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Medical evaluation for electroconvulsive therapy

Medical evaluation for electroconvulsive therapy
Authors:
Anjala Tess, MD
Gerald W Smetana, MD
Section Editor:
Andrew D Auerbach, MD, MPH
Deputy Editor:
Lisa Kunins, MD
Literature review current through: Feb 2022. | This topic last updated: Jul 30, 2021.

INTRODUCTION — Electroconvulsive therapy (ECT) is a commonly performed procedure in the United States. Use of ECT is rising, and psychiatrists often request medical evaluation before ECT since many eligible patients are older adults with multiple medical comorbidities. This topic review will discuss the use, indications, anesthetic technique, procedure, and morbidity of ECT, as well as risk assessment and strategies to reduce the risk of the procedure.

Additional discussion of ECT in adults can be found elsewhere. (See "Overview of electroconvulsive therapy (ECT) for adults".)

INDICATIONS — The primary indication for electroconvulsive therapy (ECT) is for the treatment of major depression that is refractory to antidepressant medications [1]. Indications listed in the American Psychiatric Association guidelines for the treatment of patients with major depressive disorder include depression with psychotic features, catatonia, persistent suicidal intent, food refusal leading to nutritional compromise or dehydration, and pregnancy and other situations where a rapid antidepressant response is required (table 1). The report also recommends ECT for patients who have previously shown a positive response to it and for those who have medical conditions that prevent the use of antidepressant medications. Other guidelines agree with these indications, including the Canadian Psychiatric Association clinical guidelines for the treatment of depressive disorders and the Royal Australian and New Zealand College of Psychiatrists professional practice guidelines for the administration of ECT [2,3]. (See "Unipolar major depression in adults: Indications for and efficacy of electroconvulsive therapy (ECT)" and "Unipolar depression in adults: Choosing treatment for resistant depression".)

Other psychiatric conditions for which ECT is effective include bipolar depression and mania [4].

TECHNIQUE AND ANESTHESIA — The technique for administering electroconvulsive therapy (ECT), including anesthesia, is discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in adults".)

MORBIDITY AND MORTALITY — Clinicians should be aware of certain potential side effects or complications of electroconvulsive therapy (ECT). (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Adverse effects'.)

The American Psychiatric Association lists the following conditions as 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

American Society of Anesthesiologists (ASA) Class 4 or 5 (table 2)

Mortality — ECT is one of the safest procedures performed under general anesthesia. With modern anesthetic technique, the mortality rate is sufficiently low and the potential life-saving benefit is compelling enough that absolute contraindications to treatment no longer exist. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Adverse effects'.)

Cardiovascular effects — The incidence of important cardiac complications are relatively rare with ECT and almost always occur in older patients and those with underlying cardiovascular disease.

A 15- to 20-second parasympathetic discharge occurs during the procedure as the patient enters the tonic phase of seizure. This can lead to arrhythmias including bradycardia with or without hypotension, atrial arrhythmias, premature atrial and ventricular contractions, atrioventricular block, and asystole. Asystole can occur with the first treatment or at any time later in a patient's course [6]; patients are at higher risk with longer periods of subconvulsive seizures [7]. In one study of older adult patients, 66 percent had asystole lasting greater than five seconds with no lasting complications [8]. A history of hypertension or evidence of ischemia on electrocardiogram (ECG) did not predict asystole, nor did current use of calcium channel blockers, nitroglycerin, angiotensin-converting enzyme (ACE) inhibitors, diuretics, or psychiatric medications (beta blockers were not included). Interestingly, patients with heart block and/or rhythm abnormalities were less likely to develop asystole (54 versus 16 percent).

The clonic phase of the seizure then leads to a catecholamine surge that causes tachycardia and hypertension. The duration of tachycardia usually correlates with the length of the seizure itself [9]. The increase in heart rate may attenuate with successive treatments in a given patient [10], suggesting that a significant tachycardic response during early treatments should not necessarily prohibit patients from completing a full course of therapy. These hemodynamic responses continue into the postictal period and usually resolve within 10 to 20 minutes of the seizure [11]. Occasionally, patients have persistent hypertension that requires treatment. (See 'Postprocedure hemodynamic changes' below.)

All patients are followed with ECG during the procedure; even healthy patients can have transient ECG changes. However, these changes are rarely significant, as illustrated by a study of 29 patients comprising a total of 80 treatments in which no one had persistent T-wave inversion, pathologic Q waves, or a demonstrable rise in cardiac enzymes at four and six hours (although some had a mild increase in creatine phosphokinase [CPK], presumably from skeletal muscle) [12].

ECT can also cause a transient depression in the ejection fraction of healthy patients [13]. A study in 53 adults undergoing ECT found that seven developed new global left ventricular (LV) systolic dysfunction and eight developed regional wall motion abnormalities [14]. Among the 14 patients who developed global or regional abnormalities after the first ECT treatment, 13 had resolution of these abnormalities after the fourth ECT treatment (generally about one week later), and there were no short-term adverse events in any of the patients with LV dysfunction.

A prospective cohort study of 100 subjects undergoing 245 ECT sessions showed increased cardiac troponin levels in eight patients, only two of whom had other evidence of myocardial ischemia or infarction [15].

