differentiating between supraventicular tachycardia and ventricular tachycardia in wide complex rhythm is always confusing and management is totally different. correct diagnosis will make dramatic difference in patient management.
Ventricular tachycardia (VT) is an arrhythmia originating in the ventricles with a heart rate over 100 beats per minute and wide QRS complexes of at least 120 ms. VT can be either idiopathic or structural, sustained or non-sustained, and monomorphic or polymorphic. The ECG can diagnose VT based on the wide QRS complexes. VT has subtypes including bundle branch reentry VT and idiopathic monomorphic VT. Treatment options include medical therapies like amiodarone, implantable cardioverter defibrillators based on major trials, and catheter ablation.
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.
The document discusses bradyarrhythmias and pacemaker selection. It provides an overview of conduction systems, mechanisms of sinus node dysfunction and AV block. It reviews evaluations for bradyarrhythmias including ECG, tests, and etiologies. Guidelines for pacemaker indications are presented for various conditions like sinus node dysfunction, AV block, bifascicular/trifascicular block, and neurocardiogenic syncope. Complications and special considerations like EMI and device settings are also mentioned.
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.
Osborn waves are positive deflections that occur at the junction between the QRS complex and the ST segment on electrocardiograms. They are usually observed in people with hypothermia below 32°C or with conditions like hypercalcemia, brain injury, or ventricular fibrillation. Osborn waves were first described in 1953 by Dr. John Osborn in his study of hypothermia in dogs and are named after him.
This document discusses various non-coronary causes of ST-elevation on electrocardiograms (ECGs) including ventricular aneurysms, pericarditis, early repolarization patterns, left ventricular hypertrophy, left bundle branch block, hypothermia, cardioversion, intraventricular hemorrhage, hyperkalemia, Brugada pattern, type 1C antiarrhythmic drugs, hypercalcemia, pulmonary embolism, hypothermia, myocarditis, and tumor invasion of the left ventricle. It then discusses left ventricular aneurysms, early repolarization, acute pericarditis, hyperkalemia, hypothermia, increased intracranial pressure, Brugada syndrome, Tak
differentiating between supraventicular tachycardia and ventricular tachycardia in wide complex rhythm is always confusing and management is totally different. correct diagnosis will make dramatic difference in patient management.
Ventricular tachycardia (VT) is an arrhythmia originating in the ventricles with a heart rate over 100 beats per minute and wide QRS complexes of at least 120 ms. VT can be either idiopathic or structural, sustained or non-sustained, and monomorphic or polymorphic. The ECG can diagnose VT based on the wide QRS complexes. VT has subtypes including bundle branch reentry VT and idiopathic monomorphic VT. Treatment options include medical therapies like amiodarone, implantable cardioverter defibrillators based on major trials, and catheter ablation.
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.
The document discusses bradyarrhythmias and pacemaker selection. It provides an overview of conduction systems, mechanisms of sinus node dysfunction and AV block. It reviews evaluations for bradyarrhythmias including ECG, tests, and etiologies. Guidelines for pacemaker indications are presented for various conditions like sinus node dysfunction, AV block, bifascicular/trifascicular block, and neurocardiogenic syncope. Complications and special considerations like EMI and device settings are also mentioned.
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.
Osborn waves are positive deflections that occur at the junction between the QRS complex and the ST segment on electrocardiograms. They are usually observed in people with hypothermia below 32°C or with conditions like hypercalcemia, brain injury, or ventricular fibrillation. Osborn waves were first described in 1953 by Dr. John Osborn in his study of hypothermia in dogs and are named after him.
This document discusses various non-coronary causes of ST-elevation on electrocardiograms (ECGs) including ventricular aneurysms, pericarditis, early repolarization patterns, left ventricular hypertrophy, left bundle branch block, hypothermia, cardioversion, intraventricular hemorrhage, hyperkalemia, Brugada pattern, type 1C antiarrhythmic drugs, hypercalcemia, pulmonary embolism, hypothermia, myocarditis, and tumor invasion of the left ventricle. It then discusses left ventricular aneurysms, early repolarization, acute pericarditis, hyperkalemia, hypothermia, increased intracranial pressure, Brugada syndrome, Tak
This document discusses ventricular tachycardia (VT), providing definitions and key characteristics. VT can be nonsustained (<30 seconds) or sustained (>30 seconds). ECG patterns include right bundle branch block (RBBB), left bundle branch block (LBBB), and various axis deviations. Idiopathic VT originates from the outflow tracts, mitral/tricuspid annuli, or fascicles. Specific VT types like bidirectional VT and torsades de pointes are also outlined. The document provides visual examples and differentiates VT from similar rhythms.
