Physiological Role and Impulse Conduction
In a healthy heart, the primary pacemaker is the sinoatrial node (SAN). The impulse generated there passes through the AV node and spreads across the ventricles.
This is demonstrated by the classic physiological experiment involving Stannius ligatures on a frog heart, which proves the existence of a decreasing gradient of automaticity from the sinus venosus to the cardiac apex (in frogs, Bidder's ganglion serves as the functional analogue of the AV node).
When an ectopic premature beat occurs in the atria (atrial extrasystole), the impulse also passes through the AV node and spreads to the ventricles via the normal pathway. On an ECG, this appears as a deformed P wave preceding the premature beat, followed by a normal (narrow) QRS complex, as intraventricular conduction is unaffected.
Autonomic Regulation of the AV Node
Conduction in the AV node is regulated by the autonomic nervous system, specifically the parasympathetic nervous system via acetylcholine and the vagus nerve (n. vagus).
- Inhibitory effect — vagal stimulation suppresses AV nodal conduction. The primary targets for acetylcholine are cardiac $M_2$ muscarinic receptors.
- Enhanced conduction — occurs when vagal tone is withdrawn (e.g., via pharmacological blockade of $M_2$ receptors).
- Vagal maneuvers — physiological stimulation of the vagus nerve decreases heart rate and frequently terminates AV nodal-dependent tachycardias.
Mechanism of AV Nodal Re-Entrant Tachycardia
In some individuals, longitudinal dissociation of the AV node occurs—a functional separation into two pathways with distinct structural and electrophysiological properties: the "fast" and "slow" pathways.
This creates the conditions for a macro-re-entry circuit within the node, leading to paroxysmal AV nodal re-entrant tachycardia (AVNRT). The trigger for this arrhythmia is a premature atrial impulse that arrives during the critical coupling interval: the precise moment when the "fast" pathway is still refractory, while the "slow" pathway has recovered excitability and is ready to conduct the signal.
Clinical Variants and Manifestations of AVNRT
Several forms of AVNRT are classified based on the direction of impulse circulation:
- Typical form (slow-fast) — antegrade conduction travels via the "slow" pathway, and retrograde conduction returns via the "fast" pathway. The time from the onset of ventricular activation to retrograde atrial depolarization (VA interval) is $\le$70 ms.
- Atypical form (fast-slow) — antegrade conduction travels via the "fast" pathway, and retrograde conduction returns via the "slow" pathway. Characterized by a long RP' interval.
- Atypical form (slow-slow) — a rare variant with a VA interval >70 ms.
Symptoms: Episodes have a sudden onset and termination ("on-off" phenomenon). Patients may experience "neck pounding" (Frog sign) due to simultaneous right atrial contraction against a closed tricuspid valve, which propels blood retrogradely into the jugular veins. Polyuria and dizziness are also common. Hemodynamically, a maximal drop in blood pressure occurs in the first 10–30 seconds, followed by a compensatory recovery.
ECG Findings: The QRS complex is usually of normal duration (less than 120 ms) unless aberrant conduction (such as bundle branch block) is present. AVNRT is the only re-entrant AV junctional tachycardia that can occasionally conduct to the ventricles with a 2:1 block if the level of block is infra-nodal.
Epidemiology: Onset typically occurs in young adulthood (mean age 23–32 years), with a female predominance. The arrhythmia usually occurs in structurally normal hearts, triggered by physical exertion, emotional stress, heavy meals, or alcohol.