2. Definition
• Atrial fibrillation (AF) is a Supraventricular
arrhythymia and characterized by disorganized,
rapid, and irregular atrial activation with loss of
atrial contraction and with an irregular
ventricular rate that is determined by AV nodal
conduction.
• In an untreated patient, the ventricular rate also
tends to be rapid and variable, between 120 and
160 beats/min, but in some patients, it may
exceed 200 beats/min.
3.
4.
5. EPIDEMIOLOGY
• Atrial FIBRILLATION IS THE MOST COMMON
SUSTAINED ARRHYTHMIA AND A MAJOR PUBLIC
HEALTH PROBLEM
• AF is slightly more common in men than women
and more common in whites than blacks.
• Prevalence increases with age and >95% of AF
patients are >60 years of age. The prevalence by
age 80 is ~10%. The lifetime risk of developing AF
for men 40 years old is ~25%.
6. • AF increases the risk of stroke by 5-fold and is
estimated to be the cause of 25% of strokes.
• AF is also associated with a 3-fold risk of HF
and a 2-fold increased risk of both dementia
and mortality
• AF occurs in up to 30% of patients recovering
from cardiac surgery, associated with
inflammatory pericarditis.
7. CLINICAL TYPES
1. Paroxysmal AF : defined by episodes that start spontaneously
and terminates within 7 days of onset. Paroxysmal AF is often
initiated by small reentrant or rapidly firing foci in sleeves of
atrial muscle that extend into the pulmonary veins (PV).
Catheter ablation that isolates these foci usually abolishes
paroxysmal AF.
2. Persistent AF : present continously for more than 7 days
3. Longstanding persistent AF: that persists for longer than one
year
4. Permanent AF : Long persistent AF refractory to
cardioversion
5. Lone atrial fibrillation : AF that occurs in patient younger than
60 years who do not have hypertension or any evidence of
structural heart disease
8. • Cardiac causes : Hypertension(usually with LVH)
,Ischemic heart disease ,Mitral Valve Disease
,Hypertrophic And Dilated Cardiomyopathy, WPW
syndrome ,Restrictive Cardiomyopathies such as
Amyloidosis ,Constrictive pericarditis and Cardiac
tumors
• Obstructive Sleep Apnea and Obesity
• Temporary & Reversible Causes: Excessive Alcohol
Intake ,Hyperthyroidism ,Open Heart or Thoracic
Surgery ,Myocardial Infarction ,Pericarditis ,Myocarditis
and Pulmonary Embolism
• Familial AF
Causes:
10. ELECTROPHYSIOLOGY
1 Automatic or triggered focus :
• The LA myocardial sleeves extending into pulmonary
veins(PV) appear to be the most frequent source
• Non-PV sites, including myocardial sleeves around the
superior vena cava (SVC) or coronary sinus.
• Heterogeneity of electrical conduction around the
pulmonary veins is theorized to promote reentry and
sustained AF
11. 2 Multiple wavelet :
• Multiple reentrant circuits meandering throughout the atria,
annihilating and reforming wavelets that perpetuates
fibrillation
• These wavelets are determined by the refractory period,
conduction velocity, and mass of atrial tissue.
• Increased atrial mass, shortened atrial refractory period, and
delayed intra-atrial conduction increase the number of wavelets
and promote sustained AF.
12. 3 Genetic Factors :
• Several mutations that causes a gain of function
of repolarization potassium currents that results
in shortening of atrial refractoriness and
facilitation of atrial reentry have been identified.
• Multiple polymorphisms in genes that affect
potassium and sodium channels, sarcolipin, the
renin-angiotensin system, connexin-40,
endothelial nitric oxide synthase, and interleukin-
10 detected .
• The end results are changes in calcium handling,
fibrosis, conduction, and inflammation that
predispose to AF.
13. Clinical Features & Examination
• 25% of patients with AF are asymptomatic
• Palpitations ,fatigue ,dyspnea ,effort
intolerance and lightheadedness
• The hallmark of AF on physical examination is
an irregularly irregular pulse.
• Pulse deficit
• Irregular jugular venous pulsations and
variable intensity of the first heart sound.
14. History:
• H/o Acute Alcohol consumption ,thyroid
disease ,Recent MI , Recent Heart or Thoracic
Surgery
15. Investigations
• ECG
• Chest radiography
• International normalised ratio ( INR )
• Renal function test
• Arterial blood gases
• Cardiac enzymes
• BNP & D-dimer
• Liver function test
• Thyroid function test
• Holter monitoring
• 2D-Echo
• Toxicology testing or ethanol level
• Electrophysiologic studies(EPS)
• Sleep Study
• Stress Test
20. TREATMENT
1. Acute Management
2. Long Term Management
3. Prevention of Thromboembolic complications
4. Nonpharmacological Management
21. Acute Management of AF
• Control of the ventricular rate is most rapidly
achieved with intravenous CCBs or Beta-blockers.
