Anti-arrhythmic Drugs Flashcards Preview

CV Quiz 2 > Anti-arrhythmic Drugs > Flashcards

Flashcards in Anti-arrhythmic Drugs Deck (63):
1

Where are fast response cells in the heart?

atria, ventricle, his-purkinje

2

Where are slow response cells in the heart?

SA and AV nodes

3

What is the major ion involved in depolarization of fast cells?

Na

4

What is the major ion involved in depolarization of slow cells?

Ca

5

What class inhibits depolarization of fast cells?

class 1 sodium channel blockers

6

What class inhibits depolarization of slow cells?

class 4 calcium-entry blockers

7

What are the 3 important differences between fast and slow response cells?

1. Diastolic Depolarization-slow response cells usually
2. Membrane Responsiveness - level of resting membrane potential determines maximum upstroke or conduction velocity (mV/msec) of the AP
3. Effective Refractory Period (ERP)-minimum interval between two propagating impulses

8

What are the 3 main mechanisms of arrhythmias?

-Increased automaticity (inappropriately excitable cells)
-Triggered automaticity (normal action potential is interrupted or followed by an abnormal)
-Reentry (abnormal impulse conduction)

9

What is early afterdepolarization (EAD)?

type of triggered automaticity that interrupts repolarization and is exacerbated by slow rate-long QT syndrome (Torsades de Pointes results)

10

What is delayed or late afterdepolarization (DAD)?

type of triggered automaticity that occurs after repolarization and is exacerbated by fast rates, high
intracellular Ca2+

11

What can trigger DAD?

Digitalis toxicity, catecholamines (NE, EPI) and ischemia

12

What are the 4 ways anti-arrhythmic drugs reduce spontaneous discharge in autonomic tissues?

decrease phase 4 slope
increase maximum diastolic potential
increase threshold potential
increased action potential duration

13

What are the 4 classes of anti-arrhythmic drugs?

1 sodium channel blockers
2 beta-adrenergic blockers
3 K channel blockers
4 Calcium channel blockers

14

What are the 3 subclasses of class 1 (Na blockers)?

1A prolong repolarization: moderate depress phase 0 and slow conduction
1B shorten repolarization: little depress phase 0 and slow conduction
1C little effect on repolarization: marked phase 0 depress and slow condution

15

What class acts on fast response cells, reduce membrane responsivness, increase threshold, reduce Vmax, and prolong refractory period?

Class 1: Na channel blockers

16

Class 1A drug?

Quinidine

17

Direct effects of quinidine?

Increase AP threshold
decrease Vmax
increase ERP (effective refractory period)

18

Indirect effects of quinidine?

Blocks K+ channels  early afterdepolarizations (EADs) & Vagolytic Effect

19

Use of quinidine?

-Atrial flutter or fibrillation
-Prevent ventricular tachycardia and fibrillation

20

Major side effects of quinidine?

Severe GI effects - Diarrhea, cramps
 Heart – vagolytic
 Inhibits P450 system (metabolism of narcotics is reduced)
 Proarrhythmic – not necessarily related to the arrhythmia being treated.
 Reduces the renal clearance of digitalis; increases plasma levels of digitalis

21

Is quinidine okay for pt with renal failure?

Yes, metabolized in liver.

22

Class 1B drug?

Lidocaine

23

Direct effects of lidocaine?

-Increase AP threshold
-Increased Block of Na+ channels ( Vmax) at high HR and in depolarized cells
-decreased AP duration and ERP

24

Side effects of lidocaine?

dizziness & seizures

25

What is lidocaine used for?

Ventricular tachycardia
Digitalis induced arrhythmias
Safe for patients with Long QT Syndrome

26

What is a class 1C drug?

Flecainide

27

What are the direct effects of flecainide?

Increase AP threshold
decreased Vmax (conduction velocity)
Variable effects on ERP dissociates from Na+ channel
slowly makes it the most potent Na channel blocker

28

Side effects of flecainide?

pro-arrhythmic

29

What is flecainide used for?

Approved for used in life-threatening situations when supraventricular and ventricular arrhythmias are resistant to other drugs

30

What kind of drugs are class 2?

beta-blockers

31

How do beta-blockers work?

