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The document discusses various classes of anti-arrhythmic drugs, their mechanisms of action, therapeutic uses, and side effects. It covers class IA drugs like quinidine, procainamide, and disopyramide; class IB drugs like lidocaine, mexiletine, and tocainide; class IC drugs like flecainide, propafenone, and moricizine; class II beta blockers; class III potassium channel blockers like amiodarone, bretylium, and sotalol; and class IV calcium channel blockers. Common side effects include cardiac toxicity, arrhythmia exacerbation, hypotension, and gastrointestinal issues.
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This document discusses antiarrhythmic drugs and their mechanisms of action. It begins by classifying arrhythmias and describing the electrophysiology of the heart. It then classifies antiarrhythmic drugs into four classes based on their mechanisms of action - sodium channel blockers (Class I), beta blockers (Class II), drugs that prolong the action potential (Class III), and calcium channel blockers (Class IV). Specific Class I drugs are discussed in detail, including quinidine, procainamide, and lignocaine. Their effects on cardiac sodium channels, action potentials, and refractory periods are summarized. Adverse effects and clinical uses are also briefly mentioned for key drugs.
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Anti arrhythmic drugs
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- 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.
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General Physiology - Action potential
The document summarizes membrane potentials and action potentials in nerve cells. It discusses:
1) The concentration gradients that give rise to resting membrane potentials via the Nernst equation and Goldman equation. Key ions like sodium, potassium and chloride contribute to a resting potential of around -90mV.
2) How action potentials are initiated when the membrane reaches a threshold potential, causing voltage-gated sodium channels to open and depolarize the membrane. Potassium channels then open to repolarize the membrane.
3) The roles of other ions like calcium and various ion pumps and channels in maintaining resting potentials and propagating action potentials down nerve fibers via saltatory conduction. Action potentials rely on precise ion concentration gradients maintained
Cardiac arrhythmias
- The document discusses the anatomy and physiology of the heart's conduction system and how it generates the normal cardiac rhythm. It describes the roles of the sinoatrial node, atrioventricular node, Bundle of His, and Purkinje fibers in conducting electrical impulses through the heart.
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The Resting Potential And The Action Potential
An action potential occurs when a neuron is stimulated enough to reach its threshold of excitation. This causes sodium channels to open, allowing sodium to rush into the neuron and depolarize it. The neuron then repolarizes as potassium leaves and the sodium-potassium pump restores the ion gradients. After an action potential, the neuron enters an absolute refractory period where it cannot fire again, followed by a relative refractory period where a stronger stimulus is needed to trigger another action potential. This process allows neurons to rapidly transmit signals down axons to synapse with other neurons.
Action potential
1. An action potential, or nerve impulse, occurs when a neuron reaches its threshold level and is stimulated to send a message along its axon.
2. The action potential involves two steps - depolarization, where sodium ions rush into the neuron, reversing the charge; and repolarization, where potassium ions rush out, restoring the charge.
3. After repolarization, the sodium-potassium pump restores the ion concentrations to prepare the neuron to fire again if stimulated. Myelin insulation allows the impulse to jump from node to node, speeding up conduction.
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This document summarizes antiarrhythmic drug therapy for pediatric patients. It discusses empiric diagnosis of arrhythmias and the Vaughn-Williams classification of antiarrhythmic drugs. Specific drug classes and agents are described including their mechanisms of action, uses, dosages, and side effects for treating arrhythmias like supraventricular tachycardia, atrial flutter, ventricular tachycardia, and ventricular fibrillation. Emphasis is placed on selecting the appropriate antiarrhythmic based on the specific arrhythmia and consulting with a cardiologist for long-term or complex cases.
