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TeachMe Physiology Part of the TeachMe Series * Subjects * Biochemistry * Growth & Death * Apoptosis * Cell Cycle * DNA Replication * Meiosis * Mitosis * Molecules and Signalling * Active Transport * Cellular Receptors * Diffusion * Endocytosis and Exocytosis * Enzyme Inhibition * Enzyme Kinetics * G-proteins * Osmosis * Protein Synthesis * Protein Structure * Transcription of DNA * Translation of DNA * ATP Production * Anaerobic Respiration * Electron Transport Chain * Gluconeogenesis * Glycolysis * TCA Cycle * Electrolytes * Calcium Regulation * External Balance of Potassium * Internal Balance of Potassium * Sodium Regulation * Histology * Cell Structures * Cell Membrane * Endoplasmic Reticulum * Golgi Apparatus * Lysosomes * Mitochondria * Nucleus * Tissue Structure * Blood Vessels * Bones * Cartilage * Cellular Adaptations * Epithelial Cells * Muscle Histology * Skin * Structure of Glands * Cardiovascular * Cardiac Output * Control of Stroke Volume * Control of Heart Rate * Cardiac 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Diffusion * Endocytosis and Exocytosis * Enzyme Inhibition * Enzyme Kinetics * G-proteins * Osmosis * Protein Synthesis * Protein Structure * Transcription of DNA * Translation of DNA * ATP Production * Anaerobic Respiration * Electron Transport Chain * Gluconeogenesis * Glycolysis * TCA Cycle * Electrolytes * Calcium Regulation * External Balance of Potassium * Internal Balance of Potassium * Sodium Regulation * Histology * Cell Structures * Cell Membrane * Endoplasmic Reticulum * Golgi Apparatus * Lysosomes * Mitochondria * Nucleus * Tissue Structure * Blood Vessels * Bones * Cartilage * Cellular Adaptations * Epithelial Cells * Muscle Histology * Skin * Structure of Glands * Cardiovascular * Cardiac Output * Control of Stroke Volume * Control of Heart Rate * Cardiac Cycle * Action Potential in Ventricular Cells * Cardiac Cycle * Cardiac Pacemaker Cells * Conduction System * Contraction of Cardiac Muscle * Circulation * Control of Blood Pressure * Capillary Exchange * Flow Within The Cardiovascular System * Regulation of Peripheral Blood Flow * Venous Return * Special Circulations * Cardiac Muscle * Cerebral * Cutaneous * Hepatic Circulation * Pulmonary * Skeletal Muscle * Respiratory * Pulmonary Ventilation * Airway Resistance * Lung Volumes * Mechanics of Breathing * Gas Exchange * Gas Exchange * Oxygen Transport in The Blood * Transport of Carbon Dioxide in the Blood * Ventilation-Perfusion Matching * Regulation of Respiration * Chemoreceptors * Cough Reflex * Neural Control of Ventilation * Respiratory Regulation of Acid-Base Balance * Responses of The Respiratory System to Stress * Gastrointestinal * Mouth * Regulation of Saliva * Secretion of Saliva * Swallowing * Stomach * Gastric Acid Production * Appetite * Gastric Mucus Production * Small Intestine * Digestion and Absorption * Histology and Cellular Function of the Small Intestine * Large Intestine * Absorption in the Large Intestine * Defecation * Large Intestinal Motility * Liver * Bilirubin Metabolism * Metabolic Functions of the Liver * Storage Functions of the Liver * Vitamins * Vitamin K * Other * Bile Production * Function of The Spleen * Exocrine Pancreas * Somatostatin * Urinary * Nephron * Glomerulus * Proximal Convoluted Tubule * Loop of Henle * Distal Convoluted Tubule and Collecting Duct * Micturition * Storage Phase of Micturition * Voiding Phase of Micturition * Regulation * Antidiuretic Hormone * Renin-Angiotensin-Aldosterone System * Urinary Regulation of Acid-Base Balance * Water Filtration and Reabsorption * Reproductive * Embryology * Development of the Reproductive System * Gametogenesis * Hormones and Regulation * Gonadotropins and the Hypothalamic Pituitary Axis * Puberty * Menstrual Cycle * Menopause * Fetal Physiology * Placental Development * Fetal Circulation * Pregnancy * Coitus * Conception * Labour * Lactation * Maternal Adaptations in Pregnancy * Neurology * Components * Cells of the Nervous System * Central Nervous System * Cerebrospinal Fluid * Neurotransmitters * Peripheral Nervous System * Synapses * Action Potential * Excitatory and Inhibitory Synaptic Signalling * Myelin * Resting Membrane Potential * Synaptic Plasticity * Synaptic Transmission * Sensory System * Ascending Tracts * Auditory Pathway * Consciousness and Sleep * Modalities of Sensation * Pain Pathways * Sensory Acuity * Visual Pathway * Motor System * Descending Tracts * Lower Motor Neurones * Muscle Stretch Reflex * Upper Motor Neurones * Ocular Physiology * Aqueous Humour * Ocular Accommodation * The