Atrial Fibrillation

Question 1

What is atrial fibrillation (AF)?

Answer 1

Most common sustained arrhythmia

Chaotic and disorganised atrial activity resulting in an IRREGULAR heartbeat

Question 2

Majority with AF?

Answer 2

Incidence increases with age

Question 3

Types of AF?

Answer 3

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)

Question 4

What is paroxysmal AF?

Answer 4

Intermittent, often recurrent and often lasting less than 48 hours

Question 5

What is persistent AF?

Answer 5

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

Question 6

What is permanent AF?

Answer 6

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

Question 7

Associated diseases/causes of AF?

Answer 7

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

Question 8

What is lone (idiopathic) AF?

Answer 8

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

Genetic suspicion

Question 9

Risks with AF?

Answer 9

Greatest risk is thromboembolism causing stroke

Question 10

Symptoms of AF?

Answer 10

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

Symptoms are often worse at the onset of AF

Question 11

Mechanism by which AF occurs?

Answer 11

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)

Question 12

Methods of terminating AF?

Answer 12

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

Electrical cardioversion (90% effective)

Spontaneous reversion to sinus rhythm

Question 13

ECG findings in AF?

Answer 13

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)

Question 14

What is the ventricular rate in AF dependent upon?

Answer 14

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

Question 15

Treatment of AF with a slow ventricular rate?

Answer 15

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

Question 16

HR in AF?

Answer 16

400 bpm or more; atria quiver instead of contracting

Question 17

What is pseudo-regularisation?

Answer 17

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

Question 18

What is atrial kick?

Answer 18

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

Question 19

How can AF result in congestive heart failure?

Answer 19

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

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

Question 20

Patients with AF and pre-excitation?

Answer 20

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

Question 21

Management of AF?

Answer 21

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)

Question 22

Treatment options for rate control of AF?

Answer 22

Digoxin
β-blockers
Verapamil, diltiazem

These can be used alone or in combination

Question 23

Treatment options for rhythm control in AF?

Answer 23

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)

Question 24

Aim of electrical cardioversion?

Answer 24

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

Question 25

Mechanism of action of anti-arrhythmic drugs?

Answer 25

Block ionic currents across cell membranes

Question 26

Classification of anti-arrhythmics?

Answer 26

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

Question 27

Examples of different class of drugs?

Answer 27

Class I- lignocaine, quinidine, flecainide Class II - propranolol Class III - amiodarone, sotalol, dronedarone Class IV - verapamil

Question 28

What is Torsades de Pointes (TdP)?

Answer 28

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

Question 29

Recognising TdP?

Answer 29

Heart rate - 200-250 bpm Rhythm - irregular Recognition - long QT interval, wide QRS and continuously changing QRS morphology

Question 30

Mechanisms of TdP development?

Answer 30

Hypokalaemia Prolongation of the AP duration (can be drug-induced) Renal impairment (increased drug levels)

Question 31

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

Answer 31

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 ```

Question 32

Describe the CHA2DS2-VASc score

Answer 32

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

Question 33

Describe the bleeding risk assessment

Answer 33

``` 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

Question 34

Why is radiofrequency ablation used in AF?

Answer 34

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

Question 35

What is atrial flutter (A-Flutter)?

Answer 35

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

Question 36

Mechanism of A-Flutter generation?

Answer 36

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

Question 37

End result of A-Flutter?

Answer 37

Usually progressed to AF May result in thrombo-embolism

Question 38

Differences in A-Flutter in peoples?

Answer 38

Patients with paroxysms of A-Flutter often have normal hearts Patients with chronic A-Flutter usually have underlying heart disease

Question 39

ECG characteristics of A-Flutter?

Answer 39

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

Question 40

A-Flutter treatment options?

Answer 40

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

Question 41

Goals in A-Flutter treatment?

Answer 41

1. Terminate the flutter and prevent recurrence | 2. Control ventricular response during the arrhythmia