Download Infark Miokard Akut (IMA)

Infark Miokard Akut (IMA)
Mohammad Saifur Rohman, dr.SpJP, PhD.FICA
Outlines
Anatomy of coronary artery
 Coronary artery disease : atherosclerosis
 Progression of CAD  IMA
 Diagnosing IMA
 IMA Treatment

Major components
Muscle; contractile apparatus
 Nerve; conducting system and innervation
 Vessel; Supporting oxygen from the blood
 Extra cellular matrix
 Endocardium; valves
 Pericardium
 Etc.

Coronary Arteries
Coronary
arteries branch off at base of aorta
& supply blood to the electrical conduction
system & myocardium.
3
main arteries:
 RCA
 LCA
 Circumflex
Coronary Arteries
Originates from the aorta
just beyond the aortic
valve
• Coronary blood flow to
the myocardium occurs
primarily during diastole
* To maintain adequate
blood flow through the
coronaries, mean
arterial pressure (MAP)
must be at least 60
mmHg
•
Coronary Arteries
•
Left main coronary artery
(LCA)
- Left anterior descending
artery (LAD)
>descends toward the
anterior wall & apex of LV
> supplies LV, ventricular
septum, chordae, papillary
muscle & RV
- Left circumflex artery
(LXA)
> descends toward the
lateral wall of LV & apex
> supplies LA, lateral &
posterior LV surfaces
*45% supplies SA node
Coronary Arteries
LCA
Branches into LAD & L Circumflex
Left Anterior Descending
 Anterior wall of LV & anterior 2/3
septum
 RBB & part of LBB
 LA
Circumflex Supplies
 AV node in 10% hearts
 SA node in 45% hearts
 Posterior surface of LV
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Coronary Arteries

Right main
coronary artery
(RCA)
- descends
toward the
apex of RV
- supplies the
RA, RV, &
inferior
portions of LV
Coronary Arteries
RCA
Supplies
 SA node in 55% of hearts
 AV node in 90% hearts
 RA & RV heart muscle
 Inferior wall of LV
 Posterior 1/3 of intraventricular
septum
 In 85% of hearts, RCA provides the
posterior descending branch.
Atherosclerosis
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Disease of cardiovascular system affecting
vessel wall.
It leads to the narrowing of arteries or
complete blockage.
Its main components are endothelial
disfunction, lipid deposition, inflammatory
reaction in the vascular wall.
Remodeling of vessel wall.
The process of atherogenesis – an overview
Risk Factors
Smoking
Hypertension
Obesity
DIABETES
Family history:
Man < 55 yo
Women < 65 yo
CV Prevention
Risk factors for CVD
Modifiable
– Smoking
– Dyslipidaemia
• raised LDL cholesterol
• low HDL cholesterol
• raised triglyceride
– Raised blood pressure
– Diabetes mellitus
– Obesity
– Dietary factors
– Thrombogenic factors
– Lack of exercise
– Excess alcohol consumption
Non-modifiable
–
–
–
–
Personal history of CVD
Family history of CVD
Age
Gender
Levels of risk associated with smoking,
hypertension and hypercholesterolaemia
Hypertension
(SBP 195 mmHg)
x3
x9
X4.5
x16
X1.6
Smoking
x6
x4
Serum cholesterol level
(8.5 mmol/L, 330 mg/dl)
(Adapted from Poulter et al, 1993)
The development of atherosclerosis
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The key event – damage to the endothelium
caused by excess of lipoproteins,
hypertension, diabetes, components of
cigarette smoke.
Endothelium becomes more permeable to
lipoproteins.
Lipoproteins move below the endothelial
layer (to intima).
Endothelium loses its cell-repelent quality.
Inflammatory cells move into the vascular
wall.
Triggers for inflammation in atherosclerosis
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LDL retained in the intima (in part by binding
to proteoglycan) undergoes oxidative
modification.
Lipid hydroperoxides, lysophospholipides,
carbonyl compounds localize in the lipid
fraction.
Oxygen free-radicals inactivate NO rapidly.
NO + superoxide (O2.-)  peroxynitrite
(ONOO-).
NO has no longer vasoprotective function.
