Atrial fibrillation is the most common type of cardiac arrhythmia. It is the leading cardiac cause of stroke https://www.youtube.com/watch?v=4pSobW-a6gQ&list=PL2XcrMWxPBLQyEdWnJuO4qSI2m-WTrglH&pp=gAQBiAQB

1. By
Dr Mohammud Ibraheem
ATRIAL FIBRILLATION

2. EPIDEMIOLOGY OF AF

3. AF is a affecting 1% of the population.
It is the commonest dysrhythmia treated in ER and
accounts for 33% of all dysrhythmia related
hospitalizations.
0.51% of worldwide population is affected wit AF, It
increased by 33% during the last 20 years.
AF affect about 2.3 million in the US.
Men and whites are more likely to have AF than women
and blacks.
In the future; AF burden may increase by >60% in 2050.
Heritability of AF is as high as 62%. (Alzahrani Z et al,2018)

4. AF carries adverse prognostic significance:
 It is association with organic heart disease
 An important risk factor for mortality
 Development of stroke and systemic embolism. The
risk of stroke is particularly high in patients with mitral
stenosis or mitral valve replacement and
permanent atrial fibrillation.

5. 17%-32% of ischemic strokes are considered
cardioembolic. Male to female ratio is 1.3:1
Atrial fibrillation represents the most common cause of
cardioembolic stroke and is a major cause of stroke in the
elderly.
AF is associated with a 3-5 folds increased risk of stroke.
The prevalence of AF increases sharply from 0.1%
among adults aged <55 years to almost 10% among
those aged >80 years.
The number of patients with AF may double and the
number of AF-related strokes may triple in the next few
decades

6. Wessler BS et al; 2015

7. MECHANISM OF AF

8. AF is a complex disease with a combination of
environmental and genetic factors.
AF is attributed to multiple wavelets with chaotic reentry
within the atria.
In many cases; firing of an ectopic focus within venous
structures adjacent to the atria is responsible for initiation
and maintenance of AF.
the atria do not contract, and the AV conduction system is
bombarded with many electrical stimuli, causing
inconsistent impulse transmission and an irregularly
irregular ventricular rate causing tachycardia rate.

10. Several genetic mutations affecting repolarization
potassium and calcium channels and myocyte proteins
have also been implicated in the genesis of familial AF.
The causative mutations for AF are the ion channel
KCNQ1, the cardiac peptide NPPA, the transcription
factor TBX5, and a motor protein MYL4.
TTN gene mutation is the most commonly associated with
AF.

11. Common gen mutations in AF

12. RISK FACTORS OF AF

13. 1) Low socioeconomic state
2) Adverse lifestyle factors
(smoking, alcohol intake, and
obesity)
3) Cardiovascular diseases as
HTN, LV hypertrophy, CHD, and
LA enlargement
4) Diabetes mellitus
5) Pulmonary disease
6) Hypothyroidism and OSA
7) Cardiothoracic surgery
8) Autoimmune diseases
1) The old age (10% of patients
over the age of 80)
2) Male gender; 1.5 more than
women
3) Caucasian population
4) Mutation involving Na and Ca
channels
5) Mutation affect myocite
proteinS
RISK FACTORS OF AF
Non modifiable Modifiable

14. HYPERTENSION
HTN is the commonest RF.
It increases arterial stiffness, LV hypertrophy and
impaired diastolic function. This leads to an increase
in LA pressures that causes fibroblast proliferation
and myocyte hypertrophy that impaire
interconnections between the muscle bundles and
increases AF inducibility.

15. HYPERTENSION
There is a linear association between severity
of HTN and risk of AF.
Nondipping pattern (blunted day-night fall in
blood pressure) is associated with a 2folds
higher risk for AF when compared with patients
who has a normal dipping pattern at night (fall
in systolic BP by ≥10% at night).
The renin–angiotensin–aldosterone system
(RAAS) play a role in HTN-induced LA
remodeling

16. DIABETES MELLITUS
DM have a 34% greater risk of developing AF and the
risk increases by 3% for every additional year of the
diagnosis.
frequent blood glucose fluctuations are more
dysrhythmogenic than sustained hyperglycemia.
DM is associated with oxidative stress and
inflammation in the form of high CRP, interleukin-6,
tumor necrosis factor-alpha levels; it also leads to
high transforming growth factor-beta (TGF-β) .

17. DIABETES MELLITUS
High levels of TGF-β accelerate formation of
advanced glycosylated end products (AGE)
which contribute to myocardial fibrosis. High
serum levels of AGE predict development of
persistent AF.
diabetic autonomic dysfunction leads to
sympathetic–parasympathetic imbalances that
implicate in the genesis of AF.

