Atrioventricular nodal reentrant tachycardia (AVNRT)

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Pathophysiology and Mechanisms

Clinical Manifestations

Diagnostic Investigations

Modality Specific Findings and Diagnostic Utility
Auscultation Physical examination during an episode reveals a perfectly regular, rapid heart rhythm that lacks the normal physiological variation typically seen with respiration.
Electrocardiogram (ECG) The classic presentation is a regular, narrow QRS complex tachycardia, reflecting normal antegrade ventricular activation via the His-Purkinje system. Because atrial and ventricular activation occur almost simultaneously, retrograde P waves are usually masked and hidden within the QRS complexes. However, a retrograde P wave may occasionally be visible at the terminal portion of the QRS in lead V1, appearing as a subtle "RSr'" pattern that is strictly absent during baseline normal sinus rhythm. The ventriculoatrial (VA) interval is very short, characteristically measuring less than 70 milliseconds.
Echocardiography Utilized to exclude underlying structural congenital heart disease and to confirm normal baseline biventricular systolic and diastolic function.
Invasive Electrophysiology (EP) Study Diagnostic programmed electrical stimulation (atrial extrastimulus testing) is used to map the pathways, demonstrating the characteristic "AH jump" indicative of dual AV nodal physiology, and to reliably induce the clinical tachycardia.

Management

Management Phase Targeted Interventions and Pharmacotherapy
Acute Termination (Hemodynamically Stable) Vagal maneuvers are the initial first-line therapy to increase parasympathetic tone and slow AV nodal conduction. In infants, applying an ice bag to the face for 15-30 seconds is effective. Older children should be instructed to perform the Valsalva maneuver, bear down, hold their breath, or perform a headstand. Ocular pressure is strictly contraindicated.
Acute Pharmacologic Cardioversion If vagal maneuvers are unsuccessful, rapid intravenous administration of Adenosine (0.1 mg/kg, maximum initial dose 6 mg; may increase to 0.2 mg/kg, maximum 12 mg) is the drug of choice. Adenosine activates the inward potassium rectifier current, leading to hyperpolarization and profound transient AV nodal blockade. The ECG characteristically shows termination of the tachyarrhythmia with a P-wave as the last electrical component. Intravenous calcium channel blockers (e.g., verapamil) may be used in older adolescents but are absolutely contraindicated in infants under 1 year of age due to the risk of severe hypotension and cardiovascular collapse.
Acute Termination (Hemodynamically Unstable) If the patient presents with cardiovascular collapse, severe hypotension, or heart failure, immediate synchronized direct current (DC) cardioversion (0.5 to 2 Joules/kg) is the mandatory first-line treatment.
Chronic Medical Prophylaxis For patients requiring chronic suppression to prevent recurrent episodes, oral beta-adrenergic blockers or calcium channel blockers are the mainstays of medical therapy.
Definitive Interventional Therapy Transcatheter ablation of the slow pathway offers a definitive cure in greater than 95% of patients and is highly recommended for older children and adolescents with symptomatic or recurrent AVNRT. Cryoablation is frequently preferred as it causes irreversible cell damage by freezing while providing a superior safety profile around the compact AV node; no permanent AV block has been reported with its use. Radiofrequency (heat) ablation carries a small but critical risk of unintended damage to the fast pathway or the AV node itself, potentially resulting in complete heart block and the lifelong need for a permanent pacemaker.