Presented at the Annual Scientific Sessions of the Heart Rhythm Society, Boston, USA, May 2024
History of the development of the concept and many ECG examples
The 2020 ESC Guidelines provide updated recommendations for the diagnosis and management of atrial fibrillation. Key changes include: recommending structured characterization of AF; screening individuals for AF with a referral platform; and routinely collecting patient-reported outcomes to improve care. The guidelines also provide new recommendations about prevention of thromboembolic events, cardioversion, catheter ablation, lifestyle interventions, and management of AF in special patient groups.
This document provides an overview of tachyarrhythmias. It begins by defining arrhythmia and tachycardia. It then discusses the etiology, pathogenesis and mechanisms of tachycardia. It describes the different types of tachyarrhythmias including supraventricular tachycardia involving the atria, AV node, and ventricular tachycardia. For each type, it provides details on definition, signs and symptoms, ECG findings, etiology, and treatment approaches. It specifically addresses atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, Wolff-Parkinson-White syndrome, premature ventricular contractions, ventricular tachycardia, and ventricular fib
This document provides an overview of various types of arrhythmias including their typical presentation, underlying causes, characteristic ECG patterns, and treatment approaches. Key types are discussed such as sinus tachycardia, atrial fibrillation, various degrees of heart block, premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, and asystole. For each, the rate, P wave, QRS complex, conduction, and rhythm are defined and potential causes and management strategies are outlined. The document serves as a guide for clinicians in identifying and treating different cardiac arrhythmias.
This document summarizes different types of cardiac arrhythmias including tachyarrhythmias and ventricular tachycardia. It discusses the mechanisms, classifications, diagnoses and treatments of supraventricular tachycardia including atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia and AV reentrant tachycardia. It also covers ventricular tachycardia mechanisms including triggered activity, enhanced automaticity and reentry. Management strategies for acute and long term treatment of these arrhythmias are provided including electrical cardioversion, antiarrhythmic drug therapy and catheter ablation procedures.
- Left bundle branch block (LBBB) is caused by conditions that damage the left bundle branch, such as hypertension, dilated cardiomyopathy, and ischemic heart disease.
- LBBB is diagnosed based on criteria including a QRS duration of over 120ms and abnormal ST segment and T wave patterns.
- The prognosis of LBBB depends on any underlying heart conditions, with LBBB increasing the risk of mortality. LBBB may resolve temporarily following a premature ventricular contraction due to resetting of the conduction system.
The document provides information about various cardiac conditions that can be identified on ECGs, echocardiograms, chest x-rays and other cardiac tests. It describes the findings and diagnoses for 12 different clinical cases, including polymorphic atrial tachycardia, preexcited atrial fibrillation, AV nodal reentrant tachycardia, Brugada syndrome, R-on-T phenomenon, hypokalemia, catecholaminergic polymorphic ventricular tachycardia, atrial lead dislodgment, atrial flutter, pulmonary and aortic pressures in ventricular septal defect, and intra-aortic balloon pump positioning.
Management of vt vf storm in advanced heart failuredrucsamal
This document discusses the management of ventricular tachycardia (VT) and ventricular fibrillation (VF) storm in advanced heart failure. It defines VT/VF storm and outlines potential substrate and trigger mechanisms. It recommends beta-blockers and amiodarone as first-line antiarrhythmic therapies. Sedation or general anesthesia may be needed when antiarrhythmic drugs fail. Left ventricular assist devices are preferable to IV inotropes for hemodynamic support. Cardiac sympathetic denervation through thoracic epidural anesthesia or stellate ganglion block/ganglionectomy has also been used successfully in some cases.
1. The document discusses the management of ventricular septal defects (VSD), including their natural history, evaluation, indications for surgical intervention, surgical approaches, and outcomes.
2. Key points include that smaller VSDs often close spontaneously while larger defects have risks of pulmonary hypertension, heart failure, and death if left unrepaired. Evaluation involves assessing defect size and location by echocardiogram and measuring pulmonary pressures.
3. Surgical closure is generally indicated for moderate to large VSDs, those with pulmonary hypertension, aortic valve prolapse, or those not closing on their own in infancy. The timing of closure depends on defect size and symptoms.
The 2020 ESC Guidelines provide updated recommendations for the diagnosis and management of atrial fibrillation. Key changes include: recommending structured characterization of AF; screening individuals for AF with a referral platform; and routinely collecting patient-reported outcomes to improve care. The guidelines also provide new recommendations about prevention of thromboembolic events, cardioversion, catheter ablation, lifestyle interventions, and management of AF in special patient groups.
