Cardiac arrhythmia is a condition in which the heart beats with an irregular or abnormal rhythm.

1. Anti-Arrhythmics
JYOTHSNA NAIDU RAVILLA
M.PHARM {PHARMACOLOGY}
19L81S0104
RIPER(AUTONOMOUS)

2. DEFINITION
▪ Cardiac Arrhythmia is a condition in which the heart beats with an
irregular or abnormal rhythm.
ABNORMAL RHYTHM
Can be of two extreme forms
BRADYCARDIA
Cardiac beats below 60 beats per
minute.
TACHYCARDIA
Cardiac beats above 100 beats per
minute.

3. Phases of Action Potential:

4. ETIOLOGY:
1)Coronary artery
disease.
2) Electrolyte imbalances
in your blood(such as
sodium and potassium.)
3) Changes in your heart
muscle.
4) Injury from a heart
attack.

5. 5) Healing process after heart
surgery.
6) Irregular heart rhythms can
also occur in normal healthy
hearts.
7) Ischemic Heart disease.
8) Drugs related.
9) others.

6. Mechanism of ARRHYTHMOGENESIS:
Abnormal impulse generation:
1. Altered normal automaticity
2. Abnormal automaticity
3. Delayed and early depolarizations.
Abnormal impulse conduction:
1. re- entry
2. Conduction block- I, II or III degree.

7. Mechanism of Arrhythmias.
1. After depolarizations:
Early after depolarizations occur before achieving full
repolarization (phase 3 of action potential).
▪ Hypoxia, hypokalaemia, acidosis
Delayed after depolarizations occur after full repolarization of the
membrane, i.e., a premature beat is initiated.
▪ Hypocalcaemia, hypokalaemia, due to digitalis or catecholamines.

8. Normal membrane potential vs membrane
potential of after depolarizations.

9. 2. Abnormal automaticity:
Ectopic foci
• Activation of beta adrenergic receptors, stretching of cardiac myocytes,
hypokalaemia.

10. 3. Reentry:
▪ Is caused due to conduction block ,
which leads to recirculating of the
impulse inside the heart
▪ For this re-entry there must be an
unidirectional block and slow
conduction in the region of
myocardium.
▪ 80-90% arrhythmias.
▪ ERP, Drugs converting unidirectional block
to bidirectional prevent re-entry.

11. TYPES OF ARRHYTHMIAS:
Tachyarrhythmias
• Due to abnormal automaticity, triggered
activity or reentry.
SUPRAVENTRICULAR:
• Originating in atria, SA node, AV node
• Extrasystoles, PSVT
• Atrial flutter (>200-350 beats/min)
• Atrial fibrillation(>300-550 beats/min)
VENTRICULAR:
• Vent. Tachycardia
• Vent. fibrillation
• Torsades de pointes
• Vent. Ectopics.
Bradyarrhythmias
• Due to failure of impulse generation in
the SA node or failure of impulse
conduction in AV node.
• Sinus bradycardia
• Bundle branch block.

12. Conduction system:

13. Delayed repolarizations:

14. Tachyarrhythmias
▪ Torsades de pointes (prolonged
QT interval)

15. PSVT

16. Atrial fibrillation Ventricular fibrillation

17. Bradyarrhythmias

18. Classification of Antiarrhythmics
▪ Vaughan Williams classified anti arrhythmics based on cardiac
cycle.
▪ CLASSIFICATION:
CLASS-I SODIUM CHANNEL BLOCKERS:
Prolong repolarization:1A
▪ Quinidine, procainamide, disopyramide, moricizine.
Shorten repolarization:1B
▪ Lignocaine, mexiletene, phenytoin
Little effect on repolarization:1C
▪ Encainide, flecainide, propafenone

19. CLASS-II β ADRENERGIC BLOCKERS:
▪ Propranolol, acebutolol, esmolol etc.
CLASS-III POTASSIUM CHANNEL BLOCKERS:
▪ Amiodarone, dronedarone, vernakalant, bretylium, sotalol,
dofetilide, ibutilide.
CLASS- IV CALCIUM CHANNEL BLOCKERS:
▪ Verapamil, diltiazem.

20. SODIUM CHANNEL BLOCKERS (CLASS IA DRUGS)
class 1a drugs
Block the Na channels
Prevent the inward movement of Na+ ions at resting, open and inactivated state.
Depression of phase 0 depolarization,
Prolonged ERP.
Slowing of conduction velocity
Suppression of abnormal automaticity.

21. QUINIDINE (CLASS 1A DRUG)
▪ Blocks sodium channels (membrane
stabilizing activity)
• Depresses automaticity
• Slows conduction
velocity
• Prolongs repolarization
and ERP
• Depresses excitability
• Reduces HR
• Depresses ectopic foci,

22. Pharmacokinetics, adverse effects and drug
interactions.
▪ PK: p.o. , 90 % bound to plasma proteins, metabolized in liver, excreted in urine.
▪ Adverse effects:
▪ CARDIAC- quinidine itself can cause arrhythmias, due to prolongation of QT
interval hence dose should be monitored.
NON CARDIAC- diarrhea, nausea, vomiting, hypersensitivity, hepatitis, higher
doses can cause cinchonism like quinine.
▪ Drug interactions:
Microsomal enzyme inhibitor.
Reduces clearance of digoxin
Potentiate the effects of SMRs
Myocardic depressant effects of β blockers, resulting in cardiac arrest.

