Acs Cardiovascular Emergency Jadi

Prof. Dr. dr.
Idris Idham, SpJP (K),

FIHA, FACC, FESC, FASCC, FSCAI
Education
SR Negeri Tabing, Padang, Tahun 1957

SMPN Kuranji, Padang, Tahun 1960
SMAN I Padang, Tahun 1963
Dokter Umum Fakultas Kedokteran Universitas Gadjah Mada; (S1)
Tahun 1972
Dokter Spesialis Jantung dan Pembuluh Darah FK UI; (S2) Tahun1983
Post Graduate Course on Invasive Cardiology, Nuclear Cardiology
Austin Hospital Melbourne, Australia, 1992
Post Graduate Course on Non-Invasive Cardiology Pacemaker
Implantation, Royal Melbourne Hospital, Australia, 1993
Pendidikan Dokter Universitas Airlangga; (S3) Tahun 2000
Guru Besar tetap Universitas Indonesia; Tahun 2004
Prof. Dr. dr. Idris Idham, SpJP (K),

FIHA, FACC, FESC, FASCC, FSCAI
Staf senior, Dept. Kardiologi & Kedokteran Vaskular FKUI &
Pusat Jantung Nasional Harapan Kita
Chief cardiologist, RS Medika BSD
Sekretaris Kolegium Pengurus Pusat Perhimpunan Dokter
Spesialis Kardiovaskular (PP PERKI) 2008-sekarang
Fellow of Indonesian Heart Association (FIHA)
Fellow of American College of Cardiology (FACC)
Fellow of European Society of Cardiology (FESC)
Fellow of ASEAN Federation of Cardiology (FAsCC)
Fellow of Society of Cardiovascular Angiography and
Intervention (FSCAI)
Head of Cardiovascular Devision Medika BSD Hospital
Cardiovascular Emergency :
Focus On Acute Coronary Syndromes
Roles of Primary Physicians
Idris Idham
RS MEDIKA BSD
Spectrum of CV Emergency
Congenital Heart Diseases
Acute Coronary Syndrome : UAP,
NSTEMI, STEMI
Acute Lung Edema
Acute Aortic Dissection
Acute Limb Ischemia
Deep Veins Thrombosis
Hypertensive Crisis : emergency,

urgency
Arrhythmia : AFRVR, SVT, VT, VF,
TAVB
Cardiomyopathy : PPCM, HCM, DCM.
CARDIOVASCULAR SPECIALIST
COMPETENCY
FRONTLINE DOCTORS
FROM PALPITATION TO CVD
Front-line medical practitioners

Play very important role in fighting
cardiovascular diseases (CVD), the no.1 killer
in Indonesia1
Front liners are doctors who first encounter
the patient, including family physicians
Patients will benefit from early diagnosis and
prompt treatment
Competent of recognizing important signs &
symptoms of CVD, e.g. chest pain
1Dept.
of Health, RI. 2002.
Chest Pain
One of the most challenging symptoms1
Diagnosis ranges from benign esophageal
reflux to fatal MCI
Failure to manage fatal conditions lead to
complications including death
Over management of low risk conditions causes
unnecessary burden
Acute or escalating chronic chest discomfort is

most challenging.
1Harrisons
principles of internal medicine: McGraw-Hill, 2005.
Evaluation Aim
To assess the general clinical condition of
patient
To determine the working diagnosis
To initiate immediate management plan
Should be performed rapidly yet
accurately
General Clinical Assessment

Stratify patient : stable vs unstable
condition; based on level of
consciousness & vital signs.
Stabilize the patient first! Secure ABC
(airway, breathing, circulation)
Determining Working Diagnosis

Largely a clinical work, accurate anamnesis
is the key.
Characteristics of chest pain should be
thoroughly explored:
Quality, duration, location, precipitating &
relieving factors, other associated features.
Based on characteristics, determine the

organ(s) or system(s) causing the pain.
Determining Working Diagnosis

Consider anatomical structure of thorax
& adjacent abdominal organs ; each
organ has typical characteristics
Important : features may not always
present ; several features may occur
simultaneously
Anatomy of Thoracic Cavity
I.I. - 09 / PDKI Pekanbaru
Features of Major Causes of

