The document discusses the myocardial action potential and mechanisms of arrhythmogenesis. It begins with an overview of the cardiac conduction system anatomy and ion channels. The myocardial action potential is then explained in detail, including the phases of depolarization, plateau, and repolarization. Mechanisms of arrhythmogenesis include abnormalities in automaticity, triggered activity, and impaired conduction. Abnormal automaticity can result from altered pacemaker sites while triggered activity involves early or delayed afterdepolarizations. Impaired conduction can cause blocks or provide the substrate for reentry arrhythmias due to tissue heterogeneity. Classification of antiarrhythmic drugs and examples of specific arrhythmias such as long QT syndrome and CPVT are also summarized.
Action potentials are short term changes in electrical potential across cell membranes in response to stimulation that allow electrical signals to propagate. They involve the movement of ions across the membrane through open channels. The cardiac action potential occurs in five phases: 1) rapid depolarization due to sodium influx; 2) early repolarization from sodium inactivation and potassium activation; 3) plateau from calcium influx; 4) rapid repolarization from potassium efflux; and 5) resting potential set by potassium equilibrium potential. Pacemaker cells additionally exhibit phase 4 diastolic depolarization driven by funny channel opening that leads to spontaneous firing.
1. Cardiac electrophysiology involves the electrical activity in the heart, including the action potential and ion currents.
2. The cardiac action potential is initiated by the opening of fast sodium channels, followed by calcium and potassium channels.
3. Pacemaker cells in the sinoatrial node generate spontaneous action potentials due to a balance of slow inward calcium and funny currents and delayed outward potassium currents.
4. Action potentials propagate from pacemaker cells through the heart via gap junctions between cardiomyocytes. Propagation speed depends on the underlying ionic currents.
This document discusses antiarrhythmic drugs used to treat abnormal heart rhythms (arrhythmias). It begins by describing normal heart rhythm and different types of arrhythmias including tachyarrhythmias (fast rhythms) and bradyarrhythmias (slow rhythms). It then discusses mechanisms of arrhythmias including abnormalities in impulse generation and conduction. The document focuses on classification of antiarrhythmic drugs and their mechanisms of action. The main classes described are Class I (sodium channel blockers), Class II (beta blockers), Class III (potassium channel blockers), and Class IV (calcium channel blockers). Representative drugs from each class are discussed along with their pharmacokinetics, uses,
1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. Disorders of impulse formation include abnormalities in automaticity and triggered activity.
2. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. Triggered activity is initiated by afterdepolarizations following an action potential.
3. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. Common reentrant arrhythmias include atrial flutter, at
Cardiac action potentials arise from the coordinated movement of ions through membrane channels in cardiac cells. The cardiac action potential has 5 phases: rapid upstroke (phase 0) due to sodium influx, early rapid repolarization (phase 1) mediated by potassium currents, plateau phase (phase 2) maintained by calcium and potassium currents, final rapid repolarization (phase 3) due to potassium currents, and resting phase (phase 4) where the cell prepares for the next action potential. Precisely regulated ion channel function underlies the generation and propagation of action potentials and ensures normal cardiac rhythm.
This document summarizes the mechanisms of cardiac arrhythmias. It describes normal cardiac electrophysiology and the five phases of the cardiac action potential. It then discusses mechanisms that can disrupt normal rhythms, including altered automaticity, triggered activity due to afterdepolarizations, and reentry due to conduction blocks or barriers that allow circuits to form. Key features that help distinguish automatic from triggered from reentrant arrhythmias are described.
cardiac ion channels and channelopathiesShivani Rao
The document discusses ion channels and their role in generating cardiac action potentials. It begins by defining ion channels as pore-forming proteins that gate the flow of ions across cell membranes. It then describes the key properties of ion channels including selectivity, gating, and their role in establishing membrane potentials. The remainder of the document details the specific ion channels involved in each phase of the cardiac action potential, including the fast sodium current underlying the upstroke in Phase 0, the potassium and chloride currents producing Phase 1 repolarization, the calcium and potassium currents maintaining the Phase 2 plateau, and the currents responsible for Phase 3 repolarization. Pacemaker cell action potentials are also discussed, noting their unique pacemaker potential in Phase 4 and lack of Phase
Action potentials are short term changes in electrical potential across cell membranes in response to stimulation that allow electrical signals to propagate. They involve the movement of ions across the membrane through open channels. The cardiac action potential occurs in five phases: 1) rapid depolarization due to sodium influx; 2) early repolarization from sodium inactivation and potassium activation; 3) plateau from calcium influx; 4) rapid repolarization from potassium efflux; and 5) resting potential set by potassium equilibrium potential. Pacemaker cells additionally exhibit phase 4 diastolic depolarization driven by funny channel opening that leads to spontaneous firing.
1. Cardiac electrophysiology involves the electrical activity in the heart, including the action potential and ion currents.
2. The cardiac action potential is initiated by the opening of fast sodium channels, followed by calcium and potassium channels.
3. Pacemaker cells in the sinoatrial node generate spontaneous action potentials due to a balance of slow inward calcium and funny currents and delayed outward potassium currents.
4. Action potentials propagate from pacemaker cells through the heart via gap junctions between cardiomyocytes. Propagation speed depends on the underlying ionic currents.
This document discusses antiarrhythmic drugs used to treat abnormal heart rhythms (arrhythmias). It begins by describing normal heart rhythm and different types of arrhythmias including tachyarrhythmias (fast rhythms) and bradyarrhythmias (slow rhythms). It then discusses mechanisms of arrhythmias including abnormalities in impulse generation and conduction. The document focuses on classification of antiarrhythmic drugs and their mechanisms of action. The main classes described are Class I (sodium channel blockers), Class II (beta blockers), Class III (potassium channel blockers), and Class IV (calcium channel blockers). Representative drugs from each class are discussed along with their pharmacokinetics, uses,
1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. Disorders of impulse formation include abnormalities in automaticity and triggered activity.
2. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. Triggered activity is initiated by afterdepolarizations following an action potential.
3. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. Common reentrant arrhythmias include atrial flutter, at
Cardiac action potentials arise from the coordinated movement of ions through membrane channels in cardiac cells. The cardiac action potential has 5 phases: rapid upstroke (phase 0) due to sodium influx, early rapid repolarization (phase 1) mediated by potassium currents, plateau phase (phase 2) maintained by calcium and potassium currents, final rapid repolarization (phase 3) due to potassium currents, and resting phase (phase 4) where the cell prepares for the next action potential. Precisely regulated ion channel function underlies the generation and propagation of action potentials and ensures normal cardiac rhythm.
This document summarizes the mechanisms of cardiac arrhythmias. It describes normal cardiac electrophysiology and the five phases of the cardiac action potential. It then discusses mechanisms that can disrupt normal rhythms, including altered automaticity, triggered activity due to afterdepolarizations, and reentry due to conduction blocks or barriers that allow circuits to form. Key features that help distinguish automatic from triggered from reentrant arrhythmias are described.
cardiac ion channels and channelopathiesShivani Rao
The document discusses ion channels and their role in generating cardiac action potentials. It begins by defining ion channels as pore-forming proteins that gate the flow of ions across cell membranes. It then describes the key properties of ion channels including selectivity, gating, and their role in establishing membrane potentials. The remainder of the document details the specific ion channels involved in each phase of the cardiac action potential, including the fast sodium current underlying the upstroke in Phase 0, the potassium and chloride currents producing Phase 1 repolarization, the calcium and potassium currents maintaining the Phase 2 plateau, and the currents responsible for Phase 3 repolarization. Pacemaker cell action potentials are also discussed, noting their unique pacemaker potential in Phase 4 and lack of Phase
Various coronary physiological measurements can be made in the cardiac catheterization laboratory using sensor-tipped guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relative coronary flow reserve, and the pressure-derived fractional flow reserve of the myocardium. Ambiguity regarding abnormal microcirculation has been reduced or eliminated with measurements of relative coronary flow reserve and fractional flow reserve. The role of microvascular flow impairment can be separately determined with coronary flow velocity reserve measurements. In addition to lesion assessment before and after intervention, emerging applications of coronary physiology include the determination of physiological responses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute myocardial infarction. Measurements of coronary physiology in the catheterization laboratory provide objective data that complement angiography for clinical decision-making
The document discusses regulation of coronary blood flow. It begins by outlining the coronary vessels and blood supply to the heart. The coronary arteries arise from the aorta and branch within the heart muscle to supply it with blood. Coronary blood flow is highest during cardiac diastole when the heart muscle is relaxed and lowest during systole when the heart contracts. Multiple factors influence coronary blood flow including physical factors like blood pressure, chemical factors such as local metabolic needs, and neural and hormonal control. The heart has an autoregulatory mechanism to maintain adequate blood flow over a range of perfusion pressures. Disruptions to this system can lead to pathological thrombosis in the coronary arteries and consequences like myocardial infarction.
