1

Abstract and Introduction

Introduction
External direct current (DC) cardioversion refers to the application of a
synchronized electrical shock across a patient's chest using a defibrillator. The
aim being to convert abnormal tachyarrhythmias back into sinus rhythm.
Anaesthetists are often requested to provide anaesthesia for cardioversion because
it is an extremely stimulating and painful procedure, which requires an
appropriate depth of anaesthesia to be tolerated without adverse psychological
consequences.[1] This may involve emergency scenarios in unfamiliar locations
such as Coronary Care Units (CCUs) and Emergency Departments, as well as the
more commonly performed elective case. Anaesthetists may also need to perform
cardioversion themselves in theatre or Critical Care settings. An understanding of
both the theoretical and practical aspects of this procedure are essential to perform
cardioversion safely and hence form the basis of this review.

Theory of Defibrillation and Cardioversion

The early 20th century saw a rapid expansion of the electrical power industry and
accidents associated with electrocution. It soon became apparent that most deaths
were due to ventricular fibrillation (VF). Ironically research at the time suggested
that alternating current (AC) was more effective at terminating VF than DC. As a
result the earliest defibrillators in the USA utilized AC shocks.

In the USSR defibrillator development followed a different path, largely due to

the work of Naum Gurvich.[2] In 1939, Gurvich and Yuniev proposed using a
single capacitor discharge to defibrillate VF. By 1952 Gurvich had designed the
first commercially available transthoracic DC defibrillator that became rapidly
utilized throughout the Soviet Union.

It was only 10 yr later in 1962 that Lown reported the successful use of DC
cardioversion to treat cardiac arrhythmias which revolutionized practice in the
USA and elsewhere.

Simple Defibrillator Function

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Modern defibrillators have become far more sophisticated than simple circuit
diagrams suggest. They still rely on a power source which charges a capacitor,
generating a potential difference of 2 0005 000 V across its plates. Discharging
the capacitor allows current to flow through the patient's chest as illustrated in
Figure 1. The current flow depends on the impedance encountered.

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(Enlarge Image)

Figure 1.

Simple capacitor circuit and graph showing exponential capacitor discharge.

Switch in position A allows capacitor (C) to charge. When the switch is moved to
position B the capacitor discharges current through the patient's chest. R
represents the impedance encountered. Impedance is the mathematical
combination of resistance (ability to resist DC flow) and reactance (ability to
resist AC flow).

It is customary to think of the 'dose of electricity' delivered from a defibrillator in

terms of the 'joules' of energy selected,[3] but it is the current and in particular the
current density achieved within the myocardium that successfully defibrillates the
heart.[2] This is determined by the impedance presented by the patient and
defibrillator. The path taken by the current is also relevant, since only 4% of the
energy delivered from the shock actually passes through the heart.[4] This
illustrates why significantly lower energy levels are required for defibrillation
when paddles are applied directly to the heart during cardiac surgery or via
percutaneous internal cardioversion techniques.

Transthoracic Impedance

The term transthoracic impedance (TTI), refers to the impedance presented by the
patient during cardioversion. In benchmark tests it is usually taken as 50 , but in
practice can vary considerably (25180 ). It can have a significant impact on
successful defibrillation.

Factors that influence TTI include:

Electrode size: increasing paddle/pad size reduces impedance and improves

current flow, but beyond a certain size a decrease in current density occurs. (812
cm diameter electrodes are generally considered optimal in humans.)

Electrode coupling with skin: appropriate salt containing gels reduce impedance.
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Paddle position: most studies report comparable success rates using either the
anteroposterior (AP) or anterolateral (AL) paddle position.

Distance between paddles: administering the shock at end expiration and firm
paddle pressure reduce impedance.

Body habitus: impedance increases with obese and emphysematous patients.

Repeated shocks: impedance reduces slightly (9%) with successive shocks and is
also influenced by the timing between shocks.

