MBBS antiarrhythmics 2012
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Transcript of MBBS antiarrhythmics 2012
Dr.U.P.RathnakarMD.DIH.PGDHM 1
Antiarrhythmic
Drugs
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AP of Pacemaker & Non-pace maker cells
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]
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How do antiarrhythmics work?Effect AP
• Change the shape of the cardiac AP.
1. Conduction velocity [CV].
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.
Ca or Na
K
B Blocker
Ca or Na
AntiarrhythmicsClassification [Singh-Vaughn-Williams]
Sodium-channel-blockers
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Beta-blockersPot.channel blockers
•↓ •↑•↓
Calcium channel blockers
•↓• ↑• ↓
•↓•↑•↓
•↓ •↑•↓
Conduction Velocity
Refractory Period
Automaticity
AntiarrhythmicsClassification [Singh-Vaughn-Williams]
Sodium-channel-blockers
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Beta-blockers
• Propranolol
Pot.channel blockers
• Amiodarone
Calcium channel blockers
• Verapamil• Diltiazem
Miscellaneous• Adenosine• Magnesium • Digitalis • Atropine
Procainamide
Sotalol
Na+ Channel blockers Class 1A.Eg. Procainamide
.CV↓RP↑
.Atria & Ventricles
.Oral & i.v.
PK:Acetylation
Uses:AF, Reentrant tachy,VT
.ADEs:
Anticholinergic
SLE
Proarrhythmic- Torse-De
Pointes
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Class 1BEg.LignocaineNa+ ChannelNo action at low HRUser dependentAPD[RP] ↓Only ventriclesi.v[bolus-infusion]Use: Vent.arrhythmiasADEs: CNSProarrhythmic-rare
Class 1CEg. Porpaafenone
↓↓↓ Conduction-V.potent
Oral
-ve inotropic
Uses: atrial & Vent.arrhythmias
ADEs: Visual disturbances
GIT effects
Reserve drug
Na+ Channel blockers Class 1A
Procainamide
Diisopyramide
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Class 1B
Lignocaine
Mexiletine[O]
Class 1C
Propafenone
[Also B-blocker]
Reserve drug
Class II-BetablockersEg.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.
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Class III-K+ channel blockersEg.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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Class III-K+ channel blockersEg.Amiodarone
• Uses:• Broad spectrum antiarrhythmic• Most effective in recurrent ventricular fibrillation• AF, reentrant tachycardias-AV nodal, WPW
syndrome• Others-Sotalol. Ibutilide, dobutilide
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Class III-K+ channel blockersEg.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
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Class IV-Ca++ channel blockersVerapamil & 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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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,
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Principles in clinical use of antiarrhythmics
• Narrow margin of safety• Proarrhythmics• Non-pharmacological measures [pacing,
cardioversion]
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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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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
Principle-3
• Minimize risks
1. Antiarrhythmics can cause arrhythmia
2. Monitor plasma concentraion
3. Pt.specific contra-indications Eg. Pulmonary disease & Amiodarone
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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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Type of arrhythmia Acute Chronic(PSVT)
AVN reentryAdenosine, B-blockers, Ca channel blockers
B-blockers, Ca channel blockers
PSVT- AV reentry Same as above K or Na channel blockers
Atrial fibrillationAtrial flutter
1. Control ventricular response: AV node block2. Restore sinus rhythm: DC cardioversion
1. AV nodal block2. Maintain normal rhythm: K+ channel block, Na+ channel block
Ventricular tachycardiaVF
Lidocaine, AmiodaroneProcainamide, DC cardioversion, Adenosine
ICDAmiodarone, K+ channel block, Na+ channel block
Torsede de pointes Mg, Isoprenaline Beta blockers, pacing
A-V block Atropine, Isoprenaline