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| AuthorBrian D Hoit, MD | Section EditorsBernard J Gersh, MB, ChB, DPhil, FRCPJames Hoekstra, MD | Deputy EditorGordon M Saperia, MD, FACC |
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The normal pericardium is a fibroelastic sac containing a thin layer of fluid that surrounds the heart. When larger amounts of fluid accumulate (pericardial effusion) or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may occur:
An important pathophysiologic feature of both tamponade and constrictive pericarditis is greatly enhanced ventricular interaction or interdependence, in which the hemodynamics of the left and right heart chambers are directly influenced by each other to a much greater degree than normal.
The physiology, clinical presentation, diagnosis, and treatment of the cardiac tamponade will be reviewed here. Issues related to pericardial constriction and the evaluation and management of pericardial diseases that do not compromise hemodynamics are discussed separately. (See "Constrictive pericarditis" and "Diagnosis and treatment of pericardial effusion" and "Evaluation and management of acute pericarditis".)
Tamponade — In tamponade, the primary abnormality is compression of all cardiac chambers due to increased pericardial pressure [2,3]. The pericardium has some degree of elasticity; but once the elastic limit is reached, the heart must compete with the intrapericardial fluid for the fixed intrapericardial volume. As tamponade progresses, the cardiac chambers become smaller and chamber diastolic compliance is reduced. The following consequences result from this increase in constraint to cardiac filling:
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