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Cardiology Exam III > Pharm: Anti-Arrhythmics Drugs > Flashcards

Pharm: Anti-Arrhythmics Drugs Flashcards

1
Q

What are the three mechanisms that can lead to tachyarrhythmias ?

A

Increased automaticity (SA, ectopic pacemaker etc)

Triggered activity

Re-entry (due to unidirectional block)

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2
Q

Increased or altered automaticity and Triggered activity are forms of altered impulse _________.

A

Formation

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3
Q

Re-entry is a form of altered impulse ________.

A

propagation

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4
Q

Bradyarrhytmias are due to __________ impulse formation and exhibit ___________ phase 4 depolarization

A

Decreased

Decreased

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5
Q

What are the mechanisms that lead to impaired conduction ?

A

Ischemic , anatomic or drug induced

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6
Q

To treat bradyarrhythmia with pharm you can give drugs that inhibit vagal tone or drugs that induce chronotropic effects of the heart. Which drug would you give to block vagal effects ?

A

Atropine

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7
Q

Which drugs would you give to induce chronotropic effects in the heart to treat bradyarrhythmia ?

A

B1-receptor agonists
Dopamine
Isoproterenol

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8
Q

How could you treat a bradyarrhythmia long term w/o drugs ?

A

Pacemaker

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9
Q

Altered automaticity leading to tachyarrhythmia results in _______ phase 4 depot on SA node AP.

A

increased

This is known as Sinus tachy.

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10
Q

The pharmacologic goal of treating tachyarrhythmia is

A

to eliminate increased automaticity

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11
Q

How do drugs eliminate automaticity when treating tachyarrhthmia ?

A
  1. Decrease the slope of phase 4 in pacemaker cells. (aka less steep phase 4, slower depolarization)
  2. Make diastolic potential more negative
  3. Make threshold potential less negative
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12
Q

Abnormal automaticity in atrial or ventricular myocytes is due to cells aquiring phase 4 depolarizations. What are two ways this can occur ?

A

Digitalis Toxicity

Increased Sympathetic tone

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13
Q

Triggered activity leads to what kind of non-typical depolarizations ?

A

Early After Depolarizations

Delayed after Depolarization

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14
Q

What is ‘triggered activity’ ?

A

A depolarization that forms after a single or multiple impulses following a preceeding depolarization

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15
Q

Early After Depolarization (EAD’s) occur due to conditions that prolong _______ interval.

A

QT

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16
Q

Due to their mechanism ,EAD predispose patients to what condition ?

A

Torsades De Pointes

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17
Q

What occurs to Phase 2 Ca++ influx in EAD’s ?

A

It is increased (leading to a longer Phase 2 –> Longer QT interval

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18
Q

What occurs to Na+influx in Phase 3 during EAD’s ?

A

It is increased, Longer Phase 3 –> Longer QT interval

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19
Q

DAD’s are theorized to occur due to …

A

Intracellular Ca++ overload

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20
Q

What are the specified goals of treating Triggered activity ?

A

Preventing EAD’s by shortening AP duration

Correct DAD’s by correcting conditions of calcium overload

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21
Q

What is required for Re-entry to occur ?

A 
Unidirectional block
Slowed conduction (retrograde)
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22
Q

What are the overall goals of treating reentry related tacchycardia ?

A

Extinguish the re-entry by impeding propagation in the slow conducting limb

Increase the refractory period of the tissue the re-entry is stimulating. (If it is total refractory it will not be able to fire)

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23
Q

Mechanism of Class I Antiarrhythmics

A

Na+ Channel Blockers

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24
Q

Mechanism of Class IA Antiarrhythmics

A

Block Na+ channels that lead to prolonged depolarization (increased refractory phase)

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25
Q

Mechanism of Class IB Antiarrhythmics

A

Shorten repolarization by blocking Na+ Channels

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26
Q

Mechanism of Class IC Antiarrhythmics

A

Blocks Na+ Channles (no real effect of AP)

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27
Q

Mechanism Class II Antiarrhythmics

A

Beta Receptor Blockers

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28
Q

MechanismClass III Antiarrhythmics

A

K+ Channel blockers, prolong the AP duration by not allowing depolarization

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29
Q

Mechanism Class IV Antiarrhythmics

A

Block Ca++ channels leading to decreased AP duration

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30
Q

List the Class IA drugs

A

Disopyramide(Minor), Quinidine , Procainamide

Pneumonic :Double Quarter Pounder

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31
Q

List the Class IB drugs

A

Lidocaine, Phenytoin, Mexelitine, Tocainide

(Pneumonic|: Lettuce, Pickle, Mayo, Tomato

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32
Q

List Class IC drugs

A

Flecainide, Propafone (Minor

Pneumonic: Fries Please

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33
Q

List Class II Drugs

A

Propanolol, Metoprolol and Esmolol

Propanolol is not Beta1 selective while the other two are.

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34
Q

List Class III drugs

A

Amiodarone, Sotalol, Bretylium, Ibutitide (minor) and Dofetitide (minor)

Note: One of the metabolites of Procainamide (1A) is N-Acetylprocainamide and has Class III actions.