Chest Pain
Angina: sensation of pressure, tightness,
squeezing, heaviness, burning ; located
retrosternal, often radiate (detailed later)
Aortic dissection : abrupt onset of tearing or
ripping sensation, knife-like pain in anterior
chest, often radiate to back
Pleuritis : pleuritic pain, influenced by
breathing ; accompanied by cough, fever.
1Harrisons
principles of internal medicine: McGraw-Hill, 2005.
Features of Major Causes of

Chest Pain
Esophageal reflux : burning, substernal or
epigastric pain, relieved by antacids
Musculoskeletal : aching, worsened by
movement, may be reproduced by localized
pressure
Herpes zoster : sharp, burning, dermatomal
distribution, with vesicular rash
Differential Diagnosis of
Chest Pain
Cardiac
Gastrointestinal
Esophageal reflux
Esophageal rupture
Gall bladder disease
Peptic Ulcer
Pancreatitis
ACS: infarct,angina
MVP
Aortic Stenosis
Hypertrophic cardiomyopathy
Pericarditis
Vascular
Aortic dissection/aneurysm
Lungs
Lung Emboli
Pneumonia
Pneumothorax
Pleuritis
Others
Musculoskeletal
Herpes zoster
General Approach for First liners

Targetted anamnesis and thorough physical
exams
Consider most likely diagnoses
If more than one, consider the worst one
Closely monitor vital signs

Administer essential first-line drugs
Refer to higher facility if required, after
patient is reasonably stabilized
Focus on:
Acute Coronary Syndromes
DEFINITION
A spectrum of clinical syndromes due to
sudden, significantly compromised coronary
circulation ranging from unstable angina to
NSTEMI and STEMI.
Further stages of stable angina pectoris
Topol EJ, ed. Textbook of cardiovascular medicine 2007.
PATHOPHYSIOLOGY
Atherosclerosis Timeline
Foam
Cells
Fatty
Streak
Intermediate
Atheroma
Lesion
Fibrous
Plaque
Complicated
Lesion/Rupture
Endothelial Dysfunction
From first decade
From third decade
Growth mainly by lipid accumulation
From fourth decade

Smooth muscle
and collagen
Thrombosis,
hematoma
Stary HC et al. Circulation 1995;92:1355-1374.
DIAGNOSIS
Presentation
(Clinical, Initial ECG)
Working
diagnosis
ST-Seg Elevation
Myocardial Infarction
Non-STSeg Elevation
Acute Coronary Syndr
Time
Evolution of
ECG &
Biomarkers
Final
diagnosis
Biomarker (+)
ST-Seg Elevation
MCI
Non-ST-segElevation MCI
Biomarker (-)
Unstable
Angina
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Algorithm in Acute Coronary Syndrome

CHEST PAIN
Working
diagnosis
Suspected ACS
ECG
Biochemistry
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Troponin,
CKMB (+)
Risk
Stratification
Risk: high / low
Management
Initial management,
revascularization
Secondary
prevention
Medical therapy,
coronary angiography
{on serial
ECG}
Performed in 10 min
Admission
- ACS unlikely
- NSTEMI
- STEMI
Modified from ESC 2007
Clinical Classification of Angina

Typical angina (definite)
substernal chest discomfort with a characteristic quality and
duration that is
provoked by exertion or emotional stress and
relieved by rest or nitroglycerin
Atypical angina (probable)
meets 2 of the above characteristics
Noncardiac chest pain

meets <=1 of the typical angina characteristics
Diamond GA. J Am Coll Cardiol 1983;1:574
UA/NSTEMI
THREE PRINCIPAL PRESENTATIONS
Rest Angina*
Angina occurring at rest and

prolonged, usually > 20 minutes
New-onset Angina
New-onset angina of at least CCS

Class III severity
Increasing Angina
Previously diagnosed angina that

has become distinctly more
frequent, Longer in duration, or
lower in threshold (i.e., increased
by > 1 CCS) class to at least CCS
Class III severity

CHEST PAIN
Working
diagnosis
Suspected ACS
ECG
Biochemistry
Persistent
ST elevation
Troponin,
CKMB (+)
No persistent
ST elevation
Troponin,
CKMB (+)
Risk
Stratification
Risk: high / low
Management
Initial management,
revascularization
Secondary
prevention
Medical therapy,
{on serial
ECG}
Performed in 10 min
Admission
- ACS unlikely
- NSTEMI
- STEMI
ECG pattern
Ischemia : ST , tall T,
inverted T
Injury : ST
Infarction : pathologic Q
EVOLVING ECG
A. Normal ECG
B. Tall or peaked T waves
C. ST
D. & E. ST with inverted T
waves
F. Abnormal Q

