Anesthesia for electroconvulsive therapy

INTRODUCTION — 

Electroconvulsive therapy (ECT), which involves passing a small brief current through the brain to induce a generalized seizure, is a procedure performed under general anesthesia, not always in elective circumstances [1]. ECT is primarily used to treat severe depression but is also indicated for selected patients with other conditions including bipolar disorder, schizophrenia, schizoaffective disorder, catatonia, and neuroleptic malignant syndrome. This topic will review the anesthetic management of patients undergoing an ECT procedure.

A separate topic addresses medical consultation and strategies to reduce risk before and after ECT. (See "Medical evaluation for electroconvulsive therapy".)

Discussions of the technique, efficacy, indications for, and adverse effects of ECT are found in other topics:

●(See "Overview of electroconvulsive therapy (ECT) for adults".)

●(See "Technique for performing electroconvulsive therapy (ECT) in adults".)

●(See "Unipolar major depression in adults: Indications for and efficacy of acute electroconvulsive therapy (ECT)".)

●(See "Bipolar disorder in adults: Indications for and efficacy of electroconvulsive therapy".)

GENERAL CONSIDERATIONS

Procedural techniques

●Scalp electrode placement – Scalp electrode placement for ECT is discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Electrode placement'.)

●Electrical stimulus – The electrical stimulus type and dose for inducing a seizure are discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Stimulus'.)

●Novel seizure therapies – Novel seizure therapies have been designed to increase spatial precision and avoid stimulating the deep brain structures involved in memory retention (eg, the hippocampus), to lessen neurocognitive side effects [2]. Examples include (see "Unipolar depression in adults: Overview of neuromodulation procedures", section on 'Convulsive therapies'):

•Individualized low amplitude seizure therapy, which aims to reduce the spread of current in the brain by titrating current amplitude during seizure titration.

•Magnetic seizure therapy (MST), which involves the use of transcranial magnetic stimulation (TMS) to better control spatial distribution and extent of stimulation [3].

Procedural location — Depending on institutional preferences, ECT is often performed in a location outside the main operating room suite such as the postanesthesia care unit (PACU) or a preoperative procedural area. As with all locations that serve patients receiving general anesthesia, standards set by the American Society of Anesthesiologists (ASA) for preparation, patient monitoring, and provision of anesthetic care should be met [4,5]. Equipment to manage emergencies (eg, cardiac arrest, difficult airway, malignant hyperthermia) must be readily available. (See "Considerations for non-operating room anesthesia (NORA)".)

PREANESTHETIC ASSESSMENT AND MANAGEMENT

Medical evaluation and risk reduction — Psychiatrists often request a medical evaluation before scheduling ECT since many eligible patients are older adults with multiple medical comorbidities [6]. In addition to American Society of Anesthesiologists (ASA) Class IV or V status (table 1), the American Psychiatric Association notes that the following conditions are associated with increased risk during ECT [7] (see "Medical evaluation for electroconvulsive therapy"):

•Unstable or severe cardiovascular disease

•Space-occupying intracranial lesion with evidence of elevated intracranial pressure

•Recent cerebral hemorrhage or stroke

•Bleeding or otherwise unstable vascular aneurysm

The medical consultation is reviewed by the anesthesiologist to ensure knowledge of the presence of medical comorbidities, proposed strategies to reduce risk, and recommended management of adverse effects after the procedure. (See 'Management of adverse effects during recovery' below.)

ECT is considered to be generally safe in pregnant patients [8-10]. Modifications in ECT procedural techniques and use of perianesthetic agents are discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Pregnancy'.)

Further discussion regarding medical and preanesthetic evaluation before ECT is available in separate topics. (See "Medical evaluation for electroconvulsive therapy" and "Preoperative evaluation for noncardiac surgery in adults".)

Management of cardiac and noncardiac implantable electronic devices

●Pacemakers and implantable cardioverter-defibrillators – Management of a patient with a cardiac implantable electronic device (CIED) such as a pacemaker or implantable cardioverter-defibrillator (ICD) is similar to that for other surgical procedures where electromagnetic interference is likely [11]. In patients who are not pacing-dependent, placing a magnet over the pulse generator of the pacemaker (to put it in an asynchronous mode) or the ICD (to suspend tachyarrhythmia detection and therapy) is safe, convenient, and reliable. In pacing-dependent patients with a pacemaker or ICD, consultation with the cardiology or institutional CIED care team is necessary to reprogram the device before and after the procedure [12]. Further details are available in a separate topic. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

●Deep brain stimulators – Although most manufacturers of implantable electronic medical devices recommend not using ECT in patients with functioning devices in the head or neck, some patients with a deep brain stimulator (DBS) device are also being treated with ECT [11,13-15].

Concerns regarding this select group of patients include heating of the DBS electrodes during application of the electrical stimulus or movement of these electrodes due to seizure-induced motor activity [13], although none of these adverse effects have been reported in patients with DBS undergoing ECT. Periprocedural management of the DBS device is done in consultation with the neurosurgical team and the device manufacturer, and may vary among centers. Some stop DBS therapy throughout the complete course of treatment, while others temporarily disable the DBS device before each procedure, with resumption of therapy immediately after each procedure [15].

Considerations for chronically administered psychotropic medications — Patients presenting for ECT are often taking multiple psychotropic medications for treatment of depression and/or other psychiatric illnesses. These agents are typically continued during the periprocedural period without compromising safety (eg, most antidepressants, antipsychotics, and lithium), as discussed separately. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Psychotropic drugs'.)

However, many psychotropic medications have synergistic effects with ECT and some have potentially dangerous interactions with medications that are routinely administered during anesthetic care. Familiarity with such interactions is necessary to recognize and appropriately treat common as well as rare but serious adverse effects.

●Antidepressants

•Selective serotonin reuptake inhibitor antidepressants – Selective serotonin reuptake inhibitor (SSRI) agents such as paroxetine, sertraline, and fluoxetine are commonly used antidepressants for treatment of mild-to-moderate depression. These agents are typically continued throughout the periprocedural period. (See "Perioperative medication management", section on 'Selective serotonin reuptake inhibitors'.)

Potentially important effects of SSRIs during ECT include:

-Effects on anesthetic agents and adjuvants – Fluoxetine and sertraline are inhibitors of cholinesterase in human serum and the erythrocyte membrane. This effect may lead to an extended duration of action for succinylcholine [16]. Fluoxetine is a potent inhibitor of CYP2D6, and may increase the plasma concentration of agents that rely on hepatic metabolism (eg, antiarrhythmics, antiemetics) [17,18].

