Effects of high-dose supplemental oxygen therapy on pulmonary haemodynamics at 3250 m in high-altitude residents at risk for pulmonary hypertension
Alessandro Vella, Julian Müller, Adilet Omuralieva, Anna Titz, Laura Mayer, Maamed Mademilov, Mona Lichtblau, Michael Furian, Talant Sooronbaev, Silvia UlrichQuestion addressed by the study
Hypoxic pulmonary vasoconstriction increases systolic pulmonary artery pressure (sPAP) and may contribute to high-altitude pulmonary hypertension (HAPH). While supplemental oxygen therapy (SOT) lowers sPAP during acute hypoxic exposure, its haemodynamic effects in permanent high-altitude residents remain unclear. In particular, the relative contribution of fixed vascular remodelling to chronically elevated sPAP is uncertain.
Participants and methods
In this open-label, non-randomised, sequential interventional trial, Kyrgyz highlanders living >2500 m with tricuspid regurgitation velocity >2.8 m/s underwent echocardiography under ambient air and after >15 min of high-dose SOT (FiO₂≈0.95, 10 L/min) at 3250 m.
Results
48 participants (56% females, mean±SD age 53±12 years) completed the study per-protocol. SOT reduced sPAP from 45±11 to 31±5 mm Hg, cardiac output (CO) from 5.1±1.2 to 4.3±1.4 L/min and total pulmonary resistance (TPR) from 9.2±2.7 to 7.5±1.5 WU (all p<0.001). In an exploratory subanalysis, a larger sPAP decrease was associated with higher baseline sPAP and younger age.
Answer to the question
High-dose SOT acutely lowers sPAP in high-altitude residents at risk for HAPH. The decrease in sPAP is driven by reductions in both CO and TPR. The decline in TPR indicates a largely reversible hypoxic-vasoconstrictor component, whereas the contribution of fixed vascular remodelling to elevated PAP appears minimal. These findings underscore the physiological potential of short-term high-dose oxygen to reduce right ventricular afterload and improve pulmonary haemodynamics in this high-altitude population at risk for HAPH.
Trial registration number