Anesthesia & Analgesia:
REVIEW ARTICLE: Review Article
Anesthesia for Electroconvulsive Therapy
Ding, Zhengnian MD, PhD*, and; White, Paul F. PhD, MD, FANZCA†
*Departments of Anesthesiology and Pain Management, First Affiliated Hospital of Nanjing Medical University, China; and †University of Texas Southwestern Medical Center at Dallas, Texas
This project was supported by White Mountain Institute of Los Altos, a not-for-profit educational and research foundation (Dr. P. F. White is the foundation’s president).
January 14, 2002.
Address correspondence to Dr. Paul F. White, Department of Anesthesiology and Pain Management, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9068. Address e-mail to email@example.com. No reprints will be available.
The use of electroconvulsive therapy (ECT) to provoke a generalized epileptic seizure was first described in 1938 and was performed without anesthesia for almost 30 yr (1). Now the number of ECT procedures performed each year under general anesthesia in the United States exceeds the number of coronary revascularization, appendectomy, and herniorrhaphy procedures (2). In recent years, ECT has assumed an increasingly important role in the treatment of severe and medication-resistant depression and mania, as well as in the treatment of schizophrenic patients with affective disorders, suicidal drive, delusional symptoms, vegetative dysregulation, inanition, and catatonic symptoms (2,3). Typically, the acute phase of ECT is performed three times a week for 6 to 12 treatments. In successful cases, initial clinical improvement is usually evident after three to five treatments (3,4). Maintenance therapy can be performed at progressively increasing intervals from once a week to once a month to prevent relapses.
To optimize the anesthetic management of patients undergoing ECT, it is important to understand the physiologic responses to the electrical stimulus, the effect of anesthetic drugs on the ECT response, and the pharmacologic effects of the drugs used to attenuate the side effects related to ECT. In 1986, Gaines and Rees (5) published a comprehensive review regarding the psychiatric and anesthetic considerations in caring for patients undergoing ECT. More recently, Folk et al. (6) reviewed the preanesthetic management of ECT patients with coexisting diseases. This review article is intended to provide an update on the anesthetic management of patients undergoing ECT.
Physiologic Responses to ECT
When an electrical current is applied to the brain via transcutaneous electrodes, the resultant electroencephalographic (EEG) spike and wave activity is accompanied by a generalized motor seizure and an acute cardiovascular response, which results in a marked increase in cerebral blood flow and intracranial pressure (7). The maximal blood flow velocity increases approximately 133% above the baseline value (8). However, the magnitude of the acute hyperdynamic response to ECT appears to be independent of the duration of the motor and EEG seizure activity (Fig. 1) (9). The hemodynamic response to ECT can produce myocardial ischemia and even infarction (10), as well as transient neurologic ischemic deficits, intracerebral hemorrhages, and cortical blindness (11,12). Short-term memory loss is common after ECT (1,3), and more serious cognitive dysfunction has been described in the ECT literature, even though there is no scientific evidence of direct neuronal damage (13). However, use of brief pulse stimulation, unilateral nondominant electrode placement, and individual stimulus titration have all been alleged to minimize cognitive dysfunction after ECT (2,3,14,15).
The typical cardiovascular response to ECT consists of generalized autonomic nervous system stimulation, with an initial parasympathetic-induced bradycardia lasting 10 to 15 s followed immediately by a more prominent sympathetic response that results in transient tachycardia and hypertension lasting 5 min or longer. The cardiovascular response is associated with the release of catecholamines and occasional cardiac arrhythmias (16,17). Systolic blood pressure (SBP) is transiently increased by 30%–40%, and heart rate (HR) is increased by 20% or more, resulting in a two- to fourfold increase in the rate-pressure product (RPP), an index of myocardial oxygen consumption (16–18). Bilateral ECT produces a larger increase in the RPP than unilateral ECT (19). Older patients typically manifest a larger increase in RPP after ECT. The peak HR and SBP values occur 3–5 min after the application of the electrical stimulus (9); the magnitude varies with the quality of the EEG seizure (20) and can provide clinically useful information for stimulus dose regulation.
Hyperventilation-induced hypocapnia (Paco2 of 2%) appears to augment the HR (47% vs 28%) and RPP (82% vs 60%) responses compared with normocapnic conditions (PET of 5%) (21). It is interesting to note that the HR and RPP responses correlated with seizure duration in hyperventilated patients, but not in patients with normal end-tidal CO2 values. In patients with compromised cardiac function, ECT can result in myocardial ischemia and infarction (10,22). As a result of the acute hemodynamic responses, ECT can result in ventricular tachycardia (23) and even cardiac rupture (24). Patients with preexisting cardiac diseases are at an increased risk of developing cardiac complications during and after ECT (25–27). Furthermore, left-ventricular systolic and diastolic function was decreased from 20 min to 6 h after ECT treatments even in patients without cardiac diseases (28,29).
In addition to acute neurologic and cardiovascular effects, the ECT-induced seizure activity is accompanied by a generalized convulsion that has resulted in fracture-dislocations (30,31) and muscle aches (32) (Table 1). Other complications related to ECT include nausea, headache, emergence agitation, and sudden death (33,34).
Anesthetic Drugs Used for ECT
The efficacy of ECT in alleviating acute depression is dependent on the duration of the induced seizure (1–3). EEG seizure activity lasting from 25 to 50 s is alleged to produce the optimal antidepressant response. Patients experiencing an initial seizure duration of <15 s or >120 s achieve a less favorable response to ECT (35). Because many of the anesthetic drugs used for ECT have anticonvulsant properties, they would be expected to decrease the duration of ECT-induced seizure activity in a dose-dependent manner. Use of larger than necessary dosages of general anesthetics will shorten the duration of ECT-induced seizure activity and could adversely affect the efficacy of the ECT treatments. Therefore, there is a delicate balance between achieving an adequate anesthetic state and an optimal duration of EEG seizure activity (Table 2). In the current health care environment, use of general anesthetic techniques with a rapid onset and recovery is essential to facilitate fast-tracking and permits the discharge of these patients within 1–2 h after the ECT treatment.
Methohexital remains the most widely used general anesthetic for ECT and is considered the “gold standard” against which all other anesthetics are compared (Table 2, Fig. 2) (36–38). Of interest, a recent regional survey from Edinburgh, Scotland (37), found that most patients received a methohexital dose (1.5 ± 0.3 mg/kg) exceeding the dose range recommended by the Royal College of Psychiatrists (0.75–0.9 mg/kg) and the American Psychiatric Association (0.75–1.0 mg/kg). An explanation for the larger methohexital dosage may relate to the concurrent chronic medications that the patients were receiving at the time of their ECT treatments, as well as to chronic consumption of alcohol and centrally active drugs (e.g., benzodiazepines) known to increase the anesthetic requirement. Minimally effective doses of methohexital compare favorably with other IV anesthetics with respect to its effect on the duration of seizure activity (Table 2). It has been suggested that divided doses of methohexital would minimize its depressant effect on seizure activities and could lead to improved outcomes after ECT (38). With respect to speed of recovery of cognitive function after ECT, propofol and etomidate offered no advantage over methohexital (36). Therefore, unless there is a specific contraindication to barbiturates (e.g., acute intermittent porphyria), methohexital should be considered the drug of choice for the induction of anesthesia in this patient population.
Compared with methohexital (0.5–1.0 mg/kg), both thiopental (1.5–2.5 mg/kg) and thiamylal (1.5–2.5 mg/kg) shorten the EEG seizure duration (39). The frequency of sinus bradycardia and premature ventricular contractions was also increased with thiopental and thiamylal compared with methohexital (39). Compared with propofol, the middle cerebral artery flow velocities immediately after ECT were significantly higher with thiopental (40), and suppression of ECT-induced hemodynamic changes with thiopental was comparable to that with sevoflurane anesthesia (41). Therefore, there is no obvious reason to use either thiopental or thiamylal for ECT procedures.
