Bradycardia pediatric

Clonidine is one of the most widely used sedating medications in pediatric and child psychiatry practice, particularly in children with sleep onset delay and ADHD. It is a central alpha2 agonist. Pharmacokinetics show rapid absorption, with an onset action within 1 h, peak effects at 2-4 h and a half-life 6-24 h. Effects on sleep architecture are fairly minimal but may include decreased REM, so that discontinuation can lead to REM rebound. Clonidine has a narrow therapeutic index, and there has been a recent dramatic increase in reports of overdose with this medication. Potentially significant side effects including hypotension, bradycardia, anticholinergic effects, irritability, and dysphoria rebound hypertension may occur on abrupt discontinuation. Tolerance often develops, necessitating increases in dose. 

Nahum E, Reish O, Naor N, Merlob P. Ranitidine-induced bradycardia in a neonate—a first report. Eur J Pediatr 1993 152(ll) 933-4. 

Little experience exists to define a minimum toxic dose. Most of the reported cases have been in the pediatric population amounts ingested in overdoses substantially larger than adult therapeutic doses have not resulted in fatalities. Manifestations of toxicity may include hypertension and tachycardia followed by hypotension and bradycardia. Ataxia, drowsiness, lethargy, or coma may be noted. Pupils may be pinpoint and not reactive to light. Diarrhea may occur. Extrapyramidal symptoms and cardiac dysrhythmias have been documented. 

Berkenbosch JW, Tobias JD. Development of bradycardia during sedation with dexmedetomidine in an infant concurrently receiving digoxin. Pediatr Crit Care Med (2003) 4, 203-5. 

Bradycardia and sinus arrest have been reported in young, healthy adults with high vagal tone and with large or rapid IV administration. Safety and efficacy have not been estabhshed in children under 18 years of age. Despite this, numerous trials have shown its use in pediatric patients. 

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