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Kaplan Pharm: Cardiac and Renal > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

Strategy when thinking of tachycardias?

A

Divide into:

ventricular
supraventricular tachycardias

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2
Q

What would be a target of ventricular tachycardias?

A

Na+ channels to block ventricular depolarization

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3
Q

Na+ channel blockers have what effects on ECG?

A

prolong the QRS interval

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4
Q

Class I drugs have what major action?

A

block Na+ channels

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4
Q

K+ channel blockers have what effect on ECG?

A

They prolong QT intervals

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5
Q

Class 1 drugs have what major MOA?

A

They block Na+ channels

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6
Q

What are the different classes of Class I antiarrythmics based on? Explain

A

their ability to dissociate from Na+ channels?

1a intermediate
1b least effect on phase 0
1c greatest phase 0 depression; therefore prolongs QRS the most

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7
Q

What causes phase 1 of fast response fibers?

A

Na+ channels inactivated

Some His Purkinje cells transient outward K+ currents with inward Cl- currents contribute to notch and overshoot

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8
Q

What are the causes of phase 2 in fast response fibers?

A

plateau phase in which a slow influx of Ca2+ (Ica-L) is balanced by late appearing outward K+ current (the delayed rectifier current Ik)

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9
Q

Are there any major antiarrythmic effects of drugs on phase 1 or 2 of fast response fibers?

A

no

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9
Q

What ion channels are responsible for phase 3 in fast response fibers?

A

repolarization phase in which the delayed rectifier K+ current rapidly increases as the Ca2+ current dies out because of time-dependent channel inactivation

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10
Q

Which class of anti-arrhythmic drugs slows the re-polarization phase?

A

class III

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11
Q

What are the phase 4 resting potential of the fast muscle fibers maintained by?

A

activity of the Na+/K+ ATPase

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12
Q

Capacity of a fast muscle fiber to depolarize is associated with what?

A

number of Na+ channels in ready state

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13
Q

The more negative the RMP in fast muscle fibers the faster or slower the response?

A

faster the response

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14
Q

What are the 3 major determinant of conduction velocity?

A
  1. Rate of phase 0 depolarization - as Vmax decreases, conduction velocity decreases and vice versa.
  2. Threshold potential- the less negative, the slower the conduction velocity
  3. The resting potential - the more negative the RP, the faster the conduction
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15
Q

What types of drugs are good for SVTs?

A

Those that target the slow response fibers

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16
Q

What is spontaneous depolarization phase 4 is caused by what?

A

not completely understood

composite of inward Na+ (If) and Ca2+ (Ica-t) currents and outward K+ currents (Ik)

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17
Q

Depolarization of slow fibers depends on what channels?

A

on activation of Ca2+ channels (Ica-L and Ica-t)

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18
Q

Which class of antiarrhythmics can slow or block phase 0 in slow response fibers?

A

class IV

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19
Q

During repolarization of slow response fibers Ca2+ currents are opposed and overcome by what?

A

delayed rectifier K+ current

phase 3

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20
Q

Which class of anti-arrythmics can slow down phases 4 in pacemaker fibers?

A

Class II and IV

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21
Q

What are class II antiarrhythmics?

A

B blockers

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22
Q

What are class IV anti-arrythmics?

A

CCBs

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23
Q

What is refractoriness?

A

the inability to respond to stimulus

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24
Q

What is ERP?

A

ERP effective refractory period
when no stimulus can elicit a response

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25
Q

How long does ERP last?

A

lasts into late stage 3 of AP because Na+ channels are effectively inactivated and not into the ready state

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26
Q

How do K+ channel blocker affect ERP?

A

they prolong ERP

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27
Q

What are RRPs? What is the purpose?

A

relative refractory period

when a strong stimulus can elicit a response but the timing will be out of sync with rest of heart and arrhythmias may occur

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28
Q

Ratio of ERP to APD is a measure of what?

A

refractoriness

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29
Q

What may decreases in ERP cause?

