This document discusses various types of cardiac arrhythmias including their mechanisms, ECG features, and treatment approaches. It covers basics of the cardiac action potential and mechanisms that can generate arrhythmias such as accelerated automaticity, triggered activity, and reentry. Specific arrhythmias summarized include:
- Supraventricular tachycardias like sinus tachycardia, AV nodal reentrant tachycardia, AV reciprocating tachycardia, atrial fibrillation, and atrial flutter.
- Ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
- Causes, diagnostic ECG patterns,
This document discusses cardiac arrhythmias including their mechanisms and types. It describes the cardiac action potential and how impulses are conducted regularly through the heart. The main types of arrhythmia are defined as bradycardia which is a slow heart rate, and tachycardia which is a fast heart rate. The mechanisms that can generate arrhythmias include accelerated automaticity, triggered activity, and reentry. Specific types of supraventricular tachycardias such as atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia are then explained in detail.
This document provides an overview of tachyarrhythmias. It begins by defining arrhythmia and tachycardia. It then discusses the etiology, pathogenesis and mechanisms of tachycardia. It describes the different types of tachyarrhythmias including supraventricular tachycardia involving the atria, AV node, and ventricular tachycardia. For each type, it provides details on definition, signs and symptoms, ECG findings, etiology, and treatment approaches. It specifically addresses atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, Wolff-Parkinson-White syndrome, premature ventricular contractions, ventricular tachycardia, and ventricular fib
1. Arrhythmias are disorders of cardiac impulse formation and propagation that are broadly divided into tachyarrhythmias and bradyarrhythmias.
2. Common arrhythmias include atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, heart blocks, and ventricular fibrillation.
3. Treatment depends on the type of arrhythmia but may include medications, cardioversion, ablation, pacemakers, or implantable cardioverter-defibrillators.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
1) Atrial tachycardias can be focal, triggered, or reentrant and include both macroreentrant circuits and focal mechanisms. Sinus node reentry is considered a specific type of focal atrial tachycardia.
2) AV nodal reentrant tachycardia (AVNRT) is a common form of reentrant tachycardia that involves dual pathways in the AV node - a fast and slow pathway. Typical AVNRT uses the slow pathway anterograde and fast pathway retrograde.
3) Other reentrant tachycardias discussed include atypical AVNRT variants, orthodromic and antidromic AV reentrant
This document provides an overview of cardiac arrhythmias, including definitions and descriptions of normal sinus rhythm and various arrhythmias. It discusses the cardiac conduction system and mechanisms that can cause arrhythmias, such as abnormal impulse formation or conduction. Specific arrhythmias summarized include sinus bradycardia, sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. For each arrhythmia, the document provides information on heart rate, rhythm, P wave presence/morphology, and other ECG characteristics.
This document discusses approaches to narrow complex tachycardia. It begins by defining narrow QRS tachycardia as having a QRS width of less than 120ms. It then classifies different types of narrow complex tachycardia by site of origin and regularity, including sinus tachycardia, inappropriate sinus tachycardia, sinus node reentrant tachycardia, atrial tachycardia, atrial flutter, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). It provides details on electrocardiogram features and diagnostic approaches for each type.
This document discusses different types of tachycardias associated with accessory atrioventricular pathways. It describes orthodromic and antidromic accessory pathway mediated tachycardias, as well as concealed accessory pathways. It also covers ventricular arrhythmias including premature complexes, accelerated idioventricular rhythm, ventricular tachycardia, and their treatment. Polymorphic ventricular tachycardia known as torsades de pointes associated with long QT is described.
This document discusses cardiac arrhythmias including their mechanisms and types. It describes the cardiac action potential and how impulses are conducted regularly through the heart. The main types of arrhythmia are defined as bradycardia which is a slow heart rate, and tachycardia which is a fast heart rate. The mechanisms that can generate arrhythmias include accelerated automaticity, triggered activity, and reentry. Specific types of supraventricular tachycardias such as atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia are then explained in detail.
This document provides an overview of tachyarrhythmias. It begins by defining arrhythmia and tachycardia. It then discusses the etiology, pathogenesis and mechanisms of tachycardia. It describes the different types of tachyarrhythmias including supraventricular tachycardia involving the atria, AV node, and ventricular tachycardia. For each type, it provides details on definition, signs and symptoms, ECG findings, etiology, and treatment approaches. It specifically addresses atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, Wolff-Parkinson-White syndrome, premature ventricular contractions, ventricular tachycardia, and ventricular fib
1. Arrhythmias are disorders of cardiac impulse formation and propagation that are broadly divided into tachyarrhythmias and bradyarrhythmias.
2. Common arrhythmias include atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, heart blocks, and ventricular fibrillation.
3. Treatment depends on the type of arrhythmia but may include medications, cardioversion, ablation, pacemakers, or implantable cardioverter-defibrillators.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
1) Atrial tachycardias can be focal, triggered, or reentrant and include both macroreentrant circuits and focal mechanisms. Sinus node reentry is considered a specific type of focal atrial tachycardia.
