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Cardiac conduction system
Cardiac conduction system
Cardiac conduction system
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Cardiac conduction system
Components of the heart's conduction system
Basic representation of cardiac electrical conduction
Details
Identifiers
Latinsystema conducens cordis
MeSHD006329
TA98A12.1.06.002
TA23952
FMA9476
Anatomical terminology

The cardiac conduction system (CCS, also called the electrical conduction system of the heart)[1] transmits the signals generated by the sinoatrial node – the heart's pacemaker, to cause the heart muscle to contract, and pump blood through the body's circulatory system. The pacemaking signal travels through the right atrium to the atrioventricular node, along the bundle of His, and through the bundle branches to Purkinje fibers in the walls of the ventricles. The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles.[2]

The conduction system consists of specialized heart muscle cells, situated within the myocardium.[3] There is a skeleton of fibrous tissue that surrounds the conduction system which can be seen on an ECG. Dysfunction of the conduction system can cause irregular heart rhythms including rhythms that are too fast or too slow.

Structure

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Graphical representation of the electrical conduction system of the heart that maintains the heart rate in the cardiac cycle

Electrical signals arising in the SA node (located in the right atrium) stimulate the atria to contract. Then the signals travel to the atrioventricular node (AV node), which is located in the interatrial septum. After a short delay that gives the ventricles time to fill with blood, the electrical signal diverges and is conducted through the left and right bundle branches of His to the respective Purkinje fibers for each side of the heart, as well as to the endocardium at the apex of the heart, then finally to the ventricular epicardium; causing the ventricles to contract.[2] These signals are generated rhythmically, which results in the coordinated rhythmic contraction and relaxation of the heart.

On the microscopic level, the wave of depolarization propagates to adjacent cells via gap junctions located on the intercalated disc. The heart is a functional syncytium as opposed to a skeletal muscle syncytium. In a functional syncytium, electrical impulses propagate freely between cells in every direction, so that the myocardium functions as a single contractile unit. This property allows rapid, synchronous depolarization of the myocardium. While advantageous under normal circumstances, this property can be detrimental, as it has potential to allow the propagation of incorrect electrical signals. These gap junctions can close to isolate damaged or dying tissue, as in a myocardial infarction (heart attack).

Development

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Main article: Heart development § Pacemaker and conduction system

Embryologic evidence of generation of the cardiac conduction system illuminates the respective roles of this specialized set of cells. Innervation of the heart begins with a brain only centered parasympathetic cholinergic first order. It is then followed by rapid growth of a second order sympathetic adrenergic system arising from the formation of the thoracic spinal ganglia. The third order of electrical influence of the heart is derived from the vagus nerve as the other peripheral organs form.[4]

Function

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Action potential generation

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Main article: Cardiac action potential

Cardiac muscle has some similarities to neurons and skeletal muscle, as well as important unique properties. Like a neuron, a given myocardial cell has a negative membrane potential when at rest. Stimulation above a threshold value induces the opening of voltage-gated ion channels and a flood of cations into the cell. The positively charged ions entering the cell cause the depolarization characteristic of an action potential. Like skeletal muscle, depolarization causes the opening of voltage-gated calcium channels and release of Ca2+ from the t-tubules. This influx of calcium causes calcium-induced calcium release from the sarcoplasmic reticulum, and free Ca2+ causes muscle contraction. After a delay, potassium channels reopen, and the resulting flow of K+ out of the cell causes repolarization to the resting state.[5][6]

There are important physiological differences between nodal cells and ventricular cells; the specific differences in ion channels and mechanisms of polarization give rise to unique properties of SA node cells, most importantly the spontaneous depolarizations necessary for the SA node's pacemaker activity.

