Pharmacology Of Dysrhythmias Flashcards
Consequences of dysrhythmia (3)
- Compromises mechanical performance
- Prodysrhythmic/dysrhythmogenic: conversion of one dysrhythmia to another, v tach to v fib
- Thrombogenesis: atrial flutter and fibrillation contribute to increased stroke incidence
Causative mechanisms for dysrhythmia generation (2)
- Disorders of impulse formation (early and delayed after-depolarizations)
- Disorders of impulse conduction (AV nodal block, ventricular re-entry, AV nodal re-entry)
Class Ia Antidysrhythmic agents (3)
- Procainamide
- Quinidine
- Disopyramide
Class Ib Antidysrhythmic agents (2)
- Lidocaine
2. Phenytoin
Class Ic Antidysrhythmic agents (1)
- Flecainide
Class II Antidysrhythmic agents (1)
- Propranolol
Class III Antidysrhythmic agents (3)
- Amiodarone
- Sotalol
- Ibutilide
Class IV Antidysrhythmic agents (2)
- Verapamil
2. Diltiazem
Class V “others” Antidysrhythmic agents (3)
- Adenosine
- Digoxin
- Atropine
Non-nodal tissues depolarize at phase 0 when there is ______ influx.
Na+
Nodal tissues depolarize at phase 0 when there is ______ influx.
Ca2+
General Class I agent MOA (3)
- Block voltage-sensitive Na+ channels to varying degrees in conductile tissues: slows phase 0
- ERP/APD increased
- Useful in varying degrees for ventricular dysrhythmia and/or digitalis or MI-induced dysrhythmia
General Class Ia agent MOA (3)
- Moderate binding to Na+ channels: slows phase 0 depolarization
- K+ channel blockade: delays phase 3 repolarization and prolongs QRS and QT interval
- Ca2+ channel blocking effect at high doses: depresses phase 2 and nodal phase 0
General Class Ib agent MOA (2)
- Weak binding to Na+ channels: weak effect on phase 0 depolarization due to rapid “on-off” receptor kinetics
- Accelerated phase 3 repolarization: shortened APD and QT, good use in digitalis and MI-induced dysrhythmia
General Class Ic agent MOA (1)
- Strongest binding to Na+ channels: slow “on-off” kinetics with marked effects on phase 0 depolarization. Lengthened QRS and APD. QT internal unchanged. Lengthened PR interval (depressed AV nodal conduction).
General Class II agent MOA (4)
- Comprised of beta antagonists (beta blockers!): beta receptors are G-protein-coupled to Ca2+ channels; beta effects primarily on nodal phase 0 depolarization
- Depresses SA nodal automaticity (phase 4)
- AV nodal conduction
- Decreased ventricular contractility
General Class III agent MOA (2)
- Multiplicity of membrane effects at K+, Ca2+, Na+, and beta receptors (direct and indirect): Prolong phase 3 repolarization, increase QT interval
- Useful for ventricular re-entry/fibrillatory dysthythmia
General Class IV agent MOA (4)
- Ca2+ channel antagonists (calcium channel blockers!): similar in utility to Class II agents with primary effects on nodal phase 0 depolarization
- Depresses SA nodal automaticity
- Depresses AV nodal conduction
- Decreases ventricular contractility
Atrial fibrillation, conversion, clinically used agents (High, Moderate, Low)
High efficacy: Ia agents
Moderate efficacy: II, III, IV agents
Low efficacy: Ib