This document provides an overview of tachyarrhythmias. It begins by defining arrhythmia and tachycardia. It then discusses the etiology, pathogenesis and mechanisms of tachycardia. It describes the different types of tachyarrhythmias including supraventricular tachycardia involving the atria, AV node, and ventricular tachycardia. For each type, it provides details on definition, signs and symptoms, ECG findings, etiology, and treatment approaches. It specifically addresses atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, Wolff-Parkinson-White syndrome, premature ventricular contractions, ventricular tachycardia, and ventricular fib
This document provides an overview of various types of arrhythmias including their typical presentation, underlying causes, characteristic ECG patterns, and treatment approaches. Key types are discussed such as sinus tachycardia, atrial fibrillation, various degrees of heart block, premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, and asystole. For each, the rate, P wave, QRS complex, conduction, and rhythm are defined and potential causes and management strategies are outlined. The document serves as a guide for clinicians in identifying and treating different cardiac arrhythmias.
This document summarizes different types of cardiac arrhythmias including tachyarrhythmias and ventricular tachycardia. It discusses the mechanisms, classifications, diagnoses and treatments of supraventricular tachycardia including atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia and AV reentrant tachycardia. It also covers ventricular tachycardia mechanisms including triggered activity, enhanced automaticity and reentry. Management strategies for acute and long term treatment of these arrhythmias are provided including electrical cardioversion, antiarrhythmic drug therapy and catheter ablation procedures.
- Left bundle branch block (LBBB) is caused by conditions that damage the left bundle branch, such as hypertension, dilated cardiomyopathy, and ischemic heart disease.
- LBBB is diagnosed based on criteria including a QRS duration of over 120ms and abnormal ST segment and T wave patterns.
- The prognosis of LBBB depends on any underlying heart conditions, with LBBB increasing the risk of mortality. LBBB may resolve temporarily following a premature ventricular contraction due to resetting of the conduction system.
The document provides information about various cardiac conditions that can be identified on ECGs, echocardiograms, chest x-rays and other cardiac tests. It describes the findings and diagnoses for 12 different clinical cases, including polymorphic atrial tachycardia, preexcited atrial fibrillation, AV nodal reentrant tachycardia, Brugada syndrome, R-on-T phenomenon, hypokalemia, catecholaminergic polymorphic ventricular tachycardia, atrial lead dislodgment, atrial flutter, pulmonary and aortic pressures in ventricular septal defect, and intra-aortic balloon pump positioning.
Management of vt vf storm in advanced heart failuredrucsamal
This document discusses the management of ventricular tachycardia (VT) and ventricular fibrillation (VF) storm in advanced heart failure. It defines VT/VF storm and outlines potential substrate and trigger mechanisms. It recommends beta-blockers and amiodarone as first-line antiarrhythmic therapies. Sedation or general anesthesia may be needed when antiarrhythmic drugs fail. Left ventricular assist devices are preferable to IV inotropes for hemodynamic support. Cardiac sympathetic denervation through thoracic epidural anesthesia or stellate ganglion block/ganglionectomy has also been used successfully in some cases.
1. The document discusses the management of ventricular septal defects (VSD), including their natural history, evaluation, indications for surgical intervention, surgical approaches, and outcomes.
2. Key points include that smaller VSDs often close spontaneously while larger defects have risks of pulmonary hypertension, heart failure, and death if left unrepaired. Evaluation involves assessing defect size and location by echocardiogram and measuring pulmonary pressures.
3. Surgical closure is generally indicated for moderate to large VSDs, those with pulmonary hypertension, aortic valve prolapse, or those not closing on their own in infancy. The timing of closure depends on defect size and symptoms.
This document provides guidance on the assessment and treatment of arrhythmias presenting in the emergency department. It outlines an approach of first determining hemodynamic stability, then distinguishing between narrow and wide complex tachycardias, and finally determining the specific arrhythmia and appropriate treatment. For unstable patients with any arrhythmia, synchronized direct current cardioversion is recommended. Further treatment is tailored based on whether the arrhythmia has narrow or wide QRS complexes and is regular or irregular.
The ACC/AHA guidelines for cardiac pacemaker and antiarrhythmia device implantation were revised based on advances in technology and new clinical evidence. The guidelines provide evidence-based recommendations (level A, B, C evidence) on appropriate patient selection and device optimization. Indications for implantation were expanded based on studies showing risks of untreated bradyarrhythmias and benefits of pacing. The guidelines emphasize the importance of adequate long-term follow-up to ensure devices provide ongoing clinical benefit.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
This document discusses different types of atrioventricular (AV) blocks. It begins by explaining how the normal conduction pathway between the atria and ventricles prevents direct electrical transmission. There are then three types of AV block described based on severity: 1) First-degree AV block causes a prolonged PR interval but all P waves are conducted, 2) Second-degree AV block causes intermittent conduction with two subtypes - Mobitz type I shows gradual PR prolongation and Mobitz type II has a fixed PR, and 3) Third-degree or complete AV block causes complete dissociation between the atria and ventricles.