This document provides an introduction to cardiac action potentials. It describes the five phases of a cardiac action potential: phase 4 (resting phase), phase 0 (depolarization), phase 1 (early repolarization), phase 2 (plateau phase), and phase 3 (rapid repolarization). It explains that cardiac action potentials are initiated by the sinoatrial node and involve movements of ions like sodium, calcium, and potassium through ion channels, causing changes in the cell's membrane potential. These potential changes can be recorded as an electrocardiogram to monitor the heart's electrical activity.
This document discusses basic terms in electrophysiology and the properties of cardiac cells. It describes two main types of cardiac cells: electrical cells that make up the conduction system and possess the properties of automaticity, excitability, and conductivity; and myocardial cells that make up the muscular walls and possess contractility and extensibility. It explains that cardiac cells at rest are polarized but become depolarized when an electrical impulse causes ions to cross the cell membrane, generating an action potential. The action potential curve consists of five phases: resting phase, rapid depolarization, plateau phase mediated by slow calcium channels, and rapid repolarization as ions return to their resting state.
This document provides an overview of cardiac arrhythmias, including definitions and descriptions of normal sinus rhythm and various arrhythmias. It discusses the cardiac conduction system and mechanisms that can cause arrhythmias, such as abnormal impulse formation or conduction. Specific arrhythmias summarized include sinus bradycardia, sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. For each arrhythmia, the document provides information on heart rate, rhythm, P wave presence/morphology, and other ECG characteristics.
This document discusses cardiac arrhythmias and the cardiac conduction system. It describes the sinoatrial node, atrioventricular node, and Purkinje fibers, which make up the cardiac conduction system. Causes of arrhythmias include enhanced automaticity, triggered activity, and re-entry. Various arrhythmias are described including sinus bradycardia, premature atrial contractions, atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and different types of atrioventricular block. The electrocardiogram is discussed as a tool to evaluate heart rate, intervals, waves, and diagnose arrhythmias.
The splanchnic circulation supplies blood to the gastrointestinal tract, spleen, and liver. It has unique features like blood from the mesenteric bed and spleen draining primarily to the liver via the portal vein. Mesenteric blood flow is regulated by local autoregulation, gastrointestinal activity, nerves, and chemicals like hormones. The spleen stores a large blood volume and its flow is regulated by sympathetic nerves. The liver receives substantial blood flow from the hepatic artery and portal vein, and its flow is regulated by various systemic and local factors. Cutaneous circulation regulates heat loss and is controlled by the hypothalamus in response to body temperature changes. The Lewis triple response describes the local vascular response to skin stimuli.
The document discusses Long QT Syndrome (LQTS), an inherited heart condition characterized by an abnormally prolonged QT interval on electrocardiograms. It describes the causes and types of LQTS, including LQT1, LQT2 and LQT3, which are associated with different genetic mutations and ECG patterns. The main symptoms of LQTS are syncope and cardiac arrest, typically in children or teenagers. Diagnosis involves measuring the QT interval and identifying risk factors. Treatment focuses on beta-blockers, lifestyle changes and implantable cardioverter-defibrillators for high-risk patients.
Effect of electrolytes on cardiac rhythmAhmad Thanin
Electrolyte imbalances can cause cardiac arrhythmias by disrupting the normal ionic balance across cardiac cell membranes. Common electrolyte disorders include hyperkalemia, hypokalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. Each has distinct ECG patterns - for example, hyperkalemia causes tall peaked T waves while hypokalemia causes ST depression and flattened T waves. Treatment involves replacing the deficient electrolyte or removing excess electrolytes.
This document discusses the electrical activity and action potentials of cardiac muscle cells. It begins by defining excitability and describing the resting membrane potentials of different cardiac tissues. It then explains the phases of the cardiac action potential in detail, including initial depolarization, initial repolarization, plateau, and final repolarization. The document also discusses the ionic basis and rhythmicity of cardiac muscle, pacemaker cells in the sinoatrial node, and differences between cardiac and nerve cell action potentials.
The document discusses atrio-ventricular (AV) block, which refers to delays or interruptions in the conduction pathway between the atria and ventricles of the heart. There are several types of AV block defined by the degree of conduction block, including first-degree, second-degree Mobitz types I and II, and third-degree AV block. The causes, ECG characteristics, and descriptions of each type of AV block are provided. The document emphasizes practicing ECG interpretation to determine the type of cardiac dysrhythmia.
This document discusses the physiology of cardiac muscle and the electrophysiology of normal cardiac rhythm. It covers topics like the cardiac action potential, impulse formation and conduction, heterogeneity of action potentials in the heart, and mechanisms of cardiac arrhythmias. The roles of ion channels and the control of rhythmicity by nerves are described. Factors that can precipitate arrhythmias are also listed.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the anatomy and physiology of the cardiac conduction system and the mechanisms of cardiac arrhythmias. It describes the following:
1. The location and function of the sinoatrial node, atrioventricular node, bundle of His, bundle branches and Purkinje fibers that make up the cardiac conduction system.
2. The mechanisms that can cause arrhythmias including disorders of impulse formation like abnormal automaticity and triggered activity, as well as disorders of impulse conduction like reentry.
3. Specific arrhythmias like atrial flutter and fibrillation that are caused by reentry mechanisms in the atria, and how conditions like ion channel abnormalities and electrical remodeling can contribute to these arrhythm
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Cardiac arrhythmias occur frequently in ICU patients, with the most common being sinus tachycardia. Arrhythmias are often seen in patients with structural heart disease and can be exacerbated by critical illness. Management involves treating any imbalances that may be triggering the arrhythmia as well as directed medical therapy. Arrhythmias in the ICU represent a major source of morbidity and increased length of stay.
Cardiac arrhythmias are abnormalities in the heart's rhythm. There are two main types: bradycardia, a slow heart rate, and tachycardia, a fast heart rate. Various arrhythmias are described including sinus bradycardia, heart block, atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ventricular fibrillation, and ventricular tachycardia. Treatment depends on the type of arrhythmia and may include medication, cardioversion, ablation, or pacemaker implantation. Diagnosis involves ECG, echocardiogram, blood tests, and other cardiac tests. Lifestyle changes and avoiding arrhythmia triggers can help management.
Cardiac arrhythmias occur when there is an abnormal heart rhythm or change from the normal sequence of electrical impulses causing the heart to beat too fast, too slow, or irregularly. The seminar report discusses the epidemiology, genetics, pathophysiology, signs and symptoms, and drug treatments for cardiac arrhythmias. Key genetic factors discussed include mutations in ion channel genes causing long QT syndrome, short QT syndrome, and Brugada syndrome. Drug treatments are classified based on their mechanism of action including class I-IV drugs that block sodium, calcium, potassium channels or have beta-blocking effects.
- 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 electrical properties of cardiac muscles including ventricular, SA node, and atrial action potentials. It examines the SA node action potential and the effect of the autonomic nervous system on the SA node action potential. Finally, it looks at ventricular action potentials and refractory periods.
This document discusses the properties of cardiac muscle. It outlines the electrical properties of excitability including resting membrane potential, action potential, and pacemaker potential. It also mentions conductivity and autorythmicity demonstrated by the Stannius ligature experiment and production of idioventricular rhythm. The mechanical properties discussed include contractility, the all or none law, refractory periods, the staircase phenomenon, the length tension relationship defined by Frank-Starling's law, and the force velocity relationship where increased load decreases velocity of shortening.