The Biphasic Waveform

For decades following Lown's original work, defibrillators used a damped

sinusoidal monophasic waveform. Current was delivered in one direction only and
an inductor smoothed the current discharge from the defibrillator. Modern
defibrillators reverse polarity and current flow after 510 ms to generate biphasic
waveforms (Fig. 2). This leads to more efficient depolarization of myocardium,
with an improved success rate and lowered complication risk. Two different
waveforms are currently in popular use, the rectilinear biphasic (RB) and the
biphasic truncated exponential (BTE) waveform (Fig. 3). In the former discharge
is limited to 10 ms with polarity reversed after 6 ms. Current flow is kept steady
and controlled by a series of sophisticated switches and resistors matched to the
patient's impedance rather than using an inductor. With the BTE waveform the
initial phase declines exponentially. Both the voltage and duration of shock are
manipulated electronically according to patient impedance. Due to higher
successful cardioversion and defibrillation rates at lower energy levels biphasic

defibrillators are considered superior to their monophasic counterparts. Recent

evaluation has suggested that the two biphasic waveforms have comparable
efficacy.[5]

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(Enlarge Image)

Figure 2.

Current flow reverses in biphasic defibrillators.

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(Enlarge Image)
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Figure 3.

A graphical comparison of the monophasic and two biphasic defibrillator

waveforms discussed in this article.

Events at Myocardial Level

A synchronized shock depolarizes the tissue involved in a re-entry circuit, making

the tissue involved refractory and no longer able to propagate or sustain re-entry.
This allows the sinus node to resume normal pacemaker activity.

The exact mechanisms responsible for terminating ventricular and atrial

fibrillation are less certain.

The critical mass theory proposes that defibrillation can be successfully achieved
by depolarization of a sufficient or critical mass of myocardium. The theory of the
upper limit of vulnerability relies on the fact that there is an upper limit to the
strength of shock that induces VF and to successfully defibrillate the heart shock
strength must be greater than this value. That is unsuccessful shocks abolish
activation fronts during VF, but also stimulate other regions of the myocardium
during their vulnerable period, giving rise to new activation fronts that reinitiate
VF.[4,6]

Synchronization

Following contraction, cardiac myocytes become temporarily unresponsive to

electrical stimulation. This phase of the cardiac cycle consists of an absolute
refractory and relative refractory period, during which electrical stimuli can
initiate re-entry circuits and precipitate VF. This is termed the vulnerable period
and corresponds to the upstroke and peak of the T wave on the electrocardiogram.
A cardioversion shock is synchronized to coincide with the R wave of the QRS
complex, avoiding this vulnerable period. This synchronization process is what
distinguishes cardioversion from defibrillation.

Indications for Cardioversion

Emergency DC cardioversion is indicated for any broad or narrow QRS complex

tachyarrhythmia that causes haemodynamic decompensation. Usually this
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represents heart rates in excess of 150 bpm associated with clinical shock, reduced
conscious level, angina or heart failure.[7]

Relatively urgent cardioversion is indicated for supra ventricular tachycardias

(SVTs) and monomorphic ventricular tachycardias that have not responded to a
trial of i.v. medical therapy.

Routine cardioversion is still frequently indicated in the management of atrial

fibrillation (AF) when a rhythm rather than rate control strategy is employed.
Indications for a rhythm strategy include a reversible cause of the AF, heart
failure primarily caused by the AF, new onset AF and situations where a rhythm
control strategy is considered more suitable based on the clinical judgement of the
attending physician.[8] Numbers attributable to this last indication appear to be
increasing probably due to the perception of better symptomatic control in active
patients and the increasing popularity of interventional procedures such as
percutaneous pulmonary vein isolation.[9] Initial success rates of 90% can be
expected following cardioversion, but unfortunately relapse is a common
problem.[3]

