Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury

Abstract

The present study was designed to evaluate if continuous positive airway pressure (CPAP) augments the effect of nitric oxide (NO) inhalation on matching between ventilation and perfusion (VA/Q) during acute lung injury. Prospective, randomized study. A research laboratory at a university medical center. Ten anesthetized mongrel dogs with oleic acid-induced lung injury. Zero or 40 parts per million of NO in the inspiratory gas, with and without 10 cm H2O CPAP in random order. Gas exchange was assessed by estimating the VA/Q distributions using the multiple inert gas elimination technique. Application of CPAP decreased blood flow to shunt units by 26 +/- 2 percent (mean +/- SD) and increased the fraction of cardiac output to normal VA/Q units (VA/Q ratio of 0.1 to 10) by 26 +/- 2 percent (p < 0.05). Inhalation of NO during CPAP accounted for a further 10 +/- 2 percent decrease in the blood flow to shunt units and an 8 +/- 2 percent increase in the fraction of the cardiac output to normal VA/Q units (p < 0.05). Inhalation of NO alone had no significant effect on the VA/Q distributions. Inhalation of NO decreased mean transmural pulmonary artery pressure (Ppatm) both without (Ppatm from 30 +/- 2 to 23 +/- 2 mm Hg; PVR from 323 +/- 44 to 228 +/- 43 dynes.s .cm-5; p < 0.05) and with CPAP (Ppatm from 25 +/- 2 to 20 +/- 2 mm Hg; PVR from 255 +/- 30 to 173 +/- 31 dynes.s.cm-5; p < 0.05). Although pulmonary vascular resistance can be lowered with NO inhalation alone, recruitment of gas exchange units with CPAP is necessary to produce a beneficial effect of NO inhalation on VA/Q matching and oxygenation. When recruitment of gas exchange units with CPAP brings gaseous NO in contact with enough pulmonary blood vessels, NO-induced vasodilation will augment VA/Q matching by a steal mechanism.