Atrial Fibrillation Flashcards

1
Q

What is atrial fibrillation (AF)?

A

Most common sustained arrhythmia

Chaotic and disorganised atrial activity resulting in an IRREGULAR heartbeat

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2
Q

Majority with AF?

A

Incidence increases with age

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3
Q

Types of AF?

A

Can be:
Paroxysmal

Persistent

Permanent/sustained (chronic) - sustained AF is facilitated by increased parasympathetic tone; atrial refractory periods are decreased, shortening wave length and making it easier for AF to sustain itself (duration of AF is prolonged after AF has been maintained for progressively longer periods of time)

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4
Q

What is paroxysmal AF?

A

Intermittent, often recurrent and often lasting less than 48 hours

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5
Q

What is persistent AF?

A

Episode of AF lasting longer than 48 hours, which can still be cardioverted to normal sinus rhythm; it is unlikely to spontaneously revert to normal sinus rhythm

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6
Q

What is permanent AF?

A

Inability of pharmacologic/non-pharmacologic methods to restore normal sinus rhythm

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7
Q

Associated diseases/causes of AF?

A
Most often occurs in the presence of cardiac disease:
Hypertension
Congestive Heart Failure
Sick sinus syndrome (slow HR)
CHD
Valvular heart disease
Congenital heart disease
Cardiac surgery

Others:
Alcohol can be a trigger, part. in younger patients
Thyroid disease
Familial
COPD, pneumonia, septicaemia, pericarditis, tumours
Obesity is a predisposing factor to AF
Vagal causes

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8
Q

What is lone (idiopathic) AF?

A

AF in the absence of any heart disease and no evidence of ventricular dysfunction; it is a diagnosis of exclusion

Genetic suspicion

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9
Q

Risks with AF?

A

Greatest risk is thromboembolism causing stroke

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10
Q

Symptoms of AF?

A
Palipitations
Pre-syncope (dizziness)
Syncope
Chest pain
Dyspnea
Sweatiness
Fatigue

Symptoms are often worse at the onset of AF

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11
Q

Mechanism by which AF occurs?

A

RE-ENTRY of multiple wavelets prevents atria from being organised; there is an ectopic focus around the pulmonary veins (a lot of AF arises in this region)

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12
Q

Methods of terminating AF?

A

Pharmacologic cardioversion with anti-arrhythmic drugs (30% effective), e.g: flecanide, sotalol, amiodarone

Electrical cardioversion (90% effective)

Spontaneous reversion to sinus rhythm

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13
Q

ECG findings in AF?

A

Atrial rate > 300 bpm
Rhythm - irregularly irregular

Ventricular rate is variable

Recognition - absence of P waves and presence of ‘f’ waves (wavy deflections replace the entire isoelectric line between QRS complexes)

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14
Q

What is the ventricular rate in AF dependent upon?

A

AV node conduction properties

Sympathetic (facilitates AV node conduction) and parasympathetic tone (inhibits AV node conduction)

Presence of drugs which act on the AV node, e.g: β-blockers and CCBs are effective at slowing conduction and prolonging refractoriness in the AV node

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15
Q

Treatment of AF with a slow ventricular rate?

A

May co-exist with periods of fast ventricular rate; a pacemaker may be required to allow for pharmacologic control of fast ventricular rate

Ventricular rates

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16
Q

HR in AF?

A

400 bpm or more; atria quiver instead of contracting

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17
Q

What is pseudo-regularisation?

A

AF with a fast ventricular response - so fast that the ECG appears regular

18
Q

What is atrial kick?

A

Atrial contraction immediately before ventricular systole acts to increase the efficiency of ventricular ejection, due to acutely increased preload

19
Q

How can AF result in congestive heart failure?

A

Lost “atrial kick” and decreased filling times (reduced diastole) result in decreased CO

Can result in CHF, esp. in the presence of diastolic dysfunction

20
Q

Patients with AF and pre-excitation?

A

WPW syndrome + AF can result in ventricular fibrillation and sudden cardiac death - pre-excitation of the ventricles broadens the QRS via an accessory pathway

21
Q

Management of AF?

A

Rhythm control - objective is to maintain sinus rhythm predominantly

Rate control - objective is to control ventricular rate (but AF is accepted)

Anti-coagulation for both approaches IF there is a high risk of thromboembolism (majority of cases)

22
Q

Treatment options for rate control of AF?

A

Digoxin
β-blockers
Verapamil, diltiazem

These can be used alone or in combination

23
Q

Treatment options for rhythm control in AF?

