Dorothy H. Kelly

Pneumograms in infants who subsequently died of sudden infant death syndrome

Victims of sudden infant death syndrome (SIDS) have occasionally been reported to have had prolonged apnea or an increased frequency of short apnea prior to their deaths. To examine the extent of these abnormalities, we compared pneumograms obtained in 17 infants who subsequently died of SIDS (10 with history of apnea) with those of 34 age- and sex-matched controls. The recordings were analyzed by a computer program that avoided observer bias. SIDS infants had significantly greater mean heart rate (P less than 0.05) and periodic breathing during quiet time (P less than 0.003) than control infants had. The apnea in SIDS infants tended to be more periodic than in control infants (P less than 0.002). In addition, the incidence of bradycardia was greater in SIDS (three infants) than in controls (none) (P less than 0.03). These differences suggest a disturbance of autonomic function prior to death in some victims of SIDS.

Sudden infant death syndrome: abnormalities in short term fluctuations in heart rate and respiratory activity.

Summary: In order to test the hypothesis that a defect in cardiorespiratory regulation contributes to death of infants from sudden infant death syndrome (SIDS), we analyzed the power spectra of heart rate and respiratory activity during 256-sec epochs of quiet sleep. Data were obtained from pneumogram recordings performed for 12 h at night on eight infants who subsequently died from SIDS and 22 age-matched control infants. We computed the heart rate and respiratory power spectra from a single epoch on each infant using an algorithm developed for an 8085 microprocessor system dedicated to this investigation. There was no statistically significant difference between SIDS and controls based on mean respiratory and heart rates. Spectral analysis revealed enhancement of low frequency power in the 0.02 to 0.1 Hz band in the heart rate power spectrum in the SIDS group compared to control (p < 0.002) and dispersion in respiratory frequency as determined by the respiratory band width (p < 0.00001). These data suggest that a predisposition to SIDS manifests itself in an abnormal pattern of fluctuations in heart rate and respiratory activity.

Sudden infant death syndrome and near sudden infant death syndrome: a review of the literature, 1964 to 1982.

During the past decade, investigators have begun to scientifically examine many of the theories that have been proposed to explain sudden infant death syndrome. The authors review the research in this area from 1964 to 1982.

Analysis of heart rate and respiratory patterns in sudden infant death syndrome victims and control infants

ABSTRACT. Retrospective analyses of patterns of breathing and heart rate variability obtained by visual inspection and spectral analysis of ECG and respiratory activity have provided markers associated with subsequent death in a referred population of infants at high risk for sudden infant death syndrome (SIDS). Such markers include breathing patterns characterized by excessive apneic pauses and periodic breathing, heart rate spectra characterized by increased low frequency oscillations, and respiratory activity spectra characterized by a widened “bandwidth” during regular breathing. To test whether such measurements could distinguish SIDS cases and randomly selected controls from a population study the data from 10 cases and 100 age-matched control subjects were analyzed blind. The code was disclosed after completion of the analysis. We found that none of the markers served to distinguish the SIDS cases from the controls in the population at large. This observation may indicate important physiological differences between infants destined to die in the referred high risk population and infants who die of SIDS at large. The possible reasons for our inability to identify the group of SIDS in the general population, as compared to the group of deaths in the referred high risk group are: (1) different disease processes in the two groups, (2) difference responses to the same disease process in the two groups, (3) a response reflecting the psychosocial setting of the referred high risk population, (4) methodological differences between this and previous studies. We conclude that these markers are not of value in screening the population at large.

The role of the QT interval in the sudden infant death syndrome.

To evaluate the role of QT interval prolongation in the genesis of the sudden infant death syndrome (SIDS), the postresuscitation electrocardiograms of 21 aborted SIDS infants were reviewed. The infants had been found apneic, cyanotic, limp and unresponsive during sleep and required vigorous physical stimulation and mouth-to-mouth resuscitation. Three subsequently experienced repeat similar episodes from which they could not be resuscitated. Extensive studies eliminated all “known” etiologies for death. The QT intervals of these infants were compared to age and sex matched normal infants as well as to established normal values in the literature; in both the aborted and the subsequent actual SIDS infants, the QT intervals were not significantly different from those of the normal population. Thus, we conclude that QT interval prolongation does not play a major role in the genesis of the aborted SIDS.

Ventilatory Chemoreceptor Response in Parents of Children at Risk for Sudden Infant Death Syndrome

Summary: We postulated that parents of infants who sustain near-death episodes associated with defective chemical regulation of breathing might share a similar defect. We, therefore, measured the ventilatory responses to progressive hypoxia and hypercapnia individually in eight sets of parents of infants who had sustained at least one near-death episode (apnea, cyanosis, pallor, limpness, and responsive only to mouth-to-mouth resuscitation); each infant had a ventilatory response to CO2 which was more than 2 S.D. below the mean normal. Ventilatory function measured by vital capacity forced expiratory volume 1.0 and flow volume curves was normal in each group. Responses to hypercapnia and hypoxemia in both fathers and mothers were similar to 11 pairs of controls. Ventilation during CO2 rebreathing normalized for surface area increased 0.87 liter/min/mm Hg in fathers, 0.94 in controls, 0.87 in mothers, and 0.75 in controls. Ventilation during progressive hypoxemia increased 88 liter/min/1/mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.Speculation: Defective chemical regulation of breathing in infants at risk of sudden infant death syndrome is not shared by their parents. This suggests that environmental influences, perhaps in utero, are responsible for this defect.

