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Subclinical pulmonary dysfunction contributes to high altitude pulmonary edema susceptibility in healthy non-mountaineers.

Subclinical pulmonary dysfunction contributes to high altitude pulmonary edema susceptibility in healthy non-mountaineers.
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Gupta RK, Soree P, Desiraju K, Agrawal A, Singh SB,


Gupta RK, Soree P, Desiraju K, Agrawal A, Singh SB, (click to view)

Gupta RK, Soree P, Desiraju K, Agrawal A, Singh SB,

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Scientific reports 2017 11 027(1) 14892 doi 10.1038/s41598-017-14947-z
Abstract

HAPE susceptible (HAPE-S, had HAPE episode in past) subjects may have subclinical cardio-pulmonary dysfunction. We compared the results of pulmonary function tests in 25 healthy HAPE-S non-mountaineers and 19 matched HAPE resistant (HAPE-R, no HAPE episode in past). Acute normobaric hypoxia (FIo2 0.12) was administered at sea level to confirm hypoxia intolerance in HAPE-S. Unlike HAPE-R, HAPE-S subjects had elevated baseline and post-hypoxia systolic pulmonary arterial pressures (20.9 ± 3 vs 27.3 ± 5 mm Hg during normoxia and 26.2 ± 6 vs 45.44 ± 10 mm Hg during hypoxia, HAPE-R vs HAPE-S). Forced vital capacity (FVC) and single breath alveolar volume (SBVA) were significantly lower in HAPE-S compared to HAPE-R (FVC: 4.33 ± 0.5 vs 4.6 ± 0.4; SBVA: 5.17 ± 1 vs 5.6 ± 1 Lt; HAPE-S vs HAPE-R). Two subgroups with abnormal pulmonary function could be identified within HAPE-S; HAPE-S1 (n = 4) showed DLCO>140% of predicted, suggestive of asthma and HAPE-S2 (n = 12) showed restrictive pattern. Each of these patterns have previously been linked to early small airway disease and may additionally represent a lower cross-sectional area of the pulmonary vascular bed, related to lower lung volumes. HAPE susceptibility in healthy non-mountaineers may be related to sub-clinical pulmonary pathology that limits compensatory rise in ventilation and pulmonary circulation during hypoxic stress.

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