• AV dissociation – independent atrial and ventricular activity
• Fusion or capture beats – hallmark of VT
• Extreme axis deviation (northwest axis)
• Concordance in precordial leads (all positive or all negative)
• RS interval > 100 ms in any precordial lead
• No initial R wave in V1/V2, or slow R/S transition

AV dissociation is a hallmark of VT. The atria and ventricles depolarize independently, a feature not seen in SVT.

Capture and fusion beats indicate intermittent atrial impulses conducting through the AV node during VT, confirming independent atrial activity.

Extreme axis deviation (northwest axis) suggests VT, especially in structurally abnormal hearts.

Positive or negative concordance across V1–V6 suggests abnormal ventricular activation, supporting VT diagnosis.

Delayed R/S transition, monophasic R wave, and notched S waves favor VT.

Josephson’s sign is a notch in the downstroke of the S wave in precordial leads, suggestive of VT.

Positive concordance refers to all upright QRS complexes in V1–V6, indicating a VT from apical origin.

It uses a stepwise approach examining absence of RS complexes, RS interval, AV dissociation, and morphology criteria to identify VT.

Vereckei is simpler with higher interobserver agreement, but Brugada is more validated. Both have ~85–90% sensitivity.

Ischemic heart disease, dilated cardiomyopathy, ARVC, hypertrophic cardiomyopathy, and sarcoidosis.

Reentrant circuits around infarct scar tissue in the subendocardium.

Triggered activity via early afterdepolarizations, leading to torsades de pointes.

Cyclic AMP-mediated triggered activity—usually idiopathic and sensitive to beta-blockers.

VT without structural heart disease; includes RVOT VT and fascicular VT.

Detects fibrosis or scar as arrhythmogenic substrate, especially in non-ischemic VT.

Entrainment response, earliest activation, reproducible induction, and successful ablation.

It enables 3D localization of VT circuits and guides catheter ablation.

Left bundle pattern, inferior axis, narrow QRS, and absence of AV dissociation.

Long QT syndrome, Brugada syndrome, CPVT, and short QT syndrome.

Immediate synchronized cardioversion with appropriate sedation.

IV Amiodarone.

Can cause hemodynamic collapse if used in structural VT (mistaken for SVT).

In VT with a pulse to prevent R-on-T phenomenon.

Recurrent VT despite meds, intolerant to drugs, or frequent ICD shocks.

ICDs reduce mortality in post-MI patients with reduced EF even without VT history.

ICD significantly reduces sudden death risk; meds like amiodarone reduce burden but not mortality.

Reduce sympathetic tone, prevent sudden death post-MI, and control PVC burden.

Sympathetic blockade (stellate ganglion block), mechanical support, or radiofrequency ablation.

1. Rule out reversible causes, 2. Optimize meds, 3. Reprogram ICD, 4. Ablation, 5. Mechanical support if refractory.