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35
Q

List Class IV drugs

A

Verapamil Diltiazem (notice how these are non-DHP CCB’s. These have more effect on the heart)

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36
Q

List the miscellaneous drugs used for Arrhythmia

A

Adenosine, digoxin, magnesium

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37
Q

What are the overall effects of Class I drugs (Na Channel Blockers)

A

Decreased automaticity
decreased conduction velocity
can prevent reentry arrhythmias

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38
Q

Indication for class IA drugs

A

wide variety of reentrant & ectopic supraventricular & ventricular tachycardias

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39
Q

Where do class IA drugs mainly have their effects in treating automaticity?

A

Purkinje Fibers and Ectopic pacemakers (actually have little effect of SA node automaticity)

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40
Q

Is it possible for Class IA drugs to convert a-flutter and A-fib to normal sinus rhythm ?

A

YES !

41
Q

How do Class IA drugs treat reentrant arrhythmias ?

A

Produce bidirectinal blocks (decreases conduction)
increase refractory period ! (UNIQUE TO 1A !!!)

(Note:Later on he says that Class III drug affect the refractory quality of the perkinje and ventricular muscle fibers, so maybe Class IA only affect atrial ?)

42
Q

What may Class IA drugs predispose a patient to ?

A

Torsades De pointes

43
Q

What is the protoype Class IA drug ?

A

Quinidine

44
Q

Quinidine (IA) has strong anti-muscarinic effects. How will this alter SA node automaticity and AV node conduction ?

A

Increase both SA and AV node automaticity

45
Q

What can you pre-treat with prior to giving quinidine to ensure minial vasolytic effects ?

A

Digoxin, BB’s or Verapamil (a CCB)

46
Q

Quinidine Side Effects

A

Diarrhea (most common, 1/3 of all patients)
Torsades de pointes
Cinchonism

47
Q

What is cinchonism ?

A

Side effect caused by quinidine resulting in : tinnitus, headache, vertigo, disturbed vision (is usually dose related)

48
Q

What are the drug interactions related to Quinidine

A

Increases digoxin levels by decreasing it’s clearance

49
Q

Procainamide (IA) is like quinidine except..

A

it is not as anti-muscarinic, meaning that it will not increase the ventricular rate as much as quinidine us would
It also has marked decrease in ability to prolong the QT interval, thus less likelyhood of Torsade de Pointes

50
Q

Adverse effects of Procainamide

A

Lupus Like Syndrome :arthralgias, rash, fever, connective tiss. inflammatio (is reversible with discontinuation)

Active metabolite N-Acteylprocainamide works like a Class III drug which may lead to QT prolongation and TdP.

51
Q

When is disopyramide contraindicated ?

A

Patients w/ heart failure due to negative inotropic effects

Not really used much anymore

52
Q

Class IB drugs are most commonly used to …

A

Supress Ventricular Arrhythmia (esp if associated w/ ischemia or digitalis)

53
Q

Class IB drugs act to inhibit re-entrant arrhythmias by ..

A

Decreasing conduction velocity

54
Q

How do IB drugs decrease automaticity of ectopic pacemakers ?

A

Raising the threshold potential so that depolarization is more difficult.

55
Q

Class IB side effects

A

Seizures
Confusion
dizziness

56
Q

Which of the IB drugs are an oral anolog of lidocaine (IB) ?

A

Mexiletine

57
Q

Adverse effects of Mexiletine

A

Tremor, nausea and seizure

58
Q

When is Phenytoin going to be used exclusively ?

A

Digitalis induced arrhythmia (delayed afterdepolarizations)

59
Q

Class IC drugs are indicated for …

A

Atrial fib, supraventricular arrhythmia in patients with otherwise healthy hearts

60
Q

Class IC drugs can be proarrhythmic by increasing what ?

A

QRS comples

61
Q

Indications for Class II

A

Suppressing arrhythmias induced by excessive catecholamines (stress: exercise, emotional), including triggered arrhythmias

A.fib/Flutters

Re-entrant rhythms involving the AV node

62
Q

Class II drugs are the only to show

A

decreased mortality by preventing recurrent infarction and sudden death in patients recovering form acute MI !

63
Q

Which Beta Blocker has Class III interactions ?

A

Sotalol

64
Q

Which of the beta-blockers have a less complete BB effects ?

A

Acebutolol, Pindolol

HAVE Intrinsic Sympathomimetic Activity (ISA)

65
Q

What is an adverse effect of Class II drugs ?

A

Beta blockers cause AV block and thus sinus bradycardia

66
Q

Class III drugs block K+ currents. This leads to

A

Prolonged AP and refractory period.

Prolonged QT interval

67
Q

Due to their effect on the QT interval, Class III drugs predispose patients to

A

TdP

68
Q

amiodarone is effective when used for

A

A.fib/flutter
Bypass tract mediated parosysmal SVT
V. Tach,

69
Q

Amiodarone is First line drug for ..

