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13 Cards in this Set

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is inflammation of the pericardium, often with fluid accumulation. Pericarditis may be caused by many disorders (eg, infection, MI, trauma, tumors, metabolic disorders) but is often idiopathic. Symptoms include chest pain or tightness, often worsened by deep breathing. Cardiac output may be greatly reduced. Diagnosis is based on symptoms, a friction rub, ECG changes, and evidence of pericardial fluid accumulation on x-ray or echocardiogram. Finding the cause requires further evaluation. Treatment depends on the cause, but general measures include analgesics, anti-inflammatory drugs, and sometimes surgery.
Acute pericarditis
tends to cause chest pain and a pericardial rub, sometimes with dyspnea. The first evidence can be tamponade, with hypotension, shock, or pulmonary edema.

Because the innervation of the pericardium and myocardium is the same, the chest pain of pericarditis is sometimes similar to that of myocardial inflammation or ischemia: Dull or sharp precordial or substernal pain may radiate to the neck, trapezius ridge (especially the left), or shoulders. Pain ranges from mild to severe. Unlike ischemic chest pain, pain due to pericarditis is usually aggravated by thoracic motion, cough, breathing, or swallowing food; it may be relieved by sitting up and leaning forward. Tachypnea and nonproductive cough may be present; fever, chills, and weakness are common. In 15 to 25% of patients with idiopathic pericarditis, symptoms recur intermittently for months or years.
Pericardial effusion
is often painless, but when it occurs with acute pericarditis, pain may be present. Typically, heart sounds are muffled. A pericardial rub may be heard. With large effusions, compression of the base of the left lung can decrease breath sounds (heard near the left scapula) and produce crackles (rales). Arterial pulse, jugular venous pulse, and BP are normal unless intrapericardial pressure increases substantially, causing tamponade.
Cardiac tamponade
The clinical findings are similar to those of cardiogenic shock: decreased cardiac output, low systemic arterial pressure, tachycardia, and dyspnea. Neck veins are markedly dilated. Severe cardiac tamponade is nearly always accompanied by a fall of > 10 mm Hg in systolic BP during inspiration (pulsus paradoxus—see Approach to the Cardiac Patient: Pulsus paradoxus). In advanced cases, pulse may disappear during inspiration. (However, pulsus paradoxus can also occur in COPD, bronchial asthma, pulmonary embolism, right ventricular infarction, and noncardiogenic shock.) Heart sounds are muffled unless the effusion is small.
Constrictive pericarditis
Fibrosis or calcification rarely produces symptoms unless constrictive pericarditis develops. The only early abnormalities may be elevated ventricular diastolic, atrial, pulmonary, and systemic venous pressures. Symptoms and signs of peripheral venous congestion (eg, peripheral edema, neck vein distention, hepatomegaly) may appear with an early diastolic sound (pericardial knock), often best heard during inspiration. This sound is due to abrupt slowing of diastolic ventricular filling by the rigid pericardium. Ventricular systolic function (based on ejection fraction) is usually preserved. Prolonged elevation of pulmonary venous pressure results in dyspnea (particularly during exertion) and orthopnea. Fatigue may be severe. Distention of neck veins with a rise in venous pressure during inspiration (Kussmaul's sign) is present; it is absent in tamponade. Pulsus paradoxus is rare and is usually less severe than in tamponade. Lungs are not congested unless severe left ventricular constriction develops.
usually refers to infection of the endocardium (ie, infective endocarditis). The term can also include noninfective endocarditis, in which sterile platelet and fibrin thrombi form on cardiac valves and adjacent endocardium. Noninfective endocarditis sometimes leads to infective endocarditis. Both can result in embolization and impaired cardiac function.
Infective endocarditis
is infection of the endocardium, usually with bacteria (commonly, streptococci and staphylococci) or fungi. It produces fever, heart murmurs, petechiae, anemia, embolic phenomena, and endocardial vegetations. Vegetations may result in valvular incompetence or obstruction, myocardial abscess, or mycotic aneurysm. Diagnosis requires demonstration of microorganisms in blood and usually echocardiography. Treatment consists of prolonged antimicrobial treatment and sometimes surgery.
Noninfective endocarditis (nonbacterial thrombotic endocarditis)
refers to formation of sterile platelet and fibrin thrombi on cardiac valves and adjacent endocardium in response to trauma, circulating immune complexes, vasculitis, or a hypercoagulable state. Symptoms are those of systemic arterial embolism. Diagnosis is by echocardiography and negative blood cultures. Treatment consists of anticoagulants.
Cor pulmonale
is right ventricular enlargement secondary to a lung disorder that produces pulmonary artery hypertension. Right ventricular failure follows. Findings include peripheral edema, neck vein distention, hepatomegaly, and a parasternal lift. Diagnosis is clinical and by echocardiography. Treatment is directed at the cause.
Dilated Congestive Cardiomyopathy
is myocardial dysfunction producing heart failure in which ventricular dilation and systolic dysfunction predominate. Symptoms include dyspnea, fatigue, and peripheral edema. Diagnosis is clinical and by chest x-ray and echocardiography. Treatment is directed at the cause; heart transplantation may be needed.
Heart failure
is a syndrome of ventricular dysfunction. Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid accumulation; both ventricles are usually involved to some extent. Diagnosis is clinical, supported by chest x-ray and echocardiography. Treatment includes diuretics, ACE inhibitors, β-blockers, and correction of the underlying disorder.
Hypertrophic cardiomyopathy
is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction but without increased afterload (eg, valvular aortic stenosis, coarctation of the aorta, systemic hypertension). Symptoms include chest pain, dyspnea, syncope, and sudden death. A systolic murmur, increased by Valsalva maneuver, is typically present in the hypertrophic obstructive type. Diagnosis is by echocardiography. Treatment is with β-blockers, verapamil, disopyramide, and sometimes chemical reduction or surgical removal of outflow tract obstruction.
Restrictive cardiomyopathy
is characterized by noncompliant ventricular walls that resist diastolic filling; one or both ventricles, most commonly the left, may be affected. Symptoms include fatigue and exertional dyspnea. Diagnosis is by echocardiography. Treatment is often unsatisfactory and is best directed at the cause. Surgery is sometimes useful.