-Development of serotonin syndrome – Serotonin syndrome is a rare but potentially lethal toxicity characterized by agitation, clonus, hyperreflexia, and hyperthermia. This syndrome may occur in patients taking SSRIs if other drugs with serotoninergic potential are administered during the perianesthetic period (eg, ondansetron [19,20], metoclopramide [21], or fentanyl and other opiates [19,21-23]). Thus, the anesthesiologist should be familiar with signs and symptoms of serotonin syndrome, emergency treatment (table 2), and potential complications (metabolic acidosis, rhabdomyolysis, seizures, kidney failure, disseminated intravascular coagulation [DIC], coma) of serotonin syndrome [21]. (See "Serotonin syndrome (serotonin toxicity)".)

•Tricyclic antidepressants – Abrupt withdrawal of tricyclic antidepressants agents (TCAs) such as amitriptyline, nortriptyline, dosulepin, imipramine, or desipramine should be avoided as this can lead to insomnia, nausea, headache, increased salivation, and sweating. (See "Perioperative medication management", section on 'Tricyclic and tetracyclic antidepressants'.)

Potentially important effects of TCAs during ECT include:

-Interaction with vasopressor agents – Since TCAs inhibit the uptake of norepinephrine and serotonin at the synaptic cleft, they can potentiate the vasopressor effects of indirect sympathomimetic agents such as ephedrine or metaraminol, and may also amplify the effects of catecholamines (eg, epinephrine, norepinephrine).

-Interaction with other drugs – The anticholinergic side effects of TCAs can be accentuated by administration of anticholinergic medications such as atropine or scopolamine during the periprocedural period, with increased likelihood of postoperative delirium. Also, tramadol and meperidine are avoided due to additive serotoninergic effects. (See "Serotonin syndrome (serotonin toxicity)".)

-Effects on the electrocardiogram – Electrocardiographic (ECG) effects include prolongation of the QTc interval (the QT interval that is corrected for heart rate), widening of the QRS complex, and conduction delays.

-Other effects – Other common side effects include postural hypotension, delayed gastric emptying, urinary retention, dry mouth, blurred vision, and sedation.

•Monoamine oxidase inhibitors – The monoamine oxidase inhibitors (MAOIs) target the monoamine oxidase (MAO) enzymes responsible for the breakdown of amine neurotransmitters (norepinephrine and serotonin). MAOIs are usually continued during the periprocedural period, particularly when the psychiatrist believes temporary withdrawal of the agent will exacerbate or precipitate a depressive syndrome. (See "Perioperative medication management", section on 'Monoamine oxidase inhibitors'.)

Potentially important effects of MAOIs during ECT include:

-Interaction with vasopressor agents – Use of indirect sympathomimetic agents such as ephedrine or metaraminol is contraindicated since their metabolism is inhibited by MAOIs with the consequent risk of an exaggerated vasopressor effect (eg, severe hypertension). Direct-acting catecholamines (epinephrine, norepinephrine) or vasopressor agents (eg, phenylephrine, vasopressin) can be used safely if they are titrated slowly and carefully.

-Interaction with other drugs – Administration of meperidine or pethidine is avoided, as interactions with these drugs may precipitate a serotoninergic reaction. (See "Serotonin syndrome (serotonin toxicity)".)

Remifentanil, fentanyl, alfentanil, and morphine can be safely used in patients taking MAOIs.

•Selective norepinephrine reuptake inhibitors – Selective norepinephrine reuptake inhibitor (SNRI) agents (eg, desvenlafaxine, duloxetine, venlafaxine, levomilnacipran, milnacipran) are typically continued throughout the periprocedural period.

Potentially important effects of TCAs during ECT include:

-Interaction with vasopressor agents – SNRI agents inhibit the reuptake of both serotonin and norepinephrine in the synaptic cleft and they have minimal direct effects on other neurotransmitters or receptors. Elevation in heart rate and blood pressure are possible because of inhibition of norepinephrine reuptake. Like TCAs, SNRI agents can potentiate the vasopressor effects of indirect sympathomimetic agents such as ephedrine or metaraminol, and may also amplify the effects of catecholamines (eg, epinephrine, norepinephrine). Because of its indirect sympathomimetic effect, ketamine should be used cautiously and carefully titrated in patients with cardiovascular compromise who are taking SNRIs and TCAs.

-Inhibition of CYP 2D6 – Venlafaxine is a weak inhibitor, and duloxetine is a moderate inhibitor of CYP2D6, and may increase the plasma concentration of agents that rely on hepatic metabolism (eg, antiarrhythmics, antiemetics) [17,18]. Desvenlafaxine, an active metabolite of venlafaxine, was developed to address this concern. (See "Perioperative medication management", section on 'Selective serotonin reuptake inhibitors'.)

●Mood stabilizers – Mood stabilizers include lithium and the anticonvulsants carbamazepine, lamotrigine, valproate, and oxcarbazepine.

•Lithium – Typically, lithium levels are reduced below the full therapeutic range at the time of each ECT treatment by withholding one or two doses prior to the treatment [24]. (See "Perioperative medication management", section on 'Mood stabilizing agents (lithium and valproate)'.)

Potentially important effects of lithium during ECT include:

-Effects on procedural outcome – Lithium has the potential to increase the adverse cognitive effects of ECT.

-Effects on anesthetic agents and adjuvants – Lithium may prolong the effects of succinylcholine (which is typically used during ECT to reduce tonic-clonic movements (see 'Neuromuscular blocking agent' below)) [25,26], as well as the effects of nondepolarizing neuromuscular blocking agents (NMBAs) [27,28]. However, these problems are not clinically significant in most cases [25].

•Anticonvulsant mood stabilizers (carbamazepine, valproate) – Most patients taking anticonvulsants such as carbamazepine and valproate for mood stabilization undergo successful treatment with ECT by withholding the drug on the evening before the procedure, rather than discontinuing it [28,29]. However, patients taking anticonvulsants for epilepsy should continue these drugs throughout the perioperative period if possible. (See "Perioperative medication management", section on 'Mood stabilizing agents (lithium and valproate)' and "Medical evaluation for electroconvulsive therapy", section on 'Epilepsy'.)

Potentially important effects of anticonvulsant mood stabilizers during ECT include:

-Effects on seizures – Anticonvulsant mood stabilizers may impact seizure induction or duration during ECT, although the effect is not consistent [29]. In one randomized trial, full dosing of anticonvulsant therapy (either carbamazepine or valproate) before a bilateral course of ECT was not associated with differences in induction or seizures or adverse cognitive outcomes compared with half dosing or discontinuation of anticonvulsant [30]. However, if seizures have been difficult to elicit or too short during previous ECT procedures in an individual patient, then the anticonvulsant is withheld on the evening before an ECT procedure [31]. In some cases, the dose is also reduced during the course of ECT treatment.

-Effects on anesthetic agents and adjuvants – Carbamazepine is a potent inducer of the cytochrome P450 3A4 enzyme system. Thus, it may increase anesthetic requirements and/or prolong the duration of action of succinylcholine [32].

-Other effects – In rare cases, valproic acid has been associated with perioperative hyperammonemia [33]. (See "Valproic acid poisoning", section on 'Hyperammonemia'.)

