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

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.