Management of Arrhythmias

Abhishek reddy

KMC Manipal

Agents classified according to•Mode of action•Site

Anti arrhythmic drugs

• 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

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.

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

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

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.

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

Class 3 drugs

o Acts by prolonging plateau phase of AP.o Hence lengthens refractory periodo Effective- atrial & ventricular tachyarrhythmiao Causes QT prolongation and predisposes to

torsade de pointes and VTo E.g. Amiodaroneo Principal drug o Also has class 1, 2, 4 activityo Most effective drug- paroxysmal AFo Uses: to prevent recurrent episodes of VTo Side effects: photosensitivity, skin discoloration,

thyroid dysfunction, nausea, vomiting etc

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

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.

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

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

Therapeutic Procedures

• External defibrillation and cardio version

• Catheter ablation • Temporary pacemakers• Permanent pacemakers• Implantable cardiac

defibrillators(ICDs)• CRT (cardiac resynchronization

therapy

External defibrillation

cardio version

Catheter ablation

Flouroscopic image showing catheter

pacemakerImplantable cardiac defibrillators(ICDs)

pacemaker ICDs

CRT (cardiac resynchronization therapy)