Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular > Antiarryhthmics > Flashcards

Antiarryhthmics Flashcards

1
Q

action Class 1A Na channel blockers

(quinidine, procainamide, dispyramide)

A

moderate 0 deepression

slowed conduction (+2)

shorten repol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

phase 2 =

A

plateau phase

blanced inward Ca and outward K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

action of Sotalol

A

block IKr channel

B block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ic na channel blockers

A

flecainide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

action class IV drugs

verapamil, diltiazem

A

Ca channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

side effects Lidocaine

A

dizziness

seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

side effects Beta blockers

A

negative ionotropic

heart block,

bradycardia

bronchospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

catecholamine impact on depolarization

A

enhance depl in slow response cells (no impact in fast response cells)

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

specific side effects, diltiazem (less so in other Ca blockers )

A

interact with digitalis to slow AV conduction > heart block (and verapamil)

compete for digitalis renal excretion (and verapamil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

indications sotalol

A

VF VT

supravent tachycardia

a fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

impact, flecainide

threshold

vmax

A

increase threshold

decrease Vmax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

main physiological effect of fleccainide

A

strongest change in depol (slight in duration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

side effects amiodarone

A

triggered arrhythmias (torases de pointes rare)

altered thyroid fxn (inhibts T4>T3) > hypothyroidism

pulmonary fibrosis (reversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

impact, Na channel blockers (Class I)

membrane responsiveness

threshold

Vmax

Refractory

A

reduce mem responsiveness

increase threshold

decrease Vmax

increase refractory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

indirect effects QUinidine, class Ia na blockers

A

block K channels early after depol (EAD)

Vagolytic effect - enahnce communication across AV > Vtach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

phase 3 =

A

rapid repolarization

(L type close while K still open)

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

indications flecainide

A

approved in life-threatenign when supraventricular and ventricular arrhythmias are resistant to other drugs

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

action of class II drugs

Propanolol, esmolol

A

beta adrenergic blockers

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

class III K channel blockers

A

amiodarone

sotalol

dofetilide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

class IV Ca channel blockers

A

verapamil

diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

since beta blockers do not _____, they are safe for pt with Long Qt

A

prolong repolarizaation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

indications Adenosine

A

supraventricular tachycardia (slows AV conduction and heart rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

1-4-dihydropyridines are not used as antiarrhythmics because,

they are used, however, to relieve

A

primarily target vascular cells (vs cardiac)

used to relieve angia pectoris to relieve chest spasms

19
Q

Class IV Ca blockers (Diltiazem and Verapamil) act primary on ___ cells
which are dependent on ___ for AP depol

A

act primarily on slow response cells (AV and SA nodes) which are dependent on Ca influx for AP

20
Q

action 1C Na blockers

flecainide

A

Marked 0 depression

slow conduction (4+)

little impact on repol

21
Q

triggered automaticity after repolarization excerbated by

A

fast rates

high intracellular Ca

23
Q

class IA Na Channel blockers

A

quinidine

procainamide

disopyramide

24
Q

action 1b Na blockers

(lidocaine)

A

minimal phase 0 depression

slow conduction (0- 1+)

shorten repol

26
Q

indications lidocain

A

Vtach

Digitalis - induced arrhthmias

Safe for pts with long QT syndrome

27
Q

indications Ca blockers

A

Atrial tachycardia

paroxysmal supraventricular tachycardia

28
Q

mechanism DIoxin

A

enhances vagal parasympathetic activity > slow conduction at AV node

29
Q

mechanism Adenosine

A

rapidly activates K channels to slow phase 4 depol at AV node

blocks cAMP enhance Ca channel activity at AV node

30
Q

nifedipine specific side effects (weaker in other Ca blockers)

A

peripheral edema

31
Q

side effects felcainide

A

pro-arrhtyhmic (CAST trial)

32
Q

all actions of amiodarone (class III)

A

**K blocker **

Modest Na, Ca blocker

modest B adenoreceptor blocker

33
Q

ach impact on depolarization

A

significantly depresses depol in slow response cells (no effect inf ast)

34
Q

indications, Beta blockers

A

arrhythmias

VF vT with high catecholamine

(SA and AV node highly innervated)

35
Q

action calsss III drugs

amiodarone, sotalol, dofetilide

A

K channel blockers

36
Q

triggered automaticity, intterupted repolarization exacerbated by

A

long QT syndrome

38
Q

phase 1

A

inactivation of fast Na chennels (or closure of L-type Ca)

39
Q

Torsade de Pointes in pt on sotalol

A

U wave likely due to long repol of purkinje fibers

post ectopic pause + long QT

40
Q

phase 4 =

A

resting membrane potential

(mostly K)

41
Q

4 ways antiarrhythmic drugs reduced spontaneous discharge

A

1 decrease phase 4 slope (slow rate)

  1. increase max diastolic potential (more negative, further from threshold)
  2. Increase threshold
  3. increase AP duration > increase refractory period
42
Q

phase 0

A

rapid depol of AP phase (Na in fast cells, Ca L-type in slow cells)

43
Q

impact, lidocaine

threshold

AP

refractory rate

A

increase threshold

decrease AP duration

decrease refractory

44
Q

Class II beta adrenergic blockers

A

propanolol, esmolol

45
Q

class IB Na channel blockers

A

Lidocaine

46
Q

verapamil side effects (less so in other Ca blockers )

A

constipation

interaction with digitalis to slow conduction velocity in AV > hear block (and verapamil)

increase plasma digitalis levels by competing for renal excertion (and verapamil)

48
Q

short, long acting B blockers

A

propanolol - long, oral

esmolol - short, IV

49
Q

indications Digoxin

A

Afib and supravent tachycardia

(to control ventricular response rate)

50
Q

major side effects Ca blockers

A

Negative chronotropic effect - decreases automaticity of SA (brady)

Negative ionotropic (decrease Ca influx)

hypotension (decrease Ca into smooth muscle)

51
Q

indication amiodarone (class III)

A

VF VT

prevention of reccurent paroxysmal a fib or flutter

52
Q

most common target of Class III (amiodarone, sotalol)

A

IKr channel (increases Refractory peirod) (possible arrhytmias)

53
Q

indications quinidine

A

atrial flutter

A fib

prevent VF VT

54
Q

action of beta blockers in presence of catecholamines

A

slow rate of diastolic (phase 4) depolarization)

55
Q

major side effects QUinidine

A

Severe GI

Vagolytic

inhibits p450s

Proarrhythmic,

reduced renal clearance of digitalis

metabolized by liver (renal failre pt OK)

Cardiovascular (39 decks)

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