Conduction system of the heart

Internodal conduction pathway

The internodal conduction pathways are a part of the intra-atrial conduction network initially described by Thomas N. James in 1963. Not only do these pathways travel within the right atrium, but they also form direct points of communication between the sinuatrial and atrioventricular nodes. The internodal conduction pathway is divided into anterior, middle and posterior branches.

The anterior internodal pathway originates from the anterior margin of the SA node. It continues anteriorly, coursing around the superior vena cava where it gives off Bachmann’s bundle. The anterior internodal band continues anteroinferiorly toward the atrioventricular (AV) node where it enters the node by way of its superior margin. 

The middle internodal pathway arises from the posterosuperior margin of the SA node. It continues behind the superior vena cava toward the border of the interatrial septum. The pathway turns caudally in the interatrial septum to enter the AV node through its superior margin.

Finally, the posterior internodal pathway emerges from the posterior margin of the sinus node. It takes a posterior course around the superior vena cava and continues across the crista terminalis toward the Eustachian ridge (valve of the inferior vena cava). The pathway then enters the interatrial septum (above the point of the coronary sinus) where it enters the AV node through its posterior surface. 

These conduction pathways transmit the action potential slightly faster than the surrounding cardiomyocytes. They contain the Purkinje-like (myofibril-poor) cells, which ensures that the action potential arrives at the AV node at an appropriate time. The blood supply of these pathways is similar to the blood supply of the right atrium – the circumflex branch of the left coronary artery.

Interatrial conduction pathway

The interatrial conduction pathway, also called Bachmann’s bundle, refers to a preferential pathway of specialized cardiomyocytes that facilitate the conduction of impulses between the atria. The pathway branches from the anterior internodal pathway at the level of the superior vena cava. The Bachmann’s bundle crosses the interatrial groove (an external landmark of the interatrial septum) and passes over the limbus of the fossa ovalis. A pad of fatty tissue separates the Bachmann’s bundle from the limbus.

The pathway bifurcates into right and left branches that travel toward the right and left atrial auricles, respectively. The right branch can be further divided into superior and inferior arms. The superior arm originates at the external junction of the superior vena cava and the atrium (near the location of the SA node). The inferior arm emerges in the vestibule of the right atrium. The left branch provides some structural support to the anterior atrial wall and continues to wrap around the left atrial auricle. Proximally, the superior part of the left branch passes in front of the openings of the left pulmonary veins. The inferior part continues caudally to the vestibule of the left atrium.

From a histological perspective, the interatrial conduction pathway is a series of parallel strands of myocardium traveling in the subepicardiac layer. The myocytes within Bachmann’s bundle are encased in thin septa made of tightly packed collagen fibrils. This uninterrupted sheath also forms inter-septal connections (the function of which is not yet clear). There are five identified cell types found within the interatrial pathway. These are:

• Myofibril-rich cells – which are the same as regular cardiomyocytes.
• Myofibril-poor cells – resemble Purkinje cells; are numerous in the pathway.
• P cells – like those described in the sinuatrial node.
• Slender transitional cells – short and narrow.
• Broad transitional cells – longer and wider than slender transitional cells.

The presence of these specialized cells facilitates rapid conduction of the action potential across the left atrium, minimizing the delay in depolarization between the atria. Bachmann’s bundle receives its blood supply from the sinuatrial nodal branch of the coronary artery.

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Bundle of His

The atrioventricular (AV) bundle (of His) is the initial segment of the AV node that penetrates through the fibrous trigone into the membranous part of the interventricular septum. On transverse section at the level of the fibrous body, the AV bundle may appear oval, quadrangular or triangular. A unique and important feature of the AV bundle is that it only allows the ‘forward’ movement of action potentials. Therefore, the retrograde transmission of electrical impulses from the ventricles to the atria is not allowed in a normal functioning heart. The AV bundle is supplied by the anterior and inferior interventricular branches of the coronary arteries.

Right and left bundle branches

As the node moves from the membranous to the muscular interventricular septum, it bifurcates into right and left bundles.

The crus dextrum, which is Latin for right bundle branch, emerges from the AV bundle in the membranous interventricular septum. It is a round group of narrow fascicles that travels in the myocardium before moving superficially to the subendocardiac layer space. It travels to the right side of the interventricular septum where it gives of branches to the ventricular walls before going on toward the ventricular apex. Here, it enters the septomarginal moderator band (septomarginal band) before reaching the anterior papillary muscles. The terminal arborization of the right branch supplies the papillary muscle and recurs to supply the rest of the ventricular wall. 

The left bundle branch or crus sinistrum (Latin) branches from the atrioventricular bundle at the start of the muscular interventricular septum. It is made up of numerous small fascicles that become flattened sheets. These fascicles occupy the left half of the muscular interventricular septum. The sheet moves to the subendocardiac space as it travels toward the ventricular apex. Here it trifurcates into posterior, septal and anterior divisions. The branches will go on to activate the anterior and posterior papillary muscles, interventricular septum and the walls of the left ventricle. 