Several studies have investigated the incidence of serious cardiac complications from ECT:

In a retrospective study of 42 patients who had undergone ECT, 12 of the 17 patients with underlying cardiac disease had cardiac complications [16]. Most of these were benign and self-limited, including atrial and ventricular ectopy and nonsustained ventricular tachycardia. There was evidence of ischemia in two patients and one cardiac arrest of unknown etiology. Seventy percent of all complications, self-limited or not, occurred in patients with cardiovascular disease identified on the history, physical examination, or ECG, and all occurred in patients greater than 50 years of age. This study did not, however, systematically document the degree of preexisting cardiac disease.

A prospective study of 40 patients with cardiac disease found that 55 percent had at least one complication with ECT [17]. These included minor complications, such as transient arrhythmias or ST segment changes, and major complications, such as persistent ECG changes accompanied by chest pain, asystole, or persistent arrhythmias. Only 7.5 percent in the control group without cardiac disease had a cardiac complication, and all were transient and minor.

A case-control study of 80 patients over the age of 50 found that the risk of major complications was 11.5 percent in patients at high risk for cardiovascular disease [18]. The patients were able to complete their course of therapy once the complications were treated.

Even patients at high risk for cardiac complications tolerate ECT well and, if complications occur and are treated, the vast majority can complete the treatment course. As an example, one study treated 80 patients, one-half of whom had preexisting cardiac disease (depressed ejection fraction, conduction disease, or frequent premature ventricular contractions) [17]. Among those with cardiac disease, eight had major complications, including chest pain, arrhythmia, ischemia, and one myocardial infarction. Anesthesiologists and cardiologists treated the complications as they occurred and 36 of 38 patients went on to complete treatment, including the patient with the myocardial infarction. Similarly, a second study treated 53 patients and, of the 27 patients at risk, 31 percent required changes in medication or pretreatment with subsequent treatments because of complications [18]. Twenty-five out of 27 patients completed the course of ECT; there were no deaths. Despite these successful outcomes, it is not known how many of the patients in these studies were on beta blockers or other antihypertensive medication prior to treatment.

Central nervous system and other effects — Several cerebral effects occur with ECT, including increases in cerebral blood flow and intracranial pressure. Memory loss, disorientation, and delirium are the primary clinical manifestations. (See "Overview of electroconvulsive therapy (ECT) for adults", section on 'Adverse effects'.)

ROLE OF THE MEDICAL CONSULTANT — The medical evaluation before electroconvulsive therapy (ECT) is similar to that of any patient undergoing a procedure that requires general anesthesia: to identify medical issues that place the patient at risk, to propose strategies to mitigate that risk, and to anticipate complications that may occur after the procedure.

Preprocedure evaluation — A complete history and physical examination will help to identify pertinent risk factors [19]. We agree with the recommendation from the American Psychiatric Association that no specific laboratory tests are required in the pre-ECT evaluation. We recommend measurement of serum electrolytes only for patients taking diuretics or other medications that increase the likelihood of an abnormality and for patients with established renal disease or congestive heart failure. We suggest an electrocardiogram (ECG) in patients over the age of 50 years, since most cardiac complications occur in older patients. There are no indications for other routine laboratory studies. (See "Preoperative medical evaluation of the healthy adult patient".)

The history should include a review of previous difficulties with anesthesia or ECT. As mentioned above, there are no absolute contraindications to ECT and most patients can have the procedure without serious complication, but clinicians should identify risk factors that may require intervention or management. Important considerations include risk factors for cardiac ischemia or arrhythmia, heart failure, and the presence of brain tumors or other neurosurgical issues. A history of skull fractures should be determined, as this may affect electrode placement.

The history should document current medications, including the use of herbal supplements. In one study, 54 percent of outpatients with psychiatric conditions used alternative medications in addition to routine pharmacotherapy [20]. Common herbal medications, including Ginkgo biloba, ginseng, St. John's wort, valerian, and kava kava have central nervous system effects which might interfere with ECT. The treating psychiatrist should be made aware of a patient's supplement use in order to determine if herbal products should be tapered prior to initiating ECT [21].

In addition, theophylline has been reported to cause status epilepticus after ECT and so should be tapered prior to treatment [22]. The treating psychiatrist may also choose to taper or discontinue antidepressants and/or other psychotropics prior to treatment.

A summary of management strategies for preexisting medical conditions is shown in a table (table 3).

Strategies to reduce the risk of cardiac complications — The 2014 American College of Cardiology (ACC)/American Heart Association (AHA) guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery assigns procedure-related risk to noncardiac surgery as low-risk if the rate of major acute cardiac event is less than 1 percent [23]. Though not explicitly mentioned in the AHA-ACC guidelines, ECT can be treated as a low-risk procedure because it is usually well tolerated, even in those at risk; the duration of hemodynamic changes is brief; and the mortality rate is low [17,18,24]. As a result, it is difficult to prove a beneficial effect of any intervention to reduce cardiovascular risk. Nevertheless, a cardiac risk assessment is warranted preoperatively. (See "Evaluation of cardiac risk prior to noncardiac surgery".)

Barring major clinical predictors of coronary risk (unstable angina, decompensated heart failure, severe valvular disease, malignant arrhythmias), most patients can undergo ECT with appropriate medical management [25]. Some have suggested that sedentary patients with intermediate risk factors should undergo further noninvasive risk stratification [26]. However, we feel that this population can proceed without further evaluation given the low morbidity of ECT and the potential use of prophylactic beta blockers.