A

formation and propagation of premature impulses

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30
Q

At what V does M gate typically close?

A

-50 mV

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31
Q

At approx. what voltage does h gate open?

A

-85mV

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32
Q

Do K+ blockers prolong APD?

A

yes

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33
Q

What are the 3 conformations of sodium channels?

A

resting or ready state, M gate closed h open
open active state M gate open h open
inactive or refractory state M gate open h closed

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34
Q

Why is rate of recovery slower in ischemic tissue?

A

because cells partly depolarized at rest

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35
Q

What is the MOA of Class 1A anti-arrythmics?

A

Na+ channel blocker (tend to target open state more than inactivated state sodium channels)
Block K+ channels

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36
Q

What are the effects of APD and ERP in Class 1A drugs?

A

increases APD and ERP

37
Q

What are the prototype Class 1A drugs?

A

Quinidine
Procainamide
Dysopyridine

38
Q

What are the prototype Class 1B drugs?

A

lidocaine

39
Q

What are the prototype Class 1C drugs?

A

Flecainide
Propafenone

40
Q

What is the mnemonic to remember Class 1A, 1B, 1C drugs?

A

Double Quarter Pounder with Lettuce and Fries Please

dysopyridine
quinidine
procainamide
lidocaine
flecainide
propafenone

41
Q

What are some properties of the drug quinidine that could give rise to specific S/E of the drug?

A

causes muscarinic receptor block: increases HR and AV conduction
causes Alpha block: causes vasodilation and reflex tachycardia

42
Q

Because Quinidine is a weak base what are some drugs you can take that would increase it’s absorption in the body?

A

increased absorption with antacids

43
Q

What are the A/E of quinidine?

A
  • cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation)
  • hypotension
  • prolongation of QRS and QT interval associated with syncope (torsade)
44
Q

What drugs can cause torsade from classes of anti-arrythmics?

A

K+ channel blockers

45
Q

Compared to quinidine, does procainamide have more or less autonomic side effects?

A

has fewer

46
Q

Why is it important to remember metabolization of procainamide?

A

because it can cause SLE in slow acetylators

47
Q

Special MOA of procainamide to remember.

A

The parent drug procainamide blocks the Na+ channels while the metabolite NAPA N acetyl procainamide blocks K+ channels

48
Q

A/E of Procainamide?

A

drug induced SLE

hematotoxicity (thrombocytopenia, agranulocytosis)

CV effects (torsade)

49
Q

Class 1B anti-arrythmics MOA.

A

target inactivated Na+ channels

50
Q

How do Class 1B anti-arrythmics affect APD?

A

decrease APD due to block of sodium window currents

51
Q

Main benefit of Class 1B drugs?

A

they increase diastole and extend time for recovery

basically takes longer to reach the next AP prolonging phase 4 RMP

52
Q

Indications for lidocaine?

A

acute treatment not prophylactic because has short half-life

post MI, open-heart surgery, digoxin toxicity-ventricular arrhythmias only

53
Q

Indications for Mexiletine?

A

can take it orally and has higher bioavailability than lidocaine so can use for more chronic management

54
Q

Why must lidocaine be given via IV?

A

because of first pass metabolism giving it short half life.

55
Q

Describe effect of Class 1C drugs on APD?

A

no effect on APD

56
Q

Do Class 1C drugs affect the ANS?

A

no

57
Q

What is the MOA of Class 1C drugs?

A

block fast Na+ channels (Ina) especially in His Purkinje

58
Q

What is the major drug to remember for Class 1C?

A

Flecainide

59
Q

Why is there limited use of Flecainide?

A

limited utility proarrythmogenic effects, leading to inc. sudden death post- MI and when used prophylactically in VT

60
Q

Indications for Flecainide?

A

used for paroxysmal A fib rhythm control, paroxysmal SVTs, sustained ventricular tachycardia

61
Q

MOA of Class II anti-arrythmics.

A

Beta blockers

62
Q

Name the nonselective and cardioselective B-blocking agents typically used as antiarrythmics.