Various coronary physiological measurements can be made in the cardiac catheterization laboratory using sensor-tipped guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relative coronary flow reserve, and the pressure-derived fractional flow reserve of the myocardium. Ambiguity regarding abnormal microcirculation has been reduced or eliminated with measurements of relative coronary flow reserve and fractional flow reserve. The role of microvascular flow impairment can be separately determined with coronary flow velocity reserve measurements. In addition to lesion assessment before and after intervention, emerging applications of coronary physiology include the determination of physiological responses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute myocardial infarction. Measurements of coronary physiology in the catheterization laboratory provide objective data that complement angiography for clinical decision-making
The document discusses regulation of coronary blood flow. It begins by outlining the coronary vessels and blood supply to the heart. The coronary arteries arise from the aorta and branch within the heart muscle to supply it with blood. Coronary blood flow is highest during cardiac diastole when the heart muscle is relaxed and lowest during systole when the heart contracts. Multiple factors influence coronary blood flow including physical factors like blood pressure, chemical factors such as local metabolic needs, and neural and hormonal control. The heart has an autoregulatory mechanism to maintain adequate blood flow over a range of perfusion pressures. Disruptions to this system can lead to pathological thrombosis in the coronary arteries and consequences like myocardial infarction.
This document provides an introduction to cardiac action potentials. It describes the five phases of a cardiac action potential: phase 4 (resting phase), phase 0 (depolarization), phase 1 (early repolarization), phase 2 (plateau phase), and phase 3 (rapid repolarization). It explains that cardiac action potentials are initiated by the sinoatrial node and involve movements of ions like sodium, calcium, and potassium through ion channels, causing changes in the cell's membrane potential. These potential changes can be recorded as an electrocardiogram to monitor the heart's electrical activity.
This document discusses basic terms in electrophysiology and the properties of cardiac cells. It describes two main types of cardiac cells: electrical cells that make up the conduction system and possess the properties of automaticity, excitability, and conductivity; and myocardial cells that make up the muscular walls and possess contractility and extensibility. It explains that cardiac cells at rest are polarized but become depolarized when an electrical impulse causes ions to cross the cell membrane, generating an action potential. The action potential curve consists of five phases: resting phase, rapid depolarization, plateau phase mediated by slow calcium channels, and rapid repolarization as ions return to their resting state.
This document provides an overview of cardiac arrhythmias, including definitions and descriptions of normal sinus rhythm and various arrhythmias. It discusses the cardiac conduction system and mechanisms that can cause arrhythmias, such as abnormal impulse formation or conduction. Specific arrhythmias summarized include sinus bradycardia, sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. For each arrhythmia, the document provides information on heart rate, rhythm, P wave presence/morphology, and other ECG characteristics.
This document discusses cardiac arrhythmias and the cardiac conduction system. It describes the sinoatrial node, atrioventricular node, and Purkinje fibers, which make up the cardiac conduction system. Causes of arrhythmias include enhanced automaticity, triggered activity, and re-entry. Various arrhythmias are described including sinus bradycardia, premature atrial contractions, atrial fibrillation, premature ventricular contractions, ventricular tachycardia, and different types of atrioventricular block. The electrocardiogram is discussed as a tool to evaluate heart rate, intervals, waves, and diagnose arrhythmias.
The splanchnic circulation supplies blood to the gastrointestinal tract, spleen, and liver. It has unique features like blood from the mesenteric bed and spleen draining primarily to the liver via the portal vein. Mesenteric blood flow is regulated by local autoregulation, gastrointestinal activity, nerves, and chemicals like hormones. The spleen stores a large blood volume and its flow is regulated by sympathetic nerves. The liver receives substantial blood flow from the hepatic artery and portal vein, and its flow is regulated by various systemic and local factors. Cutaneous circulation regulates heat loss and is controlled by the hypothalamus in response to body temperature changes. The Lewis triple response describes the local vascular response to skin stimuli.
The document discusses Long QT Syndrome (LQTS), an inherited heart condition characterized by an abnormally prolonged QT interval on electrocardiograms. It describes the causes and types of LQTS, including LQT1, LQT2 and LQT3, which are associated with different genetic mutations and ECG patterns. The main symptoms of LQTS are syncope and cardiac arrest, typically in children or teenagers. Diagnosis involves measuring the QT interval and identifying risk factors. Treatment focuses on beta-blockers, lifestyle changes and implantable cardioverter-defibrillators for high-risk patients.
Effect of electrolytes on cardiac rhythmAhmad Thanin
Electrolyte imbalances can cause cardiac arrhythmias by disrupting the normal ionic balance across cardiac cell membranes. Common electrolyte disorders include hyperkalemia, hypokalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. Each has distinct ECG patterns - for example, hyperkalemia causes tall peaked T waves while hypokalemia causes ST depression and flattened T waves. Treatment involves replacing the deficient electrolyte or removing excess electrolytes.
This document discusses the electrical activity and action potentials of cardiac muscle cells. It begins by defining excitability and describing the resting membrane potentials of different cardiac tissues. It then explains the phases of the cardiac action potential in detail, including initial depolarization, initial repolarization, plateau, and final repolarization. The document also discusses the ionic basis and rhythmicity of cardiac muscle, pacemaker cells in the sinoatrial node, and differences between cardiac and nerve cell action potentials.
The document discusses atrio-ventricular (AV) block, which refers to delays or interruptions in the conduction pathway between the atria and ventricles of the heart. There are several types of AV block defined by the degree of conduction block, including first-degree, second-degree Mobitz types I and II, and third-degree AV block. The causes, ECG characteristics, and descriptions of each type of AV block are provided. The document emphasizes practicing ECG interpretation to determine the type of cardiac dysrhythmia.
This document discusses the physiology of cardiac muscle and the electrophysiology of normal cardiac rhythm. It covers topics like the cardiac action potential, impulse formation and conduction, heterogeneity of action potentials in the heart, and mechanisms of cardiac arrhythmias. The roles of ion channels and the control of rhythmicity by nerves are described. Factors that can precipitate arrhythmias are also listed.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the anatomy and physiology of the cardiac conduction system and the mechanisms of cardiac arrhythmias. It describes the following:
1. The location and function of the sinoatrial node, atrioventricular node, bundle of His, bundle branches and Purkinje fibers that make up the cardiac conduction system.
2. The mechanisms that can cause arrhythmias including disorders of impulse formation like abnormal automaticity and triggered activity, as well as disorders of impulse conduction like reentry.
3. Specific arrhythmias like atrial flutter and fibrillation that are caused by reentry mechanisms in the atria, and how conditions like ion channel abnormalities and electrical remodeling can contribute to these arrhythm
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Cardiac arrhythmias occur frequently in ICU patients, with the most common being sinus tachycardia. Arrhythmias are often seen in patients with structural heart disease and can be exacerbated by critical illness. Management involves treating any imbalances that may be triggering the arrhythmia as well as directed medical therapy. Arrhythmias in the ICU represent a major source of morbidity and increased length of stay.
Cardiac arrhythmias are abnormalities in the heart's rhythm. There are two main types: bradycardia, a slow heart rate, and tachycardia, a fast heart rate. Various arrhythmias are described including sinus bradycardia, heart block, atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ventricular fibrillation, and ventricular tachycardia. Treatment depends on the type of arrhythmia and may include medication, cardioversion, ablation, or pacemaker implantation. Diagnosis involves ECG, echocardiogram, blood tests, and other cardiac tests. Lifestyle changes and avoiding arrhythmia triggers can help management.
Cardiac arrhythmias occur when there is an abnormal heart rhythm or change from the normal sequence of electrical impulses causing the heart to beat too fast, too slow, or irregularly. The seminar report discusses the epidemiology, genetics, pathophysiology, signs and symptoms, and drug treatments for cardiac arrhythmias. Key genetic factors discussed include mutations in ion channel genes causing long QT syndrome, short QT syndrome, and Brugada syndrome. Drug treatments are classified based on their mechanism of action including class I-IV drugs that block sodium, calcium, potassium channels or have beta-blocking effects.
