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Acute Pericarditis !!navigator!!

History !!navigator!!

Chest pain, which may be intense, mimicking acute MI, but characteristically sharp, pleuritic, positional (relieved by leaning forward). Pain is usually retrosternal or left precordial, radiating to neck, left shoulder, trapezius ridge, and/or arms; fever and palpitations are common. Typical pain may not be present in slowly developing pericarditis (e.g., tuberculous, post-irradiation, neoplastic, uremic).

Physical Examination !!navigator!!

Rapid or irregular pulse, coarse pericardial friction rub (may come and go); is loudest with pt sitting forward.

Laboratory ECG !!navigator!!

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 ST returns to baseline and T-wave inversion then develops (see Table 118-2 ECG in Acute Pericarditis vs Acute ST-Elevation MI and Fig. 118-1. Electrocardiogram in Acute Pericarditis). Distinguish from acute ST elevation MI (in which ST elevations are upwardly convex with reciprocal ST depression in opposite leads, PR depression does not occur, and T wave inversions appear while ST segments are still elevated). Differentiate from ECG of early repolarization (ER) (ratio of ST elevation/T wave height <0.25 in ER, but >0.25 in pericarditis). Atrial premature beats and atrial fibrillation are common.

CXR !!navigator!!

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

Echocardiogram !!navigator!!

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

TREATMENT

Acute Pericarditis

Aspirin 650-975 mg qid or other NSAIDs (e.g., ibuprofen 600-800 mg tid or indomethacin 25-50 mg tid; at higher doses, consider gastric protection, e.g., omeprazole 20 mg daily); addition of colchicine 0.5 mg bid (0.5 mg once daily if weight <70 kg) enhances response and reduces frequency of recurrences. For severe, refractory pain, glucocorticoids (e.g., prednisone) can be prescribed. Intractable, prolonged pain or frequently recurrent episodes may require pericardiectomy. Anticoagulants are relatively contraindicated in acute pericarditis because of risk of pericardial hemorrhage.

Cardiac Tamponade !!navigator!!

Life-threatening condition resulting from accumulation of pericardial fluid under pressure; impaired filling of cardiac chambers and decreased cardiac output.

Etiology !!navigator!!

Previous viral/idiopathic pericarditis, metastatic tumor, uremia, cardiac trauma, myocardial perforation during intravascular procedures, tuberculosis.

History !!navigator!!

Symptoms of hypotension; subacute symptoms include dyspnea, weakness, confusion.

Physical Examination !!navigator!!

Tachycardia, hypotension with pulsus paradoxus (inspiratory fall in systolic blood pressure >10 mmHg), jugular venous distention with preserved x descent but loss of y descent; distant heart sounds. If tamponade develops subacutely, peripheral edema, hepatomegaly, and ascites may be present.

Laboratory: ECG !!navigator!!

Low limb lead voltage; large effusions may cause electrical alternans (alternating size of QRS complex due to swinging of heart).

CXR !!navigator!!

Enlarged cardiac silhouette if large (>250 mL) effusion present.

Echocardiogram !!navigator!!

Swinging motion of heart within large effusion; high pericardial pressure causes cyclical RA indentation and RV diastolic collapse. Doppler shows marked respiratory variation of transvalvular flow velocities.

Cardiac Catheterization !!navigator!!

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

TREATMENT

Cardiac Tamponade

Pericardiocentesis and IV volume expansion.

Constrictive Pericarditis !!navigator!!

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 !!navigator!!

Gradual onset of exertional dyspnea, fatigue, lower extremity edema, abdominal swelling; symptoms of LV failure are uncommon.

Physical Examination !!navigator!!

Tachycardia, jugular venous distention (with prominent y descent) that increases further on inspiration (Kussmaul sign); hepatomegaly, ascites, peripheral edema are common; pulsus paradoxus in 1/3 of pts. A sharp diastolic sound (pericardial knock) following S2 is sometimes present.

Laboratory ECG !!navigator!!

Low limb lead voltage and atrial arrhythmias are common. Atrial fibrillation may appear.

CXR !!navigator!!

Rim of pericardial calcification may be detected (most common in chronic tuberculous pericarditis).

Echocardiogram !!navigator!!

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

CT or MRI !!navigator!!

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

Cardiac Catheterization !!navigator!!

Equalization of diastolic pressures in all chambers; ventricular pressure tracings show “dip and plateau” appearance. Differentiate from restrictive cardiomyopathy (Table 118-3 Noninvasive Features That Differentiate Constrictive Pericarditis from Restrictive Cardiomyopathy).

TREATMENT

Constrictive Pericarditis

Surgical removal of the pericardium. Progressive improvement ensues over several months.

APPROACH TO THE PATIENT

Asymptomatic Pericardial Effusion of Unknown Cause

If careful history and physical examination do not suggest etiology, the following may lead to diagnosis:

  • Testing for tuberculosis (Chap. 97 Tuberculosis and Other Mycobacterial Infections)
  • Serum albumin and urine protein measurement (nephrotic syndrome)
  • Serum creatinine and BUN (uremia)
  • Thyroid function tests (myxedema)
  • Antineutrophil antibodies (SLE and other collagen vascular diseases)
  • Search for a primary tumor (especially lung and breast)

Outline

Section 8. Cardiology