Obstructive sleep apnea is a serious medical disorder which has been associated with sudden death during sleep. Sleep-associated decreases in the electromyographic activity of the pharyngeal dilators allow the subatmospheric pressures generated during inspiration to collapse the upper airway. During these episodes of upper-airway occlusion, arterial oxyhemoglobin saturation (Sa02) decreases in association with concomitant elevations in systemic and pulmonary blood pressures. Throughout the apneic period, heart rate slows in proportion to the duration of apnea and the degree of oxyhemoglobin desaturation. Increased vagal efferent activity plays a significant role in mediating these reductions in heart rate, as atropine usually ameliorates the apnea-related bradycardias. The resumption of ventilation is associated with rapid cardioacceleration, which is considered to result from a decrease in vagal tone, probably combined with hypoxia-mediated increases in sympathetic neural activity. This repetitive sequence of events is responsible for the prominent sinus arrhythmia which is frequently observed during sleep in these patients. Marked sinus bradycardia (heart rate less than 40 beats per minute) and sinus pauses lasting from 2 to 17 seconds have been reported by different investigators to occur in as few as 9 percent to as many as 30 percent of the patients with obstructive sleep apnea. While severe bradyar-rhythmias are a potential mechanism for sudden death during sleep, repetitive ventricular ectopy degenerating to ventricular fibrillation is considered to be the more common dysrhythmia leading to sudden death. Because the relationship of ventricular ectopy to ap-neic events is less well established, the present study was undertaken to examine the relationship between ventricular ectopic activity and the severity of oxyhemoglobin desaturation in patients with obstructive sleep apnea.
Materials and Methods
The population under study consisted of 31 male patients referred for diagnostic polysomnography because of clinically suspected obstructive sleep apnea. Routine spirometric testing was performed in each patient using a wedge spirometer (Med-Science). Thoracic gas volume at functional residual capacity (FRC) was determined with a body plethysmograph (Warren E. Collins). Values were expressed as a percentage of previously published normal values. Following informed consent, all subjects underwent venipuncture for measurement of hemoglobin concentration and levels of blood urea nitrogen, creatinine, and electrolytes, as well as arterial puncture for blood gas analysis (Instrumentation Laboratories model 813). Posteroanterior chest roentgenograms were obtained, along with standard 12-lead electrocardiograms. Why do people snore hile sleeping? Sometimes the reason is obstrutive sleep apnea and More info about diseases and hot news – Canadian health&care Mall – canadianhealthcaremallinc.net.
All patients underwent overnight polygraphic sleep study. A polygraphic recorder (Beckman R411) was used to record electroen-cephalographic activity using standard central leads, respiratory airflow with both oral and nasal thermistors, thoracoabdominal movement by impedance pneumography, and electrocardiographic activity using chest leads CC5 and CM5. All of the cardiopulmonary data were recorded (Honeywell VR-16 recorder), and the data were stored on electromagnetic tape (Ampex PR500) for subsequent off-line computer-assisted analysis. A time code signal, generated with a real-time clock (Hewlett-Packard), a desktop computer (system 9835), and a multiprogrammer (model 6940), was simultaneously recorded on both the electromagnetic tape and the sleep record. This time code permitted accurate identification of the segments of the taped cardiopulmonary data which occurred during rapid eye movement (REM) and nonrapid eye movement (NREM) sleep.
Analysis of Sleep Data
The sleep record was scored using 60-second epochs according to standard criteria. Apneas and hypopneas were scored by the criteria of Block et al. Apnea and hypopnea indexes were computed as the number of events per hour of sleep. Mean high SaOz was determined as the average of the baseline values of Sa02 prior to the onset of oxygen desaturation and mean low Sa02 as the average of the values at the nadir of the desaturations. The times spent in each categoric level of Sa02 were obtained by computer analysis of the taped Sa02 data using a sampling frequency of one second and appropriate sorting routines. The mean values for Sa02 during REM and NREM sleep were determined as the average of the values obtained at one-second intervals throughout the respective sleep states. The number of PVCs within each categoric level of Sa02 were determined by visually identifying all PVCs on a hard copy of the electrocardiographic data and ascertaining the values for Sa02 at the time the PVCs occurred. The PVC frequency (number per hour) was then computed from these data and knowledge of the time spent in each categoric level of Sa02.
Data are presented as means ± standard deviation. The paired f-test was used to test for differences in PVC frequency and Sa02 between REM and NREM sleep. Analysis of variance for repeated measures (blocked design) was employed to test for significant differences in PVC frequency across categoric levels of Sa02. Tukey’s honestly significant difference (HSD) test was employed to test for differences in PVC frequency between categoric levels when analysis of variance detected a significant trend.