Basic approach to AF

2.  Most common arrhythmia
 ECG feat: Irregularly irregular R-R
intervals, with no distinct P waves

3. Risk Factors and disease
associations
 HTN
 CHD
 RHD
 Heart failure
 Hypertrophic cardiomyopaty
 Congenital heart disease
 Venous thromboembolic disease – DVT, PE
 Other cardiopulmonary disease – COPD, peripartum CM,
Lupus myocarditis, pericarditis, OSA
 Obesity
 DM
 Metabolc syndrome
 CKD
 Surgeries
 Hyperthyroidism

4. Basic atrial physiology and
Mechanism of AF
Atrial myocardium  “Fast response
tissues”
 Shorter AP duration
 Cellular reactivation occurs fast due to
short refractory period
 Very rapid electrical conduction
 Refractory period shortens with
increasing rate

5.  Risk factors (HTN, CAD, VHD, DM, Age, NYHA II - IV)  Left
atrial dilatation  Leads to formation of substrate
 Trigger: Rapid firing from substrate (mostly from
pulmonary vein)
 Maintainence of AF: by one or more
abnormalities in atrial tissue
- Atrial remodelling: AF begets AF
- Electrical remodelling: Progressive
decrease in refractoriness
- ANS
- Fibrosis
- Re-enterant mechanism: Multiple
wandering wavelets

8. Classification
 Paroxysmal AF: Self limiting , intermittent.
Duration < 7days. Spontaneously or with
intervention
 Persistent AF: >7 days
 Long standing persistent AF: >12 months
 Permanent AF: Patient and doctor jointly
agrees not to pursue rhythm control
 Lone AF: Patients with AF who have no
structural heart disease. ≤60yrs. CHA2DS2 VASc
score of 0
 Subclinical AF: Incidental diagnosis.

9. EVALUATION

10. History and examination
 Not all patients with AF are
symptomatic

12. Signs
 Look for contributory factors
◦ Eg. Murmurs of MS s/o RHD
◦ Signs of HF
◦ Features of MI

13. Investigations
 ECG
 ECHO: TTE - Size of atria and function
TEE - To identify left atrial
thrombus
Holter monitoring
 Lab: TSH, FT4, CBC, S. Creat,
Proteinuria, FBS, Markers of ischaemia
(Trop)

14. ECG
 Lack of discrete P waves
◦ Fibrillatory or ‘f’ waves are present at rate b/w
350 – 600/min
◦ vary in amplitude, morphology & intervals
◦ recent onset AF: coarse f waves (>2mm)
◦ long duration AF: fine f waves (<1mm)
 Ventricular response
◦ Irregularly irregular R-R interval. Rate: 90 –
170/min
 Narrow QRS complex

18. MANAGEMENT

19. For each pt AF, the two principal goals
of therapy are 1) symptom control and
2) prevention of thromboembolism
Newly diagnosed Previously
diagnosed
Need for
anticoagulation
Rate or Rhythm
control
Assesment of
adequacy of Rx

20. 1. Rate control
a. Beta blockers
b. Non dihydropyridine CCBs (Diltiazem,Verapamil)
c. Digoxin
d. Amiodarone
2. Rhythm control
a. Cardioversion (Electrical or Pharmacological)
b. Anti-arrhythmic drug treatment
c. Percutaneous catheter ablation
d. And/or surgical procedures
3. Anticoagulation
a. Newer anticoagulants (Non Vit K antagonist OAC)
b. Warfarin
c. Heparin

21. Unstable patient – Urgent Mx
 3circumstances for which immediate
or urgent cardioversion is required
1. Active Ischaemia : Symptomatic (eg.
angina) or ECG evidence
2. e/o organ hypoperfusion/shock: Cold
clammy skin, confusion, AKI
3. Severe manifestations of HF (eg. Pul.
Odema)

22. Imp points in Urgent Mx
 Before cardioversion atleast part of
the cause for initiation of AF must be
addressed eg. Pul. odema should not
be cardioverted without diuresis, O2,
BP control and other measures –
chance of failure or recurrence
 If longer duration (>48h) or unknown
duration  increased risk of stroke
◦ Cardiovert only - TEE guided + with Anti-
coagulation

