Journal of Applied Physiology
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J Appl Physiol 63: 521-530, 1987;
8750-7587/87 $5.00
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Journal of Applied Physiology, Vol 63, Issue 2 521-530, Copyright © 1987 by American Physiological Society

ARTICLES

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen

B. M. Groves, J. T. Reeves, 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.

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l-1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.


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