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Pericarditis
Often local manifestation of another disease May present as: Acute pericarditis Pericardial effusion Constrictive pericarditis

Acute Pericarditis
Acute inflammation of the pericardium Cause often unknown, but commonly caused by infection, uremia, neoplasm, myocardial infarction, surgery or trauma. Membranes become inflamed and roughened, and exudate may develop

Symptoms:
Sudden onset of severe chest pain that becomes worse with respiratory movements and with lying down. Generally felt in the anterior chest, but pain may radiate to the back. May be confused initially with acute myocardial infarction Also report dysphagia, restlessness, irritability, anxiety, weakness and malaise
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Signs
Often present with low grade fever and sinus tachycardia Friction rub (sandpaper sound) may be heard at cardiac apex and left sternal border and is diagnostic for pericarditis (but may be intermittent) ECG changes reflect inflammatory process through PR segment depression and ST segment elevation.
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Its killing me softly.

Treatment
Treat symptoms Look for underlying cause If pericardial effusion develops, aspirate excess fluid Acute pericarditis is usually self-limiting, but can progress to chronic constrictive pericarditis

Pericardial effusion
Accumulation of fluid in the pericardial cavity
May be transudate May be exudate May be blood

Not clinically significant other than to indicate underlying disorder, unless: Pressure becomes sufficient to cause cardiac compression cardiac tamponade

Outcome depends on how fast fluid accumulates.

If development is slow, pericardium can stretch If develops quickly, even 50 -100 ml of fluid can cause problems When pressure in pericardium = diastolic pressure, get filling of right atrium, filling of ventricles, cardiac output circulatory collapse.
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Clinical manifestations
Pulsus paradoxus B.P. higher during expiration than inspiration by 10 mm Hg Distant or muffled heart sounds Dyspnea on exertion Dull chest pain Observable by x-ray or ultrasound

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Treatment
Pericardiocentesis Treat pain Surgery if cause is aneurysm or trauma

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Constrictive (chronic) pericarditis

Years ago, synonymous with T.B. Today, usually idiopathic, or associated with radiation exposures, rheumatoid arthritis, uremia, or coronary bypass graft

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Pathophysiology:
Fibrous scarring with occasional calcification of pericardium Causes parietal and visceral layers to adhere Pericardium becomes rigid, compressing the heart C.O. Stenosis of veins entering atria Always develops gradually
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Symptoms and Signs

Exercise intolerance Dsypnea on exertion Fatigue Anorexia

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Clinical manifestations
Weight loss Edema and ascites Distention of jugular vein (Kussmaul sign) Enlargement of the liver and/or spleen ECG shows inverted T wave and atrial fibrillation Can be seen on imaging
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Treatment
Drugs and diet Digitalis Diuretics Sodium restriction Surgery to remove restrictive pericardium

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Cardiomyopathies
Disorders of the heart muscle Most cases idiopathic Many due to ischemic heart disease and hypertension. Three categories:
Dilated ( formerly, congestive) Hypertrophic Restrictive

Heart loses effectiveness as a pump

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Dilated cardiomyopathy

C.O.; thrombi formation ; contractility, and mitral valve incompetence, arrhythmias Tx: relieve symptoms of heart failure, decrease 18 workload, and anticoagulants; transplants

Hypertrophic Cardiomyopathy

C.O. is normal, inflow resistance, and mitral valve incompetence, arrhythmais and sudden death.
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Restrictive cardiomyopathy

Reduced diastolic compliance of the ventricle. C.O. is normal or; formation of thrombi, dilation of left atrium, and mitral valve 20 incompetence.

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Disorders of the Endocardium: Valvular dysfunction

Endocardial disorders damage heart valves Changes can lead to : Valvular Stenosis = too narrow Valvular Regurgitation = too leaky (or insufficiency or incompetence)

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Valves that are most often affected are the mitral and aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve. Heart Murmur sound caused by turbulent blood flow through damaged valves.

