Upper airway and respiratory muscle responses to continuous negative airway pressure

Aronson, Robert H.; Önal, Ergün; Carley, David W.; Lopata, Melvin

doi:10.1152/jappl.1989.66.3.1373

Cited by 55 publications

(49 citation statements)

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“…More recently, methods have been developed for quantifying active neuromuscular responses in sleeping subjects, and a defect in these active responses has been demonstrated in patients with sleep apnea compared with normal subjects. This defect in neuromuscular control was independent of age, obesity, and sex (86), and may be caused by sleep-related reductions in dilator activity during sleep compared with wakefulness (87,88) or by a loss of compensatory responses during sleep (87)(88)(89)(90)(91)(92)(93)(94)(95)(96)(97)(98)(99). Thus, current evidence indicates that sleep apnea is associated with fundamental disturbances in upper airway mechanical (68,100,101) and neuromuscular control (80,(102)(103)(104)(105)(106)) (see Figure 1, left), and suggests that a combined defect is required to produce sleep apnea (86).…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 98%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

574

395

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Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

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Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 98%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

574

395

View full text Add to dashboard Cite

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“…Respiratoryrelated evoked potentials did not change after OSAS treatment. (21); (2) the fact that the upper airway response to disparate stimuli, such as hypercapnia and inspiratory loading, is similar (22); (3) the rapid timing of the response compared with voluntary activation (23); and (4) changes in the response to loading during sleep compared with wakefulness (24). The upper airway contains pressure receptors in the mucosa of the nasopharynx and larynx (25).…”

Section: Upper Airway Neuromotor Controlmentioning

confidence: 99%

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Huang¹,

Marcus²,

Davenport³

et al. 2013

Am J Respir Crit Care Med

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Rationale: Children with obstructive sleep apnea syndrome (OSAS) have impaired cortical processing of respiratory afferent stimuli, manifested by blunted sleep respiratory-related evoked potentials (RREP). However, whether this impairment is limited to respiratory stimuli, or reversible after successful treatment, is unknown. We hypothesized that, during sleep, children with OSAS have (1) abnormal RREP, (2) normal cortical processing of nonrespiratory stimuli, and (3) persistence of abnormal RREP after treatment. Objectives: To measure sleep RREP and auditory evoked potentials in normal control subjects and children with OSAS before and after treatment. Methods: Twenty-four children with OSAS and 24 control subjects were tested during N3 sleep. Thirteen children with OSAS repeated testing 4-6 months after adenotonsillectomy. Measurements and Main Results: RREP were blunted in OSAS compared with control subjects (N350 at Cz 227 6 15.5 vs. 247.4 6 28.5 mV; P ¼ 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment 225.1 6 7.4 vs. 229.8 6 8.1 posttreatment). Auditory evoked potentials were similar in OSAS and control subjects at baseline (N350 at Cz 258 6 33.1 vs. 266 6 31.1 mV), and did not change after treatment (N350 at Cz 267.5 6 36.8 vs. 6 20.3).Conclusions: Children with OSAS have persistent primary or irreversible respiratory afferent cortical processing deficits during sleep that could put them at risk of OSAS recurrence. OSAS does not seem to affect the cortical processing of nonrespiratory (auditory) afferent stimuli during sleep.Keywords: evoked potentials; children; auditory; respiratory; obstructive sleep apnea syndromeThe pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS) is not clear. In most children, OSAS is related to adenotonsillar hypertrophy or obesity. However, these structural factors cannot fully explain the degree of upper airway collapsibility (1, 2). Studies have shown that upper airway neuromotor tone and reflexes during sleep play an important role in maintaining airway patency during sleep in the pediatric population (3, 4). Recently, it has been shown that central nervous system processing of upper airway respiratory stimuli is abnormal during sleep in children with OSAS (5). However, it is not known whether this abnormal afferent processing is limited to respiratory stimuli, or whether it is an indicator of broader abnormalities in stimulus processing, secondary to the hypoxemia, hypercapnia, and sleep fragmentation of OSAS. Furthermore, it is not known whether this deficit resolves after treatment of OSAS. Determining reversibility would help elucidate whether the blunted responses were a primary and perhaps predisposing abnormality, or were secondary to the OSAS.Respiratory-related evoked potentials (RREP) have been used to study the central nervous system processing of upper airway stimuli (6, 7). Auditory evoked potentials (AEP) are a useful tool to investigate cortical responses to nonrespiratory stimuli and produce the same set of longer...

