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Diagnostics

Atrial fibrillation in the Wolff-Parkinson-White syndrome:

ECG recognition and treatment in the ED

Brian T. Fengler MD, William J. Brady MD, Claire U. Plautz MD*

Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA

Received 27 September 2006; accepted 13 October 2006

Abstract Estimated to occur in 0.1% to 0.3% of the population, Wolff-Parkinson-White syndrome

(WPW) is a condition where atrial impulses bypass the atrioventricular node and activate the ventricular

myocardium directly via an accessory pathway. Clinical clues to the diagnosis include a young patient

with previous episodes of palpitations, rapid heart rate, or syncope. Although several different rhythm

presentations are possible, atrial fibrillation is a not infrequent dysrhythmia seen in the WPW patient.

Electrocardiographic features suggestive of WPW atrial fibrillation include irregularity of the rhythm; a

very rapid ventricular response; presence of a delta wave; and a wide, bizarre QRS complex. Stable

patients suspected of having this condition should not receive agents that predominantly block

atrioventricular conduction, but they may be treated with procainamide or ibutilide. If instability is

present, electrical cardioversion is required.

D 2007 Elsevier Inc. All rights reserved.

1. Introduction

In the Wolff-Parkinson-White syndrome (WPW), which

is estimated to occur in 0.1% to 0.3% of the population,

there is an accessory pathway (AP) by which atrial impulses

can bypass the atrioventricular (AV) node and activate the

ventricular myocardium directly. The electrocardiographic

triad for WPW includes a PR interval less then 0.12 seconds,

slurring and slow rise of the initial QRS complex (delta

wave), a widened QRS complex with a total duration greater

than 0.12 seconds, and secondary repolarization changesreflected as ST segment–T wave changes that are generally

directed o pposite the major delta wave and QRS complex

(Fig. 1A) [1]. For a diagnosis of WPW, these electrocar-

diographic findings must be noted within the setting of a

documented dysrhythmia.

These electrocardiogram (ECG) changes are easily

understood if considered from the perspective of WPW

pathophysiology (Fig. 1B). An impulse generated in the

atria conducts rapidly and nondecrementally down the AP.

This impulse reaches the ventricle and begins to depolarize

a portion of the ventricular myocardium before activation of

the His-Purkinje system by the AV node. This area of

ventricular myocardium, which depolarizes earlier than

anticipated, creates the delta wave that then fuses with the

QRS complex that is subsequently produced, resulting in a

minimally widened QRS complex.Accessory pathways likely form during embryologic

growth because of faulty development of the AV ring, with

strands of myocardium f ound within the normally insulating

fibrous AV annulus [2]. In most cases, the APs conduct

impulses in a nondecremental manner, meaning it does not

have the ability to reduce the number of impulses

transmitted to the ventricles over a unit time. In contrast,

conduction through the AV node is decremental and only

0735-6757/$ – see front matter D 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.ajem.2006.10.017

* Corresponding author.

E-mail address: [email protected] (C.U. Plautz).

American Journal of Emergency Medicine (2007) 25, 576–583

www.elsevier.com/locate/ajem

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allows a certain number of atrial impulses to pass to the

ventricles per period.

The electrophysiologic properties of APs vary tremen-

dously from one individual to another and appear to be

affected by age, autonomic stage, anatomic location, and

medication effect [3]. Accessory pathways can conduct

impulses anterograde, from atria to ventricle, or retrograde,

from ventricle to atria. Some APs may only be able toconduct impulses in a retrograde manner, meaning that they

will be silent on the sinus-rhythm ECG, with normal PR

interval, QRS length, and no delta wave, and only becoming

apparent during periods of reentrant tachycardia.

The most frequently encountered dysrhythmia in patients

with WPW is the AV reciprocating tachycardia, where a

reentry circuit develops between the atria, AV node,

ventricles, and AP. In patients with WPW, 90% of AV

reciprocating tachycardias are orthodromic (anterograde),

where the reentry circuit runs from the atria through the AV

node to the ventricles and is returned to the atria through the

AP, producing a narrow-complex tachycardia. In 10% of patients, the AV reciprocating tachycardia is antidromic

(retrograde), with the reentry circuit running from the atria

down the AP to the ventricles and retrograde through AV

node to the atria, resulting in a wide-complex tachycardia.

