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Anesthetic Considerations in Electroconvulsive Therapy

Editor: Bryan Rondeau Updated: 8/5/2023 9:14:49 AM


Electroconvulsive therapy (ECT) is a treatment option for patients with pharmacotherapy-resistant depression, catatonia, bipolar disorder, and other psychiatric disorders, with depression being the most common reason for receiving this treatment.[1] 

First introduced in the 1930s, this procedure involves a patient undergoing general anesthesia and receiving an electrical stimulus to one or both brain hemispheres from an external device to induce a generalized seizure. Patients often see improvements in their mental health after these procedures.[2] The goal of anesthesia for ECTs is to provide hemodynamic stability, amnesia, and muscle relaxation to allow effective patient treatment.

Anatomy and Physiology

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Anatomy and Physiology

During ECT, a seizure is induced by an external electrical device while the patient is under general anesthesia. This results in a generalized tonic-clonic seizure with a duration that is variable. Seizures cause profound autonomic nervous system activity. First, the parasympathetic nervous system is activated, resulting in possible bradycardia and even asystole. The bradycardia is typically short-lived and followed by a sympathetic surge that causes hypertension and tachycardia. This sympathetic stimulation can last for anywhere from 5 to 10 min after the seizure has been induced.

The effect of a seizure causing a parasympathetic surge increases the risk of myocardial ischemia if the bradycardia is severe enough for too long. Glycopyrrolate, an anticholinergic medication, can be given to counteract the parasympathetic response such as increased salivation and bradycardia. Unfortunately, the administration of anticholinergic medications causes the opposite effect of producing tachycardia, which is exacerbated during the sympathetic response.

During the sympathetic discharge, prolonged tachycardia and hypertension increase the risk of cardiovascular events due to increased myocardial demand and oxygen consumption. Sympathetic stimulation and the seizure itself cause an increase in cerebral blood flow and an increase in cerebral metabolic rate of oxygen, resulting in increased intracranial pressure. Increases in intraocular and intragastric pressure occur as well. Esmolol can be used to blunt the sympathetic response.[3] Patients can also have postictal states with stroke-like symptoms or cognitive agitation, which can confuse the clinical picture as they are also recovering from general anesthesia at the same time.[4]


Providing general anesthesia for ECT is essential in every case and is only done without anesthesia in developing countries where proper equipment and personnel are not available. ECT is a first-line treatment for several disorders. When psychotic features and suicide risk are high, ECT is a useful initial treatment.  If a patient's depression has caused catatonia or psychomotor retardation involving the inability to eat or drink, then ECT is a viable treatment. It can provide fast relief if it is effective. One report indicates that for severe psychomotor depression, ECT provides up to 90% relief within two weeks.[5] Neuroleptic malignant syndrome is also an indication for ECT. Severe depression and psychotic features in pregnancy are conditions where ECT is used preferentially when medications can be harmful to the patient or the developing fetus.[6] 

ECT as a second-line treatment is mainly used when pharmacotherapy is ineffective or the patient's symptoms worsen.[7] In certain conditions, ECT is considered an experimental treatment with promising benefits such as treatment-resistant epilepsy, Parkinson disease, depression and tremors, and Tourette syndrome.[8][9][10]


There are several contraindications to ECT. Most contraindications are relative and need special consideration. The anesthesia provider must take into account each patient's comorbidities and address how a generalized seizure will affect them.  In most cases, pheochromocytoma and elevated intracranial pressure with mass effect at baseline are absolute contraindications.[11]  

An increase in intracranial or intraocular pressure is not tolerated very well for a patient with intracranial mass, retinal detachment, or intracerebral aneurysms. Patients with myocardial disease, cardiac arrhythmias, bleeding disorders, and pheochromocytoma may not tolerate the hemodynamic instability from extreme parasympathetic and sympathetic stimulation during the procedure.[12][13]


