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Central Sleep Apnea^*

Pathophysiology and Treatment

^* From the Division of Sleep Medicine, Sleep Disorders Program and Harvard Medical School (Drs. Eckert, Jordan, and Merchia), and Division of Pulmonary/Critical Care Medicine (Dr. Malhotra), Brigham and Women’s Hospital Boston, MA.

Correspondence to: Danny J. Eckert, PhD, Brigham and Women’s Hospital, Division of Sleep Medicine, Sleep Disorders Program @ BIDMC, 75 Francis St, Boston, MA 02115; e-mail: deckert{at}rics.bwh.harvard.edu

Abstract

Central sleep apnea (CSA) is characterized by a lack of drive to breathe during sleep, resulting in repetitive periods of insufficient ventilation and compromised gas exchange. These nighttime breathing disturbances can lead to important comorbidity and increased risk of adverse cardiovascular outcomes. There are several manifestations of CSA, including high altitude-induced periodic breathing, idiopathic CSA, narcotic-induced central apnea, obesity hypoventilation syndrome, and Cheyne-Stokes breathing. While unstable ventilatory control during sleep is the hallmark of CSA, the pathophysiology and the prevalence of the various forms of CSA vary greatly. This brief review summarizes the underlying physiology and modulating components influencing ventilatory control in CSA, describes the etiology of each of the various forms of CSA, and examines the key factors that may exacerbate apnea severity. The clinical implications of improved CSA pathophysiology knowledge and the potential for novel therapeutic treatment approaches are also discussed.

Key Words: apnea threshold • arousal • chemoresponsiveness • control of breathing • hypercapnia • hypoxia • sleep-disordered breathing

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