Parental Reports of Apnea and Bradycardia: Temporal Characteristics and Accuracy

PEDIATRICS ◽  
1991 ◽  
Vol 88 (6) ◽  
pp. 1100-1105
Author(s):  
Alfred Steinschneider ◽  
Vicki Santos
Keyword(s):  
Heart Rate ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Event Recorder ◽  
External Stimulation ◽  
Temporal Course ◽  
Prolonged Apnea ◽  
Parental Reports ◽  
Objective Event ◽  
Objective Recording

A prospective examination was made of the temporal course of parental observations in response to a monitor alarm of apnea (apnea setting of 20 seconds) or bradycardia (bradycardia setting of 80 beats per minute). Data were obtained from 155 subsequent sudden infant death syndrome siblings followed up at home, during the first 20 weeks of life, on an apnea/bradycardia monitor with an attached event recorder. In addition, parental reports were compared to an objective recording of the pattern of cardiorespiratory activity surrounding each monitor alarm. Only those parental observations were considered which reported the infant to be asleep with no apparent equipment malfunction following an apnea alarm (with or without pallor, cyanosis, or the provision of external stimulation) or a low heart rate alarm associated with pallor, cyanosis, or stimulation. Observations were analyzed within each of five age periods (<29, 29 through 56, 57 through 84, 85 through 112, 113 through 140 days). The percentage of infants reported to have prolonged apnea, prolonged apnea with stimulation, or bradycardia with stimulation was found to decrease with age. An examination of the linked event recordings failed to document an episode of apnea as long as 15 seconds for any of the reported episodes of apnea. Furthermore, bradycardia as long as 5 seconds in duration could be documented in only 3 of 422 reported episodes of bradycardia. These results indicate the potential for considerable error when total reliance is placed on parental observations and point to the necessity for objective event recordings when using home monitors in the clinical management of at-risk infants.

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

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.

Prolonged Apnea, Vagal Overactivity, and Sudden Infant Death

PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman
Keyword(s):  
At Risk ◽  
Vagus Nerve ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Vagal Stimulation ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Prolonged Apnea ◽  
Stimulation Of

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3

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.

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.

PROLONGED APNEA AND THE SUDDEN INFANT DEATH SYNDROME: CLINICAL AND LABORATORY OBSERVATIONS

PEDIATRICS ◽  
1994 ◽  
Vol 93 (6) ◽  
pp. 944-944
Author(s):  
Alfred Steinschneider
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Critical Role ◽  
Warning System ◽  
Sudden Infant Death ◽  
Serial Killer ◽  
Medical Examiner ◽  
Sudden Infant ◽  
Pediatric Pathology ◽  
Prolonged Apnea

A 25-Year Trail to Murder Charges—... The first suspicions were raised in 1985 by Dr. Linda Norton, a former medical examiner for Dallas County, Texas, and an expert on pediatric pathology, who had been a consultant in the VanDerSluys case. "You may have a serial killer in Syracuse," she told the prosecutor in giving him a copy of an October 1972 article in Pediatrics (1972;50(4)) called "Prolonged Apnea and the Sudden Infant Death Syndrome: Clinical and Laboratory Observations." In the report Dr. Steinschneider described his work with the syndrome and how two children in a family plagued with the affliction had died within hours of their release from his Syracuse research project. In his paper, Dr. Steinschneider concluded that the family, which he still identifies only as "H," showed that victims suffered from real if almost undetectable physical abnormalities. In a proposal that was radical then but is now accepted, he suggested that the syndrome had a genetic component and was therefore inherited. He suggested that scientists could identify the abnormalities and thereby devise a warning system. "But the paper indicated a more sinister possibility to Dr. John F. Hick of Minnesota. In a letter to the journal, he wrote that the case offered "circumstantial evidence suggesting a critical role for the mother in the death of her children." (See below.) But his warning was dismissed, until Mr. Fitzpatrick read the paper 15 years later. "The medical records described two happy, healthy, perfectly normal kids," he said. "It convinced me that these children were murdered."

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