No Correlation between Pulmonary Artery Pressure and Markers of Pulmonary Interstitial Fluid Accumulation at Altitude

Abstract

PURPOSE: A previous study yielded indirect evidence by changes in closing volume that “subclinical” high altitude pulmonary edema (HAPE) occurs in a large number of mountaineers after ascent to 4559 m. Since an abnormal increase of pulmonary artery pressure (PAP) in hypoxic environment is the key mechanism of pulmonary fluid accumulation, we hypothesized that markers of interstitial pulmonary fluid accumulation correlate with the increase in PAP at high altitude. METHODS: We therefore performed pulmonary function testing by body plethysmography and measured lung compliance by oesophageal pressure measurements and systolic PAP by echocardiography in 34 healthy subjects at baseline at low altitude (LA) and after rapid ascent to 4559 m. Measurements at high altitude (HA) were performed 2–4 h (HA1), 20 h (HA2) and 44 h (HA3) after arrival at 4559 m. RESULTS: HAPE was diagnosed by clinical examination and chest x-ray in 4 subjects, which were excluded from the further analysis presented here. Pulmonary function testing showed normal values for all subjects at LA and there were no differences for the whole group in measurements at high altitude for total lung capacity, vital capacity, diffusion capacity, closing volume and dynamic or static compliance. PAP also was normal in all subjects at LA (22 ± 4 mmHg) and significantly increased by 16 ± 8 (HA1), 14 ± 6 (HA2) and 12 ± 6 (HA3), respectively (p<0.001). Maximum values of systolic PAP at high altitude varied from 30 to 60 mmHg between subjects. There was no correlation in any parameter of pulmonary function testing with the increase in systolic PAP. CONCLUSIONS: In contrast to previous studies we found that lung volumes, diffusion capacity, closing volume, and pulmonary compliance are unchanged at high altitude, which indicates that no relevant interstitial fluid accumulation occurred in our subjects despite a wide range in elevation of PAP. The lack of correlation of systolic PAP and decrements in pulmonary function parameters is evidence against the claim that the majority of climbers ascending to altitudes in the range of 4000 to 5000 meters develop subclinical HAPE.