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The Effect of Upper Airway Obstruction and Arousal on Peripheral Arterial Tonometry in Obstructive Sleep Apnea

Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland

Correspondence and requests for reprints should be addressed to Christopher P. O'Donnell, Ph.D., Room 4B61, Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Baltimore, MD 21224. E-mail: codonnel{at}jhmi.edu

We evaluated the effects of airflow limitation and arousal on digital vascular tone in 10 patients with obstructive sleep apnea (OSA) using the recently developed, noninvasive technique of peripheral arterial tonometry (PAT). Subjects were maintained at a therapeutic level of continuous positive airway pressure, and nasal pressure was acutely dropped for three to five breaths during nonrapid eye movement sleep over a range of pressures from 9.3 ± 1.3 to 1.9 ± 1.3 cm H₂O, leading to increasing airway obstruction and decreasing levels of inspiratory airflow. In the absence of a detectable electroencephalographic (EEG) arousal, severe reductions of inspiratory airflow to below 200 ml/second caused significant decreases in PAT amplitude (1.000 ± 0.007 to 0.869 ± 0.007 arbitrary units; p < 0.001), whereas mild airflow limitation (> 200 ml/second) had no effect (1.000 ± 0.009 to 1.011 ± 0.007 arbitrary units). The presence of an EEG arousal accentuated the response to airflow obstruction, such that the PAT amplitude decreased more (p < 0.001) in the presence of arousal (1.000 ± 0.007 to 0.767 ± 0.010 arbitrary units) than in the absence of arousal (1.000 ± 0.007 to 0.923 ± 0.007 arbitrary units). We conclude that airflow obstruction in patients with OSA causes an acute digital vasoconstriction that is accentuated in the presence of an EEG arousal.

Key Words: arterial hemoglobin saturation • autonomic nervous system • continuous positive airway pressure • nonrapid eye movement sleep

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