1. The document discusses various types of bradycardia and conduction blocks including sinus bradycardia, sick sinus syndrome, different degrees of AV block, bundle branch blocks, and fascicular blocks.
2. It provides details on the characteristics, causes, and electrocardiographic features of each type of block. First degree AV block results in a prolonged PR interval while second degree block causes intermittent failure of conduction.
3. Third degree or complete heart block results in independent atrial and ventricular rhythms. Bundle branch blocks involve the right or left bundle branches and fascicular blocks occur in the fascicles of the left bundle branch. Bifascicular and trifascicular blocks involve multiple levels of block
Bundle branch blocks occur when the left or right bundle branch is blocked, preventing normal conduction of electrical impulses through the ventricles. Right bundle branch block is usually benign but can worsen prognosis in acute myocardial infarction by indicating occlusion of the proximal left anterior descending artery. Left bundle branch block is more serious as it can mask signs of myocardial infarction and worsen prognosis in acute infarction. The Sgarbossa criteria can help diagnose myocardial infarction in the presence of left bundle branch block. Left anterior and posterior hemiblocks involve conduction abnormalities localized to one side of the ventricles.
The document discusses the diagnosis and management of various cardiac arrhythmias, outlining the assessment of patients' histories, ECG findings, and treatment options including medications, referral indications, and procedures. Case studies are provided examining scenarios involving bradycardias, conduction abnormalities, tachycardias, and their management in both stable and unstable patients.
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.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
- 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.
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.
1. The document discusses various types of bradycardia and conduction blocks including sinus bradycardia, sick sinus syndrome, different degrees of AV block, bundle branch blocks, and fascicular blocks.
2. It provides details on the characteristics, causes, and electrocardiographic features of each type of block. First degree AV block results in a prolonged PR interval while second degree block causes intermittent failure of conduction.
3. Third degree or complete heart block results in independent atrial and ventricular rhythms. Bundle branch blocks involve the right or left bundle branches and fascicular blocks occur in the fascicles of the left bundle branch. Bifascicular and trifascicular blocks involve multiple levels of block
Bundle branch blocks occur when the left or right bundle branch is blocked, preventing normal conduction of electrical impulses through the ventricles. Right bundle branch block is usually benign but can worsen prognosis in acute myocardial infarction by indicating occlusion of the proximal left anterior descending artery. Left bundle branch block is more serious as it can mask signs of myocardial infarction and worsen prognosis in acute infarction. The Sgarbossa criteria can help diagnose myocardial infarction in the presence of left bundle branch block. Left anterior and posterior hemiblocks involve conduction abnormalities localized to one side of the ventricles.
The document discusses the diagnosis and management of various cardiac arrhythmias, outlining the assessment of patients' histories, ECG findings, and treatment options including medications, referral indications, and procedures. Case studies are provided examining scenarios involving bradycardias, conduction abnormalities, tachycardias, and their management in both stable and unstable patients.
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.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
- 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.
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 contains a quiz with multiple choice questions about ECG interpretations. Some key findings included in the questions are right bundle branch block with left posterior hemiblock, third degree atrioventricular block, left bundle branch block with Cabrera's sign indicating possible myocardial infarction, Wolff-Parkinson-White syndrome type A, ventricular tachycardia, atrial fibrillation, premature ventricular contractions, left ventricular hypertrophy, anterior myocardial infarction, hyperkalemia, and more. The document also includes explanations of ECG patterns and signs such as bundle branch blocks, ventricular tachycardia criteria, Wellens' phenomenon, hyperacute T waves, and more.
This document discusses ECG changes that occur due to cardiac chamber enlargement, including left atrial, right atrial, biatrial, left ventricular, right ventricular, and biventricular abnormalities. For each type of chamber enlargement, the document outlines the mechanisms, diagnostic ECG criteria, and examples of ECG patterns. Key findings include prolonged P waves and biphasic P waves in leads indicating left and right atrial enlargement, increased QRS voltages and ST-T wave changes indicating left ventricular pressure overload, and tall R waves in right-sided leads indicating right ventricular hypertrophy. The document provides a detailed reference for understanding ECG manifestations of different cardiac structural abnormalities.
This document summarizes the evaluation of aortic valve stenosis using echocardiography. It describes the normal aortic valve anatomy and various types of aortic valve stenosis including calcific, bicuspid, rheumatic, and supravalvular or subvalvular stenosis. Doppler echocardiography is used to evaluate aortic valve stenosis severity based on valve area, mean gradient, and peak jet velocity. Stress echocardiography with dobutamine can help distinguish true severe from pseudo-severe low-flow, low-gradient aortic stenosis.
Dr. Abraham discusses sinus node dysfunction and atrioventricular block. Key points include:
- The sinus node is usually located in the right atrium and receives blood supply from the right coronary artery or left circumflex artery.
- Symptoms of sinus node dysfunction range from asymptomatic ECG changes to tachycardia, bradycardia, and tachy-brady syndrome.
- Treatment options include pharmacotherapy with drugs like atropine or theophylline for short term use, and pacemaker implantation for long term treatment of sinus node disease.
- The atrioventricular node receives innervation from the arteries of Koch and shows minimal autonomic innervation. AV block can be first,
This document provides an overview of cardiac arrhythmias including their classification, mechanisms, clinical manifestations, diagnostic approaches and management strategies. It discusses various specific arrhythmias in detail such as atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular arrhythmias, sick sinus syndrome and heart block. Treatment options covered include pharmacological therapies using different classes of antiarrhythmic drugs, procedures like cardiac ablation and use of devices like pacemakers.
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.
AV heart blocks can be caused by drug therapy, ischemic heart disease, degeneration due to age, aortic sclerosis, or cardiac surgery. First degree heart block involves slowed conduction through the AV node, prolonging the PR interval without dropped beats. Second degree heart block involves intermittent conduction, with Mobitz type I (Wenkebach) showing progressively prolonging PR intervals until a dropped beat, and Mobitz type II a constant PR interval with occasional dropped beats. Third degree heart block is a complete failure of AV node conduction, with dissociation between the P wave and QRS complex rates.
The document discusses various electrocardiogram (ECG) criteria for differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy presenting with a wide QRS complex tachycardia. It outlines criteria from Sandler and Marriott (1965), Wellens (1978), Kindwall (1988), Brugada (1991), Vereckei (2008) and Pava (2010). Key criteria that favor VT include QRS duration >140ms, extreme left axis, AV dissociation, monophasic R wave in V1, R/S ratio <1 in V6, and notching of the S wave in V1.
This document discusses various tachyarrhythmias, including:
- Supraventricular tachycardias like atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia.
- Ventricular arrhythmias including ventricular tachycardia and ventricular flutter.
- Irregular rhythms such as atrial fibrillation.
