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Filling in the Gaps: The Role of Noninvasive Adaptive Servoventilation for Heart Failure-Related Central Sleep Apnea

Lee K. Brown, MD, FCCP
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Albuquerque, NM

Correspondence to: Lee K. Brown, MD, FCCP, Professor of Medicine and Pediatrics and, Vice Chair, Department of Internal Medicine, University of New Mexico School of Medicine, UNMH Sleep Disorders Center, 1101 Medical Arts Ave NE, Building 2, Albuquerque, NM 87102; e-mail: lkbrown@alum.mit.edu


Chest. 2008;134(1):4-7. doi:10.1378/chest.07-3019
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Effective management of central sleep apnea, whether isolated or as part of what can be termed complex sleep apnea syndrome (CompSAS) remains one of the most challenging aspects of sleep medicine. Central sleep apnea is now commonly defined as sleep-disordered breathing with either a pattern of abrupt cessations and resumptions of respiratory effort or the well-known Cheyne-Stokes configuration. Complex sleep apnea is less well defined, often being used to describe several different patterns of abnormality that are encountered in patients with sleep-disordered breathing. For some authors and clinicians, CompSAS is a variable combination of obstructive, mixed, and central apneas and hypopneas, with the predominant mechanism that is manifest at any given time dependent on sleep stage, sleep posture, or other (often unknown) variables.12 Frequently, these are patients with comorbid congestive heart failure (CHF) or CNS disease, or are receiving treatment with medications that depress respiratory drive, so that combinations of obstructive and central events are not unexpected. For other authors, CompSAS has a more restricted definition. Obstructive and central events are both present, but the central events are most evident when positive airway pressure therapy is applied (called treatment-emergent central apneas).5 The subfield of sleep-disordered breathing science that includes central and complex sleep apnea has become a topic of extreme interest for the following several reasons: (1) these respiratory events can be vexingly resistant to treatment, since central sleep apnea is notoriously difficult to suppress and the degree of positive pressure that prevents upper airway obstruction may provoke more central events; (2) patients with CHF and central or complex sleep apnea who are not effectively treated for their sleep-disordered breathing may experience worse outcomes, not withstanding the disappointing results of the Canadian Positive Airway Pressure Trial for Congestive Heart Failure patients with Central Sleep Apnea (CANPAP)67; and (3) physicians with an analytic bent regarding control of breathing are fascinated by these phenomena, and the convoluted interactions between pathophysiology and possible treatment modalities.

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