Rhythmical Excitation of Heart Guyton

Heart system special for: 1 generating rhythmical electrical impulses to cause rhythmical contraction of the heart muscle 2 conducting the impulses rapidly through heart Atria contract approx. 1/6 second ahead of ventricles allows time for ventricles to fill up. System allows all portions of ventricles to contract almost simultaneously to create effective pressure in ventricles. Sinus Node (SA) Small flattened strip of specialized cardiac muscle located in superior posterolateral wall of right atrium immediately below and slightl lateral to opening of superior vena cava Not contractile but fibers connect with atrial muscle fibers so Aps spread Fibers of SA node have capability of self-excitation can cause automatic rhythmical discharge and contraction. Mechanism of Sinus Nodal rhythmicity RMP of Sinus node fiber is about -60 while ventricular fiber is -90. This is because the CM of sinus fibers are leaky to Na+ and Ca2+ Cardiac muscle has 3 types of ion channels : 1. Fast sodium channels 2. Slow sodium-calcium channels 3. Potassium channels Opening of fast Na channels for few 10,000ths of sec is resp for rapid upstroke spike of AP observed in ventricular muscle rapid influx of +ve NA ions. Then plateau of ventricular AP caused by slower opening of slow sodium-calcium channels for about 0.3 second. Finally opening of potassium channels allows K+ to move out and returns to RMP. Difference of channels in Sinus nodal fiber: RMP is higher -55 vs -90mV. At -55mV the fast Na+ channels have become inactivated/blocked any time MP becomes more ve than -55mV for more than few millisecs the inactivation gates for fast NA channels close. Only slow sodium

calcium channels can open and cause APtherefore the atrial nodal AP is slower to develop than ventricular AP. Also, after AP occurs repolarization is also slower than ventricular. Self-Excitation of Sinus Nodal Fibers: High [Na+] in ECF outside nodal fiber and number of already open NA channels Positive NA ions leak inside. Between heartbeats, influx of +ve charged Na ions causes slow rise in RMP. Therefore resting MP gradually rises and when threshold of -40mV reached, the sodiumcalcium channels are activated causing AP. The leakiness of SA node fibers to sodium and calcium causes self-excitation. How does leakiness to Na and Ca not cause SA node fibers to remain depolarized? 1. Sodium calcium channels become inactivated about 100-150 milliseconds after opening 2. At same time many K+ channels open Influx of +ve Na and Ca ceases and K+ diffuses out Also, K+ channels remain open for a few extra tenths of secon HYPERPOLARISATION to -60mV Potassium channels start closing and sodium + calcium ion influx inbalances outward K+ causing the resting MP to rise again.

Internodal Pathways and Transmission of the cardiac impulse through Atria: Sinus nodal fibers connect directly with surrounding atrial muscle fibers, APs travel outwards from SA node to atria and eventually to AV node. Velocity of conduction in atrial muscle is ~0.3m/s but in some small bands of atrial fibers ~1m/s. Anterior inter-atrial band: passes around anterior atrial walls to left atrium. 3 small bands: curve thru anterior, lateral and posterior atrial walls &terminate at AV node These bands have specialized conduction fibers similar to Purkinje Atrioventricular Node and Delay of Impulse Conduction from Atria to ventricles: Cardiac impulse doesnt travel from atria to ventricles quickly delay allows time for atria to drain into ventricles before ventricular contraction.

Av node is located in posterior wall of right atrium immediately behind the tricuspid valve. After travelling through intermodal pathways, the impulse reached the AV node about 0.03 seconds after its origin at SA node. Then there is a delay of 0.09secs in AV node before entering the penetrating portion of the AV bundle where it passes to ventricles. A final delay of 0.04 seconds occurs in the penetrating AV bundle (composed of many small fascicles passing through fibrous tissue separating atria from ventricles) Total delay in AV nodal and AV bundle system is ~~ 0.13 seconds. Therefore 0.13+0.03 seconds = 0.16 delay for impulse to reach ventricle muscles from SA. CAUSE OF SLOW CONDUCTION: In transitional, nodal and penetrating AV bundle due to less gap junctions greater resistance to conduction of excitatory ions Rapid Transmission in Ventricular Purkinje System: Special purkinje Fibres lead from AV node thru AV bundle to ventricles The rapid AP transmission by purkinje fibers very high gap junction permeability at intercalated discs. No or very little contraction as impulse travels through ONE WAY CONDUCTION THROUGH AV BUNDLE: Atrial muscle is separated from ventricular muscle everywhere except for at AV bundle. Insulative barrier DISTRIBUTION OF PURKINJE FIBERS IN VENTRICLES THE LEFT AND RIGHT BUNDLE BRANCHES After penetrating the fibrous tissue the distal portion of AV bundle passes in ventricular septum for 5-15 mm towards heart apex then bundle divides into right and left branches beneath endocardium on two sides of septum. Each brunch spreads downwards towards apex of each ventricle and divides into smaller branches. Branches course sideways around ventricle chamber and back towards base of heart. These Purkinje fibers penetrate 1/3 into muscle mass becoming continuous with muscle fibers. From when Cardiac impulse enters the bundle branches in ventricular septum until it reaches termination of the fibers only 0.03 seconds pass. As it enters Purkinje fibers, the Impulse spreads almost immediately to entire ventricular muscle mass.

