Conduction System of the Heart

The conducting system of the heart consists of cardiac muscle cells and conducting fibers (not nervous tissue) that are specialized for initiating impulses and conducting them rapidly through the heart (see the image below). They initiate the normal cardiac cycle and coordinate the contractions of cardiac chambers. Both atria contract together, as do the ventricles, but atrial contraction occurs first.

The conducting system provides the heart its automatic rhythmic beat. For the heart to pump efficiently and the systemic and pulmonary circulations to operate in synchrony, the events in the cardiac cycle must be coordinated. ^{[1, 2]}

Schematic illustration of the cardiac conduction system.

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See also Heart Anatomy, Aortic Valve Anatomy, Mitral Valve Anatomy, Pulmonic Valve Anatomy, Tricuspid Valve Anatomy, Anatomy of the Nerves of the Heart, and Anatomy of the Autonomic Nervous System.

Sinoatrial node

The sinoatrial (SA) node is a spindle-shaped structure composed of a fibrous tissue matrix with closely packed cells. It is 10-20 mm long, 2-3 mm wide, and thick, tending to narrow caudally toward the inferior vena cava (IVC). The SA node is located less than 1 mm from the epicardial surface, laterally in the right atrial sulcus terminalis at the junction of the anteromedial aspect of the superior vena cava (SVC) and the right atrium (RA).

The artery supplying the sinus node branches from the right coronary artery in 55-60% of hearts or the left circumflex artery in 40-45% of hearts. The artery approaches the node from a clockwise or counterclockwise direction around the SVC–RA junction. ^[3]

The SA node is densely innervated with postganglionic adrenergic and cholinergic nerve terminals. Neurotransmitters modulate the SA node discharge rate by stimulation of beta-adrenergic and muscarinic receptors. Both beta₁ and beta₂ adrenoceptors subtypes are present in the SA node. The human SA node contains a more than 3-fold greater density of beta-adrenergic and muscarinic cholinergic receptors than the adjacent atrial tissue. ^[4]

Internodal and intra-atrial conduction

Anatomic evidence suggests the presence of 3 intra-atrial pathways: (1) anterior internodal pathway, (2) middle internodal tract, and (3) posterior internodal tract.

The anterior internodal pathway begins at the anterior margin of the SA node and curves anteriorly around the SVC to enter the anterior interatrial band, called the Bachmann bundle (see the image below). This band continues to the left atrium (LA), with the anterior internodal pathway entering the superior margin of the AV node. The Bachmann bundle is a large muscle bundle that appears to conduct the cardiac impulse preferentially from the RA to the LA.

Schematic illustration of the cardiac conduction system.

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The middle internodal tract begins at the superior and posterior margins of the sinus node, travels behind the SVC to the crest of the interatrial septum, and descends in the interatrial septum to the superior margin of the AV node.

The posterior internodal tract starts at the posterior margin of the sinus node and travels posteriorly around the SVC and along the crista terminalis to the eustachian ridge and then into the interatrial septum above the coronary sinus, where it joins the posterior portion of the AV node. These groups of internodal tissue are best referred to as internodal atrial myocardium, not tracts, as they do not appear to be histologically discrete specialized tracts. ^{[3, 5]}

Atrioventricular node

The compact portion of the atrioventricular (AV) node is a superficial structure located just beneath the RA endocardium, anterior to the ostium of the coronary sinus, and directly above the insertion of the septal leaflet of the tricuspid valve. It is at the apex of a triangle formed by the tricuspid annulus and the tendon of Todaro, which originates in the central fibrous body and passes posteriorly through the atrial septum to continue with the eustachian valve (see the images below).

The stippled area adjacent to the central fibrous body is the approximate site of the compact atrioventricular node. (Illustration based on Janse MJ, Anderson RH, McGuire MA, Ho SY. "AV nodal" reentry: Part I: "AV nodal" reentry revisited. J Cardiovasc Electrophysiol. 1993 Oct;4(5):561-72.)

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Drawing of a normal human heart showing the anatomic landmarks of the triangle of Koch. This triangle is delimited by the tendon of Todaro superiorly, the fibrous commissure of the flap guarding the openings of the inferior vena cava and coronary sinus, by the attachment of the septal leaflet of the tricuspid valve inferiorly, and by the mouth of the coronary sinus at the base. (Illustration based on Janse MJ, Anderson RH, McGuire MA, Ho SY. "AV nodal" reentry: Part I: "AV nodal" reentry revisited. J Cardiovasc Electrophysiol. 1993 Oct;4(5):561-72.)

