Acute cardiac tamponade.

N Engl J Med 2003;349:684-90. Copyright © 2003 Massachusetts Medical Society. ardiac tamponade is life-threatening, slow or rapid compres sion of the heart due to the pericardial accumulation of fluid, pus, blood, clots, or gas, as a result of effusion, trauma, or rupture of the heart. 1,2 Because the causes of pericardial disease 1 and thus of tamponade are diverse, clinicians must choose the most probable diagnosis, always anticipating surprises. Thus, traumatic tamponade is most apt to follow cardiac surgery, and tuberculous tamponade is relatively common in Africa but rare in the United States. Understanding the physiological changes produced by tamponade is essential to diagnosis and treatment. 3-12 The primary abnormality is rapid or slow compression of all cardiac chambers as a result of increasing intrapericardial pressure. The pericardial contents first reach the limit of the pericardial reserve volume 6 — the volume that would just distend the pericardium — and the rate of expansion then increases, soon exceeding that of pericardial stretch. Although the pericardium stretches normally over time, at any instant it is inextensible, making the heart compete with the increased pericardial contents for the fixed intrapericardial volume. 6,10 As the chambers become progressively smaller and myocardial diastolic compliance is reduced, cardiac inflow becomes limited, ultimately equalizing mean diastolic pericardial and chamber pressures. 1-3 Key elements are the rate of fluid accumulation relative to pericardial stretch and the effectiveness of compensatory mechanisms. Thus, intrapericardial hemorrhage from wounds or cardiac rupture occurs in the context of a relatively stiff, unyielding pericardium and quickly overwhelms the pericardial capacity to stretch before most compensatory mechanisms can be activated, whereas in the case of a slow increase in pericardial volume as a result of inflammation, 2 liters or more may accumulate before critical, life-threatening tamponade occurs. 13