British Journal of Anaesthesia 1997; 79: 198–202
Peri-arrest arrhythmias
D. CHAMBERLAIN
Many victims of cardiac arrest suffer the event in the
context of a critical illness complicated by malignant
rhythm disorders. Moreover, almost all patients who
are resuscitated initially from a cardiac arrest have a
subsequent course characterized by bradyarrhythmias
or tachyarrhythmias which are likely to need treat-
ment to restore an adequate circulatory state or to
prevent further collapse. Thus competence in the
management of cardiac arrest per se is an incomplete
skill for those—usually not cardiologists—who aspire
to practice advanced cardiac life support. They
should also be able to recognize and treat cardiac
arrhythmias that are of their nature potentially
malignant or that may become life threatening in
some clinical contexts—notably in the aftermath of
cardiac arrest. The term “peri-arrest arrhythmias”
encompasses all rhythm disorders in these situations.
Guidelines on the management of peri-arrest
arrhythmias published by the European
Resuscitation Council1 and subsequently revised2
offer advice at three levels: treatment modalities that
might reasonably be expected from any individual
treating a cardiac arrest; when expert help should
ideally be sought; and advanced management
strategies that might be considered when expert help
is not immediately available.
Peri-arrest arrhythmias that may lead to or
complicate cardiac arrest are considered under three
broad headings: bradycardias and two types of
tachycardias. The designation of bradycardia usually
relates to disorders of heart rhythm with a rate of less
than 60 beat min91. But this can usefully be
extended beyond the conventional definition to
include the concept of “relative bradycardia”,
applicable to heart rates that are greater than 60 beat
min91 yet inappropriately slow within the clinical
context. A heart rate, for example, of 70 beat min91
may be the modal value in healthy adults yet
abnormally slow to a degree that calls for treatment
in the presence of cardiogenic shock. Tachy-
arrhythmias are conventionally divided into those
that arise within the ventricle (ventricular tachy-
cardia) or above (supraventricular tachycardia). This
classification has merit based on principles of
(Br. J. Anaesth. 1997; 79: 198–202).
Key words
Heart, arrhythmia. Complications, arrhythmia.
Complications, cardiac arrest.
pathological substrate, aetiology, treatment, prog-
nosis and usage, but is presented in the guidelines in
a modified form to take account of diagnostic diffi-
culties.10 Ventricular tachycardia characteristically
has a broad QRS complex reflecting delayed
depolarization through abnormal pathways, but a
minority of tachycardias arising below the AV node
may show complexes with a width that lies within the
normal range. Supraventricular tachycardia, on the
other hand, characteristically shows a narrow QRS
complex that is often very similar in shape to that of
the usual beats, but two common exceptions cause
confusion. First, normal conduction is not possible
at very high rates, in particular the right bundle may
fail under these conditions so that the pattern of
depolarization may be abnormal with a wide QRS of
a right bundle branch block pattern even in rhythm
disorders arising in the atrium or within the AV
node. This so-called rate-related aberration is more
common in the presence of heart disease. Second, a
pattern of depolarization that is abnormally pro-
longed during an individual’s normal rhythm is at
least as prolonged during tachycardia. Thus the
width of the QRS complex during tachycardia does
not reliably distinguish ventricular from supraven-
tricular origin. Many other features may indicate the
true origin of a tachycardia, but accurate classifica-
tion may be difficult and may not always be possible
from the surface electrocardiogram. The guidelines
therefore make no assumption that the origin of a
tachycardia has been defined accurately. Recom-
mendations for treatment are based instead on the
simple classification of narrow complex tachycardias
(which are usually supraventricular and may be
treated as such with acceptable safety) and broad
complex tachycardias (which should be assumed to
be ventricular for purposes of treatment as this is the
safer strategy).
Separate algorithms are available for bradycardia,
narrow complex tachycardia and broad complex
tachycardia. The principles of treatment are similar
to those used in any clinical context, but the follow-
ing points should be noted:
! The algorithms are designated specifically for the
peri-arrest situation but they cannot encompass all
situations that may arise.
! The algorithms are intended for physicians (or
those working under the direction of a physician)
DOUGLAS CHAMBERLAIN, CBE, MD, DSC (HON), FRCP, FRCA, FESC,
FACC, Royal Sussex County Hospital, Eastern Road, Brighton
BN2 5BE.
Peri-arrest arrhythmias 199

