Antiarrhythmic Drugs and its side effect.pptx

Antiarrhythmic Drugs and its side effect.pptx

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  Antiarrhythmic Drugs By: MuhammadAurangzeb Lecturer-INS/KMU
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  By the endof this unit learners, will be able to: • Discuss pharmacological management of arrhythmias. • Discuss nursing implication in relation to antiarrhythmic drugs. • Calculate the drug dosage accurately while administering oral and parenteral medication Objectives
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  Arrhythmia • Arrhythmia isdeviation of heart from normal rhythm. • Normal Rhythm 1)HR- 60-100 2) Should origin from SA Node 3) Cardiac impulse should propagate through normal conduction pathway with normal velocity.
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  100 60 Normal range 150 Simpletachyarrythmia 200 Paroxysmal TA . 500 Atrial fibrillation 350 Atrial flutter 40 Mild bradyarrhythmias 20 moderateBA Severe BA Classification of Arrhythmias
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  Arrhythmias Sinus arrythmia Atrial arrhythmia Nodal arrhythmia (junctional) Ventricular arrhytmia Supra Ventricular Tachycardia
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  Types of cardiactissue (on the basis of impulse generation) • Automatic/ pacemaker/ conducting fibers (Ca++ driven tissues)  Includes SA node, AV node, bundle of his, purkinje fibers  Capable of generating their own impulse  Normally SA node acts as pacemaker of heart • Non-automatic myocardial contractile fibers (Na+ driven tissues)  Cannot generate own impulse  Includes atria and ventricles
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  Electrophysiology of cardiactissue • Impulse generation and transmission • Myocardial action potential • Depolarization and repolarization waves as seen in ECG
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  Impulse generation andtransmission
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  Myocardial action potential Inautomatic tissues In non-automatic tissues (See video for it) https://www.youtube.com/watch?v=9xSqezC MHnw
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  Arrhythmia • Definition: – Disturbancesin the heart rate, rhythm, impulse generation or conduction of electrical impulses responsible for membrane depolarization – These disturbances can lead to alterations in overall cardiac function that can be life threatening. • Antiarrhythmic drugs: – Compounds used to prevent or treat cardiac arrhythmias
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  Mechanism of arrhythmias •Disturbances in impulse generation may be due to – Abnormal automaticity – Delayed after depolarization • Disturbances of impulse conduction – The impulse may recirculate in heart causing repeated activation (re-entry) – Conduction blocks
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  Re-entry phenomenon
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  Phases of actionpotential of cardiac cells Phase 0 rapid depolarisation (inflow of Na+) Phase 1 partial repolarisation (inward Na+ current deactivated, outflow of K+) Phase 2 plateau (slow inward calcium current) Phase 3 repolarisation (calcium current inactivates, K+ outflow) Phase 4 pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) ‘autorhythmicity’ Refractory period (phases 1-3) Phase 4 II Phase 0 Phase 1 Phase 3 0 mV -80mV I III IV Phase 2
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  Cont… • Phase 0:Fast sodium channels are responsible for initial rapid depolarization • Phase 1: Early fast repolarization (K+ efflux) • Phase 2: Prolonged depolarization “plateau” due to slow calcium influx • Phase 3: Repolarization due to closing of the calcium channels and potassium efflux • Phase 4: Resting membrane potential is restored
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  Goals of Treatment •The goal of treatment for patients with arrhythmias is preferably to return the heart to sinus rhythm, or failing that, at least to stabilize the rate. • Treatment options are pharmacological (eg, amiodarone, lidocaine, atenolol), ablative (destruction of the malfunctioning tissue) or electrical to correct the rhythm.
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  Drug therapy • Anti-arrhythmicdrug therapy is used to control the frequency and severity of arrhythmias, with the aim of maintaining sinus rhythm where possible. • The drugs can be grouped according to their electrophysiological effects at a cellular level, using a system known as the Vaughan Williams classification. • Alternatively, drug therapies can be divided according to their main sites of action within the heart.
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  Vaughan Williams classification •All anti-arrhythmic drugs act by altering the movement of electrolytes within the electrical conduction pathways of the myocardium. • The Vaughan Williams classification system groups drugs according to their ability to block the movement of one or more of these ions across the myocardial cell membrane.
