Abstract

Abstract : The objective of this study was to determine if the magnitude of the sea level pre-ascent resting ventilation and hypoxic ventilatory depression (HVD) are selective in identifying subjects who are susceptible to AMS. We hypothesized that individuals with lower effective alveolar ventilation, i.e., high resting end-tidal carbon dioxide partial pressure (PETCO2), and high HVD will be more likely to develop AMS during subsequent exposure to 4300 m. Twenty volunteers spent 24 h in a hypobaric chamber at sea level undergoing baseline measurements. During this baseline period, the subjects completed sea level resting ventilation and HVD procedures. The next morning, the chamber was decompressed to simulated altitude (PB 430 or 446 mmHg) for approximately 32 h. Resting ventilation was measured after about 4 hours exposure to high altitude and AMS assessed using the Environmental Symptoms Questionnaire at 8-hour intervals throughout the altitude exposure. At sea level, all subjects had normal levels of ventilation and exhibited no evidence of hypoxemia. There was a wide distribution in the resting PETCO2, and HVD. At about 4 hours exposure to high altitude, both SaO2 and PETCO2 were lower (p < 0.002) compared to sea level. The distribution of PETCO2 and particularly SaO2 widened at high altitude. The sea-level normoxic PETCO2 was positively correlated to the high altitude PETCO2. Sixty percent of the volunteers developed AMS (AMS+) at some point during their altitude exposure. The resting SaO2 in the AMS+ group tended (p = 0.193) to be lower than the 40% not developing AMS (AMS-). The sea level HVD was significantly higher in the AMS+ group compared to the AMS- group; but there was a wide overlap in its distribution between the groups. None of the other sea level ventilatory measurements were meaningfully different between the AMS+ and AMS- groups.

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