INTRODUCTION: The electrocardiographic (ECG) differential diagnosis of tachycardia with a broad QRS complex (BCT) represents a challenge for physicians but is important for adequate treatment and risk evaluation. Differentiated algorithms have been established and can increase the specificity of the diagnosis in individual patients but are often hampered by complexity and yield a pragmatic ECG approach. METHODS AND RESULTS: Irregular BCTs (irregular R-R distances) despite the patient being hemodynamically stable are almost always due to atrial fibrillation with bundle branch block (pre-existing or functional) or conduction via accessory pathways. In contrast, sustained polymorphic ventricular tachycardia (VT) is always associated with hemodynamic collapse. In regular BCT the following mechanisms must be differentiated: (1) VT, (2) supraventricular tachycardia (SVT) with bundle branch block or (3) SVT with pre-excitation via accessory pathways, e.g. Wolff-Parkinson-White (WPW) syndrome. The presence of an underlying structural heart disease, specifically a history of myocardial infarction is suggestive of VT. For a differentiated analysis in hemodynamically stable patients a 12-lead ECG is essential. CONCLUSION: Identification of signs of atrioventricular (AV) dissociation or a negative precordial concordance of QRS are indicative of VT. In V1 positive BCTs a positive precordial concordance, QRS width > 140 ms, superiorly directed QRS axis, monophasic or biphasic QRS complexes in V1 and deep S wave in V6 are indications of a VT. In V1 negative BCTs, QRS width > 160 ms, right-sided QRS axis, broad R peak (> 40 ms) in V1/V2, slurred S downstroke in V1/V2 and any Q peak in V6 are all indications of VT as the mechanism.
INTRODUCTION: The electrocardiographic (ECG) differential diagnosis of tachycardia with a broad QRS complex (BCT) represents a challenge for physicians but is important for adequate treatment and risk evaluation. Differentiated algorithms have been established and can increase the specificity of the diagnosis in individual patients but are often hampered by complexity and yield a pragmatic ECG approach. METHODS AND RESULTS: Irregular BCTs (irregular R-R distances) despite the patient being hemodynamically stable are almost always due to atrial fibrillation with bundle branch block (pre-existing or functional) or conduction via accessory pathways. In contrast, sustained polymorphic ventricular tachycardia (VT) is always associated with hemodynamic collapse. In regular BCT the following mechanisms must be differentiated: (1) VT, (2) supraventricular tachycardia (SVT) with bundle branch block or (3) SVT with pre-excitation via accessory pathways, e.g. Wolff-Parkinson-White (WPW) syndrome. The presence of an underlying structural heart disease, specifically a history of myocardial infarction is suggestive of VT. For a differentiated analysis in hemodynamically stable patients a 12-lead ECG is essential. CONCLUSION: Identification of signs of atrioventricular (AV) dissociation or a negative precordial concordance of QRS are indicative of VT. In V1 positive BCTs a positive precordial concordance, QRS width > 140 ms, superiorly directed QRS axis, monophasic or biphasic QRS complexes in V1 and deep S wave in V6 are indications of a VT. In V1 negative BCTs, QRS width > 160 ms, right-sided QRS axis, broad R peak (> 40 ms) in V1/V2, slurred S downstroke in V1/V2 and any Q peak in V6 are all indications of VT as the mechanism.