Requirements for effective pumping

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In order to maximize efficiency of contractions and cardiac output, the conduction system of the heart has:

  • Substantial atrial to ventricular delay. This will allow the atria to completely empty their contents into the ventricles; simultaneous contraction would cause inefficient filling and backflow. The atria are electrically isolated from the ventricles, connected only via the AV node which briefly delays the signal.
  • Coordinated contraction of ventricular cells. The ventricles must maximize systolic pressure to force blood through the circulation, so all the ventricular cells must work together.
    • Ventricular contraction begins at the apex of the heart, progressing upwards to eject blood into the great arteries. Contraction that squeezes blood towards the exit is more efficient than a simple squeeze from all directions. Although the ventricular stimulus originates from the AV node in the wall separating the atria and ventricles, the Bundle of His conducts the signal to the apex.
    • Depolarization propagates through cardiac muscle very rapidly. Cells of the ventricles contract nearly simultaneously.
    • The action potentials of cardiac muscle are unusually sustained. This prevents premature relaxation, maintaining initial contraction until the entire myocardium has had time to depolarize and contract.
  • Absence of tetany. After contracting, the heart must relax to fill up again. Sustained contraction of the heart without relaxation would be fatal, and this is prevented by a temporary inactivation of certain ion channels.

Electrical activity

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Further information: Electrocardiogram
Different wave shapes generated by different parts of the heart's action potential
The ECG complex. P=P wave, PR=PR interval, QRS=QRS complex, QT=QT interval, ST=ST segment, T=T wave
Principle of ECG formation. The red lines represent the depolarization wave, not bloodflow.

An electrocardiogram is a recording of the electrical activity of the heart.

SA node: P wave

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Under normal conditions, electrical activity is spontaneously generated by the SA node, the cardiac pacemaker. This electrical impulse is propagated throughout the right atrium, and through Bachmann's bundle to the left atrium, stimulating the myocardium of the atria to contract. The conduction of the electrical impulses throughout the atria is seen on the ECG as the P wave.[5][7]

As the electrical activity is spreading throughout the atria, it travels via specialized pathways, known as internodal tracts, from the SA node to the AV node.[8]

AV node and bundles: PR interval

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The AV node functions as a critical delay in the conduction system. Without this delay, the atria and ventricles would contract at the same time, and blood wouldn't flow effectively from the atria to the ventricles. The delay in the AV node forms much of the PR segment on the ECG, and part of atrial repolarization can be represented by the PR segment.

The distal portion of the AV node is known as the bundle of His.[9] The bundle of His splits into two branches in the interventricular septum: the left bundle branch and the right bundle branch. The left bundle branch activates the left ventricle, while the right bundle branch activates the right ventricle.

The left bundle branch is short, splitting into the left anterior fascicle and the left posterior fascicle. The left posterior fascicle is relatively short and broad, with dual blood supply, making it particularly resistant to ischemic damage. The left posterior fascicle transmits impulses to the papillary muscles, leading to mitral valve closure. As the left posterior fascicle is shorter and broader than the right, impulses reach the papillary muscles just prior to depolarization, and therefore contraction, of the left ventricle myocardium. This allows pre-tensioning of the chordae tendinae, increasing the resistance to flow through the mitral valve during left ventricular contraction.[5] This mechanism works in the same manner as pre-tensioning of car seatbelts.

Purkinje fibers/ventricular myocardium: QRS complex

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The two bundle branches taper out to produce numerous Purkinje fibers, which stimulate individual groups of myocardial cells to contract.[5]

The spread of electrical activity through the ventricular myocardium produces the QRS complex on the ECG.

Atrial repolarization occurs and is masked during the QRS complex by ventricular depolarization on the ECG.

Ventricular repolarization

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The last event of the cycle is the repolarization of the ventricles. It is the restoring of the resting state. In the ECG, repolarization includes the J point, ST segment, and T and U waves.[10] The transthoracically measured PQRS portion of an electrocardiogram is chiefly influenced by the sympathetic nervous system. The T (and occasionally U) waves are chiefly influenced by the parasympathetic nervous system guided by integrated brainstem control from the vagus nerve and the thoracic spinal accessory ganglia.

An impulse (action potential) that originates from the SA node at a relative rate of 60–100 bpm is known as a normal sinus rhythm. If SA nodal impulses occur at a rate less than 60 bpm, the heart rhythm is known as sinus bradycardia. If SA nodal impulses occur at a rate exceeding 100 bpm, the consequent rapid heart rate is sinus tachycardia. These conditions are not necessarily bad symptoms, however. Trained athletes, for example, usually show heart rates slower than 60 bpm when not exercising. If the SA node fails to initialize, the AV junction can take over as the main pacemaker of the heart. The AV junction consists of the AV node, the bundle of His, and the surrounding area; it has a regular rate of 40 to 60 bpm. These "junctional" rhythms are characterized by a missing or inverted P wave. If both the SA node and the AV junction fail to initialize the electrical impulse, the ventricles can fire the electrical impulses themselves at a rate of 20 to 40 bpm and will have a QRS complex of greater than 120 ms. This is necessary for the heart to be in good function.

