Rythm disturbance

1. ATRIAL FIBRILLATION
By TRUPTHI, MED PG
MODERATOR : DR. NAVEEN M
CHAIR PERSON : DR. BALACHANDRA

2. CONTENTS
1. Definition
2. Epidemiology and risk factors
3. Classification and pathophysiology
4. Clinical features – hemodynamics, symptoms, signs
5. Differential diagnoses
6. Complications
7. Management

3. DEFINITION
• Atrial fibrillation is 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
• There is no atrial contraction, but only fibrillation
• AF is the most common sustained arrhythmia and is a major
public health problem

4. Epidemiology and risk factors
• Prevalence increases with age, >95% of the AF patients
are >60 years of age. Prevalence by age 80 years is ~10%
• The lifetime risk of developing AF in men >40 years old is
~20%
• AF is slightly more common in men than women, and more
common in whites than blacks
• Other risk factors: hypertension, diabetes mellitus, cardiac
disease, obesity and sleep apnea

5. • AF is associated with a 1.5 to 1.9 fold increased risk of
mortality after controlling for underlying heart disease
• AF is also associated with a risk of developing heart
failure and vice-versa
• AF increases the risk of stroke by 5-fold and is estimated
to be the cause of 25% of strokes, also increases the risk
of dementia and silent strokes detected by MRI

6. Etiology
• Rheumatic heart disease (specially MS)
• IHD ( specially Acute MI)
• Hypertension
• Thyrotoxicosis
• Congenital heart disease ( specially ASD )
• Cardiomyopathy
• Pericardial diseases
• Others :Alcohol, PTE, chronic lung disease, electrocution, exercise,
LONE AF: AF occurring in the absence of clinical or echocardiographic
evidence of hypertension or any cardiac disease, usually in patients <60yrs
of age

7. Classification and Pathophysiology
1. Paroxysmal AF
2. Persistent AF
3. Long persistent AF
4. Permanent AF

8. Paroxysmal AF Persistent AF Long persistent AF Permanent AF
Episodes that start
spontaneously and stop
within 7 days of onset
Generally lasts >7days and
often requires electric/
pharmacologic cardioversion
AF that has been continuous
at least for an year
Failed cardioversion, further
attempts to terminate AF
have been futile
• Initiated by small re-
entrant or rapidly firing
foci in atrial muscle
sleeves that extend into
the PVs.
• In elderly patients/
severe underlying heart
disease, initiating foci
could in non PV sites
• Initiated by rapidly firing
foci within PVs
• Non PV sites including
myocardial sleeves
around SVC or coronary
sinus
• Structural and
electrophysiological
atrial abnormalities like
fibrosis
• Significant fibrosis that
uncouples atrial fibres
and promotes reentry,
focal automaticity
• Longstanding AF results
in loss of
myofibrils,accumulation
of glycogen granules,
disruption in cell-to-cell
coupling at gap
junctions and organelle
aggregates
• Thus AF itself seems to
produce a variety of of
atrial architecture that
further contribute to
atrial remodeling,
mechanical dysfunction,
and perpetuation of
fibrillation, a concept of
AF begetting more AF.

10. CLINICAL MANIFESTATIONS
• Clinical presentation of AF may relate to the AF itself or its
consequences (thromboembolism and tachycardia induced
cardiomyopathy)
• Patients may exhibit none to disabling symptoms

11. • Most common symptoms include: anxiety, palpitations,
dyspnea, dizziness, chest pain, exercise intolerance and
fatigue
• Several hemodynamic derangements, including rapid
ventricular rates, loss of organized atrial contraction,
irregularity of cardiac rhythm and bradycardia ( resulting
particularly from sinus pauses when AF episodes terminate),
may be the underlying cause of these symptoms

12. Hemodynamics
• Atria fire the impulses at the rate of 350-600/min, many of them
reach AVN in its refractory period and are hence not conucted
• A variable number of impulses however are conducted to the
ventricles (abt 100-150/min) at irregular intervals – irregularly
irregular rhythm of heart and pulse
• The irregular rhythm of heart results in varying durations of
diastole and hence the varying EDV and cardiac output –
giving rise to a varying volume of pulse and apex-pulse deficit

13. • The ventricular rate may be very rapid(>300/min) in WPW
syndrome, with conduction over accessory pathways (wide
preexcited QRS complexes), having short anterograde
refractory periods
• Where as, a regular slow ventricular response during AF
suggests an AV junctional rhythm, either as an escape
mechanism with complete AV block or as an accelerated AV
junctional pacemaker

14. SIGNS
• Irregularly irregular pulse
• Varying volumes of pulse
• Pulse deficit
• Varying intensity of S1
• Loss of atrial contraction leads to- absence of a wave on JVP,
disappearance of presystolic accentuation of MDM of MS,
disappearance of S4
• Hypotension

