Cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy.
The pericardium envelopes the cardiac chambers and under physiological conditions exerts subtle functions, including mechanical effects that enhance normal ventricular interactions that contribute to balancing left and right cardiac outputs. Because the pericardium is non-compliant, conditions that cause intrapericardial crowding elevate intrapericardial pressure, which may be the mediator of adverse cardiac compressive effects. Elevated intrapericardial pressure may result from primary disease of the pericardium itself (tamponade or constriction) or from abrupt chamber dilatation (eg, right ventricular infarction). Regardless of the mechanism leading to increased intrapericardial pressure, the resultant pericardial constraint exerts adverse effects on cardiac filling and output. Constriction and restrictive cardiomyopathy share common pathophysiological and clinical features; their differentiation can be quite challenging. This review will consider the physiology of the normal pericardium and its dynamic interactions with the heart and review in detail the pathophysiology and clinical manifestations of cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy.
Goldstein
James A
JA
Division of Cardiology, William Beaumont Hospital,3601 West Thirteen Mile Road, Royal Oak, MI 48073, USA, jgoldstein@beaumont.edu
D000465:Algorithms; D002305:Cardiac Tamponade / Q000503:physiopathology; D002313:Cardiomyopathy, Restrictive / Q000503:physiopathology; D015150:Echocardiography, Doppler; D006439:Hemodynamics; D006801:Humans; D010490:Pericardial Effusion; D010494:Pericarditis, Constrictive / Q000503:physiopathology; D010496:Pericardium / Q000502:physiology