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Pharm Exam 2 > Topic 11 > Flashcards

Topic 11 Flashcards

1
Q

Arrhythmia Definition

A 
Abnormalities in the electrical impulse
generation or conduction through the
heart.
...too slow, too fast, irregular, wrong direction,
wrong origin, etc
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2
Q

___% of anesthetized patients have arrhythmias

A

> 50%

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3
Q

___% of patients with MIs have arrhythmias

A

80%

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4
Q

___% of patients on CPB will be affected with arrhythmias!

A

100%

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5
Q

Virtually all antiarrhythmics work by altering the

A

ionic transmembrane balance (Na⁺,Ca⁺⁺, K⁺) or the sympathetic tone to the heart. …which alters the shape of this graph!

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6
Q

4 Classes of antiarrhythmics

The Vaughan Williams Classification

A

Na+ channel blocker
B-Adrenoreceptor blocker
K+ channel blocker
Ca++ channel blocker

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7
Q

Class I : Na⁺ Channel Blockers: Preferentially bind to

A

open Na⁺ channels rather than to fully repolarized Na⁺ channels.

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8
Q

Class I (Na+ Channel Blockers) drugs preferentially block

A

conduction in tissues that are depolarizing more frequently. This is called “use-dependence” blockade.

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9
Q

Class I : Na⁺ Channel Blockers: Ia=

A

Shorten the action potential and affect QRS complexes

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10
Q

Class I : Na⁺ Channel Blockers: Ib=

A

Shorten the action potential without affecting QRS

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11
Q

Class I : Na⁺ Channel Blockers: Ic=

A

Do not shorten the action potential

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12
Q

Class Ia: Na⁺ Channel Blockers: Shift the action potential (AP) to the

A

right by slowing Phase 0 depolarization (hence their

nickname, “membrane stabilizers”).

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13
Q

Class Ia: Na⁺ Channel Blockers: inhibit some

A

K⁺ channels (Class III activity) which widens the AP causing prolonged QT intervals.

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14
Q

Class Ia: Na⁺ Channel Blockers: Drug names

“Double Quarter Pounder”

A

Disopyramide (Norpace)
Quinidine (Quinidex)
Procainamide (Pronestyl, Procan)

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15
Q

Disopyramide

A

(Norpace)

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16
Q

Quinidine

A

(Quinidex)

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17
Q

Procainamide

A

(Pronestyl, Procan)

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18
Q

Quinidine is given ____ and used for_____

A

Orally

various tachyarrhythmias

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19
Q

Quinidine: Rarely used because of

A

toxic side effects

  • Cinchonism
  • Torsades de pointes
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20
Q

Torsades de pointes=

A

“Polymorphic Ventricular Tachycardia”
•Usually resolves spontaneously
•May devolve into V-fib

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21
Q

Disopyramide: Like Quinidine, but more

A

negative inotropic effects and increased SVR

-Dont use on a sick heart- might precipitate HF!

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22
Q

Most widely used Ia

A

Procainamide

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23
Q

Procainamide is derived from

A

procaine (a local anesthetic)

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24
Q

Procainamide is given

A

orally, IV, IM

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25
Q

Procainamide Adverse effects similar to

A

Quinidine (although less severe) but may cause reversible lupus erythematosus

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26
Q

Class Ib: Na⁺ Channel Blockers: Shift the action potential (AP) to the

A

left by shortening Phase 3 repolarization.

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27
Q

Class Ib: Na⁺ Channel Blockers: have their greatest effect on heart cells with

A

long action potentials like Purkinje fibers and ventricular myocytes

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28
Q

Class Ib: Na⁺ Channel Blockers: Drug names

Lettuce Mayo Tomato

A

Lidocaine (Xylocaine)
Mexiletine (Mextil)
Tocainide (Tonocard)

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29
Q

Lidocaine

A

(Xylocaine)

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30
Q

Mexiletine

A

(Mextil)

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31
Q

Tocainide

A

(Tonocard)

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32
Q

Lidocaine is a

A

Local anesthetic

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33
Q

Lidocaine is given ONLY

A

parenterally

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34
Q

Lidocaine therapeutic index is

A

Wide

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35
Q

Lidocaine Major toxic side effect (at high doses) is

A

cardiac depression

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36
Q

Lidocaine Extends refractory period further into

A

diastole in depressed cardiomyocytes than in healthy ones.

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37
Q

Lidocaine ***D.O.C. for

A

ventricular arrhythmias (PVCs), particularly those associated with “sick hearts” with arrhythmias like post-MI.

