PROLONGED INHALATION OF LOW CONCENTRATIONS OF NITRIC-OXIDE IN PATIENTS WITH SEVERE ADULT-RESPIRATORY-DISTRESS-SYNDROME - EFFECTS ON PULMONARY HEMODYNAMICS AND OXYGENATION

Background: Nitric oxide (NO) inhalation selectively decreases pulmona ry artery hypertension and improves arterial oxygenation in patients w ith the adult respiratory distress syndrome (ARDS). In this study of p atients with severe ARDS, we sought to determine the effect of inhaled NO dose and time on pulmonary artery pressure and oxygen exchange and to determine which patients with ARDS are most likely to show this re sponse. Methods: Thirteen patients with severe ARDS (hospital mortalit y 67%) inhaled 0-40 parts per million (ppm) NO. Seven of these patient s continued to breathe 2-20 ppm NO for 2-27 days. Results: Inhaling 5- 40 ppm NO decreased mean pulmonary artery pressure in a dose-related f ashion (from 34 +/- 7 to 30 +/- 7 mmHg at 20 ppm NO). Systemic arteria l pressure did not change. The ratio of arterial oxygen tension to ins pired oxygen fraction increased (from 126 +/- 36 to 149 +/- 38 mmHg) a nd the venous admixture decreased (from 31.2 +/- 5.5 to 28.2 +/- 5.2%) without a clear dose-response effect. During prolonged NO inhalation, 2-20 ppm KO effectively reduced mean pulmonary artery pressure (38 +/ - 7 vs. 31 +/- 6 mmHg) and increased arterial oxygen tension (79 +/- 1 0 vs. 114 +/- 27 mmHg) without evidence of tachyphylaxis. The decrease of pulmonary vascular resistance during NO inhalation correlated with the level of pulmonary vascular resistance without NO (r = -0.72). Th e reduction of venous admixture correlated with the level of venous ad mixture without NO (r = -0.78). Conclusions: Long-term NO inhalation a t low concentrations selectively decreases mean pulmonary artery press ure and improves arterial oxygen tension in patients with ARDS. The se lective pulmonary vasodilation effect is most pronounced in ARDS patie nts with the greatest degree of pulmonary vasoconstriction.