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Cardiology > Anti-Arrythmics > Flashcards

Anti-Arrythmics Flashcards

1
Q

Unlike other regions of the heart, where phase 0 is driven by Na+ channels, the SA node and AV node have slower action potentials driven by

A

Ca2+ channels

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2
Q

Antiarrhythmic drug actions generally fall into 4 classes. Class 1 action is

A

Na+ channel blocker

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3
Q

Pronlong the PD and dissociate from the channel w/ intermediate kinetics and exhibit moderate blockade

A

Class 1A

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4
Q

The prototype class 1A drug is

A

Procainamide

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5
Q

Shorten the APD in some tissues of the heart and dissociate from the channel w/ rapid kinetics

A

Class 1B

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6
Q

The prototype class 1B drug is

A

Lidocaine

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7
Q

Have minimal effects on the APD and dissociate from the channel w/ slow kinetics

A

Class 1C

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8
Q

The prototype class 1C drug is

A

Flecainide

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9
Q

Class 2 action is sympatholytic and the prototypes are

A

Propranolol and esmolol

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10
Q

Prolongs the APD by blocking phase 2 K+ current

A

Class 3

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11
Q

What are the prototype class 3 drugs?

A

Sotalol, ibutilide, and amiodarone

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12
Q

Class 4 action is blockade of the cardiac

A

Ca2+ current

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13
Q

The prototype class 4 drugs are?

A

Verapamil and diltiazem

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14
Q

The prototype is procainamide but others are quinidine and disopyramide

A

Class 1A

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15
Q

Causes a slow upstroke of AP and prolongs the action potential duration

A

Class 1A drugs

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16
Q

Class 1A drugs can be used for

A

Atrial fibrillation or stable V-tach

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17
Q

Reduces peripheral vascular resistance

A

Procainamide

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18
Q

Slowing of conduction and AP prolongation increases the risk of

A

Torsade de pointes, syncope, and arrhythmias

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19
Q

Can cause a syndrome resembling lupus in 1/3 of patients receiving long-term therapy

A

Procainamide

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20
Q

Can cause atropine-like adverse effects such as urinary retention and dry mouth, as well as worsening of preexisting glaucoma

A

Class 1A drugs

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21
Q

Eliminated by hepatic metabolism to a metabolite which has class 3 activity

-accumulation of this metabolite can cause torsade de pointes

A

Procainamide

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22
Q

Class 1A prolongs the

A

Refractory period

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23
Q

Blocks activated and inactivated Na+ channels w/ rapid kinetics

A

Lidocaine

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24
Q

SHORTEN AP duration and the refractory period

A

Class IB drugs

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25
Q

Increased inactivation and slow unwinding kinetics results in the selective depression of conduction in depolarized cells. This is called

A

State Dependent Block

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26
Q

Toxicity causes parethesia, tremor, nausea, lightheaded ness, and hearing disturbances

A

Class 1B toxicity

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27
Q

Has extensive first pass metabolism

-Only 3% of orally administered lidocaine appears in the plasma

A

Class 1B

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28
Q

Used for arrhythmias associated w/ MI and used for termination of V-tach/prevention of V-fib

A

Class 1B

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29
Q

Ineffective for supraventricular tachycardias, atrial fibrillation, and atrial flutter

A

Class 1B drugs

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30
Q

An orally active congener of lidocaine used in the treatment of ventricular arrhythmias

-Also used for chronic pain from diabetic neuropathy and nerve injury

A

Mexiletine

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31
Q

Bind readily to activated channels (phase 0) or inactivated channels (phase 2) but bind poorly to rested channels

A

Use-dependent or State-dependent Drugs

32
Q

Block electrical activity when there is fast tachycardia or when there is a significant loss of the resting potential

A

Use-dependent or State-dependent drugs

33
Q

Selectively targets channels in depolarized tissue

A

Lidocaine

34
Q

Have slow unblocking kinetics

A

Class 1C drugs

35
Q

Have little effect on the action potential duration except for in the AV node and bypass tracts

A

Class 1C drugs

36
Q

Toxicity cause provocation or exacerbation of potentially lethal arrhythmias including the acceleration of ventricular rate in patients w/ atrial flutter

A

Class 1C

37
Q

Used for supraventricular arrhythmias and pharmacologic conversion of AF

A

Class 1C drugs

38
Q

Shown in a study to increase mortality in patients convalescing from MI

A

Flecainide and propafenone (Class 1C drugs)

39
Q

Can cause heart failure in patients with heart abnormalities

A

Class 1C Drugs

40
Q

Decrease pacemaker activity and slow conduction through the AV node to increase the effective refractory period

A

Beta-blockers

41
Q

A non selective beta-blocking drug that prolongs the action potential and is usually categorized as a class 3 drug

