Effect of inhaled nitric oxide on gas exchange in patients with congestiveheart failure - A randomized, controlled trial

Background: Conventional vasodilators increase ventilation-perfusion mismat ch and do not improve gas exchange even though they reduce pulmonary hypert ension. However, the effects of nitric oxide inhalation on ventilatory and gas exchange values in patients with congestive heart failure are not known . Objective: To investigate the effect of nitric oxide inhalation on gas exch ange in patients with congestive heart failure. Design: Randomized, controlled trial. Setting: University hospital. Patients: 16 patients with congestive heart failure (New York Heart Associa tion class II or III). Interventions: Patients inhaled nitric oxide gas at graded concentrations ( n = 8) or were given intravenous isosorbide dinitrate, 2.5 mg (n = 8). Measurements: Hemodynamic and ventilatory variables and blood gases were me asured 5 minutes after inhalation of different doses of nitric oxide and 10 minutes after administration of isosorbide dinitrate. Results: Nitric oxide inhalation reduced the mean pulmonary arterial pressu re in a dose-dependent manner without altering the mean arterial pressure o r cardiac output. At a dose of 40 parts per million, nitric oxide inhalatio n increased PaO2 (change from baseline, 12.0 mm Hg [95% CI, 2.3 to 21.7 mm Hg]; P = 0.014) and decreased the alveolar-arterial difference in partial p ressure of oxygen (change, -8.6 mm Hg [CI, -16.8 to -0.4 mm Hg]; P = 0.038) and the ventilatory equivalent for carbon dioxide output (change, -6.7 [CI , -10.3 to -3.1]; P < 0.001). Although isosorbide dinitrate similarly decre ased pulmonary arterial pressure, it did not alter gas exchange or ventilat ory variables. Conclusions: Because nitric oxide inhalation improved gas exchange, it may be used as a supportive therapy when other conventional vasodilators worsen gas exchange.