What causes a wide QRS (Quaternary Response System) complex?

Causes of Wide QRS Complex

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

Main Causes of Wide QRS Complex

1. Ventricular Tachycardia (VT)

• Most common cause of wide QRS complex tachycardia, especially in patients with structural heart disease 2
• Characterized by ventricular-atrial (VA) dissociation with ventricular rate faster than atrial rate 1
• Fusion complexes (merger between conducted sinus impulses and ventricular depolarization) are pathognomonic for VT 1
• QRS width >140 ms with right bundle branch block (RBBB) pattern or >160 ms with left bundle branch block (LBBB) pattern suggests VT 1
• RS interval >100 ms in any precordial lead is highly suggestive of VT 1
• Negative concordance pattern in precordial leads is diagnostic for VT 1

2. Supraventricular Tachycardia (SVT) with Bundle Branch Block

• Bundle branch block may be pre-existing or may occur during tachycardia when one bundle branch is refractory due to rapid rate 1
• Most bundle branch blocks are rate-related and due to a long-short sequence of initiation 1
• Can occur with any supraventricular arrhythmia 1
• If rate-related BBB develops during orthodromic AVRT, tachycardia rate may slow if the BBB is ipsilateral to bypass tract location 1
• Typically shows "typical" bundle branch block morphology in leads V1 and V6 2

3. SVT with AV Conduction Over an Accessory Pathway

• Can occur during atrial tachycardia, atrial flutter, atrial fibrillation, AVNRT, or antidromic AVRT 1
• Antidromic AVRT involves anterograde conduction over accessory pathway and retrograde conduction over AV node 1
• Wide QRS complex with LBBB morphology may be seen with anterograde conduction over atriofascicular, nodofascicular, or nodoventricular tracts 1
• Difficult to distinguish from VT based on QRS configuration alone 1
• Absence of negative precordial concordance or deep q waves in precordial leads other than V1 suggests preexcited tachycardia 2

4. Other Causes

• Bundle branch reentry can cause ventricular tachycardia even in patients without myocardial or valvular dysfunction 3
• Isolated conduction abnormalities in the His-Purkinje system can lead to bundle branch reentry 3, 4
• Antiarrhythmic drugs (particularly class Ia and Ic) can slow intraventricular conduction, resulting in QRS widening 2
• Electrolyte abnormalities, particularly hyperkalemia, can cause QRS widening 1

Diagnostic Approach to Wide QRS Complex

ECG Criteria Suggestive of VT

• AV dissociation with ventricular rate faster than atrial rate 1, 5
• QRS width >140 ms with RBBB or >160 ms with LBBB pattern 1, 5
• RS interval >100 ms in any precordial lead 1, 5
• Concordant precordial pattern (absence of RS complexes in precordial leads) 2
• Fusion and/or capture beats 2
• Axis deviation less than -90° or between +180° and -180° 6

Clinical Context

• History of previous myocardial infarction strongly suggests VT 5
• First occurrence of wide QRS tachycardia after infarction suggests VT 5
• Stable vital signs during tachycardia are not helpful for distinguishing SVT from VT 1, 5

Clinical Implications and Management

• If diagnosis of SVT cannot be proven or easily made, treat as if VT is present 1, 5
• Intravenous medications for SVT (particularly verapamil or diltiazem) may precipitate hemodynamic collapse if given to patients with VT 1
• Immediate DC cardioversion is recommended for hemodynamically unstable patients 5
• For stable patients with presumed VT, IV procainamide, sotalol, or amiodarone may be used 5
• Adenosine can be used for stable, regular, monomorphic wide-QRS tachycardia for both diagnosis and treatment 5
• Patients should be referred to an arrhythmia specialist after successful termination of wide QRS-complex tachycardia of unknown etiology 5

Pitfalls in Diagnosis

• Relying solely on QRS morphology can lead to misdiagnosis, as previous myocardial infarction can result in "atypical" bundle branch block even in SVT 2
• Age, hemodynamic status, heart rate, and regularity of R-R intervals may be misleading and should not be used as primary diagnostic criteria 2
• P waves can be difficult to recognize during wide-QRS tachycardia, making VA dissociation hard to identify 1
• No single criterion is 100% sensitive or specific; a holistic approach using multiple criteria is recommended 2
• Misdiagnosis of VT as SVT with aberrancy is common and potentially dangerous 6