US EPA

3978579 

Journal Article 

Effects of low dose midazolam on bradycardia and sedation during dexmedetomidine infusion 

Bang, YunSic; So, E; Kim, S; Chun, DukHee 

2016 

Yes 

International Journal of Clinical and Experimental Medicine
ISSN: 1940-5901 

9 

6 

11838-11844 

WOS:000379157300129 

Dexmedetomidine is a sedative which does not cause respiratory depression. But the initial loading dose of dexmedetomidine can lead to bradycardia which requires intervention. We tried to evaluate the effect of low dose midazolam on bradycardia and sedation during dexmedetomidine infusion. 72 patients were randomly assigned to the Dex 1.0 group or Dex 0.5 group. After intrathecal anesthesia, the Dex 1.0 group received an initial loading dose of 1.0 mu g/kg of dexmedetomidine. The Dex 0.5 group was given midazolam 0.025 mg/kg and 0.5 mu g/kg of dexmedetomidine. Heart rate (HR), blood pressure, respiratory rate, bispectral index (BIS), and the Observer's Assessment of Alertness/Sedation Scale (OAA/S) were recorded at ten time points (baseline, after anesthesia, before dexmedetomidine administration, 5, 10, 15, 20, 40, 60, 80 min after dexmedetomidine administration). The incidence of bradycardia requiring atropine was significantly higher in the Dex 1.0 group than in the Dex 0.5 group (15/33 vs. 5/32, P = 0.009). The Dex 0.5 group had a significantly lower BIS and OAA/S score than the Dex 1.0 group (P = 0.002 and P = 0.000, respectively) 5 min after dexmedetomidine administration. HR was significantly lower in the Dex 1.0 group (P = 0.003) 10 min after dexmedetomidine administration. But BIS and OAA/S score were lower in the Dex 0.5 group (P = 0.034 and P = 0.001, respectively). Other hemodynamic variables at other time points were similar between two groups. Low dose midazolam with halved loading dose of dexmedetomidine was superior in terms of bradycardia and sedation than dexmedetomidine alone. 

Dexmedetomidine; bradycardia; midazolam