THEME

Pharmacologic
Arrhythmias

management of
tachycardia
Peter M Kistler BACKGROUND
Cardiac arrhythmias may present with palpitations, chest pain, shortness of breath, dizziness and syncope. Diagnosis may
MBBS, PhD, FRACP,
is a cardiologist and be complicated by an inability to document the arrhythmia particularly when symptoms are infrequent and short lived.
electrophysiologist,
OBJECTIVE
Department of Cardiology,
The Alfred Hospital, and This article aims to provide an overview of the pharmacological management of supraventricular tachycardia including
Department of Clinical atrial flutter and haemodynamically stable ventricular tachycardia. Management of atrial fibrillation is discussed in a
Electrophysiology Research, companion article in this issue.
The Baker Heart Research
Institute, Melbourne, Victoria. DISCUSSION
[email protected] Antiarrhythmic medications are effective in reducing symptoms, however, side effects are frequent. Fortunately
Manoj N Obeyesekere nonpharmacological strategies such as catheter ablation have evolved which offer long term cure in the majority of
MBBS, MRCP, is a cardiology patients. However, despite technological advances, pharmacotherapy retains an important place in the therapeutic
advance trainee, Department of approach to cardiac arrhythmias in many patients. It is important to remember that pharmacological management should
Cardiology, The Alfred Hospital, also address any underlying cardiac disease process.
and Department of Clinical
Electrophysiology Research,
The Baker Heart Research
Institute, Melbourne, Victoria.
Arrhythmias may be responsible for worsening paroxysmal AT) and macro re-entrant (atrial flutter). The
heart failure, stroke, myocardial infarction or sudden most common sustained arrhythmia: atrial fibrillation (AF)
death. They may be primary or occur secondary to is the subject of a separate review.
underlying cardiac, pulmonary or endocrine disease. Ventricular arrhythmias also include ectopic beats
It is important to remember that pharmacological and tachycardia. Further management of ventricular
management is not confined to modulation of the tachycardia (VT) requires assessment of underlying
cardiac ion channel but should also address any cardiac function. This is important in determining the risk
underlying cardiac disease process. of sudden cardiac death and the need for an implantable
cardioverter defibrillator (ICD).
An understanding of the underlying mechanism and
categorisation according to cardiac chamber assists
Supraventricular tachycardia
the therapeutic approach to cardiac arrhythmias. Atrial Acute management
arrhythmias include:
• ectopy Management depends on the accurate diagnosis of a
• supraventricular tachycardia (SVT) due to narrow complex tachycardia (QRS width <120 ms) typically
– atrioventricular (AV) nodal re-entry tachycardia (AVNRT) without discernible P waves. Broad complex tachycardia
– AV re-entrant tachycardia (AVRT), or (QRS width >120 ms) should be managed as VT unless
– atrial tachycardia (AT) (Figure 1a–d). there is strong evidence to support alternate diagnoses.
Atrial tachycardia is further divided according to If the patient is hemodynamically compromised, electrical
electrophysiological mechanism into focal (previously cardioversion should be considered.

500 Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007
 If the patient is stable, carotid sinus massage or
Valsalva manoeuvre may be useful in producing transient A B
AV block and terminating tachycardia. However this Atrium Atrium
manoeuvre will be ineffective for arrhythmia circuits that
Fast pathway
do not include the AV node.
The most effective approach in terminating SVT is the Slow pathway
AV AV
node node
administration of adenosine �(Figure 2a)����������������
. Adenosine has
a half life of 10 seconds and requires cardiac monitoring
during intravenous (IV) administration. Monitoring is not Accessory
pathway
only important in terminating arrhythmias safely, but (retrograde
provides diagnostic information regarding arrhythmia conduction)