When compared with methohexital, thiopental, and propofol, anesthetic induction with etomidate (0.15–0.3 mg/kg) is generally associated with a longer seizure duration and may be helpful in patients with short seizure times (<20 s) despite a maximal electrical stimulus (36,42,43). As a result of etomidate’s reduced cardiovascular depressant properties and ability to enhance seizure activity, the acute hemodynamic response to ECT is accentuated compared with the barbiturates and propofol. Furthermore, early recovery after etomidate can be delayed because of post-ECT confusion and an increased incidence of emetic symptoms compared with methohexital and propofol.
Propofol appears to have more potent anticonvulsant effects during ECT than other IV anesthetics (Table 2) (36,44–48). However, the use of a minimally hypnotic dose of propofol (0.75 mg/kg) was associated with a seizure duration that was comparable to standard hypnotic doses of methohexital (Fig. 2) (36). The ECT seizure duration after larger dosages of propofol (1.0–1.5 mg/kg) was significantly shorter than after methohexital, etomidate, and thiopental (36,40). However, even the largest doses of propofol (1.5 mg/kg) may result in a duration of EEG seizure activity that is considered clinically acceptable (45,46). Furthermore, the measurements of seizure quality (including postictal suppression index and mean integrated amplitude) after propofol anesthesia were not significantly different from those after methohexital (45).
Because use of propofol can significantly shorten the duration of seizure activity, its effect on the antidepressant action of ECT has been a concern (47–49). Two reports have compared the antidepressant efficacy of ECT by using the Hamilton Rating Scale for Depression (a 17-item scale that evaluates mood, vegetative and cognitive symptoms of depression, and comorbid anxiety symptoms) and the Beck Depression Inventory (a 21-item self-report rating inventory that measures characteristic attitudes and symptoms of depression) when propofol or methohexital was administered as the primary anesthetic (48,49). Even though the seizure duration was consistently shorter with propofol (versus methohexital), the Hamilton Rating Scale for Depression scores were improved to a similar degree in both anesthetic groups after they completed a standard series of ECT treatments. The magnitude of improvement in the patients’ depression symptoms was apparently unrelated to either the total duration of seizure activity during the series of ECT treatments or the concurrent use of tricyclic antidepressant (TCA) drugs (47). Given the well known cardiovascular depressant effects of propofol, the acute hemodynamic response during the ECT procedure is reduced with propofol compared with etomidate, methohexital, and thiopental (36,39). However, emergence from propofol anesthesia is only marginally faster than with other IV anesthetics (36,39,48), and recovery of cognitive function is similar to methohexital during the early recovery period (36,50).
Ketamine, a unique IV anesthetic with sedative and analgesic properties, has also been used to induce a hypnotic state for ECT (51). With ketamine, hemodynamic variables are increased compared with those of other IV drugs because of its intrinsic sympathomimetic activity. Surprisingly, the EEG seizure duration was decreased compared with methohexital, even with small doses of ketamine. Although there were no adverse psychological reactions to ketamine, the enhanced hemodynamic response and resultant increase in intracranial pressure make ketamine less desirable than methohexital and propofol for routine ECT treatments.
Use of benzodiazepines can alter both the ECT seizure threshold and the duration of seizure activity. Although the administration of lorazepam before ECT was not associated with a change in the seizure threshold, the seizure duration was significantly decreased (52). Nevertheless, in patients with catatonia, the concurrent use of lorazepam has been associated with a superior response to ECT treatments (53). When IV midazolam was compared with thiopental for ECT, it significantly reduced the duration of seizure activity (54). In a case report, the anticonvulsant effect produced by large doses of lorazepam or midazolam was successfully reversed with flumazenil given immediately before the ECT treatments (55). Because of their prominent anticonvulsant activity, benzodiazepines should be avoided before ECT.
Because most ECT procedures are performed in locations remote from the operating room, IV anesthetics are considered preferable to the inhaled (volatile) anesthetics. Nevertheless, sevoflurane (1.7%) in combination with nitrous oxide 50% in oxygen was comparable to thiopental in suppressing the acute hemodynamic response during ECT (41). The use of a larger concentration of sevoflurane (3.4%) was more effective than thiopental in blunting the acute hemodynamic response without producing cardiac arrhythmias. The seizure duration and recovery time after ECT with sevoflurane were similar to those with thiopental. Although this volatile anesthetic can be used to produce an adequate anesthetic state for ECT, it is more time consuming and possesses no obvious advantage when compared with the commonly used IV anesthetics, except for women requiring ECT in the late stages of pregnancy, when it may reduce post-ECT uterine contractions (56).
When ECT is performed without any muscle relaxant, the patient will require vigorous physical restraint during the seizure and will experience severe muscle pain after the procedure. To prevent myalgias (32), as well as more serious musculoskeletal complications (e.g., bone fractures or dislocations) (30,31), muscle relaxants are often administered during ECT procedures.
Succinylcholine remains the most commonly used muscle relaxant to reduce the intense muscle contractions associated with ECT-induced seizure activity (37). Although the dose recommended by the Royal College of Psychiatrists is 0.5 mg/kg, larger dosages (0.75–1.5 mg/kg) are often used in clinical practice (57). In patients with a history of post-ECT agitation related to increased levels of plasma lactate, increasing the dose of succinylcholine may decrease the emergence delirium (58). However, use of larger dosages of succinylcholine should be avoided in patients with a history of bradyarrhythmias (59). Even small doses of this rapid and short-acting muscle relaxant can produce side effects (e.g., myalgias, hyperthermia, and hyperkalemia) in at-risk patients with a history of susceptibility to malignant hyperthermia (MH), neuroleptic malignant syndrome (NMS), catatonic schizophrenia, and organophosphate poisoning (60–62). Therefore, an ultra-short-acting nondepolarizing muscle relaxant would be a valuable addition to the anesthesiologist’s armamentarium.
Mivacurium is the drug most often administered as an alternative to succinylcholine during ECT (57,60,63–65). In a patient with NMS who developed an MH-like reaction after succinylcholine administration for ECT (60), mivacurium was used during subsequent treatments and resulted in effective attenuation of muscle contractions without producing acute increases in muscle enzyme levels. In another report, mivacurium was successfully used in three older patients with severe osteoporosis, amyotrophic lateral sclerosis, and cardiac arrhythmias (65). When mivacurium (0.08 mg/kg) was compared with succinylcholine (0.5 mg/kg), succinylcholine was more effective than mivacurium in preventing muscle contractions during ECT (63). Fredman et al. (57) performed a dose-ranging assessment of mivacurium in a patient with a history of NMS and found that only a full intubating dose of mivacurium (0.2 mg/kg IV) was associated with effective muscle relaxation during ECT-induced seizures. Gitlin et al. (65) also found that mivacurium doses of 0.15–0.25 mg/kg IV were required for ECT in patients with myasthenia gravis. Of concern, a full intubating dose of mivacurium can be associated with clinically significant histamine release and occasional hypotension and requires the use of anticholinesterase drugs to reverse residual paralysis after ECT.
Patients receiving atracurium 0.5 mg/kg IV had significantly fewer ECT-induced moderate to severe muscle contractions compared with patients receiving a 0.3 mg/kg dose (16% vs 86%) (66). As expected, patients receiving atracurium 0.5 mg/kg IV required more time to achieve a train-of-four ratio of 0.5 compared with patients receiving the 0.3 mg/kg dose (9.2 ± 0.8 min vs 4.3 ± 0.4 min). These investigators recommended that a small dose of atracurium be used if one needs to avoid using succinylcholine and mivacurium for ECT treatments. However, a small dose of atracurium (10–15 mg) in a patient with atypical plasma cholinesterase (67) had an onset of action of 6 min, and the time to 90% first twitch recovery was 16 min (even after reversal with edrophonium and atropine). Although the use of atracurium has been largely replaced by cisatracurium in clinical practice, there are no clinical reports describing the use of this improved formulation of atracurium for ECT.
