CONDUCTIVITY&EXCITABILITY
MAGDI AWAD SASI
Objectives
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Illustrate the action potential of the ordinary (atrial and ventricular
)cardiac muscle fibers.
Identify its different parts and discuss the possible mechanisms for
such shape.
Relate the excitability changes of the ventricular muscle fibers to
their action potential and account for such relations
Discuss the factors affecting the excitability of cardiac muscle
fibers



.
Describe the conduction of the cardiac excitation wave fro SAN to
the ventricular muscles
Mention the different conduction velocities of the various parts of
the heart and discuss the mechanisms underlying such variation.
Discuss the factors affecting the conductivity of cardiac
muscle fibers.
Conduction system
► The
specialized heart cells of the cardiac conduction
system generate and coordinate the transmission of
electrical impulses to myocardial cells.
► The
result is sequential atrioventricular contraction
which provides for the most effective flow of blood ,
thereby optimizing cardiac out put.
Conducting System
►3
Components to cardiac conduction
(nodal) system.
 Sinoatrial (SA) node
 Atrioventricular (AV) node
 Conducting cells
►From SA node to
 Atrial myocardium
 AV node along internodal pathways
►From
AV node to ventricular myocardium
4
Changes in ion concentrations in a cardiac muscle fiber following depolarization
What causes the
muscle resting
membrane
potential to
change initially?
What would be
happening with a
skeletal muscle at this
point?
AP’s in Contractile Myocardial Cells

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
Phase 4: Resting Membrane Potential is -90mV
Phase 0: Depolarization moves through gap junctions
 Membrane potential reaches +20mV
Phase 1: Initial Repolarization
 Na+ channels close; K + channels open
Phase 2: Plateau
 Repolarization flattens into a plateau due to
 A decrease in K + permeability and an increase in Ca +2
permeability
 Voltage regulated Ca +2 channels activated by
depolarization have been slowly opening during phases 0
and 1
 When they finally open, Ca +2 enter the cell
 At the same time K + channels close
 This lengthens contraction of the cells
 AP = 200mSec or more
Phase 3: Rapid Repolarization
 Plateau ends when Ca +2 gates close and K + permeability increases
again
PHASE
0 = Rapid Depolarization
(inward Na+ current)
1
0
1
2
2 = Plateau
(inward Ca++ current)
3 = Repolarization
(outward K+ current)
0
3
4 = Resting Potential
4
-90
TIME
Electrical Properties of Myocardial Fibers
1. Rising phase of action potential
•
Due to opening of fast Na+ channels
2. Plateau phase
•
•
•
•
Closure of sodium channels
Opening of calcium channels
Slight increase in K+ permeability
Prevents summation and thus tetanus of cardiac
muscle
3. Repolarization phase
•
•
Calcium channels closed
Increased K+ permeability
Phase 0 (Rapid depolarization): It is caused by the
rapid influx of Na+ into the cell.
Phase 1 (Early partial repolarization): During this
phase, the permeability of the membrane to Na+ is
rapidly reduced, but the membrane permeability for
both Ca2+ and K+ increases. The overall effect is a small
change in the membrane potential toward the resting
membrane potential (repolarization).
Phase 2 (Plateau of the action potential): This
coincides with an increased permeability for Ca2+.
The inward movement of Ca2+ and the decreased
efflux of K+ maintain the membrane potential near
zero during this phase of the action potential.
Phase 3 (Rapid repolarization): due to a
reduction of the inward Na+ and Ca2+ currents and
a large increase in the outward K+ current.
Phase 4 (Complete repolarization): the
membrane goes back to the resting level (- 90
mV). Na+-K+ pump works to drive the excess Na+
out and the excess K+ in.
Action Potential of Myocyte
1) Na+ gates open
2) Rapid
depolarization
3) Na+ gates close
4) Slow Ca2+
channels open
5) Ca2+ channels
close, K+ channels
open
19-12
Contraction of Myocardium
► Myocytes
have stable resting potential of -90 mV
► Depolarization (very brief)
 stimulus opens voltage regulated Na+ gates, (Na+ rushes
in) membrane depolarizes rapidly
 action potential peaks at +30 mV
 Na+ gates close quickly
► Plateau
- 200 to 250 msec, sustains contraction
 slow Ca2+ channels open, Ca2+ binds to fast Ca2+
channels on SR, releases Ca2+ into cytosol: contraction
► Repolarization
- Ca2+ channels close, K+ channels
open, rapid K+ out returns to resting potential
19-13
Action potential in contractile fibers
14
Enumerate the cardiac ion channels.
1- voltage –gated
►
► Na+
channels
►
►
fast
Outer m► activated
slow
K+ channels
Ca++ channels
Inner hinactivated
T-(transient) L-(long lasted
Complete the Produces the
prepotential
AP
► 2-
Ligand-gate K+ Channels
Ca++
activated
Arachidonic acid
activated
►
Na+
activated
Ach
activated
ATP-sensitive
Refractory period
►
►
►
►
Long refractory period (250
msec) compared to skeletal
muscle (3msec)
During this period
membrane is refractory to
further stimulation until
contraction is over.
It lasts longer than muscle
contraction, prevents
tetanus
Gives time to heart to relax
after each contraction,
prevent fatigue
17
AP in skeletal muscle : 1-5 msec
AP in cardiac muscle :200 -300 msec
Locations of autorythmic cells