It provides details on characteristics like rate, morphology, underlying causes, and treatment approaches for each type of tachycardia. Emphasis is placed on distinguishing ventricular tachycardia from supraventricular tachycardia with aberrancy in clinical evaluation.
This document provides information on cardiac arrhythmias, including:
- The normal cardiac conduction system and blood flow through the heart.
- Definitions and characteristics of various normal and abnormal sinus rhythms, atrial rhythms, junctional rhythms, and ventricular rhythms based on heart rate, rhythm, P wave presence and morphology, PR interval, and QRS width.
- Key arrhythmias summarized include normal sinus rhythm, sinus bradycardia, sinus tachycardia, premature atrial contractions, atrial fibrillation, atrial flutter, premature junctional contractions, junctional tachycardia, premature ventricular contractions, ventricular tachycardia, and ventricular flutter.
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.
Antiarrhythmic drugs work by altering the conduction of electrical signals in the heart and changing the refractory periods of cardiac cells. They are classified into four classes based on their effects. Class IA drugs like quinidine and procainamide work by slowing the rise of the action potential upstroke, decreasing conduction velocity, and prolonging the refractory period. They have moderate potassium channel blocking effects. Class IA drugs are used for supraventricular arrhythmias and ventricular tachycardia but can cause toxicity like heart block or dangerous arrhythmias.
The ECG records the electrical activity of the heart over time and is the gold standard for diagnosing cardiac arrhythmias and conduction abnormalities. It detects three main waves - the P wave from atrial depolarization, the QRS complex from ventricular depolarization, and the T wave from ventricular repolarization. Abnormalities in conduction through the AV node can cause first-, second-, or third-degree heart block visible on the ECG. Higher degrees of block impair conduction more severely and require treatment such as pacemaker implantation.
The document discusses electrocardiogram (ECG) patterns associated with cardiac chamber enlargement, specifically right atrial enlargement (RAE) and left atrial enlargement (LAE). RAE is suggested by a tall, peaked P wave in leads II, III, AVF and a positive P wave in V1. LAE results in prolongation of the left atrial component of the P wave, increased posterior deviation of the left atrial vector, and left axis deviation of the P wave. The diagnostic accuracy of ECG findings for chamber enlargement is limited but can provide clues when correlated with imaging studies.
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.
Echocardiography is a useful tool for diagnosing and monitoring heart failure patients. It can assess left ventricular ejection fraction, ventricular sizes and wall thickness, valve function, diastolic function, and pulmonary pressures. New techniques such as 3D echocardiography and strain imaging provide more accurate measurements of cardiac structure and function compared to older 2D techniques. Echocardiography is also used to differentiate the causes of heart failure, monitor for complications, and predict patient outcomes. It remains an important part of the evaluation and management of patients with heart failure.
This document discusses various types of conduction disturbances including sinoatrial exit block, AV blocks, bundle branch blocks, and fascicular blocks. It provides details on the definitions, electrocardiogram findings, causes and prevalence of each type. The document concludes with guidelines on indications for permanent pacemaker implantation for acquired AV block, bifascicular/trifascicular block, and after myocardial infarction.
1. The document describes various EKG abnormalities including early repolarization, pericarditis, fascicular blocks, ventricular hypertrophy, electrolyte abnormalities, prolonged QT interval, and more.
2. Key details are provided on differentiating early repolarization from anterior MI and pericarditis. Stages of pericarditis are outlined.
3. Fascicular blocks are described along with their characteristic axis deviations and block locations. Different forms of ventricular hypertrophy and their EKG patterns are also summarized.
This document discusses cardiac arrhythmias and their treatment. It defines normal cardiac rhythm and atrial arrhythmias. It describes the cardiac action potential and ECG waves. It explains the differences between pacemaker and non-pacemaker cell action potentials. The document discusses mechanisms of arrhythmias including disorders of impulse formation and conduction. It provides an overview of antiarrhythmic drug classes and mechanisms of action including sodium channel blockade, beta-blockade, and calcium channel blockade.
This document provides an overview of how to interpret common ECG abnormalities through 3 sentences or less summaries:
1) It outlines how to measure rate, rhythm, intervals, complexes, and waves on an ECG and identifies what is considered normal.
2) Key abnormal rhythms, rates, intervals, and waves are defined along with their potential causes, such as sinus bradycardia, atrial fibrillation, various heart blocks, ventricular tachycardia, ST segment changes, T wave inversions, bundle branch blocks, and more.
3) Methods for localizing myocardial infarctions and abnormalities seen in conditions like hyperkalemia and hypothermia are also summarized.
This document discusses bradyarrhythmias and approach to treatment. It defines various types of sinus node dysfunction and AV conduction blocks including sick sinus syndrome, sinus pause, sinus arrest, tachy-brady syndrome, and different degrees of AV block. It describes evaluation of sinus node function including intrinsic heart rate, sinus node recovery time and SA conduction time. It discusses reversible and irreversible causes of bradyarrhythmias and guidelines for pacemaker implantation for sinus node and AV node dysfunction. Treatment options including medications and permanent pacing are outlined.
This document provides guidance on electrocardiogram (ECG) interpretation. It begins with descriptions of normal ECG appearances and measurements. It then discusses approaches to reading an ECG, including evaluating heart rate, rhythm, axis, and abnormalities. Common conduction abnormalities and what parts of the heart different abnormalities indicate are defined. The document concludes with descriptions of abnormalities in various ECG components like ST segments, T waves, and Q waves as well as the typical evolution of a myocardial infarction on ECG.
This document contains a quiz with multiple choice questions about ECG interpretations. Some key findings included in the questions are right bundle branch block with left posterior hemiblock, third degree atrioventricular block, left bundle branch block with Cabrera's sign indicating possible myocardial infarction, Wolff-Parkinson-White syndrome type A, ventricular tachycardia, atrial fibrillation, premature ventricular contractions, left ventricular hypertrophy, anterior myocardial infarction, hyperkalemia, and more. The document also includes explanations of ECG patterns and signs such as bundle branch blocks, ventricular tachycardia criteria, Wellens' phenomenon, hyperacute T waves, and more.
This document discusses ECG changes that occur due to cardiac chamber enlargement, including left atrial, right atrial, biatrial, left ventricular, right ventricular, and biventricular abnormalities. For each type of chamber enlargement, the document outlines the mechanisms, diagnostic ECG criteria, and examples of ECG patterns. Key findings include prolonged P waves and biphasic P waves in leads indicating left and right atrial enlargement, increased QRS voltages and ST-T wave changes indicating left ventricular pressure overload, and tall R waves in right-sided leads indicating right ventricular hypertrophy. The document provides a detailed reference for understanding ECG manifestations of different cardiac structural abnormalities.
