High Altitude Pulmonary Edema Medical Slides

Present the three-stage mechanism: (1) Exaggerated hypoxic pulmonary vasoconstriction (HPV) — HAPE-susceptible individuals have ~2x greater pulmonary artery pressure response to hypoxia. (2) Heterogeneous arteriolar constriction leads to regional overperfusion of unprotected capillary beds with pressures exceeding capillary strength. (3) Capillary stress failure causes high-permeability leak — protein-rich edema fluid (not hydrostatic edema). Key distinction: HAPE is NOT ARDS — no inflammation initially, no diffuse alveolar damage on pathology. This explains the rapid resolution with oxygen and descent.

Present the evidence: Nifedipine SR 30 mg twice daily (Bärtsch 1991, gold standard for HAPE prevention in susceptible individuals) — reduces pulmonary artery pressure. Tadalafil 10 mg twice daily (Maggiorini 2006, NEJM) — reduced HAPE incidence from 56% to 10% in HAPE-susceptible subjects. Dexamethasone 8 mg twice daily (Maggiorini 2006) — also reduced HAPE, may work via decreased capillary leak. Salmeterol 125 μg inhaled twice daily — 50% reduction (Sartori 2002) but less reliable than systemic agents. For known HAPE-susceptible individuals: nifedipine is first-line prophylaxis per Wilderness Medical Society guidelines.

Present the treatment algorithm by resource availability: (1) Descent — most effective treatment, descend ≥300-1000 m; clinical improvement often within hours. (2) Supplemental oxygen — maintain SpO2 >90%; equally effective as descent if adequate supply. (3) Portable hyperbaric chamber (Gamow bag) — simulates descent of 1500-2500 m, used when evacuation is impossible. (4) Nifedipine 30 mg SR every 12 hours — reduces PAP, useful as adjunct or when oxygen/descent unavailable. (5) CPAP/EPAP — non-pharmacological alternative improving oxygenation. Emphasize that HAPE is rapidly reversible if treated early — mortality <1% with prompt management.