There are several items needed before performing ECT. The American Society of Standard of care for monitoring a patient under general anesthesia includes monitoring heart rhythm with an electrocardiogram and monitoring heart rate, oxygenation, ventilation, and blood pressure. A tourniquet should be used on one of the patient's extremities to prevent the muscle relaxant from affecting that extremity, which allows monitoring of the effectiveness of the motor portion of the seizure.  Electroencephalogram (EEG) monitors, or processed EEG, monitor the status of the brain during the seizure. Emergency airway equipment should be readily available. A soft bite block is provided in the oropharynx to prevent tongue and tooth injury, as a generalized epileptic seizure has been shown to cause such trauma even in the setting of muscle relaxation.[14] A bag-valve mask and a simple oxygen face mask should be available to administer oxygen. A suctioning device is a necessity to help clear secretions.


The personnel required for ECT are a psychiatrist, a nurse, and a trained anesthetic provider who can perform general anesthesia for the patient. These requirements vary by state and governing body.

Technique or Treatment

An intravenous catheter (IV)  is placed before the induction of anesthesia. Typically, a patient breathes 100% oxygen before induction of anesthesia. The patient's vital signs are monitored throughout the procedure. The intravenous anesthetic of choice is administered, followed by hyperventilation with a bag mask to induce hypocapnia which lowers cerebral blood flow and reduces the seizure threshold. After general anesthesia is successfully induced, a muscle relaxant is given to prevent myalgias and musculoskeletal injuries during the seizure. A tourniquet is commonly placed on one of the lower extremities to block muscle relaxants from reaching the area. This helps monitor the motor portion of the seizure by allowing personnel to observe the tonic and clonic activity of the lower extremity. A soft bite block is then placed to prevent the patient from developing an oral injury during the seizure.  The electrical stimulus is then administered to induce the seizure and is monitored by a processed EEG.

The goal is for the seizure to last around 25 to 75 seconds but no shorter than 15 seconds.[15][16] More prolonged seizures can be desirable if the patient has had ECTs that were less than 15 seconds in the past. The patient is then recovered in a post-anesthesia unit having their neurological status and hemodynamics monitored until it is appropriate for them to return home or to their assigned hospital room.

There are a variety of anesthetic agents and muscle relaxants that are used to induce anesthesia for ECT. Most dosing regimens for medications administered should be used in the lowest effective dose.

Methohexital is considered the gold standard for induction of anesthesia for ECT. It is a barbiturate that stimulates Gamma-aminobutyric acid (GABA) receptors which are the main inhibitory receptors in the brain. Methohexital produces anesthesia for approximately 4 to 7 minutes, which is ideal for ECT. It does not affect seizure threshold and, compared to propofol, does not shorten seizure length.[17] Methohexital causes moderate cardiac depression, which helps counteract the sympathetic discharge produced by a seizure. The initial dose is usually 1 to 1.5 mg/kg.[18] 

Etomidate is a unique drug that also works by activating GABA receptors in the brain. Studies have shown that it tends to produce a longer seizure compared to propofol.[19]  Etomidate does not cause cardiac depression, so the sympathetic discharge tends to be elevated when used as the sole anesthetic for ECT. Supplementing with an intravenous opioid such as remifentanil or a beta-blocker like esmolol to inhibit sympathetic discharge is common. Etomidate is known to cause adrenal suppression and should be avoided in patients with known adrenal insufficiency or critical illness. A dose of 0.3 mg/kg of etomidate is given to induce general anesthesia, lasting around 5 to 10 minutes.[20][21] 

Propofol also acts as a GABA agonist. However, it tends to shorten seizure duration as it increases the seizure threshold. It is used in ECT as an anesthetic agent when previous seizures induced by ECTs have been prolonged and when a rapid onset is needed. Propofol is dosed at 1.5 to 2 mg/kg.[22] 

Ketamine is N-methyl-D-aspartate (NMDA) antagonist, and it causes dissociative anesthesia as well as analgesia. It is not often used in ECT as it tends to increase seizure length and causes indirect myocardial stimulation. Ketamine also has antidepressant properties, and studies are ongoing determining its effectiveness as an adjunct for the treatment of depression. Doses of 1 to 2 mg/kg are typically used to induce adequate anesthesia.[23] Ketamine has the potential side effect of causing psychomimetic delirium during recovery, vivid dreams, and hallucinations. This is often pretreated with a benzodiazepine.[24][25] Recovery from ketamine is the slowest, followed by etomidate, methohexital, propofol when given for a short period.