CHEST PAIN
Working
diagnosis
Suspected ACS
ECG
Biochemistry
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Troponin,
CKMB ()
Risk
Stratification
Risk: high / low
Management
Initial management,
revascularization
Secondary
prevention
Medical therapy,
{on serial
ECG}
Performed in 10 min
Admission
- ACS unlikely
- NSTEMI
- STEMI
Biomarkers
Recommendation : CK, CKMB & Troponin upon admission
and serial in 6-12 hours
LDH, SGOT/SGPT and other enzymes not recommended
Increase of plasma CK plasma & CK-MB happens early, but
less specific
Increase of TnI & TnT are more specific in diagnosing marker
MI ; its level corresponds with prognosis (higher value, worse
prognosis)
Multiple of the AMI cutoff limit
Biomarkers
Early release myoglobin of

CKMB isoform
50
Cardiac troponin after classical

myocardial infarction
20
CK-MB after myocardial infarction
10
Cardiac troponin after microinfarction
5
2
1
0
Day after onset of AMI

Time-course of the different cardiac biochemical markers. From Wu AH et al. Clin Chem
1999 ; 45 : 1104, with permission

CHEST PAIN
Working
diagnosis
Suspected ACS
ECG
Biochemistry
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Troponin,
CKMB ()
Risk
Stratification
Risk: high / low
Management
Initial management,
revascularization
Secondary
prevention
Medical therapy,
{on serial
ECG}
Performed in 10 min
Admission
- ACS unlikely
- NSTEMI
- STEMI
High Risk
Repetitive or prolonged (> 10 minutes) pain
Elevated level of cardiac biomarker (troponin or
creatine kinase-MB isoenzyme);
Persistent or dynamic ST depression 0.5 mm or new
T-wave inversion
Transient ST-segment elevation (0.5 mm) in more
than two contiguous leads
Haemodynamic compromise
Guideline ACS 2006 National Heart Foundation Australia
High Risk
Sustained ventricular tachycardia

Syncope
LV systolic dysfunction (ejection fraction <40%);
Prior PCI or CABG within 6 months or prior
Diabetes
Chronic kidney disease (estimated GFR< 60 mL/min)
Guideline ACS 2006 National Heart Foundation Australia

Admission
ECG
Biochemistry
Risk
Stratification
Management
Secondary
prevention
Suspected ACS
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Troponin,
CKMB ()
{on serial
ECG}
Performed in 10 min
Working
diagnosis
CHEST PAIN
- ACS unlikely
- NSTEMI
- STEMI
Risk: high / low

Initial management,
reperfusion
Medical therapy,
Initial Management
Monitor and support ABCs

Check vital signs, including O2 saturation
Establish IV access
Administer
Oxygen 4L/min
Aspirin 160-325 mg chewed
Clopidogrel loading dose 300 mg
ISDN 5 mg sublingual, nitroglycerine iv if necessary
Morphine if pain not relieved with NTG
Caution: hemodynamic instability due to pump

failure &/ malignant arrhythmia
Anticoagulation & Reperfusion

Heparin administration (LMWH or UFH)
Reperfusion in STEMI
Fibrinolysis or primary percutaneous coronary
intervention (PCI). GPs should be trained to give
fibrinolytic
Assess onset (12 hours) and contraindication
(bleeding, etc)
Door to needle time: 30 min
Door to balloon time: 90 min
Fibrinolytic Absolute Contraindication
Hemorrhagic stroke, or stroke of unknown origin

Ischemic stroke in preceding 6 months
Central nervous system trauma or neoplasm
Recent major trauma/surgery/head injury (within
preceding 3 weeks)
Gastro-intestinal bleeding within the last month
Known bleeding disorder
Aortic dissection
Non-compressible punctures (e.g liver biopsy, lumbar
puncture)
ESC Guidelines of STEMI, 2008
Algorithm in ACLS

CHEST PAIN
Working
diagnosis
Suspected ACS
ECG
Biochemistry
Risk
Stratification
Management
Secondary
prevention
Persistent
ST elevation
No persistent
ST elevation
Troponin,
CKMB (+)
Troponin,
CKMB ()
{on serial
ECG}
Performed in 10 min
Admission
- ACS unlikely
- NSTEMI
- STEMI
Risk: high / low

