The cardiac conduction system is a continuum of specialised cardiomyocytes that initiates the heartbeat, coordinates atrial activation, delays transmission at the atrioventricular junction, and distributes excitation rapidly through the ventricular myocardium. Its principal components are the sinus node, atrial conduction pathways, atrioventricular node, penetrating and non-branching atrioventricular bundle, branching bundle, right and left bundle branches, and peripheral Purkinje network. These structures cannot be understood as isolated dots and lines. Their position reflects the architecture of the atrial walls, fibrous skeleton, ventricular septum, and arterial roots. [1-4]

Modern pacing, ablation, and transcatheter valve procedures have made millimetric anatomical variation clinically decisive. Histology remains the reference for identifying specialised tissue, whereas electrograms and imaging provide indirect but clinically usable localisation. The atlas should therefore distinguish structures demonstrated histologically from procedural surrogates and should display the system in attitudinally appropriate orientation. [2-6]

1  The sinus node

The sinus node is a subepicardial structure located at the superior cavoatrial junction, usually along the terminal groove. It is not confined to the point traditionally marked at the junction of the superior caval vein and right atrial appendage. The nodal body may be crescentic or spindle-shaped and commonly gives rise to superior and inferior extensions. Its long axis follows the superior cavoatrial junction, while its exact relation to the terminal crest and epicardium varies. [1,3,4]

Histologically, the node is composed of small specialised cardiomyocytes embedded within a fibrous connective-tissue matrix. Transitional cells and working atrial myocardium surround the nodal tissue without forming a sharply circumscribed capsule. The nodal artery usually passes centrally or eccentrically through the node and can arise from either the right coronary or circumflex artery. The right phrenic nerve descends nearby on the lateral surface of the superior caval vein and right atrium, an important relation during epicardial or endocardial ablation near the node. [1,3]

The earliest atrial activation site does not invariably identify the entire anatomical node. Rate, autonomic state, disease, and prior ablation can shift the leading pacemaker within the nodal complex. Procedures for inappropriate sinus tachycardia must account for its extensions, the thickness of the terminal crest, the nodal artery, and the phrenic nerve.

2  Atrial activation and internodal conduction

Atrial excitation spreads from the sinus node through ordinary atrial myocardium organised into preferentially aligned bundles. In the right atrium, the terminal crest distributes activation towards the pectinate muscles, while septal and inferior pathways converge on the atrioventricular nodal region. The term internodal tracts should not imply insulated cables equivalent to the His-Purkinje system. Preferential conduction reflects myocardial architecture, fibre orientation, thickness, and intercellular coupling. [1,3]

Bachmann’s bundle is the most prominent superior interatrial muscular connection. It arises from broad right atrial myocardium near the superior cavoatrial junction, crosses the interatrial groove anterior to the superior caval vein and ascending aorta, and fans into the left atrial roof and appendage. It is a widespread muscular continuum rather than a narrow isolated cord. Additional interatrial connections exist through the rims of the oval fossa, the coronary sinus musculature, and inferior atrial myocardium. Consequently, interatrial conduction persists through multiple pathways and can change after surgical or ablation lesions. [1]

3  The atrioventricular node and its atrial inputs

The compact atrioventricular node lies within the atrial wall forming the floor and apex of the triangle of Koch. The triangle is bounded by the hinge of the septal tricuspid leaflet, the tendon of Todaro, and the coronary sinus ostium together with the septal isthmus. These landmarks define a right atrial surface area; they do not create a true atrial septum. Beneath the atrial wall lies the fibro-adipose inferior pyramidal space, separating it from the crest of the muscular ventricular septum. [1,2,5]

Atrial myocardium approaches the node through multiple inputs. The deeper left-sided septal input and the inferior extensions of nodal tissue are particularly relevant to slow-pathway physiology. The rightward inferior extension occupies the septal vestibule towards the coronary sinus ostium, while a leftward extension can approach the mitral vestibule. These extensions are variable and should not be represented as a single fixed slow pathway. The clinical slow pathway is a functional construct arising from the interaction of nodal and transitional tissues with surrounding atrial inputs. [2,4]

The atrioventricular nodal artery commonly enters the inferior pyramidal space from the dominant coronary artery near the crux. It passes through fibro-adipose tissue towards the compact node. Ablation in the inferior triangle of Koch is directed away from the compact node and penetrating axis, yet local anatomy varies: the size of the triangle, coronary sinus ostium, sub-Thebesian recesses, and distance to the nodal artery all influence safety.

