What is sleep apnea hypoventilation syndrome?

  Sleep apnea hypoventilation syndrome (Obstructivesleepapnea/hypopneasyndrome, OSAHS) is a temporary narrowing collapse and obstruction of the upper airway repeatedly during sleep, resulting in apnea or hypoventilation with snoring during sleep, causing frequent nocturnal blood oxygen drop, hypercapnia, sleep fragmentation and sleep structure disorder, and Daytime drowsiness and reduced quality of life. The most important pathophysiological changes are based on the narrowing of the upper airway and the decrease of neuroregulatory function, resulting in repeated collapse of the upper airway during sleep, which in turn leads to a decrease in hypoventilation and oxygen saturation, and eventually leads to the impairment of systemic multi-organ function.  The pathophysiological mechanism of OSAHS pathogenesis includes three major factors: anatomical abnormalities, inflammatory response and neuromodulatory dysfunction. The anatomical abnormalities are the basis for the narrowing of the upper airway, the inflammatory factors can aggravate the narrowing of the upper airway, and over time the function of the neuromodulatory pharyngeal opening muscle decreases, further aggravating the obstruction. The long-term interaction and transformation between the three factors form the basis for the pathogenesis of upper airway ventilation dysfunction. In long-term OSAHS clinical studies, it was found that pharyngeal cavity obstruction was the main site causing clinical symptoms. However, it was found in the follow-up that the relief of pharyngeal obstruction in some patients did not completely relieve the upper airway ventilation dysfunction during sleep.  Studies of nasal anatomy, imaging, and pathophysiology revealed that increased respiratory airflow, increased resistance to nasal ventilation, displacement of the soft palate, collapse of the pharyngeal cavity, obstruction, and triggered open-mouth breathing in nasal stenosis. It is thus hypothesized that nasal stenosis may be the source initiating factor for upper airway obstruction.