Excitation & Conduction تفريغ PDF

EXCITATION & CONDUCTION Doctor explanation Key information If you have any Writer\ Abdullah Afif Alshakhs Abbreviation questions or...

EXCITATION & CONDUCTION Doctor explanation Key information If you have any Writer\ Abdullah Afif Alshakhs Abbreviation questions or Explanation concerns regarding this document. Writer\ Walaa Alamer 219-220 notes Mnemonic Book Deleted References  ‫ﻣﯾﺣرﻻ ﻧﻣﺣرﻻ ﷲ ﻣﺳب‬ Excitation & Conduction Dr. Aliya Elamin B1.3, Theme: 16 Reference: Guyton 14th edition, Unit 111, Ch.:9, PP: 113-116, Ch.10, PP: 127-132 27.1. 2022  Learning Objectives At the end of the lecture students should be able to describe: 1.Which ion currents contribute to the different phases of the action potential of a pacemaker cell, for example a cell in the SA node? - Which ion currents contribute to the different phases of the action potential of a ventricular muscle cell? PP: (127-129) 2. Which accounts for the long duration for the cardiac action potential? What is the advantage of the long plateau of the cardiac action potential? Chap: 9, PP: ( 115) 3.What is the normal sequence of depolarization in the heart? What is the role played by specialized cells? What is the consequence of a conduction failure in one of these areas? PP: (129-132) 4.Why is the AV node the only electrical pathway between the atria and ventricles in the normal situation? What is the functional relevance of the slow conduction through the AV node? PP: (130-131) 5.Why does the SA node function as the cardiac pacemaker in the normal situation? P: ( 130) 6. What is the relationship between an action potential and mechanical a activity in a cardiac muscle fiber and skeletal muscle fiber? -Why do tetanic contractions not occur in a healthy heart in a normal biochemical environment ? Chapter 9, PP:(116-117) 7. What is the influence of the sympathetic & parasympathetic nervous system on cardiac function? - Which arm of the autonomic nervous system is dominant at rest & during exercise? Chap:9, pp (124-125), CHap10, PP (132)  Excitation & conduction system of the Heart The heart has a specialized excitatory and conductive system which is made up of specialized cardiac muscles. The function of this system is to: 1- Generates: Rhythmical electrical impulses → Initiate rhythmical contraction of heart muscle 2- Conducts: Impulses rapidly through the heart CONDUCTION of the impulse from one part to another to achieve excitation in all heart muscles (Atria and ventricles) So control: Rhythmic self-excitation & Repetitive contraction 100,000 times / day or 3 billion /life  Specialized Excitatory & Conductive System 1. Sinus node (sinoatrial [S-A] node): Why does the AV node delay Generates normal rhythmical impulses (pacemaker) the impulse before passing it to the ventricles ? It is located in the the superior posterolateral wall of right atrium below and This delay allows time for the slightly lateral to the opening of the superior vena cava (SVC). atria to empty their blood into the ventricles before ventricular contraction begins. 2. Internodal pathways : 80% of the blood in the Conduct impulses from (S-A) node → ( A-V) node ventricle is filled passively. which are considered as bands that transmit the 20% of the blood in the impulse from the SA node to the AV node ventricle is filled due to the atrial contraction. 3. [A-V] node: As a result, the atria contract about one sixth of a second In which impulses from atria are delayed before passing → before ventricular contraction ventricles It is located in the posterior wall of the right atrium immediately behind the tricuspid valve.  Specialized Excitatory & Conductive System 4. A-V bundle: Conducts impulses from atria → ventricles The two atria are separated from the two ventricles by fibrous tissue that insulates the impulse and prevents it from passing from the atria to the ventricle. That’s why we have the AV bundles that can conduct (Transport) the impulse. So, it is the only way for the impulse to be transported to the ventricles. 