Cardiovascular System Is One of the Systems of the Human Organism , That Is Responsible For: 1
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16 the Heart
Physiology Unit 3 CARDIOVASCULAR PHYSIOLOGY: THE HEART Cardiac Muscle • Conducting system – Pacemaker cells – 1% of cells make up the conducting system – Specialized group of cells which initiate the electrical current which is then conducted throughout the heart • Myocardial cells (cardiomyocytes) • Autonomic Innervation – Heart Rate • Sympathetic and Parasympathetic regulation • �1 receptors (ADRB1), M-ACh receptors – Contractility • Sympathetic stimulus • Effects on stroke volume (SV) Electrical Synapse • Impulses travel from cell to cell • Gap junctions – Adjacent cells electrically coupled through a channel • Examples – Smooth and cardiac muscles, brain, and glial cells. Conducting System of the Heart • SA node is the pacemaker of the heart – Establishes heart rate – ANS regulation • Conduction Sequence: – SA node depolarizes – Atria depolarize – AV node depolarizes • Then a 0.1 sec delay – Bundle of His depolarizes – R/L bundle branches depolarize – Purkinje fibers depolarize Sinus Rhythm: – Ventricles depolarize Heartbeat Dance Conduction Sequence Electrical Events of the Heart • Electrocardiogram (ECG) – Measures the currents generated in the ECF by the changes in many cardiac cells • P wave – Atrial depolarization • QRS complex – Ventricular depolarization – Atrial repolarization • T wave – Ventricular repolarization • U Wave – Not always present – Repolarization of the Purkinje fibers AP in Myocardial Cells • Plateau Phase – Membrane remains depolarized – L-type Ca2+ channels – “Long opening” calcium channels – Voltage gated -
Cardiovascular Physiology
CARDIOVASCULAR PHYSIOLOGY Ida Sletteng Karlsen • Trym Reiberg Second Edition 15 March 2020 Copyright StudyAid 2020 Authors Trym Reiberg Ida Sletteng Karlsen Illustrators Nora Charlotte Sønstebø Ida Marie Lisle Amalie Misund Ida Sletteng Karlsen Trym Reiberg Booklet Disclaimer All rights reserved. No part oF this book may be reproduced in any Form on by an electronic or mechanical means, without permission From StudyAid. Although the authors have made every efFort to ensure the inFormation in the booklet was correct at date of publishing, the authors do not assume and hereby disclaim any liability to any part For any inFormation that is omitted or possible errors. The material is taken From a variety of academic sources as well as physiology lecturers, but are Further incorporated and summarized in an original manner. It is important to note, the material has not been approved by professors of physiology. All illustrations in the booklet are original. This booklet is made especially For students at the Jagiellonian University in Krakow by tutors in the StudyAid group (students at JU). It is available as a PDF and is available for printing. If you have any questions concerning copyrights oF the booklet please contact [email protected]. About StudyAid StudyAid is a student organization at the Jagiellonian University in Krakow. Throughout the academic year we host seminars in the major theoretical subjects: anatomy, physiology, biochemistry, immunology, pathophysiology, supplementing the lectures provided by the university. We are a group of 25 tutors, who are students at JU, each with their own Field oF specialty. To make our seminars as useful and relevant as possible, we teach in an interactive manner often using drawings and diagrams to help students remember the concepts. -
Non-Coding Rnas in the Cardiac Action Potential and Their Impact on Arrhythmogenic Cardiac Diseases
