ATRIAL FIBRILLATION

Dr Anil kumar Sah

 INTRODUCTION & EPIDEMIOLOGY
• rapid, irregular, continuous atrial electrical activation, resulting in loss of
organized atrial mechanical contraction (usually Atrial rate 300-600/min)
• Proportion of the impulse  via AV node  conducted to ventricle: vent
rate: -100-160 /min mostly
• MC arrhythmia: occur in 1-2 % of general popn.
• Prevalence increases with age, with >95% of AF patients >60 years of age.
• The lifetime risk of developing AF for men aged 40 years old is ~25%.
• AF is slightly more common in men than women
• AF causes >25% of all stroke. The risk of dementia increases with AF
 RISK FACTORS
• Age
• Majority of pt have hypertension with Left ventricular hypertrophy. Other
are: Ischemic Heart disease, Mitral valve disease, HOCM, DCM, congestive
heart failure. Less common: restrictive cardiomyopathies such as
amyloidosis, constrictive pericarditis & cardiac tumors
• DM, Hyperthyroidism, excess alcohol intake
• Family Hx of AF
• obesity, and OSA.
• AF occur in 1/3 of pt after cardiac surgery. It usually manifests during the
first 4 days and is a/w increased morbidity and mortality, largely due to
stroke and circulatory failure,
• If NO cause is found it is called ‘lone’, or ‘idiopathic’ AF.
PATHOPHYSIOLOGY
• Incompletely understood
• Multifactorial
• Any condition resulting in raised atrial pressure, increased atrial
muscle mass, atrial fibrosis, or inflammation and infiltration of the
atrium may cause AF
• Alterations in regulation of membrane channels and other proteins
result in abnormal electrical excitability. Atrial tissues, in particular
pulmonary vein musculature, exhibit enhanced automaticity
ectopic beats (premature atrial contractions Bouts of rapid atrial
ectopy  initiate either atrial tachycardia or AF
MECHANISM
• Re-entry: is the primary mechanism
• rapidly discharging autonomic foci: AF is triggered and/or maintained by
rapidly firing foci in the pulmonary veins

AF is triggered and/or maintained by rapidly firing foci in the pulmonary

veins.
In persistent AF, changes in the atrial substrate, including interstitial fibrosis
that contributes to slow, discontinuous, and anisotropic conduction, may give
rise to wandering or stationary reentry. y. It is for this reason that the
outcomes of AF ablation targeted at the pulmonary veins (PVs) alone results
in lower efficacy.
 TYPES OF AF: DEFINED BY PATTERN OF EPISODES
• Paroxysmal AF: AF terminate in <_ 7 days
• Persistent AF: >7 days but < 1 year
• Long standing persistent AF: > 1 year
• Permanent: continuous, with a joint decision between the patient and the
physician to cease further attempts to regain sinus rhythm.

NOTE: lone’, or ‘idiopathic’ AF

• No underlying cause, Sx or comorbidities
• Younger pt: < 60 y
• a/w Genetics genes a/w sodium channel, potassium channel, gap
junction proteins, right–left isomerism& linked to chromosomes 10, 6, 5
and 4
Paroxysmal AF can further be classified as:
• Vagotonic AF: AF is initiated in the setting of high vagal tone, typically
in the evening when the patient is relaxing or during sleep. Drugs
exerting a vagotonic effect (e.g., digitalis) can aggravate vagotonic AF
• Adrenergic AF: high sympathetic tone, as during strenuous exertion.
Here, beta blockers not only provide rate control but may prevent
episodes of AF.
• Most patients have a mixed or random form of paroxysmal AF, with
no consistent pattern of onset.
CLINICAL FEATURES: Results from
1. Due to Irregular rapid ventricular rate
• Palpitation
• Irregular
• Occurs randomly or at particular times (e.g., during sleep),
• Frequency & duration

2. Due to fall in Cardiac output

• loss of contribution of atrial systole to CO & d/t irregular ventricular rates, variable
ventricular filling  variable stroke volume.
• Exercise intolerance, fatigue, weakness, presyncope, or dyspnea
• Exacerbation of Sx in pt with HOCM, CAD, HF
3. consequences of cardioembolic phenomena
• Stroke
• Dementia: Thrombus formation in LA appendage recurrent
thromboembolism to the brain though Asx, thought to be the cause of
dementia

4. impact of AF on cardiovascular function over time

• Prolong rapid ventricular rate  tachycardia-induced cardiomyopathy
• LA: dilated & fibrotic;
• noncompliant, fibrotic LA, including elevated LA filling pressures, volume
overload, & CHF, described as “stiff left atrial syndrome.
DIAGNOSIS
PULSE:
irregularly irregular;
pulse apex deficit: >10

