INTRODUCTION — Electroconvulsive therapy (ECT), which involves passing a small brief current through the brain to induce a generalized seizure, is performed under general anesthesia. 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 anesthetic management for 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, and indications for performing ECT are found in other topics:
●(See "Technique for performing electroconvulsive therapy (ECT) in adults".)
●(See "Overview of electroconvulsive therapy (ECT) for adults".)
●(See "Unipolar major depression in adults: Indications for and efficacy of electroconvulsive therapy (ECT)" and "Bipolar disorder in adults: Indications for and efficacy of electroconvulsive therapy".)
TECHNICAL CONSIDERATIONS
Procedural location — Depending on institutional preferences, ECT is performed under general anesthesia in a variety of offsite or remote locations, including the post-anesthesia care unit (PACU), preoperative procedural areas, or a dedicated suite for ECT. As with all locations that serve patients receiving general anesthesia, the standards set by the American Society of Anesthesiologists (ASA) for provision of anesthetic care and monitoring should be met [1]. Equipment to manage emergencies (eg, cardiac arrest, difficult airway, malignant hyperthermia) should be readily available.
Standard preparations — Standard preparations for a general anesthetic are necessary, including checkout of the anesthesia machine, if present, and preparation of routinely administered anesthetic and adjuvant drugs, as well as equipment for advanced airway management. (See "Induction of general anesthesia: Overview", section on 'Preparation for anesthetic induction'.)
Since ECT is administrated under general anesthesia, standard American Society of Anesthesiologists (ASA) monitoring is necessary for these procedures [2]. (See "Basic patient monitoring during anesthesia", section on 'Standards for monitoring during anesthesia'.)
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 – Electrical stimulus type and dose for inducing a seizure are discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Stimulus type' and "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Stimulus dose'.)
●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), in order to lessen neurocognitive side effects [3]. Examples include:
•Individualized low amplitude seizure therapy (iLAST), which aims to reduce 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 [4].
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. 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 [5]:
●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
●Severe pulmonary condition
The medical consultation is reviewed by the anesthesiologist to ensure knowledge of the presence of medical comorbidities, proposed strategies to reduce risk, and recommended treatments for complications after the procedure [6]. In particular, identification of patients at risk of cardiovascular complications is necessary for decisions regarding pre-emptive administration of beta blockers or other agents to minimize tachycardia and hypertension that typically occurs due to sympathetic responses to seizure induction. (See 'Sympathetic responses' below and "Medical evaluation for electroconvulsive therapy", section on 'Cardiovascular effects'.)
ECT is considered to be generally safe in pregnant patients [7,8]. Modifications in procedural techniques and use of perianesthetic agents are discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Pregnancy'.)
Additional information regarding medical and preanesthetic evaluation is available in separate topics. (See "Medical evaluation for electroconvulsive therapy" and "Preoperative evaluation for anesthesia for noncardiac surgery".)
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 [6]. 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.
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 manufactures 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 [6,9,10].
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 [9], 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 [11].
Management of chronically administered medications
Psychotropic medications: Anesthetic considerations — Patients presenting for ECT are often taking multiple psychotropic medications for treatment of depression and/or other psychiatric illness. Many psychotropic medications have synergistic effects with ECT and are usually continued during the periprocedural period without compromising safety (eg, most antidepressants, antipsychotics, and lithium). The patient’s morning dose is administered on the same day of the procedure, shortly after recovery from general anesthesia has occurred. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Psychotropic drugs'.)
However, some psychotropic agents 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.
Recommendations for psychotropic medications that patients undergoing ECT may be taking include:
●Antidepressants – Antidepressants can improve the efficacy of ECT, and are generally safe to continue during the periprocedural period.
•Selective serotonin reuptake inhibitors – Selective serotonin reuptake inhibitor (SSRI) agents such as paroxetine, sertraline, and fluoxetine are the most commonly used antidepressants for treatment of mild to moderate depression. These agents are usually continued throughout the periprocedural period; stopping these agents can exacerbate mood and other disorders. These drugs block reuptake of serotonin at the presynaptic membrane. Since they have relatively little effect on the adrenergic, cholinergic, and histaminergic systems there are few associated side effects. (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 [12]. Fluoxetine is a potent inhibitor of CYP2D6, and may increase the plasma concentration of agents that rely on hepatic metabolism (eg, antiarrhythmics, antiemetics) [13,14].
