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Asystole in 2 Pediatric Patients During Dexmedetomidine Infusion
Katrin Lichtsinn1, Ila Sehgal1, Alexandra Wilson2
1Pediatrics, 377659University of Texas at Austin Dell Medical School Program, Austin, TX, USA.
Insights
Dexmedetomidine infusions can rarely cause asystole in pediatric patients. Two cases of pediatric patients developed asystole, potentially due to increased vagal tone exacerbated by dexmedetomidine.
Area of Science:
- Pediatric Critical Care Medicine
- Pharmacology
- Cardiology
Background:
- Bradycardia is a known side effect of dexmedetomidine.
- Asystole is a rare but serious adverse event associated with dexmedetomidine infusions.
Purpose of the Study:
- To report two cases of pediatric patients who developed asystole during dexmedetomidine sedation.
- To explore potential mechanisms for dexmedetomidine-induced asystole in pediatric patients.
Main Methods:
- Case report of two pediatric patients receiving dexmedetomidine for sedation.
- Detailed clinical presentation, medication dosages, and cardiac monitoring data were reviewed.
- Echocardiograms were performed to assess cardiac function.
Main Results:
- Two pediatric patients developed asystole (one lasting 6 seconds, the other 15 seconds) while on dexmedetomidine infusions.
- Asystole resolved within hours of discontinuing dexmedetomidine in both cases.
- Neither patient had pre-existing cardiac conduction defects or was on medications known to potentiate dexmedetomidine's effects on heart rate.
Conclusions:
- Dexmedetomidine can be associated with rare but severe cardiac events like asystole in pediatric patients.
- Increased patient-related vagal tone may be a contributing factor, exacerbated by dexmedetomidine.
- Careful monitoring of cardiac rhythm is crucial in pediatric patients receiving dexmedetomidine.
Introduction:
Bradycardia is a known side effect of dexmedetomidine. Reports of sinus pauses or asystole, however, are rare. We present 2 cases of pediatric patients who developed asystole on a dexmedetomidine infusion.
Summary Of Cases:
An 8-week-old male with RSV bronchiolitis and acute hypoxemic respiratory failure was started on dexmedetomidine for sedation at 0.2 mcg/kg/h with a maximum dose of 0.7mcg/kg/h. On Hospital day (HD) 4, on dexmedetomidine at 0.7 mcg/kg/h, he developed intermittent episodes of bradycardia with heart rates in the 60 s. Echocardiogram on HD 6 showed normal function. On HD 7, he began having periods of asystole lasting up to 6 seconds. Dexmedetomidine was discontinued, with the resolution of episodes of asystole after 6 hours. A 27-month-old male with a congenital left diaphragmatic hernia and pulmonary hypertension who had been weaned off sildenafil 6 months earlier underwent re-repair of left diaphragmatic hernia. Postoperatively he remained intubated and paralyzed. Dexmedetomidine was started at 0.3 mcg/kg/h for sedation, with a maximum dose of 1.2 mcg/kg/h. An echocardiogram on HD 3 showed good function with mild to moderate pulmonary hypertension. That evening, with dexmedetomidine at 1.1 mcg/kg/h, he developed a 15 second period of asystole requiring CPR. Dexmedetomidine was discontinued, and he was started on a midazolam infusion with no further episodes.
Discussion:
Both cases occurred in patients without cardiac conduction defects or on negative chronotropic or sympatholytic medications that have been associated with dexmedetomidine-induced asystole. We hypothesize that both episodes of asystole were due to increased patient-related vagal tone exacerbated by dexmedetomidine.
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