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Prof. Dr. dr. Idris Idham, SpJP (K),
FIHA, FACC, FESC, FASCC, FSCAI
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
Education
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.
1Harrison’s 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.
1Harrison’s 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 • ACS: infarct,angina
• MVP
• Aortic Stenosis
• Hypertrophic cardio-
myopathy
• Pericarditis
Lungs • Lung Emboli
• Pneumonia
• Pneumothorax
• Pleuritis
Gastrointestinal •Esophageal reflux •Esophageal rupture •Gall bladder disease •Peptic Ulcer •Pancreatitis
Vascular •Aortic dissection/aneurysm
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
I.I. - ’09 / PDKI Pekanbaru
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.
DEFINITION
PATHOPHYSIOLOGY
Foam Cells
Fatty Streak
Intermediate Lesion Atheroma
Fibrous Plaque
Complicated Lesion/Rupture
Endothelial Dysfunction
Smooth muscle and collagen
From first decade From third decade From fourth decade
Growth mainly by lipid accumulation Thrombosis, hematoma
Stary HC et al. Circulation 1995;92:1355-1374.
Atherosclerosis Timeline
DIAGNOSIS
Presentation (Clinical, Initial ECG)
ST-Seg Elevation Myocardial Infarction
Non-STSeg Elevation Acute Coronary Syndr
ST-Seg Elevation MCI
Non-ST-seg- Elevation MCI
Unstable Angina
Working diagnosis
Time
Evolution of ECG &
Biomarkers
Final diagnosis
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Biomarker (-) Biomarker (+)
I.I. - ’09 / PDKI Pekanbaru
CHEST PAIN Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management, ±
revascularization
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (+)
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 Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (+)
EVOLVING ECG
A. Normal ECG
B. Tall or peaked T waves
C. ST ↑
D. & E. ST ↑ with inverted T
waves
F. Abnormal Q
ECG pattern
• Ischemia : ST ↓, tall T, inverted T
• Injury : ST ↑
• Infarction : pathologic Q
CHEST PAIN Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management, ±
revascularization
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (±)
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)
0 1 2 3 4 5 6 7 8
50
20
10
5
2
1
Early release myoglobin of CKMB isoform
Cardiac troponin after “classical” myocardial infarction
CK-MB after myocardial infarction
Cardiac troponin after “microinfarction”
Mu
ltip
le o
f th
e A
MI c
uto
ff li
mit
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
Biomarkers
CHEST PAIN Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (±)
I.I. - ’09 / PDKI Pekanbaru
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
CHEST PAIN Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management, ±
reperfusion
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (±)
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
I.I. - ’09 / PDKI Pekanbaru
CHEST PAIN Admission
Working diagnosis
Bio- chemistry
Risk Stratification
Management
Secondary prevention
Suspected ACS
Persistent ST elevation
No persistent ST elevation
Troponin, CKMB (+)
Risk: high / low
Algorithm in Acute Coronary Syndrome
Modified from ESC 2007
- ACS unlikely - NSTEMI - STEMI
ECG
Initial management,
±revascularization
Medical therapy,
coronary angiography
Perform
ed in 10 min
{on serial ECG}
Troponin, CKMB (±)
A Aspirin and Anticoagulants B Beta blockers and Blood Pressure C Cholesterol and Cigarettes D Diet and Diabetes E Education and Exercise F Fun and Faith
Secondary Prevention Strategy
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
I.I. - ’09 / PDKI Pekanbaru
ANTIPLATELET
•ASPIRIN •CLOPIDOGREL •TICLOPIDINE
•Gp IIb / IIIa inhibitor
I.I. - ’09 / PDKI Pekanbaru
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)
I.I. - ’09 / PDKI Pekanbaru
Adenosine Diphosphate Inhibitors
• ADP disekresi oleh platelet (aktivasi dan agregasi platelet)
• P2T cell surface receptors
• Ticlodipine
• Clopidogrel
• Efek samping : Neutropenia, trombositopenia
I.I. - ’09 / PDKI Pekanbaru
COX (cyclo-oxygenase) ADP (adenosine diphosphate) TXA2 (thromboxane A2)
CLOPIDOGREL
ASA COX
ADP
ADP
C
GPllb/llla (Fibrinogen receptor)
Collagen thrombin
TXA 2
Activation
TXA 2
ASA
Synergistic Mode of Action with Clopidogrel and ASA1
1. Schafer AI. Am J Med 1996; 101: 199–209.
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
Anti Ischemia
•NITRAT
•B BLOKER
•ANTAGONIS KALSIUM
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
Beta-bloker
Metoprolol IV
Metoprolol oral
Atenolol oral
Propranolol oral
Bisoprolol oral
Carvedilol 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
I.I. - ’09 / PDKI Pekanbaru
Antagonis kalsium
• Pd UAP atau NSTEMI bila ada indikasi kontra B-bloker
• Tidak ada bukti manfaatnya pada pencegahan infark miokard.
• Memberikan hasil yang baik dalam jangka pendek pada episode iskemik.