Clinical significance

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Arrhythmia

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Main article: Arrhythmia

An arrhythmia is an abnormal rhythm or speed of rhythm of the heartbeat. A slow heart rate of 60 or less beats per minute is defined as bradycardia. A fast heart rate of more than 100 beats per minute is defined as tachycardia. An arrhythmia is defined as one that is not physiological such as the lowered heart rate that a trained athlete may naturally have developed; the resting heart rates may be less than 60 bpm.

When an arrhythmia cannot be treated by medication (or other standard cardioversion measures), an artificial pacemaker may be implanted to control the conduction system.

See also

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This article uses anatomical terminology.

References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Cardiac conduction system

View on Grokipedia
from Grokipedia
The cardiac conduction system is a specialized network of cells within the heart that generates electrical impulses and coordinates the rhythmic contractions of the atria and ventricles to ensure efficient pumping of blood. This system comprises key components including the sinoatrial (SA) node, atrioventricular (AV) node, , bundle branches, and , which together form an intrinsic pacemaker and conduction pathway independent of external neural input, though modulated by the . The SA node, located in the upper right atrium near the , serves as the primary pacemaker by spontaneously depolarizing at a rate of 60-100 times per minute, initiating atrial contraction and propagating the impulse across both atria via internodal pathways. The electrical signal then reaches the AV node, situated at the base of the right atrium within the triangle of Koch near the , where it is delayed for approximately 0.1 seconds to allow complete atrial emptying before ventricular filling. From the AV node, the impulse travels through the , which penetrates the fibrous between the atria and ventricles, and divides into left and right bundle branches that course along the . The bundle branches terminate in an extensive Purkinje fiber network that ramifies through the ventricular myocardium, rapidly distributing the wave to synchronize ventricular contraction from apex to base, achieving a conduction up to 4 meters per second—far faster than in ordinary myocardial cells. This coordinated sequence ensures atrial precedes ventricular , optimizing , and the system's activity can be monitored noninvasively via (ECG) to detect rhythm disorders such as or arrhythmias. Dysfunctions in this system, often due to aging, ischemia, or , can lead to conduction blocks or ectopic pacemakers, underscoring its critical role in maintaining cardiovascular .

Anatomy and development

Structural components

The sinoatrial (SA) node is a crescent-shaped structure located subepicardially in the right atrium at the junction with the , with its tail extending 10-20 mm along the . Its intramural architecture features a central body approximately 15 mm long and 4 mm wide, with radiating projections toward the terminal crest, pectinate muscles, and , enclosed partly by myocardium and epicardial fat. The node consists of specialized nodal cells organized into central and peripheral zones, including pacemaker (P) cells that are small, ovoid, and pale-staining with sparse myofibrils, and transitional (T) cells that bridge to atrial myocardium. These P cells exhibit fewer myofibrils and fewer gap junctions compared to surrounding contractile myocytes, supporting while allowing controlled impulse transmission to the atria. The atrioventricular (AV) node resides at the apex of the triangle of Koch in the right atrium, positioned posterior to the septal leaflet of the and adjacent to the ostium. It comprises a compact nodal portion (N region) of small, pale cells with low expression, transitioning to the penetrating portion that extends anteriorly through the central fibrous body, and the nodo-His region with mixed profiles. Histologically, AV nodal cells are smaller than contractile myocytes, with reduced myofibrils and low expression, contributing to slow conduction and electrical isolation from adjacent atrial tissue. The emerges as the continuation of the AV node's penetrating portion, traversing the fibrous to bifurcate into the right and left bundle branches on the . The right bundle branch forms a narrow, ribbon-like tract descending along a septal trabeculation, while the left bundle branch spreads as a broad, trifascicular sheet (anterior, posterior, and septal fascicles) across the left septal . These branches connect to an extensive network, which ramifies as fine, low-density strands on the ventricular endocardial surfaces, denser on the left side in a cone-like distribution toward the apex and papillary muscles. consist of elongated cells with fewer myofibrils and abundant gap junctions relative to contractile ventricular myocytes, optimizing conduction velocity. Interatrial synchronization is supported by specialized tracts, including internodal pathways from the SA node along the and , and Bachmann's bundle, a prominent muscular band of parallel myocardial strands crossing the anterior interatrial groove from right to left atrium. These structures feature aligned cardiomyocytes with enhanced density compared to ordinary atrial myocytes, aiding efficient spread of impulses.

