NO - COPD AND BEYOND

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 vasconstriction in those pat ients where this mechanism contributes to ventilation-perfusion ((V) o ver dotA/(Q) over dot) matching. Method. We studied 13 patients with a dvanced chronic obstructive pulmonary disease (COPD). We compared thei r responses to breathing room air, NO at 40 parts per million in air, and 100% O-2. Changes in pulmonary haemodynamics, blood gases, and (V) over dotA/(Q) over dot distributions were assessed. Findings. NO inha lation decreased the mean (SE) pulmonary artery 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 from worsening of (V) over do tA/(Q) over dot distributions, as shown by a greater dispersion of the blood-flow distribution (logSD (Q) over dot) from 1.11 (0.1) to 1.22 (0.1) (p=0.018). O-2 breathing reduced the mean pulmonary arterial pre ssure to 23.4 (2.1) mm Hg and caused greater (V) over dotA/(Q) over do t mismatch (logSD (Q) over dot, 1.49 [0.1]). The intrapulmonary shunt on room air was small (2.7 [0.9]%) and did not change when breathing N O or O-2. interpretation. We conclude that in patients with COPD, in w hom hypoxaemia is caused essentially by (V) over dotA/(Q) over dot imb alance rather than by shunt, inhaled NO can worsen gas exchange becaus e of impaired hypoxic regulation of the matching between ventilation a nd perfusion.