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Published on: November 2, 2015
Postnatal development of ventilatory and arousal responses to hypoxia in human infants
Rosemary S C Horne1, Peter M Parslow, Richard Harding
1Ritchie Centre for Baby Health Research, Monash University, Level 5, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia. rosemary.horne@med.monash.edu.au
Insights
Infant hypoxic ventilatory response (HVR) matures in the first year, but remains immature compared to adults. Maternal smoking and sleep state impact HVR and arousal, potentially increasing SIDS risk.
Area of Science:
- Neonatal physiology
- Respiratory control
- Sudden Infant Death Syndrome (SIDS) research
Background:
- The hypoxic ventilatory response (HVR) undergoes significant maturation during infancy.
- Healthy term infants exhibit an immature HVR until at least six months of age compared to adults.
- Limited studies exist on sleep state's effect on infant HVR, suggesting an initial lack of difference followed by a trend towards adult patterns.
Purpose of the Study:
- To investigate the impact of sleep state on the hypoxic ventilatory response (HVR) in infants.
- To examine the influence of maternal cigarette smoking on infant HVR and arousal responses to hypoxia.
- To assess the relationship between HVR, arousal responses, and SIDS risk.
Main Methods:
- Analysis of hypoxic ventilatory response (HVR) and arousal patterns in infants across different sleep states (REM, NREM, QS, AS).
- Comparison of HVR and arousal thresholds between different sleep states and age groups.
- Evaluation of the effects of maternal smoking history on infant HVR and arousal.
Main Results:
- Infant HVR shows developmental changes, with a trend towards adult patterns where the response is blunted in REM sleep compared to NREM sleep.
- Arousal responses to hypoxia differ between sleep states: infants arouse in Active Sleep (AS) but frequently fail to arouse in Quiet Sleep (QS).
- Maternal smoking is associated with a depressed HVR and arousal response to hypoxia in infants, particularly in QS, potentially increasing SIDS risk.
Conclusions:
- Depressed arousal responses to hypoxia in Active Sleep (AS) may pose life-threatening risks for infants.
- Infants at increased risk for SIDS demonstrate both depressed ventilatory and arousal responses to hypoxia.
- Maternal smoking significantly impacts infant HVR and arousal, highlighting a potential mechanism contributing to SIDS.
Abstract:
During the first year of life there is significant maturation of the hypoxic ventilatory response (HVR) in human infants. Compared with adults, healthy term infants have an immature HVR until at least 6 months of age. There are few studies in infants on the effects of sleep state on the HVR but these suggest that at early postnatal ages there is initially no sleep-state related difference; this is followed by a developmental trend towards the adult situation in which the response is depressed in REM sleep compared with NREM. Maternal cigarette smoking is a major risk factor for SIDS and the mechanism for this may involve a depressed HVR in the exposed infant; however studies are limited and the wide variation in cigarette consumption makes interpretation of results difficult. Arousal responses to hypoxia are of vital importance and a failure to arouse has been implicated in SIDS. Sleeping infants frequently fail to arouse in response to hypoxia in QS, whereas in AS they invariably arouse; furthermore arousal latency is longer in QS compared with AS. The oxygen saturation at which infants arouse is not different between sleep states, suggesting that desaturation is more rapid in AS. In QS younger infants arouse more readily than at older ages and arousal is depressed by maternal smoking. These findings suggest that depression of the arousal response to hypoxia in AS may have life-threatening consequences. Infants at increased risk for SIDS have been shown to have both depressed ventilatory and arousal responses to hypoxia, thus they may be at even greater risk.
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