Impulse Generation

• The heart is composed of three

types of muscles
SANode
• Atria & ventricles
AVNode
• Form the working myocardium
• They do the mechanical work of
Bundle
of His pumping

Purkinje
fibers

13-Jun-23 Physiology of the heart 2

 Impulse Generation
• The specialized tissues
• Excitatory & conducting tissues
SANode
• Sino atrial node
• Atrio-ventricular node
AVNode • Bundle of his
Bundle
• Purkinje fibers
of His

Purkinje
fibers

13-Jun-23 Physiology of the heart 3

Depolarization and Impulse Conduction

• Heart is autorhythmic
• Depolarization begins in sinoatrial (SA) node
• Spread through atrial myocardium
• Delay in atrioventricular (AV) node

13-Jun-23 Physiology of the heart 4

13-Jun-23 Physiology of the heart 6
SINO ATRIAL NODE
• Small ,flattened , ellipsoid strip of specialized cardiac muscle
• Located in the superior posterolateral wall of the right atrium
immediately below the opening of the vena cava
• Automatic electrical rhythmicity of sinus fibers is caused by self-
excitation

13-Jun-23 Physiology of the heart 7

Sinoatrial node(SA node)
• It is located in the right atrium, near the
entrance of the superior vena cava.
• It acts as the heart’s natural pacemaker, i.e.
initiates heart beat and the heart rate with
help from autonomic NS.
• The SA node is a muscle in itself consisting
of cells which are involved in contraction of
the heart muscle.
• For a muscle to contract, its cells have to
first depolarize, that is, move from being
negatively charged to being positively
charged. The same has to happen for the SA
node.
• The SA node is able to depolarize on its
own without the help of other cells, which is
referred to as automaticity.
• The SA node is connected to the
neighboring heart muscle cells through gap
junctions, which allow for transmission of
signals from the SA node to the muscle
cells.
• When the SA node depolarizes, it spreads a
wave of depolarization throughout the atrial
muscle cells.
MECHANISM OF SINUS NODAL RHYTHMICITY

• Resting membrane potential of sinus nodal fiber is between -55 to -60

millivolts
• The cause of this less negativity is due to the leakiness of cell
membranes of sinus fibres to sodium and calcium ions .This therefore
neutralizes some of the intracellular negativity

13-Jun-23 Physiology of the heart 11

THE HEART

13-Jun-23 Physiology of the heart 12

 INTERNODAL AND INTERATRIAL PATHWAYS
The end of sinus fibers connects to atrial muscle fibers
Therefore, action potential originating in the sinus
node travels into atrial muscle fibers
Action potential therefore spreads through the entire
muscle and eventually to the atrial-ventricular node
There are four bands for conduction;
i. Anterior interatrial band; passes through the
anterior walls of the right atrium to the left atrium
ii. Anterior ,middle , posterior bands; passes
respectively through the atrial wall and terminates to
atrial-ventricular nodes

13-Jun-23 Physiology of the heart 13

13-Jun-23 Physiology of the heart 14
The AV Node
• Its located in the interatrial septum near the atrioventricular valve.
• It serves as an electrical gateway to the ventricles.
• It receives signals from the SA node, and delays their transmission to
the bundle of His for about 0.1 seconds.
• This ensures that the atria have ample time to completely contract and
empty all their contents into the ventricles, before the ventricles start
contracting.

13-Jun-23 Physiology of the heart 15

DELAYED IMPULSE CONDUCTION FROM THE ATRIA TO THE VENTRICLES
AT THE ATRIO-VENTRICULAR NODE

The delay is to allow time for the atria to empty their blood into the
ventricles before ventricular contraction begins
This delay is caused by Atrial-ventricular node and its adjacent conductive
fibers
The Atrial-ventricular node is located in the posterior wall of the right
atrium below the tricuspid valve
From the sinus through the inter-nodal pathways ,the impulse reaches the
Atrial-ventricular node after about 0.03 second
There is a delay of 0.09 second in the atrial-ventricular node itself before
the impulse enters the atrial-ventricular bundle where it passes into the
ventricles

13-Jun-23 Physiology of the heart 16

13-Jun-23 Physiology of the heart 17
The Bundle of His
• It is found spread out in the interventricular septum, down to the
apex of the heart.
• It is divided into the right and left branches which conduct impulses
from the AV node to the apex of the heart.
• These impulses are then transmitted to the Purkinje fibers.