●Antipsychotics – Antipsychotic agents include chlorpromazine, clozapine, quetiapine, olanzapine, risperidone, thioridazine, perphenazine, and haloperidol. These agents are well-tolerated during ECT and are typically continued throughout the periprocedural period since they may provide a synergistic antipsychotic effect [34]. In fact, ECT has been used in combination with clozapine for treatment-resistant schizophrenia [35,36].

Potentially important effects of antipsychotic agents during ECT include:

•Effects on anesthetic agents and adjuvants – Antipsychotics may enhance the effects of central nervous system (CNS) depressants, thereby lowering anesthetic dose requirements [32].

•Effects on beta blocking agents – Antipsychotics have selectivity for the CYP2D6 isoform, which primarily metabolizes beta blockers. Thus, the efficacy of beta blockers used to treat hypertension and tachycardia during ECT may be altered [37]. (See 'Sympathetic responses' below.)

•Other common side effects – All antipsychotic agents are associated with an increased risk of extrapyramidal syndromes (eg, akathisia, tardive dyskinesia, parkinsonian tremor).

•Other rare side effects – A rare (incidence between 0.02 and 3.23 percent) but life-threatening side effect of antipsychotic agents is neuroleptic malignant syndrome (NMS) [38], characterized by hyperthermia, muscle rigidity, autonomic instability (diaphoresis, labile blood pressure), and mental status changes (agitation, delirium, or coma) that last for hours to weeks. This can be mistaken for malignant hyperthermia. Complications of NMS can include myoglobinuria, kidney failure, cardiac failure, disseminated intravascular coagulation, pulmonary embolus, and cognitive sequelae caused by hypoxemia and prolonged hyperthermia. (See "Neuroleptic malignant syndrome" and "Malignant hyperthermia: Diagnosis and management of acute crisis", section on 'Differential diagnosis'.)

●Benzodiazepines – Benzodiazepines have anxiolytic, sedative, anticonvulsant, and antinociceptive effects [39]. Chronically administered benzodiazepines (eg, clonazepam, alprazolam, diazepam, lorazepam) are typically tapered and discontinued before a planned ECT procedure. Furthermore, administration of short-acting benzodiazepines such as midazolam is avoided before performing an ECT procedure.

Potentially important effects of benzodiazepines during ECT include:

•Effects on seizures – Benzodiazepines are likely to interfere with ECT by impacting seizure induction and decreasing seizure duration. However, results are inconsistent and may be partially dependent on ECT technique [40,41].

•Effects on anesthetic agents and adjuvants – Benzodiazepines have synergistic effects with most other anesthetic agents.

Administration of prophylactic medications

Headache prophylaxis — Headache is the most common adverse effect of ECT, occurring in 26 to 85 percent of patients [42-45]. In a systematic review of post-ECT headache, the weighted mean incidence in patients was 33 percent [45]. For those who present with a history of post-ECT headache responsive to over-the-counter analgesics, a prophylactic dose of acetaminophen [46], and/or non-steroidal anti-inflammatory drug (NSAIDs) such as ibuprofen [47,48], is often administered before the procedure. A preoperative dose of intravenous (IV) ketorolac 30 mg is an alternative prophylactic agent for patients with a history of severe headaches who are unresponsive to conventional analgesics [49].

Nausea prophylaxis — Transient post-procedure nausea occurs in approximately 25 percent of patients after ECT [11]. Prophylaxis and/or treatment with IV ondansetron 4 to 8 mg is reasonable for patients with a history of significant post-ECT nausea. In refractory cases of severe nausea that were not prevented by routine prophylaxis and were resistant to treatment from multiple antiemetics after previous general anesthetics, we typically plan to use propofol as the induction agent. (See "Postoperative nausea and vomiting", section on 'Prevention'.)

Anticholinergic prophylaxis — We administer an IV anticholinergic agent (either glycopyrrolate 0.2 mg or atropine 0.2 to 0.4 mg) for patients with previous episodes of severe bradycardia (or asystole) and/or excessive salivation during ECT [50-52]. Such low doses of an anticholinergic agent are associated with significantly less bradycardia during ECT, without significant changes in baseline heart rate [53,54] (see 'Parasympathetic responses' below). Furthermore, the QTc interval was reduced by administration of atropine in a small observational study (a consideration in patients with risk factors for the development of torsades de pointes) [55]. (See "Perioperative arrhythmias", section on 'Polymorphic ventricular tachycardia (torsades de pointes)'.)

A larger dose of atropine (0.4 to 1 mg) is necessary to prevent asystole in some patients with prior episodes of peri stimulus asystole, possibly due to a centrally driven parasympathetic output that is greater than the typical autonomic reflex arc [56,57].

However, we do not routinely administer an anticholinergic agent to all patients undergoing ECT. Undesirable side effects include dry mouth.

Beta blockers — For rare patients at very high risk for complications from transient hypertension or tachycardia (eg, those with intracranial aneurysm, severe ischemic heart disease, or recent myocardial infarction) pre-emptive administration of a short-acting beta blocker (eg, esmolol, landiolol) to minimize the tachycardia and hypertension that typically occurs due to sympathetic responses to seizure induction may be recommended after medical consultation. Further discussion is available below and in a separate topic. (See 'Sympathetic responses' below and "Medical evaluation for electroconvulsive therapy", section on 'Prophylactic beta blockers'.)

ANESTHETIC MANAGEMENT FOR THE ECT PROCEDURE — 

Choice of anesthetic agents, management of the physiological changes that occur during and immediately after the therapeutic seizure, and good communication between the anesthesiologist and the proceduralist can impact safety, efficacy, and the overall patient experience for an ECT procedure [11].

Preoxygenation — The patient should be preoxygenated with supplemental oxygen (O₂) via nasal cannula or preferably with a face mask during spontaneous ventilation before induction of general anesthesia, with the goal of maintaining (O₂) saturation at or near 100 percent during the induced seizure. However, O₂ desaturation under 90 percent was noted in 29 percent of ECT procedures in one study, with obesity and seizure duration as the main predictors [56,58].

Interventions to prevent O₂ desaturation by increasing the functional residual capacity (FRC) and oxygen reserves allow for a longer safe apnea period. These include use of:

•Head up position

•Apneic oxygenation

•Noninvasive positive pressure ventilation

•High flow nasal oxygen delivery

Such interventions are especially important in patients with a high body mass index (BMI) and/or obstructive sleep apnea [58].

Management of desaturation includes shortening the seizure duration if clinically possible, as well as strategies to improve oxygen reserve. (See 'Management of oxygenation and ventilation' below.)

Choice of induction agent

General considerations — The quality of the seizure is an important factor for ECT efficiency. Qualities of the ideal hypnotic induction agent include [59]:

●Provision of adequate anesthesia

●Rapid induction and recovery

●No interference with the quality of the seizure

●Maintenance of hemodynamic stability

●Minimal drug-related postoperative side effects

Most anesthetic induction agents have profound dose-dependent anticonvulsant properties. Thus, deep anesthesia should be avoided during ECT. Minimizing dosage of the agent before stimulation allows induction of a more adequate seizure and earlier treatment success without increasing the electrical stimulation energy and consequent side effects [60].

