Anesthesia for Electroconvulsive Therapy
A 64-year-old man with depression refractory to drug therapy is scheduled for electroconvulsive therapy (ECT).
The electroconvulsive shock is applied to one or both cerebral hemispheres to induce a seizure. Variables include stimulus pattern, amplitude, and duration. The goal is to produce a therapeutic generalized seizure 30-60 sec in duration. Electrical stimuli are usually administered until a therapeutic seizure is induced. A good therapeutic effect is generally not achieved until a total of 400-700 seizure seconds have been induced. Because only one treatment is given per day, patients are usually scheduled for a series of treatments, generally two or three a week. Progressive memory loss often occurs with an increasing number of treatments, particularly when electrodes are applied bilaterally.
Why is anesthesia necessary?
When the efficacy of ECT was discovered, enthusiasm was tempered in the medical community because drugs were not used to control the violent seizures caused by the procedure, thus engendering a relatively high incidence of musculoskeletal injuries. Moreover, when an NMB was used alone, patients sometimes recalled being paralyzed and awake just prior to the shock. The routine use of general anesthesia to ensure amnesia and neuromuscular blockade to prevent injuries has renewed interest in ECT. The current mortality rate for ECT is estimated to be one death per 10,000 treatments.
What are the physiological effects of ECT-induced seizures?
Seizure activity is characteristically associated with an initial parasympathetic discharge followed by a more sustained sympathetic discharge. The initial phase is characterized by bradycardia and increased secretions. Marked bradycardia (<30 beats/min) and even transient asystole (up to 6 s) are occasionally seen. The hypertension and tachycardia that follow are typically sustained for several minutes. Transient autonomic imbalance can produce arrhythmias and T-wave abnormalities on the electrocardiogram. Cerebral blood flow and ICP, intragastric pressure, and intraocular pressure all transiently increase.
Are there any contraindications to ECT?
Contraindications are a recent myocardial infarction (usually <3 months), a recent stroke (usually <1 month), an intracranial mass, or increased ICP from any cause. More relative contraindications include angina, poorly controlled heart failure, significant pulmonary disease, bone fractures, severe osteoporosis, pregnancy, glaucoma, and retinal detachment.
What are the important considerations in selecting anesthetic agents?
Amnesia is required only for the brief period (1-5 min) from when the NMB is given to when a therapeutic seizure has been successfully induced. The seizure itself usually results in a brief period of anterograde amnesia, somnolence, and often confusion. Consequently, only a short-acting induction agent is necessary. Moreover, because most induction agents (barbiturates, etomidate, benzodiazepines, and propofol) have anticonvulsant properties, small doses must be used. Seizure threshold is increased and seizure duration is decreased by all of these agents.
Following adequate preoxygenation, methohexital, 0.5-1 mg/kg, is most commonly employed. Propofol, 1-1.5 mg/kg, may be used, but higher doses reduce seizure duration. Benzodiazepines raise the seizure threshold and decrease duration. Ketamine increases seizure duration, but is generally not used because it also increases the incidence of delayed awakening, nausea, and ataxia and is also associated with hallucinations during emergence. Use of etomidate also prolongs recovery. Short-acting opioids, such as alfentanil, are not given alone because they do not consistently produce amnesia. However, alfentanil (10-25 mg/kg) can be a useful adjunct when very small doses of methohexital (10-20 mg) are required in patients with a high seizure threshold. In very small doses, methohexital may actually enhance seizure activity. Increases in seizure threshold are often observed with each subsequent ECT.
Neuromuscular blockade is required from the time of electrical stimulation until the end of the seizure. A short-acting agent, such as succinylcholine (0.25-0.5 mg/kg), is most often selected. Controlled mask ventilation, using a self-inflating bag device or an anesthesia circle system, is required until spontaneous respirations resume.
Can seizure duration be increased without increasing the electrical stimulus?
Hyperventilation can increase seizure duration and is routinely employed in some centers. Intravenous caffeine, 125-250 mg (given slowly), has also been reported to increase seizure duration.
What monitors should be used during ECT?
Monitoring should be similar to what is appropriate with the use of any other general anesthetic. Seizure activity is sometimes monitored by an unprocessed electroencephalogram. It can also be monitored in an isolated limb: a tourniquet is inflated around one arm prior to injection of succinylcholine, preventing entry of the NMB and allowing observation of convulsive motor activity in that arm.
How can the adverse hemodynamic effects of the seizure be controlled in patients with limited cardiovascular reserve?
Exaggerated parasympathetic effects should be treated with atropine. In fact, premedication with glycopyrrolate is desirable both to prevent the profuse secretions associated with seizures and to attenuate bradycardia. Nitroglycerin, nifedipine, and α- and β-adrenergic blockers have all been employed successfully to control sympathetic manifestations. High doses of β-adrenergic blockers (esmolol, 200 mg), however, are reported to decrease seizure duration.
What if the patient has a pacemaker?
Patients with pacemakers may safely undergo electroconvulsive treatments, but a magnet should be readily available to convert the pacemaker to a fixed mode, if necessary.