Review Non-Coding RNAs in the Cardiac Action Potential and Their Impact on Arrhythmogenic Cardiac Diseases Estefania Lozano-Velasco 1,2 , Amelia Aranega 1,2 and Diego Franco 1,2,* 1 Cardiovascular Development Group, Department of Experimental Biology, University of Jaén, 23071 Jaén, Spain; [email protected] (E.L.-V.); [email protected] (A.A.) 2 Fundación Medina, 18016 Granada, Spain * Correspondence: [email protected] Abstract: Cardiac arrhythmias are prevalent among humans across all age ranges, affecting millions of people worldwide. While cardiac arrhythmias vary widely in their clinical presentation, they possess shared complex electrophysiologic properties at cellular level that have not been fully studied. Over the last decade, our current understanding of the functional roles of non-coding RNAs have progressively increased. microRNAs represent the most studied type of small ncRNAs and it has been demonstrated that miRNAs play essential roles in multiple biological contexts, including normal development and diseases. In this review, we provide a comprehensive analysis of the functional contribution of non-coding RNAs, primarily microRNAs, to the normal configuration of the cardiac action potential, as well as their association to distinct types of arrhythmogenic cardiac diseases. Keywords: cardiac arrhythmia; microRNAs; lncRNAs; cardiac action potential Citation: Lozano-Velasco, E.; Aranega, A.; Franco, D. Non-Coding RNAs in the Cardiac Action Potential 1. The Electrical Components of the Adult Heart and Their Impact on Arrhythmogenic The adult heart is a four-chambered organ that propels oxygenated blood to the entire Cardiac Diseases. Hearts 2021, 2, body. It is composed of atrial and ventricular chambers, each of them with distinct left and 307–330. -
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M. Baumgarten, Ph.D. OBJECTIVES: 1. Describe the basic characteristics of cardiac electrical activity and the spread of the action potential through the heart 2. Compare the characteristics of action potentials in different parts of the heart 3. Describe how serum K modulates resting potential 4. Describe the ionic basis for the cardiac action potential and changes in ion currents during each phase of the action potential 5. Identify differences in electrical activity across the tissues of the heart 6. Describe the basis for normal automaticity 7. Describe the basis for excitability 8. Describe the basis for conduction of the cardiac action potential 9. Describe how the responsiveness relationship and the Na+ channel cycle modulate cardiac electrical activity I. BASIC ELECTROPHYSIOLOGIC CHARACTERISTICS OF CARDIAC MUSCLE A. Electrical activity is myogenic, i.e., it originates in the heart. The heart is an electrical syncitium (i.e., behaves as if one cell). The action potential spreads from cell-to-cell initiating contraction. Cardiac electrical activity is modulated by the autonomic nervous system. B. Cardiac cells are electrically coupled by low resistance conducting pathways gap junctions located at the intercalated disc, at the ends of cells, and at nexus, points of side-to-side contact. The low resistance pathways (wide channels) are formed by connexins. Connexins permit the flow of current and the spread of the action potential from cell-to-cell. C. Action potentials are much longer in duration in cardiac muscle (up to 400 msec) than in nerve or skeletal muscle (~5 msec). -
Two Components of the Cardiac Action Potential I
Two Components of the Cardiac Action Potential I. Voltage-time course and the effect of acet.flcholine on atrial and nodal cells of the rabbit heart ANTONIO PAES de CARVALHO, BRIAN FRANCIS HOFFMAN, and MARILENE de PAULA CARVALHO From the Instituto de Biofisica da Universidade Federal do Rio de Janeiro, Rio de Janeiro (GB), Brazil, and the Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York 10032 ABSTRACT Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (I?, V or phase-plane display). Acetylcholine was applied to the record- ing site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the rela- tive magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (¢) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow com- ponent, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current hav- ing a positive equilibrium potential, coupled to a decrease in the resting potas- sium conductance. -
Cardiac Muscle: Structure and Properties