- 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 electrical properties of cardiac muscles including ventricular, SA node, and atrial action potentials. It examines the SA node action potential and the effect of the autonomic nervous system on the SA node action potential. Finally, it looks at ventricular action potentials and refractory periods.
This document discusses the properties of cardiac muscle. It outlines the electrical properties of excitability including resting membrane potential, action potential, and pacemaker potential. It also mentions conductivity and autorythmicity demonstrated by the Stannius ligature experiment and production of idioventricular rhythm. The mechanical properties discussed include contractility, the all or none law, refractory periods, the staircase phenomenon, the length tension relationship defined by Frank-Starling's law, and the force velocity relationship where increased load decreases velocity of shortening.
This document provides an overview of cardiac muscle structure and function. It defines key terms related to the properties of cardiac muscle such as rhythmicity, excitability, conductivity, and contractility. It describes the cardiac syncytium and normal conduction pathway in the heart. It explains excitation-contraction coupling in cardiac muscle and compares it to skeletal muscle. It also compares action potentials in the sinoatrial node and ventricular muscle. Finally, it discusses the significance of the plateau and refractory period in ventricular muscle action potentials.
The document discusses the structure and function of the cardiac muscle and heart. It describes the heart chambers, valves, and blood flow through the heart. It explains that the heart pumps blood through contraction and relaxation in a cardiac cycle. It details the conducting system of the heart which generates and spreads the electrical impulse for heart contraction. This includes the sinoatrial node, atrioventricular node, bundle of His, and Purkinje fibers. It notes that cardiac muscle cells are striated like skeletal muscle but have specialized ion channels and gap junctions allowing rapid impulse transmission.
Structure of cardiac muscle excitation contraction coupling properties of car...Rajesh Goit
This document summarizes the structure and properties of cardiac muscle. It describes the three types of cardiac muscle - atrial, ventricular, and specialized excitatory and conductive fibers. It explains that cardiac muscle contracts similarly to skeletal muscle but with a longer duration. The document also notes that cardiac muscle fibers are interconnected in a lattice formation and contain the same actin and myosin filaments as skeletal muscle. Finally, it lists and briefly describes several key properties of cardiac muscle, including automaticity, rhythmicity, contractibility, and its functioning as a syncytium.
Cardiac muscle consists of cross-striated cardiomyocytes that are joined end-to-end by specialized junctions called intercalated discs. These discs contain desmosomes and gap junctions. Desmosomes bind cells together while gap junctions allow action potentials to spread between cells, causing the heart to contract as a syncytium. Within intercalated discs are also Purkinje fibers, which are modified cardiac muscle cells that conduct electrical signals faster than normal cardiomyocytes. This allows for coordinated contraction of the heart.
The document summarizes cardiac physiology, including:
1) The circulatory system consists of the heart, blood vessels, and blood, with the heart serving as a pump that establishes blood pressure.
2) The heart has two main functions - generating blood pressure and routing blood flow between the pulmonary and systemic circulations to ensure one-way flow.
3) An electrocardiogram (ECG) provides a non-invasive record of the heart's electrical activity and can help identify conditions like arrhythmias.
This document discusses cardiac myocytes and the cardiac action potential. It covers topics such as cardiac myofilaments, cell-cell conduction, excitation-contraction coupling, the sliding filament theory, resting membrane potential, ion pumps and exchangers, and the action potential of pacemaker and ventricular cells.
Brief description of drugs which are used to alter cardiac action potential in arrythmic patients. It focuses on understanding of action potentials in short descriptions as possible.
This document summarizes a review on ivabradine, a drug that lowers heart rate by selectively inhibiting funny (If) channels in the sinoatrial node. It discusses the pathophysiology of elevated heart rate and heart rate control. Ivabradine is a selective If current inhibitor that reduces heart rate without affecting contractility or blood pressure. Clinical trials such as BEAUTIFUL showed ivabradine reduced rates of hospitalization for heart failure and myocardial infarction in patients with coronary artery disease and heart rates over 70 beats per minute. Ivabradine may provide benefit as an add-on to standard heart failure therapy in select patient groups.
The cardiovascular system includes the heart and blood vessels. The heart weighs 200-400 grams and pumps around 7,751 litres of blood daily. It is located behind the sternum and is surrounded by membranes. Blood enters and exits the heart through major vessels while valves regulate flow between chambers. The heart muscle generates electrical impulses and contractions to circulate blood throughout the body. Cardiac output is regulated intrinsically through preload and afterload as well as extrinsically through the nervous and endocrine systems.
Cardiac muscle tissue is found only in the walls of the heart. It has a unique branching and weaving structure with overlapping regions between fibers called intercalated discs. Each cardiac muscle fiber contains one centrally located nucleus and lighter striations than skeletal muscle. Contractions are rhythmic and involuntary due to inherent pacemaker cells in the heart.
Cardiac Pacemakers: Function,
Troubleshooting, and Management
Part 1 of a 2-Part Series
Siva K. Mulpuru, MD, Malini Madhavan, MBBS, Christopher J. McLeod, MBCHB, PHD, Yong-Mei Cha, MD,
Paul A. Friedman, MD
Perioperative managment of neurological patientsnagy shenoda
This document provides guidance on the perioperative management of patients with various neurological diseases. It outlines considerations for patients with cerebrovascular stroke, epilepsy, neuromuscular disorders, muscle diseases, peripheral neuropathies, Parkinson's disease, multiple sclerosis, and Alzheimer's disease. Key recommendations include continuing antiplatelet therapies for stroke patients during many procedures, maintaining epilepsy patients' regular anticonvulsant medications, assessing respiratory function for neuromuscular disease patients, and timing Parkinson's disease medications around surgery to avoid complications. Careful planning is needed to minimize risks for each condition.
This document discusses an echocardiogram of a patient with a quadricuspid pulmonary valve. The echocardiogram shows opening of the pulmonary valve during atrial contraction, indicating low pulmonary artery pressure and ruling out pulmonary stenosis. Pulmonary flow Doppler measurements initially showed a gradient of 29 mmHg but were underestimated based on M-mode findings and misalignment of the pulmonary jet. Repeating the measurement from a subcostal view yielded a gradient of 41 mmHg, still considered an underestimate.
pre and post transplant echo , contrast echo Leonardo Vinci
This document discusses the use of contrast echocardiography for pre- and post-operative evaluation of heart transplant patients. It outlines how echocardiography is used to evaluate donor hearts prior to transplantation, assess for complications immediately after transplantation, and monitor cardiac structure and function long-term. Contrast echocardiography helps improve endocardial border visualization and allows for more accurate assessment of parameters like ventricular volumes and ejection fraction both before and after transplantation. The document also discusses the role of echocardiography in diagnosing issues like rejection and transplant coronary artery disease.
The document discusses updates to guidelines for defining and diagnosing pulmonary hypertension from the 5th World Symposium on Pulmonary Hypertension held in 2013. Key points include: maintaining the general definition of PH as a mPAP over 25 mm Hg, collecting more data on borderline PH cases with mPAP between 21-24 mm Hg, and not reintroducing exercise-induced PH criteria due to a lack of suitable definition. Recommendations are also provided on measuring and interpreting pulmonary vascular resistance and pulmonary artery wedge pressure during right heart catheterization.
Anesthesia for coronary artery bypass graftingaparna jayara
Anesthesia for coronary artery bypass grafting (CABG) has evolved significantly since the first open heart surgery in 1952. Key developments include the first successful CABG without bypass in 1961, widespread use of cardiopulmonary bypass in the 1960s-1970s, and the clinical introduction of off-pump CABG and minimally invasive techniques in the late 1990s. CABG is commonly performed for symptomatic multi-vessel coronary artery disease. Precise intraoperative monitoring and optimization of patient comorbidities are important for reducing complications of CABG.
The SIGNIFY trial investigated the effects of ivabradine in 19,102 patients with stable coronary artery disease without heart failure. It found that ivabradine reduced heart rate but did not improve cardiovascular outcomes and increased adverse events compared to placebo. However, ivabradine was found to improve angina symptoms in patients who had angina at baseline. The results contrast with previous studies and suggest that reducing heart rate may not benefit stable coronary artery disease as it does heart failure.
