The normal conduction pathway begins with the SA node generating an action potential that is conducted to the atria and AV node. The impulse is then delivered to the purkinje fibers and conducted to the ventricles. There are different types of cardiac action potentials and phases as well as different types of arrhythmias. Antiarrhythmic drugs work by decreasing conduction velocity, changing refractory periods, or suppressing abnormal automaticity to restore normal sinus rhythm.
1. The document discusses the normal conduction pathway of the heart and the action potential of pacemaker and non-pacemaker cells.
2. It describes types of arrhythmias including supraventricular and ventricular arrhythmias. Mechanisms of arrhythmogenesis include early and delayed afterdepolarizations.
3. The document outlines the classification of antiarrhythmic drugs according to their effects on sodium, potassium, calcium, and beta-adrenergic receptors. It provides details on class IA, IB, IC, II, and III drugs and their mechanisms and uses.
Antiarrhythmic therapy for supraventricular arrhythmiasKyaw Win
This document provides an overview of anti-arrhythmic drug therapy for supraventricular arrhythmias. It discusses the electrophysiology of the heart, definitions of arrhythmias, and classifications of anti-arrhythmic drugs. The four main classes of anti-arrhythmic drugs are described along with their mechanisms of action and uses for treating different types of supraventricular tachyarrhythmias. Guidelines for treating atrial fibrillation and some supraventricular tachycardias are also presented.
This document discusses antiarrhythmic drug therapy and summarizes the following key points:
- Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on the cardiac action potential. Classes I-III work by blocking sodium, calcium or potassium channels.
- Class I drugs like quinidine and procainamide work by blocking fast sodium channels, reducing the rate of depolarization. Class II drugs like propranolol are beta blockers that reduce heart rate and conduction velocity.
- Common arrhythmias treated include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardias. Drug choice is based on the arrhythmia type
This lecture covers the electrophysiology of the heart and classification of arrhythmias and antiarrhythmic drugs. Key points:
1. The lecture outlines topics on electrophysiology, arrhythmia mechanisms/types, classification of antiarrhythmic drugs, and treatment of some arrhythmias.
2. Arrhythmias are caused by abnormalities in impulse formation and conduction in the myocardium. They can be classified based on the anatomical site of abnormality: atria, AV node, or ventricles.
3. Antiarrhythmic drugs are classified into four classes based on their effects on the cardiac action potential. Class I drugs block sodium channels, class II are beta blockers,
This document discusses cardiac antidysrhythmic drugs. It notes that the use of these drugs is limited due to the potential to depress heart function and trigger new arrhythmias. The drugs are principally used to treat atrial fibrillation and flutter. They work by blocking sodium, potassium, and calcium ion channels in the heart. The drugs are classified into four classes based on their mechanism of action and effects on cardiac action potentials. Common side effects include worsening arrhythmias, heart block, and prolonged QT interval with risks of torsades de pointes.
cardiac arrhythmias are abnormal heart rhythms that occur when the electrical signals controlling the heart beat are not working properly.
these can include tachycardia ,Bradycardia,atrial fibrillation and more.
This document summarizes different classes of antiarrhythmic drugs and their mechanisms of action. It discusses how classes I-IV drugs work by altering sodium, potassium, calcium, or beta receptor channels and currents to modify cardiac automaticity, conduction, or refractoriness. Specific drugs like amiodarone, atenolol, digoxin, diltiazem, flecainide, lignocaine, metoprolol, propafenone, quinidine, sotalol, verapamil are mentioned along with their indications, dosages, and potential side effects in treating arrhythmias like atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and cardiac
1. The document discusses the normal conduction pathway of the heart and the action potential of pacemaker and non-pacemaker cells.
2. It describes types of arrhythmias including supraventricular and ventricular arrhythmias. Mechanisms of arrhythmogenesis include early and delayed afterdepolarizations.
3. The document outlines the classification of antiarrhythmic drugs according to their effects on sodium, potassium, calcium, and beta-adrenergic receptors. It provides details on class IA, IB, IC, II, and III drugs and their mechanisms and uses.
Antiarrhythmic therapy for supraventricular arrhythmiasKyaw Win
This document provides an overview of anti-arrhythmic drug therapy for supraventricular arrhythmias. It discusses the electrophysiology of the heart, definitions of arrhythmias, and classifications of anti-arrhythmic drugs. The four main classes of anti-arrhythmic drugs are described along with their mechanisms of action and uses for treating different types of supraventricular tachyarrhythmias. Guidelines for treating atrial fibrillation and some supraventricular tachycardias are also presented.
This document discusses antiarrhythmic drug therapy and summarizes the following key points:
- Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on the cardiac action potential. Classes I-III work by blocking sodium, calcium or potassium channels.
- Class I drugs like quinidine and procainamide work by blocking fast sodium channels, reducing the rate of depolarization. Class II drugs like propranolol are beta blockers that reduce heart rate and conduction velocity.
- Common arrhythmias treated include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardias. Drug choice is based on the arrhythmia type
This lecture covers the electrophysiology of the heart and classification of arrhythmias and antiarrhythmic drugs. Key points:
1. The lecture outlines topics on electrophysiology, arrhythmia mechanisms/types, classification of antiarrhythmic drugs, and treatment of some arrhythmias.
2. Arrhythmias are caused by abnormalities in impulse formation and conduction in the myocardium. They can be classified based on the anatomical site of abnormality: atria, AV node, or ventricles.
3. Antiarrhythmic drugs are classified into four classes based on their effects on the cardiac action potential. Class I drugs block sodium channels, class II are beta blockers,
This document discusses cardiac antidysrhythmic drugs. It notes that the use of these drugs is limited due to the potential to depress heart function and trigger new arrhythmias. The drugs are principally used to treat atrial fibrillation and flutter. They work by blocking sodium, potassium, and calcium ion channels in the heart. The drugs are classified into four classes based on their mechanism of action and effects on cardiac action potentials. Common side effects include worsening arrhythmias, heart block, and prolonged QT interval with risks of torsades de pointes.
cardiac arrhythmias are abnormal heart rhythms that occur when the electrical signals controlling the heart beat are not working properly.
these can include tachycardia ,Bradycardia,atrial fibrillation and more.
