthy people may have a right bundle branch block and it does not appear to cause any harm
Paroxysmal Supraventricular Tachycardia Supraventricular tachycardia (SVT), a common clinical condition, is any tachyarrhythmia that requires Atrial and/or Atrioventricular (AV) nodal tissue for its initiation and maintenance. Paroxysmal Supraventricular Tachycardia (PSVT) is episodic, with an abrupt onset and termination. It is usually a narrow-complex tachycardia that has a regular, rapid rhythm Exceptions include Atrial Fibrillation (AF) and Multifocal Atrial Tachycardia (MAT). Aberrant conduction during SVT results in a wide-complex tachycardia. SVT occurs in persons of all age groups, and treatment can be challenging.
Manifestations of SVT are quite variable; patients may be asymptomatic or they may present with minor palpitations or more severe symptoms.
Paroxysmal Supraventricular Tachycardia
Premature Beats •
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Most common type of arrhythmia. They're harmless most of the time and often don't cause any symptoms. When symptoms do occur, they usually feel like fluttering in the chest or a feeling of a skipped beat Most of the time, premature beats need no treatment, especially in healthy people.
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Premature beats that occur in the atria are called premature atrial contractions, or PACs. Premature beats that occur in the ventricles are called premature ventricular contractions, or PVCs. In most cases, premature beats occur naturally, not due to any heart disease. But certain heart diseases can cause premature beats. They also can happen because of stress, too much exercise, or too much caffeine or nicotine.
PVC’s_________ ________
Ventricular Tachycardia
Ventricular Tachycardia • •
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Wide-complex tachycardia; V tach; Ventricular tachycardia (VT) is a rapid heartbeat that starts in the ventricles Defined as HR of 100 + bpm + 3 irregular heartbeats in a row May develop as an early or late complication of an M.I. Major cause of sudden cardiac death.
May occur in pts w/ • • • • • •
Cardiomyopathy Heart failure Heart surgery Myocarditis Valvular heart disease pts w/ no cardiac disease
Can also be caused by: • •
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Anti-arrhythmic medications Changes in blood chemistry Hypokalemia Changes in pH (acid-base) Hypoxia
Symptoms • • • • •
Chest discomfort (angina) Syncope dizziness Palpitations Shortness of breath
Note: Symptoms may start and stop suddenly. In some cases, there are no symptoms. Signs: • • • •
Absent pulse Loss of consciousness Normal or low blood pressure Rapid pulse
_________________ Treatment Treatment depends on the symptoms, and the type of heart disorder - may not need treatment. Emergency V Tach: CPR Defibrillation / Cardioversion Anti-arrhythmic medications 1. Lidocaine 2. Procainamide - IV 3. Sotalol - IV 4. Amiodarone – IV • • •
Long-term treatment may require the use of oral anti-arrhythmic medications 1. Procainamide 2. Amiodarone 3. Sotalol •
Radiofrequency Catheter Ablation curative
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Preferred treatment for many chronic VT -
Implantable Cardioverter Defibrillator (ICD).
Torsades de Pointes Polymorphic ventricular tachycardia with a characteristic twist of the QRS •
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Ventricular Tachycardia that is often due to congenital heart disease or the use of certain medications. "twisting of the points".
TdP can be: •
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Inherited as congenital mutations of ion channels carrying the cardiac impulse/action potential Acquired as a result of drugs that block these cardiac ion currents.
Common causes •
Diarrhea
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Hypomagnesemia
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Hypokalemia.
________________________ Other Causes: • • •
Can also be the side effect of anti-arrhytmic medications such as Sotalol, Procainamide and Quinidine.
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Familial long QT syndrome Class IA antiarrhythmics Class III antiarrhythmics Hypocalcemia Hypoxia Acidosis Heart failure Left ventricular hypertrophy Slow heart rate Female gender Hypothermia Subarachnoid hemorrhage Malnourishment Chronic alcoholics. Drug interactions: Erythromycin or Moxifloxacin, taken concomitantly Nitroimidazol Various medications like methadone, lithium, tricyclic antidepressants or phenothiazines may also contribute
Ventricular Fibrillation Ventricular fibrillation (VF) begins as a quasiperiodic reentrant pattern of excitation in the ventricles with resulting poorly synchronized and inadequate myocardial contractions. The heart consequently immediately loses its ability to function as a pump. As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD). Sudden cardiac death can be viewed as a continuum of electromechanical states of the heart: ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and Asystole. VF is the most common initial state, and, because of insufficient perfusion of vital cardiac tissues, it degenerates to Asystole if left untreated.
Fibrillation is an uncontrolled twitching or quivering of muscle fibers (fibrils). When it it is occurs in the lower chambers of the heart, called ventricular fibrillation. During ventricular fibrillation, blood is not removed from the heart. Sudden cardiac death results. The most common cause of VF is a heart attack. However, VF can occur whenever the heart does not get enough oxygen or if a person has other heart disorders.
Ventricular Fibrillation (continued)
Ventricular Fibrillation (continued) Conditions that can lead to VF include: • •
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Symptoms
Congenital heart disease Electrocution accidents or injury to the heart Heart attack Heart muscle disease, including Cardiomyopathy
A person who has a VF episode will suddenly collapse or become unconscious, because the brain and muscles have stopped receiving blood from the heart.
Heart surgery Ischemia Sudden cardiac death typically occurring in athletes after a trauma over the surface of the heart
hour before the collapse:
The following symptoms may occur within 1
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Most people with VF have no history of heart disease. However, many have risk factors for cardiovascular disease, such as smoking, high blood pressure, and diabetes.
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Treatment External defibrillator. Medicines may be given to control the heartbeat and heart function. • •
Ventricular Flutter Tachycardia affecting the ventricles with a rate over 200 beats/min. It is characterized on the ECG by a sinusoidal waveform without clear definition of the QRS and T waves. It is considered transition stage between Ventricular Tachycardia and V. Fibrillation Critically unstable arrhythmia that can result in sudden cardiac death.
Chest pain Dizziness Nausea Rapid heartbeat Shortness of breath
Congenital Heart Diseases
Atrial Septal Defect “Hole in the Heart”
Congenital Heart Diseases
Congenital heart defect in which the wall that separates the upper heart chambers (atria) does not close completely ASD is not very common.
The 3 major types of Atrial Septal defect (ASD) •
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Ostium secundum: The most common type of ASD accounting for 75% Ostium primum: The second most common type of ASD commonly associated with Mitral valve abnormalities. Sinus venosus: The least common of the three
Treatment •
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ASD may not require treatment if there are few or no symptoms, or if the defect is small. Surgical closure of the defect is recommended if the defect is large, the heart is swollen, or symptoms occur.
Murmur •
Widely Split, Fixed S2
In fetal circulation, there is normally an opening between the two atria to allow blood to bypass the lungs. This opening usually closes around the time the baby is born. If the ASD is persistent, blood continues to flow from the left to the right atria. This is called a shunt. If too much blood moves to the right side of the heart, pressures in the lungs build up. The shunt can be reversed so that blood flows from right to left. Small Atrial Septal defects often cause very few problems and may be found much later in life In advanced and severe cases with large shunts the increased pressure on the right side of the heart would result in reversal of blood flow (now from right to left). This usually results in significant shortness of breath. When the person has no other congenital defect, symptoms may be absent, particularly in children. Symptoms may begin any time after birth through childhood. Individuals with ASD are at an increased risk for developing a number of complications including: • • • • •
Atrial fibrillation (in adults) Heart failure Pulmonary over-circulation Pulmonary hypertension Stroke
Coarctation of Aorta
Coarctation of Aorta 3 Types Aortic coarctation is a congenital narrowing of part of the aorta - whereby the Aorta narrows in the area where the Ductus Arteriosus inserts.Coarctation means narrowing. •
The pulse in the femoral (groin) area or feet will be weaker than the pulse in the arms or the carotid (neck). Sometimes, the femoral pulse may not be felt at all.
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Preductal Coarctation: o
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The blood pressure in your legs is usually weaker than in the arms. Blood pressure is usually higher in the arms after infancy.
Hallmark o
Notching of the ribs
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Hypertension in the upper extremities, and weak pulses in the lower extremities.
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This is the type seen in approximately 5% of infants with Turner Syndrome.
Ductal Coarctation: o
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The narrowing is proximal to the ductus arteriosus..
The narrowing occurs at the insertion of the ductus arteriosus Usually appears when the ductus arteriosus closes.
Postductal Coarctation: o
The narrowing is distal to the insertion of the ductus arteriosus.
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Notching of the ribs Hypertension in the upper extremities, and weak pulses in the lower extremities. This type is most common in adults
Patent Ductus Arteriosus
Patent Ductus Arteriosus
Physical Condition where the Ductus Arteriosus (the blood vessel joining the Pulmonary Artery to the Aorta) fails to close after birth, causing a left to Tachypnea right shunt with blood continuing to flow from Tachycardia the aorta to the Pulmonary Artery. Diaphoresis When the Ductus Arteriosus is small, no Cyanosis symptoms are present. Bounding peripheral pulses A Ductus Arteriosus with a moderate-to•
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large left-to-right shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, Atelectasis, or pneumonia. •
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Prematurity
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Low birth weight
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Prostaglandins
Murmur •
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Maternal rubella in thetofirst pregnancy is thought be atrimester cause ofofthe seasonal incidence of PDA.
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Clubbing
When the defect is large, CHF with Dyspnea and poor weight gain or failure to thrive are the main presentations.
Causes
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Wide Pulse Pressure
High altitude and low atmospheric oxygen tension have been associated with persistence of the PDA.
Systolic Thrill Continuous or Machinery Murmur is best heard at the upper left sternal border or left Infra-Clavicular area.
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Systolic Ejection Murmur
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Crescendo / Decrescendo
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Hypoxia
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Occasionally, auscultation of the PDA reveals numerous clicks or noises resembling shaking dice or a bag of rocks. An apical diastolic rumble with a large left to right shunt may be present.
Patent Ductus Arteriosus
Patent Ductus Arteriosus Treatment •
General measures Pulmonary support Oxygen to correct hypoxemia Sodium and fluid restriction Correction of anemia o o
Pediatric surgery Indications for surgical treatment include the following: Failure of Indomethacin treatment •
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Medical management consists of amelioration of CHF symptoms. No exercise restriction is required in the absence of pulmonary hypertension.
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Signs and symptoms of CHF
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PDA found in an older infant.
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Prophylaxis against infective Endocarditis is recommended.
Medication •
Medication use in PDA is based upon the clinical status of the patient. Prostaglandins are utilized to maintain the patency of the Ductus Arteriosus until surgical ligation is performed.
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When surgical ligation is not indicated, prostaglandin inhibitors (e.g., NSAIDs) are used to close the Ductus Arteriosus. •
Indomethacin is currently the drug of choice for closure of the Ductus in premature infants. Other studies have shown equal effectiveness with ibuprofen.
Contraindications to medical therapy (e.g., thrombocytopenia, renal insufficiency)
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Infants found to have an asymptomatic PDA after the neonatal period should undergo surgical ligation preferably before the age of 1 year to prevent future complications of a PDA. Ductal closure is indicated for cardiovascular compromise and for reduction of the risk of Infective Endocarditis Contraindications to surgery include pulmonary vascular obstructive disease. Timing of surgery is at 1-2 years or whenever the diagnosis is made in an older infant. In infants with CHF, failure to thrive, pulmonary hypertension, or recurrent pneumonia, the operation is more urgent (i.e., within 3-6 months).
Tetralogy of Fallot
Tetralogy of Fallot Congenital heart defect which is a complex combination of four birth defects of the heart: 1. 2. 3. 4.
Ventricular Septal Defect, Pulmonary Stenosis, Overriding Aorta Right Ventricular Hypertrophy.
Symptoms • •
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Most Common form of Congenital
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Cyanotic Heart Disease
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At birth, infants may not show signs of cyanosis.
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Clubbing of fingers Cyanosis, which becomes more pronounced when the baby is upset Difficult feeding Failure to gain weight Passing out Poor development Squatting during episodes of cyanosis Almost always a Heart Murmur.
Treatment Tet Spells - bluish skin from crying or feeding.
Factors that increase the risk for this condition during pregnancy include: •
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Alcoholism in the mother Diabetes
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Mother who is over 40 years old
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Poor nutrition during pregnancy
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Surgery is done when the infant is very young. Corrective surgery is done to widen part of the narrowed pulmonary tract and close the VSD
Complications •
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Rubella or other viral illnesses during pregnancy •
Delayed growth and development Arrhythmias Seizures during periods when there is not enough oxygen Death
There is a high incidence of chromosomal disorders in children with Tetralogy of Fallot, such as Down syndrome
Ventricular Septal Defect
Ventricular Septal Defect
Ventricular Septal Defect describes one or more Symptoms Shortness of breath holes in the wall that separates the right and left ventricles of the heart. Fast breathing •
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In utero, the right and left ventricles of the heart are not separate. As the fetus grows, a wall forms to separate these two ventricles. If the wall does not completely form, a hole remains.
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Paleness
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Failure to gain weight
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Fast heart rate
VSD is one of the most common congenital
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Sweating while feeding
heart defects.
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Frequent respiratory infections
May be asymptomatic, and the hole can eventually close
Treatment •
If the hole is large, too much blood will be pumped to the lungs, leading to heart failure. •
In adults, VSD is a rare but serious complication of heart attacks. These holes are related to heart attacks - not a result from a birth defect.
Murmur •
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Pathognomonic holo- or pansystolic murmur
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Widely Split S2 Best heard over the “tricuspid area”, or the lower left sternal border, with radiation to the right lower sternal border
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Except for the case of heart-attack-associated VSD, this condition is always present at birth. Drinking alcohol and using the Anti-seizure medicines Depakote and Dilantin during pregnancy been associated with increased incidence ofhave VSDs.
Babies with a large VSD who have symptoms related to heart failure may need medicine to control the symptoms and surgery to close the hole. Medications may include Digitalis (Digoxin) and diuretics. If symptoms continue despite medication, surgery to close the defect w/ a Gore-Tex patch is needed. Surgery for a VSD with no symptoms is controversial.