This document provides an outline for a lecture on basic cardiac electrophysiology. It covers:
1. The anatomy and physiology of the heart and cardiac myocytes.
2. Electrical activity in cardiac myocytes, including ion concentrations, membrane potential, and action potentials.
3. Cardiac pacemakers, including the sinoatrial node, factors affecting pacemaker firing rates, and overdrive suppression.
4. Cardiac impulse conduction, including the normal conduction pathway and factors affecting conduction velocity.
1) The document discusses the electrophysiological considerations of cardiac contraction, including the parts of the cardiac conduction system, spread of conduction through the heart, cardiac action potentials, and ECG.
2) It describes the key components of the conduction system - the sinoatrial node, atrioventricular node, bundle of His, Purkinje fibers - and their roles in generating and conducting cardiac impulses.
3) It explains cardiac action potentials, including the differences between fast response and slow response potentials, the ion channels involved in each phase, and how they support coordinated heart contraction and relaxation.
Anti-arrhythmic drugs can be used to terminate or prevent arrhythmias. They work by blocking ion channels involved in cardiac action potentials. Class 1 drugs block sodium channels, prolonging the action potential. Class 1A drugs like procainamide and quinidine prolong the action potential. Class 1B drug lidocaine has rapid sodium channel blocking kinetics. Class 2 drugs like esmolol are beta blockers that reduce automaticity. Class 3 drugs like amiodarone and dofetilide block potassium channels, prolonging the action potential. Calcium channel blockers like verapamil are Class 4 drugs that suppress arrhythmias by blocking calcium channels, especially in the SA and AV nodes. Choice of drug depends
2009 terni, università di medicina, i farmaci nel trattamento delle tachicar...Centro Diagnostico Nardi
This document discusses drugs used to treat ventricular tachyarrhythmias. It begins by describing cardiac electrophysiology, including the cardiac action potential and ion channels. It then discusses various classes of antiarrhythmic drugs, including class I drugs that block sodium channels, class II drugs that block beta-adrenergic receptors, class III drugs that prolong the action potential by blocking potassium channels, and class IV drugs that block calcium channels. The document emphasizes that while antiarrhythmic drugs can effectively treat arrhythmias, they may also cause arrhythmias as a side effect if not carefully monitored.
The document summarizes the anatomy and physiology of the cardiac conduction system and mechanisms of arrhythmia formation. It describes:
1) The key structures of the cardiac conduction system including the sinoatrial node, atrioventricular node, bundle of His, bundle branches and Purkinje fibers.
2) The electrophysiology of the cardiac action potential and the roles of ion channels and intracellular calcium handling.
3) The two main mechanisms that can cause arrhythmias - disorders of impulse formation from abnormal automaticity or triggered activity, and disorders of impulse conduction from conduction block or reentry. Abnormalities in calcium regulation are implicated in several arrhythmia conditions.
This slide set provides an introduction at new learner to intermediate level to some of the most common drugs that are used clinically to modulate the rate and force of contraction of the heart. Created by Prof. JA Peters, University of Dundee School of Medicine.
This document provides an overview of tachyarrhythmias, including:
- Definitions of tachyarrhythmias as disturbances in heart rhythm over 100 beats per minute.
- Anatomy and electrophysiology of the heart's conduction system.
- Mechanisms of arrhythmogenesis including disorders of impulse formation and conduction.
- Diagnostic approach involving history, physical exam, ECGs, monitoring, and invasive studies.
- Treatment modalities including antiarrhythmic drugs and ablation procedures for various specific arrhythmias like atrial fibrillation, supraventricular tachycardias, and ventricular arrhythmias.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
The document describes the physiology of the heart, including its muscular wall, conductive system, cardiac action potential, and excitation-contraction coupling. It discusses how electrical signals are initiated in the heart and conducted between cells, causing contraction. Finally, it summarizes how different anesthetics can impact the heart's electrical and mechanical functions by altering ion channels and calcium handling.
Dronedarone is a newer antiarrhythmic drug that is structurally similar to amiodarone but was designed to have fewer side effects. It blocks multiple ion channels including potassium, sodium, and calcium channels. This results in antiarrhythmic effects such as reducing automaticity, prolonging the action potential duration, and slowing conduction velocity. However, dronedarone has a better safety profile compared to amiodarone with less risks of thyroid and lung problems.
This document discusses antiarrhythmic drugs, including their classification, mechanisms of action, uses, and side effects. It begins by covering the electrophysiology of the heart and types of cardiac tissue. It then details the Vaughan-Williams classification system for antiarrhythmic drugs, including Class I sodium channel blockers like quinidine, Class II beta blockers, Class III potassium channel blockers, and Class IV calcium channel blockers. Specific drugs are discussed within each class. The document aims to provide guidelines for the treatment of cardiac arrhythmias.
This document provides an overview of cardiovascular physiology and ECG monitoring. It discusses the coronary circulation and conduction system of the heart. It describes the different cardiac cell types and their functions. Topics covered include the action potential, automaticity, conduction speed, the phases of the cardiac cycle, and pressure-volume loops. The document also discusses regulation of the cardiovascular system through neural mechanisms, hormones, and the renin-angiotensin-aldosterone system. Finally, it provides guidance on interpreting ECGs, including identifying rates, durations, abnormalities, and determining the location of myocardial infarction.
The document discusses the heart and cardiac arrhythmias. It begins by describing the structure and function of the heart, including the specialized conducting system that coordinates contraction and pumping of blood. It then discusses factors that can disrupt normal cardiac rhythm and cause arrhythmias through various mechanisms like changes in automaticity, triggered activity, and abnormal conduction. Various types of arrhythmias are described like tachycardias and bradycardias. Treatment of arrhythmias aims to restore normal rhythm and cardiac output when compromised. Antiarrhythmic drugs are classified based on their mechanisms of action like sodium channel blockade, calcium channel blockade, and beta blockade.
1. The cardiac electrical system is led by the sinoatrial node which acts as the primary pacemaker at 60 beats per minute. The atrioventricular node and Purkinje fibers can also act as secondary and tertiary pacemakers.
2. There are different types of action potentials in cardiac muscle depending on the region. Sinoatrial and atrioventricular nodes have slow action potentials without phases 1 and 2 due to different ion channel expression compared to ventricular myocytes.
3. Drugs like calcium channel blockers, potassium channel blockers, sodium channel blockers, and beta blockers can be used to pharmacologically manipulate heart rate and conduction velocity by affecting ion channels.
This document provides an overview of cardiovascular physiology. It begins with a brief history of the field and introduces the concept of the heart as a pump. It then discusses the anatomy of the heart including the chambers, valves, conduction system, and cardiac muscle structure. Next, it covers the autorhythmic pacemaker cells, cardiac action potentials, excitation-contraction coupling, and the cardiac cycle. It also discusses neural and hormonal control of the heart, coronary circulation, hemodynamic calculations, and cardiac reflexes.
Treatment of various arrhythmias can involve pharmacological, device-based, surgical, and interventional approaches depending on the type of arrhythmia. For paroxysmal supraventricular tachycardia, acute management may include vagal maneuvers, adenosine, or beta blockers. Long term management can be ablation of the accessory pathway or medications like verapamil, diltiazem, and beta blockers. Atrial flutter is treated with antiarrhythmic drugs or cardioversion while atrial fibrillation requires rate or rhythm control strategies.
This document provides an overview of electrocardiography (ECG) and arrhythmias. It discusses what an ECG is and how it works, lead placements, normal ECG components and intervals. Mechanisms of arrhythmias like automaticity, triggered activity and reentry are explained. Specific arrhythmias like ventricular tachycardia, atrial fibrillation, multifocal atrial tachycardia and accessory pathway tachycardias are described. Clinical uses of ECG and limitations are noted. Management of unstable tachycardic patients and various arrhythmias is also outlined.
