Resuscitation Council (UK)

8 Peri-arrest arrhythmias

Introduction
Cardiac arrhythmias are relatively common in the peri-arrest period. They are common
in the setting of acute myocardial infarction and may precipitate ventricular fibrillation
(VF) or follow successful defibrillation. The treatment algorithms described in this
chapter have been designed to enable the non-specialist advanced life support (ALS)
provider to treat the patient effectively and safely in an emergency; for this reason they
have been kept as simple as possible. If patients are not acutely ill there may be several
other treatment options, including the use of drugs (oral or parenteral) that will be less
familiar to the non-expert. In this situation there will be time to seek advice from
cardiologists or other senior doctors with the appropriate expertise.

Guideline changes
There are relatively few changes from Guidelines 2005. Initial assessment of patients
with suspected peri-arrest arrhythmias now uses the ABCDE approach (see the
preventing cardiac arrest chapter). A single set of adverse features for tachy- and
brady-arrhythmias has been introduced for consistency.

Sequence of actions
Assess the patient using the ABCDE approach. In all cases, give oxygen and insert an
intravenous cannula and assess the patient for adverse features. Whenever possible,
record a 12-lead ECG; this will help determine the precise rhythm, either before
treatment or retrospectively, if necessary with the help of an expert. Correct any
electrolyte abnormalities (e.g. K+, Mg++, Ca++).

When you assess and treat any arrhythmia address two factors: the condition of the
patient (stable versus unstable – determined by the absence or presence respectively of
adverse features) and the nature of the arrhythmia.

Adverse features
The presence or absence of adverse symptoms or signs will dictate the appropriate
treatment for most arrhythmias. The following adverse features indicate that a patient is
potentially unstable because of the arrhythmia:

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 Shock – hypotension (systolic blood pressure < 90 mmHg), pallor, sweating,

cold, clammy extremities, confusion or impaired consciousness.
 Syncope – transient loss of consciousness due to global reduction in blood
flow to the brain.
 Myocardial ischaemia – typical ischaemic chest pain and/or evidence of
myocardial ischaemia on 12-lead ECG.
 Heart failure – pulmonary oedema and/or raised jugular venous pressure
(with or without peripheral oedema and liver enlargement).

Treatment options
Depending on the nature of the underlying arrhythmia and clinical status of the patient
(in particular the presence or absence of adverse features) immediate treatments can
be categorised under four headings:
1. Electrical (cardioversion for tachyarrhythmia or pacing for bradyarrhythmia)
2. Simple clinical intervention (e.g., vagal manoeuvres, fist pacing)
3. Pharmacological (drug treatment)
4. No treatment needed

Most drugs act more slowly and less reliably than electrical treatments, so electrical
treatment is usually the preferred treatment for an unstable patient with adverse
features.

If a patient develops an arrhythmia during, or as a complication of some other condition

(e.g. infection, acute myocardial infarction, heart failure), make sure that the underlying
condition is assessed and treated appropriately, involving relevant experts if necessary.
Once an arrhythmia has been treated successfully, repeat a 12-lead ECG to detect any
abnormalities that may require treatment in the longer term.

Tachycardias
If the patient is unstable
If the patient is unstable and deteriorating (i.e., has adverse features caused by the
tachycardia) synchronised cardioversion is the treatment of choice. In patients with
otherwise normal hearts, serious signs and symptoms are uncommon if the ventricular
rate is < 150 min-1. Patients with impaired cardiac function, structural heart disease or
other serious medical conditions (e.g. severe lung disease) may be symptomatic and
unstable during arrhythmias with heart rates between 100 and 150 min-1. If
cardioversion fails to restore sinus rhythm, and the patient remains unstable, give
amiodarone 300 mg IV over 10 - 20 min and re-attempt electrical cardioversion. The
loading dose of amiodarone can be followed by an infusion of 900 mg over 24 h.