who do not regard themselves as experts in

arrhythmia management. Therefore, management
strategies that are complex or potentially dangerous
when used inappropriately are omitted as far as
possible.
! The algorithms have to be broadly applicable in
all European countries notwithstanding different
traditions of antiarrhythmic therapy. Some drugs
have been omitted as options because they are not
universally available, and alternatives have been
offered where it is necessary to do so.
! The algorithms assume that oxygen is being
administered and i.v. access is available.
! The arrows indicating progression from one
treatment to the next are to be followed only if the
arrhythmia is still present.
! All antiarrhythmic strategies (physical
manoeuvres,22 drugs13 or electrical treatment7) can
be proarrhythmic. Deterioration may therefore
occur as a result of treatment rather than as a
consequence of lack of effect. Moreover, the use of
multiple antiarrhythmic drugs or high doses of a
single drug can cause myocardial depression and
hypotension. How far sequential treatments should
be pressed in the face of these risks may be a matter
for careful clinical judgment.
! The algorithms provide doses based on average
body weight and may need adjustment, particularly
for small individuals. Doses expressed in mg/kg
body weight are judged inappropriate for use in Figure 1 Algorithm for bradycardia.
emergency situations because calculations are more
likely than usual to introduce error.
complete atrioventricular block implies that the sub-
sidiary pacemaker cannot conduct through the usual
Bradycardia pathways and may therefore be below the division of
The algorithm for bradycardia is shown in figure 1. the bundle of His into its bundle branches (unless
The apparent complexity is misleading because the there is pre-existing bundle branch block or the rare
management principles are simple and may be phenomenon of bradycardia-dependent bundle
summarized thus: if there is a risk of asystole, pace as branch block). Mobitz type II AV block which is the
soon as possible; if there is no perceived risk of last of the criteria requires more explanation. During
asystole but the haemodynamic state of the patient is the evolution of AV block a phase usually occurs
poor, give atropine and pace only if this is ineffective; when some beats are conducted and some are not.
if there is no perceived risk of asystole and the patient This is known as second degree block but there are
is not compromised haemodynamically to an important two types: for a “benign” block in the region of
degree then only observation is required. The algorithm, the AV node, intermittent failure of conduction is
however, provides more information around this characterized by dropped beats in Wenckebach
framework. periods (also known as Mobitz I block); alterna-
The first and most important decision relates to tively, when the failure is within the bundle branch
whether or not there is a perceived risk of asystole. system, the dropped beats occur unpredictably:
Observed performance of the heart rhythm provides there is no “warning” PR prolongation. Another
a guide. A history of asystole is a self-evident risk marker of problems within the bundle branch system
factor in this regard. A pause longer than 3 s also is also present and very obvious. Intermittent failure
causes concern because reliable subsidiary pace- of a depolarization wave to conduct through the
makers should provide escape beats within a briefer bundle branch system occurs only if one of the
interval. Other criteria in the presence of heart block bundle branches has previously failed, so that even
are based on indications that the site of block is the conducted beats show bundle branch block of
either in the region of the AV node itself (in which some type. Mobitz type II second degree AV block is
case reliable and adequate subsidiary pacemaker therefore characterized by wide QRS complexes in
tissue should still be available to drive the ventricle) the conducted beats, together with intermittent
or alternatively below the AV node (in which case abrupt failure of conduction. The risk is clear: one
any subsidiary pacemakers may be irregular, are bundle branch has already failed and the other is
likely to be unduly slow and are certainly unreliable). indicating it may do so with no reliable pacemaker
Thus complete heart block with a narrow QRS tissue available at a lower level.
complex is not in itself an indication for treatment. If any of the warning signs are present indicating
Conversely, an abnormally wide QRS complex with that asystole is a definite risk, transvenous pacing
200 British Journal of Anaesthesia

