Continuous positive airway pressure modulates effect of inhaled nitric oxide on the ventilation-perfusion distributions in canine lung injury.

Abstract

OBJECTIVES: 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. DESIGN: Prospective, randomized study. SETTING: A research laboratory at a university medical center. SUBJECTS: Ten anesthetized mongrel dogs with oleic acid-induced lung injury. INTERVENTIONS: Zero or 40 parts per million of NO in the inspiratory gas, with and without 10 cm H2O CPAP in random order. MEASUREMENTS AND MAIN RESULTS: 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). CONCLUSIONS: 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.