Pathophysiology of obstructive sleep apnea-hypopnea syndrome

Hypopnea can be characterized by recurrent episodes of upper airway obstruction during sleep. They are commonly associated with the so called recurrent oxyhemoglobin desaturation and frequent arousals from sleep. The term obstructive sleep apnea-hypopnea syndrome (OSAHS) is frequently used when such episodes are associated with excessive daytime sleepiness.

The majority of patients with obstructive sleep apnea-hypopnea syndrome demonstrate upper airway obstruction, either at the level of the soft palate or at the level of the tongue. Anatomic factors include enlarged tonsils, macroglossia, or abnormal positioning of the maxilla and mandible. They decrease the cross-sectional area of the upper airway and increase the pressure surrounding the airway, both of which predispose the airway to collapse.

Upper airway neuromuscular activity decreases with sleep, that is more pronounced in patients with sleep apnea or hypopnea. Reduced ventilatory motor output to upper airway muscles is believed to be the critical initiating event leading to upper airway obstruction. Central breathing instability has been well established as a contributor to the development of central sleep apnea, particularly in patients with severe congestive heart failure. There’s a good ground to believe that central breathing instability also contributes to the development of obstructive sleep apnea-hypopnea syndrome. First of all, there is upper airway obstruction in the absence of ventilatory motor output. Second of all, reduction in pharyngeal dilator activity is associated with periodic breathing and hypocapnia in subjects with evidence of inspiratory flow limitation. Third of all, there is the evidence of increased prevalence of OSAHS in men, as they are more susceptible to the development of hypopnea and central sleep apnea and have a more decreased responsiveness to carbon dioxide than woman.