-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 [15,16], metoclopramide [17], or fentanyl and other opiates [15,17-19]). Thus, the anesthesiologist should be familiar with signs and symptoms of serotonin syndrome, emergency treatment (table 2), and potential complications (metabolic acidosis, rhabdomyolysis, seizures, renal failure, disseminated intravascular coagulation [DIC], coma) of serotonin syndrome [17,20]. (See "Serotonin syndrome (serotonin toxicity)".)
•Selective norepinephrine reuptake inhibitors – Selective norepinephrine reuptake inhibitor (SNRI) agents (eg, desvenlafaxine, duloxetine, venlafaxine, levomilnacipran, milnacipran) treat depression by initially blocking presynaptic serotonin and norepinephrine transporter proteins. Considerations regarding continuation of SNRIs during the periprocedural period are similar to those with SSRIs, although there are limited specific data for SNRIs. (See "Perioperative medication management", section on 'Selective serotonin reuptake inhibitors'.)
•Tricyclic antidepressants – Tricyclic antidepressant agents (TCAs) such as amitriptyline, nortriptyline, dosulepin, imipramine, and desipramine inhibit the presynaptic reuptake of serotonin and norepinephrine. They also have antimuscarinic, antihistaminergic, and anti-alpha-1 adrenergic effects. These agents are usually continued throughout the periprocedural period to avoid worsening of depression. Abrupt withdrawal of tricyclic antidepressants should be avoided as this can lead to insomnia, nausea, headache, increased salivation, and sweating [21]. (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 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 slowly and carefully titrated.
-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.
●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 [22]. (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 agents' below)) [23,24], as well as the effects of nondepolarizing neuromuscular blocking agents (NMBAs) [25]. However, these problems are not clinically significant in most cases [23].
•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 [26]. 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 [27]. 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 [28]. 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 [29]. 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 [30].
-Other effects – In rare cases, valproic acid has been associated with perioperative hyperammonemia [31]. (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 [32]. In fact, ECT has been used in combination with clozapine for treatment-resistant schizophrenia [33,34].
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 [30].
•Effects on beta blocking agents – Antipsychotics have selectivity for the CYP2D6 isoform, which primarily metabolizes beta blockers. Thus, the efficacy of beta blocker use to treat hypertension and tachycardia during ECT may be altered [35]. (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 [36]) but life-threatening side effect of antipsychotic agents is neuroleptic malignant syndrome (NMS). It is 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. Complications of NMS can include myoglobinuria, renal failure, cardiac failure, disseminated intravascular coagulation, pulmonary embolus, and cognitive sequelae caused by hypoxemia and prolonged hyperthermia [37]. (See "Neuroleptic malignant syndrome".)
Some antipsychotic drugs have been linked with cardiomyopathy and myocarditis [38].
●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.
Other chronically administered medications — Management of other chronically administered medications is discussed in detail in a separate topic. (See "Perioperative medication management".)
Preanesthetic medications — Preanesthetic medications may be administered in selected patients to prevent or minimize common adverse effects associated with ECT. However, we avoid administration of any benzodiazepine such as midazolam before performing an ECT procedure, due to known anticonvulsant properties that would make seizure induction more difficult.
Headache prophylaxis — Headache is the most common adverse effect of ECT, occurring in 26 to 85 percent of patients [42-44]. In a systematic review of post-ECT headache, the weighted mean incidence in patients was 32.8 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], or ibuprofen [47], 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 that are unresponsive to conventional analgesics [48].
Nausea prophylaxis — Transient post-procedure nausea occurs in approximately 25 percent of patients after ECT [6]. Prophylaxis and/or treatment with IV ondansetron 4 to 8 mg is reasonable for patients with 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.
Anticholinergic administration — Severe bradycardia with hypotension may occur during ECT and is most common during the first ECT treatment, when there is a greater chance of administering a subconvulsive stimulus that leads to parasympathetic discharge. Excessive oral and respiratory secretions may also occur due to this parasympathetic response. However, routine prophylaxis with an anticholinergic agent is unnecessary, and undesirable side effects include higher heart rates in patients with ischemic heart disease, memory impairment in older adults, and discomfort due to dry mouth. Furthermore, in one observational study of 32 patients undergoing ECT, atropine significantly reduced the QTc interval, which may be a consideration in patients with risk factors for development of torsades de pointes [49]. (See "Arrhythmias during anesthesia", section on 'Polymorphic ventricular tachycardia (torsades de pointes)'.)