Embryological origins

The cardiac conduction system originates during early embryogenesis from the cardiac crescent, a mesodermal structure that forms around the third week of (approximately day 21-23 in humans), which gives rise to the primary heart tube and initiates rhythmic contractions through peristaltic waves. This primitive conduction begins with the primordial atrium serving as the initial pacemaker, transitioning to the as the heart tube elongates and loops between weeks 3 and 4. By the end of week 3, precursors of the conduction system are specified within the myocardial wall of the heart tube, setting the stage for regional differentiation into pacemaker and conductive tissues. The sinoatrial (SA) node develops from tissues of the right common cardinal vein and , which incorporate into the right atrium during heart looping around week 5. These venous pole structures express early pacemaker markers like Hcn4 and Tbx3, forming the mature SA node that becomes the primary pacemaker in the adult heart. In contrast, the atrioventricular (AV) node and His bundle derive from the AV canal myocardium and associated , which undergo epithelial-to-mesenchymal transformation to contribute to the insulating annulus fibrosus and conductive axis by weeks 5-7. The AV canal's slow-conducting properties persist in the AV node, ensuring timed ventricular activation. Purkinje fibers emerge later, during mid-to-late fetal stages (around weeks 8-10), through differentiation and migration from the subendocardial ventricular myocardium, guided by epicardial-mesenchymal interactions involving epicardium-derived cells. These cells secrete factors that promote Purkinje network expansion across the ventricles, forming a rapid-conducting subendocardial meshwork. Specification of the conduction system is tightly regulated by transcription factors such as Tbx5 and Nkx2.5, which promote AV bundle and Purkinje fiber development while repressing chamber-like gene expression in conductive tissues. Signaling pathways, including Wnt (which inhibits Nkx2.5 to maintain SA node identity) and Notch (which drives Purkinje differentiation via Bmp10 upregulation), further refine these lineages during heart tube maturation. Disruptions in these processes can lead to congenital anomalies, such as Wolff-Parkinson-White syndrome from genetic mutations (e.g., PRKAG2 in humans) causing accessory pathways, or persistent left superior vena cava altering SA node positioning and function.

Physiology

Action potential mechanisms

The action potential in cells of the cardiac conduction system, particularly pacemaker cells, differs from that in contractile myocardial cells, enabling spontaneous electrical activity essential for initiating heartbeats. In pacemaker cells such as those in the sinoatrial (SA) node and atrioventricular (AV) node, the action potential consists of three main phases, lacking the distinct early (phase 1) and plateau (phase 2) seen in ventricular myocytes. Phase 0 involves rapid , but unlike the fast sodium-driven upstroke in working myocardium, it relies primarily on calcium influx through L-type calcium channels, resulting in a slower upstroke of approximately 10-20 V/s compared to 200-500 V/s in ventricular cells. Phase 3 is driven by efflux, while phase 4 is characterized by spontaneous diastolic , which progressively brings the to the threshold for the next , conferring to these cells. This phase 4 is mediated by the "funny" current (I_f), a hyperpolarization-activated mixed sodium- inward current, alongside contributions from calcium clock mechanisms involving calcium release. Key differences between pacemaker and working myocardial action potentials arise from distinct ion channel expression and function. Pacemaker cells exhibit low expression of the Kir2.1, which underlies the stable (I_{K1}) in ventricular myocytes, preventing a true resting phase and allowing phase 4 drift. In SA and AV nodal cells, phase 0 depends on L-type calcium channels (Cav1.2) rather than voltage-gated sodium channels (Nav1.5), which are sparsely expressed or inactivated at nodal diastolic potentials, leading to slower conduction and reduced excitability compared to the rapid, sodium-mediated propagation in atrial or ventricular tissue. The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, particularly HCN4 in the SA node, conduct I_f, activating upon hyperpolarization at the end of to initiate phase 4 with slow kinetics that contribute to the timing of subsequent beats. These mechanisms establish a of among conduction system components, ensuring the SA node dominates rhythm generation under normal conditions. The SA node exhibits the fastest intrinsic firing rate of 60-100 beats per minute, followed by the AV node at 40-60 beats per minute, and at 20-40 beats per minute, with dominance determined by the steepest phase 4 slope reaching threshold first. This hierarchy relies on graded differences in I_f density and activation kinetics, with higher HCN expression and faster diastolic depolarization in the SA node.

