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Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is now performed on 1,000,000 patients per year world-wide with 100,000 of those in the United States [6]. ECT is an effective therapeutic modality for severe and treatment-resistant depression, psychosis, bipolar disorder, and catatonia. It also shows promise in treating Parkinson’s disease, and severe autism associated with self-injurious behavior [7]. The procedure involves passing small electric currents through the brain to generate a generalized, tonic seizure under anesthesia. While it is generally thought to be a safe procedure, there are major risks associated with ECT including myocardial infarction, stroke, and death, so the anesthesiologist must be intimately familiar with the physiologic effects of ECT, the propensity for the administered drugs to interfere with the treatment and the methods required to keep patients safe [8]. This review will cover the physiologic effects of ECT and the anesthetic management of patient prior to, during, and after ECT. Additionally, we will briefly describe special populations and their considerations prior to ECT.  

The cardiovascular response to ECT is mediated by activation of the autonomic nervous system. Following electrical stimulation, there is an initial parasympathetic discharge lasting 10-15 seconds that results in bradycardia, hypotension, and rarely asystole. A prominent sympathetic response quickly follows causing a 30-40% increase in SBP, and a 20% increase in heart rate that typically peaks at 3-5 minutes. The severity of this impulse may result in cardiac arrhythmias [2]. Cerebral oxygen consumption, blood flow, and intracranial pressure all increase as a result of increased neuronal firing. Rare but serious cerebral complications include transient ischemic deficits, cortical blindness, intracranial hemorrhage, and prolonged seizures. More common complications are cognitive adverse effects (more common in underlying dementia) like disorientation, impaired attention, and memory problems linked to the post-ictal state that may last several weeks. These complications occur in up to 50% of patients. Retrograde and anterograde amnesia often occurs, and permanent memory loss is possible, but most patients typically recover within 6 months. The cognitive symptoms can be reduced by altering the stimulus intensity or waveform, using unilateral electrode placement, and lengthening the time between sessions [3]. Finally, there is an increase in both intraocular and intragastric pressures.  

Many ECT patients are elderly, have a variety of co-morbidities, and can be poor historians because of their depression, making their preoperative assessment especially important. Myocardial infarction or cerebrovascular accidents within 3 months are relative but not absolute contraindications to ECT. Evaluation for increased intracranial pressure is also important as it can be a manifestation of ECT. Untreated deep vein thrombosis, poorly controlled heart failure, an unstable major fracture, severe osteoporosis, pheochromocytoma, retinal detachment, and glaucoma are all relative contraindications [3]. Cochlear implants are a contraindication that may be circumvented with unilateral ECT. ECT is quicker in onset than other treatment modalities and potentially lifesaving in severe catatonia with no oral intake, so the relative contraindications should be weighed against the risks of severe psychiatric illness. Physical examination should seek evidence of heart failure, severe valvular disease, dysrhythmias, uncontrolled hypertension, poor dentition, or dehydration requiring fluid therapy. Blood tests, electrocardiograms, and other investigations should be performed as clinically indicated. Any attempt to optimize conditions should also be weighed against the acute risk of severe depression.  

The goal of anesthesia for ECT should be rapid onset and offset of unconsciousness with muscle relaxation while minimizing physiologic complications. Premedication with benzodiazepines should be avoided in ECT as they interfere with seizure generation and delay emergence. Methohexital is the most common induction agent and is considered the “Gold Standard” for ECT. It benefits from a long history of use, but its use is limited by availability. Etomidate is also used commonly because it results in longer seizure duration and may reduce the seizure threshold [5]. Finally, some anesthesiologists will use propofol in low doses for induction, but this is generally avoided as propofol raises the seizure threshold.  

Neuromuscular blocking agents are used to reduce convulsions and decrease the risk of injury. Succinylcholine is the most commonly used paralytic and is often dosed at 0.5mg/Kg.  Larger doses up to 1.5mg/Kg are warranted in patients at high-risk for musculoskeletal injuries such as those with severe cachexia, osteoporosis, and a pre-existing skeletal injury. Rocuronium and vecuronium have only been used as pre-curarizing agents in the past, but with the advent of sugammadex, they may be used more frequently. 

Glycopyrrolate and atropine may be used to control parasympathetic effects. Glycopyrrolate is preferred as it has superior anti-sialagogue effects, lacks CNS effects, and results in less post-ECT tachycardia [3]. Atenolol may be given pre-procedure to cut down on sympathetic effects, and esmolol or labetalol may be used intra-procedure for the same purpose. Dexmedetomidine blunts the hyperdynamic response. IV lidocaine has been tried and was found to be ineffective at decreasing sympathetic effects.  

Prior to the procedure, patients should be preoxygenated. Intubation is rarely indicated unless there is a high-risk of aspiration. Following induction, a facemask may be used to gently assist with ventilation. Hyperventilation may be useful in prolonging seizure duration and lowering the seizure threshold. A bite block is useful in preventing damage to the teeth, lips, and tongue. Gentle manual ventilation is typically needed until spontaneous ventilation resumes.  

Common postoperative complications include confusion, agitation, violent behavior, amnesia, headache, myalgia, nausea, and vomiting. A trained escort or family member is reassuring to patients and may reduce these complications. Most patient recover quickly and can be discharged the same day if they are outpatients. The most challenging problem postoperatively is emergence agitation. If a secluded and calm recovery environment is inadequate to manage the agitation, small doses of midazolam may help.  

Patients with cerebral aneurysms are at risk of enlargement and rupture. Patients with intracranial masses are at a higher risk that can be mitigated with hyperventilation and pretreatment with steroid and diuretics. Patients with pacemakers should have them changed to fixed-rate pacing during the procedure, though the risks are low due to the distance between the stimulus and the pacemaker. Internal cardioverter-defibrillators should be deactivated prior to the procedure and reactivated in the recovery period. ECT in pregnant patients is safe and effective and may be preferable to some forms of drug therapy in pregnant patients. However, they are also at increased risk of aspiration, premature labor, and spontaneous abortion. Prophylactic tocolytics may be used in patients with a history of premature labor. Sevoflurane may reduce the risk of uterine contractions in later stages of pregnancy [3].  

The unique physiologic effects of ECT and the pharmacology involved are fascinating. Anesthesia providers caring for patients requiring ECT need to be intimately familiar with these effects to assure patients have safe and effective treatment.  Administered appropriately, ECT is usually safe and potentially lifesaving.  


  1. Scot AIF. The ECT Handbook, 2nd Edn. Glasgow: The Royal College of Psychiatrists, 2005 
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  1. Individualized Anesthetic Management for Patients Undergoing Electroconvulsive Therapy: A Review of Current Practice 
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