Atrioventricular Nodal Reentrant Tachycardia
A sudden, rapid heart rate caused by an electrical 'short circuit' inside the heart's AV node, starting and stopping abruptly.
Emergency Management: If the patient with AVNRT is hemodynamically UNSTABLE (systolic BP < 90, ischemic chest pain, altered LOC), immediate synchronized direct current (DC) cardioversion (50-100 Joules) is required, bypassing medications.
Atrioventricular Nodal Reentrant Tachycardia (AVNRT) is the most common type of paroxysmal supraventricular tachycardia (SVT). It is a rapid, regular, narrow-complex arrhythmia caused by a microscopic electrical reentry circuit located entirely within or immediately adjacent to the atrioventricular (AV) node.
Detailed Overview
AVNRT occurs in patients born with dual AV nodal physiology—meaning their AV node has two distinct electrical pathways: a 'fast' pathway (conducts electricity quickly but recovers slowly) and a 'slow' pathway (conducts slowly but recovers quickly). Usually, a premature atrial contraction (PAC) arrives when the fast pathway is still refractory (recovering) but the slow pathway is ready. The impulse travels down the slow pathway. By the time it reaches the bottom of the node, the fast pathway has recovered, allowing the impulse to travel backwards (retrogradely) up the fast pathway. This creates a continuous, self-sustaining loop (reentry circuit) that fires the ventricles and atria almost simultaneously at rates typically between 150-250 beats per minute.
Epidemiology & Demographics
The most common SVT, accounting for ~60% of cases. Most frequently presents in young healthy adults (20s-40s). Strikingly more common in women (approximately 75% of cases).
Etiological Mechanism
Congenital presence of dual AV nodal pathways. The arrhythmia is typically triggered by a premature atrial complex (PAC), caffeine, stress, or exertion.
Primary Causes
An electrical structural anomaly within the heart tissue itself. Not caused by coronary artery disease or structural heart muscle disease.
In typical AVNRT (Slow-Fast configuration, >90% of cases), antegrade conduction (down to ventricles) goes via the slow pathway, and retrograde conduction (up to atria) goes via the fast pathway. This results in the atria and ventricles depolarizing almost exactly at the same time. On an ECG, the retrograde P wave is often completely hidden within the QRS complex, or seen as a tiny terminal deflection at the end of the QRS (a pseudo r' in V1 or pseudo S wave in inferior leads). The rapid ventricular rate impairs diastolic filling, dropping stroke volume, which can cause symptoms of poor perfusion.
Diagnostic Criteria & Guidelines
Electrocardiogram (ECG) during an episode showing a regular, narrow QRS tachycardia (QRS < 120 ms) with absent P waves (hidden in QRS) or retrograde P waves causing pseudo r' in V1. Definitive diagnosis is via Electrophysiology (EP) study.
For acute termination of a stable episode: Vagal maneuvers (Valsalva maneuver, carotid sinus massage, cold water to the face). If vagal maneuvers fail, Adenosine is the drug of choice. Administer 6 mg IV rapid push via a large proximal vein, followed by a 20 mL saline flush. If ineffective, repeat with a 12 mg dose. Adenosine transiently completely blocks the AV node, breaking the reentry circuit.
Second-Line & Adjunctive Therapy
For acute termination if adenosine fails: IV Non-dihydropyridine Calcium Channel Blockers (Verapamil 2.5-5 mg IV or Diltiazem 15-20 mg IV) or IV Beta-blockers (Metoprolol 5 mg IV). For long-term prevention (chronic management) if episodes are infrequent: oral beta-blockers (Metoprolol succinate 25-50 mg daily) or Calcium channel blockers (Verapamil 120 mg ER daily).
Surgical & Procedural Management
Radiofrequency Catheter Ablation is the definitive, curative treatment of choice. During an EP study, the slow pathway is located and destroyed using radiofrequency energy (burning) or cryoablation (freezing). It has a success rate of >95% and is considered first-line for patients who do not want to take lifelong medications.
Patient Counseling & Advice
Warn the patient about the side effects of IV Adenosine before giving it: they will experience a few seconds of intense chest pressure, flushing, and a terrifying 'feeling of impending doom' as their heart briefly pauses (asystole) before restarting normally.
Follow-Up & Monitoring Schedule
Outpatient Holter or event monitor if the diagnosis was suspected clinically but not caught on a 12-lead ECG. Post-ablation, routine follow-up with EP cardiology at 1 and 6 months.
Preventive Strategies
Catheter ablation prevents future episodes permanently in 95% of patients. Medication therapy only suppresses episodes as long as it is taken.
Excellent. It is a benign arrhythmia that does not cause sudden cardiac death. Curable with ablation. The only major risk during ablation is a <1% chance of complete AV block requiring a permanent pacemaker.