Acute hemodynamic changes by breathing hypoxic and hyperoxic gas mixtures in pulmonary arterial and chronic thromboembolic pulmonary hypertension

Abstract

In patients with PAH/CTEPH, very short-term exposure to moderate hypoxia similar to 2600 m altitude or during commercial air travel did not deteriorate hemodynamics. These results encourage studying the response of PAH/CTEPH during daytrips to the mountain or air travel.

Right and Left Heart Function in Lowlanders with COPD at Altitude: Data from a Randomized Study

“…Even though our COPD patients had values corresponding to those in healthy subjects at very high altitude, they tolerated the exposure to this altitude well, which might be explained by an as yet unknown RV adaptation to hypoxia caused by their underlying pulmonary disease [29]. The higher PAP in COPD patients is most likely due to both restriction of the pulmonary vascular bed due to parenchymal destruction of the lung and a greater degree of hypoxemia with excessive hypoxic pulmonary vasoconstriction.…”

Into Thin Air

“…Exercise time during hypoxia could be predicted by previously assessed pulmonary vascular resistance, so that noninvasive hemodynamic measures may have underestimated subtle hypoxia-induced decrease in cardiac output during exercise. 7 The current study paves the way for further investigations at high altitude in a natural environment that may help to identify predictors of deterioration and measures to prevent altitude-related illness in patients with PH. As a pulmonary physician working at the foot of the Alps, I am much interested in evidence-based recommendations for patients with cardiopulmonary diseases who wish to travel up into our beautiful mountains.…”

“…This has been challenged recently because a short exposure of patients with PH to normobaric hypoxia corresponding to an altitude of approximately 2,500 m was not associated with a rise in pulmonary vascular resistance, unlike in healthy control subjects, possibly due to a decreased reactivity of the remodeled pulmonary vasculature after long-standing PH. 7 In another recent study of patients with PH, a 2-day stay at 2050 m was well-tolerated by the majority of patients with only minor changes in pulmonary hemodynamics, despite marked increase of hypoxemia compared with baseline at 490 m. 8 In this issue of the CHEST, Schneider et al 9 have gone one step further and studied patients with PH during exercise under hypoxic conditions simulating an altitude of 2,500 m (FIO 2 , 15%). Compared with ambient air, hypoxia reduced exercise time by 10 minutes (6.7 vs 16.9 min) and decreased PaO 2 by 1.7 kPa at the end of exercise, although dyspnea, echocardiographically determined tricuspid pressure gradient, and estimated pulmonary vascular resistance remained unaltered.…”

Altitude Travel in Patients With Pulmonary Hypertension: Randomized Pilot-Trial Evaluating Nocturnal Oxygen Therapy

“…A nonrandomized small study in patients with PAH exposed for 20 min to normobaric hypoxia with an inspiratory oxygen fraction (FiO 2 ) of 15% corresponding to an altitude of ≈2,500 m revealed that resting PAP assessed by echocardiography did not increase ( 7 ). Moreover, we recently showed that exposure to normobaric hypoxia (FiO 2 15%) during right heart catheterization did not significantly change invasive pulmonary hemodynamics at rest in patients with PAH/CTEPH despite a decrease in arterial oxygen tension from 9.5 to 7.0 kPa ( 8 ). It is not known whether and to what extent environmental hypoxia during hours to days as in air travel or altitude sojourns is harmful for patients with PH, and potential risk factors are not identified.…”

“…It is not known whether and to what extent environmental hypoxia during hours to days as in air travel or altitude sojourns is harmful for patients with PH, and potential risk factors are not identified. In our previous short-duration study with normobaric hypoxia, PH patients revealed an even smaller fall in arterial oxygen tension compared to unaffected controls while breathing hypoxia during 15′, related to increased hyperventilation as indicated by the significant decrease in arterial partial pressure of carbon dioxide (PaCO 2 ) ( 8 ). In healthy volunteers, exercise performance is gradually impaired with increasing hypoxia/altitude ( 9 ) and even more in patients with COPD ( 10 , 11 ) and improves with adaptation ( 12 ).…”