Cardio Antiarrhythmic Pharma

Front 1

The most common arrhythmias are due to re-entry, and antiarrhythmics for reentry work primarily in two ways, either by slowing conduction (increase AP threshold), or by prolonging the refractory period between beats (increase AP duration).

By which of these methods do K+ channel blockers work?

Back 1

K+ channel blockers prolong the refractory period.

Road block:
Imagine K as a man holding it's arms up in front of a car (car = electrical activity) blocking it from re-entering the road.

Front 2

The most common arrhythmias are due to re-entry, and antiarrhythmics for reentry work primarily in two ways, either by slowing conduction, or by prolonging the refractory period between beats.

By which of these methods do Na+ channel blockers work?

Back 2

Na+ channel blockers slow conduction.

Slow driving:
Imagine you are electrical activity trying to drive over a salty road in winter. It would take longer because of all the bumps of salt rocks you're driving over.

Front 3

At what phase of channel activity (or state) can Na blockers work?

Back 3

Na+ works on open or inactivated channels, but NOT resting channels.

This means that Na blockers work most during systole, when Na channels would typically be open.

Relevance is that during tachycardia, with shortened diastole, Na blockers are particularly effective.

Front 4

At what phase of channel activity (or state) can K blockers work?

Back 4

K+ works during channels at rest ONLY.

This means K blockers work mostly in diastole.

Clinical relevant because K block will be more effective at PREVENTING a tachyarrhythmia than at stopping it.

Front 5

What is Class I antiarrhythmic a synonym for?

Back 5

Na channel blocker

Front 6

Which is the relective effectiveness of Class I antiarrhythmic subclasses (IA, IB, IC)?

Back 6

IA>IC>IB

IC are the most commonly used.

Front 7

In what AA class does procainamide work?

Back 7

IA, but also has Class III (K block) activity in it's liver-acetylated form, NAPA.

Front 8

What arrhythmia might you see on an EKG of someone with renal failure taking procainamide?

Back 8

Torsade de pointes, due to NAPA accumulation

Front 9

What side effects make long-term procainamide use of limited value?

Back 9

Lupus syndrome in 30% of long-term users
Blood disorders
NV in 25%
Hypotension subsequent to catecholamine depletion from ganglia

Front 10

For what patient would you most likely want to use procainamide?

Afib
Aflutter
Vfib
Vtach

Back 10

Afib - will help control ventricular rate.

Front 11

For which of the following arrhythmias would you most likely want to use lidocaine?

-Afib
-Aflutter
-Vfib

Back 11

IV lidocaine is good for ischemic myocardium, or Vfib, and useless for Afib.

Na block will raise threshold and shorten action potential - it's already short in Afib.

Front 12

What is the Class IB drug mexiletine equivalent to?

Back 12

Oral lidocaine. Weak effect and used mostly with other agents

Front 13

In what body system are lidocaine toxicities focused?

Back 13

CNS: tremor, delirium and nystagmus

Front 14

Flecainide, a commonly rx'd IC Na channel blocker, is very effective at preventing what kind of arrhythmia?

Back 14

Afib. But it's good at promoting other arrhythmias and increases mortality in patients with hx MI.

flecainide --> :(

Front 15

What are the class II antiarrhythmics?

Back 15

Beta blockers.

Front 16

Through what mechanisms do Class II antiarrhymics (beta blockers) work?

Back 16

Slow SA / AV node, and decrease contractility of the heart

(negative inotropic, chronotropic and dromotropic effects)

Front 17

What kinds of arrhythmias are beta blockers effective for?

Back 17

Lots!

Sinus tach, Afib, SVT (AV node reentry), idiopathic VTach and polymorphic VTach (torsade de pointes)

Front 18

What are the class III antiarrhythmics?

Back 18

K blockers

Front 19

What does amiodarone block?

Back 19

Technically Class III - K blocker, but really blocks "Everything" - Ikr, Na, Ca, and beta receptors

Front 20

For what arrhythmias is amiodarone most effective?

Back 20

AF - most potent drug
VT, VF

Front 21

Amiodarone blocks liver metabolised drugs, has poor availability, is slow to work and accumulates in fat.

What is one thing it usually DOESN'T do that might make you want to use it?

Back 21

Amiodarone has very little proarrhythmia, and bradycardia if anything.

Front 22

What very commonly prescribed heart meds does amiodarone interact with?

Back 22

Warfarin and Digoxin

Front 23

What class III AA is approved ONLY for Afib?

Back 23

Dofetilide

Front 24

What are Class IV antiarrhythmics?

Back 24

Calcium channel blockers

Front 25

There are multiple Ca channel blockers that are used in angina and ACS. Only 2 are used for antiarrhymia. Which 2 are these?

Back 25

Diltiazem and Verapamil.

Anything that ends "-dipine" (amlodipine, nifedipine) is a dihydropyridine and is not an AA.

Front 26

What arrhythmia are verapamil and diltiazem primarily used for?

Back 26

SVT

Front 27

How does adenosine work as an antiarrhythmic?

Back 27

-Activates outward rectifying K current in SN and atrium

-Decreases calcium current

Front 28

What is adenosine's half life?

Back 28

10 seconds - RBCs suck it up and deaminate it.

Front 29

What arrhythmia is adenosine primarily used for?

Back 29

SVT involving AV node.

Front 30

What are adenosine's potentially serious side effects?

Back 30

bronchospasm and vasodilation

Front 31

What are digoxin's main AA effects?

Back 31

Increased contractility and vagotonicity (so not good for young people who exercise)

Front 32

What is digoxin indicated for?

Back 32

Refractory Afib

Front 33

What are Digoxin's toxicities?

Back 33

Brady or tachycard, other arrhythmias

Enhanced automaticity

Front 34

What makes digoxin's toxicities worse?

Back 34

HypoK, HypoMg, HyperCa,
Renal dysfxn and muscle wasting