Pericardial influences on ventricular filling in the conscious dog. An analysis based on pericardial pressure.

Abstract

SUMMARY. Twenty-five dogs were chronically instrumented to investigate the effects of the normal pericardium on cardiac function. Pulse-transit ultrasonic transducers were implanted to measure multiple ventricular dimensions. The pericardium was incised transversely at the base of the heart and precisely reapproximated, so as to disturb its characteristics minimally. One week later, the dogs were studied in the conscious state, and left ventricular, right ventricular, pericardial, and pleural pressures were measured with matched micromanometers. Data were recorded before and after blood volume expansion. Absolute end-diastolic pericardial pressure varied directly with pleural pressure during the respiratory cycle. Transpericardial pressure (pericardial-pleural pressure) varied little with respiration and was related directly to ventricular diameter during the cardiac cycle with peak transpericardial pressure uniformly occurring at end-diastole. With volume infusion, normalized end-diastolic minor axis diameter and left ventricular transmural pressure (left ventricular-pleural pressure) increased significantly from 0.14 ± 0.01 and 9.5 mm Hg ± 1.0 mm Hg, respectively, in the control state to 0.20 ± 0.01 and 19.3 mm Hg ± 1.2 mm Hg after volume loading. End-diastolic transpericardial pressure also increased significantly from 2.3 ± 0.5 mm Hg to 4.1 ± 0.3 mm Hg, and represented approximately 21% of transmural left ventricular pressure. When measurements were obtained sequentially after implantation, transpericardial pressure was initially high but decreased with time, presumably due to pericardial creep. After volume loading, right ventricular end-diastolic transmural pressure averaged 9.6 mm Hg, and pericardial pressure constituted 42% of right ventricular pressure. Thus, pericardial restraining effects may predominantly influence right ventricular filling and affect the left ventricle through series interaction. In the normal conscious dog, transpericardial pressure remains low over the entire physiological range, and the direct influence of the normal pericardium on diastolic filling of the left ventricle appears to be minimal. (Circ Res 54:173-184, 1984)

Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

“…This procedure allowed us to remove the heart gently while leaving most of the pericardial sac intact. After instrumenting the heart (as described below), we popped it back into the pericardial sac and loosely sutured the incision from its inferior margin to the level of the inferior border of the great vessels (Tyson et al, 1984).…”

Right heart pressure does not equal pericardial pressure in the potassium chloride-arrested canine heart in situ.

“…Based on these concepts and direct measurement of pericardial surface pressure with flat balloons, it has been variously suggested that right heart pressure equals3' 4 or nearly equals intrapericardial surface pressure.3 '5 However, if right heart pressure equals the pericardial surface pressure, then the right heart transmural pressure must be zero. From results presented in several earlier reports, one can infer that this is not the case; that is, there seems to be a nonzero transmural right heart pressure.6 10 Unfortunately, none of these experi-ments was designed specifically to test the equality of right heart and pericardial pressures and all of them can be faulted in some way when interpreted in this manner. Nonetheless, this discrepancy suggests the need for a well-controlled experiment designed specifically to test the hypothesis that right heart and pericardial surface pressures are equal.…”

Doppler Echocardiographic Assessment of Right Ventricular Filling Characteristics in Hemodynamically Significant Right Ventricular Infarction

“…early in diastole occurred in the acutely dilated left ventri cle with elevated filling pressures which was induced by microsphere embolization of the left main coronary ar tery and that this redistribution was mediated by pericar dial restraint. Because the pericardial restraining effects predominantly influence the right ventricular filling [20], redistribution of diastolic filling to early in diastole is con sidered to occur much more easily in the right ventricle. Thus, an increased E and a decreased A/E noted in the patients with acute right ventricular infarction would be explained by the pericardial restraint.…”