Ethan O. Bryson, MD

Ketamine has long been used as an alternative anesthetic agent for ECT. Recently, there has been considerable excitement about its intrinsic antidepressant qualities when given at subanesthetic doses, intravenously or intranasally. We review the clinical use of ketamine as the anesthetic induction agent in ECT and discuss the evidence that it augments antidepressant response and reduces cognitive adverse effects.

Modern ECT practice involves full, albeit brief, general anesthesia, hyperventilation with oxygen, and muscle relaxation with succinylcholine. Anesthesia technique is intimately related to the quality of ECT, not only from the standpoint of patient comfort and safety, but also because the quality and effectiveness of the seizure are affected by the anesthetic agent and airway management.

The most commonly used induction agents in the US are methohexital and propofol. Sodium thiopental, etomidate, and ketamine are less commonly used alternatives. Many anesthetics are anticonvulsant, including all the barbiturates and propofol. While this is not an optimal characteristic for an ECT induction agent, for the vast majority of patients, both methohexital and propofol are satisfactory choices.

Methohexital is often considered the ECT anesthetic of choice because of its many favorable characteristics: rapid onset, short duration of action, moderate anticonvulsant properties, predictable effectiveness, good hemodymanic profile, and low cost. Unfavorable properties of methohexital include pain on intravenous injection and less “smooth” emergence than with propofol. Methohexital is sufficiently anticonvulsant to be recommended as the agent of choice in terminating prolonged ECT seizures.

Propofol, a milky white solution, has an onset and duration of action similar to that of methohexital, a good hemodynamic profile, and “smoother” emergence, with a lesser incidence of postictal agitation. It is similarly painful on injection but is much more potently anticonvulsant, a property that may make it unsuitable for use in certain patients with high seizure thresholds and/or very short seizures. Several studies have concluded that despite propofol’s anticonvulsant activity, using it for ECT anesthesia does not result in inferior antidepressant outcomes.

 Its anticonvulsant property may make propofol a preferred induction agent for young patients receiving ECT.

Thiopental, less commonly used in the US than abroad, is half as potent as methohexital. It has a slower onset of action but a longer duration of action than methohexital. Etomidate is often used when a less anticonvulsant induction agent is preferred or when hemodynamic stability is of primary concern. Disadvantages of etomidate include the potential for repeated doses to cause adrenal suppression and a high incidence of myoclonus during the induction period.

Ketamine has a long history of use as an alternative anesthetic induction agent in ECT when seizure enhancement is desired. More recently, it has been tried with the goals of directly enhancing the antidepressant effect of ECT or reducing cognitive effects.

Ketamine is a “dissociative” anesthetic, a noncompetitive 

-methyl-D-aspartate (NMDA) receptor antagonist developed in 1964 as a derivative of phencyclidine. It is currently used either as a drug to induce general anesthesia or as an adjunct to inhaled or infused general anesthetics to provide analgesia for surgery or other painful procedures.

When ketamine is administered as an intravenous bolus dose of approximately 1 mg/kg, peak plasma levels are reached and it reliably induces a state of general anesthesia, typified by unresponsiveness to voice commands or to painful stimulus, usually within 60 to 90 seconds, rarely requiring up to 5 minutes. Nystagmus is a key physical sign induced by ketamine, which may help establish depth of anesthesia during a ketamine induction. The ECT team should be prepared to wait longer for the patient to become fully unconscious with ketamine than with methohexital; the time of injection of the succinylcholine may also have to be delayed. In addition to its NMDA effects, ketamine causes a moderate sympathomimetic action via increased catecholamine release and decreased reuptake, resulting in tachycardia and hypertension.

For patients who cannot tolerate the clinical effects of ketamine, the ketamine and propofol combination drug, colloquially referred to as “ketofol” may be more appropriate. By administering propofol and ketamine simultaneously, less of each agent is required to induce general anesthesia. The simultaneous use of these two medications allows for the capitalization on the different therapeutic and adverse-effect profiles of each: ketamine’s proconvulsant effect, and possible antidepressant effect, and propofol’s smoother induction and wake-up properties, as well as its ability to counteract the hypertension caused by ketamine. A lower dose of propofol reduces the potential negative impact on seizure elicitation.

 found no seizure-enhancing effect of ketamine (dose range, 1 to 3 mg/kg) in a case series of 10 patients, Krystal and colleagues,

 in a study that compared ketamine with methohexital, found that ketamine (mean dose, 1.3 mg/kg) increased seizure duration in 30 of 36 patients, and it also increased midictal amplitude of the EEG. One patient in whom a seizure could not be elicited with methohexital had a seizure when ketamine was used.