This document discusses pre-excitation syndrome, specifically Wolff-Parkinson-White (WPW) syndrome and Lown-Ganong-Levine (LGL) syndrome. It defines pre-excitation syndrome as having a short PR interval and usually an abnormal QRS complex due to an accessory pathway in the cardiac conduction system. Accessory pathways can connect different parts of the heart and have faster conduction velocities than the atrioventricular node. WPW syndrome is the most common type, affecting about 1.5 per 1000 people. Common symptoms include palpitations and chest discomfort due to paroxysmal tachyarrhythmias like atrioventricular reentrant tachycardia. Management involves catheter ablation
Cardiac arrhythmias refer to any abnormality in the rate, regularity, or site of origin of the cardiac electrical impulse. They can be caused by disorders of impulse formation or conduction and may lead to symptoms like palpitations, dizziness, or sudden death. The document discusses various types of arrhythmias including bradyarrhythmias like sinus bradycardia, tachyarrhythmias, and premature beats. Perioperative factors, electrocardiographic features, mechanisms, and management approaches for different arrhythmias are provided. Routine intraoperative measures and considerations for anesthetic management are also outlined.
Heart arrhythmia, also known as irregular heartbeat or cardiac dysrhythmia, is a group of conditions where the heartbeat is irregular, too slow, or too fast. Arrhythmias are broken down into: Slow heartbeat: bradycardia. Fast heartbeat: tachycardia. Irregular heartbeat: flutter or fibrillation.
This document provides an overview of stress echocardiography including objectives, indications, protocols, interpretation, and complications. Key points include: stress echo can evaluate CAD using exercise or pharmacologic stress with dobutamine; it has good sensitivity and specificity for CAD compared to nuclear imaging; and provides prognostic information on cardiac events. Interpretation focuses on changes in wall motion, ejection fraction, and detection of ischemia. Stress echo helps evaluate multiple conditions including viability, valvular disease, and cardiomyopathies.
Cardiac arrhythmias and mapping techniquesSpringer
This document provides an overview of clinical cardiac electrophysiology. It discusses the history and development of the field, including the first recordings of intracardiac electrograms in the 1940s-1960s and the development of programmed electrical stimulation in the 1960s-1970s which allowed investigation of arrhythmia mechanisms. It describes the methodology used in electrophysiology studies, including equipment for recording cardiac activity and electrical stimulation, as well as study protocols for evaluating conduction intervals, refractory periods, and inducing/terminating arrhythmias. It outlines the diagnostic and therapeutic indications for electrophysiology studies in evaluating bradycardias, tachycardias, guiding catheter ablation and medical therapy, and risk stratification of conditions like WPW
This document describes the electrocardiographic features of atrial flutter. It discusses:
- Typical atrial flutter involves a macroreentrant circuit around the tricuspid valve that rotates either clockwise or counterclockwise.
- Atypical flutter has a less well defined circuit and rate over 350 bpm.
- ECG shows sawtooth flutter waves at 250-350 bpm without isoelectric segments. The ventricular response is typically 2:1 but can be variable.
- Counterclockwise flutter has negative flutter waves in inferior leads and positive in V1. Clockwise is reversed.
- Right versus left atrial flutter can be distinguished by the polarity of flutter waves in V1
This document provides an overview of diagnosing myocardial infarction (MI) using electrocardiograms (ECGs). It discusses that an MI is best diagnosed using a 12-lead ECG rather than just a rhythm strip. The 12-lead ECG views the heart from 12 angles and can identify ST elevation in different regions to locate the MI. Anterior MIs involve leads V1-V4, lateral MIs involve leads I, aVL, V5-V6, and inferior MIs involve leads II, III, and aVF. The document walks through examples of anterior, lateral, inferior, and anterolateral MIs.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
This document discusses pacemakers and their implications for anesthesia. It provides a brief history of pacemaker development from large abdominal devices in 1980 to today's small pectoral devices. It covers pacemaker indications, types of pacing modes, factors affecting pacing thresholds, preoperative evaluation, intraoperative management considerations, and the effect of magnet application. Pacemaker dependent patients require ECG monitoring and backup pacing during anesthesia given risks of electromagnetic interference or inappropriate pacing inhibition or triggering.
