Architecture of the cardiac conduction system
Architecture of the cardiac conduction system
As we learned in the last section, the heart, in the simplest sense, is a muscular pump that circulates blood around the body. It achieves this by rhythmically generating electrical impulses that spread through the heart muscle (“exciting” it) and trigger muscular contraction, ensuring efficient pumping of blood.
Below, we detail the architecture of the heart that enables myocardial excitation, from the microscopic to the macroscopic scale. Fair warning: this section is a bit lengthy and dense, but knowing this will pay off down the line. The concepts and terminology introduced here are referenced ad nauseum throughout this website, and certainly in ECG literature as a whole. Internalizing the lingo now will save you from a lot of confusion later. Buckle up.
Note: If you’re short on time or want to take a cursory glance at what’s covered, click the button below:
The cardiac parenchyma is made of specialized cells known as cardiomyocytes (Figure 1). Like other cells, cardiomyocytes have features such as an outer cell membrane (which is comprised of a potpourri of ion channels, pumps, receptors), cytoplasm, as well as organelles such as nuclei, endoplasmic reticula, and mitochondria. These cells hang out within an extracellular matrix, which provides structural support and facilitates the exchange of resources (i.e., glucose, oxygen) and waste products between the cells and the systemic circulation. Additionally, myofibroblasts are present around the cardiomyocytes; they make the extracellular matrix proteins and play a crucial role in repair and remodeling of cardiac tissue, particularly after injury.
There are several distinctive features of cardiomyocyte microanatomy worth noting:
The bottom line is: cardiomyocytes are electrically and mechanically coupled, forming a network of fibres that act as a functional syncytium, meaning electrical activation in one cell spreads to others in a coordinated manner. This electrical activation triggers the sarcomeres inside each cell to contract. This is the key to how cardiac contraction occurs.
Cardiomyocytes can be divided into two major categories based on their function: contractile and conductive cardiomyocytes.
Contractile cardiomyocytes (also known as working cardiomyocytes) make up the vast majority (~99%) of the cardiac parenchyma. In case the name didn’t already clue you into it, these cells are mainly responsible for contracting in response to electrical signals. To do this effectively, they’re equipped with a high density of sarcomeres for force generation, abundant mitochondria to meet the considerable energy demands of contraction (they are, of course, the powerhouse of the cell), and an extensive sarcoplasmic reticulum for calcium handling during excitation-contraction coupling.
While contractile cardiomyocytes aren’t the primary drivers of electrical impulse generation, they possess the ability to do so under specific circumstances, which will be explored later. These cells also conduct electrical signals, though not particularly fast (~0.5 m/s). This makes sense, since these cells are built to ensure well-coordinated contraction, not rapid signal transmission.
In contrast, conductive cardiomyocytes make up only ~1% of the cardiac mass. These cells primarily generate and propagate the electrical signals necessary for timely and synchronized cardiac contraction. Unlike their contractile counterparts, they don’t contribute much to the heart’s pumping force. Instead, their unique physiology is optimized for electrical conduction.
In case things hadn’t been subclassified enough to satiate you, here are some of the main functional subcategories of conductive cardiomyocytes:
That said, not all conductive cardiomyocytes are optimized solely for speed. For instance, cells within the atrioventricular node have fewer gap junctions, resulting in deliberately slower conduction velocities (~0.05 m/s). This slower conduction allows for a crucial delay, the importance of which will be discussed later.
To further complicate matters, some cardiomyocytes exhibit intermediate properties, blending characteristics of both conductive and contractile cells.
This section will start with a big-picture overview of the conduction system, and then progressively escalates in complexity.
The heart’s conduction system consists of several key structures (as shown in Figure 4) that control how electrical activity spreads throughout the heart.
Electrical impulses normally originate in the sinus node (also called the sinoatrial node), located at the top of the right atrium. These signals spread through the atria, with specialized pathways such as Bachmann’s bundle expediting conduction to the left atrium, and the internodal tracts ensuring efficient transmission within the right atrium.
