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High altitude, air travel, and heart disease

Troy Tuttle, MS
Asif Ali, MD
David Filsoof, MD
Section Editors
Heidi M Connolly, MD, FASE
David R Fulton, MD
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editors
Judith A Melin, MA, MD, FACP
Gordon M Saperia, MD, FACC


The number of individuals exposed to high altitude through air travel and recreational activities has been greatly increasing in the past few decades, with tens of millions of people per year traveling to high-altitude destinations [1]. Changes in physiological functions during high altitude exposure vary with an individual’s physical fitness, rate of ascent, severity and/or duration of exposure, cultural habits, geographical locations, and genetic variation [2]. While high altitude is well tolerated by most individuals, patients with cardiovascular disease are at risk of complications caused by tissue hypoxia and reduced oxygen delivery, sympathetic stimulation, increased myocardial demand, paradoxical vasoconstriction, and alterations in hemodynamics that occur with exposure to high altitude [3-5]. The duration of travel, ascent profile, degree of exertion, and any prior cardiovascular history can each impact the health of a patient with cardiovascular disease who is considering traveling to high altitude.

High altitude provides a unique physiologic challenge to the cardiovascular system. The cardiovascular response to high altitude in both healthy individuals and in patients with cardiovascular disease will be reviewed here. A general overview of high altitude disease will also be included to provide a comprehensive understanding. (See "High altitude illness: Physiology, risk factors, and general prevention".)

Most importantly, this topic will discuss the impact of high altitude on the heart. Altitude exposure can also lead to a variety of well-described clinical syndromes including some not directly involving the cardiovascular system, such as acute mountain sickness (AMS), high altitude pulmonary edema, high altitude cerebral edema, and high altitude retinal hemorrhage. These maladies are discussed in detail within this report. (See "High altitude pulmonary edema" and "Acute mountain sickness and high altitude cerebral edema" and "High altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)


When moving from sea level to high altitude, there are reductions in atmospheric pressure, oxygen pressure, humidity, and temperature [4]. It is noteworthy to point out that significant changes occur beyond the critical height of 2500 meters (8200 feet) above sea level [6]. Factors such as degree of change in elevation, degree of hypoxia, rate of ascent, level of acclimatization, exercise intensity, previous history of severe high-altitude illness, genetics, and age significantly affect the physiological change that the human body will experience during ascents [7]. One study involving Chinese men aged 18 to 35 years noted that increased age (those 26 to 35 years old) was an independent risk factor for acute mountain sickness (AMS) upon rapid ascent to high altitude (from 500 to 3700 m) and that the prevalence of AMS also increased with increasing age [8]. Hypoxia induces peripheral vasodilation and a pulmonary vasoconstriction, leading to changes in systemic blood pressure and an increase in pulmonary blood pressure that can also contribute to high altitude pulmonary edema [9].

Although altitude is the most obvious determinant of barometric pressure and its resulting physiologic stress, other factors can contribute to a reduction in barometric pressure and can increase the physiologic consequences of altitude:

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Literature review current through: Nov 2017. | This topic last updated: Jul 27, 2017.
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