• J T Reeves and J V Weil.
• The Department of Pediatrics, University of Colorado Health Sciences Center, Denver, USA.
• Adv Exp Med Biol. 2001 Jan 1; 502: 419-37.

AbstractChronic mountain sickness (CMS) is a poorly understood syndrome, characterized by hypoxemia and polycythemia and occurring in persons residing at high altitude. To better characterize the disorder, we have reviewed measurements in more than 750 men and 200 women living at altitude as published and as submitted by colleagues. In men, blood hemoglobin concentration (Hb) and arterial oxygen saturation (SaO2) related to altitude (r=0.72). There was greater variability in both SaO2 and hemoglobin above than below 3000 m, largely due to inter-individual variations in effective ventilation. For the entire cohort, a linear relationship (r=0.72) of an index of hematopoietic response (Hb) to an index of stimulus (SaO2) was independent of age, altitude, duration of altitude residence greater than one year, ethnic origin, geographic location, presence or absence of CMS and nearly independent of gender. A potentially important and usually unrecognized variation in the hypoxic stimulus was desaturation during sleep. Contributions to variation in response include ingested toxins, such as cobalt, and nutritional deficiencies, including iron. Pulmonary hypertension was related to chronic hypoxia, with an uncertain contribution from polycythemia. In CMS there were profound hypoxemia at night, decrease in cerebral blood flow, and loss of cerebral blood flow regulation, possibly causing the cerebral symptoms. We speculate that the relationship of Hb to SaO2 is more useful than of hemoglobin to altitude, that hypoventilation awake and asleep are the primary causes accentuating altitude-hypoxia, and that the brain is the primary target organ in the disorder.

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