Deficient hypoxia awakening response in infants of smoking mothers: Possible relationship to sudden infant death syndrome

Lewis, Kathleen; Bosque, Elena

doi:10.1016/s0022-3476(95)70155-9

Cited by 177 publications

(66 citation statements)

References 32 publications

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“…These findings are consistent with other studies using different respiratory stimuli (26,27) and somatosensory stimuli (21,22,28,29). Our finding that infants frequently fail to arouse in QS has previously been reported by us (30) and others (31)(32)(33)(34)(35)(36)(37)(38), and the novel finding that infants always aroused in AS highlights the importance of arousal in this state. Arousal from sleep is accompanied by an increase in heart rate, arterial pressure, and ventilation (39), and, importantly, a behavioral response is evoked, allowing body movements aimed at avoiding the life-threatening challenge (40).…”

Section: Discussionsupporting

confidence: 93%

Variability of the Initial Phase of the Ventilatory Response to Hypoxia in Sleeping Infants

et al. 2006

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ABSTRACT:Most of the available data on the hypoxic ventilatory response (HVR) in infants has been obtained in quiet sleep (QS), and only one study has made repeated tests in the same infant. We aimed to gain a more complete knowledge of the maturation and consistency of the initial phase of the HVR by performing multiple tests in both QS and active sleep (AS) over the first 6 mo of life in term infants. Fifteen healthy term infants were studied with daytime polysomnography longitudinally at 2-5 wk, 2-3 mo, and 5-6 mo after birth. Each infant received multiple hypoxic (15% O 2 , balance N 2 ) challenges (three or more) in both AS and QS. In AS, infants consistently aroused to hypoxia; however, in QS, infants both aroused and failed to arouse. The initial phase of the HVR varied considerably between infants with the changes in ventilation/kg [SD of inspired minute ventilation per kilogram of body weight (V I /kg)] being more variable during AS than QS at all three ages and overall decreasing with postnatal age in both sleep states. The variability between replicate V I /kg measurements was also significantly greater in AS compared with QS at 2-5 wk postnatal age. There was no evidence of habituation to repeated hypoxic tests in either sleep state. Our study has demonstrated that the initial phase of the HVR is variable both between and within term infants in both AS and QS, with responses being markedly more variable during AS, and becoming more consistent with increasing postnatal age. By performing only one test or by failing to account for arousal responses, previous studies may not have detected the natural variation of the infant HVR. (Pediatr Res 59: 700-704, 2006) D uring sleep, the regulation of respiration undergoes important changes in both adults and infants. Sleep is associated with hypotonia of various respiratory muscles such as the genioglossus, masticatory, and deep neck muscles (1), and this can lead to increased upper airway resistance (2) and reduced functional residual capacity (3). Minute ventilation is also decreased during sleep (by approximately 8%-15% in adolescents and adults) when compared with wakefulness (4). With a loss of the wakefulness drive to breathing and the variability of respiratory control between different sleep states, responses to respiratory stimuli are altered during sleep (5); thus, physiologic challenges such as hypoxia, hypercapnia, and airway obstruction can pose a greater risk when asleep than when awake.The HVR is a key protective mechanism aimed at maintaining adequate blood oxygen levels. In adults, the response consists of a prompt increase in ventilation, which peaks within 3-5 min of exposure to hypoxia, followed by a period of sustained hyperventilation for 15-30 min (6). In contrast, studies in infants have reported an increase in ventilation during the first 1-2 min of hypoxic exposure, followed by a reduction to or below normoxic levels within 5 min, suggesting an immature HVR that is biphasic in nature. This biphasic response has been demonstrated in bot...

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Section: Discussionsupporting

confidence: 93%

Variability of the Initial Phase of the Ventilatory Response to Hypoxia in Sleeping Infants

et al. 2006

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“…The effect of prenatal nicotine on respiratory physiology is controversial. Maternal cigarette smoking has been reported to have no effect on ventilatory responses to hypoxia or hypercapnia (Lewis and Bosque, 1995) and diminish the hypoxic ventilatory responses and respiratory drive (Ueda et al, 1999). Similarly, it is reported that prenatal nicotine exposure both does not alter (Bamford et al, 1996) and attenuates the ventilatory response to hypoxia or hypercapnia in rats (Simakajornboon et al, 2004).…”

Section: Discussionmentioning

confidence: 98%

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

Huang

Griffioen²,

Wang³

et al. 2006

J. Neurosci.

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Hypercapnia evokes a strong cardiorespiratory response including gasping and a pronounced bradycardia; however, the mechanism responsible for these survival responses initiated in the brainstem is unknown. To examine the effects of hypercapnia on the central cardiorespiratory network, we used an in vitro medullary slice that allows simultaneous examination of rhythmic respiratory-related activity and inhibitory synaptic neurotransmission to cardioinhibitory vagal neurons (CVNs). Hypercapnia differentially modulated inhibitory neurotransmission to CVNs; whereas hypercapnia selectively depressed spontaneous glycinergic IPSCs in CVNs without altering respiratory-related increases in glycinergic neurotransmission, it decreased both spontaneous and inspiratory-associated GABAergic IPSCs. Because maternal smoking is the highest risk factor for sudden infant death syndrome (SIDS) and prenatal nicotine exposure is proposed to be the link between maternal smoking and SIDS, we examined the cardiorespiratory responses to hypercapnia in animals exposed to nicotine in the prenatal and perinatal period. In animals exposed to prenatal nicotine, hypercapnia evoked an exaggerated depression of GABAergic IPSCs in CVNs with no significant change in glycinergic neurotransmission. Hypercapnia altered inhibitory neurotransmission to CVNs at both presynaptic and postsynaptic sites. Although the results obtained in this study in vitro cannot be extrapolated with certainty to in vivo responses, the results of this study provide a likely neurochemical mechanism for hypercapnia-evoked bradycardia and the dysregulation of this response with exposure to prenatal nicotine, creating a higher risk for SIDS.

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“…Thirdhand smoke refers to residual contamination from tobacco smoke after the cigarette has been extinguished 206 ; there is no research to date on the signifi-cance of thirdhand smoke with regards to SIDS risk. Smoke exposure adversely affects infant arousal [207][208][209][210][211][212][213] ; in addition, smoke exposure increases risk of preterm birth and low birth weight, both of which are risk factors for SIDS. The effect of tobacco smoke exposure on SIDS risk is dosedependent.…”

Section: Smoking During Pregnancy In the Pregnant Woman's Environmenmentioning

confidence: 99%

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

Moon¹

2011

Pediatrics

217

115

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Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a nonprone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death occurring during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from being only SIDS-focused to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths including SIDS. The recommendations described in this report include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunization, consideration of a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in this technical report. The recommendations are published in the accompanying “Policy Statement—Sudden Infant Death Syndrome and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment,” which is included in this issue (www.pediatrics.org/cgi/doi/10.1542/peds.2011-2220).

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Deficient hypoxia awakening response in infants of smoking mothers: Possible relationship to sudden infant death syndrome

Cited by 177 publications

References 32 publications

Variability of the Initial Phase of the Ventilatory Response to Hypoxia in Sleeping Infants

Variability of the Initial Phase of the Ventilatory Response to Hypoxia in Sleeping Infants

Differential Control of Central Cardiorespiratory Interactions by Hypercapnia and the Effect of Prenatal Nicotine

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

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