AV Node Anatomy and Function: Atrioventricular Conduction

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

The atrioventricular node is a compact cluster of specialized pacemaker cardiomyocytes in the lower interatrial septum, just above the tricuspid valve, that receives the electrical impulse from the atria and passes it to the ventricles after a deliberate delay of roughly 0.1 seconds. That delay is the node's signature contribution: it lets the atria finish emptying before the ventricles begin to contract, so the heart works as a coordinated pump rather than a twitching mass of muscle.

The atrioventricular node matters because it is the only normal electrical gateway between the upper and lower chambers. Every heartbeat in every mammal passes through it. When it fails, the ventricles lose their atrial signal and fall back on slower escape rhythms. When it is injured during surgery, the result can be a permanent pacemaker. Understanding its anatomy and its conduction properties is foundational for veterinary anatomy, cardiology, anesthesia, and surgery.

What the AV Node Is and Where It Sits

The atrioventricular node (AV node) is one of the specialized tissues of the cardiac conduction system, a hierarchically organized network that initiates and coordinates the electrical activation of the heart [1]. The conduction system is built from modified cardiomyocytes that are specialized for electrical signaling rather than contraction [2].

Anatomically, the node lies in the lower part of the interatrial septum, in the region known as Koch's triangle, close to the septal leaflet of the tricuspid valve. Modern anatomical work places it within the atrial walls of the inferior pyramidal space, a wedge of tissue formed where the atrial and ventricular septal structures meet [3]. From there it continues as the non-branching component of the atrioventricular conduction axis, penetrating the plane of atrioventricular insulation to enter the inferoseptal recess of the left ventricular outflow tract [3].

The node is not a single uniform structure. It is formed by contributions from both the tricuspid and mitral vestibules, with extensive additional inputs from the base of the atrial septum [3]. That mixed origin helps explain why the node behaves as a convergence point rather than a simple relay.

Blood Supply

The AV node has a dedicated arterial supply, and its anatomy is clinically important because injury to that artery during cardiac surgery can produce conduction block. In a study of 55 human hearts, the AV node artery arose from the right coronary artery in 73% of cases and from the left coronary artery in 27% of cases [4]. The left-sided variant runs close to the mitral valve attachment, particularly near the left proximal part of the posterior leaflet, which places it at risk during mitral valve procedures [4].

The arterial supply is more variable than that of the sinus node. An additional descending AV node artery was found in 22.4% of 116 hearts examined by microdissection, and an interatrial septal branch extending to Koch's triangle was found in 11.2% of cases, findings that aligned with a histologically verified incidence of 35.7% [5]. Kugel's artery supplied the AV node in 40% of 20 dissected human hearts, and the right descending superior artery supplied it in 70% [6].

Development

The atrioventricular conduction axis arises in part from a drape of trabecular cardiomyocytes on the septal crest, which remodels into the branching and non-branching bundles, and it also includes the so-called primary ring [7]. During fetal development, expansion of the atrioventricular junctions produces the inferior pyramidal space, centralizes the compact AV node, and disrupts most nodoventricular pathways [7]. The node's final position is therefore the product of active remodeling, not a fixed embryonic address.

The Conduction Delay and Why It Exists

The AV node introduces a delay of about 0.1 seconds between atrial activation and ventricular activation. This delay is the reason the atria can empty their blood into the ventricles before the ventricles contract. Without it, atrial and ventricular contractions would overlap and ventricular filling would be compromised.

The delay is not a passive property of slow tissue. It is produced by slow, yet safe conduction shaped by specialized cellular architecture, connexin gradients, and dual-pathway organization [1]. Connexins are the protein channels that form gap junctions between cells, and their distribution determines how quickly current spreads from one cell to the next. The node's slow-conducting phenotype is built from a specific mix of these channels, and the dual-pathway arrangement (a slow pathway and a fast pathway) gives the node its characteristic conduction behavior [1].

The node also acts as a filter. It protects the ventricles from very fast atrial rates by failing to conduct every impulse when the atria fire rapidly. This property is described in terms of the node's refractory period and conduction delay, both of which are modulated by the autonomic nervous system [8]. The node is therefore both a delay line and a rate limiter.

Step by Step Conduction

1. The sinoatrial node fires and the impulse spreads across the atria.
2. Atrial myocardium delivers the impulse to the AV node through the base of the atrial septum and the tricuspid and mitral vestibules [3].
3. The node slows conduction, producing the roughly 0.1 second delay.
4. The impulse exits as the non-branching component of the atrioventricular conduction axis and crosses the plane of atrioventricular insulation [3].
5. The bundle of His and its branches deliver the impulse rapidly to the ventricular myocardium.
6. Purkinje fibers distribute the impulse through the ventricular walls so the ventricles contract in a coordinated sequence.

