Abstract
Increasing the ratio of tissue oxygen delivery (DO2) to oxygen consumption can improve the survival of critically ill patients, including those with acute respiratory failure. However, under conditions of ventilation/perfusion mismatch, the use of inotropic or vasodilator drugs to augment cardiac output could, in turn, worsen venous admixture. In a canine model of asymmetric oleic acid-induced pulmonary edema, we examined this possibility by studying the effect of 20 and 40-micrograms/kg doses of parenteral nifedipine on oxygenation variables, venous admixture, and intrapulmonary blood flow distribution. After oleic acid injury, nifedipine caused significant increases in cardiac index by 70% as systemic vascular resistance decreased proportionately by 61%. Stroke volume index (SI) and mean pulmonary arterial pressure increased, while venous admixture and the distribution of intrapulmonary blood flow did not change with nifedipine. However, nifedipine significantly improved the tissue DO2 index so that the coefficient of DO2 increased. Thus, nifedipine significantly increased SI in a dose-dependent manner, thereby improving the tissue oxygen supply-demand balance.
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