Complications •
Prevention
If the defect is small, no treatment is usually needed.
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Heart failure Infective Endocarditis Aortic insufficiency Damage to the electrical conduction system of the heart during surgery (causing arrhythmias) Delayed growth and development (failure to thrive in infancy) Pulmonary hypertension leading to failure of the right side of the heart
Congestive Heart Failure
Congestive Heart Failure “Heart failure” is a global term for the physiological state in which cardiac output is insufficient in meeting the needs of the body and lungs. This occurs most commonly when the cardiac output is low
Fluid overload is a common problem for people with heart failure but is not synonymous with it. Patients with treated heart failure will often be euvolaemic (a term for normal fluid status), or more rarely, dehydrated.
Congestive Heart Failure Heart failure (HF) is generally defined as inability of the heart to supply sufficient blood flow to meet the body's needs
Congestive Heart Failure Left-sided failure •
Occurs as a result of: Depressed cardiac contractility w/ fluid retention & impaired cardiac output or Diastolic dysfunction with fluid retention __________________________________
Backward failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature.
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There are many different ways to categorize heart failure, including: •
The side of the heart involved -Left Heart Failure versus Right Heart Failure
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Left heart failure compromises aortic flow to the body and brain. Right heart failure compromises pulmonic flow to the lungs. Mixed presentations are common, especially when the cardiac septum is involved. Systolic dysfunction vs. Diastolic dysfunction - Whether the abnormality is due to insufficient contraction and/or relaxation of the heart Whether the problem is primarily increased venous back pressure (behind) the heart Afterload, or failure to supply adequate arterial perfusion (in front of) the heart Preload
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Backward failure can be subdivided into failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea on exertion, and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, Paroxysmal nocturnal dyspnea o a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigueability and exercise intolerance "Cardiac asthma" or wheezing may occur. Chronic Non-Productive Cough Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest. Progresses from DOE to Orthopnea to Dypsnea at Rest
Congestive Heart Failure
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Low cardiac output with high systemic vascular resistance Right-sided failure (low-output heart failure) vs. Backward failure of the right ventricle High cardiac output with low vascular leads to congestion of systemic resistance capillaries. (high-output heart failure) •
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the degree of Functional Impairment conferred by the abnormality
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Functional classification generally relies on the N.Y. Heart Association Functional Classification •
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Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities. Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion. Class III: marked limitation of any activity; the patient is comfortable only at rest. Class IV: any physical activity brings on discomfort and symptoms occur at rest.
Acute exacerbations of Chronic CHF are caused by •
Patient non-compliance to meds
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Excessive salt and fluid intake
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Excessive Activities
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Pulmonary Embolus
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Intercurrent Infection
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causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down •
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Arrhythmias
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Progression of Underlying Disease
This generates excess fluid accumulation in the body. This causes peripheral edema or anasarca) and usually affects the dependent parts of the body first -
Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and hepatomegaly (enlargement of the liver) may develop. Significant liver congestion may result in impaired liver function, and jaundice and even coagulopathy (problems of decreased blood clotting) may occur. Chronic Passive Congestion of the Liver causes Anorexia and Nausea
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Tachycardia
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Hypotension
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Reduced Pulse Pressure Cold Extremities Diaphoresis Long-standing CHF causes Cachexia / Cyanosis
Congestive Heart Failure
Congestive Heart Failure Common causes of heart failureinclude myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy.
Physical Exam Findings •
LV Failure 1. Crackles at Lung Bases 2. Pleural Effusions
"High output cardiac failure"occurs when the body's requirements for oxygen and nutrients are increased and demand outstrips what the heart can provide
3. Basilar Dullness on Percussion
High Output CHF is caused by:
6. Enlarged & Sustained LV Impulse
4. Expiratory Wheezes and Rhonchi 5. Parasternal Lift
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Thyrotoxicosis
7. Diminished First Heart Sound
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Sepsis
8. S3 and S4 Gallop
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•
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Beriberi – Thiamine (B1) deficiency Severe Anemia
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RV Failure
AV Shunting / Malformations
1. Jugular Vein Distention
Paget’s disease
2. Abnormal Pulsations 3. Hepatic Enlargement 4. Heptojugular Reflux
Systolic Dysfunction is caused by: •
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6. Peripheral Pitting Edema ETOH Abuse Long-standing HTN
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Viral Myocarditis, including HIV
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Chaga’s Disease - tropical parasite
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5. Ascites
Myocardial Infarction
Idiopathic Dilated Cardiomyopathy
Differential Diagnosis •
Pneumonia •
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Diastolic Dysfunction is associated with: •
Abnormal filling of Left Ventricle
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“Stiff Ventricle”
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Chronic HTN
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LV Hypertrophy Diabetes
COPD
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Cirrhosis Peripheral Venous Insufficiency Nephrotic Syndrome
Labs •
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CBC BUN / Creatinine / LFT’s / Electrolytes TSH BNP (B-Natriurectic Peptide) – elevation is sensitive indicator symptomatic CHF, but may be nonsensitive in women and older patients
Congestive Heart Failure
Congestive Heart Failure Left-sided failure
Imaging Studies •
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1. Cardiomegaly 2. Venous Dilation 3. Perivascular / Interstitial Edema
Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema. Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged)
4. Alveolar Fluid 5. Pleural Effusion •
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• •
a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow, or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g., mitral regurgitation) of the heart failure.
Echocardiography Radionuclide Angiography – measures LV Ejection Fraction Stress Test Left Heart Catheterization – r/o Valvular Disease, delineate extent of CAD Right Heart Catheterization – to select / monitor pts that are refractory to Tx
Other Considerations •
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CXR
Common respiratory signs are tachypnea and increased work of breathing (nonspecific signs of respiratory distress).
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Salt Restriction Restrict Activity Level – only as tolerated Monitor pts of diuretics and ACE Inhibitors for Hypokalemia / Renal Failure
Complications
Right-sided failure •
Physical examination can reveal pitting peripheral edema, ascites, and hepatomegaly.
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Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by the hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength.
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MI Arrhythmias – symptomatic / asymptomatic, esp. V-Tach Syncope Sudden Death
Prevention •
Control HTN
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Control Lipids
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Early Detection and Treatment of Valvular Lesions
Congestive Heart Failure
Congestive Heart Failure
Diagnosis
Biventricular failure •
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Framingham criteria Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the By the Framingham criteria, diagnosis of congestive heart failure (heart failure with development of a pleural effusion. impaired pumping capability) requires the simultaneous presence of at least 2 of the Though it can occur in isolated left- or following major criteria or 1 major criterion in right-sided heart failure, it is more conjunction with 2 of the following minor criteria: common in biventricular failure because pleural veins drain both into the systemic Major criteria: and pulmonary venous system. When unilateral, effusions are often right sided.
• • • •
TREATMENT Treatment commonly consists of lifestyle measures, such as smoking cessation, light exercise including breathing protocols, decreased salt intake and other dietary changes, and medications, and sometimes devices or even surgery.
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• • •
Cardiomegaly on chest radiography S3 gallop (a third heart sound) Acute pulmonary edema Paroxysmal nocturnal dyspnea Crackles on lung auscultation Central venous pressure of more than 16 cm H2O at the right atrium Jugular vein distension Positive abdominojugular test Weight loss of more than 4.5 kg in 5 days in response to treatment (sometimes classified as a minor criterium
Minor criteria: Medications •
Diuretic + ACE Inhibitor (Lasix + Catopril)
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• • •
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Aldosterone Blockers - (Aldactone)
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Angiotensin Receptor Blockers
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B Blockers – start at low doses
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Digoxin
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Dobutamine – has limited use for
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hypoperfusion •
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Anticoagulation w/ A Fib or hx of MI Rigorous HTN Control Monitor Renal Function and K+ levels
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Tachycardia of more than 120 beats per minute Nocturnal cough Dyspnea on ordinary exertion Pleural effusion Decrease in vital capacity by one third from maximum recorded Hepatomegaly Bilateral ankle edema
Congestive Heart Failure Surgery •
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Left Ventricular Failure
Coronary Revascularization may improve symptoms and slow progression
1. Exertional Dypsnea
Bypass Surgery better that Catheterization for Revascularization
3. Fatigue
Heart Transplant for Advanced CHF
5. Paroxysmal Nocturnal Dypsnea
Implantable Defibrillators to guard against syncope / sudden death
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2. Cough
4. Orthopnea
6. Cardiac Enlargement 7. Rales 8. Gallop Rhythm
Prognosis •
Congestive Heart Failure
Poor – 5% mortality in Stable pts, 3050% mortality w/ advanced
9. Pulmonary Venous Congestion
Right Ventricular Failure
50% of Hospitalized Pts will be readmitted within one year
1. Elevated Venous Pressure 2. Hepatomegaly
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Transplant Pt - 1 year survival rate 90%, 5 year survival rate 70%
3. Dependent Edema 4. Usually due to LV Failure
Hypertension
Essential / Secondary / Malignant
Essential Hypertension Classification
Systolic
Normal
90–119
60–79
Prehypertension
120–139
81–89
Stage 1 HTN
140–159
90–99
Stage 2 HTN
≥160
Diastolic
≥100
Persistently high blood pressures requiring: 3 separate measurements, 1 week apart
Hypertension
Essential / Secondary / Malignant
Essential Hypertension “no identifiable cause” aka Primary or Idiopathic HTN Most common type of hypertension, affecting 95% of hypertensive patients Tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age Individuals with relatively high blood pressures at younger ages are at increased risk for the subsequent development of hypertension.
Secondary Hypertension Refers to high blood pressure caused by another medical condition or medication ___________ __________
Secondary Hypertension
Secondary hypertension may be due to:
Diabetic nephropathy -Diabetes can damage the kidneys' filtering system
Polycystic kidney disease– genetic condition forming renal cysts that prevent the kidneys from working normally, and can raise blood pressure.
Glomerular Disease - Renal Glomeruli filter waste and sodium become swollen and can't work normally, raising blood pressure.
Pheochromocytoma. This rare tumor, usually found in an adrenal gland, increases production of the hormones adrenaline and noradrenalin, which can lead to long-term high blood pressure or short-term spikes in blood pressure.
Hyperparathyroidism. The parathyroid glands regulate levels of calcium and phosphorus in your body. If the glands secrete too much parathyroid hormone, the amount of serum calcium rises, & triggers a rise in blood pressure.
Coarctation of the aorta -forces the heart to pump harder to get blood through the aorta and to the rest of the body, thus raises blood pressure — particularly the upper extremities
Sleep apnea – Hypoxia may damage the lining of the blood vessel walls making blood vessels less effective in regulating blood pressure. Also sleep apnea causes part of the nervous system to be overactive and release certain chemicals that increase blood pressure.
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Cocaine use
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Diabetes (if it causes kidney damage)
Obesity – with weight gain, the amount of circulating blood increases putting added pressure on arterial walls, increasing blood pressure. Excess weight often is associated with an increase in heart rate and a reduction in the capacity of blood vessels to transport blood.
Medications Appetite suppressants Birth control pills Certain cold medications Corticosteroids Migraine medications
Secondary hypertension may be due to: •
Alcohol abuse
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Renal artery stenosis - narrowing of Renal Arteries can cause severe hypertension & irreversible kidney damage.
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Pregnancy. Pregnancy can make existing high blood pressure worse, or may cause high blood pressure Pre-Eclampsia - Pregnancy-induced HTN Atherosclerosis Autoimmune Disorders Periarteritis Nodosa Chronic kidney disease
Endocrine Disorders Adrenal tumors Pheochromocytoma Thyroid disorders Cushing's syndrome. In this condition, corticosteroid medications, a pituitary tumor or other factors cause the adrenal glands to produce too much of the hormone cortisol. This raises blood pressure.
Aldosteronism. In this condition, a tumor in the adrenal gland, increased growth of normal cells in the adrenal gland or other factors cause the adrenal glands to release an excessive amount of the hormone Aldosterone – causing the kidneys to retain salt and water and lose too much potassium, which raises blood pressure.
Medications and supplements.Various prescription medications — from pain relievers to antidepressants and drugs used after organ transplants — can cause or aggravate high blood pressure in some people. Birth control pills, decongestants and certain herbal supplements, including ginseng and St. John's wort, may have the same effect. Many illegal drugs, such as cocaine and methamphetamine, also increase blood pressure.
Malignant Hypertension Malignant hypertension is a sudden and rapid development of extremely high blood pressure.
Malignant Hypertension Tests to determine damage to the kidneys: BUN Creatinine Arterial blood gas analysis Urinalysis • • •
The lower (diastolic) blood pressure reading, which is normally around 80 mmHg, is often above 130 mmHg. To diagnose Malignant Hypertension, Papilledema must be present.
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CXR: • •
Lung congestion Rnlarged heart.
This disease may also alter Causes
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The disorder affects about 1% of people with high blood pressure, including both children and adults.
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Aldosterone Cardiac enzymes EKG Renin
Urinary casts (sediment) It is more common in younger adults, especially African American men. It also Treatment occurs in women with toxemia of pregnancy, and persons with kidney Patients with malignant hypertension usually disorders or collagen vascular disorders. are admitted to an intensive care unit for continuous cardiac monitoring and frequent You are at high risk for malignant assessment of Neurologic status and urine hypertension if you have had kidney output. failure or renal hypertension caused by renal artery stenosis. Intravenous medications are the main focus of Malignant hypertension is a medical emergency.
therapy. - Nitroprusside and Nitroglycerin. A number of blood tests will also be checked, probably several times, to assess the status of the kidneys and other organs.