Antiarrythmic drugs part ii
This document discusses antiarrhythmic drugs, their mechanisms of action, uses, and adverse effects. It covers five classes of antiarrhythmic drugs: Class I sodium channel blockers like quinidine and lidocaine; Class II beta blockers; Class III potassium channel blockers like amiodarone; Class IV calcium channel blockers like verapamil; and miscellaneous drugs like adenosine. Amiodarone has multiple effects including sodium, potassium, calcium channel blocking and beta blocking actions. It is effective for many arrhythmias but can cause pulmonary and thyroid toxicity with long term use. Choice of antiarrhythmic depends on the presenting arrhythmia, its mechanism, the drug's pharmacokinetic
Antiarrhythmic agent
Antiarrhythmic agents are used to treat abnormal heart rhythms. They are classified into 5 classes based on their mechanism of action:
Class I agents block sodium channels. Common examples are quinidine, procainamide, and lidocaine.
Class II agents are beta blockers that block sympathetic nervous system activity. Examples include propranolol and atenolol.
Class III agents prolong the heart's repolarization by blocking potassium channels. Amiodarone, sotalol, and ibutilide are examples.
Class IV agents like verapamil and diltiazem block calcium channels and slow conduction through the AV node.
Class V agents work through other mechanisms and include
Pharmacotherapy of Cardiac arrhythmias
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
This document discusses antiarrhythmic drugs and their mechanisms of action. It begins by describing the cardiac action potential and differences between automatic and non-automatic tissues. It then covers the Vaughan Williams classification of antiarrhythmic drugs and discusses drugs from each class in detail, including their electrophysiological effects, indications, dosages, and adverse effects. The classes covered are Class IA (quinidine, procainamide), Class IB (lidocaine, mexiletine, phenytoin), Class IC (flecainide, propafenone), Class II (beta blockers), and Class III (amiodarone, sotalol).
SVTagents
This document discusses the mechanisms of action and side effects of various antiarrhythmic drugs used to treat supraventricular tachycardia. It classifies the drugs according to the Vaughn-Williams classification system based on their effects on ion channels and receptors. Key drugs discussed include adenosine which acts on A1 receptors, procainamide which blocks sodium channels, amiodarone which has effects on multiple ion channels, and verapamil which slows conduction in the sinus and atrioventricular nodes. All antiarrhythmic drugs carry a risk of proarrhythmia, so careful patient selection and monitoring is important when using these agents.
Anti arrhthymic drugs
Spurthi BS completed her Doctor of Pharmacy degree from Mallige College of Pharmacy. Her document discusses various classes of antiarrhythmic drugs, their mechanisms of action, examples, and side effects. It covers sodium channel blockers, beta blockers, potassium channel blockers, calcium channel blockers, digoxin, and adenosine. The classes are compared in terms of their effects on cardiac action potential phases and conduction. Specific drugs are also described in terms of their uses, dosages, and contraindications.
Antiarrhythmic drugs
This document discusses antiarrhythmic drugs used to treat arrhythmias. It begins by defining arrhythmias as abnormalities in heart rate, rhythm or conduction. It then discusses the normal physiology of the heart including the properties of cardiac muscle cells and the conduction system. It explains the mechanisms of arrhythmias and classification of antiarrhythmic drugs. The major classes of antiarrhythmic drugs are discussed in detail including mechanisms of action, indications, dosages and side effects. Class I drugs block sodium channels, Class II are beta blockers, and Class III block potassium channels.
Antiarrhythmic Drugs and its side effect.pptx
Antiarrhythmic drugs are used to treat and prevent cardiac arrhythmias. They work by altering the movement of ions through cardiac cell membranes. The Vaughan Williams classification system groups antiarrhythmics based on their effects on sodium, potassium, calcium, and beta-adrenergic channels. Common antiarrhythmics include amiodarone (blocks multiple channels), beta-blockers, calcium channel blockers, and sodium channel blockers. Nurses must closely monitor patients taking these drugs for effectiveness and potential adverse effects like hypotension, bradycardia, and prolonged QT interval.