This document summarizes different classes of antiarrhythmic drugs and their mechanisms of action. It discusses how classes I-IV drugs work by altering sodium, potassium, calcium, or beta receptor channels and currents to modify cardiac automaticity, conduction, or refractoriness. Specific drugs like amiodarone, atenolol, digoxin, diltiazem, flecainide, lignocaine, metoprolol, propafenone, quinidine, sotalol, verapamil are mentioned along with their indications, dosages, and potential side effects in treating arrhythmias like atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, and cardiac
This document discusses antiarrhythmic drugs, their mechanisms of action, indications, and side effects. It covers the Vaughan-Williams classification system for antiarrhythmic drugs (Classes I-IV) and describes examples from each class such as quinidine, amiodarone, beta blockers, calcium channel blockers, and others. The mechanisms by which these drugs treat arrhythmias include blocking sodium, potassium, or calcium channels or suppressing automaticity. Adverse effects and considerations for use are also outlined.
This document discusses various types of cardiac arrhythmias and drugs used to treat them. It describes the cardiac conduction system and action potential, and how sympathetic and parasympathetic nervous systems regulate heart rate. Various classes of antiarrhythmic drugs are outlined based on their mechanisms and examples are provided. Adenosine, digoxin, calcium channel blockers, beta blockers and amiodarone are discussed in more detail for treating specific arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. The importance of considering each drug's side effects and contraindications is emphasized.
This document discusses various types of cardiac arrhythmias and drugs used to treat them. It describes the cardiac conduction system and action potential, and how sympathetic and parasympathetic nervous systems regulate heart rate. Various classes of antiarrhythmic drugs are outlined based on their mechanisms and examples are provided. Adenosine, digoxin, calcium channel blockers, beta blockers and amiodarone are discussed in more detail for treating specific arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. The importance of considering each drug's side effects and contraindications is emphasized.
This document discusses antiarrhythmic drugs and their classification and mechanisms of action. It begins by defining arrhythmia and describing the normal cardiac conduction pathway and rhythm. It then classifies antiarrhythmic drugs according to the Vaughan-Williams classification system into Classes I-IV based on their effects on cardiac ion channels and action potentials. Class I drugs are sodium channel blockers and are further divided into IA, IB and IC subgroups based on their binding properties and effects on cardiac tissue. Representative drugs from each subclass are described in detail including their mechanisms of action, uses, dosages and adverse effects.
Pharmacotherapy of Cardiac arrhythmiasDrSnehaDange
This document provides an overview of pharmacotherapy for cardiac arrhythmias. It discusses the normal conduction pathway in the heart and mechanisms of arrhythmogenesis. Cardiac arrhythmias are classified and characteristics of different types are described including extrasystoles, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia and ventricular fibrillation. Antiarrhythmic drugs are classified according to the Vaughan Williams system with details provided on mechanisms and examples for Class IA, IB, IC, II, III and IV drugs.
Antiarrhythmic drugs are used to prevent or treat irregularities in cardiac rhythm caused by disturbances in the heart's electrical impulses. The drugs work by reducing abnormal pacemaker activity or modifying conduction to disable reentrant circuits. Quinidine is a Class IA drug that blocks sodium channels, prolonging the action potential and increasing the refractory period. It can treat both atrial and ventricular arrhythmias but causes side effects like cinchonism. Procainamide is also a Class IA drug that works similarly to quinidine to treat ventricular and some supraventricular arrhythmias but has more ganglionic blocking effects and can cause lupus-like symptoms.
This document discusses heart arrhythmias and how anti-arrhythmic drugs work to treat them. It provides details on:
1) The electrophysiology of normal heart contraction and how disturbances can cause arrhythmias.
2) Classification systems for anti-arrhythmic drugs based on their mechanisms of action, such as blocking specific ion channels.
3) How different classes of drugs can alter properties like conduction velocity, refractoriness, and automaticity to restore normal rhythm or prevent dangerous arrhythmias.
This document discusses anti-arrhythmic drugs, describing the physiology of normal cardiac rhythm, mechanisms of arrhythmias, classification of anti-arrhythmic drugs, and important drugs including their mechanisms and characteristics. It covers drugs like lidocaine, flecainide, amiodarone, adenosine, verapamil and digoxin; their uses in treating arrhythmias; potential adverse effects; and non-pharmacological treatments. Management of arrhythmias involves assessing the patient and diagnosing the type of arrhythmia to determine appropriate acute or prophylactic treatment.
Dronedarone is a newer antiarrhythmic drug that is structurally similar to amiodarone but was designed to have fewer side effects. It blocks multiple ion channels including potassium, sodium, and calcium channels. This results in antiarrhythmic effects such as reducing automaticity, prolonging the action potential duration, and slowing conduction velocity. However, dronedarone has a better safety profile compared to amiodarone with less risks of thyroid and lung problems.
This document discusses antiarrhythmic drugs used to treat cardiac arrhythmias. It begins by defining arrhythmias and describing the causes. It then discusses the Vaughan Williams classification system for antiarrhythmic drugs. Class I drugs like quinidine, procainamide and flecainide work by blocking sodium channels. Class II drugs like propranolol are beta blockers. Class III drugs like amiodarone work by prolonging the action potential. The document provides details on specific drugs, their mechanisms of action, uses, doses and side effects. It emphasizes restoring normal rhythm and rate while preventing more dangerous arrhythmias.
