The cardiac conduction system generates and conducts electrical impulses throughout the heart to coordinate rhythmic contractions. It includes the sinoatrial node, which acts as the pacemaker, along with pathways that conduct impulses from the atria to the ventricles. The atrioventricular node introduces a delay between atrial and ventricular contractions. The bundle of His and Purkinje fibers then rapidly conduct impulses through the ventricles to allow for synchronized contraction. The system receives inputs from the autonomic nervous system that can alter heart rate.
The conduction system of the heart generates and conducts electrical impulses to coordinate the rhythmic contraction of the heart muscles. It consists of the sinoatrial node, internodal pathways, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node acts as the natural pacemaker by initiating electrical impulses. These impulses then travel through the internodal pathways to the atrioventricular node, where they are delayed to allow the atria to contract before the ventricles. The impulse then travels down the bundle of His which splits into right and left bundle branches to coordinate simultaneous contraction of the ventricles.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
Anatomy & physiology for the EP professional part II 8.4.14lpesbens
This document provides an overview of cardiac anatomy and physiology. It identifies the venous system of the heart including the coronary sinus. It describes the specialized conduction system including the sinoatrial node, atrioventricular node, His bundle, and Purkinje fibers. It lists the properties of cardiac cells and identifies the internal structures of the atria and ventricles. It also describes cardiac innervation and how the autonomic nervous system influences heart rate, conductivity and contractility. Key concepts covered include cardiac output, stroke volume, preload, afterload, and the Frank-Starling law of the heart.
Konduksi Listrik Jantung dan Gangguannya
1) The document discusses the electrical conduction system of the heart, including the sinoatrial node, atrioventricular node, Bundle of His, and Purkinje fibers.
2) It explains how electrical impulses are normally generated by the sinoatrial node and conducted through the conduction system to coordinate heart contractions.
3) Abnormalities in the heart's electrical rhythm or conduction can cause arrhythmias or dysrhythmias such as bradycardia or tachycardia. The document discusses potential causes and manifestations of arrhythmias.
1. The document summarizes the anatomy of the right and left atria with a focus on electrophysiology. It describes important anatomical landmarks like the terminal crest, triangle of Koch, and pulmonary veins.
2. The pulmonary veins have muscular sleeves that connect at the venoatrial junction, which is an important area for arrhythmias. Ablation targets in the atria include the pulmonary vein antra, complex fractionated electrograms, and linear lesions at the roof and mitral isthmus.
3. Perforation risks during ablation include the thin areas of the atrial walls near valves and arteries. Nearby structures like the esophagus and vagus nerves must also be considered.
1) The document discusses various circuits involved in AV nodal reentrant tachycardia (AVNRT) and accessory pathway mediated tachycardias.
2) It describes the anatomy of the AV node and its divisions. It also discusses various types of AVNRT including slow-fast and fast-slow forms.
3) Accessory pathways are described which can lead to orthodromic and antidromic forms of AV reentrant tachycardia. Other preexcitation syndromes like Lown-Ganong-Levine are also summarized.
Autonomic Nervous System effects on the heart and.pptxAtulKaushik40
This document summarizes the effects of the autonomic nervous system on the heart's conduction system. It discusses how the sympathetic and parasympathetic nervous systems innervate and modulate the sinus node, AV node, His-Purkinje system, atria and ventricles through the release of neurotransmitters like acetylcholine and norepinephrine. Activation of the sympathetic nervous system increases heart rate and conduction velocity through beta receptor stimulation, while activation of the parasympathetic nervous system decreases heart rate and conduction velocity through muscarinic receptor stimulation. The complex interplay between the two divisions of the autonomic nervous system helps regulate heart rate and rhythm.
The conduction system of the heart generates and conducts electrical impulses to coordinate the rhythmic contraction of the heart muscles. It consists of the sinoatrial node, internodal pathways, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node acts as the natural pacemaker by initiating electrical impulses. These impulses then travel through the internodal pathways to the atrioventricular node, where they are delayed to allow the atria to contract before the ventricles. The impulse then travels down the bundle of His which splits into right and left bundle branches to coordinate simultaneous contraction of the ventricles.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
Anatomy & physiology for the EP professional part II 8.4.14lpesbens
This document provides an overview of cardiac anatomy and physiology. It identifies the venous system of the heart including the coronary sinus. It describes the specialized conduction system including the sinoatrial node, atrioventricular node, His bundle, and Purkinje fibers. It lists the properties of cardiac cells and identifies the internal structures of the atria and ventricles. It also describes cardiac innervation and how the autonomic nervous system influences heart rate, conductivity and contractility. Key concepts covered include cardiac output, stroke volume, preload, afterload, and the Frank-Starling law of the heart.
Konduksi Listrik Jantung dan Gangguannya
1) The document discusses the electrical conduction system of the heart, including the sinoatrial node, atrioventricular node, Bundle of His, and Purkinje fibers.
2) It explains how electrical impulses are normally generated by the sinoatrial node and conducted through the conduction system to coordinate heart contractions.
3) Abnormalities in the heart's electrical rhythm or conduction can cause arrhythmias or dysrhythmias such as bradycardia or tachycardia. The document discusses potential causes and manifestations of arrhythmias.
1. The document summarizes the anatomy of the right and left atria with a focus on electrophysiology. It describes important anatomical landmarks like the terminal crest, triangle of Koch, and pulmonary veins.
2. The pulmonary veins have muscular sleeves that connect at the venoatrial junction, which is an important area for arrhythmias. Ablation targets in the atria include the pulmonary vein antra, complex fractionated electrograms, and linear lesions at the roof and mitral isthmus.
3. Perforation risks during ablation include the thin areas of the atrial walls near valves and arteries. Nearby structures like the esophagus and vagus nerves must also be considered.
1) The document discusses various circuits involved in AV nodal reentrant tachycardia (AVNRT) and accessory pathway mediated tachycardias.
2) It describes the anatomy of the AV node and its divisions. It also discusses various types of AVNRT including slow-fast and fast-slow forms.
3) Accessory pathways are described which can lead to orthodromic and antidromic forms of AV reentrant tachycardia. Other preexcitation syndromes like Lown-Ganong-Levine are also summarized.
Autonomic Nervous System effects on the heart and.pptxAtulKaushik40
This document summarizes the effects of the autonomic nervous system on the heart's conduction system. It discusses how the sympathetic and parasympathetic nervous systems innervate and modulate the sinus node, AV node, His-Purkinje system, atria and ventricles through the release of neurotransmitters like acetylcholine and norepinephrine. Activation of the sympathetic nervous system increases heart rate and conduction velocity through beta receptor stimulation, while activation of the parasympathetic nervous system decreases heart rate and conduction velocity through muscarinic receptor stimulation. The complex interplay between the two divisions of the autonomic nervous system helps regulate heart rate and rhythm.
CONDUCTIVE SYSTEM OF HEART .pptx BY MRS. WINCY THIRUMURUGAN .PROFESSOR.NURSIN...WINCY THIRUMURUGAN
MEANING.
The conducting system of the heart consists of cardiac muscle cells and conducting fibers (not nervous tissue) that are specialized for initiating impulses and conducting them rapidly through the heart.
It provides the heart its automatic rhythmic beat.
The purpose is to
Generating rhythmical electrical impulses to cause rhythmical contraction of the heart muscle. Conducting these impulses rapidly throughout the heart.
