RHYTHMICITY AND CONDUCTIVITY OF THE CARDIAC MUSCLE بسم الله 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)

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

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 90 -100 beats/ min No fast Na+ current Ca2+ current underlies upstroke Ca2+ current underlies conducted AP

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

AV-NODE posterior septal wall of RA immediately behind tricuspid valve Delay of impulses to ventricles by 0.12sec -( 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

(after German physician Wilhelm His Jr., 1863-1934 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 Septal branch

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

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 60-80 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 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

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.

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.

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. .

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) 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

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

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

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

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,.

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