Vecuronium has been used for pretreatment in patients with severe succinylcholine-induced myalgias (32). There have been no clinical reports describing the use of rocuronium for ECT. Given the pharmacodynamic profiles of these aminosteroid nondepolarizing muscle relaxants, it does not appear that these drugs offer any advantages in the ECT setting.
Rapacuronium is a newer amino-steroid muscle relaxant with a rapid onset and short duration of action. This nondepolarizing muscle relaxant has been used for ECT treatments in a patient with a positive family history of MH (68). Rapacuronium dosages of 0.6–0.8 mg/kg provided effective muscle relaxation for ECT, and this was readily reversible with edrophonium and atropine at the end of the seizure. Unfortunately, the occurrence of respiratory complications (e.g., bronchospasm) when rapacuronium was administered as part of a rapid-sequence induction technique led to its withdrawal from the market in the United States (69).
Drugs Used to Control Cardiovascular Responses
Because acute cardiovascular responses secondary to ECT can result in serious complications (10,11,25–27), many different drugs have been used to attenuate the acute parasympathetic and sympathetic responses (16–18). The parasympathetic effects of ECT often result in increased salivation, transient bradycardia, and occasionally even asystole, especially when repeated stimuli are administered as part of a seizure threshold determination (70). The sympathetic effects of ECT typically result in tachycardia, hypertension, and occasionally even myocardial ischemia and infarction, as mentioned previously. Anticholinergic drugs are often used to block the parasympathetic responses, whereas the acute sympathetic responses are attenuated with β-blockers, calcium channel blockers, α2 agonists, and direct-acting vasodilators. Rapid, short-acting opioid analgesics also possess sympatholytic effects and have recently been investigated as adjuvants during ECT. Some of these drugs can produce adverse effects on the duration of the ECT-induced seizure activity (Table 2). Therefore, the selection of adjuvants should be tailored to the needs of the individual patient.
When atropine was administered as premedication before ECT, it resulted in significantly higher RPP values (71). However, Mokriski et al. (39) reported that atropine 0.6 mg IV given before the induction of anesthesia decreased the frequency of premature atrial contractions and bradycardia and increased the frequency of tachycardia after ECT.
Glycopyrrolate is an anticholinergic drug that lacks central nervous system activity. As a result of its ability to reduce oral secretion and bradycardia during ECT without producing post-ECT side effects, glycopyrrolate has become the anticholinergic drug of choice for ECT. In an elderly population (72), no significant post-ECT complications were reported when patients received glycopyrrolate for premedication. In a placebo-controlled study, cognitive function after ECT was similar in patients receiving glycopyrrolate (0.2 mg IV) or saline (73). Because the primary benefit of using an anticholinergic drug appears to be its antisialagogue effect, glycopyrrolate (0.1–0.3 mg IV) is a better choice than atropine for ECT because it would be associated with less post-ECT tachycardia.
To attenuate the acute sympathetic response to ECT, both esmolol (a short-acting β1-receptor blocker) and labetalol (a mixed α- and β-blocker) have been most extensively studied. When esmolol (1–1.3 mg/kg) or labetalol (0.1–0.2 mg/kg) was administrated before the induction of anesthesia, they both produced significant amelioration of the acute cardiovascular response to ECT (74). However, SBP values were significantly lower during the early recovery period with labetalol (versus esmolol) pretreatment.
In a placebo-controlled, double-blinded study (75), pretreatment with esmolol (1.0 mg/kg) or labetalol (0.3 mg/kg) immediately before the induction of anesthesia significantly reduced the hemodynamic response to ECT compared with fentanyl (1.5 μg/kg) or lidocaine (1.0 mg/kg) (Fig. 3). It is interesting to note that esmolol more effectively attenuated the blood pressure response than labetalol. In contrast to esmolol, pretreatment with labetalol, fentanyl, or lidocaine significantly reduced the EEG seizure duration and increased the frequency with which a second electrical stimulus was required (Table 3) (75). However, there is controversy about the relative effects of esmolol and labetalol on the duration of seizure activity (Table 2) (76–78). To minimize the potential adverse effect of labetalol on the duration of seizure activity, labetalol can be administered immediately before or after the electrical stimulation is applied.
Calcium channel blockers.
When the acute blood pressure response to ECT was not adequately controlled with labetalol alone (79), nifedipine combined with labetalol was found to be safe and resulted in more effective control of the hemodynamic response in older patients. In patients with hypertension, sublingual nifedipine 10 mg, given 20 min before their ECT treatments, also attenuated the acute increase in the mean arterial blood pressure (MAP) (80).
The effects of nicardipine alone and in combination with labetalol have also been investigated with respect to its ability to control the acute hyperdynamic response to ECT (Fig. 4) (81). When administered as a rapid infusion, nicardipine (5 mg IV) produced a significant decrease in MAP. It is interesting to note that larger doses of nicardipine (10–15 mg) failed to produce a significantly larger decrease in MAP than the 5-mg dose. Bolus administration of nicardipine 1.25–5 mg IV produced a rapid onset of its hemodynamic effects without exacerbating the cardiovascular depressant effects of methohexital (1 mg/kg IV) (81). Unfortunately, the decrease in MAP after the 5-mg bolus dose was accompanied by a reflex increase in HR. Therefore, the acute hyperdynamic response to ECT was most effectively controlled by a bolus dose of 1.25 to 2.5 mg IV in combination with labetalol 10 mg IV. This combination produced a 20% decrease in MAP immediately before ECT and produced a lower MAP at the time of discharge from the recovery area compared with labetalol alone. It is important to note that the use of small-dose nicardipine did not alter the ECT-induced seizure duration (81).
In a placebo-controlled study, diltiazem (10 mg IV) significantly reduced HR and MAP after the induction of anesthesia and reduced the increases in these variables after the ECT stimulus (82). However, the use of diltiazem was associated with a shortened seizure duration. Therefore, small-dose nicardipine (or nifedipine) in combination with labetalol (0.1–0.2 mg/kg IV) appears to be a more effective regimen for controlling the acute hemodynamic response in older hypertensive patients undergoing ECT.
The acute hemodynamic effects of the α2-adrenergic agonist dexmedetomidine have been investigated in patients undergoing ECT (83). Dexmedetomidine 0.5 or 1.0 μg/kg IV, given 10–30 min before the induction of anesthesia, produced dose-related increases in the level of the patient’s pre-ECT sedation. However, dexmedetomidine failed to decrease the peak MAP and HR responses after the ECT stimulus and prolonged the recovery time after ECT. Although it had no effect on seizure duration, dexmedetomidine did not appear to be beneficial in controlling the acute hyperdynamic response associated with ECT.
The α2-adrenergic agonist/antagonist clonidine has also been investigated in the ECT setting (84). Oral clonidine (0.05–0.3 mg) given 60 to 90 min before the induction of anesthesia produced a dose-related antihypertensive effect by decreasing the MAP values immediately before the electrical stimulus was applied. However, clonidine produced no significant change in either the HR or the magnitude of the increase in MAP after the stimulus was applied. Clonidine produced no adverse effects on the duration of motor and EEG seizure activity or prolongation of the recovery time.
Finally, a recent study (85) reported that the postsynaptic α1-adrenergic antagonist urapidil (25 mg IV) was as effective as labetalol (0.2 mg/kg IV) in attenuating the increase in blood pressure associated with ECT but did not prevent the increase in HR. Therefore, it would appear that clonidine, a mixed α2 agonist/antagonist, is the most beneficial drug in this class for achieving hemodynamic stability during ECT. However, careful dose titration is required to achieve the optimal outcome.