Vt in normal and abnormal hearts my ppt copyRahul Chalwade
This document discusses ventricular tachycardia (VT) in normal and abnormal hearts. It begins by defining VT and describing its classification based on ECG morphology, duration, mechanism, and etiology. In normal hearts, VT can be due to reentry, automaticity, or triggered activity. Common types of idiopathic VT in normal hearts include outflow tract VT, fascicular VT, and automatic VT. Outflow tract VT often originates from the right ventricular outflow tract and has a good prognosis. Fascicular VT originates from the left posterior fascicle. In abnormal hearts post-myocardial infarction, VT is commonly due to reentry within scar tissue. The 12-lead ECG can provide
Properties of CM, Plateau Potential & Pacemaker.pptxPandian M
Cardiac muscle has unique properties that allow the heart to function as a syncytium.
1) Cardiac cells are branched and joined by intercalated discs containing desmosomes and gap junctions, allowing action potentials to spread between cells.
2) The heart has specialized pacemaker cells in the sinoatrial node that generate action potentials spontaneously due to unstable membrane potentials and funny channels.
3) Cardiac action potentials have a plateau phase due to calcium influx through L-type calcium channels, allowing the heart to contract forcefully for over 200ms.
This document discusses antiarrhythmic drug therapy and summarizes the following key points:
- Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on the cardiac action potential. Classes I-III work by blocking sodium, calcium or potassium channels.
- Class I drugs like quinidine and procainamide work by blocking fast sodium channels, reducing the rate of depolarization. Class II drugs like propranolol are beta blockers that reduce heart rate and conduction velocity.
- Common arrhythmias treated include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardias. Drug choice is based on the arrhythmia type
Similar to Myocardial action potential and Basis of Arrythmogenesis (20)
This document discusses the no-reflow phenomenon, which occurs when restoration of coronary artery patency after procedures like primary percutaneous coronary intervention (PCI) does not translate to improved tissue perfusion. No-reflow occurs in 30% of patients after reperfusion for acute myocardial infarction and is associated with worse outcomes. It is caused by microvascular obstruction from distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Methods to diagnose no-reflow include angiography, coronary Doppler, cardiac MRI, and myocardial contrast echocardiography. Prevention strategies target reducing ischemic time, microvascular spasm, and distal embolization through early reperfusion, pharmacological agents, and ischemic conditioning techniques.
The document discusses various techniques for coronary artery bypass grafting (CABG), including conventional on-pump CABG using cardioplegic arrest and cardiopulmonary bypass (CPB), and minimally invasive techniques like off-pump CABG (OPCAB) and mid-cabinal CABG (MIDCAB) without use of CPB. It summarizes the technical concepts of different graft conduits, procedures like MIDCAB using stabilization devices, and clinical trials comparing on-pump CABG to off-pump techniques. The largest trial found no difference in major cardiovascular outcomes between on-pump and off-pump CABG, though off-pump was associated with less bleeding, transfusions, and acute kidney injury
1. Low flow aortic stenosis can be caused by either low or normal ejection fraction and is an important entity that is often underdiagnosed.
2. Evaluation of low flow AS involves calculating aortic valve area using continuity equation in addition to gradients, as well as tests like dobutamine stress echocardiogram, CT calcium scoring, and novel markers of left ventricular function.
3. Treatment depends on symptom status and severity of stenosis, with aortic valve replacement generally recommended for symptomatic patients or asymptomatic patients with low ejection fraction, even in the presence of low flow and gradients.
Management of hypertrophic cardiomyopathyDeep Chandh
The document discusses the management of hypertrophic cardiomyopathy (HCM). It covers the diagnosis of HCM using echocardiography, cardiac MRI, and genetic testing. Treatment options discussed include medical management with beta blockers and verapamil, as well as interventional strategies like alcohol septal ablation and myectomy surgery to relieve outflow tract obstruction in severe cases. The goal of treatment is to reduce symptoms from LV outflow tract obstruction and prevent sudden cardiac death through risk stratification and ICD placement if needed.
1. The document outlines a 6 step approach to diagnosing and treating vasculitis.
2. Step 1 is to learn to recognize vasculitis based on common features like purpura, pulmonary infiltrates, glomerulonephritis.
3. Step 2 is to rule out secondary causes of vasculitis like infections, malignancies, drugs.
4. Step 3 involves determining the pattern of vessel involvement - large, medium, or small vessels.
This document summarizes newer anticoagulants that are alternatives to traditional agents like heparin and warfarin. It discusses the mechanisms and properties of newer oral anticoagulants like rivaroxaban and dabigatran which directly inhibit thrombin or Factor Xa. Clinical trials showed these drugs were as effective as enoxaparin or warfarin for preventing blood clots after knee or hip surgery with lower rates of bleeding complications. The RE-LY trial found dabigatran 150mg twice daily reduced strokes by 35% compared to warfarin in atrial fibrillation patients.
The document discusses various cases of metabolic and respiratory acidosis and alkalosis. It analyzes each case's primary disorder, compensation mechanism, and any resulting secondary disorder. The cases cover scenarios such as metabolic alkalosis with an adequate compensatory increased PCO2 leading to no secondary disorder. Another example is respiratory acidosis with compensation of increased HCO3 leading to a secondary metabolic alkalosis. The document examines each component of acid-base balance for different clinical presentations.
This document provides an overview of the approach to evaluating and diagnosing ataxia. It begins with definitions of ataxia and discusses tests to differentiate various systems that can cause ataxia-mimicking symptoms. It then covers approaches to evaluating cerebellar ataxia, including assessing mode of onset, progression, focal vs symmetric involvement, and localizing the lesion. Common etiologies of acquired, inherited, autosomal dominant and recessive ataxias are summarized. The document provides a step-wise algorithm for evaluating and categorizing ataxia.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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2. SYNOPSIS
• Anatomy of the Conduction System
• Ion channels and Clinical Implications
• Myocardial Action Potential
• Basis of Arrythmogenesis
• ECG examples of Arrythmias
• Concept of Entrainment
5. SA NODE
• Spindle shaped, 10-20 mm, jxn. Of SVC and
Right Atrium in the sulcus terminalis
• 60% RCA,
• Spindle and spider cells possess pacemaker
characteristics
• Β1, B2, M2 receptors
• Neurotransmitters- Neuropeptide Y, VIP
• Postvagal Tachycardia
7. AV NODE
• Inferior nodal extension,
Compact Portion,
Penetrating bundle
• Koch’s triangle
• AV nodal artery from
crux of RCA (90%)
• Slow propagation
velocity
8. Bundle of HIS
• Continuation of the penetrating bundle of AV
node
• Located in the upper portion of IVS
• Dual blood supply
• Resistant to ishemia
CONDUCTION AV NODE HIS BUNDLE
ATROPINE IMPROVES WORSENS
9. Bundle branches
• Right BB continuation of HIS bundle
• LBB has 2-3 fascicles which are not exactly
bundles, variable anatomy
• LP fascicle resistant to ischemia, dual blood
supply
10. Purkinje Fibres
• Interweaving networks of fibres on the
endocardial surface penetrating 1/3 rd of
endocardium
• Concentrated more at apex and less at base
