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Impulse Generation 2-May-17 CVS Impulse generation 1 Impulse Generation The heart is composed of three types of muscles Atria & ventricles 2-May-17 CVS Impulse generation Form the working myocardium They do the mechanical work of pumping 2 Impulse Generation The specialized tissues Excitatory & conducting tissues 2-May-17 CVS Impulse generation Sino atrial node Atrio-ventricular node Bundle of his Purkinje fibers 3 Myocardium Myocardial fibers Excitable tissue Have a resting membrane potential Mechanism of genesis of RMP Between –60 to –90 mv Similar to that in skeletal muscles Cardiac muscle respond To supra threshold stimuli by 2-May-17 Generating an action potential Capable of propagating it CVS Impulse generation 4 Myocardium Excitation arising in atrium or ventricles 2-May-17 Spread over the unexcited tissue Works as a syncytium CVS Impulse generation 5 Cardiac Action Potential +20 mv 1 General properties of cardiac AP 2 0 mv 3 Special permeability differences 0 Similar to that of nerve & skeletal muscle Lead to difference in shape of cardiac AP 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation 6 Cardiac Action Potential +20 mv 1 In the cardiac cells after the initial spike 2 0 mv 3 0 Membrane remains deoplarized for About 0.2 sec in atria About 0.3 sec in ventricles Exhibiting a plateau 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation 7 Cardiac Action Potential +20 mv Depolarization 1 2 0 mv 3 0 4 - 85 mv Due to in Na+ conductance Opening of fast sodium channels Initial repolarization Due to closure of sodium channels 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation 8 Cardiac Action Potential +20 mv The plateau phase 1 2 0 mv 3 0 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation Due to slow prolonged opening of Voltage gated Ca++ channels Become activated at potential of –30 to – 40 mv Also known as Slow calcium channels Calcium – sodium channels 9 Cardiac Action Potential +20 mv 1 2 0 mv 3 0 Large amount of Ca++ & Na+ Flow through these channels Prolong the period of plateau phase 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation 10 Cardiac Action Potential +20 mv 1 2 0 mv 3 0 At the end of plateau phase Slow calciumsodium channels close Influx of Ca++ & Na+ ceases 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation 11 Cardiac Action Potential +20 mv 1 2 0 mv Permeability of cardiac muscle to K+ increases 3 0 4 - 85 mv 0 = depolarization 2-May-17 1 = initial repolarization 2 Plateau phase 3 repolarization CVS Impulse generation Efflux of K+ Return the membrane potential to its resting value 12 Refractory Period +20 mv 1 During the action potential 2 0 mv 3 0 4 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 Cardiac muscle is refractory to restimulation Cardiac impulse cannot re-excite an already excited area Relative refractory period 0.05 sec CVS Impulse generation 13 Refractory Period +20 mv 1 2 Normal refractory period 0 mv 3 0 4 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 0.25 to 0.3 seconds Approx equal to duration of action potential Relative refractory period 0.05 sec CVS Impulse generation 14 Refractory Period +20 mv 1 Relative refractory period 2 0 mv During this period 3 0.05 seconds 0 Muscle is more difficult to excite But can be excited 4 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 Relative refractory period 0.05 sec CVS Impulse generation 15 Refractory Period +20 mv 1 Refractory period 2 0 mv 3 Is due to inactivation of sodium channels 0 During prolonged depolarization 4 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 Relative refractory period 0.05 sec CVS Impulse generation 16 Refractory Period +20 mv 1 Not until the membrane 2 0 mv 3 Has repolarized to – 50 to –60 mv Does sodium channels recover 0 4 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 Relative refractory period 0.05 sec CVS Impulse generation 17 Refractory Period +20 mv The cells in SAN 1 2 0 mv Have transmembrane potential of 3 0 - 85 mv Absolute refractory period 0.25 – 0.3 sec 2-May-17 SAN cells membrane 4 -55 to –60 mv between discharges Naturally leaky to Na+ Relative refractory period 0.05 sec CVS Impulse generation 18 