• C D Brown, E Chow, and D J Farrar.
• Department of Cardiac Surgery, California Pacific Medical Center, San Francisco 94115.
• Am. J. Physiol. 1993 Nov 1; 265 (5 Pt 2): H1663-9.

AbstractTo 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.

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