5.Anti-Arrhythmic Drugs.pdf
This document provides an overview of anti-arrhythmic drugs and their pharmacology. It begins with an introduction to arrhythmias and their causes. It then discusses various classes of anti-arrhythmic drugs including Class I sodium channel blockers, Class II beta-blockers, Class III potassium channel blockers, and Class IV calcium channel blockers. Individual drug mechanisms and uses are explained for lidocaine, amiodarone, propranolol, and verapamil. Non-pharmacological treatments for arrhythmias like ablation and implantable defibrillators are also mentioned. Expected exam questions focus on classification of anti-arrhythmics and details of specific drugs.
5.Anti-Arrhythmic Drugs.pdf
Scope: This subject is intended to impart the fundamental knowledge on various aspects
(classification, mechanism of action, therapeutic effects, clinical uses, side effects and
contraindications) of drugs acting on different systems of body and in addition,emphasis
on the basic concepts of bioassay. Objectives: Upon completion of this course the student should be able to
1. Understand the mechanism of drug action and its relevance in the treatment of
different diseases
2. Demonstrate isolation of different organs/tissues from the laboratory animals by
simulated experiments
3. Demonstrate the various receptor actions using isolated tissue preparation
Antiarrhythmicdrug therapy Dr Vinay Verma
This document discusses antiarrhythmic drug therapy. It describes the normal cardiac conduction pathway and how arrhythmias disrupt normal rhythm. There are several classes of antiarrhythmic drugs that work by different mechanisms, such as blocking sodium, potassium, calcium channels or beta receptors. The drugs have various uses for treating supraventricular and ventricular arrhythmias. Adverse effects and drug interactions are also reviewed for specific antiarrhythmic medications.
Cardiac drugs
Telmisartan is an angiotensin II receptor blocker used to treat hypertension. It works by selectively blocking angiotensin II receptors, which prevents the constricting and aldosterone-secreting effects of angiotensin II. Side effects include diarrhea and hypotension. Nurses should monitor the patient's blood pressure closely, especially after starting the drug, and watch for orthostatic hypotension in patients undergoing dialysis.
Antiarrhythmics modified
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
Preoperative preparation of a Pheochromocytoma
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3. Cardiac Arrythmias ppt
Cardiac arrhythmias refer to irregularities in the heart's electrical activity and rhythm. This document discusses the definition, physiology, types, diagnosis, and treatment of various cardiac arrhythmias including:
- Supraventricular tachycardias like atrial flutter and atrial fibrillation which originate above the ventricles.
- Ventricular arrhythmias including ventricular tachycardia and ventricular fibrillation. Causes include coronary artery disease and cardiomyopathy.
- Other arrhythmias like sinus tachycardia, junctional tachycardia, and multifocal atrial tachycardia. Diagnosis involves electrocardiograms and treatment depends on the type and severity
1- Anti-arrhythmic drugs.pdf
This document provides an overview of the cardiovascular system module presented by Dr. Mohamed Farouk Ahmed. It discusses normal cardiac rhythm, cardiac cell action potentials, definitions and causes of arrhythmias, classification of antiarrhythmic drugs, and specific drugs from each class including their mechanisms of action, uses, and side effects. The goals of antiarrhythmic therapy and classification systems for arrhythmias and drugs are explained. Supraventricular and ventricular arrhythmias as well as individual drug profiles are outlined in detail.
Antiarrhythmics
This document discusses various types of antiarrhythmic drugs. It begins by describing the different types of cardiac tissue and the cardiac action potential. It then categorizes antiarrhythmic drugs into five classes based on their mechanisms of action. For each drug discussed, it provides information on pharmacological properties, metabolism, side effects, indications, and status of current use. The document focuses on quinidine, procainamide, disopyramide, lidocaine, mexiletine, propafenone, and flecainide, describing their electrophysiological effects, pharmacokinetics, adverse effects, and clinical applications.
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Syllabus
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Chapter 3
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Chapter 6
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Editd anti arrhythmic
- 1. ANTI-ARRHYTHMIC DRUGS Ma. Janetth B. Serrano, M.D.,DPBA
Editor's Notes
- S,