Wide Complex Tachycardias: Demystifying the Differential Diagnosis

In this next installment of the ECG 101 section, the author describes wide complex tachycardias, which can be a challenge to diagnose based on the 12-lead ECG alone.

Case Report

A 20-year-old male presents to the Emergency Department with complaints of a sudden onset of palpitations. He states he was studying for his final exams when he had palpitations associated with mild chest discomfort and shortness of breath. He drank two glasses of water without relief and finally called 911. Per the record, the paramedics found him to be agitated and anxious. His blood pressure was 110/80 and his pulse was 190 beats/min. His ECG at the time of presentation showed a wide complex tachycardia (WCT) with a heart rate of 200 bpm (Figure 1). He was instructed to perform a Valsalva maneuver by holding his breath and bearing down. On the third attempt, the tachycardia suddenly abated and an ECG was again recorded (Figure 2). His physical exam and laboratory assessments were unremarkable. An echocardiogram demonstrated normal ventricular function and wall motion without any valvular abnormalities. He was discharged home and asked to follow up with his primary care physician.

Discussion

A wide complex tachycardia is defined as a rhythm disturbance with a rate greater than 100 beats/min and a QRS complex duration of 0.12 seconds or more in the adult patient. WCTs can be divided into two broad categories: ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy or preexisting or rate-related bundle branch block. WCTs are generally due to ventricular tachycardia until proven otherwise. Supraventricular tachycardias can also have wide complexes if there is a preexisting bundle branch block, ventricular preexcitation, or rate dependant (phase III) aberration. Patient symptoms during tachycardia are not necessarily reliable and could provide false assurances assuming that a hemodyamically stable WCT is always supraventricular in origin. An immediate diagnosis made on the basis of the electrocardiogram alone may not be apparent, but an assessment of the patient, knowledge of the differential diagnosis, and a key understanding of certain electrocardiographic clues can help simplify the approach and lead to an accurate and sometimes lifesaving diagnosis and treatment plan.¹ The differential diagnosis must first be known before an actual diagnosis or analysis of the ECG can even be made. A simple differential diagnosis of common causes of a WCT includes SVT with aberrancy, VT (mono or polymorphic), orthodromic tachycardia with preexisting bundle branch block, and antidromic atrioventricular reentry tachycardia. VT is generally the most common cause and must be considered to be the diagnosis until proven otherwise, especially in patients with coronary artery disease and/or structural heart disease. A WCT that is not hemodynamically compromising may still be VT. The clinician should remember that VT can be tolerated in younger people without evidence of structural heart disease. SVTs conducting orthodromically through the atrioventricular nodal tissue can present as WCTs because of block or delay in the His-Purkinje system causing aberrancy. Any SVT such as atrial tachycardia, atrial fibrillation or flutter, atrioventricular nodal reentry tachycardia, orthodromic atrioventricular reciprocating tachycardia, junctional tachycardias, and other more rare SVTs can present as a WCT if there is delay/block in the His-Purkinje network. Preexcitation may also manifest as a WCT. It is very helpful to have a baseline ECG tracing to assess for both a delta wave in the initial upstroke of the QRS complex and a short PR interval. These findings suggest an antidromic SVT to be the most likely cause of the WCT. The delta wave represents an “accessory” atrioventricular nodal tissue with a pathway that allows conduction to occur antegradely while bypassing the AV node altogether. Sometimes the WCT may be rate dependant since atrioventricular nodal block (Wenckebach periodicity) may allow conduction to be antidromic via an accessory pathway. Other less common causes of a WCT include pacemaker-mediated tachycardia, ECG artifact, severe hyperkalemia with sinus tachycardia, and any narrow complex tachycardia with concurrent use of sodium channel blocking antiarrhythmic agents. For example, drugs such as tricyclic antidepressants and diphenhydramine block the fast gated Na+ channel resulting in prolongation of phase 0 of the action potential (increasing the QRS width on the surface ECG), and this may also result in PR interval prolongation. Answers to the following questions regarding specific ECG features can help distinguish a VT from an SVT with a wide complex morphology:

