Postnatal development of ventilatory and arousal responses to hypoxia in human infants.

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.

Respiratory control and arousal in sleeping infants.

Control of the cardiovascular and respiratory systems undergoes rapid maturation during infancy. Sleep is at a lifetime maximum during this period and has a marked influence on cardiorespiratory function. The mechanisms leading to sudden infant death syndrome (SIDS) may include a failure in the neural integration of the cardiovascular and respiratory systems, with a concomitant failure to arouse from sleep. Studies have shown that sleep states exert a marked influence on respiratory control and arousability. Infants are more arousable in active sleep compared with quiet sleep from both somatosensory and respiratory stimuli. Post-natal and gestational age at birth also have a marked influence on arousability. Arousability is depressed by the major risk factors for SIDS (prone sleeping, maternal smoking, prematurity and recent infection) and is increased by factors that decrease the risk for SIDS (e.g. use of dummies, breastfeeding).

Arousal and ventilatory responses to hypoxia in sleeping infants: effects of maternal smoking.

Our aim was to determine whether maternal cigarette smoking affects arousal and ventilatory responses to hypoxia in infants. Infants born to non-smoking (NS, n = 15) and smoking mothers (SM, n= 9) were studied at 2-5 weeks, 2-3 and 5-6 months. Ventilatory responses to 15% O(2) were determined preceding arousal. At each age and in both groups, infants aroused more frequently and earlier to hypoxia in active sleep (AS) than quiet sleep (QS). Arousal latency was longer in SM infants (in QS) at 5-6 months (P < 0.05). Baseline respiratory parameters were not different between groups, except that, at 2-3 months, SM infants had higher SP(O2) during AS than NS infants. Maternal smoking did not affect ventilatory responses preceding hypoxia-induced arousal in either sleep-state at any age. We conclude that mild hypoxia stimulates ventilation and arousal in infants up to 6 months and that arousability is depressed in SM infants at 5-6 months; however, ventilatory responses preceding arousal are not adversely affected by smoking.

Arousal responses and risk factors for sudden infant death syndrome.

BACKGROUND: Failure to arouse from sleep has been postulated as a mechanism to explain the final pathway of sudden infant death syndrome (SIDS). METHODS: We have reviewed the effects of the major risk factors for SIDS, prone sleep position, maternal smoking, prematurity and recent infection on arousability from sleep. In human infants it has been consistently demonstrated that arousal from sleep in response to a variety of stimuli is more difficult to induce from quiet sleep (QS) compared to active sleep (AS) over the first 6 months of life. RESULTS: In the prone position both stimulus-induced and spontaneous arousability from both QS and AS were impaired at 2-3 weeks and 2-3 months, but not at 5-6 months of age in both term and preterm infants. In term infants exposed to maternal smoking during pregnancy both stimulus-induced and spontaneous arousability were impaired when infants slept supine in QS at 2-3 months of age. Healthy preterm infants showed no impairment in arousability compared with term infants at matched postconceptional ages. However, preterm infants with a history of apnoea and bradycardia of prematurity showed decreased arousal responses in both QS and AS and this impairment was positively correlated to their 'perinatal risk score'. Infants who had recently suffered an infection requiring hospitalization showed decreased arousability in QS on the day of discharge when compared to 2 weeks later when they were completely well. CONCLUSIONS: In summary it has been found that the major risk factors for SIDS identified from epidemiological studies also decrease arousability from sleep in infants. We propose that this decreased arousability from sleep may be involved in the final pathway of SIDS.