Effects of High Altitude

Hypoxia is the main physiological complication when ascending to high altitudes. The percentage of oxygen in the atmosphere stays the same, but the partial pressure and barometric pressure begin to drop on rising to a higher altitude. The level of altitude, rate of ascent, and duration of exposure all determine the body’s response to hypoxia. The physiological responses to high altitude hypoxia are divided into two categories. First there are acute responses known as accommodation, which refers to the immediate reflex adjustments of the respiratory and cardiovascular systems to hypoxia. Second there are long term responses called acclimatization, which refers to the changes in body tissues in response to long term exposure to hypoxia. While long term responses occur within a cell, the acute physiologic responses are necessary for letting the cells adjust. The most significant acute response to hypoxia is sustained hyperventilation triggered by chemoreceptors in the carotid and aortic bodies. With this prolonged hyperventilation a high alveolar P02 is produced, but with that there is a lowered alveolar PCO2 that results in respiratory alkalosis. This wants to decrease the ventilation, but renal compensation is activated, secreting bicarbonate and reabsorbing hydrogen which gradually brings the blood PH back to normal and allows further increase in ventilation. This acute hypoxic ventilatory response takes approximately 4 days.
In addition to changes in ventilation, cardiovascular or circulatory changes take place that increase oxygen delivery to the tissues. When ascending to high altitude, the sympathetic nervous system is stimulated, leading to an increased resting heart rate, cardiac output, and a mild increase in blood pressure. This happens by hypoxic pulmonary vasoconstriction, the pulmonary arteries constrict, and redirect the blood flow to alveoli with a higher oxygen capacity. This in turn improves ventilation/perfusion matching and arteriole blood flow,