Background Breathing is controlled by a negative-feedback systemin which an increase in the partial pressure of arterial carbondioxide stimulates breathing and a decrease inhibits it. Althoughenhanced sensitivity to carbon dioxide helps maintain the partialpressure of arterial carbon dioxide within a narrow range duringwaking hours, in some persons a large hyperventilatory responseduring sleep may lower the value below the apneic threshold,thereby resulting in central apnea. I tested the hypothesisthat enhanced sensitivity to carbon dioxide contributes to thedevelopment of central sleep apnea in some patients with heartfailure.
Methods This prospective study included 20 men who had treated,stable heart failure with left ventricular systolic dysfunction.Ten had central sleep apnea, and 10 did not. The patients underwentpolysomnography and studies of their ventilatory response tocarbon dioxide.
Results Patients who met the criteria for central sleep apneahad significantly more episodes of central apnea per hour thanthose without central sleep apnea (mean [±SD], 35±24vs. 0.5±1.0 episodes per hour). Those with sleep apneaalso had a significantly larger ventilatory response to carbondioxide than those without central sleep apnea (5.1±3.1vs. 2.1± 1.0 liters per minute per millimeter of mercury,P=0.007), and there was a significant positive correlation betweenventilatory response and the number of episodes of apnea andhypopnea per hour during sleep (r=0.6, P=0.01).
Conclusions Enhanced sensitivity to carbon dioxide may predisposesome patients with heart failure to the development of centralsleep apnea.
Source Information
From the Pulmonary Service, Veterans Affairs Medical Center, and the Department of Medicine, University of Cincinnati College of Medicine both in Cincinnati.
Address reprint requests to Dr. Javaheri at the Pulmonary Section (111F), VA Medical Center, 3200 Vine St., Cincinnati, OH 45220, or at javaheri,shahrokh{at}cincinnati.va.gov.
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