The process of atherogenesis
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Lipid entry into the arterial wall is a key
process in atherogenesis.
Hypercholesterolemia – factor for VCAM-1
and MCP-1 induction.
LDL and VLDL are most atherogenic, enter
vascular wall more easily.
LDL – in plasma are protected against
oxidation by vit. E, ubiquinon, plasma
antioxidants (b-carotene, vit. C).
Out of plasma, LDL phospholipides and fatty
acids oxidize.
The process of atherogenesis
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Activated macrophages produce enzymes –
lipoxygenases, myeloperoxidase, NADPH
oxidase  ROS
Oxidized LDL are cytotoxic to endothelial
cells, mitogenic for macrophages.
Oxidized LDL apolipoprotein apoB100 bind to
the scavenger receptor.
Scavenger receptors are not subjected to
regulation by intracellular cholesterol level.
Macrophages take up oxidized LDL, overload
with lipids.
The process of atherogenesis
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Foam cells ruptured (apoptosis).
Lipid release to intima and their acumulation
becomes centre of atherosclerotic plaques.
• The lipid center and fibrous cap
are the main parts of a mature
atherosclerotic plaque.
• Plaque emerges from the
structurally changed vascular
wall.
• So-called vulnerable plaque
ruptures easily.
•The thrombus formed at the
rupture site.
The process of atherogenesis
Morphologic stages:
Type I – Fatty dots - Foam cells
 Type II – Fatty streak
 Type III – Extracellular lipid pool
 Type IV – Atheroma – Core of lipid
 Type V – Fibroatheroma – Fibrotic layer
 Type VI – Complicated – Ulcer, Ca+
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Hemorrhage, thrombus, embolism,
aneurysm.
Stages of Atheroma - Aorta
Stage
VI
III
II
Morphologic types:
Fatty dots
F.Atheroma Plaques
Complicated
Aterosklerosis Acute Coronary Syndrome (ACS)
Chest Pain
Plaque Rupture Toward
Occlusion
Spektrum ACS
Unstable Angina Pectoris :
(EKG normal, Trop T/I (-))
 Acute Non ST-Elevation Myocardial Infarction
(NSTEMI) :
(EKG normal/ST depresi/T inversi dan Trop
T/I (+))
 Acute ST-Elevation Myocardial Infarction
(STEMI) :
EKG ST elevasi dan Trop T/I(+)
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Prevalensi IMA
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Di Amerika : kejadian IMA lebih 1 Juta/tahun
200,000 – 300,000 pasien IMA meninggal
sebelum sampai RS
Total : Warga negara Amerika mengalami IMA
setiap 29 detik dan meninggal setiap menit.
Indonesia ?
Tahun 2008: PJN Harapan Kita 7 pasien ACS ,
50-60% IMA
10% IMA < 40 thn
Penyebab kematian no 2 di UGD RSSA
Topol EJ. CV med 2009
Saifur et al. unpublished data, 2008, 2011
Bagaimana Diagnosa ACS ?
Nyeri dada ACS?
1. Cardiac or non cardiac
 2. Cardiac : Ischemic non Ischemic
 3. Ischemic : Coronary non Coronary
 4. Angina pektoris stabil atau ACS
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Nyeri (tidak enak) dada ….. ?
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Sifat :Berat/ tertindih (pressure, tightness, or heaviness,
strangling, constricting, or compression), Panas
(burning) ; Masuk angin, Sesak,”maag”
Lokasi: Di dada kiri/tengah tidak bisa ditunjuk
Penjalaran : ke bahu/lengan, leher, dagu,
belakang,epigastrium
Lama : 5-30’
Pencetus :aktifitas/stres/dingin
Berkurang: Nitrat/Istirahat
Tidak khas: Pingsan/kejang/tidak sadar/berdebar
ESC guidelines for SAP 2006
ESC AMI ST elevation guidelines 2008
Angina Pectoris
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A syndrome resulting from myocardial
ischemia
Demand and supply imbalance
Careful history taking; mode of onset,
location, quality of pain, duration, precipitating
factors, pattern of disappearance, risk factor,
etc
Stable vs. Unstable
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Stable : There is no substantial deterioration
in symptoms over several weeks. Stability or
quiescence of an atherosclerotic plaque;
depending on increased oxygen demand
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Unstable : symptom pattern worsen abruptly
without an obvious caused of increased
oxygen consumption, decreased supply .
