Cardiac tamponade in dogs with normal coronary arteries. I. Effect of changing intravascular volume on hemodynamics and myocardial blood flow

Abstract

Intravascular volume expansion has been shown to improve cardiac output in experimental cardiac tamponade. To determine the limitations of intravascular volume manipulation, acute tamponade was created in 20 anesthetized, spontaneously breathing dogs. The intrapericardial volume causing tamponade was determined for each animal, and kept constant. Hemodynamics were recorded with and without tamponade at multiple levels of intravascular volume. During cardiac tamponade, intravascular volume expansion increased cardiac output only in animals which were initially volume-depleted. Volume expansion of normovolemic or hypervolemic animals caused minimal changes in cardiac output, but increased atrial and aortic pressures. Intravascular volume depletion of the normovolemic animal caused a significant decline in cardiac output, in contrast to the trend towards an increased output following phlebotomy of the volume-expanded animals. In general, the benefit of intravascular volume expansion during cardiac tamponade could only be demonstrated when atrial pressures were below 12 mm Hg.

Cardiac tamponade in dogs with normal coronary arteries. II. Myocardial flow and metabolism with moderate and severe hemodynamic impairment

“…Because of the inconsistency of past reports it was considered desirable to measure tissue blood flow and distribution as well as biochemical indices of myocardial ischemia in the same experimental animals. The present results and those reported previously (7) demonstrate that under diverse conditions (normal hemoglobin and blood volume, hemodilution and normovolemia, and hemodilution and hypervolemia) myocardial blood flow during cardiac tamponade is indeed decreased, but in proportion to the fall in cardiac output and myocardial oxygen consumption. Furthermore, there is no evidence of an abnormal left ventricular I/O flow ratio or selective endocardial hypoperfusion, often considered to be the hallmarks of myocardial ischemia, and no change in lactate substrate utilization by the myocardial tissue.…”

N-terminal pro-B-type natriuretic peptide as a marker of disease severity in patients with pericardial effusions

“…It is well known that elevated BNP and NT-proBNP levels may be the result of cardiac ischemia via reduced coronary flow 28) . However, although coronary blood flow is reduced in tamponade, there is no ischemic component because the coronary flow remains in proportion to the reduced work of the heart 29) . Therefore, reduced coronary flow may not be the main impetus behind the elevated NT-proBNP levels observed in the present study.…”