Open Journal of Depression
2013. Vol.2, No.3, 32-34
Published Online August 2013 in SciRes (
Copyright © 2013 SciRes. 32
Depression and Electroconvulsive Therapy: Review of
Current Anesthesia Considerations
Peter Choi, Sergey Pisklakov*, Vasanti Tilak, Ming Xiong
Department of Anesthesiology and Perioperative Medicine, University of Medicine and Dentistry of
New Jersey, New Jersey Medical School, Newark, USA
Email: *
Received June 19th, 2013; revised July 20th, 2013; accepted July 27th, 2013
Copyright © 2013 Peter Choi et al. This is an open access article distributed under the Creative Commons At-
tribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited.
Electroconvulsive therapy (ECT) is becoming increasingly popular in the treatment of medication-resis-
tant depression. Understanding the concepts behind the physiological changes brought upon by the sti-
mulus as well as the rationale behind the various pharmacologic agents used during the procedure is cru-
cial in providing safe and effective ECT. This review will discuss the general principles of perioperative
management of anesthesia for ECT with particular focus on currently used pharmacologic agents during
the procedure.
Keywords: Anesthesia for Electroconvulsive Therapy; Medications Currently Used for Anesthesia for
Electroconvulsive Therapy
ECT has been used to successfully treat a number of Axis I
disorders such as major depressive disorders, mania, and schi-
zophrenia (Kenning et al., 2012). It is a popular modality of
treatment for refractory cases of many psychiatric disorders.
Approximately 100,000 patients in the United States receive
ECT annually. Much of this rise in popularity can be attribu-
ted to the advances in perioperative anesthesia technique dur-
ing ECT, subsequently improving the safety profile of the
procedure (Kellner & Bryson 1998). This article is intended to
review the current literature on perioperative anesthesia ma-
nagement during ECT administration.
Physiological Responses to ECT
Both the psychiatrist and the anesthesiologist must have an
understanding of the physiological changes accompanying the
administration of ECT to limit complications. Cardiovascular
events account for most of the morbidity associated with ECT
(Calarge et al., 2003). The electrical current delivered during
ECT stimulates the parasympathetic nervous system via the
neuronal stimulation of the vagal nerve, resulting in transient
bradycardia or even asystole. This is followed by a sympathetic
response due to the release of catecholamines, resulting in in-
creases of heart rate, blood pressure, and the emergence of car-
diac arrhythmias (Mayo et al., 2010). Cerebral oxygen consum-
ption is increased due to the increased metabolic demand of the
brain during the induced seizure of ECT (Uppal et al., 2010).
As a result, there is a corresponding increase in blood velocity
via the middle cerebral artery (Wagner et al., 2005). The car-
diovascular response of increased peripheral blood pressure
may result in the auto-regulatory system being overwhelmed,
which in turn may lead to increased intracranial pressures as
well (Mayo et al., 2010).
Although there are no reported absolute contraindications to
the use of ECT, physiological changes during the procedure
warrant several relative contraindications. These may include
space-occupying cerebral lesions, cerebral aneurysms, arterio-
venous malformations (AVM), recent intracerebral hemorrhage,
pheochromocytoma, recent myocardial infarction (Birmaher et
al., 2010).
Preoperative Assessment
Preoperative assessment must begin with a thorough history
and physical of the patient. The relative risk of the identified
psychiatric illness left untreated must be weighed against the
risk of anesthesia and ECT. Cardiovascular comorbidities should
result in a thorough cardiovascular evaluation by a cardiologist,
while any history of CNS pathology warrants a proper neurolo-
gic assessment (Folk et al., 2010). Preoperative fasting must be
confirmed with the patient prior to general anesthetic admini-
stration. Documentation of allergies, current medications, air-
way examination, laboratory workup, as well as informed con-
sent is all important components of the preoperative assess-
Concomitant Medications
Concomitant anticonvulsant use can increase the seizure
threshold or affect the clinical efficacy of ECT; therefore its do-
sage is generally lowered as clinically tolerated (Weiner, 2001).
