Atrioventricular node

Physiological role and impulse conduction

In a healthy heart, the primary pacemaker is the sinoatrial node (SAN). The impulse generated in it passes through the AVN and spreads to the ventricles.

This is confirmed by the classic physiological experiment involving the placement of Stannius ligatures on the frog heart, which proves the existence of a decreasing gradient of automaticity from the sinus venosus to the apex of the heart (in frogs, the analogue of the AVN is Bidder's ganglion).

When an ectopic excitation occurs in the atria (atrial extrasystole), the ectopic impulse also passes through the AVN and spreads to the ventricles via the normal pathway. On the ECG, this manifests as a deformed P wave preceding the extrasystole and a normal (narrow) QRS complex, since intraventricular conduction is not impaired.

How is AV nodal function regulated?

Conduction in the AV node is regulated by the cholinergic system (acetylcholine, vagus nerve — n. vagus).

• Inhibitory effect — the vagus nerve suppresses the node's activity. The target for acetylcholine is the $M_2$ muscarinic receptors of the heart.
• Improved conduction — occurs when the inhibitory effect of the vagus is removed (e.g., during pharmacological blockade of $M_2$ receptors).
• Vagal maneuvers — physiological stimulation of the vagus nerve slows down the heart rate and often helps terminate tachycardia attacks associated with the node.

Mechanism of AV nodal re-entrant tachycardia

In some cases, longitudinal dissociation of the AV node occurs — its functional division into two pathways (zones of differentiated conduction) that are structurally and functionally heterogeneous: the "fast" and "slow" pathways.

This creates conditions for a macro-re-entry mechanism (circulating excitation) within the node and the development of paroxysmal reciprocating atrioventricular nodal tachycardia (AVNRT). The triggering condition is a premature atrial impulse that arrives during the critical coupling interval: the moment when the "fast" pathway is still in a refractory state, while the "slow" pathway has already recovered and is ready to conduct the signal.

Clinical variants and manifestations of AVNRT

Several forms of tachycardia are distinguished depending on the direction of impulse circulation:

• Typical form (slow-fast) — antegrade conduction occurs via the "slow" pathway, and retrograde conduction via the "fast" pathway. The time from the onset of ventricular activation to retrograde atrial depolarization (VA interval) is 70 ms or less.
• Atypical form (fast-slow) — antegrade conduction via the "fast" pathway, retrograde conduction via the "slow" pathway. Characterized by a long RP' interval.
• Atypical form (slow-slow) — a casuistically rare variant with a VA interval of more than 70 ms.

Symptoms: Attacks have a sudden onset and termination ("on-off" phenomenon). Patients may experience "neck pounding" (Frog sign) due to blood regurgitation into the jugular veins during right atrial contraction when the tricuspid valve is closed. Polyuria and dizziness are characteristic. Hemodynamically, in the first 10–30 seconds, there is a maximal decrease in blood pressure with a subsequent tendency toward recovery.

ECG findings: The QRS complex is usually of normal duration (less than 120 ms), except for cases of aberrant conduction (e.g., right bundle branch block). AVNRT is the only macro-re-entrant AV tachycardia in which 2:1 conduction to the ventricles is possible (if the block is located below the AV node).

Epidemiology: Disease onset most commonly occurs at a young age (average 23–32 years), predominantly in women. Usually, the arrhythmia is not associated with structural heart disease, and triggering factors include physical exertion, emotional stress, digestive disorders, or alcohol.

Class and exam questions

What else to study on this topic

• Sinoatrial node (SAN)
• Gradient of heart automaticity
• Atrial extrasystole
• Autonomic regulation of the heart

Other topics in "Physiology concepts"

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