JVP:
irregular jugular venous pulsations; No a waves, No x descend

Heart sound:
S1: Variation in intensity.
S2: may not be heard if the ventricular contraction is too weak to open the
semilunar valves
ECG
• HR: no. of QRS complex in 30 large boxes * 10
• Fibrillating(f) wave: 300-600 beats/min variable in amplitude, shape, and
timing. In lead V1 , f waves sometimes appear uniform and can mimic flutter
waves
• Note: Atrial flutter: 250-350 b/m constant in timing & morphology
• Ventricular rate: 100-160 b/m
• All atrial beats are not conducted d/t refractory period in the AV node, and
conduction is variably timed,  irregular ventricular rate. If the ventricular
rate is > 100 beats/min, a rapid ventricular response is said to be present .
• Pt with WPW syndrome: ventricular rate can exceed 250 b/m because of
conduction over the accessory pathway
• Rhythm: irregular
• No P wave
24 hr holter monitoring
LAB
• TFT
• LFT
• RFT
• CXY- if the history or physical examination is suggestive of pulmonary
disease

ECHO: to evaluate atrial size and LV function and to look for LV

hypertrophy, congenital heart disease and VHD
TREATMENT
AIMS
1. control of patient Sx via rate control and/or rhythm control;
2. Reduce thromboembolic risk
3. Addressing modifiable risk factors for progression of AF
ACUTE ATTACK
HEMODYNAMICALLY UNSTABLE:

Hypotension, respiratory distress, MI is present, immediate

Electrical (transthoracic) cardioversion is done
- QRS synchronous DC shock,
- Biphasic defibrillator used over monophasic
- Without TEE since hemodynamic compromised
- anterior patch electrode: just right of the sternum 3rd or 4th ,
with second electrode: just below the left scapula posteriorly. If
PPM, at least 6 cm away from it. Direct contact with the patient
or the bed should be avoided. Atropine (1 mg IV) should be
readily available to treat prolonged pauses
- 150-200 J, if unsuccess360 J, if unsuccess Inj Ibutilide then
shock bcz it improve success rate & lower defibrillating energy
requirement
- requires 4 weeks of therapeutic anticoagulation after cardioversion to
prevent thromboembolism related to atrial stunning
ACUTE ATTACK:
HEMODYNAMICALLY
STABLE
 ACUTE ATTACK: HEMODYNAMICALLY STABLE
Ventricular Rate control
- Aim: to allow more diastolic filling time improve cardiac output
- Oral or I.V B-blocker &/or CCB (verapamil/diltiazem)
- Metoprolol:
- Inj 2.5-5 mg I.V bolus over 2 min (total 3 doses, repeat dose every 5 min
upto total 15 mg)
- T metoprolol 50-100 mg (can be given upto 400 mg daily)
- Propranolol
- I.V 1 mg over 1 min. repeat every 2 min as needed upto 3 doses.
- T 10-40 mg po TDS/QID
- Diltiazam
- I.v 0.25 mg/kg over 2 min f/b 0.35 mg/kg over 2 min if needed.
- T 120-360 mg po od
- Verapamil
- I.V 0.0075-0.15 mg/kg over 2 min f/b 10 mg bolus after 15-30 min if needed.
- T 180-480 mg od