should be established as soon as possible. The

responder who is not an expert in arrhythmia
management may wish to do no more than establish
i.v. access and give atropine in a dose of 500 ␮g to
3 mg while waiting for expert help from others with
the necessary specific skills. In this situation,
however, the use of atropine is frequently unsuccess-
ful. When a patients’s condition is critical, external
pacing8 with appropriate sedation should be con-
sidered: it is simple to implement provided the
equipment is available. The judicious use of isopre-
naline is an alternative strategy, with the usual
starting dose of 1 ␮g min91 which may be increased
10-fold or more in a desperate situation, always
having regard to the risk of precipitating or
worsening ventricular arrhythmias and increasing
myocardial oxygen consumption. Orciprenaline is
an alternative chronotropic catecholamine used in
some countries.
The second decision for those not at immediate
risk of asystole is based on the presence or absence of
adverse haemodynamic signs. Clinical evidence of
low cardiac output, hypotension (arterial pressure
less than 90 mm Hg) and overt heart failure are self-
evident factors. Heart rate less than 40 beat min91 is
included because complications are likely to occur
even if such a slow rhythm is tolerated temporarily.
The last of the criteria relate to prognostically or
haemodynamically important ventricular arrhyth-
mias—either complex forms of ventricular
extrasystoles or non-sustained runs of ventricular
tachycardia—which occur frequently with or as a
complication of an underlying bradycardia. These
are best treated by increasing the underlying rate. If
an antiarrhythmic is used in this setting, bradycardia
is likely to become worse and thus increase the risk
from ventricular arrhythmia. In the presence of any Figure 2 Algorithm for broad complex tachycardia.
of the five adverse haemodynamic signs, atropine
should be administered, starting with an initial i.v.
dose of 500 ␮g repeated to a maximum of 3 mg a broad complex tachycardia without adverse
which provides virtually complete vagal blockade.6 haemodynamic disturbance, routine antiarrhythmic
This usually produces a satisfactory response at least therapy should be used, with cardioversion only
temporarily, but if necessary expert help would be if this fails. The algorithm provides further
needed with a view to transvenous pacing. Only information around this framework.
rarely does a patient’s haemodynamic condition The first decision relates to the presence or
justify the use of external pacing or the risky absence of a palpable pulse, with the implication that
chronotropic catecholamines while awaiting a victim with an absent pulse is also unconscious and
definitive treatment. clinically in cardiac arrest. When this is not the case,
Bradycardias that do not carry a risk of asystole a second decision is reached, relating to adverse
and are not likely to have important adverse haemo- signs. These include hypotension (arterial pressure
dynamic effects require no treatment. Indeed, in the less than 90 mm Hg) and heart failure as for brady-
context of myocardial infarction they may have a cardia, but also the presence of chest pain which
favourable influence by limiting myocardial oxygen might either be the result or the cause of the rhythm
requirement disorder, and any rate faster than 150 beat min91
because this is likely to presage problems even if it
does not do so at the onset. If any of these signs
Broad complex tachycardia are present the situation must be regarded as an
The algorithm for broad complex tachycardia is emergency and expert help should be sought even
shown in figure 2 and can be summarized into three before sedation and synchronized shock are con-
possible treatment policies: if there is no pulse as a sidered. Energies less than 100 J should not be used
result of the arrhythmia the condition should be because they may have proarrhythmic effects, so
treated as cardiac arrest using the ventricular fibrilla- attempts at restoration of a more satisfactory rhythm
tion/ventricular tachycardia algorithm for cardiac should use sequentially 100 J, 200 J and 360 J. In the
arrest; if there is a pulse but inadequate perfusion, unlikely event of cardioversion being unsuccessful,
cardioversion is required as soon as possible. If there is the algorithm recommends the use of lignocaine
Peri-arrest arrhythmias 201

50 mg over 2 min, repeated every 5 min to a total

dose of 200 mg with an infusion of 2 mg min91 set
up after the first bolus dose. If the concentration of
potassium is known to be less than 3.6 mmol litre91,
especially in the presence of recent infarction,15
potassium chloride should be given in a dose of up to
60 mmol, but the maximum infusion rate should
never exceed 30 mmol h91. Magnesium concentra-
tions should be assumed to be deficient in the
presence of hypokalaemia, and this is corrected by
magnesium sulphate i.v.24 in a dose of 10 ml of a
50% solution over 1 h. If the arrhythmia persists,
further shocks should be attempted when lignocaine
200 mg has been administered: in the presence of
adverse signs it is inappropriate to delay electrical
treatment for full correction of electrolyte deficien-
cies. Other drugs that may be used if cardioversion is
not successful after lignocaine include amiodarone,16
procainamide,14 flecainide,20 propafenone17 or
bretylium3: any one of these may sometimes reverse
the arrhythmia or act as successful adjuncts to car-
dioversion. Clearly every drug that is administered
unsuccessfully adds to myocardial depression, and
polypharmacy can be justified only in desperate
situations. Overdrive pacing25 is a method of con-
trolling ventricular tachycardia without a persistent
adverse effect on heart function, but it calls for
considerable expertise in arrhythmia management.
For broad complex tachycardia that is not causing
appreciable adverse signs, the lignocaine regimen
should be started before any attempts at cardio-
version, and hypokalaemia is treated concurrently. If
this is not successful expert help should be sought.
The management is then likely to consist of synchro-
nized shock (100 J, 200 J, 360 J), with amiodarone as
the recommended adjunctive therapy if shock alone
is unsuccessful or if the arrhythmia is recurrent.21
The time for completion of the amiodarone infusion
is more than 1 h, but assessment of urgency on
clinical grounds will determine how long should
elapse before further shocks are given after the first
set of three have been unsuccessful.
Figure 3 Algorithm for narrow complex tachycardia.