Propagation and synchronization

The electrical impulse in the heart originates in the sinoatrial (SA) node and propagates through a specialized conduction pathway to ensure coordinated contraction. From the SA node, the impulse travels rapidly across the atria via internodal pathways, depolarizing the atrial myocardium and leading to atrial . The impulse then reaches the atrioventricular (AV) node, where it is briefly delayed to allow complete atrial emptying, before proceeding through the His bundle, which divides into left and right bundle branches. These branches further ramify into the Purkinje fiber network, distributing the impulse swiftly to the ventricular myocardium for synchronized ventricular contraction. Efficient propagation along this pathway relies on low-resistance electrical coupling between cardiomyocytes, primarily mediated by gap junctions composed of proteins. In the atria and conduction system, connexin 40 (Cx40) predominates, forming channels that support rapid intercellular current flow, while connexin 43 (Cx43) is more abundant in the ventricular working myocardium, ensuring reliable signal transmission. These gap junctions create a functional , minimizing conduction delays and maintaining the integrity of the impulse as it traverses from specialized tissues to contractile cells. Synchronization of atrial and ventricular contractions is critical for optimal , with atrial preceding ventricular to enhance ventricular filling during late . This "atrial kick" contributes approximately 20-30% of ventricular , stretching myocardial fibers and invoking the Frank-Starling mechanism, whereby increased preload augments contractile force. Disruptions in this timing could impair filling and reduce , underscoring the conduction system's role in temporal coordination. Conduction velocities vary along the pathway to achieve this: atrial tissue conducts at about 0.4 m/s, sufficient for orderly atrial activation, while the Purkinje system achieves 2-4 m/s, enabling near-simultaneous ventricular from apex to base. The conduction system also maintains dominance of the primary pacemaker through overdrive suppression, where faster rhythmic activity from the SA node inhibits subsidiary pacemakers. This occurs via hyperpolarization of the in slower foci during accelerated firing, temporarily raising their threshold for spontaneous and preventing ectopic rhythms. Such a mechanism ensures stable control under normal conditions.

Electrophysiology

Atrial depolarization and SA node

The sinoatrial (SA) node serves as the primary pacemaker of the heart, initiating the through its intrinsic . Located at the junction of the and the right atrium, the SA node generates spontaneous action potentials that propagate as an electrical wavefront across the atria, coordinating their contraction prior to ventricular activation. This process ensures efficient atrial emptying and sets the rhythm for the entire heart, typically at a rate of 60-100 beats per minute in adults under normal conditions. The electrical activity originating from the SA node manifests on the electrocardiogram (ECG) as the , which represents the of the atrial myocardium. Normally, the P wave has a duration of 80-100 ms and an of less than 2.5 in the limb leads, reflecting the rapid and synchronous spread of the wavefront from the right to the left atrium. This wavefront is facilitated by preferential conduction pathways in the atrial myocardium, sometimes described in anatomical studies as internodal tracts—including the anterior internodal tract (extending from the anterior margin of the SA node around the to Bachmann's bundle), the middle internodal tract (also known as Wenckebach's tract, running along the ), and the posterior internodal tract (coursing posteriorly near the )—though their existence as specialized structures composed of clusters of conducting fibers remains debated, with electrophysiological evidence supporting efficient conduction via ordinary atrial fibers. Although the SA node dominates under normal circumstances, ectopic atrial foci—abnormal sites of within the atrial myocardium—can potentially override it if they exhibit a faster firing rate. Such foci, often located near the pulmonary veins or , may suppress SA node activity and assume pacemaker control, leading to rhythms like ectopic when their rate exceeds that of the sinus node. Histologically, the high of SA node cells arises from their specialized structure, including sparse expression of the inward rectifier current (IK1) channels, which reduces hyperpolarization after and allows for gradual diastolic . These cells are smaller, with fewer myofibrils and a higher of mitochondria compared to working atrial myocytes, supporting their role in spontaneous impulse generation.

AV conduction and delay

The atrioventricular (AV) node, located at the base of the , serves as the primary site for delaying the cardiac impulse originating from the , ensuring sequential atrial and ventricular contraction. This AV nodal conduction time is approximately 50-120 ms, allowing for complete atrial and emptying of blood into the ventricles before ventricular activation begins, optimizing ventricular preload and . On the electrocardiogram (ECG), the —encompassing intra-atrial conduction, AV nodal conduction time, and initial His bundle activation—is measured from the onset of the (atrial ) to the start of the (ventricular ), with a normal duration of 120-200 ms. A prolonged exceeding 200 ms indicates first-degree AV block, reflecting slowed conduction through the AV node without impulse blockage. Conduction decrements at the AV node manifest as second-degree AV blocks, including Wenckebach (Mobitz I) and Mobitz II types. In Mobitz I, the progressively lengthens with each successive beat until a P wave fails to conduct, resulting in a dropped ; this pattern typically arises within the AV node and is often benign, associated with high . In contrast, Mobitz II features a constant with abrupt non-conducted P waves, usually originating in the infranodal His-Purkinje system and carrying a higher risk of progression to complete . Following the AV nodal conduction, the impulse rapidly propagates through the His-Purkinje system, a specialized network of fibers including the , bundle branches, and , which conducts at high speeds (up to 4 m/s) to synchronize ventricular . This efficient distal conduction ensures near-simultaneous contraction of the ventricular myocardium, minimizing dyssynchrony. AV nodal conduction is modulated by the , with sympathetic stimulation via beta-adrenergic receptors accelerating impulse transmission by enhancing calcium influx and shortening the refractory period, thereby reducing the . Conversely, parasympathetic (vagal) input slows conduction through of the IK,ACh potassium current, prolonging the action potential and increasing the delay, which can exacerbate blocks during heightened .

Ventricular activation and repolarization

Ventricular activation begins following the atrioventricular delay, with the electrical impulse traveling from the bundle branches into the , a subendocardial system of specialized conducting cells that rapidly distributes the wavefront across the ventricular myocardium. This network ensures near-simultaneous activation from to epicardium, optimizing synchronized contraction and by minimizing dyssynchrony. The facilitate this by conducting at velocities up to 4 m/s, far exceeding the 0.5-1 m/s of myocardial cells, allowing for efficient propagation despite the ventricles' large mass. On the electrocardiogram (ECG), ventricular manifests as the , a series of deflections typically lasting less than 120 ms in duration under normal conditions. The sequence of activation proceeds from the (initial leftward Q wave), to the apical regions of both ventricles (prominent R wave reflecting bulk myocardial ), and finally to the basal portions ( as the wavefront reaches the upper ventricles). This septal-to-apical-to-basal progression, driven by the Purkinje system's arborization, ensures coordinated ventricular contraction from apex toward base, promoting effective blood ejection. Ventricular repolarization follows depolarization and is represented by the on the ECG, which typically peaks 200-300 ms after the QRS complex onset, corresponding to the recovery of the myocardial cells to their resting state. The 's polarity—usually upright in most leads—reflects the repolarization sequence, where epicardial cells recover earlier than endocardial cells, creating a vector opposite to depolarization; this transmural gradient results in a positive deflection as the recovery wavefront moves from epicardium to endocardium. The entire process of ventricular electrical activity, from depolarization onset to repolarization completion, is captured by the , measured from the start of the Q wave to the end of the . To account for heart rate variations, the corrected QT interval (QTc) is calculated using Bazett's formula: QTc = QT / √RR, where RR is the interval between consecutive R waves in seconds, allowing standardized assessment of repolarization duration. Disruptions in the conduction pathway, such as bundle branch blocks, alter ventricular activation and prolong the beyond 120 ms. In (RBBB), the right ventricle is activated belatedly via transseptal spread from the left, producing an rsR' pattern in right precordial leads (V1-V2) and wide S waves in lateral leads. (LBBB), conversely, delays left ventricular activation, resulting in broad, notched R waves in lateral leads (I, aVL, V5-V6) and absent septal Q waves, with secondary ST-T changes discordant to the QRS direction. These blocks desynchronize ventricular contraction, potentially impairing , though isolated RBBB often has less clinical impact than LBBB.