Methohexital — Methohexital is the induction agent of choice, administered intravenously (IV) at a dose of 0.75 to 1 mg/kg.

●Advantages – Methohexital is a short-acting barbiturate derivative with several characteristics that make it especially suitable for use in ECT: minimal anticonvulsant effects (so that the induced seizure is not affected), rapid onset of action, short duration, rapid recovery, and low cost. The recommended dose of approximately 1 mg/kg of ideal body weight produces an appropriate level of anesthesia in 20 to 30 seconds [61]. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

●Disadvantages – Adverse effects of methohexital include pain on injection. (See "General anesthesia: Intravenous induction agents", section on 'Disadvantages and adverse effects'.)

Notably, an older barbiturate, thiopental, is no longer available in most nations. (See "General anesthesia: Intravenous induction agents", section on 'Thiopental'.)

Propofol — Despite some disadvantages, propofol is used as an alternative to methohexital in some institutions and may be preferentially selected for certain patients (eg, those with a history of prolonged seizures, postictal agitation, or severe postoperative nausea and vomiting [PONV]).

●Advantages – Advantages of propofol include its rapid onset (20 to 30 seconds), short duration of action (8 to 10 minutes), and antiemetic effects, compared with other induction agents [62]. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

●Disadvantages – Disadvantages of propofol in the setting of ECT procedures include its significant anticonvulsant properties; thus, a higher stimulus dose (voltage) is required to achieve adequate seizures [63,64], seizure duration may be reduced [59,65], and more severe cognitive side effects may occur after use of propofol for ECT [66]. Also, propofol has been associated with a shorter seizure duration and less improvement of depression than methohexital [59,65]. Furthermore, similar to methohexital, propofol is associated with pain on injection. (See "General anesthesia: Intravenous induction agents", section on 'Disadvantages and adverse effects'.)

●Combinations of propofol with other agents

•Combinations of propofol and ketamine – Some clinicians use a combination of propofol and ketamine to minimize the side effects of using either ketamine or propofol alone, a combination of lower doses of ketamine and propofol has been employed by some clinicians for ECT procedures. Studies have noted that ketamine mixed with propofol are equivalent to the use of propofol alone. Inclusion of propofol mitigates some of the side effects of ketamine such as PONV, sympathomimetic effects, and psychotomimetic effects including recovery agitation, while inclusion of ketamine mitigates propofol-induced hypotension [67,68]. (See 'Ketamine' below.)

•Combinations of propofol and remifentanil – Some data suggests that addition of remifentanil to propofol anesthesia may significantly alter seizure indices, reduce the amount of propofol required, and improve clinical response, as discussed below [69-71]. (See 'Remifentanil' below.)

•Combinations of propofol and dexmedetomidine – Some clinicians use a combination of propofol and dexmedetomidine, which is an alpha-2 agonist (see "Monitored anesthesia care in adults", section on 'Dexmedetomidine'). A 2018 meta-analysis of the use of dexmedetomidine to supplement propofol induction for ECT procedures (six studies; 166 patients) noted that it did not interfere with seizure duration (measured with motor or electroencephalographic [EEG] parameters) and did not significantly prolong recovery time, but was associated with decreases in mean arterial pressure (MAP) and heart rate (HR) [72]. Other small trials have reported that preinduction dexmedetomidine use reduced the acute hyperdynamic responses to ECT (see 'Management of hemodynamic responses' below), with no effect on seizure duration but at the possible expense of a delayed recovery and discharge [73-76]. Additional small studies and case reports have also noted that dexmedetomidine reduces the incidence of post-ECT adverse effects such as headache, agitation, postictal delirium, or pain associated with propofol injection [73,76-79].

Ketamine — Ketamine has been used as an alternative or adjunctive anesthetic for ECT procedures when combined with propofol. (See 'Propofol' above.)

●Advantages – Ketamine may enhance efficacy of ECT by increasing seizure duration as it is less anticonvulsant than other anesthetic induction agents, which may facilitate dose reduction of the electrical current delivered to the brain [80-83]. Other studies suggest that subanesthetic doses of ketamine (0.3 mg/kg) modulate the antidepressant efficacy of ECT by accelerating onset of its effects, thereby potentially reducing the number of ECT sessions required to obtain response, remission, and suicidal ideation reduction [80,84-88].

However, these benefits of ketamine dissipate quickly, with no end of treatment cycle differences. Post-ECT outcomes (eg, depressive symptoms, cognitive improvement) are similar after ketamine administration compared with other anesthetic agents [82,83,85-87,89-91]. (See "Ketamine and esketamine for treating unipolar depression in adults: Administration, efficacy, and adverse effects".)

Other advantages of ketamine include its analgesic properties. Also, ketamine is potentially useful for patients with severe asthma because of its bronchodilating properties. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

●Disadvantages – Potential adverse effects of ketamine include postprocedure delirium (marked by confusion, restlessness, hallucinations, dissociation, delusions, or psychosis), dizziness, headache, nausea and/or vomiting [88,91-95]. Also, the sympathomimetic effects of ketamine typically cause mild tachycardia and hypertension, which may increase myocardial O₂ demand [89]. Thus, it is usually avoided in patients with ischemic heart disease. In addition, ketamine increases salivation, which may be a problem in patients who do not have an endotracheal tube. For these reason, glycopyrrolate is typically administered as a premedication when ketamine use is planned. (See "General anesthesia: Intravenous induction agents", section on 'Disadvantages and adverse effects' and 'Anticholinergic prophylaxis' above.)

Furthermore, ketamine has been associated with QTc prolongation, an effect that may be particularly important in patients chronically receiving psychotropic medications that also prolong the QTc interval [96]. (See 'Considerations for chronically administered psychotropic medications' above.)

Etomidate — Etomidate has also been used as an alternative for ECT procedures.

●Advantages – Etomidate is a short-acting induction agent with a favorable hemodynamic profile compared with methohexital (ie, fewer cardiac side effects such as bradycardia and cardiac arrhythmias); thus, it is a good choice in patients who may develop cardiovascular instability during ECT [97]. (See "General anesthesia: Intravenous induction agents", section on 'Advantages and beneficial effects'.)

Also, etomidate is associated with longer seizures compared with propofol [98].

●Disadvantages – Adrenal medullary suppression is a concern with use of etomidate. Although this side effect would theoretically render etomidate less useful for patients receiving multiple treatments, etomidate has not been specifically associated with clinically significant adrenocortical suppression during courses of ECT treatments [99]. Other adverse side effects include a higher incidence of PONV, myoclonus, and, similar to methohexital and propofol, pain on injection. (See "General anesthesia: Intravenous induction agents", section on 'Disadvantages and adverse effects'.)

