simple guideline for acute coronary syndrome prof bambangirawan
DESCRIPTION
guidelineTRANSCRIPT
Curriculum Vitae. Prof dr Bambanq Irawan FIHA FAsCC FInaSIM
• Internist [ PB PAPDI ] 1981 • Internist Cardiovascular Consultant [ PB PAPDI ] 1996
• Cardiologist and FIHA [ PP PERKI ] 2004• Cardiologist Consultant [ PP PERKI ] 2005
• Profesor in Cardiology [ DIRJEN DIKTI ] 2006
• FAsCC [ Asean Society of Cardiology ] 2008• FinaSIM [ PB PAPDI ] 2009
Bambang Irawan SpPD[K], SpJP[K], FIHA, FInaSIM, FAsCC
Divisi Cardiology Departement of Cardiology
Faculty of Medicine Gadjah Mada University
Simple Guideline for Acute Coronary Syndrome (ACS)
Coronary Heart Disease
Ischemic heart disease : epidemiology
• Annual incidence of angina: 213/100.000 population > 30 years old
• Ischemic heart disease (IHD) is the main cause of death in Europe and USA
• Cardiovascular mortality in patients with chronic stable angina: 1.3-10 %/year
• Chronic stable angina is the initial symptom of IHD
Murray CJL.,ed,Lopez AD. The Global Burden of Disease: a Comprehensive Assessment of Mortality and Disability fromdisease, Injurues and Risk Farctors in 1990 and projected to 2020.Cambridge, Mass:Harvard University Press;1996
Supply-Demand Mismatch
Oxygen Supply -Blood Flow -O2 Carrying Capacity
Oxygen Demand -Heart rate -Contractility -Wall stress
Heart rate
Afterload
wall stress
Heart size
Contractility
Exercise
Spasm
Collaterals
O2 O2Demand Supply Vasoconstriction
Ischemic Oxygen Balance
VS
Hb Level
O2 Content
Coronary blood flow
O2 Saturation
CLINICAL CLASSIFICATION OF CHEST PAIN
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
Diamond GA. J Am Coll Cardiol 1983;1:574
Atypical angina (probable)meets 2 of the above characteristics
Noncardiac chest painmeets <=1 of the typical angina characteristics
CCS Classification
• I : Angina occurring with strenous but not ordinary physical activity
• II : Slight limitation of ordinary physical activity• III : Marked limitation of ordinary physical
activity• IV : Inability to carry on any physical activity
without discomfort, symptoms may be present at rest.
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
Karakteristik Angina pd ACS
• Terlokalisir terutama (tapi tidak selalu) di daerah prekordium
• Menyebar ke lengan, leher, punggung, atau epigastrium
• Tidak berubah dengan posisi atau pergerakan• Sering terasa seperti menekan, “constricting”
atau “crushing”• Episode > 20 menit • Diikuti sesak, pusing, mual, atau berkeringat
Possible presentation of ACS
• Angina at rest, with pain episodes lasting > 20 min
• New onset ( within < 2 months ) exertional angina of at least CCSC III
• Recent increase ( < 2 months ) in anginal severity to at least CCSC III
• Angina post MCI
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
CHARACTER OF
ANGINAL PAIN
• Localized usually at precordium• Radiate to arm, neck, shoulder, back or
epicardium• Feels like being pressed by heavy object, or
constricting or crushing.• Episode > 20 min• Concomitant systemic symptoms: dyspnea,
dizziness, nausea, diaphoresis
The Grip of Angina
Atherosclerosis Timeline
FoamCells
FattyStreak
IntermediateLesion Atheroma
FibrousPlaque
ComplicatedLesion/Rupture
Endothelial DysfunctionFrom first decade From third decade From fourth decade
Growth mainly by lipid accumulation Smooth muscleand collagen
Thrombosis,hematoma
Stary HC, et al. Circulation. 1995;92:1355-74. Artery wall often gets larger with increasing plaque-Glagov NEJM 1987
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
ELEKTROKARDIOGRAMEKG 12 Sandapan Pertama
TENTUKAN:•Irama
•Elevasi SEGMENT ST ?•Depresi SEGMENT ST ?
•LEFT BUNDLE BRANCH BLOCK (BARU)?•T inverted ?
•Gelombang Q ?•NON DIAGNOSTIK atau EKG normal
3
.
• .
