Neural respiratory drive to the diaphragm in patients with COPD during sleep

Patients with COPD may develop hypoxia and hypercapnia during sleep, in particular in REM stage although normal ventilation is usually sustained during daytime. Reduction of neural respiratory drive during sleep was hypothesized to be an important mechanism underling hypoxia and hypercapnia. However healthy subjects do not develop hypoxia during sleep. To determine whether change of neural respiratory drive in patients with COPD differed from that in normal subjects, we studied nine patients with COPD (age 58.6±11.8 years; FEV1%pred 49±18) and six normal subjects (Age 58.9±10.1 years; FEV 1 %pred 98.0%±10.5%). We recorded the diaphragm EMG from a multipair esophageal electrode during overnight full polysomnography including recording of airflow which was measured by pneumotachograph. Sleep efficiency in both groups was low mainly because of interference of face mask and pneumotachograph. Sleep efficiency in COPD group was worse than that in normal group (52.8 ±16.1 vs 69.5±13.7). Tidal volume (ml/kg) in patients with COPD decreased by 32.2%±21.3% in NREM stages and further decreased by 45.6%±16.6% in REM stage compared with wakefulness. The decrease of tidal volume from wakefulness to sleep in COPD was significantly larger than that in normal subjects. Diaphragm EMG decreased by 30.0%±21.4% and 37.1%±20.0% from wakefulness to NREM and REM respectively in patients with COPD. However, diaphragm EMG in normal subjects remained the same or only slightly decreased during sleep when compared with wakefulness. We conclude that reduction in neural drive during sleep in patients with COPD is greater than that normal subjects and may be responsible for hypoxia in patients with COPD.