L17- AAST- Cardiac Excitability and conductivity.pdf

L17 Properties of Cardiac Muscle Myocardial Excitability and Conductivity ILOs By the end of this lecture, students will be able to 1. Define myocardial excitability and describe the absolute and relative refractory periods. 2. Explain the importance of the long refractory period of the heart. 3. De...

L17 Properties of Cardiac Muscle Myocardial Excitability and Conductivity ILOs By the end of this lecture, students will be able to 1. Define myocardial excitability and describe the absolute and relative refractory periods. 2. Explain the importance of the long refractory period of the heart. 3. Describe the all-or-None principle as applied to the heart. 4. Define myocardial conductivity and describe transmission of cardiac impulses through the heart. 5. Correlate the different conduction velocities in the heart to function. The cardiac muscle (myocardium) has four properties: I- Automaticity. II- Excitability. III- Conductivity. IV- Contractility. II- Myocardial Excitability It is defined as the ability of the cardiac muscle to respond to an adequate stimulus by generating an action potential followed by contraction. The general features of the excitability of the heart are like those described for the nerve and the voluntary muscle, but there are certain differences which are of fundamental significance in relation to the function of the heart. The excitability of the cardiac muscle is less than that of the skeletal muscle, but it is higher than that of the plain muscle. Excitability changes during cardiac activity Refractory Period of Cardiac Muscle It is the interval of time during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle. Different degrees of refractoriness are encountered during an action potential, reflecting the number of fast Na+ channels that have recovered from their inactive state and are capable of reopening. So, the cardiac muscle refractory period may also be defined as the time from phase 0 until the next possible depolarization of a myocyte, i.e. once enough fast Na+ channels have recovered. 1 Cardiomyocytes have a longer refractory period than the skeletal muscle cells given the long plateau in their action potential from the slow Ca2+ channels (phase 2). It includes the following two phases: 1- Absolute Refractory Period (ARP): It is the period during which the cardiac muscle does not respond to restimulation whatever the strength of the stimulus Action may be. Na+ channels are closed, therefore, stimulation of the potential muscle during this phase cannot produce further action potential. It corresponds to depolarization and approximately the first ⅔ of repolarization (phases 0, 1, 2 and beginning of phase 3). Mechanical response Mechanically, it occupies the whole period of systole and early diastole. Its duration is 0.25- 0.3 s in the ventricles and 0.15 s in the atria. 2- Relative Refractory Period (RRP): It is the period during which the cardiac muscle can respond to restimulation by a greater than normal stimulus, which will depolarize the cell and cause an action potential followed by a premature contraction (The cell exhibits reduced sensitivity to additional stimulation). It corresponds to approximately the last ⅓ of repolarization (the rest of phase 3). Mechanically, it occupies the middle of the diastole. Its duration is ≈ 0.05 s in the ventricles and 0.03 s in the atria. * Significance of long refractory period of the cardiomyocytes: The long cardiac refractory period, which lasts almost as long as the entire systole (≈ 300 msec), prevents sustained tetanic contractions. So, unlike the skeletal muscle, the heart can’t be tetanized. This is a physiological mechanism allowing sufficient time for the ventricles to empty and then refill prior to the next contraction which is essential for the pumping function of the heart. 2 Action potentials of a single nerve or skeletal muscle fiber All-or-None principle as applied to the heart: The all-or-none principle in general states that the excitable tissue either responds maximally, if the stimulus is threshold or above, or not all if the stimulus is subthreshold. This rule is applied to the single nerve fiber and the single skeletal muscle fiber. In the heart and due to the presence of intercalated discs with their gap junctions between adjacent cardiac myocytes, stimulation of any single atrial muscle fiber causes the action potential to travel over the entire atrial mass and similarly stimulation of any single ventricular fiber causes excitation of the ventricular muscle mass. Thus, each cardiac muscle sheet (atrial or ventricular) behaves as a functional syncytium and obeys the "all or none rule" like a single skeletal muscle fiber. Factors affecting myocardial excitability: 1. Innervation: a) Sympathetic stimulation leads to increased excitability (which may cause premature contractions or tachyarrhythmias). b) Parasympathetic (Vagal) stimulation decreases excitability (may inactivate atrial ectopic foci). 2. Extracellular fluid (ECF) ions concentration: - K+: Hyperkalemia is clinically a dangerous condition. It causes partial depolarization which increases excitability initially. However, if it is sustained it results in inactivation of Ca2+ and K+ channels causing loss of excitability leading to cardiac arrest and the heart stops in diastole. Hypokalemia decreases the excitability and is a serious condition, but it is not as rapidly fatal as hyperkalemia. - Ca2+: Hypercalcemia is seldom of clinical concern regarding cardiac function. It decreases excitability. 