Antiarrhythmic classifications Flashcards
Class I
block sodium channels
Class II
reduce adrenergic activity of the heart
Class III
K+ channel inhibitors
Class IV
CCBs
Misc
Adenosin
Digoxin
Magnesium
Potassium
Class IA drugs
Quinidine
Procainamide
Quinidine
Class IA
Procainamide
Class IA
Class IB drug
Lidocaine
Lidocaine
Class IB
Flecainide
Class IC
Class IC drug
flecainide
Quinidine MOA
referentially block open/activated sodium channels, lengthening duration of action potential
Blocking activated sodium channels
lengthens the duration of action potential
Procainamide MOA
referentially block open/activated sodium channels, lengthening duration of action potential
Lidocaine MOA
block inactivated sodium channels, shortening duration of action potential
Flecainide MOA
bind all sodium channels, no effect on duration of action potential
Binding all sodium channels…
has no effect on duration of action potential
blocking inactivated sodium channels…
shortens duration of action potential
K+ channel inhibition….
increases effective refractory period
Amiodarone
K+ channel inhibitor
Sotalol
K+ channel inhibitor (and non-selective B blocker)
CCBs MOA
Block slow L-type cardiac Ca++ channels
Propranolol
non-specific B blocker
Acebutolol
B1 specific B blocker
Esmolol
B1 specific B blocker
Amiodarone has a bunch of other effects:
Blocks Na+ channels (class I) B-blocker (class II) Some Ca+ channel blocking (Class IV) Alpha blocker
Block slow L-type cardiac Ca++ channels…
decreases HR and contractility
Adenosine MOA
Enhanced K+ conduction and inhibition of cAMP-induced Ca++ influx→ hyperpolarization→ heart “resets”
Potassium MOA
membrane potential stabilizing action by increased K+ permeability: hyperpolarizing
Hyperpolarizing the myocyte effects:
→ decreased action potential duration
→ decreased conduction
→ decreased pacemaker rate
→ decreased pacemaker arrhythmogenesis
