Site of Airway Collapse in Obstructive Sleep Apnea after Uvulopalatopharyngoplasty

2000 ◽  
Vol 109 (6) ◽  
pp. 581-584 ◽  
Author(s):  
Wayne C. Farmer ◽  
Stanley C. Giudici
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Collapse ◽  
Obstructive Sleep

scholarly journals Much Ado about Sleep: Current Concepts on Mechanisms and Predisposition to Pediatric Obstructive Sleep Apnea

Children ◽  
2021 ◽  
Vol 8 (11) ◽  
pp. 1032
Author(s):  
Ashley L. Saint-Fleur ◽  
Alexa Christophides ◽  
Prabhavathi Gummalla ◽  
Catherine Kier
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Biomechanical Properties ◽  
Primary Role ◽  
Airway Narrowing ◽  
Airway Collapse ◽  
Upper Airway Collapse ◽  
Obstructive Sleep ◽  
Review Current

Obstructive Sleep Apnea (OSA) is a form of sleep-disordered breathing characterized by upper airway collapse during sleep resulting in recurring arousals and desaturations. However, many aspects of this syndrome in children remain unclear. Understanding underlying pathogenic mechanisms of OSA is critical for the development of therapeutic strategies. In this article, we review current concepts surrounding the mechanism, pathogenesis, and predisposing factors of pediatric OSA. Specifically, we discuss the biomechanical properties of the upper airway that contribute to its primary role in OSA pathogenesis and examine the anatomical and neuromuscular factors that predispose to upper airway narrowing and collapsibility.

Induction of airway collapse with subatmospheric pressure in awake patients with sleep apnea

1984 ◽  
Vol 57 (1) ◽  
pp. 140-146 ◽  
Author(s):  
P. M. Suratt ◽  
S. C. Wilhoit ◽  
K. Cooper
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Obstruction ◽  
Supine Position ◽  
Face Mask ◽  
Subatmospheric Pressure ◽  
Pharyngeal Airway ◽  
Airway Collapse ◽  
Obstructive Sleep ◽  
Obese Control

To determine whether the pharyngeal airway is abnormal in awake patients with obstructive sleep apnea (OSA), we measured the ability of the pharyngeal airway to resist collapse from subatmospheric pressure applied to the nose in awake subjects, 12 with OSA and 12 controls. Subatmospheric pressure was applied to subjects placed in the supine position through a tightly fitting face mask. We measured airflow at the mask as well as mask, pharyngeal, and esophageal pressures. Ten patients developed airway obstruction when subatmospheric pressures between 17 and 40 cmH2O were applied. Obstruction did not occur in two patients with the least OSA. Obstruction did not occur in 10 controls; one obese control subject developed partial airway obstruction when -52 cmH2O was applied as did another with -41 cmH2O. We conclude that patients with significant OSA have an abnormal airway while they are awake andthat application of subatmospheric pressure may be a useful screening test to detect OSA.

Control of segmental upper airway resistance in patients with obstructive sleep apnea

1993 ◽  
Vol 74 (6) ◽  
pp. 2694-2703 ◽  
Author(s):  
M. J. Wasicko ◽  
J. S. Erlichman ◽  
J. C. Leiter
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Normal Subjects ◽  
Emg Activity ◽  
Electromyographic Activity ◽  
Resistive Load ◽  
Airway Collapse ◽  
Upper Airway Collapse ◽  
Obstructive Sleep

We sought to determine if the upper airway response to an added inspiratory resistive load (IRL) during wakefulness could be used to predict the site of upper airway collapse in patients with obstructive sleep apnea (OSA). In 10 awake patients with OSA, we investigated the relationship between resistance in three segments of the upper airway (nasal, nasopharyngeal, and oropharyngeal) and three muscles known to influence these segments (alae nasi, tensor veli palatini, and genioglossus) while the patient breathed with or without a small IRL (2 cmH2O.l–1.s). During IRL, patients with OSA exhibited increased nasopharyngeal resistance and no significant increase in either the genioglossus or tensor veli palatini activities. Neither nasal resistance nor alae nasi EMG activity was affected by IRL. We contrasted this to the response of five normal subjects, in whom we found no change in the resistance of either segment of the airway and no change in the genioglossus EMG but a significant activation of the tensor palatini. In six patients with OSA, we used the waking data to predict the site of upper airway collapse during sleep and we had limited success. The most successful index (correct in 4 of 6 patients) incorporated the greatest relative change in segmental resistance during IRL at the lowest electromyographic activity. We conclude, in patients with OSA, IRL narrows the more collapsible segment of the upper airway, in part due to inadequate activation of upper airway muscles. However, it is difficult to predict the site of upper airway collapse based on the waking measurements where upper airway muscle activity masks the passive airway characteristics.

S300 – Comparison of Endoscopy Diagrams for Obstructive Sleep Apnea

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P175-P175
Author(s):  
Masami Nakajima ◽  
B Tucker Woodson
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Muscle Tone ◽  
False Negative ◽  
Upper Airway ◽  
Endoscopic Examination ◽  
Exact Matching ◽  
Airway Collapse ◽  
Obstructive Sleep ◽  
Muscle Groups

Objectives Most methods of waking and sedated sleep endoscopy evaluating the upper airway in obstructive sleep apnea inconsistently predict surgical results. Goals of exam have been to identify levels of obstruction or levels of tissue vibration. Examinations provide little information on airway structure. A novel method of describing airway collapse using airway structures has been developed. The objectives of this study are to compare sleep and wake examination: 1) during inspiration, and 2) expiration. Methods A retrospective review evaluated waking and sedated clinical endoscopic endoscopy. Clinical endoscopic examination was performed supine at end expiration. Sedated endoscopy used propofol anesthesia evaluated the airway during both inspiration, expiration, and with elimination of airway mechanoreceptors. Defined structural butressess included salpingo/palatopharyngeus, levator, and uvular muscle groups for the epi-pharynx and the epiglottis, lateral hypopharynx, vallecular and proximal tongue base for the hypopharynx. Structures were scored on 3 and 4 point scales with agreement indicating exact matching. Results Severity of obstruction scored higher on sedated exam than clinical exam. Structural agreement in epipharynx was 52%, 29%, and 24%, and in hypopharynx, 48%,24%, and 38%. False negative and positive assessment occurred in epipharynx (levator 30% and uvula 40%) but not in hypopharynx. Conclusions Consistent with a greater loss of muscle tone during sleep, exact agreement between wake and sleep exams was low, however, supine end expiratory exam predicted patterns of airway collapse in hypopharynx. Pattern of collapse in epipharynx is confounded by ventilation during wake.

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