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

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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.

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 electrocardiographic 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 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 allows a certain number of atrial impulses to pass to the ventricles per period.

The electrophysiologic properties of APs vary tremendously 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 (AF) is not uncommon in patients with WPW, presenting with a wide-complex, irregular tachycardia. Wolff-Parkinson-White syndrome AF is the focus of this report, in which diagnosis and management issues are reviewed.

Section snippets

Case presentation

A 42-year-old man with a history of panic disorder presented to the emergency department (ED) complaining of “palpitations” 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 “clammy” 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

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

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. Electrocardiographic 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

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