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
do not combine with CYP2d6 and CYP3A4 inhibitors
propafenone
26
increases RR interval
class 2 drugs
27
increases PR interval and decreases Ca overload
class 2 drugs
28
does not prolong AP duration, QT interval on ECG, but does prolong QRS interval duration
class 1c drugs
29
blocks inactivated Na channels blocks potassium channels, does NOT block QT duration on ECG
class Ib drugs
30
prolongs QRS and QT intervals on the ECG
class 1A drugs
31
agranulocytosis, pleuritis, arthritis, hepatitis, pulmonary dx
procainamide
32
thrombocytopenia, cinchonism, n/v
quinidine
33
may cause HypoT--> tachycardia
quinidine
34
recurrent ventricular arrhythmias
disopyramide
35
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
disopyramide
36
preferentially binds to depolarized cells and no effect on conduction in normal tissue
class 1B drugs
37
class 1 drug that may shorten AP
class 1B
38
VERY efficiency in arrythmias associated with acute MI
lidocaine
39
extensive 1st pass metaboilsm, used only by the intravenous route
lidocaine
40
least toxic of all class 1 drugs
lidocaine
41
neurological effects: parasthesias, tremor, slurred speech, convulsion
lidocaine
42
used for ventricular arrhythmias and to reduce pain in diabetes associated neuropathy
mexiletine
43
orally active drug in class 1
mexiletine
44
1. metallic taste, constipation, exacerbation of ventricular arrythmias
propafone
45
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
class 2 drugs
46
half life is 10 minutes because it's hydrolyzed in the blood so quickly. how is it administered?
esmolol: administered via continuous IV infusion
47
used to tx arrhythmias associated with thyrotoxicosis
esmolol
48
used to tx arrhythmias in acute MI and mycocardial ischemia
esmolol
49
MOA: blocks K channels
class 3 drugs
50
prolongs AP duration and QT interval on ECG
class 3 drugs
51
action potential depolarization is rate dependent, and has the most marked effect at slow rates
class 3 drugs
52
prolongs refractory period
class 3 drugs
53
prolongs QT interval and ADP uniformly over a wide range of heart rates
amiodarone
54
a class 3 drug that blocks inactivated Na channels
amiodarone
55
possesses adrenolytic activity
amiodarone
56
has calcium channel blocking activities
amiodarone
57
class 3 drug that induces peripheral vasodilation
amiodarone
58
two clinical uses for amiodarone
tx of ventricular arrhythmias and atrial fib (although the FDA does not approve of the latter)
59
class 3 drug metabolized by CYP3A4
amiodarone
60
two drugs that alter amiodarone's metabolism
cimetidine (CYP3A4 inhibitor) and rifampin (CYP3A4 inducer)
61
amiodarone metabolism produces what
active metabolite, whose half life is weeks to months
62
up to how long can you still find amiodarone in the body?
up to a year
63
ADE of amiodarone
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
amiodarone derivative
dronedarone but without iodine moiety
65
MOA dronedarone
1. blocks multiple potassium channels 2. blocks L type Ca current --> decreased nodal conduction-->bradycardia 3. prolongs AV refractory period--> increases PR interval
66
in terms of adrenergics, how does dronedarone differ from amiodarone?
dronedarone has strong anti-adrenergic effects
67
T/F: dronedarone is weaker than amiodarone in maintaining sinus rhythm in AFIB/flutter patients
T
68
what are the advantages of dronedarone's toxicology profile?
shorter half life, no iodine moiety, less drug interactions
69
AE of dronedarone
abdominal pain, n/v, diarrhea
70
black box warning for dronedarone
increases risk of mortality in patients with decompensated HF and those with HF requiring hospitalization
71
dofetilide
blocks rapid