Severe Bradycardia After Anesthesia Before Electroconvulsive Therapy Tom K. Birkenha ¨ger, MD, PhD,* Esther M. Pluijms, MD,* Theo H. Groenland, MDÞ and Walter W. van den Broek, MD, PhD* Abstract: Postanesthesia bradycardia or asystole before electrocon- vulsive therapy (ECT) occurs very infrequently but is a potentially fatal complication of pre-ECT anesthesia. The optimal strategy for the pre- vention of its recurrence is unclear because the use of premedication with atropine may not always be successful. In this article, we present the case of a 21-year-old man with schizophrenia who developed bradycardia directly after receiving succinylcholine during the first 3 ECT sessions. Replacing succinylcholine with mivacurium seemed to be a successful strategy in preventing bradycardia during the final 9 ECT sessions. Key Words: electroconvulsive therapy, complications, bradycardia, succinylcholine (J ECT 2010;26: 53Y54) P oststimulus bradycardia and asystole during electrocon- vulsive therapy (ECT) are regularly reported. 1 Poststimulus bradycardia has been explained by both an increase in vagal tone due to stimulation of the hypothalamus and the Valsalva process of forced expiration against a closed glottis during the stimulus. 2 Postictal bradycardia and asystole occur directly after tachy- cardiac seizure ceases. Atropine is very effective in both treat- ment and prevention of poststimulus bradycardia. In contrast to postictal bradycardia, postanesthesia brady- cardia or asystole before ECT seems to occur very infrequently. To our knowledge, it has been reported only twice. 3,4 The patient we describe showed bradycardia directly after receiving succinylcholine and before ECT. A complicating fac- tor is the use of 400 mg of clozapine as concomitant medication. CASE REPORT This patient is a 21-year-old man, hospitalized with a diagnosis of schizophrenia and cannabis abuse. He had been experiencing auditory hallucinations for 18 months before ad- mission and was convinced that microphones had been placed in the plants at his home. He received treatment with 2 mg of risperidone as an outpatient, with initial favorable response. Four weeks before admission, the patient stopped taking risperidone. Subsequently, the auditory hallucinations reappeared, and he behaved violently toward his mother. He was admitted to the psychosis unit of the department of psychiatry at the Erasmus Medical Centre. Treatment with 5 mg of haloperidol daily was given during 4 weeks but without effect on the psychotic symptoms. He was switched to treatment with 600 mg of quetiapine, which was continued for an additional 4 weeks, again without response. Subsequently, quetiapine was switched to 400 mg of clozapine. After treatment with clozapine for 4 weeks, the patient showed only minimal improvement and still experienced auditory hallucinations and paranoid delusions. The patient agreed to a trial of inpatient ECT. Clozapine at 400 mg was continued during the ECT course. His medical history was unremarkable. The result of a pre-ECT physical examination was completely normal. Laboratory tests results including com- plete blood cell count; serum electrolyte, serum urea nitrogen, creatinine, and thyrotropin levels; and an electrocardiogram showed no abnormalities. At the time of his first treatment, he was taking 400 mg of clozapine. During the ECT course, the plasma level of clozapine varied between 240 and 300 Kg/L. Anesthesia consisted of intravenous (IV) administrations of metoclopramine at 10 mg, glycopyrrolate at 0.2 mg, alfentanil at 0.5 mg, etomidate at 16 mg, and succinylcholine at 90 mg. Preinduction vital signs were normal. The ECG indicated a sinus rhythm with a heart rate of 92 beats per minute (bpm), blood pressure was 125/85 mm Hg, and oxygen saturation was 100%. About 15 seconds after receiving succinylcholine, the patient developed severe bradycardia (30 bpm), which normalized to 76 bpm after the administration of IV atropine at 0.5 mg. The patient received ECT without further complications. During both the second and third ECT sessions, the patient again developed severe bradycardia after receiving 90 mg of IV succinylcholine. From the fourth ECT until the end of the ECT course, succinylcholine was replaced with 12 mg of mivacurium as muscle relaxant. The doses of the remaining anesthetic drugs remained unchanged. Except for the third and fourth sessions, there was no need for administration of atropine. The patient received 9 additional treatments during which post- anesthesia bradycardia did not occur again. The ECT added to clozapine led to a remarkable improvement of psychosis; all positive symptoms disappeared, and only some of the negative symptoms remained. DISCUSSION Postanesthesia bradycardia has been reported very infre- quently. 3,4 McCall 3 described a 45-year-old man who showed tachycardia after the infusion of 60 mg of methohexital, whereas the infusion of 100 mg of succinylcholine led to bradycardia (30 bpm) in the 13th session and to a 10-second asystole in the following session. Four additional uncomplicated ECT sessions were given after 0.8 mg of IV atropine was prescribed as standard pre- medication. Russ and Bailine 4 described a 44-year-old woman who developed a 6-second asystole within 30 seconds after receiving 80 mg of IV succinylcholine in her first treatment session. The asystole was followed by bradycardia (30 bpm), which reverted to sinus rhythm after 0.5 mg of IV atropine was given. In their patient, because IV atropine premedication did not CASE REPORT Journal of ECT & Volume 26, Number 1, March 2010 www.ectjournal.com 53 From the Departments of *Psychiatry, and †Anaesthesiology, Erasmus Medical Centre, Rotterdam, The Netherlands. Received for publication May 5, 2009; accepted May 6, 2009. Reprints: Tom K. Birkenha ¨ger, MD, PhD, Department of Psychiatry, Erasmus Medical Centre, PO Box 2040, 3000 CA, Rotterdam, the Netherlands (e-mail: t.birkenhager@erasmusmc.nl). Copyright * 2010 by Lippincott Williams & Wilkins Copyright @ 20 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 10