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cardiac conduction system.pptx

  1. Cardiac conduction system anatomy and physiology Dr Srikrishna S
  2. • The heart is endowed with a special system for (1) generating rhythmical electrical impulses to cause rhythmical contraction of the heart muscle (2)conducting these impulses rapidly through the heart. • The Atria contract about one sixth of a second ahead of ventricular contraction • All portions of the ventricles to contract almost simultaneously
  4. SA NODE of Keith & Flack • The sinus node is a crescent-shaped, subepicardial specialized muscular structure located posterolaterally in the right atrium (RA) free wall. • The sinus node lies within the epicardial groove of the sulcus terminalis at the junction of the anterior trabeculated RA appendage with the posterior smooth-walled venous component • - tadpole-shaped structure with a head, central body, and tail with nodal extensions representing multiple limbs. • In adults the sinus node measures 8 to 22 mm long and 2 to 3 mm wide and thick
  5. The sinus node is a complex of weakly coupled, heterogeneous cells, including the principal pacemaker cells as well as nonpacemaker cells embedded in a dense supporting connective matrix Within the sinus node, pacemaker cells may be divided Into three major classes: (1) “elongated spindle-shaped cells,” - long, multinucleated 80 microns (2) “spindle cells,” mononuclear, shorter than spindle cells, 40 microns (3) “spider cells,” - irregularly shaped branches with blunt ends.
  6. • Pacemaker of the heart Current models involve the concept of a “pacemaker hierarchy” head- body - tail Sympathetic stimulation shifts the leading pacemaker site superiorly, resulting in an increase in heart rate. • Artery to SA node – 55% - Right coronary artery - 45% - Circumflex branch of LCA The sinus nodal artery typically passes centrally through the length of the sinus body, and it is disproportionately large, which is considered physiologically important in that its perfusion pressure can affect the sinus rate. Distention of the artery slows the sinus rate, whereas collapse causes an increase in sinus rate.
  7. The sinus node is densely innervated with postganglionic adrenergic and cholinergic nerve terminals. The right vagus nerve predominantly affects sinus node function. • Vagal responses begin after a short latency and dissipate quickly. • The rapid onset and offset of responses to vagal stimulation allow dynamic beat-to-beat vagal modulation of the heart rate • Enhanced vagal activity can produce sinus bradycardia, sinus arrest, and sinoatrial exit block. • Responses to sympathetic stimulation begin and dissipate slowly. • The slow temporal response to sympathetic stimulation precludes any beat-to-beat regulation by sympathetic activity. • Increased sympathetic activity can increase the sinus rate and reverse sinus arrest and sinoatrial exit block.
  8. INTERNODAL CONDUCTION PATHS • There are three preferential anatomic conduction pathways from the sinus node to the AV node • These groups of internodal tissue are best referred to as internodal atrial myocardium, not tracts, because they do not appear to be histologically recognizable specialized tracts, only plain atrial myocardium. • ANTERIOR-------- BACHMAN • MIDDLE-------------WENCKEBACH • POSTERIOR-------THOREL
  9. The anterior “internodal atrial myocardium” begins at the anterior margin of the sinus node, curves anteriorly around the superior vena cava (SVC) to the interatrial septum, and then splits into two bundles one passes to the left atrium (LA) (Bachmann bundle), while the second bundle descends along the interatrial septum and connects to the superior margin of the AVN. Bachmans bundle It connects the anterosuperior RA an LA behind the ascending aorta, just beneath the epicardium, and Is the preferential path of LA activation during sinus rhythm. Three other interatrial conduction pathways have been described: 1. Muscular bundles on the inferior atrial surface near the coronary sinus (CS) 2. Transseptal fibres in the fossa ovalis 3. Posteriorly in the vicinity of the right pulmonary valves
  10. The middle “internodal atrial myocardium” begins at the superior and posterior margins of the sinus node, travels posteriorly behind th SVC to the crest of the interatrial septum, and descends within the interatrial septum to the superior margin of the AVN. The posterior “internodal atrial myocardium” starts at the inferoposterior margin o the sinus node, travel inferiorly through the crista terminalis to the eustachian ridge, and then into the interatrial septum above the CS os, where it joins the posterior portion of the AVN.