1. AVNRT and AVRT are types of supraventricular tachycardia involving abnormal pathways for electrical conduction between the atria and ventricles.
2. AVNRT is caused by a reentry circuit within the AV node, while AVRT involves an accessory pathway bypassing the AV node.
3. There are different subtypes of AVNRT and AVRT depending on which pathways are involved in the antegrade and retrograde directions. Typical AVNRT involves a slow-fast pathway while typical AVRT involves orthodromic conduction over an accessory pathway.
crème de la crème basics to understand electrocardiographic analysis in an easy & simple way with some specifications to its use in Emergency medicine/clinical toxicology practice.
This document provides information on various types of supraventricular tachyarrhythmias including AV nodal reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT), atrial tachycardia, junctional tachycardias, Wolff-Parkinson-White (WPW) syndrome, and atrial fibrillation. It discusses the mechanisms, ECG patterns, symptoms, diagnostic approaches, and management options for these arrhythmias in 1-3 sentences per type of arrhythmia.
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.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.
The document provides an overview of electrocardiography (ECG) interpretation. It discusses the heart's electrical conduction system and action potential, as well as the basics of reading an ECG including assessing rhythm, rate, axis, P waves, QRS complex, ST segment, and T waves. It outlines common abnormalities and provides examples of ECG interpretations for case scenarios involving myocardial infarction, left ventricular hypertrophy, sinus arrhythmia, and atrial fibrillation. The goal is to teach readers how to systematically evaluate an ECG tracing and identify potential cardiac issues.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy. The document outlines the following approach:
1. Obtain history, physical exam, and 12-lead electrocardiogram (ECG) findings to help determine VT vs SVT. Features like AV dissociation or axis deviation favor VT.
2. Use criteria/algorithms like Wellens, Brugada, Vereckei (incorporating lead aVR) to analyze ECG morphology. A majority of criteria must be met to diagnose VT.
3. Consider electrophysiological testing like measuring His-ventricular intervals
This document provides a 100 step guide to electrocardiogram (ECG) interpretation written by Dr. S. Aswini Kumar. It begins with basic definitions of an ECG, the machine used to record it, and how the paper is formatted. It then explains how to analyze various aspects of the ECG including heart rate, rhythm, electrical axis, P wave, PR interval, QRS duration, ST segment, T wave, and conditions like myocardial infarction. The document provides criteria for interpreting abnormalities and identifying conditions. It concludes with examples of analyzing ECG findings and providing an impression.
This document provides an overview of atrial fibrillation (AF) and atrial flutter. It discusses the characteristics, mechanisms, ECG features, causes and clinical outcomes of AF. It also covers the classification, mechanisms, ECG patterns and examples of atrial flutter. Key points include that AF is characterized by disorganized atrial activation and irregular ventricular rhythm, while flutter involves a reentrant circuit in the right atrium causing a regular atrial rate of 300 bpm. Complications of AF include increased risk of stroke, heart failure and cardiac death.
Wolff-Parkinson-White syndrome is caused by an abnormal accessory electrical pathway between the atria and ventricles that can bypass the AV node and allow rapid conduction, potentially causing palpitations, dizziness and other symptoms; the condition is usually asymptomatic but can cause tachyarrhythmias due to orthodromic or antidromic conduction along the accessory pathway; treatment involves catheter ablation to destroy the accessory pathway or medications to control the heart rate during arrhythmias.
1. The document describes 4 ECG findings from patients presenting with various symptoms. The first case shows ventricular bigeminy in a patient with chest pain. The second case shows sinus tachycardia with S1Q3T3 pattern in a bedridden patient with breathlessness, indicating pulmonary embolism. The third case shows ventricular tachycardia in a patient recently diagnosed with myocardial infarction. The fourth case provides the Brugada criteria used to diagnose Brugada syndrome.
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.
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.
This document discusses various types of supraventricular tachycardias (SVTs), including their causes, mechanisms, diagnosis, and treatment. It covers atrial fibrillation, atrial flutter, atrial tachycardia, and AV nodal reentrant tachycardia. For each type, it discusses epidemiology, mechanisms, classification, evaluation with tests like ECG and echocardiogram, anticoagulation measures, and treatment options like medications, cardioversion, and catheter ablation. Rate control is emphasized as usually preferable to rhythm control for atrial fibrillation.
