• The heart is endowed with a special system for
(1) generating rhythmical electrical impulses to cause
rhythmical contraction of the heart muscle
(2)conducting these impulses rapidly through the heart.
• The Atria contract about one sixth of a second ahead of ventricular
• All portions of the ventricles to contract almost simultaneously
CONDUCTION SYSTEM OF
1. SINO ATRIAL NODE
2. INTERNODAL ATRIAL
4. BUNDLE OF HIS
5. PURKINJEE SYSTEM
SA NODE of Keith & Flack
• The sinus node is a crescent-shaped, subepicardial specialized
muscular structure located posterolaterally in the right atrium (RA)
• The sinus node lies within the epicardial groove of the sulcus
terminalis at the junction of the anterior trabeculated RA
appendage with the posterior smooth-walled venous component
• - tadpole-shaped structure with a head, central body, and tail with
nodal extensions representing multiple limbs.
• In adults the sinus node measures 8 to 22 mm long and 2 to 3 mm
wide and thick
The sinus node is a complex of weakly coupled, heterogeneous cells, including the
principal pacemaker cells as well as nonpacemaker cells embedded in a dense
supporting connective matrix
Within the sinus node, pacemaker cells may be divided
Into three major classes:
(1) “elongated spindle-shaped cells,” - long, multinucleated 80 microns
(2) “spindle cells,” mononuclear, shorter than spindle cells, 40 microns
(3) “spider cells,” - irregularly shaped branches with blunt ends.
• Pacemaker of the heart
Current models involve the concept of a “pacemaker hierarchy” head- body - tail
Sympathetic stimulation shifts the leading pacemaker site superiorly, resulting in an
increase in heart rate.
• Artery to SA node – 55% - Right coronary artery
- 45% - Circumflex branch of LCA
The sinus nodal artery typically passes centrally through the length of the sinus body, and it is disproportionately
large, which is considered physiologically important in that its perfusion pressure can affect the sinus rate.
Distention of the artery slows the sinus rate, whereas collapse causes an increase in sinus rate.
The sinus node is densely innervated with postganglionic adrenergic
and cholinergic nerve terminals.
The right vagus nerve predominantly affects sinus node function.
• Vagal responses begin after a short
latency and dissipate quickly.
• The rapid onset and offset of
responses to vagal stimulation allow
dynamic beat-to-beat vagal
modulation of the heart rate
• Enhanced vagal activity can produce
sinus bradycardia, sinus arrest, and
sinoatrial exit block.
• Responses to sympathetic stimulation
begin and dissipate slowly.
• The slow temporal response to
sympathetic stimulation precludes any
beat-to-beat regulation by
• Increased sympathetic activity can
increase the sinus rate and reverse
sinus arrest and sinoatrial exit block.
• There are three preferential anatomic conduction pathways from
the sinus node to the AV node
• These groups of internodal tissue are best referred to as
internodal atrial myocardium, not tracts, because they do not
appear to be histologically recognizable specialized tracts, only
plain atrial myocardium.
• ANTERIOR-------- BACHMAN
The anterior “internodal atrial myocardium” begins at the anterior margin of the
sinus node, curves anteriorly around the superior vena cava (SVC) to the
interatrial septum, and then splits into two bundles one passes to the left atrium
(LA) (Bachmann bundle), while the second bundle descends along the interatrial
septum and connects to the superior margin of the AVN.
It connects the anterosuperior RA an LA behind the ascending aorta, just beneath
the epicardium, and Is the preferential path of LA activation during sinus rhythm.
Three other interatrial conduction pathways have been described:
1. Muscular bundles on the inferior atrial surface near the coronary sinus (CS)
2. Transseptal fibres in the fossa ovalis
3. Posteriorly in the vicinity of the right pulmonary valves
The middle “internodal atrial myocardium” begins at the superior and posterior margins of the sinus node, travels
posteriorly behind th SVC to the crest of the interatrial septum, and descends within the interatrial septum to the
superior margin of the AVN.
The posterior “internodal atrial myocardium” starts at the inferoposterior margin o the sinus node, travel inferiorly
through the crista terminalis to the eustachian ridge, and then into the interatrial septum above the CS os, where it
joins the posterior portion of the AVN.