Malignant H ypertension Symptoms •
• •
Abnormal sensation (numbness) of the arms, legs, face, or other areas Blurred vision Change in mental status Restlessness Anxiety Decreased alertness, decreased ability to concentrate
Malignant Hypertension Outlook (Prognosis) After leaving the hospital, it is common for patients prescribed medicines like beta blockers or ACE inhibitors to keep the blood pressure under control in the future.
o o o
Many body systems are in serious risk due to the extreme rise in blood pressure. Multiple organs of the body, including the brain, eyes,
o
Fatigue Sleepiness, stuporous, lethargic Confusion Chest pain Mid-chest location most common Crushing or pressure sensation Cough Decreased urinary output Headache Nausea or vomiting Seizure Shortness of breath Weakness of the arms, legs, face, or other areas o o
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o o
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Exams and Tests
blood vessels, and kidneys may be are damaged. The heart, blood vessels of the kidney highly susceptible to damage caused by pressure, and kidney failure may develop, which may be permanent, requiring dialysis (kidney machine). If treated promptly, malignant hypertension is often controlled without permanent complications. If it is not treated promptly, complications may be severe and lifethreatening. Possible Complications •
Brain damage due to: o
A physical exam commonly shows: Extremely high blood pressure Possible swelling in the lower legs and feet Abnormal heart sounds and fluid in the lungs Changes in mental status, sensation, muscle ability, and reflexes
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An eye examination will reveal changes that indicate high blood pressure: Swelling of the optic nerve, Retinal bleeding, Narrowing of the blood vessels in the eye area,
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Coma Hypertensive encephalopathy Intracerebral hemorrhage (bleeding in the brain) Seizures Spasm or constriction of the arteries of the brain Stroke Swelling Heart damage, including: Heart attack Angina (chest pain due to narrowed blood vessels or weakened heart muscle) Heart rhythm disturbances Kidney failure o
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o
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other problems with the Retina. Kidney Failure may develop as a complication of malignant hypertension. Other complications may also develop.
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Permanent edema blindness Pulmonary
Hypotension Abnormally low blood pressure. This is best understood as a physiologic state, rather than a disease. Often associated with shock, though not necessarily indicative of it. Hypotension is generally considered as systolic blood pressure less than 90 mm Hg or diastolic less than 60 mm Hg
Hypotension •
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1. Orthostatic Hypotension, including Postprandial Orthostatic Hypotension 2. Neurally Mediated Hypotension (NMH) 3. Severe hypotension brought on by a sudden loss of blood (shock) _________________________________
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Orthostatic hypotension is brought on by a sudden change in body position, usually when shifting from lying down to standing - lasts only a few seconds or minutes.
If the blood pressure is sufficiently low, fainting and often seizures will occur.
Symptoms may include:
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Three main types:
The cardinal symptom of hypotension is lightheadedness or dizziness.
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Blurry vision Confusion Dizziness Fainting (syncope) Light-headedness Sleepiness Weakness
Treatment The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs will increase venous return, thus making more blood available to critical organs at the chest and head. The Trendelenburg position, though [6] used historically, is no longer recommended.
The treatment of hypotensive shock always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed in which hypotension is corrected. In parentheses are the still debated methods for achieving, and benchmarks for evaluating, progress in correcting hypotension. A study on NMH most often affects young adults and Early Goal Directed Therapy provided the children. It occurs when a person has delineation of these general principles. been standing for a long time. Children However, since it focuses on hypotension due usually outgrow this type of hypotension. to infection, it is not applicable to all forms of severe hypotension
After eating, it’s called Postprandial Orthostatic Hypotension - commonly affects elderly, those with high blood pressure, & persons w/Parkinson's disease.
Hypotension
Hypotension
Low blood pressure is commonly caused by drugs such as:
Treatment (Continued) 1. Volume resuscitation - Crystalloid
• • • • • • •
Alcohol Anti-anxiety medications Antidepressants Diuretics HTN and CAD Meds Medications used for surgery Painkillers
Other causes: Advanced diabetes Dehydration / Hypovolemia Anaphylaxis Arrhythmias Dehydration Fainting Heart attack Heart failure Shock (from severe infection, stroke, anaphylaxis, major trauma, or heart attack) _________________________________ • • • • •
2. Blood pressure support Norepinephrine or equivalent 3. Ensure adequate tissue perfusion maintain SvO2 >70 with use ofBlood or Dobutamine 4. Address the underlying problem (i.e. antibiotic for infection, stent or CABG for infarction, steroids for adrenal insufficiency •
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Blood sugar control (80-150 by one study) Early nutrition (by mouth or by tube to prevent ileus)
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Expectations (prognosis) Low blood pressure can usually be treated with success.
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Avoiding alcohol Avoiding standing for a long time (if you have NMH) Drinking plenty of fluids Getting up slowly after sitting or lying down Using compression stockings to increase blood pressure in the legs
Treatment depends on the cause of low blood pressure.
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Prevention If you have low blood pressure, your doctor may recommend certain steps to prevent or reduce your symptoms. This may include:
Steroid support Hypotension in a healthy person that does not cause any problems usually doesn't require treatment.
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Severe hypotension caused by shock is a medical emergency. Orthostatic hypotension caused by medicines, change the dose or switch to a different drug Increasing fluids to treat dehydration Wearing elastic hose to boost blood pressure in the lower part of the body. Those with NMH should avoid triggers, such as standing for a long periods In severe cases, Fludrocortisone.
Cardiogenic Shock •
Cardiogenic shock is based upon an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively.
Cardiogenic Shock Diagnosis Electrocardiogram An electrocardiogram helps establishing the exact diagnosis and guides treatment, it may reveal: 1. Cardiac arrhythmias 2. Signs of Cardiomyopathy •
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Insufficient perfusion of tissue leading to cell death from oxygen starvation 1. Hypoxia 2. Hypoglycemia - (Nutrient starvation) May lead to cardiac arrest Definition - sustained hypotension with tissue hypoperfusion despite adequate left ventricular filling pressure. Signs of tissue Hypoperfusion 1. Oliguria (<30 mL/h) 2. Cool Extremities 3. Altered Mental Status
Etiology •
Cardiogenic shock is caused by the failure of the heart to pump effectively.
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•
It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes: 1. Arrhythmia 2. Cardiomyopathy 3. Ventricular outflow obstruction (eg. Aortic Stenosis) 4. Aortic dissection 5. Hypertrophic Cardiomyopathy 6. Systolic Anterior Motion (SAM) 7. Ventriculoseptal defects.
Ultrasound Echocardiography may show poor ventricular function, signs of PED, ventricular septal rupture (VSR), an obstructed outflow tract or cardiomyopathy. •
Swan-ganz catheter The Swan-ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics. •
Biopsy In case of suspected cardiomyopathy a biopsy of heart muscle may be needed to make a definite diagnosis. but biopsy should only be done when third space is suspected •
Cardiogenic Shock Signs and Symptoms •
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Anxiety, restlessness, altered mental status due to decreased cerebral perfusion and subsequent hypoxia.
Cardiogenic Shock Treatment •
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Hypotension due to decrease in cardiac output. A rapid, weak, thready pulse due to decreased circulation combined with
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tachycardia. •
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Cool, clammy, and mottled skin (cutis marmorata), due to vasoconstriction and subsequent hypoperfusion of the skin.
Absent pulse in tachyarrhythmia. Pulmonary edema, involving fluid backup in the lungs due to insufficient pumping of the heart..
Anti-arrhythmic agents 1. Adenosine 2. Verapamil 3. Amiodarone 4. β-blocker
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Rapid and deep respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis. Fatigue due to hyperventilation and hypoxia.
IV Dobutamine, which acts on β1 receptors of the heart leading to increased contractility and heart rate.
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Distended jugular veins due to increased jugular venous pressure. Oliguria (low urine output) due to insufficient renal perfusion if condition persists.
Fluid Infusion
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Glucagon Positive inotropic agents, which enhance the heart's pumping capabilities, are used to improve the contractility and correct the hypotension
Intra-aortic balloon pump(which reduces workload for the heart, and improves perfusion of the coronary arteries) Left Ventricular Assist Device(which augments the pump-function of the heart).
Orthostatic / Postural Hypotension Blood pressure suddenly falls when the person stands up. Decrease is typically greater than 20/10 mm Hg
Orthostatic Hypotension Causes of Orthostatic Hypotension •
May be most pronounced after resting incidence increases with age.
Signs and Symptoms Symptoms occur after sudden standing
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Consequences of insufficient blood pressure and cerebral perfusion. • • • • • • • • • • • •
Dizziness Euphoria or Dysphoria Bodily dissociation Distortions in hearing Lightheadedness Nausea Headache Blurred or dimmed vision Momentary Blindness) Numbness/tingling and fainting “Coat hanger” pain (neck / shoulders) Vasovagal syncope
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Orthostatic hypotension is primarily caused by gravity-induced blood pooling in the lower extremities, which in turn compromises venous return, resulting in decreased cardiac output and subsequent lowering of arterial pressure The overall effect is an insufficient blood perfusion in the upper part of the body. Still, the blood pressure does not normally fall very much, because it immediately triggers a vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. Therefore, a secondary factor that causes a greater than normal fall in blood pressure is often the pathology. Such factors include hypovolemia, diseases, medications, rarely, safety harnesses Heat exhaustion can also be a cause of postural hypotension.
Hypovolemia
Diagnosis •
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Lying, Sitting, Standing BP / HR measurements. Tilt table test
1. 2. 3. 4. 5. 6. 7.
Blood Lose Diuretics Vasodilators Other drugs Dehydration Prolonged bed rest Anemia.
Orthostatic Hypotension Management
Orthostatic Hypotension Diseases associated with OH 1. Addison's disease
Medical
2. Atherosclerosis Diabetes
Fludrocortisone (Florinef) and
3. Pheochromocytoma
Erythropoietin to aid in fluid retention
4. Neurological disorders
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Vasoconstrictors like Midodrine.
5. Multiple system atrophy
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Pyridostigmine bromide (Mestinon)
6. Dysautonomia
Selective serotonin reuptake inhibitors (SSRI's)
7. Ehlers-Danlos Syndrome – (genetic
Serotonin-Norepinephrine reuptake inhibitors (SNRI's)
8. Parkinson's Disease resulting from sympathetic denervation of the heart or as a side effect of dopaminomimetic therapy
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Stimulants - Adderall or Ritalin Benzodiazepines
mutations disrupt the production of collagen, a chief component of connective tissue)
9. Low level of norepinephrine but an excess of dopamine
Lifestyle factors •
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Standing up more slowly can give the blood vessels more time to constrict properly. This can help avoid incidents of syncope (fainting).
11. Cerebrospinal fluid leakage Breathing deeply and flexing the 12. Inner ear problems, esp w/ elderly abdominal muscles while rising – (contraindicated in individuals with Stage 2 hypertension) Medication side effect: "Dangle" legs before rising from bed Sodium supplements or electrolyteenriched drinks Maintaining proper fluid intake. Eating more, smaller meals can help, as digestion lowers blood pressure
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10. Quadriplegics / Paraplegics due to multiple system inability to maintain a normal blood pressure and blood flow to the upper part of the body
Take extra care when standing after eating. hypovolemia due to medications may be reversed by adjusting the dosage or by discontinuing the medication.
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Anti-depressants 1. Tricyclics 2. MAOIs
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Anti-psychotics Alpha1 adrenergic blocking agentsinhibition of vasoconstriction normally initiated by the baroreceptor reflex upon postural change and the subsequent drop in pressure
Orthostatic Hypotension Management (Continued) •
When the condition is caused by prolonged bed rest, improvement may occur by sitting up with increasing frequency each day. In some cases, physical counterpressure such as elastic hose (stockings) or whole-body inflatable suits may be required.
•
Ability toadopt recognize theposition" symptoms and quickly a "squat •
Avoiding bodily positions that impede blood flow, such as sitting with knees up to chest or crossing legs, can help prevent incidents.
Orthostatic Hypotension Harnesses •
The use of a safety harness can also contribute to orthostatic hypotension in the event of a fall. While a harness may safely rescue its user from a fall, the leg loops of a standard safety or climbing harness further restrict return blood flow from the legs to the heart, contributing to the decrease in blood pressure.
Other risk factors • • •
• • •
Postpartum mothers Bedrest Teenagers because of their large amounts of growth in a short period of time Anorexia Nervosa Bulimia Nervosa Alcohol consumption - (dehydrating effects)
Ischemic Heart Disease
Acute Myocardial Infarction •
Acute Myocardial Infarction
Signs and Symptoms Most commonly due to occlusion of a coronary artery following the rupture of a Onset of symptoms is usually gradual, vulnerable atherosclerotic plaque over several minutes, and rarely causing damage or death of myocardium instantaneous. •
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Classical symptoms sudden chest pain typically radiating to the left arm or left side of the neck shortness of breath, nausea, vomiting, indigestion, and fatigue, palpitations, sweating, and anxiety
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Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms.
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and is often described as a sensation of Tightness, Pressure, or Squeezing. •
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Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, and various blood tests - creatine kinase-MB (CK-MB) fraction and the troponin levels
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Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin. Can be classified into:
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ST Elevation MI(STEMI) versus Non-ST Elevation MI - (NSTEMI)
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STEMI (ST elevation MI) are treated with Thrombolysis or Percutaneous Coronary Intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable
Chest pain is the most common symptom
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•
Chest pain due to ischemia is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, It may mimic heartburn. Levine's sign, patient localizes the chest pain by clenching their fist over the sternum, Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Symptoms induced by a massive surge of catecholamines from the sympathetic nervous system 1. Diaphoresis 2. Weakness 3. Light-headedness 4. Nausea, Vomiting 5. Palpitations. Loss of consciousness - due to inadequate cerebral perfusion and cardiogenic shock Sudden Death - frequently due to the development of ventricular fibrillation
Acute Myocardial Infarction
Acute Myocardial Infarction
Risk factors: •
Cardiovascular disease
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Older age
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Smoking
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High Triglycerides and LDL
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Low levels of HDL
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•
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possible and to prevent complications, thus the phrase "time is further muscle".
Chronic kidney disease
Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI
Heart failure Excessive alcohol consumption
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Cocaine and Methamphetamine
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High stress levels
There are two basic types of acute myocardial infarction:
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An MI is a medical emergency which requires immediate medical attention. Treatment attempts to salvage as much myocardium as
Diabetes, HTN Obesity
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Heparin given to people who have heart conditions like unstable angina and some forms of heart attack reduces the risk of having another heart attack.