13-Jun-23 Physiology of the heart 18

• Another delay of about 0.04 second occurs in this penetrating Atrial-
ventricular bundle
• Thus the total delay in the Atrial-ventricular nodal and Atrial-
ventricular bundle system is about 0.13 second
• This delay in addition to initial conduction of 0.03 second from the
sinus node makes 0.16 second before impulses reaches the ventricles

13-Jun-23 Physiology of the heart 19

• Cause of slow conduction; caused by diminished numbers of gap
junctions between successive cells in the conducting pathways
• So there is a great resistance to conduction of excitatory ions from
one conducting fiber to the next

13-Jun-23 Physiology of the heart 20

Rapid Transmission In The Ventricular Purkinje Fibers
• Purkinje fibers lead from A-V node to the A-V bundle into the ventricles
• They have functional characteristics opposite to those of A-V Nodal fibers;-they
are very large fibers
-they transmit A.P at a velocity of about 6 times that of ventricular
muscles and 150 times than in some of A-V Nodal fibers
• This velocity allows almost instantaneous transmission throughout the remainder
part of ventricular muscles
• The rapid transmission by Purkinje fibers is believed to be due to:
Very high level of permeability of the gap junctions at the intercalated discs
between successive cells that make up Purkinje fibers
Purkinje fibers have very few myofibrils which means that they contract little or
not at all during the course of impulse transmission

13-Jun-23 Physiology of the heart 21

One-Conduction through the A-V Bundle

• Special characteristic of A-V Bundle-inability of action potentials to

travel backwards from ventricles to the atria
• Presence of a continuous fibrous barriers acts as an insulator to
prevent passage of the cardiac impulse backwards
• Everywhere except the A-V Bundle , the atrial muscle is separated
from the ventricular muscle by this continuous fibrous barrier

13-Jun-23 Physiology of the heart 22

Distribution of the Purkinje Fibers In The Ventricles

• After penetrating the fibrous tissue between atrial and ventricular

muscle , the distal portion of the A-V bundle passes downwards in the
ventricular septum towards the apex of the heart
• The bundles divides into left and right bundle branches that lie
beneath the endocardium on the two respective sides of ventricular
septum
• Each branch spreads downwards towards the apex of ventricles
dividing into smaller branches

13-Jun-23 Physiology of the heart 23

• These branches in turn course sideways around each ventricular
chamber and back towards the base of the heart
• The total elapsed time averages only 0.03 seconds from the time the
cardiac impulse enters the bundle branches in the ventricular septum
until it reaches the termination of Purkinje fibers

13-Jun-23 Physiology of the heart 24

Transmission of cardiac impulse in the ventricular
muscle
• Once the impulse reaches end of Purkinje fibers it is transmitted
through the ventricular muscle mass by the ventricular muscle fibers
• The velocity is about 0.3-0.5m/sec
• The cardiac muscle wraps around the heart in a double spiral with
fibrous septum between spiraling layers

13-Jun-23 Physiology of the heart 25

• Cardiac impulse therefore angulates towards the surface along the
direction of the spirals
• This transmission requires about 0.003secs almost equal to time
required for transmission through the entire ventricular portion of
Purkinje system

