Update in respiratory sleep disorders: Epilogue to a modern review series.

Abstract

SERIES EDITORIAL—PROLOGUE: RESPIRATORY SLEEP DISORDERS SERIES EDITORS: PETER R EASTWOOD, MARY J MORRELL AND ATUL MALHOTRA Update in respiratory sleep disorders: Prologue to a modern review series Key words: sleep apnoea, sleep disorders. Abbreviations: CANPAP, Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure; COPD, chronic obstructive pulmonary disease; OSA, obstructive sleep apnoea; P4, personalized, predictive, preventative and participatory; PAP, positive airway pressure; PREDICT, Continuous Positive Airway Pressure in Older People with Obstructive Sleep Apnoea Syndrome; REM, rapid eye movement; SASM, Society of Anesthesia and Sleep Medicine; SAVE, Sleep Apnea Cardiovascular Endpoint; SERVE-HF, Treatment of Sleep-Disordered Breathing with Predominant Central Sleep Apnea by Adaptive Servo Ventilation in Patients with Heart Failure; STAR, Stimulation Therapy for Apnea Reduction. Sleep is a period of great vulnerability for ventilation. Pharyngeal muscle tone decreases, particularly during rapid eye movement (REM) sleep, resulting in upper air- way narrowing and collapse in predisposed individuals. Pharyngeal reflexes are also dampened, compromising the capacity of the upper airway muscles to activate in response to airway narrowing and collapse. A sleep- related loss in chest wall muscle activation results in reduced end-expiratory lung volume which, in turn, reduces longitudinal traction on the upper airway, which also acts to increase its collapsibility. Furthermore, low end-expiratory lung volumes are associated with atelec- tasis in the dependent parts of the lung, compromising gas exchange. Notably, these effects are aggravated by obesity, which is associated with exaggerated sleep- related decreases in lung volume. In addition to sleep- related effects on upper airway stability and gas exchange, the decreased muscle activation of sleep can lead to hypoventilation and the loss of the behavioural effects of wakefulness can result in periodic breathing in those prone to it, even if this problem is not manifest when awake. While these various sleep-related problems can occur in isolation, they may be seen in combination, for example coexistent obstructive sleep apnoea (OSA) and sleep hypoventilation in morbid obesity. Sleep and breathing are governed by complex inter- related physiological mechanisms. The key protective mechanism in response to sleep-related breathing events is arousal from sleep, with transient restoration of wakefulness homeostasis. Absence of protective arousal responses, as is seen during general anaesthe- sia, creates a vulnerability to asphyxia, with mainte- nance of airway patency and adequate ventilation often dependent on the use of mechanical aids, utilized by the attending anaesthetist. The post-operative period presents additional challenges, as opioids and sedatives © 2016 Asian Pacific Society of Respirology may cause depression of protective respiratory responses, a hazard in unmonitored environments. Sleep compounds these drug effects. The parallels between sleep and anaesthesia, including concerns regarding the vulnerability of patients with sleep- related breathing disorders to perioperative respiratory complications, have led to the formation of a new pro- fessional body, the US-based Society of Anesthesia and Sleep Medicine (SASM), whose mission is to advance standards of care for clinical problems shared by anaesthesiology and sleep medicine. Sleep is a whole-body state and so problems with it can affect many organ systems (e.g. cardiovascular, metabolic and endocrine) and aggravate the effects of other diseases (e.g. asthma, heart failure, COPD and dementia). The daytime consequences of sleep-related breathing disorders are now well appreciated (e.g. feelings of sleepiness and fatigue, impaired cogni- tion, mood and psychomotor function, impaired pro- ductivity, increased accident risk, hypertension, vascular disease, metabolic disturbance and depres- sion). While the prevalence of these disorders appears to be increasing in some parts of the world, at least in part due to increasing obesity and an ageing popula- tion, so is our understanding of their pathogenesis. For example, OSA was for many years attributed to poor pharyngeal anatomy. Today, it is widely accepted that the pathogenesis of OSA is multifactorial in nature, with the effects of unfavourable anatomy augmented by other variable influences including lung volume, pharyngeal muscle responsiveness, arousal thresholds and stability of ventilatory control. 1 Improved understanding of the mechanisms under- lying sleep-related breathing disorders, and apprecia- tion of their complex multifactorial nature has driven the development of a variety of treatment options. While positive airway pressure (PAP) therapies are a mainstay, they are not suitable for all patients and compliance with them is problematic for many. Alter- native treatments include oral appliances, body posi- tioning devices, hypoglossal nerve stimulation, a diversity of surgical procedures and lifestyle modifica- tion including weight loss. Better understanding of neurophysiology may, in time, lead to useful pharma- cological approaches, although there is little to offer for these disorders clinically at present. The multiple potential contributors to the pathogen- esis of sleep-related breathing disorders and their co-morbidities and their variable influence between individuals are reflected in the mixed results of several high profile multicentre therapeutic trials. Studies such Respirology (2016) doi: 10.1111/resp.12959