This an excellent lecture about Atrial fibrillation for undergraduates and postgraduates.

1. Atrial fibrillation: Review of
Principles
Jwan Ali Ahmed AlSofi
HMU-College of Medicine
Supervisor: Dr. Abdulkarim AlOthman

2. Why AF?
• Atrial fibrillation (AF) is the most common sustained
cardiac arrhythmia.
• Overall prevalence of 0.5% in the adult population of
the UK.
• The prevalence rises with age, affecting 1% of those
aged 60–64 years, increasing to 9% of those aged
over 80 years.
• It is associated with significant morbidity and a
twofold increase in mortality. This is mainly
because of:
– its association with underlying heart disease
– its association with systemic embolism and stroke.

3. Pathogenesis
• AF is a complex arrhythmia
characterised by both:
1. abnormal automatic firing
2. the presence of multiple
interacting re-entry circuits
looping around the atria.
• Episodes of AF are:
1. initiated by rapid bursts of
ectopic beats arising from
conducting tissue in the
pulmonary veins or from
diseased atrial tissue.
2. It becomes sustained
because of re-entrant
conduction within the atria or
sometimes because of
continuous ectopic firing.

4. Atria in AF
• Re-entry is more likely to occur in atria that
are enlarged or in which conduction is slow,
as is the case in many forms of heart
disease.
• During episodes of AF, the atria beat rapidly
but in an uncoordinated and ineffective
manner.
• The ventricles are activated irregularly at a
rate determined by conduction through the
AV node. This produces the characteristic
‘irregularly irregular’ pulse.

5. ECG findings in AF
• normal
• irregular QRS complexes
• no P waves
• the baseline may show irregular
fibrillation waves

6. ECG findings in AF
A. Onset AF:
– There is usually a fast ventricular rate, between
120 and 160/min.
B. Chronic AF:
– the ventricular rate may be much slower, due to
the effects of medication and AV nodal fatigue.

7. Classification of AF:
1. Paroxysmal:
– intermittent episodes that self-terminate within 7
days
2. Persistent:
– prolonged episodes that can be terminated by
electrical or pharmacological cardioversion
3. Permanent:
– is atrial fibrillation for which efforts to terminate
either are not made or are not successful
 It can be difficult to identify what type of AF
patients have at first presentation but this
usually becomes clearer as time progresses.

8. Progression of AF
• Unfortunately for many patients, paroxysmal
AF becomes permanent as the underlying
disease process progresses. This is because
of:
• Within a few hours of the onset of AF:
– electrophysiological changes occur in the atria
which tend to maintain fibrillation: a process called
electrical remodelling.
• When AF persists for a period of months:
– structural remodelling also occurs, leading to atrial
fibrosis and dilatation that predispose to chronicity
of the AF.

11. Causes of atrial fibrillation
• Cardiac:
– Coronary artery disease
(including acute MI)
– Valvular heart disease,
especially rheumatic mitral
valve disease
– Hypertension
– Sinoatrial disease
– Cardiomyopathy
– Congenital heart disease
– Pericardial disease
• Pulmonary:
– Pulmonary embolism
– Chest infection
– chronic lung disease
• Metabolic:
– Hyperthyroidism
– Alcohol
• Idiopathic (lone atrial
fibrillation):
– Is persistent or permanent
AF have structurally normal
hearts.

12. Clinical features of AF
• The typical presentation is with palpitation, breathlessness
and fatigue.
• In patients with poor ventricular function or valve disease, AF
may precipitate or aggravate cardiac failure because of loss
of atrial function and heart rate control.
• A fall in BP may cause lightheadedness.
• Chest pain may occur with underlying CAD.
• In older patients, AF may not be associated with a rapid
ventricular rate and may be asymptomatic, only to be
discovered as a result of a routine examination or an ECG.
• Asymptomatic AF may also present with systemic
embolism and is a major cause of stroke in the elderly.

13. Variable intensity of S1

14. Investigations of AF
o 12-lead ECG
o echocardiogram
o Thyroid function tests to exclude
thyrotoxicosis

15. Management of AF
• Management depends on whether the AF is
transient or persistent and whether there is a clear
precipitating factor.
• When AF complicates an acute illness such as a
chest infection or pulmonary embolism, treatment of
the underlying disorder will often restore sinus
rhythm.
• Where AF does not resolve, the main
• objectives are to control heart rate during periods of
AF, restore sinus rhythm, prevent recurrence of AF
and reduce the risk of thromboembolism.

