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SummaryThe QT interval was measured in 12 normal and 7 aborted sudden infant death syndrome (SIDS) infants in rapid eye movement (REM) and quiet sleep at monthly intervals through the age of 4 months. An accuracy of better than 2 msec was assured by high resolution of the digitized signal and calibration of each Q T measurement'with an accurately ge-nerated time code. In contrast to current speculations, the QT index was significantly smaller in the infants with aborted SIDS than in the normal infants in both REM and quiet sleep ( P < 0.05). In addition, as in normal infants, the QT, was smaller in REM than in quiet sleep ( P < 0.01).Although these results offer no support for the hypothesis that SIDS results from prolongation of the QT interval, they suggest that aborted SIDS infants have a functional abnormality in the autonomic nervous system. requiring vigorous physical stimulation for resuscitation; mouthto-mouth resuscitation was required in five. At the time of the episode, four of the seven infants were clearly asleep; the level of consciousness was not known in the remaining three infants. Detailed clinical and laboratory assessment failed to reveal an explanation for the aborted SIDS episode. The laboratory evaluation included hematologic profile, serum glucose, calcium, magnesium, sodium, potassium, and chloride, acid-base and blood gas analysis, a chest x-ray, a conventional 12-lead electrocardiogram, an electroencephalogram, and a roentgenographic study i f the upper gastrointestinal tract after swallowing barium. Although the precise relationship between massive gastroesophageal reflux and the cardiorespiratory collapse of the aborted SIDS episode is not well understood, we excluded four infants with massive gastroesophageal reflux because their recurrent aborted SIDS episodes were eliminated by thickening the feedings and placing the infants SpeculationWe suggest that 1) the shortening of the QT interval in the aborted SIDS infants results from a uniform increase in the sympathetic outflow to the cardiac ventricles or an increase in circulating levels of catecholamines; and 2) an imbalance between the left and the right sympathetic outtlow to the ventricles of aborted SlDS infants, as has been previously hypothesized, is not likely since the QT, was not larger in REM sleep, a sleep state in which an increase in sympathetic activity occurs.Experimentally induced imbalance in the sympathetic outflow to the ventricles causes prolongation of the QT interval (24,25). Such a prolongation of the QT interval is associated with increased vulnerability to ventricular arrhythmias and sudden death. The clinical counterpart of these experimental observations is the long QT syndrome in which infants, as well as adults, die suddenly and unexpectedly after physical or emotional stress (8,16, 17). Recently, it has been postulated that infants dying in the first few months of life of the SIDS might have an asymmetrical development of the sympathetic innervation of the ventricles, causing an imbalance in the ventric...

SummaryThe relationship of beat-tebeat heart rate variability (delta RR) and instantaneous heart rate was studied in eight normal infants while asleep during the first four months of life. The sleep state (REM or quiet) was determined using neurophysiologic and behavioral criteria. The results of regression analyses indicated that the delta RR values were positively correlated with the instantaneous heart rate (RR intervals). The correlation coefficient range was 0.49 to 0.92 in quiet sleep and 0.50 to 0.93 in REM sleep. Regression analyses supported-a linear approximation of the delta RR to RR relation over the RR range investigated (400 to 520 msec). The median slope was 0.124 k REM Pad 0.117 in quiet sleep. The slopes of these linear functions were similar in both sleep states and at all ages. If beat-tebeat variability is to be used as an index of the integrity of the autonomic nervous system, these results suggest that delta RR be corrected for RR. A model is presented which relates the demonstrated positive correlation of delta RR to RR with the physiology of cardiac output control. SpeculationThe positive correlation of delta RR with RR is consistent with the view that beat-tebeat heart rate variability is a homeostatic mechanism required for control of cardiac output.Beat-to-beat or short-term heart rate variability (delta RR) is used for identification of fetal distress and is believed to reflect the integrity of the autonomic nervous system in the fetus and newborn (6, 11,18). Autonomic dysfunction may be manifested by decreased short-term variability as seen in hypoxic newborn infants at delivery (15) and in infants of mothers given parasympatholytic drugs (7,8,13,14).Short-term vrcriability may also prove to be a useful parameter for monitoring autonomic function during early infancy. However, as in the fetus (7, 8), short-term variability of the heart rate might be a function of the instantaneous heart rate (instantaneous heart rate defined as the inverse of the RR interval of the electrocardiotrocardiograms done after each study were normal. The procedures and objectives of the study were explained to the parents. and informed consent was obtained. A total of four or five studies, lasting one to two hr, were performed on each infant while it was asleep. Serial studies were performed during the first two wk of life and subsequently at monthly intervals through four months of age. Each study was done in a quiet laboratory environment after a usual midmorning feeding. MEASUREMENT OF THE RR INTERVALSElectrocardiogram surface electrodes were positioned on the chest to obtain a unidirectional polygraph recording with a single prominent R wave which had a sharp peak. Each RR interval of this wide-band electrocardiogram signal (0.5 to 2000 Hz) was measured with an accuracy of 200 p e c using a digital preprocessor designed in this laboratory (17). The data was carefully reviewed, and less than 0.1% of the 10,000 to 15,000 of each study RR intervals were rejected as artifact. SLEEP STAGINGSurface electrodes...

