Update Article

Narrow Complex Tachycardia: Recognition and

Management in the Emergency Room
IB Ray

Abstract
Cardiac arrhythmias often present as urgent medical conditions requiring immediate care. Patient
presenting with a tachyarrhythmia is a common finding in the emergency room. They also occur
commonly in patients undergoing non-cardiovascular procedures including surgeries. It is thus pertinent
that the physician handling such cases must be appropriately trained to diagnose and provide emergency
management till the case is referred to a specialist. Most cases present as narrow or a wide complex
tachycardia. The differential diagnosis is arrived at by deciding on the ECG morphology alongwith relevant
history and physical examination where feasible. This article describes the bedside approach to diagnose
and treat an arrhythmia presenting as a narrow complex.

INTRODUCTION

ardiac tachyarrhythmias often present as urgent medical

conditions requiring immediate care. With any type
tachycardia, the first step is the assessment of the vital signs,
to differentiate between tachycardias with or without
hemodynamic instability. The arrhythmia may be the primary
cause of hemodynamic instability, or a concomitant symptom
of another serious condition. In this series of a two part article
we shall take a panoramic view of recognizing and treating
arrhythmias that present with either a narrow complex ECG or
a wide complex tachycardias (WCT) in an emergency setting.
This differentiation of WCT (QRS duration 120 msec) and
narrow (QRS duration <120 msec) is practical and easily
determined even in an emergency setting where time is an
important constraint to make a diagnosis and apply
appropriate therapy.
In the case of hemodynamic instability at presentation, or
at any time during the treatment of cardiac tachyarrhythmias,
electrical cardioversion should be immediately considered as
a life-saving measure. Cardioversion is a safe and effective
therapy for almost all tachyarrhythmias. History taking and a
comprehensive physical examination is important but can be
done later after the patient stabilizes. If the patient does not
require immediate cardioversion, a thorough physical
examination along with relevant history-taking is mandated
alongwith a 12-lead ECG. The ECG interpretation should
always be made in the light of history and physical
Cardiac Arrhythmia Service, Division of Cardiology, Massachusetts
General Hospital, Harvard Medical School, Harvard University, 55
Fruit Street, GRB 109, Boston, MA, USA 02114.
Received : 1.4.2004; Accepted : 28.8.2004

816

examination. In the haste to treat the arrhythmia itself,

concomitant treatment of the underlying cause and
precipitating factors, as well as supportive care should not
be delayed. Pharmacological antiarrhythmic therapy can be
considered if the patient is hemodynamically stable, and/or
electrical cardioversion is not feasible, desirable or successful.
To determine the appropriate therapy, the first step however
is to classify tachycardias as regular or irregular, narrow or
wide QRS complex; the latter may be monomorphic or
polymorphic.

NARROW QRS COMPLEX TACHYCARDIA

(NCT)
Once a NCT is identified the first step is to determine
whether the rhythm is regular or irregular. The differential
diagnosis of a NCT is given in Table 1.
Irregular narrow QRS complex tachycardia
The commonest arrhythmia in clinical practice with this
Table 1: Differential diagnosis of narrow complex
tachycardia
Narrow complex tachycardia
Irregular

Regular

Atrial fibrillation

AVNRT

Atrial flutter
with variable
block
MAT

AVRT

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Atrial tachycardia/
flutter

JAPI VOL. 52 OCTOBER 2004

type of ECG is atrial fibrillation.

ATRIAL FIBRILLATION
Atrial fibrillation is the most common sustained arrhythmia
encountered in clinical practice. Approximately 0.4 percent
of persons in the general population have permanent or
intermittent atrial fibrillation, and the prevalence of the
arrhythmia increases to 6 percent in persons older than 80
years.1 Atrial fibrillation can result in serious complications,
including congestive heart failure, myocardial infarction, and
thromboembolism. Considerable evidence has accumulated
that atrial fibrillation occurring in a background of rheumatic
heart disease, as is rampant in India, is decidedly associated
with increased risk of stroke. In the Framingham Heart Study,
patients with rheumatic heart disease and AF had a 17-fold
increased risk of stroke compared with age matched controls,
and the attributable risk was five times greater than in those
with nonrheumatic AF.2 In recent years, management strategies
for atrial fibrillation have expanded significantly, and new
drugs for ventricular rate control and rhythm conversion have
been introduced.3 Physicians, handling such cases in the
emergency room thus have the challenge of keeping current
with recommendations on heart rate control, antiarrhythmic
drug therapy, cardioversion, and relevant antithrombotic
therapy.
Diagnosis
The diagnosis of atrial fibrillation should be considered in
patients who present with complaints of shortness of breath,
dizziness, or palpitations. The arrhythmia should also be
suspected in patients with acute fatigue or exacerbation of
congestive heart failure.4 In some patients, atrial fibrillation
may be identified on the basis of an irregularly irregular pulse
or an electrocardiogram (ECG) obtained for the evaluation of
another condition. Cardiac conditions commonly associated
with the development of atrial fibrillation include rheumatic
mitral valve disease, coronary artery disease, congestive heart
failure, and hypertension. Noncardiac conditions that can
predispose patients to develop atrial fibrillation include
hyperthyroidism, hypoxia, alcohol intoxication, and surgery.4
The ECG is the mainstay for diagnosis of atrial fibrillation
(Fig. 1). An irregularly irregular rhythm, inconsistent R-R
interval, and absence of P waves are usually noted on the
cardiac monitor or ECG. Atrial fibrillation waves (f waves),
which are small, irregular waves seen as a rapid-cycle baseline
fluctuation, indicate rapid atrial activity (usually between 450
and 600 beats per minute) and are the hallmark of the
arrhythmia, although they may not always be visible on a

