F Pericardial disease
This section focuses on the pathophysiology, clinical presentation, and anesthetic implications of three primary pericardial disease processes: acute pericarditis, constrictive pericarditis, and cardiac tamponade.
The pericardium surrounds the heart and anchors it to its anatomic position, concomitantly reducing contact between it and surrounding structures. It consists of an inner visceral layer, which envelops the surface of the heart, and an outer parietal layer. The pericardial space between these layers usually contains 20 to 25 mL of clear fluid, which under normal circumstances can accommodate gradual volume fluctuations. Rapid accumulation of pericardial fluid in the pericardial space can result in cardiac tamponade and cardiovascular collapse.
Etiology
Acute inflammation of the pericardium is caused by a number of disorders. The most common cause of acute pericarditis is viral infection. Post-MI syndrome (Dressler syndrome), postcardiotomy, metastatic disease, irradiation, tuberculosis, and rheumatoid arthritis represent the remaining primary predisposing conditions that contribute to the development of this process.
Pathophysiology
It is common for a serofibrinous inflammatory reaction associated with a small intrapericardial exudative effusion to evolve. This may result in adherence of the two layers of the pericardium. The sequelae are largely dependent on the severity of the reaction as well as on the specific cause. Most often when the condition is left untreated or undiagnosed, complete resolution is the end result. Infrequently, however, extended organization of fibrinous exudate within the pericardial sac may lead to encasement of the heart by dense fibrous connective tissue (chronic constrictive pericarditis) or to the accumulation of a large amount of pericardial fluid and consequent cardiac tamponade, usually when fluid levels exceed 1 L. Constrictive pericarditis and cardiac tamponade result in impaired diastolic filling and subsequent diminution of CO.
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