MINICOURSE ON ACUTE CORONARY SYNDROME ( Sindrom Koroner Akut )

TUJUAN KURSUS
Selesai kursus diharapkan peserta: Lebih mengerti ttg patofisiologi dan mekanisme SKA Bisa menegakkan diagnosis SKA dengan : -Membedakan simptom SKA dari sakit dada lain -Mengerti beberapa gambaran EKG pada SKA -Mengerti tentang beberapa petanda iskemia akut Mengerti peran, manfaat, dan penggunaan beberapa obat yang digunakan pd SKA: fibrinolitik, antitrombotik. antiskemik,dan obat-obat penunjang

Bisa merencanakan tatalaksana dini SKA dan rencana lanjutannya dg menggunakan algoritme
Kemampuan ini akan memungkinkan dokter peserta membantu peran dokter Sp Jantung dan P.Darah dlm menangani SKA

Psn Nyeri Dada Rwyat nyeri dada khas

SINDROM KORONER AKUT

Aspirin 300 mg dikunyah dan Nitrat s.l.

* EKG 12 sandapan Petanda biokimia

EKG Non diagnostik Petanda biokimia (-) Nyeri dada (-) Perubahan ST/T Petanda biokimia (+) Nyeri dada menetap

Elevasi seg ST

EKG tdk berubah Petanda(-) Nyeri dada(-) Pulang

Risiko rendah Risko tinggi Periksa di Periksa Rawat jalan segera

Observasi EKG serial Ulang petanda 6-12 jam stlh

onset nyeri dada* Perubahan seg ST Petanda (+) Nyeri dada menetap

Evaluasi utk reperfusi

Rawat Terapi Nitrat ASA Clopidogrel UFH/LMWH (+/- Antagonis Receptor GPIIb/IIIa

APTS/NSTEMI

DEFINISI DAN PATOFISIOLOGI SINDROM KORONER AKUT

SINDROM KORONER AKUT Merujuk pd sekumpulan keluhan dan tanda klinis yang sesuai dengan iskemia miokard akut Mencakup Infark miokard akut ( dgn elevasi /depresi segmen ST , gelombang-Q dan non gel Q) dan angina tidak stabil ( UAP)

Sindrom Koroner Akut

Tanpa elevasi ST NSTEMI Elevasi ST

Angina Tdk Stabil

Infark Miokard Akut NQMI Qw MI

Kursus SKA k

Angina Stabil Angina Tidak stabil Infark Miokard Akut Gagal Jantung

Kematian

Atherogenesis and Atherothrombosis: A Progressive Process

Normal Fatty Streak Fibrous Plaque Atherosclerotic Plaque Plaque Rupture/ Fissure & Thrombosis

Myocardial Infarction Ischemic Stroke Critical Leg Ischemia

Clinically Silent

Angina Transient Ischemic Attack Claudication/PAD

Cardiovascular Death

Increasing Age
3

Acute Coronary Syndrome (ACS) is a Classic Manifestation of Atherothrombosis

Unstable angina Non-Q-W MI Q-W MI Stroke PAD

Common underlying atherothrombosis

Plaque rupture

Platelet activation and aggregation

Thrombus formation

Atherothrombotic event
(MI, stroke, vascular death)

PATOFISIOLOGI

Stable Plaque

Unstable Plaque

Disrupted Plaque

Braunwald E et al. J Am Coll Cardiol 2000;36:9701062.

Kursus SKA

Coronary Artery Disease : Acute Manifestation of Atherothrombosis

Angiogram of the left coronary artery and its branches

Faxon (1996) 1998 McGraw-Hill. All rights reserved.

Faktor resiko Aterosklerosis

faktor genetik/riwayat keluarga kandung merokok dislipidemia hipertensi diabetes obesitas usia Dll. *Pernah infark miokard dan/atau stroke

PATOFISIOLOGI

Stable Plaque

Unstable Plaque

Disrupted Plaque

Braunwald E et al. J Am Coll Cardiol 2000;36:9701062.

