No evidence for interstitial lung oedema by extensive pulmonary function testing at 4,559 m

Abstract

The aim of the present study was to better understand previously reported changes in lung function at high altitude.Comprehensive pulmonary function testing utilising body plethysmography and assessment of changes in closing volume were carried out at sea level and repeatedly over 2 days at high altitude (4,559 m) in 34 mountaineers.In subjects without high-altitude pulmonary oedema (HAPE), there was no significant difference in total lung capacity, forced vital capacity, closing volume and lung compliance between low and high altitude, whereas lung diffusing capacity for carbon monoxide increased at high altitude. Bronchoconstriction at high altitude could be excluded as the cause of changes in closing volume because there was no difference in airway resistance and bronchodilator responsiveness to salbutamol. There were no significant differences in these parameters between mountaineers with and without acute mountain sickness. Mild alveolar oedema on radiographs in HAPE was associated only with minor decreases in forced vital capacity, diffusing capacity and lung compliance and minor increases in closing volume.Comprehensive lung function testing provided no evidence of interstitial pulmonary oedema in mountaineers without HAPE during the first 2 days at 4,559 m. Data obtained in mountaineers with early mild HAPE suggest that these methods may not be sensitive enough for the detection of interstitial pulmonary fluid accumulation.

Acute high-altitude sickness

“…However, there is a large overlap of individual values [7] and statistically significant differences can only be obtained in studies of large groups. These blood gas changes might be due to a mild interstitial oedema not visible on chest radiographs [8], but suggested by a slight decrease of vital capacity and increase of closing volume [9,10]; however, these are inconsistent findings [11]. Furthermore, a lower ventilatory drive in hypoxia might contribute to more severe hypoxaemia in AMS, at least in some individuals [12,13].…”

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

“…Hypoxia induces pulmonary vasoconstriction, an adaption that reduces ventilation-perfusion mismatch and optimizes the lung diffusion and perfusion matching (8,36). But exercise in the hypoxic environment is associated with a deterioration of ventilation-perfusion matching, which is only partly corrected by hypoxic vasoconstriction (36).…”

Exposure at high altitude and exercise altered membrane diffusion capacity of the lung

“…Guénard points out a discrepancy of the transfer factor of the lung for carbon monoxide (TL,CO) measurements between data published in his group's abstract [1] and data we reported recently [2]. DE BISSCHOP et al [1] observed a small but significant decrease in TL,CO in acclimatised subjects after maximal exercise at 5,000 m, which H. Guénard considers to be in disagreement with the small increase we found in nonacclimatised subjects at rest at 4,559 m. He suggests that the discrepancy is due to an erroneous calculation of diffusing capacity of the lung for carbon monoxide (DL,CO) on our part.…”

“…Guénard points out a discrepancy of the transfer factor of the lung for carbon monoxide (TL,CO) measurements between data published in his group's abstract [1] and data we reported recently [2]. DE BISSCHOP et al [1] observed a small but significant decrease in TL,CO in acclimatised subjects after maximal exercise at 5,000 m, which H. Guénard considers to be in disagreement with the small increase we found in nonacclimatised subjects at rest at 4,559 m. He suggests that the discrepancy is due to an erroneous calculation of diffusing capacity of the lung for carbon monoxide (DL,CO) on our part. Furthermore, he points out that transfer factor of the lung for nitric oxide (TL,NO), which was also slightly decreased in the study of DE BISSCHOP et al [1], is a better measure of diffusion than TL,CO, since nitric oxide uptake is dependent only on membrane conductance and is not influenced by blood conductance.…”