12 Classification of antiarrhythmics (based on mechanisms of action) Class I – blocker’s of fast Na+ channelsSubclass IACause moderate Phase 0 depressionProlong repolarizationIncreased duration of action potentialIncludesQuinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory periodProcainamide - increases refractory period but side effectsDisopyramide – extended duration of action, used only for treating ventricular arrthymias
16 Classification of antiarrhythmics (based on mechanisms of action) Subclass IBWeak Phase 0 depressionShortened depolarizationDecreased action potential durationIncludesLidocaine (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmiasMexiletine - oral lidocaine derivative, similar activityPhenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocaine
18 Classification of antiarrhythmics (based on mechanisms of action) Subclass ICStrong Phase 0 depressionNo effect of depolarizationNo effect on action potential durationIncludesFlecainide (initially developed as a local anesthetic)Slows conduction in all parts of heart,Also inhibits abnormal automaticityPropafenoneAlso slows conductionWeak β – blockerAlso some Ca2+ channel blockade
24 Classification of antiarrhythmics (based on mechanisms of action) Class II – β–adrenergic blockersBased on two major actions1) blockade of myocardial β–adrenergic receptors2) Direct membrane-stabilizing effects related to Na+ channel blockadeIncludesPropranololcauses both myocardial β–adrenergic blockade and membrane-stabilizing effectsSlows SA node and ectopic pacemakingCan block arrhythmias induced by exercise or apprehensionOther β–adrenergic blockers have similar therapeutic effectMetoprololNadololAtenololAcebutololPindololSotalolTimololEsmolol(i.v. Χορήγηση, χρόνος ημίσιας ζωής 9 min)
26 Classification of antiarrhythmics (based on mechanisms of action) Class III – K+ channel blockersDeveloped because some patients negatively sensitive to Na channel blockers (they died!)Cause delay in repolarization and prolonged refractory periodIncludesAmiodarone – prolongs action potential by delaying K+ efflux but many other effects characteristic of other classesIbutilide – 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 infarctionDofetilide - prolongs action potential by delaying K+ efflux with no other effects
32 Classification of antiarrhythmics (based on mechanisms of action) Class IV – Ca2+ channel blockersslow rate of AV-conduction in patients with atrial fibrillationIncludesVerapamil – blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardiaDiltiazem
35 Miscellaneous Antiarrhythmic Drugs AdenosineAdenosine activates A1-purinergic receptors decreasing the SA nodal firing and automaticity, reducing conduction velocity, prolonging effective refractory period, and depressing AV nodal conductivityIt is the drug of choice in treatment of supra-ventricular tachycardiaIt is used only by intravenous routeIt has only low-profile toxicity being ultra-short acting of 15 seconds duration
37 Digoxin – General Facts (δακτυλίτιδα) Half-life: 36 ώρεςΚυρίως νεφρική απέκκρισηΣημαντικές αλληλεπιδράσεις με φάρμακαVerapamilQuinidineAmiodaronePropafenone<Αντίδοτο> Digibind & DigifabDigibind/fab use impacts digoxin levels
38 Digoxin Επιβραδύνει την καρδιακή συχνότητα και την αγωγή στον Κκ κόμβο Aναστολή Να/Κ ATPασηςΠαρασυμπαθητικομιμητική δράσηΕνδείκνυται στην κολπική μαρμαρυγή(Rapid Atrial Fibrillation )Φόρτιση(δακτυλιδισμός)First Dose: 0.5 mg IVSecond and Third Dose: 0.25 mg IV q6h for 2 dosesΔιατήρησηDose: to mg IV or PO qdΘεραπευτικά επίπεδα
42 VERNAKALANTIntravenous 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-dependentNa+ channels.
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