•Action potentials originating in the
sinus node travel outward into atrial
•The velocity of conduction in most
atrial muscle is about 0.3 m/sec, but
conduction is more rapid, about 1
m/sec in tracts
• The AVN is an interatrial structure, measuring approximately 5 mm long, 5 mm wide, and 0.8 mm thick in adults.
• The AVN is located beneath the RA endocardium at the apex of the triangle of Koch
• Slightly more anteriorly and superiorly is where the His bundle (HB) penetrates the AV junction through the central
fibrous body and the posterior aspect of the membranous AV septum.
• When traced inferiorly, toward the base of the triangle of Koch, the compact AVN area separates into twoc(rightward
and leftward) posterior extensions, usually with the artery supplying the AVN running between them.
• The rightward posterior extension has been implicated in the so-called slow pathway in the typical atrioventricular
nodal reentry tachycardia (AVNRT) circuit
• Artery to AV node – 90% - Right coronary artery
- 10 % - Circumflex branch of
LCA Delay of about 0.12 sec in conduction through
• As with the SA node, the AV node has extensive autonomic
and an abundant blood supply.
• The AV node consists of three regions— distinguished by functional
and histologic differences
1) The transitional cell zone
2) Compact node
3) Penetrating bundle
The AVN and perinodal area are composed of at least three electrophysiologically distinct cells:
1. The atrionodal (AN)
2. Nodal (N)
3. Nodal-his (NH) cells
The AN region corresponds to the cells in the transitional region that are activated shortly after the atrial cells.
The N region corresponds to the region where the transitional cells merge with mid nodal cells and formd compact
1. Conduction is slower through the N region in the compact AVN than in the AN and NH cell zones.
2. The n cells exhibit diastolic depolarization and are capable of automatic impulse formation.
3. The n cells in the compact avn appear to be responsible for the major part of av conduction delay
4. They are likely the site of wenckebach block and the site at which calcium channel blockers delay av conduction.
The NH region corresponds to the lower N cells, typically distal to the site of Wenckebach block, connecting to the
insulated penetrating portion of the HB.
Cause of the Slow Conduction
• The slow conduction in the transitional, nodal, and penetrating A-V
bundle fibres is caused mainly by diminished numbers of gap
junctions between successive cells in the conducting pathways
greater resistance to conduction of excitatory ions from one
conducting fibre to the next.
Functions of AV node
1. The main function of the AVN is modulation of atrial impulse
transmission to the ventricles; it introduces a delay between atrial
and ventricular systole.
2. To limit the number of impulses conducted from the atria to the
3. Fibers in the lower part of the AVN can exhibit automatic impulse
formation, serving as a subsidiary pacemaker
• The AV nodal tissue merges with the His bundle, which runs through
the inferior portion of the membranous interventricular septum, and
then in most cases, continues along the left side of the crest of the
muscular interventricular septum.
• The proximal part of the His bundle rests on the right atrial-left
ventricular (RA-LV) part of the membranous septum and the more
distal part travels along the right ventricle-left ventricular (RV-LV)
part of the membranous septum immediately below the aortic root.
• The His bundle usually receives a dual blood supply from both
nodal artery and branches of the LAD.
• Unlike the SA and AV nodes, the bundle of His and Purkinje
relatively little autonomic innervation.
Right Bundle Branch(RBB)
• The right bundle branch (RBB) originates from the His bundle.
• It is a narrow compact structure – band like
• crosses to the right side of the IVS and extends along the RV endocardial
surface to the region of the anterolateral papillary muscle of the RV, where it
divides to supply the papillary muscle, the parietal RV surface, and the
lower part of the RV surface.
• The proximal portion of the RBB is supplied by branches from the AV nodal
artery or the LAD artery, whereas the more distal portion is supplied mainly
by branches of the LAD artery.
• Anatomically much less discrete
than the RBB.
• The LBB may divide immediately
as it originates from the bundle of
His or may continue for 1 to 2 cm
as a broad ribbon before dividing.
• The predivisional portion of the LB penetrates the membranous
portion of the interventricular septum under the aortic ring and then
divides under the septal endocardium into two branches: the LAF and
• An estimated 65% of individuals have a third fascicle of the LB, the left
median fascicle (LMF).
• The thin LAF crosses the anterobasal LV region toward the
anterolateral papillary muscle and terminates in the Purkinje system of
the anterolateral LV wall.