This pathway is made up of 5 elements:
The sino-atrial (SA) node.
The atrio-ventricular (AV) node.
The bundle of His.
The left and right bundle branches.
The Purkinje fibers.
SINOATRIAL NODE
The sinoatrial (SA) node is a collection of specialized cells (pacemaker cells), and is located in the upper wall of the right atrium, at the junction where the superior vena cava enters.
These pacemaker cells can spontaneously generate electrical impulses. The wave of excitation created by the SA node spreads via gap junctions across both atria, resulting in atrial contraction (atrial systole) – with blood moving from the atria into the ventricles.
The SA node is supraventricular and is sensitive to parasympathetic and sympathetic influence.
The SA node generates impulses and influenced by the Autonomic Nervous System:
Sympathetic nervous system – increases firing rate of the SA node, and thus increases heart rate.
Parasympathetic nervous system – decreases firing rate of the SA node, and thus decreases heart rate
THE INTER NODAL PATHWAYS consist of three bands (anterior, middle, and posterior) that lead directly from the SA node to the next node in the conduction system, the atrioventricular node. The impulse takes approximately 50 m s (milliseconds) to travel between these two nodes.
Bachmann's bundle (BB), also known as the interatrial bundle, myocardial strands connecting the right and left atrial walls and is considered to be the main pathway of interatrial conduction.
THE AV NODEThe AV node is located in the posterior wall of the right atrium immediately behind the tricuspid valve.
Cause of Slow Conduction in the A-V Node
What is the significance of AV nodal delay?
The cardiac impulse does not travel from the atria to the ventricles too rapidly.
It is primarily the AV node and it’s adjacent fibers that delay this transmission into the ventricles
AV BUNDLE OR BUNDLE OF HIS
From the AV node arises a special conducting pathway .
RIGHT AND LEFT BUNDLE BRANCHES
FASCICLE
The right bundle branch contains one fascicle.
The left bundle branch into three fascicles:
The left anterior,
The left posterior, and
The left septal fascicle.
PURKINJE FIBRES
The LT and RT bundle branches divides in turn course sidewise around each ventricular chamber and back toward the base of heart.
The ends of Purkinje fibers penetrate about one third of the way into muscle mass and finally become continuous with cardiac muscle fibers
,abundant with glycogen and extensive gap junctions, rapidly transmit cardiac action potentials in 0.03sec
The cardiac conduction system is a network of specialized cardiac muscle cells that initiate and transmit the electrical impulses responsible for the coordinated contractions of each cardiac cycle. These special cells are able to generate an action potential on their own (self-excitation) and pass it on to other nearby cells (conduction), including cardiomyocytes.
The document discusses the anatomy of the atrioventricular junctions. It describes that the junction comprises the right and left parietal junctions and a small septal component. It also discusses the triangle of Koch located in the right atrium, which contains specialized conduction tissues and borders. The document further summarizes the structure of the atrioventricular node, its components including the compact node and extensions, and the pathways for conduction through the node including the fast and slow pathways. It relates the anatomical structures to the functional pathways and discusses developments that increase the likelihood of arrhythmias during aging.
The cardiac conduction system generates and coordinates the contraction of the heart muscle. It is made up of specialized cardiac muscle cells located in the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node initiates each heartbeat by spontaneously generating an electrical impulse. This impulse then travels through the internodal pathways and atria to the atrioventricular node, which slows conduction before passing the impulse to the ventricles via the bundle of His and Purkinje fibers, causing synchronized ventricular contraction and pumping of blood. Defects or damage to the conduction system can lead to cardiac arrhythmias.
- Koch's triangle delineates the location of the atrioventricular node. It is bounded posteriorly by the tendon of Todaro, anteriorly by the tricuspid valve septal leaflet, and inferiorly by the coronary sinus ostium.
- The atrioventricular node and His bundle are located near the apex of the triangle where the His bundle penetrates the central fibrous body. Catheter ablation for atrioventrial nodal reentrant tachycardia often targets the slow pathway region within the triangle.
- The dimensions and structures within Koch's triangle can vary between individuals, which is clinically relevant for catheter ablation procedures guided by anatomic landmarks in this region.
The document discusses the anatomy of cardiac structures and the conducting system in relation to electrophysiology studies. It describes in detail the structures of the right atrium including the appendage, venous component, vestibule, crista terminalis, openings of the superior and inferior vena cava. It also discusses the left atrium and pulmonary vein openings. Understanding the normal anatomy and variants is important for electrophysiology studies and interventional procedures to interpret signals and avoid complications.
Anatomy of cardiac structures & conducting system inRamachandra Barik
The document discusses the anatomy of various cardiac structures and the conducting system in relation to electrophysiology studies. It covers the anatomy of the right atrium, left atrium, atrial septum, interatrial connections, atrioventricular junctions, and importance for electrophysiology procedures. Key structures discussed include the crista terminalis, triangle of Koch, isthmuses, pulmonary veins, atrial septum, Bachmann bundle, and atrioventricular junction. A better understanding of cardiac anatomy is essential for interpreting electrophysiology studies and performing interventional procedures.
Right Ventricle Anatomy, Physiology & ECHO Assessment by Dr. Vaibhav Yawalka...vaibhavyawalkar
This document provides an overview of right ventricle anatomy, physiology, and echocardiographic assessment. It describes the irregular shape and trabeculated structure of the right ventricle. The physiology section covers the RV's adaptation to volume overload through distensibility and compliance. Echocardiographic assessment techniques are outlined, including measurements of RV dimensions, fractional area change, TAPSE, tissue Doppler imaging, and the TEI index. The document provides a detailed but technical summary of right ventricular structure and function.
The document summarizes key aspects of heart anatomy and physiology. It describes the location and layers of the heart walls. It details the four chambers of the heart and the valves that prevent backflow of blood. It explains the pulmonary and systemic blood circulation circuits. It also outlines the specialized conduction system that controls heart rhythm, including the sinoatrial node, atrioventricular node, and Purkinje fibers. In addition, it discusses how sympathetic and parasympathetic nerves regulate heart rate and conduction.
The document summarizes the anatomy and physiology of the heart and circulatory system. It describes the structure and function of the heart chambers and valves. It explains how blood flows through the heart in two separate circuits for pulmonary and systemic circulation. It also discusses the coronary arteries and blood supply to the heart muscle itself.
The document summarizes cardiac impulse conduction through different parts of the heart. It discusses how the impulse is transmitted from the sinoatrial node to the atria, then to the atrioventricular node where it is delayed by 0.13 seconds as it travels through the node and bundle of His. It then describes how the common bundle divides into right and left branches that further divide and transmit the impulse to the ventricles via Purkinje fibers. The transmission through the ventricles occurs in a specific pattern from the septum to the anterior and apical regions and finally the posterobasal region.
The conducting system of the heart consists of specialized cardiac muscle tissue that generates and transmits electrical impulses to initiate and coordinate heart muscle contraction. It includes the sinoatrial node, atrioventricular node, bundle of His, Purkinje fibers and their left and right branches. These structures work together to conduct electrical signals from the upper to lower chambers and allow synchronized, rhythmic pumping of blood throughout the body. Damage to parts of this system can lead to arrhythmias or require treatment like artificial pacemakers.
