P024: PUMP THE BRAKES: SEVERE BRADYCARDIA FOLLOWING LARGE BOLUSES OF DEXMEDETOMIDINE IN A YOUNG HEALTHY PATIENT
Shayla A McMahon, DO; Tyler Chonis, MD; Jackeline Porto, MD
HCA Kendall Hospital
Introduction: Dexmedetomidine is a selective α2-adrenergic agonist widely used in anesthesia for its sedative, analgesic, and sympatholytic properties. While commonly administered as a continuous infusion to mitigate hemodynamic side effects, intraoperative bolus dosing is frequently employed for rapid sedation. We present a case of profound bradycardia following multiple large boluses of Dexmedetomidine in a healthy adolescent, requiring pharmacologic intervention.
Methods: A 17-year-old male underwent general anesthesia for an elective procedure. To supplement anesthesia and prevent postoperative agitation, multiple large boluses of Dexmedetomidine were administered instead of the standard continuous infusion. Shortly after administration, the patient developed severe bradycardia, with a heart rate dropping to the low 30s. Initial treatment with glycopyrrolate was ineffective, necessitating the administration of atropine to restore an adequate heart rate.
Results: Following atropine administration, the patient’s heart rate gradually increased, and he remained hemodynamically stable for the remainder of the procedure. No further episodes of bradycardia were observed, and the patient had an uneventful emergence and recovery. This case highlights the potent sympatholytic effects of Dexmedetomidine and the risk of exaggerated vagal responses when administered in large boluses, particularly in young, healthy patients with high vagal tone.
Discussion/Conclusion: This case underscores the importance of cautious dosing strategies when using Dexmedetomidine intraoperatively. Dexmedetomidine acts on the alpha 2 adrenoceptors in the locus coeruleus in the brainstem, which leads to decreased sympathetic outflow. This leads to greater vagal activity which slows conduction through the SA node of the heart causing bradycardia. Dexmedetomidine may also have a direct depressant effect on the SA node. While bolus administration is common in clinical practice, it can lead to significant hemodynamic instability, particularly in young, healthy patients prone to exaggerated vagal responses. In younger and healthier individuals there is a higher baseline vagal tone making them more susceptible to profound bradycardia. Continuous infusion remains the safer approach for titration, minimizing the risk of profound bradycardia. Anesthesiologists should remain vigilant for severe bradycardia following Dexmedetomidine boluses and be prepared to intervene with appropriate pharmacologic agents if necessary. Pharmacologic agents to treat the bradycardia can include glycopyrrolate, atropine or even low doses of epinephrine in severe or persistent cases. This case serves as a reminder that even well-tolerated anesthetic adjuncts require thoughtful administration to balance efficacy with safety.