J. Ringler et al., SYSTEMIC BLOOD-PRESSURE ELEVATION AFTER AIRWAY OCCLUSION DURING NREM SLEEP, American journal of respiratory and critical care medicine, 150(4), 1994, pp. 1062-1066
Citations number
22
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
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 desig
ned 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. Episod
ically, a stopcock was closed, occluding the inspiratory circuit. In E
xperiment 1, data were recorded on tape. Occlusions were initiated dur
ing Stage 2 NREM sleep and released coincident with arousal. Subjects
were than awakened and instructed to trace the displayed, taped Pes pr
ofile creating occulsions of identical duration to those recorded duri
ng sleep. In five subjects, the mean BP elevation (preocclusion to pea
k) 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 delaye
d 6 to 12 s after arousal. In five subjects, these occlusions were ass
ociated with BP elevations that peaked coincident with arousal, not wi
th 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.