Pacemaker Potential +20 mv Na+ tend to leak into the cell 0 mv Transient (T) Ca++ channels open -50 mv Responsible for the initial phase of pace maker potential Entry of Ca++ -60 mv Completes the prepotential phase Pacemaker potential Ca++ Na+ Ca++ Na+ 2-May-17 CVS Impulse generation 19 Pacemaker Potential +20 mv 0 mv The long lasting (L) Ca++ channels then open Ca++ More Ca++ influx Which produces the impulse -50 mv -60 mv Pacemaker potential Ca++ Na+ Ca++ Na 2-May-17 + CVS Impulse generation 20 Pacemaker Potential K+ +20 mv K+ At the peak of each impulse 0 mv Ca++ K+ ion channels open Efflux of K+ ions Brings about repolarization -50 mv -60 mv Pacemaker potential Ca++ Na+ Ca++ Na 2-May-17 + CVS Impulse generation 21 Pacemaker Potential K+ +20 mv K+ The potassium channels then close 0 mv Ca++ Na+ ions leak into the cell Causing the initial phase of prepotential -50 mv -60 mv Pacemaker potential Ca++ Na+ Ca++ Na 2-May-17 + CVS Impulse generation 22 Pacemaker Potential K+ +20 mv K+ Calcium ions channels then 0 mv Ca++ Open Calcium influx Completing another deplorization -50 mv -60 mv Pacemaker potential Ca++ Na+ Ca++ Na 2-May-17 + CVS Impulse generation 23 Spread of Excitation Depolarization initiated in SAN Atria depolarization 2-May-17 Spread radially through atria Then converge to AVN CVS Impulse generation Complete in 0.1 second 24 Spread of Excitation Conduction in AVN is slow Cause 0.1 sec delay Then the excitation 2-May-17 AVNodal delay CVS Impulse generation Spread to bundle of His Then to purkinje fibers To the ventricular myocardium 25 Spread of Excitation The conducting system is such that Gives time for 2-May-17 Cardiac impulse will not travel from atria to ventricle too rapidly CVS Impulse generation Atrial emptying before Ventricle contraction begins 26 Control of Excitation in Heart The pacemaker cells Why does the SAN SANode, AVNode, Purkinje cell All exhibit rythmicity Become the dominant pacemaker Why not 2-May-17 The AVNode or Purkinje fibers dominate CVS Impulse generation 27 Control of Excitation The normal rate of discharge from these cells 2-May-17 SAN = 70 to 80 per minute AVN = 40 to 60 per minute Purkinje fibers = 15 to 40 per minute CVS Impulse generation 28 Control of Excitation In all these cells To change from “resting” to threshold potential Thus threshold is reached much faster 2-May-17 Require a change of 20 to 25 mv In SAN than in Purkinje fibers CVS Impulse generation 29 Factors Affecting the Rate of Pacemaker +20 mv 0 Rate established by pacemaker cells depend on c - 40 mv - 60 mv b d f Threshold pot Time required for membrane pot a To change from resting to threshold For generation of AP e Normal time 2-May-17 CVS Impulse generation 30 Factors Affecting the Rate of Pacemaker +20 mv 0 Change in heart rate will be mediated by c - 40 mv - 60 mv b d f Threshold pot a Magnitude of initial “RMP” Rate of depolarization Threshold value e Normal time 2-May-17 CVS Impulse generation 31 Factors Affecting the Rate of Pacemaker +20 mv If the “RMP” becomes more negative 0 It takes longer to reach threshold c - 40 mv - 60 mv b d f Threshold pot From (e to f) as compared from (a to b) Thus the heart rate a Shift from (a to e) Decreases e Normal time 2-May-17 CVS Impulse generation 32 Factors Affecting the Rate of Pacemaker +20 mv 0 An increase in the rate of depolarization c - 40 mv - 60 mv b d f Threshold pot a e It takes shorter to reach threshold From (a to c) Compared from (a to b) The heart rate will increase Normal time 2-May-17 CVS Impulse generation 33 Factors Affecting the Rate of Pacemaker +20 mv A shift of threshold potential 0 c - 40 mv - 60 mv b d f Threshold pot To a more negative value Will cause an increase in heart rate a e Normal time 2-May-17 CVS Impulse generation 34 Cardiotonic Agents Chronotropic agents Alter the excitability of Positive chronotropic agents Lead to increase in heart rate Negative chronotropic agents 2-May-17 Pacemaker Conducting system Lead to decrease in the heart rate CVS Impulse generation 35 Cardiotonic Agents Inotropic agents Positive inotropic agents Affect the contractility of the cardiac muscles Lead to increase in contraction Negative inotropic agents 2-May-17 Lead to decrease in contraction