Central Sleep Apnea

Understanding respiratory control during sleep is fundamental to understanding the approach to the diagnosis and management of central sleep apnea (CSA).

CSA is not one disease but rather a syndrome resulting from a heterogeneous group of etiologies. There are complex chemical, metabolic, mechanical, and neural contributions that can cause dysregulation in loop gain, decreased central respiratory drive, or both. The traditional dichotomy between obstructive versus central sleep apnea is overly simplistic. Conventional CSA is the extreme end along a continuum between obstructive and central phenotypes of sleep apnea. In addition to assessing CSA severity from sleep study data, new approaches, including computational analytics and the use of wearable technologies, are increasingly aimed at extrapolating additional information to characterize CSA etiology. Various positive airway pressure modalities are available to treat CSA, but residual disease is common. There is a better understanding of drugs as causes and as treatments of CSA. Phrenic nerve stimulation is a new treatment option. Multimodal therapy is the likely future of CSA therapy.

CSA can be mechanistically divided into hypercapnic and hypocapnic CSA, with the six CSA syndromes in the International Classification of Sleep Disorders (Third Edition, Text Revision) falling under one or both of these categories depending on their etiology. Understanding the obstructive-central continuum of sleep apnea, in which the degree of contribution from each underlying sleep apnea driver, known as endotypes, predicts the relative central disease of a given patient on this continuum, can enhance comprehensive management.