mechanism (Table 1, Figure

���������
2b). Patients should be warned
Ventricle Ventricle
of the sense of impending doom before the administration
AVNRT AVRT
of adenosine. Approximately 90% of tachycardia due
to AVNRT and AVRT are terminated by a 12 mg dose of
adenosine.1 A rebound sinus tachycardia is commonly C D
Atrium Atrium
seen following termination of SVT by adenosine. If
Macro re-entrant
adenosine is contraindicated or ineffective, IV verapamil pathway around TV
or a beta blocker is also effective and helps prevent
early recurrence.
Atrioventricular nodal blocking agents should not be AV AV
Atrial focus node node
used in patients with:
• broad complex tachycardia, or
• evidence of pre-excit ation on baseline
electrocardiogram (ECG) (Wolff-Parkinson-White
[WPW] syndrome, ie. antegrade conduction via an
accessory pathway) as blocking the AV node leads to Ventricle Ventricle
unopposed conduction down the accessory pathway Focal AT Atrial flutter
which can result in ventricular fibrillation (VF).2 The
treatment of choice is IV procainamide. Flecainide Figure 1. Mechanisms of SVT
is also effective but should only be used if coronary A. Common AVNRT conduction occurs via the slow pathway and retrograde conduction via the
fast pathway. Atria and ventricles are activated synchronously (retrograde P wave rarely seen).
artery disease and structural heart disease have In uncommon AVNRT the antegrade conduction occurs via the fast pathway and retrograde via
the slow pathway (retrograde P wave)
been excluded. Intravenous sotalol and amiodarone
B. Orthodromic AVRT occurs when the AV node conducts antegradely to the ventricle and the
are also effective agents. accessory pathway conducts retrogradely (retrograde P wave). Antidromic AVRT occurs when
the accessory pathway conducts antegradely to the ventricle (resulting in pre-excitation, WPW
DC cardioversion is an alternative at any stage in the pattern with delta wave on ECG) and the AV node conducts retrogradely (retrograde P wave)
management algorithm for SVT and is indicated if all C. Focal AT results when impulse arises from a nonsinus node atrial origin
prior means have failed or hemodynamic compromise D. Typical atrial flutter is due to a large re-entrant circuit circumnavigating the tricuspid valve

develops (Figure 3).

to low energy electrical reversion or atrial overdrive pace
Atrial flutter
termination. It is the atrial mechanical ‘stunning’ as a
A narrow complex tachycardia at a ventricular rate of 150 result of the termination of atrial flutter that determines
bpm is likely to represent atrial flutter with 2:1 AV block. stroke risk rather than the means in which sinus rhythm
Assessment of the patient’s risk of thromboembolic is restored. Under deep sedation, direct current reversion
complication is of utmost importance before deciding (DCR), typically with 50 J, is the most effective means of
on a strategy of restoring sinus rhythm (‘rhythm control’) restoring sinus rhythm. If there is uncertainty regarding
versus control of ventricular rate (‘rate control’). At initial arrhythmia duration then rate control and anticoagulation
assessment low molecular weight or unfractionated should be pursued. If cardioversion is required in
heparin should be administered. If the duration of a patient with uncertain duration of atrial flutter then
atrial flutter can be established as less than 48 hours, transoesophageal echo should be performed to exclude
cardioversion may be considered. Atrial flutter is relatively the presence of left atrial thrombus.
insensitive to pharmacologic cardioversion but sensitive The ventricular response to atrial flutter or ‘rate

Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007 501
 THEME Pharmacologic management of tachycardia

control’ is an effective alternative strategy to acute Long term management

cardioversion. Drugs acting at the AV node (beta blockers, Investigations in patients with SVT are usually limited to
verapamil, diltiazem or digoxin) will reduce the ventricular a 12 lead ECG in sinus rhythm. Echocardiography may be
response but not terminate the arrhythmia (Figure 2b). indicated in patients with right sided accessory pathways
to exclude Ebstein anomaly. In patients with palpitations,
Focal atrial tachycardia
efforts should be directed at documenting tachycardia
Focal AT is due to a rapidly firing non-sinoatrial (SA) before embarking on specific therapy. Not all patients
nodal atrial focus that is typically remote to the AV with a single episode or recurrent SVT require long term
node. Therefore most forms of AT do not respond to IV treatment. The most effective form of therapy is catheter
adenosine and may be recognised by a continuation of ablation, however this may not be available or warranted
the tachycardic P waves during a period of adenosine in all patients. In patients with infrequent episodes a ‘pill
induced AV block. Pharmacologic treatment can be in the pocket’ approach may be useful. 4 This involves
difficult and requires the use of antiarrhythmic drugs that confining the administration of antiarrhythmic medication
act on the atrial myocardium. These include class IA (eg. to the period of the arrhythmia. Therefore the strategy
procainamide), class IC (eg. flecainide) or class III agents does not prevent episodes but aims to reduce symptoms.
(amiodarone, sotalol).3 DC cardioversion is effective in Patients with SVT should be instructed on Valsalva
termination, however early recurrence is common. techniques and the avoidance of precipitants. Referral is
warranted in the following circumstances (Table 2).