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Both types of valve disorders:

Cause increased cardiac work, and increased volumes and pressures in the chambers. This leads to chamber dilation and hypertrophy. Chamber dilation and myocardial hypertrophy are compensatory mechanisms to increase the pumping capability of the heart. Eventually, the heart fails from overwork
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Aortic Stenosis
Three common causes:
Rheumatic heart disease -Streptococcus infection damage by bacteria and autoimmune response Congenital malformation Degeneration resulting from calcification

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Aortic Stenosis
Blood flow obstructed from LV into aorta during systole Causes increased work of LV LV dilation & hypertrophy as compensation prolonged contractions as compensation Finally heart overwhelmed increased pressures in LA, then lungs, then right heart
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Clinical manifestations
Develops gradually Decreased stroke volume Reduced systolic blood pressure Narrowed pulse pressure Heart rate often slow and pulse faint Crescendo-decrescendo heart murmur Angina, dizziness, syncope, fatigue Can lead to dysrhythmias, myocardial infarction, and left heart failure
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Mitral Stenosis
Most common of all valve disorders Usually the result of rheumatic fever or bacterial endocarditis During healing the orifice narrows, the valves become fibrous and fused, and chordae tendineae become shortened Get decreased flow from LA to LV during filling Results in hypertrophy of LA
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By causing LA to become pump: Get increased pulmonary vascular pressures; pressures increase through LA into lung pulmonary congestion lung tissue changes to accommodate increased pressures increased pressure in pulmonary artery increased pressure in right heart right heart failure
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Clinical Manifestations
Atrial enlargement can be seen on x-ray Rumbling decrescendo diastolic murmur, and accentuated first heart sound Dyspnea Tachycardia and risk of atrial fibrillation Other signs and symptoms are of pulmonary congestion and right heart failure
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Aortic Regurgitation
Caused by acute or chronic lesion of rheumatic fever, bacterial endocarditits, syphilis, hypertension, connective tissue disorder (e.g.Marfan syndrome) or atherosclerosis

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 Reflux of blood from aorta to LV during ventricular relaxation. Causes LV to pump more blood w/ each contraction LV hypertrophy LV takes on globular shape increased pressures in LA, lung, right heart

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Clinical manifestations
Widened pulse pressure Prominent carotid pulsations and throbbing peripheral pulses Palpitations Fatigue Dyspnea Angina High-pitched or blowing heart sound during diastole
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Mitral Regurgitation
Causes: mitral valve prolapse, rheumatic heart disease, infective endocarditis, connective tissue disorders, and cardiomyopathy Permits backflow of blood from the LV into the LA during ventricular systole Loud pansystolic murmur that radiates into the back and axilla
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Causes blood to flow simultaneously to aorta and back to LA. Both LV and LA pump harder to move same blood twice
LV hypertrophy and dilation as compensation Compensation works awhile, then see C.O. heart failure Also LA hypertrophy
increased pressures through lungs pressures in right heart right heart failure

Can see edema, shock

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Clinical Manifestations
Weakness and fatigue Dyspnea Palpitations

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Mitral Valve Prolapse

Cusps of valve billow upward into the LA during ventricular systole Mitral regurgitation can occur Most common valve disorder in U.S. Studies suggest an autosomal dominant inheritance pattern Many cases completely asymptomatic Regurgitant murmur or midsystolic click
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Clinical manifestations
Palpitations Tachycardia Light-headedness, syncope, fatigue, weakness Chest tightness, hyperventilation Anxiety, depression, panic attacks Atypical chest pain
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Once considered to be a psychiatric malady May have an autonomic dysfunction in which large quantities of catecholamines are produced. May be a normal variant Can see:
chorda rupture ventricular failure systemic emboli and sudden death

actually associated with minimal morbidity and mortality

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Management
Echocardiography for diagnosis Related to degree of regurgitation Antibiotics before invasive procedures blockers to relieve syncope, severe chest pain, or palpitations Avoid hypovolemia Surgical repair
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General Treatment for Valve disorders

Antibiotics for Strep Anti-inflammatories for autoimmune disorder Analgesics for pain Restrict physical activity Valve replacement surgery

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Heart failure
Definition When heart as a pump is insufficient to meet the metabolic requirements of tissues. Acute heart failure
65% survival rate

Chronic heart failure

Most common cause is ischemic heart disease
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Ischemic Heart Disease

Coronary Artery Disease (CAD), myocardial ischemia and myocardial infarction are progression of conditions that impair the pumping ability of the heart by depriving it of oxygen and nutrients.
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Coronary Artery Disease

Any vascular disorder that narrows or occludes the coronary arteries. Most common cause is atherosclerosis

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The arteries that supply the heart are the first branches off the aorta Coronary artery disease decreases the blood flow to the cardiac muscle. Persistent ischemia or complete occlusion leads to hypoxia. Hypoxia can cause tissue death or infarction, which is a heart attack, which accounts for about one third of all deaths in U.S.

