Hypocapnia is not a predictor of central sleep apnea in patients with cirrhosis.

Abstract

During sleep, maintenance of rhythmic breathing is critically dependent on the level of PCO(2), such that if the prevailing spontaneous PCO(2) 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 PCO(2) (Pa(CO(2))) increases the likelihood of developing CSA during sleep. We therefore sought to determine if a low Pa(CO(2)) is a predictor of CSA in patients with cirrhosis of the liver and with normal left ventricular systolic function. In 13 hypocapnic (Pa(CO(2)) < 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 (Pa(CO(2)) < 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, Pa(O(2)), Pa(CO(2)), minute and alveolar ventilation, and ventilatory responses to CO(2) between the two groups. We conclude that, in contrast to SHF, presence of hypocapnia does not predict CSA in cirrhosis.