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Related Experiment Videos

Tolerance to severe hypoxia: lessons from Mt. Everest.

J B West1

  • 1Department of Medicine, University of California San Diego, La Jolla.

Acta Anaesthesiologica Scandinavica. Supplementum
|January 1, 1990
PubMed
Summary

High altitude expeditions reveal that extreme hypoxia is tolerated via increased ventilation, but can cause central nervous system impairment. This impairment, linked to cerebral vasoconstriction, can persist long after returning to sea level.

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Area of Science:

  • Physiology
  • High Altitude Medicine
  • Environmental Health

Background:

  • Human tolerance to chronic severe hypoxia at extreme altitudes is a critical area of research.
  • Previous studies, including the 1981 American Medical Research Expedition to Everest and Operation Everest II, provide insights into physiological adaptations.
  • Understanding these adaptations is crucial for managing health risks associated with high altitude environments.

Purpose of the Study:

  • To elucidate human tolerance to chronic severe hypoxia.
  • To investigate the physiological responses to extreme altitude conditions.
  • To examine the impact of high altitude on central nervous system function.

Main Methods:

  • Analysis of data from two high-altitude studies: the 1981 American Medical Research Expedition to Everest and Operation Everest II (simulated ascent).

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  • Measurement of ventilation, alveolar and arterial partial pressures of oxygen (Po2) and carbon dioxide (Pco2).
  • Assessment of cardiac function and central nervous system (CNS) function in participants.

    • Main Results:

    • Extreme hypoxia is tolerated through significant increases in ventilation, maintaining alveolar Po2 despite reduced inspired oxygen.
    • Severe hypoxia leads to low arterial Pco2, causing respiratory alkalosis, which enhances hemoglobin oxygen affinity.
    • Cardiac function remains well-maintained, with preserved myocardial contractility, but significant CNS impairment, particularly motor coordination deficits, persists long-term, potentially linked to cerebral vasoconstriction in individuals with higher ventilation rates.

    Conclusions:

    • The human body employs substantial hyperventilation to cope with extreme altitude hypoxia, with beneficial effects on oxygen loading.
    • Despite preserved cardiac function, severe hypoxia induces CNS impairment, notably motor coordination deficits, which can be long-lasting.
    • Increased ventilation at high altitude may be associated with greater CNS impairment due to cerebral vasoconstriction.