Unstable plaque: ACS
Stable Angina Pectoris
Canadian Class :
 I Ordinary physical activity does not cause
angina
 II Slight limitation of ordinary activity
 III Marked limitation of ordinary activity
 IV Inability to carry on any activity without
discomfort
Nyeri dada khas ACS
Angina awitan baru derajat 3 menurut
klasifikasi kanada kardiovaskuler group
( nyeri dada timbul pada aktifitas ringan
sehari-hari)
 Angina saat istirahat > 20 menit
 Perburukan derajat angina menjadi derajat
3 dalam beberapa hari – 1 bln terakhir
(Crescendo angina)
 Atypical
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Hati-hati : Angina Equivalent
Indigestion, belching, dyspnea
 DM, wanita, manula (post operative)
 Didapatkan 5% dari ACS
 2% dipulangkan ternyata ACS
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Braunwalds Heart Disease 8th Ed 2008
DD Chest pain
Ischemic
 Stenosis Aorta
 Regurgitasi Aorta
 Hypertrophic Cardiomyopathy
 Angina pada Hypertensi
 Hipertensi pulmonal berat
11th ed Hurst’s the heart 2005
DD Chest Pain
Non Ischemic
 Diseksi Aorta
 Pericarditis
 Mitral valve prolaps
11th ed Hurst’s the heart 2005
DD Chest Pain
Gastro intestinal
 Esophageal spasm/reflux/rupture
 Peptic Ulcer
Neuromusculoskeletal
 Costochondritis
 Herpes zoster
 Chest wall pain dan tenderness etc
11th ed Hurst’s the heart 2005
DD chest pain
Pulmonary
 Pulmonary emboli
 Pneumothorax
 Penumonia with pleural involvement
Pleurisy
Psychogenic
 Axiety/depression/cardiac psychosis etc
11th ed Hurst’s the heart 2005
Non Angina Pain
Hanya terasa pada sebagian kecil dada
kiri/kanan (bisa di tunjuk)
 Berkahir berjam jam sampai berhari hari.
 Biasanya tidak berkurang dengan
nitrogliserin
 Mungkin dicetuskan oleh debaran.
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ESC guidelines for SAP 2006
ESC AMI ST elevation guidelines 2008
EKG
Secepat mungkin – 10’ setelah pasien tiba
 Diulang apabila meragukan adanya
kenaikan segmen ST (ST televasi)
 Bandingkan denga EKG sebelumnya
 Pasang monitor EKG
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EKG : Gambaran aktifitas listrik jantung
EKG pada ACS
EKG dapat menentukan adanya:
 Old/Recent/Acute infarction
 Pericarditis
 Arrhythmias
 Pembesaran jantung
ST-T changes in STEMI
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The acute phase is marked by ST segment
elevations (current of injury pattern) and
sometimes tall positive T waves (hyperacute
T waves)
Within several hour, myocytes death leads to
loss of R amplitude and Q wave appeared
During the 1-2 days ST remains elevated, T
inverted , Q wave deepen
Several days later ST segment return to
baseline, T remains inverted,
Weeks to months following infarct, Q persist
Gambaran EKG pada Iskemik/AMI
UAP/Acute NSTEMI
Acute NSTEMI
Acute STEMI- Evolution
Systolic Current Theory
Diastolic current Theory
Leaky K+
 Never fully repolarize
 Relatively more negative than normal
 Current directed away from infarct area
 Baseline shift downward
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Acute STEMI-Q wave
ECG subsets and correlated infarctrelated artery
Category
Anatomy of Occlusion
ECG Findings
Proximal LAD
Proximal to septal
perforator
ST elevation V1-6, I, avL,
and fascicular or bundle
branch block
Mid LAD
Proximal to large diagonal
but distal to first septal
perforator
ST elevation V1-6, I, avL
Distal LAD or diagonal
Distal to large diagonal or
diagonal itself
ST elevation V1-4, or I, avL,
V5-6
Moderate to large inferior
(posterior, lateral, right
ventricular)
Proximal RCA or left
circumflex
ST elevation II, III, avF, and
any of the following:
a. V1, V3R, V4R
b. V5-6
c. R>S in V1-2
Small inferior
Distal RCA or left circumflex ST elevation II, III, avF only
branch
Occluded artery
Anterior STEMI
ECG demonstrates large anterior infarction
Inferior STEMI
Proximal large RCA occlusion
ST elevation in leads II, III, aVF, V5, and V6
with precordial ST depression
Inferior STEMI
Small inferior distal RCA occlusion
ECG changes in leads II, III, and aVF
Peningkatan Enzym jantung
Troponin T/Troponin I
 CKMB
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Pemeriksaan Fisik
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Sadar-Koma
TD: Hypertensi-Normal-Hypoptensi
HR: Regular-irregular/ Bradycardia-Tachycardia
pulseless
RR: Tachypnea-apnea
Cor: Regular-iregular, murmur, gallop
Pulmo: Normal-Rales- wheezing
Ext: dingin/hangat, edema+/-, etc.
