Electroconvulsive Therapy in a Patient with Left Main and Triple Vessel Coronary Artery Disease (CAD): Anaesthetic Management : Annals of Cardiac Anaesthesia

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Electroconvulsive Therapy in a Patient with Left Main and Triple Vessel Coronary Artery Disease (CAD)

Anaesthetic Management

Waikar, Hemant Digambar; Mendis, Nirosha1; Neema, Praveen Kumar2

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Annals of Cardiac Anaesthesia 26(1):p 102-104, Jan–Mar 2023. | DOI: 10.4103/aca.aca_144_21
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Electroconvulsive therapy (ECT) is a safe and effective treatment for many psychiatric disorders.[1] ECT is still widely used in the United States of America, Austria, Canada, Denmark, Netherlands, Germany, and India. It is indicated in selected patients with catatonia, major depressive disorders, bipolar disorders, schizophrenia, and other disorders like anxiety associated with depression. The passage of electrical current lead to hemodynamic alterations which may be detrimental to patients with severe coronary artery disease (CAD). We describe perioperative anesthetic management of a patient who had LMCAS with TVD.


A 64-yrs-old male patient with LMCAS with TVD was under psychiatric treatment for depression and anxiety disorder. He had no history of myocardial infarction; ejection fraction (EF) was 55%. He was advised of urgent coronary artery bypass graft surgery (CABG). He was on aspirin, clopidogrel, statins, ACE I, and bisoprolol. A psychiatric disorder was treated with Venlafaxine –XR (Serotonin-Norepinephrine receptor inhibitor), 37.5 mg nocte, Mirtazapine (antidepressant which blocks adrenergic and serotonin receptors) 15 mg nocte, and Risperidone (Atypical antipsychotic drugs used for treating schizophrenia & bipolar disorders) 1 mg nocte. His psychiatrist opined that the patient will not cooperate with major heart surgery and suggested a minimum of three sittings of ECT. His laboratory investigations were normal. The risk of severe heart failure, heart blocks, arrhythmias, and cardiac arrest was explained to relatives.

On the day of the procedure, emergency medications, temporary pacemaker (TPM), and Intra-Aortic Balloon Pump (IABP) were kept ready. He was premedicated with oral Diazepam 10 mg one hour before the procedure His heart rate was 74/minute, NIBP 130/80 mmHg, and SPO2 was 100%. Two peripheral venous access were secured; and after preoxygenation, Glycopyrrolate 0.2 mg, Tramadol 50 mg, etomidate 0.2 mg/kg followed by suxamethonium bromide 40 mg were administered, and ECT shock was delivered by Thymatron TM System IV (Dantecmedical, UK); seizure activity induced which lasted for 45 seconds. Bradycardia (50 bpm), and hypertension (NIBP 170/100) occurred but settled within 2-3 minutes. He woke-up in 5 min, and was monitored for 45 minutes. He received three sittings of ECT with increasing energy percentages of 25, 30, and 40%. His symptoms improved and scheduled for CABG later.


