Cardiac conduction

system

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]
 Cardiac conduction system

Components of the heart's conduction

system

Details

Identifiers

Latin systema conducens

cordis

MeSH D006329 (https://mes

hb.nlm.nih.gov/recor
d/ui?ui=D006329)

TA98 A12.1.06.002 (http://

 www.unifr.ch/ifaa/Pu
blic/EntryPage/TA9
8%20Tree/Entity%20T
A98%20EN/12.1.06.0
02%20Entity%20TA9
8%20EN.htm)
FMA 9476 (https://bioporta
l.bioontology.org/onto
logies/FMA/?p=class
es&conceptid=http%3
A%2F%2Fpurl.org%2F
sig%2Font%2Ffma%2
Ffma9476)

Anatomical terminology

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

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

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

Action potential generation

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

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
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

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.

AV node and bundles: PR interval

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.[8] 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

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
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.[9]
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 100bpm, 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 60bpm 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 60bpm. 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

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 arrythmia 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 an artificial pacemaker may be
implanted to control the conduction
system.
See also
Impedance cardiography
Intraventricular block
Stannius ligature

References
1. Mantri S, Wu SM, Goodyer WR (July 2021).
"Molecular Profiling of the Cardiac
Conduction System: the Dawn of a New
Era". Curr Cardiol Rep. 23 (8): 103.
doi:10.1007/s11886-021-01536-w (https://
doi.org/10.1007%2Fs11886-021-01536-
w) . PMID 34196831 (https://pubmed.ncbi.
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S2CID 235690734 (https://api.semanticsch
olar.org/CorpusID:235690734) .
2. "How the Heart Works - How the Heart
Beats | NHLBI, NIH" (https://www.nhlbi.nih.
gov/health/heart/heart-beats) .
www.nhlbi.nih.gov. Retrieved 24 August
2022.
3. Goodyer, WR; Beyersdorf, BM; Paik, DT;
Tian, L; Li, G (2 August 2019).
"Transcriptomic Profiling of the Developing
Cardiac Conduction System at Single-Cell
Resolution" (https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC6675655) . Circulation
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4. "Innervation of the heart" (https://web.archi
ve.org/web/20200218164512/http://www.
embryology.ch/anglais/pcardio/funktion0
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ab6e-3ef2482e3e22@7.16:127/Anatomy_&
_Physiology) . OpenStax CNX: Anatomy &
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6. "Cardiac Muscle Fibers" (https://web.archiv
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8. Anderson, Robert H.; Mori, Shumpei (2016).
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 9. Yan GX, Lankipalli RS, Burke JF, Musco S,
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