Electrical

conduction system
of the heart
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The electrical conduction system of the

heart transmits signals generated usually
by the sinoatrial node to cause contraction
of the heart muscle. The pacemaking
signal generated in the sinoatrial node
travels through the right atrium to the
atrioventricular node, along the Bundle of
His and through bundle branches to cause
contraction of the heart muscle. This
signal stimulates contraction first of the
right and left atrium, and then the right and
left ventricles. This process allows blood
to be pumped throughout the body.
 Electrical conduction system of the
heart

Heart; conduction system. 1. SA node. 2. AV

node. 3. Bundle of His. 8. Septum

Details

Identifiers

Latin systema conducens cordis

TA A12.1.06.002

FMA 9476
 Anatomical terminology

The conduction system consists of

specialised heart muscle cells, and is
situated within the myocardium. 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, fast, or slow
heart rhythms.

Structure

Overview of the system of electrical conduction which

Overview of the system of electrical conduction which
maintains the rhythmical contraction of the heart

Electrical signals arising in the SA node

(located in the right atrium) stimulate the
atria to contract and travel to the
atrioventricular node (AV node), which is
located in the interatrial septum. After a
delay, the stimulus diverges and is
conducted through the left and right
bundle 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.[1]
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 (not to be confused with a true
"syncytium" in which all the cells are fused
together, sharing the same plasma
membrane as in skeletal muscle). 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.[2]

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.[3][4]
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 important, 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.

ECG

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. Note that 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.[3][5]

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 PR segment.

The distal portion of the AV node is known

as the bundle of His.[6] 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.[3] 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.[3]
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.[7]
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 - 100bpm is known as normal
sinus rhythm. If SA nodal impulses occur
at a rate less than 60bpm, 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 40bpm 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' refers to an abnormal

rhythm or speed of rhythm of the
heartbeat. An abnormal rhythm or speed is
defined as one which is not physiological.

Speed
A resting heart that beats slower than 60
beats per minute, or faster than 100 beats
per minute, is regarded as having an
arrhythmia. A heartbeat slower than 60
beats per minute is known as bradycardia,
and a heartbeat faster than 100 is known
as a tachycardia.

Physiological

Some individuals, for example trained

athletes, may have heart beats slower than
60 beats per minute 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
"surrounds" the AV node (the AV node is
not able to initialize its own impulses) and
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.

Pacemakers

In the event of arrhythmia, a pacemaker

may be surgically inserted into the
conduction system.
See also

References
1. "Your Heart's Electrical System" .
National Heart, Lung, and Blood Institute.
National Institutes of Health. November 17,
2011. Retrieved January 1, 2015.
2. "Innervation of the heart" . Human
Embryology: Organogenesis: Functional
development of the heart.
3. "Cardiac Muscle and Electrical Activity" .
OpenStax CNX: Anatomy & Physiology.
OpenStax CNX. November 7, 2014.
Retrieved January 2, 2015.
4. "Cardiac Muscle Fibers" . ZY 560
Mammalian Physiology. Auburn University.
Archived from the original on June 1,
2005. Retrieved January 2, 2015.
5. "Cardiac Cycle" . ECG Tutorial. University
of Michigan Health System. Retrieved
January 2, 2015.
6. Anderson, Robert H.; Mori, Shumpei
(2016). "Wilhelm His Junior and his
bundle". Journal of Electrocardiology.
doi:10.1016/j.jelectrocard.2016.06.003 .
ISSN 0022-0736 .
7. Kowey, P., Yan, Gan-Xin. "Ventricular
repolarization components on the
electrocardiogram" . Retrieved 2013-03-08.
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