In 1934, the Hungarian neuropathologist Landilas Joseph von Meduna initiated the modern era of chemical convulsive therapy (CCT) by using intramuscular injection of camphor and Penthylenetetrazol to treat catatonic schizophrenia.[2] In 1938, Italian psychiatrist Lucio Bini and neurologist Vgo Carletti introduced the induction of generalized seizures by electrical stimulation. During ECT, an electrical current is applied transcutaneously to the brain via two electrodes positioned either bilaterally or unilaterally. Bilateral ECT is used more commonly when the speed of clinical recovery takes priority. Unilateral ECT is performed on the non-dominant hemisphere and has the advantage of less cognitive adverse effects; the aim is to induce generalized seizures. The optimum seizure duration remains unclear; too short (<10 s) or too long (>120 s) duration may reduce its clinical efficiency. ECT affects multiple central nervous system components, including hormones, neuropeptides, neurotrophic factors, and neurotransmitters.[3] Its efficiency is related to the “hyper-connectivity hypothesis”, where it is suggested that the patients with depression experience a localized increase in connectivity within the left dorsolateral prefrontal cortex. After ECT cognitive functions are affected; disorientation, impaired attention, and memory problems do occur in more than 50% of patients. Both retrograde and ante grade amnesia can occur but intelligence and judgment are spared. Initially, ECT was practiced without anesthesia and muscle relaxants resulting in musculoskeletal (fractures and dislocations) complications including fracture of vertebras in as many as 40% of patients. Tongue bite and dental damage are also possible and must be prevented by safety measures. Earlier, ECT was performed without anesthesia; since 1950, several refinements in anesthetic medications and muscle relaxants were introduced to increase the safety and acceptability of the procedure.[4] The main objective of anesthesia is to provide a rapid onset of unconsciousness and muscle relaxation for the duration of electrical stimulus with minimal physiological and physical side effects and emergence from both. Various anesthetic agents are used like methohexitol, thiopental, etomidate, ketamine, fentanyl, its analogs, and propofol. The duration of EEG and motor seizures are longest after etomidate and shortest after propofol. Moderate hyperventilation (20 breaths/minute with ETCO2 around 30 mmHg) can augment seizure duration. However, there is diminished drive to breathe, particularly in chronic obstructive pulmonary disease patients. Etomidate may reduce the seizure threshold. The seizure duration of propofol is shortest, this does not alter seizure quality and efficiency. Sevoflurane with proconvulsant and anticonvulsant properties at different doses may be an option but its use is uncommon; however, it should be avoided in patients with prolonged QT intervals as it may precipitate life threatening arrhythmias.[5] Muscle relaxation is achieved with suxamethonium chloride (0.25 mg/kg). A non-depolarizing relaxant may be indicated in patients with pseudocholinesterase deficiency, hyperkalemia, severe neuromuscular disease, osteoporosis, or a family history of malignant hyperthermia.

The ECT affects mainly the cardiovascular, cerebral systems, and skeletal muscles due to seizure activity. Electrical stimulus leads to intense parasympathetic discharge lasting for 10-15 s which may result in bradycardia, hypotension, and even asystole. This is followed by an intense sympathetic surge increasing arterial pressure by 30 to 40% and heart rate by 20 to 30% leading to increased myocardial oxygen consumption resulting in myocardial ischemia and infarction, particularly in patients with CAD. The maximum effect is seen at 3-5 minutes. The left ventricular systolic and diastolic function can remain depressed up to 6 hours. Cardiac rupture has also been reported. Patients with cardiac pacemakers and implantable cardioverter defibrillators can safely undergo ECT with due precautions.[6] It has also been used after a heart transplant.[7] The major issue is cardiac arrhythmias and QT Prolongation. ECT per se can cause an acute rise in QT interval leading to arrhythmias. All induction agents used for ECT prolong QT intervals.

In our case the psychiatrist decided to administer three sittings of ECT in spite of CAD; he believed; the patient would not cooperate in the postoperative period. Cardiovascular (arrhythmias and myocardial infarction), and pulmonary (laryngospasm and aspiration) are common causes of death and serious morbidity. Therefore, ECTs were given adequate monitoring and readiness of TPM, and IABP.

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Conflicts of interest

There are no conflicts of interest.


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2. Gazdag G, Ungvari GSAmerican Psychiatrist Association. The practice of electroconvulsive therapy: Recommendations for treatment, training and privilaging. A Task Force Report of the American Psychiatric Association. 20012nd ed American Psychiatric Publishing
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6. Dolenc TJ, Barnes RD, Hayes DL, Rasmussen KG. Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators Pacing Clin Electrophysol. 2004;27:1257–63
7. Fusar-Poli P, Picchioni M, Martinelli V, Bhattacharyya S, Cortesi M, Barale F, et al Anti-depressive therapies after heart transplantation J Heart Lung Transplant. 2006;25:785–93

Anti-psychotic therapy; bipolar disorder; coronary artery disease; electroconvulsive therapy

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