Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

Abstract

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (Ͼ10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean Ϯ SE: age, 25 Ϯ 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P Ͻ 0.001) and a significant decrease in R-R interval at 3 s (P Ͻ 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 Ϯ 3 to 104 Ϯ 3 mmHg; O, 86 Ϯ 3 to 105 Ϯ 3 mmHg; P ϭ 0.99. R-R interval: C, 1.12 Ϯ 0.03 to 0.89 Ϯ 0.04 s; O, 1.11 Ϯ 0.02 to 0.87 Ϯ 0.02 s, P ϭ 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P Ͻ 0.001); this increase was not different between the two conditions (C: 4.40 Ϯ 0.29 to 6.76 Ϯ 0.61 l/min, O: 4.35 Ϯ 0.34 to 7.65 Ϯ 0.73 l/min; P ϭ 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men. blood pressure; heart rate SPONTANEOUS AROUSAL FROM SLEEP is associated with large surges in both heart rate and blood pressure (13,42,49). In patients with obstructive sleep apnea (OSA), the surges in sympathetic activity that occur during an arousal from sleep at the termination of an apnea are more than double in size compared with a spontaneous arousal (2,29,40). Frequent cardiovascular surges in OSA have been implicated in the increased prevalence of both nocturnal and diurnal hypertension associated with OSA (37, 41). The mechanisms responsible for the augmentation of the cardiovascular response to arousal at the termination of an apnea potentially include stimulation of the chemoreceptors (hypercapnia, hypoxia), stimulation of upper airway (UA) mechanoreceptors (occlusion), stimulation of the pulmonary stretch receptors (increasing negative intrathoracic pressure, lung inflation), or arousalrelated central activation of autonomic centers. Our laboratory has previously reported in this journal that combined stimulation of the central and peripheral chemoreceptors (using hypercapnic hypoxia) does not significantly augment the cardiovascular response to arousal from sleep in healthy human subjects (39).Brief inspiratory occlusion evokes cortical activity during wakefulness (12, 15) and sleep (1, 51). Additionally, during sleep, complete airway occlusion can rapidly induce arousal, most likely as a result of afferent activity from UA mechanoreceptors to the brain stem respiratory centers (24). Altering this afferent activity, by topical anesthes...

The heart rate response to spontaneous arousal from sleep is reduced in children with Down syndrome referred for evaluation of sleep-disordered breathing

“…Thus the HR response to a spontaneous arousal is a fixed response. This has been demonstrated in adults (7,29,30,40), and importantly, this is also demonstrated in our two groups of children without DS.…”

“…Arousal causes large transient increases in HR, BP, and ventilation that are beyond functional requirements (3,40). In the healthy individual, the magnitude of the cardiorespiratory response to arousal from sleep is remarkably consistent and is not altered by chemoreceptor or upper airway mechanoreceptor stimulation (7,29,30). Autonomic blockade studies performed in dogs have shown that arousal from sleep is associated with both acute cardiac sympathetic activation as well as parasympathetic withdrawal (20).…”

The Cardiovascular Response to Arousal from Sleep Decreases with Age in Healthy Adults

“…The continuous inspiratory resistance measurement for each breath was divided into 10 data points, the middle 8 of which were averaged to provide a single resistance measurement for each breath. 16,[18][19][20] CPAP was titrated in older adults using the online measurement R L , which was matched to values previously obtained in the younger adult group. For the older adults in whom Pes was not measured (n=11), CPAP was titrated to eliminate any flow limitation and upper airways resistance which was inferred from the shape of the inspiratory flow signal.…”

“…The study conformed to the standards set by the Declaration of Helsinki and was approved by The Brompton and Harefield Ethics Committee. Data from the 15 young male adults in the current study has been previously published as the control group 16 ; both studies used the same methodology.…”

Obstructive Sleep Apnoea, Congestive Heart Failure and Cardiovascular Disease

“…Isolated arousals in the absence of an apnoea are associated with a small and transient increase in blood pressure with a small sympathetic discharge. 19 An arousal associated with apnoea termination results is at least twice the haemodynamic response as a Heart Lung and Circulation Obstructive sleep apnoea, congestive heart failure and cardiovascular disease 2005;14S:S2-S7 result of increased sympathetic tone, vasoconstriction and increased cardiac output. Experiments in dogs have shown that arousal appears to have a direct effect on cardiac sympathetic activity independent from effects of arterial blood gases, lung volume or ventilation.…”