NO: COPD and beyond

Background Inhalation of nitric oxide (NO) causes selective pulmonary vasodilation and improves arterial oxygenation in acute respiratory distress syndrome. But some patients do not respond or gas exchange worsens when inhaling NO. We hypothesised that this detrimental effect might be related to the reversion of hypoxic vasconstriction in those patients where this mechanism contributes to ventilation-perfusion ((V) over dotA/(Q) over dot) matching. Method. We studied 13 patients with advanced chronic obstructive pulmonary disease (COPD). We compared their 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 inhalation 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 dotA/(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 pressure to 23.4 (2.1) mm Hg and caused greater (V) over dotA/(Q) over dot 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 NO or O-2. interpretation. We conclude that in patients with COPD, in whom hypoxaemia is caused essentially by (V) over dotA/(Q) over dot imbalance rather than by shunt, inhaled NO can worsen gas exchange because of impaired hypoxic regulation of the matching between ventilation and perfusion.