PURPOSE: Dexmedetomidine is thought to activate an endogenous pathway that naturally promotes non-rapid eye movement (NREM) sleep. Dexmedetomidine may induce restorative sleep, that is, NREM stage 3 and 4 (slow wave sleep; SWS) or sleep continuity in mechanically ventilated patients. Few data have been published, however, on the sleep characteristics of mechanically ventilated patients during dexmedetomidine infusion. METHODS: We recorded polysomnography (PSG) for 24 h in mechanically ventilated patients sedated with dexmedetomidine. Dexmedetomidine (0.2-0.7 μg/kg/h) was administered intravenously to maintain the Richmond Agitation-Sedation Scale between -1 and -4 only during the nighttime (9:00 p.m. to 6:00 a.m.). During the daytime, we interrupted the sedatives and analgesics unless the patient complained of discomfort. When this occurred midazolam or opioids were administered intermittently. Sleep stages and the frequency of arousal/awakening during the nighttime were analyzed using Rechtschaffen and Kales criteria. RESULTS: For the ten mechanically ventilated adult patients recruited into the study, the median total sleep time (TST) during the night was 4.7 h (IQR, 4.2-8.1 h), and 78 % of sleep occurred during the night (median 78 %, IQR: 69-88 %). Sleep architecture was exclusively NREM sleep stage 1 (median 28.9 % of TST) and stage 2 (median 71.2 % of TST). Neither SWS (median 0 % of TST) nor rapid eye movement (REM) sleep (median 0 % of TST) was observed. Median frequency of arousals/awakenings was 9.3/h (IQR, 3-19.5/h). CONCLUSIONS: In mechanically ventilated patients, nighttime infusion of dexmedetomidine preserved the day-night cycle of sleep but induced severely disturbed sleep architecture without evidence of SWS or REM sleep.
PURPOSE:Dexmedetomidine is thought to activate an endogenous pathway that naturally promotes non-rapid eye movement (NREM) sleep. Dexmedetomidine may induce restorative sleep, that is, NREM stage 3 and 4 (slow wave sleep; SWS) or sleep continuity in mechanically ventilated patients. Few data have been published, however, on the sleep characteristics of mechanically ventilated patients during dexmedetomidine infusion. METHODS: We recorded polysomnography (PSG) for 24 h in mechanically ventilated patients sedated with dexmedetomidine. Dexmedetomidine (0.2-0.7 μg/kg/h) was administered intravenously to maintain the Richmond Agitation-Sedation Scale between -1 and -4 only during the nighttime (9:00 p.m. to 6:00 a.m.). During the daytime, we interrupted the sedatives and analgesics unless the patient complained of discomfort. When this occurred midazolam or opioids were administered intermittently. Sleep stages and the frequency of arousal/awakening during the nighttime were analyzed using Rechtschaffen and Kales criteria. RESULTS: For the ten mechanically ventilated adult patients recruited into the study, the median total sleep time (TST) during the night was 4.7 h (IQR, 4.2-8.1 h), and 78 % of sleep occurred during the night (median 78 %, IQR: 69-88 %). Sleep architecture was exclusively NREM sleep stage 1 (median 28.9 % of TST) and stage 2 (median 71.2 % of TST). Neither SWS (median 0 % of TST) nor rapid eye movement (REM) sleep (median 0 % of TST) was observed. Median frequency of arousals/awakenings was 9.3/h (IQR, 3-19.5/h). CONCLUSIONS: In mechanically ventilated patients, nighttime infusion of dexmedetomidine preserved the day-night cycle of sleep but induced severely disturbed sleep architecture without evidence of SWS or REM sleep.
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