2013-09-26 Antiarrhythmic Drugs Flashcards

1
Q

Generally, how are antiarrhythmics arrythmogenic? What type of arrhythmias do they cause?

A

Antiarrhythmics, esp Class III and Ia agents, can cause significantly prolonged QT and thus Torsade de Pointes

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2
Q

What is the only AAD that has even been shown to improve mortality in the post-MI pt?

A

beta-blockers

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3
Q

What is the preferred tx in the tx of high risk arrhythmia pts?

A

Empiric ICD

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4
Q

How do you risk stratify pts at risk for arrhythmia?

A

Pts w/ an EF <35% and/or who have had runs of sustained VT/VF

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5
Q

What ion flux causes ventricular myocyte depolarization?

A

Na+ in

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6
Q

Uniqueness of SA node electrophysiology

A

intrinsic property is that they spontaneously depolarize thanks to combines Na+/K+ funny channels

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7
Q

Name three main mechanisms that cause arrhythmias. Which is most common?

A
Reentry (most common)
Enhance automaticity (occasionally)
Triggered automaticity (rarely except for proarrhythmia)
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8
Q

What conditions must be met in order to have reentry?

A

For reentry to occur, certain conditions must be met that are related to the following:

  1. the presence of a unidirectional block within a conducting pathway
  2. slowed conduction
  3. recovery of the tissue just proximal to the block so that when the AP reenters it finds excitable tissue
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9
Q

Generally, how would you prolong depolarization?

A

Block Na+ entry

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10
Q

Generally, how would you prolong the refractory period?

A

Block K+ leaving the cell

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11
Q

What are four ways you could decrease automaticity?

A
  1. decrease the slope of the slow depolarization of the membrane due to funny channels (e.g. in SA nodal cells)
  2. increase the threshold needed to fire an AP
  3. increase the max diastolic potential (hyperpolarize a little?)
  4. lengthen the AP itself
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12
Q

disopyramide

A
Class IA (moderate Na+ channel blocker)
Rang 5.01
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13
Q

procainamide

A
Class IA (moderate Na+ channel blocker)
See Rang 5.01 (disopyramide)
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14
Q

quinidine

A
Class IA (moderate Na+ channel blocker)
See Rang 5.01 (disopyramide)
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15
Q

lidocaine

A
Class IB (weak Na+ channel blockers)
Rang 5.02
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16
Q

mexilitene

A
Class IB (weak Na+ channel blockers)
See Rang 5.02 (lidocaine)
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17
Q

Flecainide

A
Class IC (strong Na+ channel blockers)
Rang 5.03
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18
Q

propafenone

A
Class IC (strong Na+ channel blockers)
See Rang 5.03 (flecainide)
19
Q

amiodorone

A
Class III (K+ channel blocker)
Rang 5.05
20
Q

sotalol

A
Class III (K+ channel blocker)
See Rang 5.05 (amiodorone)
21
Q

Adenosine

A

Rang 5.07

22
Q

Digoxin

A

Rang 8.01

23
Q

Calcium Channel blockers (see Verapamil)

A

Rang 5.06

24
Q

dronedarone

A

See Rang 5.05 (amiodorone)

25
Q

dofetilide

A

Class III w/ amiodorone; have to have special training to prescribe

26
Q

Which of the following antiarrhythmic classes is most likely to significantly prolong repolarization (QT interval), and possibly result in Torsade de Pointes as a form of proarrhythmia?

A) Lidocaine and Mexilitine (Class 1B)
B) Flecainide and Propafenone (Class 1C)
C) Beta blockers (Class 2)
D) Sotalol and Dofetilide (Class 3)
E) Calcium channel blockers (class 4)
A

D (K+ channel blockers)

27
Q

Generally, what are Classes I-IV?

A
I = sodium-channel blockers (IA is moderate, IB is weak, IC is strong)
II = beta-blockers
III = potassium-channel blockers
IV = calcium-channel blocker
28
Q

Class I basics

A

Na-channel blockers

Class IAs (moderate blockade, ALSO BLOCK K+ channels e.g. quinidine) - prolong both conduction and re-polarization (and therefore refractory period)

Class IBs (weak blockade, e.g. lidocaine) - blocks inward Na current; decreases effective refractory period

Class ICs (strong blockade) - no ∆in refractory period

29
Q

Class II basics

A

extend (i.e. decreases the slope) of the slow depolarization in SA node cells

30
Q

Class III Basics

A

K-channel blockers (and Type IA Na Channel blockers)

31
Q

Class IV basics

A

Calcium Entry Blockers (e.g. diltiazem & verapamil)

acts primarily on SA & AV node which are dependent on Ca2+ influx for Phase 0 of AP

32
Q

Pharm Tx strategy for SVT

A

**can effective prevent arrhythmias but increases risk of TdP and therefore DEATH!

take advantage of the fact that the AV node is involved by giving negative dromotropic drugs

  • adenosine
  • beta-blockers
  • calcium channel blockers
  • digoxin
  • –allows termination and prevention of AV nodal reentrant tachy (AVNRT) and AV reciprocating tachy (AVRT)
  • –control the rate Atrial flutter and fib
33
Q

Adenosine

A

prolongs AV node conduction by hyperpolarizing cell

34
Q

What can ablation be used for?

A

SVT: >90% success for: WPW, A. tachy, A, flutter,

~70% for A. Fib

35
Q

Key point from this lecture

A

“ICDs help people, drugs tend to kill them exception = beta blockers”

36
Q

Which AAD has been shown to reduce mortality post MI?

A) quinidine
B) flecainie
C) propanolol
D) amiodarone
E) mexilitine
A

C

37
Q

EAD

A
Early afterdepolarizations
--arise during the refractory plateau
= proarrythmia
-causes TdP
-caused by Class III (K+ blockers) and Class 1a (Na+ blockers w/ some K+ blockade)
38
Q

Which tx has lower mortality in pts w/ sustained VF and/or VT?

a) drugs
b) ICD

A

b) ICD!

39
Q

What is the most effective tx strategy for reducing mortality in a pt w/ a low EF and sustained VT or cardiac arrest?

A) EP-guided antiarrhythmic therapy
B) Holter-guided antiarrhythmic therapy
C) empiric sotalol
D) empiric amiodarone
E) empiric ICD
A

E) empiric ICD

40
Q

What is the best prophylaxis tx to prevent SCD in pts w/ EF of <30%?

A) Empiric amiodarone
B) EP studies to guide Rx (drugs or ICD)
C) empiric ICD
D) none of the above

A

c) Empiric ICD

41
Q

What is acute tx for VT until definitive therapy can be instituted?

A

IV lido or amiodarone

42
Q

When is chronic anti-arrhythmia therapy appropriate?

A

To control sx after ICD implantation or ablation

43
Q

Other types of drugs that can be pro-arrhythmic?

A

GI motility
psych drugs
anti-histamines
some antibiotics