Physiology Note - Conducting System of the Heart
CONDUCTING SYSTEM OF THE HEART
The conducting system of the heart
consists of sinoartrial (SA) node, internodal pathways, atrioventicular (AV)
node, His bundle, bundle branches and purkinje fibers.
Cardiac action potentials (Fig 1)
There are two types of action potential
(AP) in the heart. Slow/brief action potential that is created in the SA and AV
nodes, and fast/long AP that occurs in the atrial and ventricular myocytes and
the specialized conducting fibers
Long action potential:
This has five phases
Phase 0:
Due to sudden and rapid opening of voltage dependant sodium channels. Sodium
enters the cells and cause depolarisation. Initially activated group of sodium
channels serve as a nidus and further activate sodium channels (autoactivation)
Phase 1:
Sodium channels closes and depolarisation halts. There occurs efflux of
potassium
Phase 2:
Characterised by efflux of potassium counter-balanced by an influx of calcium
(Ca) ions via L type Ca channels, making the membrane potential remains the
same (the plateau phase). This phase gives time for the ventricle to contract.
Phase 3:
Occurs due to closure of of calcium channels and there occurs an increase in
potassium (K) efflux via rapid and slow delayed rectifier K currents , inwardly
rectifier K current and transient outward K+ current.
Phase 4: Aims at
restoring resting membrane potential via inwardly rectifier K currents
Slow action potential:
Slow action potential is quite similar to
that of fast action potential with the following key differences
phase 0 has fewer slope
amplitude,
Phase 1 does not exist,
phase 2 is shorter and
not flat,
phase 4, is less negative
and is not constant so that a slow diastolic depolarization occurred during
this phase results in the spontaneous and rhythmic activity of the heart.
Pacemaker potential
The resting membrane potential that depolarizes is called
as the prepotential (a/k/a pacemaker potential) as it brings the membrane
potential to the threshold level, which then triggers the action potential.
In the initial phase of the action
potential within nodal tissues, repolarization is primarily mediated by
potassium ion efflux.
Potassium conductance rises at the peak of each action potential.
As repolarization nears
completion, conductance declines, a phenomenon referred to as
potassium decay.
At this juncture, “f” channels open and
facilitate the onset of membrane depolarization.
In the later phase of the pacemaker
potential, calcium entry through T-type channels completes the pacemaker
potential and elevates the membrane potential to the threshold, thereby
triggering a subsequent action potential.
The upstroke of the action potential is
then mediated by the opening of long-lasting calcium channels.
This phenomena of potaassium decay and
calcium influx is called as the ‘membrane voltage clock’. Alongside,
spontaneous diastolic depolarization occurs via rhythmic release of Ca2+ from
the sarcoplasmic reticulum through the ryanodine type 2 receptor called the
‘calcium clock’
Prepotential is hyperpolazied by vagal
stimulation and the converse happens with sympathetic stiumulation (fig 2) upon
muscarinic type 2 mediated potassium channel conductance.
Fig 1: Panel A(left) - Slow and fast
action potential, Panel B(right) - Pacemaker potential
(Barrett KE, Barman SM, Boitano S, Brooks
HL. Ganong's Review of Medical Physiology. 23rd ed. New York: McGraw-Hill
Medical; 2010)
Fig2: Effect of sympathetic and
parasympathetic stimulation on the membrane potential of the SA node
(Barrett KE, Barman SM, Boitano S, Brooks
HL. Ganong's Review of Medical Physiology. 23rd ed. New York: McGraw-Hill
Medical; 2010)
SA node
The SA node is the primary pacemaker of
the heart situated in the crescent-shaped fibromuscular ridge on the inner wall of the right atrium
between the superior and inferior vena cava opening called the crista
terminalis.
It is about 1.5 cm long and 0.5 cm wide in
human beings.
The SA node has complex 3-dimensional
structure and can be described as a bunch of pacemaker cells with central and
peripheral components (Fig 3) made up of distinct ion channel and gap junction
expression profiles.
Fig 3: SA node at
Crista terminalis with central and peripheral structure
(Unudurthi SD, Wolf RM,
Hund TJ. Role of sinoatrial node architecture in maintaining a balanced
source-sink relationship and synchronous cardiac pacemaking. Front Physiol.
2014;5:446.)
These cells have heterogenous action
potential characteristics and conduction properties by itself. Experimental and
computational models showed SA node heterogeneity is necessary to maintain
normal automaticity and impulse conduction.
The velocity of conduction of impulse in
internodal pathways is about 0.05 m/s
As mentioned earlier, human mutations
affecting the voltage clock (SCN5A and HCN4), calcium clock (RYR2 and CASQ2),
or both mechanisms (ANKB) have been identified that negatively affect sinus
node function
Internodal Pathways
There are three internodal pathways that
connect SA node and AV node
The anterior pathway - tract of Bachman,
the middle pathway - tract of Wenckebach,
and
the posterior internodal pathway - tract
of Thorel.
These pathways merge into the AV node. The
velocity of conduction of impulse in internodal pathways is about 1 m/s. From
SA node, a conducting tract arises and directly enters into the left atrium.
This is called interatrial tract or Bachman’s bundle.
These bundles are non-insulated
structures, lacking any discernible fibrous or connective tissue sheath. The
absence of such insulation permits depolarisation of adjacent atrial myocardium as depolarization
propagates along their course.
Atrial myocytes
They are randomly arranged specialised
cells functioning just to pass on the signal from SA node which under normal
physiological conditions, do not depolarise on its own.
