SLEEP-DISORDERED BREATHING DIAGNOSIS AND TREATMENTkapak

PHYSIOPATHOLOGY OF OBSTRUCTIVE SLEEP APNEA SYNDROME

Ali Rıza Yağmur

Ankara Lokman Hekim University, Faculty of Medicine, Department of Otorhinolaryngology, Ankara, Türkiye

Yağmur AR. Physiopathology of Obstructive Sleep Apnea Syndrome. In: Özcan KM, editor. Sleep-Disordered Breathing: Diagnosis and Treatment. 1st ed. Ankara: Türkiye Klinikleri; 2025. p.15-23.

ABSTRACT

Obstructive Sleep Apnea Syndrome (OSAS) is a complex sleep disorder resulting from repeated blockages of the upper airway. Its pathophysiology involves several mechanisms that vary in significance among individuals. This chapter focuses on the key mechanisms contributing to OSAS, emphasizing the interplay of upper airway narrowing, reduced dilator muscle tone, ventilatory control instability (loop gain), low arousal threshold, obesity, and genetic or structural predispositions. Anatomical factors play a significant role in the pathophysiology of OSAS. Anatomical factors that cause narrowing at various levels in the upper airway may play a role in its pathophysiology. Adenotonsillar hypertrophy is the most common cause of narrowing in children. In adults, hypertrophy of the lateral pharyngeal bands and tonsils, which cause narrowing in the oropharyngeal region, and developmental deficiencies of the maxilla and mandible due to maxillofacial anomalies play a significant role in the development of OSAS. Tongue hypertrophy due to various causes, as well as fatty tissue accumulation in the lateral pharyngeal region and tongue due to obesity, cause upper airway narrowing. One of the fundamental mechanisms in the pathophysiology is decreased pharyngeal muscle activity. Numerous dilator muscles maintain the pharyngeal lumen. While dilator muscle activity is high during wakefulness, dilator muscle activity decreases after falling asleep, particularly during REM sleep. In combination with anatomical factors, apnea and hypopneas can occur in patients with pronounced decreased dilator muscle activity. Critical airway closure pressure (Pcrit) is another important mechanism. Upper airway patency is maintained through the balance between intraluminal pressure and extraluminal forces. Patients with elevated Pcrit are prone to airway collapse. The excessive response to increased partial pressure of carbon dioxide resulting from a defect in the respiratory control system (loop gain) is known as high loop gain and is known to play a role in the pathophysiology of OSAS. A lower arousal threshold, or shallower sleep or wakefulness response to respiratory events during sleep, is a significant factor in the development of the disease in some patients. Understanding these mechanisms is essential not only for establishing a diagnosis but also for performing a holistic assessment of the patient. This comprehensive approach facilitates identification of dominant pathophysiological contributors and supports selection of individualized treatment strategies. Ultimately, a solid grasp of OSAS pathophysiology enhances the development of targeted and effective therapies that address the root causes of the disorder and improve long-term outcomes.

Keywords: Obstructive sleep apnea syndrome; Pathophysiology; Airway resistance; Arousal; Obesity

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