Atrioventricular (AV) Node

The atrioventricular node, commonly abbreviated as the AV node, is a specialized collection of cardiac conduction cells located in the lower part of the interatrial septal region of the right atrium. It forms a critical electrical connection between atrial activation and the specialized conduction system of the ventricles.

The AV node receives electrical excitation after it has spread through the atrial myocardium from the sinoatrial node. Conduction through the AV nodal region is deliberately slow, producing the AV nodal delay that allows atrial contraction and late ventricular filling to occur before ventricular activation.

After passing through the AV nodal region, excitation enters the atrioventricular bundle (bundle of His), which penetrates the fibrous skeleton and conducts the impulse toward the right and left bundle branches and Purkinje network.

Location

The AV node is located in the right atrium near the inferior portion of the interatrial septum.

Its anatomical position is classically described within the triangle of Koch, an important landmark in the right atrium.

Triangle of Koch

The triangle of Koch is an anatomical region used to identify the location of the AV node and surrounding conduction tissue.

It is particularly important during electrophysiological procedures and cardiac surgery because injury to the AV nodal region can impair conduction between the atria and ventricles.

Boundaries of the Triangle of Koch

Boundary or Landmark	Relationship
Tendon of Todaro	Forms an important superior or posterior boundary
Septal leaflet of tricuspid valve	Forms an anterior or inferior boundary
Coronary sinus ostium	Forms a major landmark at the base of the triangle

Tendon of Todaro

The tendon of Todaro is a fibrous continuation associated with structures of the right atrium and forms an important landmark of the triangle of Koch.

Its relationship to the tricuspid annulus and coronary sinus ostium helps define the region containing the AV node.

Coronary Sinus Ostium

The coronary sinus opens into the right atrium near the inferior interatrial septal region.

Its ostium is an important landmark for locating the triangle of Koch and the nearby AV nodal conduction tissue.

Relationship to the Tricuspid Valve

The AV nodal region lies close to the septal portion of the tricuspid valve.

This anatomical relationship is clinically important because interventions involving the septal tricuspid annulus or adjacent structures may place conduction tissue at risk.

Structure

The AV node is composed of specialized cardiomyocytes adapted primarily for electrical conduction rather than forceful mechanical contraction.

These cells are generally smaller and contain fewer contractile elements than ordinary working myocardial cells.

Specialized Conduction Cells

AV nodal cells have electrophysiological properties that differ from those of atrial and ventricular working myocardium.

Their membrane currents produce relatively slow impulse conduction and allow the AV node to function as both a conduction pathway and a secondary pacemaker.

Functional Regions

The AV junction is not simply a single compact group of identical cells. It includes transitional atrial tissue, compact nodal tissue, and tissue leading toward the penetrating atrioventricular bundle.

These regions contribute differently to conduction and delay through the atrioventricular junction.

Electrical Pathway to the AV Node

The normal cardiac impulse begins in the sinoatrial node and spreads through the right and left atrial myocardium.

Atrial activation ultimately reaches the AV nodal region, which serves as the normal electrical gateway to the ventricular conduction system.

Normal Conduction Sequence

Order	Structure
1	Sinoatrial node
2	Atrial myocardium and atrial conduction pathways
3	Atrioventricular node
4	Atrioventricular bundle
5	Right and left bundle branches
6	Purkinje fibers
7	Ventricular myocardium

AV Nodal Delay

One of the most important functions of the AV node is to slow conduction between the atria and ventricles.

This delay helps ensure that atrial systole occurs before ventricular systole and allows the atria to complete their contribution to ventricular filling.

Why Conduction Is Slow

AV nodal cells conduct impulses more slowly than the rapidly conducting His-Purkinje system.

Their small cellular dimensions, electrophysiological properties, and patterns of intercellular electrical coupling contribute to slow conduction through the nodal region.

Physiological Importance of the Delay

If atrial and ventricular contraction occurred simultaneously, coordinated sequential filling and ejection would be impaired.

The AV nodal delay therefore contributes to efficient mechanical timing of the cardiac cycle.

PR Interval

The PR interval on the electrocardiogram extends from the beginning of the P wave to the beginning of the QRS complex.

It reflects conduction from the atria through the AV junction and specialized conduction system before ventricular depolarization begins.

PR Segment

The PR segment is the relatively isoelectric portion between the end of the P wave and the beginning of the QRS complex.

AV nodal conduction contributes substantially to the delay represented within this interval of atrioventricular conduction.

