Left ventricular unloading decreases rate of isovolumic right ventricular pressure decline.

To determine whether direct ventricular interaction affects right ventricular (RV) relaxation, we compared the minimum rate of change of RV pressure (dP/dtmin) and the time constant, tau, of isovolumic RV pressure decline in open-chest, anesthetized pigs following a normal left ventricular (LV) contraction and an acutely unloaded LV contraction. Rapid removal of blood via the LV apex into a prosthetic ventricle during a single systole decreased the LV pressure-time integral 68.3% and peak systolic pressure 49.9% without changing RV end-diastolic conditions. Micromanometers measured ventricular chamber pressures during single RV isovolumic beats, which were produced by transient pulmonary artery occlusion in both the control and the LV-unloaded states. When the LV was unloaded, RV tau rose significantly from 41.7 +/- (SD) 7.1 to 49.8 +/- 9.4 ms, P < 0.005 (pericardium intact) and 42.9 +/- 10.8 to 51.8 +/- 13.9 ms, P < 0.005 (pericardium opened). Simultaneously, RV dP/dtmin decreased from -400.5 +/- 136.6 to -288.3 +/- 46.8 mmHg/s, P = 0.14 (pericardium intact), and -342.4 +/- 104.2 to -241.2 +/- 118.9 mmHg/s, P < 0.01 (pericardium opened). These data indicate that LV systolic unloading decreases the rate of RV relaxation. We conclude that RV relaxation is influenced by direct anatomic ventricular interaction.