Atrioventricular block carbamazepine

Cardiac dysrhythmias induced by anticonvulsants are rare and occur mainly in patients other than those known to be at high risk of sudden death (14). Phenytoin has been rarely associated with bradydysrhythmias, almost exclusively after intravenous dosing, and some of these have been fatal. Hypotension can also complicate intravenous phenytoin. Carbamazepine can depress cardiac conduction, mostly in elderly or otherwise predisposed patients. Third-degree atrioventricular block occurred in one patient with pre-existing right bnndle branch block treated with topiramate, but a cause-and-effect relation was uncertain (SEDA-21, 76). 

Carbamazepine can depress the cardiac conducting system (SEDA-16, 71). There have been a few reports of reversible atrioventricular block (SED-12,130) (2-4), and asystole has been described in a patient with GuiUam-Barre syndrome (SEDA-18, 62). 

Three cases of carbamazepine-induced Stokes-Adams attacks caused by intermittent total atrioventricular block, sinoatrial block with functional escape rhythm, and intermittent asystole have been described it was suggested that cardiac conduction should be assessed if syncope or changes in seizure tjrpe occur in patients taking carbamazepine (5). 

Four additional cases of carbamazepine-induced sinus node dysfunction (n = 3) and atrioventricular block (n = 1) were described in elderly Japanese women taking 200-600 mg/day. In two of the three patients rechallenged, sinus arrest recurred within 48 hours (8). 

Takayanagi K, Hisauchi I, Watanabe J, Maekawa Y, Fujito T, Sakai Y, Hoshi K, Kase M, Nishimura N, Inoue T, Hayashi T, Morooka S. Carbamazepine-induced sinus node dysfunction and atrioventricular block in elderly women. Jpn Heart J 1998 39(4) 469-79. 

Carbamazepine is the antiepileptic drug that is most often associated with cardiac dysrhythmias. Soon after it was marketed it was observed that it not only had antidysrhythmic properties but might also be dysrhythmogenic in some subjects [16" ], with reports of sinus bradydysrhythmias [17 ] and atrioventricular block [18, 19, 20, 21, 22, 23 ]. 

Morooka S. Carbamazepine-induced sinus node dysfunction and atrioventricular block in elderly women. Jpn Heart J 1998 39(4) 469-79. 

Kumada T, Hattori H, Doi H, Shiraishi K, Yamanaka Y, Kato T, Nakahata T. Postoperative complete atrioventricular block induced by carbamazepine in a patient with congenital heart disease. No To Hat-tatsu 2005 37(3) 257-61. 

Ide A, Kamijo Y. Intermittent complete atrioventricular block after long term low-dose carbamazepine therapy with a serum concentration less than the therapeutic level. Intern Med 2007 46(9) 627-9. 

Carbamazepine toxicity is manifested by drowsiness, nausea and vomiting, gait disturbance, nystagmus, confusion, neuromuscular excitability, and seizures (Menkes, 1999). Overdose with CBZ can be lethal (Arana et ah, 1986). In a retrospective study of 307 intoxicated patients, 41 (13%) had a fatal outcome (Schmidt and Schmitz-Buhl, 1995). Doses exceeding 24 g were important indicators of fatality. The management of CBZ overdose is primarily supportive, to prevent potential atrioventricular (AV) block (Arana et ah, 1986), possible respiratory depression (Schmidt and Schmitz-Buhl, 1995), stupor, and coma. 

A. Ataxia, nystagmus, ophthalmoplegia, movement disorders (dyskinesia, dystonia), mydriasis, and sinus tachycardia are common with mild to moderate overdose. With more serious intoxication, myoclonus, seizures (including status epilepticus), hyperthermia, coma, and respiratory arrest may occur. Atrioventricular (AV) block and bradycardia have been reported, particularly in the elderly. Based on Its structure similarity to tricyclic antidepressants, carbamazepine may cause QRS and QT interval prolongation and myocardial depression however, in case reports of overdose, QRS widening rarely exceeds 100-120 msec and Is usually transient. 

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