Chapter 116: Pericardial Disease

Etiologies

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 (See Table 116-1). Typical pain may not be present in slowly developing pericarditis (e.g., tuberculous, post-irradiation, neoplastic, uremic).

Physical Examination

Rapid or irregular pulse, coarse pericardial friction rub, which may vary in intensity and is loudest with pt sitting forward.

Laboratory ECG

Diffuse ST elevation (concave upward) usually present in all leads except aVR and V₁; PR-segment depression (and/or PR elevation in lead aVR) may be present; days later (unlike acute MI), ST returns to baseline and T-wave inversion develops (See Table 116-2 and Fig. 116-1). Atrial premature beats and atrial fibrillation may appear. Differentiate from ECG of early repolarization (ER) (ratio of ST elevation/T wave height <0.25 in ER, but >0.25 in pericarditis).

CXR

Symmetrically increased size of cardiac silhouette if large (>250 mL) pericardial effusion is present.

Echocardiogram

Most readily available test for detection of pericardial effusion, which commonly accompanies acute pericarditis.

Life-threatening condition 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, viral or idiopathic pericarditis), cardiac trauma, or myocardial perforation during intravascular procedures.

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 may be 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. Doppler shows marked respiratory variation of transvalvular flow velocities.

Cardiac Catheterization

Confirms diagnosis; shows elevated pericardial pressure with equalization of diastolic pressures in all cardiac chambers.

Condition in which a rigid pericardium impairs cardiac filling, causing 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 (mostly in developing nations), previous cardiac surgery, collagen vascular disorders, uremia, neoplastic, and radiation-associated pericarditis are potential causes.

History

Gradual onset of dyspnea, fatigue, pedal edema, abdominal swelling; symptoms of LV failure uncommon.

Physical Examination

Tachycardia, jugular venous distention (with prominent y descent) that increases further on inspiration (Kussmaul 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 is most common in tuberculous pericarditis.

Echocardiogram

Thickened pericardium, normal ventricular contraction; abrupt halt in ventricular filling in early diastole. Dilatation of IVC is common. Dramatic effects of respiration are typical: During inspiration the ventricular septum shifts to the left with prominent reduction of blood flow velocity across mitral valve; pattern reverses during expiration.

CT or MRI

More precise than echocardiogram for demonstrating thickened pericardium (present in >80% of pts with constrictive pericarditis).

Cardiac Catheterization

Equalization of diastolic pressures in all chambers; ventricular pressure tracings show “dip and plateau” appearance. Differentiate from restrictive cardiomyopathy (Table 116-3).