Normal Functions of the Pericardium
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 239-1). There are four principal diagnostic features:
Chest pain is an important but not invariable symptom in various forms of acute pericarditis (Chap. 12); 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.
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. 227); 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 is often inconstant, and the loud to-and-fro leathery sound may disappear within a few hours, possibly to reappear on the next day. A pericardial rub is heard throughout the respiratory cycle, whereas a pleural rub disappears when respiration is suspended.
The electrocardiogram (ECG) in acute pericarditis without massive effusion usually displays changes secondary to acute subepicardial inflammation (Fig. 239-1). It typically evolves through four stages. In stage 1, there is widespread elevation of the ST segments, often with upward concavity, involving two or three standard limb leads and V2 to V6, with reciprocal depressions only in aVR and sometimes V1, as well as depression of the PR segment below the TP segment reflecting atrial involvement. Usually there are no significant changes in QRS complexes. In stage 2, after several days, the ST segments return to normal, and only then, or even later, do the T waves become inverted (stage 3). Ultimately, weeks or months after the onset of acute pericarditis, the ECG returns to normal in stage 4. In contrast, in AMI, ST elevations are convex, and reciprocal depression is usually more prominent; QRS changes occur, particularly the development of Q waves, as well as notching and loss of R-wave amplitude, and T-wave inversions are usually seen within hours before the ST segments have become isoelectric. Sequential ECGs are useful in distinguishing acute pericarditis from AMI. In the latter, elevated ST segments return to normal within hours (Chaps. 244 and 245).
Early repolarization is a normal variant and may also be associated with widespread ST-segment elevation, most prominent in left precordial leads. However, in this condition the T waves are usually tall and the ST/T ratio is <0.25; importantly, this ratio is higher in acute pericarditis.
Pericardial effusion is usually associated with pain and/or the ECG changes mentioned above, as well as with an enlargement of the cardiac silhouette. Pericardial effusion is especially important clinically when it develops within a relatively short time as it may lead to cardiac tamponade (see below). Differentiation from cardiac enlargement may be difficult on physical examination, but heart sounds may be fainter with pericardial effusion. The friction rub may disappear, and the apex impulse may vanish, but sometimes it remains palpable, albeit medial to the left border of cardiac dullness. The base of the left lung may be compressed by pericardial fluid, producing Ewart's sign, a patch of dullness and increased fremitus (and egophony) beneath the angle of the left scapula. The chest roentgenogram may show a “water bottle” configuration of the cardiac silhouette (Fig. 239-2) but may be normal.
Table 239-1 Classification of Pericarditis
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Table 239-1 Classification of Pericarditis
I. Acute pericarditis (<6 weeks)
- A. Fibrinous
- B. Effusive (serous or sanguineous)
II. Subacute pericarditis (6 weeks to 6 months)
- A. Effusive-constrictive
- B. Constrictive
III. Chronic pericarditis (>6 months)
- A. Constrictive
- B. Effusive
- C. Adhesive (nonconstrictive)
I. Infectious pericarditis
- A. Viral (coxsackievirus A and B, echovirus, mumps, adenovirus, hepatitis, HIV)
- B. Pyogenic (pneumococcus, streptococcus, staphylococcus, Neisseria, ...
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