Initial management,
revascularization
Medical therapy,
Secondary Prevention Strategy

A
Aspirin and Anticoagulants
Beta blockers and Blood Pressure
Cholesterol and Cigarettes
Diet and Diabetes
Education and Exercise
Fun and Faith
Invasive Strategy
As secondary prevention
Early catheterization (before discharge):
for patients with moderate-high risk not
receiving primary percutaneous coronary
intervention
Later catheterization: for low risk
patients
Summary
Acute Coronary Syndrome as one of
potentially fatal cardiovascular emergency
should be recognized immediately
Early diagnosis and prompt treatment should
be managed to overcome good results and
avoid myocardial damage (Time is muscle)
Thank You
OKSIGEN
Pemberian suplemen O2 diberikan pada pasien
dengan desaturasi O2 (SaO2 <90%)
Suplemen O2 mungkin membatasi injury miokard
atau bahkan mengurangi elevasi ST
Pemberian suplemen O2 rutin > 6 jam pertama pd
kasus tanpa komplikasi, belum terdapat landasan
ilmiah yang kuat.
ACC/AHA Guideline of STEMI 2004

ANTIPLATELET
ASPIRIN
CLOPIDOGREL
TICLOPIDINE
Gp IIb / IIIa inhibitor
Aspirin
MANFAAT : menurunkan angka reinfark
50% dalam 30hari ; 20% penurunan
mortaliti dlm 2 tahun
Dosis 81-325 mg P.O.
Trials: ISIS (88), Antiplatelet Trialist Group
(94), HART (90)
Aspirin kunyah segera diberikan meskipun

belum ada hasil EKG
(non coated/slow released)
Adenosine Diphosphate
Inhibitors
ADP disekresi oleh platelet (aktivasi dan
agregasi platelet)
P2T cell surface receptors
Ticlodipine
Clopidogrel
Efek samping : Neutropenia, trombositopenia
Synergistic Mode of Action with

Clopidogrel and ASA1
CLOPIDOGREL
ADP
ADP
GPllb/llla
Activation
(Fibrinogen receptor)
ASA
ASA
COX
TXA
COX (cyclo-oxygenase)
ADP (adenosine diphosphate)
TXA2 (thromboxane A2)
1. Schafer AI. Am J Med 1996; 101: 199209.
Collagen thrombin
TXA 2
Clopidogrel
Gol Thienopyridine yg memblok P2Y reseptor ADP
Menghambat aktivasi platelet
Digunakan pada pasien UA/NSTEMI :

Diberikan pada semua pasien
Bukan kandidat CABG
Pasien yg direncanakan kateterisasi dlm
24-36 jam stlh masuk
Glycoprotein IIb/IIIa Inhibitors
50,000 receptors per platelet

Aggregation final common pathway
Passivation; stops deposition
Abciximab (Reopro); tirofiban (Aggrastat);
eptifibatide (Integrilin) and lamifiban (Canada)
Pre-PCI/ Procedural Coronary Intervention
Anti Ischemia
NITRAT
B BLOKER
ANTAGONIS KALSIUM
Nitrat
Indikasi : pada Anterior MI, iskemja persisten, CHF, hipertensi
Manfaat: dapat memperbaiki perfusi koroner
Hati-hati pd: inferior MI dengan perluasan atau keterlibatan
RV
Trials: GISSI-3 (94), ACC/AHA (96)
Pemberian Sublingual
Pemberian per IV
Dosis awal 5Ug/mnt ditingkatkan tiap 5 menit
disesuaikan dengan gejala klinis dan EKG
Beta-bloker
Effektif untuk pengobatan simtomatik dan
pencegahan infark miokard.
Vasokonstriktor moderat
Dipilih obat yang kardio-selektif
Berhubungan dengan nitrat.