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
Sinoatrial node (SA node)
Specialized region in right atrial
wall near opening of superior
vena cava.
Atrioventricular node (AV node)
Small bundle of pecialized
cardiac cells located at base of
right atrium near septum
Bundle of His (atrioventricular
bundle)
Cells originate at AV node and
enters interventricular septum
Divides to form right and left
bundle branches which travel
down septum, curve around tip
of ventricular chambers, travel
back toward atria along outer
walls
Purkinje fibers
Small, terminal fibers that
extend from bundle of His and
spread throughout ventricular
myocardium
18
Rate of generation of AP at different sites of the heart
SITE
RATE
(Times/min)
SA node
100
AV node
40 - 60
AV bundle, bundle
branches,& Purkinje
fibres
20 - 35
SA node acts as heart pacemaker because it has the fastest
rate of generating action potential
Nerve impulses from autonomic nervous system and
hormones modify the timing and strength of each heart beat
but do not establish the fundamental rhythm.
20
Automaticity
– 60-90 /min
►AV – node – 40-60 /min
►Hiss bundle – 30-40 /min
►Purkinje fibers - <20 /min
►SA-node
Impulse Conduction to the
Myocardium
node signal travels at 1 m/sec through atria
► AV node slows signal to 0.05 m/sec
► SA
 thin myocytes with fewer gap junctions
 delays signal 100 msec, allows ventricles to fill
► AV
bundle and purkinje fibers
 speeds signal along at 4 m/sec to ventricles
► Ventricular
systole begins at apex, progresses up
 spiral arrangement of myocytes twists ventricles slightly
19-22
Internodal Pathway
Located in the walls of the atria.
► Links the SA node to the AV node.
► Distributes the action potential to the
contractile cells of the atria.
►
Specialized Conduction
System
► Atrioventricular
(AV) node
► Delays
electrical
signal due to a
decreased number
of gap junctions.
Sherwood’s Human Physiology 9-11 (9-8 6th Edition)
Atrioventricular Node
► Larger
than SA node.
► In floor of R atrium Located in the bottom of
the right atrium near the septum( near
opening of coronary sinus).
► Cells in the AV node conduct impulses more
slowly, so there is a delay as impulses travel
through the node.
► This allows time for atria to finish contraction
before ventricles begin contracting.
The impulse picked up by the A-V node is
delayed for 0.1 – 0.15 second, then
passed on to the A-V bundle.
The A-V bundle conducts the impulses to
the buddle branches.
Tissue
Conduction
rate (m/s)
Atrial
muscle
0.3
Atrial
pathways
1
AV node
0.05
Bundle of
His
1
Purkinje
system
4
Ventricular
muscle
0.3-0.5
27
Conduction Delay
► Atrioventricular
fibrous tissue
 Acts as an insulator
► Takes
0.03s from SA node to AV node
► 0.12 before crossing into ventricle
► Into Bundle of His .16s from when SA
node fired
► Delay makes sure the atria contract first
Guyton’s Textbook of Medical Physiology 10-3
The AV nodal delay of conduction
(0.13 sec.) is important to:
delay the start of ventricular
contraction till the end of all
atrial contraction
2. Protect the ventricle from
high atrial abnormal rhythm
1.
Important functional
characteristics of the A-V node
The A-V node is characterized by:
Very slow conductivity: This delays the transmission
of impulses to the ventricles (A-V nodal delay). This
delay allows the atria to finish with their systole
before passing the impulse to the ventricles to start
ventricular systole.
Long absolute refractory period after conducting an
impulse: This limits the number of impulses that
can be transmitted from the atria to the ventricles
to 230 impulse/min. This protects the ventricles
from receiving high frequency of impulses from the
atria.
Timing of Atrial &
Ventricular Excitation
► SA
node setting pace since is the fastest
► In 50 msec excitation spreads through both
atria and down to AV node.
► 100 msec delay at AV node due to smaller
diameter fibers- allows atria to fully contract
filling ventricles before ventricles contract
► In 50 msec excitation spreads through both
ventricles simultaneously
AtrioVentricular Bundle
► “Bundle
of His”
 From the AV node,
impulses travel
through to the right
and left bundle
branches
 These branches
extend to the right
and left sides of the
septum and bottom of
the heart.
Atrioventricular Bundle
 These branch a lot to
form the Purkinje fibers
that transmit the impulses
to the myocardium
(muscle tissue)
 The bundle of His, bundle
branches and Purkinje
fibers transmit quickly and
cause both ventricles to
contract at the same time
 Like a “phone tree”
► To
transmit
impulses to the
largest chamber of
the heart, the left
bundle branch
bifurcates into the
left anterior and left
posterior bundle
branches
Factors affecting excitability
► 1.
Temperature :
► 2.
Ionic changes:
► Na
and K+
►
low  low excitability
High high
• 3. Autonomic nervous system :
Sympathetic
parasympathetic
Increase excitability
decrease excitability
► 4.
Hormones e.g. thyroxin increase
excitability.
► 5. Drugs e.g. caffeine increase excitability
► 6.Others: Ischaemia , hypoxia and bacterial
toxins → decrease excitability.
3. Conductivity
►It
is the ability of the cardiac
muscle to conduct the
excitation wave from S.A.N to
all parts of the heart.
Sherwood’s Human Physiology 9-10 (9-7 6th Edition)
https://www.youtube.com/watch?v=-Iloe-s7COo
https://www.youtube.com/watch?v=0Lx-s5wxfCU
Guyton’s Textbook of Medical Physiology 10-3
► Pejković, B.; Krajnc, I.; Anderhuber, F.; Kosutić, D. (2008). "Anatomical aspects of
the arterial blood supply to the sinoatrial and atrioventricular nodes of the human
heart". The Journal of international medical research. 36 (4): 691–698
►