Ventilatory Response to Induced Auditory Arousals During NREM Sleep

Badr, M. Safwan; Morgan, Barbara J.; Finn, Laurel; Toiber, F.; Crabtree, David C.; Puleo, Dominic S.; Skatrud, James B.

doi:10.1093/sleep/20.9.707

Cited by 38 publications

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“…Badr et al (4) reported that ventilation was unchanged during the first breath of an auditory-induced arousal and that the arousalrelated increase in ventilation occurred during the second breath of the arousal. First-breath inhibition of ventilation after arousal has also been demonstrated in dogs (19).…”

Section: Discussionmentioning

confidence: 99%

“…Although auditory stimuli have been widely used in studies investigating the autonomic response to arousal (4,10,13,33,42), it is unlike the endogenous stimuli that induce arousal at the termination of an obstructive apnea. We chose to use the auditory stimulus because occlusion alone is unlikely to induce arousal on all occasions, and it was a standardized method of rapidly inducing cortical arousal during the two conditions.…”

Section: Discussionmentioning

confidence: 99%

“…The effects of time and of C vs. O on cardiovascular and ventilatory responses to arousal were tested by using ANOVA with repeated measures. Statistical analysis was performed on all postarousal data, specifically breaths 1-6 and seconds [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]. A paired t-test was used to compare the mean peak negative intrathoracic pressure measured on the first breath postarousal between the two conditions.…”

Section: Subjectsmentioning

confidence: 99%

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

O'Driscoll

Κostikas²,

Simonds³

et al. 2005

Journal of Applied Physiology

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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...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

See 1 more Smart Citation

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

O'Driscoll

Κostikas²,

Simonds³

et al. 2005

Journal of Applied Physiology

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“…The arousal response is important for survival of the affected patient; however, the sleep fragmentation induced by repetitive arousals and the physiological events that surround the arousal response also have adverse consequences which contribute to the pathophysiology and clinical manifestations of SDB [5]. Arousals are characterized by abrupt changes in central nervous system activity that produce electroencephalogram (EEG) activation and marked changes in a wide range of autonomic nervous system parameters such as heart rate (HR), blood pressure (BP), ventilation and peripheral vascular resistance [6][7][8][9][10]. Arousals are typically evident and conventionally detected as changes in cortical EEG activity, a labor-intensive approach associated with high interscorer variability [11].…”

Section: Introductionmentioning

confidence: 99%

Obstructive sleep apnea syndrome: effect of respiratory events and arousal on pulse wave amplitude measured by photoplethysmography in NREM sleep

et al. 2005

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Obstructive sleep apnea syndrome: effect of respiratory events and arousal on pulse wave amplitude measured by photoplethysmography in NREM sleep Abstract The objective of the study is to evaluate changes in finger pulse wave amplitude (PWA), as measured by photoplethysmography, and heart rate (HR), related to obstructive respiratory events and associated arousals during sleep. We analyzed 1,431 respiratory events in NREM sleep from 12 patients according to (1) the type of event (apnea, hypopnea, upper airway resistance episode) and (2) the duration of the associated EEG arousal (>10, 3-10, <3 s). Obstructive respiratory events provoked a relative bradycardia and vasodilation followed by HR increase and vasoconstriction. Relative PWA changes were significantly greater than HR changes. These responses differed significantly according to EEG-arousal grades (time×arousal interaction, p<0.0001), with longer arousals producing greater responses, but not to the type of respiratory event (time×event interaction, p = ns). Obstructive respiratory events provoke HR and PWA changes, the magnitude seemingly related to the intensity of central nervous activation, with PWA changes greater than HR. PWA obtained from a simple pulse oxymeter might be a valuable method to evaluate sleep fragmentation in sleep breathing disorders.

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“…Of five separate studies that have investigated the breath-by-breath ventilatory responses to auditory-induced arousals in healthy subjects (10)(11)(12)(13)(14), not one found a period of significant hypoventilation (ventilation reduced .10% below baseline) after the initial hyperventilatory response, despite some subjects having flow limitation during stable sleep. In addition, airway resistance (10,11) was reduced and dilator muscle activity increased (10,14) for approximately 20-30 seconds after the brief arousal in these healthy individuals.…”

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confidence: 99%

Termination of Respiratory Events with and without Cortical Arousal in Obstructive Sleep Apnea

Jordan

Eckert²,

Wellman³

et al. 2011

Am J Respir Crit Care Med

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Rationale: A total of 20-30% of respiratory events in obstructive sleep apnea are terminated without clear arousal. Arousals are thought to predispose to further events by promoting hyperventilation, hypocapnia, and upper-airway dilator muscle hypotonia. Therefore, events terminated without arousal may promote stable breathing. Objectives: To compare physiologic changes at respiratory event termination with American Sleep Disorders Association (ASDA) Arousal to No Arousal, and determine whether secondary respiratory events are less common and have higher dilator muscle activity after No Arousal compared with ASDA Arousal. Methods: Patients with obstructive sleep apnea wore sleep staging, genioglossus (EMG GG ), and tensor palatini (EMG TP ) electrodes plus a nasal mask and pneumotachograph. During stable sleep, continuous positive airway pressure (CPAP) was lowered for 3-minute periods to induce respiratory events. Physiologic variables were compared between events terminated with (1) ASDA Arousal, (2) No Arousal, or (3) sudden CPAP increase (CPAPinc, control). Measurements and Main Results: Sixteen subjects had adequate data. EMG GG , EMG TP , and heart rate increased after ASDA Arousal (340 6 57%, 215 6 28%, and 110.7 6 2.3%) and No Arousal (185 6 32%, 167 6 15%, and 108.5 6 1.6%) but not CPAPinc (90 6 10%, 94 6 11%, and 102.1 6 1%). Ventilation increased more after ASDA Arousal than No Arousal and CPAPinc, but not after accounting for the severity of respiratory event. Fewer No Arousals were followed by secondary events than ASDA Arousals. However, low dilator muscle activity did not occur after ASDA Arousal or No Arousal (EMG GG rose from 75 6 5 to 125 6 7%) and secondary events were less severe than initial events (ventilation rose 4 6 0.4 to 5.5 6 0.51 L/min). Conclusions: Respiratory events that were terminated with ASDA Arousal were more severely flow-limited, had enhanced hyperventilation after event termination, and were more often followed by secondary events than No arousal. However, secondary events were not associated with low dilator muscle activity and airflow was improved after both No Arousal and ASDA Arousal.Keywords: pharyngeal muscle activity; upper airway obstruction; genioglossus; tensor palatini; obstructive respiratory event Approximately 20-30% of respiratory events in obstructive sleep apnea (OSA) do not end with clear arousal from sleep (1-4). Whether subcriterion arousals are present or not has been debated in the literature and is not yet resolved (1, 2, 4, 5). However, the presence of cortical arousal results in enhanced hyperventilation on termination of respiratory events (4). This greater hyperventilation is expected to result in hypocapnia and dilator muscle hypotonia on the return to sleep (because dilator muscle activity, and presumably muscle tone, varies proportionately with respiratory drive), predisposing to further airway obstruction. However, whether dilator muscle activity is reduced in this setting has not been assessed.The concept that arousal-induced hyperventilatio...

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Ventilatory Response to Induced Auditory Arousals During NREM Sleep

Cited by 38 publications

References 0 publications

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

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

Obstructive sleep apnea syndrome: effect of respiratory events and arousal on pulse wave amplitude measured by photoplethysmography in NREM sleep

Termination of Respiratory Events with and without Cortical Arousal in Obstructive Sleep Apnea

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