Pathophysiology of High Altitude Pulmonary Edema

• Published in: Nihon Kyōbu Shikkan Gakkai zasshi Vol. 26; no. 3; pp. 205 - 213
• Main Author: Kusama, Shozo
• Format: Journal Article
• Language: Japanese
• Published: Japan The Japanese Respiratory Society 01.03.1988
• Subjects: Adult; Altitude Sickness - physiopathology; Female; High altitude; Humans; Hypoxia; Hypoxia - physiopathology; Hypoxic pulmonary vasoconstriction; Hypoxic ventilatory response; Male; Middle Aged; Oxygen - blood; Platelet Count; Pulmonary Circulation; Pulmonary edema; Pulmonary Edema - physiopathology; Thromboxane B2 - metabolism
• ISSN: 0301-1542; 1883-471X
• DOI: 10.11389/jjrs1963.26.205

To determine whether there is any constitutional susceptibility underlying the development of high altitude pulmonary edema (HAPE), a field study was carried out in twelve subjects with a history of HAPE (HAPE-susceptible subjects (HAPE-SS) and control subjects living in the mountains (from 2740m to 2920m above sea level) of the Japan Alps for 4 successive days. Ventilatory response, and the pulmonary hemodynamic response to acute hypoxia were evaluated at low altitude (610m above sea level). The incidence of acute mountain sickness (AMS) of HAPE-SS in field studies, identified by using the Environmental Symptoms Questionnaire III, was higher than that in control subjects. HAPE-SS had lower oxygen saturation than controls at any given altitude. Platelet counts in HAPE-SS decreased significantly. Thromboxane B2 in HAPE-SS increased significantly, while those in controls did not increased. In both RAPE-SS and controls. 6-keto-PGF1 decreased at high altitudes. HAPE developed in one of twelve HAPE-SS on the 4th day. Pulmonary edema was confirmed by chest X-ray films. Hypoxic ventilatory response in eight HAPE-SS was significantly lower than that in nine controls, but there was no significant difference in hypercapnic ventilatory response between HAPE-SS and controls. Enhanced pulmonary vascular reactivity to hypoxia in HAPE-SS was demonstrated, using pulsed Doppler echocardiography. These findings suggest that the susceptibility to HAPE plays an important role in the pathogenesis of HAPE.