ECG criteria
- Regular tachycardia with a heart rate typically of 150–250 bpm
- Wide QRS complex, ≥ 120 ms, morphology does not match typical RBBB/LBBB
- QRS has a maximally pre-excited, often bizarre morphology; reliability of distinguishing antidromic AVRT from VT based on morphology alone is low
- Absence of an isoelectric interval before the wide QRS prevents reliable differentiation between antidromic AVRT and VT
- Retrograde P wave may be hidden within the QRS or visible after it (in ST or T); RP interval duration is variable and does not confirm the antidromic mechanism on its own
- Sudden onset and termination of the episode (paroxysmal nature)
- In patients with previously documented WPW, sinus rhythm outside the episode shows a short PQ interval and a delta wave
- Typical antidromic AVRT is usually characterized by a 1:1 atrioventricular relationship, but this sign is nonspecific and does not rule out VT or atrial flutter with 1:1 conduction
What it looks like on ECG
During an episode — regular tachycardia with a rate typically of 150–250 bpm and a wide QRS complex (≥ 120 ms). The QRS shape can differ sharply from typical bundle branch blocks, showing a bizarre morphology because the ventricular complex is largely formed by conduction through the accessory pathway. However, there is no strict rule: the QRS is maximally pre-excited and may resemble either bundle branch block or VT; typical bundle branch block morphology does not rule out antidromic AVRT.
The P wave is usually difficult to identify: the retrograde P wave may be hidden within the QRS itself or appear after it, within the ST segment or the T wave of the same complex. The RP interval duration is variable—it depends on the conduction time around the entire re-entry circuit rather than solely on the AV nodal conduction velocity, so a short RP alone does not prove an antidromic mechanism.
The onset and termination of the paroxysm are distinct and sudden. Outside of the episode, if sinus rhythm was previously recorded, classic features of WPW can be seen: a short PQ interval (< 120 ms) and a delta wave at the beginning of the QRS.
| Sign | Antidromic AVRT |
|---|---|
| HR | 150–250/min |
| QRS | wide, ≥ 120 ms |
| QRS morphology | maximally pre-excited, often atypical |
| P wave | hidden within QRS or visible after it, RP is variable |
| Rhythm | strictly regular |
Mechanism
The mechanism involves macro-re-entry utilizing an atrioventricular accessory pathway (historically, the Kent bundle for the typical pathway). In the antidromic variant, the circuit travels in the reverse direction compared to orthodromic tachycardia: the impulse descends from the atria to the ventricles via the accessory pathway (bypassing the AV node), activation begins through it, and then propagates through the ventricular myocardium, bypassing the normal sequence via the His-Purkinje system. The retrograde limb of the circuit is usually the His-Purkinje system and the AV node, but retrograde conduction through another accessory pathway is also possible if the patient has multiple pathways. Because the initial and major part of ventricular depolarization does not travel via the normal conduction system, the QRS is wide and aberrant, often maximally pre-excited. Partial participation of the His-Purkinje system in the antegrade limb is also possible, altering the specific morphology. This variant is significantly rarer than the orthodromic form (which accounts for the majority of AVRT in WPW).
Causes
- WPW syndrome with an accessory pathway capable of antegrade conduction (from atria to ventricles)
- More commonly detected in right-sided, septal, or multiple accessory pathways, although there is no reliable localization pattern for ECG diagnosis
- Triggering factors for the episode: extrasystoles (atrial or ventricular), emotional or physical stress, sometimes without an obvious trigger
Differential diagnosis
- Ventricular tachycardia: also presents with a wide QRS and regular rhythm; points in favor of antidromic AVRT include a known history of WPW and maximally pre-excited QRS morphology, but neither the absence of an isoelectric interval nor a 1:1 ratio allows reliable differentiation from VT. Definitive differentiation on a single ECG is often impossible, and in case of doubt, it should be managed as VT.
- Orthodromic AVRT with aberrant conduction (functional bundle branch block): in orthodromic tachycardia, the QRS is typically narrow unless a concomitant bundle branch block is present; a wide QRS there has the shape of typical RBBB or LBBB rather than a bizarre, maximally pre-excited morphology.
- Atrial fibrillation in WPW: irregular rhythm, varying QRS width and shape, rate may exceed 250 bpm — unlike strictly regular antidromic AVRT.
- Atrial flutter with conduction over an accessory pathway: with antegrade conduction through the accessory pathway, flutter may conduct stably at 1:1 and be strictly regular, mimicking antidromic AVRT; in some cases, slight RR variability or flutter waves are directly visible on the ECG. Vagal maneuvers and adenosine are not recommended as a diagnostic tool when pre-excitation is suspected: AV nodal blockade does not slow conduction through the accessory pathway, and adenosine carries the risk of inducing pre-excited AF with a very rapid ventricular response, up to ventricular fibrillation.