Kursus SKA

Patofisiologi
Seiring waktu, plak membesar, komponen lipid dan seluler bertambah secara progresif sampai menghambat pembuluh darah. Sewaktu obstruksi mencapai 75 %, timbullah angina stabil (stable angina ). Dulu dianggap :semakin sempit semakin berberbahaya. Sekarang : semakin tidak stabil plak, semakin mudah pecah, semakin berbahaya
Kursus SKA

Jika aliran menurun dengan cepat akibat sumbatan (obstruksi) seperti pada:
aterosklerosis vasokonstriksi bekuan darah konstriksi (spasme)

Suplai O2 menurun tidak dapat memenuhi demand

Setelah lewat suatu batas waktu, jaringan iskemik akan mati (nekrosis), dan akhirnya digantikan oleh jaringan parut yang

non-fungsional

Infark Miokard

Kursus SKA

Infark miokard non gelombang Q (NQwMI)

NQwMI sama seperti U.A., disebabkan oleh obstruksi akibat ruptur plak; namun oklusi yang terjadi lebih besar, mungkin disebabkan perlukaan yang lebih luas pada permukaan plak. NQMI ditandai dengan kerusakan jaringan
ireversibel yang terlokalisir.

Unstable Angina manifestation of temporary occlusion of the coronary artery (less than 20 minutes) Non Q myocardial infarction manifestation of longer occlusion (20 minutes to 2 hours) ST elevation /Q wave MCI manifestation of occlusion more than 2 hours

Unstable coronary artery disease

Thrombus forms and extends into the lumen

Thrombus

Lipid core

Adventitia

Infark Miokard (Q Wave Myocardial

Infarction dengan elevasi segmen ST)
Pecahnya plak diikuti trombosis berlebihan, dengan akibat oklusi total. IMA menyebabkan oklusi arteri koroner secara tiba-tiba, bukan bertahap Oklusi total arteri koroner menyebabkan iskemia yang dapat menyebabkan kematian jaringan jantung. Kebanyakan kematian sel terjadi pada 6 jam pertama setelah onset gejala. Insidens trombosis oklusi koroner, ditentukan dengan angiografi selama 4 jam pertama setelah onset gejala sebesar 87 %.

Untuk melindungi jaringan miokardium: LISIS

ANGINA PEKTORIS

INFARK MIOKARD

Pathway to Thrombosis

DIAGNOSIS SINDROM KORONER AKUT

Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS Diagnosis Kerja ECG Biochemistry Stratifikasi risiko Pengobatan Pencegahan sekunder Esc/EHJ 2002 SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap Troponin CK/CKMB Tanpa Elevasi ST menetap Troponin Normal atau Tdk dpt ditentukan ECG Troponin 2 X negative
Mungkin bukan SKA

Risiko tinggi Risiko rendah

*INITIAL ASSESMENT
1.ANAMNESIS/Targeted history Chest pain / history of chest pain/

angina pectoris
Risk factors Other disease ( concomitant disease ) Medications

2.VITAL SIGNS & Focused PHYSICAL EXAMINATION 3. ELECTROCARDIOGRAM : 12 Leads

*BIOCHEMICAL MARKERS *Chest X-Ray

Keluhan :SAKIT DADA/ANGINA PECTORIS

Sifat & kualitas Lokasi Penjalaran Lama Keluhan dan Gejala penyerta
Anamesis harus terarah
Kursus SKA

Angina:
Gejala angina dapat dibedakan dari nyeri non jantung atau nyeri kardiogenik lain, berdasarkan anamnesis, dan k/p ditunjang pemeriksaan fisik EKG,dan laboratorium. Berkaitan dengan kejadian iskemia pada otot jantung
Kursus SKA

Angina Pectoris Stabil

ANGINA STABIL, ditandai nyeri dada atau rasa tidak enak sewaktu adanya beban (aktivitas, beban mental) dimana kebutuhan miokardium tidak dapat dipenuhi dengan suplai yang cukup. Angina Stabil dapat diprediksi dan dapat hilang atau berkurang dengan istirahat dan nitrogliserin.