When nitroglycerin (NTG) 3 μg/kg IV was given 2 min before ECT, post-ECT hemodynamic variables were all significantly lower compared with esmolol 2 mg/kg IV (86). It is important to note that neither NTG nor esmolol produced a change in the ECT-induced seizure duration. In another study, the administration of NTG 0.4 mg as a sublingual spray before ECT significantly attenuated the acute hypertensive response after the ECT stimulus (87). When 2% NTG ointment was applied 45 min before ECT (88), it also effectively attenuated the increase in HR and MAP after ECT, and it should be considered for ECT patients who are at a high risk of developing myocardial ischemia. It is interesting to note that NTG partially inhibits the increase in cerebral blood flow velocity associated with ECT (8).
Nitroprusside, another peripheral-acting vasodilator, has been used in patients with intracranial aneurysms, dissecting aortic aneurysm, and critical aortic stenosis requiring ECT (89–91). The combination of a β-blocker and an infusion of nitroprusside prevented tachycardia and hypertension and attenuated the expected increase in flow velocity in the middle cerebral artery after ECT (8). Furthermore, there is no evidence that nitroprusside decreases the ECT-induced seizure duration (92).
Trimethaphan, a ganglionic blocker, administered by IV bolus injection in doses of 5, 10, and 15 mg, is able to control the hyperdynamic responses during ECT without altering the duration of seizure activity (93). It is important that no rebound hypertension, post-ECT hypotension, cardiac arrhythmias, or other side effects were noted.
Lidocaine has also been administered to blunt the cardiovascular responses after ECT (9,75). Despite producing dose-related decreases in the duration of both motor and EEG seizure activity (Table 4) (9), lidocaine (1 mg/kg IV) failed to effectively attenuate the acute hemodynamic response associated with ECT (Fig. 3) (75).
Alfentanil was evaluated in combination with methohexital or propofol during anesthesia for ECT (94,95). In an observer-blinded, prospective, randomized, cross-over study, alfentanil (10 μg/kg IV) reduced the doses of methohexital and propofol required to induce unconsciousness by 33%, resulting in a prolongation of the ECT-induced seizure duration (95). In this interaction study, the durations of motor and EEG seizure durations were longest with the methohexital/alfentanil combination and shortest with propofol alone. However, recovery times were shorter in patients receiving propofol alone compared with methohexital/alfentanil and methohexital alone. In another report (94), alfentanil (25 μg/kg IV) in combination with methohexital (20 mg IV) was associated with a 45% increase in the EEG seizure duration compared with a standard 0.75 mg/kg dose of methohexital alone. In a recent study (96) comparing the effect of a methohexital (0.5 mg/kg) and remifentanil (1 μg/kg) combination with that of methohexital (0.75 mg/kg) alone, the anesthetic-sparing effect of remifentanil resulted in prolongation of the seizure time from 27 to 38 s. However, the hemodynamic changes and recovery times were similar in both groups.
It is interesting to note that when fentanyl (1.5 μg/kg IV) was administered with a standard 0.75 mg/kg dose of methohexital, the seizure duration was reduced (Table 3) (75). Fentanyl also failed to attenuate the acute hemodynamic response to ECT (Fig. 3). Therefore, the increased seizure duration associated with the short-acting opioid analgesics alfentanil and remifentanil appears to be related to a reduction in the IV anesthetic dosage requirements. In ECT patients with borderline seizure times, adjunctive use of a potent rapid and short-acting opioid analgesic could be very beneficial.
Standard General Anesthetic Technique
The essential elements of anesthesia for ECT include rapid loss of consciousness, effective attenuation of the hyperdynamic response to the electrical stimulus, avoidance of gross movements, minimal interference with seizure activity, and prompt recovery of spontaneous ventilation and consciousness. Therefore, the use of rapid and short-acting anesthetic drugs (e.g., methohexital, propofol, succinylcholine, esmolol, and labetalol) facilitates the ECT procedure. Although the rapid and short-acting opioid analgesics (e.g., alfentanil and remifentanil) have anesthetic-sparing properties, their role in ECT is yet to be clearly defined.
Although patients are required to fast overnight for solid food, clear liquids are allowed for taking oral medication up to 1 h before the procedure. Patients with cardiovascular disease should be encouraged to take all chronic antihypertensive medications before ECT. To prevent post-ECT myalgias, patients can be premedicated with enteric-coated aspirin (650 mg orally) or acetaminophen (650 mg orally). In younger patients at risk for severe ECT-induced myalgias, headaches, or both, ketorolac 30 mg IV can also be administered before the induction of anesthesia. Finally, to minimize the pain on injection of methohexital and propofol, lidocaine 0.5–1 mL can be injected into the IV catheter immediately before administering the induction drug.
Because ECT is typically performed three times a week for 3–4 wk and each procedure lasts only a few minutes, tracheal intubation is not recommended except in very specific situations (e.g., late pregnancy or emergency treatments with full-stomach precautions). In a recent series (97) evaluating anesthesia outcome in obese patients undergoing elective ECT, there was no evidence of regurgitation or aspiration in >650 consecutive general anesthetics administered at 2 major medical centers.
Ventilation is assisted with a face mask with a standard circle or a simple bag-valve-mask system. For obese patients with sleep apnea syndrome, a Guedel oral airway can be used to facilitate assisted ventilation during the procedure. Appropriate resuscitative equipment must be available, as must a laryngoscope, tracheal tube, and laryngeal mask airway for management of an airway emergency. Noninvasive hemodynamic monitoring is recommended except in rare cases in which arterial cannulation is required to control blood pressure in patients with cerebral aneurysms. Standard EEG and electromyographic monitoring (or a tourniquet technique to isolate the circulation to an extremity before the muscle relaxant is administered) are used to quantify the durations of the motor and EEG seizure activity. A bite-block should be carefully placed before application of the electrical stimulus to protect the patient’s teeth and to minimize the risk of lacerating the tongue.
During the recovery period, the most common side effects are confusion, agitation, amnesia, and headache. Because headaches occur in up to 45% of patients receiving ECT (98), intranasal administration of the 5-hydroxytryptamine-1 agonist sumatriptan may be beneficial in patients developing post-ECT headaches despite prophylaxis with ketorolac. Nausea and vomiting, as well as dizziness, are infrequent complications after ECT. Rare complications after ECT include acute cardiovascular (10,26) and neurologic (11,12) events, splenic rupture (99), and pulmonary edema (100). Standard noninvasive hemodynamic variables and oxygen saturation should be monitored for 15–30 min after ECT (101). Emergence agitation after ECT is usually treated by administering a small dose of midazolam (0.5–1 mg IV) (102). However, increasing (or decreasing) the dose of the succinylcholine and adding a small bolus of methohexital (10 mg IV) at the end of the seizure may also be helpful in reducing the incidence of post-ECT agitation.
Special Patient Populations
Patients with Cerebral Aneurysms
Because ECT provokes abrupt changes in both systemic and cerebral hemodynamics, the cerebrovascular changes increase wall stress in aneurysms, leading to enlargement or rupture (34). The increase in cerebral blood flow velocity during ECT is generally less with propofol than thiopental (40). Although nicardipine (0.02 mg/kg) failed to block the increase in cerebral blood flow velocity associated with ECT (8), both β-blockers and NTG partially inhibit the increase in cerebral blood flow velocity. In a patient with a cerebral aneurysm, administration of nitroprusside 30 μg/min IV in combination with atenolol 50 mg orally effectively controlled the acute cardiovascular changes associated with ECT (103).
