CASE REPORT

A. 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

B. ANAMNESIS

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

C. 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 +/+

D. SUPPORTING EXAMINATION
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

Troponin I <0,01 <0,01

Troponin T <0,05

CK 202 <190

CKMB 38 <25

Natrium 138 136 145

 Kalium 5,1 3,5 - 5,1

Klorida 112 97 111

Asam Urat 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 (September 12th 2015 (1st day of treatment)

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

E. DIAGNOSIS
CHF NYHA III

Atrial Fibrilasi
MR, AR moderate

F. 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
 Atrial Fibrillation
A. Definition

Atrial fibrillation is a disorder of the heart (arrhythmia) characterized by irregularity

rhythm of the heart rate and increase in heart rate, which amounted to 350-650 x / min. Basically
atrial fibrillation is a supraventricular tachycardia with uncoordinated atrial activation and
deteriorisasi atrial mechanical function. This situation led to the ineffectiveness of a mechanical
process or blood heart pump.

B. Classification
According to the AHA (American Heart Association), the classification of atrial
fibrillation can be divided into 4 types, that is:

a. The first detection AF

All patients with AF always begins with the first phase detection AF. This stage is the
stage which has not been detected previously and a new AF was first detected.
b. Paroxysmal AF
AF lasting less than 7 days or AF who have a first episode of less than 48 hours is called
the paroxysmal AF. This type AF also has a tendency to heal itself in less than 24 hours
without the help of cardioversion.
c. Persistent AF
AF who are settled and lasted more than 48 hours but less than 7 days. In contrast to
paroxysmal AF, persistent AF need the use of cardioversion to restore sinus rhythm back
to normal.
d. Chronic / permanent AF
AF who are settled and lasted more than 7 days. On permanent AF, use of cardioversion
considered less significant, because it is considered quite difficult to return to a normal
sinus rhythm.
 Figure 1. Pattern Classification of Atrial Fibrillation
Besides classification according to the AHA (American Heart Association), AF is also
frequently classified according to the length of time the course, namely acute AF and chronic
AF. Acute AF categorized by the time the course or the onset of less than 48 hours, whereas the
reverse chronic AF, the AF lasting more than 48 hours.

C. Etiology
Etiology associated with AF is divided into several factors, including that is:
a. Increased pressure / resistance atrium
1. Valvular heart disease
2. Abnormalities charging and discharging atrium space
3. cardiac hypertrophy
4. cardiomyopathy
5. pulmonary hypertension (chronic obstructive pulmonary disease and chronic
pulmonary cast)
6. Tumor intracardiac
b. Infiltrative and inflammatory processes
1. pericarditis / miocarditis
2. Amyloidosis and sarcoidosis
3. Factors increasing age
c. The infection process
1. Fever and all kinds of infections
d. Endocrine disorders
1. Hyperthyroidism
2. Pheochromocytoma
e. neurogenic
1. Stroke
2. subarachnoid hemorrhage
f. ischemic Atrium
1. Infarction miocardial
g. Drugs
1. Alcohol
2. Caffeine
h. Heredity / genetic

D. 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.

E. Risk factor

Some people have risk factors for AF, which are:

a. Diabetes mellitus

b. Hypertension

c. Coronary heart disease

d. Mitral Valve Disease

e. Thyroid disease

f. Chronic Lung Disease

g. Post. Heart surgery

h. Age 60 years

i. Life Style

F. Pathophysiology

AF mechanism consists of two processes, namely the processes of local activation and
multiple wavelet reentry. 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.

While multiple wavelet reentry, an action potential repetitive process and involves the
circuit / track depolarization. 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, namely the 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 trigger the occurrence of AF.
 Figure 2. A. Local Activation Process B. Process Atrial Fibrillation and Atrial
Fibrillation Multiple Reentry Wavelets

G. Management

The main target in the management of AF is to control heart rhythm irregularity,

lowering increased heart rate and avoid / prevent complications of thromboembolism.
Cardioversion is one that can be done for the treatment of AF. According to the understanding,
cardioversion itself is a governance that serves to control the rhythm irregularity and lowers the
heart rate. Basically cardioversion is divided into two, namely pharmacological treatment
(Pharmacological Cardioversion) and electrical treatment (Electrical cardioversion)

a. Prevent blood clots (thromboembolism)

The prevention of blood clotting is a treatment to prevent complications of AF.

Medications used type of anticoagulant or antithrombotic, this is because the drug is used for
reducing the risk of thrombus formation in blood vessels and branches of vascularization.
Medications are often used to prevent blood clots consists of various kinds, such as:

1. Warfarin

Warfarin is an anticoagulant drug class include that function in the process of formation
of fibrin blockage to reduce or prevent coagulation. Warfarin is given orally and is very rapidly
absorbed reaching peak plasma concentrations within 1 hour with 100% bioavailability.
Warfarin in metabolism by oxidation (L shape) and reduction (form D), followed by conjugation
glukoronidasi with working long 40 hours.