• The LPF appears as an extension of the main LB and is broad in its
initial course. It then fans out extensively toward the posterior
papillary muscle and terminates in the Purkinje system of the
posteroinferior LV wall
• The LBB and its anterior fascicle have a blood supply similar to
that of the proximal portion of the RBB – LAD and AV nodal
• The left posterior fascicle is supplied by branches of the AV
nodal artery, the posterior descending artery, and the
circumflex coronary artery.
Rapid Transmission in the Ventricular Purkinje System
• Special Purkinje fibres lead from the A-V node through the A-V
bundle into the ventricles.
• They are very large fibres, even larger than the normal ventricular
muscle fibres, and they transmit action potentials at a velocity of 1.5
to 4.0 m/sec, a velocity about 6 times that in the usual ventricular
muscle and 150 times that in some of the A-V nodal fibres.
• This allows almost instantaneous transmission of the cardiac
impulse throughout the entire remainder of the ventricular muscle
Characteristics of Cardiac
• Automaticity: Ability to initiate an electrical impulse
• Excitability: Ability to respond to an electrical impulse
• Conductivity: Ability to transmit an electrical impulse from one
• The “threshold potential” is the lowest Em at which opening of
enough Na+ channels (or Ca2+ channels in the setting of nodal cells)
is able to initiate the sequence of channel openings needed to
generate a propagated action potential.
• Electrical changes in the action potential follow a relatively fixed time
and voltage relationship that differs according to specific cell types.
Two types of action potentials in heart
Fast response action potentials
• Seen in normal atrial and ventricular myocytes and in his-purkinje
• Action potentials have very rapid upstrokes, mediated by the fast
Slow response action potentials
• Seen in in the normal sinus and atrioventricular nodal cells and many
types of diseased tissues
• Have very slow upstrokes, mediated by a slow inward, predominantly
l-type voltage-gated ca2+ current (iCal)
Fast Response Action Potential
Phase 4: The Resting Membrane Potential
• The K+ (Kir) channels underlie an outward K+ current (IK1) responsible for maintaining the resting potential
• It remains near the equilibrium potential for K+ (EK).
• The resting membrane potential is negative during phase 4 (about -90 mV) because potassium channel are
open (K+ conductance K+ currents [IK1] are high).
• The resting Em is also powered by the Na+-K+ adenosine
triphosphatase (the Na+-K+ pump)
• The Na+-K+ pump transports two K+ ions into the cell against its
chemical gradient and three na+ ions outside against its
electrochemical gradient at the expense of one ATP molecule.
• The Na+-K+ pump is electrogenic and generates a net outward
movement of positive charges
• Phase 0: The Upstroke—Rapid Depolarization
• On excitation of a cardiomyocyte by electrical stimuli from adjacent
cells, its resting Em (approximately −85 mV) depolarizes, leading to
opening (activation) of Na+ channels
• A large and rapid influx of Na+ ions (inward INa) occurs into the cell
down their electrochemical gradient.
• Once an excitatory stimulus depolarizes the Em beyond the threshold
for activation of Na+ channels (approximately −65 mV), the activated
INa is regenerative and no longer depends on the initial depolarizing
INa in phase 0
• Activation of Na+ channels is transient
• Fast inactivation (closing of the channel pore) starts simultaneously
• Inactivation is slightly delayed relative to activation, the channels
remain transiently (less than 1 millisecond) open to conduct INa
during phase 0 of the action potential before it closes
ICal in phase 0
• The threshold for activation of ICaL is approximately −30 to −40 mV.
• ICaL is much smaller than the peak INa.
• The amplitude of ICaL is not maximal near the action potential peak
because of the time-dependent nature of ICaL activation.
• Therefore ICaL contributes little to the action potential until the fast
INa is inactivated, after completion of phase 0.
• As a result, ICaL affects mainly the plateau of action potentials
recorded in atrial and ventricular muscle and His- Purkinje fibers.
