The Science Journal of the American Association for Respiratory Care

1997 OPEN FORUM Abstracts

Inhaled Nitric Oxide in Adults

Richard Branson, RRT, Saturday, December 7, 1997.

Nitric Oxide (NO) is a molecule with remarkable biologic activity. Structurally, NO is a small, unstable, diatomic radical. Recent work has shown NO to be important in a wide variety of biologic functions including vasodilatation, platelet adhesion, cytotoxicity and neurotransmission. Prior to the current flurry of activity surrounding NO, it was known as a common environmental pollutant and a contaminant during the manufacture of nitrous oxide. Nitric Oxide is present in the atmosphere at 10 - 100 parts per billion (ppb), is produced in the nasopharynx at 100 - 1000 ppb, and in cigarette smoke at up to 1000 parts per million (ppm).

The interest in inhaled nitric oxide for the treatment of lung disease relates to it's properties as a vasodilator. When inhaled, NO becomes a selective pulmonary vasodilator. That is, the effects of NO occur in ventilated alveoli which better matches ventilation and perfusion. Additionally, because NO is deactivated by hemoglobin these vasodilatory effects are only seen in the pulmonary circulation with no systemic effects.

The primary effects of inhaled nitric oxide are reduced pulmonary artery pressures, increased arterial oxygenation, and an improvement in intrapulmonary shunt. These effects are achieved at doses between 1 and 80 ppm. Improvements in oxygenation typically occur at lower doses (less than 10 ppm) while decreases in pulmonary artery pressure often require higher doses.

The unique effects of inhaled nitric oxide make it an attractive adjunctive therapy in the treatment of acute respiratory distress syndrome and diseases resulting in pulmonary hypertension. Numerous studies have demonstrated the ability of inhaled NO to improve oxygenation in patients with ARDS. Results of an early clinical trial failed to show a reduction in mortality, but did demonstrate reductions in ventilator and ICU days. A second clinical trial is currently underway in adults to determine any further benefits.

Pulmonary hypertension may result from ARDS, end stage liver disease, primary pulmonary hypertension, and other idiopathic mechanisms. The ability of nitric oxide to reduce pulmonary artery pressures in these instances makes it an attractive therapy. This would include patients undergoing cardiac and/or lung transplant. The use of long term NO therapy by nasal cannula may also prove beneficial in patients with primary pulmonary hypertension.

Potential complications of NO included the production of methemoglobin, the generation of NO_{2}, and increased bleeding times. Rapid changes in pulmonary artery pressure may also cause increased left ventricular filling pressures and heart failure in patients with cardiac disease. Rapid withdrawal of NO may also result in rebound hypoxemia and pulmonary hypertension.

Inhaled NO is a promising new therapy which requires the expertise of the RCP. This therapy typically results in improved oxygenation in more than half the patients with ARDS and as yet is fairly free of complications.

AARC 50th Anniversary, December 6 - 9, 1997, New Orleans, Louisiana.

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