acs emergenci

7/30/2019 acs emergenci

1/95

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 CardiologyAustin Hospital Melbourne, Australia, 1992

Post Graduate Course on Non-Invasive Cardiology PacemakerImplantation, Royal Melbourne Hospital, Australia, 1993

Pendidikan Dokter Universitas Airlangga; (S3) Tahun 2000

Guru Besar tetap Universitas Indonesia; Tahun 2004

Education


2/95

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 andIntervention (FSCAI)

Head of Cardiovascular Devision Medika BSD Hospital


3/95

Cardiovascular Emergency :

Focus On Acute Coronary Syndromes

Roles of Primary Physicians

Idris Idham

RS MEDIKA BSD


4/95

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


5/95

Hypertensive Crisis : emergency,urgency

Arrhythmia : AFRVR, SVT, VT, VF,

TAVB Cardiomyopathy : PPCM, HCM, DCM.


6/95

CARDIOVASCULAR SPECIALIST

COMPETENCY

FRONTLINE DOCTORS

FROM PALPITATION TO CVD


7/95

Front-line medical practitioners

Play very important role in fightingcardiovascular 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.


8/95

Chest Pain

One of the most challenging symptoms1

Diagnosis ranges from benign esophageal

reflux to fatal MCI

Failure to manage fatal conditions lead tocomplications 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.


9/95

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


10/95

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)


11/95

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 theorgan(s) or system(s) causing the pain.


12/95

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


13/95

Anatomy of Thoracic Cavity

I.I. - 09 / PDKI Pekanbaru


14/95

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.


15/95

Features of Major Causes of

Chest Pain

Esophageal reflux : burning, substernal or

epigastric pain, relieved by antacids

Musculoskeletal : aching, worsened bymovement, may be reproduced by localized

pressure

Herpes zoster : sharp, burning, dermatomaldistribution, with vesicular rash


16/95

Differential Diagnosis of

Chest Pain

Cardiac ACS: infarct,angina

MVP

Aortic Stenosis Hypertrophic cardio-

myopathy

Pericarditis

Lungs Lung Emboli

Pneumonia

Pneumothorax

Pleuritis

GastrointestinalEsophageal reflux

Esophageal rupture

Gall bladder disease

Peptic UlcerPancreatitis

VascularAortic dissection/aneurysm

OthersMusculoskeletal

Herpes zoster


17/95

General Approach for First liners

Targetted anamnesis and thorough physicalexams

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, afterpatient is reasonably stabilized


18/95

Focus on:

Acute Coronary Syndromes



19/95

A spectrum of clinical syndromes due to

sudden, significantly compromised coronary

circulation ranging from unstable angina toNSTEMI and STEMI.

Further stages of stable angina pectoris

Topol EJ, ed. Textbook of cardiovascular medicine 2007.

DEFINITION


20/95

PATHOPHYSIOLOGY


21/95

FoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/Rupture

Endothelial Dysfunction

Smooth muscleand collagen

From first decade From third decade From fourth decade

Growth mainly by lipid accumulationThrombosis,hematoma

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

Atherosclerosis Timeline


22/95


23/95


24/95

DIAGNOSIS


25/95

Presentation

(Clinical, Initial ECG)ST-Seg Elevation

Myocardial Infarction Non-STSeg ElevationAcute Coronary Syndr

ST-Seg Elevation

MCI

Non-ST-seg-

Elevation MCI

Unstable

Angina

Workingdiagnosis

Time

Evolution ofECG &

Biomarkers

Finaldiagnosis

National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006

Biomarker (-)Biomarker (+)



26/95

CHEST PAINAdmission

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

Performedin10min

{on serial

ECG}

Troponin,

CKMB (+)


27/95

Clinical Classification of Angina

Typical angina (definite)

substernal chest discomfort with a characteristic quality andduration 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


28/95

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


29/95

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

revascularization

Medical therapy,


Performedin10min

{on serial

ECG}

Troponin,

CKMB (+)


30/95

EVOLVING ECGA. 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


31/95

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

revascularization

Medical therapy,


Performedin10m

in

{on serial

ECG}

Troponin,

CKMB ()


