EFFECT OF INHALED NITRIC-OXIDE ON RIGHT-VENTRICULAR FUNCTION IN ADULT-RESPIRATORY-DISTRESS-SYNDROME

To determine whether inhaled nitric oxide (NO) affects pulmonary circulation, thereby improving right ventricular (RV) function in adult respiratory distress syndrome (ARDS), we studied 13 patients with both a lung injury severity score of 2.5 or more and a mean pulmonary artery pressure higher than 30 mm Hg. RV function was assessed by a thermodilution technique using a pulmonary artery catheter equipped with a rapid response thermistor before and 15 min after initiation of inhalation of NO (5 ppm). At baseline, stroke volumes were in a normal range(46 +/- 14 ml/m(2)), with a RV dilation (end-diastolic volume = 142 +/- 36 ml/m(2)). Inhaled NO was followed by an improvement in arterial oxygenation (Pa-O2/Fl(O2) = 103 +/- 47 versus 142 +/- 63, p < 0.05) and a drop in pulmonary artery pressure (36.1 +/- 4.5 versus 31.3 +/- 6.1 mm Hg, p < 0.01); stroke volumes and heart rates did not change. The resulting fall in pulmonary vascular resistance (211 +/- 43 versus 180 +/- 59 dyn-s/cm(5), p < 0.05) was associated with an increase in RV ejection fractions (32 +/- 5 versus 36 +/- 6%, p < 0.05), a trend toward decreased RV end-systolic (96 +/- 25 versus 85 +/- 19 ml/m(2), NS) and end-diastolic(142 +/- 36 versus 131 +/- 27 ml/m(2), NS) volumes, and a decrease in right atrial pressures (10.9 +/- 2.9 versus 9.6 +/- 3.2 mm Hg, p < 0.05). No relationship was seen between the improvement in arterial oxygenation and the decrease in pulmonary vascular resistance. We conclude that in patients with ARDS who did not have RV failure, inhaled NO reduces the loading conditions of the RV without changing RV output. The hemodynamic effects of inhaled NO, however, are not closely related to the improvement in arterial oxygenation.