1. RHYTHMICITY AND CONDUCTIVITY OF THE CARDIAC MUSCLE
بسم الله الرحمن الرحيم
RHYTHMICITY AND CONDUCTIVITY OF THE CARDIAC MUSCLE
Dr QAZI IMTIAZ RASOOL

2. OBJECTIVES Describe the characters auto-rhythmicity of the cardiac muscle 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 Compare and explain the slow versus the rapid conduction of cardiac waves. 5. Discuss factors affecting rhythmicity and conductivity of cardiac muscle.

3. 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)

4. Special conducting tissue
SA Node
Right Atrial Tracts*
Anterior
Internodal
Pathway*
Middle
Internodal
Pathway*
Posterior
Internodal
Pathway*
Anterior interatrial
myocardial band
(Bachmann’s Bundle)
Left Atrium
AN Region N Region NH Region
AV Node
Bundle of His
Right Bundle Branch
Left Bundle Branch
Septal Division
Anterior Division
Posterior Division

5. Sinoatrial node (SA node)
W. J. Lederer -- Cardiac electrophysiology
Sinoatrial node (SA node)
Specialized region in R atrial wall near opening
of superior vena cava
Small, flattened , shape of a crescent ,P+T CELLS
15 X 5 X 1 mm
Cells are self-excitatory, (pacemaker cells).
Intrinsic rate of beats/ min
No fast Na+ current
Ca2+ current underlies upstroke
Ca2+ current underlies conducted AP

6. Internodal pathway- -Tract of kent Connect 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

7. AV-NODE posterior septal wall of RA immediately behind tricuspid valve
Delay of impulses to ventricles by sec
-( 0.09 at AVN & 0.03 at AV bundle)
2. Causes of delay-
i) smaller size of fibers
ii) smaller number of gap junctions
iii) more negative RMP
Significance-
a) atria contracts 0.1sec earlier than ventricle
b) limits the no impulses transmitted to ventricles- <230/min

8. (after German physician Wilhelm His Jr., 1863-1934
Bundle of His-
(after German physician Wilhelm His Jr.,
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

9. Conduction System of the Heart
Septal branch
Septal branch

10. Jan Evangelista Purkinje (Czech; 1787-1869)
Purkinje fibers-
Jan Evangelista Purkinje (Czech; )
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
Purkinje fibers
Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium

11. Of impulses in different tissue
Generation
Of impulses in different tissue
This intrinsic rhythm is primarily influenced by ANS nerves
A- vagal influences being dominant over sympathetic influences at rest.   This "vagal tone" reduces the resting heart rate down to beats/min.
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 beats/min.

12. 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

13. Conduction velocity in different tissue
Conduction rate (m/s)
SA node
0.05
Atrial muscle
0.3
Atrial pathways 1
AV node
Bundle of His
Purkinje system 4
Ventricular muscle
Msec.
Msec.

14. Action potential in sinoatrial cardiac cells
Very similar to the ventricular cardiac cells
with a few major exceptions
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.
Activated by hyperpolarization
As the membrane repolarizes after the action potential the threshold for opening of the funny channel is reached at about -50 mV
The channel opens and allows Na+ to preferentially flow into the cell
Also called the HCN channel or hyperpolarization, cyclic nucleotide gated ion channel
cAMP can have dramatic influences on this channel and shift its threshold of activation from -50 mV to -40 mV.
The funny channel actually looks very much like a voltage-gated K+ channel but has differences in its pore to allow Na+ influx and in the voltage sensing/opening mechanism.

15. FUNNY CHANNEL ( If) Also called the HCN channel or hyperpolarization, cyclic nucleotide gated ion channel
Activated by hyperpolarization
As membrane repolarizes after AP the threshold for opening of the If is reached at about -50 Mv
If opens and allows Na+ to preferentially flow into the cell
cAMP can influences ( If) and shift threshold of activation from - 50 to -40 mV. .

16. PACEMAKER ACTIVITY IN SA NODE
T-type
L type
pacemaker depolarization
Diastolic depolarizaton

17. (Nodal) Action Potential
Inward Na+ and Ca+ + ions (depolarization)
Outward K+ current (repolarization) 3
Increased HR)
threshold 4
Slow spontaneousInward Na+ ions
(d HR)
Automaticity - a pacemaker cell’s ability to spontaneously depolarize, reach threshold, and propagate an AP

20. Cardiac Action Potential Types Are Either Fast Or Slow Response
Fast-response action potentials
Atrial myocardial fibers
Ventricular myocardial fibers
Purkinje fibers
Slow-response action potentials
Sinoatrial node
Atrioventricular node
Bundle of his
4. Atrial internodal tracts
5. Bundle branches

21. Differences between fast and slow cardiac action potentials:
1.Phases
Fast response – all present
Slow response – 1 & 2 absent
2. RMP
Slow > Fast
Fast response – voltage constant
Slow response – voltage slowly decreases
3. Slope of upstroke
Fast > Slow
4.Amplitude of action potential
5. Overshoot of action potential

23. STEPS OF CARDIAC EXCITATION
Cardiac impulse originates at SA node
AP spreads throughout R and L atria
Impulse passes from atria into ventricles through AV node (only 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

25. Electrical Activity of Myocardium

26. 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,.

27. SUMMARY Comparison of APs
W. J. Lederer -- Cardiac electrophysiology
SUMMARY Comparison of APs
-80 mV
AP from VENTRICULAR MUSCLE
AP from ATRIAL MUSCLE
AP from SA node or AV node
spontaneous
depolarization
conducted AP
to cell triggers
depolarization
conducted AP
to cell triggers
depolarization
pacemaker
depolarization
maximum
diastolic
potential
No pacemaker
depolarization
No pacemaker
depolarization