• If the patient is hemodynamically unstable(within
48hrs), immediate transthoracic cardioversion
may be appropriate.
• If the AF has been present for longer than 48
hours or if the duration is unclear than
Cardioversion should be preceded by TEE to rule
out a left atrial thrombus.
22. • In Hemodynamically stable, the decision to
restore sinus rhythm by cardioversion is based
on several factors, which includes difficulty in
achieving adequate rate control, younger
patient age, tachycardia-mediated
cardiomyopathy, first episode of AF, AF
precipitated by an acute illness, and patient
preference
23. Cardioversion
1. Early vs Delayed Cardioversion :
• Early cardioversion results in rapid relief of
symptoms
• Avoidance of the need for TEE
• No need of anticoagulation for 3 to 4 weeks
before cardioversion if cardioversion is performed
within 48 hours of AF onset
• Lower risk of early AF recurrence because of less
atrial remodeling.
24. Early Cardioversion should be
Avoided If
• Unavailability of TEE in an unanticoagulated
patient with AF of unclear duration
• Duration more than 48 hours.
• left atrial thrombus by TEE
• Correctable cause of AF (hyperthyroidism)
25. 2. Pharmacological vs Electrical Cardioversion:
• Pharmacologic cardioversion has the advantage of not
requiring general anesthesia or deep sedation.
• Probability of an immediate recurrence of AF is lower.
• However, pharmacologic cardioversion is associated
with the risk of adverse drug effects and is not as
effective as electrical cardioversion.
• Pharmacologic cardioversion is unlikely to be effective
if the duration of AF is longer than 7 days.
26. Acute pharmacologic cardioversion of AF (Pill-in-
the-Pocket Therapy) :
• Patients without structural heart disease.
• Propafenone (300 to 600 mg) and Flecainide (100
to 200 mg).
• It is prudent to administer these drugs under
surveillance at first use.
• If no adverse drug effects are observed, the
patient may then be an appropriate candidate for
episodic, self-administered AAD therapy on an
outpatient basis.
27. Electrical or Transthoracic
Cardioversion
• The efficacy of transthoracic cardioversion is
approximately 95%.
• Biphasic waveform shocks better than
monophasic waveform
• 150 to 200 J biphasic waveform, followed by
higher output shocks if needed.
• If Transthoracic cardioversion fails than
• an increase in shock strength or
• infusion of ibutilide often results in successful
repeat cardioversion.
28. Anticoagulation with Cardioversion
• If the duration of AF is less than 48 hours,
Cardioversion can be performed without
anticoagulation(24 hour cutoff)
• In patients with comorbidities(CHA2DS2-VASc>2)
even when the AF duration is less than 48 hours,
and anticoagulation for 4 weeks is appropriate
• 3 weeks before and 4 weeks after cardioversion
to prevent thromboembolic complications if the
AF is of more than 48 hours duration
29.
30.
31. Longterm Management of AF
1. Pharmacological therapy:
Rate Control versus Rhythm Control
2. Nonpharmacological therapy:
32. Rate Control
• Beta blockers, Calcium channel
antagonists(NonDHPs), Digitalis and amiodarone.
• First-line agents are beta blockers and the
calcium channel antagonists.
• Digitalis & Amiodarone in patients with AF and
Heart failure
• AV node Catherter Ablation with Permanent
Pacemaker pacing when pharmacological therapy
fails
33. • At rest, the ideal ventricular rate during AF is
in the range of 60 to 80 beats/min.
• During mild to moderate exertion (e.g., rapid
walking), the target rate should be 90 to 115
beats/min.
• During strenuous exercise, the ideal rate is in
the range of 120 to 160 beats/min.
39. • The best options for drug therapy to suppress AF depend on the
patient's comorbidities.
• In patients with lone AF or minimal heart disease (e.g., mild left
ventricular hypertrophy), flecainide, propafenone, sotalol, and
dronedarone are reasonable first-line drugs
• In patients with substantial left ventricular hypertrophy (left
ventricular wall thickness >15 mm), the hypertrophy heightens the
risk of ventricular proarrhythmia , and the safest choices for drug
therapy are amiodarone and dronedarone.
• In patients with coronary artery disease (CAD),the safest first-line
options are dofetilide and sotalol, with amiodarone reserved for
use as a second-line agent.
• In patients with heart failure, the only two drugs known to have a
neutral effect on survival are amiodarone and dofetilide.