In a retrospective chart review that included 16 patients who received ketamine, no difference in seizure duration was found.

 However, ketamine resulted in higher concordance (the ratio of motor seizure duration to EEG seizure duration), a possible marker of seizure quality. Similarly, there was no increase in seizure duration in 22 patients treated with 0.5 mg/kg of ketamine (versus saline placebo) added to thiopentone anesthesia.

Nor were there differences in seizure threshold or duration in 16 patients given 0.4 mg/kg of S-ketamine (versus saline placebo) added to propofol anesthesia.

In a study that compared the effects of thiopental with those of ketamine, Yoosefi and colleagues

 found longer seizure duration and less electrical charge needed for patients who were treated with 1 to 2 mg/kg of ketamine. Results from a recent study by Rasmussen and colleagues

 showed that patients who received 1 mg/kg of ketamine had longer motor seizure duration than patients who received methohexital.

A large retrospective chart review compared ECT seizure quality induced by ketamine, thiopental, etomidate, and propofol. Findings indicate that compared with propofol or thiopental, ketamine and etomidate induced higher-quality seizures.

Ketamine has also been used for ECT anesthesia in an attempt to decrease cognitive effects. Post-ECT reorientation times were shorter in patients who received ketamine than in those treated with methohexital.

 There was less initial decline in Mini-Mental State Examination (MMSE) scores and greater final improvement in patients treated with ketamine than in those treated with thiopentone.

 After 6 sessions of ECT, patients who received 1 mg/kg of ketamine were able to recall words better than those who received etomidate.

However, when ketamine 0.5 mg/kg (versus saline placebo) was added to thiopentone or propofol, no cognitive advantage was seen on a fairly extensive neuropsychological test battery in 22 patients.

 In addition, there were no differences in MMSE or post-ECT reorientation scores between ketamine and methohexital.

The recent excitement about the intrinsic antidepressant properties of ketamine, a result of pioneering work by groups from the NIMH, Yale, and the Icahn School of Medicine at Mount Sinai, has led to the reexamination of whether this phenomenon might be synergistic with ECT. Marked immediate mood improvement was reported in a patient who received ketamine anesthesia for ECT, in whom the first 2 sessions failed to elicit a seizure.

 Similarly, a dramatic mood improvement was seen in a patient after a single ECT procedure preceded by a sedating dose of intramuscular ketamine.

 reported a statistically significant greater decrease in Hamilton Depression Rating Scale (HAM-D) scores after the fourth ECT session in 11 patients treated with ketamine versus propofol, but this advantage was gone by the end of the ECT course. In an unusual study design in which patients received a single ECT and were then observed for a week, statistically significantly greater decreases in HAM-D scores at days 1, 2, and 3 were reported for patients who received ketamine alone or ketamine plus propofol than for those who received propofol alone.

 But the advantage was gone by the end of the week.

Patients treated with ketamine 0.5 mg/kg (versus saline placebo) added to thiopentone or propofol had a modest increase in antidepressant effect over the first week, but not after the overall course.

 Abdallah and colleagues17 reported that 0.5 mg/kg of ketamine added to thiopental did not result in enhanced antidepressant effect compared with thiopental anesthesia alone. Similarly, no antidepressant advantages were seen when S-ketamine was added to propofol.

Early antidepressant response was seen in patients treated with ketamine versus thiopental, but this difference had disappeared by the end of the ECT course.

 failed to show any enhanced antidepressant response in patients treated with ketamine compared with those treated with methohexital.

A substantial body of clinical evidence supports the overall safety and tolerability of ketamine as an alternative anesthetic induction agent for ECT. Although there is a greater incidence of hypertension and dissociative/hallucinatory effects, these are manageable and not sufficiently common to be serious impediments to its use.

There is general agreement that ketamine is either less anticonvulsant than methohexital and propofol, or even slightly pro-convulsant, and therefore has a role in seizure enhancement for ECT patients with high seizure thresholds, very short seizures, or poor seizure expression.

