Pulmonary hemodynamics: implications for high altitude pulmonary edema (HAPE). A review

Abstract

The role of pulmonary hemodynamics is central to the pathogenesis of high altitude pulmonary edema (HAPE). High pulmonary artery pressure is a marker of HAPE susceptibility in hypoxia and to a lesser extent in normoxia. Compared to non-susceptible subjects high pulmonary artery pressure is present not only at rest, but also during exercise and sleep. The reasons for elevated pulmonary artery pressure in HAPE susceptible subjects include increased vasomotor tone, severe hypoxic vasoconstriction and diminished capacity of the pulmonary circulation. Overperfusion of some parts of the capillary bed and wave reflections in the pulmonary circulation may result in pressure transients in the peripheral circulation which are considerably greater than the pressure in the main arteries. The mechanism by which pulmonary hypertension causes the pulmonary circulation to leak involves hydraulic stress. Patchy vasoconstriction may expose parts of the capillary bed to high pressure resulting in stress failure of the capillary wall. The development of an inflammatory process may then occur after the initiation of the leak.