Postprocedure hemodynamic changes — Short-acting beta blockers are used to quickly treat persistent or severe tachycardia and hypertension after ECT. Other agents that have been useful for the treatment of postprocedure hypertension are intravenous (IV) nitroglycerin [27], nicardipine [28], and clonidine [11,25].

Prophylactic beta blockers — While treatment of postprocedure hemodynamic changes is indicated, use of prophylactic beta blockers to reduce risk for patients undergoing ECT is controversial.

We do not advise the routine use of beta blockers in low-risk patients, given the theoretical risks and unclear benefit. The overall risk of cardiovascular complications due to ECT is low, and no studies have documented reduced cardiac complications with the use of short-acting beta blockers before ECT. In addition, there is some evidence that beta blockers might result in a decrease in seizure length and potentially decrease the efficacy of ECT [29,30], although this has not been found in all studies [31,32]. Several authors have raised concern regarding widespread use of beta blockers because these drugs have been implicated in cases of prolonged asystole [7,33,34]. However, in these reported cases, atropine was not used and in some cases patients had subconvulsive treatments that can also cause bradycardia.

We advise the use of prophylactic short-acting IV beta blockers for patients at very high risk of complications from transient hypertension (eg, intracranial aneurysm, unstable angina, or recent myocardial infarction) [19]. Collaboration with the treating psychiatrist, an anesthesiologist, and a cardiologist is useful in such patients.

Short-acting beta blockers, such as IV esmolol or labetalol, can be used to prevent transient and persistent hypertension and tachycardia [27-29,35-38]; glycopyrrolate is administered to prevent bradycardia in these individuals. A review of 20 randomized trials of beta blockers and ECT suggested use of esmolol if a beta blocker was indicated [39]. The review found that esmolol had been studied relatively often compared with labetalol and landiolol and had consistent hemodynamic effects across the included studies. Increased doses of esmolol appeared to decrease seizure duration, but most studies were able to achieve at least a 30-second seizure, which is generally considered adequate. Another study of the use of beta blockers during ECT found that labetalol produced dose-dependent reduction in heart rate and rate pressure product using 5 and 10 mg doses, compared with placebo [40].

Typical bolus doses of labetalol are 5 to 20 mg IV and, for esmolol, 10 to 50 mg IV. It is not necessary to prevent the transient hypertension and tachycardia associated with the seizure in most patients; the main goal of the use of these agents is to reduce the risk of myocardial ischemia (a possible result of the increased oxygen demand associated with tachycardia) in patients with coronary artery disease. Other agents, such as calcium channel blockers or nitroglycerin, are sometimes given during ECT [41].

Other prophylactic medications — Medications other than beta blockers have been used to try to prevent postprocedure hemodynamic changes. As an example, a small randomized trial found that prophylactic IV nicardipine was effective in a dose-dependent fashion at minimizing the acute hemodynamic response to ECT without shortening the duration of seizure [42].

Coexisting cardiac disease

Hypertension — The American Psychiatric Association recommends that patients with unstable hypertension be stabilized prior to starting ECT [5]. Patients with stable hypertension should receive their routine antihypertensive (other than diuretics) with a small sip of water approximately two hours before ECT. Diuretics should not be given, because it is better for the bladder to be empty during the procedure to prevent the patient from soiling himself as a result of the seizure. Patients on longstanding diuretics should have electrolytes checked before proceeding to ensure potassium and magnesium are replete.

Coronary heart disease — Antianginals such as nitrates and beta blockers should be continued in patients with documented coronary heart disease who are already taking them. Patients taking long-acting beta blockers may receive atropine or glycopyrrolate with induction, given the potential increase in the risk of bradycardia and a small study that showed that atropine should be protective [8]. This should be discussed with the anesthesiologist. If ECG changes or chest pain occur during the treatment period, treatments should be postponed until the patient is evaluated and treated for potential cardiac ischemia [25,43].

For patients with a history of myocardial infarction, in general, the longer one waits after a myocardial infarction the safer it is to perform ECT. The key factors in this assessment are the extent of myocardial damage and subsequent healing and the residual functional cardiac status. For patients who have had a myocardial infarction and are not at imminent risk from their depressive episode, we advise waiting a minimum of three months prior to starting a course of ECT. However, patients at high risk of death due to their depression can be treated sooner. For severely depressed patients, treatment with ECT on an emergent basis may be indicated [44]. Cardiology consult is advised for these patients.

Heart failure and valvular disease — ECT should be delayed in patients with decompensated heart failure or significant valvular disease, pending cardiology consultation and completion of a thorough evaluation and optimization of cardiac status. One report of 10 patients who completed ECT (total of 144 ECT sessions) with severe aortic stenosis (valve area 0.7 to 1.0 cm2) noted good control of blood pressure and heart rate with continuation of chronic antihypertensive medications and/or addition of a short-acting beta blocker [45]. All patients were asymptomatic and tolerated ECT. There were no deaths attributable to ECT or aortic stenosis. Two patients had reductions in blood pressure requiring intervention, and seven patients required IV medication to control systolic blood pressure >180 mmHg. In patients with severe aortic stenosis, a cardiologist should be consulted, and clinicians should strive for tight control of blood pressure and heart rate with attention to avoiding excessive preload or afterload reduction. Little data are available for management of patients with less severe valvular disease, though ECT can be performed safely, with appropriate precautions, in most patients with underlying cardiac conditions [46].

