Upper airway pressure-flow relationships in obstructive sleep apnea

Smith, Philip L.; Wise, Robert A.; Gold, Avram R.; Schwartz, Alan R.; Permutt, S.

doi:10.1152/jappl.1988.64.2.789

Cited by 391 publications

(260 citation statements)

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“…In early studies, upper airway collapsibility during sleep was found to vary along a continuum from health to disease (54)(55)(56). The severity of upper airway obstruction during sleep is related to quantitative differences in pharyngeal collapsibility, as reflected by elevations in the critical closing pressure (Pcrit).…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 99%

“…These responses can restore airway patency by recruiting muscles that dilate and elongate the airway (63,65,66,67,(78)(79)(80)(81)(82)(83)(84). In patients with sleep apnea, impaired neural responses to airway obstruction account for the marked elevation in Pcrit during sleep compared with normal individuals (54)(55)(56). A disturbance in neuromuscular control is further suggested by comparisons of critical pressures measured during sleep (54-56) with those assessed in paralyzed, anesthetized subjects (69,85).…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 99%

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Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

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570

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: 99%

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 99%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

Self Cite

570

395

View full text Add to dashboard Cite

show abstract

“…This has been reported in healthy subjects [12], as well as in heavy snorers [2] and OSA patients [2,13]. Inspiratory flow limitation during quiet breathing and snoring has been found in apnoeic and nonapnoeic snorers during sleep [2,13]. These changes have been attributed to a sleep-related decrease in muscle tone resulting in reduction of the crosssectional area of UA.…”

Section: Discussionmentioning

confidence: 68%

Influence of gas density on simulated snoring

Liistro¹,

Veriter²,

Stănescu³

1999

Eur Respir J

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According to a recent theoretical model, snoring is related to instability of the upper airway (UA). Factors promoting UA instability include increased gas density. The aim of this study was to test the influence of gas density on simulated snoring production and supraglottic resistance.Supraglottic pressure and flow rate (V ') were measured in 10 healthy seated subjects during simulated snoring. Subjects breathed three different gas mixtures: Helium±oxygen, He 79%±O 2 21% (He±O 2 ); air; and sulphur hexafluoride±oxygen, F 6 S 79%±O 2 21% (F 6 S±O 2 ) administered in a random order. Supraglottic resistance (Rsg) was measured on its linear range during quiet breathing and V ' was measured at the onset and middle of snoring.Linear Rsg increased and V ' conversely decreased with gas density. These data are in agreement with predictions of a mathematical model of the upper airway showing that snoring occurs at lower flow rates when gas density is increased. Eur Respir J 1999; 13: 679±681. Snoring is a cardinal symptom of obstructive sleep apnoea (OSA) syndrome and a frequent finding in otherwise healthy subjects [1]. Previous studies from the authors' laboratory have shown that simulated and spontaneous snoring are characterized by high-frequency oscillations of the soft palate associated with a decrease in oropharyngeal calibre. Reduction of the pharyngeal cross-sectional area increases supraglottic resistance (Rsg) and is associated with flow limitation [2,3].The influence of gas density and viscosity on the upper airway (UA) pressure±flow relationship has not been studied before, except in animals [4].Recently, GAVRIELY and JENSEN [5], based on a theoretical model of UA, found that among other factors, increases in UA resistance and gas density, as well as decrease in UA size promote UA instability and snoring.In this study, the influence of gas density on supraglottic resistance and flow rate (V ') was tested during quiet breathing and during simulated snoring. Materials and methodsTen healthy (five females) nonsmoker subjects aged 22± 30 yrs with normal spirometric data [6] and all nonobese (meanSD body mass index, 32.42.9 kg . m -2 ), volunteered for this study. They were nonsnorers and free of any UA pathology. Written, informed consent was obtained and the experiments were approved by the Ethics Committee of the hospital.V ' was measured with a Fleish No. 2 pneumotachograph (Fleicsh, Lausanne, Switzerland), attached to a tightly fitting silicone face mask. Pressure drop across the pneumotachograph was measured by a 5 cmH 2 O Validyne pressure transducer (Northridge, CA, USA). The airtightness of the mask was verified by measuring the helium level around the border of the mask when the subjects were breathing a 79% He±21% O 2 mixture. The pneumotachograph was calibrated for the three gas mixtures: helium±oxygen, He 79%±O 2 21% (He±O 2 ); air; and sulphur hexafluoride±oxy-gen, F 6 S 79%±O 2 21% (F 6 S±O 2 ) by passing these gases through the pneumotachograph in series with a dry gasometer (Parkinson ...

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“…In fact, it was believed that ON-CPAP would not work in patients with OSA. 5,6 However, in 1994 two papers were published asserting that ON masks might be an acceptable treatment alternative for OSA. The first paper was authored by Glen Prosise and myself 7 and the second a few months later by Sanders and coworkers.…”

Section: Two Articlesmentioning

confidence: 99%

Retrospective: When Were Oronasal Masks First Used to Treat Obstructive Sleep Apnea?

Berry

2017

Journal of Clinical Sleep Medicine

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Upper airway pressure-flow relationships in obstructive sleep apnea

Cited by 391 publications

References 0 publications

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Influence of gas density on simulated snoring

Retrospective: When Were Oronasal Masks First Used to Treat Obstructive Sleep Apnea?

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