Altitude sickness pathophysiology

	Altitude sickness Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Altitude sickness caused by an increase in pulmonary artery pressure due to the normal pulmonary vasoconstriction induced by hypoxia. Hypoxia leads to increase oxygen delivery to the tissues and increases ventilation, cardiac output and haemoglobin concentrations. These changes improve ventilation-perfusion matching and gas exchange and lead to high altitude pulmonary hypertension.

Abbreviations: CBV= Cerebral blood volume, CBF= Cerebral or coronary blood flow, Pcap= Pulmonary capillary pressure, HACE= High-altitude cerebral edema, HAPE= High-altitude pulmonary edema ^[1]^[2]^[3]^[4]

Altitude hypoxemia

Brain

Lung

Vasodilation

Uneven vasoconstriction

↑CBV

↑CBF

↑PAP

Overperfusion

Focal/regional overperfusion

↑Pcap

Vasogenic edema

Capillary leak

HACE

HAPE

↑ Imray C, Wright A, Subudhi A, Roach R (2010). "Acute mountain sickness: pathophysiology, prevention, and treatment". Prog Cardiovasc Dis. 52 (6): 467–84. doi:10.1016/j.pcad.2010.02.003. PMID 20417340.
↑ Taylor AT (January 2011). "High-altitude illnesses: physiology, risk factors, prevention, and treatment". Rambam Maimonides Med J. 2 (1): e0022. doi:10.5041/RMMJ.10022. PMC 3678789. PMID 23908794.
↑ Hackett PH (1999). "High altitude cerebral edema and acute mountain sickness. A pathophysiology update". Adv. Exp. Med. Biol. 474: 23–45. PMID 10634991.
↑ Murdoch D (March 2010). "Altitude sickness". BMJ Clin Evid. 2010. PMC 2907615. PMID 21718562.