antiarrhythmic agents3 Flashcards
what are the clinical uses of Ca blockers as antiarrhythmics?
- effective in tx of reentrant arrhythmias involving AV node
- decreases ventricular reate in atrial flutter/ fibrillation
what is the effect of Ca blockres on ;
- conduction
- refractory period
- automaticity
- slow conduction
- increase refractory period
- decrease automaticity.
what type of Ca blockers are the only ones with antiarrhythmic effects
nondihydropyrimidines
what are the adverse effects of Ca blockers taken for arrhythmias
- hypotension
- worsen HF (decrease FOC)
- bradycardia or heart block
- constipation (w/ verapamil)
what class of antiarrhythmic is digoxin?
fits in none of them
what is digoxins MOA
vagotonic effects (chronotropic) = amplifies parasympathetic tone in the AV node 2. positive inotropic effects results from inhibition of the Na/K/ATPase pump, increasing intracellular Ca++
why is digoxin not useful without combo therapy in active patients.
increases parasympathetic activity; this is overcome by sympathetic stimulation
what happens to digoxin concentration if plasma level is taken too early?
falsely high; hasnt had time to enter tissue
what are 3 major toxicities of digoxin
- GI toxicity (typically first)
- visual problems (blurred vision)
- nephrotoxicity (potentially fatal)
all antiarrhythmics can cause what?
arrhythmia
anything that slows AV node can cause what?
what drugs may do this?
sinus bradycardia
digoxin (increases vagal tone)
ca channel blockers
BB’s (sympatholytic properties)
what drugs can cause tachyarrhythmias?
beta blocker withdrawal
digoxin (atrial tachycardia)
why should dofetilide and levaquin not be combined
can cause torsades.
-don’t combine any drugs that are associated with QT elongation
