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Antiarrhythmic Drugs 2.ppt
- 1. Class 1(A) Quinidine: Cinchonaplant Block open & inactivated sodium channel Block potassium channel -ve inotropic effect Antimuscarinic effect duration of action potential & refractory periods of atrium & ventricles. Hypotensive
- 3. ECG changes ProlongQ-T interval Widening QRS complex
- 4. Phrmacokinetics Well absorbedorally Highly bound to plasma proteins Metabolized in liver ( active metabolite) 20% excreted unchanged in urine Usually given as slow release formulation I.M. painful, I.V(marked hypotension)
- 5. Clinical uses Atrial flutter& fibrillation it returns the rhythm back to normal sinus rhythm. Used in treatment of ventricular arrhythmia.
- 6. Adverse effects 1- Cardiaceffects A) Due to antimuscarinic effect ,in A.F.or A.F. may precipitate ventricular tachycardia B) Syncope C)Torsade de pointes D) Cardiac stand still (asystole) in patients with sick sinus syndrome .
- 7. Extracardiac adverse effects Hypotension Cinchonism (headache, dizziness,tinnitus,deafness ) Hypersensitivity reactions (hepatitis,thrombocytopenia) GIT, diarrhea,nausea,vomiting
- 8. Drug interactions Quinidineincreases the plasma level of digoxin by : a) displacement from tissue binding sites b) decreasing digoxin renal clearance
- 9. Procainamide As quinidine but: Less hypotensive Less antimuscarinic Less cardiotoxic Can be given safely by I.M. or I.V. Metabolized in liver and give active metabolite which has a class 111 activity .
- 10. Continue Eliminated throughkidney . More effective in ventricular arrhythmias , it is the second drug of choice after lidocaine in treament of ventricular arrhythmia follow acute M.I. Effective in A.F. or A.F. due to Wolff Parkinson White syndrome
- 11. Adverse effects Systemic lupuserythematosus like syndrome. GIT : Nausea , diarrhea Torsade de pointes Hypotension
- 12. Class 1(B) Lidocaine Shorten the duration of A.P.& R.P. Effective in ventricular arrhythmias.
- 13. Pharmacokinetics Well absorbedafter oral administration . Only 3% reach general circulation. Given only by I.V. route Excreted via kidney . Half-life 2hrs.
- 14. Therapeutic uses First drugof choice in treatment of ventricular arrhythmias due to Acute myocardial infarction Digitalis toxicity Anaesthesia Open heart surgery
- 15. Adverse effects Neurological effects: (contraindicated in epileptic patients ). Arrhythmias uncommon Hypotension
- 16. Mexiletine Effective orally Half-life (8-20hrs ). Used in chronic treatment of ventricular arrhythmias. Effective in relieving chronic pain due to diabetic neuropathy& nerve injury.
- 17. Adverse effects Neurologicside effects
- 19. Amiodarone A) cardiaceffects Sodium channel blocking Potassium channel blocking Calcium channel blocking β- adrenoceptor blocking
- 20. Continue B) Extracardiaceffect Peripheral vasodilation
- 21. Pharmacokinetics Given orally Slow onset of action Long half-life(13-103 hrs ). Cumulative drug Is highly lipophilic , is concentrated in many tissues. Eliminated by liver mostly as active metabolites.
- 22. Clinical uses Recurrent& refractory ventricular & supraventricular arrhythmias . Arrhythmias associated with Wolff Parkinson syndrome. In maintaining sinus rhythm in patients with AF.
- 23. Adverse effects Gray-blue skin discoloration & photodermatitis . Corneal microdeposits corneal opacity ,optic neuritis, blindness pulmonary fibrosis
- 24. Continue hypo orhyperthyroidism Nausea & constipation Hepatic impairment neurological effects A-V block & bradycardia Hypotension
- 25. Drug interactions Oralanticoagulant bleeding Digoxindigoxin toxicity β- blockers additive effect