Effects of high altitude

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Chapter 12 Effects of high altitude

ALTITUDE AND OXYGEN TRANSPORT

Effects of altitude on plasma oxygen uptake

The standard atmospheric pressure of 760 mmHg (101 kPa) at sea level reflects the weight exerted by the gas molecules that make up the air, under gravitational force. As one ascends from sea level, the air becomes progressively less compressed and so the constituent gas molecules become less tightly packed. In consequence, a given volume of inspired air contains fewer molecules of all gases, including oxygen. The relationship between altitude and atmospheric pressure is not a strictly linear one because the air volume increases in 3 dimensions but, in rough terms, pressure falls by around 100 mmHg for every 1000 m (3300 ft) of ascent up to 3000 m (10 000 ft) (Fig. 12.1).

The absolute change in oxygen availability imposed by a given ascent can be calculated easily. Since oxygen represents 21% of normal air, the partial pressure of oxygen (PO2) at sea level is (21%.760) or 160 mmHg. Once inspired, the air becomes saturated with water vapour (partial pressure 47 mmHg) so that the total gas pressure is reduced to 713 mmHg and PO2 falls to (21%.713) or 150 mmHg. In the alveoli, the oxygen is diluted further by approximately 50 mmHg, due primarily to the presence of carbon dioxide, resulting in a local PO2 (PAO2) of around 100 mmHg: at equilibrium with the plasma, arterial PO2 (PaO2) is, therefore, usually also around 100 mmHg.

At an atmospheric pressure of 560 mmHg, which corresponds to an altitude of around 2300 m (7600 ft) or just higher than Mexico City, PAO2 can be estimated to be around 60 mmHg (21%.[560–47] – 50). Many of the major ski resorts like Aspen and Zermatt involve slopes at heights in excess of 3500 m (11 000 ft), where atmospheric pressure is 500 mmHg and so PAO2 will be around (21%.[500–47] – 50) or 45 mmHg, while permanent settlements in the Himalayas and Andes are found as high as 5000 m (17 500 ft) where atmospheric pressure is only 390 mmHg and calculated PAO2 is around 25 mmHg.

Effects of altitude on oxygen carriage

Because of the sigmoid shape of the haemoglobin dissociation curve, the falls in PaO2 associated with acute exposure to altitudes up to around 2000 m (6700 ft) cause only a slight reduction in haemoglobin saturation (Fig. 12.2) and so do not reduce oxygen delivery at rest. During exercise, however, the combination of reduced binding and reduced pulmonary capillary transit time leads to a greater degree of desaturation that is proportional both to altitude and to cardiac output. Thus, the threshold altitude for oxygen limitation of maximum exercise in sedentary individuals is typically around 1500 m (5000 ft), but, in trained athletes with substantially greater cardiac outputs, maximum work capacity begins to fall at much lower altitudes (Johnson et al 1994). In the only Summer Olympics held at a significant altitude, in Mexico City in 1968, winning times for all track events longer than 800 m were well above the existing records.

COMPENSATION FOR HYPOXIA

Respiratory stimulation

The reduced oxygen carriage associated with moderate altitude results in more rapid fatigue during exercise, but no respiratory compensation occurs because ventilation is still driven by the central chemoreceptors. These respond to rises in local proton concentration (that is, reduced pH) secondary to arterial carbon dioxide diffusing into the hindbrain, but are insensitive to hypoxia. The peripheral chemoreceptors responsible for monitoring arterial oxygen status are triggered only when PaO2 falls to around 60 mmHg which, as we saw earlier (p. 145), corresponds to an approximate altitude of 2300 m or 7600 ft. At or above this height, chemoreceptor stimulation initiates increased minute ventilation the magnitude of which depends both on the initial PaO2 and on whether increased ventilation is able to restore PaO2 to a value above 60 mmHg.

This acute ventilatory compensation for hypoxia occurs very rapidly, but is itself able to produce only a moderate improvement in oxygen availability. The reason is that increased ventilation necessarily results in carbon dioxide being blown off at a greater rate than before, leading to a fall in arterial carbon dioxide (PaCO2) (hypocapnia) and, therefore, to a rise in hindbrain pH and reduced central chemoreceptor drive, inhibiting the stimulant effect of the hypoxic drive.

With maintained exposure to the hypoxic environment, the inhibition of central chemoreceptor drive diminishes over the next several days. Most rapidly, there is over 1–2 days’ diffusion of excess bicarbonate ions out of the interstitial fluid around the central chemoreceptors that reduces buffering of interstitial protons. Over the next 2–3 days, renal bicarbonate excretion amplifies this process and restores central pH and respiratory drive to normal despite the maintained hypocapnia, although arterial pH remains slightly more alkaline than normal. As a result of these adjustments, minute ventilation rises progressively over the first week of hypoxic exposure, with an associated progressive increase in work capacity that is due both to the increased inspired air volume and to the fact that the enhanced ventilation has reduced alveolar PCO2 further and, therefore, the oxygen tension of alveolar air rises. At very high altitudes, the decrease in air density may also contribute to increased capacity for maximum ventilation.