Contraindications
There are two main contraindications to DC cardioversion
Digitalis toxicity and associated tachycardia. This is due to the high risk of
provoking refractory ventricular arrhythmias and fibrillation.
Stable atrial fibrillation of > 48 h duration without anticoagulation or TOE
exclusion of atrial thrombus. This is due to the risk of thromboembolism and
stroke.
DC cardioversion is also unlikely to prove successful in conditions associated
with increased automaticity such as catecholamine induced tachyarrhythmias and
multifocal atrial tachycardia, where efforts are best directed at addressing the
underlying precipitating cause.[10]

TOE Guided Cardioversion Strategy and Anticoagulation

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Atrial fibrillation is associated with thrombus formation in the left atrium and
atrial appendage. Early experience with cardioversion was associated with a high
risk of thromboembolism and stroke, which was significantly reduced by effective
anticoagulation (5.30.8%).[2] As a result conventional practice dictates that AF
and flutter patients should be fully anticoagulated for a minimum of 3 weeks prior
to DC cardioversion and at least 4 weeks thereafter.[8]

An alternative strategy is to exclude the presence of an atrial thrombus prior to

DC cardioversion using echocardiography. Unfortunately due to the posterior
location of the left atrium this requires transoesophageal (TOE) rather than a
transthoracic examination, which cannot reliably exclude atrial thrombi.

A TOE guided strategy has been shown to have a similar risk of

thromboembolism (0.5%), but a reduced incidence of bleeding complications
compared to conventional practice.[11]

NICE guidelines suggest considering this approach when experienced staff and
appropriate facilities are available and a minimum period of precardioversion
anticoagulation is indicated from patient choice or increased bleeding risk.[8]

If a TOE guided strategy is employed, the patient must still be fully

anticoagulated at the time of cardioversion and for 4 weeks thereafter. Conversion
to sinus rhythm often increases the intensity of spontaneous echo contrast (smoke)
in the left atrium indicating the existence of a prothrombotic state. The atrium also
takes a number of weeks to regain effective contractile function following
cardioversion.

Consideration must also be given to the 14% of patients in whom an atrial

thrombus will be detected. This finding mandates abandonment of the procedure
and repeat TOE examination 4 weeks later.[11]

Despite its more invasive nature TOE guided cardioversion appears to be

relatively common practice in a number of European centres.[12]

Procedural Considerations

Patient Preparation
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Most DC cardioversions are performed as elective day case procedures on patients

with AF.

Significant cardiovascular and respiratory disease, along with diabetes, obesity

and obstructive sleep apnea are common.

All patients should have received the following investigations:

Full blood count (anaemia)

Urea and electrolytes (hypokalaemia often associated with diuretics)

Electrocardiogram (accurate diagnosis of arrhythmia, conduction abnormalities)

Echocardiogram (assess underlying structural heart disease and myocardial

function)

Thyroid function tests (thyrotoxicosis is a known cause of AF and thyroid

function can be disturbed by amiodarone therapy)

Assessment of anticoagulationinternational normalized ratio (INR)

Point-of-care coagulometers are now frequently utilized to check adequacy of

anticoagulation (INR must be >2), but increasingly patients are taking the new
oral anticoagulant drugs (dabigatran, apixaban, and rivaroxaban). Pretreatment
with 4 weeks amiodarone or other antiarrhythmics is now commonplace. It is
essential that these drugs are continued on the day of cardioversion.

We usually omit angiotensin-converting enzyme (ACE)-inhibitors and

angiotensin 2 receptor antagonists for two days prior to cardioversion due to the
risk of an exaggerated hypotensive response to anaesthetic agents, although hard
evidence to back this approach appears limited. Digoxin is also commonly
omitted, but digoxin therapy itself does not contraindicate cardioversion when
levels lie within the therapeutic range with no signs of toxicity.