In patients with a previous experience of severe bradycardia and/or excessive salivation during ECT, premedication with an IV anticholinergic agent (either glycopyrrolate 0.2 mg or atropine 0.2 to 0.4 mg) may be beneficial to prevent vagally-mediated bradycardia and asystole, as well as excessive secretions. Low doses of atropine have been shown to result in significantly less bradycardia during ECT, without significant changes in baseline heart rate [50,51]. (See "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Cardiovascular medication' and 'Parasympathetic responses' below.)
ANESTHETIC MANAGEMENT FOR THE ECT PROCEDURE — Choice of anesthetic agents and management of the physiological changes that occur during and shortly after the therapeutic seizure can impact safety, efficacy, and the overall patient experience for an ECT procedure. Good communication between the anesthesiologist and the proceduralist facilitates tailoring a patient-specific anesthetic plan [6].
Preoxygenation — The patient is preoxygenated with supplemental oxygen via nasal cannula or face mask during spontaneous ventilation before induction of general anesthesia, with the goal of maintaining oxygen (O2) saturation at or near 100 percent. Adequate preoxygenation improves safety of the ECT procedure compared with spontaneous occurrence of an epileptic 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 [52]. (See 'Management of oxygenation and ventilation' below.)
Choice of induction agent — The selected anesthetic agent should not interfere with inducing an effective grand mal seizure. In a large retrospective study of the effects of different doses of anesthetic induction agents, low doses were associated with increased rates of response to ECT [53]. The investigators concluded that deep anesthesia should be avoided during ECT for major depressive disorder in order to achieve optimal ECT treatment effect.
●Methohexital – Methohexital is the induction agent of choice, administered intravenously (IV) at a dose of 0.75 to 1 mg/kg. Methohexital is a short-acting barbiturate derivative with several characteristics that make it especially suitable for use in ECT: rapid onset of action, short duration, minimal anticonvulsant effects, 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 [54]. Adverse effects of methohexital include pain on injection. (See "General anesthesia: Intravenous induction agents", section on 'Methohexital'.)
Notably, an older barbiturate, thiopental, is no longer available in most nations.
●Propofol – Propofol has a rapid onset, inducing general anesthesia within 20 to 30 seconds after the bolus injection, with a duration of action of 8 to 10 minutes. Propofol is associated with a better recovery and hemodynamic effects compared with other induction agents [55,56].
However, since propofol has significant anticonvulsant properties, a higher stimulus dose (voltage) is required to achieve adequate seizures [57,58], seizure duration may be reduced [55,59,60], and more severe cognitive side effects may occur after use of propofol for ECT [61]. Also, propofol has been associated with a shorter seizure duration and less improvement of depression than methohexital [55,59,60]. Furthermore, similar to methohexital, propofol is associated with pain on injection.
Despite these 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]). (See "General anesthesia: Intravenous induction agents", section on 'Propofol'.)
●Etomidate – 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 [62-64]. Also, etomidate is associated with longer seizures compared with propofol [65].
However, 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 [66]. 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 'Etomidate' and "General anesthesia: Intravenous induction agents", section on 'Disadvantages and adverse effects'.)
●Ketamine – Ketamine is not often selected for use during an ECT procedure. However, in the last two decades, subanesthetic doses of ketamine (typically 0.5 mg/kg over 40 minutes) have been studied as a treatment for major depression or bipolar depression refractory to treatment, with successful diminishing of severity in selected patients within hours to one day after administration [67-69]. The intrinsic antidepressant effects of ketamine have led to investigation of its use as a sole anesthetic agent or as an adjunct in anesthesia for ECT. Although some studies have noted that ketamine in this setting increases seizure duration or results in significant cognitive improvement compared with other anesthetic agents [70-73], these findings are not consistent [74-76]. A 2020 meta-analysis noted that ketamine enhances seizure duration, thereby facilitating reduced dosing of the electrical current delivered to the brain [77]. However, ketamine did not enhance the antidepressant effect of ECT [77]. Similarly, a 2017 meta-analysis noted that ketamine was not associated with greater improvement in depressive symptoms or higher rates of clinical response or procognitive effects compared with barbiturate anesthetic induction agents [75]. Thus, use of ketamine is reasonable when ECT seizures are suboptimal. However, some newer studies suggest that subanesthetic doses of ketamine (0.3 mg/kg) could modulate the antidepressant efficacy of ECT by accelerating onset of its effects, thereby reducing the number of ECT sessions required to obtain response, remission, and suicidal ideation reduction [78,79]. (See "Ketamine and esketamine for treating unipolar depression in adults: Administration, efficacy, and adverse effects".)
Advantages of ketamine include its analgesic properties; thus, is often used as the sole agent for short painful procedures, particularly in patients with opioid tolerance or hyperalgesia. 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'.)
