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The normal pericardium is a double-layered sac; the visceral pericardium is a serous membrane that is separated by a small quantity (15–50 mL) of fluid, an ultrafiltrate of plasma, from the fibrous parietal pericardium. The normal pericardium, by exerting a restraining force, prevents sudden dilation of the cardiac chambers, especially the right atrium and ventricle, during exercise and with hypervolemia. It also restricts the anatomic position of the heart, minimizes friction between the heart and surrounding structures, prevents displacement of the heart and kinking of the great vessels, and probably retards the spread of infections from the lungs and pleural cavities to the heart. Nevertheless, total absence of the pericardium, either congenital or after surgery, does not produce obvious clinical disease. In partial left pericardial defects, the main pulmonary artery and left atrium may bulge through the defect; very rarely, herniation and subsequent strangulation of the left atrium may cause sudden death.




Acute pericarditis, by far the most common pathologic process involving the pericardium, may be classified both clinically and etiologically (Table 22-1). There are four principal diagnostic features:


  1. Chest pain is an important but not invariable symptom in various forms of acute pericarditis (Chap. 4); it is usually present in the acute infectious types and in many of the forms presumed to be related to hypersensitivity or autoimmunity. Pain is often absent in slowly developing tuberculous, postirradiation, neoplastic, and uremic pericarditis. The pain of acute pericarditis is often severe, retrosternal and left precordial, and referred to the neck, arms, or left shoulder. Often the pain is pleuritic, consequent to accompanying pleural inflammation (i.e., sharp and aggravated by inspiration and coughing), but sometimes it is a steady, constricting pain that radiates into either arm or both arms and resembles that of myocardial ischemia; therefore, confusion with acute myocardial infarction (AMI) is common. Characteristically, however, pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine. The differentiation of AMI from acute pericarditis becomes perplexing when, with acute pericarditis, serum biomarkers of myocardial damage such as creatine kinase and troponin rise, presumably because of concomitant involvement of the epicardium in the inflammatory process (an epi-myocarditis) with resulting myocyte necrosis. However, these elevations, if they occur, are quite modest given the extensive electrocardiographic ST-segment elevation in pericarditis. This dissociation is useful in differentiating between these conditions.

  2. A pericardial friction rub is audible in about 85% of these patients, may have up to three components per cardiac cycle, is high pitched, and is described as rasping, scratching, or grating (Chap. 9); it can be elicited sometimes when the diaphragm of the stethoscope is applied firmly to the chest wall at the left lower sternal border. It is heard most frequently at end expiration with the patient upright and leaning forward. The rub ...

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