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Objective: Little is known about the mechanism of death during sudden infant death. To study the mechanism, we obtained data on six infants who died while on a memory-equipped cardiorespiratory monitor., Methods: Waveforms of respiration and heart rate trend were available for five infants; an alarm log only was available for the sixth. These printouts were reviewed with attention to mechanism and time to death., Results: All infants were born prematurely; autopsies reported the cause of death as sudden infant death syndrome in three cases and bronchopulmonary dysplasia in the others. Bradycardia, which played a more prominent role than central apnea, was preceded by tachycardia in two deaths. Resuscitation occurred within 1 minute in four cases; no response to alarms occurred in the other two cases, apparently because the parents were desensitized by prior meaningless alarms. Five patients died within 20 minutes, whereas one death due to sudden infant death syndrome was prolonged., Conclusion: Bradycardia is an important feature in all six of these infant deaths. Although its etiology is unknown, hypoxemia or obstructive apnea may precede bradycardia. Home monitors equipped to detect these possible antecedents will yield further insight into sudden infant death.

Many children older than 12 months of age are now on home monitors. Home pneumograms performed on normal infants have established standards, and have been used to evaluate infants during their first year. However, no standards have been described for infants older than 12 months. We, therefore, recorded the standard pneumogram on 88 full-term healthy infants who were 12-18 months of age. We analyzed the recordings for average respiratory and heart rates, apnea (greater than or equal to 6 seconds) density, longest apnea, periodic breathing, and bradycardia for 12 hours. We compared the values in males vs. females and in infants 12-14.9 months vs. 15.0-18.0 months of age. Since there was no difference in any parameter measured in any group, we combined the values to determine the normal values for this population.

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.

The pediatric pneumogram is a frequently used tool in the diagnosis and management of apnea during infancy. We analyzed 287 pneumographic recordings from 123 full-term infants (63 males) obtained during the first 12 months of life to establish normative values for apnea, periodic breathing, and bradycardia. The results of the analysis were compared by sex and age. The number of infants who exhibited periodic breathing decreased significantly over time (78% at 0-2 weeks vs 29% at 39-52 weeks; P less than 0.05). However, for those infants who did breathe periodically, the percent of sleep time spent in this breathing pattern did not change with age. No apnea greater than or equal to 15 seconds was recorded in any infant, and apnea density (total apnea greater than or equal to 10 seconds in minutes/100 minutes sleep time) did not change with age or sex. Using our definitions, no bradycardia was identified. Normal full-term infants occasionally have apnea of 10, 11, or 12 seconds, and, until 6 months of age, the majority will have a small amount of periodic breathing (less than 1% of sleep time) during sleep at home.

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 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 divided by mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.