Benzodiazepines, commonly used as anxiolytics prior to cases,
also have a propensity to increase the seizure threshold as well,
and are also avoided if possible (Mayo et al., 2010; Boylan et
*Corresponding author.
al., 2010). The use of lithium during ECT has been a topic of
much debate. Reports have cited associated risks of excessive
cognitive disturbance, prolonged apnea, and spontaneous sei-
zures. However a case series conducted by Dolenc and Ras-
mussen reports that the concomitant use of lithium with ECT
may be used safely and with optimal efficacy in (Dolenk & Ra-
smussen, 2005). Bupropion is known to lower the seizure thres-
hold and thus cessation of its use is recommended as to avoid
possible complications such as prolonged seizure activity and
convulsive status epilepticus following ECT (Kenning 2012;
Conway 2001). Theophylline use, common in patients with con-
current COPD, can also produce similar effects of prolonging
seizure activity with an increased risk of post-ECT status epi-
lepticus (Schak et al., 2001).
Induction Agents
Methohexital remains the most commonly used induction
agent and is regarded as the “golden standard” by the American
Psychiatry Association (Weiner, 2001). It is favored due to its
rapid onset and short duration of action, as well as its low car-
diac toxicity (Chanpattana, 2001). A recent systematic review
showed that methohexital was superior to other anesthetics with
regard to motor seizure duration (Hooten & Rasmussen, 2008).
Methohexital has the advantage of being easily titrated. How-
ever, due to a lack of availability, other induction agents have
begun to become more widely used (Mayo et al., 2010).
Thiopental is also a commonly used barbiturate used as an
induction agent, but has greater anticonvulsant effects thus re-
sulting in shorter seizure durations (Mayo et al., 2010). Typical
induction dose is 2 - 4 mg/kg (Krystal, 2010). A double blind
study conducted by Hiatt showed decreased ambulatory and
waking times as well as an early return of pharyngeal reflexes
with methohexital as opposed to thiopental for induction (Hiatt,
1963). Induction agents such as thiopental, propofol, and keta-
mine have received scrutiny by various authors for their poten-
tial cardiotoxicities. However, a randomized trial of anesthetic
induction agents in patients with coronary artery disease and
left ventricular dysfunction suggested that these agents can be
used safely as anesthetics for patients with CAD and left ven-
tricular dysfunction. Possibly, it is the speed of injection, route,
dose and experience of the clinician, rather than the property of
the agent itself that influences the outcome of the anesthetic
induction (Choudhury et al., 2010).
Ketamine, a derivative of phencyclidine, has a relatively high
safety profile with regards to the preservation of airway refle-
xes and hemodynamic stability. Subsequently, these properties
have led ketamine to it be the induction agent choice in certain
parts of the world that have limited availability of resuscitation
equipment (Morgan et al., 2012). However, ketamine is known
to have a slower onset than methohexital and is notoriously
known for its proclivity to induce post-emergence delirium
(Spitalnic et al., 2000). Despite this well-documented compli-
cation, ketamine can be used as a means to potentiate the ef-
fects of ECT as it appears to have less anticonvulsant effects
when compared to methohexital (Rasmussen et al., 1996). As a
result, ketamine may be an appropriate induction agent in cases
where eliciting a seizure with methohexital anesthesia is limited
even with the use of the maximum available stimulus intensity
(Krystal, 2010). The typical therapeutic dose ranges from 1.5 -
2 mg/kg for adults (Mankad et al., 2010).
Propofol, a potent anticonvulsant, results in shorter seizure
duration when compared to methohexital but still provides ade-
quate therapeutic benefit during induction for ECT (Wagner et
al., 2005). Various studies have shown that propofol is associ-
ated with a decrease in intensity and duration of seizure, despite
the use of larger stimulus charges during the course of ECT.
This finding did not result in any difference in treatment re-
sponse with propofol during ECT compared with other induc-
tion agents such as etomidate and methohexital (Eranti et al.,
2010). Due to its anticonvulsant properties, propofol may serve
as a useful induction agent for adolescents and young adults
who have a very low seizure threshold or prolonged seizures
(25). Propofol is also associated with less nausea after ECT as
well as faster recovery times (Bailine et al., 2003). Therapeutic
doses range from 2 - 4 mg/kg (Walder et al., 2001).
Etomidate causes seizures of longer duration than metho-
hexital and propofol (Mayo et al., 2010). However, its use is
also associated with increased confusion and recovery time
after ECT (Ding & White, 2002). Etomidate also carries the
advantage of minimally affecting hemodynamic stability, thus
is well-tolerated in patients with decreased cardiac output (Ja-
bre et al., 2009). The therapeutic dose is 0.15 - 0.3 mg/kg (Ma-
yo et al., 2010).
