Atrial fibrillation is an irregular heartbeat caused by uncoordinated electrical activity in the atria. It can cause blood clots, heart failure, and stroke. Diagnosis involves an ECG and testing to check for underlying causes like thyroid problems. Treatment focuses on rate control with medications and preventing clots with anticoagulants. Rhythm control methods include cardioversion, medications, and ablation procedures to restore normal sinus rhythm or slow the heart rate. Long term anticoagulation is often needed due to the risk of stroke.

1. 
Atrial Fibrillation
By Dr Joshua Walinjom ( Cardiologist)

2. Plan
 Intro
 BG
 Symptoms
 Diagnosis
 Treatment

3. BACKGROUND
 Definition:
 AF is A supraventricular tachyarrhythmia with uncoordinated
atrial electrical activation and consequently ineffective atrial
contraction.
 Electrocardiographic characteristics of AF include:
• Irregularly irregular R-R intervals (when atrioventricular
conduction is not impaired),
• Absence of distinct repeating P waves, and
• Irregular atrial activations.

4. BACKGROUND
 Attributed to multiple wavelets with chaotic reentry within the
atria.
 firing of an ectopic focus within venous structures adjacent to the
atria (usually the pulmonary veins) is responsible for initiation and
perhaps maintenance of atrial fibrillation.

5. BACKGROUND

6. BACKGROUND

7. BACKGROUND
 In atrial fibrillation, the atria do not contract, and the
atrioventricular (AV) conduction system is bombarded with many
electrical stimuli, causing inconsistent impulse transmission and
an irregularly irregular ventricular rate, which is usually in the
tachycardia rate range.

8. BACKGROUND
 In atrial fibrillation, the atria do not contract, and the
atrioventricular (AV) conduction system is bombarded with many
electrical stimuli, causing inconsistent impulse transmission and
an irregularly irregular ventricular rate.
 Prevalence increases with age; almost 10% of people > 80
years are affected.

9. BACKGROUND
 The exact mechanisms by which cardiovascular risk factors
predispose to AF are not understood fully but are under
intense investigation. Catecholamine excess, hemodynamic
stress, atrial ischemia, atrial inflammation, metabolic stress,
and neurohumoral cascade activation are all purported to
promote AF.

10. BACKGROUND
 In atrial fibrillation, the atria do not contract, and the
atrioventricular (AV) conduction system is bombarded with many
electrical stimuli, causing inconsistent impulse transmission and
an irregularly irregular ventricular rate.
 Prevalence increases with age; almost 10% of people > 80
years are affected.

11. BACKGROUND

12. BACKGROUND

13. BACKGROUND

14. BACKGROUND

15. BACKGROUND

16. Complications of atrial fibrillation
 Stroke
 HF

17. Etiology of Atrial Fibrillation
 Hypertension
 Coronary artery disease
 Cardiomyopathy
 Valvular heart disorders: mitral stenosis, mitral regurgitation,
tricuspid regurgitation
 Hyperthyroidism
 Binge alcohol drinking (holiday heart)

18. Etiology of Atrial Fibrillation
 Pulmonary embolism
 Atrial septal defects and other congenital heart defects
 Chronic obstructive pulmonary disease (COPD)
 Myocarditis
 Pericarditis
 Lone atrial fibrillation is atrial fibrillation without an identifiable
cause in patients < 60 years.

19. Classification of Atrial Fibrillation
 Paroxysmal AF is atrial fibrillation that lasts < 1 week having
converted spontaneously or by an intervention to normal sinus
rhythm. Episodes may recur.
 Persistent AF is continuous atrial fibrillation that lasts > 1 week.
 Long-standing persistent AF lasts > 1 year, but there is still the
possibility of restoring sinus rhythm.

20. Classification of Atrial Fibrillation
 Permanent atrial fibrillation cannot be converted to sinus rhythm
(the term also includes patients for whom a decision has been
made not to attempt conversion to sinus rhythm).

21. Symptoms and Signs of Atrial Fibrillation
 palpitations
 vague chest discomfort
 symptoms of heart failure
 Stroke

22. Diagnosis of Atrial Fibrillation
 Electrocardiography (ECG)
 Echocardiography
 Thyroid function tests

23. Diagnosis of Atrial Fibrillation
 Electrocardiography (ECG)
 Echocardiography
 Thyroid function tests

24. Ashman Phenomenon
 Ashman phenomenon describes an aberrant ventricular
conduction, usually of RBBB morphology, which follows a
short R-R interval and preceding relatively prolonged R-R interval
 Typically seen with atrial fibrillation but can also occur
with other supraventricular arrhythmias
 Clinically on its own is asymptomatic and does not require any
specific treatment

25. Diagnosis of Atrial Fibrillation
 Electrocardiography (ECG)
 Echocardiography
 Thyroid function tests

26. Treatment of Atrial Fibrillation
 Rate control with medications or AV node ablation
 Sometimes rhythm control with synchronized cardioversion,
medications, or atrial fibrillation substrate ablation
 Prevention of thromboembolism

