Pharm 1 - Antiarrythmic Therapy (Holzberger)

Front 1

3 main mechanisms of arrythmias

Back 1

Re-entry (abnormal impulse conduction)

Enhanced automaticity

Triggered automaticity/activity (normal action potential is interrupted or followed by an abnormal depolarization)

Front 2

Re-entry needs what three things?

Back 2

Unidirectional block
Slowed conduction
Recovery of blocked tissue

Front 3

Automaticity mechanism

Back 3

Spontaneous generation of an AP

It is an intrinsic property of all myocardial cells.

Front 4

Triggered activity mechanism

Back 4

Impulse initiation caused by a repolarization

Due to enhanced Na or Ca influx of blockage of K+ efflux.

Front 5

2 ways to prevent re-entry

Back 5

Prolong refractory period of the area of unidirectional block to inhibit retrograde conduction (block K leaving - prolong phase 2-3)

Prolong conduction velocity of the normal limb so the retrograde impulse will collide with the next incoming antegrade impulse in the area of the block (block Na entering - extend phase 0)

Front 6

Way to prevent automaticity

Back 6

Depress autonomic firing rate of spontaneously discharging ectopic sites and minimally affecting the rate of normal sinus node.

Front 7

How to prevent triggered activity

Back 7

Remove...
If early after depol - class 3 or 1A agents.
If delayed after depol - Digoxin

Prevent bradycardia, hypokalemia, catecholamines.

Front 8

Class II

Back 8

beta blockers

Front 9

Class III

Back 9

K-channel blockers
Delay phase 3 repolarization and thereby increase AP duration and effective refractory period.

Front 10

Class IV

Back 10

calcium entry blockers.
Most effective at SA and AV nodes.

Front 11

All class I drugs...

Back 11

Reduce phase 0 slope and peak of AP

Front 12

Class IA

Back 12

Moderate reduction in phase 0 slope, increase in APduration, increase in effective refractory period.

Front 13

Class IB

Back 13

Small reduction in phase 0 slope and reduction of AP duration and decrease in effective refractory period.

Front 14

Class IC

Back 14

Pronounced reduction in phase 0 slope, no effect on action potential duration or effective refractory period.

Front 15

Drugs in class IA

Back 15

Quinidine, procainamide, disopyramide

Front 16

Drugs in class IB

Back 16

Lidocaine, mexilitine (for VT only)

Front 17

Drugs in class IC

Back 17

flecainide, propafenone

Front 18

Drugs in class III

Back 18

sotalol, dofetilide, amiodarone, dronedarone, ibutilide*

* - activates inward Na+ current.

Front 19

Drugs in class IV

Back 19

aside from the ones you know, adenosine (for SVT only)

Front 20

Which drug least likely to prolong repolarization (QT) significantly?

Back 20

A: Quinidine
B: Flecainide****
C: Sotalol
D: Amiodarone
E: Procainamide

Front 21

Tx of SVT

Back 21

Take advantage of the AV node.
Slow conduction with negative dromotropic drugs like adenosine, beta blockers, ca++ channel blockers, digoxin.

This allows termination and prev of AVNRT (atrioventricular nodal reciprocating tachycardia) and AVRT (atrioventricular reciprocating tachycardia)

Controls the rate of atrial tachycardia, flutter and fib.

Front 22

How is adenoisne administered?

Back 22

rapid IV bolus

Front 23

In tx of SVT if negative dromotropics don't work...

Back 23

Use traditional antiarrythmics. The following have effects on AV node, accessory tissue and atrial myocardium.

Ibutilide
Quinidine, Procainamide, Disopyramide
Flecainide, Propafenone
Sotalol, Dofetilide, Dronedarone, Amiodarone

Front 24

For SVT - what is the best thing to do today?

Back 24

Ablation, unless it is atrial fibrillation.

Front 25

Genereal rule for ventricular tachycardia

Back 25

ICDs help people, drugs tend to kill them (except beta blockers)

Amiodarone may SLIGHTLY reduce mortality risk too.

Front 26

Which antiarrythmic has been shown to reduce mortality?

Back 26

A) Quinidine
B) Flecainide
C) Mexilitine
D) Amiodarone
E) Propranalol*****

Front 27

Tx of sustained VT - which drugs are superior to other drugs?

Back 27

sotalol and amiodarone

Front 28

The best treatment in the prevention of SCD in this patient with sustained VT or cardiac arrest is:

Back 28

A) EP or Holter guided Quinidine
B) EP or Holter guided Sotalol
C) Empiric Sotalol
D) Empiric Amiodarone
E) Empiric ICD*****

Front 29

Role for antiarrythmic drug therapy for VT

Back 29

Acute treatment with IV Lidocaine or Amiodarone till definitive therapy can be instituted

Chronic treatment has been relegated to secondary role (after ICD) in cardiac disease - with the exception of beta blockers

Ablation rapidly supplanting the limited role of antiarrhythmics in the treatment of VT

Front 30

Antiarrythmics safe in renal disease:

Back 30

Amiodarone, quinidine and mexilitine

Front 31

Antiarrythmics that don't prolong refractory periods (Torsade)

Back 31

IC (flecainide, propafenone)
IB (lidocaine, mexilitine)

Front 32

Antiarrythmics that have major drug rxns

Back 32

Amiodarone with warfarin and digoxin

Front 33

take home points

Back 33

Antiarrhythmics (with the exception of Flecainide and Propafenone - the 1C’s , and Lidocaine and Mexilitine -the 1B’s) can significantly prolong repolarization and therefore can result in Torsade de Pointe as a form of Proarrhythmia.

The only antiarrhythmic that has ever been shown to improve mortality in the postinfarct patient is a beta blocker

The empiric use of an ICD is preferable to any antiarrhythmic in the treatment of high risk arrhythmia patients (low EF <40% or with sustained VT)