‫بسم هللا الرحمن الرحيم‬
RHYTHMICITY AND CONDUCTIVITY OF
THE CARDIAC MUSCLE
Dr QAZI IMTIAZ RASOOL
OBJECTIVES
1. Describe the characters auto-rhythmicity of the cardiac muscle.
2. Describe the mechanism of sinus nodal rhythmicity and
illustrate the pace-maker potential.
3.Describe the pathway of conduction of cardiac excitation wave
through the conducting system of the heart.
4. Compare and explain the slow versus the rapid conduction of
cardiac waves.
5. Discuss factors affecting rhythmicity and conductivity of cardiac
muscle.
Special conducting tissue
Autorhythmicity
Definition: the ability of the heart to initiate its beat
continuously and regularly without external stimulation
-----1% of the cardiac muscle fibers
Functions
1. Act as a pacemaker (set the rhythm of electrical excitation)
2. Form the conductive system (network of specialized
cardiac muscle fibers that provide a path for each cycle of
cardiac excitation to progress through the heart)
3
Special conducting tissue
SA Node
Right
Atrial
Tracts*
Anterior
Internodal
Pathway*
AV Node
Middle
Internodal
Pathway*
Posterior
Internodal
Pathway*
Anterior interatrial
myocardial band
(Bachmann’s Bundle)
Left Atrium
AN Region
N Region
NH Region
Bundle of His
Right Bundle
Branch
Left Bundle
Branch
Septal
Division
Anterior
Division
Posterior
Division
Sinoatrial node (SA node)
Specialized region in R atrial wall near opening
of superior vena cava
1.
2.
3.
4.
5.
6.
7.
Small, flattened , shape of a crescent ,P+T CELLS
15 X 5 X 1 mm
Cells are self-excitatory, (pacemaker cells).
Intrinsic rate of 90 -100 beats/ min
No fast Na+ current
Ca2+ current underlies upstroke
Ca2+ current underlies conducted AP
Internodal pathwayConnect SA Node and AV Node
Faster conduction than Atrial muscles•
NORMAL
Anterior- Bachman’s bundle
Middle-Wenkebach’s bundle
Posterior-Thorell’s bundle
ABNORMAL
-Tract of kent
-James tract
AV-NODE
posterior septal wall of
RA immediately behind tricuspid valve
1. Delay of impulses to ventricles by 0.12sec
-( 0.09 at AVN & 0.03 at AV bundle)
2. Causes of delayi) smaller size of fibers
ii) smaller number of gap junctions
iii) more negative RMP
Significancea) atria contracts 0.1sec earlier than ventricle
b) limits the no impulses transmitted to
ventricles- <230/min
Bundle of His(after German physician Wilhelm His Jr., 1863-1934
begins from AV Node, passes downwards in the
intraventricular septum for 5-15mm
along each side of the septum,(divides into R+L bundle
branches)
Left branch divides 3 fasciculus
- anterior
-posterior
- septal
Both divide repeatedly and Lie sub-endocardially
Conduction System of the Heart
Septal branch
Purkinje fibersJan Evangelista Purkinje (Czech; 1787-1869)
origin from terminal divisions of bundle branches
that diverge to the inner sides of the ventricular walls
2. Largest and Fastest conducting
3.1-2mm thick
4. Passes impulses to ventricular myocytes
Generation
Of impulses in different
tissue
intrinsic rhythm -influenced by ANS
nervesA- vagal influences
being dominant over
sympathetic influences at
rest. This "vagal tone"
reduces the resting heart
rate down to 60-80
beats/min.
latent pacemakers
NOTE;-Non-SA nodal tissues are latent pacemakers that can take
over (at a slower rate), should the normal pacemaker (SA node )fail
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Conduction velocity in different tissue
Tissue
Conduction
rate (m/s)
SA node
0.05
Atrial muscle
0.3
Atrial pathways
1
AV node
0.05
Bundle of His
1
Purkinje system
4
Ventricular muscle
1
Msec.