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 Assess using the ABCDE approach
Adult tachycardia (with pulse)  Give oxygen if appropriate and obtain IV access
algorithm  Monitor ECG, BP, SpO2 , record 12-lead ECG
 Identify and treat reversible causes (e.g. electrolyte abnormalities)

Adverse features?
Synchronised DC Shock Yes / Unstable  Shock
Up to 3 attempts  Syncope
 Myocardial ischaemia
 Heart failure
 Amiodarone 300 mg IV over 10-20 min
and repeat shock; followed by: No / Stable
 Amiodarone 900 mg over 24 h
Broad Is QRS narrow (< 0.12 s)? Narrow

Irregular Broad QRS Regular Regular Narrow QRS Irregular

Is rhythm regular? Is rhythm regular?

 Use vagal manoeuvres Irregular Narrow Complex

 Adenosine 6 mg rapid IV bolus; Tachycardia
if unsuccessful give 12 mg;
Probable atrial fibrillation

!
Seek expert help if unsuccessful give further 12 mg.
 Monitor ECG continuously Control rate with:
 -Blocker or diltiazem
 Consider digoxin or amiodarone
Sinus rhythm restored? if evidence of heart failure

Possibilities include: If ventricular tachycardia

Yes No
AF with bundle branch block (or uncertain rhythm):
 Amiodarone 300 mg IV
!
treat as for narrow complex Seek expert help
over 20-60 min;
Pre-excited AF then 900 mg over 24 h Probable re-entry paroxysmal SVT:
consider amiodarone  Record 12-lead ECG in sinus
Polymorphic VT If previously confirmed rhythm
(e.g. torsade de pointes - SVT with bundle branch block:  If recurs, give adenosine again &
give magnesium 2 g over 10 min)  Give adenosine as for regular consider choice of anti-arrhythmic Possible atrial flutter
narrow complex tachycardia prophylaxis  Control rate (e.g. -Blocker)

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Synchronised cardioversion
Carry out cardioversion under general anaesthesia or conscious sedation, administered
by a healthcare professional competent in the technique being used. Ensure that the
defibrillator is set to synchronised mode. For a broad-complex tachycardia or atrial
fibrillation, start with 120-150 J biphasic shock (200 J monophasic) and increase in
increments if this fails. Atrial flutter and regular narrow-complex tachycardia will often be
terminated by lower energies: start with 70-120 J biphasic (100 J monophasic).

If the patient is stable

If there are no adverse features consider using drug treatment in the first instance (if
any treatment is required). Assess the ECG and determine the QRS duration. If the
QRS duration is greater than 0.12 s (3 small squares on standard ECG paper speed of
25 mm s-1), this is a broad-complex tachycardia. If the QRS duration is less than 0.12 s,
it is a narrow-complex tachycardia.

Broad-complex tachycardia
Broad-complex tachycardias (QRS ≥ 0.12 s) are usually ventricular in origin. Broad-
complex tachycardias may be also caused by supraventricular rhythms with aberrant
conduction (bundle branch block). In the unstable, peri-arrest patient assume that the
rhythm is ventricular in origin and attempt synchronised cardioversion as described
above. Conversely, if a patient with broad-complex tachycardia is stable, the next step
is to determine if the rhythm is regular or irregular.

Regular broad-complex tachycardia

A regular broad-complex tachycardia is likely to be VT or a supraventricular rhythm with
bundle branch block. In a stable patient, if there is uncertainty about the source of the
arrhythmia, give adenosine using the strategy described below.

If the broad complex tachycardia is thought to be VT, treat with amiodarone 300 mg
intravenously over 20-60 min, followed by an infusion of 900 mg over 24 h. If a regular
broad-complex tachycardia is known to be a supraventricular arrhythmia with bundle
branch block, and the patient is stable, use the strategy indicated for narrow-complex
tachycardia (below).

Irregular broad-complex tachycardia

This is most likely to be atrial fibrillation (AF) with bundle branch block, but careful
examination of a 12-lead ECG (if necessary by an expert) may enable confident
identification of the rhythm. Other possible causes are AF with ventricular pre-excitation
(in patients with Wolff-Parkinson-White (WPW) syndrome), or polymorphic VT (e.g.
torsade de pointes), but polymorphic VT is unlikely to be present without adverse
features. Seek expert help with the assessment and treatment of irregular broad-
complex tachyarrhythmia.

