Pressure-Volume Correlates of Left Ventricular Oxygen Consumption in the Hypervolemic Dog

Volume changes in the intact functioning canine left ventricle were induced by whole blood infusion and were measured by the thermodilution technic. Multiple regression analyses were performed to detect significant correlations between hemodynamic variables and left ventricular oxygen consumption. Hemodynamic variables, in addition to the pressure-time integral, ventricular volume, and ventricular work, included estimates of myocardial stress, force, and shortening. The most significant individual correlates of oxygen consumption were the pressure-time integral ( r =0.91) and ventricular end systolic volume ( r =0.81), whereas the interaction of volume with pressure-time, thus approximating wall stress and force, was the most significant variable overall (r=0.93). A number of multiple linear regression models were tested for the prediction of ventricular oxygen consumption. The equation (model E) with the greatest multiple regression coefficient (R=0.947) included heart rate, pressure-time per beat, pressure-time per minute, end systolic volume, and (end systolic volume) 2/3 as independent variables. A less elaborate regression equation including only pressure-time per minute and end systolic volume as independent variables was, however, nearly as accurate as model E in the prediction of oxygen consumption. The addition of estimates of left ventricular work and shortening to these regression models did not further improve the ability to predict oxygen consumption accurately. The relationships between these hemodynamic variables and ventricular oxygen consumption were not altered by pericardiotomy or catecholamine depletion. In the hypervolumic heart acute ventricular dilatation did not occur following pericardiotomy. The results of this study confirm the postulate that an increase in ventricular volume, as well as pressure, will be accompanied by an increase in ventricular oxygen consumption. This in turn implies a relationship between the wall stress or force generated by the myocardium and the energy requirement of contraction.