CARDIOVASCULAR SYSTEM: CARDIAC MUSCLE: STRUCTURE AND PROPERTIES For: Semester II CC2TH/ GEN 2TH Prepared and Compiled By: OLIVIA CHOWDHURY DEPARTMENT OF PHYSIOLOGY SURENDRANATH COLLEGE April 29, 2020 OLIVIA CHOWDHURY •Anatomy of The Heart April 29, 2020 OLIVIA CHOWDHURY •The Layers Of The Heart Three layers: • Epicardium . Pericardium – a double serous membrane . Visceral pericardium (Next to heart) . Parietal pericardium (Outside layer) . Serous fluid fills the space between the layers of pericardium . Connective tissue layer • Myocardium . Middle layer . Mostly cardiac muscle • Endocardium . Inner layer . Endothelium April 29, 2020 OLIVIA CHOWDHURY • The Heart Valves Allows blood to flow in only one direction Four valves: Atrioventricular valves– between atria and ventricles Bicuspid/ Mitral valve between LA and LV Tricuspid valve between RA and RV Semilunar valves between ventricles and arteries Pulmonary semilunar valve Aortic semilunar valve April 29, 2020 OLIVIA CHOWDHURY •Direction Of Blood Flow In The Heart April 29, 2020 OLIVIA CHOWDHURY Right side of the heart: • receives venous blood from systemic circulation via superior and inferior vena cava into right atrium • pumps blood to pulmonary circulation from right ventricle Left side of the Heart: • receives oxygenated blood from pulmonary veins • pumps blood into systemic circulation April 29, 2020 OLIVIA CHOWDHURY •The Cardiac Muscle Myocardium has three types of muscle fibers: Muscle fibers which form contractile unit of heart Muscle fibers which form the pacemaker Muscle fibers which form conductive system April 29, 2020 OLIVIA CHOWDHURY •The Cardiac Muscle Striated and resemble the skeletal muscle fibre Sarcomere is the functional unit Sarcomere of the cardiac muscle has all the contractile proteins, namely actin, myosin, troponin tropomyosin. -
Are Ryanodine Receptors Important for Diastolic Depolarization in Heart?
ARE RYANODINE RECEPTORS IMPORTANT FOR DIASTOLIC DEPOLARIZATION IN HEART? A Dissertation submitted in partial fulfillment of the requirement for the Degree of Doctor of Medicine in Physiology (Branch – V) Of The Tamilnadu Dr. M.G.R Medical University, Chennai -600 032 Department of Physiology Christian Medical College, Vellore Tamilnadu April 2017 Ref: …………. Date: …………. CERTIFICATE This is to certify that the thesis entitled “Are ryanodine receptors important for diastolic depolarization in heart?” is a bonafide, original work carried out by Dr.Teena Maria Jose , in partial fulfillment of the rules and regulations for the M.D – Branch V Physiology examination of the Tamilnadu Dr. M.G.R. Medical University, Chennai to be held in April- 2017. Dr. Sathya Subramani, Professor and Head Department of Physiology, Christian Medical College, Vellore – 632 002 Ref: …………. Date: …………. CERTIFICATE This is to certify that the thesis entitled “Are ryanodine receptors important for diastolic depolarization in heart?” is a bonafide, original work carried out by Dr.Teena Maria Jose , in partial fulfillment of the rules and regulations for the M.D – Branch V Physiology examination of the Tamilnadu Dr. M.G.R. Medical University, Chennai to be held in April- 2017. Dr. Anna B Pulimood, Principal, Christian Medical College, Vellore – 632 002 DECLARATION I hereby declare that the investigations that form the subject matter for the thesis entitled “Are ryanodine receptors important for diastolic depolarization in heart?” were carried out by me during my term as a post graduate student in the Department of Physiology, Christian Medical College, Vellore. This thesis has not been submitted in part or full to any other university. -
Cardiovascular Physiology
Dr Matthew Ho BSc(Med) MBBS(Hons) FANZCA Cardiovascular Physiology Electrical Properties of the Heart Physiol-02A2/95B4 Draw a labelled diagram of a cardiac action potential highlighting the sequence of changes in ionic conductance. Explain the terms 'threshold', 'excitability', and 'irritability' with the aid of a diagram. 1. Cardiac muscle contraction is electrically activated by an action potential, which is a wave of electrical discharge that travels along the cell membrane. Under normal circumstances, it is created by the SA node, and propagated to the cardiac myocytes through gap junctions (intercalated discs). 