15. ECG FINDINGS
1. An irregularly irregular rhythm of QRS complexes
2. Absent P waves
3. Small, irregular fibrillatory waves at a rate of 350-600/min that
are difficult to see on ECG- fine AF
4. At lower rates(150-300) , coarse fibrillatory waves –coarse AF

17. Differential diagnoses
1. Atrial Flutter

18. 2. Multifocal Atrial Tachycardia

19. Complications of AF
• Thromboembolism : Stroke is the most common clinical
thromboembolic event in AF, due to reduced flow velocity
within the LA appendage
• Tachycardia induced cardiomyopathy : specially in
asymptomatic AF, they have high ventricular rates for a long
period and then present as CHF secondary ventricular
dysfunction due to cardiomyopathy

20. Management of AF
AF with hemodynamic instability :
• New onset AF that produces severe hypotension, pulmonary
edema, or angina should be electrically cardioverted starting
with a QRS synchronous shock of 200J, ideally after sedation or
anesthesia is achieved
• Greater shock energy and different electrode placements can
be tried if the shock fails to terminate AF
• Administration of IV ibutilide lowers the energy required, and
may be useful if AF terminates and reinitiates

21. If the patient is hemodynamically stable
• Immediate management involves rate control, to alleviate or
prevent symptoms, and consideration of whether
anticoagulation is needed to reduce the stroke risk
• Consideration is given to whether therapy is warranted to
restore and maintain sinus rhythm or whether the patient will be
allowed to continue in AF, managed with rate control and
measures for stroke prevention
• It is critical to consider the risk of stroke when attempting to
restore sinus rhythm

22. RATE CONTROL
Acute rate control:
• The goal of acute rate control is to reduce the heart rate to
less than 100/min
• Acute rate control is achieved with the drugs that prolong the
conduction through AV node
1. Beta blockers and/or the
2. CCBs -Verapamil and Diltiazem
3. Digoxin – added particularly in heart failure patients, if
negative inotropic and other adverse effects of Beta blockers
and CCBs limit their use

23. Drugs Loading dose Onset of
action
Maintenance Class
Esmolol IV: 500mcg/kg
over 1min
2-10 min 50mcg/kg/min II
Metoprolol IV: 5mg over 3-5
min, upto 15mg
20 min 1.25-5 mg q6h II
Verapamil 5-10mg over 3-5
min
3-5min 2.5-10mg/hour IV
Diltiazem 0.25mg/kg over 3-
5 min, upto 20mg
3min 5-15mg/hour IV
Digoxin 0.25mg q2h until
1mg total
5-60min 0.125-0.25mg/d -

24. Chronic rate control
• The initial goal is a resting heart rate <80/min that increases to
<100/min with light exertion, such as walking
• If it is difficult to control HR to that degree, resting rate upto
110/min is acceptable provided it doesn’t cause symptoms
and ventricular function is normal
• Exertion related symptoms are often an indication of
inadequate rate control
• Adequate rate control increases the cardiac output, decreases
the metabolic demand of the heart and avoids the potentially
dangerous side effects of the rhythm control drugs

25. Drugs Oral dose Half-life, hrs Class Metabolism
Metoprolol 25-100mg q6h 3-8 II Hepatic
Atenolol 25-100mg/day 6-9 II Renal
Verapamil 80-120mg q6-8h 4.5-12 IV Hepatic/Renal
Diltiazem 30-60mg q6h 3-4.5 IV Hepatic
Digoxin 0.125-0.25mg qd 38-48 - Renal

26. DIGOXIN
• Digoxin can be useful in controlling the resting ventricular rate in AF, in
the setting of LV dysfunction and CHF when other agents fail. It’s utility in
other clinical setting is limited by reduced efficacy of rate control during
exertion and significant concerns of toxicity
Digitalis toxicity – characterized by
• Nausea, abdominal pain, vision changes, confusion and delirium
• Paroxysmal atrial tachycardia with varying degrees of AV block and
bidirectional VT- most common arrhythmia
• Rx: supportive – withhold the drug, temporary pacemaker for prolonged
AV block, and IV phenytoin for bidirectional VT

27. Non pharmacologic rate control in AF
• Catheter ablation of the AV junction to create heart block and
implantation of a permanent pacemaker reliably achieves rate
control without the need of AVN blocking agents, but
mandates permanent pacing
• This strategy should be reserved for patients deemed to be in
permanent AF, who have failed pharmacologic rate control
and in whom rhythm control is either ineffective or
contraindicated

28. RHYTHM CONTROL
• In general, patients who maintain sinus rhythm have better
survival than those who continue to gave AF
• AF is a marker of disease severity
• Rhythm control strategy is mainly guided by patient
symptoms and preferences regarding the benefits and risks
of therapies