Atrial fibrillation (AF) is not uncommon in patients with

WPW, presenting with a wide-complex, irregular tachycar-

dia. Wolff-Parkinson-White syndrome AF is the focus of

this report, in which diagnosis and management issues

are reviewed.

2. Case presentation

A 42-year-old man with a history of panic disorder

presented to the emergency department (ED) complaining of

b palpitations Q for approximately 18 hours. He states that he

has had a long history of palpitations and panic attacks, but

none have lasted this long. He also complains of nausea and

bclammy Q hands but denies any chest pain or dyspnea. He

denies of having any history of coronary disease, and he

does not smoke or take any medications. On examination,

the patient was found to have an irregular pulse with a rate

approaching 200. The electrocardiographic rhythm strip

demonstrated a widened QRS complex, irregular tachycar-

dia (Fig. 2). Although he appeared uncomfortable, the patient was not in any respiratory distress, and the remainder

of his physical examination was within normal limits.

Fig. 1 Normal sinus rhythm in the WPW. A, The electrocardio-

graphic triad seen in the WPW patient: shortened PR interval, delta

wave, and widened QRS complex. B, Impulse conduction in a

patient in normal sinus rhythm in the WPW. Impulses are

generated in the sinoatrial node (SAN). These impulses have

2 potential pathways to the ventricles, the AV node (AVN), and the

AP. The large atrial arrow indicates those impulses that travel to the

ventricles via the AP, bypassing the AVN. The impulses that

traverse the AP arrive in the ventricular myocardium sooner than

anticipated (multiple small ventricular arrows), causing a portion of

the ventricles to depolarize markedly earlier than the remainder of

the ventricular myocardium (shaded area), which is manifested

on the ECG by the delta wave. The impulse then travels throughout

the ventricular myocardium via inefficient myocte-myocyte con-

duction. Simultaneously, the impulses that traversed the AVN

travel throughout the ventricle via the intraventricular conduction

system (dotted ventricular arrows). The final result, ventricular

depolarization, occurs less efficiently (and therefore less rapidly)

than if the event had been triggered via the AVN and His-Purkinje

system; this less-than-efficient depolarization is manifested on the

ECG by a minimally widened QRS complex.

Atrial fibrillation in the WPW 577

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A 12-lead ECG was performed (Fig. 3) and interpreted

by the emergency physician as AF with rapid ventricular rate, for which the patient was initially treated with

intravenous (IV) b-blocker (metoprolol 5 mg). The patient’s

heart rate subsequently increased to approximately

300 beats/min (Fig. 4). The patient remained hemodynam-

ically stable and continued to complain only of mild chest

discomfort from the palpitations. Intravenous procainamide

was started at this point, with subsequent conversion to

normal sinus rhythm. This ECG revealed a shortened PR

interval and prominent delta waves, which established the

diagnosis of WPW (Fig. 5).

The patient was subsequently transferred to a tertiary

care center, where electrophysiologic mapping revealed aleft lateral AP that was successfully ablated with radio-

frequency. Interestingly, the patient’s 3-year-old daughter

was recently diagnosed with b panic attacks Q 6 months

before this presentation; hence, further evaluation of the

child was planned.

3. Discussion

The most frequently encountered tachyarrythmia in

patients with WPW is AV reciprocating tachycardia, where

a reentry circuit develops between the atria, AV node,

ventricles, and AP. In patients with WPW, 90% of AVreciprocating tachycardias are orthodromic (anterograde),

where the reentry circuit runs from the atria through the AV

node to the ventricles and is returned to the atria through the

AP. The ECG during such an episode will show a narrow

complex tachycardia (as the ventricles are activated down

the normal His-Purkinje system) with rates of 160 to

220 beats/min and no delta wave. Occasionally, a P wave

may be seen after the QRS complex, which represents

retrograde activation of the atria.

In 10% of patients, the AV reciprocating tachycardia is

antidromic (retrograde), with the reentry circuit running from

the atria down the AP to the ventricles and retrograde throughAV node to the atria. In this situation, the ECG shows a rapid,

regular, wide-complex tachycardia that is indistinguishable

from monomorphic ventricular tachycardia.

