Atrial Fibrilation Flashcards

1
Q

What is AF?

A

Chaotic and disorganised atrial activity resulting in irregularly irregular heat beat

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2
Q

What is the most common cause of AF?

A

Ectopic foci in the muscle sleeves in the atria of the pulmonary veins

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3
Q

AF is the most common sustained arrythmia. True or false?

A

True

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4
Q

All AF is symptomatic. True or false?

A

False

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5
Q

How is AF terminated?

A

1) Pharmacological cardioversion with anti-arrythmic drugs is 30% effective
2) Direct current cardioversion (DCCV) is 90% effective

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6
Q

What antiarrhythmic drugs can be used to terminate AF?

A

Flecainide, Sotalol, Amiodarone

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7
Q

What is paroxysmal AF?

A

AF lasting less than 48 hours but often recurring

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8
Q

What is persistent AF?

A

AF lasting more than 48 hours which can still be cardioverted to NSR

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9
Q

What is permanent AF?

A

AF which cannot be restored to NSR by pharmacological and non pharmacological methods

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10
Q

What are the associated diseases which can lead to AF?

A

Hypertension, CCF, CAD, Obesity, Thyroid disease, Familial, Septicaemia, COPD, Pneumonia, Alcohol abuse, Congenital heart disease, Cardiac srgery, Pericarditis, Tumours.

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11
Q

What is sick sinus syndrome?

A

Tachy brady syndrome found in older people

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12
Q

Which group of people with AF are at the highest risk of stroke?

A

Those with cardiac valve disease

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13
Q

What is idiopathic AF?

A

Absence of any heart disease and no evidence of ventricular dysfunction. Could be genetic or familial.
Its the diagnosis of exclusion. Have a high risk of stroke

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14
Q

What are the common symptoms of AF?

A

Palpitations, presyncope, syncope, dyspnoea, fatigue, chest pain, sweatiness.
Some people are assymptomatic.

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15
Q

If AF is paroxysmal, are symptoms worse at onset or delayed?

A

At onset due to associated anxiety

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16
Q

What is hypertensive heart disease?

A

AF and left ventricular hypertrophy

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17
Q

What is the mechanism of AF?

A

Multiple wavelets of re-entry or ectopic focus around the pulmonary veins

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18
Q

What are the ECG findings for AF?

A

Atrial rate >300bpm
Irregularly irregular rhythm
Absent P waves- just disorganised atrial activity
Ventricular rate is variable

19
Q

In AF, the ventricular rate is variable. What is it dependent on?

A

AV node conduction properties
Sympathetic and parasympathetic tone
Presence of drugs acting on the AV node

20
Q

What is the management for AF with a slow ventricular rate?

A

Pacemaker as you cannot give beta blockers for AF as it may lead to heart block

21
Q

What is pseudo-regularisation?

A

AF with a fast ventricular rate therefore you cannot appreciate the irregularly irregular heart rate

22
Q

What are the complications of AF?

A

Heart failure and reduced cardiac output => low BP

23
Q

What are the 2 branches to AF management and which is better?

A

1) Rhythm control- aim to maintain sinus rhythm
2) Rate control- Accept AF but aim to control ventricular rate. (higher risk of thromboembolism and stroke)
Decision is not outcome driven as there is no evidence to show one is better. Treatment is symptom driven

24
Q

What is involved in AF rate control?

A

Pharmacological therapy to slow down AV node conduction.

Digoxin, beta blockers, verapamil/diltiazam

25
Q

What is involved in AF rhythm control?

A

Restoration and maintenance of normal sins rhythm.

26
Q

How can NSR be restored?

A

1) Pharmacologic cardioversion with anti-arrhythmic drugs (amiodarone or flecainide)
2) DCCV (patient anethatised as its painful) sets all cells back to phase 4 of the AP

27
Q

How can NSR be maintained?

A

1) Anti-arrhythmic drugs
2) Radiofrequency ablation of atrial foci or pulmonary veins
3) Surgery (maze procedure)

28
Q

What is the target of class 1 antiarrhythmic drugs and give some examples?

A

Reduce the Na+ channel current (phase 0)

Lignocaine, Flecainide, Quinidine, Propafenone

29
Q

What is the target of class 2 antiarrhythmic drugs and give some examples?

A

Beta blockers targeting B1 adrenoreceptors (phase 4)

Propranolol, Bisoprolol, Atenolol

30
Q

What is the target of class 3 antiarrhythmic drugs and give some examples?

A

K+ channel blockers to prolong the AP (phase 3)

Amiodarone, Satalol, Dronedarone

31
Q

What is the target of class 4 antiarrhythmic drugs and give some examples?

A

Ca++ channel blockers (phase 2)

Verapamil and Diltiazam

32
Q

How is thromboembolism prevented in AF?

A

Anticoagulants

33
Q

Which groups of people are at high risk of thromboembolism and need anti coagulation?

A
Valvular heart disease (esp mitral valve isease
Age >75 (esp female)
Hypertension
Heart failure
Previous VTE/stroke
CAD or DM and >60
Thyrotoxicosis
34
Q

How can RFCA be used in AF?

A

To maintain sinus rhythm- ablate the AF focus

For rate control- Ablation of the AV node to stop fast conduction

35
Q

What are the ECG changes of Torsades de pointes?

A

HR =200-250bpm with an irregular rhythm
Long QT interval and wide QRS
Continually changing QRS morphology

36
Q

What can cause Torsades de pointes?

A

Hypokalemia
Drug induced prolonging of the AP duration
Undiagnosed congenital long QT syndrome
Renal impairment increasing drug circulation levels

37
Q

What is atrial flutter?

A

Rapid irregular form of atrial tachycardia 200-300bpm.

38
Q

What is the usual mechanism of atrial flutter?

A

Usually paroxysmal and sustained by a macro re-entrant current. The circuit is confined to the right atrium.

39
Q

How long can an episode of atrial flutter last?

A

Seconds to years

40
Q

Is chronic atrial flutter likely to progress to AF?

A

Yes

41
Q

Does atrial flutter carry the same risk of stroke as AF?

A

Yes

42
Q

What is the EGC pattern of atrial flutter?

A

Saw tooth pattern and the AV node repolarises more slowly so you get a 2:1 P wave to QRS complex

43
Q

What is the treatment for atrial flutter?

A

1) Radiofrequency ablation (80-90% long term success)
2) Pharmacological therapy to slow ventricular rate, restore NSR and then maintain it.
3) DCCV
4) Anticoagulation to prevent thromboembolism
Similar to AF treatment

44
Q

What are the main goals in AF management?

A

Symptom control and improve CV outcomes through stroke prevention, optimal treatment of co-existing CVD and lifestyle modification.