Although prolonged apnea has long been suspected to be the primary mechanism responsible for the Sudden Infant Death Syndrome (SIDS), recent studies have failed to uncover a definitive link between the two. On the other hand, recent work by others have suggested the potentially important roles of other factors, such as arousability from sleep and heart rate variability. As such, we have continued to focus our investigative efforts on better understanding the interaction between respiration and cardiovascular control and how this interaction is affected by sleep-wake state. Over the past year, we have tested our improved method of quantifying respiratory sinus arrhythmia (RSA), described in last year's progress report, on experimental data. Due to inaccuracies in the measurements of infant respiration available to us, we chose to conduct initial tests of our method using data obtained from adult subjects. The following variables were monitored in 3 normal volunteers and 6 patients with sleep apnea syndrome: respiratory airflow (integrated to yield tidal volume), changes in esophageal pressure (taken to represent changes in pleural pressure), instantaneous heart rate (converted from beat-to- beat Rrintervals in the electrocardiogram, EEG), EOG and chin EMG. The sleep apneics were studied without and with continuous positive airway pressure (CPAP) administered through a nasal mask. RSA transfer functions were computed between the esophageal pressure swings and heart rate. Compared to the normals, the RSA transfer function of the sleep apnea patients without CPAP was significantly lower at all but the lowest frequencies. With CPAP application, the RSA transfer function of the sleep apneics increased slightly, but remained clearly lower than normal. Thus, our results suggest that parasympathetic control of heart rate is substantially decreased in sleep apneics.
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