Physiopathology of High-Altitude Pulmonary Edema.

Abstract

The air-blood barrier is well designed to accomplish the matching of gas diffusion with blood flow. This function is achieved by maintaining its thickness at ∼0.5 µm, a feature implying to keep extravascular lung water to the minimum. Exposure to hypobaric hypoxia, especially when associated with exercise, is a condition potentially leading to the development of the so-called high-altitude pulmonary edema (HAPE). This article presents a view of the physiopathology of HAPE by merging available data in humans exposed to high altitude with data from animal experimental approaches. A model is also presented to characterize HAPE nonsusceptible versus susceptible individuals based on the efficiency of alveolar-capillary oxygen uptake and estimated morphology of the air-blood barrier.