Sodium & Beta Blockers Flashcards
General effect of sodium channel blockers
Alters AP duration and kinetics of Na channel
General effect of K+ channel blockade
Prolonged effective refractory period
General effect of beta blockers
Blockade of SNS effects in heart
General effect of Ca channel blockers
Slows conduction in cells with calcium-dependent depolarization
What do class I drugs bind? What is the result?
Bind to fast sodium channels –> slow the usually rapid depolarization (phase 0) in fast response cardiac action potentials –> decreased conduction velocity in non-nodal tissue
What is the effect of sodium channel blockers on nodal cells?
No direct effect (they depend on Ca for depolarization)
What accounts for the effects on ERP with class I drugs?
Not the sodium blockade but rather the non-specific secondary activity of them on efflux of K+ (phase 3)
What are the class I drug subdivisions? How does each subclass differ?
IA: (Quinidine) moderate sodium channel blockade, increase ERP
IB: (Lidocaine) weak sodium channel blockade, decreased ERP
IC: (Flecainide) strong sodium channel blockade, no ERP effect
Rank the class I subclasses from greatest to least sodium blockade
IC > IA > IB
Rank the class I subclasses: ____ increases ERP, ____ does not affect ERP, ___ decreases ERP
IA
IC
IB
Examples of subclass IA
Quinidine, procainamide, disopyramide
Examples of subclass IB
Lidocaine, Mexilitine, Tocainide
What are state-dependent drugs?
Only bind readily to activated or inactivated channels, not resting
Examples of subclass IC
Flecainide, Propafenone, Moricizine
When are state-dependent drugs helpful in CV situations
Fast tachycardia (many activations and inactivations) or significant loss of RMP (more channels inactivated instead of resting)