- Digoxin:
- as it lacks –ve inotrophic effect seen with B-blocker/CCB, has been used for
rate control, particularly in pt with CCF.
- Its used is declined d/t inc mortality.
- I.V 0.25-0.5 mg over several min. Repeat 0.25 mg every 6 hr to max 1.5 mg
in 24 hr.
- Amiodarone
- Used both as a rate control / rhythm control
- I.V 150 mg over 10 min followed by 1 mg/min for 6 hr f/b 0.5 mg/min for 18 hr
- T 100-200 mg od
 ACUTE ATTACK: HEMODYNAMICALLY STABLE
Rhythm control
- Antiarrhythmic or cardioversion
- If cardioversion is decided upon for a hemodynamically stable patient,
decisions must be made: early versus delayed cardioversion and
pharmacologic versus electrical cardioversion
- . Pharmacologic cardioversion:
- Adv-Donot require general anesthesia or deep sedation. And immediate recurrence
of AF is lower than with electrical
- Disadv- pharmacologic cardioversion is associated with the risk of adverse drug
effects. Unlikely to be effective if AF > 7 days.
- Drugs: Ibutiliode: efficacy-60-70%; usesd limited d/t risk of QT prolong & torsades
de pointes . Should be limited to pt with LVEF: >35%
- Amiodarone: efficacy 40-50%; Procainamide: efficacy-30-40%
- Transthoracic cardioversion: efficacy: >95%
• Regardless of whether cardioversion is performed pharmacologically or electrically,
therapeutic anticoagulation is necessary for 3 weeks or more before cardioversion
to prevent thromboembolic complications if the AF has been ongoing for more than
48 hours.
• If the time of onset of AF is unclear, for the sake of safety, the AF duration should be
assumed to be > 48 hours. These patients should be therapeutically anticoagulated
for 4 weeks after cardioversion to pre - vent thromboembolic complications
• If the patient’s stroke risk profile is elevated, anticoagulation should be continued
indefinitely.
• If the duration of AF is known to be < 48 hours, cardioversion can be performed
without anticoagulation.
• When AF > 48 hours or is unclear, an alternative to 3 weeks of therapeutic
anticoagulation before cardioversion is anticoagulation with heparin and a TEE to
check for a left atrial thrombus. If no thrombi are seen, the patient can be
cardioverted safely but still requires 4 weeks of therapeutic anticoagulation after
cardioversion to prevent thromboembolism
 LONGTERM Mx
RATE CONTROL
• B-blocker alone or combined with CCB
• Adequate rate control: resting HR: <80b/m that increases to <100 b/m
with light exercise such as walking.
• If difficult to control rate, resting HR 110 b/m is acceptable provided it
doesnot cause any Sx & ventricular function is normal

• If adequate rate control is difficult to achieve

• Catheter ablation of AV junction (to create permanent AV block) & implant
Permanent pacemaker so called “ablate & pace” stategy. Biventricular pacing or
direct pacing of bundle of his or LBB may be used.
RHYTHM CONTROL:
• Indication: In pt with difficult rate control, symptomatic Pt (Sx P. AF,
recurrent Sx persistent AF), AF that aggravate HF
• Class I antiarrhythmic drug for pt w/o st heart disease. E.g.: Flecanide,
propafenone
• Class III: Sotalol in pt with CAD or St heart disease. Amiodarone is preserved
for CAD, HF, LVH.

• Catheter ablation:
• Avoids antiarrhythmic drug toxicity, . Pt with recurrent P. AF, it is superior to drug
• Percutaneous (via femoral vein), transatrial septal puncture, radiofrequency ablation
of LA around the pulmonary vein. Extensive area of ablation is required.
• S/E: stroke(0.5-1%); cardiac tamponade(1%); phrenic nerve paralysis, bleeding from
femoral access
CHA2DS2VASc SCORE point HAS-BLED SCORE point
(Bleeding risk assessment)
C-CHF 1 H-HTN 1
H-HTN 1 A-Abnormal RFT/LFT 1-2
A-Age>_75y 2 S-Stroke 1
D-DM 1 B-Bleeding Hx/anemia 1
S-Stroke/TIA/Embolus 2 L-Labile INR 1
V-Vascular disease 1 E-Elderly: >75 y 1
A-Age 65-75 y 1 D-Drugs(antiplatelet/NSAIDS/Alcohol 1-2

S-Sex: female 1
SCORE: SCORE
0- no anticoagulant required 0-1: low risk (<2%/year)
1-Aspirin 2-3: Moderate risk (2-4%/year)
>_2-Anticoagulant: warfarin in men & >_ 3 in women >_4: High risk (>4% ?year)
>_4: high risk of annual stroke rate

AHA 2019: Aspirin is no longer recommended for stroke prevention in AF patients. In patients with a low CHA2DS2 - VASc
score, the recommended options for stroke prevention are now an anticoagulant versus no therapy
Aspirin: not effective for preventing thromboembolic complications in patients with AF

Warfarin:
• warfarin reduced the risk of all strokes (ischemic and hemorrhagic) by approximately
60%
• The target INR should be 2.0 to 3.0. This range of INRs provides the best balance
between stroke prevention and hemorrhagic complications
• Maintaining the INR at a level of 2.0 or higher is important because even small
decrease in INR from 2.0 to 1.7 more than doubles the risk of stroke.
• The annual risk of a major hemorrhagic with warfarin is 1% - 2%, and a strong
predictor of major bleeding events is an INR > 3.0. Some studies have indicated that
advanced age can be a risk factor for intracranial hemorrhage in patients with AF
treated with warfarin.
• Bridging therapy with LMWH should be continued until the INR is 2.0 or higher
Direct- Acting Oral Anticoagulants(DOAC)
Advantage:
• fixed dosing regimen that eliminates the need for monitoring the INR,
• rapid onset and offset,
• equal or greater efficacy for stroke prevention,
• lower risk of intracranial hemorrhage,
• no interactions with dietary factors such as alcohol or vitamin- K containing foods, and
• far fewer drug interactions.

