Respiratory system
Responses to low atmospheric pressures

All of the above influences of low atmospheric pressures on breathing are accommodated primarily by breathing deeper and faster (hyperpnea). The exact degree of hyperpnea is determined by the blood gas homeostat, which regulates the partial pressures of oxygen and carbon dioxide in the arterial blood. This homeostat prioritizes the regulation of the arterial partial pressure of carbon dioxide over that of oxygen at sea level. That is to say, at sea level the arterial partial pressure of CO is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial partial pressure of O, which is allowed to vary within a very wide range of values, before eliciting a corrective ventilatory response. However, when the atmospheric pressure (and therefore the partial pressure of O in the ambient air) falls to below 50-75% of its value at sea level, oxygen homeostasis is given priority over carbon dioxide homeostasis. This switch-over occurs at an elevation of about 2500 m (or about 8000 ft). If this switch occurs relatively abruptly, the hyperpnea at high altitude will cause a severe fall in the arterial partial pressure of carbon dioxide, with a consequent rise in the pH of the arterial plasma. This is one contributor to high altitude sickness. On the other hand, if the switch to oxygen homeostasis is incomplete, then hypoxia may complicate the clinical picture with potentially fatal results.
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