A

Restoration of normal sinus rhythm:
Pharmacological cardioversion, i.e: anti-arrhythmic drugs like amiodarone
Direct Current Cardioversion (DCCV)

Maintenance of normal sinus rhythm:
Anti-arrhythmic drugs
Catheter ablation of atrial focus/pulmonary veins, i.e: rid of origin
Surgery (maze procedure)

24
Q

Aim of electrical cardioversion?

A

Immediate restoration of sinus rhythm by delivery of a dose of electrical current to the heart at a specific moment in the cardiac cycle

Require sedation/general anaesthesia

25
Q

Mechanism of action of anti-arrhythmic drugs?

A

Block ionic currents across cell membranes

26
Q

Classification of anti-arrhythmics?

A

Class I (A, B, C) - Na+, act on phase 0 of the AP and are mainly used for rhythm control in AF; reduce the Na+ channel current and prolonged of teh QR interval

Class II - β-blockers, act on phase 4 of the AP and are mainly used for rate control in AF; QT interval prolonged

Class III - K+, act on phase 3 of the AP and are mainly used for rhythm control in AF; action potential prolongation; QT interval prolonged

Class IV - Ca2+, act on phase 2 of the AP and are mainly used for rate control in AF

27
Q

Examples of different class of drugs?

A

Class I- lignocaine, quinidine, flecainide

Class II - propranolol

Class III - amiodarone, sotalol, dronedarone

Class IV - verapamil

28
Q

What is Torsades de Pointes (TdP)?

A

Rapid, distinct ventricular tachycardia with a twisting configuration of the QRS morphology, assoc. with prolonged repolarisation

May be acquired of congenital but is a very deadly form of VT

29
Q

Recognising TdP?

A

Heart rate - 200-250 bpm

Rhythm - irregular

Recognition - long QT interval, wide QRS and continuously changing QRS morphology

30
Q

Mechanisms of TdP development?

A

Hypokalaemia

Prolongation of the AP duration (can be drug-induced)

Renal impairment (increased drug levels)

31
Q

Patients that have a high risk of thromboembolism and in whom anti-coagulation is required?

A

Valvular AF in mitral valve disease, e.g: mitral stenosis and mitral regurgitation

Non-valvular AF if:
Age >75 (esp. females have higher incidence)
Hypertension
Heart failure
Previous thromboembolism/stroke
CAD or diabetes and >60 years old
Thyrotoxicosis
32
Q

Describe the CHA2DS2-VASc score

A

Congestive heart failure/LV dysfunction - 1

Hypertension - 1

Age > or equal to 75 years - 2

Diabetes mellitus - 1

Stroke (TIA/TE) - 2

Vascular disease,e e.g: previous MI, PAD, aortic plaque) - 1

Age 65-74 years - 1

Sex (female) - 1

Score of 2 and above is considered high

33
Q

Describe the bleeding risk assessment

A
Hypertension - 1
Abnormal renal or liver function - 1/2
Stroke - 1
Bleeding - 1
Iabile INRs - 1
Elderly (age > 65 yrs) - 1
Drugs/alcohol - 1/2

Score >= 3 is considered high risk

34
Q

Why is radiofrequency ablation used in AF?

A

To maintain sinus rhythm by ablating AF focus (usually in the pulmonary veins) - creates non-conducting scar tissue

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

35
Q

What is atrial flutter (A-Flutter)?

A

Rapid and regular form of atrial tachycardia that is usually paroxysmal; episodes can lost seconds/years

36
Q

Mechanism of A-Flutter generation?

A

MACRO-REENTRANT circuit that is confined to the right atrial myocardium is sustained by a critical isthmus

37
Q

End result of A-Flutter?

A

Usually progressed to AF

May result in thrombo-embolism

38
Q

Differences in A-Flutter in peoples?

A

Patients with paroxysms of A-Flutter often have normal hearts

Patients with chronic A-Flutter usually have underlying heart disease

39
Q

ECG characteristics of A-Flutter?

A

Atrial rate approx 300 bpm and ventricular rate approx 150 bpm

SAW-TOOTH ‘F’ WAVE

QRS is normal

Conduction is normal but there is physiological 2:1

Rhythm is regular but may be variable

40
Q

A-Flutter treatment options?

A

RF ablation has a high long-term success rate

Pharmacological therapy to:
Slow ventricular rate
Restore sinus rhythm
Maintain sinus rhythm once converted

Cardioversion

Warfarin for prevention of thrombo-embolism; can also use NOACs but not in patients with prosthetic heart valves

41
Q

Goals in A-Flutter treatment?

A
  1. Terminate the flutter and prevent recurrence

2. Control ventricular response during the arrhythmia