[Gas exchange and hemodynamic effects of nitric oxide inhalation in patients with acute respiratory distress syndrome].

Background: To analyze the effects on gas exchange and hemodynamics of nitric oxide inhalation in patients with acute respiratory distress syndrome.

Patients And Methods: Prospective study including 16 acute respiratory distress syndrome patients. We analyzed the acute and short-term (5 days) effects of inhaling 5 parts per million (ppm) nitric oxide on gas exchange and hemodynamics.

Results: After nitric oxide inhalation, PaO2/FiO2 ratio changed from 81 +/- 25 to 126 +/- 57 mmHg (p = 0.0001), mean pulmonary artery pressure decreased from 30.1 +/- 8.2 to 27.3 +/- 6.6 mmHg (p = 0.002), intrapulmonary shunt decreased from 44.6 +/- 11% to 34.1 +/- 7.9% (p = 0.002) and cardiac index did not change. Thirteen out of 16 patients (81.2%) presented at least a 20% improvement in PaO2/FiO2 ratio. In the 10 patients treated over 5 consecutive days, we observed that those who improved (increase in PaO2/FiO2 ratio higher than 20% after inhaling 5 ppm nitric oxide) showed a lower cardiac index, a higher mean pulmonary artery pressure and a higher pulmonary vascular resistance index than those who did not: Cl 3.9 +/- 0.81 vs 4.9 +/- 0.81 l/min/m2 (p < 0.001), mean pulmonary artery pressure 32.4 +/- 7 vs 25.3 +/- 4.2 mmHg (p = 0.001), and pulmonary vascular resistance index 421 +/- 199 vs 241 +/- 106 dyn.s.cm5/m2 (p = 0.003). Mean levels of methemoglobin were 1.1 +/- 0.24% (range: 0.4-1.6%), and NO2 concentration was always lower than 100 parts per billion.

Conclusions: Low doses of inhaled nitric oxide induce a selective pulmonary vasodilatation and significant improvement of oxygenation in the majority of acute respiratory distress syndrome patients, although those with a hyperkinetic hemodynamic status are less likely to improve the oxygenation. These effects are maintained for at least 5 days. We did not observe rebound effects.