18. HEART FAILURE
HF is the most common cause of death in
anticoagulated patients with AF.
Prevalence of AF is 13 to 41% in HF patients.
AF prevalence is higher in patients with preserved EF
than patients with reduced or mid-range EF.
The mechanism link HF and AF is that the connective
tissue disruption resulting from increased LA pressure
and size causes local ischemia, interstitial fibrosis, and
slowing of conduction.

19. HEART FAILURE
The RAAS system is upregulated and
contributes to atrial fibrosis.
Endothelin-1 (a mediator with dysrhythmogenic
properties ) increase in AF and HF. Serum
levels of endothelin-1 correlate with degree of
LA remodeling and the clinical severity of both
HF and AF and has been postulated as a
mechanistic link between these two states.

20. OBESITY
AF is prevelant in obese. Increased epicardial fat
thickness play a role in geneses of AF.
sustained weight loss with avoiding weight fluctuations
cause a reduction in AF and improve success in
maintaining sinus rhythm.
The ACC/AHA/HRS 2019 guidelines recommended
the initiating of weight loss measures combined with
RF modification in patients with AF.

21. OBSTRUCTIVE SLEEP APNEA
OSA increase AF incidence. The hypoxia
caused by OSA increases the autonomic tone
and causes HTN.
The recurrence of AF at 1 year following
cardioversion is higher in patients not
adequately treated with nocturnal positive-
pressure ventilation (82%) versus patients who
have been adequately treated (42%).

22. DYSLIPIDEMIA
The Framingham cohorts reported an
independent effect of low HDL and high
triglycerides on increase in AF incidence. This is
related to the anti-inflammatory and antioxidant
properties of HDL, while higher AF risk with
elevated triglycerides could be a reflection of the
deleterious effects of metabolic syndrome.
statins reduce AF incidence due to its pleiotropic
antiinflammatory properties.

23. SMOKING
Smokers have a 32% increased risk of AF.
nicotine increases oxidative stress, inflammation,
and resulting atrial fibrosis.
Nicotine increases arterial stiffness causing HTN
and causes sympathetic stimulation with
catecholamine release. This leads to alterations in
atrial myocyte ion channels and increase in
effective refractory period.
There is a dose response relationship between
years of smoking and AF risk.
.

24. ALCOHOL USE
Alcohol use has been implicated to trigger AF.
“Holiday heart” syndrome has been described
in the literature and refers to the occurrence of
AF in patients after heavy alcohol use.
AF risk increased to 39% in subjects consuming
more than 21 drinks per week and up to 45%
with more than 35 drinks per week

25. LOW CARDIORESPIRATORY FITNESS
The association of CRF by regular exercise and
AF is complex.
The Cardiovascular Health Study reported a
28% reduction in AF with light-to-moderate-
intensity regular exercise when compared with
no exercise, but no benefit was observed with
regular high-intensity exercise.
This due to favorable cardiovascular risk profile,
lower body mass, and reduced systemic
inflammation with regular exercise.

26. LOW CARDIORESPIRATORY FITNESS
Vigorous, long-duration endurance training has been
reported to be associated with increase incidence of AF.
This could be related to left atrial and ventricular
remodeling and high vagal tone seen in endurance
athletes.
A prospective study from Finland assessed the
relationship between maximal oxygen uptake (marker
of CRF) and incident AF in 1950 middle-aged men over
a follow-up period of 20 years. There was a decrease in
incidence of AF with higher CRF levels and a modest
increase in AF incidence at very high CRF levels (>
40.6mL/kg/min).

28. HEALTH OUTCOMES

29. A. Prognosis
AF is associated with around a 1.5–2-fold increase
in cardiovascular and all-cause mortality.
B. AF and hypertension
Hypertension is probably the largest single
contributor to the development of AF in a
population. The presence of hypertension alone
increases the risk of developing AF by 70–80% and
causes fifth of the AF in the developed world.

30. D. Stroke and AF
AF is a major independent risk factor for stroke,
and increases the risk by 3-5 folds. Strokes
associated with AF are more severe, resulting in
a higher likelihood of dying, longer hospital
stays, more neurological damage, and greater
disability.
E. Heart failure and AF
Heart failure and AF have revealed an
incestuous relationship, Over a third of patients
with a diagnosis of HF will develop AF at some
stage, and the presence of AF alone increases
the risk of HF by around four- to sixfolds.

