Cardiopulmonary adaptation to high altitude

Abstract

The reduction in inspired oxygen pressure with increasing altitude triggers a full array of mechanisms allowing the human body to adapt to the lower oxygen availability. The adrenergic system is activated via the stimulation of peripheral chemoreceptors, leading to an increase in heart rate and cardiac output. With acclimatization, the cardiac response to adrenergic activation is blunted leading to an autoregulation of cardiac function that protects the heart against an imbalance between O2 availability and O2 consumption. Altogether, the cardiac inotropic function in normal subjects is not altered by altitude exposure, while diastolic filling might be slightly impaired. Hypoxia induces a pulmonary vasoconstriction that may be harmful when pulmonary hypertension develops, favoring the occurrence of High Altitude Pulmonary Edema. No major change is observed in the peripheral circulation except a transient increase in cerebral blood flow. High altitude natives may develop with aging an excessive polycythemia frequently associated with pulmonary hypertension that might lead to cardiac failure. In sea-level cardiac patients, oxygen lack might be detrimental although there is very little evidence of aggravated cardiovascular diseases at least at low and moderate altitudes.