The heart at high altitude.

On August 8, 1786 Michel Gabriel Paccard, the village doctor in Chamonix, with his guide Jacques Balmat, made the first ascent of Mont Blanc, and reached a height at which scientific opinion of the day considered life to be insupportable. Since that date the ways in which the body adapts to high altitude have interested in turn the physiologist, the mountaineer, the aviator, and now the cardiologist. The problem of acclimatization to high altitude is that of adjustment to a diminished atmospheric oxygen tension, which is halved at about 18,000 feet and is reduced to one-third of the pressure at sea level at 27,000 feet, less than the height of Mount Everest. It is remarkable that the human body can tolerate such a wide environmental change. Several mechanisms are involved in maintaining the oxygen supply to the cells of the body as height is gained, some of which are immediate while others take several days or weeks to reach their full effect. Respiration becomes faster and deeper. This occurs even with 'passive' ascent, as in a decompression chamber or in an aeroplane, and still more so of course when the climb is made on foot. The effect of deeper breathing is to improve alveolar ventilation, so that the alveolar oxygen tension, which is always lower than atmospheric oxygen tension, falls less in proportion than the partial pressure of oxygen in the atmosphere, and the respiratory exchange becomes more efficient. The heart rate quickens and cardiac output increases, at any rate initially, so that more haemoglobin passes through the lungs per minute. The oxygen dissociation curve of haemoglobin is such that a considerable fall in alveolar oxygen tension produces a relatively small percentage drop in haemoglobin oxygen saturation, while in the tissues a small drop in the oxygen tension is accompanied by a large release of oxygen. This effect is further enhanced by a shift of the dissociation curve 'to the left' due to the respiratory alkalosis which follows the loss of carbon dioxide