Kursus SKA

KELUHAN UTAMA SINDROM KORONER AKUT Sakit dada atau nyeri hulu hati yang berat, asalnya non-traumatik, dengan ciri-ciri tipikal iskemia miokard atau infark: Dada bgn tengah/substernal rasa tertekan atau sakit seperti diremas Rasa sesak, berat/tertimpa beban , mencengkeram, terbakar,sakit sakit perut yg tdk dpt dijelaskan, sendawa, nyeri hulu hati Penjalaran ke leher, rahang, bahu, punggung atau 1 atau ke 2 lengan Disertai sesak Disertai mual dan/atau muntah Disertai berkeringat

Stat ECG

DIAGNOSIS DIFERENSIAL SAKIT DADA

Cardiac
ACS : Infarct,angina MVP Aortic Stenosis Hypertrophic cardiomyopathy Pericarditis

Gastrointestinal
Reflux esofagus Ruptur esofagus Gall bladder disease Peptic Ulcer Pancreatitis

Lungs
Lung Emboli Pnemonia Pneumothorax Pleuritis

Vascular
Aortic dissection/aneurysma

Others
Musculoskeletal Herpes zoster

SAKIT DADA KARDIAK: Tidak dipengaruhi pernapasan atau batuk Tidak dipengaruhi posisi tubuh atau gerakan Tidak ada kaitan dengan kondisi lain seperti herpes zoster, trauma, etc

Angina Tidak Stabil & Infark Miokard Non Q

3 Kemungkinan penampilan: Nyeri/angina wkt istirahat ( biasanya terus > 20 minutes) Angina baru-New Onset (<2 bulan). angina waktu aktifitas-derajat Class III dari Canadian Cardiovascular Society Classification (CCSC) Atau Angina baru yang meningkat-accelerated angina (<2 months) yang ditunjukkan dgn peningkatan keparahan sekrg2nya 1 Kelas CCSC, minimal sampai Kelas III CCSC.

CONTOH CONTOH
Seorang pria 54 thn datang ke IGD dengan keluhan: sakit dada bagian tengah menjalar ke punggung sejak dua setengah jam yang lalu, saat bekerja di kantor. Berulang tetapi semakin sering Seorang pria 55 tahun datang di IGD dengan keluhan: merasa sesak tadi pagi waktu subuh ( 4 jam smrs ).Lama nya k.l 10 menit.Hilang, tetapi sejak 45 menit yg lalu timbul kembali dan terasa seperti ditimpa beban berat Badan berkeringat dan lemas. Seorang wanita 60 tahun mengeluh dada terasa berat sejak kemarin,lalu dikerik karena dikiran masuk angin, tetapi sakit tidak hilang,malahan terasa menjalar ke punggung dan ke bahu kiri.

*PENILAIAN AWAL
1.ANAMNESIS ( yang terarah) Nyeri dada ariwayat nyeri dada

angina pectoris
Faktor risiko Penyakti penyerta lain Obat-obat

2.TANDA VITAL & Pemeriksaan Fisik Terfokus 3. ELEKTROCARDIOGRAM : 12 sandapan

*Petanda Biokimia
*Chest X-Ray

Pemeriksaan Fisik
Tanda Vital Untuk menelaah kelainan lain Menentukan Klasifikasi Killip pd AMI
Kelas I : Tidak ada disfungsi VK, Mortalitas di RS 8% Kelas II: Gallop S3 dan/atau kongesti paru ringan-sedang.Mortalitas di RS 30% Kelas III:Edema paru akut. Mortalitas di RS 40% Kelas IV: shock; SBP<90, ronki diseluruh lapangan paru. Mortalitas 80-90%

ELECTROKARDIOGRAM
EKG 12 Sandapan Pertama

Dalam 10 menit !!
Tentukan: Irama Elevasi SEGMENT ST ? Depresi SEGMENT ST ? BUNDLE BRANCH BLOCK (BARU )? Gelombang Q ? NON DIAGNOSTIC or NORMAL ECG

LOKASI ISKEMIA BERDASARKAN PERUBAHAN DI SANDAPAN EKG

SANDAPAN
II

LOKASI ISKEMIA / INFARK Inferior Anteroseptal Anterior Anterior ekstensif Lateral Apikal Posterior Ventrikel kanan

