Hypoxia refers to the reduced partial pressure of oxygen at altitude. It thus represents an indirect effect of altered atmospheric pressure. The clinical manifestations at a given altitude are influenced primarily by duration of exposure, rate of ascent, and individual tolerance. However, the level of physical activity, the degree of health, physical conditioning, altitude acclimatization, and such factors as temperature, wind, and humidity may all modify the response in varying degrees.
The transfer of gases between lung, blood, and tissues depends upon differences in partial pressures. Alveolar air is saturated with water vapor, which exerts a constant pressure of 47 mm. of mercury. Carbon dioxide normally contributes about 40 mm. of mercury pressure to total alveolar pressure. Although total alveolar pressure is in equilibrium with atmospheric pressure, the space available for oxygen and other components of inspired air is approximately 87 mm. of mercury less than existing atmospheric pressure.
Mixing of inspired with residual air further reduces alveolar partial-pressure of oxygen from that in the atmosphere. The alveolar pressure constantly contributed by water vapor and C02 occupies an increasingly large proportion of alveolar pressure as
atmospheric pressure declines. At sea level (alveolar Po2 = 103 mm. of mercury) hemoglobin is normally 95 to 98 per cent saturated. Not until altitudes of 10,000 feet (PB = 523 mm. of mercury and alveolar Po2 = 61 mm. of mercury) does hemoglobin saturation begin to fall below 90 per cent. Thereafter saturation declines rapidly with further increase in altitude and decline in alveolar partial pressure of oxygen.
The first important physiologic effect of hypoxia occurs at about 5000 feet, when night vision begins to be impaired. Ventilatory and cardiovascular adjustments are minimal until about 10,000 feet, above which respiratory rate and depth and heart rate increase progressively to increase alveolar Po2 and cardiac output. Exertional dyspnea may appear, and in some people mental concentration becomes difficult. Vagal cardioinhibitory reflexes may lead to bradycardia and sometimes ectopic cardiac rhythms, and may precipitate syncope. Headache, slight giddiness, and restlessness are common.
Above 15,000 feet some persons experience lassitude and indifference whereas others exhibit increased activity, irritability, euphoria, and other disturbances of affect.
The impairment of judgment that begins at these altitudes jeopardizes the safety of fliers and mountain climbers. Cyanosis, loss of peripheral vision,’ dimming of vision, and variable degrees of muscular incoordination appear at altitudes of around 18,000 feet. Somewhere between this level and 25,000 feet, consciousness can nc* longer be retained for more than a few minutes. Rapid descent or administration of oxygen is essential to prevent death. If corrective action is taken soon enough, recovery is rapid and complete.
High-flying jet aircraft make it possible for many people of various ages and states of health to be exposed to the potential hazard of sudden hypoxia from rapid decompression. Should cabin pressure be abruptly lost at high altitudes, only a short period of consciousness would be possible with the breathing of ambient air.
At altitudes between 30,000 feet and 45,000 feet oxygen transfer across alveolar walls would be reversed, and the duration of consciousness would shorten progressively, from aboul 1 minute to 15 seconds, or the lung-to-brain circulation time of about 9 seconds plus around 6 seconds from oxygen already present in brain tissue. Rapid donning of oxygen masks and descent of the aircraft would shorten the period of severe hypoxia and minimize the possibility of serious injury.