Treat torsade de pointes VT immediately by stopping all drugs known to prolong the QT
interval. Correct electrolyte abnormalities, especially hypokalaemia. Give magnesium

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sulphate 2 g IV over 10 min (= 8 mmol, 4 ml of 50% magnesium sulphate). Obtain

expert help, as other treatment (e.g. overdrive pacing) may be indicated to prevent
relapse once the arrhythmia has been corrected. If adverse features develop, which is
common, arrange immediate synchronised cardioversion. If the patient becomes
pulseless, attempt defibrillation immediately (ALS algorithm).

Narrow-complex tachycardia
Examine the ECG to determine if the rhythm is regular or irregular.

Regular narrow-complex tachycardias include:262

 sinus tachycardia;
 AV nodal re-entry tachycardia (AVNRT) – the commonest type of regular
narrow-complex tachyarrhythmia;
 AV re-entry tachycardia (AVRT) – due to WPW syndrome;
 atrial flutter with regular AV conduction (usually 2:1).

An irregular narrow-complex tachycardia is most likely to be AF or sometimes atrial

flutter with variable AV conduction (‘variable block’).

Regular narrow-complex tachycardia

Sinus tachycardia
Sinus tachycardia is not an arrhythmia. This is a common physiological response to
stimuli such as exercise or anxiety. In a sick patient it may occur in response to many
conditions including pain, infection, anaemia, blood loss, and heart failure. Treatment is
directed at the underlying cause; trying to slow sinus tachycardia that has occurred in
response to most of these conditions will make the situation worse. Do not attempt to
treat sinus tachycardia with cardioversion or anti-arrhythmic drugs.

AVNRT and AVRT (paroxysmal supraventricular tachycardia)

AV nodal re-entry tachycardia is the commonest type of paroxysmal supraventricular
tachycardia (SVT), often seen in people without any other form of heart disease. It is
relatively uncommon in the peri-arrest setting. It causes a regular, narrow-complex
tachycardia, often with no clearly visible atrial activity on the ECG. The heart rate is
commonly well above the typical range of sinus rhythm at rest (60-100 min-1). It is
usually benign, unless there is additional, co-incidental, structural heart disease or
coronary disease, but it may cause symptoms that the patient finds frightening.

AV re-entry tachycardia occurs in patients with the WPW syndrome, and is also usually
benign, unless there is additional structural heart disease. The common type of AVRT is
a regular narrow-complex tachycardia, usually having no visible atrial activity on the
ECG.

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Atrial flutter with regular AV conduction (often 2:1 block)

This produces a regular narrow-complex tachycardia. It may be difficult to see atrial
activity and identify flutter waves in the ECG with confidence, so the rhythm may be
indistinguishable, at least initially, from AVNRT or AVRT.

Typical atrial flutter has an atrial rate of about 300 min-1, so atrial flutter with 2:1
conduction produces a tachycardia of about 150 min-1. Much faster rates (160 min-1 or
more) are unlikely to be caused by atrial flutter with 2:1 conduction. Regular tachycardia
with slower rates (e.g. 125-150) may be due to atrial flutter with 2:1 conduction, usually
when the rate of the atrial flutter has been slowed by drug therapy.

Treatment of regular narrow-complex tachycardia

If the patient is unstable, with adverse features caused by the arrhythmia, attempt
synchronised electrical cardioversion. It is reasonable to give adenosine to an unstable
patient with a regular narrow-complex tachycardia while preparations are being made
for synchronised cardioversion. However, do not delay electrical cardioversion if
adenosine fails to restore sinus rhythm.