The following flowchart summarizes this pathway.

flowchart TD
    A[Sinoatrial node fires] --> B[Atrial myocardium activates]
    B --> C[Impulse reaches AV node]
    C --> D[AV node delays conduction]
    D --> E[Bundle of His activates]
    E --> F[Right and left bundle branches]
    F --> G[Purkinje fibers]
    G --> H[Ventricular myocardium contracts]

Intrinsic Rate and the Backup Pacemaker Role

Every part of the conduction system has an intrinsic rate, meaning the rate at which it will fire if left to itself. The sinoatrial node is the fastest and therefore normally dominates. The AV node has an intrinsic rate of roughly 40 to 60 beats per minute in humans, slower than the sinoatrial node but faster than the His-Purkinje system.

This hierarchy is what makes the AV node the backup pacemaker. If the sinoatrial node fails, slows excessively, or its impulse never reaches the atria, the AV node can take over and drive the ventricles at its own intrinsic rate. The result is a slower heart rate than normal, but it is a rate that can sustain circulation. If the AV node also fails, the His-Purkinje system provides a still slower escape rhythm.

The AV node's pacemaker cells have distinct electrical properties. Human pluripotent stem cell-derived AV node-like pacemaker cells exhibit pacemaker action potentials and unique AV node-like conduction properties, and when transplanted into the guinea pig heart they replicate the functional properties of the AV node [9]. This confirms that the node's pacemaker and conduction functions are intrinsic to its cells, not imposed by surrounding tissue.

Comparison Table: Conduction System Components

The sinoatrial node is almost consistently positioned on the sulcus terminalis and varies in size and shape [10]. The AV node and the structures distal to it vary more frequently in shape, size, and position relative to conventional landmarks [10].

Comparative Anatomy Across Species

Species differences in the atrioventricular conduction system are substantial, and they matter for anyone extrapolating from animal models to humans or from one domestic species to another.

Birds

The avian heart has a different conduction arrangement from the mammalian heart. Comparative anatomical work shows marked differences between humans and most mammals and birds not only in the position of the atrioventricular conduction system relative to surrounding structures but also in its morphology [10]. Experimental data obtained in most mammals and birds are therefore difficult to apply directly to humans, and animals whose morphology is similar to that of the mature human conduction system should be used for experimental and developmental research if the results are intended for human application [10]. For veterinary students, the practical point is that the avian conduction axis should not be assumed to follow the mammalian template.

Horses

The equine AV node is large relative to the node in humans and small mammals. This size difference is consistent with the general pattern that the atrioventricular conduction system varies in shape and size across species [10]. A larger node in a larger heart is part of how conduction timing is preserved across a wide range of body sizes.

General Mammalian Pattern

Across mammals, the node's position relative to the atrial and ventricular septal structures varies, and this variability has historically contributed to misunderstandings about its anatomy [3]. The node is consistently found in the lower interatrial septum near the tricuspid valve, but the precise geometry of the surrounding structures differs between species.

How the AV Node Is Studied and Observed

The AV node cannot be seen directly with routine clinical imaging. Its location can be predicted using anatomical landmarks and three-dimensional cardiac computed tomography, which is now able to accurately predict the location of the sinus and atrioventricular nodes along with the preferential pathways of electrical atrial activation [11]. This approach has practical value for pacing procedures and for surgical planning.

In congenital left ventricular outflow tract and aortic valve surgery, preoperative cardiac computed tomography has been used to estimate the position of the AV node, the His bundle course, and the left bundle branch origin relative to the aortic virtual basal ring plane, and to guide avoidance during surgery [12]. In a series of 53 patients, the AV node landmark was located at a mean depth of 11.8 mm inferior to the aortic virtual basal ring plane, the His bundle at 3.3 mm, and the left bundle branch origin at 1.5 mm [12]. Only one patient (1.9%) developed high-grade atrioventricular block requiring permanent pacemaker insertion [12].

Histologically, the node is studied by serial sectioning of the atrial and ventricular septal structures. Microdissection and serial histological sections have been used to characterize the arterial supply and the incidence of additional AV node arteries [5]. Comparative studies using gross dissection alongside virtual dissection of living datasets have helped resolve long-standing questions about the node's location [3].

Electrophysiologically, the node's conduction properties can be assessed by modeling its refractory period and conduction delay from recorded signals. A network model of the AV node combined with a particle filter and smoothing algorithm has been used to estimate these properties beat by beat, with the estimated refractory period and conduction delay matching simulated ground truth within a mean absolute error of about 169 ms for the fast pathway refractory period and 131 ms for the fast pathway conduction delay [8].

