Posthyperventilation apnea in awake dogs during metabolic acidosis and hypoxia.

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Abstract
The ventilatory response to lowered PcO2 [CO2 tension] (following mechanical hyperventilation) and to elevated PcO2 were studied in 3 dogs with permanent tracheostomies and carotid artery loops. Apnea was invariably obtained following hyperventilation, even in the presence of a base deficit of 9. 2 mEq/1 (NH4CI by mouth 12-16 g 4-5 times daily for 3-5 days) or acute hypoxia (PAO2 45 mm Hg for 10 min.). The role of the vagus was excluded by showing that after brief, rapid, shallow hyperventilation, a few breaths preceded apnea. The resting PAO2 [arterial CO2 tension] fell from a control of 37. 0 to 30. 7 after 10 min. of hypoxia, and to 32. 6 after 3-5 days of acidosis (average pH 7. 32 when studied). The CO2 response curve slope increased from the control of 1.49 liter min per mm Hg PCO2 with PAo2 250-300 mm Hg, to 2. 02 dur ng hypoxia but was 1. 50 during acidosis. The PcO2 at the "apneic threshold," determined by steady-state mild hyperventilation, fell from a control of 34.4 to 28.1 during hypoxia and to 29. 2 with acidosis. Both posthyperventilation apnea and the shift of the apneic threshold with hypoxia and acidosis appear to be more readily demonstrated in the dog than in man.