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Antiarrhythmic Drugs PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Antiarrhythmic drugs".

This medical PowerPoint presentation talks about antiarrhythmic drugs. Antiarrhythmic drugs are a class of medications used to treat abnormal heart rhythms, also known as arrhythmias. These drugs work by controlling the electrical activity of the heart, either by slowing down or regulating the heart rate, or by restoring the normal heart rhythm.

There are different types of antiarrhythmic drugs, which are classified based on their mechanisms of action and their effects on the heart.

Tags : Antiarrhythmic drugs, abnormal heart rhythms, arrhythmias, cardiology

Published on : Mar 17, 2023 | Views : 1491 | Downloads : 4

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Slide 1-

Antiarrhythmic drugs Pharma team
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LECTURE’S OUTLINE: Electrophysiology of the heart Arrhythmia: definition, mechanisms, types Drugs :class I, II, III, IV Guide to treat some types of arrhythmia Questions
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Physiology of the normal heart 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
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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
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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
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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
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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
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Arrhythmia Arrhythmia /dysrhythmia: abnormality in the site of origin of impulse, rate, or conduction 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
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Mechnisms of Arrhythmogenesis Delayed afterdepolarization Early afterdepolarization ↑AP from SA node AP arises from sites other than SA node
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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)
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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
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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)
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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
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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
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Pharmacologic Rationale & Goals The ultimate goal of antiarrhythmic drug therapy: Restore normal sinus rhythm and conduction 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
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Antyarrhythmic drugs 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
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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
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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 Mechanism of action They make the slope more horizontal
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Class IA Drugs They possess intermediate rate of association and dissociation (moderate effect) with sodium channels. Pharmacokinetics: Procainamide metabolized into N-acetylprocainamide (NAPA) (active class III) which is cleared by the kidney (avoid in renal failure)
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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
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Class IA Drugs Toxicity Systemic lupus erythromatosus (SLE)-like symptoms: arthralgia, fever, pleural-pericardial inflammation. Symptoms are dose and time dependent Common in patients with slow hepatic acetylation
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Notes: Torsades de pointes: twisting of the point . Type of tachycardia that gives special characteristics on ECG At large dosesof 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
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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
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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, convulstion, 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
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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.
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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 proarrhythmogenic drugs causing: severe worsening of a preexisting arrhythmia 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
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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
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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)
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Class II ANTIARRHYTHMIC DRUGS Propranolol (nonselective): was proved to reduce the incidence of sudden arrhythmatic 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
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Class III ANTIARRHYTHMIC DRUGSK+ 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
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Uses: Ventricular arrhythmias, especially ventricular fibrillation or tachycardia Supra-ventricular tachycardia Amiodarone usage is limited due to its wide range of side effects
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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
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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 Most common include GI intolerance, tremors, ataxia, dizziness, and hyper-or hypothyrodism Corneal microdeposits may be accompanied with disturbed night vision Others: liver toxicity, photosensitivity, gray facial discoloration, neuropathy, muscle weakness, and weight loss The most dangerous side effect is pulmonary fibrosis which occurs in 2-5% of the patients
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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
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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
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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
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Miscellaneous Antiarrhythmic Drugs Adenosine Adenosine activates A1-purinergic receptors decreasing the SA nodal firing and automaticity, reducing conduction velocity, prolonging effective refractory period, and depressing AV nodal conductivity It is the drug of choice in the treatment of paroxysmal supra-ventricular tachycardia It is used only by slow intravenous bolus It only has a low-profile toxicity (lead to bronchospasm) being extremly short acting for 15 seconds only
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Treatment of atrial flutter/fibrillation 1st: Reduce thrombus formation by using anticoagulant warfarin 2nd: Prevent the arrhythmia from converting to ventricular arrhythmia: First choice: class II drugs: After MI or surgery Avoid in case of heart failure Second choice: class IV Third choice: digoxin Only in heart failure of left ventricular dysfunction 3rd: Conversion of the arrhythmia into normal sinus rhythm: Class III: IV ibutilide, IV/oral amiodarone, or oral sotalol Class IA: Oral quinidine + digoxin (or any drug from the 2nd step) Class IC: Oral propaphenone or IV/oral flecainide Use direct current in case of unstable hemodynamic patient
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Treatment of ventricular arrhythmia First choice: class II IV followed by oral Early after MI Second choice: amiodarone Avoid using class IC after MI  ↑ mortality Treatment of ventricular tachycardia First choice: Lidocaine IV Repeat injection Second choice: procainamide IV Adjust the dose in case of renal failure Third choice: class III drugs Especially amiodarone and sotalol Premature ventricular beat (PVB)
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تجميعات: (IA, IC, class III)  torsades de pointes. Classes II and IV  bradycardia (don’t combine the two) In atrial flutter use (1st ↓impulses from atria to ventricular to prevent ventricular tachycardia) Class II Class IV Digoxin. (على الترتيب) 2nd convert atrial flutter to normal sinus rhythm use: Ibutilide Sotalol IA or IC. (على الترتيب) If you use quinidine combine it with digoxin or β blocker (because of its anti muscarinic effect) Avoid IC in myocardial infarction because it ↑ mortality
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questions 1- In ventricular tachycardia and stable hemodynamic which drug to be used? A- propranolol B- procainamide C- quinidine D- verapamil 2- Mr.Green devloped an arrhythmia and was treated. A month later, he has arthralgia, fever, pleural inflammation. What was the treatment of arrhythmia? A- esmolol B- class III C- procainamide D- propafenone 3- Cinchonism occurs with digoxin A- pulmonary fibrosis diltiazem B- bradycardia amiodarone (F)