This document provides an overview of cardiac pacemakers, including:
- A brief history of the development of pacemakers from the first implant in 1958 to modern devices.
- The components, functions, and types of pacemakers including single vs dual chamber and permanent vs temporary pacing.
- Measurements taken during pacemaker implantation like impedance, sensing threshold, and pacing threshold to ensure proper function.
- Modes of pacing like VVI, DDD and indications for different modes. Potential complications of pacemaker therapy are also outlined.
The document serves as an introduction to pacemaker terminology, components, functions and the implantation process.
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
ST segment elevations can be seen in acute myocardial infarction (AMI) but also have other causes. Non-AMI causes of ST elevation include left bundle branch block, left ventricular hypertrophy, pericarditis, Brugada syndrome, and early repolarization. The morphology, distribution, and magnitude of ST elevations, as well as other ECG features, can help differentiate AMI from other causes of ST elevation. It can be challenging to diagnose AMI using ECG criteria alone, as around half of AMI cases present without typical ST elevation patterns.
This presentation describes the emergency department management of sinus tachycardia, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia and ventricular ectopic
This document discusses various types of tachyarrhythmias categorized by their anatomical location and electrophysiological mechanisms. It describes atrial arrhythmias including sinus tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. It also discusses atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia, junctional tachycardia, and ventricular arrhythmias including monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation. Key features and mechanisms of each type are outlined to aid in diagnosis and classification.
1. Ask the patient to say "99" and observe for pulsation.
2. Ask the patient to take a deep breath and hold it. Observe for distension.
3. Ask the patient to bear down and observe for collapse.
Examiner:
1. Observe for pulsation, distension and collapse.
2. Measure the height of pulsation above the sternal angle.
3. Note the character of pulsation.
4. Note any abnormal pulsations.
12/09/2022 26
JVP waves and descents:
12/09/2022 27
- a wave: corresponds to atrial contraction during ventricular filling.
- c wave:
This document discusses atrial fibrillation (AF), including its characteristics, prevalence, types, management, and pathophysiological mechanisms. Some key points include:
- AF is characterized by uncoordinated atrial activation and deterioration of atrial function. Prevalence increases with age, affecting over 8% of those over 80 years old.
- Types include paroxysmal, persistent, and permanent AF based on duration and frequency. Management may involve rate control, cardioversion, or rhythm control strategies.
- Pathophysiological mechanisms involve atrial fibrosis, dilation, and inflammation promoting reentrant wavelets within the atria leading to the uncoordinated activation seen in AF.
1. Right bundle branch block (RBBB) results from a defect in the heart's electrical conduction system where there is a delay or failure of impulses traveling down the right bundle branch.
2. This causes the right ventricle to depolarize more slowly than usual, resulting in a characteristic wide and notched QRS complex on ECG.
3. RBBB is generally not treated unless it progresses to heart block, in which case further testing may be needed.
This ECG shows a woman with alternating right bundle branch block (RBBB) and left bundle branch block (LBBB) during episodes of atrial ectopy. The mechanism is alternating phase 3 block in the bundle branches due to the relative refractory periods of the left and right bundle branches. Premature atrial contractions conduct down one bundle branch, making it relatively refractory due to the long-short sequence, which then causes the next premature contraction to conduct down the other bundle branch, resulting in the alternating pattern seen. This phenomenon indicates a relative functional delay rather than a diseased conduction system.
This document provides guidance on the assessment and treatment of arrhythmias presenting in the emergency department. It outlines an approach of first determining hemodynamic stability, then distinguishing between narrow and wide complex tachycardias, and finally determining the specific arrhythmia and appropriate treatment. For unstable patients with any arrhythmia, synchronized direct current cardioversion is recommended. Further treatment is tailored based on whether the arrhythmia has narrow or wide QRS complexes and is regular or irregular.
The ACC/AHA guidelines for cardiac pacemaker and antiarrhythmia device implantation were revised based on advances in technology and new clinical evidence. The guidelines provide evidence-based recommendations (level A, B, C evidence) on appropriate patient selection and device optimization. Indications for implantation were expanded based on studies showing risks of untreated bradyarrhythmias and benefits of pacing. The guidelines emphasize the importance of adequate long-term follow-up to ensure devices provide ongoing clinical benefit.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
This document discusses different types of atrioventricular (AV) blocks. It begins by explaining how the normal conduction pathway between the atria and ventricles prevents direct electrical transmission. There are then three types of AV block described based on severity: 1) First-degree AV block causes a prolonged PR interval but all P waves are conducted, 2) Second-degree AV block causes intermittent conduction with two subtypes - Mobitz type I shows gradual PR prolongation and Mobitz type II has a fixed PR, and 3) Third-degree or complete AV block causes complete dissociation between the atria and ventricles.