The cardiovascular system consists of the heart and blood vessels. The heart has four chambers and pumps blood through two circuits. Blood is pumped from the right ventricle to the lungs via the pulmonary circulation and from the left ventricle to the body via the systemic circulation. The heart's rhythmic beating is controlled by pacemaker cells located in the sinoatrial node which generate electrical impulses that cause cardiac muscle contraction and propagate through specialized conduction pathways to the atrioventricular node and ventricles. Cardiac valves ensure one-way blood flow through the heart.
The cardiovascular system consists of the heart and blood vessels. The heart has four chambers and pumps blood through two circuits. It is innervated by the autonomic nervous system. The cardiac cycle involves atrial and ventricular contraction and relaxation. Factors such as hormones, temperature, exercise and the autonomic nervous system regulate heart rate and cardiac output.
This document summarizes the anatomy of the cardiac conduction system. It describes the locations and functions of the key components, including the sinus node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It also discusses the histological characteristics that define the conduction system and how impulses are conducted through each component to coordinate ventricular depolarization.
The document describes the anatomy and physiology of the heart. It discusses the location and size of the heart, its chambers including the right and left atria and ventricles, and major blood vessels. It explains the coronary circulation including the right and left coronary arteries, areas of distribution, collateral circulation, and coronary dominance. It also covers the layers of the heart wall, conduction system, valves, coronary venous drainage and lymphatics. Finally, it summarizes the regulation of coronary blood flow including autoregulation, perfusion pressure, vascular resistance, and neural and humoral control.
The coronary arteries develop from three elements: sinusoids, an in situ endothelial network, and coronary buds on the aortic sinuses. The right coronary artery arises from the right sinus and the left coronary artery arises from the left sinus. The left main coronary artery bifurcates into the left anterior descending artery and left circumflex artery. The LAD supplies the anterior walls and septum. The LCx supplies the lateral and posterior walls. There are typically variations in the number of branches but the main coronary arteries maintain consistent vascular territories.
The cardiac conduction system sends signals through specialized cardiac muscle cells to coordinate the rhythmic contraction of the heart. It includes the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node acts as the pacemaker by spontaneously generating electrical impulses that spread through the internodal pathways and cause the atria to contract. The impulse then travels to and through the atrioventricular node and bundle of His before reaching the Purkinje fibers, which trigger fast, coordinated ventricular contraction.
ORIGIN OF THE HEARTBEAT & THE ELECTRICAL ACTIVITY OF THE HEART.pptxshreya730959
The heartbeat originates in the sinoatrial (SA) node, which acts as the heart's natural pacemaker. Impulses from the SA node spread through the conduction system to the atria and ventricles. The SA node discharges spontaneously at the fastest rate, setting the heartbeat. Impulses pass from the SA node through the atria to the atrioventricular (AV) node and bundle of His, then via Purkinje fibers to ventricular muscle. Vagal stimulation slows the heartbeat by inhibiting the SA and AV nodes, while sympathetic stimulation increases the heart rate by facilitating impulse propagation. Digitalis depresses the conduction system like vagal stimulation and is used clinically to improve heart function and control
The conduction system of the heart controls the rate and rhythm of the heart. The sinoatrial node located in the upper right chamber initiates the heartbeat, and the impulse spreads through the atria and reaches the atrioventricular node above the tricuspid valve. The impulse then travels down the bundle of His and through its branches to the Purkinje fibers, which carry the impulse to the ventricles and cause them to contract.
This study evaluated outcomes of patients with diabetes mellitus (DM) treated with bioresorbable vascular scaffolds (Absorb BVS) compared to durable polymer everolimus-eluting stents (Xience EES) in routine percutaneous coronary intervention (PCI). The primary outcome was target vessel failure at 3 years, with secondary outcomes including death, myocardial infarction, and revascularization. Among patients with DM, target vessel failure at 3 years was higher compared to those without DM, regardless of device used. Overall, Absorb BVS was non-inferior to Xience EES for outcomes in patients with DM at 3 years follow-up.
echo evaluation of coronary arteries.pptxAbhinay Reddy
1) Echocardiographic evaluation of the coronary arteries is technically challenging due to the small size of the arteries and their motion.
2) Recent improvements in ultrasound technology have enabled direct visualization and Doppler assessment of multiple segments of the main coronary arteries.
3) Transthoracic echocardiography can be used to evaluate coronary artery patency, stenosis, and blood flow velocities. Segmental evaluation of the left main, left anterior descending, left circumflex, and right coronary arteries is possible in many patients.
CONDUCTIVE SYSTEM OF HEART .pptx BY MRS. WINCY THIRUMURUGAN .PROFESSOR.NURSIN...WINCY THIRUMURUGAN
MEANING.
The conducting system of the heart consists of cardiac muscle cells and conducting fibers (not nervous tissue) that are specialized for initiating impulses and conducting them rapidly through the heart.
It provides the heart its automatic rhythmic beat.
The purpose is to
Generating rhythmical electrical impulses to cause rhythmical contraction of the heart muscle. Conducting these impulses rapidly throughout the heart.
This pathway is made up of 5 elements:
The sino-atrial (SA) node.
The atrio-ventricular (AV) node.
The bundle of His.
The left and right bundle branches.
The Purkinje fibers.
SINOATRIAL NODE
The sinoatrial (SA) node is a collection of specialized cells (pacemaker cells), and is located in the upper wall of the right atrium, at the junction where the superior vena cava enters.
These pacemaker cells can spontaneously generate electrical impulses. The wave of excitation created by the SA node spreads via gap junctions across both atria, resulting in atrial contraction (atrial systole) – with blood moving from the atria into the ventricles.
The SA node is supraventricular and is sensitive to parasympathetic and sympathetic influence.
The SA node generates impulses and influenced by the Autonomic Nervous System:
Sympathetic nervous system – increases firing rate of the SA node, and thus increases heart rate.
Parasympathetic nervous system – decreases firing rate of the SA node, and thus decreases heart rate
THE INTER NODAL PATHWAYS consist of three bands (anterior, middle, and posterior) that lead directly from the SA node to the next node in the conduction system, the atrioventricular node. The impulse takes approximately 50 m s (milliseconds) to travel between these two nodes.
Bachmann's bundle (BB), also known as the interatrial bundle, myocardial strands connecting the right and left atrial walls and is considered to be the main pathway of interatrial conduction.
THE AV NODEThe AV node is located in the posterior wall of the right atrium immediately behind the tricuspid valve.
Cause of Slow Conduction in the A-V Node
What is the significance of AV nodal delay?
The cardiac impulse does not travel from the atria to the ventricles too rapidly.
It is primarily the AV node and it’s adjacent fibers that delay this transmission into the ventricles
AV BUNDLE OR BUNDLE OF HIS
From the AV node arises a special conducting pathway .
RIGHT AND LEFT BUNDLE BRANCHES
FASCICLE
The right bundle branch contains one fascicle.
The left bundle branch into three fascicles:
The left anterior,
The left posterior, and
The left septal fascicle.
PURKINJE FIBRES
The LT and RT bundle branches divides in turn course sidewise around each ventricular chamber and back toward the base of heart.
The ends of Purkinje fibers penetrate about one third of the way into muscle mass and finally become continuous with cardiac muscle fibers
,abundant with glycogen and extensive gap junctions, rapidly transmit cardiac action potentials in 0.03sec
The cardiac conduction system is a network of specialized cardiac muscle cells that initiate and transmit the electrical impulses responsible for the coordinated contractions of each cardiac cycle. These special cells are able to generate an action potential on their own (self-excitation) and pass it on to other nearby cells (conduction), including cardiomyocytes.