A 22-year-old male presented with acute onset breathlessness, palpitations, and profuse sweating. His ECG showed tachycardia at a rate of 200 bpm with a right bundle branch block pattern. This wide complex tachycardia was determined to be ventricular tachycardia based on Brugada criteria and AVR criteria, including the absence of an RS complex in leads V1-V6, a QRS duration greater than 100 ms, and a ventricular activation-velocity ratio greater than 1. The patient was diagnosed with ventricular tachycardia based on the ECG findings and treated accordingly.
This document provides an overview of sinus of Valsalva aneurysm (SOVA). Key points include:
- SOVA is a thin-walled bulge that originates from the aortic sinuses, most commonly the right sinus. It can rupture into the right heart chambers.
- Presentation depends on rupture status - ruptured SOVA causes a continuous murmur while unruptured can cause arrhythmias or embolism. Imaging helps confirm diagnosis.
- Surgery is the standard treatment, involving a median sternotomy, cardiopulmonary bypass, and patch closure of the defect from inside the aorta and heart chambers. Device closure is also possible. Outcomes are generally good but
This document provides a history of the electrocardiogram (EKG/ECG) and describes how it is used to evaluate cardiac electrical activity and identify various cardiac conditions. Some key points:
- The EKG was developed in the late 19th/early 20th century, with scientists like Matteucci, Marey, and Einthoven contributing to its invention and clinical use.
- An EKG records the heart's electrical activity through electrodes on the skin and can be used to detect arrhythmias, ischemia, infarction, and other conditions.
- It analyzes the P wave, QRS complex, ST segment, and T wave to evaluate conduction and identify abnormalities.
This document provides an overview of ECG interpretation, including conduction pathways, a systematic method of interpretation, and common abnormalities seen in critical care. It discusses supraventricular and ventricular arrhythmias, bundle branch blocks, heart block, and life-threatening arrhythmias such as ventricular tachycardia, ventricular fibrillation, and asystole. It also covers the basics of 12-lead ECG interpretation including lead placement and axis.
An electrocardiogram (ECG or EKG) records the electrical signal from your heart to check for different heart conditions. Electrodes are placed on your chest to record your heart's electrical signals, which cause your heart to beat. The signals are shown as waves on an attached computer monitor or printer
This document discusses ventricular tachycardia (VT), providing definitions and key characteristics. VT can be nonsustained (<30 seconds) or sustained (>30 seconds). ECG patterns include right bundle branch block (RBBB), left bundle branch block (LBBB), and various axis deviations. Idiopathic VT originates from the outflow tracts, mitral/tricuspid annuli, or fascicles. Specific VT types like bidirectional VT and torsades de pointes are also outlined. The document provides visual examples and differentiates VT from similar rhythms.
1. AVNRT and AVRT are types of supraventricular tachycardia involving abnormal pathways for electrical conduction between the atria and ventricles.
2. AVNRT is caused by a reentry circuit within the AV node, while AVRT involves an accessory pathway bypassing the AV node.
3. There are different subtypes of AVNRT and AVRT depending on which pathways are involved in the antegrade and retrograde directions. Typical AVNRT involves a slow-fast pathway while typical AVRT involves orthodromic conduction over an accessory pathway.
crème de la crème basics to understand electrocardiographic analysis in an easy & simple way with some specifications to its use in Emergency medicine/clinical toxicology practice.
This document provides information on various types of supraventricular tachyarrhythmias including AV nodal reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT), atrial tachycardia, junctional tachycardias, Wolff-Parkinson-White (WPW) syndrome, and atrial fibrillation. It discusses the mechanisms, ECG patterns, symptoms, diagnostic approaches, and management options for these arrhythmias in 1-3 sentences per type of arrhythmia.
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.
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.
The document provides an overview of electrocardiography (ECG) interpretation. It discusses the heart's electrical conduction system and action potential, as well as the basics of reading an ECG including assessing rhythm, rate, axis, P waves, QRS complex, ST segment, and T waves. It outlines common abnormalities and provides examples of ECG interpretations for case scenarios involving myocardial infarction, left ventricular hypertrophy, sinus arrhythmia, and atrial fibrillation. The goal is to teach readers how to systematically evaluate an ECG tracing and identify potential cardiac issues.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy. The document outlines the following approach:
1. Obtain history, physical exam, and 12-lead electrocardiogram (ECG) findings to help determine VT vs SVT. Features like AV dissociation or axis deviation favor VT.