Fig: 1 : ECG showing Atrial fibrillation. Note varying RR intervals. No

discrete P waves are seen. Undulating baseline is due to fibrillatory f
waves
JAPI VOL. 52 OCTOBER 2004

surface ECG. Atrial fibrillation should also be distinguished

from atrial tachycardia with variable atrioventricular block,
which usually presents with an atrial rate of 120-200 beats per
minute. In this condition, the atrial rate is regular (unlike the
irregular disorganized f waves of atrial fibrillation), but
conduction to the ventricles is irregular. The resultant
irregularly irregular ventricular rhythm may be difficult to
differentiate from atrial fibrillation. However for emergency
practice it is useful to consider any irregularly irregular
tachycardia with no clear p waves seen as atrial fibrillation
unless proven otherwise.
Treatment
Ventricular rate control
Ventricular rate control may be the only therapy needed if
electrical or pharmacological cardioversion is not planned.
However, in patients with recent onset atrial fibrillation (24h),
intravenous rate control with a beta-blocker or a calcium
antagonist, followed by pharmacological cardioversion is a
reasonable strategy. This protocol has two predominant
advantages; it will decrease the risk of 1:1 conducted atrial
flutter induced by class 1C drugs (such as flecainide) if used.
Second, it will result in immediate symptom relief until
cardioversion takes place.
Intravenous beta-blocker (metoprolol, propranolol, esmolol
or other agents), or calcium-blocker (verapamil, diltiazem)
therapies have both been shown in randomized controlled
trials to be effective in ventricular rate control in patient with
preserved left ventricular function, with a rapid onset of
action. However, beta-blockers and calcium antagonists
should be used with caution in patients with CHF. A small
study suggested that intravenous diltiazem is safe in patients
with moderate to severe CHF. Verapamil should not be used
in patients with left ventricular dysfunction given its negative
inotropic effect.1 Table 2 summarizes the drugs used for rate
control.
Digoxin has been used for many years for the treatment of
recent onset atrial fibrillation. However, neither oral, nor
intravenous digoxin is more effective than placebo for the
restoration of sinus rhythm and it may even prolong the
duration of atrial fibrillation. 1,5 Although digoxin may reduce
the resting ventricular rate, its efficacy is reduced in
conditions with high sympathetic tone, and its onset of
therapeutic effect only begins at 60 minutes, peaking at 6
hours. Digoxin can be a useful addition to beta blockade or
calcium channel blockade for the treatment of atrial fibrillation
with rapid ventricular response, especially in the setting of
atrial fibrillation associated with congestive heart failure.
Intravenous amiodarone is also effective in ventricular
rate control; however, it may lead to cardioversion and
therefore the risk of thromboembolism should be considered
before its application. A recent randomized trial compared iv.
amiodarone with diltiazem in critically ill patients.6 Amiodarone
and diltiazem were both effective in achieving rate control at
4 hours; diltiazem caused hypotension more frequently. Thus,
amiodarone may be especially useful in patients with left

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<48hrs = cardioversion no anticoag

>48hrs/unknown = 3/52 anticoag or TOE

ventricular dysfunction.
Pharmacological cardioversion
Patients with atrial fibrillation or flutter that is clearly of no
more than 48 hours duration may be cardioverted electrically
or pharmacologically without anticoagulation with minimal
risk of stroke. If the duration of arrhythmia is more than 48
hours, or unknown, cardioversion should only be attempted
after three weeks of therapeutic anticoagulation, or after
performing a transesophageal echocardiogram (TEE), to
exclude the presence of atrial thrombi, and with concomitant
heparin therapy.1 Whether pre-procedural anticoagulation or
Table 2 : Drugs used for rate control.(Source: Basu Ray I.
Keeping up pace, atrial fibrillation in clinical practice.
Perspectives in Cardiology 2003;19;5: 33-43 with
permission.)
Drug

