CASE PRESENTATION

ACUTE CORONARY SYNDROME

(ACS)
FATMAWATI
C 111 05
160
SUPERVISOR:
Prof.Dr.dr.Ali Aspar Mappahya,Sp.PD,Sp.JP(K).FIHA.FAsCC
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PATIENT IDENTITY
Name
: Mrs. H
Age
: 70 y.o
Gender
: female
Address
: Maros
Date of admittance: 7 th June 2009
No.MR
: 390622

History Taking
Chief Complaint : chest pain
The complaint has been felt since 24 hours ago and
became worsen in last 2 hours. Pain was felt on the left
side of chest,but didnt spread to the shoulder and left
hand. It felt more than 20 minutes and not relieved by
medication. Chest pain occurred when she was taking a
rest.
She had history of chest pain before. No shortness of
breath and 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.
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Past Medical History

Hypertension (+) since 10 years ago,
uncontrolled regularly
DM (-)
Cardiovascular disease (+) since 5 years
ago, she controls to the doctor regularly.
History hospitalized at Maros Hospital with
chest pain for 1 day before patient was
referred to Wahidin Sudirohusodo Hospital
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PHYSICAL EXAMINATION
Status Present : Moderate illness/normal weight/composmentis
Vital Sign :
- Blood Pressure
:150/80 mmHg
- Pulse
:86 bpm
- Inspiratory rate
:24 bpm
- Body temperature
:36,80C
Head Examination
- Eyes
: Anemia-/- Lip : no Cyanosis
- Neck
: No mass, no tenderness, JVP R -2 cmH2O
Chest Examination
- Inspection : Symmetric
- Palpation
: No mass, no tenderness
- Percussion : Sonor
- Auscultation : Breath sound :bronchovesicular
Additional sound : Ronchi -/-, Wheezing -/-

PHYSICAL EXAMINATION
Cardiac Examination
Inspection
Palpation
Percussion
Auscultation

: Ictus cordis was invisible

: ictus cordis was unpalpaple
: widening of heart size
: Heartsound Pure SI and SII sound regular.

Abdominal
- Inspection
: Normal
- Auscultation
: Peristaltic sound +, normal
- Palpation
: No mass, no tenderness, hepar and
spleen unpalpable
- Percussion
: tymphani, ascites (-)
Extremities
: No swelling
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LABORATORY ASSESMENT
COMPLETE BLOOD COUNT

07/06/09
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

CARDIAC MARKER

Natrium : 129
Kalium : 3,1
Cloride : 108

CK
: 310
CK MB : 27

LIPID PROFILE
Cholesterol total
Cholesterol HDL
Cholesterol LDL
Triglyseride

: 190
: 32
: 134
: 89
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ELECTROCARDIOGRAPHY

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Interpretation
- Sinus Rhythm
- HR 63 bpm
- LAD
- LVH
- Anterior Wall Myocardial Ischemia

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ECHOCARDIOGRAM

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Interpretation
- Diastolic dysfunction
- LVH (+)
- EF = 55%

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USG ABDOMEN

Interpretation
Normal

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

- Atherosclerosis aortae

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DIAGNOSE
Acute Coronary Syndrome (ACS)

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THERAPY
Heart diet
IVFD NaCl 0,9 % 10 dpm
Fasorbid 10 mg 1-1-1
Aspilet 80 mg 0-1-0
Captopril 12,5 mg 1-0-1
Ranitidine 1 amp/12h/iv

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DISCUSSION

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Acute Coronary Syndrome (ACS)

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

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Acute Coronary Syndrome (ACS)

Ischemic heart disease accounts for
500,000 deaths annually in the U.S.
CAD and myocardial ischemia
contribute to > 5 million ER visits yearly
for chest pain
15% of patients with chest pain will
have acute MI and 25-30% will have
unstable angina
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CARDIAC RISK FACTORS

Age over 40
male
postmenopausal
females
family history
cigarette smoking
hypertension

High cholesterol
truncal obesity
sedentary lifestyle
diabetes
previous cardiac
history

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PATHOPHYSIOLOGY
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

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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
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STEMI (ST elevation myocardial infarction)

Cardiac marker evidence of myocardial necrosis(positive
CK-MB or Troponin)
New or presumably new(if no prior EKG available) STsegment elevation on admission EKG

NSTEMI (Non STEMI)

Cardiac marker evidence such as positive CK-MB or
Troponin
No new ST-segment elevation

Unstable Angina
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Unstable Angina - Definition

angina at rest (> 20 minutes)
new-onset (< 2 months) exertional
angina (at least CCSC III in severity)
recent (< 2 months) acceleration of
angina (increase in severity of at least
one CCSC class to at least CCSC class
III)
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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
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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)
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Unstable Angina
Risk Stratification
Intermediate Risk
prolonged chest pain
diagnosis of rule-out MI
Management
observe in the ER or Chest Pain Unit
monitor clinical status and ECG
obtain cardiac enzymes (troponin T or
I) every 8 to 12 hours
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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

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

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MEDICAL MANAGEMENT OF ACS

Anti-Ischemic therapy
Oxygen:maintain Sao2 >90%
Nitrates
Morphine
Beta blockers
ACE Inhibitors

Anti platelet therapy

Cycloxygenase inhibitors: ASPIRIN
Adenosine Diphosphate receptor antagonist: CLOPIDOGREL
Glycoprotein IIb/IIIa receptor inhibitors

Anti coagulant therapy

Low molecular weight heparin: ENOXAPARIN

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THANK YOU.
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