2) AV nodal reentrant tachycardia (AVNRT) is a common form of reentrant tachycardia that involves dual pathways in the AV node - a fast and slow pathway. Typical AVNRT uses the slow pathway anterograde and fast pathway retrograde.
3) Other reentrant tachycardias discussed include atypical AVNRT variants, orthodromic and antidromic AV reentrant
This document provides an overview of cardiac arrhythmias, including definitions and descriptions of normal sinus rhythm and various arrhythmias. It discusses the cardiac conduction system and mechanisms that can cause arrhythmias, such as abnormal impulse formation or conduction. Specific arrhythmias summarized include sinus bradycardia, sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. For each arrhythmia, the document provides information on heart rate, rhythm, P wave presence/morphology, and other ECG characteristics.
This document discusses approaches to narrow complex tachycardia. It begins by defining narrow QRS tachycardia as having a QRS width of less than 120ms. It then classifies different types of narrow complex tachycardia by site of origin and regularity, including sinus tachycardia, inappropriate sinus tachycardia, sinus node reentrant tachycardia, atrial tachycardia, atrial flutter, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). It provides details on electrocardiogram features and diagnostic approaches for each type.
This document discusses different types of tachycardias associated with accessory atrioventricular pathways. It describes orthodromic and antidromic accessory pathway mediated tachycardias, as well as concealed accessory pathways. It also covers ventricular arrhythmias including premature complexes, accelerated idioventricular rhythm, ventricular tachycardia, and their treatment. Polymorphic ventricular tachycardia known as torsades de pointes associated with long QT is described.
This document provides an overview of various tachyarrhythmias including their conduction pathways, pathophysiology, ECG characteristics, and treatment approaches. Key points covered include:
- The conduction system of the heart and action potentials across cardiac tissues.
- Causes of tachyarrhythmias including increased automaticity, triggered activity, and reentry.
- Algorithm for evaluating and treating stable vs. unstable tachyarrhythmias.
- Characteristics and management of common tachyarrhythmias like atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and ventricular tachycardia.
- Use of synchronized cardioversion for unstable rhythms
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. Evaluation involves analyzing the ECG for P wave presence and morphology, QRS duration and morphology, and the relationship between P waves and QRS complexes. Treatment involves vagal maneuvers, adenosine, calcium channel blockers, beta blockers
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. It provides guidance on evaluating the ECG and patient response to determine the mechanism and appropriate treatment. Treatment options discussed include vagal maneuvers, adenosine, calcium channel blockers, beta blockers, and cardioversion for 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.
This document discusses different types of cardiac arrhythmias including bradyarrhythmias which are slow heart rhythms and tachyarrhythmias which are fast heart rhythms. It describes specific arrhythmias like sinus bradycardia, atrial fibrillation, atrial flutter, atrioventricular reciprocating tachycardia, ventricular fibrillation, and ventricular tachycardia. It also discusses diagnostic studies, management through lifestyle changes and medications, and treatment options like cardioversion, pacemakers, surgery, and ablation for various arrhythmias.
This document discusses algorithms and ECG parameters for differentiating between types of narrow complex tachycardia, including atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Key parameters discussed include the presence of pseudo waves, retrograde P wave morphology and position, and the RP interval. The Jaeggi algorithm uses these parameters to differentiate AVNRT from AVRT based on ECG analysis alone in 76% of cases. Retrograde P wave morphology varies depending on the location of the accessory pathway in cases of AVRT.
Arrhythmias refer to abnormalities in the cardiac rhythm. There are two main types: bradycardia where the heart rate is slow, and tachycardia where the heart rate is fast. Specific arrhythmias include sinus bradycardia, various types of heart block, atrial fibrillation, atrial flutter, AV nodal re-entry tachycardia, ventricular tachycardia, and ventricular fibrillation. Diagnosis involves electrocardiography and other tests. Treatment depends on the type of arrhythmia but may include medications, catheter ablation, pacemaker implantation, or cardioversion. Lifestyle modifications and avoiding arrhythmia triggers can also help management.
1. Tachyarrhythmias are abnormal heart rhythms with a rate over 100 beats per minute. They can originate from the atria, AV node, or ventricles.
2. Common supraventricular tachycardias include sinus tachycardia, atrial fibrillation, atrial flutter, and AV nodal reentrant tachycardia. Atrial fibrillation is characterized by irregularly irregular rhythm without P waves.
3. Ventricular arrhythmias include premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation. Polymorphic ventricular tachycardia can degenerate into ventricular fibrillation and requires immediate defibrillation.
Cardiac arrhythmia refers to any abnormal heart rhythm and can cause the heart rate to be too fast, too slow, or irregular. Common types include sinus tachycardia, ventricular tachycardia, sinus bradycardia, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, premature atrial contractions, premature ventricular contractions, and nodal rhythm. Treatment depends on the specific arrhythmia but may include medications, cardioversion, pacemakers, ablation, or defibrillation.
This document summarizes various cardiac arrhythmias including supraventricular arrhythmias like premature atrial complexes, atrial fibrillation, and atrial flutter as well as ventricular arrhythmias such as premature ventricular complexes and ventricular tachycardia. For each arrhythmia, it describes the characteristic ECG patterns including P wave morphology, QRS width, and rhythm irregularity. It also discusses distinguishing features, causes, and clinical implications of different arrhythmias.
