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Therapeutics Module 3 > Atrial Arrhythmias > Flashcards

Atrial Arrhythmias Flashcards

1
Q

What is atrial fibrillation

A

Essentially it is electrical impulses triggered from multiple locaitosn in the atria

Electrical activity is chaotic rather than organized where the atrial walls quiver.

EF is reduced

Ventricular rate is generall elevated

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2
Q

What is atrial flutter?

A

Coordinated electrical activity in the atria. We see rapid rate of contraction

Rate is too fast to allow each impulse to be conducted through the AV node

Generally about every 2nd beat gets through

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3
Q

What is the most common sustained cardiac arrhythmia?

A

Atrial fibrillation

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4
Q

What components of A-FIB that are irregular

A
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5
Q

What is the general incidence of A-Fib

A

◦ 0.4% of adults < 60 years old
◦ 2-5% in those over the age of 60 ◦ >6% in those over the age of 80

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6
Q

What is the morbidity and mortality of AF?

A

Rarely a life threatening condition, but AF is associated with decreased health related quality of life as well as increased morbidity and mortality

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7
Q

What are the symptoms of AF?

A

◦ Fatigue
◦ Palpitations
◦ Chest Pain
◦ dyspnea
◦ Dizziness

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8
Q

What is the general pathogenesis of AF?

A

ectopic foci that generate electrical impulses

rapid irregular and uncoordinated contractions

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9
Q

What is the classifications of AF?

A

Valvular
Non-Valvular
Lone (Absence of clinical or echocardiographic findings)

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10
Q

What is Paroxysmal AF?

A

lasting longer than 30 seconds and self-terminating within 7 days of recognized onset

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11
Q

What is persistent AF?

A

continuous AF episode lasting longer than 7 days but less than 1 year

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12
Q

What is longstanding persistent AF?

A

continuous AF equal or greater than 1 year in who rhythm control

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13
Q

Risk factors of A-FIB (Figure on next slide)

A
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14
Q

What is poor health outcome that AF can lead to?

A

Stroke

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15
Q

What increases the likely hood of Afib

A

Age

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16
Q

What is the Goal of therapy in AF?

A

◦ Prevent stroke or systemic thromboembolism

◦ Cardiovascular risk reduction

◦ Improve symptoms, functional capacity and quality of life

◦ Prevent complications (eg. LV dysfunction and falls)

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17
Q

What is the CHADS2 score?

A
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18
Q

If someone has a CHADS2 score >2 what do we start them on?

A

OAC therapy

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19
Q

If someone is over the age of 65 what therapy is started?

A

OAC therapy

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20
Q

If someone does not pass the chads2 score <2, but has CAD?

A

Antiplatelet therapy such as clopidogrel

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21
Q

If someone has a BMI of greater then 50kg/m2 which DOAC do we use?

A

warfarin

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22
Q

Look at the next chart for DOAC dosing for stroke prevention and renal function

A
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23
Q

What is the dosing of Apixaban and Dabigatran?

A

Twice Daily

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24
Q

What is the dosing pattern of Edoxaban and Rivaroxaban?

A

once daily

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25
Q

Is a DOAC preferred over a warfarin?

A

DOAC yes.

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26
Q

What is BMI associated with?

A

Lower stroke rates higher bleeding rates

27
Q

In DOAC therapy what is recomended?

A

Generally BMI >=50 we want to use warfarin,

We can use other DOAC but with caution

28
Q

Which medication requires food for absorption?

A

Rovaroxaban

29
Q

What drugs does Dabigatran and edoxaban interaction with?

A

strong inhibitors or inducers of P-
glycoprotein (P-gp)

30
Q

What medicaitons does Apixaban and rivaroxaban interact with?

A

avoid combining with strong
inhibitors or inducers of both CYP 3A4 and Pglycoprotein (P-gp)

31
Q

Which medications have a an antidote?

A

Dabigatran (Idarucizumab)

Factor Xa inhibitors (Andexanet)

32
Q

What is the dosing pattern of apixaban and dabigatran?

A

Twice daily

33
Q

What is the dosing pattern of edoxaban and rivaroxaban?

A

Once daily

34
Q

When do DOACs not have a place in therapy?

A

Mechanical heart valves
Pregnancy and lactation
Pediatrics

35
Q

Other then lab values what other patient factors need to be monitored?

A

Adherence
Adverse effects
S and S
Regualr SCr, CrCl, Hgb

36
Q

If we have someone who has persistent AF what should be considered?

A

Initiate rate-control therapy and consider long-term treatment

37
Q

What drugs do we use for LVEF >40 if the individuals have high HR?

A

Beta blockers and ND-CCB

38
Q

Which CCB has rhythm control properites/

A

NDCCB

39
Q

What medications are considered first line if someone has LVEF of less then 40?

A

beta blockers

40
Q

Where is Digoxins place in therapy for long term rate control?

A

Secondary addition

41
Q

If someone requires acute rhythm control what is usually started?

A
42
Q

What are the SA NODE and AV node?

A

Slow conducts that are activated by calcium

43
Q

What are the conduction fibers?

A

Fast conductors and are generally activated by sodium

44
Q

What are the 2 general types of cardiac action potentials?

A

Pacemaker cells
Non-pacemaker cells

45
Q

What causes rapid depolarization?

A

Na influx

46
Q

What begins initial repolarizaiton?

A

K eflux

47
Q

What causes a slow depolarizaiton?

A

Ca2+

48
Q

What causes repolarizaiton? after the initial depolarization phase?

A

Potassium

49
Q

What are the two types of arrhythmias?

A

Impulse generation
Impulse conduction

50
Q

Take some time to look at this next graph

A
51
Q

What are the two ND-CCB we should know?

A

verapami, diltiazem

52
Q

What is the MOA of Digoxin

A

Increases AV node refractoriness

53
Q

What is bradyarrythmias

A

Slow heart rate less then 60

54
Q

What is the life threatening form of Ventricular tachyarrhythmia?

A

Torsade de Pointes

55
Q

What is the treatment for Torsade de Pointes

A

Magnesium sulfate, Cardioversion

56
Q

What scale can be used to identify individual patient risk of QT prolongation?

A

Tisdale score

57
Q

What are the components of the Tisdale score?

A
58
Q

What are we worried about with QT prolongation?

A

Torsade De Pointes

59
Q

What are the Sodium channel blocking medications?

A
60
Q

What are the potassium channel blocking medications?

A
61
Q

What are the ndp-ccb

A

Verapamil, diltiazem

62
Q

What do the sodium channel blocking medications do?

A

Increases depolarization event of the ventricle in some matter

63
Q

What does the potassium blocking medications do to ventricular action potential?

A

prolong the refactor period

64
Q
A

Therapeutics Module 3 (6 decks)

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