Breathing at altitude Atmospheric pressure decreases with the height above sea level (altitude) and since the alveoli are open to the outside air through the open airways, the pressure in the lungs also decreases at the same rate with altitude. At altitude, a pressure differential is still required to drive air into and out of the lungs as it is at sea level. The mechanism for breathing at altitude is essentially identical to breathing at sea level but with the following differences: The atmospheric pressure decreases exponentially with altitude, roughly halving with every rise in altitude. The composition of atmospheric air is, however, almost constant below 80 km, as a result of the continuous mixing effect of the weather. At sea level, where the
ambient pressure is about 100
kPa, oxygen constitutes 21% of the atmosphere and the partial pressure of oxygen () is 21 kPa (i.e. 21% of 100 kPa). At the summit of
Mount Everest, , where the total atmospheric pressure is 33.7 kPa, oxygen still constitutes 21% of the atmosphere but its partial pressure is only 7.1 kPa (i.e. 21% of 33.7 kPa = 7.1 kPa). Consequently, at sea level, the
tracheal air (immediately before the inhaled air enters the alveoli) consists of: water vapor ( = 6.3 kPa), nitrogen ( = 74.0 kPa), oxygen ( = 19.7 kPa) and trace amounts of carbon dioxide and other gases, a total of 100 kPa. In dry air, the at sea level is 21.0 kPa, compared to a of 19.7 kPa in the tracheal air (21% of [100 – 6.3] = 19.7 kPa). At the summit of Mount Everest tracheal air has a total pressure of 33.7 kPa, of which 6.3 kPa is water vapor, reducing the in the tracheal air to 5.8 kPa (21% of [33.7 – 6.3] = 5.8 kPa), beyond what is accounted for by a reduction of atmospheric pressure alone (7.1 kPa). The
pressure gradient forcing air into the lungs during inhalation is also reduced by altitude. Doubling the volume of the lungs halves the pressure in the lungs at any altitude. Halving the sea level air pressure (100 kPa) results in a pressure gradient of 50 kPa but doing the same at 5500 m, where the atmospheric pressure is 50 kPa, a doubling of the volume of the lungs results in a pressure gradient of the only 25 kPa. In practice, because we breathe in a gentle, cyclical manner that generates pressure gradients of only 2–3 kPa, this has little effect on the actual rate of inflow into the lungs and is easily compensated for by breathing slightly deeper. The lower
viscosity of air at altitude allows air to flow more easily and this also helps compensate for any loss of pressure gradient. 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 and . This
homeostatic mechanism prioritizes the regulation of the arterial over that of oxygen at sea level. That is to say, at sea level the arterial is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial , 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 ) 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 . If this switch occurs relatively abruptly, the hyperventilation at high altitude will cause a severe fall in the arterial 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.
Breathing at depth Pressure increases with the depth of water at the rate of about one
atmosphere – slightly more than 100 kPa, or one
bar, for every 10 meters. Air breathed underwater by
divers is at the ambient pressure of the surrounding water and this has a complex range of physiological and biochemical implications. If not properly managed, breathing compressed gasses underwater may lead to several
diving disorders which include
pulmonary barotrauma,
decompression sickness,
nitrogen narcosis, and
oxygen toxicity. The effects of breathing gasses under pressure are further complicated by the use of one or more
special gas mixtures. Air is provided by a
diving regulator, which reduces the high pressure in a
diving cylinder to the ambient pressure. The
breathing performance of regulators is a factor when choosing a suitable regulator for the
type of diving to be undertaken. It is desirable that breathing from a regulator requires low effort even when supplying large amounts of air. It is also recommended that it supplies air smoothly without any sudden changes in resistance while inhaling or exhaling. In the graph, right, note the initial spike in pressure on exhaling to open the exhaust valve and that the initial drop in pressure on inhaling is soon overcome as the
Venturi effect designed into the regulator to allow an easy draw of air. Many regulators have an adjustment to change the ease of inhaling so that breathing is effortless. ==Respiratory disorders==