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Overview of Cardiac Conduction Control of Ones Heart Rate Cardiac Action Potentials Gap Junctions Atrioventricular Node and Bundle of His Summary and References

Overview of Cardiac Conduction

The sinoatrial node is located in the upper part of the right atrium in the healthy heart, and serves as the natural pacemaker (Figure 1). These nodal cells manifest spontaneous depolarizations and are thus responsible for generating the normal cardiac rhythm; such a heart rate can also be described as intrinsic or automatic. Importantly, the frequency of this earliest cardiac depolarization is well modulated by both sympathetic and parasympathetic efferent innervation. In addition, the nodal rate can also be modulated by local changes within perfusion and/or the chemical environment (i.e., neurohormonal, nutritional, oxygenation, etc.). Although the atrial rhythms normally emanate from the sinoatrial node, variations in the initiation site of atrial depolarization have been documented outside of the histological nodal tissues, particularly when high atrial rates are elicited, and may include paranodal tissue [10-14].

One of the most conspicuous features of sinoatrial nodal cells is that they possess poorly developed contractile apparati (a common feature to all myocytes specialized for conduction), comprising only about 50% of the intracellular volume [1,10,15]. In general, although it typically cannot be seen grossly, the location of the sinoatrial node is on the roof of the right atrium at the approximate junction of the superior vena cava, the right atrial appendage, and the sulcus terminalis. In the adult human, the node is approximately 1 mm below the epicardium, 10-20 mm long, and up to 5 mm thick [1,16].

Figure 1

Figure 1. The conduction system of the heart. Normal excitation originates in the sinoatrial (SA) node, then propagates through both atria (internodal tracts shown as dashed lines). The atrial depolarization spreads to the atrioventricular (AV) node, passes through the bundle of His (not labeled), and then to the Purkinje fibers which make up the left and right bundle branches; subsequently all ventricular muscle becomes activated.

After initial sinoatrial nodal excitation, depolarization spreads throughout the atria. The exact mechanisms involved in the spread of impulses (excitation) from the sinoatrial node across the atria are still today, somewhat controversial [1,17]. However, it is generally accepted that: 1) the spread of depolarizations from nodal cells can go directly to adjacent myocardial cells; and 2) preferentially ordered myofibril pathways allow this excitation to rapidly transverse the right atrium to both the left atrium and the atrioventricular node (Figure 1). It is believed by many that there are three preferential anatomic conduction pathways from the sinoatrial node to the atrioventricular node [1,18]. In general, these can be considered as the shortest electrical routes between the nodes. Note that there are microscopically identifiable structures, appearing to be preferentially oriented fibers, that provide a direct node-to-node pathway. In some hearts, pale staining Purkinje-like fibers have also been reported in these regions. More specifically, the anterior tract is described as extending from the anterior part of the sinoatrial node, bifurcating into the so-called Bachmann's bundle which importantly delivers impulses to the left atrium and with a second tract that descends along the interatrial septum that connects to the anterior part of the atrioventricular node. The middle (or Wenckebach's pathway) extends from the superior part of the sinoatrial node, runs posteriorly to the superior vena cava, then descends within the atrial septum, and may join the anterior bundle as it enters the atrioventricular node. The third pathway is described as being posterior (Thorel's) which, in general, is considered to extend from the inferior part of the sinoatrial node, passing through the crista terminalis and the Eustachian valve past the coronary sinus to enter the posterior portion of the atrioventricular node. In addition to excitation along these preferential conduction pathways, general excitation spreads from cell to cell throughout the entire atrial myocardium via the specialized connections between cells, the gap junctions, that typically exist between all myocardial cell types (see below).

It then follows that towards the end of atrial depolarization, the excitation reaches the atrioventricular node via the aforementioned atrial routes, with the final result being excitation of the atrioventricular node. Further, these routes are known as the slow or fast pathways, which are considered to be functionally and anatomically distinct. The slow pathway typically crosses the isthmus between the coronary sinus and the tricuspid annulus; it has a longer conduction time, but a shorter effective refractory period. The fast pathway is commonly a superior route, emanating from the interatrial septum, and has a faster conduction rate but, in turn, a longer effective refractory period. Normal conduction during sinus rhythm occurs along the fast pathway, but higher heart rates and/or premature beats are often conducted through the slow pathway, since the fast pathway may be refractory at these rates.

Though the primary function of the atrioventricular node may seem simple, that is to relay conduction between the atria and ventricles, its structure is very complex [1]. As a means to describe these complexities, mathematical arrays and finite element analysis models have been constructed to elucidate the underlying structure-function relationship of the node [19].