  11. •Action potentials originating in the sinus node travel outward into atrial muscle fibres. •The velocity of conduction in most atrial muscle is about 0.3 m/sec, but conduction is more rapid, about 1 m/sec in tracts
  12. Location of AV node
  13. • The AVN is an interatrial structure, measuring approximately 5 mm long, 5 mm wide, and 0.8 mm thick in adults. • The AVN is located beneath the RA endocardium at the apex of the triangle of Koch • Slightly more anteriorly and superiorly is where the His bundle (HB) penetrates the AV junction through the central fibrous body and the posterior aspect of the membranous AV septum. • When traced inferiorly, toward the base of the triangle of Koch, the compact AVN area separates into twoc(rightward and leftward) posterior extensions, usually with the artery supplying the AVN running between them. • The rightward posterior extension has been implicated in the so-called slow pathway in the typical atrioventricular nodal reentry tachycardia (AVNRT) circuit
  14. • Artery to AV node – 90% - Right coronary artery - 10 % - Circumflex branch of LCA Delay of about 0.12 sec in conduction through AV node
  15. • As with the SA node, the AV node has extensive autonomic innervation and an abundant blood supply. • The AV node consists of three regions— distinguished by functional and histologic differences 1) The transitional cell zone 2) Compact node 3) Penetrating bundle
  16. histology The AVN and perinodal area are composed of at least three electrophysiologically distinct cells: 1. The atrionodal (AN) 2. Nodal (N) 3. Nodal-his (NH) cells The AN region corresponds to the cells in the transitional region that are activated shortly after the atrial cells. The N region corresponds to the region where the transitional cells merge with mid nodal cells and formd compact node. 1. Conduction is slower through the N region in the compact AVN than in the AN and NH cell zones. 2. The n cells exhibit diastolic depolarization and are capable of automatic impulse formation. 3. The n cells in the compact avn appear to be responsible for the major part of av conduction delay 4. They are likely the site of wenckebach block and the site at which calcium channel blockers delay av conduction. The NH region corresponds to the lower N cells, typically distal to the site of Wenckebach block, connecting to the insulated penetrating portion of the HB.
  17. Histology of AV Node
  18. Cause of the Slow Conduction • The slow conduction in the transitional, nodal, and penetrating A-V bundle fibres is caused mainly by diminished numbers of gap junctions between successive cells in the conducting pathways  greater resistance to conduction of excitatory ions from one conducting fibre to the next.
  19. Functions of AV node 1. The main function of the AVN is modulation of atrial impulse transmission to the ventricles; it introduces a delay between atrial and ventricular systole. 2. To limit the number of impulses conducted from the atria to the ventricles. 3. Fibers in the lower part of the AVN can exhibit automatic impulse formation, serving as a subsidiary pacemaker
  20. Bundle of His • The AV nodal tissue merges with the His bundle, which runs through the inferior portion of the membranous interventricular septum, and then in most cases, continues along the left side of the crest of the muscular interventricular septum. • The proximal part of the His bundle rests on the right atrial-left ventricular (RA-LV) part of the membranous septum and the more distal part travels along the right ventricle-left ventricular (RV-LV) part of the membranous septum immediately below the aortic root.
  21. • The His bundle usually receives a dual blood supply from both the AV nodal artery and branches of the LAD. • Unlike the SA and AV nodes, the bundle of His and Purkinje system have relatively little autonomic innervation.
  22. Blood supply of the conduction system
  23. Right Bundle Branch(RBB) • The right bundle branch (RBB) originates from the His bundle. • It is a narrow compact structure – band like • crosses to the right side of the IVS and extends along the RV endocardial surface to the region of the anterolateral papillary muscle of the RV, where it divides to supply the papillary muscle, the parietal RV surface, and the lower part of the RV surface. • The proximal portion of the RBB is supplied by branches from the AV nodal artery or the LAD artery, whereas the more distal portion is supplied mainly by branches of the LAD artery.
  24. Left Bundle Branch(LBB) • Anatomically much less discrete than the RBB. • The LBB may divide immediately as it originates from the bundle of His or may continue for 1 to 2 cm as a broad ribbon before dividing.
  25. • The predivisional portion of the LB penetrates the membranous portion of the interventricular septum under the aortic ring and then divides under the septal endocardium into two branches: the LAF and the LPF. • An estimated 65% of individuals have a third fascicle of the LB, the left median fascicle (LMF). • The thin LAF crosses the anterobasal LV region toward the anterolateral papillary muscle and terminates in the Purkinje system of the anterolateral LV wall. • The LPF appears as an extension of the main LB and is broad in its initial course. It then fans out extensively toward the posterior papillary muscle and terminates in the Purkinje system of the posteroinferior LV wall
  26. • The LBB and its anterior fascicle have a blood supply similar to that of the proximal portion of the RBB – LAD and AV nodal artery • The left posterior fascicle is supplied by branches of the AV nodal artery, the posterior descending artery, and the circumflex coronary artery.
