CONTINUOUS POSITIVE AIRWAY PRESSURE MODULATES EFFECT OF INHALED NITRIC-OXIDE ON THE VENTILATION-PERFUSION DISTRIBUTIONS IN CANINE LUNG INJURY

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 now 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 now 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 (Ppa(tm)) both without (Ppa(tm) 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 (Ppa(tm) 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.