One study examined the safety of ECT in patients with compensated heart failure with reduced ejection fraction (range of 15 to 40 percent) [47]. In 35 patients receiving a total of 513 treatments, all patients tolerated the procedure well and with no cardiac complications after treatment. Consistent with other studies looking at cardiac complications, three patients suffered non-life-threatening transient arrhythmias. Eighty percent of treated patients did receive prophylactic beta blockers if they had experienced prolonged hypertension or tachycardia with prior treatments.

In patients with a remote history of heart failure or compensated disease, we advise a baseline echocardiogram, if not recently performed, to assist with periprocedure management. In those with compensated systolic dysfunction, one may simply continue diuretics and vasodilator therapy and minimize volume overload. In patients with diastolic dysfunction, control of blood pressure should limit the occurrence of flash pulmonary edema. This group will benefit from prompt treatment of post-seizure hypertension if it develops.

Pacemakers and implantable defibrillators — Patients with pacemakers and automatic implantable cardiac defibrillators (AICDs) can safely undergo ECT. As an example, in a case series of ECT in 26 patients with pacemakers and three patients with AICDs there was only one serious cardiac event, an episode of supraventricular tachycardia [48].

The clinical team should be prepared to deactivate pacemakers with a magnet if any aberrant signals occur [25]. A cardiologist should deactivate AICDs before induction and reactivate the device after the seizure is complete to avoid excessive charge. The patient should have continuous ECG monitoring while the defibrillator is deactivated [49], and the team should be prepared to defibrillate should the patient develop an unstable rhythm.

Coexisting pulmonary disease — Optimizing pulmonary status before ECT is important. The anesthesiologist manipulates the patient's airway during ECT using a bag and mask circuit and there is a risk of inducing bronchoconstriction. Patients at risk for desaturation should receive supplemental oxygen via nasal cannula or facemask, initiated a few minutes prior to each treatment [50].

Elective intubation is not indicated for ECT, except in rare circumstances in which the anesthesiologist assesses that intubation would be exceptionally difficult should the airway become compromised.

Coexisting neurologic and neurosurgical disease

Brain tumors — Early recommendations considered brain tumors and other space-occupying lesions to be absolute contraindications to ECT [51]. This concern was based upon the observation that ECT raises cerebral blood flow, which in the presence of a brain tumor could translate into an increase in intracranial pressure (ICP) and neurologic deterioration.

These concerns were illustrated in a review of 35 patients with brain tumors undergoing ECT, 74 percent of whom had major adverse neurologic and cognitive side effects, with a one-month mortality of 28 percent [52]. Notable characteristics of patients who suffered neurologic deterioration included the presence of a depressive illness, no previous psychiatric illness or ECT, headache, and the presence of even, soft neurologic findings on exam. However, this study may have had a selection bias, given that only one patient was known to have a tumor before treatment.

One group reviewed 10 cases of successful treatment [53-56]. Eight patients had meningiomas in differing locations, and two patients had metastatic breast cancer. No one had abnormal neurologic examinations or evidence of increased ICP at baseline, and four had normal spinal fluid measurements. There were no adverse events other than a prolonged seizure after one treatment. A case report described successful treatment of a patient with primary brain cancer and documented elevated ICP [57]. He was treated with steroids and short-acting beta blockers to minimize edema and elevations in blood pressure during the clonic phase of seizure.

Based on this information, ECT is probably safe in patients with brain tumors as long as there is no evidence of elevated ICP. Given that the available safety data are in the form of case series or reports, we agree with the American Psychiatric Association that the decision should be made on a case-by-case basis with the involvement of neurologic and possibly neurosurgical consultants [5]. Evaluation should consist of a detailed history and physical examination to seek evidence suggestive of elevated ICP, such as headache, papilledema, or abnormal neurologic examination. Any such evidence should prompt further investigation such as head computed tomography (CT) or magnetic resonance imaging (MRI). Although data are limited, providers have successfully used steroids to minimize edema [56,57], and neurologic consultants may consider using them in patients in whom elevated ICP cannot be ruled out [58,59].

Stroke — Patients who have suffered a stroke have a high rate of depression. In a study of 14 patients with completed strokes undergoing ECT one month or more after the event, none had deleterious neurologic sequelae [60]. Similarly, a second study of 24 patients with a history of stroke found no difference in the efficacy or cardiac complication rate compared with controls [61]. Rates of delirium were similar in both groups, although within the study group all patients with delirium had their strokes within the preceding year. Adequate blood pressure control is important for such patients.

Dementia — Reports exist of successful ECT in depressed patients with dementia and organic brain disease, with efficacy rates similar to that of non-demented patients [62,63]. In a review of 135 patients with organic and depressive dementia, 21 percent developed delirium or cognitive and memory deficits; all but one had cleared by time of discharge from the hospital [62].

The severity of delirium correlates with the degree of underlying dementia or organic brain syndrome but is transient and does not interfere with treatment [63]. The clinical staff should be aware that delirium is a potential side effect in demented patients. These patients can often be managed with reassurance and alterations in level of supervision [64].

