quality:correction
Breathing at altitude

All of the above effects of low atmospheric pressure on breathing are normally accommodated by increasing the respiratory minute volume (the volume of air breathed in — or out — per minute), and the mechanism for doing this is automatic. The exact increase required is determined by the respiratory gases homeostatic mechanism, which regulates the arterial P and P. This homeostatic mechanism prioritizes the regulation of the arterial P over that of oxygen at sea level. That is to say, at sea level the arterial P is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial P, 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 atmospheric P) falls to below 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 2,500 metres (8,200 ft). If this switch occurs relatively abruptly, the hyperventilation at high altitude will cause a severe fall in the arterial P with a consequent rise in the pH of the arterial plasma leading to respiratory alkalosis. 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.