• Phase 1: Early Repolarization
• Early repolarization during which the membrane repolarizes rapidly and
transiently to almost 0 mV - early notch due to
1. Inactivation of INa
2. Concomitant activation of several outward currents.
a) The transient outward K+ current (Ito) is mainly responsible for phase 1
of the action potential. Ito rapidly activates and then rapidly inactivates
b) Na+ outward current through the Na+-Ca2+ exchanger operating in
reverse mode likely contributes to this early phase of repolarization
Phase 2: The Plateau
Phase 2 (plateau) represents a delicate
• The depolarizing inward currents
2. Small residual component of inward
• Repolarizing outward currents (outward
1. Ultrarapidly activating [IKur]
2. Rapidly activating[IKr]
3. Slowly activating [IKs] delayed
• Phase 2 is the longest phase of the action potential
• The plateau phase is unique among excitable cells and marks the phase of Ca2+ entry into the cell.
• ICaL is activated by membrane depolarization, is largely responsible
for the action potential plateau, and is a major determinant of the
duration of the plateau phase.
• ICaL also links membrane depolarization to myocardial contraction.
• L-type Ca2+ channels activate on membrane depolarization to
potentials positive to −40 mV.
• ICaL peaks at an Em of 0 to +10 mV
• Ikr activates relatively fast and inactivation thereafter is very fast.
• The fast voltage-dependent inactivation limits outward current
through the channel at positive voltages and thus helps to maintain
the action potential plateau phase that controls contraction and
prevents premature excitation.
• IKs activates slowly compared with action potential duration, it is also
• Hence the contribution of IKs to the net repolarizing current is
greatest late in the plateau phase, particularly during action
potentials of long duration.
• This allows IKs channels to accumulate in the open state during rapid
successive action potentials and mediate the faster rate of
• IKs plays an important role in determining the rate-dependent
shortening of the cardiac action potential
• IKur is detected only in human atria but not in the ventricles.
• Predominant rectifier current responsible for atrial repolarization and
is a basis for the much shorter duration of the action potential in the
• IKur activates rapidly on depolarization in the plateau range and
displays outward rectification, but it inactivates slowly during the
time course of the action potential.
• Phase 3: Final Rapid Repolarization
• Phase 3 is the phase of rapid repolarization that restores the Em to its
• Phase 3 is mediated by the
1. Increasing conductance of the delayed outward rectifying currents
(IKr and IKs)
2. The inwardly rectifying K+ currents (IK1 and acetylcholine-activated
K+ current [IKACh])
3. Outward K+ current (IK1
4. Time-dependent inactivation of ICaL .
• Phase 4: Restoration of Resting Membrane Potential
• restoration of transmembrane ionic concentration gradients to the
baseline resting state is necessary.
• This is achieved by the
1. Na+-K+ ATPase (Na+-K+ pump, which exchanges two K+ ions inside
and three Na+ ions outside)
2. Na+-Ca2+ exchanger (INa-Ca, which exchanges three Na+ ions for
one Ca2+ ion)
Atrioventricular Heterogeneity of the Action
• Compared with the atrium, ventricular myocytes
1. Maintain a slightly more hyperpolarized resting em (approximately −85 mv
vs. −80 mv).
2. The action potential duration is longer
3. The plateau phase reaches a more depolarized em (approximately +20 mv),
4. Phase 3 repolarization curve is steeper in ventricular myocytes as compared
with the atrial action potential
1. The density of Ito is twofold higher in the atria
compared with ventricular myocytes.
2. Ito subtypes (Ito,f and Ito,s) are differentially
expressed in the heart. Ito,f is the principal subtype
expressed in human atrium
3. IKur is detected only in human atria and not in the
This accelerates the early phase of repolarization and lead to lower
plateau potentials and shorter action potential durations in atrial as
compared with ventricular cells
IK1 density is much higher in ventricular than in atrial
• Explains the steep repolarization phase in the
• The hyperpolarized resting Em in ventricular
myocytes, and prevents the ventricular cell from
exhibiting pacemaker activity
Slow Response Action Potential
• Slow response action potentials are characterized by a more
depolarized Em at the onset of phase 4 (−50 to −65 mV)
• Slow diastolic depolarization during phase 4
• Reduced action potential amplitude.
• The rate of depolarization in phase 0 is much slower than that
in the working myocardial cells, resulting in reduced
conduction velocity of the cardiac impulse in the nodal regions
• The sinus and AV nodal cells lack the inward rectifier K+ current (IK1),
which acts to stabilize the resting Em
• Sinus and AV nodal excitable cells exhibit a spontaneous, slow, and
progressive decline in the Em during diastole (spontaneous diastolic
• Once this spontaneous depolarization reaches threshold
(approximately −40 mV), a new action potential is generated
Phase 4: Diastolic Depolarization
• If is a hyperpolarization-activated inward current that is carried
largely by Na+
• Once activated, It depolarizes the membrane to a level where the
Ca2+ current activates to initiate an action potential.
