Obesity and obstructive sleep apnoea: Mechanisms for increased collapsibility of the passive pharyngeal airway

ArticleinRespirology 17(1):32-42 · January 2012with28 Reads
DOI: 10.1111/j.1440-1843.2011.02093.x · Source: PubMed
Epidemiological evidence suggests there are significant links between obesity and obstructive sleep apnoea (OSA), with a particular emphasis on the importance of fat distribution in the development of OSA. In patients with OSA, the structure of the pharyngeal airway collapses. A collapsible tube within a rigid box collapses either due to decreased intraluminal pressure or increased external tissue pressure (i.e. reduction in transmural pressure), or due to reduction in the longitudinal tension of the tube. Accordingly, obesity should structurally increase the collapsibility of the pharyngeal airway due to excessive fat deposition at two distinct locations. In the pharyngeal airway region, excessive soft tissue for a given maxillomandibular enclosure size (upper airway anatomical imbalance) can increase tissue pressure surrounding the pharyngeal airway, thereby narrowing the airway. Even mild obesity may cause anatomical imbalance in individuals with a small maxilla and mandible. Lung volume reduction due to excessive central fat deposition may decrease longitudinal tracheal traction forces and pharyngeal wall tension, changing the 'tube law' in the pharyngeal airway (lung volume dependence of the upper airway). The lung volume dependence of pharyngeal airway patency appears to contribute more significantly to the development of OSA in morbidly obese, apnoeic patients. Neurostructural interactions required for stable breathing may be influenced by obesity-related hormones and cytokines. Accumulating evidence strongly supports these speculations, but further intensive research is needed.
    • "Therefore, obesity and male gender share similar mechanisms that increase the propensity of upper airway collapse by promoting tongue enlargement and pharyngeal lengthening (Fig. 3). Although we did not have information regarding the presence of sleep disordered breathing or OSA in our cohort, our findings help support recent evidence linking tongue adiposity to OSA and its relationship to obesity [4,18] . Importantly, there is evidence that weight loss may improve upper airway patency. "
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    • "This is also one of the reasons for difficult mask ventilation and obstructive sleep apnoea. [9] Larynx It serves as a sphincter, transmitting air from oropharynx and nasopharynx to trachea. "
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    • "This is further complicated in obese patients, in whom the gross enlargement of pharyngeal soft tissue structures (Horner et al., 1989; Shelton et al., 1993) along with increased fatty tissue in the soft palate, uvula, tongue and mandibular structures (Schwab et al., 2003; Stauffer et al.,1989) leading to further narrowing of the airway. In addition to the airway disorder, the lung volume is also additionally affected by the reduction in tracheal tractional and pharyngeal wall tension forces (Isono, 2012). More so, obesity related reduction of leptin responsiveness further interferes with breathing via neuro-anatomical interference (Polotsky et al., 2012). "
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