Most puzzling, and frankly disappointing, is the failure to demonstrate any more than a modest additive antidepressant effect when combined with ECT. Partly, this may be due to a “ceiling effect,” in which the antidepressant effect of ECT is so potent, it is hard to show dramatic improvement. Theoretically, if ketamine and ECT were to have identical mechanisms of action on the glutamate system, it would be unrealistic to expect huge synergism, again because of the potency of ECT. Another possibility is that the dose range of ketamine when used as the sole induction agent for ECT, typically twice that of ketamine infusions for depression, is not in the optimal range for antidepressant effect, although some ECT studies have used comparable doses.

Finally, it must be stated that, the above research notwithstanding, there has yet to be a large-scale, methodologically rigorous clinical trial of ketamine anesthesia in ECT. There are signals of enhanced antidepressant efficacy and decreased cognitive effects. There are many theoretical reasons why this combination should work well. Future research may guide how to best synergize the effects of ECT and ketamine.

Dr Kellner is Professor of Psychiatry and Dr Bryson is Associate Professor of Anesthesiology and Associate Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai in New York. The authors report no conflicts of interest concerning the subject matter of this article.

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 Vaidya PV, Anderson EL, Bobb A, et al. A within-subject comparison of propofol and methohexital anesthesia for electroconvulsive therapy. 

 Rasmussen KG, Jarvis MR, Zorumski CF. Ketamine anesthesia in electroconvulsive therapy. 

 Krystal AD, Weiner RD, Dean MD, et al. Comparison of seizure duration, ictal EEG, and cognitive effects of ketamine and methohexital anesthesia with ECT. 

 Kranaster L, Kammerer-Ciernioch J, Hoyer C, Sartorius A. Clinically favourable effects of ketamine as an anaesthetic for electroconvulsive therapy: a retrospective study. 

 Loo CK, Katalinic N, Garfield JB, et al. Neuropsychological and mood effects of ketamine in electroconvulsive therapy: a randomised controlled trial. 

 JÃ¤rventausta K, Chrapek W, Kampman O, et al. Effects of S-ketamine as an anesthetic adjuvant to propofol on treatment response to electroconvulsive therapy in treatment-resistant depression: a randomized pilot study. 

 Yoosefi A, Sepehri AS, Kargar M, et al. Comparing effects of ketamine and thiopental administration during electroconvulsive therapy in patients with major depressive disorder: a randomized, double-blind study. 

 Rasmussen KG, Kung S, Lapid MI, et al. A randomized comparison of ketamine versus methohexital anesthesia in electroconvulsive therapy. 

 Hoyer C, Kranaster L, Janke C, Sartorius A. Impact of the anesthetic agents ketamine, etomidate, thiopental, and propofol on seizure parameters and seizure quality in electroconvulsive therapy: a retrospective study. 

 McDaniel WW, Sahota AK, Vyas BV, et al. Ketamine appears associated with better word recall than etomidate after a course of 6 electroconvulsive therapies. 

 Ostroff R, Gonzales M, Sanacora G. Antidepressant effect of ketamine during ECT. 

 Goforth HW, Holsinger T. Rapid relief of severe major depressive disorder by use of preoperative ketamine and electroconvulsive therapy. 

 Okamoto N, Nakai T, Sakamoto K, et al. Rapid antidepressant effect of ketamine anesthesia during electroconvulsive therapy of treatment-resistant depression: comparing ketamine and propofol anesthesia. 

 Wang X, Chen Y, Zhou X, et al. Effects of propofol and ketamine as combined anesthesia for electroconvulsive therapy in patients with depressive disorder.

 Kellner CH, Briggs MC, Pasculli RM, Bryson EO. Antidepressant effect of the first electroconvulsive therapy with ketamine and/or propofol. 

 Abdallah CG, Fasula M, Kelmendi B, et al. Rapid antidepressant effect of ketamine in the electroconvulsive therapy setting. 

Articles

The authors review the clinical use of ketamine as the anesthetic induction agent in ECT and discuss the evidence that it augments antidepressant response and reduces cognitive adverse effects. 

Ketamine Anesthesia for Electroconvulsive Therapy

Electroconvulsive therapy (ECT) has been a safe and effective treatment for severe depression and other psychiatric illnesses since its introduction into clinical practice in 1938.

“Anesthesia Advances Add to the Safety of ECT”

), we described how modern anesthesia techniques make ECT safe. Here we discuss how advancements in anesthesia techniques and ECT procedures make ECT more comfortable and tolerable for patients.

