Oxygen Transport and Cardiovascular Function at Extreme Altitude: Lessons from Operation Everest II

Abstract

Operation Everest II was designed to examine the physiological responses to gradual decompression simulating an ascent of Mt Everest (8,848 m) to an inspired PO₂ of 43 mmHg. The principal studies conducted were cardiovascular, respiratory, muscular-skeletal and metabolic responses to exercise. Eight healthy males aged 21-31 years began the “ascent” and six successfully reached the “summit”, where their resting arterial blood gasses were PO₂ = 30 mmHg and PCO₂ = 11 mmHg, pH = 7.56. Their maximal oxygen uptake decreased from 3.98 ± 0.2 L/min at sea level to 1.17 ± 0.08 L/min at PIO₂ 43 mmHg. The principal factors responsible for oxygen transport from the atmosphere to tissues were (1) Alveolar ventilation - a four fold increase. (2) Diffusion from the alveolus to end capillary blood - unchanged. (3) Cardiac function (assessed by hemodynamics, echocardiography and electrocardiography) - normal - although maximum cardiac output and heart rate were reduced. (4) Oxygen extraction - maximal with PvO₂ 14.8 ± 1 mmHg. With increasing altitude maximal blood and muscle lactate progressively declined although at any submaximal intensity blood and muscle lactate was higher at higher altitudes.

Key words

Altitude - exercise - cardiac output - hypobaric chamber - pulmonary circulation