Anesthesia for electroconvulsive therapy

Published on 07/02/2015 by admin

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Last modified 22/04/2025

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Anesthesia for electroconvulsive therapy

Joseph J. Sandor, MD

Convulsive therapy for psychiatric disorders has been used since 1934. Electroconvulsive therapy (ECT), modified over the years to incorporate monitoring, intravenous administration of anesthetic drugs, neuromuscular blockade, and the use of supplemental O₂, is both safe and effective for the treatment of endogenous depression in patients whose symptoms have failed to respond to an adequate course of antidepressant drugs, who may be jeopardized by adverse events associated with the use of pharmacologic agents, who have severe melancholia, or who are suicidal.

Mechanism of action

Seizures induced by ECT are similar to grand mal seizures. A 2-sec to 3-sec latent phase is followed by a tonic phase lasting 10 to 12 sec, then a clonic phase of 30 to 50 sec. Both the duration of individual seizures and cumulative seizure time correlate with clinical improvement of depression. The number of treatments is determined by the patient’s clinical response.

Physiology

The physiologic mechanisms responsible for the therapeutic benefit of ECT are unknown; however, a variety of theories have been posited (Box 171-1).

The cardiovascular response to ECT is secondary to autonomic nervous system discharge. Parasympathetic discharge is immediate and may cause asystole, bradycardia, premature ventricular contractions, hypotension, and ventricular escape. Sympathetic discharge then follows within seconds, possibly manifesting as increased heart rate, premature ventricular contractions, bigeminy, trigeminy, sinus tachycardia, and severe hypertension. A marked increase in myocardial O₂ consumption frequently occurs.

An initial constriction of cerebral vessels is followed by increased cerebral blood flow (1.5 to 7 times baseline) from increased cerebral O₂ consumption and elevated blood pressure. Preoxygenation is used to prevent cerebral hypoxia.

The neuroendocrine response to ECT is manifest by increased levels of corticotropin, cortisol, and catecholamines. The effects on glucose levels vary; thus, patients with diabetes should have their glucose levels monitored before and after ECT.

Miscellaneous effects of ECT of importance to the anesthesia provider include increased intragastric pressure and increased intraocular pressure.

Morbidity and mortality rates

The mortality risk from ECT is 0.03%. Other complications include transient arrhythmias (10%-40%), gastric aspiration (2.5%), and musculoskeletal disorder (0.4%), including fractures. In addition, adverse events following ECT may include pulmonary edema, headache, memory disturbance, and agitation.

Anesthetic management

Contraindications

A variety of contraindications to ECT, both absolute and relative, are of particular note to anesthesia providers (Box 171-2).

Preoperative assessment

Preoperative assessment should document cardiopulmonary, neurologic, and endocrine status; risk of gastrointestinal reflux; and history of earlier drug therapy. Ideally, monoamine oxidase inhibitors and tricyclic antidepressants should be discontinued 2 weeks before ECT. Patients receiving lithium therapy have a decreased chance of successful treatment and may experience delayed awakening, memory loss, and postictal confusion.

Anesthesia technique

Depending on the patient’s comorbid conditions, pharmacologic intervention to reduce the risks of aspiration of gastric contents may be indicated. At a minimum, the American Society of Anesthesiologists’ standards for monitoring should be followed. Patients should be adequately preoxygenated after intravenous access is established. A small dose of methohexital or etomidate should be administered to produce hypnosis; 25 to 50 mg of succinylcholine is given to prevent musculoskeletal injuries; and 0.1 to 0.2 mg of glycopyrrolate is given to blunt parasympathetic response. Esmolol, in bolus doses of 2 to 3 mg/kg, can be given to diminish the sympathetic response in patients with a coronary artery disease or hypertension; a calcium channel blocker may be the preferred agent if the patient has a history, or is having an acute exacerbation, of reactive airway disease.

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