Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs.

To assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia. Prospective, randomized, crossover experimental trial. A total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation). Dogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg–1 minute–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg–1 minute–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05). When administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments. Lidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs. [ABSTRACT FROM AUTHOR]