Electrocardiographic and electrophysiologic effects of dexmedetomidine on children

Dexmedetomidine (DEX) is a highly selective alpha-2-adrenergic agonist approved for short-term sedation and monitored anesthesia care in adults. Its effects on the electrocardiography and cardiac conduction tissue are not well described in the literature. Therefore, we aimed to characterize the electrocardiographic and electrophysiologic effects of DEX in children.

Twenty children (11 boys and nine girls) between the ages of eight and 17 undergoing electrophysiology study and ablation of the supraventricular tachycardia had hemodynamic and cardiac electrophysiologic variables measured before and during the administration of DEX (1 microgram/kg IV over 10 minutes followed by a 10-minute continuous infusion of 0.5 microgram/kg/h).

A significant decrease in heart rate was seen after the administration of DEX, but the systolic-diastolic-mean arterial pressure, respiratory rate, and end-tidal carbon dioxide did not change. Corrected sinus node recovery times and baseline sinus cycle lengths, which are markers of sinus nodal function, were both lengthened with the administration of DEX. Atrioventricular (AV) nodal function, as evidenced by the Wenckebach cycle length, the ventriculoatrial block cycle length, and AV nodal effective refractory periods, was lengthened significantly. We also found that DEX increased the atrial refractory period and diminished atrial excitability.

DEX significantly depressed sinus and AV nodal function in pediatric patients without significant electrocardiogram interval changes, other than a trend toward lower heart rates. Although no spontaneous AV nodal block and no clinically significant bradycardia were seen, we recommend that DEX be used with caution in patients at risk for bradycardia and/or AV nodal dysfunction due to its associated comorbidities.