32/95

Biomarkers

Recommendation : CK, CKMB & Troponin upon admissionand serial in 6-12 hours

LDH, SGOT/SGPT and other enzymes not recommended

Increase of plasma CK plasma & CK-MB happens early, butless specific

Increase of TnI & TnT are more specific in diagnosing markerMI ; its level corresponds with prognosis (higher value, worseprognosis)


33/95


34/95

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

Multipleofth

eAMIcutofflimit

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


35/95

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

revascularization

Medical therapy,


Performedin10m

in

{on serial

ECG}

Troponin,

CKMB ()



36/95

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 newT-wave inversion

Transient ST-segment elevation (0.5 mm) in more

than two contiguous leads

Haemodynamic compromise

Guideline ACS 2006 National Heart Foundation Australia


37/95

High Risk

Sustained ventricular tachycardia

Syncope

LV systolic dysfunction (ejection fraction


38/95

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

reperfusion

Medical therapy,


Performedin10m

in

{on serial

ECG}

Troponin,

CKMB ()


39/95

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 pumpfailure &/ malignant arrhythmia


40/95

Anticoagulation & Reperfusion

Heparin administration (LMWH or UFH)

Reperfusion in STEMI

Fibrinolysis or primary percutaneous coronaryintervention (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


41/95

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

Al ith i ACLS


42/95

Algorithm in ACLS


Al ith i A t C S d


43/95

CHEST PAINAdmission

Working

diagnosis

Bio-

chemistry

Risk

Stratification

Management

Secondary

prevention

Suspected ACS

Persistent

ST elevation

No persistent

ST elevation

Troponin,

CKMB (+)

Risk: high / low



- ACS unlikely

- NSTEMI

- STEMI

ECG

Initial management,

revascularization

Medical therapy,


P

erformedin10m

in

{on serial

ECG}

Troponin,

CKMB ()


44/95

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


45/95

Invasive Strategy

As secondary prevention Early catheterization (before discharge):

for patients with moderate-high risk not

receiving primary percutaneous coronaryintervention

Later catheterization: for low risk

patients


46/95

Summary

Acute Coronary Syndrome as one ofpotentially 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)


47/95


48/95

OKSIGEN

Pemberian suplemen O2 diberikan pada pasiendengan desaturasi O2 (SaO2 6 jam pertama pd

kasus tanpa komplikasi, belum terdapat landasan

ilmiah yang kuat.

ACC/AHA Guideline of STEMI 2004



49/95

ANTIPLATELET

ASPIRIN

CLOPIDOGREL

TICLOPIDINE

Gp IIb / IIIa inhibitor



50/95

Aspirin

MANFAAT : menurunkan angka reinfark50% 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 meskipunbelum ada hasil EKG

(non coated/slow released)



51/95

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


52/95

COX (cyclo-oxygenase)ADP (adenosine diphosphate)

TXA2 (thromboxane A2)

CLOPIDOGREL

ASA COX

ADP

ADP

C

GPllb/llla

(Fibrinogen receptor)

Collagen thrombin

TXA2

Activation

TXA 2

ASA

Synergistic Mode of Action with

Clopidogrel and ASA1

1. Schafer AI.Am J Med1996; 101: 199209.



53/95

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



54/95

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



55/95

Anti Ischemia

NITRAT

B BLOKER

ANTAGONIS KALSIUM



56/95

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



57/95

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



58/95

Beta-bloker

Metoprolol IV

Metoprolol oralAtenolol oral

Propranolol oral

Bisoprolol oralCarvedilol oral

5 15 mg

2 x 25 100 mg1 x 25 100 mg

3 x 20 80 mg

1 x 5 10 mg1 x 25 mg



59/95

Antagonis kalsium

Pd UAP atau NSTEMI bila ada indikasi kontra B-

bloker

Tidak ada bukti manfaatnya pada pencegahaninfark miokard.

Memberikan hasil yang baik dalam jangka pendekpada episode iskemik.