2. Aspirin
 Aspirin is irreversible disabling of platelet cyclo-oxygenase (COX2) by means of
acetylation of the terminal amino acid serine. The effect of this is to inhibit the production of
COX2 endoperoksida and thromboxane (TXA2) in platelets. This is why no formation of platelet
aggregation. However, the use of aspirin for long periods can lead to a reduction in circulating
levels of blood clotting factors, especially factors II, VII, IX and X.

b. Reduce heart rate

There are 3 types of drugs that can be used to lower increased heart rate, ie the drug
digitalis, -blockers and calcium antagonists. These drugs can be used individually or in
combination.

1. Digitalis

This drug is used to improve cardiac contractility and decrease heart rate. This makes the
performance of the heart becomes more efficient. In addition, digitalis also slow the abnormal
electrical signals from the atria to the ventricles. This results in increased ventricular filling of
abnormal atrial contraction.

2. -blockers

-blocker drug is a drug that inhibits the effects of the sympathetic nervous system.
Cardiac sympathetic nerves at work to increase the heart rate and cardiac contractility. This
effect will result in the efficiency of cardiac performance.

3. Calcium Antagonists

Calcium antagonist drugs cause a decrease in cardiac contractility due to the denial of
Ca2 + from the extracellular to the intracellular Ca2 + channel passes contained in the cell
membrane.

c. Restore heart rhythm

Cardioversion is one that can be done for the treatment of cardiac rhythm menteraturkan.
According to the understanding, cardioversion itself is a governance that serves to control the
rhythm irregularity and lowers the heart rate. Basically cardioversion is divided into two, namely
pharmacological treatment (Pharmacological Cardioversion) and electrical treatment (Electrical
cardioversion).
1. Pharmacological Cardioversion (anti-arrhythmia)
a. Amiodarone
b. Dofetilide
c. Flecainide
d. Ibutilide
e. Propafenone
f. Quinidine

2. 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).

3. Operative

a. Catheter ablation This procedure uses a surgical technique membuatan incision in the thigh
area. Then the catheter is inserted into a blood vessel up into the heart UTMA. At the end there is
an electrode catheter that functions destroy ectopic focus that is responsible for the occurrence of
AF.

b. Maze operation Maze procedure is almost the same operation with catheter ablation, but the
maze operation, will result in a "maze" that serve to help menormalitaskan conduction system
sinus SA.

c. Artificial pacemaker Artificial pacemaker is a pacemaker that is placed in the heart, which
controls the rhythm and heart rate.

H. Discussion

AF is actually a part of the arrhythmia, a condition of the heart rhythm abnormality

characterized by the release pattern of electrical signals very quickly and repeatedly. This objec
in general can be caused by interference action potential, conduction disturbances or be
interference from both. At AF, interference occurs in cardiac rhythm dysfunctions and increased
heart rate. In general, AF interference can be regarded as tachycardia, because the heart rate in
AF to more than 100x / min. Tachycardia itself can be categorized into two, namely
supraventricular tachycardia and ventricular tachycardia. AF is a supraventricular tachycardia, in
which the action potential disruption or conduction conduction system above comes from his
file, which includes the SA node, the AV node and file of his own. While the ventricular
tachycardia is caused not only of the conduction system of Purkinje fibers, but also the role of
supraventricular tachycardia can cause ventricular tachycardia.

Tachycardia supravenrikuler not only AF, but include Atium extrasystoles, atrial flutter,
and supraventricular tachycardia. At AF, the mechanism through two processes, namely the local
activation or multiple wavelets reentry. At the local activation is predominantly due to an ectopic
focus on superior pulmonary vein, while the reentry of multiple wavelets are more likely to be
caused by atrial enlargement, shortening of the refractory period and a decrease in conduction
velocity. In addition, there are actually other factors that influence the occurrence of AF, the
heart rate of premature, autonomic nervous activity, atrial ischemia, conduction anisotropic and
increasing age.

The occurrence of AF will cause cardiac hemodynamic dysfunction, ie loss of

coordination mechanical activity of the heart, disorder, irregularity of the ventricular response
and heart rate. These three things will affect the decrease in cardiac output, due to contraction of
the heart is not perfect despite repetitive depolarization process. Loss of coordination due to the
mechanical process is more rapid and frequent depolarization. Rapid and repetitive
depolarization in AF have a nature that is not perfect, so the process of cardiac contractility can
not maximal. In addition, the increase in depolarization and heart rate in atrial be responded
physiologically by the ventricle with decreased heart rate. It aims to reduce the potential increase
in the action that causes the atria to the ventricles irregularity acceptance rate. A decrease in
ventricular rate occurs because of the physiological processes that played by the AV node
system. AV node will mediate this process by improving the performance of the parasympathetic
nervous system and degrade the performance of the sympathetic nervous system AV conduction.
As for the irregularity of the heartbeat due to AF, it resulted from the increase in depolarization
and entry of electrical signals repeatedly.

The effect of the occurrence of AF in addition to irregularities in heart rate and increased
heart rate, thromboembolism is also a harmful effect on the heart as a result of AF.
Thromboembolism occurs as a result of three factors, namely static, endothelial dysfunction and
hypercoagulable. This mechanism occurs from static and blood endothelial damage due to
contraction and blood flow is not perfect. Besides the hypercoagulable improve the process of
blood clot that forms part of the cause of thromboembolism.