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ANTIMΕΤΩΠΙΣΗ ΑΡΡΥΘΜΙΩΝ
(αντιαρρυθμικά φάρμακα)
ΦΑΝΗ ΖΑΓΚΛΗ
Καρδιολόγος
Επεμβατική αντιμετώπιση
ταχυαρρυθμίες
βραδυαρρυθμίες
βηματοδότης
ταχυαρρυθμιες
Κατάλυση(ablation)
κυρίως σε υπερκοιλιακές
και ιδιοπαθείς κοιλιακές
ταχυκαρδίες
Εμφύτευση
απινιδωτή(icd) σε
κοιλιακή ταχυκαρδία
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
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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
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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
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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
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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 supraventricular tachycardia
It is used only by intravenous route
It has only low-profile toxicity being ultrashort acting of 15 seconds duration
ΥΠΕΡΚΟΙΛΙΑΚΗ ΤΑΧΥΚΑΡΔΙΑ
Digoxin – General Facts
(δακτυλίτιδα)
• Half-life: 36 ώρες
• Κυρίως νεφρική απέκκριση
• Σημαντικές αλληλεπιδράσεις με
φάρμακα
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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.