Ventilation

Defense of alveolar PaO2 through increased ventilation is the primary initial adaptation. The hypoxic ventilatory response (HVR) is effected by the carotid body, which senses a decrease in arterial oxygenation and inputs to the central respiratory center in the medulla to increase ventilation. The vigor of this inborn response is related to successful acclimatization and increased performance. Respiratory depressants or stimulants may affect HVR, as does chronic hypoxia, which eventually blunts the response. A low hypoxic drive may allow extreme hypoxemia to develop during sleep. The initial hyperventilation is quickly attenuated by respiratory alkalosis, which acts as a brake on the respiratory center. As renal excretion of bicarbonate compensates for the respiratory alkalosis, pH returns toward normal, and ventilation continues to increase. This process of maximizing ventilation, termed ventilatory acclimatization, culminates after four to seven days at a given altitude. With continuing ascent to higher altitudes, the central chemoreceptors reset to progressively lower P CO2 values, and the completeness of acclimatization can be gauged by the arterial PCO2. Acetazolamide, which forces a bicarbonate diuresis, greatly facilitates this process. An appreciation of the normal values for blood gases and acid-base status with acclimatization at various altitudes is necessary in order to distinguish abnormalities ( Table 191-1).

TABLE 191-1 Blood Gases and Altitude

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