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Inferior Wall ST

Elevation (STEMI)
Onset 4 hours
Killip I
By :
L. M. Isvan Davis
C 111 07 221

Supervisor :
Prof. Dr. dr. Ali Aspar Mappahya, Sp.PD, Sp.JP(K), FIHA,
FAsCC, FINASIM, FICA

Patients Identity
Name
Age
Gender
Address
No. 8,

:
:
:
:

Mr. B
54 years old
Male
Jl . Karunrung Raya 2
Makassar

Medical Record : 586234


Date of admission : 29 December
2012

History Taking
Chief complaint : Chest Pain
Chest pain has been experienced
since 4 hours before prior to
admission at hospital, pain like
pressure on the chest, does not
radiated, the pain is felt for 10
minutes, felt increasingly become
heavy.

History Taking
Dizziness (-), Headache (-) , Fever (-)
Shortness of breath (-), cough (-)
Cold sweating (+), palpitations (-)
Nausea (-), vomiting (-), epigastric pain
(+)
Urination and defecation normal

Past Medical History


History of high blood pressure (+),
since 2 year ago, but not regular
treatment
History of Diabetes mellitus (-)
History of Heart disease (-)
Family history with cardiovascular
disease (-)
History of Smoking (-)

Risk Factor
1. Modifiable :
a. Hypertension
b. Physical inactivity

2. Non-modifiable :
a. Gender : Male
b. Age : 56 years old

Physical Examination
General status :
Moderate illness
Nutritional Status
kg/m)
Weight
Height
Consciousness
Vital sign :
Bood Pressure
Pulse Rate
Respiratory Rate
Temperature

: Overweight (BMI: 23.8


: 65 kg
: 165 cm
: Conscious

:
:
:
:

140/80 mmHg
78 bpm
20 bpm
36.8 0C

Physical Examination
Head and Neck Examinations:
Eye

: Conjunctiva anemic (-/-), sclera icteric (-/-)

Lip

: Cyanosis (-)

Neck

: No mass, no tenderness, JVP : R + 1 cmH2O

Chest Examination
Inspection

: Symmetric left = right

Palpation
left=right

: No mass, no tenderness, vocal fremitus

Percussion
: Sonor left = right, lung-liver border in ICS
VI right anterior
Auscultation

: Breath sound

: Vesicular

Physical Examination
Cardiac Examination
Inspection : Apex was not visible
Palpation : Apex was not palpable
Percussion
:
Dull, normal heart size
Upper border : left 2nd ICS
Bottom border : left 5th ICS
Right border : right parasternalis line
Left border : left midclavicular line
Auscultation : Heart Sounds : S I/II pure regular
Additional sound : murmur (-)

Physical Examination
Abdominal Examination
Inspection :
Auscultation
Palpation :
palpable
Percussion :

Flat, following breath movement


: Peristaltic sound (+), normal
No mass, no tenderness, no
liver and spleen
Tympani (+), ascites (-)

Extremities Examination
Pretibial edema -/ Dorsum pedis edema -/-

Electrocardiogram

29/12/2012
SR, HR 88 bpm, ST Elevation at Lead
II, III & AVF

Back

29/12/2012

Right

29/12/2012

Post Trombolitik

29/12/2012

Electrocardiogram

03/01/2013

Interpretation

Sinus Rhythm
QRS Rate
: 88 bpm
Regular
: regular
PR interval
: 0,12 sec
Axis
: 50 o (normal)
P Wave
: normal
QRS complex : 0,04 sec
ST segment : elevated at II,III, AVF
depression at AVL, V2, V3, V4, V5

Conclusion :
INFERIOR WALL STEMI

Chest X Ray
29 / 12 / 2012
Conclusion
Normal
pulmonary
CTI Normal
Dilation and
elongation of
aorta

Echocardiography
03/01/2013
Conclusion :
Normal function of
LV
Trivial MR
Hypokinetic of mid
posterior e/c Susp.
CAD

Laboratory
29 / 12 / 2012
Complete blood count
WBC
RBC
HGB
HCT
PLT

Enzymes
CK
CK-MB
Troponin T

Result
13,25
4,73
13,5
41,5
154

Result
230
20
Negative

Blood chemistry

Result

PT
INR

10,1
0,80

APTT
GDS
Ureum
Kreatinin
GOT
GPT
Kolesterol total
HDL
LDL

22,3
168
23
0,9
19
17
230
36
106

Diagnosis
INFERIOR WALL STEMI
ONSET 4 HOURS KILLIP I

Therapy

O2 3 -4 Lpm
IVFD Nacl 10 gtt/ i
Streptokinase 1,5 juta IU / 100 cc D5 % / 1 jam
Farsorbid 5 SL
Aspilet 80 mg - 4 tab
Plavix 75 mg - 8 tab
Arixtra 25 mg / 24 / SC
Alprazolam 0,5 mg 0-0-1
Laxadin syrup 0-0-1

DISCUSSION :
STELEVATION
MYOCARDIALINFRACTION

ACUTE CORONER
SYNDROME
Acute coronary
syndrome (ACS)
refers to a spectrum
of clinical
presentations
ranging from those
for
ST-segment
elevation myocardial
infarction (STEMI)
nonST-segment
elevation myocardial
infarction (NSTEMI)
unstable angina.