Atrial fibr illation is not uncommon in patients with

WPW (Fig. 6) and has been noted to occur in 11.5% to 39%

[4]. This dysrhythmia is usually precipitated by an episode

of AV reentrant tachycardia, but they may also occur alone

[5]. Atrial fibrillation in the presence of WPW is potentially

dangerous in that a rapid ventricular response can be

generated from nondecremental conduction down the AP

and can degenerate into ventricular fibrillation. This

Fig. 2 Electrocardiographic rhythm strip demonstrating an irregular, wide QRS complex tachycardia.

Fig. 3 12-lead ECG in 42-year-old male demonstrating a rapid, irregular, wide QRS complex tachycardia. Note the significant variations in

both the RR intervals and QRS complexes. A delta wave is also seen in numerous complexes, particularly in leads V1 to V4. This ECG

demonstrates AF in WPW.

B.T. Fengler et al.578

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sequence is thought to be the most common cause of sudden

cardiac death in patients with WPW, occurring at a rate up to

0.6% per year [6,7]. The refractory period of the AP is an

important factor in determining the risk of ventricular

fibrillation during AF, with values below 250 milliseconds

identifying patients at particular risk [8]. Furthermore, short

R-R intervals between consecutive preexcited complexes

are associated with rapid ventricular rates that can degen-

erate into ventricular fibrillation [9]. The AP lacks the

feature of slow, decremental conduction that the AV node possesses; thus, the AP can conduct atrial beats at a rate that

can approach or exceed 300 beats/min. With ventricular

responses at or above 300 beats/min, the risk of ventricular

fibrillation is greatly increased for the reasons outlined

above [8].

The clinician should consider WPW AF in patients with

an irregular, wide QRS complex tachycardia. Important

clues that can suggest the diagnosis of WPW AF are the

irregularity of the rhythm, the rapid ventricular response

(much too rapid for conduction down the AV node), and the

wide, bizarre QRS complex, signifying conduction down

the aberrant pathway. Occasionally, a narrow QRS can beseen, representing conduction through the AV node.

Interpretation of the ECG should take place within the

context of the clinical presentation. Consideration of WPW

AF in a patient who presents with a wide-complex

tachycardia should be made when the patient is young in

age (age b50) with a previous history of palpitations, rapid

heart rate, or syncope—or documented history of WPW.

Rate and QRS complex duration independently are poor

discriminators between WPW AF and other dysrhythmias,

as the presence of these electrocardiographic characteristics

alone is not sufficient to diagnose WPW AF. The inclusionof bizarre QRS complex morphologies with significant beat-

to-beat variations in configur ation, however, is more

suggestive of WPW AF (Fig. 7). Combining the variables

of a rapid rate, widened QRS complex, and unusual/

changing QRS complex morphologies in a young patient

strongly suggest the diagnosis. The use of these same

electrocardiographic characteristics can also be made in the

older patient, although a certain degree of caution is advised

because of the increased presence of other dysrhythmias

such as supraventricular tachycardia with aberrant ventric-

ular conduction, monomorphic ventricular tachycardia, and

polymorphic ventricular tachycardia, including the torsadesde pointes subtype.

Fig. 4 Electrocardiographic rhythm strip demonstrating an increased rate of the irregular, wide QRS complex tachycardia after

metoprolol administration.

Fig. 5 Twelve-lead ECG after conversion to sinus rhythm. Note the shortened PR interval, delta wave, and minimally widened QRS

complex consistent with WPW syndrome.


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Distinguishing WPW AF from other wide-complex

tachycardias is paramount such that proper treatment can be

initiated. The electrocardiographic differential diagnosis for a

patient presenting with an irregular, wide-complex tachycar-

dia consists of AF with aberrant conduction, WPW AF, and

polymorphic ventricular tachycardia (VT), including torsades

de pointes. Differentiation of these rhythms represents a

challenge for even the most experienced physician. As noted

in the case above, improper classification of a patient’s

rhythm can lead to therapeutic misadventures and potentially

poor outcomes. Discriminating WPW AF from polymorphic

VT and AF with aberrant conduction is challenging. Age and

past medical history can certainly add to the clinician’s

consideration of the patient presentation, with young healthy

individuals being more likely to have WPW AF, whereas

older individuals with a past cardiac history experience

ventricular tachycardia more often. Polymorphic VT has very

similar ECG characteristics as WPW AF: a widened QRScomplex, changing R-R intervals with a frequency of 150 to

300 beats/min, and a QRS complex that changes frequently.

