Increasing RV pressures causes diastolic RV-to-LV interdependence dependent on an intact pericardium, whereas increasing LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium.
The determinants of systolic and diastolic ventricular interdependence differ, with diastolic RV-to-LV interdependence depending on an intact pericardium, while systolic LV-to-RV interdependence is pericardium-independent.
New Findings What is the central question of this study? Are the mechanisms that cause ventricular interdependence different when due to primary right to left ventricular pressure loading? What is the main finding and its importance? An instantaneous selective increase in aortic pressure causes an immediate increase in right ventricular end‐systolic pressure independent of the pericardium, whereas a selective increase in pulmonary artery pressure decreases left ventricular diastolic compliance owing to a subsequent increasing right ventricular end‐diastolic volume as a function of an intact pericardium limiting biventricular volume. Changes in contraction synchrony of either ventricle do not appear to be causing these effects. Abstract I characterized the dynamic factors determining ventricular interdependence with and without the pericardium. I measured right (RV) and left ventricular (LV) pressures and volumes simultaneously using conductance catheters in seven pentobarbitone‐anaesthetized open‐chested 5‐ to 7‐week‐old piglets. I studied these effects during apnoea, inferior vena caval occlusion and rapid partial aortic and pulmonary arterial occlusions. Conductance catheter‐defined long‐axis regional volumes were assessed to define regional contractile synchrony. Closed‐pericardium measures were made from an initial (baseline) volume, then after two 20 ml kg −1 fluid loads followed by an open‐pericardium step. Baseline RV and LV volumes were similar. Aortic occlusion increased LV pressures and volumes and RV end‐systolic pressure such that RV end‐systolic elastance increased without changes in RV contraction synchrony, not affected by the pericardium. Pulmonary artery occlusion increased RV end‐systolic pressure but not end‐systolic volume. On the subsequent beat, RV end‐diastolic pressure increased, whereas LV end‐diastolic volume and diastolic compliance decreased. These effects were attenuated by opening the pericardium. Contraction synchrony across longitudinal segments was unaltered by either aortic or pulmonary artery occlusion. I conclude that the determinants of systolic and diastolic ventricular interdependence are different. Increasing RV pressures causes diastolic RV‐to‐LV interdependence, decreasing LV diastolic compliance and dependent on an intact pericardium. An increase in LV end‐systolic pressure increases RV end‐systolic elastance independent of the pericardium and has a minimal effect on RV diastolic function or contraction synchrony.
Michael R. Pinsky (Thu,) conducted a other in Ventricular interdependence (n=7). Aortic and pulmonary arterial occlusions vs. Baseline / intact pericardium was evaluated on Right and left ventricular pressures and volumes. Increasing RV pressures causes diastolic RV-to-LV interdependence dependent on an intact pericardium, whereas increasing LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium.