High Altitude Pulmonary Edema (HAPE)

High-altitude pulmonary edema is an acute, non-cardiogenic accumulation of fluid in the lungs after ascent. The initiating problem is hypoxic pulmonary vasoconstriction, not left-ventricular failure or excess circulating volume. In a susceptible person, low inspired oxygen produces an excessive and uneven rise in pulmonary vascular resistance. Some lung regions constrict more than others. Blood is redirected through less-constricted regions, raising regional capillary pressure. The resulting mechanical stress disrupts the alveolar-capillary barrier, allowing protein-rich fluid and red blood cells to enter the air spaces. This is primarily a pressure-driven process; inflammation is not the initiating cause. Hypoxia can also impair sodium-dependent alveolar fluid clearance, allowing fluid to persist. This mechanism explains two priorities. First, oxygen and descent reduce the hypoxic stimulus and pulmonary vascular pressure. Second, routine diuresis is inappropriate: many patients with HAPE have intravascular volume depletion, and further volume loss can cause hypotension. The nurse should therefore connect worsening breathlessness after ascent with impaired oxygenation and pulmonary vascular pressure rather than assume cardiogenic fluid overload.