• Other ionic currents gated by membrane depolarization (i.e., ICaL
and T-type Ca2+ current [ICaT]), and a current generated by the Na+-
Ca2+ exchanger have also been proposed to be involved in
TISSUE RATE OF IMPULSE
SA NODE 70-80/MIN
AV NODE 40 – 60/MIN
BUNDLE OF HIS 40/MIN
PURKINJE SYSTEM 24/MIN
Phase 0: The Upstroke—Slow Depolarization
• Action potential upstroke is mainly achieved by ICaL.
• L-type Ca2+ channels activate on depolarization to potentials positive
to −40 mV, and ICaL peaks at 0 to +10 mV.
• The peak amplitude ICaL is less than 10% that of INa, and the time
required for activation and inactivation of ICaL is slower than that for
• As a consequence, the rate of depolarization in phase 0 (dV/dt) is
much slower and the peak amplitude of the action potential is less
than that in the working myocardial cells.
• Excitability of a cardiac cell describes the ease with which the cell responds to a
stimulus with a regenerative action potential
• The most important determinant of reduced excitability is the reduced
availability of Na+ channels.
• The more negative the Em is, the more Na+ channels are available for
activation, the greater the influx of Na+ into the cell during phase 0, and the
greater the conduction velocity.
• Reduced excitability is physiologically observed during the relative refractory
period (occurring during phase 3 of the action potential, before full recovery of
• Initiation of a propagating action potential will require a larger-than-normal
• Reduced membrane excitability can occur in certain pathophysiological
1. Genetic mutations that result in loss of na+ channel function
2. Na+ channel blockade with class I antiarrhythmic drugs
3. Acute myocardial ischemia.
• Once an action potential is initiated, the cardiomyocyte becomes inexcitable to
stimulation for a time.
• Refractoriness is determined by
1. The action potential duration
3. The number of Na+ channels that have recovered from their inactive state.
• Permits relaxation of cardiac muscle before subsequent activation.
• The refractory period acts as a protective mechanism by preventing multiple,
compounded action potentials from occurring.
• Shorter refractoriness facilitates reentry and arrhythmias
• The absolute refractory period (which extends over phases 0, 1, 2, and part of phase 3 of the action potential
• After the absolute refractory period, a stimulus can cause some cellular depolarization, but it does not lead
to a propagated action potential. The sum of this period and the absolute refractory period is termed the
effective refractory period
• The relative refractory period, which extends over the middle and late parts of phase 3 to the end of phase 3
of the action potential.
• During the relative refractory period, initiation of a second action
potential is more difficult but not impossible
• A larger-than-normal stimulus can result in activation of the cell and
lead to a propagating action potential
• However, the upstroke of the new action potential is less steep and of
lower amplitude and its conduction velocity is reduced compared
• In pacemaking tissues, INa is predominantly absent and excitability is
mediated by the activation of ICaL.
• After inactivation, the transition of Ca2+ channels from the inactivated to
the closed resting state (i.e., recovery from inactivation) is relatively slow.
• As a result, excitability in pacemaking cells may not be recovered by the
end of phase 3 of the action potential
• Sinus and AV nodal cells remain refractory for a time interval that is longer
than the time it takes for full membrane repolarization to occur.
• May prevent premature excitation
• May be involved in development of blocks during ischemia
• Conduction velocity refers to the speed of propagation of the action
potential through cardiac tissue.
• The conduction velocity varies in cardiac tissues,
TISSUE CONDUCTION RATE
AVN 0.02 – 0.05 LEAST
BUNDLE OF HIS 1
PURKINJE SYSTEM 4 HIGHEST
VENTRICULAR MUSCLE 1
• Intracellular Propagation
• The velocity of propagation increases with
1. Increasing cell diameter
2. Action potential amplitude
3. The initial rate of the rise of the action potential.
• Propagation of action potentials from one cell to adjacent cells is achieved by direct ionic current spread via
specialized, low resistance intercellular connections (gap junctional channels) located mainly in arrays within
the intercalated disks.
• The heart behaves electrically as a functional syncytium, resulting in a
• coordinated mechanical function.