13-Jun-23 Physiology of the heart 26

Control of excitation and conduction in the heart

• SAN is the normal pacemaker of the heart because it has a high

impulse velocity
• Some parts of the heart can also exhibit intrinsic rhythmical excitation
in the same way as the sinus e.g A-V Nodal and Purkinje fibers
• When not stimulated from outside source the A-V Node discharge at
40-60 times per minute and the Purkinje fibers discharge at 15-40
times per minute
• Since the sinus discharge rate is higher than both the A-V Node and
Purkinje fibers , its impulses are discharged to both before the self
excitation of either A-V Node or Purkinje fibers
13-Jun-23 Physiology of the heart 27
Abnormal or Ectopic pacemakers
• This is a pacemaker elsewhere than the SAN
• A-V Node or Purkinje fibers may abnormally have a higher discharge
than sinus node hence become the pacemaker. This causes;
• Abnormal sequence of contraction of different part of the heart
• Debility of the heart pumping
• Blockage of transmission of the cardiac impulse from SAN to other parts of
the heart

13-Jun-23 Physiology of the heart 28

• When A-V Bundles blocks Purkinje fibers continues as pacemaker
• After sudden A-V bundle block the Purkinje system does not begin to
emit its intrinsic rhythmical impulses until 5-20 secs later because
before blockage Purkinje fibers had been overdriven by the rapid SAN
impulses and consequently are in a suppressed state.
• During these secs the ventricles fail to pump blood and the person
faints after the first 4-5 secs because of lack of blood flow to the brain
• This delayed pick up of heartbeat is called STOKES-ADAMS
SYNDROME

13-Jun-23 Physiology of the heart 29

Role of the Purkinje system in causing synchronous
contractions of ventricular muscle
• The rapid conduction of Purkinje fibers permits the cardiac impulse
to all ventricles and arrives after 0.03sec and contracts for about
another 0.3sec
• Effective pumping by the ventricular chambers requires this
synchronous type of contraction

13-Jun-23 Physiology of the heart 30

Mechanism of sinus node rhythmicity

• Resting membrane potential of sinus nodal fiber is between -55 to -60

millivolts unlike that of ventricular and atrial muscle cells which is -
90millivolts.
• The cause of this less negativity is due to the leakiness of cell
membranes of sinus fibers to sodium and calcium ions .
• This therefore neutralizes some of the intracellular negativity (-90 in
other excitable tissues).

13-Jun-23 Physiology of the heart 31

• The cells in SAN cell membrane are naturally leaky to Na+.
• Na+ tend to leak into the cell and this is responsible for the initial
phase of pace maker potential.
• Transient (T) Ca++ channels open and there is entry of Ca++ which
completes the pre-potential phase.
• The long lasting (L) Ca++ channels then open with resultant influx of
more Ca++ resulting in rapid depolarization.

13-Jun-23 Physiology of the heart 32

• At the peak of each impulse, K+ ion channels open, there is rapid
efflux of K+ ions which brings about repolarization.
• The K+ channels then close and Na+ ions leak into the cell causing the
initial phase of pre-potential, then the transient Ca++ channels with
the process repeating itself.

13-Jun-23 Physiology of the heart 33

13-Jun-23 Physiology of the heart 34
Control of heart rhythmicity and impulse conduction by
cardiac nerves
Parasympathetic Simulation
• Stimulation of parasympathetic nerves to the heart causes
Acetylcholine release
• Hormone has two major effects;
• Decreases rate of rhythm of SAN
• Decreases excitability of A-V junctional fibers between atrial musculature and
A-V Node thereby slowing transmission of cardiac impulse into ventricles

13-Jun-23 Physiology of the heart 35

Ventricular Escape

• Strong stimulation of Vagi can stop completely excitation of sinus

node or block transmission of impulse from atria to ventricles through
A-V Node
• Ventricles may stop beating for 5-20 secs but the ventricular septal
portion of the A-V bundle develops a rhythm of its own and causes
ventricular contraction at a rate of 15-40 beats per minute

13-Jun-23 Physiology of the heart 36

Mechanism of vagal effect
• The acetylcholine release at the vagal nerve ending increases the
permeability of potassium out of the conductive fibers
• Causes hyperpolarization making tissue much less excitable
• At SAN it causes more negativity than the normal -65 to -75