Remifentanil — Remifentanil is a potent mu-opioid receptor agonist with intense analgesic properties and a short duration of action due to rapid degradation via ester hydrolysis. It has been used as an alternative or adjunctive anesthetic for ECT procedures when combined with methohexital or propofol. (See 'Methohexital' above and 'Propofol' above.)

●Advantages – Remifentanil as an anesthetic induction agent or as a supplemental agent during ECT to reduce the induction agent dose, enhance analgesia during the procedure, and possibly also increase seizure duration [69,70,100-103]. Thus, it is useful for patients who are refractory to seizure induction after standard methohexital or propofol anesthetic dosing. In one small retrospective study, 24 patients who had become completely or relatively refractory to maximum settings on the ECT device after receiving bilateral ECT with a standard methohexital-based anesthetic, switching to remifentanil as the sole induction agent for subsequent ECT procedures was tried [104]. The stimulus dose was significantly lower with a remifentanil anesthetic induction in these patients, resulting in significantly longer motor and EEG seizure duration compared with methohexital. Remifentanil also attenuates the hypertensive response to ECT [102]. However, remifentanil at usual doses does not have intrinsic properties to enhance ECT seizures [71].

●Disadvantages – Repeated use for ECT may have short-term side effects such as dizziness, nausea, and headache, without demonstrable benefits in speed of response and remission rates [103].

Inhalation agents for induction — Although general anesthesia for ECT is usually induced with IV agent(s), the volatile inhalation anesthetic sevoflurane is rarely used for induction in select patients (eg, those with needle phobia or severe agitation that prevents IV catheter placement) [105].

●Advantages – Sevoflurane is the agent of choice for an inhalation induction because of its rapid onset and low incidence of airway irritation [106]. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)

●Disadvantages – Sevoflurane may be associated with a shorter motor seizure duration compared with methohexital, although a longer seizure duration compared with propofol [107,108]. This undesirable effect on seizure duration may be attenuated by discontinuing its administration after induction of anesthesia.

Safety issues to consider when employing an inhalational induction in a location used for ECT are ensuring the ability to treat complications that may occur during an inhalation induction (eg, laryngospasm, arrhythmias, hypotension) if there is no IV catheter, as well as the availability of a gas scavenging system to avoid environmental contamination. (See "Considerations for non-operating room anesthesia (NORA)", section on 'Preparation of anesthetic equipment'.)

Neuromuscular blocking agent — Administration of a neuromuscular blocking agent (NMBA) as a component of general anesthesia has made ECT more widely accepted and safer by minimizing the risk of physical trauma associated with uncontrolled tetanic muscle contractions. Paralysis in one foot is prevented by wrapping a standard blood pressure (BP) cuff or tourniquet around an ankle and inflating it at 20 percent above the systolic pressure before administering the NMBA to the anesthetized patient. Thus, seizure activity can be monitored in that foot. (See 'Neuromonitoring' below.)

Succinylcholine is the NMBA of choice for ECT procedures because of its rapid onset, short duration of action, and rapid recovery (see "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Succinylcholine'). Several studies suggest that a dose of 1 mg/kg provides acceptable conditions for the procedure in most patients [61,109,110]. However, there is some variability in responsiveness to succinylcholine. Therefore, in patients who have a high risk of injury (eg, older adults with significant osteoporosis), the succinylcholine dose is typically increased by 40 to 50 percent [111]. This dose increase minimizes risk of excessive uncoordinated muscular contractions which may lead to bone fractures.

Also, there is considerable variability in time to relaxation between patients. Thus, simply timing the stimulus application after administration of succinylcholine (one minute for younger patients and two minutes for older patients) is not adequate. Electrical stimulation to produce the seizure should be applied only when maximal neuromuscular blockade has been achieved, as monitored with a peripheral nerve stimulator. While 50 percent twitch depression is found to provide optimal conditions for endotracheal intubation, near complete twitch suppression is necessary for optimal neuromuscular blockade during an ECT-induced seizure [109]. Furthermore, even in the absence of twitch response to peripheral nerve stimulation, the ECT stimulus should only be applied once muscle fasciculations in the distal extremities have subsided completely, and the plantar reflex on the side without the ankle tourniquet has been abolished [112]. (See "Monitoring neuromuscular blockade".)

Contraindications to succinylcholine include prolonged immobilization, muscular dystrophy, burns, malignant hyperthermia, and paralysis (eg, after a stroke) (see "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Adverse effects of succinylcholine'). For these patients, a nondepolarizing NMBA should be selected to achieve complete muscular relaxation for ECT. Rocuronium at a dose of 0.3 to 0.6 mg/kg offers a good alternative to succinylcholine [109,113]. Compared with succinylcholine, a disadvantage for use of rocuronium or any other nondepolarizing NMBA is a longer time from injection to complete muscle relaxation. Another disadvantage is a longer duration of action compared with succinylcholine. We employ sugammadex for reversal of rocuronium after ECT. Compared to reversal of rocuronium with neostigmine, use sugammadex reduces recovery times measured by train of four (TOF) stimulation [114], and postprocedure complaints such as myalgia and headache [115,116]. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Nondepolarizing neuromuscular blocking agents'.)

Complete return of neuromuscular function before allowing emergence from general anesthesia is ensured by using quantitative monitoring of the degree of residual blockade, ideally with monitoring of the hand muscles supplied by the ulnar nerve [117]. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block' and "Monitoring neuromuscular blockade".)

Airway management — Airway management is critically important during ECT, both to ensure patient safety during the general anesthetic and to facilitate hyperventilation and purposeful hypocapnia and hyperoxia as a strategy for augmentation of the ECT-induced seizures. In addition to routine airway management during induction of general anesthesia (see "Airway management for general anesthesia in adults"), it is important to protect against dental and oral soft tissue injuries that can occur during seizures [118]. Furthermore, some ECT patients have poor dentition that is prone to injury [119-121]. Also, forceful jaw clenching cannot be prevented by using a NMBA because the temporalis, masseter, and pterygoid muscles are directly stimulated by the electrodes that induce the seizure.

To prevent dental and alveolar bone damage as well as soft tissue injury, the American Psychiatric Association (APA) recommends using a bite guard made of flexible material with maximal cushioning in the molar area and inserted prior to electrical stimulation [122]. Proper technique is to ensure that the tongue is pushed inferiorly and posteriorly in the mouth, and that the chin is held firmly against the bite block (picture 1).

Management of oxygenation and ventilation — The combination of hyperoxia and hypocapnia is desirable to increase seizure intensity and duration, thereby optimizing ECT stimulus efficiency while minimizing postictal side effects [123-127]. Studies suggest that hyperoxia and hypocapnia (with a moderately low partial pressure of carbon dioxide [PaCO₂]) act synergistically to improve seizure quality and reduce the electrical charge required to generate a therapeutic convulsion [124,126].