,III, aVF V1,V2,V3 V1-V4 V1- V6 I,aVL ,V5,V6 I, V6 V7-V9 V4R

Rekomendasi
Pada pasien yg dicurigai penyakit jantung iskemik akut 1. Harus diperiksa Troponin T atau I waktu masuk dan ,bila normal, diulangi 6-12 jam lagi 2. Mioglobin dan/atau CKMB mass boleh diperiksa pada pasien keluhan yang baru ( < 6 jam ) sebagai petanda dini infark miokard akut dan pada pasien dengan iskemia berulang setelah 2 minggu infark untuk mendeteksi infark yg lebih lanjut Level of evidence : A

ESC/ EHJ 2002

Creatinine Phosphokinase
Positif 4-12 jam Iso forms CK-MB1 dan CK-MB 2 CK-MB1/CK-MB 2

Troponin T and I
Tropomyosin complex Microinfarction Pertama terdeteksi dlm 2-4 jam Nilai Prognostik Cut-off point TnT 0.01 ng/ml

Chest X-Ray
Hanya sebagai alat bantu Tidak menentukan pada fase awal Hasil memerlukan waktu

STRATIFIKASI RISIKO

TIMI Risk Score for UA / NSTEMI

HISTORICAL Age 65 3 CAD risk factors
POINTS 1 1 1
RISK OF CARDIAC EVENTS (%) BY 14 DAYS IN TIMI 11B*
RISK SCORE DEATH OR MI DEATH, MI OR URGENT REVASC

(FHx, HTN, chol, DM, active smoker)

Known CAD (stenosis 50%) 1 ASA use in past 7 days PRESENTATION Recent ( 24H) severe angina 1 cardiac markers 1 ST deviation 0.5 mm 1 RISK SCORE = Total Points (0 - 7)
Low = 0-2 points, Medium = 3-4 points High = 5-7 points
Antman et al JAMA 2000; 284: 835 - 842

0/1 2 3 4 5 6/7

3 3 5 7 12 19

5 8 13 20 26 41

*Entry criteria:UA or NSTEMI defined as ischemic pain at rest within past 24H, with evidence of CAD (ST segment deviation or +marker)

RISIKO TINGGI
Sekurang-kurangnya 1 dari berikut hasus ada: 1. Anamnesis Simtom nyeri dada iskemik meningkat cepat dalam 46 jam terakhir Prolonged rest pain (berlangsung >20 min) 2. Temuan klinis Tanda edema paru S3 atau rhonki baru / bertambah Hypotensi,bradikardia,takicardia Usia > 75 yrs 3. ECG Angina waktu istirahat dgn perubahan transien segm ST >0.05 mV,BBB (baru a diperkirakan baru ),Sustained VT 4. Cardiac markers : kenaikanTnT or TnI >0.1ng/ml

Treatment /Pengobatan

Mengapa SKA harus diobati?

Dalam 2 minggu setelah diagnosa, Infark
miokard terjadi pada 12% pasien dengan U.A. Pada U.A risiko menjadi infark miokard atau kematian mencapai 20% dalam 30 hari f.u. Dalam SATU tahun hampir setengah kematian terjadi pada 4 minggu pertama setelah diagnosa. Setidaknya 250.000 kematian sehubungan infark miokard terjadi dalam 1 jam setelah onset gejala dan sebelum terapi dimulai

Psn Nyeri Dada Rwyat nyeri dada khas

SINDROM KORONER AKUT

Aspirin 300 mg dikunyah dan Nitrat s.l.

* EKG 12 sandapan Petanda biokimia

EKG Non diagnostik Petanda biokimia (-) Nyeri dada (-) Perubahan ST/T Petanda biokimia (+) Nyeri dada menetap

Elevasi seg ST

EKG tdk berubah Petanda(-) Nyeri dada(-) Pulang

Risiko rendah Risko tinggi Periksa di Periksa Rawat jalan segera

Observasi EKG serial Ulang petanda 6-12 jam stlh

onset nyeri dada* Perubahan seg ST Petanda (+) Nyeri dada menetap

Evaluasi utk reperfusi

Rawat Terapi Nitrat ASA Clopidogrel UFH/LMWH (+/- Antagonis Receptor GPIIb/IIIa

APTS/NSTEMI

TREATMENT OF ACUTE CORONARY SYNDROMES HOPITALIZATION 1. Anti ischemic Therapy Nitrates Beta Blockers CCB* Pain killer Tranquilizer 2. Antiplatelet and anticoagulation Aspirin,Ticlopidine, Clopidogrel Heparin Low Molecular Weight Heparin Hirudin 3.Fibrinolytics** 4. Coronary Revascularization POST HOSPITAL CARE