Neuromuscular disease and movement disorders — In patients with neuromuscular disease, particularly post-polio syndrome, depolarizing muscle relaxants such as succinylcholine may lead to severe hyperkalemia and circulatory collapse [65,66]. Thus, depolarizing muscle relaxants should be avoided in these patients. Those with neuromuscular disease may receive short-acting, nondepolarizing agents for neuromuscular blockade [67]. Patients with Parkinson disease (PD) can safely undergo ECT, although there may be an increased risk of post-procedure delirium. In an observational study including 50 subjects, there was a 2.5-fold increase in the incidence of delirium in PD patients compared with those without PD (52 versus 20 percent), suggesting they should be monitored closely after treatment [68,69].

Epilepsy — While anticonvulsants may interfere with the efficacy of ECT, patients with epilepsy should continue their anticonvulsants during a course of ECT. Clinicians should consider reducing the dose if seizures are difficult to elicit or withholding a dose the evening or night before the ECT treatment.

Cranial metallic objects — The safety and tolerability of ECT in patients with cranial metallic objects is not known. Theoretical concerns include potential warming of brain issue immediately surrounding the metallic object, treatment-induced changes in intracranial circulation causing vascular complications, and preexisting device-induced epilepsy [70]. Most providers assume that inert metals do not heat up surrounding tissue.

No complications from ECT were reported in a case series of 24 cases of patients with cranial metallic objects (eg, aneurysm clips, endovascular coils, deep brain stimulators, metal skull plate, shrapnel) [70]. Most (22 patients) had ECT ≥2 months after cranial metallic objects were placed, and 10 had modified lead placement. While this study is reassuring regarding the safety of ECT in such patients, we consult a neurosurgeon prior to the procedure, and if possible we avoid performing ECT immediately after any neurosurgical procedure.

Other structural brain abnormalities — Patients with structural abnormalities of the cerebellum or brainstem, such as Chiari I malformation with no evidence of increased ICP, have safely undergone ECT [71-73]. However, such patients should have neurosurgical evaluation prior to ECT. (See "Chiari malformations", section on 'Classification'.)

Diabetes — There is no clear evidence of an effect of ECT on blood sugar control in diabetic patients. In a small study of 19 patients with insulin-requiring type II diabetes mellitus, ECT itself did not lead to significant acute changes in blood sugar [74]. Individual patients who developed hyperglycemia or hypoglycemia after ECT were found to have changed their behaviors (eating or activity) in response to resolving depression, and these behavioral changes were thought to be responsible for the change in blood sugar control.

Patients generally do not take anything by mouth on the morning of ECT. As a general rule, we recommend holding oral hypoglycemic agents on the morning of the procedure. For insulin-requiring diabetics, on the morning of the procedure we recommend giving half of the usual total morning insulin dose (both intermediate and short-acting) as intermediate-acting insulin and withholding short-acting insulin. If the ECT will happen in the early morning, where breakfast is likely only delayed, then patients may delay taking their usual morning insulin until after ECT and before eating. A more detailed discussion of these issues can be found elsewhere. (See "Perioperative management of blood glucose in adults with diabetes mellitus".)

Anticoagulation — The safety of ECT in patients who are anticoagulated is controversial because of concerns about a possible increase in the risk of intracerebral hemorrhage [75]. However, intracerebral hemorrhage is rarely seen after ECT, making it difficult to judge whether anticoagulation increases the risk significantly. In a case series of 35 patients receiving long-term anticoagulation with warfarin who underwent 284 ECT treatments, no major adverse effects occurred [76]. The international normalized ratio (INR) on the day of ECT was subtherapeutic (below 2.0) 36 percent of the time and supratherapeutic (above 3.5) only 3 percent of the time. In addition, case reports suggest that ECT can be safely administered to patients taking the newer oral anticoagulants, such as rivaroxaban and dabigatran [77,78]. In the absence of guiding data in this evolving area, we recommend that clinicians assess the risks and benefits for each individual patient based on their CHA2DS2-VASc score (calculator 1) and their propensity for hypertension in the post and interictal setting. If a patient has a higher CHA2DS2-VASc score (>1) or another strong indication for anticoagulation, continuing anticoagulation with attention to keeping INR less than 3.5 for patients on warfarin is reasonable. For patients who have persistent repeated hypertension with ECT, discussion with anesthesia regarding possible need for IV beta blockers with treatment is reasonable regardless of CHA2DS2-VASc score.

Clinicians should assess the risks of temporarily discontinuing anticoagulation (table 4). In general, we temporarily discontinue anticoagulation (until ECT is complete) if the thrombotic risk is low (eg, atrial fibrillation with CHA2DS2-VASc score (calculator 1) of 1 or less and no prior stroke). However, we do not discontinue anticoagulation in patients with higher thrombotic risk, as courses of ECT can be months long. Decisions can be made on a case-by-case basis in discussion with the outpatient provider or specialist who is managing the patient’s anticoagulation plan.

Separate topic reviews discuss the management of intracerebral hemorrhage associated with anticoagulants and reversal of anticoagulation in warfarin-associated intracerebral hemorrhage. (See "Management of bleeding in patients receiving direct oral anticoagulants", section on 'Anticoagulant reversal' and "Reversal of anticoagulation in intracranial hemorrhage".)