2. Use criteria/algorithms like Wellens, Brugada, Vereckei (incorporating lead aVR) to analyze ECG morphology. A majority of criteria must be met to diagnose VT.
3. Consider electrophysiological testing like measuring His-ventricular intervals
This document provides a 100 step guide to electrocardiogram (ECG) interpretation written by Dr. S. Aswini Kumar. It begins with basic definitions of an ECG, the machine used to record it, and how the paper is formatted. It then explains how to analyze various aspects of the ECG including heart rate, rhythm, electrical axis, P wave, PR interval, QRS duration, ST segment, T wave, and conditions like myocardial infarction. The document provides criteria for interpreting abnormalities and identifying conditions. It concludes with examples of analyzing ECG findings and providing an impression.
This document provides an overview of atrial fibrillation (AF) and atrial flutter. It discusses the characteristics, mechanisms, ECG features, causes and clinical outcomes of AF. It also covers the classification, mechanisms, ECG patterns and examples of atrial flutter. Key points include that AF is characterized by disorganized atrial activation and irregular ventricular rhythm, while flutter involves a reentrant circuit in the right atrium causing a regular atrial rate of 300 bpm. Complications of AF include increased risk of stroke, heart failure and cardiac death.
Wolff-Parkinson-White syndrome is caused by an abnormal accessory electrical pathway between the atria and ventricles that can bypass the AV node and allow rapid conduction, potentially causing palpitations, dizziness and other symptoms; the condition is usually asymptomatic but can cause tachyarrhythmias due to orthodromic or antidromic conduction along the accessory pathway; treatment involves catheter ablation to destroy the accessory pathway or medications to control the heart rate during arrhythmias.
1. The document describes 4 ECG findings from patients presenting with various symptoms. The first case shows ventricular bigeminy in a patient with chest pain. The second case shows sinus tachycardia with S1Q3T3 pattern in a bedridden patient with breathlessness, indicating pulmonary embolism. The third case shows ventricular tachycardia in a patient recently diagnosed with myocardial infarction. The fourth case provides the Brugada criteria used to diagnose Brugada syndrome.
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.
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.
This document discusses various types of supraventricular tachycardias (SVTs), including their causes, mechanisms, diagnosis, and treatment. It covers atrial fibrillation, atrial flutter, atrial tachycardia, and AV nodal reentrant tachycardia. For each type, it discusses epidemiology, mechanisms, classification, evaluation with tests like ECG and echocardiogram, anticoagulation measures, and treatment options like medications, cardioversion, and catheter ablation. Rate control is emphasized as usually preferable to rhythm control for atrial fibrillation.
A 22-year-old male presented with acute onset breathlessness, palpitations, and profuse sweating. His ECG showed tachycardia at a rate of 200 bpm with a right bundle branch block pattern. This wide complex tachycardia was determined to be ventricular tachycardia based on Brugada criteria and AVR criteria, including the absence of an RS complex in leads V1-V6, a QRS duration greater than 100 ms, and a ventricular activation-velocity ratio greater than 1. The patient was diagnosed with ventricular tachycardia based on the ECG findings and treated accordingly.
This document provides an overview of sinus of Valsalva aneurysm (SOVA). Key points include:
- SOVA is a thin-walled bulge that originates from the aortic sinuses, most commonly the right sinus. It can rupture into the right heart chambers.
- Presentation depends on rupture status - ruptured SOVA causes a continuous murmur while unruptured can cause arrhythmias or embolism. Imaging helps confirm diagnosis.
- Surgery is the standard treatment, involving a median sternotomy, cardiopulmonary bypass, and patch closure of the defect from inside the aorta and heart chambers. Device closure is also possible. Outcomes are generally good but
This document provides a history of the electrocardiogram (EKG/ECG) and describes how it is used to evaluate cardiac electrical activity and identify various cardiac conditions. Some key points:
- The EKG was developed in the late 19th/early 20th century, with scientists like Matteucci, Marey, and Einthoven contributing to its invention and clinical use.
- An EKG records the heart's electrical activity through electrodes on the skin and can be used to detect arrhythmias, ischemia, infarction, and other conditions.
