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pharm exam 2 > Topic 11 Antiarrhythmics > Flashcards

Topic 11 Antiarrhythmics Flashcards

1
Q

Abnormalities in the electrical impulse
generation or conduction through the
heart

A

antiarrhythmic

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2
Q

> 50% of anesthetized patients have what?

A

arrhythmias

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3
Q

What % of patients with MIs have arrhythmias

A

80%

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4
Q

but darned-near what % of patients on CPB will be affected with arrhythmias?

A

100%

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5
Q

Virtually all antiarrhythmics work by altering what?

A

the ionic transmembrane balance (Na⁺,Ca⁺⁺, K⁺) or the sympathetic tone to the heart

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6
Q

The Vaughan Williams Classification

1A, 1B, and 1C mechanism of action?

A

Na+ channel blocker

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7
Q

The Vaughan Williams Classification

II mechanism of action?

A

Beta-Adrenoreceptor blocker

inhibits phase 4 depolarization in SA and AV nodes

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8
Q

The Vaughan Williams Classification

III mechanism of action?

A

K+ channel blocker

Prolongs phase 3 repolarization in ventricular muscle

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9
Q

The Vaughan Williams Classification

IV mechanism of action?

A

Ca++ channel blocker

Inhibits action potential in SA and AV nodes

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10
Q

Class I : Na⁺ Channel Blockers Preferentially bind to what channels? Thus ?

A

open Na⁺ channels rather than to
fully repolarized Na⁺ channels.
-Consequently Class I drugs preferentially block conduction in tissues that are depolarizing more frequently.
This is called “use-dependence” blockade

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11
Q

What is “use-dependence” blockade, in Class 1: Na+ Channel Blockers?

A

Class I drugs preferentially block conduction in tissues that are depolarizing more frequently (open Na⁺ channels).

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12
Q

Class I (Na⁺ Channel Blockers) antiarrhythmics three subclasses?

A

Ia: Shorten the action potential and affect QRS complexes
Ib: Shorten the action potential without affecting QRS.
Ic: Do not shorten the action potential

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13
Q

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1a do what to the AP

A

Shorten the action potential and affect QRS complexes
Shift the action potential (AP) to the right by slowing Phase 0 depolarization (hence their nickname, “membrane stabilizers”).
-Ia’s also inhibit some K⁺ channels (Class III activity) which widens the AP causing prolonged QT intervals

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14
Q

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1b

A

Shorten the action potential without affecting QRS
Shift the action potential (AP) to the left by shortening Phase 3 repolarization.
-Ib’s have their greatest effect on heart cells with long action potentials like Purkinje fibers and ventricular myocytes

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15
Q

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1c

A

Do not shorten or shift the action potential
-Ic’s even have profound effects on normal hearts.
Recent studies indicate some are very dangerous and are not used when better/safer alternatives exist

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16
Q

Disopyramide

A

Norpace

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1a- Shift the action potential (AP) to the right by slowing Phase 0 depolarization

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17
Q

Quinidine

A

Quinidex

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1a- Shift the action potential (AP) to the right by slowing Phase 0 depolarization

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18
Q

Procainamide

A

Pronestyl,Procan

Class I (Na⁺ Channel Blockers) antiarrhythmics subclass 1a- Shift the action potential (AP) to the right by slowing Phase 0 depolarization

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19
Q

Ia Drugs?

Na⁺ Channel Blockers) antiarrhythmics

A

(Double Quarter Pounder)
Disopyramide -Norpace
Quinidine -Quinidex
Procainamide -Pronestyl, Procan

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20
Q

Quinidine (Quinidex)- used for what?

A
  • Been around forever. Given orally.

* Used for various tachyarrhythmias

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21
Q

Quinidine (Quinidex) – how often is it used ?

A

Rarely used because of toxic side effects (get ready!)

  • Cinchonism
  • Torsades de pointes
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22
Q

Quinidine (Quinidex) toxic effects?

A
  • Cinchonism

* Torsades de pointes

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23
Q

What is Cinchonism?

A

toxicity due to quinidine alkaloid overdosage; symptoms are tinnitus and slight deafness, photophobia and other visual disturbances, mental dullness, depression, confusion, headache, and nausea.