Kontraindikasi:vasospastik angina, blok SV derajat II
atau III, asma, gagal jantung dlm
dekompensasi,penyakit arteri perifer yg berat
Beta-bloker
Metoprolol
Metoprolol
Atenolol
Propranolol oral
Bisoprolol
Carvedilol
IV
oral
oral
oral
oral
5 15 mg
2 x 25 100 mg
1 x 25 100 mg
3 x 20 80 mg
1 x 5 10 mg
1 x 25 mg
Antagonis kalsium
Pd UAP atau NSTEMI bila ada indikasi kontra Bbloker
Tidak ada bukti manfaatnya pada pencegahan
infark miokard.
Memberikan hasil yang baik dalam jangka pendek
pada episode iskemik.
Antagonis kalsium
Diltiazem
Lepas cepat :30 -120 mg 3x/hr

Lepas lambat: 100-360 mg 1x/hr
Verapamil
Lepas cepat : 40 160 mg/hr

Lepas lambat: 120-480 mg 1x/hr
PAIN KILLER
Morfin:
2.5mg-5 mg IV pelan.
Hati hati pada : inferior MCI,
asthma , bradikardia
Pethidin : 12.5-25 mg IV pelan
ANTITROMBOTIK DAN
ANTIKOAGULAN
Heparin ( Unfractionated Heparin)
Low Molecular Weight Heparin
Heparin (UFH)
Terikat pada AT III (anti-thrombin III)
,menginaktivasi trombin
Tidak ada efek pada Factor Xa
Hospitalization/ PTT/ bleeding
Benefit in UA/ rebound effect
Anti-Xa: Anti-thrombin 1:1
Memperpanjang APTT
Low Molecular Weight Heparin

Depolimerasi dari UFH standar dengan
berat molekul lebih kecil dari pada UFH
SQ injections/ 90% bioavailable/predictable
Anti-Xa: Anti-thrombin 2-4:1
FDA menyetujui pemakaian enoxaparin/
dalteparin untuk SKA
UFH
LMWH
KELEMAHAN UFH
Bioavailability kurang baik
Tidak dapat menghambat trombin yang terikat pada
bekuan (clot-bound thrombin)
Tergantung pada kofaktor AT III
Efek variabel
Monitor APTT berkala untuk mendapatkan kadar
terapeutik
Rebound iskemia setelah penghentian
Risiko heparin-induced thrombocytopenia (HIT)
Panduan Terapi SKA tanpa ST Elevasi PERKI 2004
KEUNGGULAN DARI LMWH
Mengurangi ikatan pada protein pengikat heparin

Efek yang dapat diprediksi lebih baik
Tidak memerlukan pengukuran APTT
Pemakaian subkutan,menghindari kesulitan dalam
pemakaian secara IV
Berkaitan dengan kejadian perdarahan yang kecil, namun
bukan perdarahan besar
Stimulasi trombosit kurang dari UFH dan jarang
menimbulkan HIT
Penghematan biaya perawatan (dari studi ESSENCE)
Panduan Terapi SKA tanpa ST Elevasi PERKI 2004

TEHNIK INJEKSI LMWH SUBKUTAN
DOSIS YANG DIREKOMENDASIKAN

UFH
Initial I.V BOLUS 60 UI/Kg max 4000 UI

Infus :12-15 UI/kg BB/jam max 1000 UI/jam
Monitor APTT : 3, 6, 12, 24 jam setelah mulai terapi
Target APTT 50-70 msec (1,5 -2 x kontrol
LMWH
1mg/kg, SC , bid
Enoxaparine
0,1 ml/10 kg , SC , bid
Nadroparine
2.5 mg
Fondaparinux
ACC/AHA 2007 Guidelines Update

for UA and NSTEMI1
Class I Recommendations for Antithrombotic Therapy*
Possible ACS
Aspirin
Likely/Definite ACS
Definite ACS with continuing

ischemia or other high-risk
features or planned PCI
SC LMWH
or
IV heparin
Aspirin
+
IV heparin/SC LMWH
+
IV GP IIb/IIIa antagonist
+ Clopidogrel
+ Clopidogrel
Aspirin
*During hospital
care
Clopidogrel should be administered to hospitalized patients who are unable to take ASA
because of hypersensitivity or major GI intolerance
Class IIa: enoxaparin preferred over unfractionated heparin, unless CABG is planned within 24 hours
1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA)
6/12/2011
Guidelines, USA: ACC/AHA; 2007.
OBAT-OBATAN LAINNYA
Tranquilizer e,g diazepam 5mg bid
Stool softener
TERAPI FIBRINOLITIK
Fibrinolitik : Indikasi
Sakit dada khas IMA 12 jam
EKG : 1 mm elevasi seg ST pada 2 sandapan yg

bersebelahan
2mm elevasi seg ST pada 2 sandapan
prekordial
Bundle branch block yg baru
Syok kardiogenik pd IMA ( bila kateterisasi dan
revaskularisasi tdk dapat dilakukan )
Fibrinolitik door to needle time < 30 menit !!
PCI pada IMA lebih unggul bila dpt dilakukan
dlm 90 30 menit
Fibrinolitik : indikasi kontra

