Anaesthesia And Electroconvulsive Therapy

Electroconvulsive therapy is used widely in psychiatric practice, with over 100 000 treatments being administered to patients in England each year under general anaesthesia; ECT is therefore an important topic for anaesthetists.

ECT is a highly successful treatment for severe depression and some other psychiatric disorders. It is often quicker, safer and more effective and has fewer side-effects than drug therapy.

Originally, seizures were induced chemically and electrical stimulation was not introduced until the late 1930s. The high incidence of trauma, such as fractures and dislocations, that occurred during unmodified fits led to the use of muscle relaxants to control convulsions. The use of succinylcholine during ECT pre-dates its use in mainstream anaesthesia by a number of years. However, ECT remains a highly emotive and controversial area of psychiatric practice dreaded by the public and demonized by the media. Its adverse image has led to a failure of commitment by psychiatrists and anaesthetists such that equipment, training and supervision remain suboptimal in some units.


The electrical stimulus produced by all ECT devices comprises brief pulses of current interrupted by longer periods of electrical inactivity. The electrical transmission lasts for only a fraction of the total stimulus duration and this results in a decrease in the amount of electrical energy required to provoke a generalized seizure.

The electrical stimulus is applied to the patient's head by handheld electrodes of low impedance. Traditionally, electrodes are placed in the bifrontotemporal region for bilateral ECT, whereas both electrodes are placed over the non-dominant hemisphere to produce unilateral ECT.


The main indication for ECT is for the treatment of severe and drug-refractory depression. ECT also has a role in the management of some other psychiatric conditions, e.g. mania and some types of schizophrenia and catatonia.

PHYSIOLOGICAL EFFECTS OF ECT (Table 49.1) Cardiovascular system

Activation of the autonomic nervous system is responsible for the profound cardiovascular changes during ECT. The autonomic disturbance consists of a parasympathetic-sympathetic sequence; this results in an initial bradycardia followed by tachycardia and hypertension secondary to intense sympathetic stimulation. In combination with the increased muscle activity of the convulsion, this increases myocardial oxygen demand and may result in myocardial ischaemia in susceptible individuals unless hypoxaemia is avoided by administration of supplementary oxygen during the convulsion.

Tabic 49,1 Physiological effects of electroconvulsive therapy

Cardiovascular effects


Parasympathetic stimulation



Late (after I min)

Sympathetic stimulation




Myocardial oxy gen

consumption increases

Cerebral effects

Cerebral oxygen consumption


Cerebral blood flow


Intracranial pressure


Intraocular pressure


Intragastric pressure


Cerebrovascular system

Cerebral blood flow increases dramatically in response to the increase in cerebral oxygen consumption that accompanies the seizure. There is an associated increase in ICP which may prove hazardous in patients with a space-occupying lesion.


ECT is a safe procedure and there are few contraindications; however, it is best avoided in those patients with an intracranial mass lesion, recent myocardial infarction or cerebrovascular accidents. Age is no barrier to treatments. ECT may be the treatment of choice in pregnancy compared with the alternative of drug therapy.


Anaesthesia for ECT is complicated by the fact that the choice of drugs used and the conduct of the anaesthetic may directly affect the success of treatment by influencing the seizure threshold and duration. Insufficient seizure duration renders ECT ineffective, but increasing seizures augment unwanted effects such as confusion and memory impairment. A technique of modified ECT has evolved in which drugs are employed to reduce the detrimental effect of ECT without the abolition of the essential beneficial effects.

Pre-anaesthetic assessment

All patients should receive a visit and evaluation by the anaesthetist before treatment. Special attention should be paid to cardiorespiratory function, symptoms of oesophageal reflux, allergies and previous anaesthetic experiences. The presence of loose or missing teeth should also be noted.

Some antidepressant drugs delay gastric emptying and the patient should be fasted for a period of at least 8 h before anaesthesia. This may seem simple, but many of these patients are extremely unreliable and occasionally uncooperative, so that careful supervision is required to ensure that fasting does occur.

Premedication with sedatives or opioids is not required and may serve only to prolong the anaesthetic recovery time. Routine administration of atropine is no longer considered to be necessary.

Table 49.2 Contraindications to electroconvulsive therapy


Recent myocardial infarction i< 3 months) Recent cerebrovascular accident - 3 months) Intracranial mass lesion


Angina pectoris Congestive cardiac failure Severe pulmonary disease Severe osteoporosis Major bone fractures Glaucoma Retinal detachment Pregnane)'

Anaesthetic management

There is no clear advantage to the use of propofol for ECT, as recovery from anaesthesia is no quicker than with barbiturates. Whilst propofol does obtund some of the cardiovascular effects of ECT, it also inhibits seizures which may impair the efficacy of ECT. Randomized controlled trials of the effect of propofol on the outcome of ECT are needed. Methohexital is the induction agent used most commonly. Thiopental offers no advantages over methohexital and prolongs the recovery time. The use of muscle relaxants in ECT has virtually eliminated the risk of fractures - succinylcholine in a dose of 0.5 mg kg~l is the most commonly used.

After induction of anaesthesia, hyperventilation of the patient's lungs by bag and mask before application of ECT stimulation lowers the seizure threshold and prolongs seizure duration.

When the limbs are flaccid, a rubber 'bite block' is inserted between the teeth before electrical stimulation is applied. During the seizure, artificial ventilation of the lungs with oxygen is continued to avoid arterial desaturation until adequate spontaneous ventilation has returned.

Patients should be recovered in the lateral position by trained nursing staff with equipment available immediately for treatment of any emergency.

Good record-keeping is vital so that any problems or changes to anaesthetic or electrical stimulus are known at the next treatment. Close cooperation between anaesthetist and psychiatrist is essential for optimal treatment.


Modified ECT in association with skilled anaesthetic management is safe and effective. Patients may complain of headache, muscle aches and confusion for 1-2 h after treatment, but memory disturbances may persist for several weeks. The latter are minimized by unilateral ECT over the non-dominant cerebral hemisphere.


Historically the provision of anaesthetic services for ECT has been a low priority for directorates. Many units have no suitably trained assistance for the anaesthetist. Standards of facilities and equipment in isolated ECT units are often inferior to those normally acceptable to an anaesthetist. For these reasons, ECT should not be left to unsupervised trainees.

Every unit should have a consultant anaesthetist responsible for ECT with an equivalent role for a psychiatrist. There should be clear departmental guidelines as to:

• Who is qualified to administer anaesthetics?

• How should they be trained?

• Who should assist the anaesthetist?

• Who should supervise recovering patients?

• What facilities and equipment should be available?

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