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In 85-90% of human hearts, the arterial supply to the AV node is a branch from the right coronary artery that originates at the posterior intersection of the AV and interventricular grooves (crux). In the remaining 10-15% of the hearts, a branch of the left circumflex coronary artery provides the AV nodal artery. Fibers in the lower part of the AV node may exhibit automatic impulse formation. The main function of the AV node is modulation of the atrial impulse transmission to the ventricles to coordinate atrial and ventricular contractions. ^{[3, 6]}

Bundle of His

The bundle of His is a structure that connects with the distal part of the compact AV node, perforates the central fibrous body, and continues through the annulus fibrosus, where it is called the nonbranching portion as it penetrates the membranous septum. Connective tissue of the central fibrous body and membranous septum encloses the penetrating portion of the AV bundle, which may send out extensions into the central fibrous body. Proximal cells of the penetrating portion are heterogeneous and resemble those of the compact AV node; distal cells are similar to cells in the proximal bundle branches.

Branches from the anterior and posterior descending coronary arteries supply the upper muscular interventricular septum with blood, which makes the conduction system at this site more impervious to the ischemic damage, unless the ischemia is extensive. ^[7]

Bundle branches

The bundle branches originate at the superior margin of the muscular interventricular septum, immediately below the membranous septum, with the cells of the left bundle branch cascading downward as a continuous sheet onto the septum beneath the noncoronary aortic cusp. The right bundle branch continues intramyocardially as an unbranched extension of the AV bundle down the right side of the interventricular septum to the apex of the right ventricle and base of the anterior papillary muscle. The anatomy of the left bundle branch system may be variable and may not conform to a constant bifascicular division. However, for clinical purposes and electrocardiography (ECG), the concept of a trifascicular system remains useful (see the images below)

Schematic representation of the trifascicular bundle branch system. A = anterior fascicle of left bundle branch; AVN = atrioventricular node; HB = bundle of His; LBB = left bundle branch; RBB = right bundle branch; P = posterior fascicle of left bundle branch.

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Structural organization of the His-Purkinje system in mouse heart. Expression of a green fluorescent protein was specifically targeted to cells of the His-Purkinje system in mice. Green fluorescent cell networks in the left ventricular chamber are shown. The left ventricular free wall (LVW) was incised from base to apex, and then the 2 parts of the LVW were pulled back to expose the left flank of the interventricular septum (LF). The dotted line demarcates the border between the LF and the LVW.A = anterosuperior fascicle of the left bundle; AVN = atrioventricular node; HB = His bundle: LBB = left bundle branch; P = posteroinferior fascicle of the left bundle branch: RBB = right bundle branch: PF = Purkinje fiber. (Illustration based on Miquerol L, Meysen S, Mangoni M, et al. Architectural and functional asymmetry of the His-Purkinje system of the murine heart. Cardiovasc Res. 2004 Jul 1;63(1):77-86.)

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Terminal Purkinje fibers

The terminal Purkinje fibers connect with the ends of the bundle branches to form interweaving networks on the endocardial surface of both ventricles, which transmit the cardiac impulse almost simultaneously to the entire right and left ventricular endocardium. Purkinje fibers tend to be less concentrated at the base of the ventricle and the papillary muscle tips. They penetrate only the inner third of the endocardium. Purkinje fibers appear to be more resistant to ischemia than ordinary myocardial fibers. ^[3]

Innervation of the AV node, His bundle, and ventricular myocardium

The AV node and His bundle are innervated by a rich supply of cholinergic and adrenergic fibers with higher densities as compared with the ventricular myocardium. Parasympathetic nerves to the AV node region enter the heart at the junction of the IVC and the inferior aspect of the LA, adjacent to the coronary sinus ostium.

The autonomic neural input to the heart demonstrates some degree of "sidedness," with the right sympathetic and vagal nerves affecting the SA node more than the AV node and the left sympathetic and vagal nerves affecting the AV node more than the SA node. The distribution of the neural input to the SA and AV nodes is complex because of substantial overlapping innervation.

