Load compensation and respiratory muscle function during sleep

Abstract

The sleeping state places unique demands on the ventilatory control system. The sleep-induced increase in airway resistance, the loss of consciousness, and the need to maintain the sleeping state without frequent arousals require the presence of complex compensatory mechanisms. The increase in upper airway resistance during sleep represents the major effect of sleep on ventilatory control. This occurs because of a loss of muscle activity, which narrows the airway and also makes it more susceptible to collapse in response to the intraluminal pressure generated by other inspiratory muscles. The magnitude and timing of the drive to upper airway vs. other inspiratory pump muscles determine the level of resistance and can lead to inspiratory flow limitation and complete upper airway occlusion. The fall in ventilation with this mechanical load is not prevented, as it is in the awake state, because of the absence of immediate compensatory responses during sleep. However, during sleep, compensatory mechanisms are activated that tend to return ventilation toward control levels if the load is maintained. Upper airway protective reflexes, intrinsic properties of the chest wall, muscle length-compensating reflexes, and most importantly chemoresponsiveness of both upper airway and inspiratory pump muscles are all present during sleep to minimize the adverse effect of loading on ventilation. In non-rapid-eye-movement sleep, the high mechanical impedance combined with incomplete load compensation causes an increase in arterial PCO2 and augmented respiratory muscle activity. Phasic rapid-eye-movement sleep, however, interferes further with effective load compensation, primarily by its selective inhibitory effects on the phasic activation of postural muscles of the chest wall. The level and pattern of ventilation during sleep in health and disease states represent a compromise toward the ideal goal, which is to achieve maximum load compensation and meet the demand for chemical homeostasis while maintaining sleep state.

Pathophysiology of Obstructive Sleep Apnea

“…1 This reduction in pharyngeal muscle tone in sleep leads to airway narrowing and increased resistance to airflow, and this effect contributes significantly to the hypoventilation and increased arterial PCO 2 of 3 to 5 mm Hg typically observed in normal sleeping subjects. 2,3 Indeed, elimination of this increased upper airway resistance reverses the major component of the normal sleep-induced hypoventilation. 2 Importantly, however, in individuals with already anatomically narrow upper airways (discussed below), this suppressant effect of sleep on pharyngeal muscle tone predisposes to significant reductions in inspiratory airflow and airflow-limitation (ie, hypopneas and snoring) and even cessation of airflow because of complete airway closure (ie, obstructive apneas) (Fig 1).…”

Recombinant human DNase nebulisation in children with cystic fibrosis: before bedtime or after waking up?

“…First, sputum after nebulisation with rhDNase might still be too viscous to allow any extra positive effect by gravity. Secondly, during sleep mucociliary clearance is depressed [16,17] and breathing patterns change, resulting in reduced minute ventilation and tidal breathing pattern [31,32] as well as an increased airway resistance [33]. If gravity and mucociliary clearance fail to mobilise the viscous sputum spontaneously, it can only be cleared by high expiratory flows [34].…”

Neural Control of the Upper Airway: Integrative Physiological Mechanisms and Relevance for Sleep Disordered Breathing

“…Either physician or patient-controlled analgesia can result in opioid effects on breathing for prolonged periods of time, including during sleep. This effect has further clinical relevance because sleep by itself causes decreased pharyngeal muscle tone, hypoventilation, and diminishes the ventilatory responses to hypoxia and hypercapnia (195,419). Moreover, the hypoventilation and blood gas changes that normally occur in sleep are exacerbated in patients with coexisting respiratory problems such as chronic obstructive pulmonary disease and obesity hypoventilation (265,418), such that further respiratory suppression produced by opioid drugs during the sleep period is also a significant clinical concern (554,585).…”

“…The respiratory function of the upper airspace assumes particular clinical relevance when it is considered that, in humans, sleep causes fundamental modifications of upper airway muscle tone and reflex responses that in normal individuals lead to airway narrowing and hypoventilation (195,223). In individuals with already narrow upper airways, these effects of sleep further predispose to inspiratory flow limitation (hypopneas), airway closure, and obstructive sleep apnea-hypopnea (OSAH) syndrome (109,435).…”