Journal of Applied Physiology
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J Appl Physiol 63: 531-539, 1987;
8750-7587/87 $5.00
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Journal of Applied Physiology, Vol 63, Issue 2 531-539, Copyright © 1987 by American Physiological Society

ARTICLES

Operation Everest II: preservation of cardiac function at extreme altitude

J. T. Reeves, B. M. Groves, J. R. Sutton, P. D. Wagner, A. Cymerman, M. K. Malconian, P. B. Rock, P. M. Young and C. S. Houston
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262.

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.


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