J Ringler, E Garpestad, RC Basner and JW Weiss
Charles A. Dana Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

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.

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