Role of respiratory control mechanisms in the pathogenesis of obstructive sleep disorders

Abstract

Obstructive sleep disorders develop when the normal reduction in pharyngeal dilator activity at sleep onset occurs in an individual whose pharynx requires a relatively high level of dilator activity to remain sufficiently open. They range from steady snoring, to slowly evolving hypopneas, to fast-recurring obstructive hypopneas and apneas. A fundamental observation is that the polysomnographic picture differs substantially among subjects with the same pharyngeal collapsibility, and even in the same subject at different times, indicating that the type and severity of the disorder is determined to a large extent by the individual's response to the obstruction. The present report reviews the various mechanisms involved in the response to sleep-induced obstructive events. When the obstructive event takes the form of mild-moderate flow limitation, compensation can take place through an increase in the fraction of time spent in inspiration (Ti/Ttot) without any increase in maximum flow (V(MAX)). With more severe obstructions, V(MAX) must increase. Recent data indicate that the obstructed upper airway can reopen reflexly, without arousal, if chemical drive is allowed to reach a threshold (T(ER)) but that this is often preempted by a low arousal threshold. The relation between T(ER) and arousal threshold, as well as the lung-to-carotid circulation time and the rate of rise of chemical drive during the obstructive event, determine the magnitude of ventilatory overshoot at the end of an event and, by extension, whether initial obstructive events will be followed by stable breathing, slow evolving hypopneas with occasional arousals, or repetitive events.