Over the past 75 years, a large number of patients have been treated successfully with ECT, but until recently, many who received ECT could expect post-treatment nausea or headache.

 Although these unpleasant effects are generally mild, for some the nausea and headache can be severe enough to cause them to avoid needed treatment. Now, even these previously common aftereffects can be prevented with medications originally developed to prevent postoperative pain and nausea. In addition to these specific anesthesia interventions, other periprocedural advancements, including liberalization of concomitant and pre-treatment medications, add to the comfort and tolerability of ECT.

Headache is the most commonly reported complaint after ECT; it may occur in about half of patients. It is typically mild and transient and usually responds to simple, over-the-counter analgesics, such as acetaminophen and ibuprofen. In some patients, however, it may be more severe, making prophylactic intervention with an intravenous agent, such as ketorolac, appropriate.

Post-ECT headache develops immediately or shortly after the patient regains consciousness following ECT.

 The headache may be associated occasionally with nausea and rarely with photophobia. It is usually bilateral and constant but may be unilateral or pulsatile.

The NSAID ketorolac can be given intravenously.

 Ketorolac is indicated for the short-term management of moderately severe acute pain that requires analgesia at the opioid lev-el, and it is frequently given to patients after they have had surgery. Although the pain-relieving properties of ketorolac are similar to those of morphine, the drug does not cause respiratory depression or cloud the sensorium.

Because ketorolac is an NSAID, it is contraindicated in anyone with sensitivity to this class of drugs or with a bleeding tendency. Because it can be administered intravenously, ketorolac can be given immediately before treatment and is very effective in significantly reducing the incidence of post-ECT headache. Generally, no prophylactic analgesic is given before the first treatment; rather, if the patient awakens with headache, he or she is offered ibuprofen or acetaminophen by mouth. If the headache turns out to be of moder-ate or severe intensity, the patient is offered prophylaxis with intravenous ketorolac at subsequent ECT sessions.

For patients with a history of migraine or other, more severe headache, the likelihood that they will experience a post-treatment headache is higher than in patients who do not have this history. For those patients, treatment of post-ECT headache may require antimigraine medications.

Nausea following ECT is less common than headache but still occurs in up to 25% of patients. Nausea may be related to the anesthetic, to the ECT treatment itself, or to air in the stomach from assisted ventilation. It may occur in conjunction with, or independently from, headache. Post-ECT nausea can prevent otherwise well patients from leaving the treatment recovery area in a timely manner and going about the rest of their day.

When nausea occurs without headache, the primary treatment is with the serotonin 5-HT3 receptor antagonist ondansetron. Since the untoward effects of prophylaxis with this medication are few, most patients at increased risk for post-ECT nausea are given ondansetron intravenously before treatment. Older antinausea medications such as the dopamine-blocking agents, including phenothiazine derivatives (eg, prochlorperazine), butyrophenones (haloperidol, droperidol), trimethabenzamide, and metoclopramide, are associated with more adverse effects (eg, sedation). These older antinausea medications are reserved for the extremely rare case in which ondansetron is not effective.

If nausea cannot be prevented by routine prophylaxis with ondansetron, switching the anesthetic agent may also be considered. For some patients with severe post-ECT nausea, propofol may be the preferred choice of anesthetic agent because it has intrinsic antiemetic properties.

Diffuse myalgias are most commonly reported after the first ECT session; they then subside or complete-ly disappear following subsequent treatments.

 They are likely caused by muscle fasciculations from the muscle relaxant agent, succinylcholine, used in ECT. Similar to what happens after an intense workout at the gym, patients may feel sore for a day or two after receiving the drug.

The incidence of myalgias after use of succinylcholine can approach 90%. Usually, the myalgias respond well to the same simple analgesics that are used for mild headache. If myalgias persist after subsequent ECT sessions, other interventions, including prophylactic intravenous ketorolac or pretreatment with a small dose of a nondepolarizing muscle relaxant (to block the fasciculations), may be considered.

In years past, an intramuscular injection of an anticholinergic agent was given at least 30 minutes before ECT; this often resulted in significantly unpleasant adverse effects, such as dry mouth and rapid heartbeat. Today, glycopyrrolate is typically administered intravenously immediately before ECT.

 Given in this fashion, glycopyrrolate safely prevents bradycardia without causing the unpleasant pre-ECT dry mouth.