This document summarizes the evaluation of aortic valve stenosis using echocardiography. It describes the normal aortic valve anatomy and various types of aortic valve stenosis including calcific, bicuspid, rheumatic, and supravalvular or subvalvular stenosis. Doppler echocardiography is used to evaluate aortic valve stenosis severity based on valve area, mean gradient, and peak jet velocity. Stress echocardiography with dobutamine can help distinguish true severe from pseudo-severe low-flow, low-gradient aortic stenosis.
Dr. Abraham discusses sinus node dysfunction and atrioventricular block. Key points include:
- The sinus node is usually located in the right atrium and receives blood supply from the right coronary artery or left circumflex artery.
- Symptoms of sinus node dysfunction range from asymptomatic ECG changes to tachycardia, bradycardia, and tachy-brady syndrome.
- Treatment options include pharmacotherapy with drugs like atropine or theophylline for short term use, and pacemaker implantation for long term treatment of sinus node disease.
- The atrioventricular node receives innervation from the arteries of Koch and shows minimal autonomic innervation. AV block can be first,
This document provides an overview of cardiac arrhythmias including their classification, mechanisms, clinical manifestations, diagnostic approaches and management strategies. It discusses various specific arrhythmias in detail such as atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular arrhythmias, sick sinus syndrome and heart block. Treatment options covered include pharmacological therapies using different classes of antiarrhythmic drugs, procedures like cardiac ablation and use of devices like pacemakers.
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.
AV heart blocks can be caused by drug therapy, ischemic heart disease, degeneration due to age, aortic sclerosis, or cardiac surgery. First degree heart block involves slowed conduction through the AV node, prolonging the PR interval without dropped beats. Second degree heart block involves intermittent conduction, with Mobitz type I (Wenkebach) showing progressively prolonging PR intervals until a dropped beat, and Mobitz type II a constant PR interval with occasional dropped beats. Third degree heart block is a complete failure of AV node conduction, with dissociation between the P wave and QRS complex rates.
The document discusses various electrocardiogram (ECG) criteria for differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy presenting with a wide QRS complex tachycardia. It outlines criteria from Sandler and Marriott (1965), Wellens (1978), Kindwall (1988), Brugada (1991), Vereckei (2008) and Pava (2010). Key criteria that favor VT include QRS duration >140ms, extreme left axis, AV dissociation, monophasic R wave in V1, R/S ratio <1 in V6, and notching of the S wave in V1.
This document discusses various tachyarrhythmias, including:
- Supraventricular tachycardias like atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia.
- Ventricular arrhythmias including ventricular tachycardia and ventricular flutter.
- Irregular rhythms such as atrial fibrillation.
It provides details on characteristics like rate, morphology, underlying causes, and treatment approaches for each type of tachycardia. Emphasis is placed on distinguishing ventricular tachycardia from supraventricular tachycardia with aberrancy in clinical evaluation.
This document provides information on cardiac arrhythmias, including:
- The normal cardiac conduction system and blood flow through the heart.
- Definitions and characteristics of various normal and abnormal sinus rhythms, atrial rhythms, junctional rhythms, and ventricular rhythms based on heart rate, rhythm, P wave presence and morphology, PR interval, and QRS width.
- Key arrhythmias summarized include normal sinus rhythm, sinus bradycardia, sinus tachycardia, premature atrial contractions, atrial fibrillation, atrial flutter, premature junctional contractions, junctional tachycardia, premature ventricular contractions, ventricular tachycardia, and ventricular flutter.
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.
Antiarrhythmic drugs work by altering the conduction of electrical signals in the heart and changing the refractory periods of cardiac cells. They are classified into four classes based on their effects. Class IA drugs like quinidine and procainamide work by slowing the rise of the action potential upstroke, decreasing conduction velocity, and prolonging the refractory period. They have moderate potassium channel blocking effects. Class IA drugs are used for supraventricular arrhythmias and ventricular tachycardia but can cause toxicity like heart block or dangerous arrhythmias.
The ECG records the electrical activity of the heart over time and is the gold standard for diagnosing cardiac arrhythmias and conduction abnormalities. It detects three main waves - the P wave from atrial depolarization, the QRS complex from ventricular depolarization, and the T wave from ventricular repolarization. Abnormalities in conduction through the AV node can cause first-, second-, or third-degree heart block visible on the ECG. Higher degrees of block impair conduction more severely and require treatment such as pacemaker implantation.
The document discusses electrocardiogram (ECG) patterns associated with cardiac chamber enlargement, specifically right atrial enlargement (RAE) and left atrial enlargement (LAE). RAE is suggested by a tall, peaked P wave in leads II, III, AVF and a positive P wave in V1. LAE results in prolongation of the left atrial component of the P wave, increased posterior deviation of the left atrial vector, and left axis deviation of the P wave. The diagnostic accuracy of ECG findings for chamber enlargement is limited but can provide clues when correlated with imaging studies.
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.
Echocardiography is a useful tool for diagnosing and monitoring heart failure patients. It can assess left ventricular ejection fraction, ventricular sizes and wall thickness, valve function, diastolic function, and pulmonary pressures. New techniques such as 3D echocardiography and strain imaging provide more accurate measurements of cardiac structure and function compared to older 2D techniques. Echocardiography is also used to differentiate the causes of heart failure, monitor for complications, and predict patient outcomes. It remains an important part of the evaluation and management of patients with heart failure.
This document discusses various types of conduction disturbances including sinoatrial exit block, AV blocks, bundle branch blocks, and fascicular blocks. It provides details on the definitions, electrocardiogram findings, causes and prevalence of each type. The document concludes with guidelines on indications for permanent pacemaker implantation for acquired AV block, bifascicular/trifascicular block, and after myocardial infarction.
1. The document describes various EKG abnormalities including early repolarization, pericarditis, fascicular blocks, ventricular hypertrophy, electrolyte abnormalities, prolonged QT interval, and more.
2. Key details are provided on differentiating early repolarization from anterior MI and pericarditis. Stages of pericarditis are outlined.
3. Fascicular blocks are described along with their characteristic axis deviations and block locations. Different forms of ventricular hypertrophy and their EKG patterns are also summarized.
This document discusses cardiac arrhythmias and their treatment. It defines normal cardiac rhythm and atrial arrhythmias. It describes the cardiac action potential and ECG waves. It explains the differences between pacemaker and non-pacemaker cell action potentials. The document discusses mechanisms of arrhythmias including disorders of impulse formation and conduction. It provides an overview of antiarrhythmic drug classes and mechanisms of action including sodium channel blockade, beta-blockade, and calcium channel blockade.
This document provides an overview of how to interpret common ECG abnormalities through 3 sentences or less summaries:
1) It outlines how to measure rate, rhythm, intervals, complexes, and waves on an ECG and identifies what is considered normal.