Action potential in sinoatrial cardiac cells
Very similar to the ventricular cardiac cells
with a few major exceptions
1.
2.
3.
4.
5.
6.
7.
Do not have a stable rest.
AP is driven by the voltage-gated Ca2+
channel in most SA cells
Rising phase is due the opening of the voltage-gated Ca2+
channel
As the Ca2+ channel inactivates the membrane is
repolarized by the delayed rectifier K+channel
Spontaneously depolarize once the delayed K+ channel
has closed
Due to presence of an ion channel that is activated by
hyperpolarization – the funny channel.
FUNNY CHANNEL ( If)
Also called the HCN channel or hyperpolarization,
cyclic nucleotide gated ion channel
1.
Activated by hyperpolarization
2.
As membrane repolarizes after
AP the threshold for opening of
the If is reached at about -50 Mv
3.
If opens and allows Na+ to
preferentially flow into the cell
4.
cAMP can influences ( If) and
shift threshold of activation from 50 to -40 mV.
.
PACEMAKER ACTIVITY IN SA NODE
T-type
L type
pacemaker depolarization
Diastolic depolarizaton
(Nodal) Action Potential
Inward Na+
and Ca+ + ions
(depolarization
)
Outward K+
current
(repolarization
)
0
3
Increased HR)
threshold
4
Slow
spontaneous
Inward Na+
ions
Automaticity - a pacemaker cell’s ability to spontaneously
depolarize, reach threshold, and propagate an AP
(d HR)
Cardiac Action Potential Types Are
Either Fast Or Slow Response
1.
Fast-response action potentials
1. Atrial myocardial fibers
2. Ventricular myocardial fibers
3. Purkinje fibers
2.
Slow-response action potentials
1. Sinoatrial node
2. Atrioventricular node
3. Bundle of his
4. Atrial internodal tracts
5. Bundle branches
Differences between fast and slow
cardiac action potentials:
1.Phases
Fast response – all present
Slow response – 1 & 2 absent
Slow > Fast
2. RMP
Fast response – voltage constant
Slow response – voltage slowly decreases
3. Slope of upstroke
4.Amplitude of action potential
5. Overshoot of action potential
Fast > Slow
Fast > Slow
Fast > Slow
STEPS OF CARDIAC EXCITATION
1. Cardiac impulse originates at SA node
2. AP spreads throughout R and L atria
3. Impulse passes from atria into ventricles through AV node (only
4.
5.
6.
7.
point of electrical contact between chambers)
AP briefly delayed at AV node (ensures atrial contraction
precedes ventricular contraction to allow complete ventricular
filling)
Impulse travels rapidly down interventricular septum by means
of bundle of His
Impulse rapidly disperses throughout myocardium by means of
Purkinje fibers
Rest of ventricular cells activated by cell-to-cell spread of
impulse through gap junctions
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Electrical Activity of Myocardium
FACTORS AFFECTING
AUTORHYTHMICITY
1.Hormonal and chemical factors ( adren. ,NE, , alkali ,
While Ach, acids, ether, bacterial toxins, chloroform
decrease.
2.T emperature ( warming increase, cooling decrease).
3.Oxygen supply ( hypoxia decrease.)
4..Autonomic nerve stimulation;- G protein
a) vagal stimulation ↓ the slope of pre-potential and ↓
the rate of impulse generation
b) sympathetic stimulation increases the slope and
increases the impulse rate
5. Ions- a) K+ b) ca++
6.Drugs Digitalis,.
-80 mV
SUMMARY
Comparison of APs
AP from VENTRICULAR MUSCLE
AP from SA node or AV node
0
spontaneous
depolarization
conducted AP
to cell triggers
depolarization
pacemaker
depolarization
-80 mV
AP from ATRIAL MUSCLE
No pacemaker
depolarization
maximum
diastolic
potential
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