31. E. Acute coronary syndromes and AF
Fifth of patients with an ACS developing AF.
F. AF and OSA
A 3.5 fold increase in the risk for the development
of AF if OSA is present.
G. AF and obesity
A linear association between increasing BMI and
the development of AF. Obese patients (BMI >
30) experience approximately a 5% increase in
their risk of developing AF for every unit of
increase in their BMI.

32. CLASSIFICATION AND ETIOLOGY

33. ACCORDING TO THE PATTERN
1) Paroxysmal (self-terminating episodes <7
days duration but usually <48 h)
2) Persistent (terminates after 7 days or
following intervention, e.g. electrical
cardioversion)
3) Permanent (no strategy to terminate the
arrhythmia)

34. ACCORDING TO VALVULAR AFFECTION
1) Valvular, the patient have a heart valve
disorder or a prosthetic heart valve, it
represent 4%-30% of all AF
2) Nonvalvular refers to AF caused by other
things, such as high blood pressure or
stress.

35. ETIOLOGY OF ATRIAL FIBRILLATION
1. Idiopathic ( ‘lone’ atrial fibrillation)-Up to 25-30% of cases of AF-
2. Increased atrial pressure (mitral valve disease, congestive heart failure, left
ventricular hypertrophy, restrictive cardiomyopathy, pulmonary embolism)
3. Atrial volume overload (atrial septal defect)
4. Myocardial ischaemia/ infarction
5. Thyrotoxicosis
6. Alcohol
7. Sinoatrial disease
8. Infiltration (constrictive pericarditis, tumour)
9. Cardiac or thoracic surgery
10. Infection
 systemic, e.g. pneumonia
 cardiac: myo/ pericarditis

36. CLINICAL EVALUATION OF AF

37. PRESENTATION
A. Asymptomatic and picked up during routine
screening
B. The onset of AF trigger palpitations, fatigue,
breathlessness, or angina in patients with
underlying coronary disease
C. Syncope is uncommon but occur in the context of
sinus node disease
D. Complications of AF as stroke.
E. Atrial fibrillation results in loss of the atrial
contribution to
F. left ventricular filling, which can result in a
worsening of heart

38. DIAGNOSIS OF AF
I. DIAGNOSIS OF AF
A. Routine ECG
1. Absence of P waves
2. Presence of f (fibrillatory) waves between QRS
complexes; f waves are irregular in timing, irregular
in morphology; baseline undulations at rates >
300/minute, usually best seen in lead V1 and not
always apparent in all leads
3. Irregularly irregular R-R intervals
it detect constant abnormalities

39. DIAGNOSIS OF AF
Irregular rhythms may resemble atrial fibrillation
on ECG:
1. Flutter wave
2. Muscle tremor or electrical interferance
3. Atrial fibrillation may also cause a
phenomenon that mimics ventricular
extrasystoles or ventricular tachycardia
(Ashman phenomenon)

40. DIAGNOSIS OF AF
B. Stress ECG
The patient is made to work hard e.g. run on a
treadmill or exercise while the leads of ECG are
placed over the chest. Those who cannot
exercise are given pills to raise their heart rate.
The ECG pattern, dysrhythmias or ischemic
changes. This usually occurs in coronary artery
disease.

41. STRESS ECG

42. DIAGNOSIS OF AF
C. Conventional 24-hour Holter monitor
It is used for detection of paroxysmal AF.
Especially, in diagnosis of the etiology of
cryptogenic stroke.
A newer option for continuous monitoring is a
small disposable wireless adhesive patch that
is worn on the chest for up to 2 weeks.

43. CONVENTIONAL 24-HOUR HOLTER MONITOR

44. DIAGNOSIS OF AF
D. Event monitor
It is used when a person must be monitored
longer than 48 hours, typically 30days. It is
similar to a Holter monitor, but it records only
when the user activates it, when symptoms
occur by pressing a button on the device or
when the device detects an abnormal heart
rhythm.

45. EVENT MONITOR

46. DIAGNOSIS OF AF
E. Cardiac telemetry
It is an observation portable device allows
continuous ECG, RR, SpO2. The patient group
requiring telemetry are children diagnosed with
a known/unknown dysrhythmia, children at risk
of an dysrhythmia, or children anticipated to be
at risk of sudden cardiac deterioration.

47. CARDIAC TELEMETRY

48. DIAGNOSIS OF AF
II. DIAGNOSIS OF THE ETIOLOGY
A. Cardiac work up
1) Echocardiography
It assess structural heart defects (eg, left atrial enlargement, left ventricular
wall motion abnormalities, valvular disorders, cardiomyopathy) and to identify
risk factors for stroke (eg, atrial blood stasis or thrombus, complex aortic
plaque).
Transoesophegeal echocardiography detect atrial thrombi in the atrial
appendages.
Agitated saline (bubble) transthoracic contrast echocardiography is
performed to diagnose intracardiac and intrapulmonary shunts.

