AF Flashcards

1
Q

What is AF?

A

Irregular/disorganised rhythm of atria

Disorganised firing of signals from atria

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2
Q

What are the causes?

A

• HTN
• T2DM
• Hyperthyroidism

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3
Q

How does AF increase the risk of stroke

A

There is a standstill of blood in the atria, which increases the risk of thrombosis (stroke)

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4
Q

What are the 3 classifications of AF?

A

• proximal
• persistent
• permanent

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5
Q

Describe Proximal AF

A

• lasts 30mins + BUT less than 7 days
• self terminating
• recurrent

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6
Q

Describe Persistent AF

A

• lasts -/+ 7 days
• requires chemical or physical Cardioversion

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7
Q

Describe Permanent AF

A

• does not terminate with Cardioversion
• or if terminates it returns within 25 hours

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8
Q

Detecting AF in people with irregular pulse, with or without:

A

• SOB
• palpitations
• chest pain
• stroke/TIA

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9
Q

Diagnosis/Investigations of AF

A

• Echo
• ECG

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10
Q

AF increases stroke risk by how many folds?

A

5 folds

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11
Q

List general ADRs of antiarythmics

A

Gi disturbances:
• nausea
• vomiting
• diarrhoea

CNS disturbances:
• hallucinations
• nightmares
• depression
• psychosis
• sezuires

Others:
• pro arrhythmic- TDP
• visual disturbances

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12
Q

List non drug therapy approaches in AF

A

• defibrillators
• cardioversion
• pacemakers
• interval Cardioversion defibrillators

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13
Q

Why may patients avoid antiarythmics?

A

• can cause new arrhythmia
• can increase the frequency of arrhythmia
• can cause ventricular tachycardia (TDP)

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14
Q

What is “Vaugh Williams classification” regarding antiarythmics?

A

These agents are classified based on their electrical activity towards myocardial cells

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15
Q

List the classes of agents

A

Class 1a = disopydramide
Class 1b = lidocaine
Class 1c = flecainide
Class 2 = beta blockers
Class 3 = amidarone
Class 4 = non-diydrophyradines - CCBs

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16
Q

Which phases of the action potential do they affect

A

Class 1 (all) - phase 0
Class 2 - phase 4
Class 3 - phase 3
Class 4 - phase 2

17
Q

What is the MOA of class 1 agents?

A

Block na ions from entering voltage gated na channels - this slowing down electrical activity/AP - during phase 0

18
Q

What is the MOA of class 2 agents?

A

Beta blockers

• inhibits effects of sympathetic nervous system
• negative inotrope
• negative chronotrope

  • during phase 4
19
Q

What is the MOA of class 3 agents

A

• blocks k channels, thus prolonging AP duration

20
Q

What is the MOA of class 4 agents?

A

Blocks ca ions - during phase 2

21
Q

What is the main reason behind managing arrhythmia?

A

Prevent/avoid stroke

^ asses stroke and bleeding risk

22
Q

CHA2DS2-VASC is used to assess what? And in which patients?

A

Stroke risk (thrombotic) in patients with the following:
• asymptomatic/symptomatic AF
• atrial flutter
• risk of recurrent arrhythmia after Cardioversion

23
Q

What does CHA2DS2-VASC stand for?

A

• congestive cardiac disease
• HTN (including history)
• Age: 75 and over
• Diabetes
• Stroke/TIA
• Vascular disease
• Age: 65-74
• Sex: female

Each score 1 point
Stroke and Age (75+) score 2 each

24
Q

CHA2DS2-VASC - when to anticoagulant

A

•Score 2 or more (both genders) = offer anticoagulants
•Score 1 in men = consider anticoagulants
•Score 1 in women = NONE
•Score 0 (both genders) = NONE

25
Q

ORBIT is used to assess what?

A

Bleeding risk when:
• starting new anticongulant OR
• review those already on it.

26
Q

List MODIFIABLE risk factors for bleeding

A

• poor control of INR
• HTN
• concurrent use of: NSAID + SSRIs + antiplatlets
• anaemia
• renal and hepatic impairment

27
Q

List NON- MODIFIABLE risk factors for bleeding

A

• older age
• hx of bleeding
• hx of stroke
• cancer
• liver disease
• dialysis

28
Q

What is the Treatment for valvular AF

A

Warfarin

29
Q

What is the Treatment for non-valvular AF

A

After calculating stroke risk with scoring system - DOACs

30
Q

Which rate controlling drugs can be given?

A

Beta blocker (not sotalol)
OR
Non dihydropyradine CCB
• diltiazem (off label)
• verapamil

31
Q

DOACs advantages and disadvantages

A

Advantages:
• quick onset of action
• therapeutic activity is predictable
• target enzyme specificity
• fewer drug-drug interactions
• as affective as warfarin, with less intercrainial haemorrhage

Disadvantage
• more frequent dosing than warfarin (reason for no compliance)
• lack of long term safety data
• expensive
• short half life
• no commercially available antidote
• no evidence for efficacy in valvular AF

32
Q

Warfarin Advantages and disadvantages

A

Advantages;
• cheap
• gold standard- used for 50> years
• antidote - vitamin K
• prescriber familiar with management and ADRs
• once daily dosing (better compaince)

Disadvantages
• drug to drug interactions
• food to food interaction
• slow onset of action
• requiring INR testing
• narrow therapeutic windows
• unpredictable therapeutic response