Three days after ascending rapidly to 4500 m, a climber develops progressive dyspnea at rest, dry cough, and crackles. Chest imaging shows patchy infiltrates with a normal-sized heart. The pathogenesis of this condition involves:

• A Left ventricular failure elevating pulmonary venous pressure
• B Hypercoagulability producing multiple small pulmonary emboli
• C Systemic vasodilation leading to transudation across the alveolar membrane
• D Uneven hypoxic pulmonary vasoconstriction causing overperfusion and stress failure of pulmonary capillaries ✓

Explanation

High-altitude pulmonary edema results from nonuniform hypoxic pulmonary vasoconstriction: poorly constricted regions receive excessive flow at high pressure, and the resulting elevated capillary stresses cause leakage and even stress failure of the capillary walls. The left atrium and left ventricle are normal, distinguishing it from cardiogenic edema, and there is no thrombotic component. Rapid descent, oxygen, nifedipine, and portable hyperbaric therapy are the mainstays of treatment.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.