Absolut
Riwayat stroke hemoragik,kapanpun terjadinya
Riwayat stroke iskemik dalam 3 bulan kecuali stroke iskemik
dengan onset < 3 jam
Neoplasma intrakranial
Perdarahan internal aktif(tidak termasuk menstruasi)
Kecurigaan suatu diseksi aorta
Luka kepala tertutup yg signifikan atau trauma facial dalam 3
bulan
Kelainan struktural atau pembuluh darah cerebral
ACC/AHA guideline of STEMI 2004

Fibrinolitik :indikasi kontra relatif

Hipertensi berat saat datang ke unit emergency yaitu BP> 180 / 110 mmHg
Pungsi vaskuler yg tak dapat dikompresi
Perdarahan internal 2 4 mgg sebelumnya
Konsumsi antikoagulan oral
prolonged CPR ( > 10 minutes) or operasi mayor dlm jangka waktu 2-4
minggu
Untuk Streptokinase : pemberian sebelumnya ( 5 hari-2 tahun) atau riwayat
reaksi alergi
Kehamilan
Active peptic ulcer
Riwayat hipertensi kronis yg tak terkontrol
Riwayat stroke iskemik lebih dari 3 bulan,demensia atau patologi serebral
lainnya yg blm tercantum dalam indikasi kontra
ACC/AHA guideline of STEMI 2004
Perbandingan terapi trombolitik

dengan terapi standar pada IMA
Mulai trombolisis
Tambahan Jiwa yg
diselamatkan per 1000
pasien yg diobati
------------------------------------------------------------------Pd jam pertama
Pd jam kedua
Pd jam ketiga
Antara jam ke 3-6
Antara jam 6-12
Antara jam 12-24
65
37
29
26
18
9
AGEN FIBRINOLITIK
Streptokinase (SK)
Actylase (tPA)
Reteplase (r-PA)
Tenecteplase (TNK-tPA)
Skema sistem fibrinolitik

Plasminogen Activators
(t-PA, u-PA)
Plasminogen Activator
Inhibitors (PA1, PA2, TAFI)
Plasminogen
Plasmin
2-Antiplasmin
Fibrin
Fibrin
degradation
Product
Braunwald, A Textbook of Cardiovascular Medicine. 6th ed
SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
Streptokinase
Actylase (tPA)
Reteplase(r-PA)
Tenecteplase
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
CARA PEMBERIAN FIBRINOLITK

Streptokinase ( Streptase )
1.5 million Unit in 100 ml D5W or 0.9% saline selama
30-60 mnt
without heparin : Inferior MCI
with heparin : anterior MCI
tPA
15 mg IV bolus kemudian 0.75 mg/Kg selama 30
mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt berikutnya
Streptokinase (SK, Streptase)

Keuntungan : lebih baik pada anterior
MCI, age <75; lebih murah
Komplikasi: antigenic, perdarahan
intraserebral pada studi GUSTO 0.6%
Trials: GISSI-1, ISIS-2 (88)
TPA Alteplase, rTPA

Keuntungan : clot specific, baik pada
anterior MCI
Komplikasi : 1% perdarahan intrakranal
Biaya: lebih mahal dari SK
Trials: ASSENT, GUSTO (93) TIMI-IIIB (94)
Complications of Acute MI
Extension / Ischemia
Expansion / Aneurysm
Mechanical
Arrhythmia
Pericarditis
Acute MI
Heart Failure
RV Infarct
Mural Thrombus
Komplikasi awal :
-aritmia
-disfungsi LV dan gagal jantung
-ruptur ventrikel
-regurgitasi mitral akut
-gagal fungsi RV
-syok kardiogenik
Komplikasi akhir :
-trombosis mural dan emboli sistemik
-aneurisma LV
-DVT
-emboli paru
-sindrome Dressler
Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS
Diagnosis
Kerja
SAKIT DADA
Curiga Sindrom Koroner Akut
ECG
Elevasi ST
menetap
Tanpa Elevasi
ST menetap
Biochemistry
Troponin
(CKMB)
Troponin
Stratifikasi
risiko
Normal atau
Tdk dpt ditentukan
ECG
Troponin
2 X negative
Risiko tinggi Risiko rendah
Mungkin bukan SKA
Pengobatan
Pencegahan
sekunder
Esc/EHJ 2002
TERAPI INTERVENSI
PADA SINDROMA
KORONER AKUT
Angioplasty
Keberhasilan Primer
85 - 95 %
Kematian
0.3 - 1.3 %
Infark Miokard
1.6 - 6.3 %
Operasi By-pass darura
1 -7%
Stenosis lebih lanjut

