Dexmedetomidine‐Associated Bradycardia Progressing to Pulseless Electrical Activity: Case Report and Review of the Literature

Abstract

Dexmedetomidine is an alpha(2)-agonist indicated for sedation in critically ill patients and procedural sedation in nonintubated patients. It is a distinctive sedative because it does not cause respiratory depression, but it may cause hypotension and bradycardia. We describe a 74-year-old man who was receiving dexmedetomidine for agitation and experienced progressive bradycardia. The patient experienced a postoperative myocardial infarction 3 days after repair of an abdominal aortic aneurysm. A dexmedetomidine infusion was started at 0.11 microg/kg/hour, without a loading dose, for agitation; the patient's heart rate was 123 beats/minute and blood pressure was 147/70 mm Hg, both within normal limits. Over the next 6 hours, the dexmedetomidine infusion rate was increased to a maximum of 0.7 microg/kg/hour; the patient's heart rate progressively decreased to 21 beats/minute, followed by pulseless electrical activity. After 2 minutes of chest compressions and an intravenous bolus of atropine 0.4 mg, the patient regained a pulse. Dexmedetomidine was discontinued, and the patient's heart rate and blood pressure returned to within normal limits. The patient was discharged home 7 days later without any cardiac or neurologic sequelae. Clinicians need to be educated about the potential for dexmedetomidine to cause bradycardia progressing to pulseless electrical activity, and patients need to be closely monitored. Patients who receive dexmedetomidine and develop a greater than 30% decrease in heart rate may be at high risk for severe bradycardia leading to pulseless electrical activity. We urge caution when using dexmedetomidine, especially in patients with significant cardiac disease.

Effective dose of dexmedetomidine as an adjuvant sedative to peripheral nerve blockade in elderly patients

“…In previous studies applying single‐ or initial‐dose dexmedetomidine sedation in elderly patients, bradycardia and hypotension were the most common side‐effects, and occurred more frequently with dexmedetomidine doses exceeding 0.5 μg/kg 8, 18, 19, 20, 21. Although a previous study reported that maintenance doses of up to 10 μg/kg per hour were tolerated,27 without producing hypotension or bradycardia, when used as a total intravenous anesthetic agent in certain patients, there are other case reports in which the use of dexmedetomidine in elderly patients was associated with the occurrence of severe bradycardia or hypotension,27, 28 sometimes even progressing to asystole. In our study, none of the patients developed clinically significant hemodynamic disturbances requiring intervention.…”

Cardiac arrest after induction of anesthesia in neurosurgical patients

“…Другой группой препаратов, опасных в отно-шении асистолии в ходе операции, считаются цен-тральные α 2 -агонисты (клонидин и дексмедитоме-дин). В отношении последнего препарата есть до-статочно настораживающие публикации [33,34]. Наконец, нам встретилось в литературе сообщение об интраоперационной асистолии после введения во время операции цитостатика адриамицина [35].…”

Anestesia loco regional más sedación con dexmedetomidina para cirugía de Mohs con reconstrucción

“…Medicamentos como la dexmedetomidina han demostrado una adecuada respuesta clínica y baja tasa de complicaciones respiratorias, así como menor incidencia de delirium (10)(11)(12)(13)(14) A pesar de los beneficios de dexmedetomidina para sedación, también se ha asociado a eventos adversos graves como bradicardia severa, hipotensión e incluso, paro cardiaco (15)(16)(17). Su uso en diferentes procedimientos, asociados a diferentes modalidades de anestesia tambien se ha visto relacionado con episodios de bradicardia, que requieren de manejo con atropina para la prevención de complicaciones hemodinámicas mas severas (18,19).…”