A Atrial ectopy
Reassurance and lifestyle modification (eg. coffee and
alcohol intake, smoking) are usually all that are required
for symptomatic patients. If symptoms remain distressing
despite these measures, beta blockers or verapamil are
effective.

Atrial flutter
B If prevention of atrial flutter is required following reversion
then antiarrhythmics or electrophysiological study and
ablation can be undertaken. Flecainide may have a
long term efficacy of 50% in maintaining SR.5 Because
flecainide can slow the flutter rate, AV nodal blocking
agents need to be used with flecainide to prevent 1:1
conduction. For maintenance of SR, sotalol or amiodarone
can also be used.
Figure 2. AV nodal block with adenosine terminating AVNRT (A) and revealing underlying atrial AV node blocking agents alone in the long term can be
flutter (B) used to affectively rate control patients with atrial flutter.
Although the risk of thromboembolism is less compared to
Table 1. Response of narrow complex tachycardia to vagal manoeuvres or adenosine AF, long term anticoagulation (INR 2–3) recommendations
are the same for atrial flutter and are presented in the
No change Consider inadequate dose/poor technique
'Management of atrial fibrillation' article in this issue.
Sudden reversion to SR* Atrioventricular re-entry tachycardia
Atrioventricular nodal re-entry tachycardia AVNRT/AVRT
Atrial tachycardia (rarely reverts)
In patients with burdensome symptoms who do not
Atrioventricular block Atrial flutter
wish to undergo catheter ablation, first line treatment
Atrial tachycardia
is AV nodal blocking agents (except in patients with
Gradual slowing and acceleration Atrial tachycardia
pre-excitation). Atrioventricular nodal blocking agents
Sinus tachycardia
in combination can also be used. A randomised trial
comparing verapamil, digoxin and propanolol failed to
* Tachycardia which terminates with a nonconducted P wave is most likely due to
reveal a superior agent over another.6
AVNRT or AVRT
Class I or class III antiarrhythmic drugs should not

502 Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007
 Pharmacologic management of tachycardia THEME