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24
Q

Torsades de pointes resolves? devolves?

A

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

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25
Q

Disopyramide (Norpace) inotropic effects?

A

Like Quinidine, but more negative inotropic
effects and ⬇️ SVR
which might precipitate HF

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26
Q

Most widely used Ia Na channel blocker antiarrhythmic

A

Procainamide -Pronestyl, Procan

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27
Q

Procainamide (Pronestyl, Procan) - adverse effects?

A

Adverse effects similar to Quinidine (although less severe) but may cause reversible lupus erythematosus

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28
Q

Procainamide (Pronestyl, Procan) derived from what?

A

Derived from procaine (a local anesthetic)

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29
Q

Ib Drugs

Na channel Blockers Antiarrhythmics

A

Lettuce, Mayo, & Tomato
Lidocaine (Xylocaine)
Mexiletine (Mextil)
Tocainide (Tonocard)

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30
Q

Lidocaine (Xylocaine) administration?

A

Only given parenterally

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31
Q

Lidocaine (Xylocaine) major toxic effect?

A

Major toxic side effect (at high doses) is cardiac depression

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32
Q

Lidocaine - is what/does what?

A

Xylocaine

Ib, Na channel Blocker antiarrhythmic
Extends refractory period further into diastole in depressed cardiomyocytes than in healthy ones

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33
Q

D.O.C. for ventricular arrhythmias, particularly those associated with “sick hearts” with arrhythmias like post-MI

A

Lidocaine (Xylocaine)

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34
Q

Lidocaine is the DOC for what?

A

ventricular arrhythmias, particularly those associated with “sick hearts” with arrhythmias like post-MI

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35
Q

Lidocaine (Xylocaine) Frequently used as a component of what?

A

cardioplegia

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36
Q

Mexiletine

A

(Mextil)

1b Na channel Blocker antiarrhythmic
Like an oral lidocaine
It is used to treat arrhythmias within the heart, or seriously irregular heartbeats. It slows conduction in the heart and makes the heart tissue less sensitive.

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37
Q

Tocainide (Tonocard) toxicity?

A

Pulmonary toxicity fairly common

—can cause pulmonary fibrosis rendering Tonocard a 2nd or 3rd line treatment!

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38
Q

Tocainide

A

Tonocard

Class 1b, Na channel blocker antiarrhythmic

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39
Q

Tocainide (Tonocard) used in what patients?

A

Used in patients resistant to &/or sensitive

to lidocaine/mexiletine

40
Q

Ic Drugs?

Na channel blockers. antiarrhythmics

A

Fries Please
Flecainide (Tambocor)
Propafenone (Rhythmol)

41
Q

Flecainide (Tambocor) suppresses what phase in the action potential?

A

Suppresses Phase 0 upstroke in Purkinje
fibers and cardiomyocytes
Dramatically slows conduction and automaticity is decreased via an increase in the threshold potential

42
Q

Flecainide (Tambocor) - used for what type of arrhythmia?

A

Used for refractory ventricular arrhythmias

particularly PVCs

43
Q

Flecainide

A

Tambocor

1c, Na channel blocker antiarrhythmic

44
Q

Flecainide (Tambocor)’s effect that worsens CHF?

A

Negative inotropic effects worsen CHF

45
Q

Flecainide (Tambocor) negative side affect?

A

Recent studies suggest Flecainide is more likely to harm than help in the long-run

46
Q

Propafenone (Rhythmol) considered what kind of antiarrhythmic?

A

Considered to be a “broad spectrum” antiarrhythmic but used mostly for supraventricular tachyarrhythmias

47
Q

Class II : Antiarrhythmics?

A

β-Adrenoceptor Blockers

48
Q

Class II : Antiarrhythmic: β-Adrenoceptor Blockers - how do they work?

A

β₁-blockers are cardioselective but many/most have other adrenergic blocker activity. Some have partial adrenergic agonist activity.
-Work by diminishing Phase 4 depolarization = ⬇️automaticity, prolonged AV conduction, negative chronotrope, negative inotrope

49
Q

Class II : Antiarrhythmic: β-Adrenoceptor Blockers diminish what phase of action potential?