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  Vaughan Williams Classification ofantiarrhythmic drugs • Class I: Sodium channel blockers • Class II: β-Adrenergic blockers – Propranolol, acebutolol, esmolol • Class III: Potassium channel blockers – Amiodarone, bretylium, sotalol • Class IV: calcium channel blockers – Verapamil, diltiazem • Miscellaneous – Adenosine, Digoxin – Atropine
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  Class I: Sodiumchannel blockers Class I drugs act by blocking the fast sodium channels and therefore delay the rise in phase 0 of the action potential. Can be subdivided into: • IA: Prolong repolarization, increase the duration of the action potential – Quinidine, procainamide, disopyramide • IB: Shorten repolarization, shorten the action potential – Lignocaine, mexiletine, phenytoin • IC: Little effect on repolarization, no effect on action potential duration – Encainide, flecainide, propafenone
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  Class I: Sodiumchannel blockers • IA: Prolong repolarization – Quinidine, procainamide, disopyramide • IB: Shorten repolarization – Lignocaine, mexiletine, phenytoin • IC: Little effect on repolarization – Encainide, flecainide, propafenone
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  Class IA
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  Quinidine • D- isomerof quinine obtained from cinchona bark • MOA: blocks sodium channels – ↓ automaticity , conduction velocity and prolongs repolarization – ↓phase 0 depolarization , ↑ APD & ↑ERP • Uses: Atrial and ventricular arrhythmias • Adverse effects: – Arrhythmias and heart block , hypotension, QT prolongation – GIT , thrombocytopenia, hepatitis , idiosyncratic reactions – High doses – cinchonism like quinine
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  • Procainamide: – Derivativeof procaine – No vagolytic or α-blocking action unlike quinidine – Better tolerated – Adverse effects: • Nausea, vomiting and hypersensitivity reactions • Higher doses can cause hypotension, heart block and QT prolongation • Disopyramide: – Significant anticholinergic properties: • Dry mouth, blurred vision, constipation, urinary retention
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  Class IB drugs Lignocaine,phenytoin, mexiletine Block sodium channels also shorten repolarization
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  Lignocaine • Local anesthetic •Raises threshold for action potential, • ↓automaticity • Suppress electrical activity of arrhythmogenic tissues, normal tissues less effected • High first pass metabolism so given parenterally • Use: ventricular arrhythmias • Adverse effects: – Drowsiness, hypotension, blurred vision, confusion and convulsions
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  • Phenytoin: – Antiepilepticalso useful in ventricular arrhythmias (not preferred) and digitalis induced arrhythmias • Mexiletine: – Can be used orally causes dose related neurological adverse events like tremors and blurred vision – Nausea is common – Used as alternative to lignocaine in ventricular arrhythmias
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  Class I Cdrugs Encainide, Flecainide, Propafenone Have minimal effect on repolarization Are most potent sodium channel blockers Risk of cardiac arrest , sudden death so not used commonly May be used in severe ventricular arrhythmias
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  Class I drugsand their primary indications Class of drug Drug Primary indication Class 1A Quinidine Procainamide Disopyramide Atrial fibrillation Ventricular arrhythmias Class 1B Lidocaine Mexilitene Phenytoin Ventricular arrhythmias Class 1C Flecainide Propafenone AV nodal re-entry Wolff-Parkinson White syndrome-related arrhythmias Ventricular arrhythmias (but increased risk of mortality
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  Class II drugs •Suppress adrenergically mediated ectopic activity • Antiarrhythmic action due to of β blockade • Depress myocardial contractility, automaticity and conduction velocity • Propranolol: – Treatment & prevention of supraventricular arrhythmias especially associated with exercise, emotion or hyperthyroidism • Esmolol: – IV short acting can be used to treat arrhythmias during surgery , following MI & other emergencies
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  ↑APD & ↑RPby blocking the K+ channels Class III drugs