A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.
Transmural: associated with atherosclerosis involving major coronary Bypass surgery may be an option. artery. It can be subclassified into anterior, posterior, or inferior. Transmural The leading cause of death for both men and women worldwide. infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart's blood supply and is more susceptible to this type of pathology
Acute Myocardial Infarction Five main types: •
•
Acute Myocardial Infarction Pathophysiology
Type 1 – Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
Lethal arrhythmias: The most serious of these arrhythmias is ventricular fibrillation V-Fib ( /VF ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. Ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping Type 2 – Myocardial infarction secondary blood effectively. Cardiac output and blood to ischaemia due to either increased pressure may fall to dangerous levels, which oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
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can lead tooffurther coronary ischemia and extension the infarct. W.H.O. Criteria fo MI: Two = Probable MI Three = Definite MI Type 3 – Sudden unexpected cardiac 1. Clinical history of ischemic type chest death, including cardiac arrest, often with pain lasting for more than 20 minutes symptoms suggestive of myocardial 2. Changes in serial ECG tracings ischaemia, accompanied by presumably 3. Rise and fall of serum cardiac new ST elevation, or new LBBB, or biomarkers such as creatine kinase-MB evidence of fresh thrombus in a coronary fraction and troponin artery by angiography and/or at autopsy, but death occurring before blood The WHO criteria were refined in 2000 to give samples could be obtained, or at a time more prominence to cardiac biomarkers before the appearance of cardiac According to the new guidelines, a cardiac biomarkers in the blood troponin rise accompanied by either typical Type 4 – Associated with coronary angioplasty or stents: Type 5 – Myocardial infarction associated with CABG
Causes Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion Acute severe infection, such as pneumonia, can trigger MI There is an association of an increased incidence of a heart attack in the morning hours
symptoms, pathological Q intervention waves, ST elevation or depression or coronary are diagnostic of MI.
Acute Myocardial Infarction
Acute Myocardial Infarction Risk factors Risk factors for atherosclerosis are generally risk factors for myocardial infarction:
Risk Decreases: • •
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Diabetes - most important risk factor
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Tobacco smoking
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Hypercholesterolemia
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Lifestyle changes BP Management Smoking cessation Regular exercise Sensible diet Limitation of alcohol intake
To reduce the risk of future MI’s, CHF, or CVA •
Hyperlipidemia - High LDL •
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Low HDL
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High Triglycerides
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High blood pressure
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Polyunsaturated fats instead of saturated fats Antiplatelet drug therapy: o o
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Family History
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Obesity- BMI of more than 30 kg/m
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Age: Men age 45, Women age 55
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First-degree male relative who suffered a coronary vascular event at or before age 55 - First-degree female relative who suffered a coronary vascular event before age 65
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Hyperhomocysteinemia - High Homocysteine, a toxic blood amino acid that is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient Stress
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Alcohol
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Socioeconomic factors such as a shorter education, lower income, unmarried cohabitation may also contribute to the risk of MI. Women who use combined oral contraceptive pills, especially in the presence of other risk factors, such as smoking
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Aspirin Clopidogrel
Beta blocker - Metoprolol or Carvedilol - beneficial in high-risk patients with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. β-Blockers improve symptoms of cardiac ischemia in NSTEMI.
ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodeling post-MI. Statin therapy has been shown to reduce mortality and morbidity post-MI.
Acute Myocardial Infarction
Acute Myocardial Infarction Risk Factors - continued •
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Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation.
Risk Decreases - continued
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The aldosterone antagonist agent Spironolactone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction,
Elevated CRP blood levels, especially •
measured with high sensitivity assays, can predict the risk of MI, •
•
•
Influenza may trigger a acute myocardial infarction Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans.
Omega-3 fatty acids, Blood donation may reduce the risk of heart disease
Angina Pectoris
Angina Pectoris Physical
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Chest pain or discomfort seen in myocardial ischemia - Coronary arteries are narrowed or blocked. Angina is a sign that someone is at increased risk of heart attack, cardiac arrest and sudden cardiac death. Angina pectoris is the most common clinical manifestation of myocardial ischemia. Pain lasts for approximately 1-5 minutes “relieved by rest”, or nitroglycerin. Angina also can occur in people with Valvular heart disease, Hypertrophic Cardiomyopathy, and uncontrolled HTN Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings Most patients with angina pectoris report of Retrosternal chest discomfort rather than frank pain
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Typical locations for radiation of pain are arms, shoulders, and neck.
A positive Levine Sign (characterized by the patient's fist clenched over the sternum when describing the discomfort) is suggestive of angina pectoris. Pain produced by chest wall pressure is usually of chest wall srcin – NOT Angina
Causes Decrease in myocardial blood supply due to increased coronary resistance in large and small coronary arteries Coronary atherosclerotic lesion in the large coronary arteries with at least a 50% reduction in arterial diameter •
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Coronary spasm - Prinzmetal’s Angina
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Abnormal constriction or deficient endothelial-dependent relaxation of resistant vessels associated with diffuse vascular disease (ie, Micro-vascular Angina)
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Syndrome X - Aka - metabolic syndrome Xis a grouping of cardiac risk factors that result from insulin resistance
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Usually described as a pressure, heaviness squeezing, burning, or choking sensation. Anginal pain may be localized primarily in the epigastrium, back, neck, jaw, or shoulders.
For most patients with stable angina, physical examination findings are normal. Diagnosing secondary causes of angina, such as aortic stenosis, is important.
Systemic Inflammatory / Collagen Vascular Disease 1. 2. 3. 4. 5.
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Scleroderma Systemic Lupus Erythematous Kawasaki Disease Polyarteritis Nodosa Takayasu Arteritis
Reduction in the oxygen-carrying capacity of blood, such as elevated Carboxyhemoglobin or Severe Anemia (Hemoglobin, <8 g/dL)
Angina Pectoris •
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Typically, angina is precipitated by exertion, eating, exposure to cold, or to emotional stress.
Chest pain lasting only a few seconds is not usually angina pectoris. The intensity of angina does not change with respiration, cough, or change in position.
Angina Pectoris Risk Factors: 1. Risk factors for Atherosclerosis: 2. LV Hypertrophy 3. Obesity 4. Elevated serum levels of 5. Homocysteine 6. Lipoprotein 7. Plasminogen Activator Inhibitor 8. Fibrinogen 9. Serum Triglycerides 10. Low HDL
Pain above the mandible and below the epigastrium is rarely anginal in nature. Angina Decubitus is a variant of angina pectoris that occurs at night while the patient is recumbent..
Precipitating Factors: 1. 2. 3. 4. 5. 6.
Stable Ischemic Heart Disease •
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People with stable angina (or chronic stable angina) have episodes of chest discomfort that are usually predictable. They occur on exertion (such as running to catch a bus) or under mental or emotional stress. Normally the chest discomfort is relieved with rest, nitroglycerin or both. Also known as effort angina, this refers to the more common understanding of angina related to myocardial ischemia.
Severe Anemia Fever Tachy-arrhythmia Catecholamines Emotional Stress Hyperthyroidism
IschemicStable Heart Disease •
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Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest. Symptoms typically abate several minutes following cessation of precipitating activities and resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms
Unstable Ischemic Heart Disease •
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In people with unstable angina, the chest pain is unexpected and usually occurs while at rest. The discomfort may be more severe and prolonged than typical angina or be the first time a person has angina.
Unstable Ischemic Heart Disease Aka - "Crescendo Angina;" It has at least one of these three features: 1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., The most common cause is reduced within the prior 4–6 weeks) blood flow to the heart muscle because the coronary arteries are narrowed 3. it occurs with a crescendo pattern by fatty buildups (atherosclerosis) (i.e., distinctly more severe, . prolonged, or frequent than An artery may be abnormally constricted previously). or partially blocked by a blood clot. Inflammation, infection and secondary ___________ causes also can lead to unstable angina. ____________ In a form of unstable angina called variant or Prinzmetal's angina, the cause is coronary artery spasm.
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Definition:
Unstable Ischemic Heart Disease is Angina Pectoris that changes or worsens
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UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. Studies show that 64% of all Unstable Anginas occur between 10 PM and 8 AM when patients are at rest. In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.
Prinzmetal’s / Variant
Prinzmetal’s / Variant Variant Angina Pectoris is also called
Diagnosis •
Prinzmetal's Angina •
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Is caused by Vasospasm •
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Unlike typical angina, it nearly always occurs when a person is at rest. It usually occurs spontaneously It doesn't follow physical exertion or emotional stress, either. Attacks can be very painful and usually occur between midnight and 8 a.m. Prinzmetal’s Variant angina is due to Transient Coronary Artery Spasm.
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Echocardiography or thallium scintigraphy is often performed. The Gold Standard is Coronary Angiography with injection of provocative agents into the coronary artery. Provocation testing agents: 1. Ergonovine 2. Methylergonovine 3. Acetylcholine. Exaggerated spasm is diagnostic of Prinzmetal angina. ECG finding will more often show ST segment elevation than ST depression. Elevation ST-segment in II, III and aVf.
Treatment
About two-thirds of people with it have severe coronary atherosclerosis in at least one major vessel.
Prinzmetal's angina typically responds to:
The spasm usually occurs very close to the blockage.
2. Calcium Channel Blockers.
1. Nitrates
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Amlodipine - (Norvasc, Lotrel)
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Bepridil - (Vascor)
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Diltiazem - (Cardizem, Tiazac)
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Felodipine - (Plendil)
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Nifedipine - (Adalat, Procardia)
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Nimodipine - (Nimotop)
• •
Nisoldipine - (Sular) and Verapamil - (Calan, Isoptin, Verelan)
Takayasu's Arteritis Aka:
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1. 2. 3. •
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Aortic Arch Syndrome Nonspecific Aorto-arteritis Pulseless Disease
A form of large vessel granulomatous vasculitis[ with massive intimal fibrosis and vascular narrowing Young or middle-aged women of Asian decent.
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Mainly affects the aorta and its branches and the pulmonary arteries. Females more than males - between 15 and 30 years of age.
Vascular Disease •
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This refers to diseases of blood vessels outside the heart and brain. It's often a narrowing of vessels that carry blood to the legs, arms, stomach or kidneys.
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Takayasu's Arteritis
There are two types of these circulation disorders: 1. Functional Peripheral Vascular Disease 2. Organic Peripheral Vascular Disease
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In the US - atherosclerosis is a more frequent cause of obstruction of the aortic arch vessels than Takayasu's arteritis. Takayasu's arteritis is similar to other forms of vasculitis, including giant cell arteritis. Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasu's arteritis can present as pulseless , absent pulses in the upper extremities - Pulseless Disease
Vascular Disease Functional Peripheral Vascular Disease 1. Do not have an organic cause 2. Do not involve defects structural vasculature 3. Usually short-term effects related to "spasm" that may come and go. 4. Reynaud’s Disease is an example. It can be triggered by cold temperatures, emotional stress, working with vibrating machinery or smoking. Organic Peripheral Vascular Disease 1. Caused by structural changes in the blood vessels, such as inflammation and tissue damage 2. Peripheral artery disease is an example. by fattyblood buildups in arteriesIt's thatcaused block normal flow.
Acute Rheumatic Fever
Acute Rheumatic Fever •
An inflammatory disease that occurs following a Group A streptococcal infection such as strep throat or scarlet fever
Diagnosis •
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Involves the heart, joints, skin, and brain Typically develops two to three weeks after a Streptococcal A infection Acute rheumatic fever commonly appears in children between theages of 5 and 17, with only 20% of first-time attacks occurring in adults
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Jones Criteria – Diagnosis of Rheumatic Fever o Two Major criteria, OR o One Major + Two Minor, o plus evidence of streptococcal infection. Exceptions are Chorea and Indolent Carditis, each of which by itself can indicate rheumatic fever.
Jones Major Criteria: •
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The illness is so named because of its similarity in presentation to rheumatism Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association recommends daily or monthly prophylaxis continue long-term, perhaps for life
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Treatment for rheumatic fever is benzylpenicillin. (Penicillin G) •
Treatment •
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The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with Penicillin G Aspirin is the drug of choice and should be given at high doses of 100 mg/kg/day. One should watch for side effects like gastritis and salicylate poisoning.
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Migratory polyarthritis: a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards. Carditis: inflammation of the heart muscle which can manifest as CHF, Pericarditis with a rub, or a new heart murmur. Subcutaneous Nodules: painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees. Erythema Marginatum: a long lasting rash that begins on the trunk or arms as macules and spreads outward to form a snake like ring while clearing in the middle. This rash never starts on the face and it is made worse with heat. Sydenham's Chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease.
Acute Rheumatic Fever •
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In children and teenagers, the use of aspirin and aspirin-containing products can be associated with Reye's syndrome, a serious and potentially deadly condition. The risks, benefits and alternative treatments must always be considered when administering aspirin and aspirin-containing products in children and teenagers. Ibuprofen for pain and discomfort and corticosteroids for moderate to severe inflammatory reactions manifested by rheumatic fever should be considered in children and teenagers. Steroids are reserved for cases where there is evidence of involvement of heart. The use of steroids may prevent further scarring of tissue and may prevent development of sequelae such as mitral stenosis. Monthly injections of longacting penicillin must be given for a period of five years in patients fever. having one attack of rheumatic
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If there is evidence of carditis, the length of Penidure therapy may be up to 40 years. Another important cornerstone in treating rheumatic fever includes the continual use of low-dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.
Heart failure Some patients develop significant carditis which manifests as congestive heart failure. This requires the usual treatment for heart failure: diuretics and digoxin. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.