Dabigatran, an oral direct thrombin inhibitor, and rivaroxaban, apixaban, and edoxaban,
which are factor Xa inhibitors, are approved by the U.S. (FDA) for prevention of stroke/
embolism in patients with nonvalvular AF
Note: Valvular AF is defined as AF in patients with a prosthetic valve or with
moderate to severe mitral stenosis
DOACs also have some disadvantages compared with warfarin:
• higher cost,
• more gastrointestinal side effects in the case of dabigatran,
• twice- daily dosing for dabigatran and apixaban,
• the absence of a readily available laboratory test to verify compliance, and
• restricted use in patients with prosthetic valves.

The onset of action of the DOACs is appro 1.5 to 2 hours after a dose. Their
half- life is approx 12 hours. The rapid onset of action and washout
eliminates the need for bridging therapy with heparin when treatment with
one of the DOACs is interrupted for a surgical or invasive medical
procedure.
SPECIFIC CLINICAL SYNDROMES
Postoperative Atrial Fibrillation
• AF is common (25% to 40%), who undergo CABG or valve
replacement. AF in this setting is associated with a twofold increase in
the risk of postoperative stroke
• Hypomagnesemia is common after open heart surgery and can
heighten the risk of AF. Magnesium administration has been reported
to decrease the risk of postoperative AF
• The incidence of AF after open heart surgery can be significantly
reduced by prophylactic treatment with amiodarone,74 sotalol, or
beta blockers
Wolff- Parkinson- White Syndrome
• d/t accessory pathway, pt can have very rapid ventricular rate during
AF. Ventricular rates > 250 to 300 b/m can result LOC or ppt V fib and
a cardiac arrest requiring transthoracic cardioversion.
• If hemodynamically stable: Procainamide may be preferable to
ibutilide because it blocks accessory pathway conduction and slows
the ventricular rate before AF has converted to sinus rhythm.
• Digitalis and CCB are C/I in patients with WPW syndrome and AF bcz
they selectively block conduction in the AV node and can result in
acceleration of conduction through the accessory pathway.
• Preferred therapy: catheter ablation of the accessory pathway.
Efficacy: 95%
Congestive Heart Failure
• AF is a common arrhythmia in pt with HF.
• AF may be the cause of heart failure in patients who present with a
nonischemic cardiomyopathy & AF with Rapid vent rate.
• It now is recognized that AF can cause HF even when the ventricular rate
is not rapid.
• . It now is recognized that AF can cause left ventricular dysfunction and
heart failure even when the ventricular rate is not rapid.
• The most appropriate rate- control drugs in patients with systolic heart
failure are beta blockers and digitalis. If necessary, amiodarone can also
be used for rate control.
• In patients with diastolic heart failure, nondihydropyridine calcium
antagonists can be used safely for rate control.
• Amiodarone and dofetilide are the only two rhythm- control drugs that
are not associated with an increased risk of death in patients with heart
failure.
• EF will remain less than 30% to 35% after optimal heart rate control, a
biventricular ICD is appropriate for primary prevention of sudden
cardiac death
• In patients with HF who undergo CRT, AF often results in intrinsic and/or
fused QRS complexes even when the rate is considered to be
adequately controlled. If this is the case in a patient with heart failure
and AF, AV node ablation is appropriate
Hypertrophic Cardiomyopathy (HCM)
• AF occurs in approximately 25% of patients with HCM
• can cause severe hemodynamic impairment because of an inadequate
diastolic filling time
• Because of a high risk of thromboembolic complications,
anticoagulation is indicated in AF patients with HCM, independent of
the CHA 2DS 2 - VASc score
Pregnancy
• Prevalence is very low. When it occurs, there often is underlying con - genital
or valvular heart disease, thyrotoxicosis, or electrolyte abnormalities.
• Pregnancy is a/w a hypercoagulable state, but there are no data that
pregnancy increases the risk of thromboembolic complications related to AF
• Anticoagulation: same criteria as in nonpregnant women. If anticoagulation is
deemed necessary, warfarin (not a DOAC) is recommended from 2nd trimester
until 1 month before the due date, and s.c LMWH is recommended during the
1st trimester and during the final month of pregnancy
• Transthoracic cardioversion is considered safe at all stages of pregnancy
• The recommended drug for acute mx of AF: I.V metoprolol for rate control. If
ineffective than digoxin. a beta blocker can be used, but only after the first
trimester. flecainide or sotalol for conversion to sinus rhythm. In the patient
with structural heart disease, amiodarone is recommended for rhythm control