  27. Rapid Transmission in the Ventricular Purkinje System • Special Purkinje fibres lead from the A-V node through the A-V bundle into the ventricles. • They are very large fibres, even larger than the normal ventricular muscle fibres, and they transmit action potentials at a velocity of 1.5 to 4.0 m/sec, a velocity about 6 times that in the usual ventricular muscle and 150 times that in some of the A-V nodal fibres. • This allows almost instantaneous transmission of the cardiac impulse throughout the entire remainder of the ventricular muscle
  28. Characteristics of Cardiac Conduction Cells • Automaticity: Ability to initiate an electrical impulse • Excitability: Ability to respond to an electrical impulse • Conductivity: Ability to transmit an electrical impulse from one cell to another
  29. Physiology • The “threshold potential” is the lowest Em at which opening of enough Na+ channels (or Ca2+ channels in the setting of nodal cells) is able to initiate the sequence of channel openings needed to generate a propagated action potential. • Electrical changes in the action potential follow a relatively fixed time and voltage relationship that differs according to specific cell types.
  30. Two types of action potentials in heart Fast response action potentials • Seen in normal atrial and ventricular myocytes and in his-purkinje fibers • Action potentials have very rapid upstrokes, mediated by the fast inward iNa. Slow response action potentials • Seen in in the normal sinus and atrioventricular nodal cells and many types of diseased tissues • Have very slow upstrokes, mediated by a slow inward, predominantly l-type voltage-gated ca2+ current (iCal)
  31. Fast Response Action Potential Phase 4: The Resting Membrane Potential • The K+ (Kir) channels underlie an outward K+ current (IK1) responsible for maintaining the resting potential • It remains near the equilibrium potential for K+ (EK). • The resting membrane potential is negative during phase 4 (about -90 mV) because potassium channel are open (K+ conductance K+ currents [IK1] are high).
  32. • The resting Em is also powered by the Na+-K+ adenosine triphosphatase (the Na+-K+ pump) • The Na+-K+ pump transports two K+ ions into the cell against its chemical gradient and three na+ ions outside against its electrochemical gradient at the expense of one ATP molecule. • The Na+-K+ pump is electrogenic and generates a net outward movement of positive charges
  33. • Phase 0: The Upstroke—Rapid Depolarization • On excitation of a cardiomyocyte by electrical stimuli from adjacent cells, its resting Em (approximately −85 mV) depolarizes, leading to opening (activation) of Na+ channels • A large and rapid influx of Na+ ions (inward INa) occurs into the cell down their electrochemical gradient. • Once an excitatory stimulus depolarizes the Em beyond the threshold for activation of Na+ channels (approximately −65 mV), the activated INa is regenerative and no longer depends on the initial depolarizing stimulus.
  34. INa in phase 0 • Activation of Na+ channels is transient • Fast inactivation (closing of the channel pore) starts simultaneously with activation • Inactivation is slightly delayed relative to activation, the channels remain transiently (less than 1 millisecond) open to conduct INa during phase 0 of the action potential before it closes
  35. ICal in phase 0 • The threshold for activation of ICaL is approximately −30 to −40 mV. • ICaL is much smaller than the peak INa. • The amplitude of ICaL is not maximal near the action potential peak because of the time-dependent nature of ICaL activation. • Therefore ICaL contributes little to the action potential until the fast INa is inactivated, after completion of phase 0. • As a result, ICaL affects mainly the plateau of action potentials recorded in atrial and ventricular muscle and His- Purkinje fibers.
