Arousal and Cardiorespiratory Responses to Airflow Obstruction in Sleeping Lambs: Effects of Sleep State, Age, and Repeated Obstruction

Harding, Richard; Jakubowska, Alexandra E; McCrabb, G. J.

doi:10.1093/sleep/20.9.693

Cited by 9 publications

(11 citation statements)

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“…9 Thus, the reduction in skeletal muscle tone during active sleep may have allowed greater forward flexion of the head on to the chest, leading to greater narrowing of the upper airway. [21][22][23] Some limitations of the current study should be considered. The study lacked power to investigate the impact of the insert on the relatively infrequent deep reductions in saturation.…”

Section: Figurementioning

confidence: 96%

Randomized Controlled Trial of a Car Safety Seat Insert to Reduce Hypoxia in Term Infants

2013

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WHAT'S KNOWN ON THIS SUBJECT: Brief periods of low oxygen saturation are common in infants while restrained in car safety seats. There is some evidence that an insert that allows the infant head to rest in a neutral position in sleep may reduce hypoxic episodes. WHAT THIS STUDY ADDS:This randomized controlled study shows that the insert reduced numbers of obstructive apneas and the severity of desaturation events but did not significantly reduce the overall rate of moderate desaturations.abstract OBJECTIVE: To test the hypothesis that a foam plastic insert that allows the infant head to rest in a neutral position in sleep may prevent obstruction of the upper airway and thus reduce episodes of reduced oxygenation in term infants in car seats. METHODS:Healthy full-term babies were randomized to be studied during sleep while restrained in an infant car safety seat either with or without the insert, with continuous polysomnographic recordings with sleep video.RESULTS: Seventy-eight infants (39 in each group) had polysomnogram recordings at a mean of 8 days of age. Both groups showed a small fall in mean hemoglobin oxygen saturation (SpO 2 ) over the first hour of sleep. There was no difference between insert and no insert in the rate of moderate desaturations (a fall in SpO 2 $4% lasting for $10 seconds, mean 6 SEM, 17.0 6 1.5 vs 17.2 6 1.5/hour), or mean SpO 2 during sleep. The insert was associated with a significant reduction in the rate of obstructive apnea (0.3 6 0.1 vs 0.9 6 1.5/hour, P , .03), the severity of desaturation events (minimum SpO 2 82% 6 1% vs 74% 6 2%, P , .001), and time with SpO 2 ,85% (0.6% 6 0.3% vs 1.8% 6 1.4%, P = .03). CONCLUSIONS:In full-term newborn infants, a car seat insert that helps the head to lie in a neutral position was associated with reduced severity of desaturation events but not the overall rate of moderate desaturations. Pediatrics 2013;132:326-331

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Section: Figurementioning

confidence: 96%

Randomized Controlled Trial of a Car Safety Seat Insert to Reduce Hypoxia in Term Infants

2013

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“…Arousal has been described as an essential safety mechanism restarting breathing effort following apnea in infants, in children and in animals [3][4][5][6]. We are not aware of any studies which have examined relationships between arousal and recovery from apnea in premature infants.…”

Section: Introductionmentioning

confidence: 99%

Physiological Parameters Evaluation following Apnea in Healthy Premature Infants

et al. 2000

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To assess responses to central and obstructive apnea, we performed 10-hour polygraphic recordings in healthy 33–34 wGA infants. Each apnea period was paired with a control period. The presence of body movements (BM) and augmented breaths (AB), the EEG, heart rate (HR), respiratory rate, phase relationships between thoracic and abdominal respiratory movements, and changes in SaO₂ were evaluated. No apnea caused awakening. Apnea were not usually followed by motor events (no significant differences with control periods), with the exception of most obstructive apnea longer than 10 s. The mean percentage of changes following apnea, normalized to baseline values, was significant for the EEG (frequency slightly increased, mainly after obstructive apnea), HR (deceleration), and respiratory rate (increased). However, the mean values masked heterogeneity across apnea in the direction of the change in each parameter. The only significant correlation was between changes in HR and SaO₂. The increases in EEG frequency and respiratory rate seen in our study can be considered markers of CNS activation, but were small and inconsistent. The heart rate decelerations and SaO₂ changes are not activation markers. Thus, mechanisms underlying restarting of breathing efforts following apnea remain unclear in premature babies. Our investigation establishes the importance of using control data to distinguish between spontaneous and apnea-related events.