Potential adverse effects of ketamine include postprocedure confusion, restlessness, hallucinations, delusions, fear, derealization, and headache [76,80-83]. Also, the sympathomimetic effects of ketamine typically cause mild tachycardia and hypertension, which may increase myocardial O2 demand. Thus, it is usually avoided in patients with ischemic heart disease. Furthermore, ketamine has been associated with QTc prolongation, an effect which may be particularly important in patients chronically receiving psychotropic medications that also prolong the QTc interval (see 'Psychotropic medications: Anesthetic considerations' above) [84]. In addition, ketamine increases salivation, which may be a problem in patients who do not have an endotracheal tube. For this 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 administration' above.)
●Combinations of ketamine and propofol – To minimize the side effects of using either ketamine or propofol alone, a combination of lower doses of ketamine and propofol (commonly known as "ketofol") has been employed by some clinicians for ECT procedures [85,86]. 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.
●Combinations of dexmedetomidine and propofol – Dexmedetomidine is an alpha-2 agonist acting predominantly in the locus coeruleus that is commonly used for procedural and intensive care unit (ICU) sedation. 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) [87]. 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 [88-91]. 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 [88,91-95].
●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. Remifentanil has been used as a supplemental agent or as a sole anesthetic during ECT, and may result in longer seizure duration in patients refractory to seizure induction after standard methohexital or propofol anesthetic dosing [96-102]. 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 [103]. 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 [101].
However, remifentanil at usual doses does not have intrinsic properties to enhance ECT seizures [104]. Furthermore, 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 [105].
●Volatile inhalation agents — Although general anesthesia for ECT is usually induced with IV agent(s), a volatile inhalation anesthetic may be used for induction in selected patients (eg, those with needle phobia, severe agitation preventing IV catheter placement, or poor tolerance of IV induction) [106]. Sevoflurane is the agent of choice for an inhalation induction because of its rapid onset and low incidence of airway irritation [107]. Although data regarding use of sevoflurane for ECT are limited, they suggest that the technique is safe, but may be associated with a shorter motor seizure duration compared with methohexital, although a longer seizure duration compared with propofol [108-110]. The undesirable effect of sevoflurane 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 "Induction of general anesthesia: Overview", section on 'Inhalation anesthetic induction' and "Inhalation anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)
Adjunct agents — Addition of a short-acting opioid such as remifentanil or alfentanil during induction of general anesthesia may reduce the necessary dose of propofol (or other induction agent), enhance analgesia during the procedure, and may also increase seizure duration.
Depth of anesthesia — The patient must be rendered unconscious to prevent awareness before a neuromuscular blocking agent (NMBA) is administered (see 'Neuromuscular blocking agents' below). An appropriate level of anesthetic is confirmed by the anesthesiologist by noting loss of response to verbal commands and/or loss of eyelash reflex (table 3 and figure 1). However, the eyelash reflex may not be lost when methohexital is used for induction even when the appropriate plane of anesthesia has been reached, and this may lead to administration of an unnecessarily high dose of methohexital, which may decrease seizure quality [111].
Processed EEG monitoring can be a useful aid to determine the optimal time for seizure induction in an unconscious patient (table 4) [112,113]. 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 [114-118]. A 2019 meta-analysis of bispectral index (BIS) monitoring during anesthesia for ECT noted that high preictal BIS values were associated with improved seizure duration and reduced incidence and magnitude of cognitive impairment after ECT [119]. However, limitations of BIS during ECT include the following (see "Neuromonitoring in surgery and anesthesia", section on 'Intravenous agents') [120]:
●The excitatory effects of ketamine may affect the validity of processed EEG-derived index values. Other combinations of anesthetic induction agents may also affect the validity of the BIS algorithm.
●Use of NMBAs interferes with BIS monitoring.
●The pretreatment awake index values on the processed EEG may decline after the first ECT treatment, suggesting that the procedure itself may induce prolonged changes in EEG parameters [121]. Thus, index values may be unreliable after the first treatment. Some patients who have received a course of ECT may have BIS values in the anesthetized range even when awake.
Neuromuscular blocking agents — Neuromuscular blockade 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. To check that the electrical stimulation has produced a tonic-clonic seizure, a standard blood pressure (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.