The document discusses pharmacotherapy for arrhythmias, describing various types of arrhythmias caused by defects in impulse generation or propagation in the heart. It covers the mechanisms of different arrhythmias and classifications of antiarrhythmic drugs, focusing on classes I-IV and how they work by blocking sodium, potassium, or calcium channels to treat arrhythmias. Examples of commonly used antiarrhythmic drugs are provided for each class along with their mechanisms of action, effects, uses, and potential adverse effects.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms. It begins by defining different types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are then explained as enhanced automaticity, triggered activity, reentry, and fractionation of impulses. Common arrhythmia conditions seen clinically are also outlined. The document then discusses the Vaughan-Williams classification system for antiarrhythmic drugs and provides details on representative drugs from each class, including their mechanisms of action and uses.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms. It begins by defining different types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are then explained as enhanced automaticity, triggered activity, reentry, and fractionation of impulses. Common arrhythmia conditions seen clinically are also outlined. The document then discusses the Vaughan-Williams classification system for antiarrhythmic drugs and provides details on representative drugs from each class, including their mechanisms of action and uses.
This document discusses antiarrhythmic drugs used to treat irregularities in cardiac rhythm. It covers various types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are discussed including enhanced automaticity, triggered activity, reentry, and fractionation of impulses. The Vaughan-Williams classification of antiarrhythmic drugs is presented along with details about specific drug classes and examples like quinidine, procainamide, lidocaine, and beta blockers. Mechanisms of action and ion channel effects are explained for different drug classes.
1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. Disorders of impulse formation include abnormalities in automaticity and triggered activity.
2. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. Triggered activity is initiated by afterdepolarizations following an action potential.
3. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. Common reentrant arrhythmias include atrial flutter, at
This document discusses cardiac arrhythmias and their treatment. It begins by describing the cardiac conduction system and action potentials in nodal and non-nodal cells. It then covers mechanisms of arrhythmias including disorders of impulse formation and conduction. Various types of tachyarrhythmias are defined including SVTs originating from the sinus node, atria, or AV node. Treatment of SVTs focuses on pharmacological agents or cardioversion. The document concludes with classifications of antiarrhythmic drugs and arrhythmias.
This document discusses various cardiac arrhythmias including their mechanisms and treatment. It begins by describing the three main mechanisms of cardiac arrhythmia: alterations in impulse initiation (automaticity), afterdepolarizations and triggered automaticity, and abnormal impulse conduction (reentry). It then discusses various specific arrhythmias in more detail, including types of heart block, tachycardias like atrial fibrillation, flutter and sinus tachycardia, as well as treatment options like antiarrhythmic drugs, catheter ablation, and pacemakers. In summary, the document provides an overview of the conduction system of the heart and covers the pathophysiology, classification, evaluation and management of different cardiac arrhythmias.
This document discusses the physiology of cardiac rhythm, classification of arrhythmias, and anti-arrhythmic drugs used to treat arrhythmias. It covers the phases of the cardiac action potential, mechanisms of arrhythmia production, Vaughan Williams classification of anti-arrhythmic drugs based on their effects on the action potential, and details several important anti-arrhythmic drugs including their mechanisms, uses, and potential adverse effects. The document concludes that treatment of arrhythmias depends on the type of arrhythmia and patient's condition, as anti-arrhythmic drugs are efficacious but can have serious side effects, and non-pharmacological therapies are also used.
Antiarrhythmic drugs work by altering the electrophysiology of the heart. They are classified into four main classes based on their mechanisms of action: Class I drugs block sodium channels, Class II block beta-adrenergic receptors, Class III prolong the heart's repolarization, and Class IV block calcium channels. While these drugs can treat arrhythmias, they may also paradoxically cause arrhythmias due to their effects on the heart's electrical activity. Pacemakers provide an alternative treatment for arrhythmias by using implanted leads and a pulse generator to electrically stimulate the heart and maintain a normal rhythm.
Cardiac arrhythmias are abnormal heart rhythms that can be caused by issues with impulse formation, conduction, or both. The document defines different types of arrhythmias and their causes. It discusses evaluation and management approaches including pharmacological therapy with antiarrhythmic drugs, electrical cardioversion, pacemaker implantation, catheter ablation procedures, and surgery. Common arrhythmias like atrial fibrillation, atrial flutter, premature beats, and ventricular tachycardia are explained in terms of their presentation and treatment.
Raw to Ready by Arham Abdullah, Class 1- purple.pptxAymanshahzad4
The document discusses raw materials and how they are transformed into finished products. It defines raw materials as basic materials that come from nature, like plants, animals and rocks. It provides examples of raw materials such as wood, fruits, cereals, cotton and animals products like wool, fish, meat and eggs. It then explains how these raw materials are processed in factories to make finished consumer goods, giving examples like paper and pencils from wood, veggie burgers from vegetables, t-shirts from cotton, and bread or pasta from cereals.
Nuclear medicine uses small amounts of radioactive tracers and imaging techniques to examine organ structure and function. It combines fields like chemistry, physics, and medicine. Nuclear imaging allows visualization of tissue structure and function by tracking how radiotracers are absorbed. Common nuclear medicine scans include thyroid scans to help diagnose thyroid abnormalities early. A thyroid scan involves administering a small amount of radioactive iodine and using a gamma camera to detect its distribution and uptake in the thyroid gland.
This document discusses antiarrhythmic drugs, their mechanisms of action, indications, and side effects. It covers the Vaughan-Williams classification system for antiarrhythmic drugs (Classes I-IV) and describes examples from each class such as quinidine, amiodarone, beta blockers, calcium channel blockers, and others. The mechanisms by which these drugs treat arrhythmias include blocking sodium, potassium, or calcium channels or suppressing automaticity. Adverse effects and considerations for use are also outlined.
This document discusses various types of cardiac arrhythmias and drugs used to treat them. It describes the cardiac conduction system and action potential, and how sympathetic and parasympathetic nervous systems regulate heart rate. Various classes of antiarrhythmic drugs are outlined based on their mechanisms and examples are provided. Adenosine, digoxin, calcium channel blockers, beta blockers and amiodarone are discussed in more detail for treating specific arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. The importance of considering each drug's side effects and contraindications is emphasized.