Sevoflurane is an option for induction of anesthesia in ECT. It has a slow onset compared to intravenous anesthetics. It can be helpful to initiate anesthesia to obtain IV access on a patient who is uncooperative awake. When used for a short period, sevoflurane has a quick recovery. In a systematic review, sevoflurane reduces seizure length more prominently than propofol, barbiturates, and ketamine.[26] Sevoflurane does not attenuate the sympathetic stimulation to the extent as other induction agents, so opioids or beta-blockers are often used to maintain hemodynamic stability.[27] Sevoflurane enhances muscular blockade compared to intravenous anesthetics. 

Succinylcholine is the preferred muscle relaxant for ECT. It is a depolarizing neuromuscular blocker and is given in doses of 1 mg/kg to produce adequate muscle relaxation for intubating conditions within 30 seconds of administration. It typically lasts 5 to 8 minutes.[28] Succinylcholine raises the serum potassium by 0.5 meq/L after IV administration. In the setting of elevated plasma potassium and conditions that can cause an exaggerated increase in serum potassium when succinylcholine is given, lethal arrhythmias occur, and succinylcholine should be avoided.[29] There is no reversal agent for succinylcholine, but typically that is not needed since its duration of action is short. Succinylcholine and sevoflurane should be avoided if the patient has a history of malignant hyperthermia, as these are triggering agents for malignant hyperthermia.

Nondepolarizing neuromuscular blocking agents are good alternatives to succinylcholine, with the most common being rocuronium. Rocuronium is given at doses of 0.6 mg/kg to produce intubating conditions. Its effects last around 35 minutes. If the patient is on an antiepileptic medication or mood stabilizer such as lithium, the anesthetic provider must be aware. Lithium can delay the onset and prolong the actions of succinylcholine and nondepolarizing neuromuscular blocking agents.[30] Antiepileptic medications acutely can prolong the effects of nondepolarizing neuromuscular blocking agents, but when chronically taken, resistance to these muscle relaxants occurs, requiring larger doses.[31]


Complications in ECT, although rare, do occur. The anesthetic provider should be monitoring the patient at all times. The most common side effects of ECTs are headaches and cognitive impairment.[1] These tend to be temporary. The cognitive impairment is compounded by the administration of general anesthesia, the underlying psychiatric disorder, and the induced seizure. A seizure that lasts too long can result in status epilepticus. This condition requires prompt treatment in the form of administering benzodiazepine or propofol until termination of seizure. Status epilepticus is more common when pretreatment with theophylline is used to prolong the seizure.[32] 

Upon induction of general anesthesia and muscle relaxation, it may be difficult to mask ventilate the patient. Depending on which medications were used, letting the patient wake up and return to spontaneous ventilation may be the best option. Endotracheal intubation may be required to prevent severe hypoxia.

During recovery in the post-anesthesia care unit, myocardial infarction, ischemic or hemorrhagic stroke are possible. Evaluation by cardiology or neurology should be implemented if these conditions are noticed. Patients emerging from anesthesia may also become agitated and experience pain. Postictal side effects such as paralysis or mania are also possible.

Patients with deep brain stimulators or cardiac devices require special considerations. Deep brain stimulators can cause electrical interference when inducing a generalized seizure and should thus be turned off. A physician specialized in deep brain stimulation should be consulted.[33] Patients with pacemakers and other cardiac devices are primarily considered safe to undergo ECT with only ECG monitoring. There is a very low likelihood that the electrical impulse interferes with the cardiac device.[34] A magnet should be readily available in case of an emergency. The anesthetic provider should communicate with the patient's cardiologist to determine the severity of illness and risk of undergoing general anesthesia.