The document discusses the anatomy of the atrioventricular junctions. It describes that the junction comprises the right and left parietal junctions and a small septal component. It also discusses the triangle of Koch located in the right atrium, which contains specialized conduction tissues and borders. The document further summarizes the structure of the atrioventricular node, its components including the compact node and extensions, and the pathways for conduction through the node including the fast and slow pathways. It relates the anatomical structures to the functional pathways and discusses developments that increase the likelihood of arrhythmias during aging.
The cardiac conduction system generates and coordinates the contraction of the heart muscle. It is made up of specialized cardiac muscle cells located in the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node initiates each heartbeat by spontaneously generating an electrical impulse. This impulse then travels through the internodal pathways and atria to the atrioventricular node, which slows conduction before passing the impulse to the ventricles via the bundle of His and Purkinje fibers, causing synchronized ventricular contraction and pumping of blood. Defects or damage to the conduction system can lead to cardiac arrhythmias.
- Koch's triangle delineates the location of the atrioventricular node. It is bounded posteriorly by the tendon of Todaro, anteriorly by the tricuspid valve septal leaflet, and inferiorly by the coronary sinus ostium.
- The atrioventricular node and His bundle are located near the apex of the triangle where the His bundle penetrates the central fibrous body. Catheter ablation for atrioventrial nodal reentrant tachycardia often targets the slow pathway region within the triangle.
- The dimensions and structures within Koch's triangle can vary between individuals, which is clinically relevant for catheter ablation procedures guided by anatomic landmarks in this region.
The document discusses the anatomy of cardiac structures and the conducting system in relation to electrophysiology studies. It describes in detail the structures of the right atrium including the appendage, venous component, vestibule, crista terminalis, openings of the superior and inferior vena cava. It also discusses the left atrium and pulmonary vein openings. Understanding the normal anatomy and variants is important for electrophysiology studies and interventional procedures to interpret signals and avoid complications.
Anatomy of cardiac structures & conducting system inRamachandra Barik
The document discusses the anatomy of various cardiac structures and the conducting system in relation to electrophysiology studies. It covers the anatomy of the right atrium, left atrium, atrial septum, interatrial connections, atrioventricular junctions, and importance for electrophysiology procedures. Key structures discussed include the crista terminalis, triangle of Koch, isthmuses, pulmonary veins, atrial septum, Bachmann bundle, and atrioventricular junction. A better understanding of cardiac anatomy is essential for interpreting electrophysiology studies and performing interventional procedures.
Right Ventricle Anatomy, Physiology & ECHO Assessment by Dr. Vaibhav Yawalka...vaibhavyawalkar
This document provides an overview of right ventricle anatomy, physiology, and echocardiographic assessment. It describes the irregular shape and trabeculated structure of the right ventricle. The physiology section covers the RV's adaptation to volume overload through distensibility and compliance. Echocardiographic assessment techniques are outlined, including measurements of RV dimensions, fractional area change, TAPSE, tissue Doppler imaging, and the TEI index. The document provides a detailed but technical summary of right ventricular structure and function.
The document summarizes key aspects of heart anatomy and physiology. It describes the location and layers of the heart walls. It details the four chambers of the heart and the valves that prevent backflow of blood. It explains the pulmonary and systemic blood circulation circuits. It also outlines the specialized conduction system that controls heart rhythm, including the sinoatrial node, atrioventricular node, and Purkinje fibers. In addition, it discusses how sympathetic and parasympathetic nerves regulate heart rate and conduction.
The document summarizes the anatomy and physiology of the heart and circulatory system. It describes the structure and function of the heart chambers and valves. It explains how blood flows through the heart in two separate circuits for pulmonary and systemic circulation. It also discusses the coronary arteries and blood supply to the heart muscle itself.
The document summarizes cardiac impulse conduction through different parts of the heart. It discusses how the impulse is transmitted from the sinoatrial node to the atria, then to the atrioventricular node where it is delayed by 0.13 seconds as it travels through the node and bundle of His. It then describes how the common bundle divides into right and left branches that further divide and transmit the impulse to the ventricles via Purkinje fibers. The transmission through the ventricles occurs in a specific pattern from the septum to the anterior and apical regions and finally the posterobasal region.
The conducting system of the heart consists of specialized cardiac muscle tissue that generates and transmits electrical impulses to initiate and coordinate heart muscle contraction. It includes the sinoatrial node, atrioventricular node, bundle of His, Purkinje fibers and their left and right branches. These structures work together to conduct electrical signals from the upper to lower chambers and allow synchronized, rhythmic pumping of blood throughout the body. Damage to parts of this system can lead to arrhythmias or require treatment like artificial pacemakers.
The cardiovascular system consists of the heart and blood vessels. The heart has four chambers and pumps blood through two circuits. Blood is pumped from the right ventricle to the lungs via the pulmonary circulation and from the left ventricle to the body via the systemic circulation. The heart's rhythmic beating is controlled by pacemaker cells located in the sinoatrial node which generate electrical impulses that cause cardiac muscle contraction and propagate through specialized conduction pathways to the atrioventricular node and ventricles. Cardiac valves ensure one-way blood flow through the heart.
The cardiovascular system consists of the heart and blood vessels. The heart has four chambers and pumps blood through two circuits. It is innervated by the autonomic nervous system. The cardiac cycle involves atrial and ventricular contraction and relaxation. Factors such as hormones, temperature, exercise and the autonomic nervous system regulate heart rate and cardiac output.
This document summarizes the anatomy of the cardiac conduction system. It describes the locations and functions of the key components, including the sinus node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It also discusses the histological characteristics that define the conduction system and how impulses are conducted through each component to coordinate ventricular depolarization.
The document describes the anatomy and physiology of the heart. It discusses the location and size of the heart, its chambers including the right and left atria and ventricles, and major blood vessels. It explains the coronary circulation including the right and left coronary arteries, areas of distribution, collateral circulation, and coronary dominance. It also covers the layers of the heart wall, conduction system, valves, coronary venous drainage and lymphatics. Finally, it summarizes the regulation of coronary blood flow including autoregulation, perfusion pressure, vascular resistance, and neural and humoral control.
The coronary arteries develop from three elements: sinusoids, an in situ endothelial network, and coronary buds on the aortic sinuses. The right coronary artery arises from the right sinus and the left coronary artery arises from the left sinus. The left main coronary artery bifurcates into the left anterior descending artery and left circumflex artery. The LAD supplies the anterior walls and septum. The LCx supplies the lateral and posterior walls. There are typically variations in the number of branches but the main coronary arteries maintain consistent vascular territories.
The cardiac conduction system sends signals through specialized cardiac muscle cells to coordinate the rhythmic contraction of the heart. It includes the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. The sinoatrial node acts as the pacemaker by spontaneously generating electrical impulses that spread through the internodal pathways and cause the atria to contract. The impulse then travels to and through the atrioventricular node and bundle of His before reaching the Purkinje fibers, which trigger fast, coordinated ventricular contraction.