Certain subtypes of polymorphic VT, such as torsades de

pointes, presents with an indulating baseline; in contrast,

WPW AF usually has a stable electrocardiographic baseline

with no alteration in the polarity of the QRS complexes.

Atrial fibrillation with aberrant conduction occurs when a

patient with a preexisting bundle branch block (or a rate-

responsive bundle branch block) has a rapid ventricular

response to AF. The ECG will show a wide complex

tachycardia of irregular rate with stable beat-to-beat QRS

configuration (Fig. 8A), contrasting the variable beat-to-beat

QRS configuration in WPW AF (Fig. 8B).

Treatment of patients with AF in WPW who are unstable

(eg, hypotension, pulmonary edema, ischemic chest pain,

and altered mentation) requires consideration for immediate

electrical cardioversion. If the patient is stable, chemical

cardioversion may be attempted with the patient being

continuously monitored and with ready access to electrical

cardioversion. Procainamide (30 mg/min, maximal dose

17 mg/kg) has traditionally been the tr eatment of choice for

patients who are stable with WPW AF [10]. By blocking fast

inward Na current and outward K current, procainamide has

been shown to prolong the effective refractory period of

atrial, ventricular, and AP tissue as well as slow antegradeand retrograde conduction in the AP. Because of the

potential for severe hypotension with rapid IV administra-

tion, procainamide requires a somewhat slow rate of

Fig. 6 Impulse conduction in a patient with AF in the WPW.

Multiple atrial impulses are generated by foci in the atria. These

impulses have 2 potential pathways to the ventricles, the AVN and

the AP. The large atrial arrow in the atria indicates that most of

these impulses travel to the ventricles via the AP, bypassing the

AVN through which fewer impulses travel (smaller atrial arrow).

The impulses that traverse the AP arrive in the ventricular myocardium sooner than anticipated (multiple small ventricular

arrows), causing a portion of the ventricles to depolarize markedly

earlier than the remainder of the ventricular myocardium (shaded

area), which is manifested on the ECG by the delta wave. The

impulse then travels throughout the ventricular myocardium via

inefficient myocte-myocyte conduction. Simultaneously, the

impulses that traversed the AVN travel throughout the ventricle

via the intraventricular conduction system (dotted ventricular

arrows). The final result, ventricular depolarization, occurs less

efficiently (and therefore less rapidly) than if the event had been

triggered via the AVN and His-Purkinje system; this less-than-

efficient depolarization is manifested on the ECG by a minimally

widened QRS complex.

Fig. 7 Atrial fibrillation in the WPW. ECG rhythm strip in

patient with WPW AF. Note the wide QRS complexes occurring in

an irregular fashion and beat-to-beat variations in the QRS

complex morphology.


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infusion and also has a relatively slow onset of action, not

reaching therapeutic blood levels for 40 to 60 minutes.

Amiodarone (150 mg IVover 10 minutes) is another agent

used by practitioners for chemical conversion of patient’s

with a wide complex tachycardia and is quoted in the 2005

American Heart Association Advanced Cardiac Life Support

guidelines as the bantiarrhythmic to consider in WPW AF

[11]. Q Although amiodarone, given orally, has been shown to be successful in treating recurrent atrial arrythmias, the

consequences of rapid IVamiodarone administration are quite

different because of its pattern of acute electrophysiologic

effects [12]. Pharmacologic studies have demonstrated that

short-term IV amiodarone administration modifies sinus and

AV node propert ies with little, if any, effect on fast-channel

tissues (ie, APs) [13]. This observation may be explained by

the pharmacokinetic fact that accumulation of amiodarone’s

desethyl metabolite is responsible for much of the long-termeffects on fast-channel tissues [14]. Administration of IV

Fig. 8 A, Atrial fibrillation with preexisting left bundle branch block. When rapid AF develops, a wide QRS complex, irregular

tachycardia develops. Note the lack of significant beat-to-beat variation in the QRS complex morphology. B, Atrial fibrillation in the WPW

syndrome. Note the widened QRS complex with rapid rate and significant beat-to-beat variation in QRS complex morphology.

Fig. 9 Therapeutic misadventure in a patient with WPW AF. A, Rapid, wide, irregular QRS complex tachycardia. The physician did not

consider the possibility of WPW and used diltiazem. B, After administration of diltiazem, an AV nodal blocking agent, the mean ventricular

rate has increased. C, Markedly increased rate approaching 300 beats/min.


