Myocardial Blood Flow and Oxygen Consumption in Man Early After Valve Replacement

Abstract

Twenty-one patients without demonstrable coronary artery disease have been studied in the first 48 hours after aortic or mitral valve replacement to determine the possible contribution of abnormalities of left ventricular myocardial blood flow and oxygen consumption to the impaired cardiac performance which is sometimes evident in such patients. In the 14 patients making an uneventful recovery (group A), the mean value for left ventricular coronary blood flow (Kety-Schmidt method) in each study period was between 105.9 and 111.2 ml·min –1 ·100 g –1 , and myocardial oxygen consumption between 11.1 and 12.7 ml·min –1 ·100 g –1 , both being higher than in normal resting man. Oxygen extraction was 59 to 69%, and coronary sinus oxygen tension 23 to 29 mm Hg. Lactate extraction was normal. Five patients (group B) required pharmacologic support because of low cardiac output; all had undergone mitral valve replacement. In them, left ventricular coronary blood flow and oxygen consumption were the same as in group A; however, oxygen extraction was greater (68 to 79%), coronary sinus oxygen tension lower (22 to 24 mm Hg) and lactate extraction lower. Patients in group A who underwent mitral replacement (N = 4) had systemic and coronary hemodynamics and metabolism that were as satisfactory as those undergoing aortic replacement, except that left atrial pressure was higher in the first study period. When heart rate was increased from 100 to 128 beats/minute by pacing in five patients in group A, and in two additional patients, myocardial oxygen consumption increased significantly, but in four patients coronary blood flow failed to increase, oxygen extraction increased, and coronary sinus oxygen levels decreased. We conclude that in patients such as those we studied, low cardiac output postoperatively is not the result of low total left ventricular coronary blood flow or myocardial oxygen supply, but may occur in some of these patients at this time from low or absent coronary reserve and added stresses such as those from tachycardia may be met only with the potentially detrimental mechanism of increasing oxygen extraction and reducing coronary venous and myocardial oxygen levels.