sblm era stent
era stent
Drug eluting stent
: 30 - 40 %
: 15-20%
: almost 0%
Primary PTCA/PCI
Keunggulan: ICH 0%,
Syarat : jumlah tindakan primary PCI>100
kasus/th/operator ;>600/yr/rumah sakit
Mortaliti: reinfark 5 vs 12% untuk TPA; 30 hari
sama dengan TPA; namun pada AMI Anterior
; age>70 pulse >100 angka 2% vs 10% for TPA
Trials: RITA, PAMI (93); MITI (96)
Treatment Delayed is Treatment Denied
Symptom
Recognition
Call to
Medical System
PreHospital
ED
Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy
Cath Lab
Options for Transport of Patients With STEMI and Initial

Reperfusion Treatment
Patients receiving fibrinolysis should be risk-stratified to identify need for

further revascularization with percutaneous coronary intervention (PCI) or
coronary artery bypass graft surgery (CABG).
All patients should receive late hospital care and secondary prevention of
STEMI.
Fibrinolysis
Not
PCI Capable
Noninvasive Risk
Stratification
Rescue
Ischemia
driven
PCI Capable
PCI or CABG
Primary PCI
Late
Hospital Care
and Secondary
Prevention
Chest pain: focus on

acute coronary syndromes
What doctors should know
IDRIS IDHAM
Department of Cardiology and Vascular Medicine
Fakultas of Medicine University of Indonesia
National Cardiovascular Center Harapan Kita
Thank you

Acs Cardiovascular Emergency Jadi

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Acs Cardiovascular Emergency Jadi

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Prof. Dr. dr.

Idris Idham, SpJP (K),

SR Negeri Tabing, Padang, Tahun 1957

Prof. Dr. dr. Idris Idham, SpJP (K),

Hypertensive Crisis : emergency,

FROM PALPITATION TO CVD

Front-line medical practitioners

of Health, RI. 2002.

Acute or escalating chronic chest discomfort is

principles of internal medicine: McGraw-Hill, 2005.

General Clinical Assessment

Determining Working Diagnosis

Based on characteristics, determine the

Determining Working Diagnosis

Anatomy of Thoracic Cavity

I.I. - 09 / PDKI Pekanbaru

Features of Major Causes of

principles of internal medicine: McGraw-Hill, 2005.

Features of Major Causes of

General Approach for First liners

Closely monitor vital signs

Acute Coronary Syndromes

I.I. - 09 / PDKI Pekanbaru

Topol EJ, ed. Textbook of cardiovascular medicine 2007.

From third decade

Growth mainly by lipid accumulation

From fourth decade

Stary HC et al. Circulation 1995;92:1355-1374.

Algorithm in Acute Coronary Syndrome

Risk: high / low

Modified from ESC 2007

Clinical Classification of Angina

Noncardiac chest pain

Angina occurring at rest and

New-onset angina of at least CCS

Previously diagnosed angina that

Algorithm in Acute Coronary Syndrome

Risk: high / low

Modified from ESC 2007

Algorithm in Acute Coronary Syndrome

Risk: high / low

Modified from ESC 2007

Multiple of the AMI cutoff limit

Early release myoglobin of

Cardiac troponin after classical

CK-MB after myocardial infarction

Cardiac troponin after microinfarction

Day after onset of AMI

Algorithm in Acute Coronary Syndrome

Risk: high / low

Modified from ESC 2007

Guideline ACS 2006 National Heart Foundation Australia

Sustained ventricular tachycardia

Guideline ACS 2006 National Heart Foundation Australia

Algorithm in Acute Coronary Syndrome

Risk: high / low

Modified from ESC 2007

Monitor and support ABCs

Caution: hemodynamic instability due to pump

Anticoagulation & Reperfusion

Fibrinolytic Absolute Contraindication

Hemorrhagic stroke, or stroke of unknown origin

I.I. - 09 / PDKI Pekanbaru

Algorithm in Acute Coronary Syndrome