Circulation, Vol 64, 553-558, Copyright © 1981 by American Heart Association
RH Beekman, AP Rocchini and A Rosenthal
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.
ARTICLES
Hemodynamic effects of nitroprusside in infants with a large ventricular septal defect
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