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 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
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)

arrhythmia management

  • 1.
  • 2.
    Agents classified according to •Modeof action •Site Anti arrhythmic drugs
  • 6.
    • Acts principallyby 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  Affectsslope 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 selectiveβ 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 oActs 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- arrhythmicdrugs  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 conductionand 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
  • 20.
    Therapeutic Procedures • Externaldefibrillation and cardio version • Catheter ablation • Temporary pacemakers • Permanent pacemakers • Implantable cardiac defibrillators(ICDs) • CRT (cardiac resynchronization therapy
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