Effect of sodium nitroprusside on ventilation-perfusion mismatching in heart failure

Sodium nitroprusside has been shown to lower arterial partial pressure of oxygen (PaO2) in patients with congestive heart failure and respiratory failure. The multiple inert gas elimination technique was used to evaluate the effect of sodium nitroprusside infusion on pulmonary gas exchange in five patients with congestive heart failure. During sodium nitroprusside infusion, mean values of cardiac output increased and mean values of arterial pressure, pulmonary artery pressure, pulmonary artery wedge pressure and pulmonary vascular resistance decreased. Cardiac output increased in each patient and PaO2 decreased in all but one patient (mean 75.6 +/- 15.1 to 68 +/- 17.5 mm Hg, p = 0.032). Distributions of ventilation and perfusion showed increased perfusion of lung units with low (less than or equal to 0.1) ventilation-perfusion ratios in all subjects during sodium nitroprusside infusion (mean 3.89 +/- 1.52 to 11.33 +/- 7.42% of cardiac output, p = 0.027, paired t test). The amount of shunt (fractional perfusion of lung units with ventilation-perfusion ratio = 0) increased in the two patients with some shunt present in the baseline measurements. The mean total low ventilation-perfusion perfusion (shunt plus ventilation-perfusion less than or equal to 0.1) was significantly increased from 4.38 +/- 1.54 to 14.7 +/- 9.37% (p = 0.023) during sodium nitroprusside infusion. Total low ventilation-perfusion perfusion was negatively correlated with mean pulmonary artery pressure and pulmonary artery wedge pressure (r = -0.949 and -0.946, respectively). Although sodium nitroprusside infusion increased cardiac output and overall oxygen transport in all patients, it worsened ventilation-perfusion mismatching. The mechanism is probably pulmonary vasodilation or increased cardiac output, or both.