Sir,Remifentanil, which is effective and easily titratable, with a rapid onset and offset of action, and no accumulation, is costeffective as it improves the quality of care, reduces the time spent on mechanical ventilation and reduces the length of stay in the Paediatric Intensive Care Unit (PICU). There have been reports, however, that remifentanil may cause hypotension in anesthetized children and decrease the cardiac index, mainly as a result of a fall in heart rate (1). In this communication, we report a sustained episode of severe bradycardia with suppressed myocardial depression after remifentanil infusion in a child during the weaning process. This is the first report of potentially life-threatening bradycardia after remifentanil infusion in a child.The patient, a 2-year-old boy, had been treated for 6 days in our PICU for a moderate closed head injury, was hemodynamically stable (cardiac frequency, >90 beats/min) and was receiving continuous midazolam and fentanyl infusions. Initial computed tomography (CT) scan showed mild brain edema and a small subdural hematoma; the intracranial pressure was kept below 15 mmHg and the cerebral perfusion pressure above 50 mmHg. After 5 days, the patient's clinical condition had improved significantly and the CT scan was normal. In order to facilitate rapid neurological assessment and to prepare the weaning process, the initial sedative/analgesic regimen was substituted with a continuous infusion of low-dose midazolam (0.1 mg/kg/h) and remifentanil (0.1 mg/kg/min). In less than 5 min, the patient's heart rate had decreased to 58 beats/min. Probable explanations, such as incorrect dilution or incorrect calculation of the infusion rate, were excluded and atropine 0.2 mg/kg was administered intravenously without an effect. The patient was normothermic and the electrocardiogram showed sinus bradycardia. An echocardiogram was performed revealing bradycardia with depressed shortening and ejection fractions (26 and 58%, respectively). Urgent magnetic resonance imaging did not show brain edema, hydrocephalus or any other expanding lesion. Although the arterial pressure remained stable at 96/46 mmHg, the heart rate decreased further to 42 beats/min. In view of the persistent bradycardia, a decision was made to discontinue remifentanil. Within 15 min, the heart rate had returned to its normal readings (more than 80 beats/min) and the myocardial contractility had improved. The patient was successfully extubated and, after uneventful neurological recovery, discharged to the ward.Remifentanil can cause bradycardia, either by parasympathetic activation or by other negative chronotropic effects. As parasympathetic inhibition by atropine does not totally prevent remifentanil's negative chronotropic effect, a direct negative chronotropic effect of remifentanil has been proposed (2). In accordance with this hypothesis, our patient developed severe bradycardia unresponsive to atropine after remifentanil infusion. Others have also reported severe bradycardia after remifentanil infusion in...