CASE

REPORT
ST Elevation
Miokard Infark
Nancy Dwi Puspita (C014182113)

Pembimbing :
Prof. dr. Peter Kabo, Ph. D, Sp. FK, Sp. JP(K), FIHA, FAsCC
CASE REPORT
ST Elevation Miokard Infark
 PATIENT’S IDENTITY
Name : Tn. E

Age : 53 Tahun

Gender : Female

Address : Enrekang

Occupation : Civil Servant

Religion : Moeslim

MR : 00875554

Admitted on : March, 2nd 2019

 HISTORY TAKING
Chief Complaint : Chest Discomfort

Recent Disease History :

 Feeling chest discomfort about +/-30 minutes before admitted to the
hospital. It can be localized by the patient. It was aggravated by heavy
activity. Chest discomfort felt like tenderness, and intermitten. It complained
heavy enough and distrub patient activity.
 There were history of diaphoresis, shortness of breath, nausea and
vomitting.
 There were no history of fever, and cough.
 HISTORY TAKING
Past Disease History
• There was no history of hipertension
• There was no history of diabetes melitus
• There was history of dislipidemia

Family History
There was no family history of cardiovascular disease

Risk Factor
• Un-modifable : Age, Gender
• Modifable : Smoking +/- 7 years ago, high consumed of fatty food
 PHYSICAL EXAMINATION
General Apparance
• Moderate illness/Adequate Nutrition/Compos mentis
• Weight : 72 kg
• Height : 160 cm
• BMI : 28,1 kg/m2 (Obes I)
• GCS : E4M6V5

Vital sign
• BP : 90/60 mmHg
• Pulse : 65x/minutes
• RR : 22x/minutes
• Temp : 36,7° C
 PHYSICAL EXAMINATION
Head and Neck Examination
Eyes : Anemic conjunctiva (-), icterus (-), isochoric (d = 2.5/2.5 mm ODS),
reflex pupil (+/+), palpebral oedema (-)
Lips : Cyanosis (-)
Neck : JVP R+2 cmH2O, lymph node enlargement (-)

Thorax
Inspection : Symmetrical
Palpation : No mass, no tenderness
Percussion : Sonor
Auscultation : Vesicular, rhonchi (-) basal bilateral, wheezing (-)
 PHYSICAL EXAMINATION
Cardiac Examination
Inspection : Inisible ictus cordis (left ICS 6)
Palpation : Palpable ictus cordis (left ICS 6)
Percussion
Right : 4th ICS right parasternal line
Left : 5th ICS anterior axillar line
Upper : 2nd ICS left parasternal
Auscultation : Regular of I/II heart sound, murmur & gallop (-)
Abdominal Examination
Inspection : Distension (-)
Auscultation : Peristaltic sound (+), normal
Palpation : No mass, no tenderness, liver and spleen are impalpable
Percussion : Tympanic
Extremities
Warm, oedema (-)
 LABORATORY RESULT
No Examination Result Reference Unit

Routine Hematology
1 WBC 11,67 4,00-10,0 10^3/ul
2 RBC 4,04 4,00-6,00 10^6/ul
3 HGB 12,5 12,0-16,0 gr/dl
4 HCT 35,7 37,0-48,0 %
5 MCV 88,4 80,0-97,0 fL
6 MCH 30,9 26,5-33,5 Pg
7 MCHC 35,0 31,5-35,0 gr/dl
8 PLT 208 150-400 10^3/ul
Coagulation

1 PT 10,8 10-14 Second

2 INR 1,04 --
3 APTT 25,9 22,0-30,0 Second
 LABORATORY RESULT
No Examination Result Reference Unit
Blood Chemistry
1 Glucose 156 140 mg/dl
2 Uric acid 3,8 P (2.4-5.7); L (3.4-7.0) mg/dl
Lipid Profile

1 Total Cholesterol 257 200 mg/dl

2 HDL 40 L (> 55), P (> 65) mg/dl
3 LDL 156 < 130 mg/dl
4 Trygliceride 182 200 mg/dl
Kidney Function

1 Ureum 19 10-50 mg/dl

2 Creatinin 0,71 L (<1,3); P( <1,1) mg/dl
Liver Function

1 SGOT 192 <38 U/L

2 SGPT 70 <41 U/L
 LABORATORY RESULT
No Examination Result Reference Unit

Immunoserology

1 Troponin I 18208,8
Laki-laki 17 – 50
ng/l
Perempuan : 8 - 29

Electrolite

1 Natrium 141
136-145 mmol/l

2 Kalium 3,7
3.5-5.1 mmol/l

3 Chlorida 114
97-111 mmol/l
 ELECTROCARDIOGRAPHY

Rhythm : Sinus rhythm PR interval : Normal, 0.10 seconds

QRS Rate : 77 bpm QRS Complex : Normal
Regularity : Regular ST Segment : Elevasi on II, III, avF
Axis : Normal axis T-wave : Normal
P-wave : Normal, duration 0.08 seconds
 ECHOCARDIOGRAPHY

 Decreased left ventricle systolic function EF 43% BIPLANE

 Dilated left atrium

 Concentric left ventricular hypertrophy

 Segmental hypokinetic

 Moderate mitral regurgitation

 Moderate ventricle diastolic dysfunction

 DIAGNOSIS
ST Elevasi Infark Miokard Inferior Onset <12 jam Killip 1

TREATMENT
• Antiplatelet : Aspilet 80mg / 24Jam / Oral

Clopidogrel 75mg / 24Jam / Oral

• Dislipidemia Agent : Atorvastatin 40g / 24Jam / Oral

• Antikoagulan : Arixtra 2,5mg /24 Jam / Subkutaneous

• Hepar Supplement : Maxiliv 1 tab/ 24 Jam / Oral

 DISCUSSION
ST ELEVATION INFARK MIOKARD
DEFINITION
Acute Coronary Syndrome (ACS) is a condition
caused by disrupted atherosclerotic plaque with
platelet aggregation and thus created
intracoronary thrombosis. Thrombosis will
become an occlusion either severe/complete or
partial occlusion and this flow disturbance will
lead to the imbalance between oxygen demand
and supply on myocardia and myocardium will
be damaged.

