What is the role of mechanical dilating in the pathophysiology of childhood obstructive sleep apnea (OSA)?

Updated: Feb 13, 2019
  • Author: Mary E Cataletto, MD; Chief Editor: Denise Serebrisky, MD  more...
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Answer

Malposition or malinsertion of specific dilating muscles is likely to have major consequences on the mechanical dilating efficiency. Therefore, even if a major weakness is not present, the mechanical disadvantage imposed by muscle shortening or by displacement of the muscle insertion on the pharyngeal wall undoubtedly results in diminished ability to stiffen the airway, thus leading to increased collapsibility or elevation of Pcrit.

Control of the upper airway size and stiffness depends on the relative and rhythmic contraction of a host of paired muscles, which include the palatal, pterygoid, tensor palatini, genioglossus, geniohyoid, and sternohyoid muscles. These muscles tend to promote a patent pharyngeal lumen and receive phasic activation in synchrony with phrenic nerve activation. Upon contraction, these muscles promote motion of the soft palate, mandible, tongue, and hyoid bone. Although the coordinated action of these muscles during the respiratory cycle has yet to be deciphered, a reasonable generalization is that inspiratory muscle output stiffens the pharynx and related structures and enlarges the lumen.

The optimal activity of these muscles depends on their anatomic arrangement; for example, airway patency is compromised during increased neck flexion by changing the points of attachment of muscles acting on the hyoid bone, such that the resulting vector of their forces may be nullified. The activity of pharyngeal muscles greatly depends on various factors within the CNS and, more particularly, on the brainstem respiratory network. Wakefulness conveys a supervisory function that ensures airway patency, and sedative agents, which compromise genioglossal muscle activity, may result in significant upper airway compromise.

Mechanoreceptor-mediated and chemoreceptor-mediated genioglossal activity is critical for maintenance of upper airway patency in healthy and micrognathic infants. Changes in genioglossal activity during transitions, from oral to nasal breathing and relative to Pcrit, suggest that genioglossus activation is critical for airway patency in micrognathic infants.


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