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.
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.
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.
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).
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).
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).
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).
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.
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