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Dexmedetomidine-related atrial standstill and loss of capture in a pediatric patient after congenital heart surgery.

OBJECTIVE: Dexmedetomidine (DEX; Precedex) is an alpha-2 adrenergic receptor agonist that produces anxiolysis and sleep-like sedation without narcosis or respiratory depression and has relatively few cardiovascular side effects. Given its favorable sedative properties combined with its limited effects on hemodynamic and respiratory function, it is widely used in pediatric intensive care and anesthesia settings.

DESIGN: Case report.

SETTING: Pediatric intensive care unit.

PATIENT: A three-yr-old girl was admitted after mitral valve replacement for persistent severe mitral insufficiency. Her prior history was significant for tetralogy of Fallot which was repaired at nine months of age. A year later the patient developed mitral and tricuspid valve insufficiency and subsequently underwent mitral and tricuspid valve repair, pulmonary valve replacement, and a maze procedure (the latter was performed for persistent atrial flutter). Following that operation she developed sinus node dysfunction and had a permanent epicardial dual-chamber pacemaker implanted. Due to remaining severe mitral insufficiency the patient had increasing pulmonary symptoms, necessitating the most recent surgery to replace her mitral valve.

INTERVENTIONS: On postoperative day two the patient was hemodynamically stable and weaning off mechanical ventilation. Tracheal extubation was anticipated to occur within the next 24 hrs. A DEX infusion of 0.6 mcg/kg/hr was initiated. A pacemaker interrogation performed on postoperative day three, 21 hrs after the initiation of DEX, revealed unsuccessful atrial capture.

MEASUREMENTS AND MAIN RESULTS: Dexmedetomidine was subsequently discontinued and the patient's pacemaker was reinterrogated. The interrogation findings were similar to those seen prior to the initiation of DEX.

CONCLUSION: As a result of these findings, caution is warranted in the administration of DEX to patients with predisposing conduction abnormalities and patients who are pacemaker-dependent.

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