Retina * Endocrine * Thyroid and Parathyroid Glands * Thyroid Gland * Parathyroid Glands * Adrenal Glands * Adrenal Medulla * Zona Glomerulosa * Zona Fasciculata * Zona Reticularis * The Pancreas * Endocrine Pancreas * Insulin * Glucagon * Hypothalamus and Pituitary * The Hypothalamus * Anterior Pituitary * Posterior Pituitary * Immunology/Haematology * Cells of the Immune System * B Cells * Phagocytes * T Cells * White Blood Cells – Summary * Innate Immune System * Barriers to Infection * Cytokines * Infection Recognition Molecules * Phagocytosis * The Complement System * Adaptive Immune System * Antibodies * Antigen Processing and Presentation * Primary and Secondary Immune Responses * T Cell Memory * Immune Responses * Acute Inflammation * Autoimmunity * Chronic Inflammation * Hypersensitivity Reactions * Immunodeficiency * Types of Immunity * Infections * Antibiotics * Pathogens * Viral Infection * Haematology * Blood Groups * Coagulation * Erythropoiesis * Iron Metabolism * Mononuclear Phagocyte System * Platelets THE ACTION POTENTIAL IN CARDIAC PACEMAKER CELLS 1. Home 2. Cardiovascular 3. Cardiac Cycle 4. The Action Potential in Cardiac Pacemaker Cells star star star star star based on 29 ratings Original Author(s): Chloe Hill Last updated: 6th February 2021 Revisions: 24 Original Author(s): Chloe Hill Last updated: 6th February 2021 Revisions: 24 format_list_bulletedContents add remove * 1 Pacemaker Cells * 2 Action potential in SA node * 2.1 Phase 4 – Pacemaker potential * 2.2 Phase 0 – Depolarisation * 2.3 Phase 3 – Repolarisation * 3 Control by the Autonomic Nervous System * 4 Clinical Relevance – Arrhythmias In the heart, electrical impulses are generated by specialised pacemaker cells and spread across the myocardium in order to produce a coordinated contraction in systole. The action potential generated is generated by a change in the potential difference between the inside and the outside of the cell. The particular action potential generated by cardiac pacemaker cells is very different from that of ventricular myocardial cells. In this article, we will discuss cardiac pacemaker cells and the action potential they generate in more detail. PACEMAKER CELLS Cardiac pacemaker cells are mostly found in the sinoatrial (SA) node, which is situated in the upper part of the wall of the right atrium. These cells have natural automaticity, meaning they can generate their own action potentials. By Madhero88 (original files); Angelito7 (this SVG version); [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons Fig 1.0 – The conduction system of the heart. The atrioventricular (AV) node and the Purkinje fibres also have cells capable of pacemaker activity, however, their natural rate is much slower than the SA node, so they are normally overridden. ACTION POTENTIAL IN SA NODE The action potential in the SA node occurs in three phases which are discussed below. PHASE 4 – PACEMAKER POTENTIAL The pacemaker potential occurs at the end of one action potential and just before the start of the next. It is the slow depolarisation of the pacemaker cells e.g. cells of the sinoatrial node, towards the membrane potential threshold. This is sometimes referred to as the ‘funny’ current, or If. The pacemaker potential is achieved by activation of hyperpolarisation activated cyclic nucleotide gated channels (HCN channels). These allow Na+ entry into the cells, enabling slow depolarisation. These channels are activated when the membrane potential is lower than -50mV. Once the membrane potential gets depolarised to reach the threshold, an action potential can be fired. PHASE 0 – DEPOLARISATION Once the HCN channels have brought the membrane potential to around -40mV, voltage-gated calcium channels open. This allows an influx of Ca2+ which produces a faster rate of depolarisation to reach a positive membrane potential (responsible for the upstroke of the action potential). HCN channels then start to inactivate. At the peak of the action potential, Ca2+ channels inactivate, and K+ channels open. PHASE 3 – REPOLARISATION Once the Ca2+ channels inactivate, and the K+ channels open, there is an efflux of K+ ions out of the cells. This results in the repolarisation of the membrane, which is seen as the downstroke of the action potential. Unlike the ventricular action potential, the opening of Ca2+ channels is not sustained, and there is no ‘plateau’ stage. Therefore, the action potential is triangular in shape. After the action potential, repolarisation must occur and the membrane potential must reach negative values. This allows the HCN channels to be reactivated again, enabling