Pathophysiological mechanisms associated with sleep disorder breathing and their influence on treatment

Abstract

This article summarizes the anatomical basis as well as the various pathophysiological mechanisms that are considered to be crucial in development of sleep-disordered breathing. The anatomic factors that predispose to the occurrence of pharyngeal collapse are considered. The collapsible tube model for understanding the behavior of human pharyngeal airway, transmural pressure, intraluminal pressure, surrounding tissue pressure, closing pressure of pharyngeal airway, and critical closing pressure are discussed. The role of nose in snoring and obstructive sleep apnea (OSA) is also touched on. The role of obesity on upper airway is outlined. These include the mechanical consequences of fat deposition within the maxillomandibular enclosure on pharyngeal collapsibility and possible influences of visceral fat on OSA. An overview of pharyngeal anatomy and musculature, pharyngeal muscle activity during wake/sleep, and neural regulation of sleep and breathing is given. Factors pertaining to the loss of pharyngeal dilator muscle activation, change in central respiratory drive, and OSA-induced neuropathy/myopathy are discussed. Abnormalities of central neuronal output and control of breathing are explained. The impact of end-expiratory lung volume on upper airway resistance is also discussed. The use of computational modeling to predict responses to upper airway surgery in OSA is discussed. Novel methods such as manipulation of the arousal threshold and measures to reduce a high loop gain (oxygen therapy, acetazolamide) are also briefly discussed.