Published ahead of print on January 18, 2005, doi:10.1164/rccm.200407-910OC
© 2005 American Thoracic Society doi: 10.1164/rccm.200407-910OC
Hypocapnia Is Not a Predictor of Central Sleep Apnea in Patients with CirrhosisPulmonary and Liver Services, Departments of Veterans Affairs Medical Center and Medicine, College of Medicine, University of Cincinnati; and Sleep Care Diagnostics, Cincinnati, Ohio Correspondence and requests for reprints should be addressed to Shahrokh Javaheri, M.D., Emeritus Professor of Medicine, Pulmonary Section (111F), VA Medical Center, 3200 Vine Street, Cincinnati, OH 45220. E-mail: shahrokh.javaheri{at}med.va.gov During sleep, maintenance of rhythmic breathing is critically dependent on the level of PCO2, such that if the prevailing spontaneous PCO2 decreases below the apneic threshold, central sleep apnea (CSA) occurs. Several studies have shown that in patients with systolic heart failure (SHF), presence of a low, awake arterial PCO2 (PaCO2) increases the likelihood of developing CSA during sleep. We therefore sought to determine if a low PaCO2 is a predictor of CSA in patients with cirrhosis of the liver and with normal left ventricular systolic function. In 13 hypocapnic (PaCO2 < 36 mm Hg, mean = 33 mm Hg) patients with SHF and a mean left ventricular ejection fraction of 23%, the mean apnea–hypopnea index, was 28/hour. CSA accounted for most of the breathing disorders. In 10 hypocapnic (PaCO2 < 36 mm Hg, mean = 32 mm Hg) patients with cirrhosis and a normal left ventricular ejection fraction (60%), the mean apnea–hypopnea index was 2/hour. The maximum central apnea index was 0.2/hour. There were no significant differences in age, demographics, pulmonary function tests, PaO2, PaCO2, minute and alveolar ventilation, and ventilatory responses to CO2 between the two groups. We conclude that, in contrast to SHF, presence of hypocapnia does not predict CSA in cirrhosis.
Key Words: apneic threshold • PCO2 • periodic breathing This article has been cited by other articles:
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