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[Postnatal development of breathing control]
1Abteilung für angewandte Physiologie, Ruhr-Universität Bochum.
Insights
Respiratory CO2 sensitivity adapts after birth, with preterm infants and those experiencing life-threatening events showing reduced responses. Impaired CO2 sensitivity can lead to hypoventilation and apneic events in infants.
Area of Science:
- Neonatal Physiology
- Respiratory Control
- Sleep Studies
Context:
- Fetal respiratory movements and EEG are established early.
- Birth triggers respiration via external stimuli, hypercapnia, hypoxia, and acidosis.
- Chemosensitive system thresholds adapt postnatally.
Purpose:
- To assess respiratory CO2-responses and hypoxic sensitivity in healthy infants, and in those with congenital central alveolar hypoventilation syndrome (CCHS) and apparently life-threatening events (ALTE).
- To investigate age-related changes in CO2-response and peripheral chemoreceptor activity.
Summary:
- Healthy infants over 2 weeks old exhibit adult-like CO2-responses during NREM sleep.
- Preterm infants show reduced CO2-response until their estimated due date.
- ALTE infants had suppressed CO2-response (17%), and CCHS children showed no response.
Impact:
- Reduced or absent respiratory CO2 sensitivity may cause apnea or hypoventilation.
- Age-related differences in CO2 and hyperoxic responses contribute to breathing control oscillations like periodic breathing.
- Findings aid in understanding and managing infant respiratory disorders.
Abstract:
Respiratory movements already occur in the fetus together with low amplitude high frequency EEG. During birth external stimuli drive respiration, supported by the development of hypercapnia, hypoxia and acidosis. The thresholds of the chemosensitive systems adapt during the first hours and days of life (CO2 sensitivity) or weeks (hypoxic sensitivity). In 180 healthy infants between 5 days and 18 months of age we performed respiratory CO2-responses during NREM-sleep and studied the immediate response to inhalation of 60% oxygen (Dejours test) as well as in 8 children with congenital central alveolar hypoventilation syndrome (CCHS) and 15 infants who experienced an apparently life-threatening event (ALTE). Infants older than 2 weeks had a mean PCO2 of 40-42 mmHg, the slope of the CO2-response showed no age trend and was found in the range of adults with a 22-38% increase in ventilation per Torr increased PCO2. Preterm infants had a significant lower CO2-response (16 vs. 33%) until they reached their estimated normal birth date. In the ALTE group the CO2-response was suppressed to 17%. Children with CCHS did not respond to CO2 by increasing their ventilation, even after years. The response to hyperoxia as a measure of peripheral chemoreceptor activity decreased from a 31% initial inhibition of ventilation at 1 month to 20% at one year. Our results indicate that temporary or lasting reduction or lack of the respiratory CO2 sensitivity may cause apneic events or hypoventilation. Different slopes of CO2- and hyperoxic responses in very young infants compared to older ones favour the occurrence of oscillations in the control of breathing such as periodic breathing during sleep.