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Cardiology Disease Profiles > Atrial Fibrillation > Flashcards

Atrial Fibrillation Flashcards

1
Q

How does the SA node usually work?

A

Produces organized electrical conductivity coordinating contraction of the atria

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2
Q

How does SA node work in A fib?

A

Contraction of atria is uncoordinated, rapid & irregular. This is due to disorganised activity from SA node

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3
Q

What does a lack of P waves on an ECG convey?

A

Lack of P waves, reflecting lack of coordinated atrial electrical conductivity
-This leads to irregular conduction of electrical impulses to ventricles

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4
Q

What does irregular conduction of electrical impulses to ventricles result in?

A
  • Irregularly irregular ventricular contractions
  • Tachycardia
  • Heart failure
  • Risk of stroke
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5
Q

Presentation of A fibrillation?

A

Patients often asymptomatic however can present with

  • Palpitations
  • SOB
  • Syncope (dizziness/fainting)
  • Symptoms of associated conditions
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6
Q

Differential diagnosis for an irregularly irregular pulse?

A
  • Atrial fibrillation

- Ventricular ectopics

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7
Q

How do you decide between A Fib and ventricular ectopics?

A

Differentiated using ECG.

Ventricular ectopics disappear when heart rate goes above a threshold for example in exercise

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8
Q

What does A Fib look like on an ECG?

A

Absent P waves
Narrow QRS complexes (tachycardia)
Irregularly irregular ventricular rhythm

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9
Q

Assumption for patients with valvular AF?

A

If they have AF but also mitral stenosis/mechanical valve the assumption is vascular pathology has lead to A Fib.

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10
Q

Non-valvular atrial fibrillation is?

A

AF without valve pathology

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11
Q

Causes of A fib + pneumonic?

A 
mrs SMITH gets AFIB
S- Sepsis
M-Mitral valve disease 
I- Ischaemic heart disease 
T- Thyrotoxicosis 
H- Hypertension
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12
Q

2 principals of treating AF?

A

Control rhythm or rate

Anticoagulation (prevents stroke)

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13
Q

Why do you need to control heart rate in AF?

A

Increased HR means less time for ventricles to fill up with blood and decreased CO
Aim is to get HR under 100BPM

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14
Q

What should all AF patients have as first line treatment?

A

Rate control

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15
Q

Reasons why rate control shouldn’t be used as first line treatment for AF?

A

AF has reversible cause
AF is of new onset
AF is causing HF
They remain symptomatic despite rate control

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16
Q

Drug options for rate control?

A
  • Beta blockers: 1st line (atenolol)
  • CCB diltiazem (not preferable in HF)
  • Digoxin (only in sedentary people)
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17
Q

Who is rhythm control for?

A

All patients who can’t have rate control for specific reasons

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18
Q

Aim of rhythm control?

A

Return patient to normal sinus rhythm

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19
Q

How is rhythm control achieved?

A

Single cardioversion event

Long term medical rhythm control

20
Q

What is immediate cardioversion?

A

AF presents less than 48 hours or patient is severely haemodynamically unstable

21
Q

What is delayed cardioversion?

A

AF presents for more than 48 hours & they are stable

22
Q

What is necessary for delayed cardioversion?

A

Patient should be on anti-coagulants for minimum 3 weeks prior & have rate control

23
Q

2 types of cardioversion?

A

Pharmacological Cardioversion

Electrical Cardioversion

24
Q

1st line pharmacological cardioversion?

A

Flecanide. amiodarone

25
Second line pharmacological cardioversion?
- Sedation/general | - Using cardiac defibrillator to drive controlled shocks until sinus rhythm
26
1st line long term rhythm control?
Beta blockers Dronedarone Amiodarone
27
What is paroxysmal AF?
AF that comes and goes in episodes of usually less than 48 hours
28
How should paroxysmal AF patients be treated?
Consider pill in pocket approach - take only when they feel AF symptoms coming on - Need to have infrequent episodes without underlying structural heart disease and also fully understand how to identify an episode and when to take treatment
29
What is usually used for paroxysmal AF?
Flecanide
30
Why do you need to take anti-coagulants in AF?
Because the uncontrolled movement of atria results in blood stagnating in left atrium which eventually leads to thrombus which then mobilises and becomes an emblous in the blood This travels to atria-ventricles-aorta- Carotid arteries- brain
31
What does an embolus eventually possibly block?
Cerebral arteries resulting in ischaemic stroke
32
What is warfarin?
Vitamin K antagonist
33
How to measure how anti-coagulated a patient is on warfarin?
INR (international normalised ratio)
34
What does an INR of 1 mean?
Normal prothrombin time
35
What does an INR of 2 mean?
Twice as long to forma blood clot
36
What are NOACs?
NOvel anticoagulants
37
Examples of DOACs?
Rivaroxaban Dabigatran Apixaban
38
What are DOACs?
Direct acting anti-coagulants | no way to reverse their effects although they lower bleeding risk and have a relatively short half life
39
Advantages of NOACs compared to warfarin?
- No monitoring required - No major interaction problems - Slightly better at preventing strokes in AF - Slightly less risk of bleeding
40
What is used to assess whether patient with AF should go on anti-coagulants?
CHA2DS2VASc score
41
Higher the CHA2DS2VASc score the -----------risk of having a stroke?
Higher
42
0 CHADSVASC score?
No anti coagulation needed
43
1 on CHA2DS2VASc score?
Consider anti-coags
44
2 on CHA2DS2VASc score?
Offer anti-coagulation
45
CHA2DS2VASc score pneumonic?
``` C- Congestive heart failure H- Hypertension A- Age over 75 (2) D- Diabetes S- Stroke/TIA (2) V- Vascular disease A- Age (65-74) S- Sex (female) ```
46
Assessment tool for establishing patients risk of major bleeding whilst on Anti-coags?
HASBLED
47
Pneumonic of HASBLED?
``` H- Hypertension A- Abnormal renal & liver function S- Stroke B- Bleeding L- Labile INRs E- Elderly D- Drugs or alcohol ```

Cardiology Disease Profiles (12 decks)

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