Muscle Relaxants
Succinylcholine is the preferred muscle relaxant for ECT
mainly because its fast action and short half-life make it ideal
(Jabre et al., 2009). Non-depolarizing agents are used when
there are contraindications to succinylcholine, such as closed
angle glaucoma, a history of malignant hyperthermia, or amyo-
trophic lateral sclerosis (Janis et al., 1995). In most cases, suc-
cinylcholine is considered superior as a muscle relaxant agent
because of the longer half-lives exhibited by non-depolarizing
agents. However, a study by Hoshi et al. showed that rocuro-
nium-sugammadex produced longer durations of seizure activ-
ity, illustrating the potential benefits of rocuronium-sugamma-
dex as an alternative to succinylcholine (Hoshi et al., 2011).
Inhalation agents, mainly sevoflurane, have also been studied
as a potential induction agent during ECT. A study by Ramsus-
sen et al. showed that sevoflurane compared favorably with thi-
opental in terms of hemodynamic stability and was also associ-
ated with better postictal orientation 20 minutes after ECT. Se-
voflurane also provides tocolytic activity thus making it ideal
for patients who are in late-pregnancy (Calarge et al., 2003).
However, some authors believe that the use of sevoflurane is
time consuming to the physician with no added benefit over
methohexital as an induction agent (Ding & White, 2002).
Anticholinergic Agents
A muscarinic-anticholinergic agent is often used to counter
the bradycardia and or asystole seen via vagal stimulation dur-
ing ECT. This primarily occurs immediately after the initial
electrical stimulation and at the end of the induced seizures
(Mankad et al., 2009). Glycopyrrolate 0.2 - 0.4 mg, and atro-
pine 0.4 - 0.8 mg IV or 0.3 - 0.6 mg IM, are the two most com-
monly used anticholinergics during ECT (Chanpattana, 2001).
Glycopyrrolate is the preferred agent for most practitioners be-
cause of its inability to cross the blood-brain barrier, which can
exacerbate post-ictal delirum, and its better antisialagogue pro-
perties (Eranti et al., 2009). However, atropine has also been re-
ported to provide more protection against bradycardia and asy-
stole when compared to glycopyrrolate (Rasmussen et al., 1999).
Copyright © 2013 SciRes. 33
Copyright © 2013 SciRes.
Cardiova scular Response Modifying Agents
Beta blockers such as labetalol and esmolol, are two of the
most commonly used agents to attenuate the ECT-induced car-
diovascular response. The starting dose of labetalol is 5 - 10 mg
and is given usually 2 minutes prior to induction. The duration
of action is about 4 - 6 hour (Chanpattana, 2001; Mankad et al.,
2009). Esmolol has a faster onset, 30 - 90 seconds, with a shor-
ter duration of action, 10 minutes, thus decreasing the likeli-
hood of post-ictal hypotension. Although both agents possess
anticonvulsant properties, esmolol is reported to shorten seizure
duration more so than labetalol (Mankad et al., 2009).
Nitroglycerine may be given sublingually several minutes
before ECT to attenuate hypertension especially for those pa-
tients suffering from pre-existing ischemic cardiac complica-
tions (Chanpattana, 2001; Mankad et al., 2009).
Calcium channel blockers such as nicardipine and nifedipine
may also be indicated to control mean arterial pressure prior to
ECT. A study showed that nifedipine did not appear to shorten
the duration of the seizure during ECT and was safely used in
conjunction with labetalol to control hypertension (Figiel et al.,
1993). A dose-ranging study found that the optimal dose of ni-
cardicpine was 40 μg/kg IV immediately before the ECT sti-
mulus (Zhang et al., 2005).
ECT is a safe and proven treatment modality for certain Axis
I psychiatric disorders refractory to pharmacologic intervention.
There must be a basic understanding of the general principles of
the physiologic responses that may arise as well as the pharma-
cologic agents used during this procedure to ensure patient sa-
fety while providing effective ECT. Communication and proper
collaboration between the anesthesiologist, psychiatrist, and the
patient are critical component to safe and successful ECT ad-
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