ATRIAL FIBRILATION

(AF)

Presented by:
Moh Gilang Fajriansyah Nohu (C11110285)

Supervisor:
Dr.dr. Muzakkir Amir,SpJP,FIHA,
CARDIOLOGY DEPARTMENT
MEDICAL FACULTY OF HASANUDDIN UNIVERSITY
MAKASSAR
2015
 PATIENT IDENTITY

Name : Mr. AS
Age : 74 years old
Gender : Male
Address : Jl. Tupolev III No.28, Mandai, Maros
MR : 640440
Date of Admission : September 12th 2015
 HISTORY TAKING
Chief Complaint : Shortness of breath
Present Illnes History :
Experienced since 2 months ago and was
advancing 1 last week. Shortness of breath
experienced by suddenly without being
influenced activity. Shortness of breath positive
history. history 4 times treated in RSWS with
swelling of the heart. no chest pain, no history of
chest pain. Patients admitted to a comfortable
bed with plenty of pillows
 PREVIOUS ILLNESS HISTORY
• History of Diabetes Melitus indisputably
• History of hypertension indisputably
• History of smoking positif
 PHYSICAL EXAMINATION
General Status
• Moderate illness/ Well nourished/ Compos mentis
• Nutritional Status:
– Weight : 50 kg
– Height : 163 cm
– BMI : 18,80 kg/m2 (normal)

Vital Sign
• Blood Pressure : 120/70 mmHg
• Pulse Rate : 105 bpm
• Respiratory Rate : 28 bpm
• Temperature : 36.6 0C (axilla)
Head and Neck Examination
• Eye : Conjunctiva anemic (-/-),
Sclera icteric (-/-)
• Lip : Cyanosis (-)
• Neck : JVP R+3 cmH20
Thorax Examination
• Inspection : Symmetric between left and right chest.
• Palpation : No mass, no tenderness.
• Percussion : Sonor between left and right chest, lung-
liver border in ICS VI right anterior.
• Auscultation:
 Respiratory sound: Vesicular
 Additional sound : Ronchi (+/+) in the median basal
lung, Wheezing -/-
Heart examination :
– Inspection : Apex invisible
– Palpation : Apex impalpable
– Percussion :
Upper heart : ICS II parasternalis linea sinistra
Bottom heart : ICS V parasternalis linea dextra
Left Heart : ICS V midclavicularis linea sinistra
Right heart : ICS IV parasternalis linea dextra
– Auscultation : heart sounds I/II regular, murmur (+)
in VRSB and apex (systolic), gallop (-)
Abdomen Examination :
• Inspection : flat, following breath movement
• Auscultation : peristaltic sound (+), normal
• Palpation : mass (-), pain (-), liver and lien
impalpable
• Percussion : tymphani (+), ascites (-)

Extremities Examination :
• Oedema Pretibial -/-
• Oedema dorsum pedis +/+
 LABORATORY FINDING
September 12th 2015 (1st day of treatment)
TEST RESULT NORMAL VALUE
GDS 84 mg/Dl <140

SGOT 46 u/L <38

SGPT 30 u/L <41

Ureum 71 10-50

Kreatinin 1,71 0,5-1,2

 LABORATORY FINDING
January 22th 2015 (1st day of treatment)
TEST RESULT NORMAL VALUE
Troponin I <0,01 <0,01
CK 202 <190
CKMB 38 <25
Natrium 138 136 - 145
Kalium 5,1 3,5 - 5,1
Klorida 112 97 - 111
Asam Urat 8.6 3,4-7,0
TEST RESULT NORMAL VALUE

WBC 7,4 x 103/uL 4.0 – 10.0 x 103

RBC 5,52 x 106/uL 4.0 – 6.0 x 106

HGB 16,4 g/dL 12 – 16

HCT 50,9% 37 – 48

PLT 181 x 103/uL 150 – 400 x 103

PT 26,1 10 – 14

APTT 37,6 22,0 - 30,0

INR 2,49
ELECTROCARDIOGRAM
 ECG INTERPRETATION
• Interpretasi
• Ritme : Asinus
• Heart Rate : 127 bpm
• Axis : 45o (Left Axis Deviation)
• Regularity : irreguler
• P wave : can not be assessed
• PR Interval : can not be assessed
• QRS complex : poor R wave progression, QRS duration
0,08 detik
• ST Segment : in the normal range
• T wave : inverted in lead AVL and V5
• Conclusion : Atrial fibrillation with a ventricular rate
of 127 beats / min (Rapid Ventricular Response), left axis
deviation without ventricular enlargement
 DIAGNOSIS

