Oxygen and pulmonary arterial hypertension: effects, mechanisms, and therapeutic benefits

Oxygen is a pulmonary vasodilator. Although treatment of pulmonary arterial hypertension (PAH) is focused on pulmonary vasodilation, treatment guidelines do not recommend O-2 therapy for patients unless they develop hypoxaemia. These guidelines point to a lack of evidence of benefit of O-2 therapy from randomized controlled trials (RCTs) and to evidence of lack of benefit in a single RCT involving patients with Eisenmenger syndrome. These guidelines did not identify major limitations with the Eisenmenger study or consider other evidence of therapeutic benefit. Recent advances in mechanistic understanding of O-2 effects on pulmonary vascular tone, along with substantial evidence of acute effects of O-2 in PAH patients, challenge the view that benefits of O-2 arise only through correction of hypoxaemia. Evidence presented in this review shows that O-2 acts as a pulmonary vasodilator in patients who are normoxaemic; that this probably involves an alveolar mechanism in addition to a blood-borne (oxyhaemoglobin) mechanism; and that therapeutic benefit of O-2 does not depend on arterial O-2 levels. This suggests that O-2 has potential therapeutic benefit for all patients with PAH. Clinical guidelines and practice related to O-2 therapy need to be reassessed, and further research is needed.

Automated summary

Oxygen acts as a pulmonary vasodilator in patients with pulmonary arterial hypertension (PAH), potentially through alveolar and blood-borne mechanisms, regardless of arterial oxygen levels. Current clinical guidelines and practices related to oxygen therapy for PAH patients need to be reevaluated, as recent evidence challenges the previous view that its benefits arise only from correcting hypoxemia. Further research is needed to better understand the therapeutic potential of oxygen in PAH.