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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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