High Altitude Exposure and Cardiovascular Circulation: Friends or Foe?

Abstract

Cardiovascular function encounter changes on exposure to altitude. The fall in arterial blood oxygen saturation, due to low quantity of breathable oxygen, caused by low atmospheric pressure at high altitude, is known as High altitude hypoxia (HAH). The human body is capable of adapting to HAH via short- and long-term mechanisms. HAH affects the vascular tone of the pulmonary and systemic vessels thereby increasing ventilation, which is the first notable change at high altitude (HA). Exposure to altitude increases cerebral and coronary blood flow and causes pulmonary hypertension. Pulmonary hypertension, is associated with a rise in pulmonary vascular resistance secondary to vasoconstriction induced by hypoxia and vascular remodeling. Initially exposure to HA decreases systolic blood pressure which increase when the sympathetic nervous system is activated. The increase in blood pressure and sympathetic nervous system activation, leads to an increase in heart rate and cardiac output, which falls to normal few days after acclimatization, but the increased heart rate is retained, while the stroke volume remains decreased. The adaptation of the cardiovascular system to chronic exposure to hypoxia involves both structural and functional changes. These include; persistent pulmonary hypertension, right ventricle (RV) hypertrophy, decrease in CBF and reduced fetal and uteroplacental volumetric blood flows. This review focuses on the adjustment of the cardiovascular system to high altitude exposure.