ORIGIN OF THE HEARTBEAT & THE ELECTRICAL ACTIVITY OF THE HEART.pptxshreya730959
The heartbeat originates in the sinoatrial (SA) node, which acts as the heart's natural pacemaker. Impulses from the SA node spread through the conduction system to the atria and ventricles. The SA node discharges spontaneously at the fastest rate, setting the heartbeat. Impulses pass from the SA node through the atria to the atrioventricular (AV) node and bundle of His, then via Purkinje fibers to ventricular muscle. Vagal stimulation slows the heartbeat by inhibiting the SA and AV nodes, while sympathetic stimulation increases the heart rate by facilitating impulse propagation. Digitalis depresses the conduction system like vagal stimulation and is used clinically to improve heart function and control
The conduction system of the heart controls the rate and rhythm of the heart. The sinoatrial node located in the upper right chamber initiates the heartbeat, and the impulse spreads through the atria and reaches the atrioventricular node above the tricuspid valve. The impulse then travels down the bundle of His and through its branches to the Purkinje fibers, which carry the impulse to the ventricles and cause them to contract.
This study evaluated outcomes of patients with diabetes mellitus (DM) treated with bioresorbable vascular scaffolds (Absorb BVS) compared to durable polymer everolimus-eluting stents (Xience EES) in routine percutaneous coronary intervention (PCI). The primary outcome was target vessel failure at 3 years, with secondary outcomes including death, myocardial infarction, and revascularization. Among patients with DM, target vessel failure at 3 years was higher compared to those without DM, regardless of device used. Overall, Absorb BVS was non-inferior to Xience EES for outcomes in patients with DM at 3 years follow-up.
echo evaluation of coronary arteries.pptxAbhinay Reddy
1) Echocardiographic evaluation of the coronary arteries is technically challenging due to the small size of the arteries and their motion.
2) Recent improvements in ultrasound technology have enabled direct visualization and Doppler assessment of multiple segments of the main coronary arteries.
3) Transthoracic echocardiography can be used to evaluate coronary artery patency, stenosis, and blood flow velocities. Segmental evaluation of the left main, left anterior descending, left circumflex, and right coronary arteries is possible in many patients.
AVNRT is the most common type of supraventricular tachycardia. It involves a reentrant circuit within the atrioventricular node utilizing two pathways - a slow pathway and a fast pathway. There are two subtypes - typical (slow-fast) AVNRT and atypical (fast-slow) AVNRT. The ECG may show retrograde P waves buried within the QRS complex or pseudo S/R waves. Treatment includes vagal maneuvers, adenosine, calcium channel blockers, beta blockers, or catheter ablation if episodes recur despite medical management.
DIFFERENTIALS OF ARRYTHMIAS WITH RBBB MORPHOLOGY.pptxAbhinay Reddy
This document discusses differentials of arrhythmias that present with right bundle branch block (RBBB) morphology on electrocardiogram (ECG). It describes the characteristics of complete RBBB, incomplete RBBB, and intermittent RBBB. It also discusses how to distinguish RBBB with left anterior fascicular block from RBBB with left posterior fascicular block based on ECG patterns. Finally, it lists various arrhythmias that can present with RBBB morphology including idiopathic ventricular tachycardia, supraventricular tachycardia, rate-related RBBB, Ashman phenomenon, supraventricular tachycardia with aberrant conduction, monomorphic ventricular tachycardia, tricyclic antidepressant
This document discusses post-myocardial infarction ventricular septal rupture (VSR). It notes that VSR incidence has decreased with improved reperfusion therapies. Surgical repair is the definitive treatment but is high risk, while percutaneous closure and mechanical support have improved outcomes. The timing and presentation of VSR depends on its pathophysiology, which can include acute or delayed rupture. Diagnosis is via echocardiography. Management involves surgical closure if stable, while unstable patients may be supported with devices or surgery delayed. Percutaneous closure is an option for inoperable cases.
This document provides guidelines for the management of patients with valvular heart disease developed by the 2020 ACC/AHA Writing Committee. It summarizes the top 10 key recommendations from the guidelines which include classifying disease stages, evaluating patients with noninvasive testing and further testing as needed, treating severe valve disease based on symptoms, involving a multidisciplinary team for severe cases, expanding indications for transcatheter interventions, and treating atrial fibrillation in patients with valvular heart disease with oral anticoagulants. It also provides tables outlining diagnostic testing, disease stages, secondary prevention of rheumatic fever, and anticoagulation recommendations for atrial fibrillation in patients with valvular heart disease.
The document provides guidelines from the European Society of Cardiology (ESC) for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. It includes recommendations on diagnosis using high-sensitivity cardiac troponin tests, risk stratification incorporating biomarkers, antithrombotic and antiplatelet treatment strategies, as well as invasive treatment approaches. New recommendations cover the use of alternative diagnostic algorithms, de-escalation of antiplatelet treatment, dual antiplatelet and anticoagulation strategies, and the timing and approach to revascularization. Major changes from previous guidelines involve diagnostic testing, stress testing, and rhythm monitoring.
Echo for transcatheter valve therapies - Copy.pptxAbhinay Reddy
This document discusses the role of echocardiography in assessing patients for and guiding transcatheter aortic valve implantation (TAVI). Echocardiography is used to evaluate aortic valve anatomy and geometry, assess suitability for different valve sizes, guide device positioning during the procedure, and evaluate complications. Key measurements include aortic annulus diameter, distance from the coronary ostia, and relationships to mitral valve and left ventricular outflow tract. Echocardiography provides real-time imaging during critical steps like valve deployment and balloon dilation to optimize positioning and identify paravalvular regurgitation. Follow up echos are important to evaluate prosthetic function and complications.
Diagnosis and Management of acute coronary syndromes-latest guidelines (1).pptxAbhinay Reddy
This document provides guidelines for the diagnosis and management of acute coronary syndromes. It discusses how to evaluate patients presenting with chest pain or discomfort, including obtaining an ECG, measuring cardiac biomarkers, and appropriate use of imaging tests. Based on the ECG, biomarker levels, and clinical presentation, patients should be stratified as high, intermediate, or low risk and managed accordingly, which may include stress testing, invasive coronary angiography, or medical management and follow-up for stable patients. The guidelines emphasize the importance of a rapid initial evaluation and provide algorithms outlining recommended diagnostic pathways and timing of tests.
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
Executive Directors Chat Leveraging AI for Diversity, Equity, and InclusionTechSoup
Let’s explore the intersection of technology and equity in the final session of our DEI series. Discover how AI tools, like ChatGPT, can be used to support and enhance your nonprofit's DEI initiatives. Participants will gain insights into practical AI applications and get tips for leveraging technology to advance their DEI goals.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
2. • The heart is endowed with a special system for
(1) generating rhythmical electrical impulses to cause
rhythmical contraction of the heart muscle
(2)conducting these impulses rapidly through the heart.
• The Atria contract about one sixth of a second ahead of ventricular
contraction
• All portions of the ventricles to contract almost simultaneously
3. CONDUCTION SYSTEM OF
THE HEART
1. SINO ATRIAL NODE
2. INTERNODAL ATRIAL
PATHWAY
3. ATRIOVENTRICULAR
NODE
4. BUNDLE OF HIS
5. PURKINJEE SYSTEM
4. SA NODE of Keith & Flack
• The sinus node is a crescent-shaped, subepicardial specialized
muscular structure located posterolaterally in the right atrium (RA)
free wall.