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“…Arousal from sleep and cardio‐respiratory compensations are powerful protective responses to respiratory stresses such as asphyxia (Campbell et al 1998), asphyxia associated with airway occlusion (Sullivan et al 1978; Igras & Fewell, 1991; Davidson & Fewell, 1994; Harding et al 1997), and the components of asphyxia, hypoxia (Phillipson et al 1978; Henderson‐Smart & Read, 1979; Jeffery & Read, 1980; Neubauer et al 1981; Berthon‐Jones & Sullivan, 1982; Fewell & Baker, 1987) and hypercapnia (Phillipson et al 1977; Douglas et al 1982; Berthon‐Jones & Sullivan, 1984; Fewell & Baker, 1989). However, indirect evidence suggests that protective arousal responses may become ineffective if the respiratory stress is repeated in sleep.…”

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confidence: 99%

“…In experimental studies, asphyxia induced by airway obstruction is a potent arousing stimulus, but it becomes less effective with repetition (Fewell et al 1988; Harding et al 1997; Brooks et al 1997). Arousal also becomes depressed after repeated exposure to one of the components of airway obstruction‐induced asphyxia, namely hypoxia (Fewell & Konduri, 1989; Johnston et al 1998).…”

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confidence: 99%

“…Some studies have demonstrated that the depressant effects upon arousal of hypoxia (Fewell & Konduri, 1989) and asphyxia (Brooks et al 1997) occur in both rapid‐eye‐movement sleep (REM sleep, or active sleep as it is termed in the newborn) and also in non‐REM (termed quiet sleep in the newborn). Others have shown that arousal depression during hypoxia (Johnston et al 1998) and airway obstruction (Fewell et al 1988; Harding et al 1997) is confined to the REM phase. As OSA occurs predominantly during active sleep in the human newborn (Kahn et al 1992) and the de‐saturations associated with OSA are more severe during this state in the adult (Sullivan & Issa, 1980; Charbonneau et al 1994), active sleep may be the more vulnerable to arousal and cardio‐respiratory depression during repetitive asphyxial stress.…”

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confidence: 99%

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The effects of repeated exposure to hypercapnia on arousal and cardiorespiratory responses during sleep in lambs

Johnston

Grant

Wilkinson

et al. 2007

The Journal of Physiology

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Arousal and cardio-respiratory responses to respiratory stimuli during sleep are important protective mechanisms that rapidly become depressed in the active sleep state when episodes of hypoxia or asphyxia are repeated: whether responses to repeated hypercapnia are similarly depressed is not known. This study aimed to determine if arousal and cardio-respiratory responses also become depressed with repeated episodes of hypercapnia during sleep and whether responses differ in active sleep and quiet sleep. Eight newborn lambs were instrumented to record sleep state and cardio-respiratory variables. Lambs were subjected to two successive 12 h sleep recordings, assigned as either sequential control and test days, or test and control days performed between 12.00 and 00.00 h. The control day was a baseline study in which the lambs breathed air to determine spontaneous arousal probability. During the test day, lambs were exposed to a 60 s episode of normoxic hypercapnia (Fractional inspired CO 2 (F ICO 2 ) = 0.08 and Fractional inspired O 2 (F IO 2 ) = 0.21 in N 2 ) during every quiet sleep and active sleep epoch. The probability of lambs arousing during the hypercapnic exposure exceeded the probability of spontaneous arousal during quiet sleep (58% versus 21%, χ 2 = 54.0, P < 0.001) and active sleep (39% versus 20%, χ 2 = 10.0, P < 0.01), though the response was less in active sleep. Exposure to hypercapnia also resulted in a significant increase in ventilation in quiet sleep (150 ± 22%) and active sleep (97 ± 23%, P < 0.05), though the increase was smaller in active sleep (P < 0.05). Small (< 5%) blood pressure increases and heart rate decreases were evident during hypercapnia in quiet sleep, but not in active sleep. Arousal and cardio-respiratory responses persisted with repetition of the hypercapnic exposure. In summary, although arousal and cardio-respiratory responses to hypercapnia are less in active sleep compared with quiet sleep, these protective responses are not diminished with repeated exposure to hypercapnia.

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Arousal and Cardiorespiratory Responses to Airflow Obstruction in Sleeping Lambs: Effects of Sleep State, Age, and Repeated Obstruction

Cited by 9 publications

References 0 publications

Randomized Controlled Trial of a Car Safety Seat Insert to Reduce Hypoxia in Term Infants

Randomized Controlled Trial of a Car Safety Seat Insert to Reduce Hypoxia in Term Infants

Physiological Parameters Evaluation following Apnea in Healthy Premature Infants

The effects of repeated exposure to hypercapnia on arousal and cardiorespiratory responses during sleep in lambs

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