Heart rate responses to non-arousing trigeminal stimulation in infants: effects of sleep position, sleep state and postnatal age.

AIMS: The aim of this study was to examine the effects of maternal smoking, sleeping position, sleep state and postnatal age on heart rate changes following non-arousing trigeminal stimulation in infants. SUBJECTS: We studied healthy term infants, 13 of whom were born to mothers who did not smoke and 11 to mothers who smoked during pregnancy. Each infant was studied using daytime polysomnography on 3 occasions: (a) 2-3 weeks, (b) 2-3 months and (c) 5-6 months after birth. Nasal air-jet stimulation was presented in both active sleep (AS) and quiet sleep (QS) when infants slept both prone and supine. RESULTS: We found no difference between infants of smoking and non-smoking mothers in any of the parameters measured. Minimum HR (MinHR) following non-arousing trigeminal stimulation was significantly lower in the supine compared to the prone sleeping position at 2-3 weeks and 2-3 months of age (p<0.05) in AS, and at all 3 ages in QS (p<0.01). MinHR was significantly lower in QS compared to AS at 2-3 months when infants slept prone and at 5-6 months when sleeping supine (p<0.01). In QS, MinHR became lower with increasing postnatal age in both sleep positions (p<0.01). In AS, there was no maturational effect. The normalized bradycardia (DeltaHR%) was significantly greater in AS than in QS at 2-3 weeks of age (p<0.05) when infants slept supine. CONCLUSION: Our study has shown that there was a decrease in heart rate (MinHR) following trigeminal stimulation in infants up to 6 months of age and this was affected by sleep position and sleep state, being larger in the supine sleeping position and the QS state.

Influences of maternal cigarette smoking on infant arousability.

Since the reduction in the incidence of the prone sleeping position, maternal cigarette smoking has become the strongest modifiable risk factor for Sudden Infant Death Syndrome (SIDS). This risk is dose dependent. Various mechanisms have been postulated to explain the increased risk of SIDS associated with maternal smoking, among these, impairment of arousal from sleep. This paper reviews the effects of maternal smoking on infant arousability from sleep, cardiorespiratory controls and sleep architecture. Infants exposed to maternal smoking have been shown to have both decreased spontaneous and evoked arousability from sleep. Such impairment of arousal has been demonstrated to be associated with changes in control of autonomic cardiac function. Sleep architecture appears not to be altered by smoking. During arousal, heart rate, blood pressure and breathing movements increase, while gross body movements occur to avoid the stimulus. Any impairment in arousability from sleep could occur when infants are exposed to maternal cigarette smoking, and could possibly contribute to the final pathway to SIDS.

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.

Effects of sleep position, sleep state and age on heart rate responses following provoked arousal in term infants.

Previous studies have suggested that autonomic dysfunction may be involved in Sudden Infant Death Syndrome (SIDS). The major risk factors for SIDS are the prone sleeping position and maternal smoking. Our aim was to examine the effects of sleeping position and maternal smoking on the postnatal maturation of autonomic function by examining heart rate responses following arousal in healthy term infants. Twenty-four infants (11 born to mothers who smoked during pregnancy and 13 to mother who did not smoke) were studied using daytime polysomnography and multiple measurements of arousal threshold (cm H(2)O) in response to air-jet stimulation applied alternately to the nares were made in both active sleep (AS) and quiet sleep (QS). We demonstrated no difference between smoking and non-smoking groups of infants in any of our measurements, and thus combined data from the groups. Baseline (BHR) was elevated in the prone compared to the supine position in quiet sleep (QS) at 2-3 weeks (p<0.001) and 5-6 months (p<0.001), and in active sleep (AS) at 2-3 and 5-6 months (p<0.05). BHR was significantly elevated in AS compared to QS in the supine position at all ages (p<0.01) and in the prone position at 2-3 (p<0.001) and 5-6 months (p<0.05). Increases in heart rate (deltaHR%) following arousal were significantly greater in the supine compared to the prone position in QS at 2-3 weeks (p<0.05) and in AS at both 2-3 (p<0.01) and 5-6 months (p<0.05). DeltaHR% was significantly greater in AS compared to QS in both supine (p<0.05) and prone (p<0.001) positions at 2-3 weeks and in the supine position at 2-3 months (p<0.001). We conclude that sleep state, sleep position and postnatal age affect the cardiac responses following arousal from sleep in healthy term infants. Impairment of heart rate control in the prone position may be important in understanding the increased risk for SIDS in this position.

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.