Anti-arrhythmic drugs Flashcards
What are the class IA vaughn williams class drugs? What channels are affected?
Disopyramide, Quinidine, Procainamide
(Double quarter pounder); Sodium and potassium channels blocked
What are the class IB Vaughn williams class drugs? Channel affected?
Lidocaine and Mexiletine
(Lettuce and mayo); Sodium channel blocked
What are the Class IC VW class drugs? Channel affected?
Propafenone and Flecainide
(Pepsi and fries); Sodium channel blocked
What are the Class II VW class drugs? Channel affected?
Metoprolol, propranolol, atenolol, timolol, esmolol
(Beta blockers); B1 receptor blocked
What are the Class III VW class drugs? Channel affected?
Amiodarone, dronaredone, dofelitide, sotalol, Ibutilide
(A drooling dog is sleeping); Potassium channel blocked
What are the Class IV VW class drugs? Channel affected?
Verapamil, diltiazem; Calcium channel blocked
What channels are blocked by adenosine?
Potassium and calcium
Which VW drugs decrease automaticity?
All of them (including adenosine)
Which VW drugs increase action potential duration, thus increasing refractory period?
Class IA and Class III
What VW drugs increase REFRACTORY PERIOD WITHOUT INCREASING ACTION POTENTIAL DURATION?
Class IA, IB, IC and Adenosine
Class IA increases refractory pd with and without APD
Which VW drugs decrease conduction velocity?
Class IA, IC, II, IV, and Adenosine
How do Class I VW drugs work by decreasing automaticity?
They block sodium channels, INCREASING THRESHOLD POTENTIAL
Note: Class IA drugs also increase AP duration via potassium channel blockage
How do Class II VW drugs work by decreasing automaticity?
They are B-anatagonists, DECREASING PHASE 4 SLOPE
How do Class III VW drugs work by decreasing automaticity?
They block potassium channels, INCREASING AP DURATION
How do Class IV drugs work by decreasing automaticity?
They block calcium channels, SLOWING SA/AV NODE DEPOLARIZATION
How does adenosine decrease automaticity?
INCREASES MAXIMUM DIASTOLIC POTENTIAL; I.e. making interior of the cell more negative between APs. It does this by promoting Potassium efflux in SA and AV nodes
Do class I drugs work on resting/closed, activated, or inactivated sodium channels?
Class IA: Activated/Open
Class IB: Inactivated/closed
Class IC: Activated/open
Class IA drugs have what effects on depolarization and refractory period?
They have a moderate affinity for blocking sodium channels and block potassium channels. They therefore prolong repolarization, prolong phase 2 and 3, leading to PROLONGED REFRACTORY PERIOD
Class IB drugs have what effects on depolarization and refractory period?
They have a weak affinity for sodium channels, and shorten repolarization. Shorten phase 2 and 3.
Class IC drugs have what affect on depolarization and refractory period?
They have a strong affinity for blocking sodium channels, but do not affect action potential duration.
What are some toxicities of Class IA VW drugs?
For a drug like procainamide, they prolong Action potential, leading to prolonged QT interval, which can lead to Torsade de pointes
What are some toxicities of Class IC VW drugs?
For flecainide and propafenone, they should not be used in patients with structural abnormalities
What are some toxicities with Class III VW drugs?
Prolonged AP, which can lead to Prolonged QT, which can lead to Torsade depointes (Note: Amiodarone is not associated with TdP)
Non-dihydropyridines act on which cells?; What are some examples?
Vascular smooth muscle AND Cardiac tissue; Verapamil, diltiazem