A

nonselective: propranolol
cardioselective: acebutolol and esmolol

63
Q

Why can’t esmolol be used prophylactically?

A

very short half life used in acute cases only

64
Q

What is the ROA for esmolol?

A

IV only

65
Q

Indications for Class II anti-arrythmics?

A

prophylaxis post-MI and SVTs
Esmolol for acute SVTs

66
Q

Class III drugs MOA?

A

K+ channel blockers

67
Q

What is the effect of the Class II drugs on APD and ERP?

A

inc. APD and ERP esp Purkinje ventricular fibers

68
Q

What are the 2 most effective anti-arrythmics that are also in Class III anti-arrhythmic class?

A

amiodarone and dronedarone

69
Q

Amiodarone and dronedarone mimic what other anti-arrhythmic classes of drug?

A

All of them

70
Q

What is the 1/2 life of amiodarone?

A

about 80 days

71
Q

1/2 life of Dronedarone?

A

about 24 hours

72
Q

Describe Vd in both Dronedarone and amiodarone?

A

High Vd

73
Q

S/E of Dronedarone and amiodarone?

A
  • interstitial pneumonitis and pulmonary fibrosis
  • phototoxicity (so look for rash on face necks sun exposed areas)
  • corneal deposits
  • hepatic necrosis

*iodine related S/Es (only amiodarone) blue skin pigmentation and thyroid dysfunction (could be hypo or hyper)

74
Q

What tests should be run when giving a person amidoarone or dronedarone?

A

PFTs
LFTs
eye exams

TFT in case of amiodarone because dronedarone doesn’t contain iodine

75
Q

Do the drugs amiodarone and dronedarone cause torsade?

A

could but not as likely as many of other K+ blocking agents

76
Q

What is the rule for drugs likely to cause torsade?

A

all class III and drugs more selective for K+ more highly likely

77
Q

What drugs are at highest risk for causing torsade in the class III category?

A

Ibutilide and Dofetilide

78
Q

What are some drugs to avoid when someone has long QT syndrome?

A
  • K+ blocking drugs (Class 1A and III)
  • antipsychotics (thioridazine)
  • TCAs
79
Q

What are some treatments for torsades that you need to remember?

A
  • correct hypokalemia
  • use Mg2+
  • correct hypomagnesemia
  • discontinue drugs that prolong QT interval
80
Q

What effect do Class IV anti-arrythmics have on ECG?

A

prolong PR interval

81
Q

What are the CCBs we used for anti-arrhythmic drugs?

A

verapamil
diltiazem

82
Q

Why can’t we use dyhydropyridines in the treatment of anti-arrythmics?

A

they are more selective for vasodilation of vascular smooth muscles and therefore could cause reflex tachy

83
Q

What are the indications of CCBs?

A

SVTs

84
Q

S/E for CCBs?

A

verapamil (constipation)
dizziness (vasodilator to some extent)
flushing
AV block
hypotension

85
Q

What are some drug interactions to remember when taking CCBs?

A
  • Digoxin and B blockers can cause additive AV block
  • verapamil can displace digoxin > toxicity
86
Q

How is adenosine used as anti-arrhythmic? (Meaning receptor type and target activity)

A

its found in nodes of heart and is Gi coupled therefore dec. cAMP > dec. SA and AV node activity

87
Q

Use of adenosine?

A

DOC for paroxysmal SVT and AV nodal arrythmias

88
Q

Describe t1/2 of adenosine?

A

short

89
Q

S/E adenosine?

A

flushing, sedation, dyspnea

90
Q

What is adenosine antagonized by? Why?

A

methylxanthines (theophylline and caffeine) because they inc. cAMP

91
Q

Can Digoxin be an antiarrythmic?

A

yes

92
Q

What are the goals in management of atrial fibrillation?

A
  1. ventricular rate control with beta blockers, CCBs, or digoxin
  2. anticoagulation

Kaplan Pharm: Cardiac and Renal (6 decks)

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