In general, the atrioventricular node is located in the so-called floor of the right atrium, over the muscular part of the interventricular septum, inferior to the membranous septum: i.e., within the triangle of Koch, which is bordered by the coronary sinus, the tricuspid valve annulus along the septal leaflet, and the tendon of Todaro (Figure 2). Following atrioventricular nodal excitation, the slow pathway conducts impulses to the His bundle, indicated by a longer interval between atrial and His activation. Currently, there is interest in the ability to place pacing leads to preferentially activate the bundle of His; in such approaches, ultrasound or other imaging modalities are used to map the electrical characteristic His potentials to position the pacing leads [20].

After leaving the bundle of His, the normal wave of cardiac depolarization spreads first to both the left and right bundle branches; these pathways rapidly and simultaneously carry depolarization to the apical regions of both the left and right ventricles (see Figure 1). Finally, the signal broadly travels through the remainder of the Purkinje fibers and ventricular myocardial depolarization spreads.

In certain pathological conditions, direct accessory connections from the atrioventricular node and the penetrating portion of the bundle of His to the ventricular myocardium have been described [21]. Yet, the function and prevalence of these connections, termed Mahaim fibers, is poorly understood. A rare bundle of Kent, an additional aberrant pathway when present, exists between the atria and ventricles and is associated with the clinical manifestation of ventricular tachycardias (also known as Wolff-Parkinson-White syndrome). Therapeutically, this accessory pathway is electrically identified and then commonly ablated as a curative procedure.

The left bundle branch splits into fascicles as it travels down the left side of the ventricular septum just below the endocardium. Its fascicles extend for a distance of 5 to 15 mm, fanning out over the left ventricle. Importantly, typically about midway to the apex of the left ventricle, the left bundle separates into two major divisions, the anterior and posterior branches (or fascicles). These divisions extend to the base of each papillary muscle as well as the adjacent myocardium. In contrast, the right bundle branch continues inferiorly, as if it were a continuation of the bundle of His, traveling along the right side of the muscular interventricular septum. This bundle branch runs proximally, just beneath the endocardium, and its course runs slightly inferior to the septal papillary muscle of the tricuspid valve before dividing into fibers that spread throughout the right ventricle. The complex network of conducting fibers that extends from either the right or left bundle branches is composed of the rapid conduction cells known as Purkinje fibers. Purkinje fibers in both the right and left ventricles act as preferential conduction pathways to provide rapid activation, so to coordinate the excitation pattern within the various regions of the ventricular myocardium. Most of these fibers travel within the trabeculations of the right and left ventricles, as well as within the myocardium itself. Due to tremendous variability in the degree and morphology of the trabeculations existing both within and between species, it is likely that variations in the left ventricular conduction patterns also exist. It should be noted that one of the most common and easily recognized conduction pathways found in mammalian hearts is the moderator band, which contains Purkinje fibers from the right bundle branch (see: Furthermore, in many human hearts, within both the right and left ventricles, one can identify conduction bands that are white in appearance (e.g., see apex videos within the right and left ventricles).

In 1910, Aschoff and Monckeberg provided three criteria for considering a myocardial cell as a specialized conduction cell, including: 1) the ability to histologically identify discrete features; 2) the ability to track cells from section to section; and 3) insulation of the cell by fibrous sheaths from the nonspecialized contractile myocardium [22,23]. It is noteworthy that only the cells within the bundle of His, left and right bundle branches, and Purkinje fibers satisfy all three criteria. No structure within the atria meets all three criteria, including the Bachmann's bundle, sinoatrial node, and atrioventricular node (which are all uninsulated tissues). Yet, with major advances in histo-molecular techniques, it is likely that new criterion will follow that better define the uniqueness of specialized conduction structures.

Figure 2

Figure 2. The conduction system of the heart. Left: Normal excitation originates in the sinoatrial (SA) node then propagates through both atria. The atrial depolarization spreads to the atrioventricular (AV) node, and passes through the bundle of His to the bundle branches/Purkinje fibers. Right: The table shows conduction velocities and intrinsic pacemaker rates of various structures within the cardiac conduction pathway. The structures are listed in the order of activation during a normal cardiac contraction, beginning with the sinoatrial node. Note that the intrinsic pacemaker rate is slower in structures further along the activation pathway. For example, the atrioventricular nodal rate is slower than the sinoatrial nodal rate. This prevents the atrioventricular node from generating a spontaneous rhythm under normal conditions, since it remains refractory at rates <55 beats per minute. If the sinoatrial node becomes inactive, the atrioventricular nodal rate will then determine the ventricular rate. Tabulation adapted from Katz AM. Physiology of the Heart, third edition. Philadelphia: Lippincott, Williams, and Wilkins, 2001.

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