CVS Impulse generation 36 Effects of Ions Calcium ions Have a positive inotropic effect In ECF Ca++ concentration leads to In force of contraction of cardiac muscle More Ca++ available for troponin In ECF Ca++ concentration reduces 2-May-17 Myocardial force of contraction CVS Impulse generation 37 Effects of Ions Calcium ions Have a chronotropic effect too In ECF Ca++ concentration 2-May-17 Slow the heart rate By elevating the excitation threshold CVS Impulse generation 38 Effects of Ions In ECF Ca++ concentration Increases the heart rate Due to increase in rate of diastolic depolarization Purkinje cells are more sensitive to Ca++ 2-May-17 Leads to development of ectopic foci CVS Impulse generation 39 Effects of Ions Sodium ions Have little effects under normal conditions A decrease in ECF Na+ concentration Slows the heart Severe reduction (10%) in Na+ concentration 2-May-17 Decrease in amplitude of AP Leads to complete loss of excitability CVS Impulse generation 40 Effects of Ions Potassium ions An increase in ECF K+ concentration Dilated heart which is flaccid Heart rate falls Impaired conduction in AVNode Lead to atrial block 2-May-17 CVS Impulse generation 41 Effects of Ions An increase in ECF K+ concentration Causes partial depolarization Shortens duration of AP Decreases amplitude & intensity of AP Hence the contraction of heart 2-May-17 Becomes progressively weaker CVS Impulse generation 42 Effects of Autonomic Nervous System Sympathetic stimulation increases 2-May-17 Rate of sinus node discharge Rate of conduction Level of excitability of myocardium Force of contraction of myocardium CVS Impulse generation 43 Nor adrenalin Nor adrenalin increases 2-May-17 The rate of SAN cells depolarization The rate of spontaneous discharge Heart rate CVS Impulse generation 44 Effect of Nor Adrenalin Ca++ Nor adrenalin 1 receptor Adenyl cyclase Nor adrenalin acts on 1 receptors GS protein ATP cAMP Increase in cAMP Activated protein kinase A Protein Kinase Ca++ Ca++ Sarcoplasmic Ret Troponin 2-May-17 CVS Impulse generation 45 Effect of Nor Adrenalin Ca++ Nor adrenalin 1 receptor Adenyl cyclase Protein Kinase A facillitates GS protein ATP cAMP Protein Kinase Ca++ Ca++ Opens long lasting Ca++ channels Influx of Ca++ into myocardial cell Leads to increase in strength of contraction Sarcoplasmic Ret Troponin 2-May-17 CVS Impulse generation 46 Parasympathetic Parasympathetic stimulation Causes release of Acetylcholine This causes a decrease Heart rate Excitability of AVN 2-May-17 Slows transmission of impulses to ventricles CVS Impulse generation 47 Parasympathetic Very strong stimulation Can stop SAN discharge Block AVN transmission Ventricle can stop contraction Vagal escape 2-May-17 Ectopic pacemaker from Purkinje fibers take over CVS Impulse generation 48 Parasympathetic Acetylcholine Activate M2 (muscarinic) receptors Through G-protein 2-May-17 Open special K+ channels Efflux of K+ Hyperpolarization CVS Impulse generation 49 Parasympathetic Activation of M2 recptors also Decrease cAMP concentration in cell Rate of diastolic depolarization is retarded 2-May-17 Slows opening of Ca++ channels It takes longer to reach threshold Heart rate is slowed CVS Impulse generation 50 Cardiac Glycosides 2Na+ 1 Ca++ 2Na+ Na+/K+ ATPase pump 2 K+ 3 Na+ 2-May-17 1 Ca++ Digitalis increase cardiac contractility Inhibits sodiumpotassium ATPase In the heart myocardium Ca++/Na++ antiport pump CVS Impulse generation There is an antiport transport mechanism 51 Cardiac Glycosides 2Na+ 1 Ca++ Cell membrane exchange ICF calcium for ECF sodium 2Na+ Na+/K+ ATPase pump 2 K+ 3 Na+ 2-May-17 1 Ca++ Ca++/Na++ antiport pump 1 Ca++ for 2 Na+ The rate of exchange CVS Impulse generation Proportional to concentration of Na+ in ICF 52 Cardiac Glycosides 2Na+ Inhibition of Na+ K+ pump 1 Ca++ 2Na+ Na+/K+ ATPase pump 2 K+ 3 Na+ 2-May-17 1 Ca++ Ca++/Na++ antiport pump CVS Impulse generation Leads to increase in Na+ concentration in ICF This interferes with antiport mechanism 53 Cardiac Glycosides 2Na+ 1 Ca++ 2Na+ Na+/K+ ATPase pump 1 Ca++ 2 K+ 3 Na+ 2-May-17 There is increase in ca++ concentration in ICF Followed by force of contraction of myocardial cells Ca++/Na++ antiport pump CVS Impulse generation 54