ECG criteria
- Regular rhythm, heart rate usually 150–250 bpm, sudden onset and termination (paroxysm)
- In orthodromic AVRT — narrow QRS (similar to sinus rhythm) unless a bundle branch block is present
- Retrograde P wave is visible after the QRS, often in the ST segment or early T wave; RP is usually longer than in typical AVNRT, but the threshold (approximately RP ≥ 70 ms) is auxiliary and not used in isolation for diagnosis
- The polarity of the retrograde P wave is variable and depends on the pathway location; a negative P wave in II, III, aVF is typical for a posteroseptal location, but not mandatory for AVRT
- In antidromic AVRT — wide QRS due to full antegrade conduction via the accessory pathway, morphology resembles a maximally prominent delta wave
- Outside of an episode, the baseline sinus ECG may show a ventricular pre-excitation pattern (short PR, delta wave, widened QRS) — supports the presence of an antegradely conducting pathway, but its absence does not rule out AVRT
- QRS amplitude alternans from beat to beat is a frequent, but not mandatory, finding
- Vagal maneuvers or adenosine typically terminate orthodromic AVRT (interrupting the circuit in the AV node)
What it looks like on ECG
Orthodromic AVRT is the most common form (about 90–95% of AVRT cases). The impulse travels antegradely through the AV node and the bundle of His (hence the QRS is narrow, as in sinus rhythm), and returns to the atria retrogradely via the accessory pathway. The retrograde P wave is usually visible shortly after the QRS, often in the ST segment or the initial part of the T wave, and sometimes partially merges with the T wave. Compared to typical AVNRT, where the P wave is usually hidden within the QRS or located immediately after it, the RP interval in AVRT is on average longer — however, this is a probabilistic difference, overlaps are possible, and the diagnosis is not made based on a single RP metric. The polarity of the retrograde P wave depends on the location of the accessory pathway: in posteroseptal locations, it is often negative in II, III, and aVF; in other locations, it may be positive, isoelectric, or variable across different leads.
Antidromic AVRT is rare (about 5–10% of AVRT cases, more common in WPW syndrome). The antegrade limb of the circuit is the accessory pathway, so the QRS is wide, deformed, and resembles ventricular tachycardia: the entire ventricle is activated via the accessory pathway without the involvement of the His-Purkinje system. The retrograde limb is usually the AV node, but a second accessory pathway is also possible (in cases of multiple pathways) — in this case, the AV node does not participate in the circuit at all, and adenosine or vagal maneuvers will not interrupt the circuit.
| Sign | Orthodromic AVRT | Antidromic AVRT |
|---|---|---|
| QRS | narrow | wide |
| Pathway antegrade | AV node | accessory pathway |
| Pathway retrograde | accessory pathway | AV node (usually) or second accessory pathway |
| Prevalence | frequent form | rare form |
Heart rate is stable throughout the episode, with sudden onset and termination (typical for re-entrant tachycardias, unlike sinus tachycardia with a gradual warm-up).
Mechanism
AVRT is a macro-re-entrant reciprocating tachycardia involving the AV node and an accessory atrioventricular pathway (e.g., the bundle of Kent in WPW syndrome). For the circuit to form, a difference in conduction and refractoriness between these two pathways is required — a premature beat (atrial or ventricular) blocks in one pathway and conducts via the other, after which the excitation returns and completes the circuit. In the orthodromic form, the circuit travels down the physiological pathway (AV node) and up the accessory pathway. In the antidromic form, the direction is reversed: down the accessory pathway and up — usually via the AV node, but if two or more accessory pathways are present, the retrograde limb may be a second accessory pathway, in which case the AV node does not participate in the circuit.
Causes
- WPW syndrome (manifest, with a delta wave on baseline ECG)
- Concealed accessory pathway — conducts only retrogradely, so the baseline sinus ECG shows no pre-excitation
- Intermittent or minimal antegrade pre-excitation — the delta wave may be absent on a single tracing, although antegrade conduction over the pathway is potentially present
- Multiple accessory pathways (increase the risk of the antidromic form, including retrograde conduction via a second accessory pathway, and predispose to AF with accessory pathway conduction)
- Congenital conduction system anomalies without structural heart disease in most patients
Differential diagnosis
- AV nodal re-entrant tachycardia — the P wave is usually hidden within the QRS or immediately follows it (very short RP, often pseudo-S in II and pseudo-R' in V1); in AVRT, the RP interval is on average longer, but with overlap, and the difference is not absolute
- Atrial tachycardia — a rhythm with an ectopic atrial P wave that precedes the QRS; P wave morphology differs from sinus rhythm, and polarity in the inferior leads may be negative, resembling a retrograde P wave in AVRT, making them indistinguishable based solely on P polarity or PR interval. Evidence favoring atrial tachycardia includes the continuation of the atrial rhythm during the development of AV block (AV dissociation with preservation of P waves at their own rate) and the response to diagnostic maneuvers (vagal maneuvers or adenosine may cause AV block without terminating the atrial rhythm, whereas AVRT is usually entirely terminated by these maneuvers)
- Ventricular tachycardia — in antidromic AVRT, it is extremely difficult to differentiate from VT on a standard ECG; QRS width alone does not reliably separate them, and antidromic AVRT can also present with a very wide QRS. A regular wide-complex tachycardia of uncertain etiology should be managed as VT until proven otherwise, using Brugada/Vereckei criteria, signs of AV dissociation, capture and fusion beats, QRS morphology, and comparison with previous ECGs. A known WPW or delta wave on a sinus ECG only supports the possibility of antidromic AVRT, but does not confirm it and does not rule out VT in the same patient