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 will provide acceptable conditions for the procedure in most patients [54,122,123]. However, there is some variability in responsiveness to succinylcholine, so in patients who have a high risk of injury (eg, older adult patients with significant osteoporosis), the dose is typically increased by 40 to 50 percent to minimize the risk of excessive uncoordinated muscular contractions which may cause bone fractures [124]. There is also 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 [125,126], near complete twitch suppression is necessary for optimal neuromuscular blockade during ECT [122]. 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 [127]. (See "Monitoring neuromuscular blockade".)
Contraindications to succinylcholine include prolonged immobilization, muscular dystrophy, burns, malignant hyperthermia, and paralysis (eg, after a stroke). For these patients, a nondepolarizing NMBA should be used 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 [122,128]. If insufficient or excessive neuromuscular blockade is noticed during the convulsion in an individual patient, then the dose of rocuronium can be adjusted by 0.05 to 0.1 mg/kg to achieve a better result. Compared with succinylcholine, a disadvantage for use of rocuronium or any other nondepolarizing NMBA is a longer time from injection to the complete muscle relaxation. Another disadvantage is a longer duration of action compared with succinylcholine. (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 [129]. We employ sugammadex for reversal of rocuronium after ECT. Use of sugammadex reduces recovery times as measured using train of four (TOF) stimulation [130], times to spontaneous ventilation and eye opening [131], and postprocedure complaints such as myalgia and headache, compared to reversal of rocuronium with neostigmine [131,132]. (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. (See 'Management of oxygenation and ventilation' below.)
Dental and oral soft tissue injuries can occur during seizures [133], and some ECT patients may have poor dentition [134]. In conscious patients, biting pressure is controlled by a feedback mechanism that prevents excessive strain, but such feedback is absent in anesthetized patients [135]. Also, forceful jaw clenching cannot be prevented by using a NMBA because the temporalis, masseter, and pterygoid muscles are directly stimulated by the electrodes. 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. 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.
Most patients are efficiently ventilated using a face mask (eg, a bag-valve-mask device with an Ambu bag or the breathing circuit on an anesthesia machine). The Mapleson D circuit is not employed as it is less efficient for lowering the partial pressure of carbon dioxide (PaCO2) [136]. Endotracheal intubation is a reliable way to secure the airway and achieve hyperventilation but it is rarely used for a brief ECT procedure. Although the laryngeal mask airway (LMA) is minimally invasive, this technique is also not used routinely [137], but may be used in patients who are difficult to ventilate with a face mask [138], especially in patients with obesity [139].
Management of oxygenation and ventilation — After preoxygenation and induction of general anesthesia (see 'Preoxygenation' above and 'Choice of induction agent' above), we typically hyperventilate the patient using a bag-valve-mask device immediately prior to delivering the electrical stimulus. This induces cerebral hypocarbia with a target end-tidal carbon dioxide (EtCO2) of 30 mmHg. Hyperoxia and hypocapnia increase seizure intensity and duration, thereby optimizing ECT stimulus efficiency while minimizing postictal side effects [102,140-144]. Some studies suggest that hyperoxia and hypocapnia (with a moderately low PaCO2) act synergistically to improve seizure quality and reduce the electrical charge required to generate a therapeutic convulsion [141,143].
Strategies to prevent O2 desaturation throughout the procedure include careful preoxygenation (see 'Preoxygenation' above), and administration of 100 percent supplemental oxygen as well as good airway control throughout the procedure, including emergence and recovery from general anesthesia [145-147]. It is thought that seizure duration is significantly impacted by the inspired oxygen concentration, although the mechanism underlying this phenomenon is not entirely clear [145]. There are no known clinically significant adverse effects of hyperoxia of short duration during ECT.
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 [142,148]. Hypocapnia may lower the seizure threshold in patients affected by an increasing seizure threshold during consecutive ECT treatment, although evidence is not consistent [149]. Hypocapnia also reduces intracranial hypertension and thereby, the incidence of postictal headache and agitation [150]. Potential adverse effects of hypocapnia include coronary and cerebral vasoconstriction and an increased the risk of arrhythmias [151].
Hypercapnia secondary to poor ventilation is avoided as it has been associated with hypertension, tachycardia, somnolence, delayed recovery from anesthesia, and a higher prevalence of postprocedure agitation and headache [152]. Notably, use of the bag-valve-mask device may not allow accurate measurement of EtCO2. Although transcutaneous CO2 pressure measurement may be an accurate noninvasive alternative, this technology is not widely available [153].
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 [154]. Asystole in the postictal period is very rare [155,156].
Asystole is often associated with chronically administered medications (see 'Management of chronically administered medications' above), administration of succinylcholine, or unusual ECT administration [157,158]. Asystole occurs more commonly after convulsive compared with nonconvulsive stimulations [154], and after electrode placement in the bitemporal or right unilateral positions compared with bifrontal electrode placement [159].