1. Is the tachycardia regular or irregular? An irregular tachycardia is more likely due to atrial fibrillation or flutter with variable block, especially if there are no discernable P waves. The wide complex morphology again can be due to rate-dependant aberrancy, bundle branch block, or conduction utilizing an accessory pathway.
2. Are there any capture or fusion beats? Capture beats (also known as a Dressler beat) and fusion beats aid in the diagnosis of a WCT. These beats imply that the WCT is ventricular tachycardia. A capture beat occurs when the atrium conducts an impulse through the atrioventricular node to activate the ventricle before the tachycardia beat (these beats are narrow complexes). This occurs during atrioventricular dissociation. A fusion beat is the collision of the tachycardia beat and the VT circuit itself.
3. Is there precordial concordance? The presence of positive precordial concordance can be associated with either a VT or SVT utilizing a posterior accessory pathway for conduction. Positive precordial concordance is not a useful criterion to differentiate VT from SVT. Negative precordial concordance, however, is usually always due to VT.
4. What is the electrical axis? A right superior (northwest) axis is VT and not SVT. There are no SVTs with a bundle branch block or fascicular in origin with a right superior axis.
5. What is the morphology of the QRS in V1? A right bundle branch block (RBBB) pattern is likely to be due to VT if the R wave is taller than the r’ wave or if the QRS complex is biphasic with an Rs or qR pattern. With a left bundle branch block (LBBB) pattern in V1, ventricular tachycardia is likely if certain criteria such as notching in the downstroke of the S wave in V1 are noted (see next paragraph).²

There are other criteria that may guide the ECG reviewer to differentiate RBBB and LBBB morphology VTs. Commonly used ECG criteria have mostly been based on QRS complex duration, axis, AV dissociation, precordial concordance, fusion beats, and absence of RS complexes in the precordial leads. The Wellens’ criteria³ favoring VT in the presence of a RBBB morphology in V1 as a diagnosis are as follows:

1. AV dissociation
2. left axis deviation
3. capture or fusion beats
4. QRS greater than 140 msec
5. precordial QRS concordance
6. monophasic QS in V63

The Kindwall ECG criteria4 for VT in the presence of a LBBB R wave in V1 or V2 of >30 ms duration are as follows:

1. any Q wave in V6
2. duration of >60 ms from the onset of the QRS to the nadir of the S wave in V1 or V2
3. notching on the downstroke of the S wave in V1 or V2⁴

The Brugada criteria⁵ can also help determine if the WCT is VT. The algorithm includes absence of RS complexes in all precordial leads, R to S interval >100 ms in one precordial lead, AV dissociation, and morphological criteria in V1–2 and V65. These features are all in favor of VT as the most likely diagnosis. None of these criteria are favored alone as each has some inherent limitation. Thus, it is important for the ECG reviewer to be familiar with each of these criteria and utilize a systematic approach when reviewing WCT ECGs.

Back to the Case

Several days went by with continued palpitations, so the patient was eventually referred to a cardiologist who immediately recommended electrophysiology consultation. The ECG with the WCT (Figure 1) clearly shows a left bundle branch QRS morphology with a left axis deviation. There was no evidence of AV dissociation, concordance, capture or fusion beats, or even notching in the S wave in V1. The baseline ECG (Figure 2) shows normal sinus rhythm with sinus arrhythmia and no evidence of baseline preexcitation or bundle branch block. There is no evidence of a RBBB pattern in V1 or ST elevation in V1-V2 to suggest the Brugada pattern. There was evidence of nonspecific ST-T changes in all leads. VT seemed unlikely to be the cause of the WCT. The vagal maneuver suggested that the AV node participated in the tachycardia circuit. The patient was taken to the EP lab. The baseline intervals were all normal. With ventricular pacing during normal sinus rhythm there was no evidence of eccentric ventricular-atrial conduction. During AV node function curve assessment, there was a greater than 50 ms “jump” in the AH interval. The WCT was easily inducible with and without isoproterenol. The VA interval during tachycardia was 60 ms. Well-timed His refractory premature ventricular complexes did not reset or terminate the WCT. Ventricular pacing 20 ms faster than the tachycardia cycle length could entrain the WCT, and when pacing stopped there was a V-A-V response. The post-pacing interval minus the tachycardia cycle length was >115 ms. All of these findings favored atrioventricular nodal reentry tachycardia as the diagnosis. The intracardiac electrogram activation showed a slow-fast AV node pathway conduction sequence. A 4-mm radiofrequency ablation catheter was placed in the area of the slow pathway, and with a single application of energy, junctional beats were noted. The WCT could not be reinduced at the end of the study with or without isoproterenol. This was a successful ablation eliminating slow pathway conduction.

Summary

WCTs are certainly diagnostically challenging based on the 12-lead ECG alone. The diagnosis can be made based on the patient’s presentation, symptoms, and careful scrutiny of the ECG. A stepwise approach to the ECG is necessary and may sometimes yield the diagnosis or at least suggest the next best step in management leading to proper therapy.

References

1. Akhtar M, Shenasa M, Jazayeri M, Caceres J. Wide QRS complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med 1988;109:905-912.
2. Lam P, Saba S. Approach to the evaluation and management of wide complex tachycardias. Indian Pacing Electrophysiol J 2002;2:120-126.
3. Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27-33.
4. Kindwall KE, Brown J, Josephson ME. Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias. Am J Cardiol 1988;61:1279-1283.
5. Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649-1659.