be administered without documentation of tachycardia

Table 2. When to refer to an arrhythmia specialist*
due to the potential for proarrhythmic effects. In patients
with structurally normal hearts and no evidence of • Tachycardia with wide QRS
coronary ischaemia, flecainide can be used. Flecainide • Pre-excitation syndrome (WPW)
is combined with an AV nodal blocking agent to reduce • Arrhythmia with burdensome symptoms
1:1 conduction if atrial flutter ensues. Flecainide appears • Patient preference to be free of medications
to be superior to verapamil in reducing the frequency • Patients intolerant to medications
of tachycardia. In one study, flecainide completely • Arrhythmia refractory to medications
suppressed episodes in 65% of patients.5 The addition of • Need to start/alter antiarrhythmic drug
a beta blocker to flecainide results in greater than 90% • Hemodynamic instability
efficacy of reducing tachycardia.5 Amiodarone7 and Sotalol8 • High risk occupation (eg. pilot)
have also been used, although their use is limited. Serum • High risk recreational pursuits (eg. diving)
potassium and renal function require monitoring to avoid • Uncertainty regarding further investigation/management
QT prolongation.
* An arrhythmia specialist refers to a electrophysiologist, cardiologist or a physician
Long term treatment in patients with pre-excitation
with an interest in arrhythmia management
should involve an arrhythmia specialist. If catheter
ablation is not possible, class I drugs (flecainide) alone
or in combination with an AV nodal blocking agent Ventricular tachycardia
are effective.
Acute management
Patients with WPW syndrome may also become
tachycardic secondary to AF, atrial flutter, AT, or AVNRT, Patients presenting with wide complex tachycardia
necessitating treatment targeting these disturbances. Atrial have VT unless there is strong evidence to the contrary.
fibrillation is potentially life threatening in patients with Alternate diagnoses include SVT with aberration or
WPW syndrome and is prevalent in up to a third of these antidromic (conduction anterograde via the accessory
patients.9 In such situations rapid conduction down the pathway and retrograde via the AV node) tachycardia.
accessory pathway can cause hemodynamic compromise. In the presence of hemodynamic compromise
For patients with occasional haemodynamically DC cardioversion should be performed. In the
stable symptoms that are burdensome, pill-in-the-pocket hemodynamically stable patient antiarrhythmic medication
therapy may be attempted. This refers to use of an may be used. Limitations include delay in onset of
agent/s only during an episode. A one off dose of diltiazem action and the risk of proarrhythmia or hemodynamic
(120 mg) and propanolol (80 mg) has been shown to reduce compromise. Intravenous amiodarone or procainamide
emergency department visits in suitable patients.10 This are both effective in terminating VT. Lignocaine is
combination has been shown to be more efficacious than particularly effective in the setting of acute cardiac
flecainide for pill-in-the-pocket therapy.10 Hypotension and ischaemia.12 Sotalol can be used in stable patients with
bradycardia are occasional complications. Pill-in-the pocket no left ventricular dysfunction.
therapy with flecainide or sotalol can be used for suitable Polymorphic VT when associated with prolonged
patients with pre-excitation. corrected QT inter vals is termed ‘torsades de
pointes’. This typically occurs in the context of a QT
Focal atrial tachycardia
prolonging drug or electrolyte disturbance (potassium,
Focal AT responds poorly to pharmacotherapy. Flecainide magnesium, calcium). Treatment involves cessation
combined with an AV blocking agent, sotalol or of the offending drug and correction of the electrolyte
amiodarone may be used. Fortunately with the advent of disturbance. When associated with bradycardia, options
radio frequency ablation this form of tachycardia, which include: isoprenaline, atropine, transvenous pacing and
often is unresponsive to drug therapy, can be treated with intravenous magnesium. If associated with hemodynamic
high long term success.11 compromise, cardioversion should be performed.
Multifocal atrial tachycardia is commonly due to
Long term management
pulmonary disease, less commonly due to metabolic
and electrolyte disturbances and seldom due to digoxin. Patients with ventricular arrhythmias require referral to
Treatment should be directed at treating the underlying an arrhythmia specialist (Table 2). The cornerstone of
causative disorder and if required calcium channel risk stratification in patients with ventricular arrhythmias
blockers may be used long term. is assessment of left ventricular function. This can be

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 THEME Pharmacologic management of tachycardia

a reduction in arrhythmic death13 but most studies have

shown no clear overall survival benefit of amiodarone in
Stable regular narrow QRS
QRS <120 msec heart failure.14 Similarly, sotalol, despite being effective in
suppressing VT, has not been shown to prolong survival.15
Beta blockers, sotalol, amiodarone and combinations
have been shown to reduce appropriate and inappropriate
SVT
ICD firing in patients with heart failure. 16 This
may become an increasingly common patient population
as ICD increases in response to increase of heart
Valsalva or carotid sinus massage failure prevalence.
IV Adenosine
IV beta blocker Ventricular ectopy
IV verapamil/diltiazem
Frequent ventricular ectopy are often benign but may
represent underlying cardiac disease. Investigations
include echocardiography and provocative testing to
No termination
determine the presence of coronary ischaemia. Therapies
may be targeted at the underlying cardiac condition (eg.
beta blockers in acute myocardial infarct [AMI] patients
Atrial tachycardia
and antihypertensive drugs in LVH). In patients with
Atrial flutter
structurally normal hearts, beta blockers are usually
effective in alleviating symptoms.

Conclusion
Amiodarone
Sotalol*^ Antiarrhythmic drugs play an important role in the
Flecainide# acute management of arrhythmias. Patients with
Procainamide# recurrent symptoms or single episodes associated
DCR† with haemodynamic compromise should be referred
to an arrhythmia specialist for consideration of long
Figure 3. Acutely managing SVT term therapy. This may include catheter ablation,
† DC cardioversion remains an alternative at any point in the
treatment regimen, as a last resort, or if hemodynamiclly
pharmacological management or device based therapy.
compromised
# Not to be used in patients with LV dysfunction Conflict of interest: none declared.
* Reduce dose in renal impairment
^ Caution should be used in patients with LV dysfunction Acknowledgment
Dr Kistler is the recipient of the Neil Hamilton Fairley Fellowship
achieved by echo, nuclear gated blood pool scan or from the National Health and Medical Research Council of Australia
left ventriculography. If LV function is compromised and National Heart Foundation.
then further assessment of underlying aetiologies
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