CARDIAC ARRHYTHMIA

1. CARDIAC ARRHYTHMIA
Ashwini somayaji
1st M.pharm
pharmacology

2. DEFINITION:
• Cardiac arrhythmia/cardiac dysrhythmia/irregular
heart beat is a group of condition in which the heart
beat is irregular,too fast or too slow.
• BRADYCARDIA:heart beat that is too slow i.e <60
beats /min
• TACHYCARDIA:heart beat that is too fast i.e >100
beats/min.

4. • Ischaemia
• Mechanial injury
• Streching
• Electrolyte and pH imbalance
• Neurogenic and drug influences
CAUSES:

5. SYMPTOMS:
Many arrhythmias have no symptoms.when
symptoms are present they include:
Palpitation(unpleasant awareness of cardiac
activity)
Sincope
Unstable haemodynamic condition.
Abnormal pulse.
Precipitation of cardiac failure.
Shortness of breath or chest pain.

6. CONTENTS:
a) Normal cardiac rhythm
b) Mechanism of arrhythmia
c) Types and ECG
d) Treatment/drugs

7. Normal cardiac rhythm:
For normal cardiac rhythm:
I. Heart rate should be 80-100
II. Impulse should originate from SA node
III. Cardiac impulse should propagate
through normal conduction pathway
IV. Normal velocity

8. CARDIAC ACTION POTENTIAL:
FAST CHANNEL AP
SLOW CHANNEL AP

10. CARDIAC CONDUCTION AND ECG:

12. MECHANISM OF CARDIAC
ARRHYTHMIA:
1) Enhanced/ectopic pacemaker activity
2) After depolarisation
i. Early after-depolarisation
ii. Delayed after depolarisation
3) Reentry
i. Circus movement type
ii. Microentry circuit
4) Increased/decreased automaticity

14. ENHANCED/ECTOPIC PACEMAKER
ACTIVITY
• An ectopic pacemaker or ectopic foci is an
excitable groups of cells that causes the
premature heart beat outside the normally
functioning SA node of human heart....

16. These are secondary depolarisation
accompanying a normal or premature action
potential.
EARLY AFTER DEPOLARISATION:
repolarisation during phase 3 is interrupted
and membrane potential oscillates.
If the amplitude of oscillation is sufficiently
large, neighbouring tissue is activated and
series of impulses are propogated
AFTER DEPOLARISATION:

17. CONTINUE........
• EAD are frequently associated with long QT
interval.
• They result from depression of delayed
rectifier K+ ion.
DELAYED AFTER-DEPOLARISATION:
• After attaining RMP a secondary deflection
occurs which may reach threshold potential
and initiate a single premature AP.
• Result from a Ca+ overload.

18. CONTINUE...
• Becaues an AP is needed to trigger after
depolarisation,arrhythmia based on these
have been called triggered arrhythmias.

19. REENTRY:
• Due primarily to abnormality of conduction,
an impulse may recirculate in the heart and
cause repetitive activation without need for
any new impulse to be generated.
i. Circus movement type
ii. Microentry circuit

20. CIRCUS MOVEMENT TYPE:

21. MICRO ENTRY CIRCUIT:

22. INCREASED OR DECREASED
AUTOMATICITY:

23. CLASSIFICATION:
NORMOTROPIC
• Sinus tachycardia
• Sinus bradychardia
• Sinus arrhythmia
ECTOPIC
• Heart block
• Extrasystole
• Paroxysmal tachycardia
• others

24. TREATMENT:

25. CLASS 1:Na+ CHANNEL BLOCKERS
FURTHER CLASSIFIED INTO:
• Class 1a-
Eg:quinidine,procainamide,disopyramide
• Class 1b-Eg:lidocaine
• Class1c-Eg:propafenone

29. CLASS 2:β BLOCKERS

30. CLASS 3:K+ channel blockers

31. CLASS 4:calcium channel blockers

33. REFERENCES:
• The pharmacological basis of therapeutics
by goodman and gilman’s
• Essentials of medical pharmacology by KD
Tripathi.
• Clinical pharmacy and therapeutics by
walker whittlesea.