Clinical significance and management
Antidromic AVRT clinically presents as a wide-complex tachycardia and may be accompanied by hemodynamic instability. Since reliable differentiation from ventricular tachycardia on a single ECG is not always possible, immediate synchronized electrical cardioversion is indicated for unstable regular wide-complex tachycardia with a palpable pulse; in polymorphic VT, ventricular fibrillation, or pulselessness, synchronization is not used — management follows the resuscitation algorithm with unsynchronized defibrillation.
In a stable patient with a known or highly probable antegradely conducting accessory pathway, adenosine is not considered a safe first step: the supraventricular origin of the signal does not in itself rule out the risk of inducing pre-excited AF with a dangerously rapid ventricular response. The drugs of choice for stable suspected antidromic AVRT are procainamide or ibutilide, or electrical cardioversion according to protocol. Adenosine may be considered separately and with caution only for uncertain regular monomorphic wide-complex tachycardia when pre-excitation has not been proven, under continuous monitoring and with readiness for immediate cardioversion.
For any unclear wide-complex tachycardia, verapamil must not be administered. Digoxin and intravenous AV nodal blockers are contraindicated primarily in pre-excited AF or atrial flutter, as they can enhance conduction through the accessory pathway and provoke ventricular fibrillation; in regular antidromic AVRT, management is determined by the mechanism and protocol, preferably after specialist consultation.
Definitive treatment is catheter ablation of the accessory pathway, which eliminates the arrhythmia substrate. Patients with confirmed WPW and episodes of tachycardia are referred for an electrophysiological study and ablation.
Common interpretation errors
- Automatically treating any wide-complex regular rhythm as VT without considering a history of WPW, or conversely, too confidently ruling out VT solely based on the presence of WPW
- Prescribing verapamil or digoxin for wide-complex tachycardia without diagnostic certainty
- Considering the 1:1 atrioventricular ratio as reliable proof of antidromic AVRT, even though it also occurs in VT and atrial flutter with 1:1 conduction
- Attempting to uncover flutter waves using vagal maneuvers or adenosine when pre-excitation is suspected, instead of accounting for the risk of accelerating the ventricular response
- Missing a P wave hidden within the QRS or ST-T segment and mistakenly interpreting the rhythm as atrioventricular dissociation
1. What happens to antegrade ventricular activation during antidromic AVRT?
Antegrade activation begins via the accessory pathway, bypassing the normal conduction system, which forms a wide, maximally pre-excited QRS.
2. Which drug must not be administered for an unclear wide-QRS tachycardia in a patient with suspected WPW?
In pre-excited AF or unclear wide tachycardia, verapamil and digoxin can enhance conduction over the accessory pathway and trigger ventricular fibrillation.
3. How does the direction of the re-entry circuit in antidromic AVRT differ from orthodromic AVRT?
In antidromic AVRT, antegrade conduction to the ventricles occurs via the accessory pathway, while the retrograde limb is typically through the His-Purkinje system and AV node (sometimes via another accessory pathway); in orthodromic AVRT, it is the reverse.
Frequently asked questions
How to distinguish antidromic AVRT from ventricular tachycardia?
It is difficult to reliably differentiate them based on a single ECG: both variants produce a regular wide-QRS tachycardia, and neither the absence of an isoelectric interval nor a 1:1 AV ratio are diagnostic features. Documented WPW may favor antidromic AVRT, but in case of any doubt, the tachycardia should be managed as ventricular tachycardia, avoiding verapamil and digoxin.
Why is the QRS wide in antidromic tachycardia?
Antegrade activation begins via the accessory pathway and bypasses the normal activation sequence through the AV node and His-Purkinje system, resulting in a wide, maximally pre-excited QRS. The exact morphology depends on the pathway location and may resemble bundle branch block or VT.
Is antidromic tachycardia dangerous?
Yes, it can present with hemodynamic instability and is easily mistaken for ventricular tachycardia. Furthermore, in a WPW patient with concomitant pre-excited atrial fibrillation, the risk of transformation to ventricular fibrillation is higher with inappropriate medical therapy—primarily when using digoxin or AV nodal blockers.
How does antidromic AVRT differ from orthodromic AVRT?
In orthodromic AVRT, the impulse travels down through the AV node (narrow QRS unless aberrancy is present) and returns via the accessory pathway. In antidromic AVRT, the direction is reversed: the impulse travels down the accessory pathway, ventricular activation does not start through the His-Purkinje system, and therefore the QRS is wide and maximally pre-excited.
Can adenosine be used in antidromic tachycardia?
In the presence of a known or highly probable antegrade-conducting accessory pathway, adenosine is not considered a safe first step: it can induce pre-excited AF with a dangerously rapid ventricular response. The drugs of choice for stable suspected antidromic AVRT are procainamide, ibutilide, or cardioversion; adenosine is reserved for select cases of undetermined regular monomorphic tachycardia, under monitoring and with readiness for cardioversion.
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Related terms
More in the section «Ventricular pre-excitation»
Sources
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Goldberger A. Clinical Electrocardiography: A Simplified Approach
- Orlov V.N. Guide to Electrocardiography
- ESC Guidelines for the management of patients with supraventricular tachycardias
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.