Initial dose

Maintenance dose

Notes

Diltiazem

15-20 mg IV
over 2 min.;
may repeat in
15 min.
5-10 mg IV
over 2 min;
may repeat in
30 min.
Bolus of 500
mcg/kg over
1 min; may
repeat in
5 min
1 mg IV over
2 min; may
repeat every
5 min to max
of 5 mg
0.25-0.5 mg
IV; then 0.25
mg IV every
4-6 hr to max
of 1 mg

5-15 mg/hr, by
continuous IV

Convenient, easy
to titrate to HR
goal

Verapamil

do not use
for CHF
Esmolol

Propranolol

Digoxin

AF+CHF

Not standardised

More myocardial
depression
and hypotension
than diltiazem
50-300mcg/kg/
Very shortmin by continuous acting, easy to
IV
titrate to HR
goal
1-3 mg IV
every hr

Short duration
of action so need
repeat dosing

0.125-0.25
mg/day IV
or orally

Adjunct therapy;
less effective for
rate control than
beta blockers or
calcium channel
blockers

IV - Intravenous; HR - Heart rate

TEE is utilized, therapeutic anticoagulation should be

continued for at least 4 weeks post-cardioversion for patients
in atrial fibrillation for >48 hours pre-cardioversion.
The success of pharmacological cardioversion is strongly
dependent on the duration of atrial fibrillation, with higher
success for shorter duration episodes and very low success
rates in chronic atrial fibrillation. Importantly, in recent onset
(<24 h) atrial fibrillation, the spontaneous cardioversion rates
are also very high, approaching 50-70% at 24 hours.7 A
description of the different drugs that can be used for medical
cardioversion is provided below (Table 3).
Propafenone
Propafenone is a Vaughan-Williams classification 1C agent
(pure Na channel blocker), available intravenously in some
countries. Intravenous propafenone was effective in the
cardioversion of recent onset (<48 h) atrial fibrillation in
randomized, placebo controlled trials, with a conversion rate
of 76.1% at 24 hours.8 A recent meta-analysis of a single dose
of oral propafenone for conversion of recent onset atrial
fibrillation also showed a high conversion rate, 72-78% within
8 hours.9 In this meta-analysis, the incidence of 1:1 conduction
atrial flutter as an adverse effect was only 0.3%. These data
further support the efficacy of oral and intravenous
propafenone in the treatment of recent onset (<48 h) atrial
fibrillation without structural heart disease.
Propafenone should be avoided in patients with CAD or
left ventricular systolic dysfunction.1,2 It has limited efficacy
for cardioversion in persistent (longer than 48 hours duration)
atrial fibrillation and in atrial flutter.1
Flecainide
Flecainide is also a drug with class IC mechanism of action.
A recent randomized study compared the efficacy of
intravenous and oral flecainide in recent onset (48 hours)
atrial fibrillation. Intravenous flecainide restored sinus rhythm
more rapidly than oral; however, at 8 hours 75% of the oral
and 72% of the intravenous flecainide group had converted.10
A recent metaanalysis showed that oral single dose flecainide

Table 3: Drugs, doses & adverse effects of pharmaceuticals used in medical conversion of atrial fibrillation. (Source:
Basu Ray I. Keeping up pace, atrial fibrillation in clinical practice. Perspectives in cardiology 2003;19;5: 33-43 with
permission.)
Drug

Intravenous

Oral

Adverse effects

Amiodarone

5 to 7 mg/Kg over 30 to 60 min,

then 1.2- 1.8 g/day continuous IV
up to 10 g in divided doses.
Maintenance of 200-400 mg/day

Inpatients: 1-2-1.8 mg/day up to

10 g in divided doses.
Maintenance of 200-400 mg/day.
Outpatients: 600 mg - 800 mg/day
up to 10 g in divided doses.
Maintenance of 200-400 mg/day
The dose is based on creatine clearance:
60 mL/min : 500 mcg bid
40-80 mL/min : 250 mcg bid
20-40 mL/min : 125 mcg bid
> 20 mL/min : contraindicated
200-300 mg

Hypertension, bradycardia, QT
prolongation. Torsade de pointes,
phlebitis (when given intravenously)

450-600 mg

Hypotension, rapidly-conducting atrial flutter

AF+LVdf

Dofetilide

Flecainide
Ibutilide
Propafenone

818

1 mg given slowly by IV over

10 min. Repeat 1 mg if required

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QT prolongation, Torsade de pointes