Purkinje fibers

The right and left bundles are populated with subendocardiac branches (Purkinje fibers). These cells can be much larger than those of the surrounding heart muscles and they function quite differently than the preceding cells in the AV node. Subendocardiac branches are found throughout the entire length of both bundles in the subendocardiac layer. They extend toward the cardiac apex, then curve upward and backward through the walls of the ventricles. 

The fibers have far more gap junctions than the AV nodal cells and surrounding myocytes. As a result, they are able to transmit impulses 6 times faster than ventricular muscles and 150 times faster than the AV nodal fibers. The increased number of gap junctions allow more ions to pass from one cell to the next, thus increasing the rate of conduction. Furthermore, there are fewer myofibrils in Purkinje cells, resulting in little to contraction (therefore shorter to absent refractory periods) within these cells. Consequently, the bundles can achieve almost instantaneous transmission of the action potential to the rest of the ventricle once it passes through the AV node. This compensates for the delay at the AV node and allows the ventricles to contract shortly after the atria. 

Note that the main branches of the atrioventricular bundle are insulated by sheaths of connective tissue. This prevents premature excitation of adjacent cardiac tissue. Therefore, the papillary muscles will depolarize first, followed by the ventricular apex, then walls. The pattern of depolarization also goes from endocardium to epicardium, since the fibers are in the subendocardiac layer.

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Sinuatrial node

Cardiomyocytes have the special ability to stimulate themselves (self-excitation or automaticity). The initiation of the action potential is dependent on ion channels that allow passage of ions into and out of the cells. In the case of cardiomyocytes, they have fast-acting sodium ion (Na+), slow sodium-calcium ion (Na+-Ca2+) and slow/fast potassium ion (K+) channels (among other important channels that maintain ionic equilibrium).

This automaticity is particularly enhanced in P cells. They have a lower resting membrane potential than the surrounding cardiomyocytes and transition cells due to the following factors:

• There is a high concentration of extracellular Na+ outside the nodal fibers.
• A relatively large amount of Na+ channels are already open.
• There is a passive diffusion of Na+ into the P cells between heartbeats due to the ‘leaky’ sodium channels.
• The passive influx of Na+ causes a slow rise in the membrane potential of the cell, bringing it progressively closer to the generation threshold of an action potential.

Therefore, cardiac P cells of the SA node are more readily depolarized than other cardiac cells. The SA node is also intimately connected with the surrounding heart muscles via the internodal and interatrial conduction pathways. Consequently, the generated action potential can be rapidly transmitted to other cells. This enables the SA node to set the pace at which the heart cells will depolarize and subsequently contract, making it the pacemaker of the heart. On average, the SA node can fire between 60 to 100 beats per minute at rest.

Atrioventricular node

Although the main role of the AV node is to facilitate passage of the depolarization wave to the ventricles, it also has additional functions. In the absence of a functioning SA node, the AV node has the ability to take over as the pacemaker of the heart. Recall that it also has P cells that are able to establish an (albeit slower) rhythm (40 to 60 beats per minute). 

The AV node is also responsible for slowing down the passage of the electrical impulse traveling to the ventricles. This important phenomenon allows more time for the ventricles to remain quiescent and fill with blood coming from the contracting atria. But how does the AV node slow down conduction? 

One key feature of the transition cells and P cells in the AV node is that they have fewer gap junctions at the intercalated discs. Consequently, there is more resistance to conduction in this part of the conduction pathway than there is in other areas. 

Impulse generation and conduction

Now let’s put all that information together and outline the cardiac conduction steps:

• The SA node generates the action potential.
• The action potential passes along the internodal and interatrial conduction pathways, causing atrial systole.
• The impulse arrives at the AV node and is slowed down to facilitate ventricular filling (ventricular diastole).
• The impulse then passes from the AV node to the AV bundle.

It is then rapidly dispersed through the bundle branches and subendocardiac tissue causing ventricular systole.

Autonomic regulation

The entire cardiac conduction system is under the influence of the autonomic pathway. Sympathetic stimulation of the conductive tissue comes from the cardiac plexus, while parasympathetic influence arises from the vagus nerve (CN X). 

Activation of the sympathetic nervous system results in the release of adrenaline (epinephrine) and other adrenergic neurochemicals. They bind to beta-1 and beta-2 receptors found in both the SA and AV nodes, as well as along the supporting conduction pathways. The overall impact of the sympathetic system is an increase in the depolarization rate of the SA node. Consequently, this elevates the overall heart rate (increased chronotropy). Since these adrenergic receptors are also present on cardiomyocytes, the sympathetic drive will act on these cells, increasing the contraction force (increased inotropy). Therefore, the overall cardiac output will be increased.

On the other hand, the parasympathetic activation of muscarinic receptors at the SA and AV nodes will have the opposite effect when compared to the sympathetic system. Parasympathetic stimulation slows down SA node activation, thus reducing the heart rate. It also reduces the contractility of the cardiomyocytes, effectively reducing the cardiac output. 

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