Atrial Fibrillation & Flutter Flashcards

1
Q

Define atrial fibrillation

A

A chaotic, irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate.

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2
Q

What does CO drop by in AF and why?

A

10-20% as ventricles aren’t reliably filled by the atria

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3
Q

What are the overall causes of AF?

A

Any condition resulting in raised atrial pressure, increased atrial muscle mass, atrial fibrosis or inflammation and infiltration of the atrial fibrillation.

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4
Q

What is the pathophysilogy of AF?

A

AF is caused by multiple “wandering” re-entry circuits within the atria, as well as some ectopics often arising from the distal pulmonary vein. These re-entry circuits are often caused by atrial enlargement as a result of an underlying pathology of the heart.

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5
Q

Give two bullet points which outline cause of AF

A
  • Re-entry circuits as a reuslt of unidirectional block

- Rapidly firing ectopic focus that drives the atria into fibrillation

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6
Q

How is the chaotic contraciton of the atria not conducted to the ventricles/

A

This chaotic rhythmn is prevented from spreading to the ventricles by refractory tissue at the AV node so that only some of the ventricles are conducted, in a very irregular fashion.

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7
Q

Give two reasons AF is potentially dangerous

A

1) Rapid ventricular rates compromising cardiac output resulting in hypotension and pulmonary congestion (especially in individuals with hypertrophied or stiff left ventricles)
2) The absence of organized atrial contraction promotes blood stasis in the atria leading to an increased risk of thrombus formation

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8
Q

Give four symptoms of AF

A
  • Chest pain
  • Palpitations
  • Dyspnoea
  • Faintness
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9
Q

When do symptoms of AF come on?

A

These symptoms will usually come on when ventricular rate is about 140-160

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10
Q

What is a pulse deficit?

A

o Apical ventricular pulse rate is often greater than the radial rate and the 1st heart sound is of variable intensity. This is because ventricle may be unable to produce contraction large enough to generate a pulse wave. This is called a pulse deficit.

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11
Q

What signs will you see in on examination in AF?

A

Patients may have pulse deficit
Patients may have signs of acute stroke due to thrombus formation
Loss of a waves in the jugular venous pulse1

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12
Q

What tests do you do to diagnose AF?

A

ECG
Echocardiography
Thyroid function tests

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13
Q

What does the ECG show in AF?

A

Absent p waves
Irregularly irregular R-R intervals
Sometimes wide QRS complex (could be WPW)

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14
Q

How do you diagnose paroxysmal AF?

A

24 hour ambulatory tape

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15
Q

What is AShman phenomenon

A

AF may cause a phenomenon which mimics ventricular extrasystoles or ventricular tachycardia due to short R-R intervals following long R-R, lengthening the refractory period of the bundle of his and causing an RBBB morphology

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16
Q

What is one looking for on electrocardiography of someone with AF

A

left atrial enlargement, left ventricular wall motion abnormalities suggesting past or present ischemia, valvular disorders and cardiomyopathy.

17
Q

What is the immediate management of acute AF?

A
  • O2
  • U+Es
  • Emergency cardioversion/IV amiodarone if unavailable
  • Treat associated illness
18
Q

How do you control ventricular rate in acute AF

A

1) Verapamil or bisoprolol
2) Digoxin or amiodarone
Start full anti-coagulation with LMWH

19
Q

What is the process of DC cardioversion in AF?

A

O2->ITU/CCU->GA or IV sedation-> 200J -> 360J -> 36J0

Relapses back into AF are common and drug cardioversion (Amiodarone/Flecainide) is often preferred

20
Q

What are the three priorities in chronic AF?

A

rate control, rhythm control and adequate anti-coagulation

21
Q

When would you want good rhythmn control and when do you not care?

A

rhythm control may be appropriate in symptomatic/younger/idiopathic/AF from a corrected metabolic abnormality.

Otherwise rate control is fine

22
Q

When is rate control prioritised?

A

Rate control is usually prioritised in patients who have the permanent form of the arrhythmia or have failed cardioversions in the past, and is usually used to produce a block at the AV node.

23
Q

When is rate considered controlled in AF?

A

HR

24
Q

What three drug classes can be used for rate control?

A
  • B blocker
  • Rate limiting Ca2+ blocker
    o Verapamil/Diltiazem
  • Digoxin
25
Q

How is DC cardioversion prepared for in AF?

A

Cardioversion is the first line for rhythm control. It is preceded by taking sotalol or amiodarone for 4 weeks if there is an increased risk of cardioversion failure.

26
Q

How can chemical cardioversion be achieved?

A
  • flecainide is 1st choice if there is no structural heart disease
  • IV amiodarone is there is structural
27
Q

Give two alternatives to chemical cardioversion

A

AV node ablation, maze procedure, pacing and pulmonary vein ablation.

28
Q

What is the acute anti-coagulation in AF?

A
  • Use heparin if AF started
29
Q

What is the chronic anticoagulation in AF?

A
  • Anticoagulation with warfarin and aim for an INR of 2-3
  • Aspirin is a less suggested alternative and is used if warfarin is contraindicated.
  • Dabigatran (a direct thrombin inhibitor) maybe an alternative to warfarin
30
Q

What scoring system is used to predict stroke risk?

A

CHAD2DS2 VASc score

31
Q

What does chad2ds2 vasc scoring measure?

A
  • Heart failure
  • Diabetes
  • Hypertension
  • Vascular disease
  • Aged> 65
  • Female
  • AND 2 points for
  • Age >75
  • Prior TIA, stroke/thromboembolism
32
Q

What is acute AF?

A

Acute AF is new-onset AF lasting

33
Q

What is paroxysmal AF?

A

Paroxysmal AF is recurrent AF that typically lasts

34
Q

What is persistent AF?

A

Persistent AF lasts > 1 wk and requires treatment to convert to normal sinus rhythm.

35
Q

What is permanent AF?

A

Permanent AF cannot be converted to sinus rhythm. The longer AF is present, the less likely is spontaneous conversion and the more difficult is cardioversion because of atrial remodeling (rapid atrial rate-induced changes in atrial electrophysiology that are dominated by a decrease in atrial refractoriness and may also include increase in spatial dispersion of atrial refractoriness slowed atrial conduction velocity, or both).

36
Q

Define atrial flutter

A

Atrial flutter is characterized by rapid, regular atrial activituy at a rate of 180-350bpm. Many of these fast impulses reach the AV node during its refractory period and do not conduct to the vevntricles.

37
Q

What is the pathophys of atrial flutter?

A

In general atrial flutter is caused by reentry over a large anatomically fixed circuit. In the common form of atrial flutter this circuit involves a specific pathway that runs through the interatrial septum and the roof and free wall of the right atrium.

38
Q

Why does atrial flutter have a saw toothed pattern?

A

The “saw toothed pattern” ocurs because large parts of the atrium are depolarized throughout the cycle given the p waves a sinusoidal appearance.

39
Q

Why does slowing of the atria in atrial flutter cause ventricular tachycardia?

A

Slowing of the atria in atrial flutter can cause a ventricular tachycardia as the atrial conduction reverts for 2:1 to 1:1.