120 PERICARDIAL DISEASE
Harrison’s Manual of Medicine
CAUSES See Table 120-1
Table 120-1 Most Common Causes of Pericarditis
HISTORY Chest pain, which may be intense, mimicking acute MI, but characteristically sharp, pleuritic, and positional (relieved by leaning forward); fever and palpitations are common.
PHYSICAL EXAMINATION Rapid or irregular pulse, coarse pericardial friction rub, which may vary in intensity and is loudest with pt sitting forward.
LABORATORY ECG (See Table 120-2 and Fig. 120-1) Diffuse ST elevation (concave upward) usually present in all leads except aVR and V1; PR-segment depression may be present; days later (unlike acute MI), ST returns to baseline and T-wave inversion develops. Atrial premature beats and atrial fibrillation may appear. Differentiate from ECG of early repolarization variant (ERV) (ST-T ratio <0.25 in ERV, but >0.25 in pericarditis).
Table 120-2 ECG in Acute Pericarditis vs. Acute (Q-wave) MI
FIGURE 120-1. Electrocardiogram in acute pericarditis. Note diffuse ST-segment elevation and PR-segment depression.
CXR Increased size of cardiac silhouette if large (>250 mL) pericardial effusion is present, with “water bottle” configuration.
Echocardiogram Most sensitive test for detection of pericardial effusion, which commonly accompanies acute pericarditis.
Aspirin 650–975 mg qid or NSAIDs (e.g., indomethacin 25–75 mg qid); for severe, refractory pain, prednisone 40–60 mg/d is used and tapered over several weeks or months. Intractable, prolonged pain or frequently recurrent episodes may require pericardiectomy. Anticoagulants are relatively contraindicated in acute pericarditis because of risk of pericardial hemorrhage.
Life-threatening emergency resulting from accumulation of pericardial fluid under pressure; impaired filling of cardiac chambers and decreased cardiac output.
ETIOLOGY Previous pericarditis (most commonly metastatic tumor, uremia, acute MI, viral or idiopathic pericarditis), cardiac trauma, or myocardial perforation during catheter or pacemaker placement.
HISTORY Hypotension may develop suddenly; subacute symptoms include dyspnea, weakness, confusion.
PHYSICAL EXAMINATION Tachycardia, hypotension, pulsus paradoxus (inspiratory fall in systolic blood pressure >10 mmHg), jugular venous distention with preserved x descent, but loss of y descent; heart sounds distant. If tamponade develops subacutely, peripheral edema, hepatomegaly, and ascites are frequently present.
LABORATORY ECG Low limb lead voltage; large effusions may cause electrical alternans (alternating size of QRS complex due to swinging of heart).
CXR Enlarged cardiac silhouette if large (>250 mL) effusion present.
Echocardiogram Swinging motion of heart within large effusion; prominent respiratory alteration of RV dimension with RA and RV collapse during diastole.
Cardiac Catheterization Confirms diagnosis; shows equalization of diastolic pressures in all four chambers; pericardial = RA pressure.
Immediate pericardiocentesis and IV volume expansion.
Rigid pericardium leads to impaired cardiac filling, elevation of systemic and pulmonary venous pressures, and decreased cardiac output. Results from healing and scar formation in some pts with previous pericarditis. Viral, tuberculosis, previous cardiac surgery, uremia, neoplastic pericarditis are most common causes.
HISTORY Gradual onset of dyspnea, fatigue, pedal edema, abdominal swelling; symptoms of LV failure uncommon.
PHYSICAL EXAMINATION Tachycardia, jugular venous distention (prominent y descent), which increases further on inspiration (Kussmaul’s sign); hepatomegaly, ascites, peripheral edema are common; sharp diastolic sound, “pericardial knock” following S2 sometimes present.
LABORATORY ECG Low limb lead voltage; atrial arrhythmias are common.
CXR Rim of pericardial calcification in up to 50% of pts.
Echocardiogram Thickened pericardium, normal ventricular contraction; abrupt halt in ventricular filling in early diastole.
CT or MRI More precise than echocardiogram in demonstrating thickened pericardium.
Cardiac Catheterization Equalization of diastolic pressures in all chambers; ventricular pressure tracings show “dip and plateau” appearance (to distinguish from restrictive cardiomyopathy; Table 119-1). Pts with constrictive pericarditis should be investigated for tuberculosis (Chap. 97).
Surgical stripping of the pericardium. Progressive improvement ensues over several months.
Approach to the Patient
With Asymptomatic Pericardial Effusion of Unknown Cause
If careful history and physical exam do not suggest etiology, the following may lead to diagnosis:
Skin test and cultures for tuberculosis (Chap. 97)
Serum albumin and urine protein measurement (nephrotic syndrome)
Serum creatinine and BUN (renal failure)
Thyroid function tests (myxedema)
ANA (SLE and other collagen-vascular disease)
Search for a primary tumor (especially lung and breast)
For a more detailed discussion, see Braunwald E: Pericardial Disease, Chap. 239, p. 1365, in HPIM-15.