Many patients are understandably anxious before an ECT session. For the vast majority, once they have had their first treatment, this anxiety subsides. For a small minority of patients, ongoing anxiety may be a problem that jeopardizes their ability to complete a course of ECT. In addition, many patients experience anxiety symptoms as part of their depressive episode and wish to continue taking benzodiazepines, at least in the beginning of their ECT course.

In the past, the amount of benzodiazepine antianxiety medication allowed during a course of ECT was strictly limited and was completely prohibited the morning before a session. Currently, the practice is much more liberal-we now recognize that low to moderate doses of benzodiazepines are very unlikely to interfere with a course of ECT.

 A common practice is to switch from a medication with a long half-life (eg, clonazepam) to one with a shorter half-life (eg, lorazepam), with the expectation that a bedtime dose will have been more fully cleared from the bloodstream by the time of ECT the next morning and, thus, will interfere minimally with seizure induction and propagation. For extremely anxious patients, a low dose of a benzodiazepine can be taken the morning of an ECT session-a patient can take 0.5 or 1 mg of lorazepam by mouth with a small sip of water, or the drug can be dissolved sublin-gually, an hour or so before the ECT procedure.

Almost all patients being considered for a course of ECT are receiving one or more psychotropic medications. Clearly, most of these drugs will have been either completely ineffective or only partially effective-hence the need to consider ECT. In the past, standard practice was to discontinue all psychotropic medications before starting ECT. This often necessitated a delay in starting ECT and sometimes led to the discomfort of withdrawal syndromes. With the recognition that many modern antidepressant medications are safe in conjunction with ECT, it is now common practice to continue medications that are well tolerated and may have been partially helpful. It is also becoming more common to initiate treatment with new antidepressant agents concurrently with a course of ECT, with the expectation of added antidepressant efficacy and a possible reduction in risk of relapse when ECT is terminated.

Contemporary anesthesia practices and ECT procedures have evolved to make ECT both safe and comfortable for patients. Unfortunately, because of lingering stigma and a low level of familiarity with ECT among many health care providers, ECT continues to be prescribed less frequently than warranted. For severely depressed patients, it remains a vital treatment option.

As practitioners, it is our responsibility to ensure that ECT is prescribed when indicated and practiced to a high standard of care, with patient safety and comfort as foremost goals. As the idealized McLean Hospital psychiatrist, Dr Nolan, said to calm her apprehensive patient, Esther Greenwood, in 

 “If it’s done properly, it’s like going to sleep.”

Kellner CH, Bryson EO. Anesthesia advances add to safety of ECT.

 American Psychiatric Association Task Force on Electroconvulsive Therapy.

 The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 

Washington, DC: American Psychiatric Association; 2001.

 Dinwiddie SH, Huo D, Gottlieb O. The course of myalgia and headache after electroconvulsive therapy. 

 Gillis JC, Brogden RN. Ketorolac. A reappraisal of its pharmacodynamic and pharmacokinetic properties and therapeutic use in pain management. 

 Markowitz JS, Kellner CH, DeVane CL, et al. Intranasal sumatriptan in post-ECT headache: results of an open-label trial. 

 Rasmussen KG, Petersen KN, Sticka JL, et al. Correlates of myalgia in electroconvulsive therapy. 

 Boylan LS, Haskett RF, Mulsant BH, et al. Determinants of seizure threshold in ECT: benzodiazepine use, anesthetic dosage, and other factors.

 Sackeim HA, Dillingham EM, Prudic J, et al. Effect of concomitant pharmacotherapy on electroconvulsive therapy outcomes: short-term efficacy and adverse effects. 

Here we discuss how advancements in anesthesia techniques and ECT procedures make ECT more comfortable and tolerable for patients.

Anesthesia Advances Add to Patient Comfort in ECT

Modern electroconvulsive therapy (ECT) is a remarkably safe and effective antidepressant treatment. It remains a critical option for urgently ill patients, many of whom do not adequately respond to antidepressant medications.

Advances in anesthesia technique are a major part of the safety and comfort profile of ECT today. In this article, we briefly review important aspects of the anesthesia used in ECT. While we do not believe that all psychiatrists need to be expert in the details, knowledge of the basics is necessary to adequately inform patients about ECT during the referral process.