Komplikasi MI
Mechanical
 Electrical
 Ischemia
 Embolic
 Inflammation
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Komplikasi Mekanik
Ventricular Septal Rupture
 Mitral Regurgitation
 Cardiac free wall rupture
 Large ventricular aneurysms
 LV pump failure and cardiogenic shock
 Dynamic LVOT obstruction
 RV failure
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Gagal Jantung (Kriteria Framingham)
Major
 Acute pulmonary edema
 PND or orthopnea
 Crackles
 S3 gallop
 HJR/Increased JVP
 Cardiomegaly
 Wt loss >4.5 kg 5d into
Rx
Minor
 Night cough
 Tachycardia >120
 Pleural effusion
 Hepatomegaly
 Ankle edema
 Vital capacity decrease
>1/3 from max
*Two major or one major and two minor*
Komplikasi Elektrik
SA Dysfunction
 Atrial Fibrillation
 First-Second degree AV block
 Total AV Block
 Left Bundle Branch Block
 Right Bundle Branch Block
 Ventricular Tachycardia
 Ventricular Fibrillation
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Komplikasi Ischemik
Perluasan Infark
 Angina Post-infark
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Komplikasi Emboli
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Systemic embolism ;
stroke, limb ischemia, renal infarction,
intestinal ischemia
Inflammation Complication
Early Pericarditis
 Late Pericarditis (Dresslers syndrome)
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Universal Definition of Myocardial Infarction
Diagnosa AMI ditegakkan apabila min memenuhi 2
dari kriteria:
 Gejala Ischemic
 Perubahan EKG
 Kenaikan/penurunan Troponin T/I
Diagnosis
NSTEMI timi risk ../7….
 Acute ant STEMI timi risk… /14 Killip…
onset j…am
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Cepat tegakkan diagnosa dan cepat
bertindak (dalam hitungan menit)
 Semakin tinggi resiko semakin agresif
terapi yang diberikan
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Killip Classification
Killip
I
II
III
IV
Characteristic
% Mortality rate
No evidence of HF
Rales, JVD, S3
Pulmonary edema
cardiogenic Shock
85
13
1
1
5.1
13.6
32.2
57.8
TIMI Risk
NSTEMI :
 Umur
 Faktor resiko >3
 Angina
 Aspirin
 Diketahui CAD (Cath)
 Enzymes
 Depresi segmen ST
TIMI Risk
STEMI
Umur
Aada/ tidak faktor resiko
Killip Class
TD sistolik
HR
Anterior STEMI/LBBB
Onset > 4 jam
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Stratifikasi Resiko
High risk
Intermediate risk
Low risk
Angina saat Istirahat
Angina > 20 kurang
dengan istirahat
Angina dengan aktivitas
ALO
Riwayat CVD
LBBB/RBBB baru
Ada Q, ST depresi
ENZYME (+)
Sedikit meningkat
ENZYM (-)
MR ATAU S3 Baru,
HYPOTENSI,
BRADIKARDI,
TAKIKARDI. VT
Usia > 70 tahun
ST DEPRESI> 0.5
T inversi
EKG TETAP
GRACE SCORE
Prinsip Terapi
Cepat (time responsif), obati penyebab 
buka sumbatan
 Terlambat: Fatal
 Monitor ketat tanda vital sejak awal
 Antisipasi dini tanda tanda perburukan dan
komplikasi
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Terapi Awal ACS
Atasi keadaan kegawat daruratan :
asistol, apneu, syock, lung edema,
gagal jantung dll.
