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Upper airway muscle dysfunction is implicated in the pathophysiology of sleep disordered breathing

Upper airway muscle dysfunction is implicated in the pathophysiology of sleep disordered breathing

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Obstructive Sleep Apnea (OSA) is the most common type of sleep disordered breathing, with an estimated prevalence of 2-4% among U.S. adults. The consequences of OSA are sever and wide ranging, from excessive daytime sleepiness to mortality from cardiovascular disease. This essay reviews the implication of upper airway muscle dysfunction in the pathophysiology of the disorder.
Obstructive Sleep Apnea (OSA) is the most common type of sleep disordered breathing, with an estimated prevalence of 2-4% among U.S. adults. The consequences of OSA are sever and wide ranging, from excessive daytime sleepiness to mortality from cardiovascular disease. This essay reviews the implication of upper airway muscle dysfunction in the pathophysiology of the disorder.

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Published by: Undergraduate Awards on Sep 01, 2012
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10/27/2013

 
Upper airway muscle dysfunction is implicated inthe pathophysiology of sleep disorderedbreathing.
ABSTRACT:
Sleep disordered breathing (SDB) describes a group of disorders that arecharacterised by abnormalities in respiration during sleep. In this review Iwill focus on the most common SBD disorder obstructive sleep apnea(OSA). Patients with OSA develop repetitive collapse of the upper airwayduring sleep and it takes arousal from sleep and sudden bursts of activityto terminate the occlusive event. The causes of OSA are multi-factorialhowever it is generally thought to occur as result of a normal statedependent decrease in upper airway muscle activity in individuals with anabnormal airway anatomy. In this review I will discuss the anatomicalabnormalities that are thought to predispose individuals to OSA. OSApatients do not experience these collapses in the upper airway duringwakefulness due to compensatory reflex responses of the upper airway. Therefore, as a result of OSA the upper airway muscles experiencemechanical trauma including increased muscle load, altered muscleactivity and hypoxia. Pathophysiology is the study of disturbances innormal function caused by a disease. In this review I will discuss howthese mechanical traumas induced by OSA affect the upper airway musclestructure and function and how it may be able to cause muscle injury.
INTRODUCTION:
 The upper airway is surrounded by a complex anatomical arrangement of skeletal muscles and soft tissues that supports the upper airways differentfunctions, such as speech, swallowing and respiration. The nonrespiratoryfunctions require the airway to be dynamic to accommodate for thechange in airway size which allows for the movement of air, liquid andsolids. Therefore the human pharynx can be considered as a collapsibletube that compromises the essential respiratory function of the upperairway, which requires the airway to be stiff. Consequently the humanpharyngeal airway is largely dependent on the upper airway muscleactivity to maintain its patency. These muscles can actively dilate andopen the airway, or may just stiffen the soft tissue structures so they areless prone to deformation by negative pharyngeal pressure, generatedduring inspiration. The principal muscles of the pharyngeal airway that are
 
involved in upper airway patency include the extrinsic tongue retractorgenioglossus muscle, the palatal muscles, the pharyngeal dilator musclesand the muscles influencing the hyoid bone position.
 
FIGURE. 1. An anatomical representation of the upper airway and the important muscles controlling airway patency. (Taken from Fogel 2004.)
Sleep disordered breathing (SDB) describes a group of disorders that arecharacterised by abnormalities in the respiratory pattern or the quantityof ventilation during sleep. Sleep disordered breathing refers to a widespectrum of sleep related breathing abnormalities such as snoring.However, obstructive sleep apnea is the most common (SDB) disorder. Itis characterised by repetitive upper airway collapse during sleep. In 1993 Young et al uncovered an alarmingly high prevalence of OSA, with anestimated 4% of men and 2% of women in the middle aged work forcelikely to meet the minimal diagnostic criteria for OSA. Normally duringsleep onset, especially rapid-eye-movement (REM) sleep, there is areduction in neuromuscular drive and reflex responses which in normalindividuals leads to upper airway narrowing and increased resistance tobreathing. However, in OSA patients the loss of the neuromuscular driveand compensatory reflex responses causes the upper airway to collapserepeatedly during sleep. So, what are the differences between OSA andhealthy individuals that predispose them to the disorder? Although thecauses of OSA are multi-factorial it is generally thought to occur as a
 
result of this sleep-related decrements in upper airway muscle activity inindividuals with an abnormal airway anatomy.
ANATOMICAL ABNORMALITIES:
Most patients with OSA in comparison to healthy individuals have ananatomically narrowed pharyngeal airway which predisposes them toOSA. The anatomical factors that produce this narrowed upper airway areusually due to soft tissue abnormalities including, hypertrophied adenoidsand tonsils, retrognathia, micrognathia, macroglossia and variations incraniofacial structures (Patil 2007). Studies using conventional computedtomography (CT) and magnetic resonance imaging (MRI) havedemonstrated nonspecific factors such as increased fatty tissue depositionand submucosal edema in the lateral walls of the pharynx which cannarrow the airway (Schwab 1995, Haponik 1983). Cephalometric X-rayimaging of the pharyngeal airway of patients with OSA have shown areduction in the length of the mandible, an inferiorly positioned hyoidbone, and a retro-position of the maxilla(Lowe 1995). In addition toalterations in the airway size of OSA patients, a number of studies haveshown a difference in airway shape that can predispose individuals toOSA. Some OSA patients have an anterior-posterior directed airway longaxis rather than laterally directed (Fogel 2004). The length of the airwayhas been implicated as an anatomical factor that determines airwaypatency, the greater the airway length the more susceptible a person is toOSA (Malhotra 2002). These anatomical abnormalities can place thepharyngeal dilator muscles at a relative mechanical disadvantage,thereby decreasing their ability to maintain airway patency. Takentogether these studies imply that all of the upper airway structuraldifferences can predispose an individual to OSA by reducing the criticalpressure needed for suction collapse (Horner 1996).It has long been recognised that there is an association between obesityand OSA which may be due to a narrowed upper airway as a result of increased fat deposition surrounding the collapsible segment of thepharynx as seen in MRI images. This increase in superficially located fatmass can also have a compressive effect on the pharynx and this couldexplain the findings that increased neck circumference correlates with theincidence and severity of OSA. Obesity may also increase pharyngealcollapsibility through reductions in lung volume which in turn canindirectly influence upper airway size and contribute to upper airwaynarrowing (Hoffstein 1984). Ray et al 2007 demonstrated that upperairway stability is reduced in obese rats compared to lean controls givingfurther evidence for the relationship between obesity and OSA.

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