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Cardiovascular Research 2006 72(1):41-50; doi:10.1016/j.cardiores.2006.07.004
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Copyright © 2006, European Society of Cardiology

High altitude-induced pulmonary oedema

Marco Maggiorini*

Intensive Care Unit, Department of Internal Medicine, University Hospital, Rämistrasse 100, CH-8091 Zürich, Switzerland

* Tel.: +41 44 255 22 04; fax: +41 44 255 31 81. Email address: klinmax{at}usz.unizh.ch

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (>300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.

KEYWORDS High altitude pulmonary oedema; Capillary pressure; Hypoxic pulmonary vasoconstriction; Trans-epithelial Na transport; Nifedipine; Tadalafil; Dexamethasone

Time for primary review 12 days


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