PPT RHYTHMICITY AND CONDUCTIVITY OF HEART BY DR QAZI

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Information about PPT RHYTHMICITY AND CONDUCTIVITY OF HEART BY DR QAZI
Education

Published on November 16, 2018

Author: IMTIAZRASOOL

Source: authorstream.com

RHYTHMICITY AND CONDUCTIVITY OF THE CARDIAC MUSCLE : RHYTHMICITY AND CONDUCTIVITY OF THE CARDIAC MUSCLE Dr QAZI IMTIAZ RASOOL بسم الله الرحمن الرحيم 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. : 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: 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 Autorhythmicity Definition : the ability of the heart to initiate its beat continuously and regularly without external stimulation PHYSIOLOGICALLY:- ( Automaticity ) a cell’s ability to spontaneously depolarize, reach threshold, and propagate an Action Potential -1% of the cardiac muscle fibers Slide4: SAN AVN Impulse conduction Impulses originate regularly at a frequency of 60-100 beat/ min Slide5: -100 -80 -60 -40 -20 0 20 Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 Na + ca ++ ATPase mv Cardiac Action Potential Resting membrane Potential Na + m Na + Na + Na + Na + Na + h K + ca ++ K + K + K + ca ++ ca ++ (Plateau Phase) K + K + K + Na + K + Depolarization Repolarization Slide6: -100 -80 -60 -40 -20 0 20 Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 Na + ca ++ ATPase mv Cardiac Action Potential R.M.P Na + m Na + Na + Na + Na + Na + h K + ca ++ K + K + K + ca ++ ca ++ (Plateau Phase) K + K + K + Na + K + Depolarization Repolarization Phase 4 (only in pacemaker cells Slide7: Sino-Atrial Node Anterior Internodal Pathway * Middle Internodal Pathway * Posterior Internodal Pathway * Anterior interatrial myocardial band Left Atrium 1.Atrio-Node Region 2.Node Region 3.Node-His Region Atrio -Ventricular Nod e Bundle of His Right Bundle Branch Left Bundle Branch Anterior Division Posterior Division Right Atrial Tracts * Septal Division Special conducting tissue Sinoatrial node (SA node) : Sinoatrial node (SA node) Specialized region in R atrial wall near opening of superior vena cava Small, flattened , shape of a crescent , P-cells (pacemaker cells ) 15 X 5 X 1 mm Cells are self-excitatory, Intrinsic rate of 90 -100 beats/ min No fast Na + current No initial repolarization Ca 2+ current underlies upstroke Ca 2+ current underlies conducted AP Internodal pathway- : Internodal pathway- Connect Sino-Atrial Node and Atrio -Ventricular 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 Atrio-Ventricular Node: Atrio -Ventricular Node Atrio-Ventricular Node: Posterior septal wall of Right Atrium near septal leaflet of tricuspid valve base of septum  in the triangle of Koch  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) A tria contracts 0.1sec earlier than ventricle b) limits the no impulses transmitted to ventricles- <230/min Atrio -Ventricular Node Slide12: 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 Bundle of His- ( after German physician Wilhelm His Jr., 1863-1934 Slide13: Conduction System of the Heart Septal branch Slide14: Normal variation of Conduction System of the Heart Bundle of kent -----WPW SYNDROME 2. James bundle Slide16: 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- Jan Evangelista Purkinje (Czech; 1787-1869) Slide17: Generation in different tissue .   This " vagal tone " reduces the resting heart rate down to 60-80 beats/min. Slide18: 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 Conduction velocity in different tissue Msec. Slide19: NOTE;- Non-SA nodal tissues are latent pacemakers that can take over (at a slower rate), should the normal pacemaker (SA node )fail latent pacemakers Slide20: latent pacemakers Cardiac Action Potential Types Are Either Fast Or Slow Response : 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 potentia ls Sinoatrial node Atrioventricular node Bundle of his 4. Atrial internodal tracts 5. Bundle branches Action potential in Sino-atrial cardiac cells : Action potential in Sino-atrial cardiac cells Very similar to the ventricular cardiac cells with a few major exceptions Do not have a stable rest . Rising phase and Action Potential is driven by the voltage-gated Ca 2+ channel in most SA cells As the Ca 2+ channel inactivates the membrane is repolarized by the delayed rectifier K + channel Spontaneously depolarize once the delayed K + channel has closed due to p resence of an ion channel that is activated by hyperpolarization – the funny channel . FUNNY CHANNEL ( If) Hyperpolarization, cyclic nucleotide HCN channel gated ion channel : FUNNY CHANNEL ( I f ) Hyperpolarization, cyclic nucleotide HCN channel gated ion channel Activated by hyperpolarization As membrane repolarizes after AP the threshold for opening of the I f is reached at about -50 Mv I f opens and allows Na + to preferentially flow into the cell cAMP can influences ( I f ) and shift threshold of activation from -50 to -40 mV. . Slide26: Slow spontaneousInward Na + ions Outward K + current (repolarization) Inward Na + and Ca + + ions (depolarization) threshold ( decreased HR ) (Increased HR) (Nodal) Action Potential 0 4 3 Slide29: 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 Fast > Slow 5. Overshoot of action potential Fast > Slow Differences between fast and slow cardiac action potentials: 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 STEPS OF CARDIAC EXCITATION 30 Electrical Activity of Myocardium: Electrical Activity of Myocardium FACTORS AFFECTING AUTORHYTHMICITY : FACTORS AFFECTING AUTORHYTHMICITY 1.Hormonal and chemical factors ( Adrenaline.NE, alkali Ach, acids, ether, bacterial toxins, chloroform 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) c a ++ 6.Drugs D igitalis,. SUMMARY Comparison of APs: 34 pacemaker depolarization spontaneous depolarization No pacemaker depolarization conducted AP to cell triggers depolarization No pacemaker depolarization conducted AP to cell triggers depolarization AP from VENTRICULAR MUSCLE -80 mV -80 mV 0 SUMMARY Comparison of APs maximum diastolic potential AP from ATRIAL MUSCLE AP from SA node or AV node

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