This document discusses pre-excitation syndrome, specifically Wolff-Parkinson-White (WPW) syndrome and Lown-Ganong-Levine (LGL) syndrome. It defines pre-excitation syndrome as having a short PR interval and usually an abnormal QRS complex due to an accessory pathway in the cardiac conduction system. Accessory pathways can connect different parts of the heart and have faster conduction velocities than the atrioventricular node. WPW syndrome is the most common type, affecting about 1.5 per 1000 people. Common symptoms include palpitations and chest discomfort due to paroxysmal tachyarrhythmias like atrioventricular reentrant tachycardia. Management involves catheter ablation
Cardiac arrhythmias refer to any abnormality in the rate, regularity, or site of origin of the cardiac electrical impulse. They can be caused by disorders of impulse formation or conduction and may lead to symptoms like palpitations, dizziness, or sudden death. The document discusses various types of arrhythmias including bradyarrhythmias like sinus bradycardia, tachyarrhythmias, and premature beats. Perioperative factors, electrocardiographic features, mechanisms, and management approaches for different arrhythmias are provided. Routine intraoperative measures and considerations for anesthetic management are also outlined.
Heart arrhythmia, also known as irregular heartbeat or cardiac dysrhythmia, is a group of conditions where the heartbeat is irregular, too slow, or too fast. Arrhythmias are broken down into: Slow heartbeat: bradycardia. Fast heartbeat: tachycardia. Irregular heartbeat: flutter or fibrillation.
This document provides an overview of stress echocardiography including objectives, indications, protocols, interpretation, and complications. Key points include: stress echo can evaluate CAD using exercise or pharmacologic stress with dobutamine; it has good sensitivity and specificity for CAD compared to nuclear imaging; and provides prognostic information on cardiac events. Interpretation focuses on changes in wall motion, ejection fraction, and detection of ischemia. Stress echo helps evaluate multiple conditions including viability, valvular disease, and cardiomyopathies.
Cardiac arrhythmias and mapping techniquesSpringer
This document provides an overview of clinical cardiac electrophysiology. It discusses the history and development of the field, including the first recordings of intracardiac electrograms in the 1940s-1960s and the development of programmed electrical stimulation in the 1960s-1970s which allowed investigation of arrhythmia mechanisms. It describes the methodology used in electrophysiology studies, including equipment for recording cardiac activity and electrical stimulation, as well as study protocols for evaluating conduction intervals, refractory periods, and inducing/terminating arrhythmias. It outlines the diagnostic and therapeutic indications for electrophysiology studies in evaluating bradycardias, tachycardias, guiding catheter ablation and medical therapy, and risk stratification of conditions like WPW
This document describes the electrocardiographic features of atrial flutter. It discusses:
- Typical atrial flutter involves a macroreentrant circuit around the tricuspid valve that rotates either clockwise or counterclockwise.
- Atypical flutter has a less well defined circuit and rate over 350 bpm.
- ECG shows sawtooth flutter waves at 250-350 bpm without isoelectric segments. The ventricular response is typically 2:1 but can be variable.
- Counterclockwise flutter has negative flutter waves in inferior leads and positive in V1. Clockwise is reversed.
- Right versus left atrial flutter can be distinguished by the polarity of flutter waves in V1
This document provides an overview of diagnosing myocardial infarction (MI) using electrocardiograms (ECGs). It discusses that an MI is best diagnosed using a 12-lead ECG rather than just a rhythm strip. The 12-lead ECG views the heart from 12 angles and can identify ST elevation in different regions to locate the MI. Anterior MIs involve leads V1-V4, lateral MIs involve leads I, aVL, V5-V6, and inferior MIs involve leads II, III, and aVF. The document walks through examples of anterior, lateral, inferior, and anterolateral MIs.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
This document discusses pacemakers and their implications for anesthesia. It provides a brief history of pacemaker development from large abdominal devices in 1980 to today's small pectoral devices. It covers pacemaker indications, types of pacing modes, factors affecting pacing thresholds, preoperative evaluation, intraoperative management considerations, and the effect of magnet application. Pacemaker dependent patients require ECG monitoring and backup pacing during anesthesia given risks of electromagnetic interference or inappropriate pacing inhibition or triggering.
This document provides an overview of cardiac pacemakers, including:
- A brief history of the development of pacemakers from the first implant in 1958 to modern devices.
