Hemodynamic effects of nitroprusside in infants with a large ventricular septal defect.

To evaluate the effect of acute vasodilator therapy, nitroprusside was administered at cardiac catheterization to five infants (ages 10 days to 6 months) with isolated ventricular septal defect and congestive heart failure. Intravenous nitroprusside was begun at a dose of 0.5 micrograms/kg/min and was increased by increments of 0.5 micrograms/kg. Hemodynamic measurements were made before nitroprusside, after 5 minutes at each dose, and 10 minutes after nitroprusside was discontinued. Baseline data were obtained before nitroprusside administration and compared with data obtained at maximal nitroprusside dose. The pulmonary-to-systemic flow ratio increased from 2.2 +/- 0.2 to 3.4 +/- 0.2 (mean +/- SEM, p less than 0.05) as a consequence of a marked decrease in systemic blood flow (5.3 +/- 0.7 to 3.6 +/- 0.51/min/m(2), p less than 0.05). Pulmonary flow did not change significantly. Mean pulmonary capillary wedge and right atrial pressures decreased by 53% (10.2 +/- 1.4 to 4.8 +/- 1.4 mm Hg [p less than 0.01] and 6.0 +/- 1.4 to 2.8 +/- 1.1 mm Hg [p less than 0.05], respectively). Decreases in mean aortic (63.6 +/- 3.0 to 54.6 +/- 2.1 mm Hg, p less than 0.05) and mean pulmonary artery pressure (41.4 +/- 6.2 to 32.0 +/- 6.7 mm Hg, p less than 0.05) were also observed. An apparently paradoxical increase in systemic resistance occurred (11.7 +/- 1.6 to 15.4 +/- 2.4 U, p less than 0.05. Our data show that nitroprusside causes a marked decrease in systemic blood flow and an increase in the pulmonary-to-systemic flow ratio in infants with a large ventricular septal defect. These findings may be related to the hemodynamic profile of these infants, in whom ventricular function, cardiac output and systemic resistance are normal.