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“…Besides, decreases in respiratory reactance have previously been observed during resistive or elastic loading, and attributed to an increase in tissue elastance resulting from increased respiratory muscle activity [27]. As it has been reported that CNAP application results in an increase in diaphragmatic and parasternal intercostal electromyographic activity [10,28], the Ers response to CNAP presently observed may be explained by the enhanced activity of inspiratory muscles. As Irs remained unchanged when the CNAP level was decreased, the signi®cant increases observed in RF directly result from those in Ers.…”

Section: Respiratory Response To Decreasing Continuous Negative Airwamentioning

confidence: 70%

“…that Rrs became more and more frequency dependent, may be attributed to: 1) the increase in Rti resulting from reduced lung volume, which has been reported to be more pronounced at the lower frequencies [25]; and 2) the occurrence and development of series and/or parallel gas redistribution [21]. Series gas redistribution is mainly due to UA shunt compliance, whose in¯uence on Rrs was probably reduced under CNAP, due to the increased activity of UA dilating muscles [10]. Consequently, it is more probable that parallel gas redistribution developed within intrathoracic airways, as a result of the pulmonary inhomogeneities promoted by the CNAPinduced decrease in lung volume.…”

Section: Respiratory Response To Decreasing Continuous Negative Airwamentioning

confidence: 96%

Respiratory impedance response to continuous negative airway pressure in awake controls and OSAS

et al. 2001

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The aim of the study was to determine whether the response of respiratory impedance (Zrs) to decreasing levels of continuous negative airway pressure (CNAP) during wakefulness, differs in controls and subjects with obstructive sleep apnoea syndrome (OSAS).Zrs was measured by the forced oscillation technique (4±32 Hz) in 15 controls and 21 patients with OSAS (apnoea/hypopnoea index >20 per sleep hour) with normal lung function, in the basal state and with application of decreasing CNAP of -5, -10, and -15 hPa. Respiratory resistance was extrapolated to 0 Hz (R0) and estimated at 16 Hz (R16) by linear regression analysis of respiratory resistive impedance versus frequency. Respiratory elastance (Ers) and inertance (Irs) were estimated by multilinear regression analysis of respiratory reactance versus frequency, and resonance frequency (RF) was determined as RF=(1/2p)(Ers/Irs) 0.5 . In both groups, R0, R16, Ers and RF signi®cantly increased as the CNAP level decreased (pv0.0001 for all). R0, Ers, and RF increased signi®cantly more in OSAS than in controls (pv0.01, 0.001, and 0.0001, respectively), independently of the severity of obesity. Receiver operator characteristic curves showed that the parameter which best detected OSAS was RF, with a sensitivity of 81% and 93% speci®city for the 13.6 Hz cut-off point.The results of the present study suggest that the response of respiratory impedance to decreasing continuous negative airway pressure levels, might allow detection of obstructive sleep apnoea syndrome in subjects with normal lung function. Obstructive sleep apnoea/hypopnoea syndrome (OSAS) is characterized by the occurrence of repetitive upper airway (UA) narrowing and/or closure during sleep. Obstructive respiratory events are generally explained by the inef®ciency of the dilating muscles in counterbalancing the tendency of the pharyngeal airway to collapse, due to the inspiratory decrease in UA transmural pressure [1]. The main factors predisposing subjects to OSAS appear to be: 1) a reduction of UA calibre [2]; 2) an increase in UA resistance, as well as in pulmonary and respiratory resistances [3±5]; 3) an increase in UA compliance [4,6,7]; and 4) dysfunction of the UA dilating muscles [8].The application of continuous negative airway pressure (CNAP) at the airway opening generates a subatmospheric intraluminal UA pressure that simulates the conditions promoting the occurrence of obstructive respiratory events. The effect of CNAP on pharyngeal cross-sectional area and resistance have been widely investigated in control and OSAS subjects [4, 8±11], but, to the authors9 knowledge, CNAPinduced changes in the respiratory mechanical parameters remain poorly documented [12]. The aim of the present study was, therefore, to investigate whether the response of respiratory mechanics to decreasing CNAP levels differs between control and OSAS subjects, and might provide a predictive index of OSAS. To this end, the forced oscillation technique (FOT) was used, which allows easy measurement of respiratory imped...

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Upper airway and respiratory muscle responses to continuous negative airway pressure

Cited by 55 publications

References 0 publications

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Respiratory and Auditory Cortical Processing in Children with Obstructive Sleep Apnea Syndrome

Respiratory impedance response to continuous negative airway pressure in awake controls and OSAS

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