Location of Procedure

DC cardioversion is performed in a variety of locations. It is mandatory that

skilled assistance and full resuscitation equipment are available. The level of
monitoring utilized should conform to AAGBI guidelines. Following
cardioversion the patient must be also be managed in an area with facilities for
suction and oxygen administration. Full resuscitation facilities should be readily
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available and appropriately trained staff in attendance until the patient has fully
recovered from the effects of anaesthesia.

Practical Considerations

Paddle Position. Defibrillator pads have largely replaced paddles due to

convenience and safety. Both anterio-posterior and anterior-lateral placement are
equally acceptable. The anterio-posterior position has the advantage of facilitating
temporary external pacing if asystole occurs.

Energy Levels. Different manufacturers advise specific energy settings which

should be checked and adhered to. In general energy settings for biphasic shocks
are about half those used in traditional monophasic defibrillators. For AF an initial
shock at 120150 J escalating to 200 J is appropriate. Atrial Flutter and
paroxysmal SVT convert more easily with initial energy settings of 70120 J
usually proving adequate.

Precautions

Check the defibrillator possesses a backup external pacing function.

Ensure that the defibrillator is set to sync. mode. Remember to disable sync. mode
if VF occurs and defibrillation is required.

Make sure all staff avoid direct contact with the patient during shock delivery.

Face mask oxygen should be moved at least 1 m away from the patient's chest
prior to shock delivery.

Choice of Anaesthetic Agent and Technique

The pharmacological agent used to facilitate cardioversion should rapidly achieve

the desired depth of anaesthesia, should wear off rapidly and should not cause
cardiovascular or respiratory side effects.

Numerous anaesthetic and sedative agents can be used for this purpose, and are
not invariably administered by anaesthetists. Attending cardiologists,[12]
Emergency physicians,[13] and appropriately trained nursing staff[9] undertake
this role in a number of centres.
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Amongst anaesthetists propofol is the most frequently utilized agent[14] with

etomidate enjoying limited popularity for haemodynamically unstable patients and
sevoflurane providing an effective inhalational alternative.[15]

The Cochrane collaboration recently conducted a systematic review aimed at

comparing the safety, effectiveness and adverse events associated with the various
anaesthetic or sedative drugs currently used for DC cardioversion.[16]

They classified currently available agents into three groups to reflect perceived
current practice:

Traditional anaesthetic induction agents: propofol, etomidate, and thiopentone.

Inhalational anaesthetic agents: sevoflurane and isoflurane.

Drugs classified as sedative agents: diazepam and midazolam.

After scrutinizing 23 studies involving 1 250 participants the reviewers found no

consistent differences between the agents studied and concluded that there was no
need for a change in current practice.

Anaesthetic Depth Required. The exact anaesthetic requirement deemed necessary

to facilitate cardioversion has been debated ever since the original description of
using thiopentone in the early 1960s.[17] No or minimal sedation can be
associated with serious psychological sequela,[1] whereas increasing anaesthetic
depth increases the risk of significant cardiorespiratory depression.

Awareness and recall were recorded in half the studies reviewed by the Cochrane
collaboration. This undoubtedly reflected the use of deep sedation to facilitate the
procedure rather than conventional general anaesthesia in a number of centres.
Deep sedation describes a level of sedation at which an individual cannot be
easily aroused, but responds purposefully to repeated or painful stimulation. It
may require airway intervention and respiratory support, but cardiovascular
function is usually maintained.[9]

Although most anaesthetists prefer utilizing a conventional depth of anaesthesia,

deep sedation seems perfectly acceptable to most patients. This level of sedation
can readily be attained by administration of a slow bolus dose of propofol (0.51
mg kg1), with further top up doses (0.25 mg kg1) as required.

This approach seems appropriate for patients with severely limited

cardiorespiratory reserve, provided they are warned about the risk of procedural
recall. The author also finds total inhalational anaesthesia using 8%
sevoflurane[15] a useful anaesthetic technique for this procedure and the judicious
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use of metaraminol (0.25 mg boluses) helpful in maintaining haemodynamic

stability.

