BACKGROUND: This study was designed to evaluate the effect of dexmedetomidine on the acute hyperdynamic response, duration of seizure activity and recovery times in patients undergoing electroconvulsive therapy (ECT). METHODS:Fourteen patients underwent a total of 84ECT sessions as a crossover design. Patients were randomly allocated to receive either dexmedetomidine (1 mug/kg IV over a period of 10 min) or saline (control). Anaesthesia was induced with propofol 1 mg/kg, and then succinylcholine 0.5 mg/kg IV was administered. Arterial blood pressure and heart rate (HR) were recorded during the study period. RESULTS: HR in the dexmedetomidine group was lower than that in the control group at 5 and 10 min after the start of study drug infusion, and at 1, 3 and 10 min after the seizure ended (P<0.05). Peak HR was lower in the dexmedetomidine group compared with that in the control group (P<0.05). The mean arterial pressure (MAP) values in the dexmedetomidine group were lower at 0, 1, 3 and 10 min after the seizure ended compared with the control group (P<0.05). Both motor and electroencephalography (EEG) seizure duration in the control group (35.65 +/- 14.89 and 49.07 +/- 9.94 s, respectively) were similar to that in the dexmedetomidine group (33.30 +/- 12.01 and 45.15 +/- 17.79 s, respectively) (P>0.05). Time to spontaneous breathing, eye opening and obeying commands were not different between the groups. CONCLUSION: A dexmedetomidine dose of 1 mug/kg IV administered over 10 min before the induction of anaesthesia with propofol may be useful in preventing the acute hyperdynamic responses to ECT without altering the duration of seizure activity and recovery time.
RCT Entities:
BACKGROUND: This study was designed to evaluate the effect of dexmedetomidine on the acute hyperdynamic response, duration of seizure activity and recovery times in patients undergoing electroconvulsive therapy (ECT). METHODS: Fourteen patients underwent a total of 84 ECT sessions as a crossover design. Patients were randomly allocated to receive either dexmedetomidine (1 mug/kg IV over a period of 10 min) or saline (control). Anaesthesia was induced with propofol 1 mg/kg, and then succinylcholine 0.5 mg/kg IV was administered. Arterial blood pressure and heart rate (HR) were recorded during the study period. RESULTS: HR in the dexmedetomidine group was lower than that in the control group at 5 and 10 min after the start of study drug infusion, and at 1, 3 and 10 min after the seizure ended (P<0.05). Peak HR was lower in the dexmedetomidine group compared with that in the control group (P<0.05). The mean arterial pressure (MAP) values in the dexmedetomidine group were lower at 0, 1, 3 and 10 min after the seizure ended compared with the control group (P<0.05). Both motor and electroencephalography (EEG) seizure duration in the control group (35.65 +/- 14.89 and 49.07 +/- 9.94 s, respectively) were similar to that in the dexmedetomidine group (33.30 +/- 12.01 and 45.15 +/- 17.79 s, respectively) (P>0.05). Time to spontaneous breathing, eye opening and obeying commands were not different between the groups. CONCLUSION: A dexmedetomidine dose of 1 mug/kg IV administered over 10 min before the induction of anaesthesia with propofol may be useful in preventing the acute hyperdynamic responses to ECT without altering the duration of seizure activity and recovery time.