60/95

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



61/95

Morfin:

2.5mg-5 mg IV pelan.Hatihati pada : inferior MCI,

asthma , bradikardia

Pethidin : 12.5-25 mg IV pelan

PAIN KILLER



62/95

ANTITROMBOTIK DANANTIKOAGULAN

Heparin ( Unfractionated Heparin)

Low Molecular Weight Heparin



63/95

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



64/95

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



65/95

UFH

LMWH



66/95

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



67/95

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, namunbukan 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



68/95

TEHNIK INJEKSI LMWH SUBKUTAN



69/95

DOSIS YANG DIREKOMENDASIKAN

UFH

LMWHEnoxaparine

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


ACC/AHA 2007 Guidelines Update


70/95

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

orIV heparin

ACC/AHA 2007 Guidelines Updatefor UA and NSTEMI1

+Clopidogrel + Clopidogrel

*During hospital careClopidogrel should be administered to hospitalized patients who are unable to take ASA

because of hypersensitivity or major GI intoleranceClass 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


71/95

OBAT-OBATAN LAINNYA

Tranquilizer e,g diazepam 5mg bid Stool softener



72/95

TERAPI FIBRINOLITIK


Fib i litik I dik i


73/95

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 blockyg 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



74/95

Fibrinolitik : indikasi kontra

Absolut Riwayat stroke hemoragik,kapanpun terjadinya

Riwayat stroke iskemik dalam 3 bulan kecuali stroke iskemikdengan 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



75/95

Hipertensi berat saat datang ke unit emergency yaitu BP> 180 / 110 mmHgPungsi vaskuler yg tak dapat dikompresi

Perdarahan internal 2 4 mgg sebelumnya

Konsumsi antikoagulan oralprolonged CPR ( > 10 minutes) or operasi mayor dlm jangka waktu 2-4

minggu

Untuk Streptokinase : pemberian sebelumnya ( 5 hari-2 tahun) atau riwayat

reaksi alergi

KehamilanActive 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 2004I.I. - 09 / PDKI Pekanbaru


76/95

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



77/95

AGEN FIBRINOLITIK

Streptokinase (SK)

Actylase (tPA)

Reteplase (r-PA)

Tenecteplase (TNK-tPA)


Skema sistem fibrinolitik


78/95

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 CardiovascularMedicine. 6th edI.I. - 09 / PDKI Pekanbaru


79/95

SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK

Streptokinase

Actylase (tPA)

Reteplase(r-PA)

Tenecteplase

(TNK-tPA)

Rendah

Tinggi

Sedang

Sangat tinggi



80/95

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 30mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt berikutnya



81/95

Streptokinase (SK, Streptase)

Keuntungan : lebih baik pada anterior

MCI, age


82/95

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


83/95

Extension / Ischemia

Complications of Acute MI

Acute MI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical Mural Thrombus



84/95

Komplikasi awal :-aritmia

-disfungsi LV dan gagal jantung

-ruptur ventrikel

-regurgitasi mitral akut

-gagal fungsi RV

-syok kardiogenik



85/95

Komplikasi akhir :

-trombosis mural dan emboli sistemik

-aneurisma LV

-DVT

-emboli paru

-sindrome Dressler


Pemeriksaan awal pada Sindrom Koroner Akut


86/95

SAKIT DADAMasuk 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 ECGTroponin

2 X negative

Risiko tinggi Risiko rendah

Esc/EHJ 2002

Mungkin bukan SKA



87/95

TERAPI INTERVENSI

PADA SINDROMAKORONER AKUT



88/95

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


89/95

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)



90/95


Treatment Delayed is Treatment Denied


91/95

Symptom

Recognition Call toMedical System EDCath LabPreHospital

Delay in Initiation of Reperfusion TherapyIncreasing Loss of Myocytes


Options for Transport of Patients With STEMI and Initial

Reperfusion Treatment


92/95

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

further revascularization with percutaneous coronary intervention (PCI) orcoronary artery bypass graft surgery (CABG).

All patients should receive late hospital care and secondary prevention of

STEMI.

Fibrinolysis

Primary PCI

Noninvasive RiskStratification

Late

Hospital Care

and Secondary

Prevention

PCI or CABG

Not

PCI Capable

PCI Capable

Rescue Ischemia

driven

Reperfusion Treatment



93/95


Chest pain: focus on


94/95

Chest pain: focus on

acute coronary syndromes

What doctors should know

IDRIS IDHAMDepartment of Cardiology and Vascular Medicine

Fakultas of Medicine University of Indonesia

National Cardiovascular Center Harapan Kita



95/95

Thank you

acs emergenci

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