Preoxygenation and Airway Management. All patients should be fully

preoxygenated for at least 3 min prior to cardioversion. This buys valuable time if
unanticipated airway difficulty or apnoea occur. Spontaneous ventilation can
usually be maintained using a conventional facemask. Assistance of ventilation by
manual ventilation or insertion of a Guedel airway/laryngeal mask rarely proves
necessary. We do not electively intubate patients with obstructive sleep apnoea or
morbid obesity, but find performing cardioversion in a semi inclined position
(30) helpful for super morbidly obese patients.

Analgesia. Cardioversion is an intensely painful and stimulating procedure, but

patients rarely experience pain following the procedure. The coadministration of
opioids is therefore unnecessary and potentially increases the risk of apnoea and
post procedural nausea and vomiting.

Special Considerations

Emergency Cardioversion

Emergency cardioversion raises the issue of administering anaesthesia to an

unfasted, haemodynamically unstable patient in an alien environment. Although
insistence on transfer to a theatre environment is instinctively preferable, this
might not be the safest overall approach.

For example, the advantages of staying on a CCU include:

No need to transfer an unstable patient

Allows earlier cardioversion

Specialist cardiology equipment and drugs are more readily available

Cardiology department skills are readily available.

The disadvantages, most of which are not insurmountable, include:

Provision of anaesthesia in a remote and unfamiliar environment

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Potentially limited monitoring equipment, anaesthetic drugs and equipment

Potentially limited assistance and recovery facilities

A further dilemma is whether to adopt a rapid sequence induction (RSI) strategy

with intubation of the trachea to protect against aspiration. Traditional anaesthetic
thinking would recommend a RSI approach,[3] but this requires greater
anaesthetic depth and complexity, presenting a greater risk of cardiovascular
depression than simply utilizing a small dose of anaesthetic agent.

This issue was investigated by means of a postal survey, when it was found that
only a one-third of emergency physicians, and significantly only two-thirds of
intensive care physicians (mainly anaesthetists) would adopt a tracheal intubation
strategy in such scenarios.[18]

In the authors' opinion both approaches should be considered acceptable and the
anaesthetic technique tailored to individual patient circumstances. If the patient is
obese, has recently ingested a large meal, has a history of oesophageal reflux and
is relatively cardiovascularly stable then a RSI approach would seem prudent. In
contrast utilization of a deep sedation technique with the avoidance of tracheal
intubation would seem preferable in a thin, frail and cardiovascularly unstable
patient.

Whichever approach is adopted the clinician must ensure that suction facilities,
full resuscitation equipment and drugs, plus appropriately skilled assistance are
directly at hand during the procedure. The patient must also be appropriately
nursed and monitored until fully recovered from the procedure.

Cardioversion During Pregnancy

DC cardioversion is recommended for haemodynamically unstable AF and flutter

occurring during pregnancy. There are a number of reports of its safe use in
pregnancy. Once fetal viability is reached fetal heart rate monitoring is advised,
with facilities for immediate Caesarean section.[19]

Anaesthetic management should not overlook the accepted obstetric precautions

of prophylactic antacid administration, pre oxygenation, RSI, cricoid pressure,
and left lateral tilt.

Patients With Pacemakers and Implantable Cardiac Defibrillators

Care must be taken to avoid damage to the pacemaker device and lead system. An
AP electrode position is recommended with the connective pads placed at least 10
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cm from the pacemaker generator, the lowest effective energy setting should be
used. It is mandatory to check pacemaker function following the procedure.