Patients with Subdural Hemorrhage and Intracranial Mass Lesion
In a case report involving a patient with a subdural hemorrhage (104), ECT was not found to extend the subdural hemorrhage or intracranial complications. These authors suggested that the use of a dose-titration method of ECT with unilateral electrode placement away from the site of the lesion minimizes the risk of adverse neurologic outcomes. The use of neuroimaging scans during and after the course of ECT was recommended. In patients with a cerebral mass lesion, special efforts should be made to reduce intracranial pressure by pretreating the patient with steroids and diuretics and by hyperventilating the patient before applying the electrical stimulus (105).
Patients with Preexisting Cardiovascular Disease
To minimize myocardial ischemia, controlling known risk factors (e.g., hypertension, angina, arrhythmias, diabetes mellitus, and congestive heart failure) are important before ECT. Although etomidate can be used for the induction of anesthesia to minimize hypotension, this anesthetic is associated with an enhanced hyperdynamic response after ECT. Pretreatment with β-blockers is strongly recommended in patients with coronary artery disease (106). In a small case series (107), ECT successfully converted atrial fibrillation (AF) to normal sinus rhythm in four of six patients. ECT was also successfully performed in a series of AF patients receiving anticoagulation therapy (107). Considering the high risk of embolization with AF, these authors recommended full anticoagulation therapy before ECT treatments in this patient population.
In patients with preexisting bradycardia (or sick sinus syndrome), pretreatment with atropine is strongly recommended, especially in patients with myasthenia gravis who are receiving pyridostigmine (59,108). In these cases, avoiding an excessively large dose of succinylcholine and threshold titration should reduce the likelihood of asystole during ECT. In patients with permanent pacemakers, a temporary conversion to fixed-rate pacing before ECT is recommended to minimize the risk of interference with pacemaker functioning as a result of inhibitory myopotentials (109). In patients with an automatic internal cardioverter-defibrillator, the device should be deactivated before the electrical current is applied and should be reactivated in the early recovery period (110).
If a depressed patient presents with severe hypertension, headaches, and episodes of flushing, the presence of a pheochromocytoma should be excluded before initiating ECT because it remains one of the few absolute contraindications to ECT (111).
Patients with NMS
NMS is a serious side effect produced by antipsychotic drugs. NMS shares some clinical similarities to MH, and well known triggering drugs (e.g., succinylcholine and sevoflurane) should be avoided (112,113). Patients with NMS will manifest increases in temperature and serum creatine kinase levels after the administration of a triggering drug (113). Nondepolarizing muscle relaxants (e.g., mivacurium) have been successfully used in place of succinylcholine in this patient population (60).
Patients with Inadequate ECT-Induced Seizure Activity
Etomidate is the induction drug of choice in patients experiencing inadequate seizure activity when a maximal electrical stimulus is applied (36). Alternatively, use of a reduced dose of methohexital in combination with alfentanil or remifentanil will prolong the duration of seizure activity (95,96). Aminophylline has also been reported to lengthen ECT-induced seizures (114). In a case report, theophylline 100–200 mg, infused approximately 30 min before the ECT treatment, prolonged the seizure duration. In 55 ECT treatment sessions, no serious cardiovascular complications were observed. Caffeine is the other drug reported to prolong seizure activity during ECT (115,116).
Pregnancy-induced depression can be successfully treated with ECT. However, there are potential complications for both the mother (e.g., aspiration and premature labor) and the fetus (e.g., spontaneous abortion and death) (117,118). In addition to securing the patient’s airway with a tracheal tube after a rapid-sequence induction with cricoid pressure, consideration should be given to the prophylactic use of tocolytic therapy in pregnant patients with a history of premature labor or uterine contractions. For parturients in the later stages of pregnancy, use of sevoflurane as an alternative to methohexital may reduce the risk of uterine contractions after ECT (56).
Patients Receiving Concurrent Psychiatric Drugs
Current practice guidelines recommend that antidepressant medications be discontinued before starting a course of ECT (3). TCAs, monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors, and lithium are all medications that are often administered to depressed patients presenting for ECT. In patients taking an MAOI, meperidine and all indirect-acting sympathomimetic drugs should be avoided. Given the intrinsic anticholinergic properties of TCA drugs, anticholinergics are unnecessary. At therapeutic doses, an MAOI can decrease MAP and increase the postural decline in MAP without affecting the HR (119). In a clinical report (120), changes in MAP and HR during ECT were not significantly different in patients receiving chronic treatment with an MAOI compared with a similar patient population not receiving these drugs.
Use of the selective serotonin reuptake inhibitor venlafaxine was compared with TCA in patients undergoing ECT (121). The seizure durations were similar in both groups, and neither drug significantly increased the MAP or produced heart rhythm abnormalities. However, a prolonged bradycardia was observed in a patient receiving venlafaxine (122), and post-ECT hypotension and bradycardia were observed in a patient receiving fenfluramine, phentermine, and fluoxetine (123). In a study involving 13 depressed patients receiving moclobemide (300 mg/d orally), a selective and reversible MAOI, there were no clinically relevant side effects during ECT treatments (124). However, the use of lithium can delay recovery from muscle relaxants (125). Chronic administration of TCA drugs and the atypical antidepressants (e.g., mianserin, iprindole, fluoxetine, zimelidine, or viloxazine) can prolong recovery from anesthesia even 2 to 5 days after the last dose.
ECT is a simple procedure performed on a highly diverse patient population with severe, drug-resistant depression and other psychiatric disorders (Table 5). Despite its proven effectiveness, ECT remains one of the most controversial treatments in all of medicine (126). When appropriately administered, ECT is an extremely safe and effective procedure in a wide variety of high-risk patient populations (127). Unfortunately, the relapse rate during the 6- to 12-mo period after completion of an acute course of ECT exceeds 50% unless the patient receives maintenance ECT or combination pharmacotherapy (128).
The anesthetic management for ECT typically involves the use of an induction dose of an IV anesthetic (e.g., methohexital or propofol) followed by a muscle relaxant (e.g., succinylcholine or mivacurium). A wide variety of cardiovascular drugs (e.g., esmolol or labetalol) are administered to minimize the acute hemodynamic changes produced by the electrical stimulus and the resultant generalized seizure activity. Standard noninvasive monitors are used during the procedure, and the airway is typically managed with a face mask. An antisialagogue (e.g., glycopyrrolate) is used to decrease oral secretion, and a Guedel airway device may be used in patients prone to upper airway obstruction (e.g., those with sleep apnea syndrome or who are morbidly obese). The availability of new brain monitors (e.g., EEG bispectral index, patient state index, auditory evoked potential index) (129) may improve the ability of anesthesiologists to titrate anesthetic drugs to optimize the conditions for ECT.
The optimal dosages of the anesthetic, muscle relaxant, and sympatholytic drugs require careful titration to the needs of the individual patient, and further adjustments should be made during the course of a series of ECT treatments on the basis of the patient’s earlier responses. In a recent editorial by Kellner (130), a simple modal approach to ECT treatment was advocated. Unfortunately, patients vary widely in their sensitivity to these drugs, depending on their age, body habitus, concurrent drug usage, and underlying medical conditions. Given the large number of elderly patients with underlying cardiovascular diseases (e.g., hypertension, coronary artery disease, and peripheral vascular disease), careful titration of the patients’ sympatholytic drugs (e.g., labetalol, esmolol, nicardipine, and clonidine) is also important to obtain the best possible outcome with ECT. The “one size fits all” approach advocated by Kellner (130) is not supported by scientific data and would result in suboptimal care for many patients undergoing ECT treatments in the future.
In conclusion, practicing anesthesiologists should be aware of the anesthetic factors that influence the duration of seizure activity, because the effectiveness of ECT treatments is predicated on achieving an adequate EEG seizure (>30 s). Because these patients may be receiving a wide variety of psychotropic and cardiovascular drugs, anesthesiologists should also be aware of potential adverse drug interactions. Despite the advanced age and presence of coexisting medical diseases in many patients undergoing ECT treatments, this therapy has remained remarkably safe and effective for treating severe depression.