Pregnancy — The treatment of psychiatric conditions in pregnancy poses challenges, as psychotropic medications may have significant side effects in both mother and fetus. However, ECT is generally thought be safe in pregnant patients by the American Psychiatric Association and the American College of Obstetricians and Gynecologists [5,77]. The safety of ECT and modifications in technique for treating pregnant patients are discussed separately. (See "Teratogenicity, pregnancy complications, and postnatal risks of antipsychotics, benzodiazepines, lithium, and electroconvulsive therapy", section on 'Electroconvulsive therapy' and "Bipolar disorder in pregnant women: Screening, diagnosis, and choosing treatment for mania and hypomania", section on 'Refractory patients' and "Technique for performing electroconvulsive therapy (ECT) in adults", section on 'Pregnancy'.)

As a pregnant patient considers ECT, the informed consent and evaluation should be performed with an obstetrician and an anesthesiologist.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Beyond the Basics topics (see "Patient education: Electroconvulsive therapy (ECT) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Perform a history and physical examination and obtain an electrocardiogram (ECG) in all patients before planned electroconvulsive therapy (ECT). Identify risk factors for cardiac complications of the procedure using one of the published cardiac risk indices or guidelines. Risk factors include coronary heart disease, valvular disease, and heart failure, as well as diabetes mellitus, hypertension, hypercholesterolemia, and advanced age. Suggestion for management of preexisting conditions is shown in a table (table 3). (See 'Preprocedure evaluation' above.)

Delay ECT for patients with unstable angina, decompensated heart failure, or severe symptomatic valvular disease until these conditions are stabilized. Cardiology consultation is advised in these patients. (See 'Coexisting cardiac disease' above.)

We do not advise routine use of prophylactic beta blockers, which might decrease the seizure duration and increase risk of asystole. However, short-acting intravenous (IV) beta blockers should be considered for patients at very high risk of complications from transient hypertension (eg, significant aortic stenosis, intracranial aneurysm, unstable angina, or recent myocardial infarction). Cardiology consultation is useful in patients at very high risk. (See 'Prophylactic beta blockers' above.)

Continue nitrates, beta blockers, and other antihypertensive drugs in patients with preexisting cardiac conditions. If a patient is on a beta blocker, use atropine with induction to reduce the risk of asystole. (See 'Coronary heart disease' above.)

ECT is likely safe for patients with intracranial metallic objects and brain tumors, as well as in patients with certain structural abnormalities like Chiari I malformation, as long as there is no evidence of increased intracranial pressure (ICP). However, we advise neurosurgical consultation in these patients before ECT. (See 'Coexisting neurologic and neurosurgical disease' above.)

Diabetic patients should generally hold oral hypoglycemics and short-acting insulin the morning of ECT. For early morning ECT, where breakfast is likely only delayed, patients may delay taking their usual morning insulin until after ECT and before eating. If breakfast and lunch are likely to be missed, then we recommend giving half of the usual total morning insulin dose (both intermediate- and short-acting) as intermediate-acting insulin. (See 'Diabetes' above.)

Warfarin therapy can be continued in patients receiving ECT who have an international normalized ratio (INR) below 3.5 and a CHA2DS2-VASc score >1 (calculator 1) or another strong indication for anticoagulation. (See 'Anticoagulation' above.)

