ECG 101: Wide Complex Tachycardias

Chirag Sandesara, MD and Brian Olshansky, MD, University of Iowa Hospitals and Clinics, Iowa City, Iowa

Chirag Sandesara, MD and Brian Olshansky, MD, University of Iowa Hospitals and Clinics, Iowa City, Iowa

Causes for wide complex tachycardia include: 1) ventricular tachycardia (VT), 2) supraventricular (and sinus) tachycardia with aberration (or with preexisting intraventricular conduction delay), and 3) preexcitation. Wide complex tachycardia can be regular or irregular in rate, monomorphic or polymorphic in QRS morphology, and similar or different from baseline tracings during slower (generally sinus) rates. Wide complex tachycardias that are regular in rate are often monomorphic ventricular tachycardia. This must be considered the most likely diagnosis if no baseline ECG is available for comparison, if the QRS complex is not typical bundle branch block morphology, and if the patient has a history of heart disease. Supraventricular tachycardias of various sorts (AV reciprocating tachycardia, sinus tachycardia, atrial tachycardia, atrial flutter with fixed AV conduction, and atrioventricular nodal tachycardia) may have wide QRS complexes and should be considered secondarily. The approach to the ECG starts with determining rate, regularity, QRS morphology, and the P-QRS relationships. The rate of a wide complex tachycardia is not an indication of the mechanism of the tachycardia since ventricular and supraventricular tachycardias can be either slow or fast. Slow, wide complex rhythms may even be ventricular in origin and are referred to as an accelerated idioventricular rhythm (Figure 1). This is not considered ventricular tachycardia. The rate is 70–110 beats per minute. If the QRS rate is regular and there is dissociation between the P wave and the QRS complex (AV dissociation), and, less likely, capture and/or fusion beats, the diagnosis is most likely ventricular tachycardia (Figure 2). These criteria will aid to distinguish VT from SVT. Careful scrutiny of all 12 leads may be required to visualize P waves. The identification of P waves may be difficult as they may be buried in the QRS complex or the T wave. Retrograde 1:1 conduction during ventricular tachycardia can complicate the diagnosis. AV dissociation is also observed with carotid massage or even adenosine if the patient is able to tolerate the tachycardia. Intermittent AV dissociation may also be present on a long rhythm strip. The next step involves evaluating QRS morphology (although this is fraught with error and is not reliable). Negative or positive concordance in leads V1-V6 suggests VT. Absence of RS complexes with the presence of tall Rs or rS complexes in all precordial leads favors VT. An RS interval > 100 ms measured from the onset of the R wave to the nadir of the S wave in any one precordial lead also adds evidence for the diagnosis of VT. Right bundle branch block (RBBB) VT may have a monophasic R wave or an R-r’ in V1 (Figure 3). If the QRS complex in lead V6 has a monophasic QS or biphasic rS morphology with an r:S ratio < 1 during a RBBB tachycardia, then VT is likely. V1 in left bundle branch block VT commonly has a notched down stroke, R width > 40 ms, and an onset of QRS to the nadir of the S wave > 70 ms. The wider the QRS width, the greater chance it is VT rather than SVT. If the QRS width is > 140 ms and the axis is left superior (so-called Northwest axis or no man’s land), VT is more likely. Careful observation for the presence of narrow QRS tachycardia beats in lieu of wide QRS beats can lend support for the diagnosis of SVT with aberration. The initiation of the tachycardia with a premature atrial beat also provides evidence for the tachycardia to be SVT. A wide complex tachycardia starting with a premature ventricular beat lends more support for VT (Figure 4). If the QRS morphology is typical for a right or left bundle branch block, then this can further support the diagnosis of SVT, especially if the QRS is the same as that seen in sinus rhythm. Any SVT can present as a wide QRS complex tachycardia. Generally, a supraventricular tachycardia with a wide QRS complex is due to the presence of a bundle branch block or aberration. Antidromic tachycardia (conduction down an accessory pathway) is also possible. Atrial fibrillation with ventricular preexcitation due to Wolff-Parkinson-White syndrome can present as an irregular wide QRS complex tachycardia due to ventricular preexcitation (intermittent or not) (Figure 5). Irregular wide complex tachycardias can be SVT or VT. Polymorphic irregular wide QRS complex tachycardias are generally VT. If the initiation is with a long QT interval, it is termed Torsades de Pointes (Figures 6 and 7). The accurate diagnosis of a wide complex tachycardia is not necessarily simple or straightforward. Clinicians must be aware of the differential diagnosis and observe the ECG tracings as described. All undiagnosed or undiagnosable wide QRS complex tachycardias should be presumed to be and treated as VT until proven otherwise if a firm diagnosis for SVT cannot be secured.