Hypotension, rapidly-conducting atrial flutter

QT prolongation, Torsade de pointes

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converted recent onset atrial fibrillation in 75-91% of the

patients at 8 hours, and it was significantly more efficacious
than placebo, and at least as efficacious as oral propafenone.11
Similar to propafenone, flecainide also can cause
proarrhythmia in the form of atrial flutter with 1:1 conduction,
or bradycardia after conversion to sinus rhythm. It should
also be avoided in patients with structural heart disease, and
it has limited efficacy in patients with atrial flutter.1
Amiodarone
Amiodarone has been utilized both for recent onset and
persistent atrial fibrillation/flutter. It can be administered in
the form of single intravenous bolus, bolus followed by
infusion, iv bolus followed by oral doses and single or divided
high oral doses for the purpose of rate control or
pharmacological cardioversion. The different dosing regimens
and clinical settings make comparison of these studies
difficult.
A recent randomized study compared intravenous
flecainide, propafenone, and amiodarone (5mg/kg, followed
by 50 mg/h) in recent onset (<48 hours) atrial fibrillation. The
conversion rates at 12 hours were 90%, 72%, 64% in the
flecainide, propafenone and amiodarone group, respectively.
The conversion rates in the propafenone and amiodarone
groups did not differ significantly (p=0.39), but flecainide
was significantly more effective than propafenone (p=0.022),
or amiodarone (p=0.002). However the conversion rates at 24
hours of study drug administration was not reported, and
there was no placebo group in this study.12
A recent meta-analysis showed that the conversion rates
of recent onset atrial fibrillation with bolus amiodarone vary
from 34-69%. Conversion rates are increased to 55-95% with
the bolus followed by infusion administration.13 Another
meta-analysis showed an average 76% conversion rate for iv.
amiodarone, 72% for other anti-arrhythmics and 60% for
placebo, respectively.14 Another recent meta-analysis of
studies of amiodarone versus placebo and IC agents was
reported.15 The 24 hour conversion rates were 82% and 56%,
for amiodarone and placebo, respectively and 66%, and 71%
for amiodarone and IC agents, respectively.
Similar to other drugs, the conversion rate with amiodarone
in patients with atrial fibrillation of longer than 7 days duration
is low,1 and its efficacy in conversion of atrial flutter is not
well established. Amiodarone can be safely used in patients
with left ventricular dysfunction and coronary artery disease.1
A reasonable strategy is to use amiodarone if rapid
conversion is not desired or necessary, especially in patients
with underlying heart disease or heart failure who require
hospital admission. In general, amiodarone is somewhat less
effective than the other agents described here at conversion
of atrial fibrillation to sinus rhythm, but is among the most
effective agents for maintenance of sinus rhythm after
cardioversion. Long term use of amiodarone is often limited
by toxicity to the thyroid, lungs and other tissues.
Ibutilide
Ibutilide is a class III antiarrhythmic agent, only available
JAPI VOL. 52 OCTOBER 2004

intravenously. It blocks the rapid component of the delayed

rectifier potassium channel (Ikr), and augments plateau
sodium current,16 thereby markedly increasing the QT interval.
In randomized trials it was effective in conversion of atrial
fibrillation and flutter of more than 7 days (3h-90 days)
duration, with conversion rates of 34.9% to 47%.17-19 The
conversion rates for atrial flutter were much higher than for
atrial fibrillation. The highest conversion rates were achieved
with short arrhythmia duration (<30 days). The incidence of
proarrhythmia due to torsades de pointes VT was 4.3%,
including 1.7% being sustained.19 In another recent trial,
ibutilide pretreatment also increased the success rate of
electrical cardioversion in persistent (mean 117 days) atrial
fibrillation.20 Sustained polymorphic tachycardia occurred in
3% of the patients, in the setting of EF<20%.
In a recent observational study, intravenous ibutilide was
administered to patients treated with long term oral amiodarone
therapy and persistent atrial fibrillation or flutter; 39 % of the
patients with atrial fibrillation and 54% of those with flutter
converted; the incidence of torsade was 1.4%.21 It should be
noted that due to the pro-arrhythmic risk of ibutilide, patient
monitoring with QT analysis must be performed for at least 6
hours post-administration of the agent.
Dofetilide
Dofetilide is a pure class III antiarrhythmic drug22 with QT
effects similar to ibutilide Randomized clinical trials of
intravenous dofetilide in patients with atrial fibrillation/flutter
of up to 6 months duration, showed conversion rates of 3038%.23-26 The conversion rates were significantly higher with
patients with atrial flutter (54-70%), and atrial fibrillation with
less than 24 hours duration (67%). The incidence of torsade
was 3-8%. The intravenous form of dofetilide is currently
only investigational.
Oral dofetilide was tested in two similar, randomized,
controlled multicenter trials, the EMERALD and SAFIRE-D
study.27,28 In these studies, patients with atrial fibrillation/
flutter from 1 week to 2 years duration were involved. The
conversion rates at 3 days were highest in the dofetilide 500
mcg bid treatment arms, 29% and 29.9%. The incidence of
torsades VT was 0.8%, and one sudden cardiac death occurred
(0.4%).
Dofetilide is thus effective in the conversion of atrial flutter,
and moderately effective in the conversion of atrial fibrillation
of longer duration, with a moderate risk of proarrhythmia; it
has a delayed onset of action, and requires in-hospital
initiation of therapy with QT monitoring.

