AVNRT on ECG

What it looks like on ECG

The main sign is a regular tachycardia with a narrow QRS without a visible separate P wave preceding the complex. Most commonly (in 90% of cases), the typical slow-fast form is encountered: the impulse travels anterogradely down the slow pathway and retrogradely up the fast pathway. Because retrograde conduction to the atria is rapid, the P wave occurs almost simultaneously with the QRS and is buried inside it.

The key interpretation technique is comparing the tachycardia ECG with the baseline sinus ECG of the same patient:

Pseudo-r' and pseudo-S waves typically appear only during tachycardia and disappear after its termination; comparison with the baseline ECG aids in diagnosis, but the absence of these features outside of an episode is not a mandatory condition for the diagnosis — a similar morphology may occasionally be part of the individual's baseline QRS or intraventricular conduction delay.

In the atypical form (fast-slow, approximately 5–10% of cases), retrograde conduction is slow, so the P wave is frequently negative in the inferior leads (II, III, aVF) and is registered closer to the following QRS complex — the retrograde P is usually visible before the next QRS, and RP is typically longer than PR; this finding is variable and nonspecific. This presentation requires differential diagnosis with atrial tachycardia and AVRT. The ST segment may show depression during tachycardia — this is often a nonspecific rate-related phenomenon, but ischemia must be assessed based on clinical presentation, ECG dynamics, and diagnostic indications. Changes must be re-evaluated after rhythm restoration.

Mechanism

AVNRT involves functional dissociation of fast and slow conduction pathways within the AV nodal region; the circuit typically includes the AV node itself and adjacent perinodal/atrial tissue, rather than being strictly confined within the compact node. In the classical model, the slow pathway has slower conduction and a shorter effective refractory period, while the fast pathway has faster conduction and a longer refractory period.

With a timely paced atrial premature beat, the fast pathway is still refractory, so the impulse travels down exclusively via the slow pathway. By the time it reaches the bottom of the circuit, the fast pathway has recovered and conducts the impulse retrogradely back to the atria. A closed re-entry loop is formed, which sustains itself until conduction conditions change. The ventricles and atria are depolarized almost simultaneously — hence the hidden or pseudo-P wave.

Causes

• Structurally normal heart in most patients (functional dissociation of conduction in the AV nodal region)
• More common in young and middle-aged adults, slightly more prevalent in women than in men
• Triggers of an episode: most commonly atrial premature beats; significantly less frequently, initiation by a premature ventricular beat is possible in the presence of appropriate retrograde conduction; other triggers include physical exertion, emotional stress, caffeine, alcohol, sleep deprivation
• Occasionally accompanies structural heart disease, but there is no specific association with any particular cardiopathology

Differential diagnosis

• Atrioventricular reentrant tachycardia (AVRT, in WPW) — the circuit utilizes an accessory pathway and the AV node; the RP interval is often longer in AVRT, but there is significant overlap; differentiation on a surface ECG is not always possible. A delta wave may be present outside of an episode, but its absence does not exclude a concealed accessory pathway.
• Atrial tachycardia — the P wave is visible separately before the QRS, its morphology differs from sinus rhythm, and the PR interval may be longer or shorter depending on the focus
• Sinus nodal reentrant tachycardia — usually starts and ends abruptly, P wave resembles a sinus P wave. Gradual “warm-up” and “cool-down” are more indicative of automatic ectopic focus tachycardia, but are not standalone diagnostic criteria
• Atrial flutter 2:1 — F waves at a rate of approximately 300 bpm, visible in some lead upon careful inspection (most often II, III, aVF, or V1), ventricular rate around 150 bpm
• Junctional tachycardia (ectopic) — focal/automatic, typically gradual onset and termination, often associated with digoxin toxicity, ischemia, or postoperative states; cardioversion may provide only temporary effect and is not a reliable differential criterion

Clinical significance and management

AVNRT typically does not cause sudden cardiac death in patients without severe structural heart disease, but it can cause marked reduction in cardiac output, ischemia, syncope, and hemodynamic instability, especially at high heart rates or with underlying structural heart disease. The ventricles are activated at a rapid regular rate; describing them as being “protected” by AV nodal refractoriness is incorrect.

For an acute episode in a stable patient: modified Valsalva maneuver as the first-line maneuver; carotid sinus massage should be performed only by trained personnel under monitoring and in the absence of contraindications (carotid bruit, known significant stenosis, previous stroke or TIA). If ineffective, intravenous bolus adenosine (terminates tachycardia via transient AV nodal block); in case of hemodynamic instability, emergency electrical cardioversion according to the tachycardia with a pulse algorithm.

For recurrence prevention and definitive treatment, catheter ablation of the slow AV nodal pathway is a highly effective and safe technique, considered the method of choice for symptomatic recurrent episodes. Medical prophylaxis (beta-blockers, non-dihydropyridine calcium channel blockers) is an alternative if ablation is refused or as a temporary measure prior to it.

Common interpretation errors

• Failing to compare the tachycardia ECG with the baseline sinus ECG — pseudo-R' in V1 and pseudo-S in inferior leads are only visible upon comparison
• Mistaking ST depression during tachycardia for myocardial ischemia — this is a frequent nonspecific phenomenon at rapid heart rates, but requires clinical and dynamic assessment
• Confusing AVNRT with ventricular tachycardia when aberrant conduction causes QRS widening
• Failing to search for atrial flutter waves when suspecting AVNRT with a heart rate around 150 bpm — this may actually be 2:1 flutter
• Overlooking the atypical form with a long RP interval, mistaking it for atrial tachycardia

Frequently asked questions

Related terms

More in the "Supraventricular Arrhythmias" section

Entire section

Sources

• Hampton J. The ECG in Practice
• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
• Orlov V.N. Guide to Electrocardiography
• Clinical Guidelines of the Russian Ministry of Health on 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.