Bind to ß-adrenergic receptors on cardiac cell membranes to competitively inhibit epinephrine and norepinephrine binding which antagonizes SNS stimulation

32

What effect to beta-blockers have on the AP curve?

slow the rate of diastolic (phase 4) depolarization.

33

What are the two beta-blockers we have to know?

propranolol and esmolol

34

What is the difference between propranolol and esmolol?

Propranolol – Long acting blocker (oral)
Esmolol – Short acting blocker (IV)

35

What are beta-blockers used for?

Used for all atrial arrhythmias, ventricular tachycardia and fibrillation

36

Are beta-blockers safe?

The beta blockers are currently the most useful antiarrhythmic drugs available due to their safety record and wide clinical applications

37

Are beta-blockers safe for people with long QT syndrome?

Yes, beta-blockers do not prolong repolarization in ventricular tissues

38

What are the major side effects of beta-blockers?

negative inotropic effect, heart block, bradycardia and bronchospasm

39

In general, what kind of drugs are class 3?

K channel blockers

40

What are the common effects of K channel blockers?

Main common property is K+ channel block; prolongs action potential repolarization (action potential duration increases); reverse use-dependence.

41

What are the two K channel blockers we have to know?

Amiodarone & sotalol

42

Which K channel do most blocker drugs target?

most common target is IKr (hERG channel)

43

Amiodarone has multiple mechanisms of action. What are they?

Potent K+ channel blocker (blocks both IKr and IKs)
 Modest Na+ channel blocker
 Modest Ca++ channel blocker
 Modest beta- adrenoreceptor blocker

44

What is amiodarone used for?

 Effective against ventricular tachyarrhythmias and fibrillation.
 Also used in the prevention of recurrent paroxysmal atrial fibrillation or flutter

45

What are the major side effects of amiodarone?

 Triggered arrhythmias (EADs); but rarely associated with Torsades de Pointes
 Altered thyroid function (inhibits conversion of T4 to T3) - hypothyroidism
 Pulmonary fibrosis – often irreversible

46

What is sotalol's MOA?

Major action is block of K+ channel (IKr) also has beta-adrenergic receptor blocking actions (secondary effect)

47

What side effect do we have to watch out for with sotalol?

triggered arrhythmias with Torsades de Pointes.

48

What is sotalol used for?

Effective against ventricular tachyarrhythmias and fibrillation.
Also used against supraventricular tachycardias, atrial fibrillation

49

Torsades de Pointes in pt with sotalol produces what changes in the EKG?

long QT interval
prominent U wave d/t prolonged repolarization
post-ectopic pause

50

What do class 4 drugs do?

Ca channel blockers

51

Where to Ca channel blockers primarily block?

Acts primarily on slow response cells (SA & AV node), which are dependent on Ca++ influx for action potential depolarization

52

What are the major effects of Ca channel blockers on the heart?

Increase threshold for AP firing in nodal cells
 Increase nodal cell refractory period
 Depress conduction velocity in the SA and AV nodes

53

What are Ca channel blockers used to treat?

Paroxysmal supraventricular tachycardia

54

What are major side effects of Ca channel blockers?

--Negative chronotropic effect – decreases automaticity of SA node (bradycardia)
--Negative inotropic effect – decreases Ca++ influx during plateau phase of ventricular action potential
--Hypotension – decreases Ca++ influx into vascular smooth muscle cells

55

What Ca channel blockers should we know?

nifedipine
verapamil
diltizaem

56

Which Ca channel blocker has the side effect of peripheral edema?

nifedipine

57

Which Ca channel blocker especially has the side effect of constipation?

verapamil

58

Which Ca channel blocker has the side effect of interacts with digitalis to slow conduction velocity in the AV node causing heart block?

verapamil
diltizaem

59

Which Ca channel blocker has the side effect of increasing plasma levels of digitalis by competing for renal excretion?

verapamil
diltizaem

60

What is adenosine's MOA?

Very rapidly activates K+ channels to slow phase 4 depolarization at AV node (T1/2=10 seconds)
 Blocks cAMP-enhanced Ca2+ channel activity at the AV node

61

What should you use adenosine for?

Indicated for supraventricular tachycardia-slows AV conduction and heart rate

62

How does Digoxin work?

Enhances vagal parasympathetic activity to slow conduction at the AV node

63

What should you use digoxin for?

Indicated for atrial fibrillation and supraventricular tachycardia to control ventricular response rate