Oxygen is vital for cellular metabolism; therefore, the hypoxic conditions encountered at high altitude affect all physiological functions. Acute hypoxia activates the adrenergic system and induces tachycardia, whereas hypoxic pulmonary vasoconstriction increases pulmonary artery pressure. After a few days of exposure to low oxygen concentrations, the autonomic nervous system adapts and tachycardia decreases, thereby protecting the myocardium against high energy consumption. Permanent exposure to high altitude induces erythropoiesis, which if excessive can be deleterious and lead to chronic mountain sickness, often associated with pulmonary hypertension and heart failure. Genetic factors might account for the variable prevalence of chronic mountain sickness, depending on the population and geographical region. Cardiovascular adaptations to hypoxia provide a remarkable model of the regulation of oxygen availability at the cellular and systemic levels. Rapid exposure to high altitude can have adverse effects in patients with cardiovascular diseases. However, intermittent, moderate hypoxia might be useful in the management of some cardiovascular disorders, such as coronary heart disease and heart failure. The aim of this Review is to help physicians to understand the cardiovascular responses to hypoxia and to outline some recommendations that they can give to patients with cardiovascular disease who wish to travel to high-altitude destinations.
Hypoxic conditions encountered at high altitude affect all physiological functions. In this Review, Richalet et al. describe the cardiovascular responses to acute and chronic exposure to hypoxia and provide recommendations that clinicians can give to patients with cardiovascular disease who wish to travel to high-altitude destinations.
Key points: Acute exposure to high altitude stimulates the adrenergic system, increasing heart rate and cardiac output; although blood pressure remains stable, pulmonary artery pressure increases owing to hypoxic pulmonary vasoconstriction.Prolonged exposure to high altitude induces a decrease in maximal heart rate through desensitization of the adrenergic pathway, as a protective mechanism against environmental conditions of low oxygen availability.Long-term exposure to high altitude results in cardiac adaptations with no obvious dysfunction; stroke volume is slightly reduced owing to decreased left ventricular filling volume secondary to right ventricular overload.High-altitude natives can develop chronic mountain sickness, associated with erythropoiesis, pulmonary hypertension and right heart failure, although genetic adaptations to hypoxia have been found in Tibetan and Ethiopian populations.Patients with cardiovascular diseases can be at increased risk of adverse events at altitudes above 2,500 m, owing to hypoxaemia, high adrenergic activity and pulmonary hypertension.Intermittent, moderate hypoxia might be useful in the conditioning of patients with cardiovascular diseases, such as coronary heart disease and heart failure.