Background: CO(2) inhalation reduces central sleep apnea (CSA) in patients with congestive heart failure (CHF) and idiopathic CSA. CO(2) is also a stimulus for cortical arousal, which has been linked to increased sympathetic nerve activity (SNA) and increased mortality in CHF patients with CSA.
Objective: We have tested the hypothesis that during sleep, inhalation of CO(2) sufficient to reduce the apnea-hypopnea index (AHI) would not reduce the arousal index (AroI).
Methods: In 10 male patients with CSA (7 with CHF and 3 with idiopathic CSA), the inspired CO(2) concentration was increased to raise the sleeping end-tidal CO(2) by 2-4 mm Hg during established stage 2 sleep. Each intervention was maintained for a 10-min period. Sleep stage was monitored with electroencephalograms, electrooculograms, submental electromyogram, airflow with pneumotachometer and respiratory effort and blood gases with oxygen saturation and end-tidal CO(2). During periods of air and CO(2) breathing, AHI and AroI were compared with paired t tests; patients acted as their own controls.
Results: Inhalation of CO(2) produced a significant reduction in AHI (mean +/- SEM) from 74.4 +/- 12.4 events/h during air breathing to 25.8 +/- 7.8 events/h with CO(2) inhalation (p = 0.002). However, the AroI was not significantly different between the two conditions, air 67.8 +/- 12.3 events/h and CO(2) inhalation 52.8 +/- 12.4 events/h (p = 0.264).
Conclusion: CO(2) inhalation reverses CSA but not arousals from sleep. Our findings highlight the need for treatment options that reduce both respiratory events and decrease arousals from sleep, with their associated SNA sequelae.