Partial Occlusion : Unstable Angina Pectoris

(UAP) and non-ST segment elevation
myocardial infraction (NSTEMI)
Total Occlusion : ST- segment elevation
myocardial infraction (STEMI)
 EPIDEMIOLOGY

.
However, reported incidence in United States
is decreasing from 133 per 100.000 in
1999 to 50 per 100.000 in 2008,

In the whole world, ischemia heart disease
has become the single common cause of
death with its frequency that keeps
increasing. STEMI in Europe is approximately
43 to 144 per 100.000 per year.
STEMI is relatively common in younger
people and occurring more in men than
women (ESC, 2017).
RISK FACTOR
Modifiable : Unmodifiable :

• Dyslipidemia • Age

• Smoking • Gender

• Hypertension • Family History

• DM • Genetic

• Less
physical
activity
 PATHOPHYSIOLOGY

ACS is the manifestation of torn or ruptured atheroma

plaque of coronary vessel
 DIAGNOSIS
Acute Coronary Syndrome is diagnosed
when 2/3 criteria is found :

1. Chest pain ±20 minutes or didn't relieve

with sublingual nitrate

2. Electrocardiography changes (EKG)

3. Elevated heart biomarker

 DIAGNOSIS
Anamnesis
The most important complain was CAD and radiated pain to
the neck, jaw, or left hand. It's also important to ask about
risk factors.

Physical Examination
To identify the trigger factors, complication, and morbidity
of ischemia, and to exclude differential diagnosis
 DIAGNOSIS
ECG
Done in 10 minutes since patient was admitted to the
hospital with chest pain
that lead to ischemia.
Assessment of ECG from ST segment elevation. Suspect
infarct if ECG with new LBBB/suspect also accompanied
by ST segment elevation ≥1 mm on positive QRS complex
and lead with positive QRS complex and ST segment
depression ≥ 1 mm in lead V3-V6
 DIAGNOSIS
Heart Enzym Examination
Creatinine kinase – MB (CK-MB) or Troponin T/I are heart
myosite necrosis
marker and becomes the biomarker to diagnose myocardial
infarction
Laboratorium
Laboratorium data, that needs to be collected in
emergency unit besides heart biomarker, are
hematology routine test, gds, electrolyte status, blood
coagulation, kidney function test, and lipid fraction.

Chest X-Ray
To determine differential diagnosis, identify complication and comorbidity.
Unstable Angina NSTEMI STEMI

Occluding thrombus Complete thrombus

sufficient to cause occlusion
Non occlusive
tissue damage & mild
thrombus
myocardial necrosis ST elevations on
Non specific ECG
ST depression +/-
ECG
T wave inversion on Elevated cardiac
ECG enzymes
Normal cardiac
enzymes
Elevated cardiac More severe
enzymes symptoms
KILLIP CLASSIFICATION
 MANAGEMENT
Fixing the chest pain
and fearness
Stabilizing the
hemodinamic (blood
pressure and perpheral
pulse control)
Reperfusion of the
myocard
 INITIAL TREATMENT
• Bed rest
• Oxygen (2-4 lpm)
• Anti platelet therapy :
 Aspirin 160-320mg chewed immediately and 80-160 mg continued indefinitely.
 Clopidogrel 300-600mg loading dose and 75mg daily continued for at least 14 days and
up to 12 months.
• Nitroglycerin :
 0.4 mg SL tablets every 3-5 min up to 3 times; if effect is not sustained, can continue
with an IV drip of 50mg in 250mL Dextrose 5%.
• Morphine 2-5mg iv (can be administered again in 5-30 minutes later)
• Fibrinolytic therapy:
 Streptokinase 1.5 million units in 100 mL dextrose 5% or NaCl 0,9% finished in 30 – 60
minutes
 Actilyse : 15 mg bolus iv
0.75mg/kg weight body in 30 minutes
and 0,5 mg/kg weight body in 60 minutes
• Anticoagulation therapy:
 Low Molecular Weight Heparins (Fluxum) 0.4cc/sc for up to 8 days post-MI.
 Unfractionated heparin
• Anti Hypertension Drugs
• Lipid Lowering Agents
PROGNOSIS
Clinical Manifestation
Aside from various typical signs such as age, diabetes
mellitus, kidney failure and other comorbidity,
prognosis also can be predicted from clinical
presentation when the patient was admitted to the
hospital. The presence of symptoms at rest will give a
worse prognosis. Besides that, a continuous pain or
often accompanied by tachycardia, hypotension, and
heart failure also markers of increased risk and need
prompt diagnosis and treatment.
COMPLICATION
THANK YOU