• CHF NYHA III

• Atrial Fibrilasi
• MR, AR moderate
 MANAGEMENT
• O2 4 lpm via nasal canule
• IVFD NacL 0,9 % 500 cc/24 hours
• Furosemide 40 mg/24 hours/IV
• Simvastatin 40 mg/24 hours/oral
• Digoksin 0,25 mg/24 hours/IV
• Warfarin 1 mg/24 hours/oral
DISCUSSION
 DEFINITION
Atrial fibrillation is a supraventricular tachyarrhythmia
characteristics uncoordinated atrial activation with
consequent deterioration of atrial mechanical function
 EPIDEMIOLOGY
• At the age of 50 years under the AF prevalence of less than 1% and
increased by more than 9% at age 80 years.
• More common in men than women
• AF is a strong independent risk factor for the incidence of embolic stroke.
• The incidence of ischemic stroke in patients with non-valvular AF found as
many as 5% per year, 2-7 times more than patients without AF
• In the Framingham study the risk of embolic stroke 5.6 times as much on
non-valvular AF and 17.6 times more on valvular AF compared with
controls.
 CLASIFICATION
According to the AHA (American Heart Association), the classification of atrial
fibrillation can be divided into four types, that is:
• The first detection AF
• paroxysmal AF
• persistent AF
• Chronic / permanent AF
 ETIOLOGY
• Peningkatan tekanan/resistensi atrium
- Penyakit katup jantung
- Aritmia jantung : takikardia atrial, fluter atrial, AVNRT, sindrom WPW, sick sinus
syndrome
- Hipertrofi jantung
- Kardiomiopati hipertrofik
- Kardiomiopati Dilatasi
- Hipertensi pulmo (chronic obstructive pulmonary disease dan cor pulmonal
chronic)
- Tumor intracardiac

• Infiltrative and inflammatory processes

- Pericarditis / miocarditis
- Amyloidosis and sarcoidosis
- Factors increasing age

• The infection process

- Fever and all sorts of infections
• lung disease
- Chronic obstructive pulmonary disease
- Primary pulmonary hypertension
- Acute pulmonary embolism
• Endocrine disorders
- hyperthyroidism
- pheochromocytoma
- Diabetes mellitus
• neurogenic
- stroke
- subarachnoid hemorrhage
- the autonomic nervous system can trigger AF in patients who are sensitive
through the elevation of vagal tone or adrenergic.
• ischemic Atrium
- infarction miocardial
• Drugs
- Alcohol
- caffeine
• Heredity / genetic
 RISK FACTOR
Some people have risk factors for AF, which are:
• Diabetes mellitus
• Congestive Heart Failure
• hypertension
• Coronary heart disease
• Rheumatic Heart Disease
• Mitral Valve Disease
• Thyroid disease
• Chronic Lung Disease
• Post. heart surgery
• A history of previous stroke or TIA (transient ischemic attack) There
is a picture of spontaneous echo contrast in the left atrium Left
atrial appendage vilowcity <20 cm / sec Complex aortic
• atheroma
• Age ≥ 60 years
• Life Style
 SIGNS AND SYMPTOMS

• Basically AF, does not provide the typical signs

and symptoms in the course of their illness.
• Generally, symptoms of AF are increased heart
rate, heart rhythm irregularity and hemodynamic
instability.
• Besides that, AF also provide other symptoms
caused by a decrease in blood oxygenation to the
tissues, such as dizziness, weakness, fatigue,
shortness of breath and chest pain. However,
more than 90% of AF episodes do not cause
symptoms
 PHATOPHYSIOLOGY
AF mechanism consists of two processes, that
is:
1. Local activation process
2. multiple wavelet reentry.
 Local activation process
• Local activation process can involve a single
depolarization processes or repetitive
depolarization.
• At the local activation process, the dominant
ectopic focus is derived from the superior
pulmonary veins.
• In addition, the ectopic focus could also come
from the right atrium, superior vena cava and
sinus coronarius.
• This raises the ectopic focus electrical signals that
influence the action potential in the atrium and
potentially interfere with the action initiated by
the SA node
 multiple wavelet reentry
• Multiple wavelet reentry mechanism does not depend
on the existence of such an ectopic focus on local
activation process, but more or less depending on the
electrical signals that affect depolarization.
• In the multiple wavelet reentry, a little amount of
electrical signal is influenced by three factors, that is
refractory period, the amount of space atrium and
conduction velocity. This can be analogous to that in
atrial enlargement will usually be accompanied by a
shortening of the refractory period and a decrease in
conduction velocity.
• The third factor is exactly what will improve the
electrical signals and cause an increase in
depolarization and precipitate AF
 DIAGNOSIS
anamnesis:
• Type FA can be determined by knowing the length of onset (first episode,
paroxysmal, persistent, permanent)
• Determine the severity of the symptoms that accompany: berdebardebar,
weakness, shortness of breath, especially on exertion, dizziness, symptoms that
indicate the presence of ischemia or congestive heart failure
• Underlying heart disease, other causes of FA for example hyperthyroidism.