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 [160]. In some cases, it is necessary to administer either atropine or glycopyrrolate to treat severe or persistent bradycardia. (See "Arrhythmias during anesthesia", section on 'Other bradyarrhythmias'.)
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 administration' above.)
Sympathetic responses — The seizure itself triggers a sympathetic response which increases plasma levels of catecholamines resulting 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 [161]. Despite these significant hemodynamic changes, major adverse cardiac events (MACE) are rare after ECT [162]. (See 'Cardiovascular complications' below.)
Preparation for management of exaggerated or prolonged responses to sympathetic stimulation and close communication with the proceduralist are 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 or treatment of tachycardia and hypertension in response to seizure-induced sympathetic stimulation (table 5) [163]. Possible 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 [163]. Other agents (eg, calcium channel blockers, direct vasodilators such as nitroglycerin or nitroprusside) may be used in selected patients to minimize the undesirable cardiovascular effects of the sympathetic response to seizure induction (table 5). (See "Hemodynamic management during anesthesia in adults", section on 'Hypertension: Prevention and treatment' and "Arrhythmias during anesthesia", section on 'Pharmacologic treatment of tachycardia'.)
Decisions regarding preemptive administration of beta blockers or other agents 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. (See "Medical evaluation for electroconvulsive therapy", section on 'Cardiovascular effects'.)
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 postprocedure 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 [164,165]. (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]. In most cases, the headache is transient and mild, peaks at two hours, and is responsive to over-the-counter analgesics such as acetaminophen or ibuprofen given after the ECT procedure [166].
Triptans are also effective for post-ECT headache [167,168]. In a study of 20 patients with post-ECT headache, eletriptan and acetaminophen both reduced post-ECT headaches, but eletriptan was superior to acetaminophen at reducing the duration and intensity of headaches [169]. Cold therapy has also been found to be successful [170].
Nausea — Transient, postoperative nausea and vomiting (PONV) may occur in approximately 25 percent of patients after ECT [6]. Causes include anesthetic agents, hyperventilation with 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'.)
Adverse effects of antiemetic agents such as ondansetron or metoclopramide include rare development of serotonin syndrome if the patient is chronically taking a selective serotonin reuptake inhibitor (SSRI) or selective norepinephrine reuptake inhibitor (SNRI) agent. Development of QTc interval prolongation is possible 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). Administration of scopolamine to treat PONV may accentuate the anticholinergic side effects of TCAs, causing increased likelihood of postoperative delirium. (See 'Psychotropic medications: Anesthetic considerations' above.)
Mirtazapine has been successfully used to treat both post-ECT nausea and headache [171]. (See "Postoperative nausea and vomiting", section on 'Antiemetics'.)
Adverse cognitive effects
●Postictal agitation – Postictal agitation is a relatively frequent clinical problem reported in 10 percent of patients undergoing ECT [172]. 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 [173]. Mild cases can be treated with supportive measures and behavioral interventions.
In patients with a history of severe postictal agitation, intravenous (IV) benzodiazepines or propofol may be administered at the end of the seizure [174,175]. Dexmedetomidine may be useful in the treatment of refractory cases [93,94].
●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 cardiovascular complications are relatively rare with ECT and almost always occur in older patients and those with underlying cardiovascular disease. Medical management of such patients is discussed separately. (See "Medical evaluation for electroconvulsive therapy", section on 'Cardiovascular effects'.)
●Major adverse cardiovascular events – Major adverse cardiac events (MACE) and death after ECT are rare, occurring in about 1 in 50 patients, and after approximately 1 in 200 to 500 ECT treatments [162]. In a 2019 meta-analysis of 82 studies that included 106,569 patients undergoing 786,995 ECT treatments, the most commonly reported 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) [162]. Notably, acute pulmonary edema after ECT may be associated with a hypertensive crisis [176-178], a cardiogenic cause [161], a neurogenic cause [179], or another etiology such as negative intrathoracic pressure associated with airway obstruction [180,181].
●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 damage [182,183]. As noted above, prophylactic administration of a short-acting beta blocking agent is useful for prevention and treatment of tachycardia and hypertension due to sympathetic responses to ECT, particularly in patients at high risk of cardiovascular complications [163,184]. (See 'Sympathetic responses' above.)
●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 women (>70 years) [185]. Limited evidence suggests that pretreatment with beta blockers would prevent recurrence during subsequent ECT procedures [186].