- It analyzes the P wave, QRS complex, ST segment, and T wave to evaluate conduction and identify abnormalities.
This document provides an overview of ECG interpretation, including conduction pathways, a systematic method of interpretation, and common abnormalities seen in critical care. It discusses supraventricular and ventricular arrhythmias, bundle branch blocks, heart block, and life-threatening arrhythmias such as ventricular tachycardia, ventricular fibrillation, and asystole. It also covers the basics of 12-lead ECG interpretation including lead placement and axis.
An electrocardiogram (ECG or EKG) records the electrical signal from your heart to check for different heart conditions. Electrodes are placed on your chest to record your heart's electrical signals, which cause your heart to beat. The signals are shown as waves on an attached computer monitor or printer
1. The document discusses electrocardiographic (ECG) interpretation including determining cardiac rate and rhythm, identifying conduction disturbances, myocardial ischemia or infarction, and other abnormalities.
2. It provides details on properly placing ECG leads and determining the cardiac axis. Common rhythms, conduction blocks, hypertrophy, and other ECG findings are explained.
3. A mnemonic device, RRAHIM, is presented to guide the systematic interpretation of an ECG, covering rate, rhythm, axis, hypertrophy, ischemia/infarction, and other findings.
This document provides an overview of how to read an electrocardiogram (ECG). It describes the basic anatomy and electrical conduction system of the heart and how the ECG machine records and displays the heart's electrical activity. It then outlines a systematic approach for interpreting an ECG, including evaluating the rhythm, rate, axes, voltages, waves, segments, intervals, and any signs of ischemia, injury, or arrhythmia. Localization of abnormalities is also addressed. Examples are provided throughout to illustrate various normal and pathological ECG patterns.
The 11-step method provides a systematic approach to reading EKGs:
1. Gather data such as heart rate, intervals, and axis.
2. Diagnose rhythm, conduction blocks, enlargement, and infarction by applying specific criteria.
3. Potential diagnoses are identified through disturbances of rhythm, conduction, hypertrophy, and ischemia. The relationship between P waves and QRS complexes helps determine block types.
The 11-step method provides a systematic approach to reading EKGs:
1. Gather data such as heart rate, intervals, and axis.
2. Diagnose rhythm, conduction blocks, enlargement, and infarction by applying specific criteria.
3. Potential diagnoses are identified through disturbances of rhythm, conduction, hypertrophy, and ischemia. The four questions framework is used to characterize rhythms.
This document provides an overview of electrocardiography (ECG), including how an ECG works, the basics of recording an ECG, ECG leads, normal ECG waveforms and intervals, interpreting an ECG, common abnormalities, and how to report an ECG. It discusses topics such as the cardiac conduction system, Einthoven's triangle, the 12-lead ECG, determining heart rate and axis, normal sinus rhythm, P waves, QRS complex, ST segment, T waves, and the QT interval.
The ECG represents the electrical activity of the heart. It can provide insight into cardiac pathophysiology by analyzing the distinctive waveforms of each cardiac event. The ECG can identify arrhythmias, ischemia, infarction, pericarditis, chamber hypertrophy, and electrolyte disturbances. The standard 12-lead ECG consists of 3 limb leads, 3 augmented limb leads, and 6 precordial leads, which provide different views of the heart. Analysis of the P wave, PR interval, QRS complex, ST segment, T wave, and QT interval can reveal normal sinus rhythm or abnormalities that require further investigation.
This document discusses left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). It defines LVH as an increase in left ventricle mass due to increased wall thickness or cavity size. There are two types of LVH - systolic overload from conditions like hypertension which compromise the left ventricle during systole, and diastolic overload from things like valvular diseases which compromise it during diastole. The document outlines ECG criteria for diagnosing LVH including Sokolov-Lyon and Cornell voltage criteria. It also discusses RVH manifestations on ECG like right axis deviation, tall R waves in right precordial leads, and an S1S2S3 pattern.
The document discusses principles of electrocardiography and interpretation of ECG tracings. It states that depolarization or repolarization waves traveling toward a positive electrode result in positive deflections, while those traveling away result in negative deflections. Perpendicular waves result in biphasic deflections. The amplitude seen depends on tissue orientation relative to electrode placement. Common ECG findings of left ventricular hypertrophy and right ventricular enlargement are also reviewed.
