Central Hypoventilation During Quiet Sleep in Two Infants

Abstract

Expired ventilation (VE), tidal volume (VT), frequency (f), and alveolar CO2 tension (PACO2) were examined in 6 normal infants at 41-52 wk post-conceptional age and in 2 infants who were apneic at birth. Their response to breathing 5% CO2 in air and to 100% O2 in quiet sleep were compared to those in rapid eye movement (REM) sleep. VE in normal infants was 259 ml/kg per min in REM and 200.2 ml/kg per min in quiet sleep, with the difference being due to decreased CO2 production and to decreased dead space. VE increased 34.4 ml/kg per min.cntdot.mm Hg of PCO2 [CO2 tension] elevation with 5% CO2 breathing during REM and was not significantly different during quiet sleep. During O2 breathing, VE fell by 32.7% at 30 s before increasing again. In the affected infants VE and PACO2 during REM at 1 and 4 mo. were normal. At 1 mo. during quiet sleep, each infant became apneic and PACO2 rose 9 and 8 mm Hg/min, respectively. At this time mechanical ventilation was begun. At 4 mo. during quiet sleep, VE was 0.064 and 0.063 ml/kg per min at PACO2 of 66 mm Hg in each infant. The change was due entirely to a decrease in VT to 2.3 and 2.5 ml/kg. At this time 5% CO2 breathing given during normal ventilation in REM produced an abrupt fall in VT to 2.0 and 2.2 ml/kg with no change in frequency. O2 breathing during REM at 1 mo. had no effect, but at 4 mo. it produced apnea requiring mechanical ventilation after 1 min. The ventilatory response to CO2 apparently is important in initiation of extrauterine ventilation and in sustaining ventilation particularly in quiet sleep. It is not necessary in sustaining ventilation awake or in REM sleep, and it represents a balance between the stimulatory and depressant effects of CO2 on the CNS.