In patients with an implantable cardiac defibrillator (ICD) in situ it is feasible to

utilize the device to issue the shock and only use external cardioversion if this
approach fails. Although an attractive strategy, a recent review concluded that the
battery drainage to the ICD device, especially when external cardioversion proved
necessary, outweighed the potentially reduced ICD damage risk with this
approach.[20]

Complications
Complications can result from the sedation or anaesthesia administered and
include, cardiorespiratory depression, airway obstruction, and aspiration.
The complications that are attributable to cardioversion itself include:
Asystole, severe bradycardia, ventricular arrhythmias, and fibrillation
Systemic arterial embolism and stroke
Cutaneous burns or irritation at the paddle site
Ischaemia and pulmonary oedema (attributed to left atrial standstill)
Myocardial necrosis, skeletal muscle injury, rhabdomyolysis, and renal failure
have been reported as complications, but should not be a feature of modern day
cardioversion.

Kowey PR. The calamity of cardioversion of conscious patients. Am J Cardiol

1988; 61: 11067

Cakulev I, Efimov IR, Waldo AL. Cardioversion: past, present and future.
Circulation 2009; 120: 162332

Stoneham MD. Anaesthesia for cardioversion. Anaesthesia 1996; 51: 56570

Adgey AA J, Walsh SJ. Theory and practice of defibrillation; (1) Atrial

fibrillation and DC conversion. Heart 2004; 90: 14938

Deakin CD, Connelly S, Wharton R, Yuen HM. A comparison of rectilinear and

truncated exponential biphasic waveforms in elective cardioversion of atrial
 13

fibrillation: a prospective randomised controlled trial. Resuscitation 2013; 84:

28691

Adgey AAJ, Spence MS, Walsh SJ. Theory and practice of defibrillation: (2)
defibrillation for ventricular fibrillation. Heart 2005; 91: 11825

Resuscitation Council (UK) Guidelines 2015. [Online] Available from

https://www.resus.org.uk/resuscitationguidelines/peri-arrest-arrhythmias/
(accessed 2 July 2016)

National Institute of Clinical Excellence. Atrial Fibrillation: Management, 2014.

[Online] Available from https://www.nice.org.uk/guidance/cg180 (accessed 2 July
2016)

Furniss SS, Sneyd JR. Safe sedation in modern cardiological practice. Heart 2015;
101: 152630

Stewart AM, Greaves K, Bromilow J. Supraventricular tachyarrhythmias and their

management in the perioperative period. CEACCP 2015; 15: 907

Klein AL, Grimm RA, Murray RD, et al. Use of transesophageal

echocardiography to guide cardioversion in patients with atrial fibrillation. N Engl
J Med 2001; 344: 141120

Hernadez-Madrid A, Svendsen JH, Lip GY, et al. Cardioversion for atrial

fibrillation in current European practice: results of the European Heart Rhythm
Association survey. Europace 2013; 15: 9158

Kaye P, Govier M. Procedural sedation with propofol for emergency DC

cardioversion. Emerg Med J 2014; 31: 9048

James S, Broome IJ. Anaesthesia for cardioversion. Anaesthesia 2003; 58: 2912

Karthikeyan S, Balachandran S, Cort J, Cross MH, Parsloe M. Anaesthesia for

cardioversion: a comparison of sevoflurane and propofol. Anaesthesia 2002; 57:
11149

Lewis SR, Nicholson A, Reed SS, Kenth JJ, Alderson P, Smith AF. Anaesthetic
and sedative agents used for electrical cardioversion. Cochrane Database Syst Rev
2015; (3): CD010824

Lown B, Kleiger R, Wolff G. The technique of cardioversion. Am Heart J 1964;

67: 2824
 14

Cumberbatch GLA, Gray L. Airway management in patients with a broad

complex tachycardia requiring electrical cardioversion: a postal survey. Emerg
Med J 2006; 23: 2168

Tromp CHN, Nanne ACM, Pernet PJM, Tukkie R, Bolte AC. Electrical
cardioversion during pregnancy: safe or not? Neth Heart J 2011; 19: 1346

Berger WR, Knops RE, de Groot JR. Internal cardioversion of persistent atrial
fibrillation in implantable cardioverter defibrillator patients: the juice is not worth
the squeeze. Neth Heart J 2013; 21: 5457