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wook · 03-12-2012, 18:29

From an electronic resource....

High altitude pulmonary edema (HAPE) is the abnormal accumulation of water in the lung due to a breakdown in the pulmonary blood-gas barrier, triggered by hypobaric hypoxia. This breakdown develops from a number of maladaptive responses to hypoxia, including poor ventilatory response, increased sympathetic tone, exaggerated and uneven pulmonary vasoconstriction (pulmonary hypertension), inadequate production of endothelial nitric oxide, and overproduction of endothelin . The end result is a patchy accumulation of extravascular fluid in the alveolar spaces that impairs respiration and can, in severe cases, prove fatal.

Genetics likely play an important role in the risk of HAPE, as suggested by the marked variability in individual susceptibility and the higher rates of recurrence among some individuals.

High mean pulmonary artery (PA) pressure, in excess of 35 to 40 mmHg, appears to be the initiating event. Specific segmental and subsegmental capillary beds with relatively less vasoconstriction are disproportionately exposed to elevated microvascular pressures (>20 mmHg) that arise from the elevated mean PA pressure. This uneven vasoconstriction and regional overperfusion result in failure of the alveolar-capillary barrier and patchy pulmonary edema.

As disruption of the alveolar-capillary barrier progresses, high molecular weight proteins, cells, and fluid leak into the alveolar space. Eventually, basement endothelial and epithelial cell membranes are disrupted, leading to alveolar hemorrhage.

A striking feature of HAPE is the rapid reversibility of this process with descent or the administration of oxygen. Pulmonary vascular resistance returns to normal within days after descent to low altitude.

High altitude pulmonary edema (HAPE) generally occurs above 2500 m (8000 ft). The incidence depends upon individual susceptibility, altitude attained, rate of ascent, and time spent at altitude. Symptoms of acute mountain sickness (AMS) develop in approximately 50 percent of those with HAPE. High altitude cerebral edema (HACE) may also occur concomitantly.

03-12-2012, 18:29	#15
wook Asset Join Date: Jul 2009 Location: MA Posts: 34	From an electronic resource.... High altitude pulmonary edema (HAPE) is the abnormal accumulation of water in the lung due to a breakdown in the pulmonary blood-gas barrier, triggered by hypobaric hypoxia. This breakdown develops from a number of maladaptive responses to hypoxia, including poor ventilatory response, increased sympathetic tone, exaggerated and uneven pulmonary vasoconstriction (pulmonary hypertension), inadequate production of endothelial nitric oxide, and overproduction of endothelin . The end result is a patchy accumulation of extravascular fluid in the alveolar spaces that impairs respiration and can, in severe cases, prove fatal. Genetics likely play an important role in the risk of HAPE, as suggested by the marked variability in individual susceptibility and the higher rates of recurrence among some individuals. High mean pulmonary artery (PA) pressure, in excess of 35 to 40 mmHg, appears to be the initiating event. Specific segmental and subsegmental capillary beds with relatively less vasoconstriction are disproportionately exposed to elevated microvascular pressures (>20 mmHg) that arise from the elevated mean PA pressure. This uneven vasoconstriction and regional overperfusion result in failure of the alveolar-capillary barrier and patchy pulmonary edema. As disruption of the alveolar-capillary barrier progresses, high molecular weight proteins, cells, and fluid leak into the alveolar space. Eventually, basement endothelial and epithelial cell membranes are disrupted, leading to alveolar hemorrhage. A striking feature of HAPE is the rapid reversibility of this process with descent or the administration of oxygen. Pulmonary vascular resistance returns to normal within days after descent to low altitude. High altitude pulmonary edema (HAPE) generally occurs above 2500 m (8000 ft). The incidence depends upon individual susceptibility, altitude attained, rate of ascent, and time spent at altitude. Symptoms of acute mountain sickness (AMS) develop in approximately 50 percent of those with HAPE. High altitude cerebral edema (HACE) may also occur concomitantly.
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