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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
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
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
:
:
:
:
140/80 mmHg
78 bpm
20 bpm
36.8 0C
Physical Examination
Head and Neck Examinations:
Eye
Lip
: Cyanosis (-)
Neck
Chest Examination
Inspection
Palpation
left=right
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 :
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)
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
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
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)
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 A
II B
II C
III A
III B
III C
Clinical Manifestation
ECG
ECG
STEMI
NSTEMI
ECG
Location of myocardial infarction by EKG
changes
No Location AMI ECG
1
Anterior
Anteroseptal
Anterolateral
Lateral
Inferolateral
Inferior
Inferoseptal
True posterior
Biomarker
Biomarker
Biochemical marker for detection of myocardial necrosis
Normal value
First rise
after AMI
Peak after
AMI
Return to
normal
CK-MB
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
3-4 h
24 36 h
5 14
days
Treatment
Prognosis
KILLIP CLASSIFICATION
Class
Description
II
III
30 - 40
IV
60 80
17
Complication
Sudden Death
Ventricular Dysfunction
Hemodynamic Disturbances
Cardiogenic shock
Pericarditis
Thank
you