From there, the signals reach the atrioventricular (AV) node, which acts as a crucial bottleneck in the conduction pathway. It intentionally slows electrical flow, creating a delay that allows the atria to contract and fully fill the ventricles before ventricular contraction begins.
After leaving the AV node, the electrical signal moves into the His bundle, which splits into the right and left bundle branches as it descends along the interventricular septum. The right bundle branch activates the right ventricle, with a part of the branch taking a detour via the moderator band to rapidly reach the lateral wall of the right ventricle. Meanwhile, the left bundle branch divides into the left anterior and posterior fascicles, which primarily supply the anterior and posterior regions of the left ventricle, respectively.
At the terminal end of the conduction system are the Purkinje fibers, which branch extensively into the ventricular myocardium to synchronously distribute the electrical signal.
The nervous system plays a crucial role in regulating the heart, as shown in Figure 4. Specifically, the autonomic nervous system exerts a significant influence on the cardiac conduction system. The parasympathetic system (PSNS), through the release of acetylcholine, slows down various aspects of conduction, while the sympathetic system (SNS), via norepinephrine, accelerates these processes. The biological tug-of-war between the SNS and PSNS determines the heart rate, and can be finely tuned in accordance to the body’s needs at any given time.
Next, we’ll take a closer look at each of the components, in painstaking detail.
The sinoatrial node (SAN) is the principal pacemaker of the heart. Resembling a tadpole, it’s found in the upper part of the right atrium, beginning at the junction of the superior vena cava and the right atrial appendage, and extending inferiorly along the crista terminalis towards the eustachian ridge (Figure 5a). The core of the SAN consists of pacemaker cells, known as P cells, which exhibit automaticity and set the heart’s pace (usually at around 60-100 bpm). Surrounding these cells is a zone of transitional cells, or T cells, that relay the electrical impulses to the rest of the atrium (Figure 5b).
The core part of the SAN is packed with P cells, creating a mosaic-like landscape of automatic cells that are clustered into “regions” of varying automaticity. The cells huddled closer to the “head” of the SAN tend to fire faster than the more leisurely cells near the “tail”. Yet, despite this range of automaticity in the P cells, the SAN must settle on one overall firing rate. It would be reasonable to assume that the fastest P cells set the pace, steamrolling the wimpier cells into submission (especially if you’ve read ahead and are familiar with overdrive suppression). But in practice, the P cells follow a more democratic process called mutual entrainment, whereby they compromise to all operate at some middle-ground rate of automaticity. The benefit of this coordination is that the SAN generates a unified, high-voltage electrical impulse, which is more effective at activating, or “capturing”, the surrounding contractile myocardium.
An interesting feature of the SAN is that the uppermost cells are more sensitive to acetylcholine than those lower down. So, with parasympathetic stimulation, the higher cells (which normally fire faster) are preferentially inhibited. As a result, the lowermost cells end up dominating the pacemaking role (so-called pacemaker shift).
The transitional cells (T cells) that border the P cells and form the “transitional zone” have intermediate properties between purely conductive and contractile cardiomyocytes. Their main job is to relay signals generated by the P cells to the surrounding atrial myocardium.
The atria contain several well-documented conduction pathways (Figure 6) that facilitate the transmission of electrical signals. Among these are three internodal tracts — anterior, middle, and posterior — connecting the SAN to the AV node.
There is one major interatrial tract, known as Bachmann’s bundle, shown in Figure 6. This tract branches off from the anterior internodal tract and runs between the superior vena cava and the aorta, ultimately landing at the left atrial appendage in the anterolateral left atrium. For the avid anatomists in the audience, while other interatrial connections have been described, they are less notable and anatomically less defined (Figure 7).
Unlike highly specialized pathways such as the Purkinje fibres, which boast distinct cellular features like unique gap junction proteins and fibrous insulation to boost signal conduction, the internodal and interatrial tracts lack comparable histologic specialization. This has sparked some pedantic debate in academia over whether they should even be classified as true specialized conduction fibres — a discussion that is, thankfully, of little consequence to the average ECG interpretation.