49. DIAGNOSIS OF AF
B. Laboratory studies :
1. Complete blood cell count (looking for anemia, infection)
2. Levels of serum electrolytes and blood urea nitrogen (BUN)/creatinine
3. Cardiac enzymes levels: Creatine kinase (CK) and/or troponin level (to
investigate myocardial infarction as a primary or secondary event)
4. B-type natriuretic peptide (BNP) level (to evaluate for congestive heart
failure)
5. D-dimer level (if the patient has risk factors to merit a pulmonary
embolism workup)
6. Thyroid function studies
7. Digoxin level
8. Toxicology testing or ethanol level

50. DIAGNOSIS OF AF
C. CT and MRI
In AF and a positive D-dimer result, chest
computed tomography angiography (CTA) is
necessary to rule out pulmonary embolus.
Three-dimensional imaging technologies (CT
scan or MRI) are helpful to evaluate atrial
anatomy if AF ablation is planned.

51. STROKE RISK ASSESSMENT

52. The National Institute for Health and Care
Excellence (NICE), American Heart Association/
American College of Cardiology/ Heart Rhythm
Society, and European Society of Cardiology
(ESC) guidelines advocate the use of CHA2DS2-
VASc to assess stroke risk.
CHA2DS2-VASc is an acronym for the stroke risk
factors. the CHA2DS2-VASc score better
discriminated stroke risk in nonvalvular AF

53. mCHADS2DS2-VASc (50-74/ 1)
It perform better than CHA2DS2-VASc
score for stroke risk stratification
CHA2DS2-VASC

54. CHA2DS2-VASc
Score
Adjusted Stroke Risk, (% per
year)
0 0
1 1.3
2 2.2
3 3.2
4 4
5 6.7
6 9.8
7 9.6
8 6.7
9 15.2
I. Score 0 low risk
II. score 1 intermediate risk
III. score ≥2 high risk
OAC or antiplatelet prophylaxis is
recommended for patients with a
score of 1
OAC use is a definite recommendation
for patients with a score of 2 or
greater
CHA2DS2-VASC

55. MANAGEMENT OF AF

56. GENERAL PRINCIPLES OF MANAGEMENT
Appropriate management of AF depends on the
presence or absence of symptoms,
haemodynamic status, duration of arrhythmia,
and the presence of factors affecting the
successful maintenance of sinus rhythm.
Management is based on the prevention of
thomboembolic complications as the initial
priority, and the use of a rate- or rhythm- control
strategy in a patient- centred and symptom-
directed approach.

57. EMERGENCY PRESENTATION
AF of recent onset may terminate
spontaneously, particularly if associated with an
acute febrile illness. Outside the context of an
acute febrile illness, an attempt to restore sinus
rhythm should be made unless the dysrhythmia
is obviously long- standing(>48 h) or is
associated with advanced organic heart
disease.
Underlying precipitating factors such as
thyrotoxicosis should be corrected before
attempting cardioversion.

58. CLASSIFICATION OF ANTIDYSRHYTHMIC
DRUGS (VAUGHAN–WILLIAMS)
1) Class I: Na channel blockers (membrane stabilizing agents)
I. IA: Drugs that moderately depress phase 0 depolarization – quinidine,
procainamide, disopyramide.
II. IB: Drugs that have minimal effect on phase 0 depolarization –
lignocaine, mexiletine.
III. IC: Drugs that markedly depress phase 0 depolarization – flecainide,
propafenone.
2) Class II (beta adrenergic blockers): Propranolol, atenolol, esmolol,
metoprolol, sotalol.
3) Class III (drugs that prolong duration of action potential): Amiodarone,
dronedarone, sotalol, dofetilide, ibutilide, bretylium.
4) Class IV (CCBs): Verapamil, diltiazem.

59. PHARMACOLOGICAL CARDIOVERSION
Class Ia agents accelerate the ventricular rate by virtue
of their anticholinergic action on the AV node and must be
used in combination with AV nodal blocking agent
(digoxin, β- blocker, or CCBs).
For patients without underlying heart disease, class Ic is
recommended (flecainide 2 mg/ kg IV over 30 min).
Class III drugs are safer in the presence of LV
dysfunction or IHD (e.g. amiodarone 300 mg
intravenously over 30 min, followed by 900 mg/ 24 h until
cardioversion).
Only one drug should be tried in any individual patient. If
drug therapy fails, DC cardioversion is commonly
effective.

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