 Terapi reperfusi : PCI, Fibrinolitik,
heparin
 Antiischemic
 Turunkan oksigen demand : Bed rest
total, pendekatan psikologis, dll
 Terapi komorbid; hipertensi, DM, dll
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Pentingnya Reperfusi
Sumbatan total15-30 menit tanpa
kolateral IMA
 Reperfusion  selamatkan miorkard
 Kematian1 bulan: 25-30% 4-6% dengan
reperfusi (PCI, fibrinolytic, antithombotic)
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ESC AMI ST elevation guidelines 2008
Kerusakan Miokard Irreversibel
Miokard tidak mengalami regenerasi
 Terlambat/tidak dibuka  Miokard mati 
Gagal Jantung  rawat ulang  biaya
besar, kualitas hidup kurang baik
 Obat gagal Jantung hanya mencegah
perburukan, tidak memperbaiki miokard
yang mati/infark
 Alternatif terapi : Stem cell
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The time is muscle
Terapi NSTEMI
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O2
Bed rest
Pain killer
Nitrate and anti-ischemia
Antiplatelet : Aspirin, Clopidogrel
Heparin
HTN
Hyperglicemia
Treat the complication etc
Tips
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Obat anti ischemik atau anti nyeri segera di berikan
Anti platelet dan heparin dimasukkan secepatnya
setelah diagnosis ACS-NSTEMI ditegakkan, jangan
di tunda
Turunkan kebutuhan/kerja jantung dengan berikan
rasa nyaman dan aman pasien dan bed rest total
Setengah duduk pada pasien dengan gagal
jantung
Pikirkan immediate/urgent PCI pada pasien resiko
tinggi/hemodinamik tidak stabil/nyeri
berkepanjangn/aritmia maligna dll
Alat diagnosis dan monitoring Perawat
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Keluhan berhubungan dengan fungsi dan
beban jantung, deteksi dini komplikasi
Monitor tanda vital, saturasi, perfusi, EKG,
intake- output, balance. dll
Kalau perlu ukur CVP, arteri line dll
Laboratorium : Enzyme jantung, analisa gas
darah, fungsi ginjal, elektrolit, komorbid (infeksi,
dm, dll)
Intervensi keperawatan
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Turunkan kebutuhan dan bebang jantung
misalnya istirahat fisik dan mental, kondisi
hangat, tenang, rasa aman, pemilihan diet : NGT
atau bantuan makanan, dilarang mengejan,
atasi febris, rasa sakit atau sesak dll
Bantu fungsi jantung: Inotropic, IABP, anti
iskemik, dll
Atasi komorbid/komplikasi: hipertensi, DM,
infeksi, gagal jantung, gangguan ginjal, dll
Atasi kekurangan atau kelebihan cairan, kalori,
oksigen, PH, elektrolit, dll
Terapi STEMI
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O2
Bed rest
Pain killer
Nitrate and anti-ischemia
Antiplatelet : Aspirin, Clopidogrel
Fibrinolytic time to neddle : 30 m/PCI
HTN
Hyperglicemia
Treat the complication etc
Fibrinolitik
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Manfaat bila onset < 12 jam, optimal bila onset <
3 jam
Bila dikirim ke RS dengan PCI > 90 menit,
fibrinolitik
Konsep baru : Fibrinolitik di Ambulan menuju RS
Perhatikan kontraindikasi fibrinolitik
Awasi ketat komplikasi fibrinolitik seperti
perdarahan, stroke, syok dll
Perhatikan tanda tanda keberhasilan: nyeri
hilang, ST elevasi turun >50%, Junctional
VES(+), bila gagal rescue PCI
Kontra Indikasi Absolut
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Any prior ICH
Known structural cerebral vascular lesion (eg, AVM)
Known malignant intracranial neoplasm (primary or
metastatic)
Ischemic stroke within 3 months EXCEPT acute
ischemic stroke within 3 hours
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed head or facial trauma within 3 months
Kontra Indikasi Relatif
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History of chronic severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (SBP greater than
