AVNRT — Atrioventricular Nodal Reentrant Tachycardia
The most common paroxysmal supraventricular tachycardia in clinical practice
Mechanism
Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular paroxysmal supraventricular tachycardia (SVT), accounting for approximately 60% of all SVTs. It results from a reentrant circuit involving two functionally and anatomically distinct pathways within the perinodal tissue of the AV junction. Understanding the dual AV nodal physiology is central to diagnosing and ablating this arrhythmia.
The fast pathway is located superiorly, near the apex of Koch's triangle, close to the compact AV node and the His bundle. It conducts rapidly but has a longer effective refractory period (ERP). The slow pathway is located anteroinferiorly, along the tricuspid annulus near the coronary sinus ostium, at the base of Koch's triangle. It conducts slowly but has a shorter ERP. Koch's triangle — bounded by the tendon of Todaro posterosuperiorly, the tricuspid annulus inferiorly, and the coronary sinus os posteriorly — defines the anatomic region in which both pathways reside.
In typical (slow-fast) AVNRT (90–95% of cases), a premature atrial beat blocks in the fast pathway (still refractory), conducts antegradely down the slow pathway, then returns retrogradely up the now-recovered fast pathway. Because atrial and ventricular activation occur nearly simultaneously (retrograde fast pathway activation arrives at the atrium just as antegrade slow pathway activates the ventricle), the P wave is buried within or immediately after the QRS complex. In atypical (fast-slow) AVNRT, the circuit reverses: antegrade conduction proceeds down the fast pathway and retrograde conduction up the slow pathway, producing a long RP tachycardia. The rare slow-slow variant uses two slow pathways with intermediate RP intervals.
- Fast pathway: superior, near apex of Koch's triangle — rapid conduction, long ERP
- Slow pathway: anteroinferior, near CS os — slow conduction, short ERP
- Koch's triangle: tendon of Todaro, tricuspid annulus, coronary sinus os
- Typical AVNRT: antegrade slow, retrograde fast (short RP)
- Atypical AVNRT: antegrade fast, retrograde slow (long RP)
Importantly, the reentrant circuit is confined to the perinodal tissue and does not require atrial or ventricular myocardium as obligatory limbs, though atrial tissue typically participates in the upper turnaround. This is why AV block can occasionally occur without terminating the tachycardia — a finding that strongly supports AVNRT over AVRT, where the atrium is an obligatory component of the circuit.
ECG Clues
AVNRT typically presents as a regular narrow-complex tachycardia at rates of 150–250 bpm with abrupt onset and termination. The hallmark is the relationship between the P wave and QRS complex, which varies with the subtype.
- Narrow QRS (<120 ms) unless pre-existing or rate-related aberrancy
- Heart rate 150–250 bpm, regular RR intervals
- RP interval <70 ms — P waves buried in or just after the QRS
- Pseudo-r′ in V1: a small upright deflection at the terminal portion of the QRS not present in sinus rhythm — retrograde P wave mimicking a terminal r′
- Pseudo-S waves in leads II, III, aVF: a small notch in the terminal QRS giving the appearance of S waves not seen in sinus
- ST depression is common (rate-related, not ischemic)
In atypical (fast-slow) AVNRT, the RP interval is longer than the PR interval (RP > PR), producing an inverted P wave well before the next QRS — a long RP tachycardia. This can mimic atypical atrial flutter, ectopic atrial tachycardia, or PJRT. In the slow-slow variant, the RP interval is intermediate, and retrograde P waves may be visible in the ST segment.
Comparing AVNRT subtypes on the surface ECG is crucial for pre-procedural localization and planning:
| Feature | Typical (Slow-Fast) | Atypical (Fast-Slow) | Slow-Slow |
|---|---|---|---|
| RP interval | <70 ms | >PR interval (long RP) | Intermediate (70–200 ms) |
| P wave location | Buried in QRS or terminal QRS | Well before next QRS | In ST segment |
| Pseudo-r′ in V1 | Common | Absent | Uncommon |
| Pseudo-S in II/III/aVF | Common | Absent | Uncommon |
| Prevalence | 90–95% | 3–5% | 1–5% |
EP Study Findings
The electrophysiology study in AVNRT is both diagnostic and therapeutic. A systematic approach to demonstrating dual AV nodal physiology, inducing the tachycardia, and differentiating from other SVTs is essential.
Demonstrating Dual AV Nodal Physiology
During atrial extrastimulus testing (decremental S1-S2 from the high right atrium), the hallmark of dual AV nodal physiology is an AH jump >50 ms for a 10 ms decrement in the S1-S2 coupling interval. This represents conduction shifting from the fast pathway (which reaches its ERP and blocks) to the slow pathway. The AH jump is often accompanied by a single echo beat or initiation of sustained AVNRT.
