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 Table of Contents    
Year : 2020  |  Volume : 62  |  Issue : 2  |  Page : 222-224
Recurrent ventricular tachycardia during the electroconvulsive therapy procedure: A case report

Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India

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Date of Submission14-Jul-2019
Date of Acceptance05-Oct-2019
Date of Web Publication17-Mar-2020

How to cite this article:
Grover S, Aggarwal S. Recurrent ventricular tachycardia during the electroconvulsive therapy procedure: A case report. Indian J Psychiatry 2020;62:222-4

How to cite this URL:
Grover S, Aggarwal S. Recurrent ventricular tachycardia during the electroconvulsive therapy procedure: A case report. Indian J Psychiatry [serial online] 2020 [cited 2020 Mar 29];62:222-4. Available from:

Electroconvulsive therapy (ECT) is one of the lifesaving treatments for patients with various severe mental disorders.[1] The initial cardiovascular response to the electrical stimulus includes initial parasympathetic upsurge, lasting for 10–15 s, during which the patient is observed to have bradycardia, hypotension, and transient asystole. This is followed by a sympathetic upsurge, which peaks at 3–5 min after the electrical stimulation, during which patients may have increased blood pressure (BP), tachycardia, and cardiac arrhythmias.[2],[3],[4] Occasional patients also develop sinus arrhythmias, atrial and ventricular premature beats, and minor ST-T changes during the postimmediate postelectrical stimulation.[3] Sustained ventricular tachycardia (VT) is rarely reported during the ECT procedure, and the literature is limited to few case reports.[5],[6],[7],[8] Here, we report a 24-year-old female patient who had VT after three consecutive ECTs.

A 24-year-old female suffering from paranoid schizophrenia since the age of 20 years presented to inpatient unit following a suicidal attempt. Her mental state examination revealed the presence of delusion of reference and delusion of persecution, auditory and somatic hallucinations, made act and thought broadcast. The patient also reported that she made suicide attempt under the influence of commanding auditory hallucinations. In the inpatient unit, she was initially treated with risperidone up to 5 mg/day for 6 weeks, but she showed minimal improvement in psychotic symptoms. While on risperidone, she showed emergence of depressive symptoms and worsening in the intensity of commanding hallucination, asking her to harm herself. Following this, ECT was considered. Her pre-ECT evaluation did not reveal any abnormality in the hemogram, serum electrolytes, liver function test, renal function test, electrocardiogram (ECG), and X-ray chest posterior–anterior view. Her ECG showed a heart rate of 70 beats/min (BPM), which was regular, and there was no evidence of any arrhythmia. Routine monitoring of BP during the week before ECT showed readings of systolic BP to vary from 110 to 124 mmHg and diastolic BP to vary from 76 to 84 mmHg. During the first ECT, she was getting the same dose of risperidone, and no new medication was added. She was given ECT, with atropine as a premedication and thiopentone and succinylcholine as the inducing agents. Immediately, after the first ECT (receiving the electrical stimulus), her heart rate decreased to 48 BPM, and she required treatment with injection atropine 0.6 mg i/v. With this, her heart rate improved, but the patient developed monomorphic VT with hypotension (BP = 60/40 mmHg), which resolved spontaneously in 30 s, without any intervention. At this point, the possibility of atropine-induced VT was considered. Her heart rate and BP were monitored for the next 3 days, which did not reveal any abnormality. Following this, she was considered for second ECT during which atropine was avoided as the premedication. However, immediately after receiving the electrical stimulus, this time, she again developed monomorphic VT, heart rate going up to 150 BPM, and her BP was recorded as 90/60 mmHg. She was immediately administered injection lignocaine 90 mg (1.5 mg/kg body weight), with which the VT resolved. She achieved sinus rhythm with heart rate of 86 BPM and her BP normalized to 110/70 mmHg. She was subjected to detailed cardiology evaluation. Her trop-I levels were found to be negative, and her creatine kinase (MB) levels were within the normal limits. Her echocardiographic evaluation revealed ejection fraction of 55% with no evidence of any regurgitation and embolism. Monitoring of her rhythm using 12-lead Holter showed a minimum heart rate of 74 BPM and a maximum rate of 119 BPM with no evidence of paroxysmal supraventricular tachycardia, supraventricular tachycardia, supraventricular premature beats, or any evidence of significant sinus pauses. All her blood investigations including the serum electrolytes did not reveal any abnormality. She was also evaluated for all the possible reversible causes of VT such as hypovolemia, hypoxia, acidosis, hypokalemia, hyperkalemia, hypoglycemia, hypothermia, toxins, cardiac tamponade, tension pneumothorax, and pulmonary and coronary thrombosis, all of which were found to be negative. At this point, possibility of ECT/risperidone-induced VT was considered, and tablet risperidone was decreased to 3 mg/day. She maintained well without cardiac complications for the next 4–5 days. In view of the continuing psychopathology, including depressive symptoms and suicidality, she was considered for the third ECT, after obtaining high-risk consent. However, she again developed VT (heart rate: 180 BPM; BP = 90/60 mmHg), immediately after the administration of electrical stimulus, which was managed with injection amiodarone 150 mg. This time, VT did not resolve for the next 4 min, following which she was managed with cardioversion with 150 Joules, which was repeated twice, with which she achieved sinus rhythm (heart rate: 78/min; BP = 100/70 mmHg). After this, the VT was attributed to ECT, and ECT was stopped. Later, she was managed with clozapine, with which she showed significant improvement and has been maintaining well for 3 years, without any cardiac complications.

