1 / 66

Antiarrhythmic Drugs

Antiarrhythmic Drugs. Learning outcomes:-. At the end of the lectures students should be able to: 1-Classify antiarrhythmic drugs 2-Identify the general characteristics of each class 3-To elaborate on clinical uses , adverse effects and drug –drug interactions of selected drugs.

nknaack
Download Presentation

Antiarrhythmic Drugs

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Antiarrhythmic Drugs

  2. Learning outcomes:- At the end of the lectures students should be able to: 1-Classify antiarrhythmic drugs 2-Identify the general characteristics of each class 3-To elaborate on clinical uses , adverse effects and drug –drug interactions of selected drugs

  3. 1- What is cardiac arrhythmia? 2-What causes cardiac arrhythmias? 3-Why do we treat cardiac arrhythmias? 4-When to treat? 5-What are the goals of therapy?

  4. CLASSIFICATION OF ANTIARRHYTHMIC DRUGS According to Vaughan-Williams

  5. Continue • Miscellaneous • Adenosine • Electrolyte supplement ( magnesium, potassium) • Digitalis • Atropine

  6. CLASS 1 • Bind & block the fast sodium channels that are responsible for rapid depolarization ( phase 0). • These drugs decrease the slope of phase 0, thus causing decrease in the amplitude of action potential.

  7. Continue This type of action potential is found in non-nodal cardiomyocytes ( atria, ventricles, purkinje tissues which are depending on sodium to start depolarization )

  8. CLASS 1 • At high concentration they have local anaesthetic • -Veinotropic effect ( cardiac depression )

  9. CLASS 1 SUBCLASSIFIED INTO : Class(1A) Slow phase 0 depolarization Decrease conduction velocity ( sodium channel blocking effect )

  10. Continue • Prolong action potential duration • Prolong Effective refractory period (ERP) { Potassium channel blocking effect Prolong QT interval in ECG

  11. Other actions of class 1A Anticholinergic effect : - Increase conduction through the A.V. node May lead to increase ventricular rate in atrial flutter. Can be prevented by administration of a drug that slow A.V. conduction such as : digoxin, β blocker calcium channel blockers. Negative inotropic effect

  12. Clinical uses of Class 1A Atrial flutter, Atrial fibrillation Supraventricular , ventricular tachyarrhythmias

  13. Examples of Class 1A : {1} Qunidine

  14. Actions of quinidine Cause α-adrenergic blocking effect cause vasodilatation and reflex sinus tachycardia This effect is seen more after I.V. I

  15. Adverse effects of quinidine GIT: anorexia, nausea, vomiting, diarrhea CARDIAC: quinidine syncope: (fainting attack) (due to torsadesdepointes developing at therapeutic plasma levels ) may terminate spontaneously or lead to fatal ventricular fibrillation

  16. Torsades de pointes

  17. Adverse effects ( continue) Anticholinergic adverse effects Cinchonism: ( tinnitus , headache & dizziness) Hypotension

  18. Adverse effects ( continue) • - At toxic concentrations, can precipitate arrhythmia and produce asystole ( cardiacarrest ) if serum concentrations exceed 5 µg/ml

  19. QUINIDINE Drug interactions: -  Increase serum concentration of digoxin: - Displacement from plasma proteins - Inhibition of digoxin renal clearance GIVEN ORALLY ....rarely given I.V. because of toxicity .

  20. {2} PROCAINAMIDE As compared to quinidine less toxic on the heart... can be given I.V. ( common route) more effective in ventricular than in atrial arrhythmias less depressant on cardiac contractility Weak anticholinergic or α-blocking actions

  21. PROCAINAMIDE Secondchoice ( after lidocaine ) in ventricular tachycardia after acute myocardial infarction

  22.  ADVERSE EFFECTS In long term therapy it cause reversible lupus erythematosus-like syndrome Hypotension Torsades de pointes Hallucination & psychosis

  23. CLASS 1 B • Shorten action potential duration and refractory period of ventricles lidocaine mexiletine

  24. LIDOCAINE USES : Drug of choice for treatment of ventricular tachycardia in emergency ..e.g. cardiac surgery , acute myocardial infarction - - NOT effective orally (3% bioavailability) - GIVEN I.V. bolus or slow infusion

  25. ADVERSE EFFECTS : hypotension neurological such as: paresthesia, tremor, dysarthria (slurred speech), convulsions T1/2 (2hrs)

  26. MEXILETINE - Given ORALLY USES : Chronic treatment of ventricular arrhythmia digitalis-induced arrhythmias chronic pain e.g. diabetic neuropathy and nerve injury ADVERSE EFFECTS : nausea , vomiting neurological hypotension t1/2 ( 10 hr)

  27. CLASS 1C • have no or little effect on action potential duration flecainide propafenone

  28. Clinical uses of class 1C Life –threatening supraventricular ( SVT) And ventricular tachyarrhythmias

  29. FLECAINIDE It is a proarrhythmic drug Can induce life-threatening ventricular arrhythmias -

  30. ADVERSE EFFECTS : CNS : dizziness, tremor, blurred vision, abnormal taste sensations, paraesthesia arrhythmias heart failure due to -veinotropic effect

  31. PROPAFENONE: - has weak beta-blocking action - cause metallic taste and constipation

  32. CLASS 11 DRUGS β- ADRENOCEPTOR BLOCKERS PHARMACOLOGICAL ACTIONS : blocking β1- receptors in the heart → reduce the sympathetic effect on the heart causing : - decrease automaticity of S.A. node and ectopic pacemakers - slow conduction of the A.V node

  33. CLINICAL USES : 1- atrial arrhythmias associated with emotion, exercise and thyrotoxicosis 2- digitalis-induced arrhythmias 3- Prophylactic or treatment of choice for post myocardial infarction arrhythmias ( Decrease the incidence of sudden death e.g. Propranolol

  34. Case

  35. Q1 1-What are the therapeutic effects of nonster . At this stage, would you initia .

  36. Q2 1-What are the therapeutic effects of nonster . At this stage, would you initia .

  37. Class III Potassium channels blocking drugs • Prolong the action potential duration & effective refractory period . (Prolong phase 3 )

  38. CLASS III AMIODARONE PHARMACOLOGICAL ACTIONS : Main effect is to prolong action potential duration and refractory period Additional actions of classes : 1, 2 & 4 vasodilating effects ( due to α- and β-adrenoceptor blocking effects and calcium channel blocking effects )

  39. Clinical uses of amiodarone Broad spectrum antiarrhythmic serious resistant ventricular arrhythmias maintenance of sinus rhythm after D.C. cardioversion of atrial flutter and fibrillation resistant supraventricular arrhythmias Re-entry arrhythmia

  40. ADVERSE EFFECTS 1-bradycardia & heart block, heart failure 2- pulmonary fibrosis 3- hyper- or hypothyroidism - 4- Skin deposits causes photodermatitis , patients should avoid exposure to the sun. may cause bluish discoloration of the skin

  41. (CONTiNUE) 5- tremor, headache, ataxia, paresthesia 6- constipation 7- corneal microdeposits 8- hepatocellular necrosis 9- peripheral neuropathy

More Related