ECT is performed under full general anesthesia and muscle relaxation. Blood pressure, pulse, ECG, and blood oxygen saturation are monitored to ensure patient safety. Supplemental oxygen is provided throughout the procedure by the anesthesiologist, who ventilates the patient using a mask and bag. Patients are not intubated for ECT, except under extremely rare circumstances.

An intravenous line is inserted in the patient’s arm, through which the anesthetic and muscle relaxant medications are administered. The sequence of administration is to give the anesthetic induction agent first, followed by the muscle relaxant, only after the patient has lost consciousness. The patient is ventilated with oxygen while the muscle relaxant takes effect (1 to 2 minutes). A foam or rubber protective device is then inserted into the patient’s mouth, and the electrical stimulus is delivered. A seizure occurs (typically 30 to 60 seconds), and the patient awakens in a few minutes as the medications wear off. The total procedure takes less than 10 minutes.

The anesthesiologist will consult with the patient before the treatment. For medically complex patients, this should be done in advance; for younger, medically healthy patients, it may be done the morning of the first treatment. Some patients who present for ECT may be poor historians or completely nonverbal; it may therefore be necessary to rely on supplemental sources of information, such as consults with other treating physicians, discussion with family members, and laboratory or other diagnostic tests.

Although ECT is generally a low-risk procedure, many ECT patients fall into the high-risk category. The pre-anesthetic assessment should therefore focus on identifying conditions that increase the risk of morbidity or mortality during treatment.

 The ECT psychiatrist and the anesthesiologist must decide which laboratory tests will need to be done before ECT. At a minimum, each patient referred for ECT should have an ECG to evaluate potential cardiac problems and to establish a baseline; a complete blood cell count to detect anemia or infection; and a basic metabolic panel to look for electrolyte imbalances, especially potassium and sodium levels.

When evaluating a potential candidate for ECT, it is particularly important to pay close attention to the patient’s cardiovascular and pulmonary status.

 The release of endogenous catecholamines associated with the therapeutic seizure typically causes transient hypertension and tachycardia. Patients with a significant cardiac history who may be at risk for myocardial ischemia under these conditions need a careful cardiac evaluation. It is also important to evaluate the patient’s pretreatment pulmonary function. Particularly close attention needs to be paid to any signs of deteriorating respiratory status or infection, such as shortness of breath, cough, fever, or low oxygen saturation on room air.

Potential interactions between psychiatric medications the patient is taking and the medications used during anesthesia need to be assessed. The patient’s current medication list needs to be reviewed and decisions made in advance about which medications to taper or stop before the procedure, which medications to continue during the course of ECT (but held until after each treatment), and which medications can safely be given with a minimum amount of water early in the morning of the ECT.

In general, medications that would interfere with the seizure (anticonvulsants and benzodiazepines) should be minimized, and medications that optimize the patient’s medical condition (most importantly antihypertensives and antireflux medi-cations) should be given before the treatment.

 There has been a recent revival of interest in concomitant use of antidepressant medications and ECT: the goal is improved antidepressant efficacy and protection against relapse when the course of ECT is completed.

 Certain medications, including MAO inhibitor antidepressants, lithium, and theophylline, present specific issues that may require modifications in ECT, anesthesia technique, or patient instructions.

 The full range of concomitant medication issues is covered elsewhere.

The 2 most commonly used anesthetic agents for ECT in the United States are methohexital and propofol. Less commonly used anesthetics are thiopental sodium, etomidate, and ketamine. An optimal anesthetic for ECT should put the patient to sleep quickly but for a short time and not interfere too much with the induction of the ECT seizure.

Methohexital is an ultrashort-acting barbiturate that has become the anesthetic of choice in ECT practice. It renders the patient unconscious quickly (in about 45 seconds) and lasts just long enough for the ECT procedure. Because it is a barbiturate, it has some anticonvulsant properties, but not enough to interfere with ECT. It is easy to dose, administered as an intravenous bolus of about 1 mg/kg of patient weight. It is quite inexpensive and is available as a generic.

Propofol is probably the second most commonly used anesthetic for ECT. It is a milky white liquid that is also given by intravenous bolus. Advantages over methohexital include a “smoother wake up” and a somewhat more favorable hemodynamic profile. Disadvantages are its much greater anticonvulsant effect and higher cost.

Etomidate is an alternative agent that has less anticonvulsant effect than methohexital. It is sometimes used when seizures are short or hard to elicit.