Clinical Significance

ECT is an effective treatment for pharmacotherapy-resistant depression and other severe psychiatric disorders. Its effects are quickly seen, but some patients may require multiple sessions of this therapy. Providing general anesthesia for ECT is standard and has been the case since the 1950s. Anesthesia for ECT provides a safe environment for a generalized epileptic seizure to take place.  Treatment of hemodynamic instability and prevention of painful and detrimental side effects are possible through a carefully planned anesthetic.

The ideal anesthetic agent provides amnesia with minimal effects on hemodynamic stability and seizure duration. An anesthetic agent that does affect seizure duration might be desirable if the patients' previous seizure during ECT was too long or short. Muscle relaxation protects the musculoskeletal system from the tonic and clonic actions of a generalized seizure. There are enough options and ways to provide anesthesia for ECT to suit most patients' needs. Alterations are made by the anesthesiologist, who recognizes reactions, patient discomfort, and side effects. Today, ECT is seldom performed without the use of general anesthesia except in developing countries. Musculoskeletal injury and post-traumatic stress disorder are not uncommon when enduring ECT without anesthesia.[35][36] Anesthesia prevents harm and trauma to the patient while enabling them to undergo a procedure that significantly improves their psychiatric disorder.

Enhancing Healthcare Team Outcomes

ECT provides patients with certain psychiatric disorders a treatment option for improvement in their mental state. Performing ECT requires an entire team composed of interprofessional colleagues, including anesthesiologists, psychiatrists, and nurses.[37][16] [Level 5]

Prior to undergoing ECT, a patient should be evaluated by an anesthetic provider to ensure the patient is safe to undergo general anesthesia and consent to the use of general anesthesia. Additionally, this allows the anesthetic provider to determine if the patient's comorbidities and current medication regimen require alterations to the anesthetic plan. The anesthesia team should also coordinate with the psychiatrist to determine the severity of the patient's psychiatric disorders and the length of seizure desired. A nurse is present before, during, and after the procedure to ensure the patient is ready for the procedure and monitored afterward. Nursing staff help to position the patient and to make sure all safety guidelines are followed. During recovery, nurses help recognize side effects and reactions to either the anesthesia or seizure.



Moksnes KM,Ilner SO, Electroconvulsive therapy--efficacy and side-effects. Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke. 2010 Dec 16;     [PubMed PMID: 21164584]


Payne NA,Prudic J, Electroconvulsive therapy: Part I. A perspective on the evolution and current practice of ECT. Journal of psychiatric practice. 2009 Sep     [PubMed PMID: 19820553]

Level 3 (low-level) evidence


Kadiyala PK,Kadiyala LD, Anaesthesia for electroconvulsive therapy: An overview with an update on its role in potentiating electroconvulsive therapy. Indian journal of anaesthesia. 2017 May;     [PubMed PMID: 28584345]

Level 3 (low-level) evidence


Gaines GY 3rd,Rees DI, Anesthetic considerations for electroconvulsive therapy. Southern medical journal. 1992 May;     [PubMed PMID: 1585198]


Petrides G,Fink M,Husain MM,Knapp RG,Rush AJ,Mueller M,Rummans TA,O'Connor KM,Rasmussen KG Jr,Bernstein HJ,Biggs M,Bailine SH,Kellner CH, ECT remission rates in psychotic versus nonpsychotic depressed patients: a report from CORE. The journal of ECT. 2001 Dec;     [PubMed PMID: 11731725]

Level 1 (high-level) evidence


Baghai TC,Möller HJ, Electroconvulsive therapy and its different indications. Dialogues in clinical neuroscience. 2008;     [PubMed PMID: 18472488]


Warneke L, Managing resistant depression. When patients do not respond to therapy. Canadian family physician Medecin de famille canadien. 1993 Apr;     [PubMed PMID: 8495142]