Jones Minor Criteria •
Fever
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Arthralgia: Joint pain without swelling
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Raised Sedimentation Rate
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Raised C-reactive protein
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Leukocytosis
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ECG showing features ofHeart block, such as a prolonged PR interval Evidence of streptococcal infection: 1. Elevated Antistreptolysin O titre 2. Elevated DNAase
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Previous episode of rheumatic fever or inactive heart disease
Aortic Aneurysm
Aortic Aneurysm An Aortic Aneurysm is a general term for any swelling / dilation of the aorta, usually representing an underlying weakness in the wall of the aorta at that location. While the stretched vessel may occasionally cause discomfort, a greater concern is the risk of rupture, which causes severe pain; massive internal hemorrhage; and, without prompt treatment, death occurs rapidly. Classification Aortic aneurysms are classified by where on the aorta they occur; aneurysms can appear anywhere. •
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Abdominal Aortic Aneurysms, the most common form of aortic aneurysm, Aortic Root Aneurysm, or aneurysm of sinus of Valsalva, appears on the sinuses of Valsalva or aortic root. Thoracic Aortic Aneurysmsare located in the Thoracic Cavity - classified as Ascending, Aortic Arch, or Descending Aneurysms depending on the location on the thoracic aorta involved.
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Thoracoabdominal Aortic Aneurysms involve both the thoracic and abdominal aorta.
Pathology •
The physical change in the aortic diameter can occur secondary to trauma, infection, an intrinsic defect in the protein construction of the aortic wall, or due to progressive destruction of aortic proteins by enzymes.
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An AAA may remain asymptomatic indefinitely Generally asymptomatic before rupture. Classic Triad of Rupture: 1. Pain 2. Hypotension 3. Mass The pain is classically reported in the abdomen, back or flank. Pain is acute, severe, constant, with radiation through the abdomen to the back Increased risk of rupture @ 5 cm diameter
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Abdominal Bruit may be heard
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Rupture is usually the first hint of AAA.
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The diagnosis of Aneurysm is confirmed at the bedside by the use of ultrasound. Rupture confirmed by Contrast CT Only 10–25% of patients survive rupture due to large pre- and post-operative mortality..
U.S. Preventive Services Task Force: •
Recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men age 65 to 75 years who have ever smoked.
Aortic Aneurysm Signs, Symptoms and Diagnosis •
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Most intact aortic aneurysms are asymptomatic As they enlarge, symptoms such as abdominal pain and back pain may develop.
Aortic Aneurysm Management Asymptomatic = Conservative Management Surveillance with a view to eventual repair, and immediate repair •
Two modes of repair for an AAA: 1. Open aneurysm repair 2. Endovascular aneurysm repair
Compression of nerve roots may cause leg pain or numbness.
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(EVAR).
Intervention recommended: Untreated, aneurysms tend to become progressively larger, although the rate of 1. Growth of 1 cm per year enlargement is unpredictable for any 2. Lesion is greater than 5.5 cm individual. 3. Indicated for symptomatic aneurysms May be found on physical examination – “Pulsatile Mass” Conservative management is indicated in patients where repair carries a high risk of Symptoms may include: anxiety or mortality and in patients where repair is unlikely feeling of stress; nausea and to improve life expectancy. vomiting; clammy skin; rapid heart rate •
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In patients presenting with aneurysm of the arch of the aorta, a common symptom is a hoarse voice as the left recurrent laryngeal nerve winds around the arch of the aorta.
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AAAs are the most common type of aortic aneurysm. Most involve all three layers - tunica intima, tunica media and tunica adventitia Erythema Nodosum - Most common sign for the aortic aneuysm - leg lesions typically found near the ankle area. Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus.
Medical therapy - Strict blood pressure
control •
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The mainstay of the conservative treatment is smoking cessation.
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Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture. As an AAA grows in diameter the risk of rupture increases. No medical / pharmaceutical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs. Blood pressure and lipids should however be treated like in any atherosclerotic condition.
Aortic Aneurysm
Aortic Aneurysm Prevention •
Attention to patient's general blood pressure, smoking and cholesterol risks helps reduce the risk on an individual basis.
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The tetracycline antibiotic Doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilising properties.
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Studies have suggested possible protective effects of therapy with ACE Inhibitors, B Blockers, and Statins Open repair is indicated in young patients as an elective procedure, or in growing or large, symptomatic or ruptured aneurysms. Endovascular repairgenerally indicated in for older, high-risk patients or patients unfit open repair.
Aortic Dissection
Aortic Dissection Symptoms:
Aortic Dissection is a potentially lifethreatening condition in which there is bleeding Abrupt, Sudden Onset of Severe Chest Pain into and along the wall of the aorta, the major artery carrying blood out of the heart. Sharp, stabbing, tearing, or ripping Sub-sternal pain radiating to shoulder, A tear in the inner wall of the aorta causes back, neck, arm, jaw, abdomen, or hip blood to flow between the layers of the wall of the aorta and force the layers apart Change position - pain typically moves to the arms and legs as the Dissection most commonly occurs in the aortic dissection gets worse Thoracic chest portion of the aorta, but may also occur in the abdominal portion. Mental Status / CNS changes •
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Type A begins in the Ascending Aorta.
Type B begins in the Descending Aorta. _____________ ______________ •
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Fainting / Nausea and vomiting
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Pallor / Diaphoresis / Hypotension / JVD
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Rapid, weak pulse / SOB
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“Blowing" murmur over the aorta
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When a tear occurs, it creates two channels: 1. Blood continues to travel 2. Blood remains still.
Blood pressure differences between the right and left arms, or between the arms and the legs
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Signs of shock, but with normal blood pressure
Aortic Dissection •
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Aortic Dissection
Treatment As the aortic dissection grows bigger, the channel with non-traveling blood can get The goal of treatment is to prevent bigger and push on other branches of the complications. Hospitalization is required. aorta. An aortic dissection may also involve abnormal ballooning of the aorta (aneurysm). The exact cause is unknown, but risks include atherosclerosis and hypertension
Traumatic injury is a major cause of aortic dissection, especially blunt trauma to the chest
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Hitting the steering wheel of a car during an accident is a common traumatic cause. Risk factors: • • • • • • • • • •
Aging Bicuspid aortic valve Coarctation (narrowing) of the aorta Connective tissue disorders Ehlers-Danlos syndrome Heart surgery or procedures Marfan’s syndrome Pregnancy Pseudoxanthoma Elasticum Vascular inflammation due to conditions such as Arteritis and Syphilis
Imaging:
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Aortic angiography Chest x-ray – mediastinal widening / pleural effusion MRI / CT Doppler Ultrasonography Echocardiogram Transesophageal Echocardiogram (TEE)
Type B - may be treated with medication first. IV Hypertensive Medications Strong pain relievers are usually needed. Beta-blockers may reduce some of the symptoms. Aortic Valve replacement, if necessary CAD Bypass, if necessary
Prognosis
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Aortic dissection is life threatening. Possibly managed surgically if prior to dissection
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Survival – less than 50%
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Complications •
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Type A - Immediate Surgery to repair the aorta.
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Aortic rupture causing rapid blood loss, shock Bleeding from the aorta Blood clots Cardiac Tamponade Heart attack Not enough blood flow past the dissection Permanent kidney failure Stroke
Arterial Embolism
Arterial Embolism •
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A sudden interruption of blood flow to an organ or body part due to an embolus adhering to the wall of an artery thus creating a blockage of blood flow distally. Thromboembolism - the major type of embolus being a blood clot
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Arterial embolism is the major cause of infarction.
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Is the combination of Thrombosis and its main complication,Embolism Thrombosis is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system.
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When a blood vessel is injured, the body uses platelets and fibrin to form a blood clot to prevent blood loss. Alternatively, even when a blood vessel is not injured, blood clots may form in the body if the proper conditions present themselves. If the clotting is too severe and the clot breaks free, the traveling clot is now known as an Embolus.
However, PE is generally classified as a form of venous embolism, because the embolus forms in veins.
Arterial Thrombosis
Arterial Thrombosis Thromboembolism
Pulmonary Embolism is sometimes classified as arterial embolism as well in the sense that the clot follows the pulmonary artery carrying deoxygenated blood away from the heart.
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Arterial thrombosis is the formation of a thrombus within an artery. Arterial thrombosis usually affects individuals who already have atherosclerosis Atherosclerosis tends to develop in areas where the Blood-flow is more turbulent, for example where blood vessels branch off. Atherosclerosis causes the walls of the arteries to ‘fur up’ with deposits of atheroma, a porridge-like substance. In most cases, arterial thrombosis follows rupture of atheroma, and is therefore referred to as atherothrombosis. Another common cause of arterial thrombosis is atrial fibrillation, which causes disturbed blood flow. Cardioversion of atrial fibrillation carries a great risk of thromboembolism
Arterial Thrombosis Causes
Arterial Thrombosis Symptoms of arterial thrombosis
Thrombosis is caused by abnormalities in one or more of the following known as:
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Virchow's Triad 1. Hypercoagulability / Thrombophilia The Composition of the Blood •
2. Endothelial Injury / Dysfunction Quality of the vessel wall •
3. Hemodynamic changes Nature of the blood flow Stasis, turbulence • •
1. Hypercoagulability •
• •
As seen with genetic deficiencies or autoimmune disorders. Cancers or malignancies like leukemia CA Treatments - Radiation, chemotherapy
2. Endothelial cell injury •
Causes of injury to the vessel's wall include trauma, surgery, infection or turbulent flow at bifurcations.
Peripheral vascular disease is a condition that usually affects the lower part of the leg. Although it is usually present in both legs, it is common for symptoms to affect one side only. Peripheral vascular disease appears to affect men more than women and usually occurs after the age of 50. It is particularly common in people with diabetes and is rare in nonsmokers. Symptoms include: •
Intermittent Claudication
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Cold extremities
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3. Disturbed blood flow •
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Stagnation of blood flow past the point of injury Atrial Fibrillation causes stagnant blood in the left atrium
_____________________ ______________ Risk factors for arterial thrombosis ● ● ● ● ● ● ● ● ●
Smoking High blood pressure Increased levels of cholesterol Diabetes Increasing age Family history Poor diet Excess body weight Physical inactivity.
The build up of atheroma causes the narrowing of the arteries, which can lead to heart disease, angina, and heart attacks, strokes or peripheral vascular disease.
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Occasionally a blood clot may lodge in one of the narrowed arteries. The leg then becomes cold, numb and pale, and loses its pulses. When this happens it is vital to restore the blood supply quickly, to prevent loss of the leg. This requires surgery to remove the clot.
CHRONIC Arterial Occlusion
CHRONIC Arterial Occlusion
Peripheral Arterial Occlusive Disease Claudication, is defined as reproducible ischemic muscle pain, is one of the most common manifestations of peripheral vascular disease caused by atherosclerosis.
This is the most common area for peripheral vascular disease.
Superficial Femoral Artery occlusionon one side Superficial Femoral Artery stenosison the Claudication occurs during physical activity and other side is relieved after a short rest. Pain develops because of inadequate blood flow. Intermittent claudication typically causes pain that occurs with physical activity. Determining how much physical activity is needed before the onset of pain is crucial. Typically, vascular surgeons relate the onset of pain to a particular walking distance in terms of street blocks (eg, 2block Claudication). •
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Other important aspects of Claudication pain are that the pain is reproducible within the same muscle groups and that
Treatment of Claudication is medical, with surgery reserved for severe cases
it ceases with a resting period of 2-5 minutes.
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Most common - Distal Superficial Femoral Artery - corresponds to Claudication in the calf muscle area
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When atherosclerosis is distributed throughout the Aorto-iliac area, thigh and buttock muscle Claudication predominates. Atherosclerosis is a systemic disease process. Patients who present with claudication due to PAOD can be expected to have atherosclerosis elsewhere.
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The goal is to impede the progression Most effective to slow progression is to stop tobacco use. Extensive evidence indicates that smoking cessation improves the prognosis. Improved walking distance and ankle pressure have been attributed to smoking cessation. Exercise plays a vital role in the treatment of Claudication. Regular walking programs result in substantial improvement (45 mins daily) Control lipids, diabetes, and hypertension
CHRONIC Arterial Occlusion Risk Factors •
The risk factors for PAOD are the same as those for coronary artery disease or cerebrovascular disease and include diabetes, hypertension, Hyperlipidemia, family history, sedentary lifestyle, and tobacco use.
CHRONIC Arterial Occlusion •
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Referral to a vascular surgeon – Reserved for Patients with limbthreatening ischemia or significant lifestyle limitations Arteriogram is reserved for severe cases warranting surgical repair.
Medications •
Smoking is the risk greatest of all the cardiovascular factors. Counseling patients on the importance of smoking cessation is paramount in PAOD management.
Physical Exam Clues to underlying PAOD: 1. Atrophy of calf muscles 2. Loss of extremity hair 3. Shiny skin 4. Thickened toenails Palpation of pulses should be attempted from the abdominal aorta to the foot, with auscultation for bruits in the abdominal and pelvic regions. •
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Daily aspirin Pentoxifylline (Trental) - 2-3 months to produce noticeable results. Clopidogrel (Plavix) Enoxaparin (Lovenox) - more research is needed to establish clinical efficacy. Cilostazol (Pletal) – may be beneficial Statins - regardless of the baseline cholesterol profile
Antiplatelet Agents Decrease overall risk of cardiovascular disease Absence of a pulse signifies arterial from myocardial infarction and stroke. Also obstruction proximal to the area palpated improve walking distance by enhancing circulation. When palpable pulses are not present, further assess withDoppler device. o
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An audible Doppler signal assures the clinician that some blood flow is perfusing the extremity. If no Doppler signals can be heard, a vascular surgeon should be immediately consulted.
Ankle-Brachial Index (ABI). ABI is calculated as the ratio of systolic blood pressure at the ankle to that of the arm.
Acute Arterial Occlusion
Acute Arterial Occlusion This results in the sudden cessation of blood flow to some area of the body.
Acute Peripheral Arterial Occlusion A sudden blockage of a peripheral artery.
The severity of ischemia and the viability of the extremity depend on:
The blockage may result from a blood 1. Clot 2. Embolism 3. Dissection 4. Trauma
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The location and extent of the occlusion The presence and subsequent development of collateral blood vessels.