Clinical significance

Arrhythmias

Arrhythmias arising from the cardiac conduction system disrupt the normal generation and propagation of electrical impulses, leading to irregular heart rhythms that can compromise and cause symptoms such as syncope, fatigue, or hemodynamic instability. These disorders primarily involve abnormalities in the sinoatrial (SA) node, atrioventricular (AV) node, His-Purkinje system, or their interconnecting pathways, resulting in bradyarrhythmias, tachyarrhythmias, or conduction delays. The immediate clinical impacts include reduced to vital organs, increased risk of in atrial arrhythmias, and potential progression to life-threatening events like . Sinus node dysfunction, also known as sick sinus syndrome, manifests as impaired SA node pacemaker activity or impulse transmission, leading to severe ( <50 bpm), sinus pauses exceeding 3 seconds, or sinoatrial exit block. In this condition, failure of pacemaker cells (P cells) or transitional cells (T cells) due to structural degeneration disrupts the heart's primary rhythm generator, causing chronotropic incompetence where the heart cannot adequately increase rate in response to physiologic demands. A common variant, tachy-brady syndrome, involves alternating bradycardia and paroxysmal supraventricular tachyarrhythmias like atrial fibrillation, affecting over 50% of patients and exacerbating symptoms through erratic rhythm transitions. Clinically, these lead to cerebral hypoperfusion, manifesting as dizziness or presyncope, with an annual incidence of associated AV block ranging from 0% to 4.5%. AV blocks represent interruptions in conduction from atria to ventricles, with second-degree and third-degree (complete heart block) forms being particularly relevant to conduction system pathology. Second-degree AV block type II features constant PR intervals with intermittent non-conducted P waves, often originating infranodally in the His-Purkinje system, while high-grade variants involve multiple consecutive dropped beats. Third-degree AV block results in complete dissociation between atrial and ventricular activity, with no impulses traversing the AV node, forcing reliance on subsidiary pacemakers. Escape rhythms emerge to maintain ventricular rate: junctional escapes from the AV node (rate 40-60 bpm, narrow QRS) or ventricular escapes from (rate 20-40 bpm, wide QRS) if junctional fails, but these slower rates often cause bradycardia-induced symptoms like hypotension and fatigue. The immediate impacts include irregular pulses, dyspnea, and risk of syncope due to inadequate cardiac output. Bundle branch blocks and fascicular blocks constitute intraventricular conduction delays within the His-Purkinje system, prolonging QRS duration and altering ventricular activation sequence. Right or left bundle branch block interrupts impulse flow in respective branches, causing sequential rather than simultaneous ventricular depolarization (QRS >0.12 seconds), while fascicular blocks affect anterior or posterior left fascicles, leading to axis deviation and milder QRS widening (<0.12 seconds). These delays arise from slowed or blocked conduction in the specialized fibers, often progressing to bifascicular or trifascicular involvement in extensive damage. Clinically, they are typically but signal underlying structural disease, increasing vulnerability to complete AV block and reducing synchrony, which impairs ventricular efficiency and elevates cardiac event risk, particularly in . Supraventricular tachycardias (SVT) linked to the conduction system, such as atrioventricular nodal reentrant (AVNRT), arise from re-entry circuits within or adjacent to the AV node. AVNRT, the most common SVT (50-60% of cases), involves dual AV nodal pathways—a fast and slow conduit—enabling a reentrant loop where anterograde conduction occurs via the slow pathway and retrograde via the fast, producing rapid rates (118-264 bpm) with near-simultaneous atrial and ventricular activation. Typical slow-fast AVNRT predominates (90%), while atypical fast-slow variants reverse the pathways. These tachycardias cause , chest discomfort, and due to abrupt hemodynamic shifts, with potential for tachycardia-mediated if sustained. Ventricular arrhythmias originating in the conduction system include premature ventricular contractions () and (VT) driven by Purkinje fiber abnormalities. PVCs are ectopic impulses from distal Purkinje sites, often triggered by delayed afterdepolarizations from calcium dysregulation in remodeled fibers post-infarction or in . VT via Purkinje re-entry forms macro-reentrant circuits involving surviving Purkinje remnants and scarred myocardium, perpetuated by slowed conduction and unidirectional block in the His-Purkinje network. These arrhythmias manifest as or hemodynamic collapse, with PVCs initiating VT/VF storms in vulnerable substrates, heightening sudden death risk in structural heart disease. Key risk factors for these conduction-related arrhythmias include ischemia, which induces electrical instability through oxidative stress and reperfusion injury, promoting re-entry in the Purkinje system. Fibrosis, prevalent in aging and heart failure, replaces conduction tissue with scar, depressing velocity and creating heterogeneous substrates for block and re-entry, particularly in the atria and nodes. Electrolyte imbalances, such as hyperkalemia, prolong conduction by elevating resting membrane potential and reducing excitability, leading to widened QRS, AV block, and ventricular arrhythmias via slowed His-Purkinje propagation.

