High-altitude pulmonary edema: pathophysiology and clinical review.
High-altitude pulmonary edema (HAPE) affects young, healthy climbers in an unpredictable fashion. It is potentially fatal, and its underlying pathophysiology is not thoroughly understood. The history and clinical presentation of HAPE, as well as the known underlying pathophysiology, are reviewed. For instance, in HAPE there is an association with blunted respiratory drives to hypoxia and accentuated hypoxic pulmonary vasoconstriction. Recent data show that HAPE is a high permeability leak of protein into the alveolar space associated with an influx of alveolar macrophages. These data have been obtained recently by fiberoptic bronchoscopy in the field setting of Mt McKinley at 4,400 m. The approach to recognition and treatment that involves primarily descent and/or oxygen is discussed.
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D000532:Altitude Sickness / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D002463:Cell Membrane Permeability; D006801:Humans; D000860:Hypoxia / Q000175:diagnosis*; D008168:Lung / Q000503:physiopathology; D010102:Oxygen Inhalation Therapy; D011175:Positive-Pressure Respiration; D011506:Proteins / Q000378:metabolism; D011654:Pulmonary Edema / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology / Q000628:therapy
D011506:Proteins