  36. • Phase 1: Early Repolarization • Early repolarization during which the membrane repolarizes rapidly and transiently to almost 0 mV - early notch due to 1. Inactivation of INa 2. Concomitant activation of several outward currents. a) The transient outward K+ current (Ito) is mainly responsible for phase 1 of the action potential. Ito rapidly activates and then rapidly inactivates b) Na+ outward current through the Na+-Ca2+ exchanger operating in reverse mode likely contributes to this early phase of repolarization
  37. Phase 2: The Plateau Phase 2 (plateau) represents a delicate balance between • The depolarizing inward currents 1. ICaL 2. Small residual component of inward INa) • Repolarizing outward currents (outward rectifying currents) 1. Ultrarapidly activating [IKur] 2. Rapidly activating[IKr] 3. Slowly activating [IKs] delayed activating) Vs • Phase 2 is the longest phase of the action potential • The plateau phase is unique among excitable cells and marks the phase of Ca2+ entry into the cell.
  38. ICal • ICaL is activated by membrane depolarization, is largely responsible for the action potential plateau, and is a major determinant of the duration of the plateau phase. • ICaL also links membrane depolarization to myocardial contraction. • L-type Ca2+ channels activate on membrane depolarization to potentials positive to −40 mV. • ICaL peaks at an Em of 0 to +10 mV
  39. Ikr • Ikr activates relatively fast and inactivation thereafter is very fast. • The fast voltage-dependent inactivation limits outward current through the channel at positive voltages and thus helps to maintain the action potential plateau phase that controls contraction and prevents premature excitation.
  40. IKs • IKs activates slowly compared with action potential duration, it is also slowly inactivated. • Hence the contribution of IKs to the net repolarizing current is greatest late in the plateau phase, particularly during action potentials of long duration. • This allows IKs channels to accumulate in the open state during rapid successive action potentials and mediate the faster rate of repolarization. • IKs plays an important role in determining the rate-dependent shortening of the cardiac action potential
  41. IKur • IKur is detected only in human atria but not in the ventricles. • Predominant rectifier current responsible for atrial repolarization and is a basis for the much shorter duration of the action potential in the atrium. • IKur activates rapidly on depolarization in the plateau range and displays outward rectification, but it inactivates slowly during the time course of the action potential.
  42. • Phase 3: Final Rapid Repolarization • Phase 3 is the phase of rapid repolarization that restores the Em to its resting value. • Phase 3 is mediated by the 1. Increasing conductance of the delayed outward rectifying currents (IKr and IKs) 2. The inwardly rectifying K+ currents (IK1 and acetylcholine-activated K+ current [IKACh]) 3. Outward K+ current (IK1 4. Time-dependent inactivation of ICaL .
  43. • Phase 4: Restoration of Resting Membrane Potential • restoration of transmembrane ionic concentration gradients to the baseline resting state is necessary. • This is achieved by the 1. Na+-K+ ATPase (Na+-K+ pump, which exchanges two K+ ions inside and three Na+ ions outside) 2. Na+-Ca2+ exchanger (INa-Ca, which exchanges three Na+ ions for one Ca2+ ion)
  44. Atrioventricular Heterogeneity of the Action Potential • Compared with the atrium, ventricular myocytes 1. Maintain a slightly more hyperpolarized resting em (approximately −85 mv vs. −80 mv). 2. The action potential duration is longer 3. The plateau phase reaches a more depolarized em (approximately +20 mv), 4. Phase 3 repolarization curve is steeper in ventricular myocytes as compared with the atrial action potential
  45. 1. The density of Ito is twofold higher in the atria compared with ventricular myocytes. 2. Ito subtypes (Ito,f and Ito,s) are differentially expressed in the heart. Ito,f is the principal subtype expressed in human atrium 3. IKur is detected only in human atria and not in the ventricles. This accelerates the early phase of repolarization and lead to lower plateau potentials and shorter action potential durations in atrial as compared with ventricular cells
  46. IK1 density is much higher in ventricular than in atrial myocytes • Explains the steep repolarization phase in the ventricles • The hyperpolarized resting Em in ventricular myocytes, and prevents the ventricular cell from exhibiting pacemaker activity
  47. Slow Response Action Potential • Slow response action potentials are characterized by a more depolarized Em at the onset of phase 4 (−50 to −65 mV) • Slow diastolic depolarization during phase 4 • Reduced action potential amplitude. • The rate of depolarization in phase 0 is much slower than that in the working myocardial cells, resulting in reduced conduction velocity of the cardiac impulse in the nodal regions
  48. • The sinus and AV nodal cells lack the inward rectifier K+ current (IK1), which acts to stabilize the resting Em • Sinus and AV nodal excitable cells exhibit a spontaneous, slow, and progressive decline in the Em during diastole (spontaneous diastolic depolarization) • Once this spontaneous depolarization reaches threshold (approximately −40 mV), a new action potential is generated
  49. Phase 4: Diastolic Depolarization • If is a hyperpolarization-activated inward current that is carried largely by Na+ • Once activated, It depolarizes the membrane to a level where the Ca2+ current activates to initiate an action potential. • Other ionic currents gated by membrane depolarization (i.e., ICaL and T-type Ca2+ current [ICaT]), and a current generated by the Na+- Ca2+ exchanger have also been proposed to be involved in pacemaking.
