Elevated Thinking: Altitude and the Heart

Take-Home Messages

  • Altitudes above 8,200 feet can cause major physiologic effects, including decreased oxygen delivery to tissues, increased pulmonary vasoconstriction, and increased sympathetic nervous outflow.
  • Responses to high altitudes differ among cardiovascular (CV) patients, but most will see an earlier onset of symptoms at higher elevations.
  • Elevated thinking: Clinicians should make their patients aware of the changes likely at higher altitudes and help patients prepare appropriately based on the activity planned as well as medication changes that may be necessary (e.g., uptitrating beta-blocker dose for rate-controlled AF patients).

When it comes to altitude, is it safe for individuals with CV disease (CVD) to be on top of the world? How about a trip to the Mile-High City?

The effects of elevated altitude on the human body are numerous. In healthy individuals, heart rate increases at rest and at submaximal exercise workloads with no change in maximal rate; similarly, increasing altitude causes a rise in systolic blood pressure and decreases arterial oxygen saturation.1 Patients with CHD showed equivalent responses.

The major CV-related effects associated with elevated altitude are:

  • Immediate decrease in oxygen delivery to the tissues, which requires a cardiac response.
  • Increase in pulmonary vascular constriction, which increases pulmonary afterload.
  • Increase in sympathetic nervous outflow, primarily by an increase in epinephrine but also norepinephrine.

High Variability

At sea level, oxygen saturation hovers around 98 to 100 percent, but at 14,000 feet, the saturation levels drops to 80 percent due to oxygen-poor air, requiring the heart to increase cardiac output, requiring a 10 to 30 percent increase in heart rate to maintain appropriate oxygen delivery to tissues. Hypoxic pulmonary vasoconstriction serves to mediate ventilation-perfusion matching in the lungs and reduce shunt fraction to improve systemic arterial oxygen tension.2 Hypoxia also results in the release of epinephrine within minutes to hours of initial exposure and the higher epinephrine levels impact cardiac output, too.

In any individual, the degree to which changes occur will depend on numerous factors, including the overall change in elevation from an individual’s normal baseline, degree of hypoxia, rate of ascent, rate of acclimation, exercise intensity, genetics and age.3 However, with most people, significant changes usually begin above 8,200 feet. For most people, airplane travel with its higher elevations should not be an issue: cabin pressurization produces a cabin altitude that is equivalent to 5,000 to 8,000 feet.

Alterations seen at high altitudes will translate differently for CVD patients depending on their condition. Those with CAD tend to have earlier symptom onset in terms of angina or ischemic ST-elevation changes than they would at sea level, due in part to impaired coronary flow reserve and lower oxygen saturation. According to John P. Higgins, MD, these patients should be warned that they are likely to experience activity-related symptoms, for example, earlier than they would at lower elevations.

Specific Populations

For patients with heart failure, the increased sympathetic activity leads to hemodynamic changes and release of vasoactive factors.4 With increasing altitude, systemic vascular resistance rises, elevating heart rate and blood pressure; likewise, pulmonary vasoconstriction produces pulmonary hypertension especially during exercise.

Other patients appear to have a genetic predisposition to high-altitude pulmonary edema (HAPE), which usually occurs within the first four days of arrival at high altitude.5 HAPE relates to increased intravascular pulmonary vasoconstriction plus pulmonary vascular endothelial dysfunction. The rapid onset of HAPE causes what Dr. Higgins calls a “full-blown episode of pulmonary edema (and) class IV heart failure,” requiring urgent yet slow descent, including supplemental oxygen to maintain a saturation >90%, pharmacotherapy (nifedipine and the phosphodiesterase inhibitors tadalafil and sildenafil have been shown to be effective), and rest/no activity.

Patients with arrhythmias will become more tachycardic and patients being rate-contolled, such as those with atrial fibrillation, may benefit from an uptitration of their beta-blocker to compensate for the increased heart rate produced by higher epinephrine levels and sympathetic activity.

High altitudes may also impact patients with adult congenital heart disease, who are at risk due to increased right-to-left shunting. These individuals should avoid going higher than 8,000 feet, if possible.

In general, clinicians should talk to their patients about the physiologic changes at high altitude and make sure they adequately prepare for the activity. In healthy patients, an exercise treadmill test may be considered for anyone over the age of 40 to assess cardiac fitness prior to the activity. Physical conditioning prior to high-altitude activity is advised, too, as is appropriate hydration and curtailing of caffeine and alcohol. For CV symptomatic patients, a clear delineation of earlier symptom onset is critical. If a patient has had a recent hospitalization for their condition, travel should be delayed until they are more stable.


  1. Morgan BJ, et al. The patient with coronary heart disease at altitude: observations during acute exposure to 3100 meters. J Wilderness Med 1990;1:147-53.
  2. Jones JG, et al. Profound hypoxemia in pulmonary patients in airline-equivalent hypoxia: roles of VA/Q and shunt. Aviat Space Environ Med 2008;79:81-6.
  3. Higgins JP, et al. Altitude and the heart: is going high safe for your cardiac patient? Am Heart J 2010;159:25-32.
  4. Negrao CE, Middlekauff HR. Adaptations in autonomic function during exercise training in heart failure. Heart Fail Rev 2008;13:51-60.
  5. Schoene RB. Illnesses at high altitude. Chest 2008;134:402-16.


Clinical Topics: Heart Failure and Cardiomyopathies, Pulmonary Hypertension and Venous Thromboembolism, Statins, Acute Heart Failure, Pulmonary Hypertension

Keywords: Phosphodiesterase Inhibitors, Purines, Norepinephrine, Blood Pressure, Nifedipine, Vasoconstriction, Caffeine, Workload, Epinephrine, Hypertension, Pulmonary, Genetic Predisposition to Disease, Exercise Test, Constriction, Pulmonary Edema, Cardiac Output, Piperazines, Sulfones, Heart Rate, Carbolines, Heart Failure, Vascular Resistance, Oxygen, Hospitalization

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