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| AuthorBrian D Hoit, MD | Section EditorsBernard J Gersh, MB, ChB, DPhil, FRCP, MACCJames Hoekstra, MD | Deputy EditorBrian C Downey, MD, FACC |
Topic Outline
INTRODUCTION
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:
In both cardiac tamponade and constrictive pericarditis, cardiac filling is impeded by an external force. The normal pericardium can stretch to accommodate physiologic changes in cardiac volume. However, after its reserve volume is exceeded the pericardium markedly stiffens. An important pathophysiologic feature of both cardiac 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 cardiac tamponade will be reviewed here. Issues related to constrictive pericarditis 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 "Clinical presentation and diagnostic evaluation of acute pericarditis".)
PHYSIOLOGY
In cardiac tamponade, the primary abnormality is compression of all cardiac chambers due to increased pericardial pressure [1,2]. 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 cardiac tamponade progresses, the cardiac chambers become smaller and chamber diastolic compliance is reduced. The following consequences result from this constrained cardiac filling:
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