OTHER IRREGULAR ARRHYTHMIAS

Multifocal atrial tachycardia (MAT) and atrial flutter with
variable AV block can produce irregularly irregular rhythm
which may be mistaken for atrial fibrillation.
MAT is a form of atrial tachycardia with at least three p
wave morphologies and often occurs in the setting of severe
metabolic disease. It can be treated by rate control with beta
blockers or calcium channel blockers to slow AV nodal

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conduction. It is not typically responsive to electrical

cardioversion, but does respond to treatment of the
underlying illness.
Atrial flutter may present either with a consistent A:V
relationship, producing a regular ventricular rhythm, or with
a variable A:V relationship, producing an irregular ventricular
rhythm. The diagnosis and treatment of atrial flutter is
discussed below.

ATRIAL FLUTTER
Classical atrial flutter is caused by a re-entrant circuit
confined to the right atrium in which the impulse travels up
the atrial septum, with epicardial breakthrough superiorly in
the right atrium where the impulse then travels inferiorly down
the right atrial free-wall to re-enter the atrial septum. When
the circulating wave-front re-enters the atrial septum, it travels
through an isthmus bounded by the inferior vena cava,
Eustachian ridge, the coronary sinus os on one side and the
tricuspid valve annulus on the other side (the cavo-tricuspid
isthmus).
Atrial flutter by this circuit is called typical atrial flutter,
although it also has been called common atrial flutter and
counterclockwise atrial flutter. A 12-lead ECG during typical
atrial flutter with characteristic negative sawtooth atrial
flutter waves in leads II, III, and aVF and upright flutter waves
in V1 as shown in Fig. 2. It is also recognized that impulses
can travel in this re-entrant circuit in the opposite direction,
so that the impulse travels down the atrial septum and breaks
through to the epicardium via the same atrial flutter isthmus
to travel up the right atrial free-wall and then re-enter the
septum superiorly. This form of atrial flutter is called reverse
typical atrial flutter, although it has in the past been called
atypical atrial flutter, clockwise atrial flutter, uncommon atrial
flutter, and rare atrial flutter. A 12-lead ECG during reverse
typical atrial flutter is with characteristic positive flutter waves
in leads II, III, and aVF. Other atrial flutter circuits have been
described originating in both the left and right atrium, often

Fig. 2 : Atrial flutter- The sawtooth waveform of atrial flutter can

usually be seen in the inferior leads II, III and aVF if one looks closely.
Sometimes the rapid atrial rate can be seen in V1. Suspect atrial
flutter with 2:1 block when you see a rate of about 150 bpm. The
atrial rate is shown to be twice the ventricular rate in the figure below.
Thus there is a 2:1 AV block. So a 300 bpm atrial rate produces half
the ventricular rate. The sawtooth waves are negative in the inferior
leads thus this is a case of typical counterclockwise flutter.
820

in patients with atrial scar related to prior surgical procedures.

These are characterized by regular flutter waves with a rate
typically between 250-350 bpm and a morphology determined
by the flutter circuit. In the ER, these can be treated in the
same way as typical atrial flutter.
Atrial flutter generally presents as narrow complex
tachycardia with a sawtooth baseline. Flutter with 2:1 A:V
conduction is common, and so atrial flutter should be
considered for any arrhythmia with narrow complexes at the
rate of 150 beats per minute. Although atrial flutter can present
with nearly any ventricular rate, 1:1 A:V conduction with
ventricular rates of up to and above 300 bpm is occasionally
encountered in the ER (either with a narrow QRS or with
aberrant conduction producing a wide QRS). This constitutes
a true medical emergency and rapid treatment with IV AV
nodal blocking agents or electrical cardioversion is generally
indicated.
Treatment
Atrial flutter is treated much like atrial fibrillation. The
mainstays of treatment include ventricular rate control and
anti-coagulation for stroke prevention. Rate and rhythm
control can be generally achieved with the same agents used
for atrial fibrillation. Electrical cardioversion is usually effective
in the acute conversion of atrial flutter although recurrence is
common. Catheter ablation is the only curative treatment for
this disorder

PSVT
Paroxysmal supraventricular tachycardia (PSVT) is a
common group of arrhythmias that present with NCT. PSVT
in the absence of structural heart disease can present at any
age but most commonly first presents between ages 12 and
30. Most patients with PSVT due to atrioventricular nodal
reentrant tachycardia (AVNRT) or atrioventricular reentrant
tachycardia (AVRT) do not have associated structural heart
disease, although exceptions (e.g., Epsteins anomaly, familial
preexcitation) do exist. Atrial tachycardias are another cause
of PSVT and are often associated with structural heart disease.
In patients without structural heart disease, the physical exam
during PSVT is significant mainly for rapid heart rate although
occasionally PSVT with very rapid ventricular rate can cause
hemodynamic instability leading to pre-syncope or syncope.
History, physical exam, and an ECG constitute an appropriate
initial evaluation. A 12-lead ECG during tachycardia is helpful
for defining the mechanism of PSVT. Patients with panic
disorder report symptoms similar to those of PSVT, and an
ECG during palpitations shows mostly sinus tachycardia thus
aiding in diagnosis.
PSVT? But what is the mechanism?
An ECG showing PSVT, but with a stable hemodynamics
should be approached by asking the question-what is the
mechanism of this arrhythmia? To answer the above question
one must examine the P waves. The different forms of PSVT
are illustrated in Fig. 3. The P-wave position relative to the
QRS complex during AVNRT depends on the types of

