Stroke volume is decreased initially, and an increased heart rate maintains cardiac output. Maximum exercising heart rate declines at altitude proportional to the decrease in maximum oxygen consumption (VO2 max). Cardiac muscle in healthy persons is able to withstand extreme levels of hypoxemia (PaO2 < 30 mmHg) without evidence of ST segment changes or ischemic events. Blood pressure is mildly elevated on ascent secondary to increased sympathetic tone.
The pulmonary circulation constricts with exposure to hypoxia. This is an advantage during regional alveolar hypoxia, such as pneumonia, but is a disadvantage during the global hypoxia of altitude exposure. As a result, pulmonary pressure increases. This degree of hypertension is quite variable, with those having a hyperreactive response much more susceptible to high altitude pulmonary edema.
Cerebral blood flow transiently increases on ascent to altitude (despite the hypocapnic alkalosis), which increases oxygen delivery to the brain. This response, however, is limited by the increase in cerebral blood volume, which may increase intracranial pressure and aggravate symptoms of altitude illness.
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