Strassnig M,Riedel M,Müller N, Electroconvulsive therapy in a patient with Tourette's syndrome and co-morbid Obsessive Compulsive Disorder. The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry. 2004 Jul;     [PubMed PMID: 15346542]

Level 3 (low-level) evidence


Regenold WT,Weintraub D,Taller A, Electroconvulsive therapy for epilepsy and major depression. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. 1998 Spring;     [PubMed PMID: 9581214]

Level 3 (low-level) evidence


Fregni F,Simon DK,Wu A,Pascual-Leone A, Non-invasive brain stimulation for Parkinson's disease: a systematic review and meta-analysis of the literature. Journal of neurology, neurosurgery, and psychiatry. 2005 Dec;     [PubMed PMID: 16291882]

Level 1 (high-level) evidence


Taylor S, Electroconvulsive therapy: a review of history, patient selection, technique, and medication management. Southern medical journal. 2007 May;     [PubMed PMID: 17534086]


Buday J,Albrecht J,Mareš T,Podgorná G,Horáčková K,Kališová L,Raboch J,Anders M, Brain Tumors and Electroconvulsive Therapy: A Literature Overview of the Last 80 Years. Frontiers in neurology. 2020;     [PubMed PMID: 32849199]

Level 3 (low-level) evidence


Pandya M,Pozuelo L,Malone D, Electroconvulsive therapy: what the internist needs to know. Cleveland Clinic journal of medicine. 2007 Sep;     [PubMed PMID: 17879522]


Chanpattana W,Kojima K,Kramer BA,Intakorn A,Sasaki S,Kitphati R, ECT practice in Japan. The journal of ECT. 2005 Sep;     [PubMed PMID: 16127301]


Jindal S,Sidhu GK,Kumari S,Kamboj P,Chauhan R, Etomidate versus Propofol for Motor Seizure Duration during Modified Electroconvulsive Therapy. Anesthesia, essays and researches. 2020 Jan-Mar;     [PubMed PMID: 32843794]


Wojdacz R,Święcicki Ł,Antosik-Wójcińska A, Comparison of the effect of intravenous anesthetics used for anesthesia during electroconvulsive therapy on the hemodynamic safety and the course of ECT. Psychiatria polska. 2017 Dec 30;     [PubMed PMID: 29432502]


Avramov MN,Husain MM,White PF, The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy. Anesthesia and analgesia. 1995 Sep;     [PubMed PMID: 7653829]

Level 1 (high-level) evidence


Martone CH,Nagelhout J,Wolf SM, Methohexital: a practical review for outpatient dental anesthesia. Anesthesia progress. 1991 Nov-Dec;     [PubMed PMID: 1842156]


Gazdag G,Kocsis N,Tolna J,Iványi Z, Etomidate versus propofol for electroconvulsive therapy in patients with schizophrenia. The journal of ECT. 2004 Dec;     [PubMed PMID: 15591855]

Level 1 (high-level) evidence


Upchurch CP,Grijalva CG,Russ S,Collins SP,Semler MW,Rice TW,Liu D,Ehrenfeld JM,High K,Barrett TW,McNaughton CD,Self WH, Comparison of Etomidate and Ketamine for Induction During Rapid Sequence Intubation of Adult Trauma Patients. Annals of emergency medicine. 2017 Jan;     [PubMed PMID: 27993308]


Forman SA, Clinical and molecular pharmacology of etomidate. Anesthesiology. 2011 Mar;     [PubMed PMID: 21263301]

Level 3 (low-level) evidence


Shah PJ,Dubey KP,Watti C,Lalwani J, Effectiveness of thiopentone, propofol and midazolam as an ideal intravenous anaesthetic agent for modified electroconvulsive therapy: A comparative study. Indian journal of anaesthesia. 2010 Jul;     [PubMed PMID: 20882170]

Level 2 (mid-level) evidence


Hooten WM,Rasmussen KG Jr, Effects of general anesthetic agents in adults receiving electroconvulsive therapy: a systematic review. The journal of ECT. 2008 Sep;     [PubMed PMID: 18628717]

