Critique of the equivalent air altitude model

  • Conkin J
  • Wessel J
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Abstract

The adverse effects of hypoxic hypoxia include acute mountain sickness (AMS), high altitude pulmonary edema, and high altitude cerebral edema. It has long been assumed that those manifestations are directly related to reduction in the inspired partial pressure of oxygen (P(I)O2). This assumption underlies the equivalent air altitude (EAA) model, which holds that combinations of barometric pressure (P(B)) and inspired fraction of O2 (F(I)O2) that produce the same P(I)O2 will result in identical physiological responses. However, a growing body of evidence seems to indicate that different combinations of P(B) and P(I)O2 may produce different responses to the same P(I)O2. To investigate this question with respect to AMS, we conducted a search of the literature using the terms hypobaric hypoxia, normobaric hypoxia, and hypobaric normoxia. The results suggest that the EAA model provides only an approximate description of isohypoxia, and that P(B) has an independent effect on hypoxia and AMS. A historical report from 1956 and 15 reports from 1983 to 2005 compare the same hypoxic P(I)O2 at different P(B) with respect to the development of hypoxia and AMS. These data provide evidence for an independent effect of P(B) on hypoxia and AMS, and thereby invalidate EAA as an ideal model of isohypoxia. Refinement of the EAA model is needed, in particular for applications to high altitude where supplemental O2 is inadequate to prevent hypoxic hypoxia. Adjustment through probabilistic statistical modeling to match the current limited experimental observations is one approach to a better isohypoxic model.

Author-supplied keywords

  • Acute mountain sickness
  • Hypobaric hypoxia
  • Hypobaric normoxia
  • Hypoxia
  • Normobaric hypoxia
  • Normobaric normoxia
  • Supplemental oxygen

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Authors

  • Johnny Conkin

  • James H. Wessel

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