Anti-arrhythmic Agents Flashcards
What is the best treatment for an asymptomatic or minimally symptomatic arrhythmia
No pharmacological treatment
what are use or state-dependent work
drugs that are more effective in blocking channels that are being used frequently (activated) or in an inactivated state (have a higher affinity for activated for inactive channels and low affinity for resting channels)
What is the MOA of the class I anti-arrhythmic agents
Na+ channel blockers
What is the MOA of the class II anti-arrhythmic agents
B-adrenergic receptor blocker
What is the MOA of the class III anti-arrhythmic agents
prolong action potential duration (K+ channel blocker)
What is the MOA of the class IV anti-arrhythmic agents
Ca++ channel blockers
What are the 3 drugs in the class 1A AAA
procainamide, quinidine, disopyramide (Intermediate kinetics)
what are the 2 drugs in the class 1B AAA
LIDOCAINE, mexiletine (Fast Kinetics)
What are the 3 drugs in the class 1C AAA
amiodarone, dronedarone, sotalol (Slow kinetics)
What is the MOA of propranolol
BB (class II)
What is the MOA of esmolol
BB (class II)
What is the MOA of amiodarone
prolong APD (K+ channel blocker)
What is the MOA of dronedarone
prolong APD (K+ channel blocker)
What is the MOA if sotalol
prolong APD (K+ channel blocker)
what is the MOA of verpamil
CCB (class IV)
what is the MOA of diltiazem
CCB (class IV)
what is the MOA of procainamide
blocks Na+ and K+ channels (intermediate kinetics - prolong APD)
What is the clinical effect of procainamide
slows upstroke of AP and conduction, prolong QRS, direct depressant action on SA/AN nodes use/state-dependent action
Indication for procainamide
atrial and ventricular arrhythmias, 2nd choice for ventricular arrhythmias post aMI
Metabolism of procainamide
half life: 3-4hrs, metabolized to NAPA and renal eliminated
Adverse effects of procainamide
Torsades des pointes, Hypotension, anti-cholenergic effects, Lupus (long term use)
MOA of quinidine
blocks Na+ and K+ channels
Adverse effects of quinidine
strong anti-cholenergic effects, Cinchonism (headache, dizziness, tinnitus), rarely used because of cardiac and extra-cardiac effects
MOA of disopyramide
blocks Na+ and K+ channels
Adverse effects of quinidine
worst anti-cholenergic effects of the class IA and requires co-administration of drugs that slow AV conduction. negative iontrophic effect may induce heart failure
Indications for quinidine
Not drug of 1st or second choice. ONLY approved for ventricular arrhythmias
MOA of Lidocaine
Na+ channel blockers use/state dependent drug action (fast kinetics - reduces APD)
Clinical effect of lidocaine
at normal resting potential: no effect on conduction, selective depression of conduction in depolarized (ischemic cells)
Indication for LIdocaine
Drug of choice for ventricular tachycardia and fibrillation after cardioversion in the setting of ischemia/infarction, highly effective for ventricular arrhythmias post MI
Adverse Effects of Lidocaine
Least cardiotoxic drug among class I drugs, neurological side effects due to local anesthetic properties
Metabolism of Lidocaine
extensive first pass metabolism, half life: 1-2hrs (3-6 hrs with liver disease)
Difference between lidocaine and mexiletine
Mexiletine is an orally active lidocaine analog with similar actions and AEs. Has a longer half life 8-20 hrs. Off label use to treat chronic pain
MOA of flecainide
Na+ and K+ blocker (Class 1C: slow kinetics)
Clincial effect of flecainide
no effect on APD. no anti-cholinergic effect
Indication for flecainide
Supraventricular arrhythmias in pts with otherwise normal hearts
Metabolism of flecainide
half life: 20hrs, renal and hepatic elimination
Adverse effects of flecainamide
increases mortality in pt with v. tach, MI and ventricular ectopy
Contraindication of flecainamide
ventricular ectopy
MOA of propafenone
potent blocker of Na+ channel and may also block K+ channels, weak BB activity
Clinical effect of propafenone
no effect on APD
Indications for propafenone
supraventricular arrhythmias in pt with otherwise normal hearts
Metabolism of propafenone
half life: 5-7hrs, hepatic elimination
Adverse Effects of propafenone
arrhythmogenic, sinus bradycardia/bronchospasm (B-blockade), metallic taste and constipation
MOA of propanolol
non-selective BB
MOA of Esmolol
selective B1 antagonist
Clinical effects of the BB on the heart
- inhibit sympathetic influenes on the the cardiac electrical activity
- reduce HR
- decrease intracell Ca overload
- decrease pacemaker activity
- Reduce conduction velocity
- decrease catecholamine induced DAD and EAD arrhythmias
Indications for the BBs
Exercise induced arrhythmias, A. fib. atrial flutter, AV nodal re-entry, prevention of recurrent infarction post MI
AE of the BBs
bradycardia, reduced exercise capacity, heart failure, hypotension, AV block, bronchospasms, masking hypoglycemia in diabetic pts.
Contraindications of BBs
Asthma/COPD, sinus bradycardia or partial AV block
