Pretrial and post-trial baseline hemodynamic values were essentially within normal limits but considerably below the optimal values empirically determined from critically ill postoperative survivors (Cl, 4.5 L/min/sq m; Do2, 600 ml/min/sq m; Vo2, 170 ml/min/sq m). Although about 75 percent of the postoperative patients achieved these goals with only therapy with fluids, all of the patients given dobutamine in the immediate postoperative period achieved these optimal goals during the titrations or in subsequent infusions of fluid and dobutamine. The relative effectiveness of both catecholamines on the disturbed circulation of the immediate postoperative state is of particular interest. The assumption here is that the lesion of peripheral circulatory postoperative shock is a maldistribution of flow from uneven vasoconstriction in which some metarterio-capillary networks are maximally constricted while others are wide open; this uneven flow pattern results in a high overall flow but inadequate oxygenation of tissues. It was assumed that the β2-adrenergic effect of dobutamine would be most clearly evident in these patients. Indeed, we found that dobutamine was most effective in the early postoperative period, and, moreover, the increases in Do2 and Vo2 were significantly greater after dobutamine than after dopamine. By contrast, the increases in Cl were smaller and not statistically significant after both dobutamine and dopamine in the elderly, in respiratory failure, in hyperdynamic states, and in patients with sepsis.
The changes in oxygen transport are clearly of major interest because deficiencies in oxygen transport are an essential part of the shock state as well as major determinants of outcome. The critically ill postoperative patient usually has inadequate tissue perfusion with impaired Vo2, despite normal or supranor-mal cardiac function. Inadequate Do2 and Vo2 are strongly related to outcome in these patients and provide sensitive predictors of survival or death. Oxygen consumption may be limited by the delivery of oxygen and oxidative substrates during disturbed circulatory states. When tissues are hypoxic because of inadequate or maldistributed flow, the increased Do2 may increase oxygen uptake. Since oxygen cannot be stored, increased Vo2 after therapy suggests the presence of a prior oxygen debt that is now at least partially corrected. The effects of dobutamine on oxygen transport may be attributed to both the β1-adrenergic effects which improve cardiac output by increased myocardial contractility and to the peripheral β2-adrenergic effects which open up previously vasoconstricted metarteriolocapillary networks. The increased Do2 and Vo2 after therapy with dobutamine indicate improved tissue perfusion from more evenly distributed flow that increases tissue oxygenation.