Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Pharm Quiz > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

1
Q

atrial arrhythmias are treated to protect the ventricles using

A
  • AV blocking drugs “nodal agents”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

example of dihydropyridines

A
  • Amlodipine- Nifedipine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class 1C ion blockers

A
  • strong Na+ blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class 1A ion blockers

A
  • moderate Na+ block- K+ block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which drug classes increase the length of the action potential duration

A
  • Class 1A- Class 3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

examples of non-dihydropyridines

A
  • Verapamil- Diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A
  • Class 1A/B/C Na+ channel blockers- adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ways to treat structural defects creating reentry circuits

A
  • increase refractory period- decrease conduction velocity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

use of class 1C drugs

A
  • proarrhythmic - should not be used in patients with structural abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

class 1A toxicities

A
  • prolonged AP- prolonged QT- Torsade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

another name for abnormal automaticity of ectopic foci

A
  • premature beats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

another name for abnormal automaticity of pacemaker cells

A
  • altered rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how you increase action potential duration

A
  • block K+ channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  • slow Ca2+ influx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

abnormal conduction due to

A
  • reentry rhythms- AV blocks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which drug classes increase the length of the AP

A
  • Class 1A: Na+ channel blockers (K+ blockers)- Class 3: K+ channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A
  • slows Ca2+ influx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

drugs that slow SA/AV node depolarization

A
  • class 4: Ca2+ channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

example of a condition where a patient has structural abnormalities

A
  • post MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Class 1C examples

A
  • flecainide- propafenoneFRIES AND PEPSI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which drug classes are AV blocking drugs “nodal agents”

A
  • Class 2: beta antagonists- Class 4: Ca2+ channel blockers- Adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

drugs that increase threshold potential

A
  • Class 1: Na+ channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

half life of adenosine

A
  • less than 30 seconds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

drugs that increase action potential duration

A
  • class 3: K+ channel blocks- class 1A: Na+ channel blockers (K+ blockers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Class III drug examples

A
  • amiodarone- dronedarone- dofetilide- sotalol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

drugs that increase maximum diastolic potential

A
  • adenosine
27
Q

selectivity of Class 1 Na+ channel blockers

A
  • selective for rapidly depolarizing tissues
28
Q

action potentials in SA/AV nodes versus action potentials in other cardiac myocytes?

A
  • electrophysiologically different
29
Q

five ways to decrease automaticity

A
  • increase threshold potential (depolarization threshold)- decrease phase 4 slope- increase AP duration- slow SA/AV node depolarization- increase maximum diastolic potential
30
Q

Class 1B drug examples

A
  • lidocaine- mexiletineLIGHT MAYO
31
Q

Class 1A effect on repolarization

A
  • prolonged repolarization
32
Q

Class 1C effect on repolarization

A
  • no change in repolarization
33
Q

two types of Ca2+ channel blockers

A
  • dihydropyridine- non-dihydropyridine
34
Q

importance of binding to Na+ channels in the open or inactive states

A
  • renders them inactive- to trigger an AP, you need a certain amount of channels open
35
Q

ways to treat defects in automaticity

A
  • decrease automaticity
36
Q

repolarization in SA/AV node due to

A
  • outflow of K+
37
Q

reentry rhythms create problems with

A
  • structural defects creating reentry circuits
38
Q

what drug is not associated with Torsade?

A
  • amiodarone
39
Q

which drugs prolong the QT interval?

A
  • class 1A- Class 3
40
Q

which Ca2+ channel blockers are anti-hypertensives?

A
  • dihydropyridines- non-dihydropyridines
41
Q

beta blocker drug examples

A
  • metoprolol- propranolol
42
Q

how do we administer adenosine

A
  • rapid I.V. bolus
43
Q

abnormal formation due to

A
  • abnormal automaticity of pacemaker cells- abnormal automaticity of ectopic foci
44
Q

Class III drug toxicities

A
  • prolonged AP- prolonged QT- Torsade
45
Q

adenosine pharmacokinetics issues

A
  • super short half life
46
Q

how does adenosine slow conduction through the AV node?

A
  • increases maximum diastolic potential (makes it more negative)
47
Q

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

A
  • slow Na+ influx- reduce phase 4 slope
48
Q

Class 1B effect on repolarization

A
  • shortened repolarization
49
Q

how do Class 1A/B/C increase the refractory period but not the action potential duration

A
  • slowing the reset of Na+ channels- takes longer for enough resting channels to be available to initiate new action potentials
50
Q

name for system where AAD are classified by their molecular mechanisms

A
  • vaughn-williams classification
51
Q

altered rate and premature beats are both defects in

A
  • automaticity
52
Q

drugs that decrease phase 4 slope

A
  • Class 2: beta antagonists (beta blockers)
53
Q

which Ca2+ channel blockers are anti-arrhytmicsselective for

A
  • non-dihydropyridines- selective for cardiac tissue
54
Q

how to AADs increase the refractory period of cardiac myocytes

A
  • increase the length of the AP- slow the recovery of Na+ channels during repolarization
55
Q

depolarization in SA/AV node due to

A
  • rapid influx of Ca2+
56
Q

cause of arrhythmias

A
  • abnormal formation- abnormal conduction
57
Q

class 1b ion blockers

A
  • weak Na+ block- K+ mechanism unclear
58
Q

how Class II Beta antagonists decrease phase 4 slope

A
  • compete for binding to beta 1 receptor with NE and E- slows rate at which funny channels depolarize (allow Na+ in)
59
Q

name for system where AAD are classified by the effects they produce

A
  • task force 1991 classification- Sicilian Gambit
60
Q

automatic slow phase 4 depolarization in SA/AV node due to

A
  • slow influx of Na+
61
Q

MOA of adenosine

A
  • promotes K+ efflux - increases diastolic membrane potential (makes more negative) in SA and AV nodes
62
Q

Class 1A drug examples

A
  • Quinidine- Procainamade- DisopyramideDOUBLE QUARTER POUNDER
63
Q

MOA of Class 1 Na+ channel blockers

A
  • slow the resetting of Na+ channels after an action potential- bind to the open or inactive states

Cardio Pharm Quiz (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions