Electroconvulsive therapy-induced asystole: Occurrence after 39 previous uneventful treatments

Abstract

Hormis l 'article de Sia et coll.,4 Electroconvulsive therapy-induced asystole: occurrence after 39 previous uneventful treatmentsTo the Editor: Asystole (defined as an absence of heartbeat for five or more seconds) is an unusual but increasingly recognized complication of electroconvulsive therapy (ECT) in older patients. 1,2 We recently provided care for a 73-yr-old man with major depression including psychotic and catatonic features who was admitted for outpatient ECT. The patient had undergone a series of 39 previous uncomplicated ECTs under general anesthesia over the previous six months, and had experienced an excellent clinical response. The patient was treated with maintenance ECT on a weekly basis, and also received chronic oral venlafaxine (300 mg·day -1 in divided doses) and aripiprazole (30 mg·day -1 in divided doses) therapy. Sodium thiopental (dose range of 1.5 to 2 mg·kg -1 ) and succinylcholine (1 to 1.5 mg·kg -1 ) were used for anesthesia, and labetalol (10 to 20 mg) or esmolol (50 to 100 mg) were used to control sympathetic nervous system stimulation during most of the previous treatments. The patient also had a past history of coronary artery disease, poorly controlled essential hypertension, and hyperlipidemia treated with oral enteric aspirin (325 mg·day -1 ), clopidogrel (75 mg·day -1 ), isosorbide mononitrate (30 mg·day -1 ), lisinopril (20 mg·day -1 ), and simvastatin (80 mg·day -1 ). A preoperative electrocardiogram indicated normal sinus rhythm with occasional premature ventricular contractions, voltage criteria for left ventricular hypertrophy, and nonspecific T wave abnormalities. These findings were stable, and no conduction abnormalities were present. The serum potassium concentration was 4.4 mEq·L -1 . The remainder of the laboratory analysis was normal.In anticipation of a hyperdynamic cardiovascular response to ECT, preoperative hypertension was treated with labetalol (20 mg iv in divided doses). Anesthesia was induced using sodium thiopental 2 mg·kg -1 iv and succinylcholine 1 mg·kg -1 iv after placement of transcutaneous bilateral cranial electrodes. An oral airway was placed, positive pressure ventilation by mask was begun using 100% oxygen, and ECT was induced (95% energy; total delivered charge of 479 mCoulomb; total seizure duration of 35 sec). Asystole was noted on the continuous electrocardiogram concomitant with the loss of the pulse oximetry and capnography signals immediately after the onset of the electrical stimulus. Radial and carotid arterial pulses were absent, chest compressions were initiated, and atropine (0.6 mg iv) was administered. Ventricular bigeminy was observed almost immediately after chest compressions were begun, lidocaine 100 mg iv was administered, and normal sinus rhythm was restored. The asystole was approximately ten seconds in duration. Arterial blood gas analysis and serum electrolyte concentrations obtained after the episode were normal. The patient emerged from anesthesia without difficulty and was drowsy but easily aroused during the first ...

Asystole During Electroconvulsive Therapy

“…Nine case reports describing 10 cases of asystole were initially included in this review 11,21–25,27–30 . However, 3 of the case reports described postictal asystole instead of asystole occurring during or right after application of the electrical stimulus.…”

“…Nine case reports describing 10 cases of asystole were initially included in this review. 11,[21][22][23][24][25][27][28][29][30] However, 3 of the case reports described postictal asystole instead of asystole occurring during or right after application of the electrical stimulus. The retrospective study and cohort studies included in this review did not describe postictal asystole.…”

Severe bradycardia at the termination of seizure during electroconvulsive therapy

“…Some cases of asystole or severe bradycardia during ECT have been reported [6][7][8][9][10]. In most of these case reports, asystole or severe bradycardia was observed immediately after electrical stimulation in the first phase of parasympathetic nerve system activity.…”

“…That report suggested that asystole or severe bradycardia could occur after seizure termination in the third phase, with a dominance of parasympathetic activity [5]. However, most reports have only described asystole or severe bradycardia immediately after electrical stimulation in the first phase of parasympathetic dominance [6][7][8][9][10]. To date, there have been few reports of asystole after seizure termination in the third phase of parasympathetic dominance during ECT [11][12][13].…”