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Ganong's Review of Medical Physiology, 23rd Edition

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618 SECTION VII Respiratory <strong>Physiology</strong><br />

Pressure (mm Hg)<br />

FIGURE 36–12 Composition <strong>of</strong> alveolar air in individuals breathing air (0–6100 m) and 100% O 2 (6100–13,700 m). The minimal<br />

alveolar PO 2 that an unacclimatized subject can tolerate without loss <strong>of</strong> consciousness is about 35–40 mm Hg. Note that with increasing altitude,<br />

the alveolar PCO 2 drops because <strong>of</strong> the hyperventilation due to hypoxic stimulation <strong>of</strong> the carotid and aortic chemoreceptors. The fall in barometric<br />

pressure with increasing altitude is not linear, because air is compressible.<br />

to definitely increase ventilation. As one ascends higher, the<br />

alveolar PO 2 falls less rapidly and the alveolar PCO 2 declines<br />

somewhat because <strong>of</strong> the hyperventilation. The resulting fall<br />

in arterial PCO 2 produces respiratory alkalosis.<br />

HYPOXIC SYMPTOMS BREATHING AIR<br />

A number <strong>of</strong> compensatory mechanisms operate over a period<br />

<strong>of</strong> time to increase altitude tolerance (acclimatization), but in<br />

unacclimatized subjects, mental symptoms such as irritability<br />

appear at about 3700 m. At 5500 m, the hypoxic symptoms are<br />

severe; and at altitudes above 6100 m (20,000 ft), consciousness<br />

is usually lost.<br />

HYPOXIC SYMPTOMS<br />

BREATHING OXYGEN<br />

0<br />

760<br />

720<br />

680<br />

640<br />

600<br />

320<br />

280<br />

240<br />

200<br />

160<br />

120<br />

The total atmospheric pressure becomes the limiting factor in<br />

altitude tolerance when breathing 100% O 2 .<br />

The partial pressure <strong>of</strong> water vapor in the alveolar air is<br />

constant at 47 mm Hg, and that <strong>of</strong> CO 2 is normally 40 mm<br />

Hg, so that the lowest barometric pressure at which a normal<br />

alveolar PO 2 <strong>of</strong> 100 mm Hg is possible is 187 mm Hg, the<br />

pressure at about 10,400 m (34,000 ft). At greater altitudes, the<br />

increased ventilation due to the decline in alveolar PO 2 lowers<br />

the alveolar PCO 2 somewhat, but the maximum alveolar PO 2<br />

80<br />

40<br />

0<br />

Altitude (m)<br />

3000 6000 9000 12,000 15,000 18,000 21,000<br />

Highest permanent<br />

human habitations<br />

(5500 m) Loss <strong>of</strong> consciousness<br />

if unacclimatized<br />

breathing air<br />

N 2<br />

O 2<br />

CO 2<br />

H 2 O<br />

Top <strong>of</strong> Mt. Everest<br />

(8854 m)<br />

Alveolar PO2 100 mm Hg<br />

(10,400 m)<br />

Alveolar PO2 40 mm Hg<br />

(13,700 m)<br />

Loss <strong>of</strong> consciousness<br />

breathing 100% O2 Body fluids boil at<br />

37° C<br />

Breathing air Breathing 100% O 2 Life impossible without<br />

pressurization<br />

that can be attained when breathing 100% O 2 at the ambient<br />

barometric pressure <strong>of</strong> 100 mm Hg at 13,700 m is about 40<br />

mm Hg. At about 14,000 m, consciousness is lost in spite <strong>of</strong><br />

the administration <strong>of</strong> 100% O 2 . At 19,200 m, the barometric<br />

pressure is 47 mm Hg, and at or below this pressure the body<br />

fluids boil at body temperature. The point is largely academic,<br />

however, because any individual exposed to such a low pressure<br />

would be dead <strong>of</strong> hypoxia before the bubbles <strong>of</strong> steam<br />

could cause death.<br />

Of course, an artificial atmosphere can be created around<br />

an individual; in a pressurized suit or cabin supplied with O 2<br />

and a system to remove CO 2 , it is possible to ascend to any<br />

altitude and to live in the vacuum <strong>of</strong> interplanetary space.<br />

Some delayed effects <strong>of</strong> high altitude are discussed in Clinical<br />

Box 36–4.<br />

ACCLIMATIZATION<br />

(19,200 m)<br />

Acclimatization to altitude is due to the operation <strong>of</strong> a variety<br />

<strong>of</strong> compensatory mechanisms. The respiratory alkalosis produced<br />

by the hyperventilation shifts the oxygen–hemoglobin<br />

dissociation curve to the left, but a concomitant increase in red<br />

blood cell 2,3-BPG tends to decrease the O 2 affinity <strong>of</strong> hemoglobin.<br />

The net effect is a small increase in P 50 . The decrease<br />

in O 2 affinity makes more O 2 available to the tissues. However,<br />

the value <strong>of</strong> the increase in P 50 is limited because when the

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