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1Clinical and Academic Unit of Sleep and Breathing, National Heart and Lung Institute, Imperial College, London SW3 6LY; 2MacKay Institute of Communication and Neuroscience, School of Life Sciences, Keele University, Keele ST5 5BG; and 3Sleep and Ventilation Unit, Royal Brompton Hospital, London SW3 6NP, United Kingdom
Submitted 18 July 2003 ; accepted in final form 23 October 2003
The cardiovascular response to an arousal occurring at the termination of an obstructive apnea is almost double that to a spontaneous arousal. We investigated the hypothesis that central plus peripheral chemoreceptor stimulation, induced by hypercapnic hypoxia (HH), augments the cardiovascular response to arousal from sleep. Auditory-induced arousals during normoxia and HH (>10-s duration) were analyzed in 13 healthy men [age 24 ± 1 (SE) yr]. Subjects breathed on a respiratory circuit that held arterial blood gases constant, despite the increased ventilation associated with arousal. Arousals were associated with a significant increase in mean arterial blood pressure at 5 s (P < 0.001) and with a significant decrease in the R-R interval at 3 s (P < 0.001); however, the magnitude of the changes was not significantly different during normoxia compared with HH (mean arterial blood pressure: normoxia, 91 ± 4 to 106 ± 4 mmHg; HH, 91 ± 4 to 109 ± 5 mmHg; P = 0.32; R-R interval: normoxia, 1.12 ± 0.04 to 1.02 ± 0.05 s; HH, 1.09 ± 0.05 to 0.92 ± 0.04 s; P = 0.78). Mean ventilation increased significantly at the second breath postarousal for both conditions (P < 0.001), but the increase was not significantly different between the two conditions (normoxia, 5.35 ± 0.40 to 9.57 ± 1.69 l/min; HH, 8.57 ± 0.63 to 11.98 ± 0.70 l/min; P = 0.71). We conclude that combined central and peripheral chemoreceptor stimulation with the use of HH does not interact with the autonomic outflow associated with arousal from sleep to augment the cardiovascular response.
hypoxia; hypercapnia; blood pressure; heart rate
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