another action potential to be generated (phase 4). By Pacemaker_potential.svg: Diberri derivative work: Silvia3 (Pacemaker_potential.svg) [CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons Fig 2 – Diagram showing the action potential in cardiac pacemaker cells and the main ion movements at each stage. CONTROL BY THE AUTONOMIC NERVOUS SYSTEM The autonomic nervous system (ANS) alters the slope of the pacemaker potential, in order to alter heart rate. Heart rate is affected by both the parasympathetic and sympathetic branches of the ANS, which innervate both the SA and AV nodes. * Parasympathetic activity is mediated via acetylcholine acting on M2 muscarinic receptors at the SA node. This lengthens the interval between pacemaker potentials, hence slowing heart rate. * Sympathetic activity is mediated via noradrenaline acting on B1 adrenoceptors. This shortens the interval between impulses by making the pacemaker potential steeper, hence increasing the heart rate. If all autonomic inputs are blocked, the intrinsic heart rate is about 100 beats per minute (bpm). The normal resting rate of about 60bpm is produced because the parasympathetic system dominates at rest. Initial increases in heart rate are brought about by a reduction in the parasympathetic outflow. Increasing sympathetic outflow allows for further increases in heart rate. CLINICAL RELEVANCE - ARRHYTHMIAS Disturbance to the natural pacemaker activity of the heart can lead to arrhythmias i.e. a heartbeat with an irregular rate and/or rhythm. Causes of arrhythmias include: * Ectopic Pacemaker Activity: This is when another area of the myocardium becomes spontaneously active and its depolarisations dominate over the SA node. A latent pacemaker region can become activated due to ischaemic damage. * After-Depolarisations: This is when abnormal depolarisations follow the action potential – thought to be caused by high intracellular Ca2+. * Re-entry loop: This occurs when the normal spread of excitation across the heart is disrupted due to a damaged area. When the conduction damage is incomplete, it allows the impulse to spread the wrong way through the damaged area and create a circle of excitation. Multiple small re-entry loops can occur in the atria, leading to atrial fibrillation. printPrint this Article star_borderRate this Article Quiz The Action Potential in Cardiac Pacemaker Cells Results Question 1 of 5 Where are the pacemaker cells that normally control the heart rate located? Right atrium Left atrium Right ventricle Septum Skip Submit check_circle Correct cancel Incorrect Next Report question Well done! You scored: 33% Skipped: 2/5 Try again to score 100%. Use the information in this article to help you with the answers. Retake Quiz close Report question thumb_upSubmit bookmarksRecommended reading 1. GDMT in HFrEF: Recap of HFSA Data and Recommendations ReachMD 2. Free CME: Strategies to Maximize GDMT & Optimize RAASi Dosing ReachMD 1. Strategies & Clinical Techniques to Maximize GDMT and Optimize RAASi Dosing for HFrEF ReachMD 2. Global Heart Failure Academy: Key Perspectives on the Evolving Role of Precision Medicine in HFrEF ReachMD Powered by * Privacy policy * Do not sell my personal information * Google Analytics settings I consent to the use of Google Analytics and related cookies across the TrendMD network (widget, website, blog). Learn more Yes No In the heart, electrical impulses are generated by specialised pacemaker cells and spread across the myocardium in order to produce a coordinated contraction in systole. The action potential generated is generated by a change in the potential difference between the inside and the outside of the cell. The particular action potential generated by cardiac pacemaker cells is very different from that of ventricular myocardial cells. In this article, we will discuss cardiac pacemaker cells and the action potential they generate in more detail. PACEMAKER CELLS Cardiac pacemaker cells are mostly found in the sinoatrial (SA) node, which is situated in the upper part of the wall of the right atrium. These cells have natural automaticity, meaning they can generate their own action potentials. [caption id="attachment_14135" align="aligncenter" width="800"] Fig 1.0 - The conduction system of the heart.