Narrow complex tachycardia acute ischaemia, with digitalis toxicity or in elderly

This is almost always supraventricular tachycardia,
and as a peri-arrest arrhythmia is less frequent and
somewhat less hazardous. Supraventricular tachy-
cardias are, however, a recognized trigger for
malignant ventricular arrhythmias in some clinical
contexts,12 including myocardial ischaemia, and
atrial fibrillation is a relatively common peri-arrest
arrhythmia.
The algorithm shown in figure 3 can be summa-
rized as follows: for regular supraventricular tachycar-
dias, vagal manoeuvres or adenosine may be tried
first, but if these are not successful in the presence
of adverse signs the first strategy is cardioversion;
without adverse signs there is a choice of routine
antiarrhythmic agents that include a short-acting
beta-blocker, digoxin, verapamil and amiodarone.
The algorithm adds further details to this outline.
Vagal manoeuvres must be considered first, but
they may not always be appropriate in peri-arrest
situations: they are dangerous in the presence of
patients, especially in those with a carotid bruit
because of vulnerability to plaque rupture with
cardiovascular complications.4 Adenosine, however,
is a comparatively safe treatment,5 using rapid bolus
administration at a starting dose of 3 mg, repeating
every 1–2 min with increments to 6 mg, then 12 mg
and, if necessary, a final second dose of 12 mg.
Ideally adenosine is given into a central vein because
its half-life is measured in seconds and a more
peripheral injection may be inactivated before it
reaches the coronary circulation. The injection
should, in any case, be given as rapidly as possible.
Even with central injections administered rapidly,
severe circulatory impairment that slows the circula-
tion may prevent an adequate concentration ever
reaching the coronary circulation. If these simple
treatments are unsuccessful, or if atrial fibrillation is
identified, then expert help should be sought.
The factors that indicate adverse signs are similar
as for broad complex tachycardia: hypotension
202
(systolic pressure less than 90 mm Hg), heart failure
and chest pain. But the list in this case includes
impaired consciousness (which may occur without
full cardiac arrest) or a rate of more than 200 beat
min91 (rather than 150 beat min91 for broad
complex tachycardia). In the presence of any of these
signs the treatment should be by synchronized
cardioversion using sequentially 100 J, 200 J and 360
J as necessary after appropriate sedation. If this fails
amiodarone should be administered at an initial dose
of 300 mg by central i.v. injection over 15 min,
followed by 300 mg over 1 h. Spontaneous reversion
may occur during the amiodarone infusion but
otherwise repeat cardioversion should be attempted.
If the need to reverse the arrhythmia is pressing, one
or more shocks may be given during the amiodarone
infusion. For refractory or recurrent atrial fibrilla-
tion, the slowing induced by amiodarone may relieve
any haemodynamic compromise and be judged a
satisfactory outcome. Occasionally controlled atrial
fibrillation may be the most stable rhythm that can
be achieved and may then be preferable to other
recurrent supraventricular rhythms.
In the absence of adverse signs there is no one
recommended “best buy”. One reasonable choice
may be esmolol23 which is a short-acting beta
blocker and can be used in a dose of 40 mg over
1 min (which may be repeated) with an infusion
starting at 4 mg min91 and increments as necessary
to 12 mg min91. Digoxin may have a role either for
the control of atrial fibrillation or for terminating
some regular supraventricular tachycardias. The
recommended dose is 500 ␮g over 30 min which can
be repeated once. Verapamil is highly effective for
narrow complex tachycardia in other situations but
should be used with great caution in the peri-arrest
situation, and is best reserved for the expert
because there are circumstances in which its use is
hazardous. These include arrhythmias associated
with Wolff–Parkinson–White syndrome,11 tachy-
cardias that are ventricular in origin,19 and some of
the supraventricular arrhythmias of childhood.18
The dose is 5–10 mg i.v. The dangers of interaction
between verapamil and beta blocking agents is of
particular concern if the drugs are used i.v.9
Amiodarone may also be used, and in this context
the appropriate dose is 300 mg over 1 h, repeated
once if necessary. Overdrive pacing can also be
effective but requires considerable expertise. It is not
appropriate in the presence of atrial fibrillation.
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