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Flashcards in Drugs-Cardiac Rhythm Deck (68):
1

Class I drugs

Local anesthetics

2

Class II drugs

Beta blockers

3

Class III drugs

Class III

4

Class IV drugs

Ca Channel Blockers

5

What channels does class IA block

Na
K

6

What is a class IA drug?

Procainamide

7

What kinds of tissues do class I drugs work on?

Fast tissues

8

What do class IA drugs do to AP duration?

Increase

9

What do class IA drugs do to resting potential?

Increase

10

What do class IA drugs do to excitability?

Decrease

11

What channels does class IB block?

Na

12

What is a class IB drug?

Lidocaine

13

What does class IB do to excitability

Decrease, esp in depolarized tissue

14

What channels does IC block?

Na

15

What is an example of IC drug?

Flecainide

16

What does class IC do to excitability?

Decrase

17

What does class IC do to ERP?

Increase in fast tissue

18

What is an example of a class II drug?

Atenolol

19

What channel is affected by atenolol?

Ca2+

20

What kind of tissues do class II drugs work on?

Slow response tissue

21

What does atenolol do to sinus rate?

Decrease

22

What does atenolol do to AV node ERP?

Increase

23

What does atenolol do to AV node excitation?

Decreases

24

When are class I drugs most potent?

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

25

Rank class I drugs from most potent to least

IC-->IA-->IB (least potent)

26

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

-Slow HRs
-Low extracellular K+ or Mg

27

What channels does class III drugs block?

Delayed rectifier K+

28

What is an example of a class III drug?

Dofetilide

29

What kinds of tissues do class III drugs work on?

Fast tissues

30

What do class III drugs do to the ERP?

Increase in fast tissue

31

What kind of tissue does class III drugs work on?

Fast tissue

32

What do class III drugs do to the AP duration?

Increase

33

What channels do class IV drugs work on?

block Ca2+ channels

34

What types of tissues do class IV drugs work on?

Slow response

35

What is an example of a class IV drug?

Verapamil

36

What does verapamil do to the sinus rate

dec

37

What does verapamil do to the AV node ERP?

Increase

38

What does verapamil do to the AV node excitability?

Dec

39

What is digoxin?

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

40

What does digoxin do to the Ca current?

Dec

41

What does digoxin do to the KAch current?

Increases

42

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

hyperpolarization of AV and SA nodes

43

What does digoxin do to the sinus rate?

dec

44

What does digoxin do to the AVnode ERP?

increase

45

What does digoxin do to the AVN excitability

dec

46

What is adenosine?

Adenosine or purinergic receptor agonist

47

What channels does adenosine work on?

Dec Ca current and increases KAch current

48

What types of tissue does adenosine and digoxin work on?

Slow response

49

Which classes of drugs work on fast response tissue?

II and IV

50

Which classes of drugs work on slow response tissue?

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

51

Which drug has a positive inotropic effect?

Digoxin (all others have negative ionotropic effects)

52

Which drug is IV only?

Adenosine

53

Is digoxin slow or fast acting?

Slow

54

Which arrhythmias involve fast tissue?

-Ventricular tachycardia
-A fib
-Some AV reentry

55

Which arrhythmias involve slow tissue?

-Av reentry
-AV nodal reentry
-Sinus tachycardia

56

What do we use class I drugs for?

Ventricular tachy, a fib, some AV reentry

57

What do we use class II drugs for?

AV reentry, AVN reentry

58

What do we use class III drugs for?

Vent tachy, a feb, AV reentry

59

What do we use class IV drugs for?

AVN reentry

60

What do we use digoxin for?

AVN reentry

61

What do we use adenosine for?

AVN reentry

62

What is an excitable gap?

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

63

What is a low safety factor?

Does not require much stimulation to cause an AP

64

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

1. Prolong ERP to cause refractory block
2. Depress excitability to cause fixed block

65

What drugs do we use for AV re entrant tachy?

IA, III (block bypass tract by prolonging ERP)
Adenosine, atenolol, digoxin (prolong AV refractory)

66

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

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

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

Longer ERPs and lower safety factors

68

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

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