The acute effect of high-dose supplemental oxygen on hemodynamics assessed by echocardiography in patients with pulmonary vascular disease living in Quito at 2850m.

<bold>Background:</bold> Worldwide, >220 Mio people live >2000m, many of whom have preexisting chronic conditions, including pulmonary vascular diseases (PVD). We investigated the acute effects of supplemental oxygen on pulmonary hemodynamics in patients with PVD permanently living at 2850m. <bold>Methods:</bold> Patients diagnosed as pulmonary arterial or chronic thromboembolic pulmonary hypertension (PAH/CTEPH), were randomly allocated to receive 10L/min supplemental oxygen (FiO2 ≈95%) or sham air given near their living altitude in Quito at 2850m (FiO2 0.21, PiO2 ≈60% of sea level). This was a randomized crossover trial with a wash-out period of >2h. After >15min breathing respective FiO2 at rest, echocardiography was performed. Systolic pulmonary artery pressure (sPAP), cardiac output (CO) and other parameters were measured. Furthermore, we assessed arterial blood gases. <bold>Results:</bold> 28-patients (24 female, 26 PAH, age 46±12yrs), treated with endothelin-receptor antagonists (N=9) or phosphodiesterase-5-inhibitors (N=27) were included. With oxygen vs. air sPAP was 57±23 vs 68±24 mmHg, mean difference -11mmHg (−15 to -6mmHg, p<0.001), CO was 3.2±0.9 vs. 3.9±1.1L/min; −0.7L/min (−0.9 to −0.4L/min, p<0.001) while other parameters like sPAP/CO, and indices of right heart function were unchanged. PaO2 was 22.5±9.7 vs. 7.6±1.5kPa, 14.9 (11.4 to 18.4kPa, p<0.001). <bold>Conclusion:</bold> High-dose oxygen therapy in prevalent patients with PVD permanently living near 2850 m significantly lowered sPAP, but also reduces CO with an unchanged pulmonary resistance. This signifies pulmonary vasodilatation due to oxygen, even in this pretreated PVD-highlander collective.