3 III- Myocardial Conductivity It is defined as the ability to transmit the cardiac impulse generated in the SAN to the rest of the heart. The atrial muscle fibers are separated from those of the ventricles by a fibrous tissue ring called Annulus fibrosis (a part of the fibrous skeleton of the heart), which effectively provides an area of insulation between the atria and the ventricles. Normally the only conducting tissue between the atria and ventricles is the AV bundle (bundle of His). Transmission of cardiac impulses through the heart: The cardiac impulse (action potential) normally originates at the SA node because it is the region of the heart with the fastest intrinsic spontaneous discharge rate. The cardiac impulse then spreads across the left and right atria due to their functional syncytial nature. It also proceeds along the internodal pathways in the atria and finally reaches the AV node (situated in the right atrium at the posterior part of the interatrial septum close to the opening of the coronary sinus). Due to the presence of annulus fibrosis, excitation must normally pass through the AV node and AV bundle (bundle of His) in order to reach the ventricles. 4 On the top of the ventricular septum the wave of depolarization spreads in the specialized rapidly conducting Purkinje fibers to all parts of the ventricles. These fibers are modified ventricular muscle cells. They have a relatively large diameter, and they are the largest of all the cells in the heart. This means they have a high conduction velocity. The depolarization passes from the AV bundle ‘bundle of His’ into the left and right bundle branches down each side of the septum before spreading out over the ventricles. As a result, depolarization of the ventricles occurs in a prescribed sequence starting with the papillary muscles and the septum and then spreading through the terminal Purkinje fibers to the endocardial (inner) part of the ventricular muscle and out towards the epicardial (outer) surface. This coordinated spread of electrical activity through the heart is responsible for the shape of the ECG. Purkinje fibers, together with the AV nodal tissue, have the longest refractory period of any cardiac cells. ▪ Conduction speeds in cardiac tissue: - The AV node has the slowest conduction velocity (0.05 m/s) and a very long ARP which leads to 0.1 s of “AV nodal delay”. This is caused by the small diameter of the nodal cells and slow conductive fibers. AV nodal delay is shortened by sympathetic stimulation and prolonged by vagal stimulation. Tissue Conduction Rate (m/s) SA node 0.05 Atrial pathways 1 AV node 0.05 Bundle of His 1 * Significance of slow conduction in AV node: Purkinje system 1) Allows the atria to complete emptying before the Ventricular muscle beginning of ventricular contraction. 2) Protects the ventricles from abnormal atrial rhythms. (acts as a gatekeeper). 4 1 Functions of AV node: a) Receives the impulse originating from S-A node and transmits it to the ventricles through the A-V bundle. b) AV nodal delay. c) Can initiate cardiac impulses but at a slower rate (40 - 60 /min= AV nodal rhythm) if SA node is damaged. 5 Functional characteristic of AV node: Its cells structurally resemble those of SA node and the shape of their action potentials is similar except: 1) Initial resting potential is ≈ - 80 mV and the depolarization ‘overshoot’ does not normally exceed + 5 to +10 mV. 2) The depolarization in phase 4 is slower because of the absence of a population of Na+ channels, hence the slower intrinsic rate of firing. - The Purkinje system has the fastest conduction velocity (4 m/s). * Significance: To ensure the simultaneous contraction of all parts of the ventricles, which is essential for the pumping function of the heart. One-way conduction through the A-V bundle: Purkinje fibers and AV node have the longest refractory period in the heart which allows only forward conduction from the atria to the ventricles. This prevents re-entry of cardiac impulses from the ventricles to the atria (except in abnormal states which results in serious cardiac arrhythmias). Cells of the conducting system are modified cardiac myocytes with few myofibrils, so they don’t contract significantly when depolarized. 6 Wolff– Parkinson–White (WPW) or pre-excitation syndrome: If there is an electrical ‘leak’ in the fibrous ring separating the atria and the ventricles, this leads to an alternative, direct route for excitation to spread from atria to ventricles, which causes a characteristic arrhythmia. Repolarization of the ventricle: It proceeds from epicardial to endocardial surface (the opposite direction to depolarization). So, QRS complex (depolarization) and T wave (repolarization) are both upwards deflections in a normal ECG (opposite polarity currents moving in opposite directions). __________________________________________ 1- Human Physiology - From Cells to Systems 7th ed – Chapter 9 2- Hall JE. Guyton and Hall Textbook of Medical Physiology, 14th. Ed. Elsevier Saunders; 2021, Chapter 9. 3- The cardiovascular system, 2ed edition, Noble A et al, Page 22-24 4- Portal resources: https://youtu.be/TnFoJ7Hhi-M https://www.youtube.com/watch?v=RYZ4daFwMa8 7