Predicting Acute Mountain Sickness

In 1910, the German physiologist, Nathan Zuntz, led a high altitude expedition to Tenerife in the Canary Islands and the members stayed in the Alta Vista Hut at an altitude of 3350 m. Joseph Barcroft was one of the participants, and he reported that he was the only member of the group who had severe mountain sickness (Barcroft 1925). In addition he was the only person who showed no significant fall in alveolar PCO₂ at the Alta Vista Hut. His PCO₂ at sea level was normally 40 mmHg and this fell only to 38 mmHg at the Hut. This was in contrast to his colleague Douglas who did not suffer from mountain sickness and whose PCO₂ fell from 41 to 32, while that of Zuntz fell from 35 to 27 mmHg. Barcroft therefore argued that since his alveolar ventilation was almost unchanged at high altitude, his alveolar PO₂ must have been lower than that than the rest of the party, and this was the cause of the mountain sickness. Although Paul Bert had demonstrated to most people's satisfaction that the physiological problems of high altitude were caused by a low PO₂ back in 1878 (Bert 1878), this was not universally accepted. In fact in 1910 Angelo Mosso still believed that mountain sickness was caused by a low PCO₂.

These early and somewhat anecdotal data gave rise to the hypothesis that a good hypoxic ventilatory response was important in tolerance to high altitude. Subjects with a low ventilatory response to hypoxia would be more hypoxic and therefore at risk, whereas those with a brisk response were able to maintain a higher alveolar and therefore arterial PO₂. It is known that there is a large range of ventilatory responses to hypoxia in normal people. For example, measurements made on climbers of the AMREE expedition in 1981 using the method described by Weil et al (1970) showed that the response ranged from about 3 to over 30 l.min⁻¹, that is a tenfold difference (Schoene et al 1984).

If a low alveolar and therefore arterial Po₂ is an important factor in the development of acute mountain sickness, we would expect this to be reflected in a lower pulse oximeter reading. This explains the Pro/Con feature on “Pulse Oximetry is Useful in Predicting Acute Mountain Sickness” that is included in this issue. Buddha Basnyat summarizes the data supporting the hypothesis whereas Jeremy Windsor and George Rodway argue the opposite. Readers can decide for themselves whether they are convinced one way or the other. However it is clear that there are cogent arguments on both sides.

Part of the problem may be in the methodology. The pulse oximeter reading can be influenced by a number of factors including the temperature of the finger and the activity of the subject, and it is well known that a short period of hyperventilation, even if the subject is unaware of this, can substantially increase the reading. Also we are all familiar with the fact that because of the shape of the oxygen dissociation curve, the pulse oximetry reading is a blunt instrument at the higher arterial PO₂ values. A reduction of arterial PO₂ from 100 to 60 mmHg may only decrease the pulse oximeter reading from only 97% to 90% depending on the position of the oxygen dissociation curve.

If AMS is actually present in a small amount (forme fruste), it would certainly not be surprising if this depressed the pulse oximeter reading. Some patients with AMS have crackles in their lung by auscultation, which presumably means that they have subclinical pulmonary edema, and this would be expected to impair gas exchange.

It would be useful to know to what extent subjects increase their ventilation when they go to high altitude. As indicated above, there is a large range in the ventilatory response to hypoxia among normal people, and intuitively it seems reasonable that those who do not increase their ventilation much, and therefore have a lower alveolar and arterial P0₂, will not tolerate high altitude well. However at the present time there is no simple non-invasive method of measuring the alveolar PO₂ and PCO₂. There is currently interest in developing a hand-held alveolar gas meter in which a subject breathes through a mouthpiece and a small sample of the expired and inspired gas is drawn into miniature oxygen and carbon dioxide analyzers and the end-tidal values are displayed. Such a device would immediately tell us whether the subject was increasing his ventilation and therefore depressing his alveolar PCO₂ at high altitude or not. With existing technology it should be possible to make a handheld, battery-operated instrument that could be used in the field. Such a device might be useful in predicting who is at risk of developing AMS.