Published ahead of print on January 18, 2005, doi:10.1164/rccm.200407-910OC Am. J. Respir. Crit. Care Med., Volume 171, Number 8, April 2005, 908-911 A more recent version of this article appeared on April 15, 2005
Submitted on July 21, 2004 Hypocapnia is not a Predictor of Central Sleep Apnea in Patients with CirrhosisShahrokh Javaheri1*,1 Pulmonary Section, Veterans Affairs Medical Center, Cincinnati, OH, USA; Department of Medicine, Sleep Care Diagnostics, University of Cincinnati, College of Medicine, Cincinnati, OH, USA, 2 Pulmonary Section, Veterans Affairs Medical Center, Cincinnati, OH, USA, 3 Liver Services, Veterans Affairs Medical Center, Cincinnati, OH, USA * To whom correspondence should be addressed. E-mail: shahrokh.javaheri{at}med.va.gov.
During Sleep, maintenance of rhythmic breathing is critically dependent upon 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 LV systolic function. In 13 hypocapnic (PaCO2 < 36 mm Hg, mean = 33 mm Hg) patients with SHF, mean LV ejection fraction of 23%, the mean apnea-hypopnea index (AHI) was 28/hr. Central sleep apnea accounted for most of the breathing disorders. In 10 hypocapnic (PaCO2 < 36 mm Hg, mean = 32 mm Hg) patients with cirrhosis and normal LV ejection fraction (60%), the mean AHI was 2/hr. The maximum CAI was 0.2/hr. 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: PCO2, periodic breathing, apneic threshold
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