Heart rate control in normal and aborted-SIDS infants

1993 ◽  
Vol 264 (3) ◽  
pp. R638-R646 ◽  
Author(s):  
S. M. Pincus ◽  
T. R. Cummins ◽  
G. G. Haddad
Keyword(s):  
Heart Rate ◽  
Rem Sleep ◽  
Rate Control ◽  
Approximate Entropy ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Normal Infant ◽  
Quiet Sleep ◽  
Heart Rate Data ◽  
High Risk Subject

Approximate entropy (ApEn), a mathematical formula quantifying regularity in data, was applied to heart rate data from normal and aborted-sudden infant death syndrome (SIDS) infants. We distinguished quiet from rapid-eye-movement (REM) sleep via the following three criteria, refining the notion of REM as more "variable": 1) REM sleep has greater overall variability (0.0374 +/- 0.0138 vs. 0.0205 +/- 0.0090 s, P < 0.005); 2) REM sleep is less stationary (StatAv = 0.742 +/- 0.110) than quiet sleep (StatAv = 0.599 +/- 0.159, P < 0.03); 3) after normalization to overall variability, REM sleep is more regular (ApEnsub = 1.224 +/- 0.092) than quiet sleep (ApEnsub = 1.448 +/- 0.071, P < 0.0001). Fifty percent of aborted-SIDS infants showed greater ApEn instability across quiet sleep than any normal infant exhibited, suggesting that autonomic regulation of heart rate occasionally becomes abnormal in a high-risk subject. There was an association between low ApEn values and aborted-SIDS events; 5 of 14 aborted-SIDS infants had at least one quiet sleep epoch with an ApEn value below the minimum of 45 normal-infant ApEn values.

Heart Rate and Respiratory Rate Differences Between Preterm and Full-Term Infants During Quiet Sleep: Possible Implications for Sudden Infant Death Syndrome

PEDIATRICS ◽  
1978 ◽  
Vol 62 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Peter G. Katona ◽  
John R. Egbert
Keyword(s):  
Heart Rate ◽  
Respiratory Rate ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Full Term ◽  
Sudden Infant ◽  
Quiet Sleep ◽  
Term Infants ◽  
The Difference

The heart rate and respiratory rate of eight preterm (average gestational age, 33.3 ± 2.2 weeks) and 13 full-term infants were determined during quiet sleep at home during the first year of life. Both heart rate and respiratory rate were greater in preterm infants throughout the first six months. The difference was maximum at age 10 weeks (21.1 beats per minute and 13.7 breaths per minute), with the difference being statistically significant, at least at the P &lt; .01 level at ages 10, 12, and 14 weeks, while P ≥.01 at all other ages. The 10-to 14-week period is precisely the same period during which the incidence of sudden infant death syndrome (SIDS) has been reported to be maximum. These results support the concept that SIDS is linked to a vulnerable phase of cardiorespiratory maturation.

Sleep State Organization in Normal Infants and Victims of the Sudden Infant Death Syndrome

PEDIATRICS ◽  
1992 ◽  
Vol 89 (5) ◽  
pp. 865-870 ◽  
Author(s):  
Vicki L. Schechtman ◽  
Ronald M. Harper ◽  
Arian J. Wilson ◽  
David P. Southall
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Early Morning ◽  
Sudden Infant ◽  
Sleep State ◽  
Quiet Sleep ◽  
Increased Risk ◽  
State Organization

Infants at increased risk of the sudden infant death syndrome (SIDS) show abnormal patterning of sleep-waking states. It was hypothesized that infants who were to die of SIDS would show abnormalities of sleep state distribution prior to their deaths. Twenty-two 12-hour recordings were obtained from infants who subsequently died of SIDS, and sleep state patterns were compared in these records and 66 records of age-matched control infants. Each 1-minute epoch was classified as quiet sleep, rapid eye movement (REM) sleep, waking, indeterminate state, or artifact-contaminated. Victims of SIDS showed less waking and more sleep than control infants during the early-morning hours. Victims of SIDS younger than 1 month of age showed significantly more epochs classified as REM sleep across the night and significantly fewer epochs contaminated by artifacts relative to control infants. Further analysis indicated that the increased number of REM epochs resulted from fewer artifact-contaminated epochs, suggesting reduced motility during REM sleep in the SIDS victims compared with the control infants. The finding of decreased waking time during the early morning is of particular importance since most SIDS deaths occur during this portion of the day. The findings of altered sleep patterns in SIDS victims suggest that central neural changes are associated with SIDS risk.

