The first ECG reveals an irregular, wide QRS complex tachycardia of unclear etiology. The differential diagnosis includes polymorphic ventricular tachycardia including torsades de pointes, ventricular fibrillation, ventricular flutter, supraventricular and atrial tachycardia with bundle branch block or aberrancy, and a tachycardia mediated by an accessory pathway.
An accessory pathway is a tract of anomalous conducting tissue in the heart that serves as a potential bypass pathway for impulse conduction. The most common tract is the atrioventricular (AV) bypass tract, but other tracts include nodoventricular, atriofascicular, and intranodal. (J Emerg Med 2003;24:72.) The AV bypass tract can produce a narrow or wide QRS complex tachycardia depending on the direction of the circuit loop if a reentrant mechanism exists. It also can produce a narrow or wide QRS complex tachycardia (or a mixture of the two) by direct conduction down the bypass tract (wide QRS complex) competing with direct conduction down the AV node (narrow QRS complex).
Normal AV nodal pathways can create a reentry circuit loop in which the ventricle is repeatedly depolarized. This type of tachycardia is known as an AV reentry tachycardia (AVRT). When the ventricles are activated down the AV node path and atria are reactivated by impulses going back up the bypass tract (orthodromic conduction), the AVRT produces a narrow QRS complex tachycardia. When the direction is the opposite, that is, the ventricles are activated by the bypass tract and the atria reactivated by impulses going retrograde up the AV node (antidromic conduction), the AVRT produces a wide QRS complex tachycardia. Due to the reentry loop, the antidromic wide QRS complex AVRT is usually regular.
The second and more common mechanism by which an accessory bypass tract produces a wide complex QRS tachycardia occurs when impulses from an atrial tachydysrhythmia are rapidly transmitted to the ventricles through the accessory pathway, bypassing the inherent AV nodal slowing effects on rapid atrial impulses. Because ventricular activation occurs through the accessory pathway, the QRS complex is wide and often bizarre in appearance. More importantly, rapid atrial tachydysrhythmias such as atrial fibrillation and flutter can result in dangerously fast ventricular responses that can provoke ventricular fibrillation because of the lack of AV nodal slowing. (N Engl J Med 1979;301:1080.)
In this particular case, the patient demonstrated an irregular, wide QRS complex tachycardia at a very rapid rate, nearly 300 beats/minute on the rhythm strip obtained in the ED. (Figure 2.) While it can occur, such an extremely fast rate is rare with ventricular tachycardia. The regularity of morphology also makes ventricular fibrillation and torsades less likely. The irregular rate argues against ventricular flutter. The QRS complex morphology is not consistent with a supraventricular tachycardia (SVT) with bundle branch block. (Pacing Clin Electrophysiol 2000;23:2040.) Moreover, the rate is higher than would be expected for SVT with aberrant intraventricular conduction because impulses would still travel through the AV node. The rapid, irregular, wide QRS complex rate suggests the possibility of atrial fibrillation in the setting of an accessory pathway, which is transmitting these rapid atrial impulses directly to the ventricles.
The ECG obtained in the ED after cardioversion supports this diagnosis. (Figure 3.) On this ECG, the patient shows evidence of pre-excitation from an AV node bypass tract. Pre-excitation is characterized by the early activation of part of the ventricular myocardium from impulses transmitted down the bypass tract, though the majority of ventricular tissue is activated through the standard AV nodal conduction pathway. As a result of this early partial ventricular activation, the ECG demonstrates a slurred upstroke of the QRS wave (delta wave), a shortened PR interval, and repolarization abnormalities of the ST segment/T wave as a result of the abnormal activation pattern. All of these features are seen on the ECG of this patient after she was cardioverted back to her baseline sinus rhythm. (Figure 3.)
The combination of pre-excitation and episodic tachydysrhythmias is known as Wolff-Parkinson-White syndrome. Pre-excitation is reportedly seen in 1.5 per 1000 persons. (Heart Disease, 6th ed. Baltimore: Williams and Wilkins. 1995.) Atrial fibrillation has been reported in as many as 10 percent to 39 percent of patients with Wolff-Parkinson-White syndrome, and therefore presentations with rapid, irregular wide QRS complex tachydysrhythmias are not uncommon. (Circulation 1971;43:520.) Caution must be exercised when treating such patients. Misdiagnosis of the tachydysrhythmia as SVT with aberrancy can result in treatment with AV nodal blocking agents such as digitalis, calcium channel blockers, beta-adrenergic blockers, or adenosine. These agents carry the risk of slowing AV nodal conduction and paradoxically accelerating bypass tract conduction, increasing the risk for rapid ventricular response rates and even ventricular fibrillation. Similar concerns have been raised regarding the misdiagnosis of such rhythms as ventricular tachycardia and the use of lidocaine as well. In many cases, the safest approach is electrical cardioversion with consideration for specific pharmacologic agents (such as procainamide) provided the patient is hemodynamically stable and tolerating the tachydysrhythmia.
After electrical cardioversion, the patient was admitted to the cardiology service. The following day, she underwent an electrophysiology study demonstrating a left posterior AV accessory pathway, which was successfully ablated. An ECG obtained after ablation revealed no evidence of delta waves and normalization of the PR interval length. (Figure 4.) The patient was ultimately discharged home without any complications or subsequent sequelae.