• The sinus node lies within the epicardial groove of the sulcus
terminalis at the junction of the anterior trabeculated RA
appendage with the posterior smooth-walled venous component
• - tadpole-shaped structure with a head, central body, and tail with
nodal extensions representing multiple limbs.
• In adults the sinus node measures 8 to 22 mm long and 2 to 3 mm
wide and thick
5. The sinus node is a complex of weakly coupled, heterogeneous cells, including the
principal pacemaker cells as well as nonpacemaker cells embedded in a dense
supporting connective matrix
Within the sinus node, pacemaker cells may be divided
Into three major classes:
(1) “elongated spindle-shaped cells,” - long, multinucleated 80 microns
(2) “spindle cells,” mononuclear, shorter than spindle cells, 40 microns
(3) “spider cells,” - irregularly shaped branches with blunt ends.
6. • Pacemaker of the heart
Current models involve the concept of a “pacemaker hierarchy” head- body - tail
Sympathetic stimulation shifts the leading pacemaker site superiorly, resulting in an
increase in heart rate.
• Artery to SA node – 55% - Right coronary artery
- 45% - Circumflex branch of LCA
The sinus nodal artery typically passes centrally through the length of the sinus body, and it is disproportionately
large, which is considered physiologically important in that its perfusion pressure can affect the sinus rate.
Distention of the artery slows the sinus rate, whereas collapse causes an increase in sinus rate.
7. The sinus node is densely innervated with postganglionic adrenergic
and cholinergic nerve terminals.
The right vagus nerve predominantly affects sinus node function.
• Vagal responses begin after a short
latency and dissipate quickly.
• The rapid onset and offset of
responses to vagal stimulation allow
dynamic beat-to-beat vagal
modulation of the heart rate
• Enhanced vagal activity can produce
sinus bradycardia, sinus arrest, and
sinoatrial exit block.
• Responses to sympathetic stimulation
begin and dissipate slowly.
• The slow temporal response to
sympathetic stimulation precludes any
beat-to-beat regulation by
sympathetic activity.
• Increased sympathetic activity can
increase the sinus rate and reverse
sinus arrest and sinoatrial exit block.
8. INTERNODAL CONDUCTION
PATHS
• There are three preferential anatomic conduction pathways from
the sinus node to the AV node
• These groups of internodal tissue are best referred to as
internodal atrial myocardium, not tracts, because they do not
appear to be histologically recognizable specialized tracts, only
plain atrial myocardium.
• ANTERIOR-------- BACHMAN
• MIDDLE-------------WENCKEBACH
• POSTERIOR-------THOREL
9. The anterior “internodal atrial myocardium” begins at the anterior margin of the
sinus node, curves anteriorly around the superior vena cava (SVC) to the
interatrial septum, and then splits into two bundles one passes to the left atrium
(LA) (Bachmann bundle), while the second bundle descends along the interatrial
septum and connects to the superior margin of the AVN.
Bachmans bundle
It connects the anterosuperior RA an LA behind the ascending aorta, just beneath
the epicardium, and Is the preferential path of LA activation during sinus rhythm.
Three other interatrial conduction pathways have been described:
1. Muscular bundles on the inferior atrial surface near the coronary sinus (CS)
2. Transseptal fibres in the fossa ovalis
3. Posteriorly in the vicinity of the right pulmonary valves
10. The middle “internodal atrial myocardium” begins at the superior and posterior margins of the sinus node, travels
posteriorly behind th SVC to the crest of the interatrial septum, and descends within the interatrial septum to the
superior margin of the AVN.
The posterior “internodal atrial myocardium” starts at the inferoposterior margin o the sinus node, travel inferiorly
through the crista terminalis to the eustachian ridge, and then into the interatrial septum above the CS os, where it
joins the posterior portion of the AVN.
11. •Action potentials originating in the
sinus node travel outward into atrial
muscle fibres.
•The velocity of conduction in most
atrial muscle is about 0.3 m/sec, but
conduction is more rapid, about 1
m/sec in tracts
14. • The AVN is an interatrial structure, measuring approximately 5 mm long, 5 mm wide, and 0.8 mm thick in adults.
• The AVN is located beneath the RA endocardium at the apex of the triangle of Koch
• Slightly more anteriorly and superiorly is where the His bundle (HB) penetrates the AV junction through the central
fibrous body and the posterior aspect of the membranous AV septum.
• When traced inferiorly, toward the base of the triangle of Koch, the compact AVN area separates into twoc(rightward
and leftward) posterior extensions, usually with the artery supplying the AVN running between them.
• The rightward posterior extension has been implicated in the so-called slow pathway in the typical atrioventricular
nodal reentry tachycardia (AVNRT) circuit
15. • Artery to AV node – 90% - Right coronary artery
- 10 % - Circumflex branch of
LCA Delay of about 0.12 sec in conduction through
AV node
16. • As with the SA node, the AV node has extensive autonomic
innervation
and an abundant blood supply.
• The AV node consists of three regions— distinguished by functional
and histologic differences
1) The transitional cell zone
2) Compact node
3) Penetrating bundle
17. histology
The AVN and perinodal area are composed of at least three electrophysiologically distinct cells:
1. The atrionodal (AN)
2. Nodal (N)
3. Nodal-his (NH) cells
The AN region corresponds to the cells in the transitional region that are activated shortly after the atrial cells.
The N region corresponds to the region where the transitional cells merge with mid nodal cells and formd compact
node.
1. Conduction is slower through the N region in the compact AVN than in the AN and NH cell zones.
2. The n cells exhibit diastolic depolarization and are capable of automatic impulse formation.
3. The n cells in the compact avn appear to be responsible for the major part of av conduction delay
4. They are likely the site of wenckebach block and the site at which calcium channel blockers delay av conduction.
The NH region corresponds to the lower N cells, typically distal to the site of Wenckebach block, connecting to the
insulated penetrating portion of the HB.
19. Cause of the Slow Conduction
• The slow conduction in the transitional, nodal, and penetrating A-V
bundle fibres is caused mainly by diminished numbers of gap
junctions between successive cells in the conducting pathways
greater resistance to conduction of excitatory ions from one
conducting fibre to the next.
20. Functions of AV node
1. The main function of the AVN is modulation of atrial impulse
transmission to the ventricles; it introduces a delay between atrial
and ventricular systole.
2. To limit the number of impulses conducted from the atria to the
ventricles.
3. Fibers in the lower part of the AVN can exhibit automatic impulse
formation, serving as a subsidiary pacemaker
21. Bundle of
His
• The AV nodal tissue merges with the His bundle, which runs through
the inferior portion of the membranous interventricular septum, and
then in most cases, continues along the left side of the crest of the
muscular interventricular septum.
• The proximal part of the His bundle rests on the right atrial-left
ventricular (RA-LV) part of the membranous septum and the more
distal part travels along the right ventricle-left ventricular (RV-LV)
part of the membranous septum immediately below the aortic root.
22. • The His bundle usually receives a dual blood supply from both
the AV
nodal artery and branches of the LAD.
• Unlike the SA and AV nodes, the bundle of His and Purkinje
system have
relatively little autonomic innervation.
24. Right Bundle Branch(RBB)
• The right bundle branch (RBB) originates from the His bundle.