Persistent VT has been rarely reported with the ECT procedure. In fact, in view of this rarity, initially, possibility of ECT-associated VT was not considered in the index case. A review of available literature revealed existence of only four case reports, which have reported similar association.[5],[6],[7],[8] Of these, in three cases, there was no past or current medical history of cardiac illness, as seen in the index case.[6],[7],[8] Detailed cardiac evaluation in these cases also did not reveal any abnormality, as in the index case.[5],[6],[7],[8] One of the reported cases had a history of ischemia, and the patient was on quinidine and digoxin at the time of receiving ECT.[8] Of the four reported cases, two cases required the use of chest compression,[5],[8] one patient had spontaneous resolution of VT,[7] and one patient was managed with cardiac massage and midazolam.[6]

Index case developed VT thrice, every time temporally related to the electrical stimulus, with no evidence of VT before, after, and during the intervening periods between the ECTs. Further, efforts were made to remove the probable offending medications during the ECT, and patients did not have any VT during the intervening period between the three ECTs, with the continuation of the same medication. All these provide further credence to this association in the index case. In the index case, VT always required interventions.

To conclude, the present case report suggests that sustained VT is a rare side effect of ECT. Accordingly, whenever a patient receiving ECT develops VT, a possibility of ECT-associated VT must be considered.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

American Psychiatric Association. Task Force on Electroconvulsive Therapy. The practice of ECT: Recommendations for treatment, training and privileging. Convuls Ther 1990;6:85-120.  Back to cited text no. 1
Welch CA, Drop LJ. Cardiovascular effects of ECT. Convuls Ther 1989;5:35-43.  Back to cited text no. 2
Chaudhary S, Rajuria SS. Effects of electroconvulsive therapy on cardiovascular system. Med J Armed Forces India 1995;51:31-3.  Back to cited text no. 3
Perrin GM. Cardiovascular aspects of electric shock therapy. Acta Psychiatr Scand Suppl 1961;36:1-45.  Back to cited text no. 4
Larsen JR, Hein L, Strömgren LS. Ventricular tachycardia with ECT. J ECT 1998;14:109-14.  Back to cited text no. 5
Heinz B, Lorenzo P, Markus R, Holger H, Beatrix R, Erich S, et al. Postictal ventricular tachycardia after electroconvulsive therapy treatment associated with a lithium-duloxetine combination. J ECT 2013;29:e33-5.  Back to cited text no. 6
Urabe K, Koguchi T, Ishikawa K, Sato H, Shinohara M, Okuda Y, et al. A case of ventricular tachycardia immediately after electroconvulsive therapy in a schinzophrenic patient. Masui 2001;50:50-2.  Back to cited text no. 7
Koga Y, Mishima Y, Momozaki M, Hiraki T, Ushijima K. A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient. J Anesth 2011;25:595-8.  Back to cited text no. 8

Correspondence Address:
Sandeep Grover
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/psychiatry.IndianJPsychiatry_412_19

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