AV Node and the ECG

ECG Feature	Relationship
P wave	Atrial depolarization before AV nodal transmission is completed
PR interval	Reflects atrial and AV conduction before ventricular depolarization
QRS complex	Ventricular depolarization after conduction through the AV junction and His-Purkinje system

Connection to the Bundle of His

The distal AV nodal region continues into the atrioventricular bundle, or bundle of His.

The bundle passes through the central fibrous body and provides the normal electrical connection from the atrioventricular junction to the ventricular conduction system.

Cardiac Fibrous Skeleton

The fibrous skeleton electrically separates most atrial myocardium from ventricular myocardium.

The atrioventricular conduction axis traverses this insulating fibrous framework, creating a controlled route for normal electrical propagation from atria to ventricles.

Electrical Insulation

Without accessory pathways, impulses cannot normally spread directly from atrial working myocardium into ventricular working myocardium across the fibrous atrioventricular junction.

This arrangement directs normal atrioventricular conduction through the specialized AV conduction axis.

Action Potential of AV Nodal Cells

AV nodal cells exhibit slow-response action potentials.

The upstroke depends primarily on calcium entry rather than the rapid sodium current responsible for the fast upstroke in ordinary atrial and ventricular myocytes and Purkinje fibers.

Phase 0 Depolarization

During phase 0 of the AV nodal action potential, calcium influx through voltage-dependent calcium channels produces depolarization.

The slower rate of this depolarization contributes to the relatively slow conduction velocity of nodal tissue.

Pacemaker Activity

AV nodal and junctional tissue can demonstrate spontaneous pacemaker activity.

Under normal conditions, this activity is suppressed by the faster rate of the sinoatrial node.

Secondary Pacemaker Function

If impulses from the sinoatrial node fail to reach the AV junction, cells in the AV junctional region may generate an escape rhythm.

This backup pacemaker function can help maintain ventricular activation when normal sinoatrial control is interrupted.

Intrinsic Rate

The intrinsic pacemaker rate of the AV junction is generally slower than that of the sinoatrial node.

For this reason, junctional escape rhythms typically produce a slower heart rate than normal sinus rhythm.

Autonomic Regulation

AV nodal conduction is strongly influenced by the autonomic nervous system.

Sympathetic and parasympathetic activity can alter conduction velocity, refractoriness, and pacemaker behavior in the AV nodal region.

Sympathetic Stimulation

Sympathetic stimulation generally increases AV nodal conduction velocity and reduces AV nodal delay.

Beta-adrenergic signaling also tends to shorten nodal refractoriness and can facilitate transmission of more frequent atrial impulses.

Parasympathetic Stimulation

Parasympathetic stimulation through the vagus nerve generally slows AV nodal conduction.

Strong vagal activity can substantially increase AV nodal delay and, in some circumstances, temporarily block conduction of atrial impulses to the ventricles.

Autonomic Effects on the AV Node

Influence	Typical Effect
Sympathetic stimulation	Faster AV nodal conduction and shorter nodal delay
Parasympathetic stimulation	Slower AV nodal conduction and longer nodal delay

Refractory Period

After activation, AV nodal tissue enters a period during which its ability to conduct another impulse is reduced.

This refractory behavior limits the number of rapidly arriving atrial impulses that can reach the ventricles.

Protective Filtering Function

The AV node can act as a functional filter during very rapid atrial rhythms.

Because nodal tissue cannot conduct every impulse at arbitrarily high rates, ventricular activation may occur at a lower frequency than atrial activation.

AV Node During Atrial Fibrillation

During atrial fibrillation, numerous irregular atrial impulses reach the AV node.

Variable AV nodal conduction and refractoriness determine which impulses are transmitted to the ventricles, contributing to the irregular ventricular rhythm.

Blood Supply

The AV node receives arterial blood from an AV nodal artery.

In most individuals, this branch arises from the right coronary artery near the crux of the heart, while in others it arises from the circumflex branch of the left coronary artery.

Coronary Dominance

The origin of the AV nodal artery is related to coronary arterial anatomy and dominance.

This relationship helps explain why ischemia affecting particular coronary territories can disturb AV nodal conduction.

AV Nodal Artery

Feature	Key Point
Target	AV nodal and adjacent conduction tissue
Common origin	Right coronary artery
Alternative origin	Circumflex coronary artery in some hearts
Clinical relevance	Ischemia may impair AV conduction

Relationship to the Central Fibrous Body

The compact AV nodal region lies near the central fibrous body of the heart.

The conduction axis then passes into the penetrating atrioventricular bundle as it traverses the fibrous tissue separating atrial and ventricular myocardium.