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JAPI VOL. 52 OCTOBER 2004

Fig. 4 : Typical AVNRT. Note narrow QRS complex tachycardia with no

p waves seen as ventricular and atrial contraction takes place almost
simultaneously thus hiding p waves within QRS.

Fig 3: PSVT: Mechanisms, typical ECG findings, and recommended

therapies. In typical AV nodal reentrant tachycardia (antegrade
conduction down the slow AV nodal pathway and retrograde
conduction up the fast pathway), the retrograde P wave may not be
seen or may be visible early after the QRS complex. When visible, it
often appears as a pseudo-R in lead V1. In AV reentrant tachycardia,
there is typically a short RP interval with the timing and morphology of
the P-wave dependent on the site and conduction velocity of the
accessory pathway. Atrial tachycardia typically produces variable RP
and PR intervals as AV conduction depends on AV nodal properties
and the tachycardia rate. In atrial tachycardia, the morphology and
axis of the P wave are influenced by atrial site of origin and
tachycardia mechanism. Acute and chronic therapies are discussed in
the text. P indicates P wave; AAD, antiarrhythmic drug.( adapted and
modified from Ferguson JD, DiMarco JP: Contemporary management
of paroxysmal supraventricular tachycardia. Circulation
2003;107:1096-9 with permission.)

pathways used. In typical, slow pathway-antegrade, fast

pathway-retrograde AVNRT, the P wave is either not seen or
is visible in the terminal portion of the QRS (especially in lead
V1). If two slow pathways or a fast antegrade pathway and a
slow retrograde pathway are used, the RP interval will be
longer than in typical AVNRT. Although uncommon, AV block
is possible during AVNRT, usually in either the distal AV
node or the bundle of His, which can lead to periods of
irregularity during AVNRT.
In AVRT, an extranodal accessory pathway connects the
atrium and ventricle. Accessory pathways may exhibit both
antegrade and retrograde conduction, or either only antegrade
(rare) or retrograde (concealed pathways) conduction. When
the pathway manifests antegrade conduction, a delta wave
may be present on the surface ECG, and a diagnosis of WolfParkinson-White syndrome is made if the patient also has
PSVT. Accessory pathways usually exhibit rapid, nondecremental conduction, but a minority of them may manifest
slow, decremental conduction. The most common form,
orthodromic AVRT, uses the accessory pathway as the
retrograde limb and the AV node-His as the antegrade limb,
which results in a narrow QRS. Functional or fixed bundle
branch block, a reversal of the circuit (antidromic AVRT), or
the presence of two accessory pathways can lead to a wide
QRS complex during AVRT. Accessory pathways can also
conduct as passive bystanders during AVNRT or atrial
tachycardias. In AVRT, the ventricle is an obligate part of the
circuit, and thus there is always a 1:1 A:V relationship.
JAPI VOL. 52 OCTOBER 2004

Atrial tachycardia is the least common form of PSVT in

normal individuals but predominates in patients with
significant atrial scarring, especially from prior atrial surgery.
Atrial tachycardias may be caused by enhanced or triggered
automaticity or by reentry. Because the AV node and ventricle
are not required participants in the arrhythmia, AV block
commonly occurs. The PR or apparent RP intervals depend
on AV conduction properties. P-wave morphology depends
on the site of origin in the atrium.
We shall now discuss each forms of PSVT in detail to
understand their characteristics which will help in recognizing
them when they present to the emergency room.
AV nodal re-entrant tachycardia (AVNRT)
AVNRT is a common arrhythmia which occurs in patients
with two functionally distinct conduction pathways through
the atrioventricular node, typically fast and slow pathways.
The slow pathway usually has a shorter refractory period
than the fast pathway. Both the fast and slow pathways are
necessary to maintain AVNRT. The common form of AVNRT
is typically initiated when an atrial premature beat blocks in
the fast pathway, conducts down the slow pathway, and
returns retrograde via the fast pathway to depolarize the
atrium, thus creating a re-entrant circuit in the AV node. During
the uncommon form of AVNRT the wave front propagates in
the opposite direction, conducting down the fast pathway
and returning via the slow pathway. The fast pathway is
located anteriorly along the septal portion of the tricuspid
annulus, near the compact atrioventricular node, whereas
the atrial insertion of the slow pathway is located more
posteriorly along the tricuspid annulus, closer to the coronary
sinus os.
ECG
Rate is in the range 120-250 beats/minute (commonly 170200). It presents as a NCT with no visible p waves. (Fig. 4).
Characteristics
It starts abruptly due to an atrial premature beat (APB)
and ends abruptly. The APB that initiates the tachycardia
generally is conducted with a prolonged PR interval.
Carotid massage can either slow or terminate the
tachycardia.
P waves are generally not seen. They are buried in the
QRS complex and are thus not seen in the most common form
of this tachycardia, i.e., the slow -fast variety, occurring in
66% cases. However, if the tachycardia occurs through the