• It is a narrow compact structure – band like
• crosses to the right side of the IVS and extends along the RV endocardial
surface to the region of the anterolateral papillary muscle of the RV, where it
divides to supply the papillary muscle, the parietal RV surface, and the
lower part of the RV surface.
• The proximal portion of the RBB is supplied by branches from the AV nodal
artery or the LAD artery, whereas the more distal portion is supplied mainly
by branches of the LAD artery.
25. Left Bundle
Branch(LBB)
• Anatomically much less discrete
than the RBB.
• The LBB may divide immediately
as it originates from the bundle of
His or may continue for 1 to 2 cm
as a broad ribbon before dividing.
26. • The predivisional portion of the LB penetrates the membranous
portion of the interventricular septum under the aortic ring and then
divides under the septal endocardium into two branches: the LAF and
the LPF.
• An estimated 65% of individuals have a third fascicle of the LB, the left
median fascicle (LMF).
• The thin LAF crosses the anterobasal LV region toward the
anterolateral papillary muscle and terminates in the Purkinje system of
the anterolateral LV wall.
• The LPF appears as an extension of the main LB and is broad in its
initial course. It then fans out extensively toward the posterior
papillary muscle and terminates in the Purkinje system of the
posteroinferior LV wall
27. • The LBB and its anterior fascicle have a blood supply similar to
that of the proximal portion of the RBB – LAD and AV nodal
artery
• The left posterior fascicle is supplied by branches of the AV
nodal artery, the posterior descending artery, and the
circumflex coronary artery.
28. Rapid Transmission in the Ventricular Purkinje System
• Special Purkinje fibres lead from the A-V node through the A-V
bundle into the ventricles.
• They are very large fibres, even larger than the normal ventricular
muscle fibres, and they transmit action potentials at a velocity of 1.5
to 4.0 m/sec, a velocity about 6 times that in the usual ventricular
muscle and 150 times that in some of the A-V nodal fibres.
• This allows almost instantaneous transmission of the cardiac
impulse throughout the entire remainder of the ventricular muscle
29. Characteristics of Cardiac
Conduction Cells
• Automaticity: Ability to initiate an electrical impulse
• Excitability: Ability to respond to an electrical impulse
• Conductivity: Ability to transmit an electrical impulse from one
cell to
another
30. Physiology
• The “threshold potential” is the lowest Em at which opening of
enough Na+ channels (or Ca2+ channels in the setting of nodal cells)
is able to initiate the sequence of channel openings needed to
generate a propagated action potential.
• Electrical changes in the action potential follow a relatively fixed time
and voltage relationship that differs according to specific cell types.
31. Two types of action potentials in heart
Fast response action potentials
• Seen in normal atrial and ventricular myocytes and in his-purkinje
fibers
• Action potentials have very rapid upstrokes, mediated by the fast
inward iNa.
Slow response action potentials
• Seen in in the normal sinus and atrioventricular nodal cells and many
types of diseased tissues
• Have very slow upstrokes, mediated by a slow inward, predominantly
l-type voltage-gated ca2+ current (iCal)
32. Fast Response Action Potential
Phase 4: The Resting Membrane Potential
• The K+ (Kir) channels underlie an outward K+ current (IK1) responsible for maintaining the resting potential
• It remains near the equilibrium potential for K+ (EK).
• The resting membrane potential is negative during phase 4 (about -90 mV) because potassium channel are
open (K+ conductance K+ currents [IK1] are high).
33. • The resting Em is also powered by the Na+-K+ adenosine
triphosphatase (the Na+-K+ pump)
• The Na+-K+ pump transports two K+ ions into the cell against its
chemical gradient and three na+ ions outside against its
electrochemical gradient at the expense of one ATP molecule.
• The Na+-K+ pump is electrogenic and generates a net outward
movement of positive charges
34. • Phase 0: The Upstroke—Rapid Depolarization
• On excitation of a cardiomyocyte by electrical stimuli from adjacent
cells, its resting Em (approximately −85 mV) depolarizes, leading to
opening (activation) of Na+ channels
• A large and rapid influx of Na+ ions (inward INa) occurs into the cell
down their electrochemical gradient.
• Once an excitatory stimulus depolarizes the Em beyond the threshold
for activation of Na+ channels (approximately −65 mV), the activated
INa is regenerative and no longer depends on the initial depolarizing
stimulus.
35. INa in phase 0
• Activation of Na+ channels is transient
• Fast inactivation (closing of the channel pore) starts simultaneously
with activation
• Inactivation is slightly delayed relative to activation, the channels
remain transiently (less than 1 millisecond) open to conduct INa
during phase 0 of the action potential before it closes
36. ICal in phase 0
• The threshold for activation of ICaL is approximately −30 to −40 mV.
• ICaL is much smaller than the peak INa.
• The amplitude of ICaL is not maximal near the action potential peak
because of the time-dependent nature of ICaL activation.
• Therefore ICaL contributes little to the action potential until the fast
INa is inactivated, after completion of phase 0.
• As a result, ICaL affects mainly the plateau of action potentials
recorded in atrial and ventricular muscle and His- Purkinje fibers.
37. • Phase 1: Early Repolarization
• Early repolarization during which the membrane repolarizes rapidly and
transiently to almost 0 mV - early notch due to
1. Inactivation of INa
2. Concomitant activation of several outward currents.
a) The transient outward K+ current (Ito) is mainly responsible for phase 1
of the action potential. Ito rapidly activates and then rapidly inactivates
b) Na+ outward current through the Na+-Ca2+ exchanger operating in
reverse mode likely contributes to this early phase of repolarization
38. Phase 2: The Plateau
Phase 2 (plateau) represents a delicate
balance between
• The depolarizing inward currents
1. ICaL
2. Small residual component of inward
INa)
• Repolarizing outward currents (outward
rectifying currents)
1. Ultrarapidly activating [IKur]
2. Rapidly activating[IKr]
3. Slowly activating [IKs] delayed
activating)
Vs
• Phase 2 is the longest phase of the action potential
• The plateau phase is unique among excitable cells and marks the phase of Ca2+ entry into the cell.
39. ICal
• ICaL is activated by membrane depolarization, is largely responsible
for the action potential plateau, and is a major determinant of the
duration of the plateau phase.
• ICaL also links membrane depolarization to myocardial contraction.
• L-type Ca2+ channels activate on membrane depolarization to
potentials positive to −40 mV.
• ICaL peaks at an Em of 0 to +10 mV
40. Ikr
• Ikr activates relatively fast and inactivation thereafter is very fast.
• The fast voltage-dependent inactivation limits outward current
through the channel at positive voltages and thus helps to maintain
the action potential plateau phase that controls contraction and
prevents premature excitation.
41. IKs
• IKs activates slowly compared with action potential duration, it is also
slowly inactivated.
• Hence the contribution of IKs to the net repolarizing current is
greatest late in the plateau phase, particularly during action
potentials of long duration.
• This allows IKs channels to accumulate in the open state during rapid
successive action potentials and mediate the faster rate of
repolarization.
• IKs plays an important role in determining the rate-dependent
shortening of the cardiac action potential
42. IKur
• IKur is detected only in human atria but not in the ventricles.
• Predominant rectifier current responsible for atrial repolarization and
is a basis for the much shorter duration of the action potential in the
atrium.
• IKur activates rapidly on depolarization in the plateau range and
displays outward rectification, but it inactivates slowly during the
time course of the action potential.
