The Response To High Altitude

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Changes in activity and the environment initiate integrated ventilatory responses that involve changes in the car-

diopulmonary system. Examples include the response to exercise (see Chapter 30) and the response to the low inspired oxygen tension at high altitudes. The importance of understanding integrated ventilatory responses is that similar interactions occur under pathophysiological conditions in patients with respiratory illnesses.

How the body responds to high altitude has fascinated physiologists for centuries. The French physiologist Paul Bert first recognized that the harmful effects of high altitude are caused by low oxygen tension. Recall from Chapter 21 that the percentage of oxygen does not change at high altitude but the barometric pressure decreases (see Fig 21.1). So the hypoxic response at high altitude is caused by a decrease in inspired oxygen tension (PlO2). At high altitude, when the PlO2 decreases and oxygen supply in the body is threatened, several compensations are made in an effort to deliver normal amounts of oxygen to the tissues. Chief among these responses to altitude is hyperventilation. Figure 22.7 shows, that hypoxia-induced hyperventilation is not significantly increased until the alveolar Po2 decreases below 60 mm Hg. In a healthy adult, a drop in alveolar Po2 to 60 mm Hg occurs at an altitude of approximately 4,500 m (14,000 feet).

Figure 22.10 shows how ventilation and alveolar Pco2 change with hypoxia. The hypoxia-induced hyperventilation appears in two stages. First, there is an immediate increase in ventilation, which is primarily a result of hypoxia-induced stimulation via the carotid bodies. However, the increase in ventilation seen in the first stage is small compared with the second stage, in which ventilation continues to rise slowly over the next 8 hours. After 8 hours of hy-poxia, minute ventilation is sustained. The reason for the small rise in ventilation seen in the first stage is that the hy-

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