ANTIMΕΤΩΠΙΣΗ ΑΡΡΥΘΜΙΩΝ (αντιαρρυθμικά φάρμακα) ΦΑΝΗ ΖΑΓΚΛΗ Καρδιολόγος

Επεμβατική αντιμετώπιση βραδυαρρυθμίες ταχυαρρυθμίες βηματοδότης

Εμφύτευση απινιδωτή(icd) σε κοιλιακή ταχυκαρδία ταχυαρρυθμιες Κατάλυση(ablation) κυρίως σε υπερκοιλιακές και ιδιοπαθείς κοιλιακές ταχυκαρδίες Εμφύτευση απινιδωτή(icd) σε κοιλιακή ταχυκαρδία

ΑΝΤΙΑΡΡΥΘΜΙΚΑ ΦΑΡΜΑΚΑ ΦΑΡΜΑΚΕΥΤΙΚΗ ΑΝΤΙΜΕΤΩΠΙΣΗ ΑΝΤΙΑΡΡΥΘΜΙΚΑ ΦΑΡΜΑΚΑ

Αντιαρρυθμικά φάρμακα(κατά Vaughan Williams)

Classification of antiarrhythmics (based on mechanisms of action) Class I – blocker’s of fast Na+ channels Subclass IA Cause moderate Phase 0 depression Prolong repolarization Increased duration of action potential Includes Quinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory period Procainamide - increases refractory period but side effects Disopyramide – extended duration of action, used only for treating ventricular arrthymias

Classification of antiarrhythmics (based on mechanisms of action) Subclass IB Weak Phase 0 depression Shortened depolarization Decreased action potential duration Includes Lidocaine (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmias Mexiletine - oral lidocaine derivative, similar activity Phenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocaine

Classification of antiarrhythmics (based on mechanisms of action) Subclass IC Strong Phase 0 depression No effect of depolarization No effect on action potential duration Includes Flecainide (initially developed as a local anesthetic) Slows conduction in all parts of heart, Also inhibits abnormal automaticity Propafenone Also slows conduction Weak β – blocker Also some Ca2+ channel blockade

Κολπική μαρμαρυγή (ταχεία κοιλιακή ανταπόκριση)

Classification of antiarrhythmics (based on mechanisms of action) Class II – β–adrenergic blockers Based on two major actions 1) blockade of myocardial β–adrenergic receptors 2) Direct membrane-stabilizing effects related to Na+ channel blockade Includes Propranolol causes both myocardial β–adrenergic blockade and membrane-stabilizing effects Slows SA node and ectopic pacemaking Can block arrhythmias induced by exercise or apprehension Other β–adrenergic blockers have similar therapeutic effect Metoprolol Nadolol Atenolol Acebutolol Pindolol Sotalol Timolol Esmolol(i.v. Χορήγηση, χρόνος ημίσιας ζωής 9 min)

Classification of antiarrhythmics (based on mechanisms of action) Class III – K+ channel blockers Developed because some patients negatively sensitive to Na channel blockers (they died!) Cause delay in repolarization and prolonged refractory period Includes Amiodarone – prolongs action potential by delaying K+ efflux but many other effects characteristic of other classes Ibutilide – slows inward movement of Na+ in addition to delaying K + influx. Bretylium – first developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial infarction Dofetilide - prolongs action potential by delaying K+ efflux with no other effects

ΚΟΙΛΙΑΚΗ ΤΑΧΥΚΑΡΔΙΑ

YΠΕΡ-ΥΠΟ/ΘΥΡΕΟΕΙΔΙΣΜΟΣ

Classification of antiarrhythmics (based on mechanisms of action) Class IV – Ca2+ channel blockers slow rate of AV-conduction in patients with atrial fibrillation Includes Verapamil – blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardia Diltiazem

Miscellaneous Antiarrhythmic Drugs Adenosine Adenosine activates A1-purinergic receptors decreasing the SA nodal firing and automaticity, reducing conduction velocity, prolonging effective refractory period, and depressing AV nodal conductivity It is the drug of choice in treatment of supra-ventricular tachycardia It is used only by intravenous route It has only low-profile toxicity being ultra-short acting of 15 seconds duration

ΥΠΕΡΚΟΙΛΙΑΚΗ ΤΑΧΥΚΑΡΔΙΑ

Digoxin – General Facts (δακτυλίτιδα) Half-life: 36 ώρες Κυρίως νεφρική απέκκριση Σημαντικές αλληλεπιδράσεις με φάρμακα Verapamil Quinidine Amiodarone Propafenone <Αντίδοτο> Digibind & Digifab Digibind/fab use impacts digoxin levels

Digoxin Επιβραδύνει την καρδιακή συχνότητα και την αγωγή στον Κκ κόμβο Aναστολή Να/Κ ATPασης Παρασυμπαθητικομιμητική δράση Ενδείκνυται στην κολπική μαρμαρυγή (Rapid Atrial Fibrillation ) Φόρτιση(δακτυλιδισμός) First Dose: 0.5 mg IV Second and Third Dose: 0.25 mg IV q6h for 2 doses Διατήρηση Dose: 0.125 to 0.375 mg IV or PO qd Θεραπευτικά επίπεδα

Digoxin(παρενέργειες) Adverse Effects Γαστρεντερικές Αρρυθμίες-ecg changes (ST depression, T wave inversion) Κεντρικό νευρικό σύστημα Διαταραχές όρασης ΤΟΞΙΚΟΣ ΔΑΚΤΥΛΙΔΙΣΜΟΣ(δηλητηρίαση) Μέτρηση επιπέδων δακτυλίτιδας(1-2ng/ml θεραπευτικά)

ΔΑΚΤΥΛΙΤΙΔΑ

VERNAKALANT Intravenous vernakalant is a relatively atrial-selective antiarrhythmic agent that has shown to be efficacious in converting recent onset AF but not atrial flutter . Vernakalant is the first in a class of new pharmacologic agents developed for the acute conversion of AF and works predominantly by blocking early-activating K+ channels and frequency-dependent Na+ channels.