Pharyngeal Patency in Response to Advancement of the Mandible in Obese Anesthetized Persons

Isono, Shiroh; Tanaka, Atsuko; Tagaito, Yugo; Sho, Yasuhide; Nishino, Takashi

doi:10.1097/00000542-199711000-00008

Cited by 122 publications

(79 citation statements)

References 18 publications

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“…Moreover, our baseline critical pressures (mouth-closed condition) were comparable with those of a recent study (Litman et al, 2002) which documented values of -8.2 ± 4.3 cm H 2 O that were obtained when the investigators lowered the nasal pressure under midazolam sedation. Nevertheless, our critical pressures under sedation were much more negative than those reported from subjects under general anesthesia and paralysis (Isono et al, 1997;Eastwood et al, 2002a), which markedly decreases or eliminates neuromuscular mechanisms involved in the maintenance of airway patency. Thus, our critical pressure measurements, obtained from subjects under midazolam sedation, suggest that upper-airway neuromuscular mechanisms remain intact during moderate midazolam sedation and are comparable with those obtained during stable non-REM sleep.…”

Section: Effect Of Midazolam Sedation On Upper-airway Patencycontrasting

confidence: 67%

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

et al. 2004

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Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to −3.6 ± 2.9 cm H2O compared with −8.7 ± 2.8 (p = 0.002) for closed mouths and −7.2 ± 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 ± 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

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Section: Effect Of Midazolam Sedation On Upper-airway Patencycontrasting

confidence: 67%

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

et al. 2004

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“…We excluded obese patients and as such omitted a group of patients in whom airway devices are often required to assist with airway management. A different result may have been produced in such a group [17]. Only one senior anaesthetist used the JawThrust-Device in this study.…”

Section: Discussionmentioning

confidence: 92%

Optimising the unprotected airway with a prototype Jaw‐Thrust‐Device – a prospective randomised cross‐over study

Goedecke

Mitterschiffthaler

Paal³

et al. 2009

Anaesthesia

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SummaryDespite being a standard procedure during induction of anaesthesia, facemask ventilation can be a major challenge especially for inexperienced anaesthetists. We manufactured a Jaw-Thrust-Device designed to keep the patient's jaws in an optimised position, and thus to maintain the airway in a permanently patent state. Using a cross over design, we compared the influence of using the Esmarch manoeuvre (bimanual jaw-thrust), a nasopharyngeal airway, an oropharyngeal airway, or the Jaw-Thrust-Device on airway physiology in 50 healthy adults with body mass index < 35 kg.m )2 , undergoing standard facemask ventilation for routine induction of anaesthesia.The main study endpoints were expiratory tidal volumes, airway resistances, and gas flow rates. The Jaw-Thrust-Device was more effective in increasing expiratory tidal volumes and peak inspiratory flow than a standard Esmarch manoeuvre, and was more effective than both nasopharyngeal and oropharyngeal airways in decreasing airway resistance.

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“…29 Furthermore, obesity, jaw position, acromegaly, tonsillar hypertrophy, and a smaller bony enclosure surrounding the pharynx have been demonstrated to predispose toward pharyngeal collapsibility. 23,[32][33][34][35][36] These studies imply that upper airway structural differences distinguish OSA patients from normal subjects, and may predispose to upper airway obstruction when protective neuromuscular mechanisms wane at sleep onset. 37 Obesity, the major risk factor for OSA, has been linked with elevations in neck circumference and increased amounts of peripharyngeal fat, 38,39 which could narrow and compress the upper airway.…”

Section: Contribution Of Anatomic Factors To Osamentioning

confidence: 95%

Adult Obstructive Sleep Apnea

Patil

Schneider

Schwartz

et al. 2007

Chest

428

169

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Obstructive sleep apnea (OSA) is a highly prevalent disease characterized by recurrent episodes of upper airway obstruction that result in recurrent arousals and episodic oxyhemoglobin desaturations during sleep. Significant clinical consequences of the disorder cover a wide spectrum, including daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease, metabolic dysfunction, and cor pulmonale. The major risk factors for the disorder include obesity, male gender, and age. Current understanding of the pathophysiologic basis of the disorder suggests that a balance of anatomically imposed mechanical loads and compensatory neuromuscular responses are important in maintaining upper airway patency during sleep. OSA develops in the presence of both elevated mechanical loads on the upper airway and defects in compensatory neuromuscular responses. A sleep history and physical examination is important in identification of patients and appropriate referral for polysomnography. Understanding nuances in the spectrum of presenting complaints and polysomnography correlates are important for diagnostic and therapeutic approaches. Knowledge of common patterns of OSA may help to identify patients and guide therapy.Keywords critical pressure; diagnosis; obstructive sleep apnea; pathophysiology Obstructive sleep apnea (OSA) is a highly prevalent disease, affecting 4% of men and 2% of women, 1 and strongly linked to the current obesity epidemic. The disorder is characterized by recurrent episodes of upper airway obstruction, and is associated with reductions in ventilation, resulting in recurrent arousals and episodic oxyhemoglobin desaturations during sleep.2 Significant clinical consequences of the disorder cover a wide spectrum including daytime hypersomnolence,3 , 4 neurocognitive dysfunction, 5 cardiovascular disease (hypertension, stroke, myocardial infarction, heart failure), 6, 7 metabolic dysfunction,8 -10 respiratory failure, and cor pulmonale. 11 The major risk factors for the disorder include obesity, male gender, postmeno-pausal status, and age, and are discussed in detail elsewhere. [12][13][14] The rising prevalence of obesity in the United States suggests that OSA will represent an escalating public health burden. 15 Therefore, knowledge and understanding of the pathogenic basis, clinical presentation, and diagnosis of OSA are essential for the development of preventive, screening, and therapeutic strategies to reduce the public health burden of the disorder. In this review, we * The manuscript was supported by grants HL50381, HL37379, and HL77137 from the National Heart, Lung, Blood Institute, National NIH Public Access Author ManuscriptChest. Author manuscript; available in PMC 2010 January 29. Published in final edited form as:Chest. Pathophysiology of Upper Airway Obstruction in OSAThe pharynx is a complex structure that serves several purposes including speech, swallowing, and respiration. The human pharynx is composed of > 20 muscles and divided into four sections that include the nas...

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Pharyngeal Patency in Response to Advancement of the Mandible in Obese Anesthetized Persons

Abstract: Mandibular advancement did not improve the retropalatal airway in obese persons.

Cited by 122 publications

References 18 publications

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

Optimising the unprotected airway with a prototype Jaw‐Thrust‐Device – a prospective randomised cross‐over study

Adult Obstructive Sleep Apnea

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