This document discusses various types of cardiac arrhythmias and drugs used to treat them. It describes the cardiac conduction system and action potential, and how sympathetic and parasympathetic nervous systems regulate heart rate. Various classes of antiarrhythmic drugs are outlined based on their mechanisms and examples are provided. Adenosine, digoxin, calcium channel blockers, beta blockers and amiodarone are discussed in more detail for treating specific arrhythmias like atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia. The importance of considering each drug's side effects and contraindications is emphasized.
This document discusses antiarrhythmic drugs and their classification and mechanisms of action. It begins by defining arrhythmia and describing the normal cardiac conduction pathway and rhythm. It then classifies antiarrhythmic drugs according to the Vaughan-Williams classification system into Classes I-IV based on their effects on cardiac ion channels and action potentials. Class I drugs are sodium channel blockers and are further divided into IA, IB and IC subgroups based on their binding properties and effects on cardiac tissue. Representative drugs from each subclass are described in detail including their mechanisms of action, uses, dosages and adverse effects.
Pharmacotherapy of Cardiac arrhythmiasDrSnehaDange
This document provides an overview of pharmacotherapy for cardiac arrhythmias. It discusses the normal conduction pathway in the heart and mechanisms of arrhythmogenesis. Cardiac arrhythmias are classified and characteristics of different types are described including extrasystoles, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia and ventricular fibrillation. Antiarrhythmic drugs are classified according to the Vaughan Williams system with details provided on mechanisms and examples for Class IA, IB, IC, II, III and IV drugs.
Antiarrhythmic drugs are used to prevent or treat irregularities in cardiac rhythm caused by disturbances in the heart's electrical impulses. The drugs work by reducing abnormal pacemaker activity or modifying conduction to disable reentrant circuits. Quinidine is a Class IA drug that blocks sodium channels, prolonging the action potential and increasing the refractory period. It can treat both atrial and ventricular arrhythmias but causes side effects like cinchonism. Procainamide is also a Class IA drug that works similarly to quinidine to treat ventricular and some supraventricular arrhythmias but has more ganglionic blocking effects and can cause lupus-like symptoms.
This document discusses heart arrhythmias and how anti-arrhythmic drugs work to treat them. It provides details on:
1) The electrophysiology of normal heart contraction and how disturbances can cause arrhythmias.
2) Classification systems for anti-arrhythmic drugs based on their mechanisms of action, such as blocking specific ion channels.
3) How different classes of drugs can alter properties like conduction velocity, refractoriness, and automaticity to restore normal rhythm or prevent dangerous arrhythmias.
This document discusses anti-arrhythmic drugs, describing the physiology of normal cardiac rhythm, mechanisms of arrhythmias, classification of anti-arrhythmic drugs, and important drugs including their mechanisms and characteristics. It covers drugs like lidocaine, flecainide, amiodarone, adenosine, verapamil and digoxin; their uses in treating arrhythmias; potential adverse effects; and non-pharmacological treatments. Management of arrhythmias involves assessing the patient and diagnosing the type of arrhythmia to determine appropriate acute or prophylactic treatment.
Dronedarone is a newer antiarrhythmic drug that is structurally similar to amiodarone but was designed to have fewer side effects. It blocks multiple ion channels including potassium, sodium, and calcium channels. This results in antiarrhythmic effects such as reducing automaticity, prolonging the action potential duration, and slowing conduction velocity. However, dronedarone has a better safety profile compared to amiodarone with less risks of thyroid and lung problems.
This document discusses antiarrhythmic drugs used to treat cardiac arrhythmias. It begins by defining arrhythmias and describing the causes. It then discusses the Vaughan Williams classification system for antiarrhythmic drugs. Class I drugs like quinidine, procainamide and flecainide work by blocking sodium channels. Class II drugs like propranolol are beta blockers. Class III drugs like amiodarone work by prolonging the action potential. The document provides details on specific drugs, their mechanisms of action, uses, doses and side effects. It emphasizes restoring normal rhythm and rate while preventing more dangerous arrhythmias.
The document discusses pharmacotherapy for arrhythmias, describing various types of arrhythmias caused by defects in impulse generation or propagation in the heart. It covers the mechanisms of different arrhythmias and classifications of antiarrhythmic drugs, focusing on classes I-IV and how they work by blocking sodium, potassium, or calcium channels to treat arrhythmias. Examples of commonly used antiarrhythmic drugs are provided for each class along with their mechanisms of action, effects, uses, and potential adverse effects.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms. It begins by defining different types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are then explained as enhanced automaticity, triggered activity, reentry, and fractionation of impulses. Common arrhythmia conditions seen clinically are also outlined. The document then discusses the Vaughan-Williams classification system for antiarrhythmic drugs and provides details on representative drugs from each class, including their mechanisms of action and uses.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms. It begins by defining different types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are then explained as enhanced automaticity, triggered activity, reentry, and fractionation of impulses. Common arrhythmia conditions seen clinically are also outlined. The document then discusses the Vaughan-Williams classification system for antiarrhythmic drugs and provides details on representative drugs from each class, including their mechanisms of action and uses.
This document discusses antiarrhythmic drugs used to treat irregularities in cardiac rhythm. It covers various types of arrhythmias including bradyarrhythmias, tachyarrhythmias, and heart block. The causes of arrhythmias are discussed including enhanced automaticity, triggered activity, reentry, and fractionation of impulses. The Vaughan-Williams classification of antiarrhythmic drugs is presented along with details about specific drug classes and examples like quinidine, procainamide, lidocaine, and beta blockers. Mechanisms of action and ion channel effects are explained for different drug classes.
1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. Disorders of impulse formation include abnormalities in automaticity and triggered activity.
2. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. Triggered activity is initiated by afterdepolarizations following an action potential.
3. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. Common reentrant arrhythmias include atrial flutter, at
This document discusses cardiac arrhythmias and their treatment. It begins by describing the cardiac conduction system and action potentials in nodal and non-nodal cells. It then covers mechanisms of arrhythmias including disorders of impulse formation and conduction. Various types of tachyarrhythmias are defined including SVTs originating from the sinus node, atria, or AV node. Treatment of SVTs focuses on pharmacological agents or cardioversion. The document concludes with classifications of antiarrhythmic drugs and arrhythmias.
This document discusses various cardiac arrhythmias including their mechanisms and treatment. It begins by describing the three main mechanisms of cardiac arrhythmia: alterations in impulse initiation (automaticity), afterdepolarizations and triggered automaticity, and abnormal impulse conduction (reentry). It then discusses various specific arrhythmias in more detail, including types of heart block, tachycardias like atrial fibrillation, flutter and sinus tachycardia, as well as treatment options like antiarrhythmic drugs, catheter ablation, and pacemakers. In summary, the document provides an overview of the conduction system of the heart and covers the pathophysiology, classification, evaluation and management of different cardiac arrhythmias.
This document discusses the physiology of cardiac rhythm, classification of arrhythmias, and anti-arrhythmic drugs used to treat arrhythmias. It covers the phases of the cardiac action potential, mechanisms of arrhythmia production, Vaughan Williams classification of anti-arrhythmic drugs based on their effects on the action potential, and details several important anti-arrhythmic drugs including their mechanisms, uses, and potential adverse effects. The document concludes that treatment of arrhythmias depends on the type of arrhythmia and patient's condition, as anti-arrhythmic drugs are efficacious but can have serious side effects, and non-pharmacological therapies are also used.
Antiarrhythmic drugs work by altering the electrophysiology of the heart. They are classified into four main classes based on their mechanisms of action: Class I drugs block sodium channels, Class II block beta-adrenergic receptors, Class III prolong the heart's repolarization, and Class IV block calcium channels. While these drugs can treat arrhythmias, they may also paradoxically cause arrhythmias due to their effects on the heart's electrical activity. Pacemakers provide an alternative treatment for arrhythmias by using implanted leads and a pulse generator to electrically stimulate the heart and maintain a normal rhythm.
Cardiac arrhythmias are abnormal heart rhythms that can be caused by issues with impulse formation, conduction, or both. The document defines different types of arrhythmias and their causes. It discusses evaluation and management approaches including pharmacological therapy with antiarrhythmic drugs, electrical cardioversion, pacemaker implantation, catheter ablation procedures, and surgery. Common arrhythmias like atrial fibrillation, atrial flutter, premature beats, and ventricular tachycardia are explained in terms of their presentation and treatment.
Raw to Ready by Arham Abdullah, Class 1- purple.pptxAymanshahzad4
The document discusses raw materials and how they are transformed into finished products. It defines raw materials as basic materials that come from nature, like plants, animals and rocks. It provides examples of raw materials such as wood, fruits, cereals, cotton and animals products like wool, fish, meat and eggs. It then explains how these raw materials are processed in factories to make finished consumer goods, giving examples like paper and pencils from wood, veggie burgers from vegetables, t-shirts from cotton, and bread or pasta from cereals.
Nuclear medicine uses small amounts of radioactive tracers and imaging techniques to examine organ structure and function. It combines fields like chemistry, physics, and medicine. Nuclear imaging allows visualization of tissue structure and function by tracking how radiotracers are absorbed. Common nuclear medicine scans include thyroid scans to help diagnose thyroid abnormalities early. A thyroid scan involves administering a small amount of radioactive iodine and using a gamma camera to detect its distribution and uptake in the thyroid gland.
X-rays are a form of ionizing radiation that are used in diagnostic imaging to identify fractures, detect diseases like cancer, and examine internal structures. An x-ray tube produces x-rays by accelerating electrons at a metal target. X-rays are penetrating and can pass through tissues to form radiographic images. Radiologists use x-rays to examine bones, teeth, organs and tissues. While low dose, repeated x-ray exposures increase cancer risks, so the diagnostic benefits are weighed against risks in each case. Shielding with lead and distance from the source reduce radiation exposure for patients and medical staff.
This document discusses several classes of psychoactive drugs, including psychomotor stimulants and hallucinogens. Psychomotor stimulants like amphetamines cause excitement and decrease fatigue by increasing motor activity and CNS stimulation. Hallucinogens like LSD and THC produce altered thought patterns and hallucinations. Many of these drugs are addictive and can have adverse effects like anxiety, insomnia, and cardiovascular issues when taken in high doses. The document provides details on the mechanisms and therapeutic and recreational uses of various stimulants and hallucinogenic drugs.
This document discusses various classes of psychoactive drugs, including their mechanisms of action, effects, uses and adverse reactions. It covers psychomotor stimulants such as caffeine, nicotine and cocaine, which cause excitement and increase motor activity. It also discusses hallucinogens like LSD, THC and PCP, which can produce changes in thought patterns and mood. The document provides details on specific drugs, outlining their therapeutic uses and risks.
The document discusses abdominal trauma care, providing definitions and signs of various abdominal injuries. It describes mechanisms of injury including blunt and penetrating trauma. Specific injuries to organs like the spleen, liver, kidneys, and hollow organs are outlined, with signs and symptoms, diagnostic tests, and treatment approaches summarized for each. General assessment, management principles and diagnostic tests for abdominal trauma are also reviewed.
1. Antidepressants work by increasing levels of neurotransmitters like serotonin and norepinephrine in the brain. They are divided into several classes including SSRIs, SNRIs, TCAs, and MAOIs.
2. SSRIs are now the most commonly prescribed due to their safer side effect profile. They work by inhibiting reuptake of serotonin. TCAs affect serotonin and norepinephrine but have more side effects.
3. Antidepressants take 2-3 weeks to start working and should be taken long term to prevent relapse of depression. Side effects are usually mild and transient but can include nausea, sexual dysfunction, and dry mouth depending on the drug class.