Recommendation for anti ischemic therapy

Class I 1. Bed rest, continuous ECG monitoring ( C ) 2. NTG s.l. or spray followed by IV adm. ( C ) 3. Oxygen ( C) 4. Morphine sulphate IV if symptoms not relieved by NTG (C) 5. Beta blocker,if there is ongoing chest pain (( B) 6. Calcium Channel blocker if BB if contraindicated (B) 7. ACE inhibitor when hypertension persists despite treatment with NTG and a BB in pts with LV systolic dysfunction or CHF and in Pts with diabetes (B) Class IIa 1. Oral long acting CCB for recurrent ischemia in the absence of contra indication and when BB and nitrates are fully used (C) 2. An ACI for all post ACS patients ( level evidence B ) 3. IABP for severe ischemia that is continuing or recurs frequently despite intensive medical Tx or for hemodynamically instabibility in pts before or after coronary angiography ACC Task Force 2002

Level of evidence of the different therapeutic options

Treatment Early benefit Early benefit Sustained Additional long reduction prevention effects of term reduction ischemia MI, death early benefit death,MI A C B A C A C B B A A B A A B B A A A A B A A A* C B

Beta blocker Nitrates Calcium antagonists Aspirin GPIIb/IIIa blockers Unfractionated heparin Low mol.weight heparin Specific anti-thrombins Revascularization

Eur Heart J 2000; 21, 1406-1432

Aspirin
Benefits: decrease 50% reinfarction @ 30dys; two-year mortality 20% reduction Doses 81-325 mg P.O. Trials: ISIS (88), Antiplatelet Trialist Group (94), HART (90)

Aspirin kunyah 160-325 mg segera diberikan meskipun belum ada hasil EKG (non coated/slow released)

Clopidogrel
Diberikan bila ada riwayat intoleransi terhadap aspirin

Synergistic Mode of Action with Clopidogrel and ASA1

CLOPIDOGREL

ADP ADP

GPllb/llla
(Fibrinogen receptor)

Activation

Collagen thrombin TXA2

ASA ASA

COX

TXA2 COX (cyclo-oxygenase) ADP (adenosine diphosphate) TXA2 (thromboxane A2)

1. Schafer AI. Am J Med 1996; 101: 199209.

Adenosine Diphosphate Inhibitors

ADP secreted by platelets (activates/aggregates platelets) P2T cell surface receptors Ticlid (ticlodipine) versus ASA Plavix (clopidogrel) CAPRIE trial Neutropenia, thrombocytopenia

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

Beta-blocker
Effektif untuk pengobatan simtomatik dan pencegahan infark miokard. Vasokonstriktor moderat
Dipilih obat yang kardio-selektif

Berhubungan dengan nitrat.

Kontraindikasi pada pada jenis angina vasospastik IV betablocker : metoprolol

Nitrates
Benefits: In AWMI, persistent ischemia, CHF, hypertension Complications: IWMI with RV extension Mortality: May improve coronary perfusion Trials: GISSI-3 (94), ACC/AHA (96)

Nitrat
Vasodilator Mengurangi konsumsi Oksigen dan menurunkan jumlah episode iskemik. Digunakan secara luas Pemberian per IV
1mg /jam Disesuaikan dengan gejala klinis dan EKG Nitrate sublingual

Calcium channel blocker

Tidak ada bukti manfaatnya pada pencegahan infark miokard.