Relationship to the Membranous Septum

The atrioventricular conduction axis is closely related to the membranous portion of the interventricular septal region.

This relationship is important during surgery or catheter-based procedures near the ventricular septum and cardiac valves.

Relationship to the Aortic Valve

The conduction axis lies near structures of the aortic root and membranous septum.

Interventions involving the aortic valve region can therefore occasionally affect atrioventricular conduction.

Clinical Significance

First-Degree AV Block

First-degree AV block is characterized by prolonged atrioventricular conduction, producing a prolonged PR interval while each atrial impulse is still conducted to the ventricles.

The delay may occur within the AV node or elsewhere in the atrioventricular conduction system.

Second-Degree AV Block

In second-degree AV block, some atrial impulses fail to conduct to the ventricles.

Different patterns of second-degree block have different electrophysiological locations and clinical implications.

Mobitz Type I

Mobitz type I, or Wenckebach block, typically shows progressive prolongation of atrioventricular conduction before an atrial impulse fails to conduct.

The site of block is commonly within the AV node.

Mobitz Type II

Mobitz type II block produces intermittent failure of ventricular conduction without the characteristic progressive PR prolongation of Wenckebach block.

The conduction abnormality is commonly located below the AV node within the His-Purkinje system.

Third-Degree AV Block

In complete or third-degree AV block, atrial impulses do not conduct normally to the ventricles.

The atria and ventricles therefore activate independently, with ventricular activity maintained by a subsidiary escape pacemaker.

AV Nodal Reentrant Tachycardia

AV nodal reentrant tachycardia (AVNRT) is a supraventricular tachycardia involving reentry within or near the AV nodal region.

It is associated with functionally distinct pathways capable of supporting a reentrant electrical circuit.

Dual AV Nodal Physiology

Some individuals have functionally distinct fast and slow conduction pathways in the AV nodal region.

Differences in conduction velocity and refractory periods can create conditions that support AV nodal reentry.

Catheter Ablation

Catheter ablation can be used to modify conduction tissue involved in AV nodal reentrant tachycardia.

Precise anatomical localization is important because excessive injury to the compact AV node or His bundle can cause clinically significant atrioventricular block.

Accessory Pathways

An accessory atrioventricular pathway creates an electrical connection between atrial and ventricular myocardium outside the normal AV nodal-His pathway.

Such pathways can bypass the physiological AV nodal delay and may participate in reentrant tachyarrhythmias.

Myocardial Ischemia

Ischemia affecting the blood supply to the AV node can slow or interrupt atrioventricular conduction.

Conduction disturbances may therefore accompany myocardial infarction involving relevant coronary territories.

Inferior Myocardial Infarction

Inferior myocardial infarction commonly involves the right coronary artery in right-dominant circulation.

Because the AV nodal artery frequently arises from the right coronary artery, transient AV nodal conduction abnormalities can occur in this setting.

Cardiac Surgery

The AV node and proximal His bundle are vulnerable during procedures performed near the septal tricuspid annulus, membranous septum, central fibrous body, and neighboring valve structures.

Knowledge of the triangle of Koch and conduction-axis anatomy helps surgeons avoid iatrogenic heart block.

Key Features of the AV Node

Feature	Key Point
Location	Inferior interatrial septal region within the triangle of Koch
Primary role	Conducts and delays atrial impulses before ventricular activation
Downstream structure	Atrioventricular bundle
Conduction velocity	Relatively slow
Action potential type	Slow-response, calcium-dependent upstroke
Pacemaker capability	Can support a secondary junctional rhythm
Autonomic regulation	Sympathetic activity accelerates and vagal activity slows conduction
Common arterial supply	AV nodal branch of the right coronary artery
Clinical importance	AV block, AVNRT, accessory pathway physiology and procedural injury

Anatomical and Physiological Importance

The atrioventricular node is a critical interface between atrial and ventricular electrical activity. Its location near the triangle of Koch places it at the transition between atrial myocardium and the specialized atrioventricular conduction axis.

The slow conduction properties of AV nodal tissue create the physiological delay required for sequential atrial and ventricular contraction. At the same time, its refractory properties limit transmission of excessively rapid atrial impulses and provide an important filtering function between the atria and ventricles.

The AV node also has major clinical importance because abnormalities of nodal conduction can produce heart block or participate in reentrant tachycardia. Its close relationship to the tricuspid valve, coronary sinus, central fibrous body, membranous septum, and proximal His bundle makes detailed anatomical knowledge essential during electrophysiological procedures and cardiac surgery.