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38
Q

Lidocaine is Frequently used as a component of

A

cardioplegia

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39
Q

Mexiletine is Like an oral

A

lidocaine

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40
Q

Mexiletine is used in what treatment

A

? look it up

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41
Q

Tocainide is given

A

Orally

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42
Q

Tocainide Used in patients resistant to &/or sensitive

to

A

lidocaine/mexiletine

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43
Q

Tocainide Pulmonary toxicity fairly common— can cause

A

pulmonary fibrosis rendering Tonocard a 2nd or 3rd line treatment

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44
Q

Class Ic: Na⁺ Channel Blockers: does what to the action potential

A

Nothing- it does NOT shift

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45
Q

Class Ic: Na⁺ Channel Blockers: have profound effects on

A

normal hearts.

–Recent studies indicate some are very dangerous and are not used when better/safer alternatives exist.

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46
Q

Class Ic: Na⁺ Channel Blockers: drug names

Fries Please

A

Flecainide (Tambocor)

Propafenone (Rhythmol)

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47
Q

Flecainide

A

(Tambocor)

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48
Q

Propafenone

A

(Rhythmol)

49
Q

Flecainide is given

A

Orally

50
Q

Flecainide Suppresses Phase…

A

ZERO upstroke in Purkinje fibers and cardiomyocytes

51
Q

Flecainide Dramatically slows

A

conduction and automaticity is decreased via an increase in the threshold pote ntial

52
Q

Flecainide used for what type of arrhythmia

A

refractory ventricular arrhythmias

particularly PVCs

53
Q

Flecainide has what effects

A

Negative inotropic effects worsen CHF

54
Q

Recent studies suggest Flecainide is more likely to

A

harm than help in the long-run

55
Q

Propafenone has similar uses as

A

quinidine

56
Q

Propafenone is given

A

Orally

57
Q

Propafenone Considered to be a “broad spectrum”

antiarrhythmic but used mostly for

A

supraventricular tachyarrhythmias

58
Q

β₁-blockers are cardioselective but

A

many/most have other adrenergic blocker activity. Some have partial adrenergic agonist activity.

59
Q

Class II : β-Adrenoceptor Blockers: work by

A 
diminishing Phase 4 depolarization =
decreased automaticity
prolonged AV conduction
negative chronotrope
negative inotrope
60
Q

Class II : β-Adrenoceptor Blockers: what arrhythmias are they used for?

A
  1. Atrial tachyarrhythmias…including AV nodal re-entrant tachyarrythmias (the most common type, particularly in women.)
  2. extensively used post-MI for ventricular arrhythmias
61
Q

Class II : β-Adrenoceptor Blockers: drug names

A

Propranolol (Inderal)
Metoprolol (Lopressor, Toprol-XL)
Esmolol (Brevibloc)

62
Q

Propranolol

A

(Inderal)

63
Q

Metoprolol

A

(Lopressor, Toprol-XL)

64
Q

Esmolol

A

(Brevibloc)

65
Q

Propranolol (Inderal): Extensively used for decades.

*Has been proven to

A

decrease incidence of mortality within the first year of an MI

66
Q

The most commonly used β-blocker for treating cardiac arrhythmias

A

Metoprolol (Lopressor, Toprol-XL)

67
Q

Very short-acting IV β-blocker commonly used during surgery and during emergencies

A

Esmolol (Brevibloc)

68
Q

Class III: K⁺ Channel Blockers: Block K⁺ channels with little effect on

A

Na⁺ channels

69
Q

Class III: K⁺ Channel Blockers: By blocking the outward flow of K⁺ during REpolarization they

A

prolong the action potential without affecting Phase 0 (depolarization).

70
Q

Class III: K⁺ Channel Blockers: have what effect

A

refractory period and “refractoriness”

71
Q

Class III: K⁺ Channel Blockers: have a prolonged action potential with

A

“normal” conduction velocity block re-entrant arrhythmias.

72
Q

Class III: K⁺ Channel Blockers: Exhibit the negative side effect of

A

“reverse use-dependence blockade” which can contribute to arrhythmias.

73
Q

Class III: K⁺ Channel Blockers: Generally prolong the

A

QT

74
Q

Class III: K⁺ Channel Blockers: drug names

A 
Amiodarone (Cordarone)
Drondarone (Multaq)
Dofetilide (Tikosyn)
Sotalol (Betapace, Sorine)
Ibutilide (Corvert)
75
Q

Amiodarone

A

(Cordarone)

76
Q

Drondarone

A

(Multaq)

77
Q

Dofetilide

A

(Tikosyn)

78
Q

Sotalol

A

(Betapace, Sorine)

79
Q

Ibutilide

A

(Corvert)

80
Q

Amiodarone is an

A

“iodinated benzofuran” which means it looks a little like thyroxine

81
Q

Amiodarone Effects all cardiac tissues, so it has a

A

broad-spectrum of antiarrhythmic activity.

