1 From the Division of Cardiology, Stanford University School of Medicine, Palo Alto, California, and the High Altitude Research Laboratory, Division of Cardiology, University of Colorado Medical Center, Denver, Colorado.
In five men with a history of susceptibility to high-altitude pulmonary edema (HAPE), hemodynamics and pulmonary gas exchange were measured at sea level, and again 24 hours following ascent to an altitude of 3,100 m. At sea level, all findings were essentially normal including a mean pulmonary arterial pressure [See Equation in PDF File] of 13.8 ± 1.9 mm Hg. None of the subjects developed clinically detectable pulmonary edema at altitude. Wedge pressures and cardiac output remained normal. [See Equation in PDF File] increased remarkably, being 38.8 ± 10.3 mm Hg at rest and 53.2 ± 11.6 mm Hg during moderate exercise. Acute relief of hypoxia only partially relieved this pulmonary hypertension. Arterial blood gases were normal at sea level. In spite of hyperventilation at altitude, arterial O2 pressure was only 50.8 ± 6.1 torr at rest and fell to 41.4 ± 3.3 torr during exercise due to a widening of the alveolar-arterial O2 pressure difference to 28.0 ± 6.8 torr. Hence, these men susceptible to HAPE developed excessive pulmonary hypertension and impaired pulmonary O2 exchange without detectable pulmonary edema following ascent to high altitude. The increase in pulmonary vascular resistance is only partially explained by hypoxic pulmonary vasoconstriction.
Submitted on January 21, 1971
© 1971 American Heart Association, Inc.
Abnormal Circulatory Responses to High Altitude in Subjects with a Previous History of High-Altitude Pulmonary Edema
Key Words: Pulmonary hypertension • Pulmonary circulation • Hypoxia • Pulmonary gas exchange
Accepted on June 19, 1971
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