Neurologic complications — Neurologic dysfunction following ECT is rare.
●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 [187]. Reported predisposing factors include electrolyte disturbance, benzodiazepine withdrawal, head trauma, pregnancy, neurologic disease, and antibiotics such as cefotiam, piperacillin, or ciprofloxacin [188-191]. 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 a confirmation by a multi-lead electroencephalogram (EEG) [192]. The first line of treatment includes IV benzodiazepines, followed by IV antiepileptic drugs if the seizure persists.
●Focal neurologic deficits – Todd phenomenon is a rare transient postictal focal neurologic deficit (eg, aphasia, hemiparesis, visual loss) with complete spontaneous recovery after ECT [187,193,194]. Other causes of focal neurologic dysfunction should be ruled out (eg, cerebrovascular ischemia [195], ruptured aneurysm [196,197]).
CONSIDERATIONS FOR ECT DURING THE COVID-19 PANDEMIC — Although elective surgical and other interventional procedures have been postponed during the novel coronavirus disease 2019 (COVID-19) pandemic, urgent and emergency procedures are necessary. Some institutions have established interdisciplinary review processes to determine which patients require urgent interventions, including electroconvulsive therapy (ECT) [198,199]. The bag-mask ventilation technique that is typically used during ECT incurs high risk for aerosol generation and consequent infection of participating clinicians, particularly anesthesia providers managing the airway. Details regarding techniques for minimizing infection risks for clinicians and the environment during airway management and provision of anesthetic care are available in a separate topic. (See "COVID-19: Perioperative risk assessment and anesthetic considerations, including airway management and infection control".)
Specific strategies and precautions to minimize risk of infection during ECT procedures have been developed, although these may vary according to local resources, and data supporting the efficacy of such strategies individually or collectively are scant [198,199]:
●Prior to ECT treatment, each scheduled patient is screened for COVID-19 infection.
●Some institutions are using a designated operating room or a designated negative pressure room to perform ECT during the COVID-19 pandemic, rather than using an open space area that is close to other patient beds (such as the post-anesthesia care unit [PACU]).
●Some institutions use a patient decolonization protocol before transport to the site where the ECT procedure will be performed with hydrogen peroxide oral rinsing, povidone-iodine nasal swabbing, and hand hygiene. A surgical mask is placed on the patient during transport.
●All health care personnel involved in the patient's care wear personal protective equipment. Details are available in a separate topic (see "COVID-19: Perioperative risk assessment and anesthetic considerations, including airway management and infection control", section on 'Infection control for anesthesia'). Specific institution-dependent recommendations for COVID-19-negative patients undergoing an aerosol-generating procedure during the COVID-19 pandemic may vary.
●In some institutions, the patient is asked to self-insert a bite block into his or her mouth, then an anesthesia mask attached to a high efficiency particulate air (HEPA) filter is applied by an anesthesia team member and held in place with a head strap. In other institutions, a supraglottic airway (SGA) with an integrated bite block is inserted after induction to limit aerosolization during controlled ventilation, rather than using a bite block.
●Preoxygenation is accomplished with a low inflow of oxygen (O2), typically two to four L/minute.
●After induction of anesthesia and electrical stimulation to induce the seizure, positive pressure ventilation is initiated if necessary. A two-person technique can be employed, with one anesthesia provider using two hands to ensure a good seal of the facemask and another provider delivering ventilation with small tidal volumes and low pressures to maintain adequate O2 saturation.
●If hyperventilation is required for seizure induction or rescue ventilation, a bite-proof SGA is typically inserted.
●Upon return of adequate spontaneous ventilation and demonstrated ability to maintain a patent airway, the patient's surgical mask is reapplied. The anesthesia circuit, anesthesia mask, and bite block are removed and placed in a biohazard bag to be discarded.
●During and after transport to a PACU, the surgical face mask is kept in place. If necessary to maintain adequate O2 saturation, supplemental O2 is administered via nasal cannula positioned under the surgical mask.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines are provided separately. (See "Society guideline links: Depressive disorders".)
SUMMARY AND RECOMMENDATIONS
●Electroconvulsive therapy (ECT) is a treatment for severe depression involving passage of a small brief current through the brain to induce a generalized seizure in a patient who is under general anesthesia. ECT may be performed in a variety of offsite or remote locations, including the post-anesthesia care unit (PACU), preoperative procedural areas, or a dedicated suite. Standard preparations for a general anesthetic are necessary. (See 'Technical considerations' above.)