A

Work by diminishing Phase 4 depolarization = ⬇️automaticity, prolonged AV conduction, negative chronotrope, negative inotrope

50
Q

Class II : Antiarrhythmic: β-Adrenoceptor Blockers work on what arrhythmias?

A

Atrial tachyarrhythmias

  • including AV nodal re-entrant tachyarrythmias (the most common type, particularly in women.)
  • Also extensively used post-MI for those nasty ventricular arrhythmias
51
Q

Propranolol

A

(Inderal)
Class II : Antiarrhythmic: β-Adrenoceptor Blockers
Extensively used for decades.
*Has been proven to decrease incidence of mortality within the first year of an MI

52
Q

The most commonly used β-blocker for treating cardiac arrhythmias (less β₂ than others)

A

Metoprolol (Lopressor, Toprol-XL)

53
Q

Metoprolol

A

Lopressor, Toprol-XL

Class II, Antiarrhythmic: β-Adrenoceptor Blockers

54
Q

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

A

Esmolol (Brevibloc)

55
Q

Esmolol

A

Brevibloc

Class II, Antiarrhythmic: β-Adrenoceptor Blockers
Very short acting, IV, used during surgery

56
Q

Class II, Antiarrhythmic: β-Adrenoceptor Blockers Drugs

A

Propranolol (Inderal)
Metoprolol (Lopressor)
Esmolol (Brevibloc)

57
Q

Class III: antiarrhythmics

A

K⁺ Channel Blockers

58
Q

Class III, K Channel Blockers, Antiarrhythmic - how do they work on the action potential?

A

Block K⁺ channels with little effect on Na⁺ channels
-By blocking the outward flow of K⁺ during repolarization they prolong the action potential without affecting Phase 0 (depolarization).
-⬆️ refractory period and “refractoriness”
Generally prolong the QT

59
Q

Class III, K Channel Blockers, Antiarrhythmic does what to the refractory period?

A

⬆️ refractory period and “refractoriness”

Generally prolong the QT

60
Q

How do Class III, K Channel Blockers, Antiarrhythmic block arrhythmias?

A

Prolonged AP with “normal” conduction velocity block re-entrant arrhythmias.

61
Q

Class III, K Channel Blockers, Antiarrhythmic exhibit neg side effects

A

Exhibit the negative side effect of “reverse use-dependence blockade”

62
Q

What is reverse use dependent blockade?

Class III, K Channel Blockers, Antiarrhythmic

A

faster rates of channel stimulation (or indeed heart rate) encourage greater dissociation than slower rates, resulting in comparatively less channel inhibition at faster than at slower rates.

63
Q

Amiodarone

A

(Cordarone)

Class III, K Channel Blockers, Antiarrhythmic

64
Q

Drondarone

A

(Multaq)

Class III, K Channel Blockers, Antiarrhythmic

65
Q

Sotalol

A

(Betapace, Sorine)

Class III, K Channel Blockers, Antiarrhythmic

66
Q

Dofetilide

A

(Tikosyn)

Class III, K Channel Blockers, Antiarrhythmic

67
Q

Ibutilide

A

(Corvert)

Class III, K Channel Blockers, Antiarrhythmic

68
Q

Amiodarone (Cordarone) - what is it chemically?

how does it affect cardiac tissues?

A

It’s an “iodinated benzofuran” which means it looks a little like thyroxine
*Effects all cardiac tissues, so it has a broad-spectrum of antiarrhythmic activity

69
Q

Amiodarone (cordarone) is often the DOC for what?

A

A-Fib

70
Q

Amiodarone (cordarone) T1/2

A

Very long half-life (20-100 days!) combined with high ability to interact with other drugs

71
Q

Amiodarone (cordarone) Used as a 2nd-line Rx for lots of what?

A

refractory arrhythmias

72
Q

Amiodarone (Cordarone) at lower dosages?

A

Less toxicity at lower dosages (100-200 mg/day)…
BUT at lower dosage it takes weeks to months to get to therapeutic levels (because of long half-life
so you have to give high loading doses (800-1600 mg/day)

73
Q

Amiodarone (Cordarone) side effects?