23.  For pts with no other options and not
responding to rate control
 Start IV Heparin or newer oral
anticoagulants before cardioversion
 Without causing delay in the emergent
cardioversion

27. Rate control
 Target rate:
◦ In symptomatic: <85/min
◦ In asymptomatic: <110/min
 Choice of drugs:
◦ Beta blockers for: Exercise induced,
angina/acute MI
◦ CCB for: COPD, Asthma
 Oral vs. IV:
◦ IV drugs are more effective
◦ Should be used if raised HR is causing
hypotention, hypoperfusion, HF

28. Rate control agents and
dosing
 Beta blockers
◦ ACUTE CONTROL
 IV Metaprolol (5mg/5ml):
 Bolus – 2.5mg to 5mg over 2 mins
 Dose may be repeated at 5 min intervals upto total of 15mg as
needed
 IV Esmolol: Rapidly acting with short duration of action
(10-20 mins).
 Bolus – 0.5mg/kg infused over 1min, followed by 50µg/kg/min
 If after 4 mins, inadequate response – give another bolus
followed by an infusion of 100µg/kg/min
 If after 4 mins still inadequate – 3rd and final bolus followed by an
infusion of 150µg/kg/min
 If needed infusion can be increased to 200µg/kg/min after 4 mins
 Alternatively, an infusion can be started at 50µg/kg/min, without
a bolus, and the rate of administration can be increasedby
50µg/kg/min every 30 mins

29.  Beta blockers
◦ ACUTE CONTROL
 IV Propranolol:
 1mg over 1 min
 Can be repeated upto 3 doses at two-minute intervals
◦ CHRONIC CONTROL
 Atenolol – 50 to 200mg OD
 Metaprolol tartarate – 25 to 100mg BD or TID
 Timolol – 10 to 30mg BD
 Pindolol – 5 to 30mg BD
 Nadolol – 40 to 160mg OD

31.  Calcium Channel Blockers
◦ ACUTE CONTROL
 IV Diltiazem:
 Bolus: 0.25mg/kg (Avg. adult dose of 20mg) over 2
mins
 In 15 min, if the first dose is tolerated but does not
produce the desired response (20% reduction in HR
from baseline or a HR ≤ 100/min 
 A second bolus: 0.35mg/kg (Avg. adult dose of 25mg)
over 2 mins
 If responding to either of boluses: Continuous infusion
rate of 5 to 15 mg/h is initiated
 This regimen usually controls the ventricular rate within
4 – 5 mins

32.  Calcium Channel Blockers
◦ ACUTE CONTROL
 IV Verapamil:
 Given acutely as 5 to 10mg over 3 mins. Can be repeated
every 15 to 30 mins, as necessary (usu. one or two doses
are necessary)
 Start maintainence infusion at rate of 5mg/h, can be
titrated upto 20mg/h
 Onset of action is within 2 mins and peaks in 10 to 15
mins
◦ CHRONIC CONTROL
 Oral Diltiazem: Started at 30mg upto120mg QID
 Oral Verapamil: Initial dose of 40mg TID or QID
increased to maximum of 360mg/day in divided
doses

33.  Digoxin(2mg/5mg)
◦ For pts who do not achieve rate control on
beta blockers alone
◦ Who cannot tolerate the addition or
increased doses of beta blockers due to
decompensated heart failure
◦ For improved control of heart failure
symptoms

34.  Slow digoxin loading
◦ Starting maintainence dose of 0.125 to 0.25mg daily
◦ A steady state will be achieved after 5 cycles of the drug
half life, approx 7 to 10 days.
 Rapid digoxin loading
◦ IV loading: Most rapid means of digitalization
 Initial IV dose of 0.25 to 0.5mg given over several mins
 Followed by 0.25mg every 6 hrs for a total loading dose of 0.75 to
1.5mg (10 to 12µg/kg lean body weight)
◦ Oral loading:
 0.5mg initially
 Followed by 0.25mg every six hrs for a total loading dose of 0.75 to
1.5mg
 Maintainence dosing
◦ For pts taking digoxin for ventricular rate control
 Between 0.125 and 0.25mg OD