●Oxygenation – Strategies to induce and maintain hyperoxia (and prevent O₂ desaturation) throughout the procedure include careful preoxygenation before induction of anesthesia (see 'Preoxygenation' above), followed by administration of 100 percent supplemental oxygen with good control of the airway throughout the procedure [128-130]. It is thought that seizure duration is significantly impacted by the inspired oxygen concentration, although the mechanism underlying this phenomenon is not entirely clear [128]. There are no known clinically significant adverse effects of hyperoxia of short duration during ECT.

●Ventilation – After induction of general anesthesia, we typically hyperventilate the patient to a target end-tidal carbon dioxide (EtCO₂) of 30 mmHg to induce cerebral hypocarbia immediately prior to delivery of the electrical stimulus by the interventionalist. Induction of hypocapnia is particularly important in patients with a history of inadequate seizure length, and some studies found that the seizure threshold is also significantly lowered by hypocapnia [125,131]. Hypocapnia may lower the seizure threshold in patients affected by an increasing seizure threshold during consecutive ECT treatment, although evidence is not consistent [132]. Hypocapnia also reduces intracranial hypertension and thereby, the incidence of postictal headache and agitation [133]. Potential adverse effects of hypocapnia include cerebral vasoconstriction, as well as coronary vasoconstriction with consequent increased risk for arrhythmias [134].

Most patients are efficiently ventilated/hyperventilated using either a bag-valve-mask device with an Ambu bag or the breathing circuit on an anesthesia machine. Notably, the use of the bag-valve-mask device may not allow accurate measurement of EtCO₂.

We do not employ the Mapleson D circuit as it is less efficient for lowering the PaCO₂ [135]. Although the laryngeal mask airway (LMA) is minimally invasive, this technique is not used routinely [136], but may be used in patients who are difficult to ventilate with a face mask [137], especially in patients with obesity [58]. Endotracheal intubation is a reliable way to secure the airway and achieve hyperventilation, but is very rarely used for ECT because the procedure is so brief.

It is important to avoid hypercapnia secondary to poor ventilation, which is associated with hypertension, tachycardia, somnolence, delayed recovery from anesthesia, and a higher prevalence of postprocedure agitation and headache [138].

Neuromonitoring

●Awareness monitoring – The patient must be rendered unconscious to prevent awareness before an NMBA is administered (see 'Neuromuscular blocking agent' above). An appropriate depth of anesthesia is determined by the anesthesia provider by noting the loss of response to verbal commands and/or loss of eyelash reflex (table 3 and figure 1) (see "Overview of anesthesia", section on 'Induction'). However, the eyelash reflex may not be lost when methohexital is used for induction (see 'Methohexital' above), even when an appropriate plane of anesthesia has been reached [139]. This may lead to administration of an unnecessarily high dose of methohexital, which can decrease seizure quality. Several studies have noted that seizure duration is best if the patient is maintained at a lighter level of anesthetic depth since intravenous induction agents have anticonvulsant properties [140-144].

Processed EEG monitoring can be a useful aid to monitor loss of awareness (table 4) [145]. A 2019 meta-analysis of bispectral index (BIS) monitoring during anesthesia for ECT noted that high values (eg, mean of 35 to 64) on the preictal BIS values were associated with improved seizure duration and reduced incidence and magnitude of cognitive impairment after ECT [146]. However, limitations of BIS during ECT include the following [147] (see "Neuromonitoring in surgery and anesthesia", section on 'Intravenous agents'):

•The excitatory effects of ketamine may affect the validity of processed EEG-derived index values.

•Use of NMBAs interferes with BIS monitoring.

•The pretreatment awake index values on the processed EEG may decline after the first ECT treatment. One study suggests that the procedure itself may induce prolonged changes in EEG parameters rendering index values unreliable in subsequent treatments [148]. Some patients who have received a course of ECT may have BIS values in the anesthetized range even when awake [148].

●Seizure activity monitoring – To check that the electrical stimulation has produced a tonic-clonic seizure, a standard BP cuff or tourniquet is wrapped around an ankle and inflated at 20 percent above the systolic pressure to prevent paralysis in the foot before the NMBA is administered to the anesthetized patient. This allows visual and tactile observation of the motor component of seizure activity in that foot.

Since processed EEG monitors can also be used to display the raw EEG, these devices can also be used to monitor the seizure and postictal EEG [149].

Management of hemodynamic responses

Parasympathetic responses — Electrical stimulation to induce the seizure initially triggers bradycardia lasting for a brief period (10 to 15 seconds). This probably occurs because of a sudden increase in parasympathetic discharge to the sinoatrial node due to electrical stimulation of the motor nucleus of the vagus nerve and nucleus ambiguous within the medulla oblongata of the brain [150]. Asystole in the postictal period is very rare [151,152].

Asystole may occur in patients taking chronically administered medications (see 'Considerations for chronically administered psychotropic medications' above) or with administration of succinylcholine [153,154]. Also, asystole may be more common after convulsive compared with nonconvulsive stimulations [150] and after electrode placement in the bitemporal or right unilateral positions compared with bifrontal electrode placement [155].

Bradycardia and/or asystole is self-limited in most patients undergoing ECT, and usually has no long-lasting effects, particularly in younger patients without significant heart disease [156]. In some patients with severe or persistent bradycardia, treatment with either atropine or glycopyrrolate is necessary, as discussed in a separate topic. (See "Perioperative arrhythmias", section on 'Sinus bradycardia'.)

Although administration of anticholinergic premedication (glycopyrrolate or atropine) typically prevents bradycardia and asystole, prophylactic anticholinergic administration is not routine because of undesirable side effects. (See 'Anticholinergic prophylaxis' above.)

Sympathetic responses — The seizure itself triggers a sympathetic response which increases plasma levels of catecholamines. This results in tachycardia with an increase in HR of approximately 20 percent, hypertension with an increase in systolic BP of approximately 30 to 40 percent, and an increase in cardiac output of approximately 80 percent, lasting for five or more minutes [157]. Despite these significant hemodynamic changes, major adverse cardiac events (MACE) are rare after ECT, as discussed in a separate topic [158]. (See "Medical evaluation for electroconvulsive therapy", section on 'Cardiovascular effects'.)

Preparation for the management of exaggerated or prolonged responses to sympathetic stimulation and close communication with the proceduralist is critically important. We typically administer esmolol 10 to 50 mg (which may be repeated every 5 to 15 minutes to achieve the desired effect) for prophylaxis against or treatment of tachycardia and hypertension in response to seizure-induced sympathetic stimulation (table 5) [159]. A theoretical reduction in seizure duration at higher esmolol doses is unlikely to be clinically significant. Limited data suggest that landiolol (a short-acting IV beta blocker with similar kinetics but greater negative chronotropic effects than esmolol) may be a suitable alternative beta blocker in this setting. Labetalol is used by some clinicians but has inconsistent cardiovascular effects during the first few minutes after the stimulation and a longer half-life than esmolol [159].

