– A chronic or acute inflammation of the parietal and visceral layers of the pericardium and outer myocardium.
Causes and Incidence
Pericarditis is most commonly idiopathic in origin but may result from viral, bacterial, fungal or parasitic pathogens from infective diseases (AIDS, tuberculosis, influenza, histoplasmosis); underlying connective tissue disorders (systemic lupus erythematosus, rheumatoid arthritis, rheumatic fever, scleroderma, periarteritis); neoplastic disease (breast cancer, lymphoma, bronchogenic cancer); metabolic disease (renal failure, myxedema); postmyocardial infarction; trauma to the chest cavity; chest surgery or hemodialysis; drugs (procainamide or phenytoin); and irradiation. Any individual with one of the above causative agents is at risk. All age groups and races and both genders are vulnerable. Pericarditis is the most common manifestation in those with AIDS.
Inflammation of the pericardium occurs by irritation or by direct extension of another disease state. The normally clear fluid in the pericardial sac is filled with an exudate of fibrin, WBCs, and endothelial cells, which coat the parietal and visceral layers of the pericardium. Friction occurs between the layers, setting up an inflammatory process in the surrounding tissues. This process may remain localized or become widespread. Pericarditis may be fibrinous or may create a pleural effusion that is serous, sanguineous, hemorrhagic, or purulent. Chronic pericarditis leads to pericardial thickening, adhesions, and scarring, which may in time calcify, rendering the pericardium useless. This impedes the diastolic filling of the heart, reduces stroke volume, and decreases cardiac output.
Retrosternal or precordial chest pain radiating to the neck and back; pleuritic pain that increases on inspiration and in a horizontal position; shallow, rapid breathing; dyspnea; dysphagia; restlessness; anxiety; fever, chills, and weakness
Asymptomatic unless constriction is present, then symptoms appear with exertional dyspnea; paroxysmal nocturnal dyspnea; fatigue; peripheral edema; orthopnea; cough
Rapidly forming effusion interferes with cardiovascular dynamics and leads to cardiac tamponade, shock, and cardiovascular collapse if not treated immediately. Chronic disease leads to cardiac and liver failure.
History of pain; elevated WBCs, erythrocyte sedimentation rate; blood or urine culture to identify organism if infectious process is involved; electrocardiography (ECG); early ST-T segment elevation, PR interval depression, QRS voltage decrease; precordial friction rub; enlarging cardiac silhouette on serial chest x-ray studies; echocardiogram to detect pleural effusion
Pericardial knock on auscultation; calcification on x-ray study; enlarged cardiac silhouette; ECG: widened P wave in leads I, II, and V6, deep Q waves, flattened or inverted T waves; magnetic resonance imaging shows thickened pericardium; echocardiogram shows presence of effusion
Pericardiocentesis to remove fluid, pus, or blood from pericardium in acute effusive disease or tamponade; pericardiectomy to remove visceral and parietal pericardium in chronic constrictive disease.
Antiinfective drugs to treat underlying infection; antiinflammatory drugs for effusion, fever, and pain; analgesics for pain; diuretics for chronic congestion; anticoagulants are contraindicated, because they can cause intrapericardial bleeding and contribute to tamponade.
Treatment of underlying disease; acute: cardiac monitoring for complications; bed rest; adequate hydration; comfort measures; chronic: restricted activity; instruction about surgery.