I.I. - ’09 / PDKI Pekanbaru
Antagonis kalsium
Diltiazem
Verapamil
Lepas cepat :30 -120 mg 3x/hr
Lepas lambat: 100-360 mg 1x/hr
Lepas cepat : 40 – 160 mg/hr
Lepas lambat: 120-480 mg 1x/hr
I.I. - ’09 / PDKI Pekanbaru
•Morfin: 2.5mg-5 mg IV pelan. Hati –hati pada : inferior MCI, asthma , bradikardia •Pethidin : 12.5-25 mg IV pelan
PAIN KILLER
I.I. - ’09 / PDKI Pekanbaru
ANTITROMBOTIK DAN ANTIKOAGULAN
•Heparin ( Unfractionated Heparin)
•Low Molecular Weight Heparin
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
Low Molecular Weight Heparin
• Depolimerasi dari UFH standar dengan berat molekul lebih kecil dari pada UFH
• SQ injections/ 90% bio-available/predictable
• Anti-Xa: Anti-thrombin 2-4:1
• FDA menyetujui pemakaian enoxaparin/ dalteparin untuk SKA
I.I. - ’09 / PDKI Pekanbaru
UFH
LMWH
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
TEHNIK INJEKSI LMWH SUBKUTAN
I.I. - ’09 / PDKI Pekanbaru
DOSIS YANG DIREKOMENDASIKAN
UFH
LMWH
Enoxaparine
Nadroparine
Fondaparinux
• 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
• 0,1 ml/10 kg , SC , bid
• 2.5 mg
I.I. - ’09 / PDKI Pekanbaru
6/12/2011
Definite ACS with continuing ischemia or other high-risk
features or planned PCI
Aspirin†
+ IV heparin/SC LMWH‡
+ IV GP IIb/IIIa antagonist
Possible ACS
Aspirin†
Likely/Definite ACS
Aspirin†
+ SC LMWH
or IV heparin
ACC/AHA 2007 Guidelines Update for UA and NSTEMI1
+ Clopidogrel + Clopidogrel
*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
Class I Recommendations for Antithrombotic Therapy*
1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA) Guidelines, USA: ACC/AHA; 2007. I.I. - ’09 / PDKI Pekanbaru
OBAT-OBATAN LAINNYA
• Tranquilizer e,g diazepam 5mg bid
• Stool softener
I.I. - ’09 / PDKI Pekanbaru
TERAPI FIBRINOLITIK
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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
Fibrinolitik :indikasi kontra relatif
ACC/AHA guideline of STEMI 2004 I.I. - ’09 / PDKI Pekanbaru
Perbandingan terapi trombolitik dengan terapi standar pada IMA
Mulai trombolisis Tambahan Jiwa yg diselamatkan per 1000 pasien yg diobati ------------------------------------------------------------------- •Pd jam pertama 65 •Pd jam kedua 37 •Pd jam ketiga 29 •Antara jam ke 3-6 26 •Antara jam 6-12 18 •Antara jam 12-24 9
I.I. - ’09 / PDKI Pekanbaru
AGEN FIBRINOLITIK
• Streptokinase (SK)
• Actylase (tPA)
• Reteplase (r-PA)
• Tenecteplase (TNK-tPA)
I.I. - ’09 / PDKI Pekanbaru
Plasminogen Activators (t-PA, u-PA)
Skema sistem fibrinolitik
Plasminogen Plasmin
α2-Antiplasmin
Fibrin Fibrin degradation Product
Plasminogen Activator Inhibitors (PA1, PA2, TAFI)
Braunwald, A Textbook of Cardiovascular Medicine. 6th ed I.I. - ’09 / PDKI Pekanbaru
SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
• Streptokinase
• Actylase (tPA)
• Reteplase(r-PA)
• Tenecteplase
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
I.I. - ’09 / PDKI Pekanbaru
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
I.I. - ’09 / PDKI Pekanbaru
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)
I.I. - ’09 / PDKI Pekanbaru
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)
I.I. - ’09 / PDKI Pekanbaru
Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm RV Infarct
Pericarditis
Mechanical Mural Thrombus
I.I. - ’09 / PDKI Pekanbaru
• Komplikasi awal :
-aritmia
-disfungsi LV dan gagal jantung
-ruptur ventrikel
-regurgitasi mitral akut
-gagal fungsi RV
-syok kardiogenik
I.I. - ’09 / PDKI Pekanbaru
• Komplikasi akhir :
-trombosis mural dan emboli sistemik
-aneurisma LV
-DVT
-emboli paru
-sindrome Dressler
I.I. - ’09 / PDKI Pekanbaru
SAKIT DADA Masuk RS
Diagnosis Kerja
ECG
Bio- chemistry
Stratifikasi risiko
Pengobatan
Pencegahan sekunder
Curiga Sindrom Koroner Akut
Elevasi ST menetap
Tanpa Elevasi ST menetap
Normal atau Tdk dpt ditentukan
Troponin (CKMB)
Troponin ECG Troponin
2 X negative
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
Esc/EHJ 2002
Mungkin bukan SKA
I.I. - ’09 / PDKI Pekanbaru
TERAPI INTERVENSI PADA SINDROMA KORONER AKUT
I.I. - ’09 / PDKI Pekanbaru
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 : 30 - 40 %
era stent : 15-20%
Drug eluting stent : almost 0% I.I. - ’09 / PDKI Pekanbaru
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)
I.I. - ’09 / PDKI Pekanbaru
I.I. - ’09 / PDKI Pekanbaru
Symptom Recognition
Call to Medical System
ED Cath Lab PreHospital
Delay in Initiation of Reperfusion Therapy
Increasing Loss of Myocytes
Treatment Delayed is Treatment Denied
I.I. - ’09 / PDKI Pekanbaru
• 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
Primary PCI
Noninvasive Risk Stratification
Late Hospital Care
and Secondary Prevention
PCI or CABG
Not PCI Capable
PCI Capable
Rescue Ischemia driven
Options for Transport of Patients With STEMI and Initial Reperfusion Treatment
I.I. - ’09 / PDKI Pekanbaru
I.I. - ’09 / PDKI Pekanbaru
Chest pain: focus on
acute coronary syndromes
What doctor’s should know
IDRIS IDHAM
Department of Cardiology and Vascular Medicine Fakultas of Medicine University of Indonesia
National Cardiovascular Center Harapan Kita I.I. - ’09 / PDKI Pekanbaru
Thank you
I.I. - ’09 / PDKI Pekanbaru