Respiratory and arousal responses to hypoxia in apnoeic infants reinvestigated

Milerad, Josef; Hertzberg, Torbjörn; Wennergren, Göran; Lagercrantz, Hugo

doi:10.1007/bf00441560

Cited by 26 publications

(9 citation statements)

References 30 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 figure is a reconstruction of the original chart. The curve for oxygen saturation has been shifted 30 s to the left and the curve for tcPCO, 1 min to the left to correct for the time lag as implied by the time constant of these recording techniques (Milerad et al, 1989).…”

Section: Resultsmentioning

confidence: 99%

Clinical and Neurophysiological Development of Unverricht‐Lundborg Disease in Four Swedish Siblings

Kyllerman¹,

Sommerfelt

Hedström

et al. 1991

Epilepsia

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Four siblings aged 12-18 years with progressive myoclonus epilepsy demonstrated a subclinical stage at the age of 9-11 years, with visual blackouts and polyspike electroencephalographic (EEG) activity on photic stimulation, an early myoclonic stage at the age of 12-15 years, with increasing segmental, stimulus-sensitive myoclonus, occasional nocturnal buildup myoclonic "cascade" seizures, slowing of EEG alpha-activity, episodic 4-6 Hz bilateral sharp waves and polyspikes with myoclonias on photic stimulation, and a disabling myoclonic stage at the age of 16-18 years, with periodic generalized myoclonias, nocturnal myoclonic "cascade" seizures, ataxia, dysarthria, mental changes, intermittent wheelchair dependency, and continuous EEG slow waves with polyspikes and intense myoclonias on photic stimulation. One of the siblings died at the age of 18 years with no apparent cause of death. Treatment with antiepileptic drugs other than valproate may have contributed but none of the siblings were ever treated with phenytoin. Extensive clinical and laboratory investigations revealed no abnormalities and excluded other known possible causes of progressive myoclonus epilepsy. The diagnosis was consistent with Unverricht-Lundborg disease and rested on typical age of onset, clinical signs, EEG, and evoked response abnormalities. Buildup myoclonic seizures are typical in advanced stages of Unverricht-Lundborg disease. We have labeled these myoclonic "cascade" seizures. A typical seizure was studied with video-EEG and cardiorespiratory monitoring. Characteristics revealed were onset with continuous arrhythmic myoclonic jerks followed by intense rhythmic myoclonus with increasing muscle tone that successively reduced the amplitude of the jerks. The EEG during the whole seizure showed intense polyspike activity. Obstructive apnea was seen at the peak of the seizure. There were no cardiac dysrhythmias. Consciousness was normal or only slightly impaired. Postictal drowsiness was not observed. Myoclonic "cascade" seizures are easily confused with generalized tonic-clonic seizures.

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“…, 1985; Hunt, 1981; Lewis and Bosque, 1995; McCulloch et al. , 1982; Milerad et al. , 1989) and may indicate that infants are better able to maintain oxygen levels in this state.…”

Section: Discussionmentioning

confidence: 99%

Arousal and ventilatory responses to mild hypoxia in sleeping preterm infants

Verbeek

Richardson

Parslow

et al. 2008

Journal of Sleep Research

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SUMMARY A failure to adequately respond to hypoxia has been implicated in the Sudden Infant Death Syndrome (SIDS). Preterm infants are at increased risk for SIDS, thus we compared ventilatory and arousal responses to mild hypoxia [15% oxygen (O 2 )] in preterm and term infants. Eight preterm and 15 term infants were serially studied with daytime polysomnography during which nasal airflow was monitored by pneumotachograph at 2-5 weeks, 2-3 and 5-6 months. At each age, in both groups, hypoxia induced a significant decrease in oxygen saturation (SpO 2 ) during both active sleep (AS) and quiet sleep (QS). Infants invariably aroused in AS; and in QS either aroused or failed to arouse. In preterm infants arousal latency in AS was longer than in term infants (P < 0.05) at 2-5 weeks. Compared with term infants, preterm infants reached significantly lower SpO 2 levels at 2-5 weeks in both AS and QS non-arousing tests and at 2-3 months in QS. A biphasic hypoxic ventilatory response was observed in QS nonarousing tests in both groups of infants at all three ages. We conclude that the greater desaturation during a hypoxic challenge combined with the longer arousal latency in preterm infants could contribute to greater risk for SIDS.

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Respiratory and arousal responses to hypoxia in apnoeic infants reinvestigated

Cited by 26 publications

References 30 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

Clinical and Neurophysiological Development of Unverricht‐Lundborg Disease in Four Swedish Siblings

Arousal and ventilatory responses to mild hypoxia in sleeping preterm infants

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