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  16. Gerring JP, Shields HM. The identification and management of patients with a high risk for cardiac arrhythmias during modified ECT. J Clin Psychiatry 1982; 43:140.
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  18. Rice EH, Sombrotto LB, Markowitz JC, Leon AC. Cardiovascular morbidity in high-risk patients during ECT. Am J Psychiatry 1994; 151:1637.
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  22. Devanand DP, Decina P, Sackeim HA, Prudic J. Status epilepticus following ECT in a patient receiving theophylline. J Clin Psychopharmacol 1988; 8:153.
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  26. Applegate RJ. Diagnosis and management of ischemic heart disease in the patient scheduled to undergo electroconvulsive therapy. Convuls Ther 1997; 13:128.
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  28. Avramov MN, Stool LA, White PF, Husain MM. Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy. J Clin Anesth 1998; 10:394.
  29. van den Broek WW, Leentjens AF, Mulder PG, et al. Low-dose esmolol bolus reduces seizure duration during electroconvulsive therapy: a double-blind, placebo-controlled study. Br J Anaesth 1999; 83:271.
  30. Howie MB, Black HA, Zvara D, et al. Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy. Anesth Analg 1990; 71:384.
  31. Howie MB, Hiestand DC, Zvara DA, et al. Defining the dose range for esmolol used in electroconvulsive therapy hemodynamic attenuation. Anesth Analg 1992; 75:805.
  32. Dannon PN, Iancu I, Hirschmann S, et al. Labetalol does not lengthen asystole during electroconvulsive therapy. J ECT 1998; 14:245.
  33. Decina P, Malitz S, Sackeim HA, et al. Cardiac arrest during ECT modified by beta-adrenergic blockade. Am J Psychiatry 1984; 141:298.
  34. Wulfson HD, Askanazi J, Finck AD. Propranolol prior to ECT associated with asystole. Anesthesiology 1984; 60:255.
  35. Castelli I, Steiner LA, Kaufmann MA, et al. Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy. Anesth Analg 1995; 80:557.
  36. Kovac AL, Goto H, Arakawa K, Pardo MP. Esmolol bolus and infusion attenuates increases in blood pressure and heart rate during electroconvulsive therapy. Can J Anaesth 1990; 37:58.
  37. Mayur PM, Shree RS, Gangadhar BN, et al. Atropine premedication and the cardiovascular response to electroconvulsive therapy. Br J Anaesth 1998; 81:466.
  38. Stoudemire A, Knos G, Gladson M, et al. Labetalol in the control of cardiovascular responses to electroconvulsive therapy in high-risk depressed medical patients. J Clin Psychiatry 1990; 51:508.
  39. Boere E, Birkenhäger TK, Groenland TH, van den Broek WW. Beta-blocking agents during electroconvulsive therapy: a review. Br J Anaesth 2014; 113:43.
  40. McCall WV, Shelp FE, Weiner RD, et al. Effects of Labetalol on Hemodynamics and Seizure Duration During ECT. Convuls Ther 1991; 7:5.
  41. Kellner CH, Pritchett JT, Beale MD, Coffey CE. Handbook of ECT, American Psychiatric Press Inc, 1997.
  42. Zhang Y, White PF, Thornton L, et al. The use of nicardipine for electroconvulsive therapy: a dose-ranging study. Anesth Analg 2005; 100:378.
  43. de Silva RA, Bachman WR. Cardiac consultation in patients with neuropsychiatric problems. Cardiol Clin 1995; 13:225.
  44. Magid M, Lapid MI, Sampson SM, Mueller PS. Use of electroconvulsive therapy in a patient 10 days after myocardial infarction. J ECT 2005; 21:182.
  45. Mueller PS, Barnes RD, Varghese R, et al. The safety of electroconvulsive therapy in patients with severe aortic stenosis. Mayo Clin Proc 2007; 82:1360.
  46. Rayburn BK. Electroconvulsive therapy in patients with heart failure or valvular heart disease. Convuls Ther 1997; 13:145.
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  48. Dolenc TJ, Barnes RD, Hayes DL, Rasmussen KG. Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators. Pacing Clin Electrophysiol 2004; 27:1257.
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  50. Saito S. Anesthesia management for electroconvulsive therapy: hemodynamic and respiratory management. J Anesth 2005; 19:142.
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  56. Zwil AS, Bowring MA, Price TR, et al. Prospective Electroconvulsive Therapy in the Presence of Intracranial Tumor. Convuls Ther 1990; 6:299.
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  58. Zwil AS, Pelchat RJ. ECT in the treatment of patients with neurological and somatic disease. Int J Psychiatry Med 1994; 24:1.
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  63. Nelson JP, Rosenberg DR. ECT Treatment of Demented Elderly Patients with Major Depression: A Retrospective Study of Efficacy and Safety. Convuls Ther 1991; 7:157.
  64. Durr AL, Golden RN. Cognitive effects of electroconvulsive therapy: a clinical review for nurses. Convuls Ther 1995; 11:192.
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  68. Moellentine C, Rummans T, Ahlskog JE, et al. Effectiveness of ECT in patients with parkinsonism. J Neuropsychiatry Clin Neurosci 1998; 10:187.
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  70. Gahr M, Connemann BJ, Freudenmann RW, Schönfeldt-Lecuona C. Safety of electroconvulsive therapy in the presence of cranial metallic objects. J ECT 2014; 30:62.
  71. Francois D, Huang T. Successful Treatment With Electroconvulsive Therapy of a Patient With Chiari Malformation Type I. J ECT 2019; 35:e6.
  72. Gerschwitz S, Tibrewal P, Bastiampillai T, et al. Electroconvulsive therapy and type 1 Chiari malformation. Asian J Psychiatr 2018; 33:86.
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  74. Netzel PJ, Mueller PS, Rummans TA, et al. Safety, efficacy, and effects on glycemic control of electroconvulsive therapy in insulin-requiring type 2 diabetic patients. J ECT 2002; 18:16.
  75. Bleich S, Degner D, Scheschonka A, et al. Electroconvulsive therapy and anticoagulation. Can J Psychiatry 2000; 45:87.
  76. Mehta V, Mueller PS, Gonzalez-Arriaza HL, et al. Safety of electroconvulsive therapy in patients receiving long-term warfarin therapy. Mayo Clin Proc 2004; 79:1396.
  77. Yonkers KA, Wisner KL, Stewart DE, et al. The management of depression during pregnancy: a report from the American Psychiatric Association and the American College of Obstetricians and Gynecologists. Obstet Gynecol 2009; 114:703.
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Topic 4817 Version 43.0

References

1 : Electroconvulsive therapy: evidence and challenges.

2 : Clinical guidelines for the treatment of depressive disorders.

3 : Royal Australian and New Zealand College of Psychiatrists professional practice guidelines for the administration of electroconvulsive therapy.

4 : Indications for the use of ECT.

5 : Indications for the use of ECT.

6 : Asystole in electroconvulsive therapy: Report of four cases.

7 : Asystole with electroconvulsive therapy.

8 : Incidence of asystole in electroconvulsive therapy in elderly patients.

9 : Duration of ECT-induced tachycardia as a measure of seizure length.

10 : Changes in cardiac autonomic nervous system activity during a course of electroconvulsive therapy.

11 : Changes in cardiac autonomic nervous system activity during a course of electroconvulsive therapy.

12 : The effects of electroconvulsive therapy on serial electrocardiograms and serum cardiac enzyme values. A prospective study of depressed hospitalized inpatients.