and papillary muscle tips
• Large surface area and resistant to ischemia
12. Heart Rhythm, Volume 11, Issue 2, Pages 321–
324, February 2014
“ Successful ablation of a narrow complex
tachycardia arising from a left ventricular false
tendon: Mapping and optimizing energy
delivery”
13. Tissues susceptible to ischemia
• SA node
• AV node
• Bundle branches
• HIS bundle, Purkinje fibres resistant to
ischemia
15. Few important concepts on
Nervous distribution
• Sidedness- Right stellate ganglion and vagal nerves
affect the SA node more,
• The left sympathetic and vagal nerves affect the
AV node more
• Tonic vagal stimulation causes greater absolute
reduction in SA rate in presence of tonic
background sympathetic stimulation—
ACCENTUATED ANTAGONISM
• Differential distribution of Sympathetic and
parasympathetic nerves- sympathetic more at
base, PS more in the inferior myocardium
(responsible for vagomimetic effects of Inferior MI)
16. SYNOPSIS
• Anatomy of the Conduction System
• Ion channels and Clinical Implications
• Myocardial Action Potential
• Basis of Arrythmogenesis
• ECG examples of Arrythmias
• Concept of Entrainment
18. Ion Channels
• Named after the Ion like Na,
K, Ca or the NT affecting the
channel like Ik.ach, Ik.atp
• Gating of channels
• Voltage dependence (RMP
of the membrane its
situated on)
• Time dependence
23. Inward Rectifying K+ channels
• I k.ATP ischemic preconditioning, nicorandil
and diazoxide open these channels,
glibenclamide inhibit
• I k.ACH decreases spontaneous
depolarisation in SA node and slows AV
conduction, ADENOSINE increases activity
24. CARDIAC PACEMAKER CHANNEL
• Pacemaker current Funny current “If”
• Encoded by HCN4 gene
• Mutation familial sinus bradycardia
25. CONNEXINS
• Proteins forming the gap junctions which are
responsible for anisotropy in heart
• Connexin 43 abundant in human cardiac
myocardium
MUTATIONS IN:
Carvajal syndrome Desmoplakin
Naxos Disease Plakoglobin
ARVD Plakophilin2
29. SYNOPSIS
• Anatomy of the Conduction System
• Ion channels and Clinical Implications
• Myocardial Action Potential
• Basis of Arrythmogenesis
• ECG examples of Arrythmias
• Concept of Entrainment
31. Heart Rhythm
Volume 11, Issue 7, Pages 1210–19, July 2014
“Synchronization of sinoatrial node pacemaker
cell clocks and its autonomic modulation impart
complexity to heart beating intervals”
32. RESTING MEMBRANE POTENTIAL
• The RMP of a cell is the same as the Nernst
potential of the predominant active ion
channels in the cell
• For Cardiac cells, that which determines the
RMP are the POTASSIUM CHANNELS
• Hence the RMP of a resting cell approximates
– 90 mv (The Nernst potential of K+ channel)
33. Action Potential
• Deviation from RMP as a result of influx and
efflux of ions, leading to increase in positive
charges (Depolarisation) and decrease in
positive charges (Repolarisation)
34. Action potential of the cardiac muscles
• The cardiac action potential is made
of 3 phases:
1. Depolarization:
2. Plateau:
3. Replarization:
35. MAP OF NODE VS MYOCARDIUM
• SA NODE
• AV NODE
• DISEASE MYOCARDIUM
• ATRIAL MUSCLE
• VENTRICULAR MUSCLE
• PURKINJE FIBRE
37. MAP OF MYOCARDIUM
• PHASE 4- THE RMP
• PHASE 0- RAPID UPSTROKE
• PHASE 1- INITIAL DOWNSTROKE
• PHASE 2- PLATEAU
• PHASE 3- FINAL DOWNSTROKE
38.
39. PHASE 4
• 3 MAIN CHANNELS
o Inward rectifying potassium channels-
Potassium efflux helps maintain negativity
o Na-Ca exchanger
o Na-K ATPase
40. PHASE 0
• 2 inward currents
• SUDDEN INCREASE IN MEMBRANE INFLUX OF
Na+
• Stimulus should be enough to take the MP
past the threshold, beyond which “the size of
AP is independent of the strength of the
stimulus- ALL OR NONE RESPONSE”
• Later part of upstroke is contributed by Slow
Inward Ca channel opening
41. • Initial curve- FAST RESPONSE Na channels
Time dependent inactivation, usually close at
around + 60 mv
• Later curve- SLOW RESPONSE L-Ca channels
Activated at around -30 mv, continue into the
plateau phase
Class 1A inhibit
Class IV inhibit
42. Phase 1-Early rapid repolarisation
• Inactivation of inward Na current
• Activation of 3 main outward currents leading
to efflux of positive charges
o K+
o Cl-
o Na/Ca exchanger
• Typical notch
44. Phase 2-Plateau phase
• Competition between the outward and inward
currents lead to Plateau phase
• Steady state phase
45. Phase 3-Final rapid repolarisation
• Time dependent inactivation of Inward L-Ca
current
• Activation of a number of K+ channels-Ikr, Iks,
Ik.ach, Ik.ca-leading to outward K+ current and
loss of positivity return to a more negative
steady state (the RMP)
46.
47. K+ channels-Ikr, Iks, Ik.ach, Ik.ca
Prolongation of plateau phase
Prolongation of action potential
LONG QT
HERG
mutation
Erythromycin
Ketoconazole
48. MAP OF SA & AV NODE
• PHASE 4- SLOW DIASTOLIC DEPOLARISATION
“PACEMAKER POTENTIAL”
• PHASE 0- SLOW UPSTROKE
• PHASE 3- DOWNSTROKE
49.
50. PHASE 4 “PACEMAKER POTENTIAL”
• SLOW DIASTOLIC DEPOLARISATION- “no REST
for SA node, AV node”
• Maintained by Funny currents “If”
• Hyperpolarisation current activated by Na and
K+, Transient Ca2+ channels
• Influenced by adrenergic and cholinergic
neurotransmitters
56. POST REPOLARISATION REFRACTORINESS
• Even after the restoration
of RMP in a cell, it
continues to remain in a
state of refractoriness to
stimuli and hence non
excitable
• This period is called
POST REPOLARISATION
REFRACTORINESS, which is
a time dependent
phenomenon
57. Classification of Antiarrhythmic Drugs
based on Drug Action
CLASS ACTION DRUGS
I. Sodium Channel Blockers
1A. Moderate phase 0 depression and
slowed conduction (2+); prolong
repolarization
Quinidine,
Procainamide,
Disopyramide
1B. Minimal phase 0 depression and slow
conduction (0-1+); shorten
repolarization
Lidocaine
1C. Marked phase 0 depression and slow
conduction (4+); little effect on
repolarization
Flecainide
II. Beta-Adrenergic Blockers Propranolol, esmolol
III. K+ Channel Blockers
(prolong repolarization)
Amiodarone, Sotalol,
Ibutilide
IV. Calcium Channel Blockade Verapamil, Diltiazem
59. Heart Rhythm
Volume 11, Issue 3, Page e1, March 2014
“Propranolol, a β-adrenoreceptor blocker, prevents
arrhythmias also by its sodium channel blocking effect”
60. SYNOPSIS
• Anatomy of the Conduction System
• Ion channels and Clinical Implications
• Myocardial Action Potential
• Basis of Arrythmogenesis
• ECG examples of Arrythmias
• Concept of Entrainment
65. ROLE OF ANS
• Alterations in vagal and sympathetic
innervation and sensitivites to the same,
can lead to heterogeneity within the
myocardium and hence serve a substrate to
various arrthymias
• AUTONOMIC REMODELLING
66. ROLE OF ANS
• Alterations in vagal and sympathetic
innervation and sensitivites to the same,
can lead to heterogeneity within the
myocardium and hence serve a substrate to
various arrthymias
• AUTONOMIC REMODELLING
72. AUTOMATICITY
• Property of a fibre to initiate an impulse
spontaneously, without need for an initial
stimulation
73. Normal Automaticity
• Normal pacemaker mechanism behaving
inappropriately
Eg:
1.Persistent sinus tachycardia at rest
2.Sinus Bradycardia during exercise
74. Abnormal Automaticity
• Escape of a latent pacemaker
• Due to abnormal ionic mechanisms, other
pacemaker sites gain predominance over SA
node
• Secondary to spontaneous submembrane Ca
elevations, abnormal electric and ionic mileu
leading to spontaneous depolarisation
(Eg-Myocardial infarction)
77. PARASYSTOLE
• Fixed rate asynchronously discharging
pacemaker
• Not altered by the dominant rhythm (Entrance
Block)
• Inter discharge interval is multiple of a basic
interval
• May be Phasic or Modulated
80. TRIGGERED ACTIVITY
• Initiated by AFTER DEPOLARISATIONS
o EARLY AFTER DEPOLARISATION
o DELAYED AFTER DEPOLARISATION
Not all after depolarisations reach the threshold
potential (all or none response), but if they do,
they would self perpetuate
81. EARLY AFTER DEPOLARISATION
• TYPE 1 -occurs during PHASE 2 of MAP
• TYPE 2 –occurs during PHASE 3 of MAP
• Substrate-
- prolonged plateau phase (action potential duration)
- leads to excess intracellular calcium,
-invokes a series of pumps (the Na+ pump), causing
depolarisation
82.
