Awake inspiratory airway occlusion in normal humans is followed by hyperpnea and hypocapnia

The ventilatory response following 15 seconds of inspiratory airway occlusion at functional residual capacity (FRC) was studied in nine normal supine awake subjects. Expired minute ventilation (Ve), CO₂ output (v̊V_CO2), tidal volume (Vt), and end-tidal P_CO2(Pet_CO2) were measured on a bbreath-by-breath basis. Alveolar P_CO2 rose 5.6 mm Hg during the apnea (P<0.001). Ventilation rose 10.8 L/min on the first breath following apnea and remained elevated above control measurements for five breaths (P<0.05). The persistent hyperpnea was due to an increase in tidal volume and was associated with alveolar hypocapnia for 6 breaths or 30 sec (P<0.05) and an increase in CO₂ output for 4 breaths (P<0.05). Changes in end-tidal P_CO2 correlated with excess CO₂ output relative to control measurements immediately prior to airway occlusion (P<0.03). After 15 sec airway occlusion at FRC, there is alveolar hypercapnia with a 2.6-fold first breath rise in ventilation. Persistent alveolar hyperventilation lasting 30 sec following airway occlusion may be due to delays in central chemoreceptor response or an afterdischarge phenomenon. This overshoot hypocapnia following airway occlusion may have some relevance to the development of central apneas following obstructive apnea episodes.