Atrial Fibrillation

2073/02/03

Bibek Raj Poudel

Intern
PAHS-SOM
 Contents
• Introduction
• Pathophysiology
• ECG finding
• Risk Factors & Etiology
• Clinical Type
• Evaluation
• Management
 Introduction
• Disorganized, rapid, and irregular atrial activation with loss of
atrial contraction
– With an irregular ventricular rate (determined by AV nodal conduction)
– Between 120 and 160 beats/min, but in some patients, it may exceed
200 beats/min

• Prevalence increases with age

– More than 95% of AF patients are older than 60 years
– Prevalence by age 80 is approximately 10%.

• Lifetime risk of developing AF for individuals 40 years old

– Approximately 25%.
 Pathophysiology

Mechanisms initiating atrial fibrillation.

(1) Ectopic beats, often arising from the pulmonary veins, trigger atrial
fibrillation.

(2) Re-entry within the atria maintains atrial fibrillation, with multiple
interacting re-entry circuits operating simultaneously
 ECG Finding
• Characteristic ‘irregularly irregular’ pulse

QRS complexes-irregular & no P waves.

A Usually a fast ventricular rate, e.g. between 120 &160/min, at

the onset of AF

B In chronic AF, ventricular rate may be much slower, due to the

effects of medication & AV nodal fatigue
 Risk Factors
• Hypertension
• Diabetes mellitus
• Cardiac disease
• Sleep apnea

• M>F
• AF is a marker for heart disease, the severity of heart
disease, and age, and
– Therefore difficult to determine the extent to which AF itself
contributes to associated increased mortality and morbidity
• AF increases the risk of stroke by 5x and is estimated
to be the cause of 25% of strokes

• Precipitating factors/Etiology
 Clinical Type
• Paroxysmal
– Recurrent AF (≥2 episodes) that terminates spontaneously in seven
days or less, usually less than 24 hours
– Up to 90% are asymptomatic

• Persistent
– Fails to self-terminate within 7 days.
– Episodes often require pharmacologic or electrical cardioversion to
restore sinus rhythm
– Progression to persistent and permanent AF occur in >50 percent
beyond 10 years despite antiarrhythmic therapy
– If last > 1year---Long standing persistent
 Clinical Type

• Permanent
– individuals with persistent atrial fibrillation where a
decision has been made to no longer pursue a
rhythm control strategy

• American College of Cardiology/American Heart Association

and the European Society of Cardiology (ACC/AHA, ESC)
UP To Date 21.6
• Persistence
– single or multiple areas of reentry facilitated by structural
and electrophysiologic atrial abnormalities

• In patients with long-standing persistent AF (>1 year)

– Significant structural changes are present in the atrium
that support reentry and automaticity,
– Making it difficult to restore and maintain sinus rhythm
• Clinical consequences are related to
– Rapid ventricular rates,
– Loss of atrial contribution to ventricular filling,
– Predisposition to thrombus formation in the left atrial
appendage with potential embolization

• Rapid rates may cause

– Hemodynamic collapse or
– Heart failure exacerbations particularly in patients with
• Impaired cardiac function,
• Hypertrophic cardiomyopathy, and
• Heart failure with preserved systolic function
• Exercise intolerance and easy fatigability are
common

• Occasionally, dizziness or syncope occurs due to

pauses when AF terminates to sinus rhythm
 Evaluation
• History
– Description of symptoms
– Precipitating cause---exercise, emotion or alcohol
– Cardiovascular or cerebrovascular disease, DM, HTN
COPD, or potentially reversible causes
(hyperthyroidism, excessive alcohol ingestion)

• Examination
 Investigations
• ECG
– Markers of nonelectrical cardiac disease (LVH), Q
wave (coronary artery disease)
– Markers of electrical heart disease (delta wave or
short PR interval) or BBB
– QT interval

• ECHO---Transthoracic----thrombus
 Management
• Primarily guided by
– Patients’ symptoms