180 mm Hg or DBP greater than 110 mm Hg)†
History of prior ischemic stroke greater than 3 months, dementia, or
known intracranial pathology not covered in contraindications
Traumatic or prolonged (greater than 10 minutes) CPR or major
surgery (less than 3 weeks)
Recent (within 2 to 4 weeks) internal bleeding
Noncompressible vascular punctures
For streptokinase/anistreplase: prior exposure (more than 5 days
ago) or prior allergic reaction to these agents
Pregnancy
Active peptic ulcer
Current use of anticoagulants: the higher the INR, the higher the risk
of bleeding
Treatment of STEMI
Percutaneous Coronary Intervention
•Primary PCI : Pasien langsung di lakukan tindakan
reperfusi dengan membuka sumbatan di
arteri koroner tanpa dilakukan fibrinilotik
terlebih dahulu
•Rescue PCI : Dilakukan PCI setelah gagal dengan terapi
fibrinolitik
•Facilitated PCI : Pasien dilakukan fibrinolitik terlebih
dahulu meskipun sudah ada rencana PCI
•Urgent PCI: As soon as possible
•Early PCI : Dalam waktu 24 jam pertama
Early/urgent PCI: Resiko tinggi, hemodinamik tidak stabil,
aritmia maligna, angina (+) dgn terapi, EF <40%,Gagal
jantung, Riwayat PCI, CABG dl 6 bl
Tim PCI
Target
1. Time to balloon : 90 m
2. Yang dibuka hanya Culprit lesion (pembuluh
darah tersumbat yang menyebabkan IMA kali ini)
saja
3. Aliran darah yang diintervensi kembali lancar
Primary PCI Case
A 53 yo man reffered from a private
hospital for primary PCI
 A typical chest after exercise 2 hr prior to
admission
 ECG send by fax
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PCI appointment via phone
 Patient directly transfer red to cath lab.
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Case 2
Mr W. 28 yo, smoker and family history
 Admit to Nearest private hospital with
chief complaint of Heaviness while he
was driving a car 30 min prior to admission
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Case 2
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ECG on admission
Case 2
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ECG on referral hospital (after double antiplatelet tx)
CABG
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Failed PCI with persistent pain or hemodynamic
instability in patients with coronary anatomy suitable for
surgery.
Persistent or recurrent ischemia refractory to medical
therapy in patients who have coronary anatomy suitable
for surgery, have a significant area of myocardium at
risk, and are not candidates for PCI or fibrinolytic
therapy.
At the time of surgical repair of postinfarction ventricular
septal rupture (VSR) or mitral valve insufficiency.
CABG
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Cardiogenic shock in patients less than 75 years old with
ST elevation, LBBB, or posterior MI who develop shock
within 36 hours of STEMI, have severe multivessel or left
main disease, and are suitable for revascularization that
can be performed within 18 hours of shock
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Life-threatening ventricular arrhythmias in the presence
of greater than or equal to 50% left mainstenosis and/or
triple-vessel disease.
Yang sering di lupakan…..
Edukasi pasien mengenai :
 Mengapa bisa sampai sakit….. Pola hidup
 Kepatuhan untuk merubah pola hidup
 Faktor resiko di kendalikan, rokok, HT, dll
 Kepatuhan minum obat
 Mencegah serangan jantung berikutnya
dengan…..merubah pola hidup, atur pola
makan, olah raga teratur dan terukur
 Reperfusi adalah awal dimulainya hidup baru
…agar koroner tetap terbuka
Simpulan
Tegakkan diagnosa dengan cepat dan
tepat
 Terapi dengan cepat dan tepat : Reperfusi
 Monitor ketat
 Cegah komplikasi
 Edukasi untuk prevensi dan rehabilitasi

…..…….Kerja keras di awal……