WORSENING OF PULMONARY GAS-EXCHANGE WITH NITRIC-OXIDE INHALATION IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

Background Inhalation of nitric oxide (NO) causes selective pulmonary vasodilation and improves arterial oxygenation in acute respiratory di stress syndrome. But some patients do not respond or gas exchange wors ens when inhaling NO. We hypothesised that this detrimental effect mig ht be related to the reversion of hypoxic vasoconstriction in those pa tients where this mechanism contributes to ventilation-perfusion (V-A/ Q) matching. Methods We studied 13 patients with advanced chronic obst ructive pulmonary disease (COPD). We compared their responses to breat hing room air, NO at 40 parts per million in air, and 100% O-2. Change s in pulmonary haemodynamics, blood gases, and V-A/Q distributions wer e assessed. Findings NO inhalation decreased the mean (SE) pulmonary a rtery pressure from 25.9 (2.0) to 21.5 (1.7) mm Hg (p=0.001) and PaO2 from 56 (2) to 53 (2) mm Hg (p=0.014). The decrease in PaO2 resulted f rom worsening of V-A/Q distributions, as shown by a greater dispersion of the blood-flow distribution (logSD Q) from 1.11 (0.1) to 1.22 (0.1 ) (p=0.018). O-2 breathing reduced the mean pulmonary arterial pressur e to 23.4 (2.1) mm Hg and caused greater V-A/Q mismatch (logSD Q, 1.49 [0.1]). The intrapulmonary shunt on room air was small (2.7 [0.9]%) a nd did not change when beathing NO or O-2. Interpretation We conclude that in patients with COPD, in whom hypoxaemia is caused essentially b y V-A/Q imbalance rather than by shunt, inhaled NO can worsen gas exch ange because of impaired hypoxic regulation of the matching between ve ntilation and perfusion.