27. Rate Control
 Rate < 100 beats/minute at rest) to control symptoms and
prevent tachycardia-induced cardiomyopathy
 AV node blockers should not be used in patients with Wolff-
Parkinson-White syndrome when an accessory AV pathway is
involved (indicated by wide QRS duration); these drugs increase
frequency of conduction via the bypass tract, possibly causing
ventricular fibrillation

28. Atrial Fibrillation and WPW Syndrome
 In Wolff-Parkinson-White syndrome,
antegrade conduction occurs over an
accessory pathway.
In Wolff-Parkinson-White syndrome, antegrade conduction occurs
over an accessory pathway. Treatment = procainamide

29. Rate Control
 Beta-blockers (eg, metoprolol, esmolol) are preferred if excess
catecholamines are suspected (eg, in thyroid disorders, exercise-
triggered cases)
 Nondihydropyridine calcium channel blockers (eg, verapamil,
diltiazem) are also effective.
 Digoxin is the least effective but may be preferred if heart failure
is present. These medications may be used orally for long-term
rate control.

30. Rate Control
 When beta-blockers, nondihydropyridine calcium channel
blockers, and digoxin—separately or in combination—are
ineffective => amiodarone may be required.

32. Rhythm control
 When beta-blockers, nondihydropyridine calcium channel
blockers, and digoxin—separately or in combination—are
ineffective => amiodarone may be required.
 In patients with heart failure or other hemodynamic compromise
directly attributable to new-onset atrial fibrillation, restoration of
normal sinus rhythm is indicated to improve cardiac output
 Conversion to sinus rhythm does not eliminate the need for
chronic anticoagulation.

33. Rhythm control
 If atrial fibrillation has been present > 48 hours, patients should
typically be given an oral anticoagulant (conversion, regardless of
method used, increases risk of thromboembolism)
 Anticoagulation should be maintained for > 3 weeks before
conversion or can be given for a shorter time before conversion if
transesophageal echocardiography (TEE) does not show left atrial
thrombus.
 Anticoagulation should be continued for at least 4 weeks after
cardioversion.
 Many patients need chronic anticoagulation

34. Rhythm control
Synchronized cardioversion:
 Efficacy and maintenance of sinus rhythm after the procedure is
improved with use of class Ia, Ic, or III antiarrhythmic medications
24 to 48 hours before the procedure.
 Cardioversion is more effective in patients with
- shorter duration of atrial fibrillation,
- lone atrial fibrillation,
- atrial fibrillation with a reversible cause; it is less effective when
the left atrium is enlarged (> 5 cm), atrial appendage flow is low,
or a significant underlying structural heart disorder is present.

35. Rhythm control
Synchronized cardioversion:
 Cardioversion is more effective in patients with
- shorter duration of atrial fibrillation,
- lone atrial fibrillation,
- atrial fibrillation with a reversible cause;
 it is less effective when :
- left atrium is enlarged (> 5 cm),
- atrial appendage flow is low, or
- a significant underlying structural heart disorder is present.

36. Rhythm control
Cardioversion:
Medications
 class Ia (procainamide, quinidine, disopyramide),
 Ic (flecainide, propafenone), and
 III (amiodarone, dofetilide, dronedarone, ibutilide, sotalol,
vernakalant)
 These medications should not be used until rate has been
controlled by a beta-blocker or nondihydropyridine calcium
channel blocker < 120 beats/minute

37. Rhythm control
 However, for paroxysmal AF that occurs only or almost only at rest
or during sleep when vagal tone is high, medications with
vagolytic effects (eg, disopyramide) may be particularly effective.
 Exercise-induced AF may be better prevented with a beta-blocker.

38. Rhythm control
recurrent paroxysmal atrial fibrillation who also can identify its
onset by symptoms, some clinicians provide a single oral loading
dose of flecainide (300 mg for patients ≥ 70 kg, otherwise 200 mg) or
propafenone
patients carry and self-administer when palpitations develop (“pill-
in-the-pocket” approach).
This approach must be limited to patients who have no sinoatrial or
AV node dysfunction, bundle branch block, QT prolongation, Brugada
syndrome, or structural heart disease

39. Rhythm control
Pill-in-the-pocket” approach:
 Its hazard (estimated at 1%) is the possibility of converting atrial
fibrillation to a slowish atrial flutter that conducts 1:1 in the 200 to
240 beat/minute range.
 This potential complication can be reduced in frequency by
coadministration of an AV nodal suppressing drug (eg, a beta-
blocker or a nondihydropyridine calcium antagonist).

40. Rhythm control
 Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II
receptor blockers (ARBs), and aldosterone blockers may attenuate
the myocardial fibrosis that provides a substrate for atrial
fibrillation in patients with heart failure
 but the role of these drugs in routine atrial fibrillation treatment
has yet to be define

42. Antiarrhythmic drugs used for long-term
maintenance of sinus rhythm in AF patients
 Amiodarone
 Flecainide
 Propafenone
 Dronedarone
 Sotalol
 Disopyramide

43. Ablation procedures for atrial fibrillation
 For patients who do not respond to or cannot take rate-controlling
medications, ablation of the AV node may be done to cause
complete heart block; insertion of a permanent pacemaker is then
necessary.
 Ablation of only one AV nodal pathway (AV node modification)
reduces the number of atrial impulses reaching the ventricles and
eliminates the need for a pacemaker, but this approach is
considered less effective than complete ablation and is rarely
used.

