Hemodynamic and gas exchange 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/FiO2ratio 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/FiO2ratio. In the 10 patients treated over 5 consecutive days, we observed that those who improved (increase in PaO2/FiO2ratio 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: CI 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.cm-5/m2(p = 0.003). Mean levels of methemoglobin were 1.1 ± 0.24% (range: 0.4-1.6%), and NO2concentration 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.