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29 Cards in this Set

  • Front
  • Back
5 ways/things that antiarrhythmic drugs alter
1. Max diastolic potential in pacemaker cells and/or the resting potential in ventricular cells

2. Phase 4 depolarization

3. Threshold potential

4. AP duration

5. Refractory period through state-dependent binding to Na channels.
All antiarrythmics are .... except class..., which... but effectively regulates channel activities
Direct ion channel blockers
4 classes of antiarrhythmics
Class 1A- Fast Na channel blockers (prefer active state)

Class 1B- Na channel blockers- perfers active and inactive

Class 1C- Na channel blockers

Class 2- beta blockers

Class 3- K channel blockers

Class 4- Ca channel blockers
Name 4 class 1A Na channel blockers
Flecainide ( FLEK-a-nide)
MA of Class 1A drugs
preferentially bind to Na channels in active state and prolong repolarization (SA node and ventricular myocytes) and prolong repolarization of the membrane (by blocking outward K current)

Decreased re-entry

block Na channels -> prolong QRS
also block K channels -> prolong repolarization (QT)
Name 3 class 1B drugs
MA of class 1B drugs
preferentially binds to Na channels in active and inactive state, shortens repolarization

weakly block Na channels -> little to no effect on QRS
actually shorten repolarization -> QT
What happens to 1B drugs bound to na channels
Dissociate very fast
3 1C Na channel blockers
Encainide ( en-KAY-nide)

strongest Na channel blockers -> prolong QRS
have no effect on repolarization -> no change to QT
Name a non-selective beta blocker
name 4 Beta 1 selective beta blockers
name 3 B1 selective beta blockers that also vasodilate.
Labetalol and carvedilol (also block alpha adenergic)

Pindolol (also beta 2 partial agonist)
What do lg. hyperpolarizing K currents do?
Shorten plateau phase and return membrane potential to resting more quickly
English: can start a new AP more quickly
So then what do K channel blockers do?
Prolong repolarization, increase refractory, decrease re-entry
*For some reason this facilitates EAD.

prolong repolarization -> long QT
don't effect depolarization -> nl QRS
What can too much prolongation of the plateau cause?
Name 4 class 3 drugs
What's special about Amioderone?
Class I, II, III, and IV drug b.c. it alters lipid membranes in which ion channels sit
What's special about Sotalol?
Class II and III drug
Name 2 class IV drugs
Diltiazem and verapamil
How does adenosine work as an antiarrythmic?
Activated Ach sensitive K+ current in the atrium and sinus and AV node
What are the consequences of adenosis
Shortend AP, hyperpolarization, and slowing of normal automaticity
Which kind of current does adenosine reduce
Ca currents
What is the consequence of adenosine slowing Ca currents
Increases AV nodal refractoriness

Inhibits DAD
How is adenosis often administered?
Bolus i.v. injection to terminate PSVT
How does digoxin work? What do you use if for?
1. Inhibits Na-K ATPase activity

2. Used for HF pts. w/reetrant tachycardia
Is it hypo or hyperkalemia that causes arrhthymias?
Hypokalemia can cause what kind of arrhythmia?
Ectopic beats in non pacemaker cells
Hyperkalemia causes arrhthymias by...
Depolarizing the membrane and slowing conduction velocity
Explain EAD
Prolongation of the repolarization delays the inactivation of the ion channels responsible for the inward flow of positive depolarizing currents. This leads to a further delay in repolarization and causes early after depolarization (EAD), the triggering event for torsade