upper airwayObstructive 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.