40. Adverse Effects:
• class IA agents (quinidine, procainamide, disopyramide)
and class III agents (sotalol, dofetilide, dronedarone,
amiodarone) results in QT prolongation and polymorphic
ventricular tachycardia (torsades de pointes).
• Class IC agents (flecainide and propafenone) manifests as
monomorphic ventricular tachycardia
• Drugs most likely to result in ventricular proarrhythmia are
quinidine, flecainide, sotalol, and dofetilide
• Adverse drug effects resulting in discontinuation of drug
therapy are fairly common with rates as high as 40%.
41. Rhythm Control with Other than antiarrthymic
drugs:
• ACEI
• ARBs
• Statins
• Omega-3 fatty acids
Limited Studies available
42. Nonpharmacological Therapy
1. Pacing: Only in patients of AF with
bradycardia
2. Catheter Ablation:
-Radiofrequency Catheter
-Cryoballoon catheter
3. Surgical Approach:
-Maze Procedure
43. Catheter Ablation Therapy:
Indication -
• When the arrhythmia substrate is well defined,
localized, and temporally stable
• symptomatic AF despite antiarrthymic drug
therapy.
• lone AF or only minimal structural heart disease.
• Patient younger than 35 with symptomatic AF
44. Contraindication :
• Left atrial thrombus
• Who cannot tolerate anticoagulation for at
least 6 to 8 weeks after ablation.
49. Aspirin Role in Throboembolism:
• When the CHA2DS2-VASc score is 1, the
guidelines recommend that either no
antithrombotic therapy or treatment with an
oral anticoagulant or aspirin may be
considered.
• In high-risk patients(CHA2D2-VASc>2) who are
not suitable candidates for warfarin or a
NOAC.
50. Low Molecular Weight Heparin:
• For initiation of anticoagulation with warfarin
in patients with AF.
• Bridging therapy with LMWH be continued
until the INR is 2.0 or higher.
• In high-risk patients for a few days before and
after a medical or dental procedure when
anticoagulation with warfarin has been
suspended.
51. Excision and Closure of the Left Atrial Appendage :
• Approx 90% of left atrial thrombi form in the left
atrial appendage (LAA)
• Either excision or closure by suturing or stapling
• Transesophageal echocardiography (TEE) should
be performed to confirm successful closure
before discontinuation of anticoagulation.
55. Atrial Fibrillation in Special
Recommendation
Postoperative AF :
• Prophylactic treatment with an oral beta
blocker
• Preoperative amiodarone is also considered
• Cardioversion, rhythm-control medications
and antithrombotic medication should be
based on the same considerations as in
nonsurgical patients.
56. Acute Myocardial Infarction :
• Electrical cardioversion is recommended if there
is hemodynamic compromise
• Intravenous (IV) amiodarone or digitalis to slow
the ventricular rate in patients and to improve LV
function in patients with an acute MI.
• If there is no LV dysfunction, bronchospasm, or
AV block, an IV beta blocker or
nondihydropyridine calcium antagonist used
57. AF in WPW syndrome :
• Catheter ablation of the accessory pathway in
symptomatic AF
• Immediate electrical cardioversion if
hemodynamic instability.
• If the patient is hemodynamically stable, IV
procainamide or ibutilide.
• IV digitalis and nondihydropyridine calcium
channel antagonists should be avoided in patients
with ventricular preexcitation during AF.
58. AF in Hyperthyroidism :
• Beta blocker as first-line therapy for rate
control
• If a beta blocker contraindicated, verapamil or
diltiazem(CCB)
59. AF during Pregnancy :
• Digoxin, a beta blocker, or a nondihydropyridine
calcium channel antagonist for rate control.
• DC cardioversion is recommended if there is
hemodynamic instability.
• Pharmacologic cardioversion in hemodynamically
stable patients
• Unfractionated or low-molecular-weight heparin
during the first trimester and last month of pregnancy
and an oral anticoagulant during the second trimester
in patients at high risk of thromboembolism.
60. AF in Hypertrophic Cardiomyopathy :
• Anticoagulation is indicated independent of
CHA2DS2-VASc score
• Either disopyramide plus a beta blocker,
verapamil, or diltiazem for rate control
• or Amiodarone alone
61. AF in Pulmonary Disease :
• Correction of hypoxemia and acidosis the
primary therapy .
• Verapamil or diltiazem is recommended for
rate control in patients with obstructive
pulmonary disease.
• Beta blockers, sotalol, propafenone, and
adenosine are not recommended in patients
with obstructive lung disease
62.
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64.
65. Refrences
• Harrison Principles of Internal Medicine 20th
Edition
• Braunwald’s Heart Disease 11th Edition
• ACC/AHA Recent Guidelines