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Cardio II Yr II > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

1
Q

Reserved for use in patients with no significant organic/structural heart disease (e.g. no evidence of coronary artery disease such as angina pectoris or previous MI) (yet are arrhythmic

A

quinidine- class 1A

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2
Q

Sustained Ventricular Arrhythmias, has unforuntate pro-arrythmia side effects,
mixed Na channel blocker & K channel blocker, decreased ectopic pacemaker activity

A

quinidine 1A

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3
Q

restore sinus rhythm in patients who are not adequately controlled by drugs that reduce the ventricular response, or to reduce the frequency of relapse into atrial fib/flutter

A

quinidine, class 1a

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4
Q

anticholinergic side effects that can decrease the AV node’s Effective Refractory Period, which can result in a rapid acceleration of ventricular rate (which is potentially dangerous in patients with coronary artery disease)

A

quinidine, class 1a

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5
Q

diarrhea, cinchonism

A

quinidine, class 1a

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6
Q

increased by coadministration of amiodarone or cimetidine

A

quinidine 1a

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7
Q

commonly develop a positive anti-nuclear antibody (ANA) titer

A

procainamide, class 1a

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8
Q

Weak ganglionic blocker (use cautiously in patients with atrial tachyarrhythmias)

A

procainamide class 1a

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9
Q

Negative inotropic effects (use cautiously in CHF)

A

procainamide class 1a

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10
Q

Effective against most atrial & ventricular arrhythmias

Life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia.

A

procainamide class 1a

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11
Q 
slurred speech
numbness (around the lips)
blurred vision
twitching, convulsions 
parasthesias
A

lidocaine

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12
Q

ventricular cardiac arrhythmias (esp. post-MI

A

lidocaine

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13
Q

weak β-blocking activity

A

propafenone

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14
Q

Treatment of paroxysmal atrial fibrillation/flutter & PSVT in patients WITHOUT structural heart disease.

A

propafenone

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15
Q

has pro-arrhythmic potential, but can be used with caution to treat ventricular arrhythmias (such as sustained VT) that are judged to be life-threatening.

A

propafenone

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16
Q

cardiac arrhythmias (atrial tachyarrhythmias induced by catecholamines, digitalis, thyrotoxicosis, or associated with Wolff-Parkinson-White syndrome; for the control of ventricular rate in patients with atrial flutter or fibrillation when digoxin is ineffective or contraindicated, ventricular arrhythmias caused by catecholamines or digoxin).

A

propanolol

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17
Q

prevention of sudden death and reinfarction after an MI.

A

propanolol

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18
Q

cutely blocks IKr, but IKs also becomes reduced with chronic therapy

A

amiodarone

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19
Q

arrythmias associated with stress

A

propanolol

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20
Q

rentrant arrythymias that involve AV node

A

propanolol

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21
Q

decreases mortality in patients suffering acute MI

A

propanolol

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22
Q

avoid in patients with pre-existing ventriculat tachyarrythmias

A

flecainide

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23
Q

avoid in patients with previous MI

A

flecainide

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24
Q

avoid in patient with ventricular ectopic rhythms

A

flecainide

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25
Q

do not combine with CYP2d6 and CYP3A4 inhibitors

A

propafenone

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26
Q

increases RR interval

A

class 2 drugs

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27
Q

increases PR interval and decreases Ca overload

A

class 2 drugs

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28
Q

does not prolong AP duration, QT interval on ECG, but does prolong QRS interval duration

A

class 1c drugs

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29
Q

blocks inactivated Na channels blocks potassium channels, does NOT block QT duration on ECG

A

class Ib drugs

30
Q

prolongs QRS and QT intervals on the ECG

A

class 1A drugs

31
Q

agranulocytosis, pleuritis, arthritis, hepatitis, pulmonary dx

A

procainamide

32
Q

thrombocytopenia, cinchonism, n/v

A

quinidine

33
Q

may cause HypoT–> tachycardia

A

quinidine

34
Q

recurrent ventricular arrhythmias

A

disopyramide

35
Q

QT prolongation, induction of torsade de pointes arrhythmia + syncope, negative inotropic effect. atropine-like symptoms, urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma

A

disopyramide

36
Q

preferentially binds to depolarized cells and no effect on conduction in normal tissue

A

class 1B drugs

37
Q

class 1 drug that may shorten AP

A

class 1B

38
Q

VERY efficiency in arrythmias associated with acute MI

A

lidocaine

39
Q

extensive 1st pass metaboilsm, used only by the intravenous route

A

lidocaine

40
Q

least toxic of all class 1 drugs

A

lidocaine

41
Q

neurological effects: parasthesias, tremor, slurred speech, convulsion

A

lidocaine

42
Q

used for ventricular arrhythmias and to reduce pain in diabetes associated neuropathy

A

mexiletine

43
Q

orally active drug in class 1

A

mexiletine

44
Q
  1. metallic taste, constipation, exacerbation of ventricular arrythmias
A

propafone

45
Q

MOA:
decreases HR by ↓ RR interval @ the SAN,
decreases ventricular contractions by ↓ AV conductance and increasing the PR interval, and decreases Ca overload in the ventricular myocardium, which prevents delayed after depolarizations

A

class 2 drugs

46
Q

half life is 10 minutes because it’s hydrolyzed in the blood so quickly. how is it administered?

A

esmolol: administered via continuous IV infusion

47
Q

used to tx arrhythmias associated with thyrotoxicosis

A

esmolol

48
Q

used to tx arrhythmias in acute MI and mycocardial ischemia

A

esmolol

49
Q

MOA: blocks K channels

A

class 3 drugs

50
Q

prolongs AP duration and QT interval on ECG

A

class 3 drugs

51
Q

action potential depolarization is rate dependent, and has the most marked effect at slow rates

A

class 3 drugs

52
Q

prolongs refractory period

A

class 3 drugs

53
Q

prolongs QT interval and ADP uniformly over a wide range of heart rates

A

amiodarone

54
Q

a class 3 drug that blocks inactivated Na channels

A

amiodarone

55
Q

possesses adrenolytic activity

A

amiodarone

56
Q

has calcium channel blocking activities

A

amiodarone

57
Q

class 3 drug that induces peripheral vasodilation

A

amiodarone

58
Q

two clinical uses for amiodarone

A

tx of ventricular arrhythmias and atrial fib (although the FDA does not approve of the latter)

59
Q

class 3 drug metabolized by CYP3A4

A

amiodarone

60
Q

two drugs that alter amiodarone’s metabolism

A

cimetidine (CYP3A4 inhibitor) and rifampin (CYP3A4 inducer)

61
Q

amiodarone metabolism produces what

A

active metabolite, whose half life is weeks to months

62
Q

up to how long can you still find amiodarone in the body?

A

up to a year

63
Q

ADE of amiodarone

A

av block brady
fatal pulmonary fibrosis
hepatitis
photodermatitis
blue-grey skin (deposits on skin) discoloration in sun exposed areas
drug-deposits in cornea
optical neuritis
blocks peripheral conversion of thyroxine to triiodothryonine- may cause hypo or hyperthyroidism
note: amiodarone DOES have an iodine moiety (inorganic)

64
Q

amiodarone derivative

A

dronedarone but without iodine moiety

65
Q

MOA dronedarone

A
  1. blocks multiple potassium channels
  2. blocks L type Ca current –> decreased nodal conduction–>bradycardia
  3. prolongs AV refractory period–> increases PR interval
66
Q

in terms of adrenergics, how does dronedarone differ from amiodarone?

A

dronedarone has strong anti-adrenergic effects

67
Q

T/F: dronedarone is weaker than amiodarone in maintaining sinus rhythm in AFIB/flutter patients

A

T

68
Q

what are the advantages of dronedarone’s toxicology profile?

A

shorter half life, no iodine moiety, less drug interactions

69
Q

AE of dronedarone

A

abdominal pain, n/v, diarrhea

70
Q

black box warning for dronedarone

A

increases risk of mortality in patients with decompensated HF and those with HF requiring hospitalization

71
Q

dofetilide

A

blocks rapid

Cardio II Yr II (18 decks)

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