[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.