Effect of nitric oxide inhalation on gas exchange in acute severe pneumonia

- We evaluated the effects of inhaled nitric oxide (NO) in acute severe pneumonia.
- Inhaled NO improved arterial oxygenation.
- NO shifted blood flow from shunt areas to normal ventilation-perfusion units.
- Effects were achieved with a low dose of 5 parts per million of inhaled NO.
- In severe pneumonia, inhaled NO may contribute to sustain temporarily gas exchange.

Inhaled nitric oxide (NO) causes selective pulmonary vasodilatation and may improve gas exchange. The study was aimed to evaluate the acute effects of inhaled NO on pulmonary gas exchange in severe unilateral pneumonia, where hypoxemia results from increased intrapulmonary shunt. We studied 8 patients without preexisting lung disease (59 ± 18 yr; 4M/4F) with early unilateral severe pneumonia and respiratory failure. Pulmonary and systemic hemodynamics and gas exchange, including ventilation-perfusion (V;A/Q;) distributions, were measured at baseline and while breathing 5 and 40 parts per million (ppm) of NO. Inhaled NO caused a dose-dependent fall in pulmonary vascular resistance (by 12% and 21%, with 5 and 40 ppm, respectively; p < 0.01, each) and improvement of PaO2 (by 25% and 23%; p < 0.05, each), owing to the reduction of intrapulmonary shunt (by 23% and 27%; p < 0.05, each), without changes in the amount of perfusion to low V;A/Q; ratio alveolar units. Patients with greater baseline intrapulmonary shunt exhibited greater improvement in arterial oxygenation (r2 = 0.55, p < 0.05). We conclude that low doses of inhaled NO improve pulmonary gas exchange in acute severe pneumonia.