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PharmSci > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

0
Q

What beta receptor(s) does Propranolol block?

A

ß-1 and ß-2

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1
Q

What is the ULTRA-short acting beta blocker?

A

Esmolol

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2
Q

What drug is a non-selective β-AR antagonist; however, it is classified as a Class III agent due to its profound ability to prolong the action potential (Potassium channel blocker)?

A

Sotolol

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3
Q

What problems can occur because amiodarone blocks alpha-1 receptors?

A

decreased bp

increased risk of hypotension

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4
Q

What is the dosing of oral amiodarone?

A

1g/day (divided doses) over 2 weeks, then 200-400 mg/day

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6
Q

What is the dosing of IV amiodarone?

A

for the acute treatment of ventricular arrhythmias: give 150 mg IV bolus, followed by 1mg/min x 6 hours, then 0.5 mg/min x 18 hours, then typically followed by 200 mg/day oral starting dose

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7
Q

What class primarily affects myocytes and purkinje fibers?

A

Class I agents (Na+ channel blockers)

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8
Q

Class I agents are essentially “____________”

A

local anesthetics

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9
Q

In normal tissue, VGNC spend most of their time in their _________ state.
A. resting
B. inactive
C. active

A

A. resting

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10
Q

In arrhythmic tissue, VGNC spend most of their time in their _________ state.
A. resting
B. inactive
C. active

A

B & C (not resting very much)

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11
Q

What state(s) do Na+ channel blockers bind to?

A

Active and inactive (phase 0-3)

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12
Q

When do Na+ channel blockers dissociate from the channel?

A

when the channel enters the resting state

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13
Q

Class Ia Agents have a Tau-recovery time of:
A. 10 sec
B. 1-10 sec
C. <1 seconds

A

B. intermediate (1-10 sec)

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14
Q

Class Ib Agents have a Tau-recovery time of:
A. 10 sec
B. 1-10 sec
C. <1 seconds

A

C. rapid (< 1 sec)

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15
Q

Class Ic Agents have a Tau-recovery time of:
A. >10 sec
B. 1-10 sec
C. <1 seconds

A

D. delayed (> 10 sec)

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16
Q

What is Tau-recovery time?

A

Tau-recovery time: the time it takes for the drug to dissociate from the VGNC once the channel enters the resting state.

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17
Q

Tau-recovery time ________ relates to the magnitude in which agents in each subclass affect the slope of Phase 0 of the cardiac myocyte action potential (AP)
A. directly
B. indirectly

A

A. DIRECTLY

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18
Q

Since Class Ic agents take a longer time to come off the VGNC, if they bind to normal tissue (not desired, but can happen) the drug can be _________

A

“PRO-ARRHYTHROGENIC.”

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19
Q 
Which of the following are Class 1A agents?
A. Quinidine
B. Mexiletine
C. Disopyramide
D. Procainamide
A

A,C,D

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20
Q 
Which of the following are Class 1B agents?
A. Quinidine
B. Mexiletine
C. Lidocaine
D. Propafenone
A

B, C

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21
Q 
Which of the following are Class 1C agents?
A. Flecainide
B. Mexiletine
C. Lidocaine
D. Propafenone
A

A,D

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22
Q

Which class IA agent has class I and III action?

A

Quinidine

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23
Q

Which class IA agent can reduce digoxin clearance by 50%?

A

Quinidine

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24
Q

What are the adverse effects of Quinidine?

A

GI (30-50%) mostly diarrhea
Cinchonism*
Antimuscarinic effects
hypotension

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25
Q

What is Cinchonism?

A

headaches, dizziness, ringing in ears

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26
Q 
Which class IB agent binds to α-1 acid
Glycoprotein and why is this important to know?
A

Lidocaine

Alpha-1 acid glycoprotein is elevated during stress or injury such as MI, post-MI or post-op (“acute phase protein”)
So, Free fraction of lidocaine may change during the course of therapy as the pt transitions from post-acute MI to a more stable condition.

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27
Q

Lidocaine is a very effective Na+ channel blocker, so why do we not use it for prophylaxis?

A

evidence now shows this increases mortality

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28
Q

When is Lidocaine used?

A

It is very effective at STOPPING Ventricular tachycardia (V-tach) in the acute post-MI setting

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29
Q

What does Mexiletine usually treat?

A

peripheral neuropathies

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30
Q

What are the 2 Class IC agents?