5. Left & right bundle branches of Purkinje fibers: Conduct impulses → all parts of the ventricles It is responsible for the rapid excitation of the two ventricles 1- sinus node: 2- internodal pathways: 3- A-V node: 4- A-V bundle: 5- left & right bundle branch: 6- Purkinje fibers: 1 4 2 5 3 Purkinje fibers 6  AV bundle: The only electrical pathway between atria & ventricles Except at A-V bundle, atrial muscle is separated from ventricular muscle by a continuous fibrous barrier This barrier normally (insulator) → prevent passage of cardiac impulse Rarely, abnormal muscle bridge penetrate the barrier→ cardiac impulse re- enter → arrhythmias Arrhythmia is a problem with the rate or rhythm of your heartbeat. It means that your heart beats too quickly, too slowly, or with an irregular pattern. When the heart beats faster than normal, it is called tachycardia. When the heart beats too slowly, it is called If we want to conduct an electrical energy between the 2 bradycardia. rooms separated by a wall , we have to make an opening in the wall. Similarly, to the rooms and wall , the atria are separated from the ventricles by continuous fibrous barrier. If we want to conduct an electrical energy between the atrium and ventricle , we must make an opening in the atrioventricular septa  Functional relevance of slow conduction throughAVN A-V Node & its adjacent conductive fibers: Delay impulse transmission → ventricles Because: ↓ No. of gap junctions between successive cells. The green structure in the image is the gap junction AV node has less number of gap junctions that’s why it’s delay Allows time for atria to empty their Blood to ventricles, before ventricular contraction begins ↑Conduction velocity of A-V Node led to decrease ventricular filling, SV & CO Stroke volume (SV), Cardiac output (CO) In case of an increase in the conduction velocity: 1-the ventricles wouldn’t be filled adequately 2-It would decrease the Stroke Volume which is the amount of blood ejecting (spew out) in one beat 3- Cardiac Output which is the amount of blood ejecting in one minute would be less. Before we continue you have to understand the following terms Depolarization Repolarization Hyperpolarization The explanation in the next slide Ion currents that produce action potential (AP) of a ventricular muscle cell A 7m video will make everything clear https://youtu.be/v7Q9BrNfIpQ Resting membrane potential (RMP) = -85 to -90 mv Fast Na+ channels (phase 0) Rapid upstroke spike of the action potential (AP) Ca ++ channels: ( L-type or “slow” Ca ++ channels) = Slow Na + - Ca ++ channels, plateau (phase 2) K + channels (efflux) phase 1,3,4 Returns MP → resting level The action potential of a ventricular muscle cell occurs in 4 phases based on three main types of membrane ion channels : ( 1- fast sodium channels, 2- calcium channels (slow sodium- calcium channels), and 3- potassium channels.Each phase indicates important process : Phase 4 ( resting phase ) : - ventricular muscle cell is relaxed. - This state happens due to the K+ efflux through K+ channel - Resting membrane potential: RMP = -85 to -90 mv. Phase 0 ( Depolarization ) : - ventricular muscle cell is contracted. This state happens due to the Na+ influx through fast Na+ channels, by entering the Na+ ions to the intracellular space, the cellular negativity decreases and becomes more positive. Once the Action potential reaches 20mv , the fast Na+ channels get closed and the cell enter phase 1 Phase 1 ( early Repolarization ) : - ventricular muscle cell starts to relax. - This state happens due to the opening of K+ channels which effluxes the K+ ions. By passing the K + ions to the extracellular space, the cellular negativity increases a little bit because it is not opening very much. Phase 2 (plateau phase ) : - ventricular muscle cell pauses the relaxation. - This state happens due to\ 1- The prolonged opening of slow Na+ / Ca + + channels which which influxes the Ca + + ions. 2-The K+ channels are not opening very much ( that mean the cell will take much more time to become more negative ). Phase 3 (Repolarization phase ) : -Ventricular muscle cell continues relaxation. -This state happens due to: -closure of calcium ion channels. - the opening of K+ channels. These channels keep open until the membrane potential reaches -90 mv.  