scholarly journals 353 HEART RATE VARIABILITY AND SUDDEN INFANT DEATH SYNDROME

1994 ◽  
Vol 36 (1) ◽  
pp. 61A-61A
Author(s):  
Francesco Perticone ◽  
Raffaele Maio ◽  
Carmela Cosco ◽  
Fabiola Pugliese ◽  
Cosima Cloro ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Sudden Infant Death ◽  
Sudden Infant

Intercostal muscle reflexes and sleep breathing patterns in the human infant

1980 ◽  
Vol 48 (1) ◽  
pp. 139-146 ◽  
Author(s):  
B. T. Thach ◽  
I. F. Abroms ◽  
I. D. Frantz ◽  
A. Sotrel ◽  
E. N. Bruce ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Cervical Spinal Cord ◽  
Human Infant ◽  
Neural Pathways ◽  
Normal Infant ◽  
Intercostal Muscle ◽  
Breathing Patterns ◽  
Quiet Sleep ◽  
Term Infants ◽  
Airway Occlusion

Breathing variability and apnea characteristic of rapid eye movement (REM) sleep was investigated in a newborn infant with complete interruption of intercostal to phrenic neural pathways due to intrapartem transection of the cervical spinal cord. Breath-to-breath variability in inspiratory duration (TI), breath duration (Ttot), tidal volume (VT), and ventilation (VI) was significantly greater in REM than in quiet sleep and was similar to the variability in these parameters seen in normal infants. In addition, brief periods of diaphragmeatic apnea were observed during REM sleep. The phenomenon of shortened TI during airway occlusion previously attributed to intercostal-to-phrenic reflexes was examined in the quadriplegic infant and in seven healthy term infants. The frequency of this response was increased when airway occlusion was delayed until after onset of inspiration. Shortening of TI by occlusion occurred no less frequently in the quadriplegic than in the control infants. The constant paradoxical inward movement of the rib cage during inspiration observed in the quadriplegic infant suggests that supraspinal innervation of intercostal muscle limits such paradoxical movements in the normal infant. The quadriplegic infant's end-expiratory volume was consistently above his passive functional residual capacity, as inferred from respiratory volume and pressure measurements.

Apnea, Hypoxemia, and Aborted Sudden Infant Death Syndrome

PEDIATRICS ◽  
1978 ◽  
Vol 62 (5) ◽  
pp. 686-691
Author(s):  
June P. Brady ◽  
Ronald L. Ariagno ◽  
John L. Watts ◽  
Steven L. Goldman ◽  
Fe M. Dumpit
Keyword(s):  
Heart Rate ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Total Duration ◽  
Periodic Breathing ◽  
Sudden Infant Death ◽  
Control Group ◽  
Sudden Infant ◽  
Nasal Catheter ◽  
End Tidal

To find out whether there is any relationship between the ventilatory response to hypoxia and the sudden infant death syndrome (SIDS), we studied the effects of mild induced hypoxia (PIO2, 120 mm Hg = 17% oxygen) in 16 infants aged 2 weeks to 6 months. Eight had recurrent apneic spells (apnea group) (five had aborted SIDS and three had recurrent apnea in the intensive care nursery) and eight were "well" preterm infants about to fly in a pressurized airplane (PIO2, 120 mm Hg) (control group). Mean birth weights were 2,245 and 1,400 gm and mean gestational ages were 35 and 30 weeks. Postconceptual ages (41.8 and 41.3 weeks) were almost identical. Heart rate was obtained from an ECG, and respiratory rate and pattern were obtained from a pneumogram. In addition, end-tidal PCO2 and PN2 or PO2 were obtained with a nasal catheter and gas analyzers. In the apnea group with inhalation of 17% oxygen, we observed an increase in periodic breathing and an increase in both rate and total duration of respiratory pauses. In the control group there were no significant changes. Heart rate and PCO2 did not change in either group. Our findings suggest that infants prone to apnea may have unique respiratory responses to mild induced hypoxia.