Nevertheless, these tracts do conduct signals faster than the adjacent atrial myocardium. For example, conduction velocity in Bachmann’s bundle clocks in at 1.7 m/s, a considerable improvement from the 0.4 m/s seen in the surrounding contractile tissue. This speed advantage can be partially explained by specialized cellular features (i.e., a lower density of contractile proteins in the way, leading to lower internal resistance to electrical flow). However, it probably has more to do with the neat alignment of fibres that streamlines signal conduction in the direction of the tracts, unlike the relatively more haphazard fibre layout in the contractile atrial myocardium.
The atrioventricular (AV) node is the next major checkpoint in the conduction pathway. This fusiform structure sits on the floor of the right atrium, nestled within an anatomical region known as the Triangle of Koch. This triangle is defined by the borders of the coronary sinus os, the septal leaflet of the tricuspid valve, and the tendon of Todaro (see Figure 8). While it makes for great fodder for the esoterica-obsessed attending physician to grill learners with on rounds, your ability to successfully interpret ECGs fortunately doesn’t hinge on committing the Triangle of Koch to memory.
The AV node is the only normal pathway for atrioventricular conduction (i.e., transmitting electrical signals from the atria to the ventricles). The fibrous skeleton usually electrically isolates the remainder of atrial tissue from the ventricular myocardium, preventing any rogue impulses from bypassing the AV node in your average heart.
The AV node is actually made of three heterogeneous regions: from proximal to distal, the atrionodal (AN), nodal (N), and nodal-His (NH) regions (Figure 9). It may also have anatomical extensions, such as the posterior nodal extension (PNE). All regions of the AV node lie within the right atrium. While subdividing the AV node into its component parts may reveal important insights about the structure, it’s generally more clinically practical to think about the AV node as a whole, rather than focusing on its individual parts.
The atrionodal (AN) region, also known as the transitional zone, is made of transitional cells that mash up properties of both the AV node proper (i.e., the nodal region) and atrial myocardium. The AN region essentially funnels atrial signals into the nodal region.
The nodal (N) region, also known as the compact AV node, is a dense bundle of interwoven conductive cells, adapted to act like an electrophysiologic speed bump that deliberately stalls atrioventricular conduction. These adaptations include a lack of fibrous insulation, fewer gap junctions, and relatively disorganized fibre orientation.
These features collectively reduce conduction velocity to a sluggish 0.05 m/s in the compact node, causing a delay in atrioventricular conduction of 50–150 milliseconds. This AV delay postpones ventricular contraction (and, consequently, closure of the atrioventricular valves) to allow sufficient time for ventricular filling following atrial contraction.
Not only is the AV node naturally slower at conducting signals, but it also exhibits decremental conduction — the more frequently the node is stimulated, the slower it conducts. This property isn’t a design flaw; on the contrary, it actually safeguards the ventricles from pathologically fast atrial rhythms. For example, if the atria decide one day to fire at 300 bpm (as is the case in atrial flutter), the AV node will slow conduction accordingly, limiting how many signals reach the ventricles and preventing the ventricles from being forced to match that rate. Though we’ve covered plenty of obscure details till now, decremental conduction is something worth remembering, as it does demystify many electrocardiographic phenomena later on. As a final takeaway on the matter, the AV node stands alone as the only tissue in the heart that normally exhibits decremental conduction.
Before we move on from the compact node, I will add that the AV node isn’t usually a single-lane route from the atria to the ventricles. Instead, it often contains two parallel pathways (or sometimes more) that signals can take, each with different properties. In most people, there exists a slow pathway and a fast pathway, named for their relative conduction velocity. The slow pathway tends to correlate anatomically to a structure depicted in Figure 10 called the posterior nodal extension (PNE), or inferior nodal extension. On the other hand, the fast pathway has a less clearly defined anatomical basis, but is thought to involve the transitional cells of the AN region and the anterolateral aspect of the compact AV node.