Causes of plateau 1. Slow, prolonged opening of the slow Na+ - Ca ++ channels, mainly Ca++ influx ↑ Ca ++ permeability & ↓ K+ permeability →Plateaus 2. Voltage-gated K+ channels: Slower, not opening very much until ending of the plateau This delays return of MP → normal -ve value [–80 to –90 mv] Long duration of cardiac AP? Plateau of ventricular AP ( ~ 0.3 sec )  Advantages of the long plateau Prolonged ventricular contraction ( 15 times > skeletal muscle) Ca ++ influx during it →contractile process Mainly, in the Slow-sodium-calcium-channels, the amount of calcium getting in is more than sodium. This calcium is very important because it makes the cardiac muscle contracts stronger. Delay in repolarization → Absolute refractory period (ARP), lasts for nearly the entire duration of contraction Inaction the refractory period for any muscle or any nerve, we cannot start another potential while there is another action potential working and that is because we don’t want to have two contractions at the same time which may cause a spasm (Lethal consequences). (The refractory period lasts longer because of the Plateau) CON… Refractory Period Prolonged RP protects the ventricular muscle from too rapid re-excitation Tetanus: prolonged contraction of a muscle caused by rapidly repeated stimuli. So heart muscle Can't tetanus during high-frequency stimulation (Tetanization →lethal) If the refractory period does not prevent the ventricular muscle from re-excitation , there will be 2nd contraction which leads to tetanus Allows them to relax long enough to be filled with blood (B)  Ion currents that produce AP of a pacemaker cell Resting membrane potential The normal cardiac pacemaker is the SA node RMP: Ventricular muscle fiber = -85 to -90 mv RMP: Sinus nodal fiber = -55 to -60 mv Less -ve ?: Cell membranes of sinus fibers naturally leaky to Na+ & Ca++ +ve charges of Na+ & Ca++ neutralize some of IC Intracellular negativity -vity At -55 mv, fast Na+ channels = blocked The slow Na+ - Ca++ channels = open (“activated”) → AP Resting Membrane Potential of Sinus nodal fiber = -55 to -60 mv Why the resting membrane potential of sinus nodal fibers are less than resting membrane potential of ventricular muscle cell ? The cell membrane of sinus fibers naturally permeable to Na+ & Ca + +. When theses ions enter the cell , their positive charges neutralize some of Intracellular negativity - sinus nodal fibers isn’t stimulated ( not active ). sinus nodal fiber becomes activated when the action potential reaches the threshold (-40 mv) due to the slow Na + influx at -55mv.  Rhythmical discharge of a sinus nodal fiber Between heartbeats: ↑ECF [Na+] + open Na+ channels → Na+ (+ve) leak → inside through inward “funny”currents Resting membrane potential Na+ influx → slow ↑ RMP in +ve direction This little elevated is because of the slow influx of sodium and we call this rise which lead to the threshold for discharge the “funny current” When P → –40 mv (Threshold) → L-type Ca ++ channels (activated ) → AP After reaching the threshold, in addition to the Na+ channels , the Na+ /Ca++ channel becomes activated which will cause influx of Ca++ until it reaches 0 mv.  Why sinus nodal fibers NOT remain depolarized all the time? 1.Na+ - Ca ++ channels → inactivated ( close) , 100 - 150 ms, after opening Milli second 2. K+ channels open (K+ efflux) Action potential Both effects ↓ MP back →its -ve value → terminate AP K+ channels remain open ( tenths of a sec) (Hyperpolarization) → RMP down (−55 to −60 mv) Repolarization starts due to the efflux of K+ The efflux of K+ continues even after reaching the threshold which cause hyperpolarization, in order to reach the resting membrane potential. Then after 100-150 milli second the slow sodium-calcium channel closes and the potassium channel opens for repolarization and to the point of Hyperpolarization (Under the resting membrane potential). -After a while, the potassium channels close and the sodium and calcium go inside and raise the resting membrane to the threshold level and slow-sodium- calcium-channels open for depolarization and then they close, and potassium channels open for hyperpolarization and so on……… (the cycle continues) CON… Then more K+ channels close The inward-leaking Na+ (“funny” current) & Ca++ once again overbalance K+ efflux → “resting” P drift upward once more → threshold = -40 mv The entire process begins again Continues indefinitely throughout a person’s life MCQ Which of the following is true concerning the electrical activity of cardiac muscle? A. RMP is due to K+ influx B. The duration of AP is shorter than that of skeletal muscle C. Hyperpolarization is due to K+ influx D. Depolarization is due to Na+ influx (the answer is D)  Cardiac