Vereckei aVR algorithm on ECG

What it looks like on ECG

The algorithm is an evaluation of QRS morphology in lead aVR, performed sequentially in four steps. It applies to regular monomorphic wide QRS tachycardia (≥ 120 ms); the result is not validated for irregular or polymorphic tachycardia.

1. Initial R wave in aVR. Normally, the initial vector of ventricular depolarization is directed from base to apex, i.e., away from aVR, so the complex in aVR begins with a negative deflection. An initial positive wave (R) in aVR is an empirical morphological criterion for VT, reflecting initial ventricular activation that is unusual for the normal conduction pathway. Its presence does not prove a specific focus location: the direction and velocity of the initial vector depend on the site of origin and exit of VT, and an initial R wave is occasionally encountered in certain variants of aberrant or pre-excited conduction. This sign significantly increases the probability of VT, but is not absolute.

1. Duration of the initial r or q in aVR. The duration of the initial R or Q wave is measured from the onset of the QRS to its end — i.e., until the transition through the peak (or trough) to the next deflection. If this initial part lasts more than 40 ms, depolarization is slow, which is typical for VT.

1. Notch on the initial negative deflection. If the complex in aVR begins with a negative wave (QS-like morphology) and its descending limb has a distinct notch, this is also a sign of VT.

1. Vi/Vt ratio (velocity initial/velocity terminal). Vi is the absolute voltage difference between the QRS onset and the point 40 ms from the onset; Vt is the absolute voltage difference between the point 40 ms before the end of the QRS and its end. Since both segments are equal in time (40 ms), this ratio essentially reflects the ratio of velocities (slopes) of the initial and terminal parts of the complex. Vi/Vt ≤ 1 is characteristic of VT, while Vi/Vt > 1 is characteristic of SVT with aberrancy.

Mechanism

In SVT with aberrant conduction, initial depolarization is triggered via the AV node and the His-Purkinje system — a fast specialized conduction system; therefore, the initial vector usually remains rapid and directed away from aVR, as normal. Deceleration due to bundle branch block manifests in the terminal part of the QRS. In VT, the impulse originates in the ventricular contractile myocardium and initially propagates cell-to-cell, bypassing the fast conduction system, which yields a slower initial vector, sometimes directed toward aVR. This is a general pattern rather than a strict rule: the specific direction and velocity of initial activation depend on the location of the VT focus and the type of aberrancy, so exceptions in both directions are possible. The Vi/Vt ratio is an empirical quantitative sign of this specific relative slowing of the initial part of the complex in VT, rather than proof of a mandatory late involvement of His-Purkinje fibers.

When to use

• Regular monomorphic wide QRS tachycardia (≥ 120 ms) of unclear origin
• Suspected VT in a patient with structural heart disease or prior myocardial infarction
• Absence of overt pre-excitation (in antidromic tachycardia via an accessory pathway, the algorithm is unreliable because the initial vector is formed differently)
• As an alternative or adjunct to the Brugada criteria for VT

The algorithm should not be used as a validated diagnostic method for irregular or polymorphic wide QRS tachycardia, atrial fibrillation with pre-excitation, and other forms of ventricular pre-excitation.

Differential diagnosis

Antidromic tachycardia in WPW: the initial QRS vector is formed via an accessory pathway rather than de novo through the ventricular myocardium; therefore, the aVR algorithm and Brugada criteria are less reliable here — additional pre-excitation signs and clinical context are needed.

Irregular or polymorphic wide QRS tachycardia: the algorithm is designed for regular monomorphic tachycardia; the result is unreliable in polymorphic VT, atrial fibrillation with pre-excitation, and other irregular rhythms.

Vi/Vt measurement artifacts: with low-amplitude or noisy QRS in aVR, the 40 ms segment assessment is inaccurate — in such cases, rely on steps 1–3 or the Brugada criteria.

Complete bundle branch block without tachycardia: the morphology resembles aberrancy, but the algorithm is used only during tachycardia, not for evaluating bundle branch blocks during sinus rhythm.

Clinical significance and management

Proper differentiation between VT and SVT with aberrancy dictates management. Unstable monomorphic VT with a pulse requires immediate synchronized electrical cardioversion. Pulseless VT is managed according to cardiac arrest protocols — CPR and unsustained/unsynchronized defibrillation. Sustained polymorphic VT with a pulse usually requires immediate unsynchronized defibrillation due to the inability to achieve reliable synchronization, as well as correction of the underlying cause (ischemia, electrolyte abnormalities, prolonged QT), though this is not equivalent to cardiac arrest if a pulse is present.

In stable regular monomorphic wide-complex tachycardia interpreted as VT, ensure monitoring, IV access, electrolyte correction, and administration of an intravenous antiarrhythmic drug according to protocol (often procainamide or amiodarone); the choice depends on structural heart disease, QT interval duration, and left ventricular function. If clinical deterioration occurs or drug therapy fails, proceed to synchronized cardioversion. Post-stabilization, evaluation is indicated to rule out structural heart disease (CAD, cardiomyopathies, post-infarction scar).

In diagnostic uncertainty, wide-complex tachycardia is provisionally treated as VT until proven otherwise. Consequently, verapamil and diltiazem should be avoided in wide-complex tachycardia of unclear etiology, especially if VT or pre-excitation is suspected, as they can precipitate hemodynamic instability and ventricular fibrillation in true VT. Adenosine in this setting may be considered only in a stable patient with regular monomorphic tachycardia in an appropriate clinical context and with immediate resuscitation equipment available, but it does not replace the fundamental rule to manage unclear wide-complex tachycardia as VT.

The Vereckei algorithm is convenient at the bedside due to the evaluation of a single lead, but a "non-VT" result merely means that SVT with aberrancy is more likely, without ruling out VT. It does not replace the full Brugada algorithm and clinical evaluation (age, history of CAD, AV dissociation, capture and fusion beats on ECG).

Common interpretation errors

• Applying the algorithm to narrow QRS tachycardia or irregular/polymorphic wide QRS tachycardia — the method is validated only for regular monomorphic wide QRS tachycardia
• Interpreting a negative result (absence of VT criteria) as proven SVT rather than a result that merely increases the probability of SVT
• Incorrect measurement of the 40 ms interval for Vi/Vt due to low recording speed or calibration
• Ignoring steps 1–3 and jumping directly to Vi/Vt, even though the first three signs are simpler and often resolve the question immediately
• Applying the algorithm in overt pre-excitation (WPW) without accounting for the method's limitations

Frequently asked questions

Related terms

More in the section "Criteria, Formulas, Algorithms"

Entire section

Sources

• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice, 6th ed.
• Hampton J. The ECG in Practice
• AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the ECG, 2009

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.