23. ▪ Procainamide:
Acute treatment of supraventricular and ventricular arrhythmias.
It has following advantages over quinidine:
1. Better tolerated than quinidine
2. Not an α- blocker
3. It has weak vagolytic property (inhibit the action of vagus nerve
on the heart, GIT and other organs).

24. USES:
▪ Atrial fibrillation
▪ Atrial flutter
▪ Ventricular arrhythmias

25. CLASS 1B DRUGS:
▪ Decrease in Action Potential Duration (APD) and ERP of purkinje fibres(in
ventricles) which suppresses the re-entry.
▪ Block Na+ channels and also shorten repolarization.
ADMINISTRATION:
Lidocaine: iv
Mexiletine and phenytoin: oral
USES:
▪ Acute Ventricular tachycardia and fibrillation (esp. during ischemia)
SIDE EFFECTS:
CNS effects: Dizziness, drowsiness.

26. Class 1C drugs:
▪ Flecainide, propafenone, moricizine.
▪ Most potent Na+ channel blockers
USES:
Effective in supraventricular arrhythmias and maintain sinus rhythm
in atrial fibrillation.
SIDE EFFECTS:
Over usage causes cardiac arrest and sudden death hence not
commonly used.

27. CLASS II: β ADRENERGIC BLOCKERS
▪ Propranolol, acebutalol, esmolol.
ADMINISTRATION:
Propranolol- i.v, oral.
Esmolol- short acting (t half- 9mins) i.v.,
EFFECTS:
▪ myocardial contractility, automaticity,
conduction velocity.
▪ slope of phase 4 depolarization,
automaticity in SA node and
purkinje fibres.
▪ Depress AV conduction by prolonging ERP
of AV node.

28. USES:
▪ Prevention of supraventricular arrhythmias.
▪ Supress sinus tachycardia, atrial and nodal extrasysytoles and
digitalis induced arrhythmias.

29. CLASS III- Potassium channel blockers
▪ These are the drugs which prolong the action potential duration
and effective refractory period and delay the repolarization by
blocking the potassium channels.
▪ Amiodarone, sotalol, ibutilide, dofetilide.
ADMINISTRATION:
Amiodarone: oral or iv (T half-3 months)
Effects:
▪ Blocks the k+ channels and prolongs APD and ERP.
▪ blocks Na and Ca channels
▪ Blocks non selective β adrenergic receptors.

30. Uses:
Effective for most arrhythmias.
Side effects:
▪ Nausea, gastrointestinal disturbances and hepatitis.
▪ Pulmonary fibrosis.
▪ Photosensitization of skin
▪ Peripheral neuropathy
▪ Hypo and hyperthyroidism

31. ▪ SOTOLOL: p.o.
EFFECTS:
▪ prolongs APD, ERP.
▪ By beta blocking depresses SA and AV nodes.
SIDE EFFECTS:
▪ bradycardia, torsade's de pointes, ventricular fibrillation, fatigue, headache, nausea and vomiting.
USES:
▪ Ventricular and supra ventricular arrhythmias
▪ Maintenance of sinus rhythm in atrial fibrillation and atrial flutter.

32. ▪ IBUTILIDE: i.v. infusion
EFFECTS:
▪ prolongs repolarization
USES:
▪ Convert atrial flutter and fibrillation to sinus rhythm.
SIDE EFFECTS:
▪ Torsade's de pointes

33. DOFETILIDE: oral
EFFECTS:
▪ prolongs APD and refractory period.
USES:
▪ maintain sinus rhythm in atrial fibrillation.
SIDE EFFECTS:
▪ Torsade's de pointes.
 AZIMILIDE – A new class III drug that prolongs cardiac repolarization.
Studied for prevention of arrhythmias in post myocardial infarction
patients.

34. CLASS IV DRUGS- CALCIUM CHANNEL BLOCKERS
▪ Verapamil , Diltiazem
VERAPAMIL:
▪ Depresses AV conduction
▪ Decrease in phase 4 depolarization in SA node and purkinje fibres.
▪ Terminates PSVT
SIDE EFFECTS:
digoxin toxicity.

35. DILTIAZEM: Oral
▪ controls ventricular rate in atrial flutter and atrial fibrillation.
▪ used to terminate PSVT.
OTHER ANTIARRHYTHMIC AGENTS:
Adenosine: i.v bolus, slows AV conduction and suppresses
automaticity.
Digoxin: enhances vagal activity, increases refractory period, slows
AV conduction and slows HR.
Atropine: selective muscarinic antagonist, blocks vagal activity to
speed AV conduction and increase HR.
Magnesium: treatment for tachycardia.