Currently proposed pathophysiology of<unk> . Though it remains a topic of intense investigation, multiple studies and reviews over the last several years have helped to elucidate the proposed mechanism of<unk> . The inciting factor of<unk>  is the decrease in partial pressure of arterial oxygen caused by the lower air pressure at<unk><unk> s<unk>  gas pressures). The resultant hypoxemia is then thought to precipitate the development of: # Increased<unk>  arterial and capillary pressures<unk>  hypertension) secondary to hypoxic<unk>  vasoconstriction. # Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as "stress failure." This leads to subsequent leakage of cells and proteins into the alveoli, aka<unk>  edema. Hypoxic<unk>  vasoconstriction (HPV) occurs diffusely, leading to arterial vasoconstriction in all areas of the lung. This is evidenced by the appearance of "diffuse," "fluffy," and "patchy" infiltrates described on imaging studies of climbers with known<unk> . Although<unk> er<unk>  arterial pressures are associated with the development of<unk> , the presence of<unk>  hypertension may not in itself be sufficient to explain the development of edema; severe<unk>  hypertension can exist in the absence of clinical<unk>  in subjects at<unk><unk> .
High-altitude pulmonary edema
High-altitude cerebral edema
Decompression sickness
Chronic mountain sickness
Monofixation syndrome
Athletic heart syndrome
Pulmonary-renal syndrome
Cardiorenal syndrome