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amiodarone to patients in AF has been shown to cause

acceleration of the ventricular rate [15,16] and degeneration

into ventricular fibrillation [17]. Taking these factors into

consideration, the use of IV amiodarone for the treatment of

patients identified as having WPW AF should be made with

caution [17].

Ibutilide is a reasonable agent for management of AF in

patients with WPW. As a class III antiarrhythmic agent,ibutilide prolongs the action potential duration and refrac-

toriness by enhancing the slow inward sodium current and

blocking delayed-rectifier outward K current, resulting in

QT interval prolongation. It is given at a dosage of 1 mg

(0.01 mg/kg for patients b60 kg) over 10 minutes and can be

repeated once after a 10-minute period. It has a very short

half-life of 4 hours; it does not interact with most of the

medications that are used for rate control (b-blockers,

diltiazem, verapamil, digoxin) [18]; its dosing requires no

concern for hepatic or renal function; it is safe in elderly

patients [19]; and it is very rapid in action, with a mean

conversion time of approximately 20 minutes [20].

In the non-WPW AF patient, the superiority of ibutilide

over procainamide in the conversion of AF/flutter has been

documented in numerous studies, with rates of conversion

with ibutilide of 32% to 51% in patients with AF and 64%

to 76% in patients with atrial flutter, compared with 0% to

21 % in AF an d 5% to 14% in atrial flutter with

procainamide [21,22]. It has also been demonstrated that

ibutilide had minimal effect on blood pressure, whereas

procainamide reduced blood pressure significantly, with

decreases in diastolic blood pressure up to 67 mm Hg [22].

The safety and success of ibutilide in the conversion of AF

to sinus rhythm in the ED were reiterated by Viktorsdottir

et al [23] when they found ibutilide converted 64% of patients presenting with AF to sinus rhythm compared with

29% conversion with rate controlling drugs.

In regard to patients with WPW, Glatter [24] showed that

ibutilide significantly prolongs the refractory period of APs

and promptly decreases the ventricular response in patients

with WPW AF. By prolonging the AP refractory period,

ibutilide decreases the likelihood of a potential fatal

ventricular arrythmia, an essential characteristic for any

drug given for treatment of WPW AF. Several case reports

have had excellent results with ibut ilide in treating wide-

complex AF [25] and WPW AF [26]. With a faster onset of

action, a better conversion rate in patient’s with AF/flutter,

prolongation of the AP refractory period, and stable blood

pressure profile, ibutilide may be superior to procainamide

for chemical conversion of WPW AF. The primary concern

with ibutilide use is the development of torsade de pointes

due to prolongation of the QT interval. Patients who present

with WPW AF, however, usually are young and have normal

ventricular function, therefore placing them at a lower risk

for ibutilide-induced arrhythmias [24].

Patients identified as having WPW AF should not be

treated with medications that prolong conduction through

the AV node, such as digitalis compounds, calcium channel

antagonists, b-adrenergic blocking agents, and adenosine.

Such medications will block conduction via the AV node

and cause preferential conduction down the AP. This

conduction pattern can increase the ventricular response to

the AF, promoting hemodynamic collapse and/or ventricular

fibrillation (Fig. 9) [8].

Disposition of patients who present with WPW AF after

resolution of their tachyarrythmia should be made withregard to the patient’s presentation, comorbidities, social

situation, and the physician’s practice environment. In a

large tertiary center, consultation with the cardiology service

for potential radiofrequency mapping and ablation can be

considered in the ED. In a smaller hospital or rural setting, if

immediate cardiology follow-up cannot be arranged, trans-

fer to a tertiary center can be considered.

4. Conclusion

Atrial fibrillation occurring in the setting of the WPW

should be in the differential diagnosis for patients presentingwith wide-complex tachycardias. Clinical clues to the

diagnosis include a young patient with previous episodes

of palpitations, rapid heart rate, or syncope. Electrocardio-

graphic features suggestive of AF in WPW include

irregularity of the rhythm; a rapid ventricular response,

often greater than 200 beats/min; a delta wave; and a wide,

bizarre QRS complex. If unstable, these patients should

undergo electrical cardioversion. If stable, an attempt at

chemical conversion to sinus rhythm may be attempted with

procainamide or ibutilide.

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