This document discusses various tachyarrhythmias classified by their electrocardiographic features and mechanisms. Broad complex tachycardias include ventricular tachycardia, ventricular flutter, torsades de pointes, and ventricular fibrillation. Narrow complex tachycardias originate from supraventricular structures and include sinus tachycardia, atrial fibrillation, atrial flutter, atrioventricular nodal reentrant tachycardia, and accessory pathway mediated tachycardias. Specific tachycardias like inappropriate sinus tachycardia, multifocal atrial tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation are also described.
1. Supraventricular tachycardia (SVT) refers to a group of tachyarrhythmias originating above the ventricles. Paroxysmal SVT is characterized by episodes of tachycardia with abrupt onset and termination.
2. The main types of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and focal atrial tachycardia. They have different mechanisms and ECG patterns that can help determine the underlying rhythm.
3. Acute management involves vagal maneuvers, medications like adenosine or beta blockers, or cardio
This document provides an overview of cardiac arrhythmias that may be seen in the surgical intensive care unit (SICU). It begins with definitions of normal sinus rhythm and mechanisms of arrhythmias including automaticity, ectopic foci, and reentry. Common arrhythmias are then described in more detail such as sinus bradycardia, atrial fibrillation, ventricular tachycardia, and various forms of heart block. Causes and management of arrhythmias are discussed with a focus on the relevant medical literature. Antiarrhythmic drug classes and their uses and side effects are also reviewed.
Arrhythmias are abnormal heart rhythms that can be caused by issues with the heart's electrical conduction system or structural problems with heart muscles or valves. Common causes include ischemia, electrolyte imbalances, cardiomyopathy, and genetic conditions. Arrhythmias are classified based on heart rate, regularity, site of origin in the heart, and ECG characteristics. They are often due to reentry circuits, abnormal automaticity, or heart block. Treatment involves medications to suppress arrhythmias or restore normal rhythm, ablation procedures, or pacemakers.
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
This document describes different types of supraventricular tachycardias (SVTs), which are rapid heart rhythms originating above the ventricles. It defines SVTs and paroxysmal supraventricular tachycardia (PSVT), and lists common symptoms. The types of SVTs are categorized based on their origin in the sinoatrial node, atria, or atrioventricular node/junction. Each type has a distinct electrocardiogram appearance and cause, such as reentry circuits, ectopic foci, or increased node automaticity. Common examples include AV nodal reentrant tachycardia, atrial fibrillation, atrial flutter, and Wolff-Parkinson-
1. This document discusses the approach to evaluating and diagnosing narrow complex tachycardias. It describes the main mechanisms that can cause tachycardias including enhanced automaticity, triggered activity, and reentry.
2. Specific tachycardia types are then discussed in detail including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), and inappropriate sinus tachycardia. The diagnostic criteria and distinguishing characteristics of each are provided.
3. A number of other arrhythmias are also briefly covered such
The document discusses various types of arrhythmias that may occur during anesthesia including narrow and broad complex arrhythmias. It defines arrhythmia and outlines the conduction pathways in the heart. For narrow complex arrhythmias it describes sinus arrhythmias, premature atrial contractions, sinus bradycardia, sinus tachycardia, junctional tachycardia, atrial flutter and fibrillation. For broad complex arrhythmias it covers ventricular ectopy, ventricular tachycardia and fibrillation. Management strategies are provided for selected arrhythmias.
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.
ECG changes, changes in intraventricular conductionDeepikaLingam2
This document provides an overview of common ECG changes seen in various cardiac conditions including:
- Intraventricular conduction abnormalities, arrhythmias, injury, infarction, electrolyte imbalances, and atrial and ventricular enlargement.
It describes sinus rhythm and arrhythmias, different types of dysrhythmias categorized by heart rate, and characteristics of junctional and ventricular dysrhythmias. Specific arrhythmias like atrial fibrillation, bundle branch blocks, AV blocks, and Wolff-Parkinson-White syndrome are outlined. Finally, ECG patterns of ischemia, injury and infarction in different areas of the heart are identified.
This document provides an overview of various tachyarrhythmias including their conduction pathways, pathophysiology, ECG characteristics, and treatment approaches. Key points covered include:
- The conduction system of the heart and action potentials across cardiac tissues.
- Causes of tachyarrhythmias including increased automaticity, triggered activity, and reentry.
- Algorithm for evaluating and treating stable vs. unstable tachyarrhythmias.
- Characteristics and management of common tachyarrhythmias like atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and ventricular tachycardia.
- Use of synchronized cardioversion for unstable rhythms
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. Evaluation involves analyzing the ECG for P wave presence and morphology, QRS duration and morphology, and the relationship between P waves and QRS complexes. Treatment involves vagal maneuvers, adenosine, calcium channel blockers, beta blockers
This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. It provides guidance on evaluating the ECG and patient response to determine the mechanism and appropriate treatment. Treatment options discussed include vagal maneuvers, adenosine, calcium channel blockers, beta blockers, and cardioversion for 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.