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Symptoms usually start suddenly
There are two principal causes of acute arterial The symptoms of an acute arterial occlusion depend on the location, duration, and severity of occlusion: the obstruction. 1. Embolism 2. Thrombus in situ Severe Pain, Paresthesia, Numbness, & Coldness Physical findings develop in the involved extremity within 1 hour. Loss of pulses distal to the occlusion • • • • • •
Cyanosis or pallor Mottling Decreased skin temperature Muscle stiffening Loss of sensation Weakness Absent deep tendon reflexes.
Paralysis may occur with severe and persistent ischemia. The list of signs and symptoms mentioned in
various sources for Acute peripheral arterial occlusion includes the 7 symptoms listed below: Severe pain Coldness Note: Paresthesias If acute arterial occlusion occurs in the Loss of sensation presence of an adequate collateral circulation, Paleness in an extremity as is often the case in acute graft occlusion, the Lack of pulse in an extremity symptoms and findings may be less impressive. Blue skin in affect limb • •
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Treatment List for Acute peripheral arterial occlusion The list of treatments mentioned in various sources for Acute peripheral arterial occlusion includes the following list. Always seek professional medical advice about any treatment or change in treatment plans. Embolectomy, Thrombolysis or Bypass Surgery •
Giant Cell Arteritis •
Giant Cell Arteritis
Giant-cell Arteritis / Temporal Arteritis Associated Conditions is an inflammatory disease of blood vessels most commonly involving large Polymyalgia Rheumatica (PMR) and medium arteries of the head. Polymyalgia Rheumatica is characterized by sudden onset of It is a form of vasculitis. pain and stiffness in muscles (pelvis, shoulder) The name – “Giant Cell Arteritis” reflects the type of inflammatory cell GCA and PMR are so closely linked that involved as seen on a biopsy. •
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they are often considered to be different manifestations of the same disease The terms "Giant-Cell Arteritis" and process. "Temporal Arteritis" are sometimes used interchangeably, because of the frequent Also: involvement of the temporal artery. 1. Systemic Lupus Erythematosus, May also involve other large vessels 2. Rheumatoid Arthritis such as the aorta in "Giant-Cell Aortitis". 3. Severe Infections. Temporal Arteritis - is also known as "Cranial arteritis" and "Horton's Disease” Physical Exam Temporal, Giant cell, and Cranial Arteritis occur when one or more arteries become inflamed and die. The condition may also be a systemic disorder, affecting many medium-to-large sized arteries anywhere in the body. The cause is unknown but is believed to be partly due to a faulty immune response. The disorder has been associated with severe infections and high doses of antibiotics. The disorder may develop along with or after Polymyalgia Rheumatica. Giant Cell Arteritis is seen almost exclusively in those over 50 years old - It is rare in people of African descent.
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Palpation of the head reveals prominent temporal arteries with or without pulsation. The temporal area may be tender. Decreased pulses may be found throughout the body. Evidence of ischemia may be noted on fundal exam.
Laboratory Tests •
Abnormal LFTs - particularly raisedALPAlkaline Phosphatase
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Elevated Erythrocyte Sed. Rate
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C-reactive protein, another inflammatory marker, is also commonly elevated.
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Platelets may also be elevated.
Giant Cell Arteritis Symptoms It is more common in females than males by a ratio of 3:1.
Giant Cell Arteritis Biopsy – Diagnostic Gold Standard (Examination for Giant Cells infiltrating the tissue) •
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The mean age of onset is about 70 years, and it is rare in those less than 50 years of age. Patients present with: • • • • •
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Bruits Fever Headache Scalp Tenderness Jaw Claudication (pain in jaw when chewing) Tongue Claudication (pain in tongue when chewing) and Tongue Necrosis Reduced Visual Acuity(blurred vision) Acute Visual Loss (sudden blindness) Diplopia Acute Tinnitus
MRI and CT - Generally Negative
Treatment This is a medical emergency •
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The inflammation may affect blood supply to the eye and blurred blindness may occur.vision or sudden
Temporal Artery Ultrasound - “Halo Sign”
In 76% of cases involving the eye, the ophthalmic artery is involved causing anterior ischemic optic neuropathy Loss of vision in both eyes may occur very abruptly and this disease is therefore a medical emergency.
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High-dose Corticosteroids, typically prednisone (40–60 mg bid), must be started as soon as the diagnosis is suspected to prevent irreversible blindness secondary to ophthalmic artery occlusion. Steroids do not prevent the diagnosis from later being confirmed by biopsy, although certain changes in the histology may be observed towards the end of the first week of treatment and are more difficult to identify after a couple of months The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9– 12 months. Oral steroids are at least as effective as intravenous steroids, except in the treatment of acute visual loss where intravenous steroids appear to offer significant benefit over oral steroids
Peripheral Vascular Disease
Peripheral Vascular Disease Peripheral artery disease is a condition of the blood vessels that leads to narrowing that supply the legs and feet.
Severe PAD • •
The narrowing of the blood vessels leads to decreased blood flow, which can injure nerves and other tissues.
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Peripheral artery disease is caused by arteriosclerosis Arterial Vasculature become stiffer and cannot dilate to allow greater blood flow when needed
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Tests • •
Progressively Worsening Claudication is main symptom, with eventual pain at rest Classic Symptoms: Pain, Fatigue, Burning, or Discomfort in the muscles of the feet, calves, or thighs. These symptoms usually appear during walking or exercise and resolve with rest. Cool, Numb, Pale Extremities, even at rest. Severe PAD: • • •
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Impotence Pain and cramps at night Pain or tingling in the feet or toes, which can be so severe that even the weight of clothes or bed sheets is painful Pain that is worse when the leg is elevated Improved by dangling legs over the side of the bed Ulcers that do not heal
Calf Muscle Atrophy Hair loss over the toes and feet Painful, non-bleeding ulcers on the feet or toes Cyanosis toes or foot Shiny, tight skin Thick toenails
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Angiography of the arteries in the legs Ankle-Brachial Index -Blood pressure measured in the arms and legs for comparison Doppler ultrasound exam of an extremity Magnetic resonance angiography or CT angiography
Treatment •
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Balance exercise with rest to improve circulation Stop smoking. Foot Care - especially w/ diabetes. Blood pressure control Reduce weight Control cholesterol Glucose Control - diabetes
Medications: 1. Aspirin 2. Clopidogrel (Plavix) 3. Cilostazol – dilates the affected artery or arteries for moderate-to-severe cases that are not candidates for surgery 4. Statins 5. Analgesics 6. Hypertensives 7. Diabetic Meds
Peripheral Vascular Disease Signs and Tests: • •
• •
Peripheral Vascular Disease Surgery:
Arterial Bruits Decreased blood pressure in the affected limb Loss of hair on the legs or feet Weak or absent pulses in the limb
May be performed if the condition is severe (pain at rest) • •
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Angioplasty and stent placement Peripheral artery bypass surgery of the leg Leg or foot amputation.
Phlebitis
Phlebitis Phlebitis is an inflammation of a vein, usually in the legs.
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May occur spontaneously, or
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Complication of a medical procedure.
Phlebitis means inflammation of a vein. •
Phlebitis can occur in both the surface (superficial) or deep veins.
Local trauma and injury to a vein also increase the risk of forming a blood clot.
Risk factors for DVT: Thrombophlebitis is phlebitis is associated with the formation of blood clots
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Thrombophlebitis is the term used when a blood clot in the vein causes the inflammation. Thrombosis usually occurs in the deep veins of the legs Can travel to the lungs, causing Pulmonary Embolisms •
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Superficial Phlebitis affects veins on the skin surface. The condition is rarely serious and, with proper care, usually resolves rapidly. Sometimes people with superficial phlebitis also get Deep Vein Thrombophlebitis, so a medical evaluation is necessary. Deep Vein Thrombophlebitisaffects the larger blood vessels deep in the legs. Blood clots (thrombi) can form, which may break off and travel to the lungs. This is a potentially life-threatening condition called pulmonary embolism.
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Prolonged inactivity Long trips in a car or airplane Bed rest after an operation or illness Sedentary lifestyle Inactivity with little or no exercise Obesity Smoking cigarettes Hormone replacement therapy or birth control pills Pregnancy Certain medical conditions, such as cancer or blood disorders, that increase the clotting potential of the blood Injury to the arms or legs Varicose veins may be associated with superficial phlebitis
Phlebitis Signs and Symptoms •
Redness (erythema) and warmth with a temperature elevation of a degree or more above the baseline
Phlebitis Vasculitis: •
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Pain or burning along the length of the vein •
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Swelling (edema
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Vein being hard, and cord-like
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Bacterial: Pathogenic organisms can gain access and stimulate inflammation. Chemical: caused by irritating or vesicant solutions. Mechanical: physical trauma from the skin puncture and movement of the cannula into the manipulation vein during insertion; any subsequent and movement of the cannula; clotting; or excessively large cannula.
If occurring due to an intravenous infusion line, then slowed infusion rate •
Medications: including celecoxib, olanzapine, antidepressants, and others.
Superficial Phlebitis •
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Usually a slow onset of a tender red area along the superficial veins on the skin. A long, thin red area may be seen as the inflammation follows the path of a superficial vein.
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Genetic / Familial Risk
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Alcohol abuse
Signs and symptoms •
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This area may feel hard, warm, and tender. The skin around the vein may be itchy and swollen.
temperature elevation of a degree or more above the baseline •
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Redness (erythema) and warmth with a
The area may begin to throb or burn.
Pain or burning along the length of the vein
Symptoms may be worse when the leg is lowered, especially when first getting out of bed in the morning.
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Swelling (edema
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Vein being hard, and cord-like
A low-grade fever may occur.
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Sometimes phlebitis may occur at the site where a peripheral intravenous (IV) line was started. The surrounding area may be sore and tender along the vein. If an infection is present, symptoms may include redness, fever, pain, swelling, or breakdown of the skin.
If occurring due to an intravenous infusion line, then slowed infusion rate
Massage is contraindicated - manipulations risks breaking loose a clot which could then travel to the lungs (pulmonary embolism) or the heart
Thrombophlebitis •
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Thrombophlebitis is phlebitis is associated with the formation of blood clots
Thrombophlebitis Deep Vein Thrombophlebitis Signs and Symptoms:
Usually occurs in leg veins, but it may occur in an arm.
1. Redness
The thrombus (clot) in the vein causes pain and irritation and may block blood flow in the veins.
3. Inflammation
2. Warmth / Tenderness
4. Calf / Leg Pain Treatment Support Stockings •
Patients at Increased Risk: •
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Being hospitalized for a major surgery or with a major illness Disorders that make you more likely to develop blood clots Sitting for a long period of time (long airplane trip)
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Antibiotics (if infection is present)
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Anticoagulants to prevent new clots
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NSAIDS to reduce pain & inflammation
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Two Types of Thrombophlebitis 1. Deep venous thrombosis (affects deeper, larger veins) 2. Superficial Thrombophlebitis (affects veins near the skin surface)
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Thrombolytic Drugs to dissolve an existing clot Apply moist heat to reduce inflammation and pain Keep pressure off of the area to reduce pain and decrease the risk of further damage
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Elevation to reduce swelling
Surgical removal, stripping, or bypass of the vein is rarely needed
Tests •
Analgesics
Blood coagulation studies Doppler ultrasound Venography
Superficial Thrombophlebitis rarely causes complications. Pulmonary Embolism – Complication Chronic Leg Pain / Inflammation - Complication Routine changing of I.V. lines helps to prevent Thrombophlebitis
Venous Thrombosis •
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Deep Venous Thrombosis is the formation of a blood clot ("thrombus") in a deep vein. It is a form of Thrombophlebitis (inflammation of a vein with clot formation)
Venous Thrombosis Signs and symptoms There may be no symptoms referable to the location of the DVT Classical symptoms of DVT include pain, swelling and redness of the leg and dilation of the surface veins.
Commonly occurs in the Femoral Vein, Popliteal Vein, or the deep veins of the To Objectivate Edema – Measure the pelvis. circumference of the and the contralateral limb at aaffected fixed point Paget-Schrötter Disease - VT occuring spontaneously in the arm
Palpate the venous tract for tenderness
Physical examination is unreliable for A DVT can occur without symptoms, but excluding the diagnosis of deep vein in many cases the affected extremity will thrombosis. be painful, swollen, red, warm and the superficial veins may be engorged. Very extensive DVTs can extend into the Iliac Veins or the Inferior Vena Cava. The most serious complication of a DVT is that the clot could dislodge and travel Diagnosis to the lungs, which is called a pulmonary embolism (PE). The gold standard is intravenous venography DVT is a medical emergency, so, all limb swellings, however trivial, should be regarded Because of its invasiveness, this test is rarely as a DVT until proven otherwise. performed. •
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Late complication of DVT is the post-thrombotic Abdominal computed tomographic scan syndrome, which can manifest itself as edema, showing a Common Iliac Vein Thrombosis. pain or discomfort and skin problems . Physical examination According to Virchow's triad, venous thrombosis occurs via three mechanisms: Homans sign: Dorsiflexion of foot elicits pain in posterior calf 1. Decreased flow rate of the blood, 2. Damage to the blood vessel wall 3. Increased tendency of the blood to clot (Hypercoagulability).
Pratt's sign: Squeezing of posterior calf elicits pain. However, these medical signs do not perform well not included in clinical prediction rulesand thatare combine best findings in order to diagnose DVT.
Venous Thrombosis Several medical conditions can lead to DVT • • • • • • • •
Compression of the veins Physical trauma Cancer Infections Inflammatory diseases Stroke Heart failure Nephrotic syndrome.
At risk for DVT: •
Surgery
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Hospitalization,
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Orthopedic cast Immobilization Traveller's Thrombosis
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Smoking
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Obesity
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Age Certain drugs Estrogen Erythropoietin Genetic Thrombophilia
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Factor V Leiden
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Pregnancy
Diagnositic Tests of DVT 1. 2. 3. 4. 5. 6. 7. 8. 9.