Decisions regarding preemptive administration of beta blockers to minimize tachycardia and hypertension are based on preoperative assessment of the individual patient’s risk of cardiovascular complications, as well as the patient's responses during previous ECT treatments. Details are discussed separately. (See "Medical evaluation for electroconvulsive therapy", section on 'Prophylactic beta blockers' and "Medical evaluation for electroconvulsive therapy", section on 'Other prophylactic medications'.)

MANAGEMENT OF ADVERSE EFFECTS DURING RECOVERY — 

As with all procedures requiring general anesthesia, recovery in a post-anesthesia care unit (PACU) or recovery area with comparable equipment and personnel is necessary. (See "Overview of post-anesthetic care for adult patients".)

Common adverse effects of ECT may be evident in the immediate post-procedure period, including headache, nausea, and postictal agitation. Major cardiovascular complications and neurologic complications are rare. Overall, medical morbidity and mortality rates after ECT treatment are low and comparable to other low-risk ambulatory procedures performed under general anesthesia [160,161]. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Adverse effects'.)

Headache — Headache is the most common side effect of ECT, occurring in 26 to 85 percent of patients [42,44]. In most cases, the headache is transient and mild, peaks at two hours, and is responsive to over-the-counter analgesics such as acetaminophen and/or non-steroidal anti-inflammatory drug (eg, ibuprofen) given after the ECT procedure [162].

Triptans are also effective for post-ECT headache [163,164]. In a study of 20 patients with post-ECT headache, eletriptan (a serotonin receptor agonist) and acetaminophen both reduced post-ECT headaches, but eletriptan was superior to acetaminophen at reducing the duration and intensity of headaches [165]. Cold therapy has also been found to be successful [166].

Nausea — Transient, postoperative nausea and vomiting (PONV) may occur in approximately 25 percent of patients after ECT [11]. Causes include anesthetic agents, hyperventilation with the introduction of air into the stomach, the ECT treatment itself, and/or severe postprocedure headache. Standard antiemetics such as ondansetron are used when treatment is necessary. (See "Postoperative nausea and vomiting", section on 'Antiemetics'.)

Potential adverse effects of intravenous (IV) antiemetic agents such as ondansetron or metoclopramide include (see 'Considerations for chronically administered psychotropic medications' above):

●Rare development of serotonin syndrome if ondansetron or metoclopramide is selected to treat PONV in a patient who is chronically taking a selective serotonin reuptake inhibitor (SSRI) or selective norepinephrine reuptake inhibitor (SNRI) agent. (See "Serotonin syndrome (serotonin toxicity)".)

●Possible development of QTc interval prolongation if a butyrophenone such as droperidol or haloperidol is selected to treat PONV in a patient who is chronically taking a tricyclic antidepressant agent (TCA). (See "Perioperative arrhythmias", section on 'QT interval prolongation'.)

●Accentuation of the anticholinergic side effects of TCAs with increased likelihood of postoperative delirium if scopolamine is selected to treat PONV. (See 'Adverse cognitive effects' below and "Perioperative neurocognitive disorders in adults: Risk factors and mitigation strategies", section on 'Intravenous agents associated with higher risk'.)

Adverse cognitive effects

●Postictal agitation – Postictal agitation is a relatively frequent clinical problem reported in 10 percent of patients undergoing ECT [167]. It is an acute confusional state characterized by disorientation, restlessness, and poor response to verbal requests. It is usually associated with amnesia and is mostly self-limiting [168]. Mild cases can be treated with supportive measures and behavioral interventions.

In patients with a history of severe postictal agitation, IV benzodiazepines or propofol may be administered after the seizure [169,170]. Dexmedetomidine may be useful in the treatment of refractory cases [78,79,171].

●Other cognitive effects – Longer-term cognitive side effects (eg, memory loss, long-term changes in cognition) are discussed separately. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Adverse cognitive effects'.)

Cardiovascular complications

●Major adverse cardiac events (MACE) and death – MACE or death after ECT is rare, and almost always occur in older patients and those with underlying cardiovascular disease. In a 2019 meta-analysis of 82 studies that included 106,569 patients undergoing 786,995 ECT treatments, these events occurred in approximately 1 in 50 patients, (in approximately 1 in 200 to 500 ECT treatments) [158]. The most common MACE diagnoses were acute heart failure (2.4 per 1000 treatments; 95% CI 1.3-4.7), arrhythmia (4.7 per 1000 treatments; 95% CI 2.2-10.1), and acute pulmonary edema (1.5 per 1000 treatments; 95% CI 0.7-3.1). Rare acute pulmonary edema after ECT may be associated with a hypertensive crisis [172,173], a cardiogenic cause [157], a neurogenic cause [174], or another etiology such as negative intrathoracic pressure associated with airway obstruction [175,176].

●Myocardial ischemia – While the incidence of MACE after ECT is low, prospective studies have demonstrated that 5 to 10 percent of ECT treatment patients develop cardiac troponin elevation indicative of myocardial injury [177,178]. However, routine monitoring of troponin is not indicated unless associated with other indicators of myocardial injury.

As noted above, prophylactic administration of a short-acting beta blocker is useful for prevention and/or treatment of tachycardia and hypertension due to sympathetic responses to ECT, particularly in patients at high risk of cardiovascular complications [159,179]. (See 'Sympathetic responses' above and "Medical evaluation for electroconvulsive therapy", section on 'Prophylactic beta blockers'.)

●Takotsubo cardiomyopathy – Takotsubo cardiomyopathy is a transient and reversible stress-induced cardiomyopathy characterized by left ventricular hypokinesis and apical ballooning associated with ST-segment elevations and increased cardiac enzymes. Seventeen case reports have described Takotsubo cardiomyopathy associated with ECT, primarily in older females (>70 years) [180]. Limited evidence suggests that pretreatment with beta blockers would prevent recurrence during subsequent ECT procedures [181].

Discussion of management of cardiovascular complications in the PACU is available in a separate topic. (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Postoperative cardiovascular complications'.)

Discussion of further medical management of patients with cardiovascular complications after ECT is available in a separate topic. (See "Medical evaluation for electroconvulsive therapy", section on 'Cardiovascular effects' and "Medical evaluation for electroconvulsive therapy", section on 'Postprocedure hemodynamic changes'.)

Neurologic complications — Neurologic dysfunction immediately following ECT is rare, but includes the following (see "Medical evaluation for electroconvulsive therapy", section on 'Central nervous system and other effects'):

●Tardive seizures – Although rare, tardive seizures are a potentially fatal complication of ECT. Either nonconvulsive or focal seizures may occur spontaneously after the termination of convulsion from ECT, or after return to full consciousness [182]. The first line of treatment includes IV benzodiazepines, followed by IV antiepileptic drugs if the seizure persists.

