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Cheyne-Stokes Respiration and Congestive Heart Failure : Are Oxygen Stores the Critical Factor?

Michael R. Littner, MD, FCCP; Steve Han, MD
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Affiliations: Los Angeles, CA
 ,  Dr. Littner is a member of the Pulmonary, Critical Care and Sleep Medicine Division, VA Greater Los Angeles Healthcare System, and Professor of Medicine, David Geffen School of Medicine at UCLA, Sepulveda. Dr. Han is a Fellow, Pulmonary, Critical Care and Sleep Medicine, Combined Program of Cedars-Sinai Medical Center, VA Greater Los Angeles Healthcare System, and Olive View-UCLA Medical Center, Los Angeles. Correspondence to: Michael R. Littner, MD, FCCP, Pulmonary, Critical Care and Sleep Medicine VAGLAHS (IIID), 16111 Plummer St, Sepulveda, CA 91343-2036; e-mail: mlittner@ucla.edu

Correspondence to: Michael R. Littner, MD, FCCP, Pulmonary, Critical Care and Sleep Medicine VAGLAHS (IIID), 16111 Plummer St, Sepulveda, CA 91343-2036; e-mail: mlittner@ucla.edu



Chest. 2003;123(1):7-9. doi:10.1378/chest.123.1.7
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Cheyne-Stokes respiration (CSR) is a pattern of increasing, followed by decreasing, ventilation leading to a period of apnea. CSR is associated with several conditions, including CNS dysfunction, ascent to high-altitude and, as investigated in this issue of CHEST (see page 59) congestive heart failure.1 Typically, CSR is most obvious during non-rapid eye movement sleep when metabolic control of breathing predominates.2 The initiation of CSR may depend on a narrow difference between the resting end-tidal CO2 (Petco2) and the apneic threshold for CO2.3 This enhances the likelihood that apnea will occur under conditions that favor a decrease in CO2 and an increase in the apneic threshold such as a transient arousal followed by the onset of sleep. As reviewed,,12 once initiated, CSR is maintained, in part, by the interactive effect of fluctuations in CO2 and O2 on central and peripheral chemoreceptors. The increasing ventilation results from progressive elevation of CO2 levels above the apneic threshold plus a progressive decrease in O2. The decreasing ventilation results from a progressive decline of CO2 and increase in O2 due to hyperpnea from chemoreceptor stimulation. As discussed, apnea is then the result of a CO2 level below the apneic threshold possibly combined with little or no hypoxic stimulation. Several factors may make CSR more likely to be present. These include a delayed circulation time from the heart to the respiratory chemoreceptors (eg, from congestive heart failure), chemoreceptors that are overly sensitive to CO2, frequent arousals, various reflexes, upper airway instability, and the interactive effect of an increase in CO2 with a decrease in O2 that is known to produce greater than additive respiratory chemostimulation.,4

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