Acs Cardiovascular Emergency Jadi

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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.

    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 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

  • 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

  • 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 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: 199209.

    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

    2-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

  • 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 doctors 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