- Atrial flutter with 2:1 conduction — flutter F waves on the tachycardia ECG may not be visible; inferior leads and V1 should be evaluated, and in a regular rhythm under monitoring, vagal maneuvers or adenosine can be used to temporarily slow AV conduction and reveal F waves; if in doubt, additional diagnostic recordings are indicated
Clinical significance and management
Orthodromic AVRT is usually hemodynamically well tolerated and terminates with vagal maneuvers or adenosine (AV nodal block interrupts the circuit). Antidromic AVRT and especially AF in a patient with an accessory pathway are potentially life-threatening conditions: a short antegrade refractory period of the pathway can lead to extremely rapid ventricular rates with the risk of degenerating into ventricular fibrillation. For wide-complex tachycardia with hemodynamic instability, synchronized cardioversion is indicated. AV nodal blocking agents must be carefully managed depending on the situation: in pre-excited AF, verapamil, digoxin, and other AV nodal blockers are contraindicated — by removing the protective function of the AV node, they can drastically accelerate conduction over the accessory pathway and provoke ventricular fibrillation. In regular wide-complex tachycardia of uncertain origin, verapamil is also avoided — not because of the "protective role" of the AV node, but because the rhythm could be VT, and calcium channel blockers in such patients pose a risk of hemodynamic deterioration. The definitive solution to the problem is catheter ablation of the accessory pathway.
Common interpretation errors
- Mistaking a retrograde P wave for part of the T wave or ST segment and failing to notice it
- Confusing AVRT with AVNRT without assessing P wave position relative to the QRS, forgetting that the difference is probabilistic
- Prescribing verapamil or digoxin in AF with suspected ventricular pre-excitation
- Failing to look for a pre-excitation pattern on the patient's prior baseline ECGs outside of an episode
- Diagnosing antidromic AVRT instead of VT based solely on a history of WPW, without considering wide-complex tachycardia differential diagnosis criteria
1. Which ECG finding during tachycardia favors orthodromic AVRT rather than typical AVNRT?
In orthodromic AVRT, the circuit includes the accessory pathway, so the retrograde conduction time to the atria is on average longer, and the P wave is visible separately, although the difference from AVNRT is probabilistic.
2. Why is the QRS complex wide in antidromic AVRT?
The entire ventricle is activated via the accessory pathway, bypassing the fast physiological conduction system, which results in a wide, deformed QRS.
3. Which drug is contraindicated in atrial fibrillation with ventricular pre-excitation?
Verapamil blocks the AV node and can sharply accelerate conduction via the accessory pathway in AF with pre-excitation, increasing the risk of ventricular fibrillation.
Frequently asked questions
How does AVRT differ from AVNRT on the ECG?
In AVRT, the retrograde P wave is usually visible separately after the QRS, and the RP interval is on average longer than in AVNRT, where the P wave is almost merged with the QRS complex. However, the distinction is probabilistic rather than absolute, and the diagnosis cannot be made based on the RP interval alone. Also, AVRT may present with baseline signs of pre-excitation on the sinus ECG.
Is atrioventricular reentrant tachycardia dangerous?
The orthodromic form is usually relatively well tolerated and terminated with vagal maneuvers or adenosine. The antidromic form and atrial fibrillation in a patient with an accessory pathway are dangerous due to the high risk of a rapid ventricular response and transition to ventricular fibrillation.
Is it possible to distinguish antidromic AVRT from ventricular tachycardia based on a single ECG of the episode?
This is difficult and often impossible to determine with certainty based solely on QRS width or history. Brugada/Vereckei criteria, signs of AV dissociation, capture beats, and fusion beats are used. When in doubt, wide regular tachycardia is managed as VT until proven otherwise.
Why should verapamil not be given when tachycardia with pre-excitation is suspected?
If it is atrial fibrillation with pre-excitation, AV nodal blockers remove its protective role and can sharply accelerate conduction through the accessory pathway, provoking ventricular fibrillation. Verapamil is also not used for unspecified wide-complex tachycardia — it may turn out to be ventricular tachycardia, and a mistake in identifying the rhythm mechanism is dangerous in itself.
How is an episode of orthodromic AVRT terminated?
Vagal maneuvers (Valsalva maneuver, carotid sinus massage) and intravenous adenosine usually terminate the tachycardia circuit by blocking conduction in the AV node.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
- Video lessons and theory for every topic
- Simulator case studies under every lesson
- Unlimited ECG simulator practice
- Study guide: "All ECGs in 25 minutes"
ECG Strip Simulator
ECG, radiology, histology, pathomorphology, pharmacology — thousands of flashcards with detailed explanations.
- Real ECG strips, not textbook drawings
- Instant answers and explanations
- Streaks and progress tracking in your dashboard
Related terms
More in the "Supraventricular Arrhythmias" section
Sources
- Hampton J. The ECG in Practice
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- AHA/ACCF/HRS Recommendations for the Standardization of ECG, 2009
- Orlov V.N. Guide to Electrocardiography
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.