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fast-slow pathway, then retrograde p waves may be visible

after the QRS complex due to slow conduction over the
retrograde pathway. It must be remembered that both the fast
and slow pathways are within the AV node.
Clinical features
AVNRT is typically found in patients with no structural
heart disease.
It may produce symptoms like palpitations, polyuria, etc.
It can also produce angina, syncope, heart failure or even
shock.
Tachycardia, typically with a regular pulse.
S1 is of constant intensity.
Prominent jugular venous pulsations due to atrial
contraction against closed AV valves may be a clue to AVNRT.
Treatment
Because PSVT will rarely be so poorly tolerated that it
requires immediate termination with electrical cardioversion,
most patients can be managed with physiological maneuvers
or drugs.
Many patients learn to terminate acute episodes of PSVT
by using vagal maneuvers early during an episode of PSVT.
Valsalva is the most effective technique in adults, but carotid
massage may also be effective.29 Facial immersion is the most
reliable method in infants. Vagal maneuvers are less effective
once a sympathetic response to PSVT has become established,
so patients should be advised to try them soon after the
onset.
Adenosine and the non-dihydropyridine calcium
antagonists verapamil and diltiazem are the intravenous (IV)
drugs of choice for termination of PSVT.29 Adenosine is an
endogenous purine nucleoside that slows AV nodal
conduction and results in transient AV nodal block.
Conduction in rapidly conducting accessory pathways is
usually not affected, but decremental pathways may exhibit
block. Exogenous adenosine is cleared extremely rapidly from
the circulation by cellular uptake and metabolism, with an
estimated half-life of <5 seconds.30 Adenosine effect is
typically seen 5 to 30 seconds after rapid peripheral infusion
as a first-pass effect. Administration via a central line requires
dose reduction; 3 mg would be the appropriate initial dose.
The effective dose range for peripheral administration in adults
is 2.5 to 25 mg. If no upper dosage limit is imposed, at least
transient termination of AV node-dependent PSVT can be
produced in all patients. The recommended adult dosage for
peripheral infusion is 6 mg, followed by a 12 mg dose and
then an 18 mg dose if needed. In pediatric patients, the dose
range is 50 to 250 g/kg administered via an upward dose
titration. Because of the ultrashort duration of action,
cumulative effects of sequential doses are not seen.
Minor side effects, including transient dyspnea or chest
pain, are common with adenosine. Sinus arrest or bradycardia
may occur but typically will resolve quickly if appropriate
upward dosing is used. With PSVT termination, atrial and
ventricular premature beats are frequently seen, and a few
822

patients with adenosine-induced polymorphic ventricular

tachycardia have been reported.29 These patients had long
baseline QT intervals and long pauses during adenosineinduced AV block. Adenosine shortens the atrial refractory
period, and atrial ectopy may induce atrial fibrillation. This
may be dangerous if the patient has an accessory pathway
capable of rapid antegrade conduction. Because adenosine
is cleared so rapidly, re-initiation of PSVT after initial
termination may occur. Either repeat administration of the
same dose of adenosine or substitution of a calcium channel
blocker will often be effective in this situation.
Adenosine mediates its effects via a specific cell surface
receptor, the A1 receptor. Theophylline and other
methylxanthines block the A1 receptor. Caffeine levels
achieved after beverage ingestion may be overcome by the
doses of adenosine used to treat PSVT. Dipyridamole blocks
adenosine elimination, thereby potentiating and prolonging
its effects. Cardiac transplant recipients are also unusually
sensitive to adenosine. If adenosine is chosen in these latter
situations, much lower starting doses (i.e., 1 mg) should be
selected.
The AV node action potential is calcium channeldependent, and the non-dihydropyridine calcium channel
blockers verapamil and diltiazem are very effective for
terminating AV node-dependent PSVT.31,32 The recommended
dosage of verapamil is 5 mg IV over 2 minutes, followed in 5
to 10 minutes by a second 5 to 7.5 mg dose. The recommended
dosage of diltiazem is 20 mg followed, if necessary, by a second
dose of 25 to 35 mg. PSVT termination should occur within 5
minutes of the end of the infusion, and over 90% of patients
with AV node-dependent PSVT respond.
As with adenosine, transient arrhythmias, including atrial
and ventricular ectopy, atrial fibrillation, and bradycardia, may
be seen after PSVT termination with calcium channel blockers.
Hypotension may occur with calcium channel blockers,
particularly if the PSVT does not terminate. Calcium channel
blockers are not recommended in infants and neonates with
PSVT because of reports of cardiovascular collapse.33
Adenosine and verapamil have been shown to have
equivalent efficacy in several randomized clinical trials.29, 30,34
Most PSVT patients can be acutely managed with either agent.
To minimize the potential for adverse effects, adenosine
should be selected in patients with severe hypotension or
heart failure, in infants and neonates, and in those at risk for
severe bradycardia. Verapamil and diltiazem should be chosen
for patients with poor venous access, patients with
bronchospasm, and those taking agents that interfere with
adenosine action or metabolism.
It should be noted that while pharmacological therapy
can be useful for acute control of symptoms of PSVT and
chronic arrhythmia suppression, catheter ablation is the only
curative therapy for recurrent arrhythmia.
Atrioventricular reentrant tachycardia (AVRT)
AVRT can present as a narrow complex tachycardia
(orthodromic AVRT) or as a wide complex tachycardia

