Antiarrhythmic drugs work by altering ion channels and fluxes, changing the shape of the cardiac action potential. This affects conduction velocity, refractory period, and automaticity. Drugs are classified based on their main ion channel targets: sodium channel blockers, beta blockers, potassium channel blockers, or calcium channel blockers. The goals of treatment are to restore normal sinus rhythm, control ventricular rate, and reduce symptoms, while minimizing risks of proarrhythmia or adverse effects. Treatment selection depends on the specific arrhythmia and acute versus chronic needs.

1. Antiarrhythmic
Drugs
Dr.U.P.Rathnakar
MD.DIH.PGDHM 1

2. AP of Pacemaker & Non-pace maker cells
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3. How do antiarrhythmics work?
• Tachyarrhythmias mediated by changes in
the cardiac action potential
• Drugs that alter the action potential alter
cardiac arrhythmias [By altering ionic
fluxes]
31

4. How do antiarrhythmics work?
Effect AP
• Change the shape of the cardiac AP.
Ca or Na
K
B Blocker
1. Conduction velocity [CV].
Ca or Na 2. Refractory period [RP]
3. Automaticity [AM]
• Antiarrhythmic drugs do this by altering the
channels that control the flow of ions across
the cardiac cell membrane. 32

5. Antiarrhythmics
Classification [Singh-Vaughn-Williams]
Sodium-channel- Pot.channel Calcium channel
blockers Beta-blockers blockers blockers
Conduction Velocity
•↓ •↓ •↓ •↓
Refractory Period
•↑ •↑ •↑ •↑
Automaticity
•↓ •↓ •↓ •↓
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6. Antiarrhythmics
Classification [Singh-Vaughn-Williams]
Sodium-channel- Beta-blockers Pot.channel Calcium channel
blockers blockers blockers
Procainamide • Propranolol • Amiodarone • Verapamil
Sotalol • Diltiazem
Miscellaneous
• Adenosine
• Magnesium
• Digitalis
• Atropine 37

7. Na+ Channel blockers
Class 1A Class 1B Class 1C
Eg.Lignocaine
.Eg. Procainamide Eg. Porpaafenone
Na+ Channel
.CV↓RP↑ ↓↓↓ Conduction-V.potent
No action at low HR
.Atria & Ventricles Oral
User dependent
.Oral & i.v. -ve inotropic
APD[RP] ↓
PK:Acetylation Uses: atrial &
Only ventricles Vent.arrhythmias
Uses:AF, Reentrant
tachy,VT i.v[bolus-infusion] ADEs: Visual disturbances
.ADEs: Use: Vent.arrhythmias GIT effects
Anticholinergic ADEs: CNS Reserve drug
SLE Proarrhythmic-rare
Proarrhythmic- Torse-De
Pointes
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8. Na+ Channel blockers
Class 1A Class 1B Class 1C
Procainamide Lignocaine Propafenone
Diisopyramide Mexiletine[O] [Also B-blocker]
Reserve drug
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9. Class II-Betablockers
Eg.atenolol,propranolol
• Mild, blunt arrhythmogenic effect
• SA Node-Phase 4 is blunted-reduces automaticity
• AV Node-slows conduction
• Protective-Prevents reentrant tachycardias
• Uses:
• Effective in arrhythmias where SA & AV nodes are involved
• AF & AFL-Reduces ventricular response
• Not effective in treating ventricular arrhythmias, but effectively
protects.
40

10. Class III-K+ channel blockers
Eg.Amiodarone
• K+ channel blocker[CL III], Na channel
blocker[CL I], betablockade[CL II], Ca channel
blockade[CL IV]
• Prolongs APD-ERP
• Large volume of dist.-slow action, loading dose
• Immediate antiarrhythmic effects are due to
non CL III effects
• Oral and i.v. administration
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11. Class III-K+ channel blockers
Eg.Amiodarone
• Uses:
• Broad spectrum antiarrhythmic
• Most effective in recurrent ventricular fibrillation
• AF, reentrant tachycardias-AV nodal, WPW
syndrome
• Others-Sotalol. Ibutilide, dobutilide
42

12. Class III-K+ channel blockers
Eg.Amiodarone
• ADEs: 15% to 50% of pts.
• Cumulative drug
• GIT-nausea, vomiting,esophageal reflux
• Reversible elevation of liver transaminases
• Pneumonitis, pulmonary fibrosis
• Iodine containing compound-prevents peripheral
conversion of T4 to T3
• Hypothyroidism or hyperthyroidism
• Cutaneous, neurological, ocular symptoms
• ADEs:Torsede-de-pointes[Not common] 43

13. 44

14. Class IV-Ca++ channel blockers
Verapamil & Diltiazem
• Low BA
• Inhibit Ca ++ dependent depolarization in SA &
AV node
• ↓Automaticity, ↓ conduction and RP
• Uses:
• Control Vent.response in atrial
tachyarrhythmias
• AV nodal and bypass reentrant arrhythmias
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15. Unclassified antiarrhythmics
• Digoxin-In AF to lower vent.response
• Adenosine-Short acting, depresses AV node,
used in reentrant tachyarrhythmi s
[Adenosine R→K Channels→Hyperpolarization
• Magnesium-Torsades-de-pointes, digitalis
toxicity
• Atropine-H.block
• Isoprenaline-H.block, Torsede de pointes
• Others-Azimilide, Dronedarone, tedisamil,46

16. Principles in clinical use of
antiarrhythmics
• Narrow margin of safety
• Proarrhythmics
• Non-pharmacological measures [pacing,
cardioversion]
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17. Principle-1
• Identify and remove precipitating factors
1. Electrolyte disturbances
2. Hypoxia
3. Ischemia
4. Digoxin
5. Other drugs used for non cardiac
conditions[Erythromycin, pentamidine,
antipsychotics]
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18. Principle-2
• Establish goals
1. Some should not be treated
Eg. Asymptomatic ventricular ectopics
2. Symptoms- Sensation of irregular beats,
Syncope, breathlessness, cardiac failure
3. Choosing therapeutic approaches-
• Restoring sinus rhythm-
• Reducing ventricular rate 49

19. Principle-3
• Minimize risks
1. Antiarrhythmics can cause arrhythmia
2. Monitor plasma concentraion
3. Pt.specific contra-indications Eg. Pulmonary
disease & Amiodarone
50

20. Principle-4
• Heart is a moving target!
1. Cardiac electrophysiology varies in a highly
dynamic fashion
Eg.autonomic tone, ischemia, cardiac stretch,
electrolyte variations
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21. Type of arrhythmia Acute Chronic
Adenosine, B-blockers, B-blockers, Ca channel
(PSVT)
Ca channel blockers blockers
AVN reentry
PSVT- AV reentry Same as above K or Na channel
blockers
1. Control ventricular 1. AV nodal block
Atrial fibrillation response: AV node 2. Maintain normal
block rhythm: K+ channel
Atrial flutter 2. Restore sinus block, Na+ channel block
rhythm: DC
cardioversion
Ventricular Lidocaine, Amiodarone ICD
Procainamide, DC Amiodarone, K+ channel
tachycardia cardioversion, Adenosine block, Na+ channel block
VF
Torsede de pointes Mg, Isoprenaline Beta blockers, pacing
A-V block Atropine, Isoprenaline 52