This document discusses different types of cardiac arrhythmias including bradyarrhythmias which are slow heart rhythms and tachyarrhythmias which are fast heart rhythms. It describes specific arrhythmias like sinus bradycardia, atrial fibrillation, atrial flutter, atrioventricular reciprocating tachycardia, ventricular fibrillation, and ventricular tachycardia. It also discusses diagnostic studies, management through lifestyle changes and medications, and treatment options like cardioversion, pacemakers, surgery, and ablation for various arrhythmias.
This document discusses algorithms and ECG parameters for differentiating between types of narrow complex tachycardia, including atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Key parameters discussed include the presence of pseudo waves, retrograde P wave morphology and position, and the RP interval. The Jaeggi algorithm uses these parameters to differentiate AVNRT from AVRT based on ECG analysis alone in 76% of cases. Retrograde P wave morphology varies depending on the location of the accessory pathway in cases of AVRT.
Arrhythmias refer to abnormalities in the cardiac rhythm. There are two main types: bradycardia where the heart rate is slow, and tachycardia where the heart rate is fast. Specific arrhythmias include sinus bradycardia, various types of heart block, atrial fibrillation, atrial flutter, AV nodal re-entry tachycardia, ventricular tachycardia, and ventricular fibrillation. Diagnosis involves electrocardiography and other tests. Treatment depends on the type of arrhythmia but may include medications, catheter ablation, pacemaker implantation, or cardioversion. Lifestyle modifications and avoiding arrhythmia triggers can also help management.
1. Tachyarrhythmias are abnormal heart rhythms with a rate over 100 beats per minute. They can originate from the atria, AV node, or ventricles.
2. Common supraventricular tachycardias include sinus tachycardia, atrial fibrillation, atrial flutter, and AV nodal reentrant tachycardia. Atrial fibrillation is characterized by irregularly irregular rhythm without P waves.
3. Ventricular arrhythmias include premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation. Polymorphic ventricular tachycardia can degenerate into ventricular fibrillation and requires immediate defibrillation.
Cardiac arrhythmia refers to any abnormal heart rhythm and can cause the heart rate to be too fast, too slow, or irregular. Common types include sinus tachycardia, ventricular tachycardia, sinus bradycardia, paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, premature atrial contractions, premature ventricular contractions, and nodal rhythm. Treatment depends on the specific arrhythmia but may include medications, cardioversion, pacemakers, ablation, or defibrillation.
This document summarizes various cardiac arrhythmias including supraventricular arrhythmias like premature atrial complexes, atrial fibrillation, and atrial flutter as well as ventricular arrhythmias such as premature ventricular complexes and ventricular tachycardia. For each arrhythmia, it describes the characteristic ECG patterns including P wave morphology, QRS width, and rhythm irregularity. It also discusses distinguishing features, causes, and clinical implications of different arrhythmias.
This document discusses various tachyarrhythmias classified by their electrocardiographic features and mechanisms. Broad complex tachycardias include ventricular tachycardia, ventricular flutter, torsades de pointes, and ventricular fibrillation. Narrow complex tachycardias originate from supraventricular structures and include sinus tachycardia, atrial fibrillation, atrial flutter, atrioventricular nodal reentrant tachycardia, and accessory pathway mediated tachycardias. Specific tachycardias like inappropriate sinus tachycardia, multifocal atrial tachycardia, polymorphic ventricular tachycardia, and ventricular fibrillation are also described.
1. Supraventricular tachycardia (SVT) refers to a group of tachyarrhythmias originating above the ventricles. Paroxysmal SVT is characterized by episodes of tachycardia with abrupt onset and termination.
2. The main types of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and focal atrial tachycardia. They have different mechanisms and ECG patterns that can help determine the underlying rhythm.
3. Acute management involves vagal maneuvers, medications like adenosine or beta blockers, or cardio
This document provides an overview of cardiac arrhythmias that may be seen in the surgical intensive care unit (SICU). It begins with definitions of normal sinus rhythm and mechanisms of arrhythmias including automaticity, ectopic foci, and reentry. Common arrhythmias are then described in more detail such as sinus bradycardia, atrial fibrillation, ventricular tachycardia, and various forms of heart block. Causes and management of arrhythmias are discussed with a focus on the relevant medical literature. Antiarrhythmic drug classes and their uses and side effects are also reviewed.
Arrhythmias are abnormal heart rhythms that can be caused by issues with the heart's electrical conduction system or structural problems with heart muscles or valves. Common causes include ischemia, electrolyte imbalances, cardiomyopathy, and genetic conditions. Arrhythmias are classified based on heart rate, regularity, site of origin in the heart, and ECG characteristics. They are often due to reentry circuits, abnormal automaticity, or heart block. Treatment involves medications to suppress arrhythmias or restore normal rhythm, ablation procedures, or pacemakers.
