Anti-arrhythmic Drugs Flashcards
Quinidine protein bindings
80-90%
Procainamide protein binding
15%
Lidocaine protein binding
55%
propranolol protein binding
90-95%
(Propranolol is Pro Proteins)
Amiodarone protein binding
96%
sotalol protein binding
0%
verapamil protein binding
90%
What triggers Torsades de pointes?
early after depolarization in a setting of delayed repolarization and increased duration of refractoriness
What is EKG characteristic of torsades?
QTc interval prolongation
What are exacerbating factors of torsades?
hypokalemia
hypomagnesemia
poor LV function
concomitant administration of QT prolonging drugs
Incessant ventricular tachycardia is more likely to occur with high doses of class ___ drugs
IC
Wide complex ventricular rhythm easily degenerates to what?
V Fib
T/F: Lidocaine increases occurence of fatal bradycarrhythmias and asystole with prophylactic treatment of acute MI
True
Is CCB recommended as routine treatment of patients with acute MI?
No
In patients with HF, ____ reduces the risk of sudden cardiac death by 29%
amiodarone
Amiodarone is associated with a 2 and 5 fold increased risk of ____ and ___ toxicity, respectively.
pulmonary; thyroid
What is the only drug that plays a role for prophylactic antiarrhythmic medication for the primary prevention of sudden cardiac death in patietns with HF?
Amiodarone
Class I drugs are ___ channel blockers
sodium
What are 3 examples of class IA drugs?
Quinidine
Procainamide
DIsopyramide
What are 3 examples of class IB drugs?
Lidocaine
Mexiletine
Tocainide
What are 2 examples of class IC drugs?
Flecainide
Propafenone
What are class II drugs?
Beat blockers
What are class III drugs?
K+ channel blockers
Name 3 class III drugs?
Amiodarone
Bretylium
Sotalol
What are class IV drugs?
Calcium channel blockers
What are 2 examples of Class IV drugs?
Diltiazem and Verapamil (CCB)
What is the MOA of class IA/Na+ channel blocking drugs?
Slows phase 0 depolarization in ventricular muscle fibers
(prolong AP)
What is the MOA of class IB/Na+ channel blocking drugs?
Shortens phase 3 repolarization in ventricular muscle fibers
(decrease duration of AP)
What is the MOA of class IC/Na+ channel blocking drugs?
Markedly slows phase 0 depolarization in ventricular muscle fibers
What is the MOA of class II drugs/BB?
Inhibits phase 4 depolarization in SA and AV nodes
What is the MOA of class III/K+ channel blocking drugs?
prolongs phase 3 repolarization in ventricular muscle fibers
(phase 0 is not altered)
What is the MOA of class IV/Ca+ channel blocking drugs?
inhibits action potential in SA and AV nodes
The QT interval is ____ with Class IA drugs
prolonged
Do Class IA drugs affect atrial arrhythmias, ventricular arrhythmias or both?
Both
What are S/S of Quinidine toxicity?
Cinchonism – HA, tinitus, thrombocytopenia, Torasades
What are S/S of procainamide toxicity?
lupus like syndrome
Class II antiarrhythmics ___ cAMP
decrease
Class II antiarrhythmics ___ Ca+ current
decrease
Class II antiarrhythmics ___ slope of phase 4
decrease
Class II antiarrhythmics ___ PR interval
increase
Class II antiarrhythmics ___ myocardial O2 consumption
decrease
What are uses for class II antiarryhtmics?
V-tach, SVT, A Fib, A flutter
What are toxicity effects of BB?
impotence, bronchospasm, bradycardia, AV block, mask hypoglycemia
Class III antiarrythmic drugs ____ AP duration
increase
Class III antiarrythmic drugs ____ effective refractory period
increase
When do you use Class III antiarrhytmic drugs?
when other antiarrhythmics fail
What is Amiodarone toxicity S/S?
Pulmonary fibrosis
Hepatotoxicity
Hypo or hyperthyroidsm
Corneal Deposits
Skin deposits
Class IV antiarrhythmics ___ conduction velocity
decrease
Class IV antiarrhythmics ___ ERP
increase
Class IV antiarrhythmics ___ PR interval
incrase
What is the use of class IV (CCB) drugs?
prevents nodal arrhythmias
In the heart, adenosine binds with _____
A1 receptor (Gi protein)
When adenosine binds to the A1 receptor, it leads to opening of what channels?
K+ channels (which in turn leads to hyperpolarization
Adenosine decreases ___ in cardiac cells –> decreased entry of ___
cAMP; Calcium
Slows HR and conduction
In vascular smooth muscle, adenosine binds to ____
A2 (Gs protein)
In vascular smooth, Adenosine causes a ___ of cAMP, which in turn causes ____
increase; vasodilation
What is the drug of choice for SVT?
Adenosine
What is the DOA of Adenosine?
15 seconds
What antagonizes adenosine?
Xanthines (Theophylline and Caffeine)
What potentiates adenosines effects?
Dipyridamole “Persantine” (adeonsine uptake inhibitor)
Digozin is what type of drug?
Cardiac glycoside
Digoxin _____ AV node conduction
decreases
Digoxin causes depression of the ___ node
SA
What are s/s of digoxin toxicity?
NVD, yellow vision, increased PR, decreased QT, T wave inversion
What electrolyte abnormality worsens Digoxin toxicity?
Hypokalemia