2) Key abnormal rhythms, rates, intervals, and waves are defined along with their potential causes, such as sinus bradycardia, atrial fibrillation, various heart blocks, ventricular tachycardia, ST segment changes, T wave inversions, bundle branch blocks, and more.
3) Methods for localizing myocardial infarctions and abnormalities seen in conditions like hyperkalemia and hypothermia are also summarized.
This document discusses bradyarrhythmias and approach to treatment. It defines various types of sinus node dysfunction and AV conduction blocks including sick sinus syndrome, sinus pause, sinus arrest, tachy-brady syndrome, and different degrees of AV block. It describes evaluation of sinus node function including intrinsic heart rate, sinus node recovery time and SA conduction time. It discusses reversible and irreversible causes of bradyarrhythmias and guidelines for pacemaker implantation for sinus node and AV node dysfunction. Treatment options including medications and permanent pacing are outlined.
This document provides guidance on electrocardiogram (ECG) interpretation. It begins with descriptions of normal ECG appearances and measurements. It then discusses approaches to reading an ECG, including evaluating heart rate, rhythm, axis, and abnormalities. Common conduction abnormalities and what parts of the heart different abnormalities indicate are defined. The document concludes with descriptions of abnormalities in various ECG components like ST segments, T waves, and Q waves as well as the typical evolution of a myocardial infarction on ECG.
This document provides guidance on electrocardiogram (ECG) interpretation. It begins with descriptions of normal ECG appearances and measurements. It then discusses approaches to reading an ECG, including evaluating the patient details, heart rate, rhythm, axis, and conduction abnormalities. Various abnormalities are described such as arrhythmias, conduction blocks, abnormal P waves, QRS complexes, ST segments, and T waves. Causes and indications of different abnormalities are provided. The document concludes with descriptions of myocardial infarction patterns on ECG over time.
This document provides a comprehensive overview of EKG interpretation. It defines the various EKG waves, intervals, segments and complexes. It describes normal values as well as abnormalities related to conditions like myocardial infarction, hypertrophy, conduction blocks, electrolyte imbalances, hypothermia and more. Causes of variations in waves, intervals and complexes are discussed in detail. Commonly seen arrhythmias and their mechanisms are also explained.
The document provides steps for analyzing electrocardiograms (ECGs). It discusses evaluating the rhythm, rate, P-wave, PR interval, QRS complex, and other aspects. The key steps are:
1. Analyze the rhythm as regular or irregular and the rate as normal, bradycardia, or tachycardia.
2. Examine the P-wave for size, shape, and abnormalities.
3. Measure the PR interval and check for abnormalities like prolongation.
4. Inspect the QRS complex for duration, amplitude, and progression.
The document discusses various cardiac rhythm disorders and mechanisms including:
1. Abnormal automaticity, triggered activity, and reentry can cause arrhythmias. Reentry requires both a substrate and a trigger.
2. Bundle branch blocks are conduction disorders involving the left or right bundle branch and are diagnosed based on specific ECG criteria including QRS width and morphology.
3. Bradyarrhythmias are classified based on whether they involve impaired impulse formation in the sinus node or conduction blocks in the AV node. Examples of each type are described briefly.
The document provides an overview of electrocardiography (ECG) basics including lead positions, ECG paper and timing, standardization, the normal ECG waves including P, PR, QRS, ST segments, T waves, and QT interval, and abnormalities. Key findings of right and left ventricular hypertrophy, atrial enlargement, bundle branch blocks, myocardial infarction, and various degrees of atrioventricular block are also summarized.
This document provides information on various types of arrhythmias including:
- Supraventricular arrhythmias like atrial flutter and atrial fibrillation which involve rapid and irregular atrial rhythms.
- Re-entry supraventricular tachycardia which is caused by an extra connection between the atria and ventricles.
- Wolff-Parkinson-White syndrome which results from an abnormal accessory pathway that can cause supraventricular tachycardia.
- Ventricular arrhythmias like ventricular tachycardia and ventricular fibrillation which involve rapid and life-threatening rhythms originating in the ventricles.
- Bradyarrhythmias including different
This document provides definitions and descriptions of various cardiac arrhythmias in 3-5 bullet points each, covering topics such as rate, P wave characteristics, QRS width, conduction patterns, rhythm, common causes, and potential treatment approaches. A total of 16 different arrhythmias are defined, including sinus tachycardia, sinus bradycardia, premature atrial contractions, atrial fibrillation, various types of heart block, bundle branch block, ventricular premature complexes, ventricular tachycardia, ventricular fibrillation, idioventricular rhythm, and asystole. The document serves as an educational guide for technicians on how to recognize and classify different arrhythmia patterns.
The document discusses several ECG tracings showing different types of arrhythmias and conduction abnormalities. It provides analysis of each case, identifying features that indicate the rhythm, site of block, underlying conditions, and clinical implications. Key details are highlighted for educational purposes to aid in ECG 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.
This document discusses arrhythmias and their classification, pathogenesis, clinical presentation, diagnosis and management. It covers topics such as:
1. Arrhythmias are abnormal heart rhythms that can cause symptoms and health risks if left untreated. They are classified as bradyarrhythmias or tachyarrhythmias.
2. Causes of arrhythmias include reentry mechanisms, enhanced automaticity of ectopic foci, and multiple enhanced foci.
3. Management depends on the specific arrhythmia but may involve rate control with medications, cardioversion, ablation procedures, or pacemaker implantation.
How to read ECG systematically with practice strips Khaled AlKhodari
This lecture simplifies the steps of reading ECG systematically. It starts with a simple heart anatomy and the logical steps that should be followed to perfect ECG reading without missing any abnormality. Finally, there are some practice ECG strips that include but not only MI, STEMI, Wellens syndrome, Pulmonary embolism, LVH, arrhythmias... and others
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 information about electrocardiogram (ECG) rhythms, intervals, abnormalities and their causes and treatments. It discusses normal sinus rhythm and various arrhythmias including sinus tachycardia, sinus bradycardia, supraventricular tachycardia, ventricular tachycardia, atrial fibrillation, atrial flutter, and heart block. It also covers abnormalities of the P-R interval, diseases of the atria and ventricles, bundle branch blocks, myocardial infarctions and localization based on ECG findings. Treatment options are provided depending on hemodynamic stability and the specific arrhythmia or condition.
Similar to Bradycardias and conduction defects (20)
Anorexia nervosa
Definition and presentation
Key features:
Weight loss, typically via restriction of caloric intake ('restricting type'). Can also be of a binge/purge type, involving behaviours such as vomiting, intense exercise, or laxative use.
Results in weight less than 85% of that expected, or BMI 17 is mild.
Fear of weight gain.
Feeling fat when thin.