- The components, functions, and types of pacemakers including single vs dual chamber and permanent vs temporary pacing.
- Measurements taken during pacemaker implantation like impedance, sensing threshold, and pacing threshold to ensure proper function.
- Modes of pacing like VVI, DDD and indications for different modes. Potential complications of pacemaker therapy are also outlined.
The document serves as an introduction to pacemaker terminology, components, functions and the implantation process.
Bradyarrhythmias are caused by problems with impulse formation in the sinus node or impulse conduction through the AV node. Sinus node dysfunction can cause sinus bradycardia, sinus pause/arrest, or chronotropic incompetence. Atrioventricular block is classified as first, second, or third degree and may be caused by conditions like CAD, drugs, or infiltrative diseases. Second degree AV block is further classified as Mobitz type I or II based on PR interval characteristics. Third degree AV block causes complete dissociation between atrial and ventricular rhythms.
ST segment elevations can be seen in acute myocardial infarction (AMI) but also have other causes. Non-AMI causes of ST elevation include left bundle branch block, left ventricular hypertrophy, pericarditis, Brugada syndrome, and early repolarization. The morphology, distribution, and magnitude of ST elevations, as well as other ECG features, can help differentiate AMI from other causes of ST elevation. It can be challenging to diagnose AMI using ECG criteria alone, as around half of AMI cases present without typical ST elevation patterns.
This presentation describes the emergency department management of sinus tachycardia, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia and ventricular ectopic
This document discusses various types of tachyarrhythmias categorized by their anatomical location and electrophysiological mechanisms. It describes atrial arrhythmias including sinus tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. It also discusses atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia, junctional tachycardia, and ventricular arrhythmias including monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation. Key features and mechanisms of each type are outlined to aid in diagnosis and classification.
1. Ask the patient to say "99" and observe for pulsation.
2. Ask the patient to take a deep breath and hold it. Observe for distension.
3. Ask the patient to bear down and observe for collapse.
Examiner:
1. Observe for pulsation, distension and collapse.
2. Measure the height of pulsation above the sternal angle.
3. Note the character of pulsation.
4. Note any abnormal pulsations.
12/09/2022 26
JVP waves and descents:
12/09/2022 27
- a wave: corresponds to atrial contraction during ventricular filling.
- c wave:
This document discusses atrial fibrillation (AF), including its characteristics, prevalence, types, management, and pathophysiological mechanisms. Some key points include:
- AF is characterized by uncoordinated atrial activation and deterioration of atrial function. Prevalence increases with age, affecting over 8% of those over 80 years old.
- Types include paroxysmal, persistent, and permanent AF based on duration and frequency. Management may involve rate control, cardioversion, or rhythm control strategies.
- Pathophysiological mechanisms involve atrial fibrosis, dilation, and inflammation promoting reentrant wavelets within the atria leading to the uncoordinated activation seen in AF.
1. Right bundle branch block (RBBB) results from a defect in the heart's electrical conduction system where there is a delay or failure of impulses traveling down the right bundle branch.
2. This causes the right ventricle to depolarize more slowly than usual, resulting in a characteristic wide and notched QRS complex on ECG.
3. RBBB is generally not treated unless it progresses to heart block, in which case further testing may be needed.
This ECG shows a woman with alternating right bundle branch block (RBBB) and left bundle branch block (LBBB) during episodes of atrial ectopy. The mechanism is alternating phase 3 block in the bundle branches due to the relative refractory periods of the left and right bundle branches. Premature atrial contractions conduct down one bundle branch, making it relatively refractory due to the long-short sequence, which then causes the next premature contraction to conduct down the other bundle branch, resulting in the alternating pattern seen. This phenomenon indicates a relative functional delay rather than a diseased conduction system.
Ohnell described this phenomenon as the “concertina
effect,” in which the QRS complex morphologies from individual
patients with WPW pattern differ owing to variation in the degree
of ventricular excitation via the accessory pathway and AV node.
Recognizing the concertina effect in WPW pattern as normal
variation is important to prevent unnecessary diagnostic and
therapeutic interventions.
Selective vs nonselective his bundle captureSergio Pinski
1) His bundle pacing can result in either selective or non-selective capture of the His bundle and surrounding ventricular myocardium.
2) The hallmark of selective His bundle pacing is changes in QRS morphology seen as the pacing output is reduced, which is not evident when only monitoring 1-2 ECG leads.
