High Altitude Pulmonary Edema (HAPE)

High-altitude pulmonary oedema is an acute, non-cardiogenic accumulation of fluid in the alveoli after ascent. The initiating problem is not left-ventricular failure. Low inspired oxygen causes pulmonary arterioles to constrict; in a susceptible person, that response is excessive and unevenly distributed. Some lung regions constrict markedly while others remain relatively open. Blood is then forced through the less-constricted regions at abnormally high pressure and flow. Pulmonary artery and capillary pressures rise until the alveolar-capillary barrier develops mechanical stress failure. Protein-rich fluid and red blood cells leak into the interstitium and alveoli, producing haemorrhagic pulmonary oedema. Inflammation may follow, but it is a secondary response rather than the initial cause. Reduced nitric oxide synthesis or bioavailability can intensify pulmonary vasoconstriction. Impaired transepithelial sodium transport also reduces alveolar fluid clearance, so leaked fluid remains in the air spaces longer. A patent foramen ovale may worsen arterial hypoxaemia by allowing right-to-left shunting when right-sided pressures rise. This mechanism explains why diuresis is not the answer. The patient may be critically hypoxaemic without being fluid overloaded; removing intravascular volume can lower blood pressure and...