The document provides an overview of electrocardiography (ECG) fundamentals. It defines what an ECG is and discusses the cardiac cycle and interpretation of different ECG components such as waves, intervals, complexes, and segments. Key points covered include the components of the ECG, abnormalities that can be identified from the ECG, cardiac electrical conduction pathways, lead placements, and common causes of ECG abnormalities.
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 ECG represents the electrical activity of the heart during the cardiac cycle. Each waveform provides insight into cardiac physiology and pathology. The ECG can be used to identify arrhythmias, ischemia, infarction, conduction abnormalities, chamber enlargement, and electrolyte disturbances. It consists of 12 leads that view the heart from different angles. The waveform intervals like P wave, PR interval, QRS complex, and ST segment must be carefully analyzed to interpret the ECG tracing.
The document provides information about electrocardiograms (ECGs), including what an ECG is, the types of pathology that can be identified from ECGs, ECG paper specifications, the anatomy of the heart and normal ECG signal, ECG leads, determining heart rate and rhythm from ECGs, P waves, the PR interval, the QRS complex, axes determination, bundle branch blocks, ventricular hypertrophy, Q waves, the ST segment, T waves, and the QT interval. Key aspects of the ECG that can help identify conditions like myocardial infarction, pericarditis, and electrolyte abnormalities are discussed.
The document discusses the history and development of electrocardiography (ECG/EKG) and summarizes the key aspects of ECG interpretation. Some of the main points covered include:
- The key individuals who contributed to the development of ECG, from its initial discovery in the 1800s to modern applications.
- The components of a standard 12-lead ECG, including the waves, intervals, leads, and their normal values and appearances.
- Common ECG abnormalities such as arrhythmias, conduction blocks, hypertrophy, ischemia, and injury patterns.
- Guidelines for proper ECG acquisition and systematic interpretation.
This document provides a summary of basics of electrocardiography (ECG/EKG). It discusses the history and development of ECG technology. It describes the components of a normal ECG waveform including the P, QRS, and T waves. It explains how to determine heart rate from an ECG and identify different arrhythmias based on the waveform. Key anatomical structures involved in heart's electrical conduction system are also outlined.
1. Sepsis is a life-threatening organ dysfunction caused by a dysregulated immune response to infection. It can progress to septic shock, which involves circulatory and metabolic abnormalities increasing the risk of death.
2. Initial management of sepsis involves screening, resuscitation, infection control, hemodynamic support, and empiric antibiotics within 1-3 hours while obtaining cultures. Ongoing care focuses on organ support, source control, and monitoring for complications.
3. Long term goals include preventing disability, addressing psychosocial needs, and smooth transition to post-acute care and follow up. Prompt recognition and treatment can reduce mortality from this medical emergency.
1. The document discusses various cardiac arrhythmias including supraventricular tachycardias, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
2. It provides details on characteristics, causes, diagnosis, and treatment of these arrhythmias based on American and European cardiology guidelines.
3. The treatment discussed includes electrical cardioversion, antiarrhythmic medications, catheter ablation, and implantable cardioverter defibrillators.
This document provides an overview of atrial fibrillation (AF) and paroxysmal supraventricular tachycardia (PSVT). It defines these conditions and describes their typical ECG patterns, mechanisms, clinical presentations, diagnostic evaluations, and treatment approaches including medications, procedures like cardioversion and ablation. Key points include: AF can be paroxysmal, persistent or permanent, and is caused by mechanisms like reentry and ectopic automaticity; evaluation involves assessing thromboembolic risk with scores like CHA2DS2-VASc; treatment focuses on rate or rhythm control with medications or ablation, while preventing thromboembolism with anticoagulation; PSVT often presents with abrupt
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
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Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
A 24-year-old woman presented with headache and left-sided weakness. Imaging showed cerebral venous thrombosis involving the superior sagittal sinus and draining veins. She was diagnosed with antiphospholipid syndrome based on recurrent pregnancy loss and positive lupus anticoagulant. She was treated with anticoagulation and anticonvulsants and showed gradual improvement over 10 days with residual mild weakness. Her long-term management plan includes lifelong anticoagulation and screening for recurrent thrombosis.
A 68-year-old male farmer presented with post-traumatic T3-T4 compression fracture and paraplegia in January 2022. He developed recurrent UTIs, hemorrhagic pleural effusion, and a retropharyngeal cyst requiring debulking. In early March, he developed cough, dyspnea, stridor and altered sensorium. He was diagnosed with right lower lobe pneumonia, sepsis and respiratory failure. Treatment included antibiotics, ventilation, and supportive care. He later developed bilateral vocal cord palsy and was discharged at family's request before further evaluation.