A

Flecainide, Propafenone

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31
Q

Flecainide and Propafenone are both metabolized by _____.

A

CYP2D6

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32
Q

ADRs of Flecainide?

A 
Blurred vision
Dizziness
Edema
Abdominal pain
Constipation
Headache
nausea & vomiting (10%)
mild negative chronotropic effect  (may exacerbate CHF)
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33
Q

ADRs of Propafenone?

A 
Mild→moderate negative inotropic effect
Rare cases of elevated liver enzymes
Common GI:
N/V
Constipation
Anorexia
Diarrhea
xerostomia
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34
Q

What do you monitor in Flecainide?

A

trough monitoring

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35
Q

Contraindications with Flecainide?

A

Flecainide + Dofetilide (b/c of risk of developing pro-arrhythmias)

Flecainide + Dronedarone (b/c dronedarone is a 2D6 inhibitor)

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36
Q

Contraindications/Drug interactions with Proparenone?

A

CI: Propafenone + Dofetilide

CI: patients with acute bronchospasm or asthma (BB activity)

Interact with CYP2D6 inhibitors (Dronedarone, some SSRIs, delavirdine)

May also interact with CYP1A2 & 3A4

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37
Q

Tobacco smoke may ________ hepatic metabolism of Flecainide

A

increase

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38
Q

Clearance of flecainide is _________ in pts with renal/hepatic insufficiency

A

decreased

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39
Q

Which Class I agent can increase warfarin plasma levels?

A

Propafenone

40
Q

Is Propafenone protein bound?

A

Yes, 85-97% protein bound (primarily to alpha-1 acid glycoprotein)

41
Q

What CYP enzyme is Propafenone a substrate and inhibitor of?

A

CYP2D6 substrate and inhibitor (possibly)

42
Q

Which Class IC agent has weak BB activity?

A

Propafenone

43
Q

How are BB useful in treating arrhythmias?

A

Suppress SA nodal depolarization & AV nodal conduction which is useful in treating AF (atrial fibrillation)

44
Q

________ are effective at preventing & treating catecholamine-induced arrhythmias (SNS-induced arrhythmias) (ex. Pheochromocytoma)

A

BB

45
Q

What is a pheochromocytoma?

A

Pheochromocytoma: catecholamine secreting tumor in adrenal medulla

46
Q

Use BB with caution in patients with:

A

asthma/COPD or diabetes

47
Q

Which BB treats rapid, short-term control of supraventricular arrhythmias (ex. Sinus tachycardia, AF)?

A

esmolol

48
Q

What BB treats essential tremor?

A

Propranolol

49
Q

What BB has Membrane-stabilizing activity (local anesthetic action) may block Na+ channels in myocardial tissue (some class I properties)

A

Propranolol

50
Q

Which agents can prolong the QT interval?

A

Class III agents

51
Q

What is Torsades de Pointes?

A

Torsades de Pointes:“twisting of the points” is a condition that occurs when K+ channels are blocked and is deadly.

52
Q

Some class ___ agents may actually increase inward current (Ca2+ & Na+) to make the AP ore positive for a longer period of time. This causes delayed repolarization and therefore prolonged AP duration

A

class III agents

53
Q

Name 5 Class III agents:

A
  1. AMIODARONE
  2. Dronedarone
  3. Sotolol
  4. Ibutilide
  5. Dofetilide
54
Q

What is the prototypical Class III agent?

A

AMIODARONE

55
Q

What is the analog of amiodarone

iodine groups are removed & methane-sufanomyl group is added → much less TH AEs

A

Dronedarone

56
Q

What is the MOA of amiodarone?

A
  1. K+ channel blocker
  2. Na+ channel blocker
  3. ß-AR antagonist (BB)
  4. CCB
  5. Inhibition of cell-cell coupling (affects gap junctions)
  6. TH & receptor effects (usually w/ chronic use)
    * has class I, II, III, & IV properties
57
Q

What does amiodarone treat?

A

wide variety of arrhythmias

58
Q

What is the half life of amiodarone?

A

Complex half-life
Rapid: 3-10 days
Slower: 50 days

59
Q

Is amiodarone lipophilic or hydrophilic?

A

Highly lipophilic (Accumulates in tissues)

60
Q

How is amiodarone metabolized?

A

CYP3A4

61
Q

What does amiodarone inhibit?

