Journal: Anesth Analg 106(1):79-83, 2008
Reprint: Dept of Anesthesia, Stanford University Medical Center, 300 Pasteur Drive, Stanford, CA 94305-5640 (GB Hammer, MD)
Faculty Disclosure: Abstracted by L. Easley, who has nothing to disclose.
Dexmedetomidine (DEX) is a highly selective α2-adrenergic agonist that is approved by the Food and Drug Administration for short-term sedation in adult patients in the intensive care unit. It is not approved for use in children; however, the use of DEX in infants and children for sedation and analgesia in the pediatric intensive care unit has been reported. It is unknown whether the cardiac effects of DEX are related strictly to interaction with α2A-adrenergic receptors in the central nervous system (CNS) and α2B-adrenergic receptors in the peripheral vascu¬lature, or whether direct interaction with α2-adrenergic receptors in the heart may play a role.
The aim of this study was to characterize the effects of DEX on cardiac conduction in children. Included in this study were 12 patients, 5-17 years of age, median age 13 yr, median weight 59.5 kg, scheduled for a cardiac electrophysiology (EP) study and ablation under anesthesia for a diagnosis of supraventricular tachycardia (SVT). Patient monitor¬ing included electrocardiogram (ECG), noninvasive mean arterial pressure (MAP), skin temperature, pulse oximetry, and capnography. After a 30-min observation period to ensure the success of the ablation and to allow offset of the isoproterenol, baseline EP data were recorded.
After recording of baseline EP data, DEX 1 µg/kg IV was administered over 10 min, followed by a con¬tinuous infusion at a dose of 0.7 µg/kg/hr for 10 min. The EP study was terminated upon completion of the monitoring and data collection period. Seven of the 12 patients received isoproterenol during the EP study. A significant increase in MAP was seen compared with baseline at 10 min but not at 20 min during administration of DEX. This was accom¬panied by a significant decrease in HR compared with baseline at 10 min but not at 20 min. Respiratory rate and end-tidal carbon dioxide (ETCO2) did not change with administration of DEX. Sinus node function was significantly depressed after administra¬tion of DEX. Atrioventricular (AV) nodal function also showed depression after administration of DEX.
The study found that DEX significantly depressed sinus and AV nodal function in pediatric patients. Sinus node recovery times and baseline sinus cycle lengths, which are markers of sinus nodal function, were both prolonged with administration of DEX. No patient developed clinically significant bradycardia during this study. The incidence of bradycardia associated with the administration of DEX in infants and children is unknown. The respiratory rate and ETCO2 did not change during the administration of DEX.
The authors recommend that DEX not be used to provide sedation for EP studies, as the effects that were observed in this study are likely to cause undesired and misleading measurements of cardiac conduction and might also interfere with the inducibility of some tachycardias. DEX should be used with caution in patients at risk for bradycardia and/or AV nodal dysfunction due to associated comorbidities. |