Diagnostic and therapeutic interventions

Diagnostic methods for assessing cardiac conduction system function primarily include (ECG), studies (EPS), and advanced imaging techniques. The 12-lead ECG serves as the cornerstone for evaluating conduction intervals, such as PR, QRS, and QT durations, enabling the identification of abnormalities like or through non-invasive surface recordings. monitoring via Holter ECG extends this assessment by capturing intermittent conduction disturbances over 24-48 hours, particularly useful for detecting paroxysmal bradyarrhythmias or tachyarrhythmias in dynamic settings. EPS involves invasive catheter-based mapping to measure conduction velocities, localize re-entry circuits, and provoke arrhythmias under controlled conditions, providing precise localization of conduction defects such as accessory pathways or slow pathway involvement in supraventricular tachycardias. This technique is indicated for risk stratification in patients with syncope or structural heart disease, with high sensitivity for identifying inducible circuits. Echocardiography complements these by revealing structural correlates to conduction abnormalities, such as valvular disease or chamber enlargement impacting the conduction pathways, through real-time visualization of myocardial motion and strain. Cardiac (MRI) excels in detecting within conduction tissues, using late enhancement and T1 mapping to quantify extracellular volume expansion, which correlates with slowed conduction and arrhythmogenic substrates in conditions like . These imaging modalities are particularly valuable in unexplained conduction disease, where MRI identifies infiltrative processes in up to 30% of cases with preserved . Therapeutic interventions target conduction disorders through and device-based or procedural approaches. Beta-blockers, such as metoprolol, are first-line for supraventricular tachycardias involving enhanced or re-entry, by prolonging atrioventricular nodal refractoriness and reducing sympathetic drive on the conduction system. Antiarrhythmic agents are classified into Vaughan-Williams classes I-IV, with Class I (e.g., ) slowing conduction in atrial or ventricular tissues, Class III potassium channel modulators (e.g., ) prolonging to prevent re-entry, and Class IV antagonists (e.g., verapamil) targeting nodal tissues. These drugs modulate ion channels directly affecting conduction velocity and excitability, though proarrhythmic risks necessitate ECG monitoring. For bradyarrhythmias due to sinoatrial or dysfunction, pacemaker implantation restores physiologic conduction by delivering paced impulses, with dual-chamber devices preferred to maintain atrioventricular synchrony and prevent . is curative for focal re-entrant arrhythmias like atrioventricular nodal reentrant tachycardia (AVNRT), targeting the slow pathway with radiofrequency energy to eliminate dual nodal physiology, achieving success rates over 95% while minimizing risks like transient . In (VT), ablation maps and ablates scar-related circuits, often guided by EPS, reducing recurrence by 70-80% in structural heart disease. Recent advances emphasize conduction-preserving therapies and molecular interventions. His-bundle pacing, a selective site pacing technique, directly activates the intrinsic conduction system distal to the , improving ventricular synchrony compared to traditional right ventricular pacing and reducing progression in patients with conduction delays. Clinical adoption has grown since 2020, with multicenter trials demonstrating lower pacing thresholds and better long-term outcomes in bradycardic patients. trials for channelopathies, such as or catecholaminergic polymorphic VT, have progressed post-2020 using adeno-associated viral vectors to deliver corrective genes (e.g., or RYR2), showing restored conduction and reduced inducibility in preclinical models and initial early-phase human trials. For instance, in July 2025, the FDA granted fast track designation to SGT-501, an AAV-based for CPVT, with first-in-human trials planned for late 2025. These approaches target genetic defects in conduction proteins, with ongoing phase I/II trials assessing safety and preliminary efficacy in restoring normal based on preclinical data.

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