Increased Respiratory Frequency and Variability in High Risk Babies Who Die of Sudden Infant Death Syndrome

ABSTRACT. We have tested the hypothesis that autonomic instability, reflected in increased variability of heart rate and respiratory frequency, characterized high risk babies who died of sudden infant death syndrome. Using computer-based methods, we compared the power spectra of instantaneous heart rate and respiration on coded tape recordings from seven asymptomatic siblings and 10 babies with symptomatic apnea who died of sudden infant death syndrome to 34 age- and sex-matched controls. We confirmed our previous observation of increased respiratory bandwidth, an index of variability in respiratory frequency (p = 0.009) but failed to confirm our finding of increased low frequency fluctuations in heart rate (p = 0.18). In addition, we found an increase in mean respiratory frequency during quiet breathing (p = 0.001) and a significant relationship between respiratory bandwidth and mean respiratory frequency (r = 0.604, (p = 0.0002). These variables along with those from a previous analysis of the same data base yield a discriminant function with 82% sensitivity and 100% specificity. These results confirm previous suggestions that high risk babies who die of sudden infant death syndrome exhibit autonomic instability.

PROSPECTIVE ANALYSIS OF HEART RATE AND BREATHING PATTERNS IN INFANTS SUCCUMBING TO SIDS AND IN CONTROLS

In studies of babies at high risk for SIDS (near-SIDS and siblings), we have identified among some who died excess periodic breathing (PB) excess variability (var) of respiratory frequency (f) and increased oscillation of heart rate (HR), at 4-7 cycles per min., (low frequency peak-LFP). The present study was planned to test the hypothesis that in an unselected prospectively studied population, these same variables might discriminate SIDS from controls. From 6914 term infants, we selected 24 hour pneumograms performed at 6 weeks on 11 SIDS and 101 random controls. One SIDS had one near-SIDS spell. Casettes were coded for blind analysis. From data recorded between 12MN and 6AM we transcribed ECG and respiratory signals onto hard copy for visual inspection and we transferred these signals during all 5 min epochs of quiet breathing (Q) onto FM tape for spectral analysis. We inspected hard copies for PB and apnea ⩾10s. Spectral analysis identified f and var, HR and var and power at f (resp. sinus arrhythmia) and at the LFP. We rank ordered results to test hypothesis 1) that PB and 2) that abnormal spectral var were markers for SIDS. We performed cluster analysis on each data set The code was then broken; neither hypothesis was correct. These results neither support nor negate the apnea hypothesis of SIDS.

Incidence and significance of primary abnormalities of cardiac rhythm in infants at high risk for sudden infant death syndrome

SummaryThe exact relationship between cardiac arrhythmias and sudden infant death syndrome (SIDS) is uncertain. Several reports have implicated both ventricular and supraventricular arrhythmias in isolated cases, but there have been no studies of the incidence or type of arrhythmias that occur in populations at risk for SIDS. Of 1699 infants at high risk for SIDS, 60 (4%) were found to have a primary cardiac arrhythmia (i.e., not associated with disordered respiration or apnea). The incidence of atrial and ventricular premature beats, supraventricular tachycardia, and Wolff-Parkinson-White syndrome was similar to the incidence found in normal infants. Primary bradycardia (defined as a heart rate less than 60 for greater than 10 s not associated with abnormal respiration) was the most common arrhythmia, occurring with a frequency and severity not seen in normal infants. Thirty-two infants experienced periodic bradycardia. In 19 of these latter infants, there were symptoms associated with these bradyarrhythmias that necessitated treatment. Heart rates as low as 20 beats/min were recorded. One infant presented with an episode of ventricular fibrillation and on further evaluation was noted to have recurrent bradyarrhythmias. In no infant was there abnormal prolongation of the QT interval.Primary bradyarrhythmias are seen at an increased incidence in infants at high risk for SIDS and may play a causal role in this syndrome. Most symptomatic infants can be adequately controlled with sympathomimetic or parasympatholytic therapy. Other cardiac arrhythmias occur at a rate similar to that in normal infants and are therefore unlikely to play a major role in SIDS.

Neonatal and Infantile Apnea

Prolonged sleep apnea, defined as apnea greater than 20 sec or less than 20 sec if accompanied by bradycardia,1 has been described in premature infants for many years2–4 and more recently in young infants5–10 and in older children.11–20 Long—term effects attributed to this condition range from neurologic abnormalities to death. Banker and Larroche, in autopsy studies of preterm infants who had experienced repeated episodes of prolonged apnea and cyanosis, noted diffuse neuronal loss in the cerebral cortex, leukomalacia in periventricular watershed zones, and spasticity in two of three infants who survived for longer than 1 month after the cyanotic event. In autopsy studies of full—term infants whose hypoxic episode occurred between 2 and 52 weeks of age, they described subcortical leukomalacia. They theorized that the specific brain lesions in the two groups of infants occur because the affected regions are border zones and have a tenuous arterial blood supply from the anterior, middle, and posterior cerebral arteries.21 Lou recently documented that cerebral perfusion pressure in the premature infant is mainly dependent on systemic blood pressure and that auto—regulation of smooth muscle tone in vessels is not present.22 This observation strengthens the argument that these areas are extremely susceptible to hypoxic injury.