At the distal end of the AV node is the nodal-His (NH) region, also called the lower nodal bundle. This region contains cells that shares characteristics with the compact node but features more adaptations that enhance conduction (i.e., fibrous insulation, high sodium ion channel density, specialized gap junctions, and parallel fibre orientation). The fibrous insulation of the NH region plays another vital role: without it, atrial signals going to the ventricles could sidestep the protective effects of decremental conduction by favouring the low-resistance lower nodal bundle over the high-resistance compact node. The lower nodal bundle then transitions into the penetrating Bundle of His, a cord-like structure that crosses the fibrous tissue separating the atria and ventricles, extending into the ventricular myocardium at the basal septum.
Finally, like the SA node, the AV node also exhibits automaticity (usually at a rate of 40-60 bpm — slightly slower than the intrinsic sinus rate). Interestingly, the compact AV node is rarely the source of physiologic automaticity; this usually arises from the NH region, but may arise from the AN region or PNE as well. The AV node is also highly innervated by the autonomic system, making its conduction properties heavily responsive to parasympathetic and sympathetic stimuli.
The ventricular portion of the conduction system comprises several major structures: the His bundle, bundle branches and related fascicles, and the Purkinje network. Together, these form the mighty His-Purkinje system (also known as the intraventricular conduction system).
The His bundle, also known as the atrioventricular bundle, is a continuation of the NH region of the AV node (Figure 11). It is a thick, cord-like structure composed of parallel cardiomyocyte fibres, insulated within a fibrous sheath. The penetrating His bundle (proximal His bundle) connects to the tail end of the AV node in the right atrium and crosses the fibrous skeleton and membranous septum to emerge as the non-penetrating portion (distal His bundle) on the left side of the interventricular septum. This represents the beginning of the ventricular conduction system and is essential for coordinated ventricular contraction.
The cardiomyocyte fibres that make up the His bundle are called Purkinje fibres. These long fibres span from the His bundle to their terminal ends in the ventricular myocardium, at the end of the His-Purkinje system. These specialized conduction fibres have several perks (I feel like a broken record at this point) that ensure rapid impulse conduction (approximately 1 m/s):
In fact, there’s evidence that collagen strands separate individual Purkinje fibres within the His bundle, creating “inter-fibre” insulation — except for a few cross-bridging connections between adjacent fibres. Sticking with road analogies, these fibres act like long, one-lane highways with barriers on both sides and zero exits. This design ensures that impulses travelling along these fibres cannot deviate from these paths, leading them to preordained destinations within the heart (Figure 12). This idea — that impulses in different fibres travel independently, each on their own fixed routes — is known as the theory of longitudinal dissociation.
At the distal end of its non-penetrating portion, the His bundle splits into the right and left bundle branches (Figure 13), each hugging the subendocardium on its respective side of the interventricular septum. These branches follow a structural hierarchy as follows:
The bundle branches ultimately conclude with an intricate Purkinje fibre network, or Purkinje system, the most specialized components of the ventricular conduction system.
Fibres in the Purkinje system are built for speed, with multiple adaptations that let them conduct at an impressive ~4 m/s. They branch extensively, forming a dense, web-like network that spans the entire ventricular subendocardium (Figure 15). While these fibres are typically confined to the subendocardial layer, in some individuals, they can extend deeper towards the epicardium.
The complexity of the Purkinje network is often oversimplified in diagrams, failing to capture just how vast it is. Figure 16a presents a computer-modelled visualization of the network’s full extent. Figure 16b reveals the scope of the Purkinje network in the murine heart using fluorescence imaging, following the staining of cells that express connexin 40, a protein that forms the fast gap junctions crucial for Purkinje fibre function.
The rapid conduction and sprawling network of Purkinje fibres ensure near-simultaneous activation of ventricular muscle, making for a far more hemodynamically efficient contraction. Unlike their more upstream counterparts, these fibres aren’t bundled in fibrous insulation, meaning they can directly interface with the working contractile myocardium.
The His-Purkinje system contains multiple sites capable of automaticity, ranging from the His bundle to the downstream Purkinje fibres. However, their automaticity rate is meagre, ranging from 20-40 bpm, making them much less potent than both the SA and AV node.
The whirlwind of information in this page can be neatly summarized as follows: