What is the MOA for Class IA antiarrhythmics?
-Binds to open and inactivated sodium channels and prevents sodium
influx
- Decreases phase 0
- Decreases myocardial excitability and conduction velocity and
myocardial contractility
- results in slowing conduction velocity and increased refractoriness
what are the adverse effects of quinidine
arrhythmias (TdP), SA and AV blockade, asystole, GI distress,
cinchonism at high doses (blurred vision, tinnitus, HA, disorientation,
psychosis), increase digoxin levels
what are some drug interactions of quinidine
antifungals (itraconazole, voriconazole, posaconazole)
What is different about disopyramide MOA?
Same as other 1A's except also has a negative inotropic effect and
peripheral vasoconstriction
what are adverse effects of Procainamide?
•Reversible lupus-erythematosus-like syndrome
•Toxic concentrations may cause asystole
•CNS side effects (depression, hallucinations, psychosis)
•Hypotension (IV)
do the class 1A drugs require dose adjustments?
, YES - adjust for renal impairment
how do you dose Disopyramide?
weight based!
> 50kg start w 300mg
<50 kg start with 200 mg
how much of the oral dose of disopyramide is excreted unchanged by
the kidneys?
1/2
what are the adverse effects of Disopyramide?
anticholinergic effects, hypotension, CHF
What agents are in the Class IB antiarrhythmics?
Lidocaine
Mexiletine
What is the MOA of Class IB antiarrhythmics?
Rapidly associates and disassociates from sodium channels with actions
manifested when the cardiac cell is depolarized or rapidly firing
Shortens phase 3 repolarization and decreases the duration of AP
how is lidocaine administered? why?
IV only due to extensive first pass metabolism
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