Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload

Abstract

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.

Fig. 1

Instrumentation of the heart. RV, right ventricle; RA, right atrium; PA, pulmonary artery; Ao, aorta: IVC, inferior vena cava.

Fig. 2

A: representative pressure-wall area loops obtained by brief occlusion of the inferior vena cava under baseline conditions (black lines, loops A–D) and at 1 h of recovery (gray lines, loops A’–D’). Only four loops are shown under each condition for clarity. Loops A (baseline) and A’ (recovery) were obtained under steady-state conditions before inferior vena cava occlusion. Note that loop A’ (recovery) has greater end-diastolic wall area and nearly identical end-diastolic pressure compared with loop A (baseline), but loop area (i.e., external work) is 24% lower and RV free wall systolic area reduction is 37% lower at 1 h of recovery compared with baseline. B: regional Frank-Starling relation derived from the data in A, demonstrating a downward and rightward shift in the relation at 1 h of recovery. The definition of preload-adjusted regional external work is shown (see text).

Fig. 3

Correlation of recovery of RV preload-adjusted regional external work 1 h after release of pressure overload with RV systolic pressure (A) or normalized RV free wall area at peak RV pressure (B) during acute pressure overload. ○, Open pericardium, no dobutamine; □, open pericardium + dobutamine; ●, closed pericardium, no dobutamine; ■, closed pericardium + dobutamine.

Fig. 4

Correlation of recovery of RV preload-adjusted regional external work with the dysfunction predictor index (see text for explanation). There was no independent effect on recovery of function due to opening or closing the pericardium or using or not using dobutamine. ○, Open pericardium, no dobutamine; □, open pericardium + dobutamine; ●, closed pericardium, no dobutamine; ■, closed pericardium + dobutamine.