Upper respiratory conditions (sinusitis) result in distortion of the upper airway, which contributes to the development of sleep apnea.
Conceptually, the upper airway is a compliant tube and, therefore, is subject to collapse. OSA is caused by soft tissue collapse in the pharynx. Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure. If transmural pressure decreases, the cross-sectional area of the pharynx decreases. If this pressure passes a critical point, pharyngeal closing pressure is reached. Exceeding pharyngeal critical pressure (Pcrit) causes a juggernaut of tissues collapsing inward. The airway is then obstructed. Until forces change transmural pressure to a net tissue force that is less than Pcrit, the airway remains obstructed.
OSA duration is equal to the time that Pcrit is exceeded. The Bernoulli effect plays an important dynamic role in OSA pathophysiology. In accordance with this effect, airflow velocity increases at the site of stricture in the airway. As airway velocity increases, pressure on the lateral wall decreases. If the transmural closing pressure is reached, the airway collapses.
The Bernoulli effect is exaggerated in areas where the airway is most compliant. Loads on the pharyngeal walls increase adherence and, hence, increase the likelihood of collapse. This effect helps to partially explain why obese patients, and particularly those with fat deposition in the neck, are most likely to have OSA. Given this information, it is abundantly clear that even a small reduction in a diameter of the upper airway will cause a collapse of the upper airway during sleep.
Fitzpatrick et al. studied the effect of nasal breathing on sleep apnea in the article Effect of nasal or oral breathing route on upper airway resistance during sleep. The author reports that healthy subjects with normal nasal resistance breathe almost exclusively through the nose during sleep. The researchers studied the resistance to the upper airway through either nasal or oral breathing and found that upper airway resistance during sleep and the propensity to obstructive sleep apnea are significantly lower while breathing nasally rather than orally.
Nasal obstruction during sleep results in mouth opening and mouth opening has been shown to increase the propensity to upper airway collapse. It has been shown that jaw opening is associated with posterior movement of the angle of the jaw, thus compromising the oropharyngeal airway diameter. This is caused by the shortening of the upper airway dilator muscles located between the mandible and the hyoid bone. In addition, jaw opening profoundly affects the diameter of the retroglossal airway.
The author has shown that there are two distinct sites of airway obstruction during sleep with oral breathing, when nasal breathing is not efficient.
The Board of Veterans’ Appeals in a decision dated December 24, 2003, Citation Nr: 0336453, Docket No. 03-00 071A, concluded that sinusitis (upper airway obstruction) significantly contributes to sleep apnea:
“While the record clearly supports a finding that the veteran suffers from sleep apnea, the record is equivocal regarding the effect that the veteran’s service-connected sinusitis has on his sleeping disorder. In the opinion of the February 2001 VA examiner the veteran’s sinusitis was not an obvious cause of the veteran’s sleep apnea. Test results appear to indicate that the veteran’s sleep apnea is positional in nature, being twice as common in the supine position. However, a more recent medical opinion from his VA primary care physician indicates that the veteran’s chronic sinusitis, if not the total cause, contributes significantly to his obstructive sleep apnea. In light of the above medical evidence showing a relationship between the veteran’s chronic sinusitis and his sleep apnea, the Board determines that 38 C.F.R. § 3.102 (2003) should be applied in this case.”