Physical examination :
• Vital signs: pulse form with regularitasnya velocity, blood pressure
• Jugular venous pressure
• Crackles in the lung suggests there may be congestive heart failure
• S3 gallop rhythm on cardiac auscultation showed the possibilities are congestive
heart failure, there is a possibility of noise on auscultation of heart valve disease
• Hepatomegaly: there is a possibility of right heart failure
• Peripheral edema: there is a possibility of congestive heart failure
• laboratory: hematocrit (anemia), TSH (thyroid disease),
cardiac enzymes if there is a suspected cardiac ischemia.
• EKG: it can be seen among others rhythms (verification FA),
left ventricular hypertrophy. Left ventricular pre-excitation,
pre-excited syndrome (WPW syndrome), identification of
iskemia.5,6
• Thoracic X-rays: Picture of pulmonary embolism, pneumonia,
COPD, cor pulmonale.
• echocardiography: to see, among others, valve lesion, the size
of the atrium and ventricle, left ventricular hypertrophy, left
ventricular function, outflow obstruction and TEE (Trans
esophago Echocardiography) to see the thrombus in the left
atrium
• Thyroid function tests: In the FA's first episode when the rate
of ventricular rhythm is difficult to control.
• Exercise test: identification of cardiac ischemia, determining
the adequacy of rate control heart rhythm. Other tests that
may be required is holter monitoring elektrofisiolagi study.
 MANAGEMENT
• The main target in the management of AF is to control heart rhythm irregularity,
lowering increased heart rate and avoid / prevent complications
thromboembolism
• divided into two, that is pharmacological treatment (Pharmacological
Cardioversion) and electrical treatment (Electrical cardioversion)

Prevent blood clots (thromboembolism)

1. warfarin
2. aspirin
Reduce heart rate
1. digitalis
2. β-blockers
3. Calcium antagonists
Restore heart rhythm
1. Pharmacological Cardioversion (anti-arrhythmia)
 electrical cardioversion
• A technique providing electrical current to the heart through two metal
plates (pads) are placed on the chest.
• The function of the electrical therapy is to restore the heart rhythm back
to normal or in accordance with NSR (node sinus rhythm).
• AF patients with hemodynamically stable ventricular rhythm due to the
rapid pace accompanied by signs of ischemia, hypotension, syncope need
immediate electrical cardioversion.
• Electrical cardioversion began with 200 Joule.
• If not successfully be raised to 300 Joules. Patients fasted and performed
anesthesia with short-acting anesthetic.

Operative
• catheter ablation
• Maze operation
• artificial pacemaker
Prophylactic treatment with antiarrhythmic drugs to Prevent Recurrence
• FA lasting more than 3 months is one of the predictors of recurrence.
• Antiartimia drug that is often used to maintain sinus rhythm
Atrial Fibrillation Treatment Algorithm
1. AF newly discovered or first episode of AF
2. AF recurrent paroxysmal
3. AF persistent recurrences
Prevention of thromboembolism
 PROGNOSIS
• Epidemiological studies have shown that patients with sinus rhythm
live longer than someone atrial abnormalities.
• Research also shows the use of anticoagulants and routine control
aims to asymptomatic in elderly patients.
• Results of these studies showed that medical therapy aimed at
controlling the heart rhythm is not making a profit compared with a
success rate control and anticoagulation therapy.
• AF therapy as a whole provide a better prognosis in
thromboembolic events, especially stroke.
• AF can trigger tachycardia cardiomiopati if not controlled properly.
• The formation of AF can cause heart failure in individuals that
depend on the components of the cardiac output atrium where
patients with hypertension and heart disease in patients with heart
valve disease are included in the high risk of heart failure occurs
when the AF.
THANK YOU