pacemaker [S-A]node Normally the discharge rate times/min of: - [S-A]node = 70 to 80 ( S-A node, A-V node, purkinje fibers) all have the ability of spontaneous discharge - [A-V]node = 40 to 60 which mean that they can produce impulses - Purkinje fibers = 15 to 40 (electrical activity) by themselves. Impulse from [S-A] node → discharges [A-V]node & Purkinje fibers, before their self-excitation occur Why S-A node is considered as the normal cardiac pacemaker? Because it has the highest discharge rate + it activates the A-V node and purkinje fibers [S-A]node : Normal pacemaker of the heart, It drives (Heart rate) HR Latent pacemakers are suppressed Latent pacemakers are A-V node and purkinje fibers, normally they are suppressed and the S-A node is the active one.  AP: action potential. Duration of Contraction AP & contractile response of a cardiac muscle fiber Cardiac muscle begins to contract a few ms after AP begins & continues to contract a few ms after AP ends Significance of long plateau phase Since the AP for cardiac muscle is very long, the contractile response will be also long because it is related directly to AP. Duration of contraction: Mainly a function of duration of AP, including – plateau Why AP duration is long? Because of plateau phase. Plateau: 0.2 s in atria & 0.3 s in ventricles The figure shows that the mechanical response (contractions) begins after the AP and continues few seconds after it ends.  Relationship between AP & mechanical activity in skeletal & cardiac muscle fiber § RP is short in skeletal muscle, but very long in cardiac muscle RP: refractory period. § So skeletal muscle can undergo summation & tetanus, via repeated stimulation § Cardiac muscle can’t sum APs or contractions & can’t be tetanized  Electrical & mechanical responses of a skeletal muscle fiber If 2nd stimulation applied after the RP, but before complete muscle relaxation, 2nd contraction is stronger than 1st The 2nd contraction is added to the 1st so it brings up a stronger contraction. 23 MCQ Normally the least discharge rate (times/min) appear in a. A-V nodal fibers b. Purkinje fibers c. Sinus nodal fibers Answer: B  Normal Sequence of Heart Depolarization Role played by specialized cells Ends of [S-A]nodal fibers connect directly with surrounding atrial muscle fibers APs originating in [S-A]node → atrial muscle fibers → [A-V]node (0.3m/sec) AP travels with longer time through atrial muscle fibres (0.3m/sec) while the small bands transport it in (1m/sec). Also by several small bands of atrial fibers (1 m/sec) CON…. The AP is transported either by atrial muscle fibers (internodal) or by interatrial band. Anterior interatrial band (Bachman’s bundle) → anterior walls of atria →left atrium Anterior, middle & posterior internodal pathways →[A-V]node More rapid velocity of conduction (1 m/sec) due to “Purkinje fibers” CON… Impulses are delayed throughout the transmission from one part of the conduction system to the next till it reaches the ventricles, these are the times of this delay. Initial conduction delay = 0.03 sec from [S-A]node → [A-V]node A delay = 0.09 sec in [A-V]node The longest delay is here. A delay = 0.04 sec in penetrating A-V bundle A total delay = 0.16 sec, before impulse finally reac hes → contracting muscle of the ventricles Delay : shortened by stimulation of symp. nerves → heart & lengthened by stimulation of the vagi Notice that we can make this delay shorter or longer.  Impulse Transmission through ventricles Special Purkinje fibers lead from [A-V] node → A-V bundle → ventricles Fibers in ventricles are very large > ventricular muscle fibers Velocity = (1.5 - 4.0 m/sec), very high level of permeability of gap junctions These fibers have high level of transmission because of its characteristics. CON… Extra picture to see the location of the bundles and purkinje fibers. From bundle branches in ventricular septum → terminations of Purkinje fibers = 0.03 sec From Purkinje fibers, it is transmitted by the ventricular muscle fibers themselves Velocity of transmission = 0.3 to 0.5 m/sec, In ventricular muscle fibers. 