Endocrine dysfunction: amenorrhea for 3 months, or ↓libido in men.
Other features:
Mental state: fatigue, impaired cognition due to cerebral atrophy, altered sleep.
Sensations: cold sensitive, dizzy.
CV: arrhythmias due to hypokalaemia, heart failure. Hypokalaemia is usually a consequence of purging behaviour.
Sexual: psychosexual problems, ↓fertility.
GI: constipation.
Skin: dry skin, fine body hair (lanugo).
Bone: osteoporosis, dental caries.
Obs: ↓temperature, ↓BP, ↓HR.
Schizophrenia
Pathophysiology and epidemiology
Dopamine theory:
Overactive dopamine system, especially in the mesolimbic area, causes the positive symptoms of schizophrenia.
Associated brain changes:
Larger lateral ventricles.
Reduced volume of the frontal lobe, parahippocampal gyrus, hippocampus, temporal lobe, and/or amygdala.
None of these changes are especially sensitive or specific.
Epidemiology:
0.5% lifetime risk.
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multiple myeloma
Pathophysiology
Malignant proliferation of plasma cells in the bone marrow.
Causes bone marrow destruction via infiltration, and bone destruction via ↑RANKL activity (causing ↑osteoclast activity).
A single clone of plasma cells produce large amounts of identical immunoglobulin (a 'paraprotein' or 'monoclonal band'), as well as free κ or λ light chains (also a 'paraprotein', or 'Bence Jones protein' if in the urine).
Classified by Ig class, with prevalence reflecting prevalence in normal blood: IgG (⅔), IgA (⅓), remainder IgM or IgD.
Immunoglobulin classes other than that of the proliferating clone are relatively low ('immunoparesis').
Epidemiology
Lifetime risk: 1/140.
Incidence steadily increases with age. Rare <55.
Slightly commoner in men.
2x commoner in blacks vs. whites.
Non-Hodgkin's lymphoma (NHL)
Definition
Lymphoma is a malignant proliferation of mature lymphocytes that accumulate in lymph nodes ± other tissue, often as a solid tumour. Differs from leukaemia, which arises in the bone marrow and is present in the blood.
Non-Hodgkin's lymphomas (NHL) represent 80% of all lymphomas, and are distinguished from Hodgkin's lymphoma by the absence of Reed-Sternberg cells on light microscopy.
NHL are a diverse group of conditions, with proliferating cells potentially accumulating in various sites, including lymph nodes, mucosa-associated lymphoid tissue (MALT), CNS, and skin.
90% are B cell proliferations, 10% T cell.
Types
Low-grade lymphoma:
Slow growing, good prognosis, but hard to cure.
Follicular lymphoma. CD20 +ve.
Marginal zone lymphoma. Various types including MALT, which can occur in stomach, lung, thyroid, or salivary/tear glands. Generally remain localised to original organ so good prognosis.
Lymphocytic lymphoma. Similar to CLL.
Waldenström's macroglobulinaemia (aka lymphoplasmacytoid lymphoma). ↑IgM production.
Speech problems
Dysphasia
Overview:
• A deficit in the higher language functions i.e. comprehension and generation.
• Aphasia is a total absence.
• Most commonly due to a left anterior circulation stroke.
• If speech is internally consistent but nonsense, it is confusion not dysphasia.
Receptive (Wernicke's) dysphasia
• Temporal lobe lesion.
• Patient can't follow a command e.g. lift a hand. If the problem is only with a series of commands, the more they can manage then the better the prognosis.
This document discusses various visual problems including field defects, diplopia, nystagmus, and vertigo. It defines these conditions and outlines their typical causes. Field defects can result from lesions anywhere along the visual pathway and present as scotomas, hemianopias or quadrantanopias. Diplopia can be binocular or monocular with various causes such as cranial nerve palsies or myasthenia gravis. Nystagmus includes jerk, pendular, and gaze-evoked types and may be congenital or acquired from vestibular or central nervous system lesions. Vertigo can be peripheral from issues like BPPV, Meniere's disease, or vestibular neur
Cranial nerve problems
Neuroanatomy
In simple terms, the cranial nerve nuclei are in 4 groups:
• Cortex: CN1 (olfactory bulb), CN2 (occipital lobe).
• Midbrain: CN3-4.
• Pons: CN5-8.
• Medulla (aka 'bulb'): CN9-12.
Upper motor neuron cranial nerve lesions
Pathophysiology
• Lesions of the cortex or corticobulbar tract.
• The corticobulbar tract supplies all the cranial nerves (except 3, 4, 6) on its way to the medulla.
Neurological examination
Limb motor examination
Mnemonic:
Observe The Patient Really F'ing Carefully.
Observation, Tone, Power, Reflexes, Function, Co-ordination.
Observation
Inspect carefully and for a good amount of time, moving around and crouching to make sure you properly look, including under feet and/or on both sides of hands (turn them over).
Look for SWIFT:
Scarring, and ask if there's any you can't see.
Wasting
Involuntary movements.
Fasciculations: take time, look in plane.
Tremor
Upper limb:
Ask if left or right handed.
Pronator drift: have them extend arms palms up, eyes closed. If there is an UMN lesion, contralateral pronation is stronger, causing pronation ± drift. If there is a cerebellar lesion, the contralateral arm may drift upwards.
Limb rebound: have them push their outstretched, upturned palms against your straight arm. If there is a cerebellar hemisphere lesion, the ipsilateral arm will jump up when you move your arm away.
Hodgkin's lymphoma is a type of lymphoma characterized by the presence of Reed-Sternberg cells. It represents 20% of lymphomas and is a B-cell cancer that commonly involves lymph nodes in the neck. Signs and symptoms include painless swollen lymph nodes and B symptoms such as weight loss, fever, and night sweats. Staging involves imaging tests and determines prognosis and treatment, which typically consists of chemotherapy and radiation therapy. Complications can include infection, superior vena cava obstruction, and secondary cancers from treatment. With treatment, 5-year survival rates are 90% for early stage disease and 75% for later stages.
Non-progressive labour
Management
Steps in managing non-progressive 1st stage are similar to induction of labour, but skipping cervical ripening:
First: analgesia, empty bladder, and ensure membranes ruptured. Artificial rupture if required.
If dilating
Non-progressive 2nd stage:
If fetal malposition (OP or OT): rotate manually, rotation ventouse, or Kielland's forceps.
If position correct(ed) (OA): oxytocin → if unsuccessful, traction ventouse or forceps.
C-section if above steps fail.
Complications
Postpartum hemorrhage.
Uterine rupture.
Fistula
Shoulder dystocia.
Hypoxia
Gestational diabetes (GDM)
Pathophysiology
↑Progesterone and cortisol → ↑insulin resistance → ↑glucose in previously non-diabetic woman.
