What causes a wide QRS (Quadrature Amplitude Modulation Signal) complex?

Causes of Wide QRS Complex

A wide QRS complex (>120 ms) is primarily caused by three mechanisms: ventricular tachycardia (most common), supraventricular tachycardia with bundle branch block or aberrant conduction, and supraventricular tachycardia with AV conduction over an accessory pathway. 1

Primary Mechanisms

Ventricular Tachycardia (VT)

• VT is the most common cause of wide QRS complex tachycardia, accounting for the majority of cases, particularly in patients with structural heart disease 2
• Characterized by ventricular-atrial (VA) dissociation where the ventricular rate exceeds the atrial rate 1
• Strongly associated with prior myocardial infarction—if a patient has a history of MI and presents with their first wide QRS tachycardia after the infarct, VT is highly likely 3, 1
• QR complexes indicate myocardial scar and are present in approximately 40% of VT patients after MI 3
• Ventricular fusion beats indicate a ventricular origin of the tachycardia 3

Supraventricular Tachycardia with Bundle Branch Block

• Bundle branch block may be pre-existing or develop during tachycardia when one bundle branch becomes refractory due to rapid rate 3, 1
• Most bundle branch blocks are not only rate-related but also occur due to a long-short sequence of initiation 3
• Can occur with any supraventricular arrhythmia 3
• If rate-related BBB develops during orthodromic AVRT, the tachycardia rate may slow if the BBB is ipsilateral to the bypass tract location 3

Supraventricular Tachycardia with Accessory Pathway Conduction

• Occurs during atrial tachycardia, atrial flutter, atrial fibrillation, AVNRT, or antidromic AVRT 3
• Antidromic AVRT involves anterograde conduction over the accessory pathway and retrograde conduction over the AV node or a second accessory pathway 3, 1
• Wide QRS with left bundle branch block morphology may occur with anterograde conduction over atriofascicular, nodofascicular, or nodoventricular tracts 3

Key Diagnostic ECG Criteria for VT

High-Specificity Features

• QRS width >140 ms with right bundle branch block pattern or >160 ms with left bundle branch block pattern strongly suggests VT 1, 4
• RS interval >100 ms in any precordial lead is highly suggestive of VT 1, 4
• Negative concordance pattern (all precordial leads showing similar QS complexes) is diagnostic for VT 3, 1
• Positive concordance does not exclude antidromic AVRT over a left posterior accessory pathway 3
• AV dissociation with ventricular rate faster than atrial rate is a key diagnostic criterion 1, 4

Clinical Context Matters

• Width and morphological criteria are less specific in patients taking certain antiarrhythmic agents, those with hyperkalemia, or those with severe heart failure 3
• Electrolyte abnormalities, particularly hyperkalemia, can cause QRS widening 1
• Drugs causing wide QRS include Vaughan-Williams class Ia and Ic antiarrhythmics (procainamide, quinidine, flecainide), cyclic antidepressants (amitriptyline), and cocaine 3

Critical Management Principle

If the specific diagnosis of a wide QRS complex tachycardia cannot be made despite careful evaluation, treat the patient as if they have VT. 3, 4 This is essential because intravenous medications given for SVT treatment, particularly verapamil or diltiazem, may precipitate hemodynamic collapse in patients with VT 3, 4

Common Pitfall to Avoid

• Stable vital signs during tachycardia do NOT help distinguish SVT from VT—hemodynamic stability is not a reliable differentiating factor 3, 4
• Despite available ECG criteria, patients with wide QRS complex tachycardia are often misdiagnosed, with only 39 of 122 VT patients correctly diagnosed initially in one large series 2