Though AV node serves as check point for
any depolarisatins, they spontaneously are depolarised in hyperkalemia, drug
induced (milrinone), heart failure.
AV node
The atrioventricular node is located in
the lower region of the right atrium just above the atrioventricular ring
within the anatomical boundaries of triangle of Koch. It measures approximately
22 mm in length, 10 mm in width, and 3 mm in thickness.
Just like the SA node, AV node are a group
of fusiform shaped cells and are functionally categorized into
three regions
1. AN
region - the transition zone from atria to AV
node
2. N
region - the core of the AV node
3. NH region
merges into the Bundle of His.
Junctional rhythm originates from NH cells, below
the slow part of the AV node, and spreads down into the ventricles. This can be
useful as a means of maintaining normal ventricular coordination in the face of
some sort of nodal or atrial dysfunction
The AV nodal fibers are narrow in diameter
and extensively branched, resulting in a slow conduction velocity of about 0.05
m/s. Consequently, the transmission of impulses through the AV node is delayed
by approximately 0.1 seconds; this phenomenon is known as the AV nodal delay.
Pathology
l Wolff
Parkinson White syndrome is distinguished by early activation of the
ventricular myocardium through an accessory pathway, known as the bundle of
Kent, which bypasses the typical slow conduction through the atrioventricular
node secondary to a missense mutation in PRKAG2.
l
Mahaim fibers are rare accessory conduction
pathways linking the atria to the ventricular conduction system, most often
located near the tricuspid annulus. They exhibit decremental conduction
properties resembling those of the atrioventricular node, which may predispose
to potentially life-threatening tachyarrhythmias. Confirmation of diagnosis
necessitates an electrophysiological study.
Bundle of His
Bundle of His (BUH) is the continuation of
the lowermost NH part of the AV node with the difference being AV node cells
are randomly placed and short whereas BUH cells are longer and parallelly
arranged.
The bundle is short (maybe 10mm), and
separates into two branches. The right continues down the subendocardial region
of the right ventricle, and the left penetrates the interventricular septum,
where it divides yet further into discrete anterior and posterior fascicles.
Purkinje fibres
This is a network of small bundles of
conducting fibers that are present throughout the sub-endocardial regions of
right and left ventricles.
1. The
cells of the Purkinje system (are also called Purkinje cells) are the largest
cells in the heart.
2. Numerous
gap junctions (low impedance electrical synapses) are present between the
cells.
3. Because
of the larger diameters of the fiber and presence of low impedance cell-to-cell
connections, the rate of impulse conduction is highest in the Purkinje fibers
Inherited defects in cardiac conduction
have been linked to mutations in SCN5A and SCN1B (both affect phase 0) and
KCNJ2 (affects phase 3 and 4).
Basis of arrythmia
Briefly, the mechanisms responsible for
cardiac arrhythmias are broadly categorized into abnormalities of impulse
generation, impulse conduction, or a combination of both.
1. Disorders
of impulse generation:
l Disturbances
of the autonomic nervous system and metabolic derangements - hyperkalemia,
acidosis, catecholamine surge
l Altered
automaticity (triggered activity) - initiated by
afterdepolarizations—oscillations in membrane potential that arise during or
immediately after a preceding action potential (AP). When these oscillations
reach the excitation threshold, a new AP is generated.
Based on timing, two forms of
afterdepolarizations are recognized:
l early
afterdepolarizations (EADs), occurring during the plateau - precipitated by
hypokalemia, hypoxia, or acidosis and may lead to torsade de pointes,
l late
repolarization phase (phase 2 or 3), and
l delayed
afterdepolarizations (DADs), which develop after full repolarization (phase 4).
Seen in conditions that increase intracellular calcium during diastole - digitalis toxicity, catecholamine excess,
electrolyte disturbances (hypokalemia, hypercalcemia), myocardial hypertrophy,
or heart failure. During calcium overload, particularly at higher heart rates
(shorter cycle lengths), DAD amplitude may increase, reaching the threshold for
spontaneous depolarization and triggering arrhythmic activity .
(EAD occurs early (phase 2) or late (phase
3), and DAD occurs during phase 4 of the action potential)
2. Disorders
of impulse propagation primarily include cardiac blocks and reentry phenomena.
Cardiac blocks result
from delayed or interrupted conduction within the cardiac conducting system and
may be caused by pharmacological agents or degenerative structural changes.
Reentry involves the
reactivation of previously depolarized myocardial tissue that has recovered
excitability while the original impulse persists. This allows a circulating
wavefront to re-excite the myocardium, sustaining arrhythmia. Prolonged
conduction time and shortened refractory periods are key facilitators of
reentry, which represents the predominant mechanism underlying clinical
arrhythmias and may occur due to both structural and functional abnormalities.
References
1. Barrett
KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology.
23rd ed. New York: McGraw-Hill Medical; 2010.
2. Pal
GK, Pal P, Nanda N. Comprehensive Textbook of Medical Physiology. 4th ed. New
Delhi: Jaypee Brothers Medical Publishers; 2025.
3. Park
DS, Fishman GI. The Cardiac Conduction System. Circulation.
2011;123(8):e469-72.
4. Yartsev
A. Excitatory, conductive and contractile elements of the heart [Internet].
Deranged Physiology. 2024. Available from:
https://derangedphysiology.com/main/cicm-primary-exam/cardiovascular-system/Chapter-002/excitatory-conductive-and-contractile-elements-heart
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