In the absence of adverse features:

 Start with vagal manoeuvres. Carotid sinus massage or the Valsalva
manoeuvre will terminate up to a quarter of episodes of paroxysmal SVT.
Record an ECG (preferably multi-lead) during each manoeuvre. If the rhythm
is atrial flutter, slowing of the ventricular response will often occur and reveal
flutter waves.
 If the arrhythmia persists and is not atrial flutter, give adenosine 6 mg as a
rapid intravenous bolus. Use a relatively large cannula and large (e.g.,
antecubital) vein. Warn the patient that they will feel unwell and probably
experience chest discomfort for a few seconds after the injection. Record an
ECG (preferably multi-lead) during the injection. If the ventricular rate slows
transiently, but then speeds up again, look for atrial activity, such as atrial
flutter or other atrial tachycardia, and treat accordingly. If there is no
response to adenosine 6 mg, give a 12 mg bolus. If there is no response
give one further 12 mg bolus. Apparent lack of response to adenosine will
occur if the bolus is given too slowly or into a peripheral vein.
 Vagal manoeuvres or adenosine will terminate almost all AVNRT or AVRT
within seconds. Failure to terminate a regular narrow-complex tachycardia
with adenosine suggests an atrial tachycardia such as atrial flutter (unless
the adenosine has been injected too slowly or into a small peripheral vein).
 If adenosine is contra-indicated, or fails to terminate a regular narrow
complex tachycardia without demonstrating that it is atrial flutter, consider
giving a calcium-channel blocker, for example verapamil 2.5 - 5 mg
intravenously over 2 min.

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Irregular narrow-complex tachycardia

An irregular narrow-complex tachycardia is most likely to be AF with an uncontrolled
ventricular response or, less commonly, atrial flutter with variable AV block. Record a
12-lead ECG to identify the rhythm. If the patient is unstable, with adverse features
caused by the arrhythmia, attempt synchronised cardioversion.263

If there are no adverse features, treatment options include:

 rate control by drug therapy;
 rhythm control using drugs to encourage chemical cardioversion;
 rhythm control by electrical cardioversion;
 treatment to prevent complications (e.g. anticoagulation).

Obtain expert help to determine the most appropriate treatment for the individual
patient. The longer a patient remains in AF the greater is the likelihood of atrial
thrombus developing. In general, patients who have been in AF for more than 48 h
should not be treated by cardioversion (electrical or chemical) until they have been fully
anticoagulated for at least three weeks, or unless trans-oesophageal echocardiography
has shown the absence of atrial thrombus. If the clinical situation dictates that
cardioversion is needed more urgently, give either regular low-molecular-weight heparin
in therapeutic dose or an intravenous bolus injection of unfractionated heparin followed
by a continuous infusion to maintain the activated partial thromboplastin time (APTT) at
1.5 to 2 times the reference control value. Continue heparin therapy and commence oral
anticoagulation after successful cardioversion. Seek expert advice on the duration of
anticoagulation, which should be a minimum of 4 weeks, often substantially longer.

If the aim is to control heart rate, the usual drug of choice is a beta-blocker. Diltiazem or
verapamil may be used in patients in whom beta blockade is contraindicated or not
tolerated. An intravenous preparation of diltiazem is available in some countries but not
in the UK. Digoxin may be used in patients with heart failure. Amiodarone may be used
to assist with rate control but is most useful in maintaining rhythm control. Magnesium is
also used but the data supporting this are limited. When possible seek expert help in
selecting the best choice of treatment for rate control in each individual patient.

If the duration of AF is less than 48 h and rhythm control is considered appropriate,

chemical cardioversion may be attempted. Seek expert help with the use of drugs such
as flecainide. Do not use flecainide in the presence of heart failure, known left
ventricular impairment or ischaemic heart disease, or a prolonged QT interval.
Amiodarone (300 mg intravenously over 20-60 min followed by 900 mg over 24 h) may
also be used but is less likely to achieve prompt cardioversion. Electrical cardioversion
remains an option in this setting and will restore sinus rhythm in more patients than
chemical cardioversion.

Seek expert help if any patient with AF is known or found to have ventricular pre-
excitation (WPW syndrome). Avoid using adenosine, diltiazem, verapamil, or digoxin in
patients with pre-excited AF or atrial flutter as these drugs block the AV node and cause
a relative increase in pre-excitation.

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Adult bradycardia algorithm

 Assess using the ABCDE approach
 Give oxygen if appropriate and obtain IV access
 Monitor ECG, BP, SpO2, record 12-lead ECG
 Identify and treat reversible causes
(e.g. electrolyte abnormalities)

Adverse features?
YES  Shock NO
 Syncope
 Myocardial ischaemia
 Heart failure

Atropine
500 mcg IV

Satisfactory YES
response?

