Atrial fibrilation Flashcards

1
Q

What is atrial flutter?

A

When the atria beats too fast but is rhythmic

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2
Q

What is the biggest danger in AF?

A

During AF, the atria is firing impulses from everywhere in the atria 400 time a second = isn’t contracting and ejecting blood properly so blood pools in the atria = risk of clots = risk of stroke

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3
Q

What would be missing on the ECG during AF?

A

P wave

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4
Q

What are the 4 types of AF?

A
  1. ) Paroxysmal - episodes come and go, don’t last longer than 48hrs
  2. ) Persistent - episodes that last longer than 7 days (without treatment)
  3. ) Long-standing - continuous AF for more than a year
  4. ) Permanent - present all the time - can’t be treated.
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5
Q

What are the symptoms?

A

Often asymptomatic - put it down to old age

  1. ) Breathlessness
  2. ) Palpitations
  3. ) Tiredness
  4. ) Dizziness
  5. ) Chest pain
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6
Q

Who are most at risk?

A

Women over 65 who have HT, atherosclerosis, heart valve issues

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7
Q

If left untreated what can AF lead to?

A

Heart failure - ventricles work too hard = become enlarged

Stroke

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8
Q

How do we diagnose AF?

A

ECG - if paroxysmal will have to wear for 24hrs

After diagnosis will have and echo to see the damage and enlargement

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9
Q

What are the three classes of drug involved in RATE CONTROL in AF? (control ventricular beating)

A
  1. ) Beta-blockers
  2. ) Rate-limiting CCB’S = dilatazem and verapamil (not the ones used in HT)
    3) Digoxin monotherapy
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10
Q

Who is digoxin monotherapy suitable for?

A

People with permanent AF and who are sedentary - digoxin slows the heart down permanently = if did any exercise would collapse.

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11
Q

What are the three types of RHYTHM CONTROL (cardioeversion)?

A
  1. ) Pharmacological carioeversion
  2. ) Electrical cardioeversion
  3. ) surgical cardioversion
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12
Q

who is rhythm control recommended for?

A
  1. ) New onset AF
  2. ) Reversible cause
  3. ) People with HF that is getting worse bc of AF
  4. ) Atrial flutter
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13
Q

What drug groups are involved in pharmacological cardioeversion?

A
  1. ) Voltage gated Na+ channel blockers - FLECANIDE
  2. ) beta blocker - SOTALOL
  3. ) K+ channel blocker - AMIODARONE
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14
Q

What is electrical caridioeversion?

A

Like defibrillation. If not done within 48hrs of presenting symptoms need to administer anticoagulant first. Mild irritation but will recover quickly. Will resolve problem for long period of time, permanently in some people.

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15
Q

What is surgical cardioeversion?

A

A catheter is put through the groin and into the heart. Identify where the problem is and kill this part of the heart via radiofrequency or chryotherapy (freezing).
in people with permanent AF OR WHERE ELECTRICAL HASN’T WORKED

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16
Q

What happens before surgical cardioeversion if the part causing the problem is near the AV node?

A

A pacemaker must be fitted

17
Q

What extra drug class should most AF patients be on?

A

Anticoagulants - risk x5 in people with non-rheumatic AF. risk is x17 if is rheumatic i.e. another disease affecting the valves

18
Q

If you have AF how many points do you have to score (CHA2DS2-VASc) to be offered an anti-coagulant?

A

2

19
Q

Why would an anti-platelet like aspirin not be offered in AF?

A

Not good at preventing strokes and has a high risk of causing bleeds

20
Q

What two scores need to be balanced before an anticoagulant can be offered

A

CHA2DS2-VASc vs HAS-BLED

= RISK OF STROKE Vs risk of bleeding

21
Q

What two classes of anticoagulants were made to try and overcome the problems associated with vitamin K antagonists?

A

NOACS (non-vitamin K antagonists_
DOACS ( direct acting oral anticoagulants) : either directly inhibit thrombin through 2A (dabigatran) or directly inhibit factor xa (rivaroxaban)

22
Q

What factors in the clotting pathway does warfarin inhibit?

A

All of them

23
Q

What are the disadvantages of warfarin?

A
  1. ) Interacts with everything
  2. ) Have to have regular INR tests to check how well blood is clotting
  3. ) Can be difficult to find initial loading dose
  4. ) Risk of bleeding in CNS (but easily monitored and reversed)
24
Q

why can we not measure INR for NOACS and DOACS?

A

only act on factorr Xa or thrombin - we can’t measure at these parts of the pathway

25
Q

What are the advantages of the NOACS AND DOACS?

A

Don’t interact with quite as much - mostly renally cleared = doesn’t go through the liver
Don’t have to go for regular INR tests
Same dose is taken everyday - don’t have to change

26
Q

What are the disadvantages of the NOACS AND DOACS?

A
  1. )Have a shorter half-life = if miss a dose if non-adherant won’t be protected against stroke
  2. )More risk of accumulation and bleeding (in GI) as can’t monitor and tell if you are bleeding
  3. ) Difficult to reverse its effects if you do bleed - monoclonal antibody = new and very expensive
27
Q

What is used to reverse small bleed on warfarin?

A

Vitamin K = INCREASE CLOTTING FACTORS

28
Q

what is the target INR and what are we balancing?

A

2.5 (range is 2-3)

The risk of bleeding (high INR) and the risk of clotting (low INR)