29. • Usually for patients with symptomatic paroxysmal AF,
recurrent episodes of symptomatic persistent AF, AF with
difficult rate control, and AF that has resulted in depressed
ventricular function or that agrravates heart failure
• Favored in younger patients than in sedentary or elderly
patients, where rate control is more easily achieved
• While beta blockers and CCBs help in rate control effectively
but hav low efficacy for preventing AF episodes, class I and III
antiarrhythmic agents are considered for rhythm control

30. Drugs Loading Maintenance Class
Quinidine 6-10mg/kg at 0.3-
0.5mg/kg/min
N/A IA
Procainamide 15mg/kg over 60min 1-4mg/min IA
Drugs Oral, mg T1/2, hrs Metabolism Class
Quinidine 300-600 q6h 6-8 Hepatic 75% IA
Disopyramide 100-300 q6-8h 4-10 Renal, Hepatic IA
Flecainide 50-200 q12h 7-22 Hepatic 75% IC
Propafenone 150-300 q8h 2-8 Hepatic IC
In patients without significant structural heart disease – class I sodium
channel blocking agents are good options, but negative inotropic and
proarrhythmic effects warrants avoidance in CAD or heart failure

31. In patients with CAD or structural heart disease – class III
agents can be admisitered, but they have ~3% risk of inducing
excessive QT prolongation and torsades de pointes. They
should be initiated only in hospital with ECG monitoring
• Ibutilide, dofetilide have high QT prolongation risks
• Dronedarone increases mortality in heart failure patients
• Amiodarone is most effective, maintains sinus rhythm in
approx. 2/3 of the patients. It can be admisitered in patients
with heart failure and CAD. On long term therapy, over 40%
patients experience amiodarone related toxicities

32. Drug Loading Maintenance Class
Amiodarone 150mg over 10min,
1mg/min for 6hrs
0.5-1mg/min III
Ibutilide 1mg over 10min if
over 60kg
N/A III
Drug Oral, mg T1/2,hours Metabolism Class
Amiodarone 100-400 qd 40-55days Hepatic III
Dronedarone 400 q12h 13-19 Hepatic III
Dofetilide 0.125-0.5 q12h 10 Renal III
Sotalol 80-160 q12h 12 Renal III

33. Amiodarone :
• Has low efficacy for acute conversion of AF
• Adverse effects of oral Amiodarone are partially dose dependent,
and occur in upto 75% of patients treated with high dose for 5yrs
• Pulmoray fibrosis
• Hypo/hyperthyroidism
• Raised hepatic transaminases
• Photosensitivity
• Peripheral neuropathy, corneal deposits, tremors
• Raises blood levels of Warfarin and Digoxin

34. Non-pharmacologic rhythm control
• Direct current cardioversion (DCCV) : safest and most
effective way of acutely restoring sinus rhythm
• Catheter ablation of AF: highly effective in younger patients
with structurally normal heart and a paroxysmal pattern of AF.
Goal is to achieve electrical isolation of PVs. Success rate is
70-80% after multiple procedures
• Surgical ablation : most frequently performed concomitant
with cardiac valve or CAD surgery, includes surgical remove
of LA appendage—reduces stroke risk. Sinus node injury is a
common complication

35. Cardioversion and anticoagulation
• If the duration of AF is <48hrs, cardioversion may proceed
without anticoagulation (provided they aren’t at a high risk for
stroke – d/t a prior embolic event, rheumatic MS, or
hypertrophic cardiomyopathy with marked LA enlargement
• If AF has persisted for >48hrs/unknown duration, patients
should be therapeutically anticoagulated for at least 3wks
before cardioversion (elective), and to be continued for a
minimum of 4weeks following a successful cardioversion

36. Alternatively, we can start anticoagulation and perform TEE to
determine if thrombus is present in the LA appendage
• If thrombus is absent, cardioversion can be performed and
anticoagulation continued for a minimum of 4weeks to
allow time for recovery of atrial mechanical function
• Long term maintenance of anticoagulation is considered
based on patient’s individual risk for stroke, commonly
assessed from the CHA2DS2 – VASc score

37. Stroke prevention in Atrial Fibrillation
• The major source of thromboembolism and stroke in AF is
formation of thrombus in LA appendage, where flow is relatively
stagnant
• Anticoagulation is warranted in patients with MS, or hypertrophic
cardiomyopathy, and those with a prior history of stroke
• Patients without MS- non valvular AF, are grouped with the help
of CHA2DS2-VASc score
• Anticoagulation is recommended for a score of >/=2

38. CHA2DS2-VASc risk assessment score

42. References :
1. Harrison’s principle of INTERNAL MEDICINE, 20th edition
2. Hurst’s the Heart- Textbook by John Willis Hurst
3. The Washington Manual of Medical Therapeutics

43. THANK YOU