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Comprehensive Overview of Anti-Arrhythmics: Mechanisms, Classification, and Key Drugs

This article provides an in-depth examination of anti-arrhythmic drugs, focusing on their mechanisms of action, including automaticity, triggered activity, and re-entry arrhythmogenic mechanisms. It covers the classification of these drugs according to the Vaughan Williams system, detailing Class I, II, III, and IV agents. Key medications such as Quinidine, Lidocaine, Amiodarone, Verapamil, and Ivabradine are discussed, highlighting their effects on ion channels and the heart's electrical activity. This informative piece serves as a vital resource for understanding arrhythmias and their pharmacological management.

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Comprehensive Overview of Anti-Arrhythmics: Mechanisms, Classification, and Key Drugs

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  1. Anti arrhythmics!!!

  2. Automaticity • enhanced automaticity • abnormal automaticity • Triggered activity • Early afterdepolarisation (EAD) • Delayed afterdepolarisation (DAD) • Re-entry Arrhythmogenic mechanisms

  3. Classification of the Anti-arrhythmics Vaughan Williams EM. "Classification of antiarrhythmic drugs." 1970

  4. Delay depolarisation – fast Na+ channels 1 2 0 0 3 Transmembrane Potential mV -90 4 Quinidine - Class Ia

  5. 1 2 0 0 3 Transmembrane Potential mV -90 4 Blocks Na+ channels in actively depolarising cells/depolarised areas. Action potential is shortened. Lidocaine (Lignocaine) – Class Ib

  6. No change in action potential duration 1 2 0 0 3 Transmembrane Potential mV -90 4 Flecainide - Class Ic

  7. K+ channel blockers: Amiodarone, dronedarone Delay repolarisation – K+ channels 1 2 0 0 3 Transmembrane Potential mV -90 4 Amiodarone - Class III

  8. Ca2+ channels blockers: Verapamil, diltiazem Reduce amplitude and shorten Phase 2 – L-type Ca2+ channels 1 2 0 0 3 Transmembrane Potential mV -90 4 Verapamil - Class IV Reduce intracellular Ca2+ and thus negatively inotropic on myocytes

  9. Verapamil Effect on SA Node

  10. Summary

  11. Ivabradine • Selective If blocker – “funny channel” • Acts only on the SA node • Slows Na+ entry • Slower pacemaker potential Na+ K+ If Channel blockers Ivabradine

  12. Usually digoxin • Inhibits the Na+/K+ ATPase pump • Increased intracellular Na+ • Ca2+ exchanged for Na+ passively • Via Ca2+/Na+ exchangers that rely on Na+ concentration gradient • Thus cytoplasmic Ca2+ increased as less extruded • (Increases vagal drive – the heart slows down) K+ [Na+] low Cardiac Glycoside: Increased force of contraction and blocks AV node ATP→ADP [Na+] high Na+ Ca2+ Na+ Inhibited by concentration gradient Na+ increases as pump blocked

  13. Speeds up the heart rate • Acetylcholine receptors in the SA and AV nodes • Blocks the effects of acetylcholine (parasympathetic blockade) → blocks the “handbrake” so heart beats faster • Used for emergency treatment of bradycardia (slow heart rate) • Because of other Ach receptors in the body • S/E: dry mouth, urinary retention, dilated pupils Atropine

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