Anesthetic Considerations in Electroconvulsive Therapy

Anatomy and Physiology

During ECT, an external electrical device induces a seizure while the patient is under general anesthesia. This results in a generalized tonic-clonic seizure with a variable duration. Seizures cause profound autonomic nervous system activity. First, the parasympathetic nervous system is activated, resulting in possible bradycardia and even asystole. The bradycardia is typically short-lived and followed by a sympathetic surge that causes hypertension and tachycardia. This sympathetic stimulation can last for anywhere from 5 to 10 min after the seizure has been induced.

The effect of a seizure causing a parasympathetic surge increases the risk of myocardial ischemia if the bradycardia is severe enough for too long. Glycopyrrolate, an anticholinergic medication, can be given to counteract the parasympathetic response, such as increased salivation and bradycardia. Unfortunately, the administration of anticholinergic medications causes the opposite effect of producing tachycardia, which is exacerbated during the sympathetic response.

During the sympathetic discharge, prolonged tachycardia and hypertension increase the risk of cardiovascular events due to increased myocardial demand and oxygen consumption. Sympathetic stimulation and the seizure itself increase cerebral blood flow and cerebral oxygen metabolic rate, resulting in increased intracranial pressure. Intraocular and intragastric pressures also increase. Esmolol can blunt the sympathetic response.[3] Patients can also have postictal states with stroke-like symptoms or cognitive agitation, which can confuse the clinical picture as they are also recovering from general anesthesia at the same time.[4]

Indications

General anesthesia is essential for ECT in every case and is used without anesthesia only in developing countries where proper equipment and personnel are unavailable. ECT is a first-line treatment for several disorders. When psychotic features and suicide risk are high, ECT is a useful initial treatment. If a patient's depression has caused catatonia or psychomotor retardation involving the inability to eat or drink, then ECT is a viable treatment. If it is effective, it can provide fast relief. One report indicates that for severe psychomotor depression, ECT provides up to 90% relief within 2 weeks.[5] Neuroleptic malignant syndrome is also an indication for ECT. Severe depression and psychotic features in pregnancy are conditions where ECT is used preferentially when medications can be harmful to the patient or the developing fetus.[6] 

ECT as a second-line treatment is mainly used when pharmacotherapy is ineffective, or the patient's symptoms worsen.[7] In certain conditions, ECT is considered an experimental treatment with promising benefits, such as treatment-resistant epilepsy, Parkinson disease, depression, tremors, and Tourette syndrome.[8][9][10]

Contraindications

There are several contraindications to ECT. Most contraindications are relative and need special consideration. The anesthesia provider must take into account each patient's comorbidities and address how a generalized seizure will affect them. In most cases, pheochromocytoma and elevated intracranial pressure with mass effect at baseline are absolute contraindications.[11]  

Patients with intracranial mass, retinal detachment, or intracerebral aneurysms do not tolerate increases in intracranial or intraocular pressure. Patients with myocardial disease, cardiac arrhythmias, bleeding disorders, and pheochromocytoma may not tolerate the hemodynamic instability from extreme parasympathetic and sympathetic stimulation during the procedure.[12][13]

Equipment

Several items are needed before performing ECT. The American Society of Anesthesiologists' standards of care for monitoring a patient under general anesthesia include monitoring heart rhythm with an electrocardiogram and monitoring heart rate, oxygenation, ventilation, and blood pressure. The use of a tourniquet on one of the patient's extremities prevents the muscle relaxant from affecting that extremity, allowing monitoring of the effectiveness of the motor portion of the seizure. Electroencephalogram (EEG) monitors, or processed EEG, monitor brain status during the seizure. Emergency airway equipment should be readily available. A soft bite block is provided in the oropharynx to prevent tongue and tooth injury, as a generalized epileptic seizure has been shown to cause such trauma even in the setting of muscle relaxation.[14] A bag-valve mask and a simple oxygen face mask should be available to administer oxygen. A suctioning device is necessary to help clear secretions.

Personnel

The personnel required for ECT include a psychiatrist, a nurse, and a trained anesthesiologist who can provide general anesthesia for the patient. These requirements vary by state and governing body.

