Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function

Abstract

Approximately 20% of patients who receive left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery have had complications of right ventricular failure. To evaluate this problem in the diseased heart we simulated an LVAD in the operating room by bypassing and unloading the left ventricle with the heart-lung machine before routine open heart surgery. Right ventricular function was assessed in 12 patients with preoperative left ventricular ejection fractions of less than 0.55 (poor left ventricular function) (mean ± SEM 0.40 ± 0.03) and 10 patients with ejection fractions greater than 0.55 (normal left ventricular function ) (0.63 ± 0.02). Measurements before and during left ventricular bypass in the normal left ventricular function group revealed no change in cardiac output (from 5.7 ± 0.6 to 5.8 ± 0.4 liters/min), with a decrease in right ventricular end-diastolic pressure (from 8 ± 2 to 6 ± 1 mm Hg). However, in the poor left ventricular function group, cardiac output was increased significantly during left ventricular bypass from 4.5 ± 0.2 to 5.3 ± 0.4 liters/min and right ventricular end-diastolic pressure was decreased significantly from 13 ± 2 to 8 ± 2 mm Hg. During bypass there were significant reductions in mean pulmonary arterial pressure from 17 ± 3 to 10 ± 2 mm Hg in the normal left ventricular function group and from 27 ± 3 to 12 ± 2 mm Hg in the poor left ventricular function group. These measurements reflect passive changes in pulmonary pressures due to reductions in left ventricular filling pressure during left ventricular bypass. The findings show that acute left ventricular unloading results in unchanged to slightly improved right ventricular function in the normal left ventricular function group and in significantly improved right ventricular function in the poor left ventricular function group, principally due to right ventricular afterload reduction. This demonstrates a potential beneficial effect to the right ventricle in patients with pulmonary venous hypertension secondary to poor left ventricular function. The data suggest that acute unloading of the left ventricle is not the cause of right ventricular failure in patients with LVADs, and the pathophysiology of other causes must be investigated.