Arrythmias

Anti arrythmics

Dr Urmila M Aswar

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Anatomy of the conducting system

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Introduction

• Definition of Arrhythmia:

The Origin, Rate, Rhythm, Conductvelocity and sequence of heartactivation are abnormal.

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Phase 4: Resting/restoring with the Na+K+ pump; RMP is -90mVPhase 0: Depolarization; Influx of Na+ through FAST Na+ channelsPhase 1: Early Rapid Repolarization: K+ efflux, Fast Na+ channels closePhase 2: Slow Repolarization (plateau phase): K+ efflux, influx of Ca++ and Na+ (SLOW Na+ channels)Phase 3: Final Rapid Repolarization: K+ efflux, Ca++ and SLOW Na+ channels close

Pathogenesis and Inducement of Arrhythmia

• Pathological heart disease

• Electrolyte disturbance and acid-base imbalance

• Physical and chemical factors or toxicosis

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Mechanism of Arrhythmia

• Abnormal impulse formation1. Ectopic pulse2. After depolarization'sa. Early after depolarizationb. Delayed after depolarization-triggered

arrythmia

• Abnormal impulse conduction1. Reentry eg Afl, PSVT2. Conduct block eg sick sinus

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Impulse generation

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Reentry block

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Types: normal

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Sinus bradycardia

• HR< 60 bpm; every QRS narrow, preceded by p wave

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Sinus tachycardia

• HR > 100 bpm, regular

• Often difficult to distinguish p and t waves

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Sick sinus syndrome

• All result in

bradycardia

• Sinus bradycardia

(rate of ~43 bpm) with

a sinus pause

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PSVT

• Refers to supraventriculartachycardia

• Occur due to re-entry

• No P wave

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Classes of antiarrythmic agents

• Classification of antiarrhythmic agents:

• Class I agents interfere/ blocks the sodium (Na+)channel.

• Class II agents are anti-sympathetic nervoussystem agents. Most agents in this class are betablockers.

• Class III agents affect potassium (K+) efflux/ K blockers.

• Class IV agents affect calcium channels/ Ca channelblockers

• Class V agents work by other or unknown mechanisms.

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