We thank our psychiatry (Drs. Mark Litle, Larry Thornton, and Mustafa Husian) and nursing (Carol Bethany, Nieva Rubiano, Brenda Small, Helen Derroush, Flo Bernardo, Ken Adams, and Tommie Tipton) colleagues at Zale Lipshy University Hospital in Dallas, TX, for their support.
1. Khan A, Mirolo MH, Hughes D, Bierut L. Electroconvulsive therapy. Psychiatr Clin North Am 1993; 16: 497–513.
2. Thompson JW, Weiner RD, Myers CP. Use of ECT in the United States in 1975, 1980 and 1986. Am J Psychiatry 1994; 151: 1657–61.
3. American Psychiatric Association Committee on Electroconvulsive Therapy. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging. 2nd ed. Washington, DC: American Psychiatric Association, 2001.
4. Segman RH, Shapira B, Gorfine M, Lerer B. Onset and time course of antidepressant action: psychopharmacological implications of a controlled trial of electroconvulsive therapy. Psychopharmacology 1995; 119: 440–8.
5. Gaines GY 3rd, Rees DI. Electroconvulsive therapy and anesthetic considerations. Anesth Analg 1986; 65: 1345–56.
6. Folk JW, Kellner CH, Beale MD, et al. Anesthesia for electroconvulsive therapy: a review. J ECT 2000; 16: 157–70.
7. Saito S, Miyoshi S, Yoshikawa D, et al. Regional cerebral oxygen saturation during electroconvulsive therapy: monitoring by near-infrared spectrophotometry. Anesth Analg 1996; 83: 726–30.
8. Saito S, Kadoi Y, Iriuchijima N, et al. Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy. Can J Anaesth 2000; 47: 767–74.
9. Fu W, Stool LA, White PF, Husain MM. Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity. J Clin Anesth 1997; 9: 653–7.
10. Lopez-Gomez D, Sanchez-Corral MA, Cobo JV, et al. Myocardial infarction after electroconvulsive therapy. Rev Esp Cardiol 1999; 52: 536.
11. Weisberg LA, Elliott D, Mielke D. Intracerebral hemorrhage following electroconvulsive therapy. Neurology 1991; 41: 1849.
12. Rikher KV, Johnson R, Kamal M. Cortical blindness after electroconvulsive therapy. J Am Board Fam Pract 1997; 10: 141–3.
13. Zachrisson OC, Balldin J, Ekman R, et al. No evident neuronal damage after electroconvulsive therapy. Psychiatry Res 2000; 96: 157–65.
14. Ng C, Schweitzer I, Alexopoulos P, et al. Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000; 16: 370–9.
15. Delva NJ, Brunet D, Hawken ER, et al. Electrical dose and seizure threshold: relations to clinical outcome and cognitive effects in bifrontal, bitemporal, and right unilateral ECT. J ECT 2000; 16: 361–9.
16. Weinger MB, Partridge BL, Hauger R, et al. Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy. II. Effects of pretreatment regimens on catecholamines, ACTH, vasopressin, and cortisol. Anesth Analg 1991; 73: 563–9.
17. 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: 557–61.
18. Wells DG, Davies GG. Hemodynamic changes associated with electroconvulsive therapy. Anesth Analg 1987; 66: 1193–5.
19. Mayur PM, Gangadhar BN, Girish K, et al. Acute post-ECT cardiovascular response: a comparison of threshold right unilateral and bilateral ECT. J ECT 1998; 14: 94–8.
20. Swartz CM. Physiological response to ECT stimulus dose. Psychiatry Res 2000; 97: 229–35.
21. Bergsholm P, Bleie H, Gran L, d’Elia G. Cardiovascular response and seizure duration as determined by electroencephalography during unilateral electroconvulsive therapy. Acta Psychiatr Scand 1993; 88: 25–8.
22. Cockey GH, Conti CR. Electroconvulsive therapy-induced transient T-wave inversions on ECG. Clin Cardiol 1995; 18: 418–20.
23. Larsen JR, Hein L, Stromgren LS. Ventricular tachycardia with ECT. J ECT 1998; 14: 109–14.
24. Ali PB, Tidmarsh MD. Cardiac rupture during electroconvulsive therapy. Anaesthesia 1997; 52: 884–6.
25. Zielinski RJ, Roose SP, Devanand DP, et al. Cardiovascular complications of ECT in depressed patients with cardiac disease. Am J Psychiatry 1993; 150: 904–9.
26. McCall WV. Asystole in electroconvulsive therapy: report of four cases. J Clin Psychiatry 1996; 57: 199–203.
27. Peterson GN. ECT risk in cardiac patients. Psychosomatics 1985; 26: 531.
28. Fuenmayor AJ, el Fakih Y, Moreno J, Fuenmayor AM. Effects of electroconvulsive therapy on cardiac function in patients without heart disease. Cardiology 1997; 88: 254–7.
29. Kadoi Y, Saito S, Seki S, et al. Electroconvulsive therapy impairs systolic performance of the left ventricle. Can J Anaesth 2001; 48: 405–8.
30. Sarpel Y, Togrul E, Herdem M, et al. Central acetabular fracture-dislocation following electroconvulsive therapy: report of two similar cases. J Trauma 1996; 41: 342–4.
31. Nott MR, Watts JS. A fractured hip during electro-convulsive therapy. Eur J Anaesthesiol 1999; 16: 265–7.
32. Herriot PM, Cowain T, McLeod D. Use of vecuronium to prevent suxamethonium-induced myalgia after ECT. Br J Psychiatry 1996; 168: 653–4.
33. Fantz RM, Markowitz JS, Kellner CH. Sumatriptan for post-ECT headache. J ECT 1998; 14: 272–4.
34. Zhu BL, Ishida K, Oritani S, et al. Sudden death following psychiatric electroconvulsive therapy: a case report. Nippon Hoigaku Zasshi 1998; 52: 149–52.
35. Sackeim HA, Devanand DP, Prudic J. Stimulus intensity, seizure threshold, and seizure duration: impact on the efficacy and safety of electroconvulsive therapy. Psychiatr Clin North Am 1991; 14: 803–43.
36. Avramov MN, Husain MM, White PF. The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy. Anesth Analg 1995; 81: 596–602.
37. Cook A, Stevenson G, Scott AI. A survey of methohexitone use by anesthetists in the clinical practice of ECT in Edinburgh. J ECT 2000; 16: 350–5.
38. Gurmarnik S, Young R, Alesker E. Divided doses of methohexitone improves ECT outcome. Can J Anaesth 1996; 43: 535.
39. Mokriski BK, Nagle SE, Papuchis GC, et al. Electroconvulsive therapy-induced cardiac arrhythmias during anesthesia with methohexital, thiamylal, or thiopental sodium. J Clin Anesth 1992; 4: 208–12.
40. Saito S, Kadoi Y, Nara T, et al. The comparative effects of propofol versus thiopental on middle cerebral artery blood flow velocity during electroconvulsive therapy. Anesth Analg 2000; 91: 1531–6.
41. Tanaka N, Saito Y, Hikawa Y, et al. Effects of thiopental and sevoflurane on hemodynamics during anesthetic management of electroconvulsive therapy. Masui 1997; 46: 1575–9.
42. Saffer S, Berk M. Anesthetic induction for ECT with etomidate is associated with longer seizure duration than thiopentone. J ECT 1998; 14: 89–93.
43. Trzepacz PT, Weniger FC, Greenhouse J. Etomidate anesthesia increases seizure duration during ECT: a retrospective study. Gen Hosp Psychiatry 1993; 15: 115–20.
44. Fredman B, Husain MM, White PF. Anaesthesia for electroconvulsive therapy: use of propofol revisited. Eur J Anaesthesiol 1994; 11: 423–5.