Ketamine is a very interesting agent that is slightly proconvulsant and has intrinsic antidepressant properties. Disadvantages include hypertension and occasional transient dissociative symptoms on wake up. If its antidepressant qualities prove to be additive with ECT, its use could increase.

Muscle relaxation to eliminate the motor component of the ECT-induced seizure has been a feature of ECT since the 1950s. Muscle relaxation during the application of the stimulus, as well as for the duration of the motor portion of the seizure, prevents musculoskeletal injury. Because of the short duration of ECT, succinylcholine is the drug of choice for neuromuscular blockade, although for patients in whom its use is contraindicated, rocuronium or other nondepolarizing agents are alternatives.

Succinylcholine is a depolarizing neuromuscular blocker with an ultrashort duration of action, slightly less than that of the anesthetic agent. The duration of muscle paralysis is thus very brief, and spontaneous respirations return shortly after the seizure ends.

Modern anesthesia technique during ECT includes careful management of the patient’s airway with the administration of 100% supplemental oxygen.

 Once general anesthesia has been induced, hyperventilation is performed using a bag and mask device during the 1 to 2 minutes before the initiation of therapy. Hyperventilation decreases the blood levels of carbon dioxide, reduces the seizure threshold, and increases seizure duration. Ventilation with 100% oxygen during this period also increases the amount of oxygen available to the brain for use during the treatment.

The anesthesiologist who manages the airway during this period is careful to protect the patient from aspiration while maintaining ventilation and oxygenation. Sometimes a soft preshaped airway device (oral airway) is placed to facilitate this. In most patients, return of spontaneous respiration occurs within 3 to 5 minutes after induction, before the effects of the anesthetic have worn off and the patient is awake. Some patients may begin breathing immediately after the seizure ceases. For others, ventilatory support is continued until the patient takes adequate breaths on his own and no longer requires assistance.

The increase in heart rate and blood pressure that typically accompany an ECT-induced seizure are easily managed with currently available short-acting intravenous medications.

The stimulus applied to the brain during the initiation of ECT results in a profound parasympathetic surge. Asystole during this period is common but temporary, even though it may persist throughout the stimulus application.

Following stimulus termination, the resulting seizure is accompanied by a profound sympathetic surge, typically associated with tachycardia and hypertension. The elevations in heart rate and blood pressure can be significant, with increases in systolic blood pressure by as much as 40% over baseline.

 Safe control of heart rate and blood pressure can easily be achieved with frequent dosing of a short-acting agent such as esmolol, labetalol, or nitroglycerin.

Modern anesthesia techniques allow ECT to be performed with a high degree of patient safety and comfort. Simple, standardized protocols ensure that it can be provided in many facilities with consistent antidepressant results and a favorable adverse-effect profile. Mental health practitioners should be knowledgeable about the basics of the procedure, including how the anesthetic is given, in order to provide accurate information for patients who may be candidates for ECT.

While only a small percentage of practitioners will actually provide ECT, many more will encounter seriously ill patients who will need to be referred to facilities in which ECT is performed. For those practitioners, we hope that this summary is helpful; for those readers who want to learn more, authoritative resources include the American Psychiatric Association’s Task Force Report on ECT as well as several excellent text books and online resources.

 American Psychiatric Association. Task Force on Electroconvulsive Therapy. 

The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging

. 2nd ed. Washington, DC: American Psychiatric Association; 2001.


 Fink M. Electroconvulsive therapy resurrected: its successes and promises after 75 years. 

 Tess AV, Smetana GW. Medical evaluation of patients undergoing electroconvulsive therapy [published correction appears in 

 Zielinski RJ, Roose SP, Devanand DP, et al. Cardiovascular complications of ECT in depressed patients with cardiac disease. 

 Sienaert P, Peuskens J. Anticonvulsants during electroconvulsive therapy: review and recommendations. 

 Dolenc TJ, Habl SS, Barnes RD, Rasmussen KG. Electroconvulsive therapy in patients taking monoamine oxidase inhibitors. 

 Dolenc TJ, Rasmussen KG. The safety of electroconvulsive therapy and lithium in combination: a case series and review of the literature. 

Rasmussen KG, Zorumski CF. Electroconvulsive therapy in patients taking theophylline. 

 Simple, standardized protocols ensure that ECT can be provided safely and comfortably in many facilities, with consistent anti-depressant results and a favorable adverse-effect profile.

Author | Ethan O. Bryson, MD

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