A

Tx. of vent. arr. during cardiac resuscitation

70
Q

Amiodarone is go for treating arrhythmias in patients with vent. sys. dysfunction because

A

less pro-arrhythmic complications than with many other agents

71
Q

Mechanism of Amiodarone action

A

Prolong AP duration & refractoriness of all cardiac fibers: blocks K+ rectifier current

72
Q

Amiodarone has effects in all classes. Explain Class I, II and IV effects

A

Significant Na+ channel blocker effect as well (Class I).

Weakly blocks Beta-rec.’s & Ca++ channels (Class 2 & 4)
Prolong PR, QRS & QT intervals
Additional firing suppression provided by these effects likely account for the absence of Torsades typically seen with agents that produce long QT intervals

73
Q

What are the extracardiac effects of amiodarone ?

A

peripheral vasodilation (noncompetitive alpha-blocker & blocks Ca++ influx in vascular smooth muscle) perhaps beneficial, rarely requires discontinuation

74
Q

Why will amiodarone accumulate in most organs ?

A

Highly lipophilic

in plasma, highly bound to proteins

75
Q

Where is amiodarone inactivated ?

A

In the liver

76
Q

Why is amiodarone difficult to discontinue ?

A

VERY SLOW ELIMINATION… prolonged effects event after it has been stopped

77
Q

Drug interactions of amiodarone

A

Increased action of Dig. & warfarin, avoid other drugs with negative chronotropic/inotropic effects (Beta-blockers, verapamil, diltiazem)

78
Q

What occurs with prolonged high dose treatmet with amiodarone ?

A

Toxicities with the most serious being PULMONARY FIBROSIS

Others include : Corneal micro-deposits
Hypo and hyperthroid problems

79
Q

Sotalol (III) is used for

A

supraventricular & ventricular arrhythmias

80
Q

what are the major side effects associated with sotolol >

A

bradycardia, AV block, CHF, bronchospasm (these are those associated with BB’s as well)

81
Q

When is Bretylium tosylate indicated ?

A

for life-threatening v. tach or v. fib when all other resuscitation attempts fail

82
Q

How does Bretylium tosylate work ?

A

initially increased release of NE at nerve terminals followed by decreased release.

Overall there is a decrease in catecholamines .R aises threshold for vent. fibrillation

83
Q

Side effect of Bretylium tosylate ?

A

Orthostatic hypotension

84
Q

Dofetilitide is a new AA drug and is unique in that it is a …

A

PURE K+ channel blocker –> Delays depolarization

85
Q

When is Dofetilide used ?

A

Conversion of A-fib & A-flutter  sinus rhythm, maintenance of rhythm after conversion

86
Q

Adverse effect of Dofetilide

A

TdP

87
Q

When are the Class IV drugs used

A

reentrant arrhythmias whose circuit involves AV node. Also decreased ventricular rate in A-flutter, A-fib

88
Q

Side effects of Class IV drugs

A

Similar effects as Betablockers (can cause bradycardia, HF, AV block)
May cause hypotension

89
Q

Adenosine is the DOC for …

A

termination of PSVT with reentrant circuits involving the AV node, including WPW syndrome

90
Q

How does Adenosine achieve its therapeutic action ?

A

Activates K+ rectifier current in SA & AV nodes
decreases Ca++ influx

Leads to hyperpolarization and inhibition of Ca++ dependent depolarization (decreases SA automaticity and AV conduction)

91
Q

What is Adenosines affect of cAMP levels and what will this cause ?

A

inhibits intracellular adenylate cyclase–>cAMP-mediated effects which occur with sympathetic stimulation

This leads to decreased inward pacemaker current (If channels)
and decreases Ca influx

92
Q

Why must Adenosine be given as an IV bolus as close to the heart as possible ?

A

Extremely short plasma t1/2 (< 10 seconds)

Rapidly cleared from the blood and thus has minimal adverse effects

93
Q

What are the side effects related to Adenosine

A

Transient asystole: common but lasts < 5 sec & is, in fact, the therapeutic goal
Rarely precipitates A-fib

94
Q

Drug interactions of Adenosine

A

Methylxanthines block adenosine receptors

Caffeine and Theophyline

95
Q

When is digoxin used ?

A

Commonly used for CHF complicated by A. Fib

Not really used much anymore due to narrow therapeutic range and side effects.

96
Q

Digoxin MOA

A

Decreases AV nodal conduction by direct depressant effect on AV node and by acting in the CNS to increase vagal impulses to the AV node.

Leads to prolonged PR interval

Decreases SA node automaticity by increasing’ing vagal activity and decreasing sympathetic activity at the node

97
Q

Digoxin has a propensity to cause arrythmias. How do you treat these ?

A

Treat dig.-induced arrhythmias with digoxin-immune F-ab (digoxin antibody fragments), lidocaine or phenytoin

98
Q

When is MgSO4 indicated ?

A

IV admin. prevents recurrent episodes of torsades de pointes

Cardiology Exam III (12 decks)

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