PERICARDIAL DISEASES - ACUTE PERICARDITIS



Inflammation of the pericardial lining around the heart from a variety of causes is termed acute pericarditis. Its typical manifesta­tions include chest pain, a pericardial friction rub, and characteristic electrocardiographic changes. Chest pain, often localized substernally or to the left of the sternum, is usually worsened by lying down, coughing, and deep inspiration, and is re­lieved somewhat by sitting up and leaning for­ward. There is often adjacent pleural involve­ment. The pericardial friction rub, diagnostic of pericarditis, is a scratchy, high-pitched sound that has from one to three components corresponding to atrial systole, ventricular systole, and early diastolic ventricular filling. The ventricular sys­tolic component is present most consistently. The rub is often transient; its absence does not exclude the diagnosis of pericarditis and its presence does not exclude the existence of a large pericardial effusion. The rub often is best heard with the dia­phragm of the stethoscope as the patient sits for­ward at forced end-expiration. Single-component friction rubs must be differentiated from systolic cardiac murmurs, skin rubbing against the dia­phragm of the stethoscope, and the crunching sound of mediastinal air.

The electrocardiogram may be diagnostic, es­pecially if obtained serially, and reveals ST seg­ment elevation with upright T waves at the onset of chest pain . The ST elevation is char­acteristic in all leads except aVR and Va. The ST segments are often concave upward in distinction to those of acute myocardial infarction, but this distinction is often difficult or impossible to make. Reciprocal ST segment depression as in acute myocardial infarction generally does not occur. Several days later the ST segments char­acteristically return to normal, and the T waves begin to flatten. Subsequently, diffuse T wave in­version develops, usually after the ST segments return to normal, in contrast to the typical pattern of myocardial infarction. Weeks to months later the T waves usually return to normal but may re­main abnormal indefinitely. The PR segment may be depressed, reflecting atrial injury. The ECG changes of acute pericarditis must be distin­guished from early repolarization. Early repolar­ization is common in young patients, usually without PR segment depression, more often as­sociated with sinus bradycardia than the sinus tachycardia of acute pericarditis, and without a characteristic evolution as described above for pericarditis. Atrial rhythm disturbances during pericarditis are common, especially intermittent atrial fibrillation; AV conduction disturbances and ventricular tachyarrhythmias are unusual and should suggest myocardial infarction. If a large pericardial effusion is present, low QRS voltage and electrical alternans may occur.
The chest x-ray is of little value in the diagnosis of acute pericarditis, but an enlarged cardiac sil­houette may be noted if a pericardial effusion is present. Calcification of the pericardium may be detected in patients with long-standing pericar­ditis, especially secondary to tuberculosis. The echocardiogram is extremely accurate for detec­tion and quantitation of pericardial fluid and is also useful to evaluate suspected hemodynamic compromise (tamponade).

Nonspecific indicators of inflammation such as elevated erythrocyte sedimentation rate and leu­kocytosis are usually present. Cardiac isoenzymes are usually normal. Other laboratory tests that may exclude specific diagnoses include blood cultures, acute and convalescent viral serologies, fungal serology (e.g., histoplasmosis), ASO titer (rheumatic fever), cold agglutinins (mycoplasma), electrical alternans may occur.
The chest x-ray is of little value in the diagnosis of acute pericarditis, but an enlarged cardiac sil­houette may be noted if a pericardial effusion is present. Calcification of the pericardium may be detected in patients with long-standing pericar­ditis, especially secondary to tuberculosis. The echocardiogram is extremely accurate for detec­tion and quantitation of pericardial fluid and is also useful to evaluate suspected hemodynamic compromise (tamponade).
Nonspecific indicators of inflammation such as elevated erythrocyte sedimentation rate and leu­kocytosis are usually present. Cardiac isoenzymes are usually normal. Other laboratory tests that may exclude specific diagnoses include blood cultures, acute and convalescent viral serologies, fungal serology (e.g., histoplasmosis), ASO titer (rheumatic fever), cold agglutinins (mycoplasma),

heterophile test (mononucleosis), thyroid func­tion tests (hypothyroidism), BUN and creatinine (uremia), and connective tissue disease screens such as ANA, rheumatoid factor, and comple­ment.
Management of the patient with acute pericar­ditis involves treating its etiology. Patients are usually hospitalized to make sure that myocardial infarction is not present and to watch carefully for the occurrence of cardiac tamponade. Salicy­lates or nonsteroidal anti-inflammatory agents are often effective to relieve, pain. Corticosteroids may be used if necessary, but long-term admin­istration should be avoided. Anticoagulants should not be administered because of the risk of hemopericardium. In rare cases, pericardiectomy may be indicated to relieve recurrent symptoms. Most causes of pericarditis are self-limited, and inflammation abates after two to six weeks. Re­current episodes of pericarditis occur in some patients. Rarely, pericarditis eventually results in pericardial constriction or a combination of ef­fusion and constriction (effusive-constrictive per­icarditis).