D-Dimer Doppler Ultrasound CBC PT PTT (Primary coagulation studies) Fibrinogen LFT’s Renal Function Electrolytes
Venous Thrombosis Management The main issue with anticoagulation in pregnancy is that warfarin, the most commonly used anticoagulant in chronic administration, is known to haveteratogenic effects on the fetus if administered in early pregnancy. Anticoagulation 1. Heparin for one week 2. Warfarin for 3- to 6-month Low molecular weight heparin is preferred Unfractionated heparin is given in patients who have a contraindication to LMWH (e.g., renal failure or imminent need for invasive procedure. •
Thrombolysis Thrombolysis is generally reserved for extensive clot, e.g. an iliofemoral thrombosis . Thrombectomy
Used is Thrombus can be removed with a mechanical thrombectomy device. •
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Compression stockings should be routinely applied Inferior vena cava filter may be used
Hospitalization Hospitalization should be considered in patients with more than two of the following risk factors • • • • • •
Bilateral DVT Renal Insufficiency Low Body Weight (<70 kg/154 lbs) Recent Immobility Chronic Heart Failure Cancer
Varicose Veins
Varicose Veins Varicose veins are veins that have become enlarged and tortuous. Leg muscles pump the veins to return blood to the heart, against the effects of gravity. When veins become varicose, the leaflets of the valves no longer meet properly, and the valves do not work. This allows blood to flow backwards and they enlarge even more Varicose veins are most common in the superficial veins of the legs, which are subject to high pressure when standing.
Signs and Symptoms •
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Ankle Edema
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Stasis Dermatitis - Redness, dryness,
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and itchiness of areas of skin Leg Cramps especially with sudden move as standing up.
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Non-surgical treatments: • • • •
Sclerotherapy Elastic stockings Elevating the legs Exercise.
Appearance of spider veins (Telangiectasia)
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Besides cosmetic problems, varicose veins are often painful, especially when standing or walking.
Aching, heavy legs - worse at night and after exercise)
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Minor injuries – prolonged bleeding / slow healing Lipodermatosclerosis - skin above the ankle may shrink because the fat underneath the skin becomes hard. Atrophie Blanche - Whitened, irregular scar-like patches can appear at the ankles
Causes Pregnancy Obesity Menopause Aging Prolonged standing Leg injury Abdominal straining Crossing legs at the knees or ankles •
Surgical Treatment:
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Vein Stripping Ambulatory phlebectomy Vein Ligation Cryosurgery
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Alternative Treatment Techniques
Treatment is Conservative • • •
Ultrasound-guided Sclerotherapy Radiofrequency Ablation Endovenous Laser Treatment Varicose veins are distinguished from
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Reticular Veins (blue veins) and Telangiectasias (spider veins) by size and location of the veins
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Elevating the legs often provides temporary symptomatic relief. Compression Stockings - Caution should be exercised in their use in patients with concurrent arterial disease. NSAIDs Regular exercise is not supported by any evidence
Valvular Diseases
Valvular Diseases
Aortic Stenosis • • • •
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Crescendo-decrescendo Harsh Systolic Best heard at the second intercostal space Right upper sternal border Radiates to one or both carotid arteries. Increased with squatting Reduced during Valsalva strain
Aortic Stenosis In adults, three conditions are known to cause aortic stenosis. 1. Progressive wear and tear of a bicuspid valve present since birth (congenital). 2. Wear and tear of the aortic valve in the elderly. 3. Scarring of the aortic valve due to rheumatic fever as a child or young adult.
Aortic Insufficiency The hallmark of Aortic Regurgitation/ Insufficiency
Aortic Insufficiency • • •
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High-pitched Decrescendo Diastolic Murmur at the Left Sternal Borderafter the Second Heart Sound.
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Mitral Stenosis Classic murmur of Mitral stenosis • • • • • •
Low-pitched, Rumbling Loud S1 Opening Snap Diastolic best heard with the bell @ Apex The length of the murmur, as opposed to the intensity, is used as a nonspecific guide to stenosis severity.
Rheumatic Fever Ankylosing spondylitis Aortic dissection Congenital (present at birth) valve problems Endocarditis High blood pressure Marfan syndrome Reiter syndrome Syphilis Systemic lupus Erythematous
Mitral Stenosis Causes of mitral stenosis include the following: • • • • • • •
Rheumatic fever Congenital Mitral stenosis Systemic lupus Erythematous (SLE) Rheumatoid arthritis (RA) Malignant Carcinoid Fabry disease Whipple disease
Mitral Insufficiency Most common cardiac problem seen in Rheumatic Heart Disease.
Mitral Insufficiency •
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Pansystolic High-pitched Blowing Apical Radiates to the left axilla.
NOTE: Pancarditis is the most serious and second most common complication of rheumatic fever
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Secondary mitral regurgitationis due to the dilatation of the left ventricle, due dilated cardiomyopathy, including aortic insufficiency, nonischemic dilated cardiomyopathy It is also called functional mitral regurgitation Acute Mitral Regurgitation most often caused byInfective Endocarditis, mainly S. aureus
Mitral Valve Prolapse Can occur in a multitude of disorders Typically reflects abenign, normal variant rather than a single disease process.
Most common cause is Mitral Valve Prolapse (MVP) Ischemic heart disease Rheumatic fever Marfan's syndrome
Mitral Valve Prolapse Causes Most cases of mitral valve prolapse are primary, idiopathic in nature, and expressed as an autosomal dominant trait that exhibits both sexand age-dependent penetrance.
Usually is asymptomatic, nonprogressive, and benign. May present as:
Connective disorders Marfan tissue syndrome Ehlers-Danlos syndrome Osteogenesis imperfecta Pseudoxanthoma elasticum Polycystic kidney disease Stickler syndrome Systemic lupus erythematosus Relapsing polychondritis Polyarteritis Nodosa • • •
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Chest pain Dyspnea Fatigue Dizziness Near-syncope symptoms Anxiety
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Muscle disorders Duchenne muscular dystrophy Fragile X syndrome Mucopolysaccharidoses Myotonic dystrophy • • • •
Mitral Valve Prolapse
Murmur: Mid-systolic click. Crescendo-Decrescendo Heard best at the apex. •
Mitral Valve Prolapse Congenital heart disease Atrial Septal defect (ASD) Epstein anomaly • •
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The click is so characteristic of MVP that even without a subsequent murmur, its presence alone is enough for the diagnosis.
Acquired heart disease •
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Papillary muscle dysfunction (eg, ischemia, Myocarditis) Cardiac trauma
Post Mitral valve surgery In stark contrast to most other murmurs, MVP is Rheumatic Endocarditis enhanced by Valsalva maneuvers and decreased by squatting. Miscellaneous • •
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Tricuspid Stenosis •
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A prominent right atrium may be palpable to the right of the sternum. Opening snap, if not obscured by
Tricuspid Stenosis •
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Mitral stenosis sounds •
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Tricuspid stenosis is almost always Rheumatic in srcin Generally accompanied by Mitral and Aortic valve involvement.
Widely Split S1
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A diastolic murmur is audible along the left sternal border or at the Xiphoid
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Most Stenotic Tricuspid Valves are associated with clinical evidence of regurgitation Stenotic Tricuspid Valves are always anatomically abnormal
Increases with inspiration. •
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Wolff-Parkinson-White syndrome Von Willebrand disease
Tricuspid Regurgitationis also present, represented by a Holosystolic murmur in a similar location.
Cause is limited to a few conditions With the exceptions of congenital causes or active Infective Endocarditis, Tricuspid Stenosis takes years to develop
Tricuspid Insufficiency •
S3 gallop:
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Jugular Venous Distention
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Prominent V wave
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Pansystolic murmur
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Heard along the lower left sternal border
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Inspiratory accentuation. Diminished peripheral pulse volume Hypotension due to therapeutic interventions used to decrease volume overload
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Pulmonary Rales
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LV dysfunction
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Mitral Stenosis RV heave S 4 gallop that increases with inspiration Ascites and Jaundice Peripheral edema Cachexia
Tricuspid Insufficiency Causes •
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Rheumatic heart disease Endocarditis Ebstein anomaly Prolapse (floppy, redundant) Carcinoid Papillary muscle dysfunction Trauma Connective-tissue diseases Medications Anatomically normal tricuspid valve 1. 2.
Dilatation of the RV cavity. The valve structures are normal;
Medical Treatment The medical therapy used in the treatment of tricuspid regurgitation is directed toward the control of CHF that is causing or contributing to the problem. Diuretics Are used to control the fluid overload associated with the process.
Atrial fibrillation Fourth intercostal Parasternal region The murmur is usually augmented during inspiration and is reduced in intensity and duration in the standing position and during a Valsalva maneuver.
Cardiac glycosides Digoxin is used to control Atrial fibrillation and to increase myocardial contractility. Angiotensin-converting enzyme (ACE) inhibitors Are used to provide afterload reduction, thereby decreasing the volume load on the right ventricle. Anticoagulants Are used to prevent thrombosis and embolization from the prosthetic valve used in the treatment of tricuspid regurgitation.
Pulmonary Stenosis •
Normal S1
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Split S2
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Systolic Ejection Click.
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The Louder on expiration.
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Left upper sternal border
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Second left intercostal space
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Crescendo-decrescendo Prominent jugular venous a wave and a right ventricular lift Cyanosis may occur
Causes Results from a Mal-development of the Pulmonic valve tissue Coexisting Cardiac Malformations
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1. 2.
Ventricular Septal Defect Atrial Septal Defect
3. 4.
Patent Ductus Arteriosus. Aberrant flow patterns in utero
Rubella Embryopathy Family history is a mild risk factor Congenital syndromes 1.
Mayer-Rokitansky-Kuster-Hauser Syndrome.
Pulmonary Stenosis Management depends on the degree of stenosis Severe stenosis requires emergent dilatation of valves by balloon valvulotomy Patients with mild Pulmonic Valvular stenosis usually do not require any treatment. Cyanotic infants with respiratory distress and hypotension/shock undergo a workup as that for septic patients. Bacterial Endocarditis prophylaxis
Pulmonary Insufficiency •
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Wide splitting of S2 Right-sided S3 may be audible and Accentuated with inspiration
Pulmonary Insufficiency Signs and Symptoms •
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Right-sided S4 may be audible and accentuated with inspiration Low-pitched murmur, usually best heard along the third or fourth intercostal
Complications •
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Etiology Pulmonary hypertension (causing insufficiency secondary to dilatation of the valve ring) •
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Infective Endocarditis
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Rheumatic heart disease
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Right heart failure
spaces adjacent to the left sternal border; Treatment may be accentuated with inspiration Pulmonary insufficiency is usually well Graham-Steell's murmur, a hightolerated pitched, blowing decrescendo murmur heard best along the left Parasternal Valvuloplasty / Valve replacement region •
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May be tolerated for years without problems Dyspnea
Congenital abnormalities (e. g., Tetralogy of Fallot, Ventral Septal Defect, Valvular Pulmonic Stenosis)
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Carcinoid heart disease
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Pulmonary valve repair
Acute Bacterial Endocarditis
Acute Bacterial Endocarditis
Medical Care Bacterial Endocarditis is a microbial infection of Bacterial Endocarditis is a disease in which the endothelial surface of the heart. complete eradication of the organism is required. Signs and symptoms of bacterial Endocarditis are diverse; therefore, the practitioner must Prolonged parenteral therapy is the only way to have a high degree of suspicion to make an achieve bactericidal serum levels for the time early diagnosis. needed to kill all the bacteria present in a Features of bacterial Endocarditis are due to bacteremia, local cardiac invasion by organisms, peripheral embolization, and the formation of immune complexes. Patients present with many nonspecific symptoms 85-99% of patients are febrile. Patients with congenital heart disease and fever require special consideration Fatigue, chills, sweats, anorexia, malaise, a cough, a headache, Myalgias, Arthralgias, and confusion. Acute - toxic, febrile illness and symptoms that have lasted less than 2 weeks.
vegetation of endocarditis. Treatment ranges from 4-8 weeks. Therapy is tailored according to the etiologic agent. Penicillin G for 4 weeks -orPenicillin or Ceftriaxone combined with Gentamicin for 2 weeks. Penicillin-resistant streptococcal Endocarditis (PRSE) - Penicillin, Ampicillin, or
Ceftriaxone for 4 weeks combined with gentamicin for the first 2 weeks . Sub acute - more nonspecific flu like illness and MRSA - infection on native valves is treated symptoms that have lasted more than 2 weeks with Vancomycin for at least 6 weeks, with or without 3-5 days of gentamicin. A history of intravenous (IV) drug usemay be Gram negative Endocarditis: elicited. HACEK - Ceftriaxone or Ampicillin plus Gentamicin for 4 weeks. S Aureus is the most common cause In neonates, Endocarditis commonly produces septic embolic phenomena, such as Osteomyelitis, Meningitis, and Pneumonia Neonates with Endocarditis may also have feeding problems, respiratory distress, tachycardia, or Neurologic symptoms.
Acute Bacterial Endocarditis Duke Criteria: used for Diagnosis: •
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Positive blood cultures Positive Echo - oscillating mass and/or vegetation, paravalvular abscess, or dehiscence of a prosthetic valve) New Valvular regurgitation Predisposition ( history of IV drug use or congenital heart disease) Fever with a temperature of more than 38°C Vascular phenomena (arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions - painless, hemorrhagic lesions on palms and soles Immunologic phenomena (Glomerulonephritis, Osler nodes, Roth spots, positive result for rheumatoid factor)
Acute Bacterial Endocarditis Surgical Care Absolute indications for surgery include progressive cardiac failure, valve obstruction, definitive Peri-Valvular abscess, Non-candidal Fungal infection, and Pseudomonas infection Relative indications bacteremia despiteincludepersistent appropriate antibiotic therapy, Candidal Endocarditis, and Vegetations larger than 10 mm. Surgery should be performed without delay in patients with severe congestive heart failure (CHF) secondary to Valvular regurgitation
Sub-Acute Bacterial Endocarditis Subacute bacterial endocarditisis a type of Infective Endocarditis Summary:
Sub-Acute Bacterial Endocarditis Prognosis Underlying structural valve disease is usually present in patients before developing subacute endocarditis.