- AH jump >50 ms for a 10 ms decrease in coupling interval = dual AV nodal physiology
- Induction typically with atrial extrastimulus (S1-S2); may require atropine or isoproterenol
- The longest S1-S2 that induces AVNRT corresponds to the fast pathway ERP
- Echo beats (single reentrant beats) often precede sustained tachycardia
- ~30% of the general population has dual AV nodal physiology without clinical AVNRT
Intracardiac Intervals During Tachycardia
During typical AVNRT, the AH interval is prolonged (typically 200–400 ms), reflecting antegrade slow pathway conduction. The VA interval is short (<70 ms), measured from the onset of the ventricular electrogram on the His catheter to the earliest atrial activation (usually on the His or CS proximal recording). A VA interval <70 ms is a hallmark of typical AVNRT and is difficult to achieve with any accessory pathway because of the additional time needed to traverse myocardial tissue to reach the AP insertion. The retrograde atrial activation sequence is typically concentric (earliest at His/CS os) because retrograde fast pathway activation exits near the apex of Koch's triangle.
Key Differential Maneuvers
Distinguishing AVNRT from AVRT (orthodromic) and atrial tachycardia requires several important maneuvers:
A premature ventricular complex (PVC) delivered when the His bundle is refractory that advances or resets the atrial activation excludes AVNRT and proves the presence of an accessory pathway (AVRT). In AVNRT, the PVC cannot reach the atrium because the His bundle blocks retrograde conduction; therefore, the tachycardia is not perturbed.
Pacing near the His bundle at high output (capturing both His and myocardium) vs low output (capturing myocardium only). In AVNRT, the stimulus-to-atrium (SA) interval and retrograde atrial activation sequence remain unchanged regardless of His capture, because retrograde activation goes through the AV node in both cases. In AVRT with a septal AP, His capture shortens the SA interval and changes the activation sequence.
Ventricular overdrive pacing during SVT: the response upon cessation is analyzed. A V-A-V response suggests AVRT. A V-A-A-V response suggests AVNRT or atrial tachycardia. The post-pacing interval minus tachycardia cycle length (PPI − TCL) from the RV apex of >115 ms favors AVNRT over AVRT.
VA linking is another useful concept: in AVNRT, the VA interval is fixed and does not change with changes in cycle length (because the VA is determined by the fast pathway conduction time, which is constant). Variability in the VA interval favors atrial tachycardia.
Ablation Targets & Strategy
Catheter ablation is the definitive treatment for AVNRT, with success rates exceeding 97% and a recurrence rate of 1–3%. The target is the slow pathway, located in the posteroinferior region of Koch's triangle, between the coronary sinus ostium and the tricuspid annulus.
Anatomic Targeting
The ablation catheter is positioned along the tricuspid annulus, just anterior and superior to the coronary sinus ostium. The region is divided into posterior, mid, and anterior zones. Most operators begin at the most posterior position (near the CS os) and move anteriorly if needed. The electrogram at the target site typically shows a small atrial signal relative to the ventricular signal (A/V ratio <0.5), often with a slow pathway potential visible between the atrial and ventricular electrograms.
- Junctional ectopy: the appearance of junctional rhythm during RF delivery is the most reliable real-time indicator of effective slow pathway modification — it indicates proximity to the AV nodal slow pathway inputs
- Non-inducibility: AVNRT is no longer inducible with or without isoproterenol
- Elimination of slow pathway: loss of the AH jump on repeat extrastimulus testing (some operators accept persistent dual physiology without inducibility)
- Single echo beat: a single echo beat without sustained AVNRT after ablation is generally considered an acceptable endpoint
Junctional Ectopy During Ablation
Junctional ectopy during radiofrequency energy delivery is the hallmark of successful slow pathway ablation. The appearance of accelerated junctional rhythm confirms that the lesion is being placed in the correct location. However, 1:1 VA conduction must be monitored during junctional ectopy — loss of retrograde VA conduction during junctional beats signals impending AV block and should prompt immediate cessation of energy delivery.
Cryoablation
Cryoablation is an alternative energy source particularly suited for AVNRT ablation when the target site is close to the compact AV node or His bundle. Cryotherapy offers the advantage of cryomapping — reversible cooling to −30°C to assess the effect on AV conduction before creating a permanent lesion (−80°C). If AV block develops during cryomapping, rewarming restores conduction. The trade-off is a slightly higher recurrence rate (3–7% vs 1–3% with radiofrequency), but the superior safety profile makes it the preferred modality in young patients and those with challenging anatomy.
Key References
- Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992;327(5):313–318. DOI: 10.1056/NEJM199207303270504
- Cosío FG, Anderson RH, Kuck KH, et al. Living anatomy of the atrioventricular junctions. A guide to electrophysiological mapping. Circulation. 1999;100(5):e31–e37. DOI: 10.1161/01.CIR.100.5.e31
- Katritsis DG, Camm AJ. Atrioventricular nodal reentrant tachycardia. Circulation. 2010;122(8):831–840. DOI: 10.1161/CIRCULATIONAHA.110.936591
- Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41(5):655–720. DOI: 10.1093/eurheartj/ehz467
- Katritsis DG, Zografos T, Katritsis GD, et al. Catheter ablation vs. antiarrhythmic drug therapy in patients with symptomatic atrioventricular nodal re-entrant tachycardia: a randomized, controlled trial. Europace. 2017;19(4):602–606. DOI: 10.1093/europace/euw064