Antiarrhythmic Drugs - Quiz 2 Flashcards

(63 cards)

1
Q

atrial arrhythmias are treated to protect the ventricles using

A
  • AV blocking drugs “nodal agents”
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2
Q

example of dihydropyridines

A
  • Amlodipine - Nifedipine
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3
Q

Class 1C ion blockers

A
  • strong Na+ blockers
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4
Q

Class 1A ion blockers

A
  • moderate Na+ block
  • K+ block
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5
Q

which drug classes increase the length of the action potential duration

A
  • Class 1A - Class 3
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6
Q

examples of non-dihydropyridines

A
  • Verapamil
  • Diltiazem
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7
Q

what drug classes slow the recovery of Na+ channels during depolarization

A
  • Class 1A/B/C Na+ channel blockers
  • adenosine
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8
Q

ways to treat structural defects creating reentry circuits

A
  • increase refractory period
  • decrease conduction velocity
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9
Q

use of class 1C drugs

A
  • proarrhythmic
  • should not be used in patients with structural abnormalities
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10
Q

class 1A toxicities

A
  • prolonged AP - prolonged QT - Torsade
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11
Q

another name for abnormal automaticity of ectopic foci

A
  • premature beats
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12
Q

another name for abnormal automaticity of pacemaker cells

A
  • altered rate
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13
Q

how you increase action potential duration

A
  • block K+ channels
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14
Q

how do Class 4 drugs slow conduction through the AV node?

A
  • slow Ca2+ influx
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15
Q

abnormal conduction due to

A
  • reentry rhythms
  • AV blocks
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16
Q

which drug classes increase the length of the AP

A
  • Class 1A: Na+ channel blockers (K+ blockers)
  • Class 3: K+ channel blockers
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17
Q

how does adenosine increase the refractory period, but not the action potential duration?

A
  • slows Ca2+ influx
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18
Q

drugs that slow SA/AV node depolarization

A
  • class 4: Ca2+ channel blockers
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19
Q

example of a condition where a patient has structural abnormalities

A
  • post MI
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20
Q

Class 1C examples

A
  • flecainide - propafenone FRIES AND PEPSI
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21
Q

which drug classes are AV blocking drugs “nodal agents”

A
  • Class 2: beta antagonists
  • Class 4: Ca2+ channel blockers - Adenosine
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22
Q

drugs that increase threshold potential

A
  • Class 1: Na+ channel blockers
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23
Q

half life of adenosine

A
  • less than 30 seconds
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24
Q

drugs that increase action potential duration

A
  • class 3: K+ channel blocks
  • class 1A: Na+ channel blockers (K+ blockers)
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25
Class III drug examples
- amiodarone - dronedarone - dofetilide - sotalol 3 DADS - AS IF MY DADDY ISSUES AREN'T PERMEATING MEDICAL SCHOOL ENOUGH
26
drugs that increase maximum diastolic potential
- adenosine
27
selectivity of Class 1 Na+ channel blockers
- selective for rapidly depolarizing tissues
28
action potentials in SA/AV nodes versus action potentials in other cardiac myocytes?
- electrophysiologically different
29
five ways to decrease automaticity
- increase threshold potential (depolarization threshold) - decrease phase 4 slope - increase AP duration - slow SA/AV node depolarization - increase maximum diastolic potential
30
Class 1B drug examples
- lidocaine - mexiletine LIGHT MAYO
31
Class 1A effect on repolarization
- prolonged repolarization
32
Class 1C effect on repolarization
- no change in repolarization
33
two types of Ca2+ channel blockers
- dihydropyridine - non-dihydropyridine
34
importance of binding to Na+ channels in the open or inactive states
- renders them inactive - to trigger an AP, you need a certain amount of channels open
35
ways to treat defects in automaticity
- decrease automaticity
36
repolarization in SA/AV node due to
- outflow of K+
37
reentry rhythms create problems with
- structural defects creating reentry circuits
38
what drug is not associated with Torsade?
- amiodarone
39
which drugs prolong the QT interval?
- class 1A - Class 3
40
which Ca2+ channel blockers are anti-hypertensives?
- dihydropyridines - non-dihydropyridines
41
beta blocker drug examples
- metoprolol - propranolol
42
how do we administer adenosine
- rapid I.V. bolus
43
abnormal formation due to
- abnormal automaticity of pacemaker cells - abnormal automaticity of ectopic foci
44
Class III drug toxicities
- prolonged AP - prolonged QT - Torsade
45
adenosine pharmacokinetics issues
- super short half life
46
how does adenosine slow conduction through the AV node?
- increases maximum diastolic potential (makes it more negative)
47
how do Class II drugs slow conduction through the AV node?
- slow Na+ influx - reduce phase 4 slope
48
Class 1B effect on repolarization
- shortened repolarization
49
how do Class 1A/B/C increase the refractory period but not the action potential duration
- slowing the reset of Na+ channels - takes longer for enough resting channels to be available to initiate new action potentials
50
name for system where AAD are classified by their molecular mechanisms
- vaughn-williams classification
51
altered rate and premature beats are both defects in
- automaticity
52
drugs that decrease phase 4 slope
- Class 2: beta antagonists (beta blockers)
53
which Ca2+ channel blockers are anti-arrhytmics selective for
- non-dihydropyridines - selective for cardiac tissue
54
how to AADs increase the refractory period of cardiac myocytes
- increase the length of the AP - slow the recovery of Na+ channels during repolarization
55
depolarization in SA/AV node due to
- rapid influx of Ca2+
56
cause of arrhythmias
- abnormal formation - abnormal conduction
57
class 1b ion blockers
- weak Na+ block - K+ mechanism unclear
58
how Class II Beta antagonists decrease phase 4 slope
- compete for binding to beta 1 receptor with NE and E - slows rate at which funny channels depolarize (allow Na+ in)
59
name for system where AAD are classified by the effects they produce
- task force 1991 classification - Sicilian Gambit
60
automatic slow phase 4 depolarization in SA/AV node due to
- slow influx of Na+
61
MOA of adenosine
- promotes K+ efflux - increases diastolic membrane potential (makes more negative) in SA and AV nodes
62
Class 1A drug examples
- Quinidine - Procainamade - Disopyramide DOUBLE QUARTER POUNDER
63
MOA of Class 1 Na+ channel blockers
- slow the resetting of Na+ channels after an action potential - bind to the open or inactive states