This document discusses antiepileptic drugs, their mechanisms of action, classifications, pharmacokinetics, indications, and adverse effects. It covers older drugs like phenobarbital, phenytoin, carbamazepine, and ethosuximide as well as newer drugs like lamotrigine, gabapentin, vigabatrin, tiagabine, and topiramate. The main mechanisms of action are enhancing GABA transmission, blocking sodium channels, and blocking calcium channels. The drugs are used to treat generalized tonic-clonic, partial, and absence seizures, as well as neuropathic pain and bipolar disorder. Common adverse effects include sedation, dizziness, rash
A mammogram is an x-ray of the breast used to detect breast cancer. Modern mammography machines use low doses of radiation that are considered safe. Screening mammograms are used to check women without symptoms, while diagnostic mammograms are used to investigate abnormalities. Mammograms produce images of breast tissue that radiologists analyze for signs of cancer such as masses or microcalcifications. The BI-RADS system is used to classify mammogram results. Mammograms can miss some cancers and detect abnormalities that turn out to be non-cancerous, but regular screening is still recommended as the best way to find cancers early.
The document discusses the pancreas and its role in producing digestive enzymes and peptide hormones like insulin, glucagon, and somatostatin. It describes the four types of diabetes, focusing on type 1 diabetes which results from an absolute deficiency of insulin due to destruction of beta cells in the pancreas. Signs and symptoms of type 1 diabetes include polydipsia, polyphagia, polyuria, and weight loss. Treatment involves administering exogenous insulin through injections to control blood glucose levels.
This document discusses several types of streptococci bacteria. S. pyogenes causes pharyngitis and cellulitis, as well as immunological diseases like rheumatic fever. S. agalactiae is a cause of neonatal sepsis and meningitis. Streptococci are catalase-negative and can exhibit alpha, beta, or gamma hemolysis on blood agar plates. Beta-hemolytic streptococci produce enzymes like streptolysin O and S. They cause disease via pyrogenic toxins, hemolysins, and cross-reacting antibodies that can damage tissues. S. pneumoniae is a cause of pneumonia and forms an alpha-hemolytic polysaccharide capsule that inhibits phag
1) MRI uses powerful magnets and radio waves to create detailed images of the inside of the body without using ionizing radiation.
2) It provides highly detailed images of soft tissues and is especially useful for imaging the brain, spine, joints, and inside of bones.
3) During an MRI scan, the patient lies inside a large tube-like scanner with a magnet and computer that produces cross-sectional images of internal organs and structures.
This document provides an overview of neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. It discusses the pathophysiology, symptoms, and pharmacological treatments for each condition. For Parkinson's, it describes how dopamine production decreases and the resulting motor symptoms. Common drugs mentioned include levodopa, dopamine agonists, COMT inhibitors, and anticholinergics. For Alzheimer's, it outlines the amyloid plaque and neurofibrillary tangle pathology and resulting cognitive decline. Cholinesterase inhibitors and memantine are the major pharmaceutical therapies discussed for Alzheimer's treatment. The document concludes by mentioning some newer investigational drugs for both conditions.
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Tele Optometry (kunj'sppt) / Basics of tele optometry.
Antiarrhythmic_drugs
1.
2. Normal conduction pathway:
1- SA node generates
action potential and
delivers it to the atria
and the AV node
2- The AV node
delivers the impulse
to purkinje fibers
3- purkinje fibers
conduct the impulse
to the ventricles
Other types of
conduction that
occurs between
myocardial cells:
When a cell is
depolarized
adjacent cell
depolarizes along
3. Action potential of the heart:
In the atria, purkinje, and
ventricles the AP curve
consists of 5 phases
In the SA node and AV
node, AP curve consists
of 3 phases
4. Non-pacemaker action potential
Phase 0: fast
upstroke
Due to Na+
influx
Phase 3:
repolarization
Due to K+ efflux
Phase 4: resting
membrane
potential
Phase 2: plateu
Due to Ca++
influx
Phase 1: partial
repolarization
Due to rapid efflux of K+
N.B. The slope of phase 0 = conduction velocity
Also the peak of phase 0 = Vmax
5. Pacemaker AP
Phase 4: pacemaker
potential
Na influx and K efflux
and Ca influx until the
cell reaches threshold
and then turns into
phase 0
Phase 0: upstroke:
Due to Ca++ influx
Phase 3: repolarization:
Due to K+ efflux
Pacemaker cells (automatic cells) have unstable
membrane potential so they can generate AP
spontaneously
6. Effective refractory period (ERP)
It is also called absolute refractory period (ARP) :
•In this period the cell can’t be excited
•Takes place between phase 0 and 3
7. Arrhythmia
If the arrhythmia
arises from the
ventricles it is
called ventricular
arrhythmia
If the arrhythmia
arises from atria,
SA node, or AV
node it is called
supraventricular
arrhythmia
Causes of
arrhythmia
arteriosclerosis
Coronary artery
spasm
Heart block
Myocardial
ischemia
8. Mechnisms of Arrhythmogenesis
1- Abnormal impulse generation
Automatic rhythms
Ectopic focus
Enhanced
normal
automaticity
Triggered rhythms
Due to abnormal leakage
of + ions into cardiac cell
Delayed
afterdepolarization
Early
afterdepolarization
↑AP from SA node
Due to increase
permibility of Na
from Membrane
AP arises from sites
other than SA node
9. 2-Abnormal
conduction
Conduction
block
1st degree 2nd degree 3rd degree
Reentry
Circus
movement
Reflection
This is when the
impulse is not
conducted from
the atria to the
ventricles
1-This
pathway is
blocked
2-The impulse
from this pathway
travels in a
retrograde fashion
(backward)
3-So the cells here will
be reexcited (first by
the original pathway
and the other from the
retrograde)
10. Here is an
accessory
pathway in the
heart called
Bundle of Kent
•Present only in small populations
•Lead to reexcitation Wolf-Parkinson-
White Syndrome (WPW)
Abnormal anatomic conduction
11. Action of drugs
In case of abnormal generation:
Decrease of phase
4 slope (in
pacemaker cells)
Before drug
after
phase4
Raises the threshold
In case of abnormal conduction:
↓conduction
velocity (remember
phase 0)
↑ERP
(so the cell
won’t be
reexcited
again)
12. Supraventricular Arrhythmias
Sinus Tachycardia: high sinus rate of 100-180 beats/min,
occurs during exercise or other conditions that lead to
increased SA nodal firing rate
Atrial Tachycardia: a series of 3 or more consecutive atrial
premature beats occurring at a frequency >100/min
Paroxysmal Atrial Tachycardia (PAT): tachycardia which
begins and ends in acute manner
Atrial Flutter: sinus rate of 250-350 beats/min.