Memberikan hasil yang baik dalam jangka pendek pada episode iskemik. Diltiazem pada infark non-Q Pd UAP bila indikasi kontra b blocker

Heparin (UFH)
Inhibits AT III (anti-thrombin III) Cannot inhibit clot bound thrombin No effect on Factor Xa Hospitalization/ PTT/ bleeding Benefit in UA/ rebound effect Anti-Xa: Anti-thrombin 1:1

HEPARIN:Mechanism of Action
Both UH and LMWH exert their anticoagulation activity by catalyzing antithrombin (AT or AT III) catalyzed AT is accelerated in its inactivation of the coagulation enzymes thrombin (factor IIa) and factor Xa. prolongs aPTT

DOSAGE UNFRACTIONATED HEPARIN

I.V BOLUS 60 UI/Kg max 4000 UI Drip/infusion : 12 UI/hour first 24-48 hrs max 1000 UI/hour = 12.000 UI/12 hours Monitor APTT : 3, 6, 12, 24 hours after start of treatment Target APTT 50-70 msec (1 1/2-2X kontrol )

Low Molecular Weight Heparin

Dissociate bleeding/ anti-thrombotic Smaller/ fractionated SC injections/ 90% bioavailable/predictable Anti-Xa: Anti-thrombin 2-4:1 FDA approved enoxaparin/ dalteparin for ACS

Enoxaparin for UA and non-Q MI

DOSAGE DURATION For the prevention of 1 mg/kg q12h SC minimum 2 days; usual duration ischemic complications with oral aspirin therapy of therapy: 2 to 8 days of unstable angina and (100 to 325 mg once daily) non-Q-wave myocardial infarction (MI) when concurrently administered with aspirin

4/00

MedSlides.com

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Advantages of LMWH over UH

Less inhibition of platelet function
potentially less bleeding risk, but not shown in clinical use

Lower incidence of thrombocytopenia and thrombosis (HIT syndrome)

less interaction with platelet factor 4 fewer heparin-dependent IgG antibodies

Advantages of LMWH over UH

Decreased heparin resistance
pharmacokinetics of UH are influenced by its bindings to plasma protein, endothelial cell surfaces, macrophages, and other acute phase reactants LMWH has decreased binding to nonanticoagulant-related plasma proteins

TEHNIK INJEKSI LOVENOX SUBKUTAN

Contoh instruksi dokter pd waktu masuk perawatan ACS

Rawat tirah baring NPO/Puasa 8 jam D5W as net Obat-obat: 1.Aspirin dst 2.Nitrat dst 3.Beta blocker/CCB 4.Heparin dst 5.Diazepam dst 6.Laksans dst ECG diulang 12 jam Ro Foto torak Lab : CKMB, Troponin Rutin : panel lipid, GD, panel renal ,electrolyte

ACC/AHA 2002 Guidelines Update for UA and NSTEMI1

Class I Recommendations for Antithrombotic Therapy*
Definite ACS with continuing ischemia or other high-risk features or planned PCI

Possible ACS

Likely/Definite ACS

Aspirin

Aspirin

+
SC LMWH or IV heparin

Aspirin + IV heparin/SC LMWH + IV GP IIb/IIIa antagonist

+ Clopidogrel
*During

+ Clopidogrel

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

3/27/2013

1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA) Guidelines, USA: ACC/AHA; 2002.

Psn Nyeri Dada Rwyat nyeri dada khas

SINDROM KORONER AKUT

Aspirin 300 mg dikunyah dan Nitrat s.l.

* EKG 12 sandapan Petanda biokimia

EKG Non diagnostik Petanda biokimia (-) Nyeri dada (-) Perubahan ST/T Petanda biokimia (+) Nyeri dada menetap

Elevasi seg ST

EKG tdk berubah Petanda(-) Nyeri dada(-) Pulang

Risiko rendah Risko tinggi Periksa di Periksa Rawat jalan segera

Observasi EKG serial Ulang petanda 6-12 jam stlh

onset nyeri dada* Perubahan seg ST Petanda (+) Nyeri dada menetap

Evaluasi utk reperfusi

Rawat Terapi Nitrat ASA Clopidogrel UFH/LMWH (+/- Antagonis Receptor GPIIb/IIIa

APTS/NSTEMI

PADA STEMI INFARK MIOKARD ELEVASI SEGMEN ST

FIBRINOLITIK / TROMBOLISIS : 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 ) Trombolisis door to needle time < 30 menit !! PCI pada IMA lebih unggul bila dpt dilakukan dlm 90 30 menit

FIBRINOLITIK/TROMBOLISIS: Contra Indication Previous hemorrhagic stroke at any time Other strokes or cerebrovascular events in the preceeding 1 yr Known intracranial neoplasm Active internal bleeding is present ( does not include menses ) Aortic dissection is suspected

TROMBOLISIS: Warnings/Relative C.I.