Usually develops at 24-28 weeks.
See separate page on diabetes management in pregnancy for women with pre-existing diabetes.
Risk factors
MACROS:
Medical or family history of GDM, macrosomia, or T2 diabetes.
Age >40 years.
Cystic: PCOS.
Race: non-white, including South Asian and black Caribbean.
Obese
Smoking
Investigations
If there are risk factors, do oral glucose tolerance test (OGTT) after fasting overnight:
Check plasma glucose, give 75 g glucose, then repeat plasma glucose after 2 hours.
≥5.6 mmol/L fasting OR ≥7.8 mmol/L at 2h = GDM.
Who and when to test:
If they have a past history of GDM or BMI ≥40, test at 18 weeks and re-test at 28 weeks if normal.
All other risk factors: test once at 24-28 weeks.
Check HbA1c at diagnosis to identify any pre-existing type 2 diabetes.
Pathophysiology and epidemiology
Implantation of a fertilised egg outside of the uterus. Almost uniformly unviable.
Affects 1/100 pregnancies.
98% are tubal, usually in the ampulla. Remainder are in the ovaries, cervix, and peritoneum, the latter sometimes carrying to the 3rd trimester.
Eventually, trophoblast invasion of the tubal wall can cause tubal rupture and potentially major haemorrhage. However, many cases resolve spontaneously without rupture.
Presentation
Typical presentation:
Patients usually present 6-8 weeks after last period, though 30% present before a missed period.
Common symptoms are PV bleeding (dark or fresh) – which can occur with or without rupture – and/or abdominal or pelvic pain. However, many patients are asymptomatic.
Other possible features:
Syncope and dizziness.
Shoulder tip pain.
Painful defecation and urination.
Diarrhoea and vomiting.
Adnexal mass or big uterus.
Cervical excitation
Sudden rupture: peritonism and shock.
Pathophysiology
Acute inflammation of the upper genital tract – the uterus or adnexa – from an ascending infection – usually chlamydia or gonorrhea (25%). May lead to epithelial damage thus allowing further pathogen entry.
Involves any combination of endometritis, salpingitis, tubo-ovarian abscess, or pelvic peritonitis.
Rarer causes: Gardnerella vaginalis, H. influenzae, Strep agalactiae (Group B Strep), CMV.
Often no pathogen is found.
Signs and symptoms
Symptoms:
Varies from asymptomatic to severe.
Pain: lower abdominal (often bilateral), lower back, and deep dyspareunia.
Systemic: fever, nausea and vomiting.
Discharge and bleeding: cervical or vaginal mucopurulent discharge, postcoital or intermenstrual bleeding.
On bimanual examination, tenderness in the uterus, adnexa, and cervix ('cervical excitation').
Cardiomyopathy
Definition
Abnormal structure or function of the myocardium.
Newer definitions require it to be unexplained by ischaemic, hypertensive, or valvular disease, with the term limited to myocardial diseases with known genetic, morphological, and/or functional characteristics.
It often leads to heart failure, and in rarer cases, sudden cardiac death.
Dilated cardiomyopathy (DCM)
Pathophysiology and epidemiology
Commonest cardiomyopathy. Exact prevalence unclear but probably more than 1/500. Can present at any age.
Features:
Dilated chambers.
Systolic dysfunction.
↓Cardiac output.
Causes:
Idiopathic
Familial, 2/3 of which are autosomal dominant.
Cardiovascular: ischaemia, HTN, valve disease. See 'Definition' above about why this isn't strictly speaking 'cardiomyopathy'.
Myocarditis: viral, Chagas disease.
Alcohol
Pregnancy: Peripartum cardiomyopathy.
Stress: Takotsubo cardiomyopathy.
Tachycardia: 'tachymyopathy', usually in chronic SVT such as atrial flutter or AF.
Multi-system disease: thyrotoxicosis, sarcoidosis, haemochromatosis.
Burn depths
Superficial epidermal (1st degree)
Commonly due to sunburn.
Red, painful, peels.
Heals in days and leaves no scar.
Dermal (2nd degree)
Defining feature: blistering.
Superficial dermal (aka partial thickness):
Pink below blister, blanches on pressure, painful.
Heals in 2–3 weeks and leaves no scar.
Deep dermal (aka full thickness):
Deep red below blister from vasodilation, or red dots (vessels) on white background. No or slow blanching.
May be sensory changes.
>3 weeks to heal, and leaves scar.
Subdermal (3rd degree)
Damage extends into subcutaneous tissue.
White (or charred), painless (insensate), leathery skin.
Heals slowly by contraction.
Definitions
Ulcer: discontinuity of skin with complete break in epidermis and possibly dermis and subcutaneous tissue.
Erosion: partial break in epidermis. Appears bright red and weepy.
Causes
Trauma and/or internal pathology.
Types: arterial, venous, vasculitis, or neuropathic. For the latter, see diabetic foot, the commonest cause of neuropathic ulceration.
Rash history
Much of the diagnosis comes from examining the rash or lesion itself, but history taking is still important.
History of presenting complaint
Features of the rash:
Evolution of rash/lesion over time.
Onset at multiple sites and/or symmetrical? Suggests an internal cause.
Does sun exposure make it worse (e.g. SLE) or better (e.g. psoriasis)?
Associated symptoms:
Itch (common) and pain (uncommon), both of which can be explored with SOCRATES.
Ooze or weeping? Suggests eczema.
Loosing sleep from discomfort?
Possible causes:
Contact with substances at work or as part of a hobby. May cause allergic or irritant contact dermatitis.
Medications.
Sun exposure history if you suspect cancer:
Do you tan/burn often?
Sunbed use.
Lived abroad?
Worked outside?
The medicos PDF app was used to collect this information. I stumbled discovered this amazing app when searching for various slides and books and decided to share it with you all. The Google Play Store has a free version of the app.
ACE inhibitors (ACEi) and angiotensin II receptor blockers (ARB)
Drugs
ACEi include enalapril, ramipril, and lisinopril.
ARBs include losartan and candesartan.
Mechanism
Reduce levels (ACEi) or effects (ARB) of angiotensin II.
Angiotensin II increases BP via systemic vasoconstriction, sodium retention, and aldosterone and ADH release.
Lower efficacy in black patients, so not 1st line in this group.
The medicos PDF app was used to collect this information. I stumbled discovered this amazing app when searching for various slides and books and decided to share it with you all. The Google Play Store has a free version of the app.
The medicos PDF app was used to collect this information. I stumbled discovered this amazing app when searching for various slides and books and decided to share it with you all. The Google Play Store has a free version of the app.
Importance for learners:
MBBS/Dental
Nursing
Pharmacy
Microbiology
BPH
MPH
MDS
MD
Ophthalmology
Paramedics
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In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
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TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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• Pitfalls and pivots needed to use AI effectively in public health
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3. Sick sinus syndrome
Aka sinus node dysfunction.