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JAPI VOL. 52 OCTOBER 2004

Atrial tachycardias

Fig. 5 : A. 12-lead ECG during tachycardia in a patient with WPW

syndrome. Note the NCT. B. Same patient in sinus rhythm. Note the
delta waves.

(antidromic AVRT or orthodromic AVRT with aberrant

ventricular conduction). The position of p waves helps to
differentiate AVRT from AVNRT. In typical AVNRT, no p waves
are seen as they are tucked inside the QRS; at times they also
may be found in the terminal part of the QRS producing a
pseudo S in lead III and a pseudo R in V1. In cases of
atypical AVNRT, p waves can be seen with a long R-P interval
which can be difficult to distinguish from AVRT
In case of AVRT the RP interval is generally at least 100
msec.
It is important in emergency room practice to identify
patients with anterograde accessory pathway conduction
(typically visualized by a delta wave) (Fig. 5) as use of
adenosine or calcium channel blockers can paradoxically
increase conduction through the accessory pathway (which
has faster conducting properties than the normal AV node in
which conduction remains blocked due to adenosine)
resulting in dangerous or fatal arrhythmias. Although AV
nodal blocking agents can be effective in terminating both
AVNRT and AVRT, these drugs can prove dangerous in
patients with anterograde conduction through an accessory
pathway who develop rapid atrial rhythms (typically atrial
fibrillation or atrial flutter). These atrial rhythms may be
conducted to the ventricles at extremely rapid rates via the
accessory pathway in the presence of these agents,
potentially leading to hemodynamic decompensation or
ventricular fibrillation. In patients with manifest accessory
pathways as identified by a delta wave, Class IA or IC agents
will generally inhibit accessory pathway conduction, and so
are safer in these patients, either when used alone or in
combination with AV nodal blocking agents. As these preexcited tachycardias produce a wide QRS complex, they will
be discussed in greater detail in the chapter on wide complex
tachycardias.
JAPI VOL. 52 OCTOBER 2004

These include different forms of tachycardia occurring

due to automatic foci or reentry in the atrium. P-wave
morphology depends on the site of origin in the atrium. If the
site of origin is within or involves the sinus node region,
sinus node reentrant or inappropriate sinus tachycardia is
identified. Left atrial tachycardia can be identified by positive
p wave morphology in lead V1 and a negative or biphasic p in
aVL (although AVRT via a left-sided accessory pathway,
producing retrograde P waves originating in the left atrium
must also be considered). Frequently there is AV block evident
in cases of atrial tachycardia and thus more P waves are seen
than QRS complexes, thus simplifying diagnosis.
Treatment
Limited data are available on acute pharmacological
therapy of atrial tachycardias. Automatic or triggered
tachycardias and sinus node reentry may respond to
adenosine, verapamil, diltiazem, or -adrenergic blockers.
Other atrial tachycardias may respond to class I or class III
antiarrhythmic drugs given orally or parenterally.35 The
response of atrial tachycardia to electrical cardioversion is
variable. Typically re-entrant forms of atrial tachycardia will
terminate with electrical cardioversion (although they may
recur), while automatic forms generally will not terminate with
cardioversion. It is often difficult to determine whether a
particular atrial tachycardia is re-entrant or automatic in origin
before initiating therapy. In the majority of cases, AV nodal
blocking agents (beta blockers and calcium channel blockers)
will slow the ventricular rate of patients presenting with atrial
tachycardia and rapid ventricular rates. Anti-arrhythmic drugs
including Type I and Type III agents and amiodarone can be
effective in suppressing atrial tachycardias when other
therapies are ineffective, and catheter ablation can prove
curative for refractory cases.

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