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
This document describes different types of supraventricular tachycardias (SVTs), which are rapid heart rhythms originating above the ventricles. It defines SVTs and paroxysmal supraventricular tachycardia (PSVT), and lists common symptoms. The types of SVTs are categorized based on their origin in the sinoatrial node, atria, or atrioventricular node/junction. Each type has a distinct electrocardiogram appearance and cause, such as reentry circuits, ectopic foci, or increased node automaticity. Common examples include AV nodal reentrant tachycardia, atrial fibrillation, atrial flutter, and Wolff-Parkinson-
1. This document discusses the approach to evaluating and diagnosing narrow complex tachycardias. It describes the main mechanisms that can cause tachycardias including enhanced automaticity, triggered activity, and reentry.
2. Specific tachycardia types are then discussed in detail including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), and inappropriate sinus tachycardia. The diagnostic criteria and distinguishing characteristics of each are provided.
3. A number of other arrhythmias are also briefly covered such
The document discusses various types of arrhythmias that may occur during anesthesia including narrow and broad complex arrhythmias. It defines arrhythmia and outlines the conduction pathways in the heart. For narrow complex arrhythmias it describes sinus arrhythmias, premature atrial contractions, sinus bradycardia, sinus tachycardia, junctional tachycardia, atrial flutter and fibrillation. For broad complex arrhythmias it covers ventricular ectopy, ventricular tachycardia and fibrillation. Management strategies are provided for selected arrhythmias.
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.
ECG changes, changes in intraventricular conductionDeepikaLingam2
This document provides an overview of common ECG changes seen in various cardiac conditions including:
- Intraventricular conduction abnormalities, arrhythmias, injury, infarction, electrolyte imbalances, and atrial and ventricular enlargement.
It describes sinus rhythm and arrhythmias, different types of dysrhythmias categorized by heart rate, and characteristics of junctional and ventricular dysrhythmias. Specific arrhythmias like atrial fibrillation, bundle branch blocks, AV blocks, and Wolff-Parkinson-White syndrome are outlined. Finally, ECG patterns of ischemia, injury and infarction in different areas of the heart are identified.
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5. Cardiac Arrhythmias
●An abnormality of the cardiac rhythm is called a
cardiac arrhythmia.
● Arrhythmias may cause sudden death, syncope,
heart failure, dizziness, palpitations or no
symptoms at all.
● There are two main types of arrhythmia:
bradycardia: the heart rate is slow (< 60 b.p.m).
tachycardia: the heart rate is fast (> 100 b.p.m).
6. Mechanisms of Cardiac Arrhythmias
Mechanisms of bradicardias:
Sinus bradycardia is a result of abnormally slow
automaticity while bradycardia due to AV block is caused by
abnormal conduction within the AV node or the distal AV
conduction system.
Mechanisms generating tachycardias include:
- Accelerated automaticity.
- Triggered activity
- Re-entry (or circus movements)
7. ACCELERATED AUYOMATICITY
• It occurs due to increasing the rate of
diastolic depolarization or changing the
threshold potential.
• Abnormal automaticity can occur in
virtually all cardiac tissues and may initiate
arrhythmias.
• Such changes are thought to produce sinus
tachycardia, escape rhythms and accelerated
AV nodal (junctional) rhythms.
8. TRIGGERED ACTIVITY
• Myocardial damage can result in oscillations of the
transmembrane potential at the end of the action potential.
These oscillations, which are called 'after depolarizations',
may reach threshold potential and produce an arrhythmia.
• The abnormal oscillations can be exaggerated by pacing,
catecholamines, electrolyte disturbances, and some
medications.
• Examples as atrial tachycardias produced by digoxin
toxicity and the initiation of ventricular arrhythmia in the
long QT syndrome.
9. Re-entry (or circus movement)
• The mechanism of re-entry occurs when a 'ring' of cardiac
tissue surrounds an inexcitable core (e.g. in a region of
scarred myocardium). Tachycardia is initiated if an ectopic
beat finds one limb refractory (α) resulting in
unidirectional block and the other limb excitable. Provided
conduction through the excitable limb (β) is slow enough,
the other limb (α) will have recovered and will allow
retrograde activation to complete the re-entry loop. If the
time to conduct around the ring is longer than the recovery
times (refractory periods) of the tissue within the ring,
circus movement will be maintained, producing a run of
tachycardia.
• The majority of regular paroxysmal tachycardias are
produced by this mechanism.
12. SUPRAVENTRICULAR TACHYCARDIAS
• Supraventricular tachycardias (SVTs) arise from the
atrium or the atrioventricular junction.
• Conduction is via the His-Purkinje system; therefore
the QRS shape during tachycardia is usually similar to
that seen in the same patient during baseline rhythm.