35.  Amiodarone (150mg/3ml)
◦ Commonly used in rhythm control strategy
◦ However it can also slow rate in patients
remaining in chronic AF
◦ Used as a second line of therapy for
chronic rate control only when other
therapies are unsuccessful or
contraindicated

36.  Magnesium sulphate (1mg/2ml)
◦ IV 2.5g over 20 mins
◦ Followed by 2.5g over 2 hrs

37. Rhythm control
 Candidates:
◦ Pts with symptomatic new onset AF
◦ Even if apparently asymptomatic – atleast
one attempt at cardioversion
 Contraindicated
◦ Patients who are completely asymptomatic,
particularly very elderly (>80yrs), multiple
comorbidities and increased risk
◦ Pts who are symptom free and have been in
AF for 3-5yrs (Dilated LA >5.5cm, review of
previous ECGs)

38.  Electrical vs. Pharmacological
cardioversion
◦ Emergency DC cardioversion if
hemodynamically compromised
◦ Elective DC for well compensated pts.
With 1st episode
◦ Anti-arrhythmic drug for long standing AF
◦ For paroxysmal AF
◦ Drugs for whom risk of sedation is high

39.  DC Cardioversion
◦ Pre treatment with anti-arrhythmic drugs
◦ Fasting for 6 hrs
◦ Good O2 saturation
◦ Normal K+ levels
◦ Anticoagulant status
◦ Procedural sedation and under monitor
 Monophasic – 200J
 Biphasic – 120 to 200J

41.  Pharmacological Cardioversion
◦ Flecanide
 2mg/kg IV over 10 mins, or
 Single 100-400mg per oral dose (Reverts in 6hrs)
◦ Propafenone
 2mg/kg IV over 10-20 mins, or
 Single 450 – 600 mg oral dose
◦ Ibutilide
◦ Defetilide
◦ Amiodarone
 Bolus: 150mg over 10 mins
 1 mg/min x 6hrs
 0.5 mg/min x 18hrs
 Oral maintainence of 100 – 200mg OD

42.  “Pill-in-the-pocket” approach
◦ To terminate out of hospital attacks
◦ Flecanide or propafenone
◦ Only to be prescribed after these drugs
have been shown to be efficacious and
safe prevously
◦ Patient first takes diltiazem or a beta
blocker 30 mins or more before the anti-
arrhythmic agent
◦ Also to use a Non-vitamin K anti
coagulant (NOAC)

43. Rate vs. Rhythm
 Rate control
◦ For asymptomatic or mildy symptomatic
AF pts who are 65yrs or older
 Rhythm control
◦ For most patients younger than 65yrs
particularly those who are symptomatic
◦ For those in whom rate control has failed
 Persistent symptoms despite adequate rate
control
 Inability to attain adequate rate control

45. Anticoagulation
 >48 hrs
◦ Atleast 3 weeks of anticoagulants
◦ Cardioversion
◦ 4 wks of further
◦ If urgent cardioversion needed – TEE guided
 < 48hrs
◦ May or may not use
 1st episode of AF
◦ Anti-coagulate based on Risk of Embolization - CHA2DS2-VASc
score
 Agents
◦ Warfarin
◦ Newer anticoagulants (NOAC) – Dabigatran, Apixaban,
Rivaroxaban and Endoxaban

49. Summary
 When a patient presents to
Casualty/OPD
◦ Assess if critical/hemodynamically stable and
obtain ECG
◦ Consider cardioversion if unstable
◦ If stable
 Evaluate (previous ECGs, Lab investigations,
ECHO, r/o MI/HF)
 Classify (Paroxysmal/persistent)
 Initially Rate control
 CHA2DS2-VASc score and requirement of
Anticoagulation
 Long term Rate vs Rhythm therapy
 Follow up

50. References
 Content from UpToDate.com
 Few slides from AF ppt by Dr.
Ravikanth Moka
https://www.slideshare.net/ravikanthm
oka/atrial-fibrillation-2016