3) During threshold testing, responses may indicate selective or non-selective His bundle capture, or myocardial capture alone. Diagnosing non-selective capture can be tricky but is important to avoid self-deception.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Cardiac channelopathies are genetic disorders characterized by altered cardiac excitability without structural heart involvement. Major channelopathies include long QT syndrome (LQTS), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), and short QT syndrome. LQTS results from mutations affecting genes controlling myocardial cell excitability and commonly involves potassium channel genes. It presents with prolonged QT interval and symptoms include syncope. Treatment involves beta-blockers and ICD implantation in high-risk patients. Brugada syndrome causes a distinctive ECG pattern and risk of sudden cardiac death. CPVT causes adrenergic-dependent ventricular arrhythmias during exercise or stress.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Electrocardiographic manifestation of "supernormal" conduction is defined as conduction that is more rapid than expected or presence of conduction when block is anticipated. It is not supernormal in the sense or being more rapid than normal. Therefore, the term relative supernormality or "supernormality" is more appropriate. The mechanism of "supernormal" conduction is conduction during a period of supernormal excitability and conduction associated with altered membrane potential. Some of the more common phenomena that are not dependent on conduction during the supernormal period but manifest better than expected conduction, thus simulating "supernormal" conduction, include dual AV nodal conduction, the "gap" phenomenon, "peeling back" of the refractory period, summation of subthreshold responses, diastolic phase 4 depolarization, and phasic autonomic influences.
Here are the key points from the case:
- A 75-year-old post-menopausal woman presented with pneumonia and chest pain
- In the last 24 hours she experienced dyspnea and sputum production
- This physical stressor of pneumonia could potentially trigger Takotsubo cardiomyopathy in this high-risk demographic
- Her symptoms of chest pain could represent Takotsubo cardiomyopathy mimicking an acute coronary syndrome
- Further workup would be needed to evaluate for potential left ventricular dysfunction and regional wall motion abnormalities consistent with Takotsubo cardiomyopathy versus other causes of her symptoms.
This document discusses strategies for interpreting EKGs in the presence of conduction abnormalities like bundle branch blocks. It provides examples of EKGs showing myocardial infarctions complicating right bundle branch block and left bundle branch block. Key points are that pathologic Q waves can still indicate infarction location, ST elevations are abnormal in bundle branch blocks, and the orientation of ST-T waves can provide clues. Recognition of infarction is still possible despite conduction delays by assessing early versus late QRS deformation.
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.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
This document discusses hyperkalemia (high potassium levels), including its causes, effects on the heart, diagnosis, and treatment. It describes a case report of a 69-year-old woman who experienced hyperkalemia after dialysis. Her symptoms included abdominal pain, fatigue, and arrhythmia. Treatment involved calcium, insulin, glucose, and emergent dialysis to lower her potassium level. The document then provides details on potassium regulation in the body, effects of high potassium on heart function, electrocardiogram changes seen with hyperkalemia, common causes, and approaches for treating acute hyperkalemia including membrane stabilization, promoting potassium influx, and potassium removal methods like dialysis or sodium polystyrene sulfonate.
This document discusses the ECG findings of a 29-year-old male with recurrent palpitations who presented to the emergency room with a prolonged episode during exercise. The ECG shows a regular, narrow complex tachycardia. P-waves are difficult to identify but appear negative in inferior leads and bimodal in V1, suggesting an accessory pathway using the right posterior pathway. The tachycardia terminated with verapamil, and the sinus rhythm ECG shows a short PR interval consistent with Wolff-Parkinson-White syndrome using a right posterior accessory pathway location. The document also discusses the evolution of terminology used to describe accessory pathway locations.
A 23-year-old female presented with episodes of feeling lightheaded and weak. She had a history of anorexia nervosa and had lost significant weight recently. Laboratory tests revealed low calcium, potassium, and other electrolyte abnormalities. During her emergency department stay, she experienced another episode where a rhythm strip was obtained. The rhythm strip showed a prolonged QT interval, likely the cause of her symptoms due to electrolyte abnormalities from her eating disorder.
1. The document discusses supraventricular tachycardia (SVT), which refers to tachycardias originating above the ventricles, with a rate over 100 bpm. Common types include atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) involving an accessory pathway.
2. AVNRT and AVRT-AP are most commonly treated by catheter ablation, which uses radiofrequency energy to destroy the abnormal tissue causing the reentry circuits. Success rates for ablation of AVNRT and AVRT-AP are over 90% and the procedures have become increasingly safer and more effective.
This document summarizes research on right bundle branch block (RBBB) in patients presenting with acute coronary syndrome (ACS). It finds that RBBB in ACS patients identifies a high-risk group with worse short- and long-term outcomes. The presence of RBBB in AMI is associated with more complex cases and obstructive coronary artery disease as well as higher rates of complications and mortality. Studies found 30-day mortality was 14% for AMI patients with RBBB compared to 2% for those without.
