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Central hypoventilation during quiet sleep in two infants
Insights
Infant breathing responses to carbon dioxide and oxygen vary by sleep state. Carbon dioxide is crucial for initiating and maintaining breathing, especially during quiet sleep, in newborns.
Area of Science:
- Neonatal Physiology
- Respiratory Control
- Infant Sleep Studies
Background:
- Investigating ventilatory control in infants is crucial for understanding respiratory development and potential issues like apnea.
- This study examines how sleep state (REM vs. quiet sleep) and gas challenges (CO2, O2) affect breathing in normal and apneic infants.
Observation:
- Expired ventilation (VE) was lower in quiet sleep compared to REM sleep in normal infants, attributed to reduced CO2 production and dead space.
- Breathing 5% CO2 increased VE in REM sleep but not significantly in quiet sleep.
- Oxygen inhalation initially decreased VE before it recovered.
- Infants with a history of apnea showed normal ventilation in REM sleep but experienced apnea and rising PACO2 during quiet sleep.
Findings:
- The ventilatory response to carbon dioxide is vital for initiating and sustaining extrauterine ventilation, particularly in quiet sleep.
- This response is less critical for maintaining ventilation during wakefulness or REM sleep.
- The study highlights the complex balance of CO2's stimulatory and depressant effects on the central nervous system.
Implications:
- Understanding these ventilatory responses can inform clinical management of respiratory distress in newborns.
- The findings emphasize the importance of sleep state in neonatal respiratory regulation.
- Further research into the central nervous system's role in CO2 sensing could lead to novel therapeutic strategies.
Abstract:
Expired ventilation (VE), tidal volume (VT), frequency (f), and alveolar PCO2 (PACO2) were examined in six normal infants at 41 to 52 weeks post-conceptional age and in two infants who were apneic at birth. Their response to breathing 5% carbon dioxide in air and to 100% oxygen in quiet sleep were compared to those in rapid eye movement (REM) sleep. VE in normal infants was 259 ml/kg/min in REM and 200.2 ml/kg/min in quiet sleep with the difference being due to decreased carbon dioxide production and to decreased dead space. VE increased 34.4 ml/kg/min/mm Hg of PCO2 elevation with 5% carbon dioxide breathing during REM and was not significantly different during quiet sleep. During oxygen breathing VE fell by 32.7% at 30 seconds before increasing again. In the affected infants, VE and PACO2 during REM at 1 and 4 months were normal. At 1 month, 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 months, during quiet sleep, VE was 0.064 and 0.063 ml/kg/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% carbon dioxide 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. Oxygen breathing during REM at one month had no effect but at 4 months produced apnea requiring mechanical ventilation after one minute. The findings suggest that the ventilatory response to carbon dioxide is (1) important in initiation of extrauterine ventilation and (2) 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 carbon dioxide on the central nervous system.