16. Paroxysmal atrial fibrillation
• Occasional attacks of AF that are well tolerated do not necessarily require treatment.
1. Beta-blockers:
– first-line therapy if symptoms are troublesome,
– they reduce the ectopic firing that normally initiates the arrhythmia.
– They are particularly useful for treating patients with AF associated with CAD, HTN and HF.
2. Class Ic drugs, such as propafenone or flecainide:
– are also effective at preventing episodes
– should not be given to patients with CAD LVD.
– Flecainide is seldom used alone, since it can precipitate atrial flutter, and is usually
prescribed with a rate-limiting β-B.
3. Class III drugs:
– amiodarone is the most effective agent for preventing AF but side-effects restrict its use to
when other measures fail.
– Dronedarone is an effective alternative but is contraindicated in patients with HF or
significant left ventricular impairment
4. Digoxin and verapamil:
– Not effective for the prevention of AF but help with rate control by slowing conduction through
the AV node.
5. Catheter ablation: drug therapy is ineffective or causes side-effects.
 Assessment of stroke risk is similar to that in patients with persistent AF

17. Persistent atrial fibrillation
• There are two options for treating persistent AF.
1. One is to attempt to restore and maintain sinus
rhythm (( Rhythm control ))
2. The second is to accept the presence of AF
and to try to control the ventricular rate
(( Rate control ))
• With both options prophylaxis against
thromboembolism is required on either a
short-term or long-term basis.

18. Rhythm control
• An attempt to restore sinus rhythm is
particularly appropriate if:
1. the arrhythmia causes troublesome symptoms
2. there is a modifiable or treatable underlying
cause
3. AF has been present for less than 3 months,
4. the patient is young
5. there is no important structural heart disease.
• Electrical DC VS pharmacological cardioversion
• Cardioversion is initially successful in most patients
but relapse is frequent.

19. Rhythm control
• If AF has been present for less than 48 hours:
– In stable patients with no history of structural heart disease
IV flecainide.
– In patients with structural or IHD  IV amiodarone.
– Cardioversion is an alternative treatment and is often
effective when drugs fail.
• If AF has been present for 48 hours or longer, or if
there is doubt about its duration:
– DC cardioversion should be deferred until the patient has been
established on effective oral anticoagulation for a minimum of 4 weeks
– and any underlying problems, such as hypertension or alcohol excess,
have been corrected.
• Consideration should be given to prophylactic treatment with
amiodarone to reduce the risk of recurrence.
• Catheter ablation is sometimes used to restore and maintain
sinus rhythm in resistant cases.

21. Rate control
• If sinus rhythm cannot be restored, treatment
should be directed at maintaining an
appropriate heart rate.
• Digoxin, β-blockers and rate-limiting calcium
antagonists, such as verapamil or diltiazem.
• Combination therapy with digoxin and a β-
blocker can help with rate control
• but CCB should not be used with β-blockers
because of the risk of bradycardia.

22. Why we need
Thromboprophylaxis in AF?
AF  Loss of atrial contraction and left atrial 
dilatation cause stasis of blood in the LA 
may lead to thrombus formation in the left atrial
appendage  predisposes patients to stroke
and other forms of systemic embolism.

23. 1- Patients undergoing cardioversion
to restore sinus rhythm
• Such patients require temporary
anticoagulation to reduce the risk of systemic
embolus.
• This can be achieved with:
– warfarin, aiming for an (INR) target of 2.0–3.0
– DOACs are used as an alternative.
• Anticoagulation should be started for at least 4
weeks before cardioversion and should be
maintained for at least 3 months following
successful cardioversion.

24. 2- Patients with chronic AF
Risk of stroke
Risk of bleeding
with anticoagulation

25. 2- Patients with chronic AF
1. Patients with AF secondary to mitral valve
disease should always be anticoagulated
because the risk is so high.
2. In other patients, clinical scoring systems
can be used to assess the risk of stroke and
bleeding.
– The risk of stroke is usually assessed by the
CHA2DS2-VASc score
– Estimate the bleeding risk by the HAS-BLED
score.

27. 3- In patients with intermittent
AF
• Stroke risk is similar to that in patients with
persistent AF when adjusted for
CHA2DS2-VASc score.
• Stroke prevention guidelines do not
distinguish between those with
paroxysmal, persistent and permanent AF.

28. Agents to reduce stroke risk
in AF:
1. Warfarin therapy:
– Target INR of 2.0–3.0 reduces the risk of stroke by
about two-thirds at the cost of an annual risk of
bleeding of 1–1.5%.
– Clinical risk factors that increase the risk of
bleeding:
• peptic ulcer, uncontrolled hypertension, alcohol misuse,
frequent falls, poor adherence and the use of other drugs
that might interact with warfarin.
– If bleeding does occur in warfarin-treated patients,
anticoagulation can be reversed by administering
vitamin K or clotting factors.

29. Agents to reduce stroke risk in
AF:
2. Directly acting oral anticoagulants, DOACs:
– The factor Xa inhibitors: rivaroxaban, apixaban and
edoxaban.
– The direct thrombin inhibitor: dabigatran
– They are used as an alternative to warfarin.
– Advantages of DOACs:
1. They are at least as effective as warfarin at preventing
thrombotic stroke
2. Are associated with a lower risk of intracranial
haemorrhage.
3. Lack of requirement for monitoring and the fact that they
have fewer drug interactions.

30. Agents to reduce stroke risk in
AF:
3. Asprin:
– Should not be used since it has little or no effect on
embolic stroke and is associated with significant
bleeding risk.

31. Any QS?