13 : Effects of electroconvulsive therapy on cardiac function in patients without heart disease.

14 : Frequency of left ventricular dysfunction after electroconvulsive therapy.

15 : High-sensitivity Cardiac Troponin Elevation after Electroconvulsive Therapy: A Prospective, Observational Cohort Study.

16 : The identification and management of patients with a high risk for cardiac arrhythmias during modified ECT.

17 : Cardiovascular complications of ECT in depressed patients with cardiac disease.

18 : Cardiovascular morbidity in high-risk patients during ECT.

19 : Medical evaluation of patients undergoing electroconvulsive therapy.

20 : Alternative therapy use by psychiatric outpatients.

21 : Implications of herbal alternative medicine for electroconvulsive therapy.

22 : Status epilepticus following ECT in a patient receiving theophylline.

23 : 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.

24 : The mortality rate with ECT.

25 : Anesthetic considerations of cardiovascular risk during electroconvulsive therapy.

26 : Diagnosis and management of ischemic heart disease in the patient scheduled to undergo electroconvulsive therapy.

27 : Intravenous nitroglycerine in the management of posttreatment hypertension during electroconvulsive therapy.

28 : Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy.

29 : Low-dose esmolol bolus reduces seizure duration during electroconvulsive therapy: a double-blind, placebo-controlled study.

30 : Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy.

31 : Defining the dose range for esmolol used in electroconvulsive therapy hemodynamic attenuation.

32 : Labetalol does not lengthen asystole during electroconvulsive therapy.

33 : Cardiac arrest during ECT modified by beta-adrenergic blockade.

34 : Propranolol prior to ECT associated with asystole.

35 : Comparative effects of esmolol and labetalol to attenuate hyperdynamic states after electroconvulsive therapy.

36 : Esmolol bolus and infusion attenuates increases in blood pressure and heart rate during electroconvulsive therapy.

37 : Atropine premedication and the cardiovascular response to electroconvulsive therapy.

38 : Labetalol in the control of cardiovascular responses to electroconvulsive therapy in high-risk depressed medical patients.

39 : Beta-blocking agents during electroconvulsive therapy: a review.

40 : Effects of Labetalol on Hemodynamics and Seizure Duration During ECT.

41 : Effects of Labetalol on Hemodynamics and Seizure Duration During ECT.

42 : The use of nicardipine for electroconvulsive therapy: a dose-ranging study.

43 : Cardiac consultation in patients with neuropsychiatric problems.

44 : Use of electroconvulsive therapy in a patient 10 days after myocardial infarction.

45 : The safety of electroconvulsive therapy in patients with severe aortic stenosis.

46 : Electroconvulsive therapy in patients with heart failure or valvular heart disease.

47 : Safety of electroconvulsive therapy in patients with a history of heart failure and decreased left ventricular systolic heart function.

48 : Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators.

49 : Implantable cardioverter-defibrillators: implications for the nonelectrophysiologist.

50 : Anesthesia management for electroconvulsive therapy: hemodynamic and respiratory management.

51 : Electroshock treatment in the psychoses

52 : Electroconvulsive therapy in the presence of brain tumor. Case reports and an evaluation of risk.

53 : The treatment of depression with ECT in the presence of brain tumor.

54 : Prospective uses of ECT in the presence of intracranial tumors.

55 : Electroconvulsive treatment of a patient with known intracranial tumor.

56 : Prospective Electroconvulsive Therapy in the Presence of Intracranial Tumor.

57 : ECT in the presence of brain tumor and increased intracranial pressure: evaluation and reduction of risk.

58 : ECT in the treatment of patients with neurological and somatic disease.

59 : ECT and Neurological Disorders.

60 : Electroconvulsive therapy for poststroke depression.

61 : ECT-induced interictal delirium in patients with a history of a CVA.

62 : Safety and Efficacy of ECT in Depressed Patients with Dementia: A Review of Clinical Experience.

63 : ECT Treatment of Demented Elderly Patients with Major Depression: A Retrospective Study of Efficacy and Safety.

64 : Cognitive effects of electroconvulsive therapy: a clinical review for nurses.

65 : Circulatory collapse following succinylcholine: report of a patient with diffuse lower motor neuron disease.

66 : Anesthetic management for patients with postpolio syndrome receiving electroconvulsive therapy.

67 : Increased potency of nondepolarizing relaxants after poliomyelitis.

68 : Effectiveness of ECT in patients with parkinsonism.

69 : Factors Associated With Delirium Following Electroconvulsive Therapy: A Systematic Review.

70 : Safety of electroconvulsive therapy in the presence of cranial metallic objects.

71 : Successful Treatment With Electroconvulsive Therapy of a Patient With Chiari Malformation Type I.

72 : Electroconvulsive therapy and type 1 Chiari malformation.

73 : Electroconvulsive Therapy With Chiari Malformation.

74 : Safety, efficacy, and effects on glycemic control of electroconvulsive therapy in insulin-requiring type 2 diabetic patients.

75 : Electroconvulsive therapy and anticoagulation.

76 : Safety of electroconvulsive therapy in patients receiving long-term warfarin therapy.

77 : The management of depression during pregnancy: a report from the American Psychiatric Association and the American College of Obstetricians and Gynecologists.

78 : Safety of electroconvulsive therapy in patients receiving dabigatran therapy.