Level 1 (high-level) evidence


Zanos P,Moaddel R,Morris PJ,Riggs LM,Highland JN,Georgiou P,Pereira EFR,Albuquerque EX,Thomas CJ,Zarate CA Jr,Gould TD, Ketamine and Ketamine Metabolite Pharmacology: Insights into Therapeutic Mechanisms. Pharmacological reviews. 2018 Jul;     [PubMed PMID: 29945898]


Jankauskas V,Necyk C,Chue J,Chue P, A review of ketamine's role in ECT and non-ECT settings. Neuropsychiatric disease and treatment. 2018;     [PubMed PMID: 29922060]


Aoki N,Suwa T,Kawashima H,Tajika A,Sunada N,Shimizu T,Murai T,Kinoshita T,Takekita Y, Sevoflurane in electroconvulsive therapy: A systematic review and meta-analysis of randomised trials. Journal of psychiatric research. 2021 Sep;     [PubMed PMID: 34171759]

Level 1 (high-level) evidence


Pekel M,Postaci NA,Aytaç İ,Karasu D,Keleş H,Şen Ö,Dikmen B,Göka E, Sevoflurane versus propofol for electroconvulsive therapy: effects on seizure parameters, anesthesia recovery, and the bispectral index. Turkish journal of medical sciences. 2016 Apr 19;     [PubMed PMID: 27513252]


Andrade C,Shah N,Tharyan P,Reddy MS,Thirunavukarasu M,Kallivayalil RA,Nagpal R,Bohra NK,Sharma A,Mohandas E, Position statement and guidelines on unmodified electroconvulsive therapy. Indian journal of psychiatry. 2012 Apr;     [PubMed PMID: 22988318]


Marsch SC,Steiner L,Bucher E,Pargger H,Schumann M,Aebi T,Hunziker PR,Siegemund M, Succinylcholine versus rocuronium for rapid sequence intubation in intensive care: a prospective, randomized controlled trial. Critical care (London, England). 2011 Aug 16;     [PubMed PMID: 21846380]

Level 1 (high-level) evidence


Hill GE,Wong KC,Hodges MR, Lithium carbonate and neuromuscular blocking agents. Anesthesiology. 1977 Feb;     [PubMed PMID: 835845]

Level 3 (low-level) evidence


Soriano SG,Martyn JA, Antiepileptic-induced resistance to neuromuscular blockers: mechanisms and clinical significance. Clinical pharmacokinetics. 2004;     [PubMed PMID: 14748617]


Devanand DP,Decina P,Sackeim HA,Prudic J, Status epilepticus following ECT in a patient receiving theophylline. Journal of clinical psychopharmacology. 1988 Apr;     [PubMed PMID: 3372714]

Level 3 (low-level) evidence


Yeoh TY,Manninen P,Kalia SK,Venkatraghavan L, Anesthesia considerations for patients with an implanted deep brain stimulator undergoing surgery: a review and update. Canadian journal of anaesthesia = Journal canadien d'anesthesie. 2017 Mar;     [PubMed PMID: 28028671]


MacPherson RD,Loo CK,Barrett N, Electroconvulsive therapy in patients with cardiac pacemakers. Anaesthesia and intensive care. 2006 Aug;     [PubMed PMID: 16913344]

Level 2 (mid-level) evidence


Payne NA,Prudic J, Electroconvulsive therapy: Part II: a biopsychosocial perspective. Journal of psychiatric practice. 2009 Sep     [PubMed PMID: 19820554]

Level 3 (low-level) evidence


Ray AK, How bad was unmodified electroconvulsive therapy! A retrospective study. Indian journal of psychiatry. 2016 Apr-Jun;     [PubMed PMID: 27385857]

Level 2 (mid-level) evidence


Shukla GD, Modified versus unmodified ect. Indian journal of psychiatry. 2000 Oct;     [PubMed PMID: 21407989]