Technique or Treatment

An intravenous (IV) catheter is placed before induction of anesthesia. Typically, a patient breathes 100% oxygen before induction of anesthesia. The patient's vital signs are monitored throughout the procedure. The intravenous anesthetic of choice is administered, followed by hyperventilation with a bag-mask to induce hypocapnia, which lowers cerebral blood flow and reduces the seizure threshold. After general anesthesia is successfully induced, a muscle relaxant is given to prevent myalgias and musculoskeletal injuries during the seizure. A tourniquet is commonly placed on one lower extremity to block muscle relaxants from reaching the area. This helps monitor the motor portion of the seizure by allowing personnel to observe the tonic and clonic activity of the lower extremity. A soft bite block is then placed to prevent the patient from developing an oral injury during the seizure. The electrical stimulus is then administered to induce the seizure and is monitored by a processed EEG.

The goal is for the seizure to last around 25 to 75 seconds but no shorter than 15 seconds.[15][16] More prolonged seizures can be desirable if the patient has had ECTs that were less than 15 seconds in the past. The patient then recovers in a post-anesthesia unit, where staff monitor neurological status and hemodynamics until it is appropriate for the patient to return home or to their assigned hospital room.

A variety of anesthetic agents and muscle relaxants are used to induce anesthesia for ECT. Most dosing regimens should use the lowest effective dose.

Methohexital is considered the gold standard for induction of anesthesia for ECT. It is a barbiturate that stimulates Gamma-aminobutyric acid (GABA) receptors, which are the main inhibitory receptors in the brain. Methohexital produces anesthesia for approximately 4 to 7 minutes, which is ideal for ECT. It does not affect seizure threshold and, compared to propofol, does not shorten seizure length.[17] Methohexital causes moderate cardiac depression, which helps counteract the sympathetic discharge produced by a seizure. The initial dose is usually 1 to 1.5 mg/kg.[18] 

Etomidate is a unique drug that also works by activating GABA receptors in the brain. Studies have shown that it tends to produce a longer seizure compared to propofol.[19]  Etomidate does not cause cardiac depression, so the sympathetic discharge tends to be elevated when used as the sole anesthetic for ECT. Supplementing with an intravenous opioid such as remifentanil or a beta-blocker like esmolol to inhibit sympathetic discharge is common. Etomidate is known to cause adrenal suppression and should be avoided in patients with known adrenal insufficiency or critical illness. A dose of 0.3 mg/kg of etomidate is given to induce general anesthesia, lasting around 5 to 10 minutes.[20][21] 

Propofol also acts as a GABA agonist. However, it tends to shorten seizure duration by increasing the seizure threshold. It is used in ECT as an anesthetic agent when previous seizures induced by ECTs have been prolonged and when a rapid onset is needed. Propofol is dosed at 1.5 to 2 mg/kg.[22] 

Ketamine is an N-methyl-D-aspartate (NMDA) antagonist, and it causes dissociative anesthesia as well as analgesia. It is not often used in ECT as it tends to increase seizure length and causes indirect myocardial stimulation. Ketamine also has antidepressant properties, and studies are ongoing to determine its effectiveness as an adjunct for the treatment of depression. Doses of 1 to 2 mg/kg are typically used to induce adequate anesthesia.[23] Ketamine has the potential side effect of causing psychomimetic delirium during recovery, vivid dreams, and hallucinations. This is often pretreated with a benzodiazepine.[24][25] Recovery from ketamine is the slowest, followed by etomidate, methohexital, and propofol when given for a short period.

Sevoflurane is an option for induction of anesthesia in ECT. It has a slow onset compared to intravenous anesthetics. It can be helpful to initiate anesthesia to obtain IV access in a patient who is uncooperative while awake. When used for a short period, sevoflurane has a quick recovery. In a systematic review, sevoflurane reduces seizure length more prominently than propofol, barbiturates, and ketamine.[26] Sevoflurane does not attenuate sympathetic stimulation to the extent of other induction agents, so opioids or beta-blockers are often used to maintain hemodynamic stability.[27] Sevoflurane enhances muscular blockade compared to intravenous anesthetics. 

Succinylcholine is the preferred muscle relaxant for ECT. It is a depolarizing neuromuscular blocker and is given at 1 mg/kg to produce adequate muscle relaxation for intubation within 30 seconds of administration. It typically lasts 5 to 8 minutes.[28] Succinylcholine raises the serum potassium by 0.5 meq/L after IV administration. In the setting of elevated plasma potassium and conditions that can cause an exaggerated increase in serum potassium when succinylcholine is given, lethal arrhythmias occur, and succinylcholine should be avoided.[29] There is no reversal agent for succinylcholine, but it is typically not needed because its duration of action is short. Succinylcholine and sevoflurane should be avoided in patients with a history of malignant hyperthermia, as these are triggering agents for malignant hyperthermia.

