Overview

AV delay≈0.09 s in the node (≈0.13 s total)

Conduction velocity≈0.01–0.05 m/s

Escape rate≈40–60/min

Location. The AV node lies just beneath the endocardium in the lower interatrial septum, at the apex of the triangle of Koch and just above the opening of the coronary sinus. The triangle is bounded by the tendon of Todaro, the attachment of the septal tricuspid leaflet and the coronary sinus ostium.

Slow conduction. Conduction through the node is very slow, about 0.01–0.05 m/s. The reasons are that its cells are small, have few gap junctions (mostly connexin 45) and fire Ca²⁺-dependent rather than Na⁺-dependent action potentials. The impulse is delayed about 0.09 s in the node and a further 0.04 s in the penetrating part of the bundle of His, a total of about 0.13 s. This delay is the main component of the PR interval.

Filtering. AV nodal conduction slows further as the rate rises (decremental conduction), and the node has a long refractory period. Together these limit how many atrial impulses reach the ventricles. This protects the ventricles during atrial fibrillation or flutter.

Back-up pacemaker. If the SA node fails, the AV junction can take over at an escape rate of about 40–60/min, producing a junctional rhythm.

Location: In the lower interatrial septum, at the apex of the triangle of Koch, just above the opening of the coronary sinus.

Anatomy

Arterial supply: AV nodal artery from the dominant coronary artery, which is the RCA in about 80–90% of people. The septal perforators of the LAD add a second supply to the adjacent bundle of His.

Function

Delays the impulse so that atrial contraction finishes before the ventricles contract.
Filters rapid atrial rhythms and protects the ventricles.
Acts as a back-up pacemaker (junctional escape rhythm, 40–60/min).

Physiology: Some people have two functional input routes into the AV node: a fast pathway with a long refractory period and a slow pathway with a short one. This dual-pathway arrangement allows AV nodal re-entrant tachycardia (AVNRT), the most common regular supraventricular tachycardia.
Regulation: The left vagus mainly supplies the AV node. Vagal stimulation slows AV conduction (negative dromotropy), and sympathetic stimulation speeds it up. Adenosine, β-blockers, non-dihydropyridine calcium channel blockers (verapamil, diltiazem) and digoxin all slow AV nodal conduction.

Clinical significance

AV block

In first-degree block the PR interval is longer than 200 ms. In Mobitz I (Wenckebach) block the PR interval lengthens progressively until a beat is dropped. It is usually caused by disease in the AV node itself and is benign. In Mobitz II block, beats are dropped without warning while the PR interval stays constant. The block lies below the node, and patients usually need a pacemaker. In third-degree (complete) block the atria and ventricles beat independently, with cannon a waves in the JVP and a slow escape rhythm.

Adenosine and SVT

An intravenous bolus of adenosine causes a brief AV block. This terminates re-entrant tachycardias that use the AV node (AVNRT, AVRT). It also slows the ventricular rate long enough to reveal atrial flutter waves.

Test yourself

Which ECG interval mainly reflects conduction delay through the AV node?

QT interval
PR interval
QRS duration
ST segment

Answer: PR interval

The PR interval runs from the start of atrial depolarisation to the start of ventricular depolarisation (normally 0.12–0.20 s). Most of it is the deliberate delay in the AV node, about 0.09 s.