BACKGROUND: We have examined the effect of dexmedetomidine, a selective alpha2-adrenoreceptor agonist, for controlling delirium in patients in the intensive care unit. METHODS: Intravenous infusion of dexmedetomidine (0.05-0.40 microg kg(-1) hr(-1)) was started at the onset of delirium, and its effect on sedation levels, circulation and respiration was examined in 111 patients. RESULTS: Nine patients were excluded from the study because of insufficient sedation and development of bradycardia requiring additional sedatives and discontinuance of dexmedetomidine infusion, respectively. The mean Ramsay score was 1.5 before starting dexmedetomidine (baseline), which was significantly increased to 3.2 4 hours after starting dexmedetomidine infusion (n=102). Heart rate and systolic arterial blood pressure significantly decreased 6 hours after starting dexmedetomidine compared with baseline. There were no differences in respiratory rate during infusion of dexmedetomidine. In 30 patients with hypoxemia (Pa(O2)/ Fi(O2) (P/F) ratio<300), respiratory rate, tidal volume, arterial blood gas data and P/F ratio were not affected by dexmedetomidine. CONCLUSIONS: Dexmedetomidine is effective for controlling delirium and provides sufficient sedation without respiratory adverse effects in patients in the intensive care unit. It is also effectively and safely used in patients with respiratory failure.
BACKGROUND: We have examined the effect of dexmedetomidine, a selective alpha2-adrenoreceptor agonist, for controlling delirium in patients in the intensive care unit. METHODS: Intravenous infusion of dexmedetomidine (0.05-0.40 microg kg(-1) hr(-1)) was started at the onset of delirium, and its effect on sedation levels, circulation and respiration was examined in 111 patients. RESULTS: Nine patients were excluded from the study because of insufficient sedation and development of bradycardia requiring additional sedatives and discontinuance of dexmedetomidine infusion, respectively. The mean Ramsay score was 1.5 before starting dexmedetomidine (baseline), which was significantly increased to 3.2 4 hours after starting dexmedetomidine infusion (n=102). Heart rate and systolic arterial blood pressure significantly decreased 6 hours after starting dexmedetomidine compared with baseline. There were no differences in respiratory rate during infusion of dexmedetomidine. In 30 patients with hypoxemia (Pa(O2)/ Fi(O2) (P/F) ratio<300), respiratory rate, tidal volume, arterial blood gas data and P/F ratio were not affected by dexmedetomidine. CONCLUSIONS:Dexmedetomidine is effective for controlling delirium and provides sufficient sedation without respiratory adverse effects in patients in the intensive care unit. It is also effectively and safely used in patients with respiratory failure.