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seminar anti-arrhythmic drugs treatment.pptx

seminar anti-arrhythmic drugs treatment.pptx

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1 Anti-Arrhythmic Drugs Dr. Kavyanshi Verma Junior Resident Department of Pharmacology
• Definition: – Disturbances in 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 Arrhythmia
Mechanism of arrhythmias • Disturbances in impulse generation may be due to – Abnormal automaticity – Delayed after depolarizations • Disturbances of impulse conduction – The impulse may recirculate in heart causing repeated activation (re-entry) – Conduction blocks
Arrhythmia Defects in impulse generation Altered automaticity escape/ectopic rhythm Triggered automaticity EAD/DAD Defects in impulse conduction RE-ENTRY obstacle Conduction blocks complete WPW syndrome
Causes of Arrhythmias • Ischemia, hypoxia • Acidosis or alkalosis, electrolyte abnormalities • Excessive catecholamine exposure, autonomic influences • Drug toxicity (eg, digitalis or antiarrhythmic drugs) • Overstretching of cardiac fibers
Phases of action potential 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
Classification • Miles Vaughn Williams and Brahma Singh • ‘Vaughn Williams classification’ • Based on the Predominant Mechanism of Action • Brahma Singh added class III • Based on action Na+ , Ca+ and K+ channels
Classification v v v v v v v
Class 1 Membrane stabilising agents • Common Mechanism of Action: Block Na+ channels  reduce slope of phase 0 reduce ectopic pacemaker activity and suppress abnormal conduction • At higher doses can also reduce normal pacemaker activity and normal conduction • Oldest available antiarrhythmic drugs • Subdivided based on their actions on action potential duration: • 1A: prolong APD • 1B: shorten APD • 1C: no significant effect on APD
Class IA
Quinidine • Dextro-isomer of quinine obtained from cinchona bark • MOA: blocks sodium channels – ↓ automaticity , conduction velocity and prolongs repolarization – ↓phase 0 depolarization , ↑ APD • Uses: Atrial and ventricular arrhythmias • Adverse effects: – QT prolongation – GIT intolerance
• Procainamide: – Derivative of 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
Class IB drugs • Lignocaine, phenytoin, mexiletine • Block sodium channels also shorten repolarization
Lignocaine • Local anaesthetic • Raises threshold for action potential, ↓automaticity • Suppress electrical activity of normal tissues • High first pass metabolism if given parenterally • Use: ventricular arrhythmias • Adverse effects: – Drowsiness, hypotension, blurred vision, confusion and convulsions
• Phenytoin: – Antiepileptic also useful in ventricular arrhythmias (not preferred) • Mexiletine: – Can be used orally causes dose related neurological adverse events like tremors and blurred vision – Used as alternative to lignocaine in ventricular arrhythmias – Additional uses: chronic pain
Class I C drugs 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
Class II drugs • Antiarrhythmic action due to of β blockade • Depress myocardial contractility, automaticity and conduction velocity • Propranolol: – Treatment & prevention of supraventricular arrhythmias especially associated with exercise, hyperthyroidism • Esmolol: – IV short acting can be used to treat arrhythmias during surgery , following MI
Class III drugs ↑APD & ↑RP by blocking the K+ channels
Amiodarone • Iodine containing long acting drug • Blocks K+ channels (class 3)prolongs APD (action potential duration)conduction is slowed • Blocks Na+ channels (class 1)suppresses ectopic automaticity • Blocks beta receptors non-selectively (class 2) slightly depresses SAN pacemaker activity • Blocks Ca2+ channels (class 4) • Alters thyroid function • Especially on IV injection: it causes (a) myocardial depression (b) hypotension
Pharmacokinetics: • Variable absorption 35-65% • Slow onset 2 days to several weeks • Duration of action : weeks to months Adverse effects: – Cardiac: heart block , QT prolongation, bradycardia, cardiac failure, hypotension – Pulmonary fibrosis – Bluish discoloration of skin – GIT disturbances, hepatotoxicity
USES Supraventricular arrhythmias • Atrial fibrillation: rhythm control • PSVT, WPW tachyarrhythmias (not first line) Ventricular arrhythmias • Ventricular tachycardia, resistant VT • Recurrent ventricular fibrillation
DRONEDARONE • Structural analogue of amiodarone, without iodine • Antiarrhythmic profile similar to amiodarone • Half life: 24 hours • Less toxic, but also less efficacious than amiodarone • No thyroid and pulmonary toxicities • Contraindicated in the presence of HF • Useful in supraventricular arrhythmias: rhythm control in AF
SOTALOL • Non-selective beta blocker with prominent K+ channel blocking action ADRs • Cardiac depression, especially in patients with HF • Torsades de pointes (prolongation of APD in reverse use- dependent fashion): contraindicated in patients with long QTc interval Uses • Life-threatening ventricular tachyarrhythmias • Rhythm control in Atrial fibrillation
OTHER DRUGS: DOFETILIDE(oral), IBUTILIDE(IV) • Pure K+ channel blockers: prolongs APD • Reverse use-dependent blockade: risk of Torsades de pointes high • Contraindicated in patients with prolonged QTc • Use: Rhythm control in Atrial Fibrillation and Atrial Flutter
Calcium channel blockers (Class IV) • Inhibit the inward movement of calcium ↓ contractility, automicity , and AV conduction. • Verapamil & diltiazem
Verapamil • Uses: – DOC:PSVT – control ventricular rate in atrial flutter or fibrillation • Drug interactions: – Displaces digoxin from binding sites – ↓ renal clearance of digoxin
OTHER DRUGS: ADENOSINE • Ultra-short acting Purine Nucleoside • T ½: 10 seconds: always given Fast/ Rapid IV MoA • Acts on A1 Adenosine receptorsActivation of inward rectifier K+ currentmarked hyperpolarization (SAN, AVN, Atria) • Inhibition of Ca2+ currentsuppression of calcium dependent AP (AVN) Actions • SAN: Bradycardia; AVN: slowing of conduction; Atria: decrease excitability
ADRs • Bronchospasm in asthmatics, Dyspnoea, chest pain, fall in BP, flushing Uses • Drug of choice for PSVT (except in asthmatics: verapamil is preferred) • Diagnosis of tachycardias dependent on A-V node • To produce controlled hypotension during surgery
Other antiarrhythmics • Digoxin: – +ve inotropic drug with AVN blocking action – Used in atrial fibrillation associated with CHF • Atropine: Used in sinus bradycardia • Digitalis: Atrial fibrillation and atrial flutter • Magnesium SO4: digitalis induced arrhythmias
Bibliography 1. Tripathi KD. Essentials of Medical Pharmacology. 8th ed. New Delhi: Jaypee Brothers Medical Publishers; 2019 2. Padmaja Udaykumar. Medical Pharmacology. CBS Publishers & Distributors Pvt Limited, India; 2019
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