Inhaled Nitric Oxide for the Adult Respiratory Distress Syndrome

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Abstract
Rossaint et al. (Feb. 11 issue)1 discussed the potential benefits of inhaled nitric oxide in the adult respiratory distress syndrome (ARDS). Their hypothesis is that inhalation of nitric oxide causes selective vasodilation of the pulmonary vascular bed in the ventilated lung regions, improving oxygenation and cardiac performance and reducing the accumulation of extravascular lung water. The study patients had a mild elevation of pulmonary-artery pressure that was of no apparent hemodynamic consequence, since their cardiac output was normal. Inhalation of nitric oxide reduced pulmonary-artery pressure slightly and did not change cardiac output. This confirms that its hemodynamic effects were inconsequential. The presence of nitrogen in the inspired air and of methemoglobin in the blood could have adversely affected arterial and tissue oxygenation. The authors could have resolved this issue by presenting data on measures of oxygen transport and tissue oxygenation.