A conservative approach to non-delivery of women with prolor ed premature rupture of membranes (PPROM) before 36 wks. was associated with congenital postural deformities and hypoplastic lungs but not with neonatal asphyxia or sepsis. PPROM> 24 hrs. occurred in 89 infants (15.8/1000 deliveries 1975-1977). Positional foot deformity (PFD), congenital dislocation of hips (CDH) and hypoplastic lungs (HL) were present only with PPROM a 28 wks. gestation or less. TOTAL 89 8118 5 1 The incidence of PFD and CDH in this group was significantly higher than in all newborns (5.5% and 1.1% vs. 0.4% and 0.5% respectively). 3/89(3.3%) of the infants were stillborn; 8/89 (9.0%) died; 8/11 perinatal deaths were ClOOO gm. There was no difference in the incidence of neonatal asphyxia in PPROM infants matched for gestational age and birth weights with non-PPROM controls. The one PPROM infant with infection survived Group B streptococcal septicemia.I£ Medicine, Depts. of Family and 1 'community Medicine, Pediatrics, and Obstetrics/Gynecology, TucsolA 5-year retrospective study of 4,430 deliveries assessed the influence of maternal obesity, pre-pregnant weight, weight gain, age, and diabetes on fetal outcome. Male babies were heavier than females (p<.05). Thus different curves may be needed to determine the designation "LGA" in some populations. Obese mothers, mothers who gained > 30 lbs. during their pregnancy, and Class A diabetics all had heavier babies and increased numbers of LGA births compared to controls (p<.01).When obesity and diabetes were present, 66.7% of the births were LGA vs. 12.1 -for controls (p<.01).The prevalence of major malformations correlated only with maternal diabetes, where there was a 4-fold increase over controls (11.3% vs. 2.7%, p<.05). Perinatal mortality was affected by maternal factors only insofar as they adversely affected birthweight or gestational age. Diabetes however, resulted in increased mortality at all birthweights and gestational ages, ant gave an overall perinatal mortality rate of 143/1000 births, which was almost 4 times greater than controls (p<.01).Maternal obesity, pre-pregnant weight, weight gain and diabetes are significant determinants of birthweight and the percentage of LGA births, whereas only maternal diabetes was found to directly increase the prevalence of major malformations or the perinatal death rate. Following our initial report regarding the use of tolazoline ir infants with persistent pulmonary hypertension, we have reviewed our subsequent experience with this drug in patients with hyalinc membrane disease (HMD) and meconium aspiration syndrome (MAS) whc had severe hypoxemia unresponsive to usual therapy. From 10/74-10/77 we infused tolazoline to infants on assisted ventilation xhen their Pa02 fell below 50 torr while in an Fi02 of 1.0 and requiring peak inspiratory pressures of > 40 cm H20. A bolus of 1-2 mg/kg was given via scalp vein, followed by 1-2 mg/kg/hr to a iaximum of 10 mg/kg/hr. Five of 15 patients with HMD who met this :riteria survived, with only one surviv...

i n 7 aborted SIOS i n f a n t s were performed during sleep i n the f i r s t four months o f l i f e . The QT index (QTc) was measured with an accuracy o f 2 msec o r b e t t e r . I n contrast t o recent suggestions, the mean QTc was s i g n i f i c a n t l y smaller i n the aborted SIDS than i n the normal i n f a n t s i n both REM and q u i e t sleep (p< 0.05, unpaired t -t e s t ) . Means SD are presented: NORMAL ABORTED SIDS

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In the belief that intercellular communication playa a role in development, we have studied beating 7-day chick embryo heart cell aggregatesand layers. In comparisonwith asynchronous controls we have shown correlations between synchronous beating and both the appearanceof gap junctionsrevealedby freeze-fractureandelectrophysiologic evidence of ionic couplingat the interfacebet!'centhem.The freeze-fracture studies reveal gap junctions which are mall, often unusual inshape and occur in clusters; these features are also characteristic of the gap junctions in intact hearts from embryos of the same age. When the interfaces between 11 synchronous and 10 asynchronous aggregate-layers were compared there were significant differences in the number of gap junctions and the total areaofgapjunctionsper cell, but no significant differences in the numberof cells containing junctions, the percent of total membrane area occupied by junctions, their density or their average size. The electrophysiological studies showed no propagation of stimulating current pulses from aggregate to layer in 16 asynchronous instances, but successful transmission in 6 of 7 synchronous aggregate-layers. These data indicate that synchronous beating is a sensitive detector of the presence of ionic coupling and of gap junctions, suggesting its usefulness in further studie~ of the role of intercellular communication in development. We report a new syndrome with the simultaneous failure of control of ventilation (Ondine's Curse), esophageal and intestinal motility (Hirschsprung's disease), and heart rate in three infants, who died in the first few months of life; two were siblings.Detailed physiologic studies were performed in one, and pathologic studies in three. Ventilation was measured by the barnmetric method or by pneumotachography. Sleep was staged using the EEG, EOG, and EMG. Minute Ventilation (V) ar.d respimtory rate (f) were lower in Ouiet sleep (~=315nl, f=18/min) than in both REM sleep (V=477ml, f=22/min) and wakefulness (V=654ml, f= 29/min). Respiratory paus$s > 5 sec occurred more frequently in Quiet than in REM sleep. V increased by 25% after IV doxapram but not following aminophylline, progesterone or imipramine. Minimal short term (beat to beat) variability of the ECG R-R interval (interquartile range(+l.5 msec.) in both Quiet and REM sleep indicated abnormal c o~t m l of heart rate. Histologic studies revealed aganglionosis of the colon in all three patients; serial sections of the brain stem in the siblings failed to reveal any abnormality. The Riley-Day Syndrome was excluded. We believe that a congenital abnormality in the autonomic nervous system is responsible for this syndrome. mass (MM). DNA and protein (Pr) content. plus disaccharidase activities were determined in groups of beagle puppies at birth (Controls; 11-61 and after 24 hours of either suckling (n-5) or artificial feeding with simulated bitch milk (n-5). Body weights of the latter 2 groups increased similarly. While neither MM, DNA nor Pr of the artificially fed group w...

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