BOOK READING

ATRIAL FIBRILASI

oleh
dr. Iswandi Darwis

Pembimbing
dr. Hasanah Mumpuni, Sp.PD, Sp.JP

SUB BAGIAN KARDIOLOGI

BAGIAN PENYAKIT DALAM
FKUGM/RSUP DR. SARDJITO
YOGYAKARTA, 2014
 Definition

Atrial Fibrillation (AF) is a supraventricular tachyarrhythmia characterized by

uncoordinated atrial activation with consequent deterioration of atrial mechanical
function

On the electrocardiogram (ECG), AF is characterized by the replacement of

consistent P waves by rapid oscillations or fibrillatory waves that vary in amplitude,
shape, and timing, associated with an irregular, frequently rapid ventricular
response when atrioventricular (AV) conduction is intact
Figure from: 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC2006 Guidelines
for the Management of Patients With Atrial Fibrillation: AReport of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines
Figure from: 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC2006 Guidelines
for the Management of Patients With Atrial Fibrillation: AReport of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines
 Hemodynamic Stress
Etiologi and
predispocing Atrial ischemia

factor Inflammatory or infiltrative atrial disease

Non cardiovascular respiratory cause

Drugs and alcohol use

Endocrine disorders

Postoperative

Advanced age

Congenital heart disease

Neurologic disorder

Idiopathic (lone AF)

Familial AF
 Minimum evaluation
History, to define

●
Presence and nature of symptoms associated with AF
●
Clinical type of AF (first episode, paroxysmal, persistent, or permanent)
●
Onset of the first symptomatic attack or date of discovery of AF
●
Frequency, duration, precipitating factors, and modes of termination of AF
●
Response to any pharmacological agents that have been administered
●
Presence of any underlying heart disease or other reversible conditions (eg, hyperthyroidism or alcohol consumption)

Physical examination to define

●
Vital sign
●
Head and neck
●
Chest examinations (pulmonary and Cardiac exxaminations)
●
Abdomen
●
Extremity
●
Neurologic

Chest x-ray

●
Evaluate cardiac size
●
pulmonary parenchymal and vascular
 Minimum evaluation
Electrocardiogram, to identify

●
Rhythm (verify AF)
●
LV hypertrophy
●
P-wave duration and morphology or fibrillatory waves
●
Preexcitation
●
Bundle-branch block
●
Prior MI
●
Other atrial arrhythmias
●
To measure and follow the R-R, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy

Transthoracic echocardiogram, to identify

●
Valvular heart disease
●
LA and RA size
●
LV size and function
●
Peak RV pressure (pulmonary hypertension)
●
LV hypertrophy
●
LA thrombus (low sensitivity)
●
Pericardial disease

Laboratory studies

●
CBC, Serum electrolite, Cardiac enzyme, Blood tests of thyroid, BNP, D-Dimer, renal,
and hepatic function, toxicology ethanol
 Management therapy

Antiarythmia drugs

●
Agents used for rate control
●
Beta blockers (Class II)
●
Nondihidropyridine calcium chanel blockers (Class IV)
●
Digoxin
●
Amiodarone (Class I, II, III and IV. Mailnly class III)
●
Agents used for rhythm control
●
Flecainide (Class I)
●
Propafenon (Class I)
●
Dofetilide (class III)
●
Amiodarone (Class I, II, III and IV. Mailnly class III)
●
Dronedarone
●
Sotalol (Class III)

Preventing Thromboembolism

●
Heparin or LWMH
●
Vitamin K Antagonis
●
Acetylsalisilic acid
●
Dabidatran (direct thrombin inhibitor)
●
Rivaroxaban (highly selective direct factor Xa inhibitor)
●
Apixaban (factor Xa inhibitor)
 Management therapy

Catheter ablation

●
Recomended as an alternative to pharmacologic therapy to prevent recurrent
paroxysmal AF in significantly symptomatic patients with little or no structureal heart
disease or severe pulmonary disease
●
Reasonable as a treatment for symptomatic persistent AF
●
Maybe reasonable as a treatment for symptomatic paroxysmal AF in patients with
some structural heart diseas
Figure from: 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC2006 Guidelines
for the Management of Patients With Atrial Fibrillation: AReport of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines
THANKS YOU
 Cardiac cycle: automaticity Rhythmic AP

SA node AV node HIS-purkinje

system
 Mechanisms of Cardiac Arrhythmia

Abnormalities in impulse generation

●
Enhanced normal automaticity
●
Abnormal automaticity
●
Effect of drugs on automaticity

Abnormalities in impulse conduction

●
Reentry
●
Effects of drugs on conduction abnormalities
 Action Potential

1
2

0 mV

0 3

-85 mV
eff refractory period

0 : depolarization 2 : Plateau phase

1 : partial repolarization 3 : repolarization
Mechanisms of AAD actions :

suppressing the initiating mechanism

slow automaticity
1. phase 4 slope β-blockers
2. threshold block of Na++, Ca++
++

3. max. diastolic potential adenosine

4. AP duration block of K++

altering the re-entrant circuit

 Altering The Re-entrant Circuit

Normal Unidirectional block

 Classification of AADs :
Classification Mechanism of Action Comment
of Drug
IA Na+ channel blocker Slows phase 0 depol

IB Na+ channel blocker Shorten phase 3 depol

IC Na+ channel blocker Slows phase 0 depol

II  Adrenorec. blocker Suppress phase 4 depol

III K+ channel blocker Prolongs phase 3 Repol

IV Ca+ + channel blocker Shortens AP

 Intrinsic Pathway COAGULATION Extrinsic Pathway
C ASCADE
Blood Vessel Injury Tissue Injury

Tissue Factor
XII XIIa

Thromboplastin
XI XIa

IX IXa VIIa VII

X Xa X

Prothrombin Thrombin
Factors affected
By Heparin Fibrinogen Fribrin monomer

Vit. K dependent Factors Fibrin polymer

XIII
Affected by Oral Anticoagulants