TRANSMISSION OF THE CARDIAC IMPULSE IN THE VENTRICULAR MUSCLE Once impulse reaches ends of the Purkinje fibers it is transmitted to ventricular muscle. Velocity of transmission is only 0.3-0.5m/s in ventricular muscle fibers. Cardiac muscle wraps around heart in double spiral, with fibrous septa between spiraling layers impulse does not travel outward toward surface of heart but moves to surface along spiral. Transmission from endocardium to epicardium requires 0.03 seconds more. Total time for impulse from initial bundle to last of ventricular muscle fibers is 0.06 seconds. SUMMARY OF SPREAD OF THE CARDIAC IMPULSE THROUGH THE HEART Pg 118.

Control of Excitation and Conduction in the Heart SINUS NODE AS PACEMAKER OF THE HEART Impulse normally arises from Sinus node, in some abnormal cases other parts of heart can exhibit intrinsic rhythmical excitation eg AV nodal and Purkinje fibers AV nodal fibers discharge at intrinsic rhythmical rate of 40-60 times per minute Purkinje fibers discharge at rate of 15-40 times per minute.

Normal sinus rate is 70-80 times per minute Since sinus rate is faster it controls the hearts rhythmicity. Each time SA node discharges it excites Av node and purkinje and SA node discharges before they can reach their own thresholds for self-excitation. Therefore SA node is the pacemaker. Abnormal Pacemakers Ectopic some part of heart develops discharge rate faster than that of SA node. (eg AV node or purkinje fibers) becomes the pacemaker. Causes an abnormal sequence of contraction sequence of contraction of the different heart parts can cause debility of heart pumping. Blockage of transmission of impulse from SA node to rest of heart also causes pacemaker shift. AV nodal fibers then take over. If AV nodal fibers block then atria continue to contract normally and Purkinje fibers form new pacemaker in ventricles which will contract at 15-40 bpm. Sudden AV block: purkinje system does not begin to emit its intrinsic rhythmical impulses until 5-20 seconds later because they had been overdriven by faster SA node and were suppressed. Person faints in first 4-5 seconds due to lack of blood flow to brain Stokes-Adams syndrome. ROLE OF PURKINJE SYSTEM IN CAUSING SYNCHRNOUS CONTRACTION OF VENTRICULE MUSCLE Normally cardiac impulse arrives at most portions of ventricles within narrow time span, exciting the first ventricular fiber 0.03-0.06 seconds ahead of last ventricular fiber. Contraction continues for 0.3 seconds. CONTROL OF HEART RHYTHMICITY AND IMPULSE CONDUCTION BY CADIAC NERVES: SYMPATHETIC and PARASYMPATHETIC NERVES Parasympathetic: Vagi most to SA and AV nodes; less to atrial muscles; least to ventricular Muscles Sympathetic: distributed to all parts of heart

PARASYMPATHETIC STIMULATION CAN SLOW OR BLOCK CARDIAC RHYTHM AND CONDUCTION Stimulation of Vagi causes hormone Acetylcholine to be released. Ach has 2 major effects on heart: Decreases rate of rhythm of SA node Decreases excitability of AV fibers between atrial muscles and AV node

Weak-moderate stimulation of parasympathetic slows down rate of heart Strong stimulation can stop completely cardiac impulse from SA node or block completely transmission of excitation from atria to ventricles. Ventricles stop contracting for 5-20 seconds but then Purkinje fibers become an ectopic pacemaker and cause ventricles to contract 15-40 bpm VENTRICULAR ESCAPE MECHANISM OF VAGAL EFFECTS: Ach released increases permeability of fiber membranes to Potassium causes hyperpolarization. In SA node this decreases the resting MP to -70 mV vs usual -55mV. Initial rise of SA nodal MP requires much more time to reach threshold. Hyperpolarisation in AV node makes it difficult for small atrial fibers to excite..large depolarization blocks conduction completely.

EFFECT OF SYMPATHETIC STIMULATION on CARDIAC RHYTHM AND CONDUCTION Opposite effects as vagal stimulation: Increases rate of SA nodal discharge Increases rate of conduction and level of excitability in all parts of heart Increases force of contraction of cardiac musculature

Maximal stimulation can triple frequency of heartbeat and increase strength of contrction twofold. Mechanism of Sympathetic Effect Stimulation of symp nerves releases Noradrenaline Noradrenaline stimulates beta-1-adrenergic receptors stimulation increases fiber permeability to sodium and calcium ions. In SA node increased Na+ & Ca2+ permeability creates more +ve RMP and increased rate of up drift of MP to threshold, increasing self-excitation and hence heart rate. In AV node easier for AP to excite fiber bundle decreasing conduction time to ventricles. Increase in CA2+ permeability increased contractile strength.