An anesthetized patient is mechanically ventilated at her normal tidal volume, but at twice her normal frequency. When mechanical ventilation is stopped, the patient fails to breathe spontaneously for 1 minute. This temporary cessation of breathing occurs because
The apnea observed in this patient following her re­moval from the ventilator resulted from a lowered cerebrospinal fluid carbon dioxide tension (PCO2), which, in turn, reduced central chemoreceptor activ­ity. Doubling the frequency of breathing while main­taining the tidal volume doubles alveolar ventilation, according to the formula:
VA = (V T - VD) f,
where VA is the alveolar ventilation per minute, VT is the tidal volume, VD is the volume of the dead space, and f is the frequency of breathing.
Increasing alveolar ventilation increases the arterial oxygen tension (Pao2) and lowers the arterial and cerebrospinal fluid PCO2. It is the low cerebrospinal fluid PCO2 and the concomitant alkalosis in the cere­brospinal fluid that is responsible for the apnea ob­served after periods of hyperventilation. Ventilation resumes after the cerebrospinal fluid PCO2 increases and returns the cerebrospinal fluid pH to normal. The peripheral chemoreceptors are relatively inactive at a normal Pao2 of 100 mm Hg. Hyperventilating and raising the Pao2 does little to influence the peripheral chemoreceptors and, therefore, ventilation.
The elevated arterial oxygen tension (Pao2) reduced peripheral chemoreceptor activity
The elevated  (Pao2) reduced central chemoreceptor activity
Low levels of nitrogen are known to inhibit ventilation
The lowered carbon dioxide tension (Pao2) reduced central chemoreceptor activity