Update in respiratory sleep disorders: Prologue to a modern review series

Sleep is a period of great vulnerability for ventilation. Pharyngeal muscle tone decreases, particularly during rapid eye movement (REM) sleep, resulting in upper airway 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 atelectasis 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.