ABSTRACT
Central sleep apnoea (CSA) is characterized by episodes of apnoea or hypopnoea related to loss of ventilatory output from the central respiratory generator located in the brainstem. However, owing to the complexity of the control of ventilation, many structures may be structurally or functionally involved in the loss of ventilatory drive, including medullary neurones, carotid bodies or feedback from respiratory muscle afferents. The nosology of CSA remains debated although several recommendations/ classifications have been published in the past 10 years.1 The reason is probably the disparity in prevalence between the different clinical entities. Although CSA is very frequent in heart failure and thus commonly seen in clinical practice,2 idiopathic CSA or tumuors and trauma-induced lesions of the brainstem are rare.3 However, it has been suggested to divide CSA into two classes based on the presence or absence of hypercapnia during daytime.4 This classification seems to be pertinent with respect to both pathophysiology
and different treatment options.3 In this chapter, we will review the classification and pathophysiology of CSA. We will also discuss CSA in heart failure, specific aetiologies such as complex sleep apnoea or opioid-induced sleep apnoea, and hypercapnic central sleep apnoea with special emphasis on the treatment issues.