Chronic myeloid leukemia (CML) is a stem cell disorder caused by the Philadelphia chromosome, which results from the fusion of the BCR gene on chromosome 22 and the ABL gene on chromosome 9. This fusion produces the BCR-ABL protein which exhibits uncontrolled tyrosine kinase activity, driving excessive proliferation of CML cells. CML progresses through chronic, accelerated and blast crisis phases as additional genetic mutations accumulate. Tyrosine kinase inhibitors (TKIs) target the BCR-ABL protein and have significantly improved survival, with a 10-year survival of 85% with TKI therapy. Monitoring response through cytogenetics, FISH and molecular testing guides treatment decisions such as changing or adding other TKIs.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
surviving sepsis guidelines - Notes are made from surviving sepsis guidelines 2016 article to assist medical students and residents to grasp subject in a easy to read format in a step wise manner. Resources: surviving sepsis guidelines 2016 (free access article)
Pulmonary embolism - Notes are made from textbook of Internal medicine to assist medical students and residents to grasp subject in totality. Resources: Harrison's 20thEd, ESC 2019 guidelines on PE
A pulmonary embolism occurs when a blood clot or other material occludes the pulmonary artery or its branches. This most commonly results from a deep vein thrombosis in the lower leg that embolizes to the lung. When a PE occurs, it causes ventilation-perfusion mismatching in the lungs. Diagnosis is difficult due to nonspecific symptoms but evaluation involves a Wells criteria assessment, D-dimer testing, echocardiogram, and CT pulmonary angiogram. Treatment consists of anticoagulation with low molecular weight heparin or novel oral anticoagulants. Fibrinolytic therapy may be used in massive PEs. Prevention focuses on prophylaxis in high risk hospitalized patients.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
2. Myocardial Cell
Atria : Myocardial Cells
Ventricle: Myocardial cells
SA Node, AV Node, Purkinjee Fibers
Gap Junctions
Myocardium : Na Ca K Dependent
SA node & AV node : Ca Dependent
Depolarization Repolarization
Plateau Phase
3. Understanding Vector
.
Atria : Myocardial Cells
Ventricle: Myocardial cells
SA Node, AV Node, Purkinjee Fibers
Positive wave towards
positive charge
+
Negative wave towards
negative charge
+
Depolarization
--
+++
Negative wave away
from positive charge
Repolarization
More cells: Larger vector
Specialized conduction: Faster vector
Direction of Vector
Stimulus
20. Left Ventricular Hypertrophy
ROMHILT ESTES POINT CRITERIA
Axis, V1, V6, Strain pattern
Atria abnormality
Other abnormalities
SOKOLOW – LYON CRITERIA
S V1 + R V5 or V6 > 35 mm ( > 3.5 mV)
R wave in V5 or V6 > 26 mm (> 2.6 mV)
37. Ectopic
Premature Atrial Ectopic
Junctional Rhythm
Premature Ventricular Ectopic
Rate
Regularity
Narrow / wide QRS
P wave morphology
Relation of P & QRS
Other Clues
• 3 to 30 seconds it is Non Sustained Tachy
• > 30 Sec it is Sustained Tachycardia
• PB follow every alternate normal beat: Bigeminy
• PB follow every second normal beat: Trigeminy
Abnormal P wave
Normal QRS complex
Incomplete Compensatory pause
Wide QRS complex
Complete Compensatory pause
Inverted P wave
Normal QRS complex
Incomplete Compensatory pause
38. Brady Arrhythmias
FAILURE OF ELECTRICAL IMPULSE
GENERATION (Sinus node Dysfunction)
FAILURE OF EFFECTIVE
CONDUCTION ( AV Node Block)
Sick Sinus Syndrome
Sinus Bradycardia
Inability to increase rate with increased sympathetic activity
Absence of escape rhythms when sinus rate slows
Tachy-brady syndrome
39. Tachyarrhythmias - Mechanisms
INCREASED
AUTOMATICITY
RE ENTRY
TRIGGERED ACTIVITY
Wide Complex Tachycardia
Ventricular tachycardia
Other: SVT with BBB
SVT with WPW syndrome
(Antidromic AVRT)
A fib/A flutter with variable conduction