Atrial Fibrillation: uncoordinated atrial depolarizations.
AV blocks
A conduction block within the AV node , occasionally in the
bundle of His, that impairs impulse conduction from the atria
to the ventricles.
Types of Arrhythmia
13. Ventricular Premature Beats (VPBs): caused by ectopic
ventricular foci; characterized by widened QRS.
Ventricular Tachycardia (VT): high ventricular rate caused
by abnormal ventricular automaticity or by intraventricular
reentry; can be sustained or non-sustained (paroxysmal);
characterized by widened QRS; rates of 100 to 200
beats/min; life-threatening.
Ventricular Flutter - ventricular depolarizations >200/min.
Ventricular Fibrillation - uncoordinated ventricular
depolarizations
Ventricular Arrhythmias
14. Pharmacologic Rationale &
Goals
The ultimate goal of antiarrhythmic drug
therapy:
o Restore normal sinus rhythm and conduction
o Prevent more serious and possibly lethal
arrhythmias from occurring.
Antiarrhythmic drugs are used to:
decrease conduction velocity
change the duration of the effective refractory
period (ERP)
suppress abnormal automaticity
15. Antiarrhythmic drugs
class mechanism action notes
I Na+ channel blocker
Change the slope of
phase 0
Can abolish
tachyarrhythmia
caused by reentry
circuit
II β blocker
↓heart rate and
conduction velocity
Can indirectly alter
K and Ca
conductance
III K+ channel blocker
1. ↑action potential
duration (APD) or
effective refractory
period (ERP).
2. Delay
repolarization.
Inhibit reentry
tachycardia
IV Ca++ channel blocker
Slowing the rate of rise
in phase 4 of SA
node(slide 12)
↓conduction velocity
in SA and AV node
•Most antiarrhythmic drugs are pro-arrhythmic (promote arrhythmia)
•They are classified according to Vaughan William into four classes according to their
effects on the cardiac action potential
16. Class I
IA IB IC
They ↓ conduction velocity in non-nodal
tissues (atria, ventricles, and purkinje fibers)
They act on open
Na+ channels or
inactivated only
Have moderate K+
channel blockade
So they are used
when many Na+
channels are opened
or inactivated (in
tachycardia only)
because in normal
rhythm the channels
will be at rest state
so the drugs won’t
work
Class I drugs
17. Slowing of the rate of rise
in phase 0 ↓conduction
velocity
↓of Vmax of the cardiac action
potential
They prolong muscle action
potential & ventricular (ERP)
They ↓ the slope of Phase 4
spontaneous depolarization
(SA node) decrease
enhanced normal
automaticity
Class IA
Quinidine Procainamide
They make the
slope more
horizontal
18. Class IA Drugs
They possess intermediate rate of association and
dissociation (moderate effect) with sodium channels.
Pharmacokinetics:
Procainamide
Good oral
bioavailability
Used as IV to avoid
hypotension
Quinidine
Good oral
bioavailability
Metabolized
in the liver
Procainamide metabolized into N-acetylprocainamide (NAPA) (active
class III) which is cleared by the kidney (avoid in renal failure)
19. Class IA Drugs
Uses
Supraventricular and ventricular arrhythmias
Quinidine is rarely used for supraventricular
arrhythmias
Oral quinidine/procainamide are used with class III
drugs in refractory ventricular tachycardia patients
with implantable defibrillator
IV procainamide used for hemodynamically stable
ventricular tachycardia
IV procainamide is used for acute conversion of
atrial fibrillation including Wolff-Parkinson-White
Syndrome (WPWS)
defibrillator
20. Class IA Drugs Toxicity
Quinidine
AV block
Torsades de pointes arrhythmia
because it ↑ ERP (QT interval)
Blurred vision
Tinnitus
Tremors
Abdominal Upset
Procainamide
Hypersensitivity
: fever,
agranulocytosis
Systemic lupus erythromatosus (SLE)-like
symptoms: arthralgia, fever, pleural-
pericardial inflammation.
Symptoms are dose and time dependent
Common in patients with slow hepatic
acetylation
21. Notes:
Torsades de pointes: twisting of the point . Type of
tachycardia that gives special characteristics on ECG
At large doses of quinidine cinchonism occurs: blurred vision, tinnitus, headache,
psychosis and gastrointestinal upset
Digoxin is administered before quinidine to prevent the conversion of atrial fibrillation or
flutter into paradoxical ventricular tachycardia
22. Class IB Drugs
They shorten Phase 3
repolarization
↓ the duration of the
cardiac action potential
They suppress arrhythmias
caused by abnormal
automaticity
They show rapid
association &
dissociation (weak effect)
with Na+ channels with
appreciable degree of use-
dependence
No effect on conduction
velocity
Class IB
lidocaine mexiletine tocainide
23. Agents of Class IB
Lidocaine
Used IV because of extensive 1st pass
metabolism
Lidocaine is the drug of choice in
emergency treatment of ventricular
arrhythmias
Has CNS effects: drowsiness,
numbness, convulsion, and nystagmus
Mexiletine
These are the oral analogs of
lidocaine
Mexiletine is used for chronic
treatment of ventricular
arrhythmias associated with
previous myocardial infarction
Uses
They are used in the treatment of ventricular arrhythmias arising during
myocardial ischemia or due to digoxin toxicity
They have little effect on atrial or AV junction arrhythmias (because they don’t
act on conduction velocity)
Adverse effects:
1- Neurological effects
2- Negative inotropic activity
24. Class IC Drugs
They markedly slow Phase 0 fast
depolarization
They markedly slow conduction in
the myocardial tissue
They possess slow rate of
association and dissociation
(strong effect) with sodium
channels
They only have minor effects on
the duration of action potential
and refractoriness
They reduce automaticity by
increasing the threshold potential
rather than decreasing the slope of
Phase 4 spontaneous
depolarization.
Class IC
Flecainide Propafenone
25. Uses:
Refractory ventricular arrhythmias.
Flecainide is a particularly potent suppressant of premature
ventricular contractions (beats)
Toxicity and Cautions for Class IC Drugs:
They are severe pro arrhythmogenic drugs causing:
1. severe worsening of a preexisting arrhythmia
2. de novo occurrence of life-threatening ventricular
tachycardia
In patients with frequent premature ventricular contraction
(PVC) following MI, flecainide increased mortality
compared to placebo.
Notice: Class 1C drugs are particularly of low safety and have
shown even increase mortality when used chronically after MI
26. Compare between class IA, IB, and IC drugs as
regards effect on Na+ channel & ERP
Sodium channel blockade:
IC > IA > IB
Increasing the ERP:
IA>IC>IB (lowered)
Because of
K+
blockade
27. Class II ANTIARRHYTHMIC DRUGS
(β-adrenergic blockers)
Uses
Treatment of increased
sympathetic activity-
induced arrhythmias such
as stress- and exercise-
induced arrhythmias
Atrial flutter and fibrillation.
AV nodal tachycardia.
Reduce mortality in post-
myocardial infarction
patients
Protection against sudden
cardiac death
Mechanism of action
Negative inotropic
and chronotropic
action.
Prolong AV
conduction (delay)
Diminish phase 4
depolarization
suppressing
automaticity(of
ectopic focus)
28. Class II ANTIARRHYTHMIC DRUGS
Propranolol (nonselective): was proved to
reduce the incidence of sudden arrhythmic death
after myocardial infarction
Metoprolol
reduce the risk of bronchospasm
Esmolol:
Esmolol is a very short-acting β1-adrenergic
blocker that is used by intravenous route in acute
arrhythmias occurring during surgery or
emergencies
selective
29. Class III ANTIARRHYTHMIC
DRUGS
K+ blockers
Prolongation of phase 3
repolarization without altering
phase 0 upstroke or the resting
membrane potential
They prolong both the duration
of the action potential and ERP
Their mechanism of action is
still not clear but it is thought
that they block potassium
channels
30. Uses:
Ventricular arrhythmias, especially ventricular
fibrillation or tachycardia
Supra-ventricular tachycardia
Amiodarone usage is limited due to its wide
range of side effects
Class III
sotalol amiodarone ibutilide
31. Amiodarone (Cordarone)
Amiodarone is a drug of multiple actions and is still not well understood
It is extensively taken up by tissues, especially fatty tissues (extensive
distribution)
t1/2 = 60 days
Potent P450 inhibitor
Amiodarone antiarrhythmic effect is complex comprising class I, II, III,
and IV actions
• Dominant effect: Prolongation of action potential duration and refractoriness
• It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak
β-adrenergic blocker
Toxicity
GI intolerance
Neuropathy, tremors, ataxia, dizziness.
Hyper-or hypo thyrodism
Corneal microdeposits may be accompanied with disturbed night vision
Liver toxicity, photosensitivity, gray facial discoloration, muscle weakness,
and weight loss
The most dangerous side effect is pulmonary fibrosis which occurs in
2-5% of the patients
32. Sotalol (Sotacor)
Sotalol also prolongs the duration of action potential and
refractoriness in all cardiac tissues (by action of K+ blockade)
Sotalol suppresses Phase 4 spontaneous depolarization and
possibly producing severe sinus bradycardia (by β blockade
action)
The β-adrenergic blockade combined with prolonged action
potential duration may be of special efficacy in prevention of
sustained ventricular tachycardia
It may induce the polymorphic torsades de pointes ventricular
tachycardia (because it increases ERP)
Ibutilide
Used in atrial fibrillation or flutter
IV administration
May lead to torsade de pointes
Only drug in class three that possess pure K+ blockade
33. Class IV ANTIARRHYTHMIC
DRUGS
(Calcium Channel Blockers)
Calcium channel blockers decrease
inward Ca2+ currents resulting in a
decrease of phase 4 spontaneous
depolarization (SA node)
They slow conductance in Ca2+
current-dependent tissues like AV
node.
Examples: verapamil & diltiazem
Because they act on the heart only
and not on blood vessels.
Dihydropyridine family are not used
because they only act on blood vessels
34. Mechanism of
action
They bind only to depolarized (open) channels prevention of repolarization
They prolong ERP of AV node ↓conduction of impulses from the atria to the
ventricles
So they act only in cases of arrhythmia because many Ca2+
channels are depolarized while in normal rhythm many of
them are at rest
More effective in treatment of atrial than ventricular arrhythmias.
Treatment of supra-ventricular tachycardia preventing the
occurrence of ventricular arrhythmias
Treatment of atrial flutter and fibrillation
Uses
35. contraindication
Contraindicated in patients with pre-existing
depressed heart function because of their negative
inotropic activity
Adverse effects
Cause bradycardia, and asystole especially when
given in combination with β-adrenergic blockers
36. Miscellaneous Antiarrhythmic Drugs
Adenosine
o Adenosine activates A1-purinergic receptors
decreasing the SA nodal firing and automaticity,
reducing conduction velocity, prolonging effective
refractory period, and depressing AV nodal
conductivity
o It is the drug of choice in the treatment of
paroxysmal supra-ventricular tachycardia
o It is used only by slow intravenous bolus
o It only has a low-profile toxicity (lead to
bronchospasm) being extremely short acting for
15 seconds only