Clinical Relevance, Limitations and Common Mistakes

The AV node is a frequent site of conduction disturbance. Atrioventricular block occurs when conduction through the node is delayed or fails, and it can be life-threatening [9]. Heart failure is often associated with AV node dysfunction, which leads to conduction delays and dyssynchrony that are related to adverse clinical outcomes [13]. The pathophysiology of AV node dysfunction in heart failure remains poorly explored, and current therapeutic approaches are an active area of review [13].

Surgical injury is a major concern. The occurrence of early postoperative AV node block after mitral valve implantation or ring annuloplasty ranged from 20% to 37% in the clinical reports compared with the morphological data on the AV node artery [4]. This is because the left AV node artery runs close to the mitral valve attachment [4]. In congenital aortic valve and left ventricular outflow tract surgery, high-grade atrioventricular block is prevalent, which is why preoperative imaging of the conduction axis is used to guide avoidance [12].

Genetic and developmental causes also exist. Bi-allelic variants in POPDC2 cause an autosomal recessive syndrome presenting with sinus node dysfunction, AV conduction defects, and hypertrophic cardiomyopathy, and single-cell RNA sequencing from human hearts showed that co-expression of POPDC1 and POPDC2 was most prevalent in AV node, AV node pacemaker, and AV bundle cells [14]. In zebrafish, POPDC1 variants cause AV node dysfunction and arrhythmogenic changes in cardiac electrophysiology and intracellular calcium handling [15]. Meis transcription factors regulate cardiac conduction system development and adult function, and elimination of Meis function in adult cardiomyocytes produced sinus node dysfunction and delayed atrioventricular conduction [16]. Heterotaxy syndromes, which result from aberrant left-right axis formation, can cause atrial and atrioventricular conduction defects through dysregulated Pitx2 expression [17].

Infection is a rare but documented cause of AV node failure. A case report described a 43-year-old man who died of an AV node abscess caused by Rhodococcus erythropolis endocarditis, with arrhythmia and heart failure [18].

Common mistakes students make:

1. Treating the AV node as a passive wire. It is an active filter with its own pacemaker cells, refractory period, and dual-pathway organization [1].
2. Forgetting the delay is purposeful. The roughly 0.1 second delay is what allows ventricular filling.
3. Assuming all species follow the human pattern. The avian heart has a different conduction arrangement, and the equine AV node is large [10].
4. Confusing the node with the bundle of His. The node is the slow, compact structure in the atrial septum. The bundle is the fast, insulated continuation.
5. Ignoring the blood supply. The AV node artery is variable and vulnerable during surgery [5][4].
6. Assuming the node is always in the same place. Its position varies with respect to conventional landmarks across species and individuals [10].

This article is educational and is not a substitute for veterinary diagnosis or treatment.

Quick Review

• The AV node sits in the lower interatrial septum near the tricuspid valve, within the inferior pyramidal space [3].
• It introduces a delay of about 0.1 seconds so the atria empty before the ventricles contract.
• Its intrinsic rate is roughly 40 to 60 beats per minute in humans, making it the backup pacemaker if the sinoatrial node fails.
• Conduction through the node is slow, safe, and shaped by connexin gradients and dual-pathway organization [1].
• The sinoatrial node, AV node, bundle of His, and Purkinje fibers differ in location, intrinsic rate, and conduction speed.
• The avian heart has a different conduction arrangement, and the equine AV node is large [10].
• The AV node artery is variable and at risk during mitral and aortic valve surgery [5][4][12].

Frequently Asked Questions

What is the atrioventricular node?

The atrioventricular node is a cluster of specialized pacemaker cardiomyocytes in the lower interatrial septum near the tricuspid valve that receives the atrial impulse and passes it to the ventricles after a short delay.

Why does the AV node delay conduction?

The delay of about 0.1 seconds lets the atria finish emptying blood into the ventricles before the ventricles contract, which preserves coordinated pumping.

What is the intrinsic rate of the AV node?

The AV node's intrinsic rate is roughly 40 to 60 beats per minute in humans, slower than the sinoatrial node but faster than the His-Purkinje system.

Can the AV node act as a pacemaker?

Yes. If the sinoatrial node fails, the AV node can take over as the backup pacemaker and drive the ventricles at its own intrinsic rate.

How does the avian heart differ from the mammalian heart?

The avian heart has a different conduction arrangement, and comparative anatomy shows marked differences between humans and most birds in the position and morphology of the atrioventricular conduction system [10].

Why is the equine AV node notable?

The equine AV node is large relative to the node in humans and small mammals, consistent with the general pattern of size variation in the atrioventricular conduction system across species [10].

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