Obstructive sleep apnea hypopnea syndrome (OSAHS) is a clinical disease in which the airflow between the nose and mouth is suspended for more than 10s during sleep. Classification】 ①Obstructive sleep apnea: sleep apnea caused by upper airway obstruction, manifested by the cessation of airflow in the oral and nasal cavities while the thoracic and abdominal breathing movements are still present. ② Central sleep apnea: airflow in the oral and nasal cavities and thoracic and abdominal respiratory movements stop at the same time. (3) Mixed sleep apnea, the above two coexist, starting with central apnea, followed by obstructive sleep apnea. The direct pathogenesis of obstructive sleep apnea syndrome is the narrowing and obstruction of the upper airway, but the pathogenesis of obstructive sleep apnea syndrome is not simply the obstruction of the airway, but also the disorder of the central neuroregulatory factors of breathing. There are many causes of upper airway narrowing and obstruction, including nasal septum curvature, nasal polyps, turbinate hypertrophy, tonsillar hypertrophy, tonsillar hyperplasia, soft palate overgrowth, palatal arch hypoplasia, mandibular arch stenosis, mandibular recession deformity, small jaw deformity, temporomandibular joint ankylosis, especially small jaw deformity secondary to joint ankylosis on both sides, tongue hypertrophy, megalingualism, hyoid bone recession, etc. Obesity, mucus edema of upper airway tissue, and oropharyngeal or hypopharyngeal tumors can also lead to obstructive sleep apnea syndrome. The pathogenesis of obstructive sleep apnea is mainly due to anatomical narrowing of the upper airway and dysfunctional respiratory control. The pharyngeal airway lacks the support of bony structures and is a muscular, soft tube with collapsibility. The main force causing the closure of the pharyngeal airway is the negative pressure in the pharyngeal airway, which is generated by the contraction of the diaphragm and other respiratory muscles during inspiration; the activity of the pharyngeal dilator muscle, mainly the chin-lingual muscle, is the main force to counteract the negative pressure in the pharyngeal cavity and maintain the opening of the upper airway. It has been found that the patient’s central respiratory drive decreases during sleep and the tone of the pharyngeal dilator muscle decreases significantly, making it difficult to overcome the negative pressure in the pharyngeal cavity during inspiration and causing passive collapse of the soft tissues of the pharyngeal airway. Together with the anatomical defects of the patient’s pharyngeal airway itself, the obstruction is further aggravated. During the development of obstructive sleep apnea, blood oxygen gradually decreases, partial pressure of carbon dioxide gradually increases, and negative pressure in the pharyngeal cavity increases, all of which cause transient awakening by stimulating the corresponding chemical and pressure receptors and excite the brainstem reticular activation system, airflow is restored, and obstructive sleep apnea ends. The reasons for the reduced sensitivity of the respiratory center during sleep may vary from primary (related to genetic factors) to secondary to certain factors.