Fascicular ventricular tachycardia is a type of ventricular tachycardia that originates in the Purkinje fibers near the fascicles of the left bundle branch. It typically presents in young males as palpitations or dizziness. The electrocardiogram shows a narrow QRS complex tachycardia with right bundle branch block morphology that is sensitive to verapamil. The reentrant circuit involves abnormal Purkinje fibers as the slow pathway and the left posterior fascicle as the fast pathway. Radiofrequency ablation targeting Purkinje potentials in the left ventricular septum is effective for treatment.
Pre-excitation Syndromes is a group of ECG and Electrophysiological abnormalities in which
The atrial impulses are conducted partly or completely, PREMATURELY, to the ventricles via a mechanism other than the normal AV-node *
Associated with a wide array of tachycardias with both normal QRS and prolonged QRS durations
1. Typical atrial flutter involves a macroreentrant circuit around the tricuspid annulus using the cavotricuspid isthmus. Activation proceeds up the septal side of the annulus and along the lateral wall before propagating through the isthmus.
2. Atrial flutter can have clockwise or counterclockwise activation with variable surface ECG patterns depending on the direction. AV conduction is usually 2:1 but can be irregular.
3. Other types of atrial tachycardias involve reentry around scars from prior surgeries or procedures, with circuits in the right or left atrium stabilized by anatomical barriers. Surface ECG patterns vary based on the location of the re
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A thorough review of supernormal conduction.pptx
1. Supernormal Conduction
Sergio L. Pinski, MD, FHRS
Medical University of South Carolina
Charleston, South Carolina, USA
@SergioPinski
2. • No conflicts of interest, besides the fact that I am Argentinian.
3. Definitions of Supernormal Conduction
A misnomer. Conduction is not better than normal.
”Impulse conduction is better than expected”
”Conduction that is better than anticipated under the circumstances”
“ Propagation succeeds early in diastole and fails later".
True only when conduction improves in relation to a supernormal phase
of excitability. Many other unrelated causes of improvement “pseudo-
supernormal conduction”
9. Causes of pseudo supernormal conduction
in AV conduction
• Gap phenomena
• Shortening of refractoriness by changing the preceding cycle length
• Peeling of refractoriness by an early beat
• Manifest or concealed nodal reentry during Wenckebach periodicity
• Dissociation with interference
• Dual AV nodal pathways
• Pulsatile changes in vagal discharge
• Facilitation of conduction by ectopic beats (summation)
10. Causes of pseudo supernormal conduction
in bundle branch block
• Gap phenomena
• Peeling of refractoriness by an early beat
• Shortening of refractoriness by changing the preceding cycle
length
• Dissipation of concealed transeptal conduction
• Wenckebach phenomenon in the bundle branches
• Bradycardia-dependent or phase 4 block
• Bilateral bundle branch delay
11. Equal delay in conduction in the bundle
branches: My pet peeve
• To my knowledge, never demonstrated. I could not find a convincing
example in a thorough literature review. I believe it unlikely to exist.
• Clinical and experimental evidence demonstrate that most cases of
bundle branch block are true “blocks”
• Given the very different length of the fascicles, the possibility that delay
will be exactly the necessary in each one to result in a narrow QRS is very
improbable
• Type 2 gap can result in pseudo supernormal conduction with a long HV.
Diligent search for a split His or a bundle branch potential reveals that
the delay is proximal.
12. Where does supernormal conduction exist?
• In depressed or injured His-Purkinje system (mainly bundle
branches)
• In not very healthy A-V accessory pathways (WPW)
• It cannot occur in the AV node. AV supernormal conduction
can only occur in infranodal block, and so it is a special
variant of supernormal conduction in His or bundle branches
13. Typical behavior of supernormal conduction
in intermittent bundle branch block
Rosenbaum et al. Cardiol Clin 1983;1:75
14. Supernormal conduction in LBB in presence
of RBBB= supernormal AV conduction
Miles & George. Cardiol Clin 2023;41:315
31. Possible 1:1 supernormal conduction in WPW
Chiale et al. J Cardiovasc Pharmacol Ther 2007;12:181
32. Conclusions
• Supernormal conduction exists in depressed His-Purkinje tissue
(generally intermittent bundle branch block) and AV accessory
pathways with poor conduction
• Generally, has little clinical significance but helps explain may puzzling
ECG findings.
• It can be casual to the rare cases of sudden death in patients with
WPW with a long baseline refractory period