45. Geretsegger C, Rochowanski E, Kartnig C, Unterrainer AF. Propofol and methohexital as anesthetic agents for electroconvulsive therapy (ECT): a comparison of seizure-quality measures and vital signs. J ECT 1998; 14: 28–35.
46. Fredman B, d’Etienne J, Smith I, et al. Anesthesia for electroconvulsive therapy: effects of propofol and methohexital on seizure activity and recovery. Anesth Analg 1994; 79: 75–9.
47. Fear CF, Littlejohns CS, Rouse E, McQuail P. Propofol anaesthesia in electroconvulsive therapy: reduced seizure duration may not be relevant. Br J Psychiatry 1994; 165: 506–9.
48. Kirkby KC, Beckett WG, Matters RM, King TE. Comparison of propofol and methohexitone in anaesthesia for ECT: effect on seizure duration and outcome. Aust N Z J Psychiatry 1995; 29: 299–303.
49. Malsch E, Gratz I, Mani S, et al. Efficacy of electroconvulsive therapy after propofol and methohexital anesthesia. Convuls Ther 1994; 10: 212–9.
50. Sakamoto A, Hoshino T, Suzuki N, et al. Effects of propofol anesthesia on cognitive recovery of patients undergoing electroconvulsive therapy. Psychiatry Clin Neurosci 1999; 53: 655–60.
51. Rasmussen KG, Jarvis MR, Zorumski CF. Ketamine anesthesia in electroconvulsive therapy. Convuls Ther 1996; 12: 217–23.
52. Boylan LS, Haskett RF, Mulsant BH, et al. Determinants of seizure threshold in ECT: benzodiazepine use, anesthetic dosage, and other factors. J ECT 2000; 16: 3–18.
53. Bush G, Fink M, Petrides G, et al. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand 1996; 93: 137–43.
54. Loimer N, Hofmann P, Chaudhry HR. Midazolam shortens seizure duration following electroconvulsive therapy. J Psychiatr Res 1992; 26: 97–101.
55. Bailine SH, Safferman A, Vital-Herne J, Bernstein S. Flumazenil reversal of benzodiazepine-induced sedation for a patient with severe pre-ECT anxiety. Convuls Ther 1994; 10: 65–8.
56. Ishikawa T, Kawahara S, Saito T, et al. Anesthesia for electroconvulsive therapy during pregnancy: case report. Masui 2001; 50: 991–7.
57. Fredman B, Smith I, d’Etienne J, White PF. Use of muscle relaxants for electroconvulsive therapy: how much is enough? Anesth Analg 1994; 78: 195–6.
58. Auriacombe M, Reneric JP, Usandizaga D, et al. Post-ECT agitation and plasma lactate concentrations. J ECT 2000; 16: 263–7.
59. Tang WK, Ungvari GS. Asystole during electroconvulsive therapy: a case report. Aust N Z J Psychiatry 2001; 35: 382–5.
60. Kelly D, Bruell SJ. Neuroleptic malignant syndrome and mivacurium: a safe alternative to succinylcholine? Can J Anaesth 1994; 41: 845–9.
61. Cooper RC, Baumann PL, McDonald WM. An unexpected hyperkalemic response to succinylcholine during electroconvulsive therapy for catatonic schizophrenia. Anesthesiology 1999; 91: 574–5.
62. Jaksa RJ, Palahniuk RJ. Attempted organophosphate suicide: a unique cause of prolonged paralysis during electroconvulsive therapy. Anesth Analg 1995; 80: 832–3.
63. Cheam EW, Critchley LA, Chiu PT, et al. Low-dose mivacurium is less effective than succinylcholine in electroconvulsive therapy. Can J Anaesth 1999; 46: 49–51.
64. Liu S, Modell JH. Anesthetic management for patients with postpolio syndrome receiving electroconvulsive therapy. Anesthesiology 2001; 95: 799–801.
65. Gitlin MC, Jahr JS, Margolis MA, McCain J. Is mivacurium chloride effective in electroconvulsive therapy? A report of four cases, including a patient with myasthenia gravis. Anesth Analg 1993; 77: 392–4.
66. Lui PW, Ma JY, Chan KK. Modification of tonic-clonic convulsions by atracurium in multiple-monitored electroconvulsive therapy. J Clin Anesth 1993; 5: 16–21.
67. Hickey DR, O’Connor JP, Donati F. Comparison of atracurium and succinylcholine for electroconvulsive therapy in a patient with atypical plasma cholinesterase. Can J Anaesth 1987; 34: 280–3.
68. Kadar AG, Kramer BA, Barth MC, White PF. Rapacuronium: an alternative to succinylcholine for electroconvulsive therapy. Anesth Analg 2001; 92: 1171–2.
69. White PF. Rapacuronium: why did it fail as a replacement for succinylcholine? Br J Anaesth 2002; 88: 1–3.
70. McCall WV, Reid S, Ford M. Electrocardiographic and cardiovascular effects of subconvulsive stimulation during titrated right unilateral ECT. Convuls Ther 1994; 10: 25–33.
71. Mayur PM, Shree RS, Gangadhar BN, et al. Atropine premedication and the cardiovascular response to electroconvulsive therapy. Br J Anaesth 1998; 81: 466–7.
72. Sommer BR, Satlin A, Friedman L, Cole JO. Glycopyrrolate versus atropine in post-ECT amnesia in the elderly. J Geriatr Psychiatry Neurol 1989; 2: 18–21.
73. Kelway B, Simpson KH, Smith RJ, Halsall PJ. Effects of atropine and glycopyrrolate on cognitive function following anaesthesia and electroconvulsive therapy (ECT). Int Clin Psychopharmacol 1986; 1: 296–302.
74. 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: 557–61.
75. Weinger MB, Partridge BL, Hauger R, Mirow A. Prevention of the cardiovascular and neuroendocrine response to electroconvulsive therapy. I. Effectiveness of pretreatment regimens on hemodynamics. Anesth Analg 1991; 73: 556–62.
76. 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: 271–4.
77. McCall WV, Zvara D, Brooker R, Arias L. Effect of esmolol pretreatment on EEG seizure morphology in RUL ECT. Convuls Ther 1997; 13: 175–80.
78. Kovac AL, Goto H, Pardo MP, Arakawa K. Comparison of two esmolol bolus doses on the haemodynamic response and seizure duration during electroconvulsive therapy. Can J Anaesth 1991; 38: 204–9.
79. Figiel GS, DeLeo B, Zorumski CF, et al. Combined use of labetalol and nifedipine in controlling the cardiovascular response from ECT. J Geriatr Psychiatry Neurol 1993; 6: 20–4.
80. Wells DG, Davies GG, Rosewarne F. Attenuation of electroconvulsive therapy induced hypertension with sublingual nifedipine. Anaesth Intensive Care 1989; 17: 31–3.
81. 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: 394–400.
82. Wajima Z, Yoshikawa T, Ogura A, et al. The effects of diltiazem on hemodynamics and seizure duration during electroconvulsive therapy. Anesth Analg 2001; 92: 1327–30.
83. Fu W, White PF. Dexmedetomidine failed to block the acute hyperdynamic response to electroconvulsive therapy. Anesthesiology 1999; 90: 422–4.
84. Fu W, Stool LA, White PF, Husain MM. Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy? Anesth Analg 1998; 86: 1127–30.
85. Blanch J, Martinez-Palli G, Navines R, et al. Comparative hemodynamic effects of urapidil and labetalol after electroconvulsive therapy. J ECT 2001; 17: 275–9.
86. O’Flaherty D, Husain MM, Moore M, et al. Circulatory responses during electroconvulsive therapy: comparative effects of placebo, esmolol and nitroglycerin. Anaesthesia 1992; 47: 563–7.
