HIGH-ALTITUDE PULMONARY EDEMA: Current Concepts

Annual Review of Medicine - Tập 47 Số 1 - Trang 267-284 - 1996
Herbert N. Hultgren1
1Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, 94305

Tóm tắt

▪ Abstract  High-altitude pulmonary edema (HAPE) occurs in unacclimatized individuals who are rapidly exposed to altitudes in excess of 2450 m. It is commonly seen in climbers and skiers who ascend to high altitude without previous acclimatization. Initial symptoms of dyspnea, cough, weakness, and chest tightness appear, usually within 1–3 days after arrival. Common physical signs are tachypnea, tachycardia, rales, and cyanosis. Descent to a lower altitude, nifedipine, and oxygen administration result in rapid clinical improvement. Physiologic studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (precapillary) resistance is elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury, with leakage of protein and red cells into the alveoli and airways. HAPE represents one of the few varieties of pulmonary edema where left ventricular filling pressure is normal.

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Annual Review of Medicine

Tập 47 Số 1

267-284

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