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CV Quiz 2 > Anti-arrhythmic Drugs > Flashcards

Anti-arrhythmic Drugs Flashcards

1
Q

Where are fast response cells in the heart?

A

atria, ventricle, his-purkinje

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2
Q

Where are slow response cells in the heart?

A

SA and AV nodes

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3
Q

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

A

Na

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4
Q

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

A

Ca

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5
Q

What class inhibits depolarization of fast cells?

A

class 1 sodium channel blockers

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6
Q

What class inhibits depolarization of slow cells?

A

class 4 calcium-entry blockers

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7
Q

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

A
  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
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8
Q

What are the 3 main mechanisms of arrhythmias?

A
  • Increased automaticity (inappropriately excitable cells)
  • Triggered automaticity (normal action potential is interrupted or followed by an abnormal)
  • Reentry (abnormal impulse conduction)
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9
Q

What is early afterdepolarization (EAD)?

A

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

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10
Q

What is delayed or late afterdepolarization (DAD)?

A

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

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11
Q

What can trigger DAD?

A

Digitalis toxicity, catecholamines (NE, EPI) and ischemia

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12
Q

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

A

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

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13
Q

What are the 4 classes of anti-arrhythmic drugs?

A

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

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14
Q

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

A

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

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15
Q

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

A

Class 1: Na channel blockers

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16
Q

Class 1A drug?

A

Quinidine

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17
Q

Direct effects of quinidine?

A

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

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18
Q

Indirect effects of quinidine?

A

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

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19
Q

Use of quinidine?

A
  • Atrial flutter or fibrillation

- Prevent ventricular tachycardia and fibrillation

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20
Q

Major side effects of quinidine?

A

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

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21
Q

Is quinidine okay for pt with renal failure?

A

Yes, metabolized in liver.

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22
Q

Class 1B drug?

A

Lidocaine

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23
Q

Direct effects of lidocaine?

A
  • Increase AP threshold
  • Increased Block of Na+ channels ( Vmax) at high HR and in depolarized cells
  • decreased AP duration and ERP
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24
Q

Side effects of lidocaine?

A

dizziness & seizures

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25
Q

What is lidocaine used for?

A

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

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26
Q

What is a class 1C drug?

A

Flecainide

27
Q

What are the direct effects of flecainide?

A 
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
Q

Side effects of flecainide?

A

pro-arrhythmic

29
Q

What is flecainide used for?

A

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

30
Q

What kind of drugs are class 2?

A

beta-blockers

31
Q

How do beta-blockers work?

A

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

32
Q

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

A

slow the rate of diastolic (phase 4) depolarization.

33
Q

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

A

propranolol and esmolol

34
Q

What is the difference between propranolol and esmolol?

A

Propranolol – Long acting blocker (oral)

Esmolol – Short acting blocker (IV)

35
Q

What are beta-blockers used for?

A

Used for all atrial arrhythmias, ventricular tachycardia and fibrillation

36
Q

Are beta-blockers safe?

A

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

37
Q

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

A

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

38
Q

What are the major side effects of beta-blockers?

A

negative inotropic effect, heart block, bradycardia and bronchospasm

39
Q

In general, what kind of drugs are class 3?

A

K channel blockers

40
Q

What are the common effects of K channel blockers?

A

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

41
Q

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

A

Amiodarone & sotalol

42
Q

Which K channel do most blocker drugs target?

A

most common target is IKr (hERG channel)

43
Q

Amiodarone has multiple mechanisms of action. What are they?

A

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

44
Q

What is amiodarone used for?

A

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

45
Q

What are the major side effects of amiodarone?

A

 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
Q

What is sotalol’s MOA?

A

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

47
Q

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

A

triggered arrhythmias with Torsades de Pointes.

48
Q

What is sotalol used for?

A

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

49
Q

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

A

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

50
Q

What do class 4 drugs do?

A

Ca channel blockers

51
Q

Where to Ca channel blockers primarily block?

A

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

52
Q

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

A

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

53
Q

What are Ca channel blockers used to treat?

A

Paroxysmal supraventricular tachycardia

54
Q

What are major side effects of Ca channel blockers?

A
  • -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
Q

What Ca channel blockers should we know?

A

nifedipine
verapamil
diltizaem

56
Q

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

A

nifedipine

57
Q

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

A

verapamil

58
Q

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

A

verapamil

diltizaem

59
Q

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

A

verapamil

diltizaem

60
Q

What is adenosine’s MOA?

A

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
Q

What should you use adenosine for?

A

Indicated for supraventricular tachycardia-slows AV conduction and heart rate

62
Q

How does Digoxin work?

A

Enhances vagal parasympathetic activity to slow conduction at the AV node

63
Q

What should you use digoxin for?

A

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

CV Quiz 2 (16 decks)

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