87. Villalonga A, Planella T, Castillo J, et al. Nitroglycerin spray in the prevention of hypertension induced by electroconvulsive therapy. Rev Esp Anestesiol Reanim 1989; 36: 264–6.
88. Parab AL, Chaudhari LS, Apte J. Use of nitroglycerin ointment to prevent hypertensive response during electroconvulsive therapy: a study of 50 cases. J Postgrad Med 1992; 38: 55–7.
89. Levin L, Wambold D, Viguera A, et al. Hemodynamic responses to ECT in a patient with critical aortic stenosis. J ECT 2000; 16: 52–61.
90. Devanand DP, Malitz S, Sackeim HA. ECT in a patient with aortic aneurysm. J Clin Psychiatry 1990; 51: 255–6.
91. Drop LJ, Bouckoms AJ, Welch CA. Arterial hypertension and multiple cerebral aneurysms in a patient treated with electroconvulsive therapy. J Clin Psychiatry 1988; 49: 280–2.
92. Sudha S, Andrade C, Anand A, et al. Nitroprusside and ECS-induced retrograde amnesia. J ECT 2001; 17: 41–4.
93. Petrides G, Maneksha F, Zervas I, et al. Trimethaphan (Arfonad) control of hypertension and tachycardia during electroconvulsive therapy: a double-blind study. J Clin Anesth 1996; 8: 104–9.
94. Dinwiddie SH, Isenberg KE. Combined alfentanil-methohexital anesthesia in electroconvulsive therapy. Convuls Ther 1995; 11: 170–6.
95. Nguyen TT, Chhibber AK, Lustik SJ, et al. Effect of methohexitone and propofol with or without alfentanil on seizure duration and recovery in electroconvulsive therapy. Br J Anaesth 1997; 79: 801–3.
96. Andersen FA, Arsland D, Holst-Larsen H. Effects of combined methohexitone-remifentanil anaesthesia in electroconvulsive therapy. Acta Anaesthesiol Scand 2001; 45: 830–3.
97. Kadar AG, Ing CH, White PF, et al. Anesthesia for electroconvulsive therapy in obese patients. Anesth Analg 2002; 94: 360–1.
98. Markowitz JS, Kellner CH, DeVane CL, et al. Intranasal sumatriptan in post-ECT headache: results of an open-label trial. J ECT 2001; 17: 280–3.
99. Gitlin MC, O’Neill PT, Barber MJ, Jahr JS. Splenic rupture after electroconvulsive therapy. Anesth Analg 1993; 76: 1363–4.
100. Tsutsumi N, Tohdoh Y, Kawana S, et al. A case of pulmonary edema after electroconvulsive therapy under propofol anesthesia. Masui 2001; 50: 525–7.
101. McCormick AS, Saunders DA. Oxygen saturation of patients recovering from electroconvulsive therapy. Anaesthesia 1996; 51: 702–4.
102. Labbate LA, Miller JP. Midazolam for treatment of agitation after ECT. Am J Psychiatry 1995; 152: 472–3.
103. Viguera A, Rordorf G, Schouten R, et al. Intracranial haemodynamics during attenuated responses to electroconvulsive therapy in the presence of an intracerebral aneurysm. J Neurol Neurosurg Psychiatry 1998; 64: 802–5.
104. Wijeratne C, Shome S. Electroconvulsive therapy and subdural hemorrhage. J ECT 1999; 15: 275–9.
105. Salaris S, Szuba MP, Traber K. ECT and intracranial vascular masses. J ECT 2000; 16: 198–203.
106. Applegate RJ. Diagnosis and management of ischemic heart disease in the patient scheduled to undergo electroconvulsive therapy. Convuls Ther 1997; 13: 128–44.
107. Petrides G, Fink M. Atrial fibrillation, anticoagulation, and electroconvulsive therapy. Convuls Ther 1996; 12: 91–8.
108. Otsuka H, Shikama H, Saito T, et al. Asystole during electroconvulsive therapy in a patient with depression and myasthenia gravis. Masui 2000; 49: 893–5.
109. Abiuso P, Dunkelman R, Proper M. Electroconvulsive therapy in patients with pacemakers. JAMA 1978; 240: 2459–60.
110. Lapid MI, Rummans TA, Hofmann VE, Olney BA. ECT and automatic internal cardioverter-defibrillator. J ECT 2001; 17: 146–8.
111. Carr ME Jr, Woods JW. Electroconvulsive therapy in a patient with unsuspected pheochromocytoma. South Med J 1985; 78: 613–5.
112. Sakamoto A, Hoshino T, Suzuki H, et al. Repeated propofol anesthesia for a patient with a history of neuroleptic malignant syndrome. Nippon Ika Daigaku Zasshi 1999; 66: 262–5.
113. Nisijima K, Ishiguro T. Electroconvulsive therapy for the treatment of neuroleptic malignant syndrome with psychotic symptoms: a report of five cases. J ECT 1999; 15: 158–63.
114. Stern L, Dannon PN, Hirschmann S, et al. Aminophylline increases seizure length during electroconvulsive therapy. J ECT 1999; 15: 252–7.
115. Francis A, Fochtmann L. Caffeine augmentation of electroconvulsive seizures. Psychopharmacology 1994; 115: 320–4.
116. Navines R, Bernardo M, Martinez-Palli G, et al. Optimization of electroconvulsive therapy: strategies for an adequate convulsion—role of caffeine. Actas Esp Psiquiatr 2000; 28: 194–201.
117. Gilot B, Gonzalez D, Bournazeau JA, et al. Case report: electroconvulsive therapy during pregnancy. Encephale 1999; 25: 590–4.
118. Echevarria Moreno M, Martin Munoz J, Sanchez Valderrabanos J, et al. Electroconvulsive therapy in the first trimester of pregnancy. J ECT 1998; 14: 251–4.
119. Goldman LS, Alexander RC, Luchins DJ. Monoamine oxidase inhibitors and tricyclic antidepressants: comparison of their cardiovascular effects. J Clin Psychiatry 1986; 47: 225–9.
120. El-Ganzouri AR, Ivankovich AD, Braverman B, McCarthy R. Monoamine oxidase inhibitors: should they be discontinued preoperatively? Anesth Analg 1985; 64: 592–6.
121. Bernardo M, Navarro V, Salva J, et al. Seizure activity and safety in combined treatment with venlafaxine and ECT: a pilot study. J ECT 2000; 16: 38–42.
122. Agelink MM, Zeit T, Klieser E. Prolonged bradycardia complicates antidepressive treatment with venlafaxine and ECT. Br J Psychiatry 1998; 173: 441.
123. Rich JM, Njo L, Roberts KW, Smith KP. Unusual hypotension and bradycardia in a patient receiving fenfluramine, phentermine, and fluoxetine. Anesthesiology 1998; 88: 529–31.
124. Becker T, Struck M, Laux G. Treatment of depression using MAO-A inhibitors: an open study of a direct switch from moclobemide to tri-tetracyclic antidepressants. Psychiatr Prax 1989; 16: 44–7.
125. Martin BA, Kramer PM. Clinical significance of the interaction between lithium and a neuromuscular blocker. Am J Psychiatry 1982; 139: 1326–8.
126. Glass RM. Electroconvulsive therapy: time to bring it out of the shadows. JAMA 2001; 285: 1346–8.
127. Rabheru K. The use of electroconvulsive therapy in special patient populations. Can J Psychiatry 2001; 46: 710–9.
128. Sackeim HA, Haskett RF, Mulsant BH, et al. Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA 2001; 285: 1299–307.
129. Tanabe T, Sakai T, Mi WD, Matsuki A. Electroconvulsive therapy decreased bispectral index: a case report. Masui 1998; 47: 1096–8.
130. Kellner CH. Towards the modal ECT treatment. J ECT 2001; 17: 1–2.
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