[/caption] The atrioventricular (AV) node and the Purkinje fibres also have cells capable of pacemaker activity, however, their natural rate is much slower than the SA node, so they are normally overridden. ACTION POTENTIAL IN SA NODE The action potential in the SA node occurs in three phases which are discussed below. PHASE 4 - PACEMAKER POTENTIAL The pacemaker potential occurs at the end of one action potential and just before the start of the next. It is the slow depolarisation of the pacemaker cells e.g. cells of the sinoatrial node, towards the membrane potential threshold. This is sometimes referred to as the 'funny’ current, or If. The pacemaker potential is achieved by activation of hyperpolarisation activated cyclic nucleotide gated channels (HCN channels). These allow Na+ entry into the cells, enabling slow depolarisation. These channels are activated when the membrane potential is lower than -50mV. Once the membrane potential gets depolarised to reach the threshold, an action potential can be fired. PHASE 0 - DEPOLARISATION Once the HCN channels have brought the membrane potential to around -40mV, voltage-gated calcium channels open. This allows an influx of Ca2+ which produces a faster rate of depolarisation to reach a positive membrane potential (responsible for the upstroke of the action potential). HCN channels then start to inactivate. At the peak of the action potential, Ca2+ channels inactivate, and K+ channels open. PHASE 3 - REPOLARISATION Once the Ca2+ channels inactivate, and the K+ channels open, there is an efflux of K+ ions out of the cells. This results in the repolarisation of the membrane, which is seen as the downstroke of the action potential. Unlike the ventricular action potential, the opening of Ca2+ channels is not sustained, and there is no ‘plateau’ stage. Therefore, the action potential is triangular in shape. After the action potential, repolarisation must occur and the membrane potential must reach negative values. This allows the HCN channels to be reactivated again, enabling another action potential to be generated (phase 4). [caption id="attachment_14134" align="aligncenter" width="960"] Fig 2 - Diagram showing the action potential in cardiac pacemaker cells and the main ion movements at each stage.[/caption] CONTROL BY THE AUTONOMIC NERVOUS SYSTEM The autonomic nervous system (ANS) alters the slope of the pacemaker potential, in order to alter heart rate. Heart rate is affected by both the parasympathetic and sympathetic branches of the ANS, which innervate both the SA and AV nodes. * Parasympathetic activity is mediated via acetylcholine acting on M2 muscarinic receptors at the SA node. This lengthens the interval between pacemaker potentials, hence slowing heart rate. * Sympathetic activity is mediated via noradrenaline acting on B1 adrenoceptors. This shortens the interval between impulses by making the pacemaker potential steeper, hence increasing the heart rate. If all autonomic inputs are blocked, the intrinsic heart rate is about 100 beats per minute (bpm). The normal resting rate of about 60bpm is produced because the parasympathetic system dominates at rest. Initial increases in heart rate are brought about by a reduction in the parasympathetic outflow. Increasing sympathetic outflow allows for further increases in heart rate. [start-clinical] CLINICAL RELEVANCE - ARRHYTHMIAS Disturbance to the natural pacemaker activity of the heart can lead to arrhythmias i.e. a heartbeat with an irregular rate and/or rhythm. Causes of arrhythmias include: * Ectopic Pacemaker Activity: This is when another area of the myocardium becomes spontaneously active and its depolarisations dominate over the SA node. A latent pacemaker region can become activated due to ischaemic damage. * After-Depolarisations: This is when abnormal depolarisations follow the action potential – thought to be caused by high intracellular Ca2+. * Re-entry loop: This occurs when the normal spread of excitation across the heart is disrupted due to a damaged area. When the conduction damage is incomplete, it allows the impulse to spread the wrong way through the damaged area and create a circle of excitation. Multiple small re-entry loops can occur in the atria, leading to atrial fibrillation. [end-clinical] close Rate this article Not selected 1 2 3 4 5 star_border star star_border star star_border star star_border star star_border star thumb_upSubmit close Edit this article Found an error? Is our article missing some key information? Make the changes yourself here! Once you've finished editing, click 'Submit for Review', and your changes will be reviewed by our team before publishing on the site. replyGo back editEdit this article TeachMePhysiology Part of the TeachMe Series The medical information on this site is provided as an information resource only, and is not to be used or relied on for any diagnostic or treatment purposes. 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