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Cardiology > Drugs-Cardiac Rhythm > Flashcards

Drugs-Cardiac Rhythm Flashcards

1
Q

Class I drugs

A

Local anesthetics

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2
Q

Class II drugs

A

Beta blockers

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3
Q

Class III drugs

A

Class III

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4
Q

Class IV drugs

A

Ca Channel Blockers

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5
Q

What channels does class IA block

A

Na

K

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6
Q

What is a class IA drug?

A

Procainamide

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7
Q

What kinds of tissues do class I drugs work on?

A

Fast tissues

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8
Q

What do class IA drugs do to AP duration?

A

Increase

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9
Q

What do class IA drugs do to resting potential?

A

Increase

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10
Q

What do class IA drugs do to excitability?

A

Decrease

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11
Q

What channels does class IB block?

A

Na

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12
Q

What is a class IB drug?

A

Lidocaine

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13
Q

What does class IB do to excitability

A

Decrease, esp in depolarized tissue

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14
Q

What channels does IC block?

A

Na

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15
Q

What is an example of IC drug?

A

Flecainide

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16
Q

What does class IC do to excitability?

A

Decrase

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17
Q

What does class IC do to ERP?

A

Increase in fast tissue

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18
Q

What is an example of a class II drug?

A

Atenolol

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19
Q

What channel is affected by atenolol?

A

Ca2+

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20
Q

What kind of tissues do class II drugs work on?

A

Slow response tissue

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21
Q

What does atenolol do to sinus rate?

A

Decrease

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22
Q

What does atenolol do to AV node ERP?

A

Increase

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23
Q

What does atenolol do to AV node excitation?

A

Decreases

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24
Q

When are class I drugs most potent?

A

In cells with depolarized resting membrane potential (this determines sodium blocking effect–>recover with repolarization).

More potent at faster HR because there is less time to repolarize and knock off the drug

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25
Q

Rank class I drugs from most potent to least

A

IC–>IA–>IB (least potent)

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26
Q

What factors increase the effect of Ik blockade on action potential duration?

A
  • Slow HRs

- Low extracellular K+ or Mg

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27
Q

What channels does class III drugs block?

A

Delayed rectifier K+

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28
Q

What is an example of a class III drug?

A

Dofetilide

29
Q

What kinds of tissues do class III drugs work on?

A

Fast tissues

30
Q

What do class III drugs do to the ERP?

A

Increase in fast tissue

31
Q

What kind of tissue does class III drugs work on?

A

Fast tissue

32
Q

What do class III drugs do to the AP duration?

A

Increase

33
Q

What channels do class IV drugs work on?

A

block Ca2+ channels

34
Q

What types of tissues do class IV drugs work on?

A

Slow response

35
Q

What is an example of a class IV drug?

A

Verapamil

36
Q

What does verapamil do to the sinus rate

A

dec

37
Q

What does verapamil do to the AV node ERP?

A

Increase

38
Q

What does verapamil do to the AV node excitability?

A

Dec

39
Q

What is digoxin?

A

Blocks Na/K pump, muscarinic receptor agonist, so it increases vagal tone

40
Q

What does digoxin do to the Ca current?

A

Dec

41
Q

What does digoxin do to the KAch current?

A

Increases

42
Q

What are the consequences of digoxin’s KAch current actions?

A

hyperpolarization of AV and SA nodes

43
Q

What does digoxin do to the sinus rate?

A

dec

44
Q

What does digoxin do to the AVnode ERP?

A

increase

45
Q

What does digoxin do to the AVN excitability

A

dec

46
Q

What is adenosine?

A

Adenosine or purinergic receptor agonist

47
Q

What channels does adenosine work on?

A

Dec Ca current and increases KAch current

48
Q

What types of tissue does adenosine and digoxin work on?

A

Slow response

49
Q

Which classes of drugs work on fast response tissue?

A

II and IV

50
Q

Which classes of drugs work on slow response tissue?

A

I and III (directly on Ca channels), digoxin and adenosine (work by enhancing parasympathetic/reduction of sympathetic stimulation)

51
Q

Which drug has a positive inotropic effect?

A

Digoxin (all others have negative ionotropic effects)

52
Q

Which drug is IV only?

A

Adenosine

53
Q

Is digoxin slow or fast acting?

A

Slow

54
Q

Which arrhythmias involve fast tissue?

A
  • Ventricular tachycardia
  • A fib
  • Some AV reentry
55
Q

Which arrhythmias involve slow tissue?

A
  • Av reentry
  • AV nodal reentry
  • Sinus tachycardia
56
Q

What do we use class I drugs for?

A

Ventricular tachy, a fib, some AV reentry

57
Q

What do we use class II drugs for?

A

AV reentry, AVN reentry

58
Q

What do we use class III drugs for?

A

Vent tachy, a feb, AV reentry

59
Q

What do we use class IV drugs for?

A

AVN reentry

60
Q

What do we use digoxin for?

A

AVN reentry

61
Q

What do we use adenosine for?

A

AVN reentry

62
Q

What is an excitable gap?

A

Amount of time tissue is excitable (ie if it’s long, it has recovered and can form an AP)

63
Q

What is a low safety factor?

A

Does not require much stimulation to cause an AP

64
Q

What are 2 ways to cause block in a fast response re entrant circuit?

A
  1. Prolong ERP to cause refractory block

2. Depress excitability to cause fixed block

65
Q

What drugs do we use for AV re entrant tachy?

A

IA, III (block bypass tract by prolonging ERP)

Adenosine, atenolol, digoxin (prolong AV refractory)

66
Q

How do we know if we blocked re entrant or AV node?

A

On EKG, the p wave associated with the last QRS will be before the QRS if blocked re entrant and after if blocked AVnode

(this makes sense! with reentry here, the impulse goes down the AV node and up the accessory pathway. If you block the AV node, the P wave will be after the accessory pathway up from the ventricles, if you block the accessory, the P wave comes before the ventricles contract)

67
Q

Post Mi, what ERP and safety factors do the dead tissues have?

A

Longer ERPs and lower safety factors

68
Q

What kinds of drugs do we want to use for ventricular tachycardia post MI?

A 
Decrease excitability (procainamide or flecainide)
Prolong ERP (1A, III)

Cardiology (16 decks)

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