ACUTE CORONARY SYNDROME

PRESENTED BY :
YUNITA CHANDRA DEWI
C11104120
SUPERVISOR :
dr. IDAR MAPPANGARA, SpPD, SpJP,
FIHA

PATIENT IDENTITY

Name
: Mrs. H
Age
: 81 y.o
Gender
: female
Address
: Pangkep
Date of admittance : 7

th

June 2009

History Taking
Chief Complaint : chest pain
It has been felt since 48 hours ago and became
worsen in last 2 hours. Pain was felt on the left
side of chest,spreaded to the shoulder. Chest
pain occurred during rest. This condition stayed
until 30 minutes and not responded with nitrat
sub lingual. She had history of chest pain
before.
No shortness of breath, no cough
The patient was sweating, felt nausea and she
vomited once at that time.There was no
headache and no fever.
Urinate and defecate were normal.

Past Medical History

Hypertension (+) since 10 years ago,
not control regularly
Diabetes Mellitus (-)
Cardiovascular disease (+) since 5
years ago, control to the doctor regularly.
Hospitalized at Pangkep Hospital with
chest pain for 2 days before patient
refered to Wahidin Sudirohusodo Hospital

PHYSICAL EXAMINATION
Status Present : Moderate illness/normal
weight/composmentis
Vital Sign :
- Blood Pressure :130/80 mmHg
- Pulse
:86 bpm
- Inspiratory rate :24x/minute
- Body temperature
:36,80C
Head Examination
- Eyes
: Anemis -/- Lip
: no Cyanosis
- Neck
: No mass, no tenderness, JVP R -1 cmH 2O
Chest Examination
- Inspection
: Symmetric
- Palpation: No mass, no tenderness
- Percussion
: Sonor
- Auscultation
: Breath sound :bronchovesicular
Additional sound : Ronchi -/-, Wheezing -/-

PHYSICAL EXAMINATION
Cardiac Examination

Inspection : Ictus cordis was invisible

Palpation : ictus cordis was unpalpaple
Percussion : widening of heart size
Auscultation: sound of I/II heart sound regular.

Abdominal
- Inspection
- Auscultation
- Palpation
:
unpalpable
- Percussion
Extremities

: Normal
: Peristaltic sound +, normal
No mass, no tenderness, hepar and spleen
: tymphani, ascites (-)
: No edema

LABORATORY ASSESMENT
COMPLETE BLOOD COUNT

WBC : 16,34 .103

/mm3
RBC : 3,97. 106/mm3
HGB : 11,5 g/dl
HCT : 35,1 %
PLT : 276. 103/l

BLOOD CHEMISTRY
ASSESMENT

Random blood
sugar : 101 mg/dL
Ureum : 34 mg/dL
Creatinin
: 0,7
mg/dL
SGOT : 16 U/l
SGPT
: 13 U/l

LABORATORY ASSESMENT
ELECTROLITE
Natrium : 129
Kalium : 3,1
Cloride : 108
LIPID PROFILE
Cholesterol total : 190
Cholesterol HDL : 32
Cholesterol LDL : 134
Triglyseride : 89
8

CARDIAC MARKER
CK
: 310
CK MB : 29

ELECTROCARDIOGRAPHY

INTERPRETATION
Sinus Rhytm
HR 63 bpm
LAD
LAH
Myocardial Ischemia

ECHOCARDIOGRAM

INTERPRETATION
Diastolyc disfunction
LVH (+)
EF = 55%

USG ABDOMEN

Interpretation
Normal

CHEST X-RAY
Interpretation :
Cardiomegaly with
dilatation et
elongation of
aortae
( appropriate for
HHD )
Atherosclerosis
aortae

DIAGNOSIS
UNSTABLE ANGINA PECTORIS

THERAPY
Heart diet
IVFD NaCl 0,9 % 10 dpm
Vasodilator : Fasorbid 10 mg 1-1-1
Anti Agregasi Trombosit :
Aspilet loading dose 2 x 80 mg, after that 0-1-0
Clopidrogel loading dose 4 x 75 mg, after that
0-1-0
Anti Hipertensi : Captopril 12,5 mg 1-0-1
H2 receptor antagonist : Ranitidin 1amp/12h/iv

18

DISCUSSION

Acute Coronary Syndrome (ACS)

Acute Coronary Syndrome is symptoms that
happen suddenly because sub total occlusion
of one or more of the coronary arteries ,
usually following plaque rupture, resulting in
decreased oxygen supply to the heart
muscle.