Nondepolarizing neuromuscular blocking agents are good alternatives to succinylcholine, with rocuronium being the most common. Rocuronium is given at doses of 0.6 mg/kg to produce intubating conditions. Its effects last around 35 minutes. If the patient is on an antiepileptic medication or mood stabilizer such as lithium, the anesthetic provider must be aware. Lithium can delay the onset and prolong the actions of succinylcholine and nondepolarizing neuromuscular blocking agents.[30] Antiepileptic medications can acutely prolong the effects of nondepolarizing neuromuscular blocking agents, but with chronic use, resistance to these muscle relaxants occurs, requiring larger doses.[31]

Complications

Complications in ECT, although rare, do occur. The anesthetic provider should be monitoring the patient at all times. The most common adverse effects of ECT are headaches and cognitive impairment.[1] These tend to be temporary. The administration of general anesthesia, the underlying psychiatric disorder, and the induced seizure compound the cognitive impairment. A seizure that lasts too long can result in status epilepticus. This condition requires prompt treatment in the form of administering benzodiazepines or propofol until termination of the seizure. Status epilepticus is more common when pretreatment with theophylline is used to prolong the seizure.[32] 

Upon induction of general anesthesia and muscle relaxation, it may be difficult to mask ventilate the patient. Depending on which medications were used, letting the patient wake up and return to spontaneous ventilation may be the best option. Endotracheal intubation may be required to prevent severe hypoxia.

During recovery in the post-anesthesia care unit, myocardial infarction and ischemic or hemorrhagic stroke are possible. If these conditions are suspected, cardiology or neurology should be consulted. Patients emerging from anesthesia may also become agitated and experience pain. Postictal side effects such as paralysis or mania are also possible.

Patients with deep brain stimulators or cardiac devices require special considerations. Deep brain stimulators can cause electrical interference when inducing a generalized seizure and should thus be turned off. Consult a physician specialized in deep brain stimulation.[33] Patients with pacemakers and other cardiac devices are generally considered safe to undergo ECT with ECG monitoring only. The likelihood that the electrical impulse interferes with the cardiac device is very low.[34] A magnet should be readily available in case of an emergency. The anesthetic provider should communicate with the patient's cardiologist to determine the severity of illness and risk of undergoing general anesthesia.

Clinical Significance

ECT is an effective treatment for pharmacotherapy-resistant depression and other severe psychiatric disorders. Its effects are often seen quickly, but some patients may require multiple sessions. Providing general anesthesia for ECT is standard and has been the case since the 1950s. Anesthesia for ECT provides a safe environment for a generalized epileptic seizure to take place. Treatment of hemodynamic instability and prevention of painful and detrimental side effects are possible through a carefully planned anesthetic.

The ideal anesthetic agent provides amnesia with minimal effects on hemodynamic stability and seizure duration. An anesthetic agent that does affect seizure duration might be desirable if the patient's previous seizure during ECT was too long or too short. Muscle relaxation protects the musculoskeletal system from the tonic and clonic actions of a generalized seizure. There are enough options and ways to provide anesthesia for ECT to suit most patients' needs. The anesthesiologist makes adjustments based on reactions, patient discomfort, and side effects. Today, ECT is seldom performed without general anesthesia, except in developing countries. Musculoskeletal injury and posttraumatic stress disorder are not uncommon when enduring ECT without anesthesia.[35][36] Anesthesia prevents harm and trauma to the patient while enabling them to undergo a procedure that significantly improves their psychiatric disorder.

Enhancing Healthcare Team Outcomes

ECT provides patients with certain psychiatric disorders a treatment option for improvement in their mental state. Performing ECT requires an interprofessional team, including anesthesiologists, psychiatrists, and nurses.[37][16]

Before undergoing ECT, an anesthetic provider should evaluate the patient to ensure they are safe for general anesthesia and can consent to its use. This also allows the anesthetic provider to determine whether the patient's comorbidities and current medication regimen require changes to the anesthetic plan. The anesthesia team should also coordinate with the psychiatrist to determine the severity of the patient's psychiatric disorders and the desired length of seizure. A nurse is present before, during, and after the procedure to ensure the patient is ready and monitored afterward. Nursing staff helps position the patient and ensures all safety guidelines are followed. During recovery, nurses help recognize side effects and reactions to either the anesthesia or the seizure.