Reported predisposing factors include electrolyte disturbance, benzodiazepine withdrawal, head trauma, pregnancy, neurologic disease, and antibiotics such as cefotiam, piperacillin (available as piperacillin-tazobactam), or ciprofloxacin [183-186]. Rarely, tardive seizures may persist as convulsive or nonconvulsive status epilepticus. One review that included 13 case reports describing nonconvulsive status epilepticus after ECT noted that this diagnosis requires a high index of clinical suspicion and confirmation by a multi-lead electroencephalogram (EEG) [187].

●Focal neurologic deficits – Todd phenomenon is a rare transient postictal focal neurologic deficit (eg, aphasia, hemiparesis, visual loss) with complete spontaneous recovery after ECT [182,188,189]. Other causes of focal neurologic dysfunction should be ruled out (eg, cerebrovascular ischemia [190], ruptured aneurysm [191,192]).

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines are provided separately. (See "Society guideline links: Depressive disorders".)

SUMMARY AND RECOMMENDATIONS

●General considerations – Electroconvulsive therapy (ECT) involves passing a small brief electrical current through the brain to induce a generalized seizure while the patient in under general anesthesia. ECT is often performed in locations outside the main operating room suite. Standards set by the American Society of Anesthesiologists for preparation, patient monitoring, and provision of anesthetic care are necessary. (See 'General considerations' above and "Considerations for non-operating room anesthesia (NORA)".)

●Preoperative assessment and management

•Medical comorbidities – Many ECT patients are older adults with multiple medical comorbidities. Preoperative evaluation is discussed separately. (See "Medical evaluation for electroconvulsive therapy".)

•Pacemakers and implantable cardioverter-defibrillators – Management of cardiac implantable electronic devices is similar to that for other surgical procedures where electromagnetic interference is likely, as discussed separately. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

•Chronically administered medications – Most psychotropic medications are continued during the periprocedural period, and may have synergistic effects with ECT (eg, selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors, antipsychotics). Specific interactions with anesthetic or vasopressor agents may occur, as discussed separately. (See 'Considerations for chronically administered psychotropic medications' above.)

•Prophylactic medications

-Headache – For patients with a history of headaches, we suggest over-the-counter analgesics (eg, acetaminophen, ibuprofen) or a preoperative dose of intravenous (IV) ketorolac (Grade 2C). (See 'Headache prophylaxis' above.)

-Postoperative nausea and vomiting (PONV) – For patients with a history of significant nausea, we suggest IV ondansetron 4 to 8 mg (Grade 2C). (See 'Nausea prophylaxis' above.)

-Anticholinergic effects – For patients with a history of severe bradycardia and/or excessive salivation, we suggest an IV anticholinergic agent (glycopyrrolate or atropine) (Grade 2C). (See 'Anticholinergic prophylaxis' above and 'Parasympathetic responses' above.)

-Beta blockers – For rare patients at high risk for complications from transient hypertension or tachycardia that typically occurs due to sympathetic responses to seizure induction (eg, those with intracranial aneurysm, severe ischemic heart disease, or recent myocardial infarction), we suggest preemptive administration of a short-acting beta blocker (eg, esmolol, labetalol) (Grade 2C). (See 'Beta blockers' above and 'Sympathetic responses' above.)

●Management during the ECT procedure

•Preoxygenation – Preoxygenation with supplemental oxygen (O₂) via nasal cannula or preferably via face mask before induction is followed by administration of 100 percent O₂ throughout the procedure. The goal is the maintenance of O₂ saturation at or near 100 percent during the seizure. (See 'Preoxygenation' above and 'Management of oxygenation and ventilation' above.)

•Induction – Anesthetic induction agent(s) should not interfere with inducing an effective grand mal seizure. In general, low doses are preferable. (See 'Choice of induction agent' above.)

Choices include:

-Methohexital – For most patients, we suggest IV methohexital rather than other induction agents (Grade 2C), administered at a dose of 0.75 to 1 mg/kg. The advantages of methohexital include minimal anticonvulsant effects, rapid onset of action, short duration, and rapid recovery. Disadvantages include pain on injection. (See 'Methohexital' above.)

-Other agents – Reasonable alternative IV induction agents include propofol, ketamine, etomidate, or remifentanil. (See 'Propofol' above and 'Ketamine' above and 'Etomidate' above and 'Remifentanil' above.)

•Neuromuscular blocking agents (NMBAs) – An NMBA is administered. (See 'Neuromuscular blocking agent' above.)

-Rational – NMBA administration minimizes the risk of physical trauma associated with uncontrolled tetanic muscle contractions during ECT.

-Technique – Paralysis in one foot is prevented by wrapping a standard blood pressure (BP) cuff or tourniquet around an ankle and inflating it to 20 percent above systolic BP before administering the NMBA. This allows monitoring of seizure activity in that foot.

-Agent – Succinylcholine is selected in patients without contraindications because of its rapid onset, short duration of action, and rapid recovery. Other NMBAs have longer durations of action that may exceed the time necessary to complete the procedure, as discussed separately. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Succinylcholine'.)

•Airway management – A bite guard made of flexible material with maximal cushioning in the molar area is inserted prior to electrical stimulation. This protects against dental and oral soft tissue injuries during seizures. (See 'Airway management' above.)

•Ventilation – We suggest hyperventilation to produce mild hypocapnia rather than maintaining normocapnia (Grade 2C), with a target end-tidal carbon dioxide of approximately 30 mmHg. Hypocapnia may increase seizure intensity and duration and is particularly important in patients with a history of inadequate seizure duration. Most patients are efficiently hyperventilated using either a bag-valve-mask device with an Ambu bag or the breathing circuit on an anesthesia machine. (See 'Management of oxygenation and ventilation' above.)

•Neuromonitoring – Appropriate depth of anesthesia is determined by noting loss of response to verbal commands and/or loss of eyelash reflex (table 3 and figure 1). Processed electroencephalogram (EEG) monitoring may be a useful aid to monitor loss of awareness (table 4). (See 'Neuromonitoring' above.)

•Management of hemodynamic responses

-Parasympathetic responses – Electrical stimulation initially triggers self-limited bradycardia and/or asystole (10 to 15 seconds). Either atropine or glycopyrrolate is administered if bradycardia is severe or persistent. (See 'Parasympathetic responses' above.)

-Sympathetic responses – Seizures trigger a sympathetic response which increases plasma levels of catecholamines, heart rate, systolic BP, and cardiac output for five or more minutes. If necessary, a short-acting beta blocker (eg, esmolol, labetalol) or other agent (eg, calcium channel blockers, nitroglycerin or nitroprusside) is administered to treat hypertension and/or tachycardia (table 5). (See 'Sympathetic responses' above.)

●Management of postoperative adverse effects – Recovery in a postanesthesia care unit (PACU) or recovery area with comparable equipment and personnel is necessary. Details are discussed separately. (See "Overview of post-anesthetic care for adult patients".)

Common adverse effects treated in the immediate postprocedure period include headache, PONV, and adverse cognitive effects. Major adverse cardiac events or neurologic complications are rare. (See 'Management of adverse effects during recovery' above.)