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Risk Factors
Hyperlipidemia Hypertension Diabetes mellitus Genetic predisposition Cigarette smoking Obesity Sedentary life-style Heavy alcohol consumption Higher risk for males than premenopausal women
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Myocardial Ischemia
Myocardial cell metabolic demands not met Time frame of coronary blockage:
10 seconds following coronary block Decreased strength of contractions Abnormal hemodynamics See a shift in metabolism, so within minutes: Anaerobic metabolism takes over Get build-up of lactic acid, which is toxic within the cell Electrolyte imbalances Loss of contractibility
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 20 minutes after blockage Myocytes are still viable, so If blood flow is restored, and increased aerobic metabolism, and cell repair, Increased contractility About 30-45 minutes after blockage, if no relief Cardiac infarct & cell death

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Clinical Manifestations
May hear extra, rapid heart sounds ECG changes:
T wave inversion ST segment depression
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Chest Pain
First symptom of those suffering myocardial ischemia. Called angina pectoris (angina pain) Feeling of heaviness, pressure Moderate to severe In substernal area Often mistaken for indigestion May radiate to neck, jaw, left arm/ shoulder
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Due to :
Accumulation of lactic acid in myocytes or Stretching of myocytes

Three types of angina pectoris:

Stable, unstable and Prinzmetal

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Stable angina pectoris

Caused by chronic coronary obstruction Recurrent predictable chest pain Gradual narrowing and hardening of vessels so that they cannot dilate in response to increased demand of physical exertion or emotional stress Lasts approx. 3-5 minutes Relieved by rest and nitrates
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Prinzmetal angia pectoris (Variant angina)

Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%) Occurs unpredictably and almost exclusively at rest. Often occurs at night during REM sleep May result from hyperactivity of sympathetic nervous system, increased calcium flux in muscle or impaired production of prostaglandin

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Unstable Angina pectoris

Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing angina May indicate a progression to M.I.

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Silent Ischemia
Totally asymptomatic May be due abnormality in innervation Or due to lower level of inflammatory cytokines

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Treatment
Pharmacologically manipulate blood pressure, heart rate, and contractility to decrease oxygen demands

Nitrates dilate peripheral blood vessels and

Decrease oxygen demand Increase oxygen supply Relieve coronary spasm
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blockers: Block sympathetic input, so Decrease heart rate, so Decrease oxygen demand

Digitalis Increases the force of contraction Calcium channel blockers Antiplatelet agents (aspirin, etc.)
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Surgical treatment
Angioplasty mechanical opening of vessels Revascularization bypass Replace or shut around occluded vessels

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Myocardial infarction
Necrosis of cardiac myocytes
Irreversible Commonly affects left ventricle Follows after more than 20 minutes of ischemia

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Structural, functional changes

Decreased contractility Decreased LV compliance Decreased stroke volume Dysrhythmias Inflammatory response is severe Scarring results
Strong, but stiff; cant contract like healthy cells
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Clinical manifestations
Sudden, severe chest pain
Similar to pain with ischemia, but stronger Not relieved by nitrates Radiates to neck, jaw, shoulder, left arm

Indigestion, nausea, vomiting Fatigue, weakness, anxiety, restlessness and feelings of impending doom. Abnormal heart sounds possible (S3,S4)

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 Blood test show several markers:

Leukocytosis Increased blood sugar Increased plasma enzymes Creatine kinase Lactic dehydrogenase Aspartate aminotransferase (AST or SGOT)

Cardiac-specific troponin

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ECG changes
Pronounced, persisting Q waves ST elevation T wave inversion

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Treatment
First 24 hours crucial Hospitalization, bed rest ECG monitoring for arrhythmias Pain relief (morphine, nitroglycerin) Thrombolytics to break down clots Administer oxygen Revascularization interventions: by-pass grafts, stents or balloon angioplasty
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