Milrinone, dobutamine, and nitroprusside

To assess their comparative effects on hemodynamics and myocardial energetics, we administered nitroprusside (1.5 ± 0.6 μ/kg-min), dobutamine (10 ± 3 μ/kg-min), and milrinone (67 ± 13 μ/kg-min) sequentially to 10 patients with severe (NYHA class III or IV) congestive heart failure. Each agent led to a significant (p = .001) increase in cardiac index (1.9 ± 0.5 to 2.7 ± 0.6 liters/min/m²; 1.7 ± 0.4 to 2.6 ± 0.6 liters/min/m²; and 1.8 ± 0.5 to 2.7 ± 0.5 liters/min/m², for nitroprusside, dobutamine, and milrinone, respectively). Dobutamine did not produce a significant change in the pulmonary capillary wedge pressure (27 ± 5 to 24 ± 6 mm Hg, NS) nor in mean arterial pressure (83 ± 9 to 86 ± 10 mm Hg, NS), but caused a significant rise in heart rate (85 ± 16 to 99 ± 17 beats/min, p .001) and in myocardial oxygen consumption (8.7 ± 2.1 to 11.1 ± 3.8 ml 02/min, p = .03). In contrast, nitroprusside and milrinone each caused a significant (p = .001) fall in the pulmonary capillary wedge pressure (27 ± 6 to 19 ± 7 mm Hg and 26 ± 6 to 19 ± 9 mm Hg, respectively), without significantly increasing either the heart rate (87 ± 18 to 85 ± 17 beats/min and 86 ± 17 to 89 ± 17 beats/min, respectively) or myocardial oxygen consumption (8.8 ± 2.3 to 7.6 ± 2.1 ml 02/min and 8.8 ± 2.1 to 8.4 ± 2.1 ml 02/min, respectively). Both nitroprusside and milrinone produced a significant fall in mean arterial pressure (81 ± 7 to 68 ± 5 mm Hg, p .001; 79 ± 8 to 73 ± 8 mm Hg, p = .03, respectively), reflecting their shared vasodilator activity. This fall in mean arterial pressure was, however, significantly (p = .05) less after milrinone than after nitroprusside, consistent with milrinone's known concomitant inotropic effect. Thus, therapy with milrinone led to a greater improvement in the pulmonary capillary wedge pressure and a lower myocardial oxygen consumption than that with dobutamine, while producing the same hemodynamic improvement as nitroprusside with less concomitant hypotension.