MBBS antiarrhythmics 2012


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  • Sinus-atrial-junctional[nodal=SVT
  • Ca blockers are not given as cell is ischemic and these produce –veionotropic effect
  • CV-ALL, RP-All except Ligno, AM-All except K
  • Anticholinergic, -ve inotropic, Hypoglycemia-increases insulin levels
  • Paralyzes GE sphincter
  • Paralyzes GE sphincter
  • Paralyzes GE sphincter
  • ICD-implantable cardiac defifibrillator
  • MBBS antiarrhythmics 2012

    1. 1. Antiarrhythmic DrugsDr.U.P.Rathnakar MD.DIH.PGDHM 1
    2. 2. AP of Pacemaker & Non-pace maker cells 30
    3. 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. 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. 5. Antiarrhythmics Classification [Singh-Vaughn-Williams] Sodium-channel- Pot.channel Calcium channel blockers Beta-blockers blockers blockersConduction Velocity •↓ •↓ •↓ •↓ Refractory Period •↑ •↑ •↑ •↑ Automaticity •↓ •↓ •↓ •↓ 35
    6. 6. Antiarrhythmics Classification [Singh-Vaughn-Williams]Sodium-channel- Beta-blockers Pot.channel Calcium channelblockers blockers blockers Procainamide • Propranolol • Amiodarone • Verapamil Sotalol • Diltiazem Miscellaneous • Adenosine • Magnesium • Digitalis • Atropine 37
    7. 7. Na+ Channel blockersClass 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.arrhythmiasUses:AF, Reentranttachy,VT i.v[bolus-infusion] ADEs: Visual disturbances.ADEs: Use: Vent.arrhythmias GIT effectsAnticholinergic ADEs: CNS Reserve drugSLE Proarrhythmic-rareProarrhythmic- Torse-De Pointes 38
    8. 8. Na+ Channel blockersClass 1A Class 1B Class 1CProcainamide Lignocaine PropafenoneDiisopyramide Mexiletine[O] [Also B-blocker] Reserve drug 39
    9. 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. 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 41
    11. 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. 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. 13. 44
    14. 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 45
    15. 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. 16. Principles in clinical use of antiarrhythmics• Narrow margin of safety• Proarrhythmics• Non-pharmacological measures [pacing, cardioversion] 47
    17. 17. Principle-1 • Identify and remove precipitating factors1. Electrolyte disturbances2. Hypoxia3. Ischemia4. Digoxin5. Other drugs used for non cardiac conditions[Erythromycin, pentamidine, antipsychotics] 48
    18. 18. Principle-2 • Establish goals1. Some should not be treatedEg. Asymptomatic ventricular ectopics2. Symptoms- Sensation of irregular beats,Syncope, breathlessness, cardiac failure3. Choosing therapeutic approaches-• Restoring sinus rhythm-• Reducing ventricular rate 49
    19. 19. Principle-3 • Minimize risks1. Antiarrhythmics can cause arrhythmia2. Monitor plasma concentraion3. Pt.specific contra-indications Eg. Pulmonary disease & Amiodarone 50
    20. 20. Principle-4 • Heart is a moving target!1. Cardiac electrophysiology varies in a highly dynamic fashionEg.autonomic tone, ischemia, cardiac stretch,electrolyte variations 51
    21. 21. Type of arrhythmia Acute Chronic Adenosine, B-blockers, B-blockers, Ca channel(PSVT) Ca channel blockers blockers AVN reentryPSVT- AV reentry Same as above K or Na channel blockers 1. Control ventricular 1. AV nodal blockAtrial fibrillation response: AV node 2. Maintain normal block rhythm: K+ channelAtrial flutter 2. Restore sinus block, Na+ channel block rhythm: DC cardioversionVentricular Lidocaine, Amiodarone ICD Procainamide, DC Amiodarone, K+ channeltachycardia cardioversion, Adenosine block, Na+ channel blockVFTorsede de pointes Mg, Isoprenaline Beta blockers, pacingA-V block Atropine, Isoprenaline 52