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Anti arrythmics
Dr Urmila M Aswar

1
Anatomy of the conducting system

2
Introduction
• Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct
velocity and sequence of heart
activation are abnormal.

3
Phase 4: Resting/restoring with the Na+K+ pump; RMP is -90mV
Phase 0: Depolarization; Influx of Na+ through FAST Na+ channels
Phase 1: Early Rapid Repolarization: K+ efflux, Fast Na+ channels close
Phase 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

4
Pathogenesis and Inducement
of Arrhythmia
•
•

•

Pathological heart disease
Electrolyte disturbance and acid-base
imbalance
Physical and chemical factors or toxicosis

5
Mechanism of Arrhythmia
•
1.
2.
a.
b.

Abnormal impulse formation
Ectopic pulse
After depolarization's
Early after depolarization
Delayed after depolarization-triggered
arrythmia
• Abnormal impulse conduction
1. Reentry eg Afl, PSVT
2. Conduct block eg sick sinus
6
Impulse generation

7
Reentry block

8
Types: normal

9
Sinus bradycardia
• HR< 60 bpm; every QRS
narrow, preceded by p
wave

10
Sinus tachycardia
• HR > 100 bpm, regular
• Often difficult to
distinguish p and t
waves

11
Sick sinus syndrome
• All result in
bradycardia
• Sinus bradycardia
(rate of ~43 bpm) with
a sinus pause

12
PSVT
• Refers to
supraventricular
tachycardia
• Occur due to re-entry
• No P wave

13
Classes of antiarrythmic agents
• Classification of antiarrhythmic agents:
• Class I agents interfere/ blocks the sodium (Na+)
channel.
• Class II agents are anti-sympathetic nervous
system agents. Most agents in this class are beta
blockers.
• Class III agents affect potassium (K+) efflux/ K blockers.
• Class IV agents affect calcium channels/ Ca channel
blockers
• Class V agents work by other or unknown mechanisms.
14

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Arrythmias

  • 2. Anatomy of the conducting system 2
  • 3. Introduction • Definition of Arrhythmia: The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormal. 3
  • 4. Phase 4: Resting/restoring with the Na+K+ pump; RMP is -90mV Phase 0: Depolarization; Influx of Na+ through FAST Na+ channels Phase 1: Early Rapid Repolarization: K+ efflux, Fast Na+ channels close Phase 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 4
  • 5. Pathogenesis and Inducement of Arrhythmia • • • Pathological heart disease Electrolyte disturbance and acid-base imbalance Physical and chemical factors or toxicosis 5
  • 6. Mechanism of Arrhythmia • 1. 2. a. b. Abnormal impulse formation Ectopic pulse After depolarization's Early after depolarization Delayed after depolarization-triggered arrythmia • Abnormal impulse conduction 1. Reentry eg Afl, PSVT 2. Conduct block eg sick sinus 6
  • 10. Sinus bradycardia • HR< 60 bpm; every QRS narrow, preceded by p wave 10
  • 11. Sinus tachycardia • HR > 100 bpm, regular • Often difficult to distinguish p and t waves 11
  • 12. Sick sinus syndrome • All result in bradycardia • Sinus bradycardia (rate of ~43 bpm) with a sinus pause 12
  • 13. PSVT • Refers to supraventricular tachycardia • Occur due to re-entry • No P wave 13
  • 14. Classes of antiarrythmic agents • Classification of antiarrhythmic agents: • Class I agents interfere/ blocks the sodium (Na+) channel. • Class II agents are anti-sympathetic nervous system agents. Most agents in this class are beta blockers. • Class III agents affect potassium (K+) efflux/ K blockers. • Class IV agents affect calcium channels/ Ca channel blockers • Class V agents work by other or unknown mechanisms. 14