83. Egs of EAD
• LONG QT SYNDROME AND ASSOCIATED
VENTRICULAR TACHYCARDIAS (inc. TdP)
- GENETIC CAUSES
- ACQUIRED CAUSES (class Ia and III
antiarrythmics, Macrolide antibiotics)
• Magnesium and Potassium channel openers
like Nicorandil suppress these EADs
87. DELAYED AFTER DEPOLARISATION
• Occur after completion of Phase 4 of MAP
• Activation of calcium sensitive inward current
Eg:
• Mutations in RYR2 gene encoding
Calsequestrinincreased sensitivity of RyR2
channel to catecholaminesDADCPVT
ABNORMAL CALCIUM HANDLING
88.
89. Proposed scheme of events leading to
delayed after depolarizations and triggered tachyarrhythmia
90. CPVT
DAD-mediated CPVT. Mutations in the ryanodine receptor (RyR) result in leakage of Ca2+
from sarcoplasmic reticulum (SR) into cytoplasm.
92. DISORDERS OF IMPULSE CONDUCTION
• Blocks
- tissue blocks, rate dependent blocks
- responsible for some of the bradyarrythmias
• Reentry
- heterogeneity in tissues
- responsible for most of the tachyarrythmias
93. Blocks
• Tissue becomes “inexcitable” and when there
is no escape to the propagating impulse, it
manifests as bradyarrythmias
• Can occur at any level of the conduction
system
• Anatomic reasons (fibrosis-degenerative or as
a consequence to the pathological process)
• Functional reasons (Rate dependent blocks)
94.
95. Rate dependent blocks
• Deceleration dependent blocks
-Reduced ‘spontaneous diastolic depolarisation’ at
slow rates is the cause
-? Role of digitalis
• Tachycardia dependent blocks
-post repolarisation refractoriness (incomplete recovery of
excitabilty when the next impulse arrives) of 1 or the other
bundle branches, is the cause
98. DISORDERS OF IMPULSE CONDUCTION
• Blocks
- tissue blocks, rate dependent blocks
- responsible for some of the bradyarrythmias
• Reentry
- heterogeneity in tissues
- responsible for most of the tachyarrythmias
99. REENTRY
• Heterogeneity in spread of depolaristion
within a tissue is the cause
• Slow and Fast pathways
• Repeated Impulse reentry into the conduction
system through an excitable pathway leads to
sustaining of the tachycardia
reentrant tachycardia/ reciprocating
tachy/circus movement/ echo beat
101. Types of Reentry
• Anatomical reentry
- 2 distinct heterogeneous pathways of
conduction, each with differrent
electrophysiological properties, creating a slow
and a fast pathway
- can occur at level of SA node, Atrium, AV node,
Ventricle, Accessory pathways (WPW pattern)
• Functional reentry
-dispersion of excitability, refractoriness or both
within a tissue
-Egs: Post Infarction, failing heart
105. Atrial Flutter
-TYPICAL FLUTTER,
counterclockwise moving
from caudocranial
direction in the interatrial
septum
-recurrence can occur in
cases of other pathways of
reeentry, specially seen in
cases like ASD with
AFlutter
107. Atrial Fibrillation
-micro entry circuits due
to spatio-temporal
disorganisation within
the atrium
-MULTIPLE WAVELET
HYPOTHESIS
-anatomic remodelling
-electric remodelling of
the atrium
-Role of Micro RNAs
-Ion channel
abnormalities
-Familial AF (KCNQ1)
108.
109. Heart Rhythm Volume 11, Issue 7,
Pages 1229–1232, July 2014
Marshall bundle reentry: A novel type of
macroreentrant atrial tachycardia
110. AV NODAL REENTRY
-Sudden onset and
termination
-Variation in cycle length
“exposes” the AV nodal
heterogeneity and stats
the reentry
•SLOW-FAST pathway
(Typical)
•FAST-SLOW pathway
•SLOW-SLOW pathway
111. AV REENTRY
Location of accessory pathways
-Accessory bundles of
conducting tissue
“Preexcitation”impulses
conducted to ventricles
thru’ these pathways
earlier than the usual
oneWPW PATTERN
117. BRUGADA
SYNDROME
BRUGADA PATTERN
-Phase 2 reentry
-Mutations in genes
encoding Na
+ channels (SCN5A gene)-
>alterations in Na channel
currentheterogeneity in
AP in RV epicardium
-ICDs are the only proven
therapies to avert SCD in
such pts.
118. • Importance of using PROPER ECG ELECTRODE
POSITIONS and HIGH PASS FILTERS (0.05-0.35 HZ)
during a recording of ECG
122. “Rotor Stability Separates Sustained
Ventricular Fibrillation From Self-Terminating
Episodes in Humans”
J Am Coll Cardiol. 2014;63(24):2712-
2721. doi:10.1016/j.jacc.2014.03.037
123. SYNOPSIS
• Anatomy of the Conduction System
• Ion channels and Clinical Implications
• Myocardial Action Potential
• Basis of Arrythmogenesis
• ECG examples of Arrythmias
• Concept of Entrainment
124. OVERDRIVE PACING
• After cessation of pacing,
- It can increase the amplitude and shorten the
cycle length of the complexes (overdrive
acceleration) suggest the mechanism of
arrythmia is DELAYED AFTER DEPOLARISATION
- It can terminate the underlying
tachycardiasuggest the underlying
mechanism of arrythmia is REENTRY
125.
126. ENTRAINMENT
• “En-training” the tachycardia simply means
increasing the rate of tachycardia by pacing
• Resetting of the reentrant circuit with the pacing
induced activation
• Resumption of the intrinsic rate of the
tachycardia when the pacing is stopped
• Implications:
-used to prove the reentrant mechanism of the
tachycardia,
-used to locate the reentrant pathway
127.
128. SUMMARY
• ANATOMY OF CONDUCTION SYSTEM
• IMPORTANT ION CHANNELS AND THEIR
CLINICAL IMPORTANCE
• MYOCARDIAL ACTION POTENTIAL
• MECHANISMS OF ARRYTHMOGENESIS
• FEW CONCEPTS-
Overdrive Pacing, Entrainment,
Drugs Causing And Treating Arrythmias
129. CONCLUSION
“An attempt should be made to study the
basis of each arryhthmia we come across, in
order to terminate it with appropriate
pharmacological/ intervention and also
prevent its recurrence”
130. REFERENCES
• BRAUNWALD TEXTBOOK
• HURST TEXTBOOK
• ZIPES’ ELECTROPHYSIOLOGY
• LITERATURE SEARCH OF 2013-2014 ISSUES
“HEART RHYTHM”, “JACC”
After cesssation of vagal stimulation, the sinus node rate accelrates transiently
GENETIC BASIS OF CARDIAC ARRYTHMIAS
Abnormalities in these….Central to many arryhtmias as we would see later…
We ld see abt them when we study MAP….
How does the sa node know that it should be beating every n th second….
-ATRIAL AND VENTRICULAR MUSCLE-SA AND AV NODE AND DISEASED MYOCARDIUM
DIAGRAM OF BOTH
Very broad concept….
Animal models
Animal models
After a disease process likde MI, Heart failure….
Each will be explained with examples of ECGs…by the end of it, we will be able to trace the underlying mechanism of many of the common arryhtmias we see in clinical practice….understanding the mechanism helps in treating them whetehr pharmacologically or with procedures like RFA…
Biological clock starts behaving inappropriately…
The dominant rhythm modulates the parasystole to slow down or speed up its rate…
Background
Bradycardia dep. Block…Paradoxical situtaion…mechanisms are not known and controversial but fr now….
AS MENTIONED EARLIER, CAN OCCUR AT ANY LEVEL….
MAGNESIUM, VERAPMAIL
Verapamil sensitive….benhassen vt s….
The rotor hypothesis states that VF is maintained by a single intra mural Mother rotor (reentry circuit), which develops blocks and breaks into daughter wavelets causing fibirllation….
Before going into egs of each of these reentrant tachycardias, we will discuss this important concept of entrainment….
IN THE COURSE OF THE PRESENTATION WE VE GINE THRU THE…….