13. Causes of SVT
Tachycardia ECG features Comment
Sinus tachycardia P wave morphology similar to sinus
rhythm
Need to determine underlying cause
AV nodal re-entry tachycardia (AVNRT) No visible P wave, or inverted P wave
immediately before or after QRS
complex
Commonest cause of palpitations in patients
with normal hearts
AV reciprocating tachycardia (AVRT) P wave visible between QRS and T
wave complexes
Due to an accessory pathway. If pathway
conducts in both directions, ECG during
sinus rhythm may be pre-excited
Atrial fibrillation Irregularly irregular RR intervals and
absence of organized atrial activity
Commonest tachycardia in patients over 65
years
Atrial flutter Visible flutter waves at 300/min (saw-
tooth appearance) usually with 2 : 1 AV
conduction
Suspect in any patient with regular SVT at
150/min
Atrial tachycardia Organized atrial activity with P wave
morphology different from sinus
rhythm
Usually occurs in patients with structural
heart disease
Multifocal atrial tachycardia Multiple P wave morphologies (≥3) and
irregular RR intervals
Rare arrhythmia; most commonly associated
with significant chronic lung disease
Accelerated junctional tachycardia ECG similar to AVNRT Rare in adults
14. SVT
Sinus tachycardia
• A condition in which the heart rate is 100-160/min
• Symptoms may occur with rapid heart rates including;
weakness, fatigue, dizziness, or palpitations.
• Sinus tachycardia is often temporary, occurring under
stresses from exercise, strong emotions, fever,
dehydration, thyrotoxicosis, anemia and heart failure.
• If necessary, beta-blockers may be used to slow the
sinus rate, e.g. in hyperthyroidism
17. Atrial Arrhythmias
Premature supraventricular contractions or
premature atrial contractions (PAC)
• A condition in which an atrial pacemaker site above the
ventricles sends out an electrical signal early. The
ventricles are usually able to respond to this signal, but
the result is an irregular heart rhythm.
• PACs are common and may occur as the result of
stimulants such as coffee, tea, alcohol, cigarettes, or
medications.
• Treatment is rarely necessary.
19. SVT
Paroxysmal Supraventricular tachycardia [HR 160-
250/min]
• Atrioventricular nodal re-entry tachycardia (AVNRT)
• It usually begins and ends rapidly, occurring in repeated periods. This
condition can cause symptoms such as weakness, fatigue, dizziness,
fainting, or palpitations if the heart rate becomes too fast.
• In AVNRT, there are two functionally and anatomically different
pathways within the AV node: one is characterized by a short effective
refractory period and slow conduction, and the other has a longer
effective refractory period and conducts faster.
• In sinus rhythm, the atrial impulse that depolarizes the ventricles
usually conducts through the fast pathway.
• If the atrial impulse (e.g. an atrial premature beat) occurs early when
the fast pathway is still refractory, the slow pathway takes over in
propagating the atrial impulse to the ventricles. It then travels back
through the fast pathway which has already recovered its excitability,
thus initiating the most common 'slow-fast', or typical, AVNRT.
20. AVNRT (continue)
The rhythm is recognized on ECG by normal regular QRS
complexes, usually at a rate of 140-240 per minute. Sometimes
the QRS complexes will show typical bundle branch block. P
waves are either not visible or are seen immediately before or
after the QRS complex because of simultaneous atrial and
ventricular activation.
21. SVT
Atrioventricular reciprocating tachycardia
(AVRT)
• In AVRT there is a large circuit comprising the
AV node, the His bundle, the ventricle and an
abnormal connection from the ventricle back to
the atrium. This abnormal connection is called an
accessory pathway or bypass tract.
• Bypass tracts result from incomplete separation of
the atria and the ventricles during fetal
development.
• Atrial activation occurs after ventricular activation
and the P wave is usually clearly seen between the
QRS and T complexes
22. PSVT
Acute Management
• Patients presenting with SVTs and haemodynamic instability
require emergency cardioversion.
• If the patient is haemodynamically stable, vagal manoeuvres,
including right carotid massage, Valsalva manoeuvre and
facial immersion in cold water can be successfully
employed.
• If not successful, intravenous adenosine (up to 0.25 mg/kg) ,
verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or
beta-blockers should be tried.
Long-term management
• It includes ablation of an accessory pathway. Also,
verapamil, diltiazem & β-blockers; are effective in 60-80%
of patients.
23. N.B.
The Wolf Parkinson White Syndrome (WPW)
►An abnormal band of atrial tissue connects the atria and
ventricles and can electrically bypass the normal
pathways of conduction; a re-entry circuit can develop
causing paroxysms of tachycardia.
►ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
►Drug treatment includes flecainamide, amiodarone or
disopyramide.
►Digoxin and verapamil are contraindicated.
►Transvenous catheter radiofrequency ablation is the
treatment of choice.
25. Atrial Arrhythmias
Atrial flutter (HR200-350/min)
• A condition in which the electrical signals come from
the atria at a fast but even rate, often causing the
ventricles to contract faster and increase the heart rate.
• When the signals from the atria are coming at a faster
rate than the ventricles can respond to, the ECG pattern
develops a signature "sawtooth" pattern, showing two
or more flutter waves between each QRS complex.
26. Atrial Arrhythmias
Atrial flutter (TREATMENT)
• Treatment of the symptomatic acute paroxysm is
electrical cardioversion.
• Patients who have been in atrial flutter more than 1-2
days should be treated in a similar manner to patients
with atrial fibrillation and anticoagulated for 4 weeks
prior to cardioversion.