A

boat-load of side-effects (particularly with long-term use) limit its use

  • increases with both high doses and long-term use
  • Sinus Bradycardia
  • Hypotension
  • ARDS & Pulmonary Fibrosis
  • Nausea, dizziness, blue/gray skin (caused by iodine), thyroid dysfunction (caused by iodine), jaundice
74
Q

Pulmonary fibrosis

A

A disease marked by scarring in the lungs. Tissue deep in the lungs becomes thick, stiff and scarred. The scarring is called fibrosis. As the lung tissue becomes scarred, it interferes with a person’s ability to breathe
SIDE EFFECT of Amiodarone (cardarone)

75
Q

Dronedarone (Multaq)

A

Like amiodarone without the iodine

Less effective than amiodarone for a-fib but has fewer of those side effects except death is one of the side effects

76
Q

Dronedarone (Multaq) T1/2

A

half-life (24 hours) than amiodarone

77
Q

Sotalol (Betapace, Sorine) does what?

A

non-selective β-blocker
*Not only does it reduce post-MI mortality (as do most β-blockers) but it also has Class III activity (lengthening of refractory period)

78
Q

Sotalol (Sorine, Betapace) is ideal for what patients? does what to myO2cardial consumption?

A

So it reduces myO₂cardial consumption and acts as a powerful antiarrhythmic.
*Helps prevent fibrillation and makes defibrillating patients easier so it’s ideal for post-MI patients

79
Q

Dofetilide Often the D.O.C. for what patients?

A

A-fib in patients with HF or low EF’

80
Q

Ibutilide has properties in what two classes of antiarrhythmics?

A

has both Class III and IA antiarrhythmic properties

81
Q

All antiarrhythmics can cause ___ and

_____ are more prone than others, particularly in causing Torsades de Pointe

A

arrhythmias

Class III

82
Q

Class IV: Antiarrhythmics

A

Ca⁺⁺ Channel Blockers

83
Q

Class IV: Ca++ Channel Blocker Antiarrhythmic decrease what phase of the action potential, and slow what?

A

Decrease the rate of Phase 4 spontaneous depolarization.

-Class IV’s also preferentially slow the rate of conduction in tissues dependent on calcium currents for depolarization

84
Q

Class IV: Ca++ Channel Blocker Antiarrhythmic Drugs in order of greatest vascular effects

A

Verapamail > Cardizem

85
Q

Verapamail and Cardizem used for what?

A

Used almost interchangeably for arrhythmias
Since they preferentially block the voltage-sensitive channels…
They are “use-dependent” (preferring to block channels on tissues depolarizing too fast) and block Ca⁺⁺ channels most effectively on the AV and SA nodes

86
Q

Verapamail and Cardizem are what kind of inotropes

A

negative inotropes so avoided in patients with HF

87
Q

Classless Antiarrhythmic Drugs

A

Digoxin
Adenosine (adenocard)
Magnesium sulfate

88
Q

Digoxin - does what to conduction?

A

shortens the refractory period in atrial and ventricular tissue while slowing conduction through the AV node
•Used to control ventricular response rates in a-fib and a-flutter
Just slows down the ventricular rate even tho atrial rate is still going cray

89
Q

Digoxin used to control what two arrhythmias?

A

a-fib and a-flutter

90
Q

Adenosine

A

(Adenocard)

91
Q

DOC for abolishing SVT

A

Adenosine (adenocard)

92
Q

Adenosine (adenocard) what it does to conductivity

A

it decreases AV node automaticity and

cardiac conduction velocity and automaticity

93
Q

Adenosine Doses -

A
  • First dose is 6 mg fast IV push in manifold wait 30 seconds…
  • If that doesn’t convert the SVT give 12 mg fast IV push
94
Q

Magnesium Sulfate DOC for?

A

D.O.C. for digoxin-induced arrhythmias

95
Q

Mg Sulfate does what for conduction?

A

Among other things, it slows the rate of SA node impulse formation and the rate at which the impulse travels through myocardium

96
Q

Mg Sulfate must be given how?

A

Must be given IV to be effective as an antiarrhythmic

pharm exam 2 (9 decks)

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