4  The penetrating atrioventricular bundle and central fibrous body

The atrioventricular node becomes the penetrating atrioventricular bundle when the axis enters the insulating fibrous tissues of the atrioventricular junctions. This transition, historically associated with the bundle of His, occurs near the apex of the triangle of Koch within the area of fibrous continuity between the mitral and tricuspid valves. The axis then continues as a non-branching bundle before reaching the crest of the muscular ventricular septum. [2,5]

The site of penetration is not constant. Serial histological and clinical studies by Cabrera, Anderson, Sánchez-Quintana and colleagues demonstrated marked variation relative to the septal tricuspid hinge, membranous septum, and apex of the triangle. The axis may penetrate on the atrial side of the hinge, at the hinge level, or on its ventricular side. The amount of atrial myocardium between the axis and right-sided endocardium also varies. A His electrogram therefore identifies electrical proximity, not a universally reproducible anatomical depth or position. [2,5]

The hinge of the septal tricuspid leaflet divides the membranous septum into atrioventricular and interventricular components, when both are present. The interventricular component may be very small or absent. The conduction axis is related to the inferior margin of this fibrous structure rather than to a simple circular annular plane. These findings explain why schematic textbook drawings are insufficient for guiding pacing or predicting procedural injury. [2,5]

5  Inferoseptal recess and relationship to the aortic root

The inferoseptal recess is an intracavitary extension of the left ventricular outflow tract between the aortic leaflet of the mitral valve and the inferoseptal ventricular structures. It must be distinguished from the inferoseptal process, which is basal left ventricular myocardium, and from the inferior pyramidal space, which is an extracavitary fibro-adipose region. These three structures are spatially related but are not interchangeable. [2,6,7]

The depth and configuration of the recess influence the relation of the non-branching conduction axis to the aortic root. In the usual human arrangement, the axis can be embedded in fibrous tissue forming the rightward wall of the recess before emerging on the crest of the muscular septum. When the recess is absent or shallow, a greater length of the non-branching axis may lie within the circumference of the left ventricular outflow tract. Variation in aortic-root rotation, membranous-septal dimensions, and septal support further modifies this relation. [6,7]

6  The branching axis and Purkinje network

At the crest of the muscular ventricular septum, the axis becomes the branching atrioventricular bundle. The right bundle branch continues as a relatively discrete cord on the right ventricular septal surface. It descends within or beneath endocardium, passes towards the base of the medial papillary complex, and commonly reaches the moderator band, which carries distal ramifications towards the anterior papillary muscle and right ventricular free wall. Its course and depth are variable. [3,4]

The left bundle branch originates as a broad sheet from the left side of the branching bundle and spreads beneath the endocardium of the left ventricular septal surface. Its fascicular organisation is better considered a branching network than an invariant two-cable system. Superior, inferior, and septal ramifications interconnect and merge with the Purkinje network. The clinical concepts of anterior and posterior fascicles remain useful for electrocardiography, but they simplify a variable three-dimensional anatomy. [3,4]

Purkinje fibres form a subendocardial network extending over both ventricles, entering papillary muscles and trabeculations and connecting with working myocardium at multiple Purkinje-muscle junctions. On the left, Purkinje fibres may run within false tendons crossing the cavity; on the right, they accompany the moderator band and other trabeculations. These tissues can participate in bundle-branch re-entry, fascicular tachycardia, post-infarction ventricular tachycardia, and triggered ventricular arrhythmias.

7  Conduction system pacing

Conduction system pacing seeks to recruit the native atrioventricular axis or ventricular conduction network. His bundle pacing targets the penetrating or non-branching axis from the tricuspid vestibule. Because penetration may occur at different levels relative to the septal leaflet hinge, mapping both atrial and ventricular aspects of the vestibule can be necessary. Selective and non-selective capture reflect the relation of the lead to specialised tissue and adjacent working myocardium, not simply a single fluoroscopic coordinate. [2,5]

Left bundle branch area pacing places the lead through the right ventricular septum towards the subendocardial left bundle network. The target is usually inferior to the His region and requires appreciation of septal thickness, aortic-root position, tricuspid valvar apparatus, right bundle course, and variable origin of the left bundle. Electrical criteria are required to demonstrate conduction-system recruitment because anatomical depth alone cannot prove capture. The term left bundle branch area pacing appropriately includes procedures in which direct left bundle capture is not conclusively demonstrated. [3,8]

8  Vulnerability during structural intervention and ablation

The conduction axis is vulnerable during transcatheter aortic valve implantation because the non-branching and branching bundle approach the membranous septum and muscular septal crest beneath the right and non-coronary aortic sinuses. Risk is influenced by prosthesis type and depth, calcification, aortic-root anatomy, membranous-septal length, inferoseptal recess configuration, and the level at which the bundle branches. Imaging can estimate anatomical risk, but it does not directly visualise the specialised cells. [6,7]

Surgery or ablation near the triangle of Koch, septal atrioventricular junctions, aortic root, ventricular septum, or paraseptal accessory pathways can injure different components of the axis. The compact node, penetrating bundle, bundle branches, and their arterial supply are not co-located. Safe intervention therefore requires identification of the intended target, its relation to the valvar hinges and fibrous tissues, and confirmation with electrical recordings or imaging appropriate to the procedure.