Consider risks vs benefits
Severe uncontrolled Hypertension on presentation BP> 180 / 110 mmHg Prior Hx of CVA or known intracerebral pathology Taking oral anticoagulant in therapeutic dose ( INR > 2-3 ) or known bleeding diathesis Recent trauma including head trauma in the preceding 2-4 weeks or prolonged CPR ( > 10 minutes) or major surgery in the preceding 2-4 weeks For Streptokinase : prior exposure ( 5 days-2 yrs ) or prior allergic reactions Pregnancy Active peptic ulcer History of chronic severe hypertension

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

FIBRINOLITIK
Streptokinase (SK) Actylase (tPA) Reteplase (r-PA) Tenecteplase (TNK-tPA)

CARA PEMBERIAN FIBRINOLITIK

Streptokinase ( Streptase ) 1.5 million Unit in 100 ml D5W or 0.9% saline over 30-60 minute without heparin : Inferior MCI with heparin : anterior MCI tPA 15 mg IV bolus then 0.75 mg/Kg over 30 min,then 0.5 mg/Kg ovr 60 minutes

Streptokinase (SK, Streptase)

Manfaat: untuk semua lokasi STEMI, usia <75; simptom < 6jam ( bisa <12 jam); relatif lbh murah Komplikasi: antigenik, Perdarahan Intra serebral
(GUSTO study 0.6%) Trials: GISSI-1, ISIS-2 (88)

TPA Alteplase, RT-PA

Manfaat : clot specific, Baik pada STEMI Anterior Komplikasi: perdarahan intraserebral 1% Harga: lebih mahal dari SK
Trials: ASSENT, GUSTO (93) TIMI-IIIB (94)

PAIN KILLER Morphin : 2 mg- 4 mg slow IV. Precaution : inferior MCI, asthma , bradycardia Pethidin : 12.5-25 mg slow I.V

OBAT Lain
Tranquilizer e,g diazepam 5mg bid Pelunak tinja

Miscellaneous
Magnesium- no benefit ISIS-4 ACE Inhibitors- benefit ISIS-4 Calcium Channel blockers- causes harm ( Diltiazem in Non-Q MI )

Contoh instruksi dokter pd waktu msk perawatan IMA anterior

Rawat tirah baring NPO/Puasa 8 jam D5W as net Obat-obat: 1.Aspirin 250 mg dikunyah,selanjutnya 160mg/hari 2.Streptokinase 1.5 juta Unit dalam 60 menit ss protokol 2.ISDN 5 mg s.l dst 3.Heparin sesuai protokol ,dst 4.Diazepam tab 5 mg bid 5.Laksans bid ECG serial Ro Foto torak Lab : CKMB serial , Troponin rutin : panel lipid, GD, panel renal ,electrolyte

Pra Rumah Sakit (oleh personil yg sudah dilatih )

Aspirin 160mg P.O. kunyah Oxygen 2-6L/min Baring, pasang IV line Pain killer ( morphin atau alternatif) Nitrogiserin-NTG 0.2mg SL / Infusion (SBP>90) EKG 12 sandapan Defibrilator / AEDs

Options for Transport of Patients With STEMI and Initial Reperfusion Treatment
Hospital fibrinolysis: Door-to-Needle within 30 min.

Not PCI capable

Onset of symptoms of STEMI 9-1-1 EMS Dispatch

EMS on-scene
Encourage 12-lead ECGs. Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min.

InterHospital Transfer

PCI capable

GOALS
5 min. Patient

8 min.
EMS

EMS Transport
Prehospital fibrinolysis EMS transport EMS-to-needle EMS-to-balloon within 90 min. within 30 min. Patient self-transport Hospital door-to-balloon within 90 min.

Dispatch 1 min.

Golden Hour = first 60 min.

Total ischemic time: within 120 min.