Risk Factors
Risk Factors That Cannot Be Modified:
Age
Men, risk increases after age 45.
Women, risk increases after age 55.
Family history of early heart disease.
Heart disease diagnosed before age 55
in father or brother.
Heart disease diagnosed before age 65
in mother or sister.

Risk Factors
Risk Factors That Can Be Modified:
High blood cholesterol
High blood pressure
Cigarette smoking
Diabetes
Overweight or obesity
Lack of physical activity

Patophysiology
ACS is caused by secondary reduction
in myocardial blood flow due to
coronary arterial spasm
disruption of atherosclerotic
plaques
platelet aggregation or thrombus
formation at site of atherosclerotic
lesion

Cascade of events leading to ACS

Rupture of unstable atherosclerotic plaque

Disruption of protective endothelial layer
Exposure of very prothrombotic subendothelial layer
Platelet adhesion to area of injury
Platelet activation
exposure of Glycoprotein(GP) IIb/IIIa receptors

Platelet aggregation
Caused by fibrinogen binding to GP IIb/IIIa receptors
Fibrin deposition - Platelet plug incorporates fibrin strands

Occlusion of coronary artery

Myocardial infarction

A c u te C o r o n a r y S y n d r o m e
Is c h e m ic ty p e d is c o m fo rt
N o n S T E le v a tio n
U n s ta b le A n g in a

N on Q w ave M I

S T E le v a tio n
N on Q w ave M I

Q w ave M I

Definition of terms used to

describe ACS
STEMI (ST elevation myocardial infarction)
Cardiac marker evidence of myocardial
necrosis(positive CK-MB or Troponin)
New ST-segment elevation on admission
ECG
NSTEMI (Non STEMI)
Cardiac marker evidence such as positive
CK-MB or Troponin
No new ST-segment elevation
Unstable Angina

Unstable Angina
Three Principal presentations
Rest angina
occurs at rest and prolonged usually >20 minutes
New-onset angina
occurs with marked limitation of ordinary physical
activity, such walking 1-2 blocks or climbing 1 flight
of stairs
Increasing angina - previously diagnosed angina that
has distinctly become
more frequent
longer in duration
lower in threshold

Causes of Unstable Angina

Reduction in oxygen supply to myocardium
Coronary artery narrowing from non-occlusive thrombus
on a disrupted atherosclerotic plaque
Dynamic obstruction by coronary vasospasm or
vasoconstriction
Severe narrowing without thrombus or spasm
progressive atherosclerosis
Restenosis after Percutaneous coronary intervention
Arterial inflammation and /infection

Increased myocardial oxygen demand in the

presence of fixed restricted oxygen supply
Fever, tachycardia, thyrotoxicosis, anemia

Unstable Angina
Risk Stratification
Low Risk
new-onset exertional angina
minor chest pain during exercise
pain relieved promptly by
nitroglycerine
Management
can be managed safely as an
outpatient (assuming close follow-up
and rapid investigation)
29

Unstable Angina
Risk Stratification
Intermediate Risk
prolonged chest pain
diagnosis of rule-out MI
Management
observe in the Chest Pain Unit
monitor clinical status and ECG
obtain cardiac enzymes (troponin T or
I) every 8 to 12 hours
30

Unstable Angina
Risk Stratification
High Risk
recurrent chest pain
ST-segment change
hemodynamic compromise
elevation in cardiac enzymes
Management
monitor in the Coronary Care Unit
31

Risk Stratification by ECG

The risk of death or MI at 30 days
is strongly related to the ECG at
the time of chest pain.
ST depression
10%
T-wave inversion
5%
No ECG changes
1-2%

32

Unstable Angina
Therapeutic Goals
Therapeutic Goals
Reduce myocardial ischemia
Control of symptoms
Prevention of MI and death

33

Medical management of ACS

Anti-Ischemic therapy

Oxygen
Nitrates
Morphine
Beta blockers
ACE Inhibitors

Anti platelet therapy

Cycloxygenase inhibitors
Adenosine Diphosphate receptor antagonist
Glycoprotein IIb/IIIa receptor inhibitors

Anti coagulant therapy

Low molecular weight heparin

THANK YOU