82
Q

Amiodarone Often the D.O.C. for

A

A-Fib

83
Q

Amiodarone Used as a 2nd-line Rx for lots of

A

refractory arrhythmias

84
Q

Amiodarone has a Very long half-life of

A

(20-100 days!) combined with high ability to interact with other drugs and a lot of side-effects (particularly with long-term use) limit its use

85
Q

Amiodarone has LESS toxicity at lower dosages of _____ but it takes weeks to months to get to therapeutic levels (because of long half-life). So you have to give high loading doses of ______

A

(100-200 mg/day)

800-1600 mg/day

86
Q

Amiodarone Potential for side effects…

A

increases with both high doses and long-term use

87
Q

Amiodarone side effects

A

Sinus Bradycardia
Hypotension
ARDS & Pulmonary Fibrosis

88
Q

Dronedarone: Like amiodarone without the

A

iodine (whew, no thyroid dysfunction or blue skin!)

89
Q

Dronedarone Much shorter half-life of ____ than ____

A

(24 hours) than amiodarone

90
Q

Dronedarone Less effective than amiodarone for

A

a-fib but has fewer of those side effects except death

91
Q

Sotalol is a

A

a non-selective β-blocker

92
Q

Sotalol Not only does it reduce post-MI mortality (as do most β-blockers) but it also has

A

Class III activity

lengthening of refractory period

93
Q

Sotalol has what effects

A

reduces myocardial O2 consumption

acts as a powerful antiarrhythmic

94
Q

Sotalol Helps prevent

A

fibrillation and makes defibrillating patients easier

so it’s ideal for post-MI patients

95
Q

Dofetilide: Often the D.O.C. for

A

a-fib in patients with HF or decreasing EF’s

96
Q

Ibutilide has both

A

Class III and IA antiarrhythmic properties

97
Q

Ibutilide: DOC for

A

? look it up

98
Q

All antiarrhythmics can cause

A

arrhythmias.

99
Q

Class III are more prone than others, particularly in causing

A

Torsade de Pointes

100
Q

Class IV: Ca⁺⁺ Channel Blockers: Decrease the rate of

A

Phase 4 spontaneous depolarization

101
Q

Class IV: Ca⁺⁺ Channel Blockers: preferentially

slow the rate of conduction in

A

issues dependent on calcium currents for depolarization

102
Q

Class IV: Ca⁺⁺ Channel Blockers: drug names

A

Verapamail
Cardizem
Nifedipine

103
Q

nifedipine can cause more

A

arrhythmias

104
Q

Verapamil & Cardizem: Used almost ______ for arrhythmias

A

interchangeably

105
Q

Verapamil & Cardizem: preferentially block the

A

voltage-sensitive channels

106
Q

Verapamil & Cardizem: are “use-dependent”=

A

preferring to block channels on tissues depolarizing too fast and block Ca⁺⁺ channels most effectively on the AV and SA nodes

107
Q

Verapamil & Cardizem: also treat what arrhythmia

A

Atrial flutter

108
Q

Verapamil & Cardizem: are both

A

negative inotropes

109
Q

Classless Antiarrhythmics include

A

Digoxin
Adenosine (Adenocard)
Magnesium sulfate

110
Q

Digoxin shortens the refractory period in

A

atrial and ventricular tissue while slowing conduction through the AV node

111
Q

Digoxin Used to control

A

ventricular response rates in a-fib and a-flutter

112
Q

Adenosine

A

(Adenocard)

113
Q

Adenosine (Adenocard) is the D.O.C. for abolishing

A

SVT

114
Q

Adenosine (Adenocard) When given fast IV push on bypass (a rarity) …it

A

decreases AV node automaticity and cardiac conduction velocity and automaticity

115
Q

Adenosine (Adenocard) Has a very short half-life of_____ and causes _____

A

(~10-15 seconds!) and causes transient hypotension

116
Q

Adenosine doses

A

First dose is 6 mg fast IV push

*If that doesn’t convert the SVT give 12 mg fast IV push

117
Q

Magnesium Sulfate: it slows the rate of

A

A node impulse formation and the rate at which the impulse travels through myocardium

118
Q

Magnesium Sulfate: DOC for

A

digoxin-induced arrhythmias

119
Q

Magnesium Sulfate: Must be given

A

IV to be effective as an antiarrhythmic

Pharm Exam 2 (9 decks)

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