In cases of subacute bacterial endocarditis, the causative organism -Streptococcus Viridans - needs a previous heart valve It is less likely to lead to septic emboli than is disease to colonize and cause such disease. acute endocarditis, but subacute endocarditis In cases of acute bacterial endocarditis, the organism can colonize on the healthy heart valve, causing the disease.
has a relatively slow process of infection and, if left untreated, can worsen for up to one year before it is fatal. Treatment
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Considered a form of Type III hypersensitivity Sub acute bacterial Endocarditis is more common in patients with an underlying congenital heart defect.
The standard treatment is with a minimum of four weeks of high-dose intravenous penicillin with an aminoglycoside such as gentamicin.
Note: Diagnosis
Penicillin G vs. Pen VK
Osler's nodes
Penicillin G Benzathine (orally and
Swelling, redness, and pain that characterize parenteral). Trade names are: Bicillin LA and these lesions of the hands and feet - The nodes Permapen. are commonly indicative of subacute bacterial Penicillin V potassium (Oral) is endocarditis. characteristically known for being stable in acid (therefore, is taken orally). Trade names are: Other signs: Ledercillin VK and SK-Penicillin VK Roth's Spots and Janeway Lesions occur on the palms and soles, can be differentiated from Osler's nodes because they are nontender. Causes Causative Agent -Streptococci Viridans bacteria that normally live in the mouth and throat - Streptococcus mutans, mitis, sanguis or milleri). Other strains of streptococci (bovis and equines) can also cause subacute endocarditis, usually in patients who have a form of gastrointestinal cancer.
Acute Pericarditis Inflammation of pericardiumcharacterized by: 1. 2. 3.
Chest pain Pericardial friction rub Serial EKG changes
Acute Pericarditis 3. Bacterial Causes Purulent Pericarditis. •
Caused by Serous or Hemorrhagic Effusion. Granulomatous pericarditis– 1. 2. 3. 4.
TB, Fungal infections Rheumatoid arthritis Sarcoidosis.
The pericardium drainage occurs via the thoracic duct and the right lymphatic duct into the right pleural space.
Bacterial pericarditis develops from direct Pulmonary Extension, Hematogenous spread, Myocardial Abscess or Endocarditis, Penetrating injury to chest wall from either trauma or surgery, or a sub diaphragmatic suppurative lesion.
. Treatment includes appropriate antibiotics for at least 4 weeks and drainage of pericardial fluid. 4. Inflammatory Disorders •
Rheumatoid arthritis
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Systemic lupus Erythematosus
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Scleroderma Pericardial effusions occur in 40% of patients with scleroderma and can be due to scleroderma, restrictive Cardiomyopathy, and renal failure. o
Pericardial physiology includes 3 functions: 1. Promotes cardiac efficiency by limiting acute dilation, maintaining ventricular compliance with
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preservation of the Starling curve, distributing hydrostatic forces. The and pericardium also creates a closed chamber with sub atmospheric pressure that aids Atrial filling and lowers transmural cardiac pressures.
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2. Through its membranous function, the pericardium shields the heart by reducing external friction and acting as a barrier against extension of infection and malignancy. 3. Through its ligamentous function, the pericardium anatomically fixes the heart.
Pericardial fluid has a protein value greater than 5 g/dL, has a low cell count, and does not demonstrate the antibodies found in RA and SLE. These patients havea poor prognosis.
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Rheumatic fever
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Sarcoidosis
Acute Pericarditis Chest pain is the cardinal symptom. 1. Sharp, dull, aching, burning, or pressing. 2. Worse during inspiration, when lying flat, or during swallowing and with body motion . Dyspnea, especially with Tamponade.
Acute Pericarditis •
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Other inflammatory conditions Sjögren syndrome Mixed connective-tissue disease Reiter syndrome Ankylosing spondylitis Inflammatory bowel disease Wegener granulomatosis Vasculitis (eg, giant cell arteritis, polyarteritis) Polymyositis o
Fever may be present.
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Abdominal pain occurs infrequently in children.
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Physical • • • • •
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Friction Rub is Pathognomonic. Tachypnea Tachycardia Patients may have fever. Beck’s Triad - (Cardiac Tamponade)
Behçet syndrome Whipple disease Familial Mediterranean fever Serum sickness
Metabolic disorders Renal failure Hypothyroidism Cholesterol pericarditis • • •
Cardiovascular diseases 1. Hypotension 2. JVD 3. Muffled heart sounds
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Especially w/ Sudden Intra-pericardial
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Myocardial infarction Dressler Syndrome Aortic dissection Takotsubo Cardiomyopathy Neoplasm
Hemorrhage) •
Pulsus Paradoxus is defined as a > 10 mm Miscellaneous causes, including iatrogenic Hg decrease in arterial systolic pressure with Drugs inspiration. Irradiation This decrease is important in patients with Post Pericardiotomy syndrome more slowly developing Tamponade Invasive cardiac procedures because they may lack findings of the Beck Trauma triad. •
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Causes 1. Idiopathic 2. Viral - the most common cause 1. Coxsackievirus B 2. 3. 4. 5. 6.
Echovirus Adenoviruses Influenza A and B HIV HSV
Cardiac Tamponade
Cardiac Tamponade
Other Symptoms Compression of the heart that occurs when blood or fluid builds up in the space Anxiety, restlessness between the myocardium and the Chest pain pericardium CP radiating to the neck, shoulder, back, or abdomen Tamponade is life-threatening CP is Sharp, stabbing Causes CP is worsened by deep breathing or coughing Blood or fluid collects in the pericardium. Difficulty breathing This prevents the ventricles from Discomfort, sometimes relieved by sitting expanding fully. The excess pressure upright or leaning forward from the fluid prevents the heart from Fainting, light-headedness functioning normally. Pale, gray, or blue skin Palpitations Due to: Rapid breathing Dissecting aortic aneurysm (thoracic) Swelling of the abdomen or other areas End-stage lung cancer Dizziness Heart attack (acute MI) Drowsiness Heart surgery Low blood pressure Pericarditis caused by bacterial or viral Weak or absent pulse infections Wounds to the heart Echocardiogram is typically used to help establish the diagnosis. Other potential causes include: •
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Heart tumors Hypothyroidism Kidney failure Placement of central lines Radiation therapy to the chest Recent invasive heart procedures Recent open heart surgery Systemic lupus Erythematous
Signs:Pulsus Paradoxical - Blood pressure may fall when the person inhales deeply Breathing may be rapid (faster than 12 breaths in an adult per minute) Heart rate may be over 100 (normal is 60 to 100 beats per minute) Heart sounds are faint during examination with a stethoscope Neck veins may be abnormally extended (distended) but the blood pressure may be low Peripheral pulses may be weak or absent Chest CT / MRI •
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Symptoms
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Beck’s Triad - (Cardiac Tamponade) 1. Hypotension 2. JVD 3. Muffled heart sounds
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Chest x-ray Coronary angiography ECG
Cardiac Tamponade
Cardiac Tamponade
Treatment Cardiac Tamponade is an emergency condition that requires hospitalization • • • •
Pericardiocentesis - fluid must be drained Surgical Pericardioectomy Fluids replacement for Hypotension The cause of the Tamponade must be identified and treated.
Wolff-Parkinson-White •
Wolff-Parkinson-White
Wolff-Parkinson-White syndrome is a heart condition in which there is an extra electrical pathway
“Delta Wave” •
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Leads to episodes tachycardia Wolff-Parkinson-White is one of the most common causes of fast heart rate disorders in infants and children.
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Patients are usually asymptomatic. However, during supraventricular tachycardia the individual may have symptoms of palpitation, dizziness, shortness of breath, and syncopy / near syncopal episodes of supraventricular tachycardia . ECG will show the telltale "Delta An wave".
CARDIAC DRUGS
CARDIAC DRUGS
Anticoagulants
Anticoagulants •
Heparin
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Warfarin
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Dalteparin
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Danaparoid
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Enoxaparin
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Tinzaparin
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Antiplatelet Agents •
Aspirin
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Clopidogrel - (Plavix)
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Ticlopidine
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Dipyridamole
Decreases the clotting ability of the blood. They do NOT dissolve existing blood clots. Used to treat certain blood vessel, heart and lung conditions. Helps to prevent harmful clots from forming in the blood vessels. May prevent the clots from becoming larger and causing more serious problems. Often prescribed to prevent first or recurrent stroke.
Antiplatelet Agents •
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Keeps blood clots from forming by preventing blood platelets from sticking together. Helps prevent clotting in patients with h/o MI, Unstable Angina, Ischemic Strokes, TIA Usually prescribed preventively, when plaque buildup is evident but there is not yet a large obstruction in the artery.
Angiotensin-Converting Enzyme (ACE) Inhibitors •
Benazepril - (Lotensin)
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Captopril - (Capoten)
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Enalapril - (Vasotec)
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Fosinopril - (Monopril)
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Lisinopril - (Prinivil, Zestril)
Angiotensin-Converting Enzyme (ACE) Inhibitors •
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Moexipril - (Univasc) Perindopril - (Aceon)
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Quinapril - (Accupril)
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Ramipril - (Altace)
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Trandolapril - (Mavik)
Angiotensin II Receptor Blockers (ARBS) •
Candesartan - (Atacand)
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Eprosartan - (Teveten)
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Irbesartan - (Avapro)
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Losartan - (Cozaar)
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Telmisartan - (Micardis)
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Valsartan - (Diovan)
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Expands blood vessels and decreases resistance by lowering levels of Angiotensin II. Allows blood to flow more easily and makes the heart's work easier or more efficient. Used to treat or improve symptoms of cardiovascular conditions including high blood pressure and heart failure. Always recommended for DM to help protect Renal Function
Angiotensin II Receptor Blockers (ARBS) •
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Rather than lowering levels of Angiotensin II (as ACE inhibitors do) Angiotensin II receptor blockers prevent this chemical from having any effects on the heart and blood vessels. This keeps blood pressure from rising. Used to treat or improve symptoms of cardiovascular conditions including high blood pressure and heart failure
Beta Blockers •
Acebutolol - (Sectral)
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Atenolol - (Tenormin)
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Betaxolol - (Kerlone)
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Bisoprolol/ HCTZ - (Ziac)
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Bisoprolol - (Zebeta)
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Carteolol - (Cartrol)
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Metoprolol - (Lopressor, Toprol XL)
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Nadolol - (Corgard)
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Propranolol - (Inderal)
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Sotalol - (Betapace) and
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Timolol - (Blocadren)
Calcium Channel Blockers •
Amlodipine - (Norvasc, Lotrel)
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Bepridil - (Vascor)
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Diltiazem - (Cardizem, Tiazac)
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Felodipine - (Plendil)
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Nifedipine - (Adalat, Procardia)
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Nimodipine - (Nimotop)
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Nisoldipine - (Sular) and
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Verapamil - (Calan, Isoptin, Verelan)
Beta Blockers •
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Decreases the heart rate and cardiac output, which lowers blood pressure and makes the heart beat more slowly and with less force. Used to lower blood pressure. Used with therapy for cardiac arrhythmias Used to treat chest pain (angina). Used to prevent future heart attacks in patients who have had a heart attack. Do NOT use ion DM patients b/c rise in glucose
Calcium Channel Blockers •
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Interrupts the movement of calcium into the cells of the heart and blood vessels. May decrease the heart’s pumping strength and relax blood vessels. Used to treat high blood pressure, chest pain (angina) caused by reduced blood supply to the heart muscle Used to treat some arrhythmias
Diuretics •
Amiloride - (Midamor)
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Bumetanide - (Bumex)
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Chlorothiazide - (Diuril)
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Chlorthalidone - (Hygroton)
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Furosemide - (Lasix)
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Hydrochlorothiazide - (Esidrix,
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Indapamide - (Lozol)
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Spironolactone - (Aldactone)
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Causes the body to rid itself of excess fluids and sodium through urination. Helps to relieve the heart's workload. Decreases the buildup of fluid in the lungs and other parts of the body, such as the ankles and legs.
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Different diuretics remove fluid at varied
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Used to help lower blood pressure.
rates and through different methods.
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Used to help reduce edema from excess buildup of fluid in the body.
Vasodilators • •
Isosorbide Dinitrate - (Isordil)
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Nesiritide - (Natrecor)
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Hydralazine - (Apresoline)
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Nitrates
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Minoxidil
Digitalis Preparations •
Digoxin
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Digitoxin
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Lanoxin
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Relaxes blood vessels and increases the supply of blood and oxygen to the heart while reducing its workload. Prescribed to patients who cannot tolerate ACE inhibitors Used to for angina
Increases the force of the heart's contractions, which can be beneficial in heart failure and for irregular heart beats. Used to relieve heart failure symptoms, especially when the patient isn't responding to ACE inhibitors and diuretics. Also slows certain types of arrhythmias, particularly Atrial fibrillation.
Statins (HMG-CoA Reductase Inhibitors) Cholesterol – Lowering drugs: 1. Statins 2. Resins 3. Nicotinic acid (Niacin), ______________________
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Statins are drugs that can lower your cholesterol. They work by blocking a substance your body needs to make cholesterol.
Gemfibrozil
Statins may also help your body reabsorb cholesterol that has built up in plaques on your artery walls, preventing
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Clofibrate Lovastatin – (Mevacor)
further blockage in your blood vessels and heart attacks.
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Pravastatin – (Pravachol)
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Simvastatin – (Zocor)
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Amlodipine / Atorvastatin) –(Caduet)
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Rosuvastatin – (Crestor)
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Fluvastatin - (Lescol)
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Atorvastatin – (Lipitor)
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Ezetimibe / Simvastatin –(Vytorin)
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Side effects Muscle and joint aches (most common) Nausea Diarrhea Constipation Liver damage o Gemfibrozil and Niacin, increase the risk of liver problems when combined with Statins o Monitor LFT’s • • • • •
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Muscle problems o Statin Myopathy o o
Rhabdomyolysis Myoglobin can damage your kidneys.
Certain drugs when taken with Statins can increase the risk of Rhabdomyolysis. These include Gemfibrozil, Erythromycin, antifungal medications, Nefazodone, Cyclosporine and Niacin.
