Antiarrhythmics II Flashcards
limitations of Vaughan Williams Classification system
primarily based on effects of drugs on electrophysiological characteristics of isolated, normal cardiac tissue. The classification is incomplete. Considers primary blocking effect only
class IA antiarrhythmic drugs mechanism
fast (open) Na channel block. prolongs effective refractory period, prolongs action potential duration
Quinidine, procainamide, disopyramide uses
secondary drug of choice for treatment of chronic Afib, PSVTs, sustained VT/VF (procainamide), acute atrial flutter/fibrillation (IV procainamide)
Class 1A toxicities
QT prolongation, TdP arrhythmias, heart block, hypotension, lupus-like syndrome. GI symptoms.
quinidine adverse effects
alpha adrenergic blockade -> hypotension, reflex tachycardia. M2 blockade, vagal inhibition. cinchonism, hepatitis, diarrhea, thrombocytopenia. CYP2D6 inhibition. drug interactions
procainamide adverse effects
no receptor antagonism, but local anesthetic action. active metabolite NAPA leads to QT prolongation and TdP. slow acetylators lead to lupus like syndrome. IV hypotension (ganglionic block)
disopyramide adverse effects
prominent anticholinergic action. heart failure.
class IB antiarrhythmic drugs
Na channel block. prefers depolarized (ischemic) tissue Na channel blockade. prefers inactivated Na channels, rapidly unbinds at rest. Lidocaine, mexiletine.
class IB clinical uses
secondary drug of choice for acute suppression of VT or VF. post-MI emergency VT/VF, cardioversion, digitalis toxicity. not used for atrial arrhythmias. no QT prolongation, may shorten APD slightly
class IB toxicities
tremor, nausea, seizures, local anesthetic action. Lidocaine is IV only. mexiletine has GI toxicity, metabolism induced by phenytoin
class IC drugs
Na channel block. slow unbinding, greatly prolongs Ina recovery which causes K channel blockaed. prolongs APD preferentially at faster heart rates. prolongs PR, QRS, QT intervals. no EADs or TdP. flecainide, propafenone, moricizine.
Clinical uses of Class IC drugs
primary use for maintenance of sinus rhythm in chronic AF or SVT in patients without structural heart disease. secondary drug of choice for management of Afib, SVT. last resort drug for refractory VT.
class IC toxicities
increase ventricular response to atrial flutter. contraindicated in heart failure, post MI. causes heart block.
class II drugs
Beta adrenergic receptor blockers, may be nonselective or b1 selective. decreases SA, AV node activity. phase 4 depolarization. non selective: propanolol, carvedilol. b1 selective: metroprolol, acebutolol, esmolol
clinical uses of class II drugs
control of ventricular rate in acute or chronic atrial flutter or fib. long term suppression of SVTs. safe and somewhat effective against PVCs. carvedilol decreases mortality in CHF.
class II toxicities
heart block, bradycardia, bronchospasm, hypotension. contraindicated in WPW
which class II is used in acute emergency?
esmolol. short half life.
class III drugs
K channel blockade. prolongs refractoriness. major toxicity is TdP arrhythmias. sotalol, ibutilide, dofetilide, amiodarone, dronedarone
clinical uses of class III drugs
maintenance of sinus rhythm in AF. long term suppression of SVT. amiodarone is primary drug of choice for VT/VF. useful against all arrhythmiaas except digitalis tox
class III tox
QT prolongation, TdP, heart block, bradycardia, hypotension, bronchospasm.
amiodarone
thyroxine analog. mixed actions mimics all antiarrhythmic classes. Na, Ca, K, alpha and beta adrenergic blocking effects. long half life of 80 days. causes thyroid effects, pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, corneal deposits, photosens, drug interactions. dont give with another QT prolonging drug
dronedarone
less effective but fewer side effects than amiodarone
ibutilide
IV for termination of atrial flutter or fib
class IV drugs
L-type Ca channel blockade. Slows SA and AV node activity. prolongs AV refractoriness. Verapamil, diltiazam, nifedipine, amlodipine etc