• Recurrent paroxysms may be prevented by class Ic and
class III agents
• The treatment of choice for patients with recurrent
atrial flutter is radiofrequency catheter ablation
28. Atrial Arrhythmias
Atrial fibrillation (AF) -
• A condition in which the electrical signals come from
the atria at a very fast and erratic rate. The ventricles
contract in an irregular manner because of the erratic
signals coming from the atria.
• The ECG shows normal but irregular QRS complexes,
fine oscillations of the baseline (so-called fibrillation or
f waves) and no P waves.
• Common causes include CAD, valvular heart disease,
hypertension, hyperthyroidism and others. In some
patients no cause can be found 'lone' atrial fibrillation.
30. Atrial Arrhythmias
Management
• When atrial fibrillation is due to an acute precipitating event such as
alcohol toxicity, chest infection or hyperthyroidism, the provoking
cause should be treated.
• Strategies for the acute management of AF are ventricular rate control
or cardioversion (± anticoagulation).
– Ventricular rate control is achieved by drugs which block the AV node
– Cardioversion is achieved electrically by DC shock or medically either by IV
infusion of an anti-arrhythmic drug such as a class Ic or a class III agent
The choice depends upon:
• How well the arrhythmia is tolerated (is cardioversion urgent?)
• Whether anticoagulation is required before considering elective
cardioversion
• Whether spontaneous cardioversion is likely (previous history?
reversible cause?).
31. Atrial Arrhythmias
Management (continue)
• Patients are anticoagulated with warfarin for 4 weeks before
cardioversion.
• Anticoagulants are used to minimize the risk of thromboembolism
associated with cardioversion unless atrial fibrillation is of less than
1-2 days' duration.
• Transoesophageal echocardiography is being used to document the
presence or absence of atrial thrombus as a guide to the necessity for
long-term anticoagulation.
32. Atrial Arrhythmias
Management
• Long-term management of atrial fibrillation include two strategies:
– Rhythm control: antiarrhythmic drugs plus DC cardioversion plus warfarin
– Rate control: AV nodal slowing agents plus warfarin
• Recurrent paroxysms may be prevented by oral medication; class Ic
agents are employed in patients with no significant heart disease and
class III agents are preferred in patients with structural heart disease.
• Rate control is usually achieved by a combination of digoxin beta-
blockers or calcium channel blockers (diltiazem or verapamil).
• Anticoagulation (target INR 2.0-3.0) This is indicated in patients with atrial
fibrillation and one of the following major or two of the moderate risk factors:
• Major risk factors: Prosthetic heart valve, Rheumatic mitral valve disease, Prior
history of CVA/TIA, Age > 75 years, Hypertension, Coronary artery disease with
poor LV function
• Moderate risk factors: Age 65-75 years, Coronary artery disease but normal LV
function, Diabetes mellitus.
33. Ventricular Tachyarrhythmias
Ventricular tachyarrhythmias can be
considered under the following headings:
• life-threatening ventricular
tachyarrhythmias (Sustained ventricular
tachycardia and ventricular fibrillation)
• torsades de pointes
• normal heart ventricular tachycardia
• non-sustained ventricular tachycardia
• ventricular premature beats
34. Ventricular Arrhythmias
Ventricular tachycardia (VT)
• A condition in which an electrical signal is sent from
the ventricles at a very fast but often regular rate.
• The ECG shows a rapid ventricular rhythm with broad (often
0.14 s or more), abnormal QRS complexes. AV dissociation may
result in visible P waves
• Treatment: in haemodynamically compromised patients,
emergency DC cardioversion may be required. If the blood
pressure and cardiac output are well maintained, intravenous
therapy with class I drugs or amiodarone is usually used. First-
line drug treatment consists of lidocaine (50-100 mg i.v. over 5
minutes) followed by a lidocaine infusion (2-4 mg i.v. per
minute). DC cardioversion is necessary if medical therapy is
unsuccessful.
36. Ventricular Arrhythmias
Ventricular fibrillation (VF)
• A condition in which many electrical signals are sent from the ventricles at a
very fast and erratic rate. As a result, the ventricles are unable to fill with
blood and pump.
• This rhythm is life-threatening because there is no pulse and complete loss of
consciousness.
• The ECG shows shapeless, rapid oscillations and there is no hint of organized
complexes
• A person in VF requires prompt defibrillation to restore the normal rhythm
and function of the heart. It may cause sudden cardiac death. Basic and
advanced cardiac life support is needed
• Survivors of these ventricular tachyarrhythmias are, in the absence of an
identifiable reversible cause (e.g. acute myocardial infarction, severe
metabolic disturbance), at high risk of sudden death. Implantable cardioverter-
defibrillators (ICDs) are first-line therapy in the management of these patients
38. Ventricular Arrhythmias
Torsades de pointes -
• This is a type of short duration tachycardia that reverts to sinus rhythm
spontaneously.
• It may be due to:
- Congenital
- Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia.
- Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics.
• It may present with syncopal attacks and occasionally ventricular fibrillation.
• QRS complexes are irregular and rapid that twist around the baseline. In
between the spells of tachycardia the ECG show prolonged QT interval.