97

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 PCI Capable Noninvasive Risk Stratification Rescue Ischemia driven Late Hospital Care and Secondary Prevention

PCI or CABG
Primary PCI

98

Reperfusion
Patient Transport Inhospital Reperfusion

Goals
D-N 30 min 5 min < 30 min D-B 90 min

Media campaign Patient education

Prehospital ECG MI protocol Critical pathway Bolus lytics Quality Greater use of improvement Dedicated 9-1-1 PCI team program Prehospital Rx

Methods of Speeding Time to Reperfusion

99

Treatment Delayed is Treatment Denied

Symptom Recognition

Call to Medical System

PreHospital

ED

Cath Lab

Increasing Loss of Myocytes

Delay in Initiation of Reperfusion Therapy

100

INTERVENSI PADA SINDROM KORONER AKUT

Angioplasti /PCI
Keberhasilan Primer : 85 - 95 %

Kematian :
Infark Miokard :

0.3 - 1.3 %
1.6 - 6.3 %

Operasi By-pass darurat :1 - 7 %

Stenosis lebih lanjut

sblm era stent: 30 - 40 % era stent : 15-20% Drug eluting stent : almost 0%

PTCA
Benefits: ICH 0%, Complications: experience counts >100 cases/yr/ea provider; >600/yr/hospital Mortality: reinfarction 5 vs 12% for TPA; 30 day same as TPA; but in AWMI; age>70 pulse >100 rates 2% vs 10% for TPA Trials: RITA, PAMI (93); MITI (96)

Lower Rate of Restenosis with Stenting (6 month follow-up)

Treatment
External elastic lamina Tunica media Internal elastic lamina

Restenosis

External elastic lamina

PTCA

Internal elastic lamina Intimal area

Treatment

Coronary stenting
Intimal area Lumen

Stent

Evolution of PCI for STEMI

AngioJet

Platelet

GP IIb/IIIa inhibitor

Embolization Protection Device

Balloon

Antiplatelet Rx

Stent

DES

Antman. Circulation 2001;103:2310.

Thrombus Removal and Distal Embolization Protection Devices

106

Operasi pintas koroner ( CABG )

Pada sindrom koroner akut Aritmia/Block ---- Kematian Mendadak Disfungsi Ventrikel Gagal Jantung Hipotensi ---- Shock Cardiogenic Mekanikal : Ruptur Ventrikel/Septum Pericarditis

Warning Arrhythmias

Antman and Rutherford. Coronary Care Medicine. Boston, MA: Martinus Nijhoff Publishing;1986:81. 109

SHOCK/HIPOTENSI/ EDEMA PARU Vide ALGORITME ACLS RUPTUR MEKANIKAL : VSD, FREE WALL
IABP OPERASI CARDIOPULMONARY BY PASS

TERIMA KASIH
Selamat mengikuti Kursus

Thrombotic Plug Formation

Vessel Wall Injury
Platelet Deposition

Platelet Activation
Platelet Recruitment

Thrombotic plug

Platelet Adhesion and Activation

Platelets adhering to damaged endothelium Normal platelets and undergoing in flowing blood activation Aggregation of platelets into a thrombus

Platelets

Platelets adhering to subendothelial space

Platelet thrombus

Endothelial cells Subendothelial space

Platelet Activation Pathways

Thrombin

Platelet
Fibrinogen Binding Site

Fibrinogen

Platelet Aggregation
Herbert. Exp Opin Invest Drugs 1994;3:449-455.
9

ADP: A Key Mediator of Platelet Activation

Fibrinogen
Platelet Aggregation
Fibrinogen Binding Site Platelet Recruitment

External ADP

ADP

ADP Platelet Activation Fibrinogen Binding Site

Internal ADP

Fibrinogen
10

Platelet Aggregation

Clopidogrel Blocks the ADP Receptor

Platelet

ADP
Fibrinogen Binding Site

Fibrinogen
Fibrinogen Binding Reduced Acts by selective inhibition of ADP binding to its platelet receptor and prevents subsequent platelet aggregation
11

Herbert. Exp Opin Invest Drugs 1994;3:449-455.

Coagulation Cascade
Intrinsic Pathway (surface contact) XIIa Extrinsic Pathway (tissue factor)

VIIa
XIa IXa
Heparin / LMWH
(AT-III dependent)

Xa
aPTT PT Thrombin (IIa)

Hirudin/Hirulog
(direct antithrombin)

Thrombin-Fibrin Clot
Courtesy of VTI