  51. Phase 0: The Upstroke—Slow Depolarization • Action potential upstroke is mainly achieved by ICaL. • L-type Ca2+ channels activate on depolarization to potentials positive to −40 mV, and ICaL peaks at 0 to +10 mV. • The peak amplitude ICaL is less than 10% that of INa, and the time required for activation and inactivation of ICaL is slower than that for INa. • As a consequence, the rate of depolarization in phase 0 (dV/dt) is much slower and the peak amplitude of the action potential is less than that in the working myocardial cells.
  52. EXCITABILITY • Excitability of a cardiac cell describes the ease with which the cell responds to a stimulus with a regenerative action potential • The most important determinant of reduced excitability is the reduced availability of Na+ channels. • The more negative the Em is, the more Na+ channels are available for activation, the greater the influx of Na+ into the cell during phase 0, and the greater the conduction velocity.
  53. • Reduced excitability is physiologically observed during the relative refractory period (occurring during phase 3 of the action potential, before full recovery of Em). • Initiation of a propagating action potential will require a larger-than-normal stimulus. • Reduced membrane excitability can occur in certain pathophysiological conditions 1. Genetic mutations that result in loss of na+ channel function 2. Na+ channel blockade with class I antiarrhythmic drugs 3. Acute myocardial ischemia.
  54. REFRACTORINESS • Once an action potential is initiated, the cardiomyocyte becomes inexcitable to stimulation for a time. • Refractoriness is determined by 1. The action potential duration 2. Em 3. The number of Na+ channels that have recovered from their inactive state. • Permits relaxation of cardiac muscle before subsequent activation. • The refractory period acts as a protective mechanism by preventing multiple, compounded action potentials from occurring. • Shorter refractoriness facilitates reentry and arrhythmias
  55. • The absolute refractory period (which extends over phases 0, 1, 2, and part of phase 3 of the action potential • After the absolute refractory period, a stimulus can cause some cellular depolarization, but it does not lead to a propagated action potential. The sum of this period and the absolute refractory period is termed the effective refractory period • The relative refractory period, which extends over the middle and late parts of phase 3 to the end of phase 3 of the action potential.
  56. • During the relative refractory period, initiation of a second action potential is more difficult but not impossible • A larger-than-normal stimulus can result in activation of the cell and lead to a propagating action potential • However, the upstroke of the new action potential is less steep and of lower amplitude and its conduction velocity is reduced compared with normal.
  57. Post-repolarization refractoriness. • In pacemaking tissues, INa is predominantly absent and excitability is mediated by the activation of ICaL. • After inactivation, the transition of Ca2+ channels from the inactivated to the closed resting state (i.e., recovery from inactivation) is relatively slow. • As a result, excitability in pacemaking cells may not be recovered by the end of phase 3 of the action potential • Sinus and AV nodal cells remain refractory for a time interval that is longer than the time it takes for full membrane repolarization to occur. • May prevent premature excitation • May be involved in development of blocks during ischemia
  58. PROPAGATION • Conduction velocity refers to the speed of propagation of the action potential through cardiac tissue. • The conduction velocity varies in cardiac tissues, TISSUE CONDUCTION RATE (m/s) RELATIVE VALUE SAN 0.05 ATRIAL PATHWAY 1 AVN 0.02 – 0.05 LEAST BUNDLE OF HIS 1 PURKINJE SYSTEM 4 HIGHEST VENTRICULAR MUSCLE 1
  59. • Intracellular Propagation • The velocity of propagation increases with 1. Increasing cell diameter 2. Action potential amplitude 3. The initial rate of the rise of the action potential. Intercellular Propagation • Propagation of action potentials from one cell to adjacent cells is achieved by direct ionic current spread via specialized, low resistance intercellular connections (gap junctional channels) located mainly in arrays within the intercalated disks. • The heart behaves electrically as a functional syncytium, resulting in a • coordinated mechanical function.
  60. • Thank you