●Patients presenting for ECT are often taking psychotropic medications (eg, selective serotonin reuptake inhibitors [SSRIs], tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), anticonvulsants [eg, carbamazepine, valproate], lithium, antipsychotic agents [eg, chlorpromazine, clozapine, quetiapine, olanzapine, risperidone, thioridazine, perphenazine, haloperidol], benzodiazepines). These drugs may have synergistic effects with ECT, and are usually continued during the periprocedural period. (See 'Psychotropic medications: Anesthetic considerations' above.)
Exceptions include benzodiazepines which are typically tapered and discontinued, while lithium or anticonvulsants such as carbamazepine and valproate are typically withheld on the evening before a planned ECT procedure.
In patients taking MAOIs, indirect sympathomimetic agents such as ephedrine or metaraminol are avoided to prevent exaggerated vasopressor effects (ie, severe hypertension), but direct-acting catecholamines (epinephrine, norepinephrine) or vasopressors (eg, phenylephrine, vasopressin) can be administered if slowly and carefully titrated.
●Preanesthetic medications may be administered in selected patients to prevent or minimize common adverse effects associated with ECT (eg, headaches, nausea, bradyarrhythmias). Benzodiazepines are avoided due to anticonvulsant properties that would make seizure induction more difficult. (See 'Preanesthetic medications' above.)
●The selected anesthetic induction agent(s) should not interfere with inducing an effective grand mal seizure. Methohexital is the agent of choice, administered intravenously at a dose of 0.75 to 1 mg/kg. Advantages include rapid onset of action, short duration, minimal anticonvulsant effects, rapid recovery, and low cost. Other anesthetic induction agents include propofol and etomidate. (See 'Choice of induction agent' above.)
●The patient must be rendered unconscious to prevent awareness before the administration of neuromuscular blocking agent (NMBA). An appropriate level of anesthetic is confirmed by the anesthesiologist by noting loss of response to verbal commands and/or loss of eyelash reflex. (See 'Depth of anesthesia' above.)
●Succinylcholine 1 mg/kg is the NMBA of choice because of its rapid onset, short duration of action, and rapid recovery. A higher dose may be used in selected patients. To check that the electrical stimulation has produced a tonic-clonic seizure, a standard blood pressure 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. This allows visual and tactile observation of the motor component of seizure activity in that foot. Electrical stimulation to produce the seizure should be applied only when maximal neuromuscular blockade has been achieved, as monitored with a peripheral nerve stimulator. (See 'Neuromuscular blocking agents' above.)
●To prevent dental and alveolar bone damage as well as soft tissue injury, a bite guard made of flexible material with maximal cushioning in the molar area is used. Most patients are efficiently ventilated using a face mask (eg, a bag-valve-mask device). (See 'Airway management' above.)
●Preoxygenation via nasal cannula or face mask during spontaneous ventilation is accomplished before induction of general anesthesia to maintain oxygen (O2) saturation at or near 100 percent. After induction of general anesthesia, the patient is typically hyperventilated immediately prior to delivering the ECT stimulus. This induces cerebral hypocarbia with a target end-tidal carbon dioxide (EtCO2) of approximately 30 mmHg. Hyperoxia and hypocapnia increase seizure intensity and duration, thereby optimizing ECT stimulus efficiency while minimizing postictal side effects. (See 'Preoxygenation' above and 'Management of oxygenation and ventilation' above.)
●Electrical stimulation to induce the seizure initially triggers bradycardia and/or asystole that is self-limited in most patients, lasting for a brief period (10 to 15 seconds). If severe or persistent, either atropine or glycopyrrolate is administered. (See 'Parasympathetic responses' above.)
●The seizure itself triggers a sympathetic response which increases plasma levels of catecholamines resulting in tachycardia with an increase in heart rate of approximately 20 percent, hypertension with an increase in systolic blood pressure of approximately 30 to 40 percent, and an increase in cardiac output of approximately 80 percent, lasting for five or more minutes. A short-acting beta blocker (eg, esmolol, landiolol, labetalol) or other agent (eg, calcium channel blockers, direct vasodilators such as nitroglycerin or nitroprusside) is used for prophylaxis or treatment of these effects if necessary (table 5). (See 'Sympathetic responses' above.)
●As with all procedures requiring general anesthesia, recovery in a PACU or recovery area with comparable equipment and personnel is necessary. Common adverse effects may be evident in the immediate postprocedure period, including headache, nausea, and postictal agitation. Major cardiovascular or neurologic complications are rare. (See 'Management of adverse effects during recovery' above.)