43. • Phase 3: Final Rapid Repolarization
• Phase 3 is the phase of rapid repolarization that restores the Em to its
resting value.
• Phase 3 is mediated by the
1. Increasing conductance of the delayed outward rectifying currents
(IKr and IKs)
2. The inwardly rectifying K+ currents (IK1 and acetylcholine-activated
K+ current [IKACh])
3. Outward K+ current (IK1
4. Time-dependent inactivation of ICaL .
44. • Phase 4: Restoration of Resting Membrane Potential
• restoration of transmembrane ionic concentration gradients to the
baseline resting state is necessary.
• This is achieved by the
1. Na+-K+ ATPase (Na+-K+ pump, which exchanges two K+ ions inside
and three Na+ ions outside)
2. Na+-Ca2+ exchanger (INa-Ca, which exchanges three Na+ ions for
one Ca2+ ion)
45.
46. Atrioventricular Heterogeneity of the Action
Potential
• Compared with the atrium, ventricular myocytes
1. Maintain a slightly more hyperpolarized resting em (approximately −85 mv
vs. −80 mv).
2. The action potential duration is longer
3. The plateau phase reaches a more depolarized em (approximately +20 mv),
4. Phase 3 repolarization curve is steeper in ventricular myocytes as compared
with the atrial action potential
47. 1. The density of Ito is twofold higher in the atria
compared with ventricular myocytes.
2. Ito subtypes (Ito,f and Ito,s) are differentially
expressed in the heart. Ito,f is the principal subtype
expressed in human atrium
3. IKur is detected only in human atria and not in the
ventricles.
This accelerates the early phase of repolarization and lead to lower
plateau potentials and shorter action potential durations in atrial as
compared with ventricular cells
48. IK1 density is much higher in ventricular than in atrial
myocytes
• Explains the steep repolarization phase in the
ventricles
• The hyperpolarized resting Em in ventricular
myocytes, and prevents the ventricular cell from
exhibiting pacemaker activity
49. Slow Response Action Potential
• Slow response action potentials are characterized by a more
depolarized Em at the onset of phase 4 (−50 to −65 mV)
• Slow diastolic depolarization during phase 4
• Reduced action potential amplitude.
• The rate of depolarization in phase 0 is much slower than that
in the working myocardial cells, resulting in reduced
conduction velocity of the cardiac impulse in the nodal regions
50. • The sinus and AV nodal cells lack the inward rectifier K+ current (IK1),
which acts to stabilize the resting Em
• Sinus and AV nodal excitable cells exhibit a spontaneous, slow, and
progressive decline in the Em during diastole (spontaneous diastolic
depolarization)
• Once this spontaneous depolarization reaches threshold
(approximately −40 mV), a new action potential is generated
51. Phase 4: Diastolic Depolarization
• If is a hyperpolarization-activated inward current that is carried
largely by Na+
• Once activated, It depolarizes the membrane to a level where the
Ca2+ current activates to initiate an action potential.
• Other ionic currents gated by membrane depolarization (i.e., ICaL
and T-type Ca2+ current [ICaT]), and a current generated by the Na+-
Ca2+ exchanger have also been proposed to be involved in
pacemaking.
52. TISSUE RATE OF IMPULSE
GENERATION
SA NODE 70-80/MIN
AV NODE 40 – 60/MIN
BUNDLE OF HIS 40/MIN
PURKINJE SYSTEM 24/MIN
53. Phase 0: The Upstroke—Slow Depolarization
• Action potential upstroke is mainly achieved by ICaL.
• L-type Ca2+ channels activate on depolarization to potentials positive
to −40 mV, and ICaL peaks at 0 to +10 mV.
• The peak amplitude ICaL is less than 10% that of INa, and the time
required for activation and inactivation of ICaL is slower than that for
INa.
• As a consequence, the rate of depolarization in phase 0 (dV/dt) is
much slower and the peak amplitude of the action potential is less
than that in the working myocardial cells.
54.
55. EXCITABILITY
• Excitability of a cardiac cell describes the ease with which the cell responds to a
stimulus with a regenerative action potential
• The most important determinant of reduced excitability is the reduced
availability of Na+ channels.
• The more negative the Em is, the more Na+ channels are available for
activation, the greater the influx of Na+ into the cell during phase 0, and the
greater the conduction velocity.
56. • Reduced excitability is physiologically observed during the relative refractory
period (occurring during phase 3 of the action potential, before full recovery of
Em).
• Initiation of a propagating action potential will require a larger-than-normal
stimulus.
• Reduced membrane excitability can occur in certain pathophysiological
conditions
1. Genetic mutations that result in loss of na+ channel function
2. Na+ channel blockade with class I antiarrhythmic drugs
3. Acute myocardial ischemia.
57. REFRACTORINESS
• Once an action potential is initiated, the cardiomyocyte becomes inexcitable to
stimulation for a time.
• Refractoriness is determined by
1. The action potential duration
2. Em
3. The number of Na+ channels that have recovered from their inactive state.
• Permits relaxation of cardiac muscle before subsequent activation.
• The refractory period acts as a protective mechanism by preventing multiple,
compounded action potentials from occurring.
• Shorter refractoriness facilitates reentry and arrhythmias
58. • The absolute refractory period (which extends over phases 0, 1, 2, and part of phase 3 of the action potential
• After the absolute refractory period, a stimulus can cause some cellular depolarization, but it does not lead
to a propagated action potential. The sum of this period and the absolute refractory period is termed the
effective refractory period
• The relative refractory period, which extends over the middle and late parts of phase 3 to the end of phase 3
of the action potential.
59. • During the relative refractory period, initiation of a second action
potential is more difficult but not impossible
• A larger-than-normal stimulus can result in activation of the cell and
lead to a propagating action potential
• However, the upstroke of the new action potential is less steep and of
lower amplitude and its conduction velocity is reduced compared
with normal.
60. Post-repolarization refractoriness.
• In pacemaking tissues, INa is predominantly absent and excitability is
mediated by the activation of ICaL.
• After inactivation, the transition of Ca2+ channels from the inactivated to
the closed resting state (i.e., recovery from inactivation) is relatively slow.
• As a result, excitability in pacemaking cells may not be recovered by the
end of phase 3 of the action potential
• Sinus and AV nodal cells remain refractory for a time interval that is longer
than the time it takes for full membrane repolarization to occur.
• May prevent premature excitation
• May be involved in development of blocks during ischemia
61. PROPAGATION
• Conduction velocity refers to the speed of propagation of the action
potential through cardiac tissue.
• The conduction velocity varies in cardiac tissues,
TISSUE CONDUCTION RATE
(m/s)
RELATIVE VALUE
SAN 0.05
ATRIAL
PATHWAY
1
AVN 0.02 – 0.05 LEAST
BUNDLE OF HIS 1
PURKINJE SYSTEM 4 HIGHEST
VENTRICULAR MUSCLE 1
62. • Intracellular Propagation
• The velocity of propagation increases with
1. Increasing cell diameter
2. Action potential amplitude
3. The initial rate of the rise of the action potential.
Intercellular Propagation
• Propagation of action potentials from one cell to adjacent cells is achieved by direct ionic current spread via
specialized, low resistance intercellular connections (gap junctional channels) located mainly in arrays within
the intercalated disks.
• The heart behaves electrically as a functional syncytium, resulting in a
• coordinated mechanical function.