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  Amiodarone • Iodine containinglong acting drug • Mechanism of action: (Multiple actions) – Prolongs APD by blocking K+ channels – blocks inactivated sodium channels – β blocking action , Blocks Ca2+ channels – ↓ Conduction, ↓ectopic automaticity • Pharmacokinetics: – Variable absorption 35-65% – Slow onset 2days to several weeks – Duration of action : weeks to months – Many drug interactions
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  Amiodarone • Uses: – Canbe used for both supraventricular and ventricular tachycardia • Adverse effects: – Cardiac: heart block , QT prolongation, bradycardia, cardiac failure, hypotension – Pulmonary: pneumonitis leading to pulmonary fibrosis – Bluish discoloration of skin – GIT disturbances, hepatotoxicity – Blocks peripheral conversion of T4 to T3 can cause hypothyroidism or hyperthyroidism
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  Other Class IIIDrugs • Bretylium: – Adrenergic neuron blocker used in resistant ventricular arrhythmias • Sotalol: – Beta blocker • Dofetilide: – Selective K+ channel blocker, less adverseevents – Oral use in AF to convert or maintain sinus rhythm • Ibutilide: – K+ channel blocker used as IV infusion in AF or flutter can cause QT prolongation
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  Calcium channel blockers(Class IV) • Inhibit the inward movement of calcium ↓ contractility, automaticity , and AV conduction. • Verapamil & diltiazem
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  Verapamil • Uses: – TerminatePSVT – control ventricular rate in atrial flutter or fibrillation • Drug interactions: – Displaces digoxin from binding sites – ↓ renal clearance of digoxin
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  Other antiarrhythmics • Adenosine: – Purine nucleotide having short and rapid action – Mechanism of action: Acetylcholine sensitive K+ channels and causes membrane hyperpolarization through interaction with A1 type of adenosine GPCRs on SAnode – IV suppresses automaticity, AV conduction and dilates coronaries – Drug of choice for PSVT – Adverse events: • Nausea, dyspnoea, flushing, headache • Atropine: Used in sinus bradycardia, AV block • Digitalis: Atrial fibrillation and atrial flutter • Magnesium SO4: digitalis induced arrhythmias
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  Classification of drugaccording to principal site of action Site of action Anti-arrhythmic drug Action AV node Verapamil, dilatiazem, adenosine, digoxin, beta- blockers Delay AV nodal conduction Useful for control of supra-ventricular tachycardias Ventricles Lignocaine, mexelitine, phenytoin Control of ventricular arrhythmias Atria, ventricles and accessory pathways Quinidine, disopyramide, amiodarone, flecainide, procainamide, propafenone Effective in both supra- ventricular tachycardia and ventricular arrhythmias
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  Nursing Considerations forAntiarrhythmic drugs • Assess for the mentioned contraindications to this drug (e.g. renal dysfunction, heart blocks, hypersensitivity, etc.) to prevent potential adverse effects. • Conduct thorough physical assessment before beginning drug therapy to establish baseline status, and to evaluate potential adverse effects. • Assess cardiac status closely (e.g. blood pressure, heart rate and rhythm, heart sounds, ec.) to determine whether change in drug dose is imperative. • Monitor laboratory test results including complete blood count, renal and liver function tests to determine the need for possible change in dose and identify toxic effects.
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  Nursing Intervention These arevital nursing interventions done in patients who are taking antiarrhythmic drugs: • Titrate the dose to the smallest amount enough to manage arrhythmia to decrease the risk of drug toxicity. • Monitor cardiac rhythm closely to detect potentially serious adverse effects and to evaluate drug effectiveness. • Ensure maintenance of emergency drugs and equipment at bedside to promote prompt treatment in cases of severe toxicity. • Educate patient on drug therapy including drug name, its indication, and adverse effects to watch out for to enhance patient understanding on drug therapy and thereby promote adherence to drug regimen.
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  References • Karch, A.M., & Karch. (2011). Focus on nursing pharmacology. Wolters Kluwer Health/Lippincott Williams & Wilkins. [Link] • Katzung, B. G. (2017). Basic and clinical pharmacology. McGraw-Hill Education. • Lehne, R. A., Moore, L. A., Crosby, L. J., & Hamilton, D. B. (2004). Pharmacology for nursing care. • Smeltzer, S. C., & Bare, B. G. (1992). Brunner & Suddarth’s textbook of medical-surgical nursing. Philadelphia: JB Lippincott