• J A Johannigman, K Davis, R S Campbell, F Luchette, J M Hurst, and R D Branson.
• Department of Surgery, University of Cincinnati Medical Center, Ohio 45267-0558, USA.
• J Trauma. 1997 Dec 1;43(6):904-9; discussion 909-10.

BackgroundInhaled nitric oxide has been shown to improve oxygenation in select patients with acute respiratory distress syndrome (ARDS).ObjectiveThe purpose of this study was to evaluate the clinical response to four concentrations of inhaled nitric oxide (NO) in 20 patients with ARDS.MethodsAll patients with ARDS were eligible for the study. ARDS was defined as (1) the presence of a predisposing factor; (2) a PaO2/FiO2 ratio < 200; (3) bilateral infiltrates on chest radiograph; and (4) absence of evidence of congestive heart failure and pulmonary artery wedge pressure < 18 mm Hg. Patients received each of four doses (1, 15, 30, and 60 ppm) in random order, each for a 3-hour period. Cardiovascular variables were continuously monitored, and arterial and mixed venous blood gas measurements were obtained at 30 minutes and 3 hours.ResultsThirteen of the 20 patients demonstrated a significant increase in their PaO2/FiO2 (> 20% increase) when treated with inhaled NO. The administration of inhaled NO was associated with an increase in oxygenation at doses of 1, 15, and 30 ppm, but not 60 ppm. Increasing NO dose to more than 1 ppm did not significantly improve response. Mean pulmonary artery pressure decreased with increasing NO concentration, but this did not reach statistical significance. Nine of the 13 responding patients and 2 of the 7 nonresponding patients survived.ConclusionInhaled NO was successful in increasing PaO2/FiO2 by > 20% in 65% of the surgical patients in this trial. Response to NO could not be predicted by initial PaO2/FiO2 or pulmonary artery pressures. A trial of inhaled NO at a dose of < 10 ppm may be helpful in ARDS patients requiring increasing FiO2 and positive end-expiratory pressure.

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