2. Cardiac action potential: a. Phase 4 – resting membrane potential: i. Usually -90mV ii. Dependent mostly on potassium permeability, and gradient formed from Na-K ATPase pump b. Phase 0 - -90mV-+20mV i. Generated by the opening of fast Na channels Na into cell potential inside rises > 65mV (threshold potential) positive feedback further Na channel opening action potential ii. Threshold potential also triggers opening Ca channels (L type) at -10mV iii. Reduced K permeability c. Phase 1 – starts + 20mV i. The positive AP causes rapid closure of fast Na channels transient drop in potential d. Phase 2 – plateau i. Maximum permeability of Ca through L type channels ii. Rising K permeability iii. Maintenance of depolarisation e. Phase 3 – repolarisation i. Na, Ca and K conductance returns to normal ii. Ca. Na channels close, K channels open 3. Threshold: the membrane potential at which an AP occurs a. Usually-65mV in the cardiac cell b. AP generated via positive feedback Na channel opening 4. Excitability: the ease with which a myocardial cell can respond to a stimulus by depolarising. -
The Fitzhugh-Nagumo System As a Model of Human Cardiac Action Potentials
THE FITZHUGH-NAGUMO SYSTEM AS A MODEL OF HUMAN CARDIAC ACTION POTENTIALS Amy D. Ngo ∗1 1Department of Mathematical Sciences, Rensselaer Polytechnic Institute, Troy, NY, USA Abstract In this paper, we aim to develop models of the action potentials of healthy human myocardial and pacemaker cells using the periodically forced Fitzhugh-Nagumo system. Pacemaker cells generate impulses which cause myocardial cells to contract, producing a heartbeat. Such impulses both cause and result from changes in membrane potential. Using eigenvalue stability analysis and the Hopf Bifurcation Theorem, we determined ranges of the two constants intrinsic to the system and the forcing amplitude for which the system has a unique, stable limit cycle. From simulations in MATLAB, we discovered that at forcing amplitudes near and greater than the maximum value which induces the limit cycle, the square wave and the cosine wave forced systems describe the behaviors of myocardial and pacemaker action potentials, respectively, with high fidelity. 1 Introduction The living heart is an example of a relaxation oscillator, a term used to describe self-sustained nonlinear oscillators that behave non-sinusoidally. The heart spontaneously generates the electrical impulses that make it pulsate, so the heartbeat is self-sustained. The rate at which the heart generates and responds to these impulses fluctuates naturally, so the heartbeat, albeit repetitive, does not have a constant period. When the body experiences a physiological stimulus, such as stress, the heart responds by beating faster or slower to supply the body with adequate blood. This change in pace can occur abruptly or smoothly, depending on how the stimulus is applied. -
Lab 2 Intrinsic Cardiac Conduction System Spring 2016 V10.Pdf
Lab 2 The Intrinsic Cardiac Conduction System 1/23/2016 MDufilho 1 Figure 18.13 Intrinsic cardiac conduction system and action potential succession during one heartbeat. Superior vena cava Right atrium 1 The sinoatrial (SA) node (pacemaker) generates impulses. Pacemaker potential Internodal pathway 2 The impulses Left atrium SA node pause (0.1 s) at the atrioventricular (AV) node. Atrial muscle 3 The Subendocardial atrioventricular conducting (AV) bundle network connects the atria (Purkinje fibers) AV node to the ventricles. 4 The bundle branches Pacemaker Ventricular conduct the impulses Inter- potential muscle through the ventricular interventricular septum. septum Plateau 5 The subendocardial conducting network depolarizes the contractile 0 100 200 300 400 cells of both ventricles. Milliseconds Anatomy of the intrinsic conduction system showing the sequence of Comparison of action potential shape at electrical excitation various locations 1/23/2016 MDufilho 2 Video • Conducting System Of The Heart 1/23/2016 MDufilho 3 Figure 18.12 Pacemaker and action potentials of pacemaker cells in the heart. 1 Pacemaker potential This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is Action Threshold never a flat line. +10 potential 0 2 Depolarization The action –10 potential begins when the 2 2 pacemaker potential reaches –20 threshold. Depolarization is due –30 3 3 to Ca2+ influx through Ca2+ –40 channels. –50 3 Repolarization is due to 1 1 2+ –60 Pacemaker Ca channels inactivating and potential K+ channels opening. This allows –70 + Membrane potential(mV) K efflux, which brings the membrane potential back to its most negative voltage. -