13-Jun-23 Physiology of the heart 37

• Initial rise of sinus nodal membrane potential requires much longer
to reach threshold potential for excitation;
• Slows rate of rhythmicity of nodal fibers
NOTE : If Vagal stimulation is strong enough it can stop entirely
rhythmical excitation of this node

13-Jun-23 Physiology of the heart 38

CONT’D
• In A-V node hyperpolarization makes it difficult for small atrial fibers
to generate enough electricity to excite nodal fibers
• Hence decrease of safety factor for transmission of cardiac impulse
through the transitional fibers into A-V Nodal fibers
• Moderate decrease simply delays conduction of the impulse
• A large decrease blocks the conduction entirely

13-Jun-23 Physiology of the heart 39

Control of Excitation in Heart
• The pacemaker cells
• SANode, AVNode, Purkinje cell
• All exhibit rhythmicity
• Why does the SAN
• Become the dominant pacemaker
• Why not
• The AVNode or Purkinje fibers dominate

13-Jun-23 Physiology of the heart 40

Control of Excitation
• The normal rate of discharge from these cells
• SAN = 70 to 80 per minute
• AVN = 40 to 60 per minute
• Purkinje fibers = 15 to 40 per minute

13-Jun-23 Physiology of the heart 41

Control of Excitation
• The rate of diastolic depolarization
• SAN = 15 to 60 mv/sec
• Purkinje fibers = 5 to 40 mv/sec
• In all these cells
• To change from “resting” to threshold potential
• Require a change of 20 to 25 mv
• Thus threshold is reached much faster
• In SAN than in Purkinje fibers

13-Jun-23 Physiology of the heart 42

Cardiotonic Agents
• Chronotropic agents
• Alter the excitability of
• Pacemaker
• Conducting system- Dromotropic effect

• Positive chronotropic agents

• Lead to increase in heart rate
• Negative chronotropic agents
• Lead to decrease in the heart rate

13-Jun-23 Physiology of the heart 43

Effects of Autonomic Nervous System
• Sympathetic stimulation increases
• Rate of sinus node discharge
• Rate of conduction
• Level of excitability of myocardium
• Force of contraction of myocardium

13-Jun-23 Physiology of the heart 44

Noradrenalin
• Noradrenalin increases
• The rate of SAN cells depolarization
• The rate of spontaneous discharge
• Heart rate

13-Jun-23 Physiology of the heart 45

Parasympathetic
• Parasympathetic stimulation
• Causes release of acetylcholine
• This causes a decrease
• Heart rate
• Excitability of AVN
• Slows transmission of impulses to ventricles

13-Jun-23 Physiology of the heart 46

Parasympathetic
• Very strong stimulation
• Can stop SAN discharge
• Block AVN transmission
• Ventricle can stop contraction
• Vagal escape
• Ectopic pacemaker from Purkinje fibers take over

13-Jun-23 Physiology of the heart 47

Parasympathetic
• Acetylcholine
• Activate M2 (muscarinic) receptors
• Through G-protein
• Open special K+ channels
• Efflux of K+
• Hyperpolarization

13-Jun-23 Physiology of the heart 48

Parasympathetic
• Activation of M2 receptors also
• Decrease cAMP concentration in cell
• Slows opening of Ca++ channels
• Rate of diastolic depolarization is retarded
• It takes longer to reach threshold
• Heart rate is slowed

13-Jun-23 Physiology of the heart 49

 Depolarization and Impulse Conduction

• Spread from
atrioventricular (AV)
node
• AV bundle
• Bundle branches
• Purkinje fibers

13-Jun-23 Physiology of the heart 50

 Depolarization and Impulse Conduction

• Depolarization in SA
node precedes
depolarization in atria,
AV node, ventricles

13-Jun-23 Physiology of the heart 51

13-Jun-23 Physiology of the heart 52
 Cardiotonic Agents
• Inotropic agents
• Affect the contractility of the cardiac muscles
• Positive inotropic agents
• Lead to increase in contraction
• Negative inotropic agents
• Lead to decrease in contraction

13-Jun-23 Physiology of the heart 53