• A Matsumoto, S Momomura, S Sugiura, H Fujita, T Aoyagi, M Sata, M Omata, and Y Hirata.
• University of Tokyo, Japan. amatsu-tky@umin.u-tokyo.ac.jp
• Ann. Intern. Med. 1999 Jan 5;130(1):40-4.

BackgroundConventional vasodilators increase ventilation-perfusion mismatch and do not improve gas exchange even though they reduce pulmonary hypertension. However, the effects of nitric oxide inhalation on ventilatory and gas exchange values in patients with congestive heart failure are not known.ObjectiveTo investigate the effect of nitric oxide inhalation on gas exchange in patients with congestive heart failure.DesignRandomized, controlled trial.SettingUniversity hospital.Patients16 patients with congestive heart failure (New York Heart Association class II or III).InterventionsPatients inhaled nitric oxide gas at graded concentrations (n = 8) or were given intravenous isosorbide dinitrate, 2.5 mg (n = 8).MeasurementsHemodynamic and ventilatory variables and blood gases were measured 5 minutes after inhalation of different doses of nitric oxide and 10 minutes after administration of isosorbide dinitrate.ResultsNitric oxide inhalation reduced the mean pulmonary arterial pressure in a dose-dependent manner without altering the mean arterial pressure or cardiac output. At a dose of 40 parts per million, nitric oxide inhalation 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 pressure 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 decreased pulmonary arterial pressure, it did not alter gas exchange or ventilatory variables.ConclusionsBecause nitric oxide inhalation improved gas exchange, it may be used as a supportive therapy when other conventional vasodilators worsen gas exchange.

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