STEMI
STEMI is when there is a
transmural infartion of the
myocardium
entire thickness of the
myocardium has undergone
necrosis - resulting in ST
elevation.
Usually due to a complete block
of a coronary artery (occlusive
thrombus). This requires the use
of thrombolytics like
Streptokinase to lyse the
thrombus.
Evidence has proven that it is
very effective and not as risky
(Benefits > Risk)

NSTEMI and UNSTABLE


ANGINA
UA or NSTEMI is when there
is a partial dynamic block to
coronary arteries (nonocclusive thrombus).
There will be no ST elevation
or Q waves on ECG, as
transmural infarction is not
seen.
The main difference between
NSTEMI and unstable angina
is that in NSTEMI the severity
of ischemia is sufficient to
cause cardiac enzyme
elevation.

Epidemiology
Acute coroner syndrome
1,5 million hospital
addmision ACS

UA/ NSTEMI

1,24 million
admission
per year

STEMI

0,33 million
admission
per year

Heart disease and stroke statistic 2007 update. Circulation 2007 ,

Etiology

Mechanism:
Coronary plaque rupture (95%)
lead to partial or total coronary occlusion
Coronary spasm
Prinzmetal angina (transient ST elevation)
Myocardial infarction (if the ischemic period is too
long)
Coronary embolisation

Risk factor
Non- Modifiable
Gender
Men > women

Modifiable
Hypertension
Diabetes Mellitus

Age
Men, increased risk after age 50
Women, increased risk after age 65

Dyslipidemia
Obesity

Family History
Lack of physical activity

Heart disease diagnosed before age 55


Diet (high fat and high
in father or brother
charbohidrat)

Heart disease diagnosed before age 65


Cigarette Smoking
in mother or sister
Stress

Pathophysiologi
Acute myocardial infarction with ST elevation
(STEMI) usually occurs when blood flow of
artery coroner suddenly decreased after
occlusive thrombus on atherosclerotic plaque
koronre plaques tend to rupture if it has a
thin fibrous cap and a lipid-rich core. In
STEMI classical pathological picture consists
of rich red fibrin thrombus, which is believed
to be the basis of so STEMI response to
thrombolytic therapy.

Pathophysiologi
At the site of plaque rupture, various agonists
(collagen, ADP, epinephrine, serotonin) triggers
platelet activity and subsequent production and
release of thromboxane A2 (a potent local
vasoconstrictor).
Coagulation cascade is activated by exposure of
tissue factor on endothelial cells are damaged.
Factor VII and X are activated, resulting in the
conversion of prothrombin to thrombin, which then
convert fibrinogen into fibrin. Artery occlusion
coroner will then experience the thrombus
composed of platelets and fibrin aggregates.

Pathophysiologi

Pathophysiologi

Diagnosis

Symptom
Chest pain
Clinical circumstance
Severity

A
Develops in
presenceof
extracardiac that
intensifies
myocardial ischemia
Secondary UA)

I new onset of severa


angina or accelerated
angina , no rest pain

B
Develops in
absence of
extracardiac
condition
(primary UA)

C
Develops I n2 weeks of acute
myocardial infarction (post
infarction UA)

IA

IB

IC

II angina at rest within


past month but not within
preceding 48 h (angina at
rest, subacute )

II A

II B

II C

III angina at rest within 48


h (angina at rest, acute )

III A

III B

III C

Braunwald classification of unstable angina

Working Diagnostic (ACS


)
Ischemic symptoms
Prolonged pain (usually >20 mins) constricting, crushing,
squeezing
Usually retrosternal location, radiating to left chest, left arm,
can be epigastric
Dyspnea
Diaphoresis
Palpitations
Nausea/vomiting
Light headedness

Clinical Manifestation

ECG

ECG
STEMI

NSTEMI

ECG
Location of myocardial infarction by EKG
changes
No Location AMI ECG
1

Anterior

ST segment elevation and / or Q waves in V1-V4/V5

Anteroseptal

ST segment elevation and / or Q waves in V1-V3

Anterolateral

ST segment elevation and / or Q waves in V1-V6 and I


and aVL

Lateral

ST segment elevation and / or Q waves in V5-V6 and


T wave inversion / ST elevation / Q-wave in I and aVL

Inferolateral

ST segment elevation and / or Q waves in II, III, aVF, and


V5-V6 (sometimes I and aVL).

Inferior

ST segment elevation and / or Q waves in II, III, and aVF

Inferoseptal

ST segment elevation and / or Q waves in II, III, aVF, V1V3

True posterior

High R wave in V1-V2 with ST segment depression in V1V3.


Upright T wave in V1-V2

Biomarker

Biomarker
Biochemical marker for detection of myocardial necrosis
Normal value

First rise
after AMI

Peak after
AMI

Return to
normal

CK-MB

< 5.0 ng/ml

4h

24 h

72 h

Myoglobin

< 82 ng/ml

2h

6-8 h

24 h

Troponin T

Negatif

4h

24 - 48 h

5 21
days

Troponin I

Detection Limit = 0.5


ng/ml
Abnormal > 2.0 ng/ml
Borderline - Not detected

3-4 h

24 36 h

5 14
days

Treatment

General Theraphy for ACS


Immediate oxygen therapy ( maintain for first 6 hours )
Aspirin
Nitroglycerin
Morphine Sulfate
Continuous cardiac monitoring
Establishment of intravenous (IV) access

Prognosis
KILLIP CLASSIFICATION

Class

Description

Mortality Rate (%)

No clinical signs of heart failure

II

Rales or crackles in the lungs, an S3,


and elevated jugular venous
pressure

III

Acute pulmonary edema

30 - 40

IV

Cardiogenic shock or hypotension


(systolic BP < 90 mmHg), and
evidence of peripheral
vasoconstriction

60 80

17

Complication

Sudden Death

Ventricular Dysfunction

Hemodynamic Disturbances

Cardiogenic shock

Pericarditis

Arrhythmia post STEMI

Thank
you