Full EKG Criteria

The atria and ventricles beat independently. P waves march at their own rate, unrelated to the QRS complexes. This proves the wide complex rhythm originates in the ventricles, because in SVT the atria and ventricles are linked. Look for P waves "walking through" the QRS complexes at a slower rate, especially visible in leads II and V1.

A hybrid QRS complex that occurs when a sinus impulse and a ventricular impulse activate the ventricles simultaneously. The resulting QRS is intermediate in morphology between the patient's normal sinus beat and the wide VT beat. Fusion beats prove two independent pacemakers are firing (sinus node and ventricular focus), which only happens in VT.

A narrow, normal-looking QRS complex that appears suddenly in the middle of a wide complex tachycardia. It occurs when a sinus impulse "captures" the ventricles through the normal conduction system during a brief window when the ventricles are not refractory. A narrow beat during a wide complex run proves the wide beats are ventricular in origin.

All six precordial leads (V1 through V6) show QRS complexes deflecting in the same direction: either all predominantly positive (positive concordance) or all predominantly negative (negative concordance). In normal conduction and typical BBB, the QRS transitions from negative to positive across the precordial leads. When all leads agree, the impulse is coming from a single ventricular focus, not through the normal His-Purkinje system.

The QRS axis falls between -90 and +180 degrees, meaning it points up and to the right. On the ECG, this produces negative QRS in both leads I and aVF. This "no man's land" axis is nearly impossible to produce through the normal conduction system, even with aberrancy, and strongly suggests a ventricular origin.

The wider the QRS, the more likely the rhythm is VT. Typical RBBB aberrancy produces a QRS of 120-140ms. LBBB aberrancy rarely exceeds 160ms. A QRS wider than 160ms suggests the impulse is spreading slowly through ventricular muscle rather than using the fast His-Purkinje conduction system. QRS >200ms in the absence of drugs or hyperkalemia is almost always VT.

Measured from the onset of the QRS to the nadir (deepest point) of the S wave in any precordial lead. If this interval exceeds 100ms, it suggests the impulse is conducting slowly through ventricular myocardium rather than the rapid His-Purkinje system. In SVT with aberrancy, the initial part of the QRS is conducted normally and reaches the S-wave nadir quickly.

A small notch or "hitch" near the nadir (lowest point) of the S wave in any precordial lead. This notching reflects slow, irregular conduction through scarred ventricular myocardium. In SVT with aberrancy, the S wave descends and returns smoothly without notching. The Josephson sign is subtle but highly specific when present.

The time from QRS onset to the peak of the R wave in lead II. In normal conduction and aberrancy, the R wave peaks quickly (<50ms) because the impulse travels through the fast conduction system. In VT, the impulse spreads slowly through ventricular muscle, so the R wave takes longer to reach its peak. Measured from the first deflection of the QRS to the tip of the R wave.

In normal conduction, at least one precordial lead (V1-V6) shows a biphasic RS complex: an initial R wave followed by an S wave. If every precordial lead shows only a monophasic complex (all R, all S, all QS, or all qR), it means no lead captures the normal transition of the wavefront across the precordium. This pattern is not possible with aberrancy and confirms VT. Part of the Brugada criteria algorithm.

If an RS complex is present in the precordial leads, measure from the onset of the R wave to the deepest point of the S wave. If this interval exceeds 100ms in any precordial lead, it indicates slow conduction through ventricular myocardium rather than the fast His-Purkinje system. This is the second step of the Brugada criteria algorithm, applied only when an RS complex is found.

The Vereckei algorithm uses lead aVR alone to distinguish VT from SVT. Four steps, applied in order: (1) Is there an initial R wave in aVR? If yes, VT. (2) Is there an initial r or q wave wider than 40ms? If yes, VT. (3) Is there a notch on the descending limb of a predominantly negative QRS? If yes, VT. (4) Measure the voltage change in the first vs last 40ms of the QRS: if the initial 40ms has less voltage change than the terminal 40ms, VT. Any positive step ends the algorithm.

In SVT with aberrancy, the wide QRS should still resemble a classic bundle branch block pattern. Typical RBBB: rsR' ("rabbit ears") in V1 with a wide S wave in V6. Typical LBBB: narrow r wave with a swift, clean descent into S in V1, and a broad R wave in V6. If the wide QRS doesn't match either of these patterns (bizarre morphology, concordant precordial leads, no typical rabbit ears), VT is far more likely.

Patients with prior myocardial infarction, cardiomyopathy, or other structural heart disease have scar tissue that creates the substrate for reentrant VT circuits. In this population, a wide complex tachycardia is VT until proven otherwise. Studies show that ~80% of wide complex tachycardias in patients with structural heart disease are VT. The pretest probability shifts dramatically with this history.

A classic triphasic rsR' ("rabbit ears") in V1 with the second R' taller than the first r, plus a wide S wave in leads I and V6. This pattern reflects normal septal depolarization (r) followed by delayed right ventricular activation (R'). When a wide complex tachycardia perfectly matches this pattern, it suggests the impulse traveled through the AV node normally but encountered a refractory right bundle branch.

In V1: a narrow initial r wave (<30ms) followed by a sharp, smooth, swift descent into a deep S wave with no notching. In V6: a tall, broad R wave. The key is the "clean" morphology. VT with LBBB-type morphology typically shows a wider initial r wave (>30ms), slurred or notched S-wave descent, and may have a q wave in V6. When the LBBB pattern is textbook-clean, aberrancy is more likely.

If the patient has a prior ECG in normal sinus rhythm that shows the same wide QRS morphology (e.g., baseline LBBB or RBBB), and the wide complex tachycardia has an identical QRS shape, the wide QRS is simply the patient's baseline conduction pattern conducted at a faster rate. The tachycardia is supraventricular. Always compare to old ECGs when available.

In a young patient without prior MI, cardiomyopathy, or known heart disease, the pretest probability of VT is lower. SVT with aberrancy, AVRT (WPW), and other supraventricular causes become relatively more likely. However, this is a probabilistic factor, not a rule. Young patients can have VT (idiopathic VT, ARVC, channelopathies). ECG morphology criteria still take priority over demographics.

Monomorphic VT is almost always regular. If a wide complex tachycardia is irregularly irregular, atrial fibrillation with aberrant conduction (baseline BBB or rate-related BBB) is much more likely. The exception: pre-excited AFib (WPW + AFib) also produces an irregular wide complex tachycardia, but with varying QRS morphology from beat to beat reflecting different degrees of pre-excitation.