A

Pgp &CYP2C9 (increase warfarin plasma conc.)

62
Q

ADRs of amiodarone?

A

Pulmonary Fibrosis
Thyroid Dysfunction
Corneal Deposits
Photodermatitis

63
Q

How long will elimination of amiodarone take once D’C?

A

MONTHS

64
Q

Which class III agent is a derivative of TH?

A

amiodarone

65
Q

Is dronedarone protein bound?

A

Yes 98% to albumin

66
Q

In which Class III agent, does BA increase with high fat meals?

A

Dronedarone

67
Q

Explain the PK properties of dronedarone with races and genders.

A

Pts > 65 YO have a 23% greater exposure to dronedarone
Females have a 30% greater exposure than males
Japanese males have a 2-fold higher exposure than Caucasian males

68
Q

When do you take dronedarone?

A

BID in morning and evening with meals

69
Q

Metabolism of dronedarone?

A

Metabolized by and inhibitor of CYP2D6 & 3A4

70
Q

ADRs of dronedarone?

A

N/V, diarrhea
May worsen HF
Skin & soft tissue rxns (rash, pruritus, eczema, atopic dermatitis)

71
Q

Can you take dronedarone while pregnant?

A

NO, pregnancy category X

72
Q

CI to dronedarone?

A

severe hepatic impairment

pregnancy

73
Q

What type of BB is stool?

A

non-selective (binds to ß-1 and ß-2)

74
Q

What drug has class II and III effects because it is a significant K+ blocker and prolongs QT interval?

A

Sotolol

75
Q

How is sotolol eliminated?

A

Eliminated almost 100% by kidneys

76
Q

ADRs of sotolol?

A

increased risk of TdP (b/c of QT prolongation)

generally well tolerated

77
Q

What class of agents Affect phase 2 of the cardiac myocyte AP (decreases Ca2+ entry & FOC) →negative inotropic effect (avoid in HF)

A

Class IV (CCBs)

78
Q

What are Class IV (CCB) Agents most useful in treating?

A

AF rate

79
Q

Use Class IV agents with caution in pts with:

A

Use with extreme CAUTION in pts with systolic HF because they decrease contractility (negative inotropes)

80
Q

What class of agents may cause peripheral VD by inhibiting VSM contraction to some extent?

A

Class IV Agents (CCBs)

81
Q

What effect might peripheral vasodilation have reflexively on the SA node?

A

Reflex tachycardia when SA node has reflex activation (negates drug action)

82
Q

What are non-DHP CCBs effective at doing?

A

significantly affect nodal tissues.

they may also be effective in calcium-dependent EADs in damaged myocardial tissues.

83
Q

ADRs of non-DHP CCBs?

A
  • Constipation (verapamil)
  • Peripheral edema (more so with DHP’s/diltiazem)

  • Gingival hyperplasia → swollen gums (verapamil/diltiazem)
  • Flushing/headache/hypotension (diltiazem)
84
Q

What are 3 agents that treat arrhythmias that are “non-classified” agents?

A
  1. Adenosine
  2. Digoxin
  3. Magnesium
85
Q

What drug can induce complete, but transient AV nodal block?

A

Adenosine

86
Q

What is the ADR of Adenosine?

A

“ sense of impending DOOM”

87
Q

How is Adenosine administered?

A

IV push only

88
Q

What is the half-life of adenosine?

A

10 seconds

89
Q

How fast must the IV push be given for adenosine?

A

within 3 seconds

90
Q

What are 2 drugs that can decreases the effect of adenosine?

A

theophylline, caffeine

91
Q 
What drug:
• inhibits Na/K ATPase membrane pump
• increases intracellular calcium
• shortens the action potential duration
• increases vagal activity?
A

Digoxin

92
Q

What is the main pharmacological property of Digoxin in treating arrhythmias?

A

its ability to decrease AV nodal conduction (Vagal-like effect) → mimics PNS

93
Q

digoxin will affect the conduction system similarly to what is seen when the PNS is activated; these tissues are primarily the ___________.

A

SA and AV nodes

94
Q

Why is Digoxin favored over Class II and Class IV agents in treating patients with supraventricular arrhythmias who also have heart failure?

A

Digoxin slows SA and AV nodes and treats HF as well because it has neg. inotropic effect.

95
Q

Study magnesium in notes

A

. . .

PharmSci (12 decks)

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