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Conduction System of the Heart

Updated: Jun 28, 2016
Author: Ramin Assadi, MD; Chief Editor: Richard A Lange, MD, MBA more...

OVERVIEW

Overview
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.

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.

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Gross Anatomy
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.

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Schematic illustration of the cardiac conduction system.

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).

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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.)

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.)

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

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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.)

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

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nodal conduction time and refractoriness when sidedness is present. Neither sympathetic nor vagal
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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]

Pathophysiologic Variants
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:

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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]

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