1/6th that in the Purkinje fibers CON… Transmission from endocardial surface → epicardial surface = 0.03sec Transmission of impulses is always from inside to outside. Total time : Impulse from initial bundle branches → last of ventricular muscle fibers = 0.06 sec Rapid conduction of AP throughout ventricles → allows efficient contraction & ejection of B Excitation of the ventricles needs 0.06 sec. 0.03 is the time of transmission from bundle branches to the purkinje fibers and 0.03 is the time needed for transmission from endocardial surface to the epicardial surface. 0.03 + 0.03 = 0.06 sec. Velocity ( m/sec) Extra picture. Time (sec) 0.09 0.04 0,3 0.03 0.3- 0.5 0.03 1.5-4 0.03  Consequence of a conduction failure in one specialized cells 1. When AVN or Purkinje fibers → abnormal, develops a rhythmical discharge rate more rapid than SAN → Pacemaker of the heart 2. Rarely a place in atrial or ventricular muscle, develops excessive excitability → Pacemaker We considered SAN as pacemaker of the heart because it has the highest discharge rate, but if there is an abnormality that lead to having more rapid discharge rate in AVN or Purkinje fibers or having excessive excitability elsewhere >they will be the pacemaker A pacemaker elsewhere than [ S-A]node = "ectopic" pacemaker → abnormal sequence of contraction Normal pacemaker (SAN)= normal sequence of contractions. Abnormal pacemaker = abnormal sequence of contractions. CON…. v Another cause of shift of pacemaker is, Blockage of transmission of impulse from [S-A]node Here at first we have the normal pacemaker but after the blockage it is shifted. The new pacemaker → at [A-V]node or in penetrating portion of A-V bundle  CON….. v In A-V block → atria continue to beat at normal rate of rhythm of SAN Block in AV means the atria separate from ventricles electrically so ventricles generate new pacemaker. A new pacemaker develops in Purkinje system → drives the ventricular muscle at a new rate between 15 - 40 beats/ min CON… vBefore blockage: Purkinje fibers "overdriven" by the rapid sinus impulses (a suppressed state) Purkinje fibers are in suppressed state so they need 5 to 20s to get activated but ventricles may fail to pump blood which lead to faints or death if it’s long. 5 to 20 s, ventricles fail to pump B → Faints (first 4 to 5 s) This delayed pickup of heartbeat = Stokes-Adams syndrome long delay → death  Influence of parasymp. stimulation on cardiac function (Parasympathetic) The vagus innervate SAN and AVN + little Reminder: sympathetic > fight or flight, parasympathetic > rest & digest. muscle fibers. (Sympathetic) innervate SAN, AVN, two atria and ventricles strongly. v Vagus nerve → acetylcholine → M2 muscarinic receptors Functions: ↓ Rate of [S-A]node rhythm ↓ Transmission of impulse → Ventricles v Mechanism? ↑ K+ efflux→ Hyperpolarization Weak to moderate vagal stimulation →↓ HR Strong stimulation → Stop completely [S-A]node rhythmical excitation or transmission If it is stopped completely, Purkinje fibers will be the pacemaker in a process called ventricular escape. Ventricular escape? Purkinje fibers 15- 40 beats/ min  Influence of symp. NS on cardiac function During exercise or stress. v Norepinephrine → beta-1 adrenergic R Functions: ↑ Rate of sinus nodal discharge ↑ Rate of conduction & level of excitability in all heart portions ↑ Force of contraction of the heart v Mechanism? ↑Permeability of fiber membrane to Na + & Ca ++  Arms of the autonomic NS dominant at rest & during exercise Both work at rest but the parasympathetic works dominantly. Symp. →↑ Effectiveness of the heart as a pump (exercise) Parasymp. → ↓ heart pumping, allowing it → rest At rest: Moderate tonic sympathetic discharge & great tonic vagal discharge (vagal tone) Strong symp., ↑HR from 70 to 180 – 200 beats/min, rarely 250 beats/min &double the force of contraction Strong parasymp.( vagus), stop heartbeat - few sec, then → ventricular escapes - Purkinje fibers - → 15 - 40 beats/min Q1) which of the following heart Q2) The resting membrane Potential of tissues possess the longest conduction the ventricular muscle fibers is: delay of the cardiac impulse: A. from -85 to -95 A. Ventricular muscle fiber B. from -75 to -85 B. AV nodal fibers 219 QB 219 QB 1)-B 2)- A Answers: Q.3) For a patient with atrioventricular block, Q.4)Which of the following structures of the doctor stated that the patient had purkinje the heart possess the fastest fiber rhythm, what is the likely heart rate of this patient? propagation of the AP? A. SA node A. 120\min B. Purkinje fibers B. 30\min C. AV node C. 60\min D. 90\min 219 QB 219 QB Answers: 1)-B 2)- B 2/14/22 43