Search

Blood pressure (BP) rises at the termination of obstructive episodes in patients with sleep apnea. Although the relationship of these BP elevations to oxygen saturation (SaO2) and arousal has been explored, the influence of sleep stage is undefined. To examine the effects of sleep stage on the postapnea BP elevation, we enrolled 12 patients with obstructive sleep apnea (OSA), and successfully collected data from seven of these (all male). Subjects slept overnight in the sleep laboratory, with full sleep and respiratory monitoring. Arterial pressure was assessed continuously with a radial artery catheter (six patients) or with digital photoplethysmography (one patient). Apneas occurring in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep were matched for duration and degree of desaturation. When mean arterial pressure (MAP) at termination of apneas during NREM sleep associated with SaO2 nadirs 78 to 82% (NREM 80%) was compared with MAP following apneas in REM with the same SaO2 nadir (REM 80%), there was a significant difference (NREM 80% 122 +/- 15.3 mm Hg, REM 80% 132 +/- 11.0; p = 0.0109). We also analyzed the effect of oxygen desaturation on MAP during REM sleep, by comparing events with SaO2 nadirs of 78 to 82% with events with nadirs of < 75% (REM < 75%). In REM, further desaturation was associated with significant lengthening of the obstructive episodes and significantly higher postapnea BP increases (REM 75% 143 +/- 19.9 mm Hg, p = 0.0392). We conclude that sleep stage alters the hemodynamic response to obstructive apneas during sleep.

Increases in arterial pressure follow obstructive sleep apneas even in the absence of hypoxemia. These blood pressure (BP) elevations could be caused by arousal from sleep, resumption of ventilation, or abrupt changes of intrathoracic pressure (ITP). To better define the relative contributions of each of these factors to the BP elevations, we designed two protocols employing six normal subjects isolating the effects of arousal from those of ventilation and ITP. BP (Penaz method), sleep stage, air flow, and esophageal pressure (Pes) were monitored. Episodically, a stopcock was closed, occluding the inspiratory circuit. In Experiment 1, data were recorded on tape. Occlusions were initiated during Stage 2 NREM sleep and released coincident with arousal. Subjects were than awakened and instructed to trace the displayed, taped Pes profile creating occlusions of identical duration to those recorded during sleep. In five subjects, the mean BP elevation (preocclusion to peak) associated with occlusion release upon arousal was 19.0 +/- 5.1 mm Hg, whereas the analogous rise for matched awake occlusions was 5.4 +/- 4.8 mm Hg (p = 0.027). In Experiment 2, occlusion release was delayed 6 to 12 s after arousal. In five subjects, these occlusions were associated with BP elevations that peaked coincident with arousal, not with resumption of ventilation (mean increase, 18.0 +/- 10.4 mm Hg). We conclude that under the conditions of these experiments, BP elevations after airway occlusion during sleep are attributable more to arousal than to resumption of ventilation.

Patients with obstructive sleep apnea experience nocturnal hemodynamic oscillations in association with repetitive respiratory events. Apnea termination (recovery) is accompanied by the nadir of arterial O2 saturation (SaO2), changes in intrathoracic pressure, and arousal from sleep. To investigate separately the contributions of hypoxemia and of arousal from sleep to changes in cardiac function, we continuously measured left ventricular stroke volume (LVSV) and mean arterial pressure (MAP) in eight subjects with severe obstructive sleep apnea (apnea-hypopnea index > 30 events/h associated with SaO2 < or = 82%) during two experimental conditions: 1) subjects slept without intervention for 1-2 h and then supplemental O2 was administered to maintain SaO2 > or = 90% (mean SaO2 nadir 92.7%) throughout the apnea-recovery cycle and 2) upper airway obstructions were abolished using nasal continuous positive airway pressure and subjects were aroused from sleep by an auditory signal. Recovery was associated with an increase in MAP and a decrease in LVSV both with and without supplemental O2. Arousal from sleep on nasal continuous positive airway pressure reproduced the postapneic elevation of MAP but not a decrease in cardiac function of the magnitude that occurred at apnea termination. We conclude that elevation of blood pressure and reduction of LVSV that occurred at apnea termination may be due to different physiological mechanisms.