Cardiovascular Physiology
Introductory Human Physiology © Copyright Emma Jakoi CV 1. HEART ELECTRICAL ACTIVTY Emma Jakoi, Ph.D. LEARNING OBJECTIVES 1. Describe the conduction system of the heart 2. Explain spontaneous electrical activity (pacemaker) in cardiac muscle. 3. Explain action potentials of ventricular cardiac muscle. 4. Explain the cardiac conduction system, pacemakers, and regulation of heart rate by the autonomic nervous system. 5. Explain the ECG and its correspondence to the cardiac action potential (AP). EXCITATION IN CARDIAC MUSCLE The cardiovascular system transports blood containing oxygen, carbon dioxide, nutrients and wastes, between the environment and the cells of the body. It consists of a heart (pump) and blood vessels which deliver nutrients to the tissues (arteries) and ferry waste products away from the tissues (veins). The heart is a muscular organ (Fig 1) which can contract in a rhythmic manner without direct stimulus from the nervous system. Each heart beat begins with the flow of ions across the plasma membrane of the cardiac muscle cell. This current is generated in specialized cells called pacemaker cells. The impulse from the pacemaker cells flows in a unidirectional manner through out the heart via specialized conducting tissue (Fig 1) and into the heart muscle. The electrical impulse results in mechanical contraction of the cardiac muscle through a series of intracellular events involving calcium. Figure 1. Electrical conduction within the heart starts at the sinoatrial (SA) node and passes sequentially to the atriaventricular (AV) node, Bundle of His, left and right bundle branches, and the Purkinje fibers. So the electrical activity moves from the base (A-V junction) to the apex (tip of ventricle) distant from the atria and then sweeps up the sides of the ventricles towards the base. -
On the Evolution of the Cardiac Pacemaker
Journal of Cardiovascular Development and Disease Review On the Evolution of the Cardiac Pacemaker Silja Burkhard 1, Vincent van Eif 2, Laurence Garric 1, Vincent M. Christoffels 2 and Jeroen Bakkers 1,3,* 1 Hubrecht Institute-KNAW and University Medical Center Utrecht, 3584 CT Utrecht, The Netherlands; [email protected] (S.B.); [email protected] (L.G.) 2 Department of Medical Biology, Academic Medical Center Amsterdam, 1105 AZ Amsterdam, The Netherlands; [email protected] (V.v.E.); [email protected] (V.M.C.) 3 Department of Medical Physiology, Division of Heart and Lungs, University Medical Center Utrecht, 3584 CT Utrecht, The Netherlands * Correspondence: [email protected]; Tel.: +31-302121892 Academic Editors: Robert E. Poelmann and Monique R. M. Jongbloed Received: 24 March 2017; Accepted: 24 April 2017; Published: 27 April 2017 Abstract: The rhythmic contraction of the heart is initiated and controlled by an intrinsic pacemaker system. Cardiac contractions commence at very early embryonic stages and coordination remains crucial for survival. The underlying molecular mechanisms of pacemaker cell development and function are still not fully understood. Heart form and function show high evolutionary conservation. Even in simple contractile cardiac tubes in primitive invertebrates, cardiac function is controlled by intrinsic, autonomous pacemaker cells. Understanding the evolutionary origin and development of cardiac pacemaker cells will help us outline the important pathways and factors involved. Key patterning factors, such as the homeodomain transcription factors Nkx2.5 and Shox2, and the LIM-homeodomain transcription factor Islet-1, components of the T-box (Tbx), and bone morphogenic protein (Bmp) families are well conserved.