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Here are the concise notes from Chapter 38 – Antiarrhythmic Drugs:
Chapter 38 — Antiarrhythmic Drugs
Definition: Drugs used to prevent or treat irregularities of cardiac rhythm.
Prevalence:
~3 out of 4 MI patients show some cardiac rhythm irregularity.
~half of patients given general anaesthesia show rhythm irregularity.
Arrhythmias are the most important cause of sudden cardiac death.
Only a few arrhythmias actually need antiarrhythmic drug treatment.
Underlying causes of arrhythmias: Abnormal automaticity, impaired conduction, or both. Triggered by ischaemia, electrolyte/pH imbalance, mechanical injury, heart failure, neurogenic and pharmacological influences (including antiarrhythmic drugs themselves).
Important Mechanisms of Cardiac Arrhythmias
A. Enhanced / Ectopic Pacemaker Activity
Phase-4 depolarization slope increases → automatic fibres fire abnormally.
Ischaemia partially depolarizes myocardial cells → injury current between these and normal fibres → initiates an impulse.
B. After-depolarizations (secondary depolarizations accompanying an AP)
EAD (Early After-Depolarization): Phase-3 repolarization is interrupted; membrane potential oscillates. If large enough, propagates extra impulses.
Associated with long Q-T interval, slow heart rate.
Caused by depression of delayed rectifier K⁺ current.
DAD (Delayed After-Depolarization): After reaching RMP, a secondary deflection occurs in phase 4; may reach threshold and fire a premature AP.
More common at fast heart rate.
Caused by Ca²⁺ overload (e.g., digitalis toxicity, ischaemia-reperfusion).
Arrhythmias from after-depolarizations = triggered arrhythmias.
C. Reentry
Impulse recirculates in the heart, causing repetitive activation without a new impulse → reentrant arrhythmias.
Circus movement reentry: Premature impulse blocked in one direction by refractory tissue → travels one-way around an obstacle (A-V node, abnormal tract) → finds the original site recovered → reexcites it, setting up a loop.
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