Usually due to idiopathic SA node fibrosis. May also be secondary to cardiomyopathy, infiltrative
disease (amyloidosis, sarcoidosis, haemochromatosis), drugs (digoxin, β-blockers), or metabolic
problems (↑K+, ↓Ca2+, ↓thyroid).
Causes sinus bradycardia, sinus arrest, or exit block. May also cause episodes of tachycardia
(tachy-brady syndrome, brady-tachy syndrome).
5. Sinoatrial exit block and sinus arrest
Failure of impulse formation (arrest) or conduction from (exit block) the SA node.
Absent P waves on ECG.
Escape rhythm may take over: junctional — narrow QRS 45–60bpm — or ventricular — wide
QRS 30–45 bpm.
Its causes overlap with those of sinus bradycardia, including sick sinus, ↑K+, inferior MI, and CV
drugs.
6. Atrioventricular (AV) block
Aka heart block.
Causes
Idiopathic
RCA infarct (inferior MI), as this supplies the AV node.
Myocarditis
Drugs: β-blockers, calcium channel blockers, adenosine, digoxin, cholinesterase inhibitors.
7. 1st degree AV block
Prolonged PR interval (>0.2 seconds, 5 small squares).
No treatment required.
8. 2nd degree AV block
Intermittent conduction of the P wave to the ventricles.
The conduction ratio is the number of P waves to QRS complexes e.g. 4:3.
A conduction ratio of 2:1 is untypable as it is hard to determine if there is progressive PR
prolongation.
High grade 2nd degree block is when 2 consecutive P waves fail to conduct to the ventricles.
The P waves are regular, distinguishing it from ectopic atrial contractions.
9. 2nd degree AV block type 1
Aka Mobitz type 1, or Wenckebach.
Progressively prolonged PR interval until a P wave fails to transmit to the ventricles.
No treatment required.
Can sometimes be hard to distinguish from Mobitz type 2 when increases in PR are small. Look
for the biggest increase, which is between the 1st and 2nd PR after the missed QRS.
10. 2nd degree AV block type 2
Aka Mobitz type 2.
Constant PR interval but intermittent failure to transmit to the ventricles.
High risk of progression to 3rd degree block so often requires pacemaker treatment.
11. 3rd degree AV block
Aka complete heart block.
No transmission of P waves into ventricles, with a ventricular escape rhythm taking over.
QRS is usually wide, but occasionally the bundle of His provides the pacemaker and thus the QRS
is narrow.
HR 20–40.
This is one cause of AV dissociation. Others include accelerated idioventricular rhythm (ectopic
focus in ventricles with HR 50–110) and VT.
Requires pacemaker.
12. Bundle branch blocks
General features
Blockage in the bundle branches, which lie between the bundle of His and the Purkinje fibres.
Depolarisation instead spreads via the (slower) myocardium, causing broad QRS complexes.
The altered depolarisation sequence also leads to altered repolarisation, and hence ST-T
changes.
13. Left bundle branch block (LBBB)
Causes:
Anterior MI (LAD). May be the initial ECG sign.
HTN
Myocarditis
Cardiomyopathy
Aortic valve disease.
14. ECG:
Deep, wide S in V1 and RSR’ (M-shaped) in V6: SLaM (LBBB).
V1: delayed LV depolarisation results in a deep, wide S wave.
V6: right to left septal depolarisation, instead of the usual left to right, leads to initial R wave in
V6 followed by a dip during RV depolarisation, then 2nd R wave as depolarisation reaches the LV.
Same pattern seen in lead I. Often the middle notch of the M is very small, such that it simply
looks like a broad R wave.
Discordant T waves in V1 and V6.
Criteria: {broad QRS} + {broad R in V6} + {broad S in V1 or 2}.
15. Right bundle branch block (RBBB)
Causes:
Increased RV pressure: primary pulmonary HTN, cor pulmonale, PE.
Acquired heart disease: anterior MI (LAD), myocarditis, cardiomyopathy.
Congenital
Iatrogenic e.g. cardiac catheterisation.
Can also be a normal ECG variant in healthy individuals.
16. ECG:
rSR in V1 (M-shaped) and QRS (W-shaped) in V6: MaRroW (RBBB).
Electrophysiology: the initial rS (V1) and QR (V6) reflect a normal left to right septal
depolarisation and LV depolarisation. The delayed RV depolarisation leads to a 2nd broad R
wave in V1 and a late ‘slurred’ S wave in V6.
Instead of rSR, sometimes V1 simply has one large R ± a small notch as it rises.
Criteria: {broad QRS} + {slurred S V6 and/or rSR V1} + {overall +ve QRS in V1}.
17. Left anterior and posterior fascicular
block
Blockage in one of the two branches of the left bundle branch.
LAFB is much commoner, and in isolation may simply be a benign feature of aging. Other causes
include anterior MI, IHD, aortic valve disease, HTN, or cardiomyopathy.
LPFB is associated with inferior MI or cardiomyopathy.
Aka left anterior and posterior hemiblocks.
18. ECG
QRS normal or slightly prolonged (80–120 ms).
LAFB:
Left axis deviation.
Small Q and tall R (qR pattern) in lateral leads (I and aVL) with prolonged R peak time (>45 ms) in
aVL.
Small R and deep S (rS pattern) in inferior leads.
LPFB is the opposite:
Right axis deviation.
Small R and deep S in lateral leads.
Small Q and tall R in inferior leads, with prolonged R peak time in aVF.
19. Bifasciular and trifascicular block
Bifascicular block:
RBBB plus {LAFB or LPFB}. Conduction is via the single remaining fascicle.
ECG: RBBB plus left or right axis deviation.
Causes: IHD (50%), HTN (25%), aortic stenosis, anterior MI, congenital, ↑K+.
Clinical significance uncertain, but carries a 1% annual risk of progression to complete heart
block.
20. Trifascicular block:
May not be a clinically useful term. It implies blockage in right bundle plus both fascicles, which
is essentially just 3rd degree AV block.
In practice, it may be used to describe an incomplete trifascicular block where there is still
partial/intermittent transmission in one of the fascicles, plus associated 1st/2nd degree AV
block. Resulting ECG shows RBBB, LAFB or LPFB, and prolonged PR.
21. Escape rhythms and ectopic beats
Definitions
Escape rhythm: a non-sinus pacemaker takes over from a non-functioning SA node. Beat
occurs after the next expected sinus beat. HR is <60, except in ‘accelerated’ escape rhythm,
which is 60–100.
Ectopic beat: a non-sinus beat occurs before the next expected sinus beat. Often irregular
ventricular ectopics, which are non-pathological; can also be regular e.g. ventricular bigeminy.