NO

Interim measures: Risk of asystole?

 Atropine 500 mcg IV  Recent asystole
repeat to maximum of 3 mg  Mobitz II AV block
YES
 Isoprenaline 5 mcg min-1 IV  Complete heart block
 Adrenaline 2-10 mcg min-1 IV with broad QRS
 Alternative drugs *  Ventricular pause > 3 s
OR
 Transcutaneous pacing NO

Seek expert help ! Observe

Arrange transvenous pacing

* Alternatives include:
 Aminophylline
 Dopamine
 Glucagon (if beta-blocker or calcium channel blocker overdose)
 Glycopyrrolate can be used instead of atropine

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Bradycardia
Bradycardia is defined as a heart rate of < 60 min-1. It may be:
 physiological (e.g., in athletes);
 cardiac in origin (e.g., atrioventricular block or sinus node disease);
 non-cardiac in origin (e.g., vasovagal, hypothermia, hypothyroidism,
hyperkalaemia);
 drug-induced (e.g., beta blockade, diltiazem, digoxin, amiodarone).

Assess the patient with bradycardia using the ABCDE approach. Consider the potential
cause of the bradycardia and look for adverse features. Treat any reversible causes of
bradycardia identified in the initial assessment. If adverse signs are present start to treat
the bradycardia. Initial treatment is pharmacological, with pacing being reserved for
patients unresponsive to pharmacological treatment or with risks factors for asystole.

Pharmcological treatment
If adverse signs are present, give atropine, 500 mcg, intravenously and, if necessary,
repeat every 3-5 min to a total of 3 mg. Doses of atropine of less than 500 mcg have
been reported to cause paradoxical slowing of the heart rate.264 In healthy volunteers a
dose of 3 mg produces the maximum achievable increase in resting heart rate.265 Use
atropine cautiously in the presence of acute coronary ischaemia or myocardial
infarction; increased heart rate may worsen ischaemia or increase the zone of
infarction. Do not give atropine to patients with cardiac transplants. Their hearts are
denervated and will not respond to vagal blockade by atropine, which may cause
paradoxical sinus arrest or high-grade AV block in these patients.266

If bradycardia with adverse signs persist despite atropine, consider cardiac pacing. If
pacing cannot be achieved promptly consider the use of second-line drugs. Seek expert
help to select the most appropriate choice. In some clinical settings second-line drugs
may be appropriate before the use of cardiac pacing. For example consider giving
intravenous glucagon if a beta-blocker or calcium channel blocker is a likely cause of
the bradycardia. Consider using digoxin-specific antibody fragments for bradycardia due
to digoxin toxicity. Consider using theophylline (100-200 mg by slow intravenous
injection) for bradycardia complicating acute inferior wall myocardial infarction, spinal
cord injury or cardiac transplantation.

Pacing
Transcutaneous pacing
Initiate transcutaneous pacing immediately if there is no response to atropine, or if
atropine is unlikely to be effective. Transcutaneous pacing can be painful and may fail to
achieve effective electrical capture (i.e. a QRS complex after the pacing stimulus) or fail
to achieve a mechanical response (i.e. palpable pulse). Verify electrical capture on the
monitor or ECG and check that it is producing a pulse. Reassess the patient’s condition
(ABCDE). Use analgesia and sedation as necessary to control pain; sedation may
compromise respiratory effort so continue to reassess the patient at frequent intervals.

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Fist pacing
If atropine is ineffective and transcutaneous pacing is not immediately available, fist
pacing can be attempted while waiting for pacing equipment.267-269 Give serial rhythmic
blows with the closed fist over the left lower edge of the sternum to stimulate the heart
at a rate of 50-70 min-1.

Transvenous pacing
Seek expert help to assess the need for temporary transvenous pacing and to intitiate
this when appropriate. Temporary transvenous pacing should be considered if there is
documented recent asystole (ventricular standstill of more than 3 s), Mobitz type II AV
block; complete (third-degree) AV block (especially with broad QRS or initial heart rate
<40 beats min-1).

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