Operation Everest II: Preservation of Cardiac Function at Extreme Altitude

摘要

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 (8840m, Pa 240 mmHg, PIO2 43 mmHg). In the 5 subjects having resting and exercise measurements at the barometric pressures of 760 (sea level), 347 (6100m), 282 (7620m), and 240 mmHg, heart rate for a given oxygen uptake rose with the progressive hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise, with arterial blood oxygen saturations below 50%. Oxygen breathing reversed hypoxemia but never increased heart rate, suggesting that depression of rate, if present, was slight. For a given oxygen uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling i.e., decreased right atrial and wedge pressures. Oxygen 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.