22. ECG findings in escape rhythms
Atrial escape rhythms: HR 40–60, P wave may be inverted.
Junctional escape rhythms: HR 40–60, P wave hidden in QRS complex
Ventricular escape rhythms: HR 20–40, broad QRS.
23. Cardiac axis deviation
Cardiac axis which is less than -30° (left axis deviation, LAD) or greater than +90°
(right axis deviation, RAD).
ECG
Look at the QRS complexes in the limb leads:
In LAD, they’re Leaving (QRS pointing away from each other): +ve QRS (dominant R) in I and aVL,
-ve QRS (dominant S) in II and aVF.
In RAD, they’re Romantic (QRS pointing towards each other): -ve QRS (dominant S) in I and aVL,
+ve QRS (dominant R) in III and aVF.
24. Causes
LAD:
Left anterior fascicular block.
LBBB
LVH
Inferior MI
RAD:
Left posterior fascicular block.
RVH
Lateral MI
Lung disease: PE, COPD.
↑K+
May be a normal variant.
WPW syndrome and ventricular ectopics can cause either.
25. Acute management of bradycardia
1. Atropine 500 mcg IV if there is cardiac ischaemia, syncope, SBP <90, or HF.
2. Further measures if there is inadequate response or risk of asystole: further atropine (up to
3 mg), transcutaenous pacing, adrenaline infusion, or isoprenaline infusion (β1 agonist). Risk
of asystole is defined as severe AV block (3rd degree or 2nd degree type 2), recent asystole,
or ventricular pauses (> 3 s).
3. Definitive management with transvenous and/or permanent pacemaker.
27. Devices and indications
Implantable cardioverter-defibrillators (ICDs) are used to prevent sudden cardiac
death (SCD) in:
{LVSD with EF ❤5%} plus {wide QRS [120–149 ms] or high SCD risk}.
Sustained VT causing syncope or haemodynamic instability.
Congenital high risk conditions e.g. long QT, Brugada, HCM.
Secondary prevention: post VF or VT cardiac arrest.
Permanent pacemakers (PPMs) are used to maintain an adequate heart rate in:
AV block: 3rd degree or 2nd degree type 2.
Sinus node dysfunction with symptomatic bradycardia.
Carotid sinus syndrome.
Cardiac resynchronization therapy (CRT, aka biventricular pacemaker):
Indication: {LVSD NYHA class 2–4 with EF ❤5%} plus {very wide QRS [>150 ms] or LBBB}.
Can be pacer only (CRT-P) or include an ICD function (CRT-D).
28. Structure and mechanism
Pulse generator — comprising a battery, control circuits, and transmitter/receiver — is placed in
the infraclavicular area (subcutaneously or submuscularly). Requires reimplantation every 5–10
years due to battery lifespan.
Pacing leads (one or two) extend from the generator, transvenously, into the right atrium and/or
ventricle (plus left ventricle in CRT), with the tips implanted in the myocardium. These leads
both sense cardiac depolarization and deliver cardiac stimulation.
PPMs can provide either a fixed impulse rate (‘asynchronous’), or an impulse in response to
absent depolarization (‘synchronous’).
ICDs respond to ventricular tachycardias with a defibrillation shock. Many devices also have a
pacer function, both to treat co-morbid arrhythmias and to deliver antitachycardia pacing before
shocking.
29. Pacemaker codes and modes
Standard 5 letter code to describe PPMs, with often just the first 3 used:
1. Where it’s pacing: Atria, Ventricles, or Dual (A+V).
2. Where it’s sensing: Atria, Ventricles, or Dual (A+V).
3. Response to sensing depolarization: Triggers pacing, Inhibits pacing (i.e. doesn’t pace), Dual
(triggers and inhibits).
4. Rate modulation: ability to adjust HR in response to physiological need.
5. Anti-tachycardia function: Pacing, Shock, or Dual (P+S).
30. Common modes:
VVI: no pacing if ventricular depolarization detected, otherwise it paces. AAI is the same for the
atria.
DDD: senses both A and V, and takes over if either don’t work.
VDD: used in AV block, as it senses both A and V but only paces V.
VOO: asynchronous pacing, which should be used during surgery as diathermy may affect
device.
31. Interpreting pacemaker ECGs
Most pacemaker leads sit in RV causing LBBB pattern, though a minority are LV and RBBB.
If patient’s heart rate is above PPM threshold, pacing spikes will be appropriately absent.
See pacemaker and ICD complications for abnormal ECG findings in presence of PPM.
32. Device interrogation and manipulation
Investigate cardiac symptoms in PPM/ICD patients as usual, including with an ECG, but specific device
interrogation may also be needed:
Should be done by specialists using specialist devices. Even in asymptomatic patients it is done
regularly e.g. 3-monthly.
Pacemaker/ICD magnets allow basic device manipulation. When placed over a PPM, it will revert
to asynchronous mode (good if device is undersensing or overpacing), and when placed over an
ICD, it will prevent shocks (but not pacing).
33. Pacemaker and ICD complications
General
Acute (post-placement): pneumothorax, infection, bleeding (including pocket haematoma).
Device-related pain.
ICD malfunctions
Inappropriate ICD shocks: may be triggered by atrial arrhythmias (AF, SVT) or device
malfunction.
Failure to shock. If this occurs, treat ventricular dysrhythmias as usual e.g. external defibrillation,
anti-arrhythmic drugs.
34. PPM malfunctions
Bradycardia
Failure to output/pace: no impulse (e.g. due to device malfunction, battery failure) and hence
no pacing artefact on ECG.
Failure to capture i.e. no response from heart (e.g. due to poor lead contact, cardiac problem).
ECG shows pacing spikes not followed by atrial or ventricular activity.
Oversensing: noise (e.g. movement artefacts) misinterpreted as cardiac activity and hence PPM
fails to pace.
35. Tachycardia
Pacemaker-mediated tachycardia: PPM forms re-entrant loop. Less common with new devices.
Sensor-induced tachycardia: noise (e.g. movement artefacts) misinterpreted as physiologically
increased heart rate and PPM increases rate. Occurs in newer devices which allow
physiologically-varied heart rate in response to need.
Can also be due to all the usual causes of tachycardia e.g. physiological response, SVT.
36. Other dysrhythmias
Undersensing (e.g. due to poor lead contact), leading to asynchronous pacing. Suggested by
pacing spikes within or just after QRS.
Pacemaker syndrome: AV dyssyncrhony due to PPM failing to perfectly replicate normal cardiac
contraction. Causes reduced cardiac output, fatigue, dizziness, and palpitations.
37. Thank You
This information was taken with the help of Medicos PDF app. You can download the app from
Google Play Store. There are tons of slides, book and articles that a medical student should
need.
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