– Hemodynamic effect of AF, the duration of AF if

there are persistent

– Risk factors for stroke, & underlying heart disease

 Principles
• Rhythm Control
• Rate Control
• Anticoagulation
• Treat underlying cause
 New Onset AF
• Causing severe hypotension, pulmonary edema or angina

• Less than 48 hours duration

– Cardioversion(QRS synchronous shock of 200 J) & anticoagulation
simultaneously

• More than 48 hours

– A month of therapeutic warfarin prior to cardioversion with a target
INR of 2.5 (range 2.0 to 3.0)

2012 ACCP and ACC/AHA/ESC guidelines

Up To Date 21.6
 Anticoagulation
• Vitamin K antagonists (Warfarin)

• Newer anticoagulants such as thrombin inhibitors

(dabigatran) or factor Xa inhibitors (rivaroxaban,
apixaban),

• But not antiplatelet agents (aspirin & clopidogrel),

which have substantially less effect
 More than 48 hrs or unknown
• Greater concern for thromboembolism with
cardioversion, even in patients considered low risk for
stroke
• Two approaches
– Anticoagulate for 3 weeks before & minimum of 4 weeks after

– Start anticoagulation and perform TEE to determine if

thrombus is present in the left atrial appendage.
• Absent---cardioversion & anticoagulation continued for a minimum of 4
weeks because recovery of atrial mechanical function after electrical or
pharmacologic cardioversion may be delayed and thrombus can form
and embolize days after cardioversion
 Rate control
• Acute control (goal < 100 bpm)
– beta blockers and/or the calcium channel blockers verapamil
and diltiazem administered either intravenously or orally

• Digoxin may be added---particularly In heart failure

– Does not have negative ionotropic effects (particularly if use
of AV nodal blocking agents is limited by poor tolerance or is
contraindicated)
 Chronic rate control
• To alleviate and prevent symptoms and prevent
deterioration of ventricular function from excessive rates
– β-Adrenergic blockers, calcium channel blockers, & digoxin

• Rate should be assessed with exertion and medications

adjusted accordingly
– Exertion-related symptoms are often an indication of
inadequate rate control
– initial goal is a resting heart rate of less than 80 beats/min that
increases to less than 100 beats/min with light exertion
 Contd…
• If rate control is difficult
– Catheter ablation of the AV junction to create
heart block and implantation of permanent
pacemaker
 Stroke prevention in AF
• More than 48 h of AF & are undergoing cardioversion,
• For patients who have a prior history of stroke, or for patients
with a CHA2DS2-VASc score of ≥2, but it may be considered in
patients with a risk score of 1

• Warfarin reduces the annual risk of stroke by 64% compared to

placebo by 37% compared to antiplatelet therapy

• Antiplatelet agents aspirin and clopidogrel are inferior to

warfarin for stroke prevention in AF and do not reduce the risk
of bleeding
 Rhythm Control
• In randomized trials,
– Administration of antiarrhythmic medications to maintain
sinus rhythm did not improve survival or symptoms
compared to a rate control strategy, and the drug therapy
group had more hospitalizations

• Uses
– Symptomatic paroxysmal AF,
– First episode of symptomatic persistent AF,
– AF with difficult rate control,
– AF that has resulted in depressed ventricular function or that
aggravates heart failure

• Young vs Old patients

• Even if sinus rhythm is apparently maintained,
anticoagulation is recommended
– According to the CHA2DS2-VASc stroke risk profile because
asymptomatic episodes of AF are common
 Pharmacologic agent

• Class I sodium channel–blocking agents (e.g.,

flecainide, propafenone, disopyramide)
– Without significant structural heart disease,

• But they have negative inotropic and proarrhythmic

effects that warrant avoidance in patients with
coronary artery disease or heart failure
 Contd…
• Class III agents sotalol and dofetilide can be
administered to
– patients with coronary artery disease or structural
heart disease but have approximately a 3% risk of
inducing excessive QT prolongation and torsades
des pointes

• CATHETER AND SURGICAL ABLATION

Summary
 Reference
• Harrison’s Principle of Internal Medicine 19E

• Davidson’s Principle & Practice of Medicine 22E

• Up To Date 21.6
Thank You!!!