Inferior Wall MI
Anterior Wall MI
New LBBB
T inverted
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
SPEKTRUM KLINIS SKA4
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
TIMI Risk Score UA / NSTEMI
Age ≥ 65≥ 3 CAD risk factors(FHx, HTN, ↑ chol, DM, active smoker)
ST deviation ≥ 0.5 mm↑ cardiac markersRecent (≤ 24H) severe angina
HISTORICAL
PRESENTATION
RISK SCORE = Total Points (0 - 7)
Known CAD (stenosis ≥ 50%)ASA use in past 7 days
1
1
11
11
POINTS
0/12345
6/7
RISKSCORE
RISK OF CARDIAC EVENTS (%)BY 14 DAYS IN TIMI 11B*
33571219
DEATH OR MI
DEATH, MI ORURGENT REVASC
5813202641
*Entry criteria:UA or NSTEMI defined as ischemic painat rest within past 24H, with evidence of CAD (ST segmentdeviation or +marker)
1
Low = 0-2 points, Medium = 3-4 pointsHigh = 5-7 points
5
SAKIT DADA
Bio-chemistry
Stratifikasirisiko
Diagnosis
Pengobatan
Curiga Sindrom Koroner Akut
Elevasi STmenetap
ST/T-abnormalities
Normal atauTdk dpt ditentukan ECG
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
STEMI NSTEMI Angina tidak stabil
Reperfusi Invasive Non-Invasive
Troponin (+) Troponin 2 kali negatif
Masuk RS
ECG
Diagnosis kerja
3
Providing relief for the ischemic heart
Reduction ofPreload
Reduction ofafterload
Reduction ofcontractility
Reduction ofHeart rate
Reduction of the oxygen demand
Elevation of oxygen supply
Reduction of the extravasalcoronary resistance
Prolongation of thediastolic interval
Dissolution or Prevention Of Intravasal obstruction
Nitrocompounds
CCBsACE-I B Blockers CCBs
Nitro vasodilatatorsACE-IIn case of HF
B BlockersCCBs
Inhibitor of pleteletAggregationThrombvolytic agents
Symptom Recognition
Call to Medical System
ER Cath LabPreHospital
Delay in Initiation of Reperfusion Therapy
Increasing Loss of Myocytes
Treatment Delayed is Treatment Denied
Immediate Assessment in ER• Vital signs, including blood pressure• Oxygen saturation• IV access• 12-leads ECG < 10 minutes• Brief, targeted history and physical exam (to
identify reperfusion candidates)• Fibrinolytic check list; check contraindications• Obtain initial cardiac markers
Immediate Assessment in ER
• Portable Chest X-ray < 30 min• Assess for the following :
-Heart rate > 100 bpm and SBP < 100 mmHg-Pulmonary edema/rales or-Signs of shock
• If any of these conditions is present, consider triage to a facility capable of cardiac catheterization and revascularization
TERAPI PADA SINDROMA KORONER AKUT PERAWATAN DI RUMAH SAKIT 1. Antiplatelet (Aspirin 160 mg)2. Pain killer (morfin)3. Suplemen O2 4. Terapi anti iskemia
Nitrat5. Antiplatelet dan antikoagulan
Clopidogrel 300 mg, TiclopidineHeparin atau Low Molecular Weight HeparinHirudin
Tranquilizer5. a. STEMI : tentukan segera pilihan revaskularisasi
( Fibrinolitik Vs PCI)b. Non STEMI : segera lakukan stratifikasi risiko
MONA
• Morfin:2.5mg-5 mg IV perlahanHati –hati pada : inferior MCI,asthma, bradikardia
• Pethidin : 12.5-25 mg IV pelan
PAIN KILLER
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
ACC/AHA Guideline of STEMI 2004
ANTI ISKEMIK •NITRAT •B BLOKER (jika tidak ada kontraindikasi)•ANTAGONIS KALSIUM (UAP/NSTEMI)
VASODILATOR •INHIBITOR ACE (EF < 40%, anterior MCI, HF)•NITRAT IV (jika AHF)
ANTITROMBOTIK DAN ANTIKOAGULAN
•Heparin ( Unfractionated Heparin)•Low Molecular Weight Heparin•Anti Xa
DOSIS YANG DIREKOMENDASIKAN
UFH
LMWHEnoxaparineFondaparinux
• 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)
• 1mg/kg, SC , bid (5 hari)• 2,5 cc , satu kali sehari (5 hari)
REVASKULARISASI PADA STEMI < 12 jam
Apa pilihan kita?FIBRINOLITIK
VS PCI
Fibrinolitik lebih dianjurkan jika: ( 3 Point)
1. Presentasi STEMI akut ≤ 3 jam2. Jika presentasi STEMI > 3 jam namun
tindakan PCI tidak bisa dikerjakan atau akan terlambat dikerjakan;
Waktu antara pasien tiba sampai dengan inflasi balon >90 menit
3. Tidak ada kontraindikasi fibrinolitik
Catatan: Fibrinolitik harus dikerjakan dalam waktu < 30 mnt
(Door to Needle time < 30 menit)
PCI primer lebih dianjurkan jika:( 5 Point )
1. Presentasi ≥3 jam2. Presentasi < 3 jam namun terdapat
kontraindikasi fibrinolitik3. Tersedia fasilitas PCI dan waktu kontak
antara pasien tiba sampai dengan inflasi balon <90 menit
4. STEMI akut dengan risiko tinggi ( gagal jantung Killip ≥3 dan syok kardiogenikl)
5. Diagnosis STEMI masih diragukan
STRATIFIKASI RISIKOpada Non-STEMI / UAP
MENENTUKAN STRATEGI TATALAKSANA NON STEMI/UAP
Strategi Invasif (angiografi akan dilakukan
dalam 48 jam)
VS
Strategi Konservatif(angiografi tidak akan
dilakukan/direncanakan elektif)
Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm RV Infarct
Pericarditis
Mechanical Mural Thrombus
Komplikasi awal :
Aritmia Disfungsi LV dan gagal jantungRuptur ventrikel Regurgitasi mitral akut Gagal fungsi RV Syok kardiogenik
Komplikasi lambat :
Trombosis mural dan Emboli sistemikAneurisma LV DVT Emboli paru Sindrome Dressler
How to reduce plaque formationIntervention on risk fact
How to reduce the risk of plaque rupture
KESIMPULAN1. Tatalaksana STEMI dimana tersedia fasilitas PCI
adalah PCI primer. Jika sarana PCI tidak tersedia diberikan trombolitik sesuai indikasi dan kontraindikasi.
2. Tatalaksana NSTEMI meliputi strategi invasif dini dan strategi konservatif sesuai stratifikasi risiko.
3. Klopidogrel direkomendasikan sebagai antiplatelet (klas 1) untuk penanganan ACS baik STEMI maupun UA/NSTEMII dan diberikan bersama ASA. Clopidogrel diberikan tunggal jika terdapat kontraindikasi ASA (ACC-AHA / ESC Guideline).
4. GPIIb-IIIa inhibitor diberikan pada pasien yang menjalani PCI primer.
5. Fondaparinux dan Enoksaparin efektif pada SKA.