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University of Cincinnati Academic Health Center
Publish Date: 10/20/99
Media Contact: AHC Public Relations, (513) 558-4553
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New Clues to Understanding Heart Failure

Cincinnati—Enhanced sensitivity to carbon dioxide (CO2) may predispose some patients with heart failure to the development of central sleep apnea, says Shahrokh Javaheri, MD, professor of medicine at the University of Cincinnati (UC) College of Medicine and director of the Veterans Affairs Medical Center Sleep Disorders Laboratory. Javaheri's findings were published in the September 23 issue of the New England Journal of Medicine.

"Normally, the rate and depth of breathing are regulated by a negative feedback system that maintains the amount of CO2 found in the arteries," says Javaheri. "When CO2 blood levels become elevated, the lungs are stimulated to ventilate and rid the blood of excess CO2."

In Javaheri's study, half of the patients studied had sleep apnea and were found to be more sensitive to increases in blood levels of CO2. "Although this protective mechanism is advantageous during waking, the increased sensitivity can potentially destabilize breathing during sleep, causing a cessation of breathing or apnea," says Javaheri.

The greater sensitivity to increased blood levels of CO2 leads to cycles of hyperventilation followed by central sleep apnea. The apnea patients in this study had at least 35 apnea episodes in which they stopped breathing for 10-16 seconds at least 35 times an hour. These patients also carried less oxygen in their blood and experienced more than twice the number of sleep disturbances.

Javaheri's earlier research showed that at least 40 percent of stable patients being treated for heart failure had central sleep apnea. His latest research shows that a patient's hypersensitivity to CO2 may cause the apnea.

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