Stimulation of the right stellate ganglion produces sinus tachycardia with less effect on AV nodal conduction, whereas stimulation of the left stellate ganglion generally produces a shift in the sinus pacemaker to an ectopic site and consistently shortens AV nodal conduction time and refractoriness, but it inconsistently speeds the SA node discharge rate. However, stimulation of the right cervical vagus nerve slows the SA node discharge rate, and stimulation of the left vagus primarily prolongs AV nodal conduction time and refractoriness when sidedness is present. Neither sympathetic nor vagal stimulation affects normal conduction in the His bundle. ^{[3, 4]}

The right vagus nerve primarily innervates the sinoatrial (SA) node, whereas the left vagus innervates the atrioventricular (AV) node; however, significant overlap can exist in the anatomic distribution.

Effects of sympathetic stimulation

Stimulation of sympathetic ganglia shortens the refractory period equally in the epicardium and underlying endocardium of the left ventricular free wall, although dispersion of recovery properties occurs (ie, different degrees of shortening of refractoriness occur) when measured at different epicardial sites. Nonuniform distribution of norepinephrine (NE) may, in part, contribute to some of the nonuniform electrophysiologic effects, because the ventricular content of NE is greater at the base than at the apex of the heart, with greater distribution to muscle than to Purkinje fibers. Afferent vagal activity appears to be higher in the posterior ventricular myocardium, which may account for the vagomimetic effects of inferior myocardial infarction. ^{[4, 8]}

Effects of vagal stimulation

The vagus modulates cardiac sympathetic activity at prejunctional and postjunctional sites by regulating the amount of NE released and by inhibiting cyclic adenosine monophosphate (cAMP) – induced phosphorylation of cardiac proteins. Tonic vagal stimulation results in a greater absolute reduction in sinus rate in the presence of tonic background sympathetic stimulation. In contrast, changes in AV conduction during concomitant sympathetic and vagal stimulation are essentially the algebraic sum of the individual AV conduction responses to tonic vagal and sympathetic stimulation alone.

Cardiac responses to brief vagal bursts commence after a short latency and dissipate quickly; conversely, cardiac responses to sympathetic stimulation begin and dissipate slowly. The rapid onset and offset of responses to vagal stimulation allow dynamic beat-to-beat vagal modulation of heart rate and AV conduction, whereas the slow temporal response to sympathetic stimulation precludes any beat-to-beat regulation by sympathetic activity. Because the peak vagal effects on sinus rate and AV nodal conduction occur at different times in the cardiac cycle, a brief vagal burst can slow the sinus rate without affecting AV nodal conduction or can prolong AV nodal conduction time and not slow the sinus rate. ^[3]

Arrhythmias

The normal sinus rate of 60-100 beat/min at rest is affected by several factors including autonomic nervous system input, medications, metabolic and electrolyte status, and pathological conditions. ^[9]

Etiologies of sinus node and atrioventricular node dysfunction are as follows:

Enhanced automaticity

• Fever
• Catecholamine release
• Stimulants
• Medications
• Hyperthyroid states
• Idiopathic

Decreased automaticity

• Increased vagal tone
• Medications
• Electrolyte abnormalities
• Obstructive sleep apnea (OSA)
• Myocarditis (inflammatory, infectious, infiltrative)
• Endocarditis
• After cardiac surgery
• Degeneration
• Fibrosis
• Valvular heart disease
• Rheumatologic
• Genetic (channelopathies, neuromuscular disorders)

Inherited forms of cardiac conduction disease are rare, however, the discovery of causative genetic mutations has enhanced our understanding of the processes underlying impulse generation and propagation.

The circadian pattern of normal heart rates widely varies; enhanced vagal tone during sleep can result in heart rates < 40 beats/min, pauses, and Wenckebach conduction block in normal individuals. However, pauses greater than 3 sec are rarely seen in normal individuals and should prompt further evaluation. Exercise conditioning can also result in a physiologically normal slow sinus rate at rest. ^[10]

Alterations in vagal and sympathetic innervation can influence the development of arrhythmias and sudden cardiac death due to ventricular tachyarrhythmias. Cardioneuropathy may develop due to damage to the nerves extrinsic to the heart, such as the stellate ganglia, as well as to intrinsic cardiac nerves from diseases that may affect primarily nerves, such as viral infections or, secondarily, from diseases that cause cardiac damage. Such neural changes may create electrical instability through various electrophysiologic mechanisms. For example, myocardial infarction can interrupt afferent and efferent neural transmission and create areas of sympathetic supersensitivity that may be conducive to the development of arrhythmias. ^[4]