Atrioventricular nodal reentrant tachycardia (AVNRT)

Definition & Pathophysiology

• Reentrant supraventricular tachycardia (SVT) utilizing two functional pathways within atrioventricular (AV) node.
• Dual AV Nodal Physiology: Requires electrophysiologically distinct pathways.
  • Slow Pathway: Short refractory period. Extends from AV node inferiorly toward coronary sinus ostium.
  • Fast Pathway: Longer refractory period. Located higher on atrial septum, extending laterally away from AV node.
• “Slow-Fast” (Typical) AVNRT Mechanism: Premature atrial beat encounters refractory fast pathway. Conduction shifts to slow pathway. Electrical impulse returns retrograde to atrium via fast pathway, establishing reentrant circuit. Represents 80–90% of AVNRT cases.
• Lacks clear anatomic correlates for functional pathways.

Epidemiology

• Dual AV nodal pathways present in ~30% of general population.
• Rare in infancy. Incidence increases during childhood and adolescence.
• More common in adolescents, young adults, and females.
• Occurs in structurally normal hearts and congenital heart disease (CHD).
• Found in adults with CHD at same frequency as general population; often identified during electrophysiology (EP) study as secondary arrhythmia.

Clinical Manifestations

• Abrupt onset and termination.
• Often triggered by exercise or stress.
• Symptoms: Palpitations, dizziness, shortness of breath, chest pain.
• Syncope: Occasional presentation.
• No increased risk of sudden cardiac death (lacks manifest accessory pathway).

Electrocardiographic (ECG) Features

• Regular, narrow QRS complex tachycardia.
• Rate: 150–250 beats/min in children and young adults.
• P-wave Morphology: Retrograde P waves. Negative axis in inferior leads (II, III, aVF).
• P-wave Location: Short RP interval. P wave often buried within or immediately following QRS complex.
• V1 Morphology: Subtle RSr’ pattern (pseudo-R’ wave) visible during tachycardia, absent during normal sinus rhythm.
• Ventriculoatrial (VA) Interval: <70 ms.

Differential Diagnosis

Tachycardia	P-Wave / AV Relationship	Response to Adenosine
AVNRT	Buried/Short RP (VA <70 ms)	Sudden termination (P-wave often last component)
AVRT (Orthodromic)	Inverted (inferior leads); VA >70 ms	Sudden termination (P-wave typically last component)
Ectopic Atrial Tachycardia	Abnormal P-wave axis; Warm-up/Cool-down	Transient AV block unmasking ectopic P-waves, or termination
Junctional Ectopic Tachycardia	AV dissociation common	Transient VA dissociation; tachycardia continues
Atrial Flutter	Saw-tooth waves; 2:1 or 3:1 conduction	Transient AV block unmasking flutter waves

Management

Acute Management

• Hemodynamic stability dictates initial intervention.

Modality	Indication / Dosage	Nuances & Adverse Effects
Vagal Maneuvers	First-line (stable)	Ice bag to face (15-30s) in infants. Valsalva, straining, head-stand in older children. Ocular pressure contraindicated. Carotid massage rarely effective.
Adenosine	Drug of choice (stable)	Rapid IV push: 0.1 mg/kg (max 6 mg). May increase to 0.2 mg/kg (max 12 mg). Requires continuous ECG and immediate direct current (DC) cardioversion availability (risk of inducing atrial fibrillation).
Calcium Channel Blockers	Alternative (older children)	Verapamil reduces cardiac output. Contraindicated in infants <1 year (causes severe hypotension/cardiac arrest).
DC Cardioversion	Hemodynamic instability	Synchronized shock: 0.5–2 J/kg.
Esophageal Pacing	Alternative termination	Pace termination using esophageal catheter.

Chronic & Definitive Management

• Medical Therapy: $\beta$-blockers represent drugs of choice for chronic suppression. Calcium channel blockers also utilized safely.
• Catheter Ablation:
  • Class IIa indication per PACES/HRS guidelines.
  • Definitive cure in >95% of patients.
  • Target: Slow pathway modification.
  • Risk: Unintended damage to fast pathway causing complete AV block, necessitating permanent pacemaker implantation.
  • Energy Source: Radiofrequency ablation or cryoablation. Cryoablation preferred near AV node; no permanent AV block reported with this energy source.

Nuances in Congenital Heart Disease (ACHD)

• AV node location highly variable in specific congenital lesions.
• High-Risk Anatomy: Atrioventricular septal defects (AVSD) and congenitally corrected transposition of the great arteries (L-TGA) feature displaced AV nodal conduction tissue.
• Single ventricle anatomy severely complicates mapping and ablation procedures.
• Medical management preferred over ablation in complex CHD variants due to high risk of inadvertent AV node injury and heart block.