A

Sotalol

42
Q

Lowers cAMP which results in reduction of both Na+ and Ca2+ currents and the suppression of abnormal pacemakers

A

Beta-blockers like propranolol

43
Q

Particularly sensitive to beta-blockers

A

AV node

44
Q

Decreases phase 4 slope and decreases myocardial oxygen demand

A

Beta-blockers

45
Q

A non-selective beta antagonist that also exhibits Na+ channel blocking in vitro

A

Propranolol

46
Q

An IV cardioselective beta-blocker that is effective in controlling the ventricular response in atrial flutter or fibrillation

A

Esmolol

47
Q

Control the ventricular rate in atrial fibrillation or flutter, suppress PVCs, and terminate and prevent recurrences of paroxysmal supraventricular tachycardias

A

Beta-blockers

48
Q

Beta-blockers are contraindicated in patients with

A

WPW syndrome

49
Q

A use-dependent drug that blocks the “funny” current in the SA node and reduces heart rate w/out affecting myocardial contractility

A

Ivabradine

50
Q

Made up of the pneumonic ISBAD which comprises ibutilide, sotalol, bretylium, amiodarone, and dofetilide

A

Class III antiarrhythmics

51
Q

Usually classified as a class III because it markedly prolongs AP duration as well as blocks sodium channels

A

Amiodarone

52
Q

Prolongs the AP duration by blockade of IK+ channels or by enhancing inward current

A

Class III drugs

53
Q

AP prolongation increases the effective refractory period and reduces the ability of the heart to respond to rapid

A

Tachycardias

54
Q

AP prolongation by many class III drugs are reverse-dependent, such that the AP prolongation is least marked at fast rates and most marked at slow rates where it can contribute to the risk of torsade de pointes. One exception to this is

A

Amiodarone

55
Q

Prolonging AP can sometimes precipitate

A

Arrhythmias

56
Q

Are more likely to develop in conditions that prolong AP duration

A

Early After Depolarizations (EADs)

57
Q

A non selective beta-blcoking drug that is more effective for many arrhythmias than other beta-blockers because of its IK+ blocking activities

A

Sotalol

58
Q

Can cause dose-related incidence of excessive QT-interval prolongation w/

A

Sotalol

59
Q

Used to treat life-threatening ventricular arrhythmias and maintenance of sinus rhythm in patients w/ A-fib

A

Sotalol

60
Q

Used therapeutically for the conversion of atrial flutter and fibrillation to normal sinus rhythm

A

Ibutilide and Dofetilide

61
Q

Effective in most types of arrhythmias and is considered the most efficacious of all antiarrhythmic drugs likely due to its ability to block Na+, Ca2+, and Beta activity

A

Amiodarone

62
Q

Is not reverse-use dependent and prolongs the AP duration over a wide range of HRs and prolongs the QT interval on the ECG by blockade of IKr

A

Amiodarone

63
Q

Causes pulmonary fibrosis, microcrystalline deposits in the cornea and skin, and thyroid dysfunction

A

Amiodarone

64
Q

Structural analogue of amiodarone, lacking iodine

-lacks major side effects of amiodarone

A

Dronedarone

65
Q

Blocks IKur, IAch, and Ito in atria and is a less potent blocker of IKr

A

Vernakalant

66
Q

Anti-ischemic drug for chronic angina

-Lessens incidences of supraventricular arrhythmias including AF

A

Ranolazine

67
Q

Ca2+ channel blockers that are not useful as antiarrhythmics

A

Nifedipine and other dihydropyridines

68
Q

Block both activated and inactivated Ca2+ channels which decreases conduction velocity and increases refractory period

A

Ca2+ channel blockers verapamil and diltiazem

69
Q

Both verapamil and diltiazem also cause

A

Peripheral vasodilation

70
Q

Major use is to prevent reentrant atrioventricular nodal re-entrant tachycardia (AVNRT) PSVT

-Contraindicated in WPW Syndrome

A

Diltiazem and Verapamil

71
Q

Ca2+ channel blockers reduce automaticity by decreasing the

A

Phase 4 slope

72
Q

Activated inward rectifier K+ current, inhibits Ca2+ and If current, and causes hyperpolarization and suppression of Ca2+-dependent APs

A

Adenosine

73
Q

Drug of choice for prompt conversion of paroxysmal supraventricular tachycardia to sinus rhythm because of its high efficacy (90-95%)

A

Adenosine

74
Q

Cofactor for Na+/K+ ATPase and antagonist of Ca2+ channels

-Deficit is known to contribute to several arrhythmias

A

Magnesium

75
Q

Used as an adjunctive agent and can help control ventricular response in A-fib and flutter and may terminate some paroxysmal (reentrant) supraventricular arrhythmias

A

Digoxin

Cardiology (27 decks)

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