Influence of adenosine A1-receptor blockade and vagotomy on the gasping and heart rate response to hypoxia in rats during early postnatal maturation

2007 ◽  
Vol 103 (4) ◽  
pp. 1234-1241 ◽  
Author(s):  
James E. Fewell ◽  
Chunfen Zhang ◽  
Anne M. Gillis
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Parasympathetic Nervous System ◽  
Age Groups ◽  
Sudden Infant Death ◽  
Severe Hypoxia ◽  
Sudden Infant ◽  
Postnatal Life ◽  
Postnatal Maturation ◽  
Rat Pups

Failure to autoresuscitate from apnea has been suggested to play a role in sudden infant death. Little is known, however, about factors that influence the gasping and heart rate response to severe hypoxia that are fundamental to successful autoresuscitation in the newborn. The present experiments were carried out on 184 rat pups to investigate the influence of the parasympathetic nervous system, as well as adenosine, in mediating the profound bradycardia that occurs with the onset of hypoxic-induced primary apnea and in modulating hypoxic gasping. On days 1 to 2, days 5 to 6, and days 10 to 11 postpartum and following bilateral cervical vagotomy (VAG) or administration of a selective adenosine A1 receptor antagonist (8-cyclopentyl-1,3-dipropylxanthine; DPCPX), each pup was exposed to a single period of severe hypoxia produced by breathing an anoxic gas mixture (97% N2-3% CO2). Exposure to severe hypoxia resulted in an age-dependent decrease in heart rate ( P < 0.001), accentuated with increasing postnatal age, that was attenuated in all age groups by DPCPX but not by VAG. Furthermore, DPCPX but not VAG decreased the time to last gasp but increased the total number of gasps in the 1- to 2-day-old and 5- to 6-day-old pups but not in the 10- to 11-day-old pups during exposure to severe hypoxia. Thus our data provide evidence that adenosine acting via adenosine A1 receptors plays a role in modulating hypoxic gasping and in mediating the profound bradycardia that occurs coincident with hypoxic-induced primary apnea in rats during early postnatal life.

Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS?

2003 ◽  
Vol 94 (5) ◽  
pp. 1883-1895 ◽  
Author(s):  
Liesbeth van der Velde ◽  
Aidan K. Curran ◽  
James J. Filiano ◽  
Robert A. Darnall ◽  
Donald Bartlett ◽  
...  
Keyword(s):  
Eye Movement ◽  
Sudden Infant Death Syndrome ◽  
Rem Sleep ◽  
Infant Death ◽  
Nrem Sleep ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Rapid Eye Movement ◽  
Ventral Medulla ◽  
Before And After

We tested the hypothesis that inhibition of neurons within the rostral ventral medulla (RVM) would prolong the laryngeal chemoreflex (LCR), a putative stimulus in the sudden infant death syndrome (SIDS). We studied the LCR in 19 piglets, age 3–16 days, by injecting 0.05 ml of saline or water into the larynx during wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep, before and after 1 or 10 mM muscimol dialysis in the RVM. Muscimol prolonged the LCR ( P < 0.05), and the prolongation was greater when the LCR was stimulated with water compared with saline ( P < 0.02). The LCR was longer during NREM sleep than during wakefulness and longest during REM sleep (REM compared with wakefulness). Muscimol had no effect on the likelihood of arousal from sleep after LCR stimulation. We conclude that the RVM provides a tonic facilitatory drive to ventilation that limits the duration of the LCR, and loss of this drive may contribute to the SIDS when combined with stimuli that inhibit respiration.

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