Article, Cardiology

Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED

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.

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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 changes reflected as ST segment-T wave changes that are generally directed opposite 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.

* Corresponding author.

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

These electrocardiogram 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 found 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

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case presentation“>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 to conduct 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 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.

Case presentation

A 42-year-old man with a history of panic disorder presented to the emergency department (ED) complaining of bpalpitationsQ 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 bclammyQ 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.

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

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 a left lateral AP that was successfully ablated with radio- frequency. Interestingly, the patient’s 3-year-old daughter was recently diagnosed with bpanic attacksQ 6 months before this presentation; hence, further evaluation of the child was planned.

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 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. 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 through AV node to the atria. In this situation, the ECG shows a rapid, regular, wide-complex tachycardia that is indistinguishable from monomorphic ventricular tachycardia.

Atrial fibrillation 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. 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.

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

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 be seen, 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 inclusion of bizarre QRS complex morphologies with significant beat- to-beat variations in configuration, 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 Torsades de pointes subtype.

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.

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.

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 , 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 QRS complex, 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 treatment 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 antegrade and 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. 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.

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.

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 properties 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-term effects on fast-channel tissues [14]. Administration of IV

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.

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 and 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 ibutilide 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 with regard 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.

Conclusion

Atrial fibrillation occurring in the setting of the WPW should be in the differential diagnosis for patients presenting with 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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