44. Ablation procedures for atrial fibrillation

45. Ablation procedures for atrial fibrillation
 Ablation procedures that accomplish electrical isolation of the
pulmonary veins from the left atrium can prevent atrial fibrillation
without causing AV block. In comparison to other ablation
procedures, pulmonary vein isolation has a lower success rate (60
to 80%) and a higher complication rate (1 to 5%).
 Accordingly, this procedure is often reserved for the best
candidates (eg, younger patients who have no significant
structural heart disease, patients without other options such as
those with medication-resistant AF, or patients with left
ventricular systolic dysfunction and heart failure.

46. Prevention of thromboembolism
 If urgent cardioversion is required because of hemodynamic
compromise, cardioversion is done and anticoagulation is started
as soon as is practical and continued for at least 4 weeks
 If the onset of the current episode of atrial fibrillation is clearly
within 48 hours, cardioversion may proceed without prior or
subsequent anticoagulation in men with a CHA2DS2-VASc score of
0 and in women with a CHA2DS2-VASc score of 1 (class IIb
recommendation).

47. Prevention of thromboembolism
 If the onset of the current episode of atrial fibrillation is not
clearly within 48 hours, the patient should be anticoagulated for 3
weeks before and at least 4 weeks after cardioversion regardless
of the patient's predicted risk of a thromboembolic event (class I
recommendation).
 Alternatively, therapeutic anticoagulation is started,
transesophageal echocardiography (TEE) is done, and, if no left
atrial or left atrial appendage clot is seen, cardioversion may be
done, followed by at least 4 weeks of anticoagulation therapy
(class IIa recommendation).

48. Prevention of thromboembolism
Long-term oral anticoagulant therapy is recommended for :
patients with rheumatic mitral stenosis, mechanical artificial heart
valve, nonvalvular atrial fibrillation with CHA2DS2-VASc scores of ≥ 2
in men and ≥ 3 in women (class of recommendation I)
and may be considered for patients with nonvalvular atrial
fibrillation and CHA2DS2-VASc scores of ≥ 1 in men and ≥ 2 in women
(class of recommendation IIb).

49. Prevention of thromboembolism
 No antithrombotic therapy is recommended for patients with
nonvalvular atrial fibrillation and CHA2DS2-VASc scores of
0 in men and 1 in women (class of recommendation IIa).
 Patients with atrial fibrillation and a mechanical heart valve(s) are
treated with warfarin.
 Patients with atrial fibrillation and significant mitral stenosis are
treated with warfarin.

50. Prevention of thromboembolism
 For patients with nonvalvular atrial fibrillation who are to be
treated with an oral anticoagulant, a class I recommendation is
given for warfarin with a target international normalized ratio
(INR) of 2.0 to 3.0, apixaban, dabigatran, edoxaban, and
rivaroxaban.
 non-vitamin K antagonist anticoagulants are preferred (class I
recommendation)

51. Prevention of thromboembolism
 The INR target recommended in evidence-based guidelines for
most warfarin indications is currently 2.5, with a range of 2.0 to
3.0.
 For patients with mechanical mitral valve replacements, a slightly
higher target of 3.0, with a range of 2.5 to 3.5, is recommended

52. Prevention of thromboembolism

53. Prevention of thromboembolism

54. Prevention of thromboembolism

55. ESC Recommendations In AF
 Pharmacological cardioversion of AF is indicated only in a
haemodynamically stable patient, after consideration of the
thrombo-embolic risk. I
 In patients with AF duration of >24 h undergoing cardioversion,
therapeutic anticoagulation should be continued for at least 4
weeks even after successful cardioversion to sinus rhythm
(beyond 4 weeks, the decision about long-term OAC treatment is
determined by the presence of stroke risk factors). IIa

56. ESC Recommendations In AF
 AF catheter ablation:
Is recommended to reverse LV dysfunction in AF patients
when tachycardia-induced cardiomyopathy is highly probable,
independent of their symptom status.

57. Conclusion
 Atrial fibrillation is an irregularly irregular atrial rhythm that may
be episodic or continuous; paroxysms of tachycardia may occur.
 QRS complexes are typically narrow; a wide complex may occur
with intraventricular conduction defects or Wolff-Parkinson-White
syndrome.
 Patients should have electrocardiography, echocardiography, and
thyroid function testing.
 Heart rate is controlled typically to < 100 beats/minute at rest;
first-line medications include beta-blockers and
nondihydropyridine calcium channel blockers (eg, verapamil,
diltiazem).

58. Conclusion
 Restoration of sinus rhythm is not as important as rate control and
does not eliminate the need for anticoagulation but may help
patients with continuing symptoms or hemodynamic compromise
(eg, heart failure); synchronized cardioversion or medication can
be used.
 Anticoagulation is usually necessary before cardioversion.
 Long-term oral anticoagulation to prevent stroke is required for
patients with risk factors for thromboembolism.

59. Thank You for your
kind attention.