• Treatment includes; correction of any electrolyte disturbances, stopping of
causative drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol
(mg2+) over 10-15 min for acquired long QT, IV isoprenaline in acquired
cases and B blockers in congenital types
• Long-term management of acquired long QT syndrome involves avoidance of
all drugs known to prolong the QT interval. Congenital long QT syndrome is
40. Ventricular Arrhythmias
Torsades de pointes -
• Acute management includes; correction of any electrolyte
disturbances, stopping of causative drug, atrial or ventricular
pacing, Magnesium sulphate 8 mmol (mg2+) over 10-15 min for
acquired long QT, IV isoprenaline in acquired cases and B
blockers in congenital types.
• Long-term management of acquired long QT syndrome involves
avoidance of all drugs known to prolong the QT interval.
Congenital long QT syndrome is generally treated by beta-
blockade, left cardiac sympathetic denervation, and pacemaker
therapy. Patients who remain symptomatic despite conventional
therapy and those with a strong family history of sudden death
usually need ICD therapy.
41. Ventricular Arrhythmias
Premature ventricular
contactions (PVCs)
• A condition in which an electrical signal originates in
the ventricles and causes the ventricles to contract
before receiving the electrical signal from the atria.
• ECG shows wide and bizarre QRS complex
• Early 'R-on-T' ventricular premature beats may induce
ventricular fibrillation
• PVCs are not uncommon and often do not cause
symptoms or problems.
• Treated only if symptomatic with beta-blockers.
43. Bradycardias
Sinus Bradycardia
• Physiological variant due to strong vagal tone or atheletic
training.
• Rate as low as 50 at rest and 40 during sleep.
• Common causes of sinus bradycardia include:
• Extrinsic causes ;Hypothermia, hypothyroidism, cholestatic
jaundice and raised intracranial pressure. Drug therapy with beta-
blockers, digitalis and other antiarrhythmic drugs.
• Intrinsic causes; Acute ischaemia and infarction of the sinus node
(as a complication of acute myocardial infarction). Chronic
degenerative changes such as fibrosis of the atrium and sinus
node (sick sinus syndrome).
45. Bradycardias
Sick sinus syndrome
• A condition in which the sinus node sends out
electrical signals either too slowly or too fast. There may
be alternation between too-fast and too-slow rates.
• This condition may cause symptoms if the rate becomes
too slow or too fast for the body to tolerate.
• Chronic symptomatic sick sinus syndrome requires
permanent pacing (AAI), with additional antiarrhythmic
drugs (or ablation therapy) to manage any tachycardia
element.
• Thromboembolism is common in tachy-brady syndrome
and patients should be anticoagulated unless there is a
contraindication.
46. Atrioventricular (AV) Block
First degree A-V Block
• Seldom of clinical significance, and unlikely to
progress.
• ECG shows prolonged PR interval.
• May be associated with acute rheumatic fever,
diphtheria, myocardial infarction or drugs as digoxin
47. Atrioventricular (AV) Block
Second degree A-V Block
Mobitz type I (Wenchebach phenomenon):
• Gradually increasing P-R intervals culminating in an
omission.
• When isolated, usually physiological and due to
increased vagal tone and abolished by exercise and
atropine.
Mobitz type II
• The P wave is sporadically not conducted. Occurs when
a dropped QRS complex is not preceded by progressive
PR interval prolongation.
• Pacing is usually indicated in Mobitz II block, whereas
patients with Wenckebach AV block are usually
monitored.
48. Second Degree AV Block
Acute myocardial infarction may produce second-degree
heart block. In inferior myocardial infarction, close
monitoring and transcutaneous temporary back-up pacing
are all that is required. In anterior myocardial infarction,
second-degree heart block is associated with a high risk of
progression to complete heart block, and temporary pacing
followed by permanent pacemaker implantation is usually
indicated.
49.
50. Atrioventricular (AV) Block
Third degree A-V Block
• Common in elderly age groups due to idiopathic
bundle branch fibrosis.
• Other causes include coronary heart disease,
calcification from aortic valve, sarcoidosis or
congenital.
• ECG shows bradycardia, P wave continue,
unrelated to regular slow idioventricular rhythm.
• Treatment is permanent pacing.
52. Atrioventricular (AV) Block
Bundle Branch Block (BBB):
• Interruption of the right or left branch of the bundle of
Hiss delays activation of the corresponding ventricle
leading to broadening of the QRS complex
• Unlike right BBB, left BBB is always associated with
an underlying heart disease.
• Both RT and LT BBB show wide deformed QRS
complex. In RBBB there is rSR pattern in lead V1,
while in LBBB there is a broad monophasic (or
notched) R wave in leads V5 and V6.
53. Atrioventricular (AV) Block
Bundle Branch Block (BBB):
Hemiblock
Delay or block in the divisions of the left bundle branch produces
a swing in the direction of depolarization (electrical axis) of the
heart. When the anterior division is blocked (left anterior
hemiblock), there is left axis deviation. Delay or block in the
postero-inferior division causes(right axis deviation).
Bifascicular block
This is a combination of a block of any two of the following: the
right bundle branch, the left antero-superior division and the left
postero-inferior division. Block of the remaining fascicle will
result in complete AV block.