This document discusses the classification and mechanisms of action of various anti-arrhythmic drugs. It describes five classes of anti-arrhythmic drugs based on their effects on cardiac ion channels and muscle fibers. Class I drugs block sodium channels, Class II drugs are beta blockers, Class III drugs prolong the cardiac action potential, and Class IV drugs block calcium channels. The uses, examples and side effects of each drug class are provided. Other therapeutic procedures for treating arrhythmias including defibrillation, cardioversion, catheter ablation, and pacemakers are also briefly mentioned.
6. • Acts principally by suppressing excitability
and slowing down conduction in atrial or
ventricular muscle.
• Blocks Na+ channels
• Contraindicated in patients w/ heart failure as
they depress myocardial function.
Class 1 drugs
7. Class 1a drugs:
• Prolongs cardiac action potential
• ↑ tissue refractory period
• Uses: atrial and ventricular arrhythmias
• E.g. Disopyramide:
• Causes anticholinergic side effects- urinary
retention, ppts glaucoma.
• Depresses myocardial function n hence
avoided in cardiac failure
• E.g. Quinidine:
• Rarely used as it increases mortality n causes
GI upset.
8. Class 1b drugs:
They shorten the AP and tissue
refractory period
Acts on ventricles so used in Ventricular
tachycardia and ventricular fibrillation.
E.g. Lidocaine, Mexiletine
9. Class 1c
Affects slope of AP w/o altering duration or
refractory period.
Uses: prophylaxis of AF, SVA, VA.
Contraindicated in patients w/ previous MI-
leads to pro- arrhythmias
E.g. Flecainide
Effective- AF
Given w/ AV node blocking drugs- β
blockers to prevent pro-arrhythmias
E.g. Propafenone
10. Class 2 drugs
Group comprises of β blockers
These drugs diminish Phase 4
depolarization, thus depresheart rate and
contractility. sing automaticity, prolonging
AV conduction, and decreasing
These reduce the rate of SA node
depolarization and causes a relative block
in AV node.
Uses: Rate control in Atrial Flutter, AF, SVA,
VT
Reduces myocardial excitability and risk of
arrhythmic death in patients w/ CHD &
heart failure.
11. Cardio selective β blockers:
Acts on myocardial β1 receptors
E.g. Atenolol, Bisoprolol, Metoprolol
Non selective β blockers:
Acts on β1 & β2 receptors
Β2 blockade- bronchospasm and peripheral
vasoconstriction
E.g. Propranolol, Nadolol, Carvedilol
Sotalol:
Causes torsade de pointes
12. Class 3 drugs
o Acts by prolonging plateau phase of AP.
o Hence lengthens refractory period
o Effective- atrial & ventricular tachyarrhythmia
o Causes QT prolongation and predisposes to torsade
de pointes and VT
o E.g. Amiodarone
o Principal drug
o Also has class 1, 2, 4 activity
o Most effective drug- paroxysmal AF
o Uses: to prevent recurrent episodes of VT
o Side effects: photosensitivity, skin discoloration,
thyroid dysfunction, nausea, vomiting etc
13. Class 4 drugs
Blocks the slow calcium channels(
important for impulse generation and
conduction in atrial and nodal tissues
Acts at the AV node
E.g. Verapamil, Diltiazem
14. Other anti- arrhythmic drugs
Atropine Sulphate (0.6 mg i.v., repeated
if necessary- maximum of 3 mgs)
↑ sinus rate and SA, AV conduction
Best choice- severe bradycardia or
hypotension due to vagal over activity.
Side effects: dry mouth, thirst, blurred
vision, atrial and ventricular extra
systoles.
15. Adenosine:
Given i.v. bolus, initially 3mg over 2 sec. If
no response after 1-2 mins, 6mg should be
given; and if needed after 1-2 mins, max
dose 12mg may be given.
Uses: terminate SVT when AV node is part
of re-entry circuit or in Atrial Flutter with 2:1
AV block or broad complex tachycardia.
Side effects: flushing, dyspnea, chest pain
Contraindications: Asthma
16. Digoxin
Slows conduction and prolongs
refractory period in AV node.
Controls ventricular rate in AF & SVT of
AV node.
Shortens refractory period and
enhances conduction and excitability in
other parts of the heart.
Side effects: GI disturbances,
xanthopsia, arrhythmias