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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 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
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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
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Cardiovascular Emergency :
Focus On Acute Coronary Syndromes
Roles of Primary Physicians
Idris Idham
RS MEDIKA BSD
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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
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Hypertensive Crisis : emergency,urgency
Arrhythmia : AFRVR, SVT, VT, VF,
TAVB Cardiomyopathy : PPCM, HCM, DCM.
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CARDIOVASCULAR SPECIALIST
COMPETENCY
FRONTLINE DOCTORS
FROM PALPITATION TO CVD
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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.
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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.
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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
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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)
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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.
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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
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Anatomy of Thoracic Cavity
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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.
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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
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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
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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
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Focus on:
Acute Coronary Syndromes
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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
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PATHOPHYSIOLOGY
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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
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DIAGNOSIS
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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 (+)
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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 (+)
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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
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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
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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 (+)
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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
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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
Performedin10m
in
{on serial
ECG}
Troponin,
CKMB ()
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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)
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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
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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
Performedin10m
in
{on serial
ECG}
Troponin,
CKMB ()
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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
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High Risk
Sustained ventricular tachycardia
Syncope
LV systolic dysfunction (ejection fraction
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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,
reperfusion
Medical therapy,
coronary angiography
Performedin10m
in
{on serial
ECG}
Troponin,
CKMB ()
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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
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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
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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
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Algorithm in ACLS
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Al ith i A t C S d
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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
P
erformedin10m
in
{on serial
ECG}
Troponin,
CKMB ()
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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
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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
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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)
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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
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ANTIPLATELET
ASPIRIN
CLOPIDOGREL
TICLOPIDINE
Gp IIb / IIIa inhibitor
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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)
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Adenosine Diphosphate
Inhibitors ADP disekresi oleh platelet (aktivasi dan
agregasi platelet)
P2T cell surface receptors
Ticlodipine
Clopidogrel
Efek samping : Neutropenia, trombositopenia
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Synergistic Mode of Action with
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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.
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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
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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
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Anti Ischemia
NITRAT
B BLOKER
ANTAGONIS KALSIUM
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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
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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
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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
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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.
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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
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Morfin:
2.5mg-5 mg IV pelan.Hatihati pada : inferior MCI,
asthma , bradikardia
Pethidin : 12.5-25 mg IV pelan
PAIN KILLER
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ANTITROMBOTIK DANANTIKOAGULAN
Heparin ( Unfractionated Heparin)
Low Molecular Weight Heparin
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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
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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
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UFH
LMWH
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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
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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
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TEHNIK INJEKSI LMWH SUBKUTAN
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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
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ACC/AHA 2007 Guidelines Update
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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
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OBAT-OBATAN LAINNYA
Tranquilizer e,g diazepam 5mg bid Stool softener
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TERAPI FIBRINOLITIK
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Fib i litik I dik i
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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
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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
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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
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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
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AGEN FIBRINOLITIK
Streptokinase (SK)
Actylase (tPA)
Reteplase (r-PA)
Tenecteplase (TNK-tPA)
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Skema sistem fibrinolitik
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Plasminogen Activators(t-PA, u-PA)
Skema sistem fibrinolitik
Plasminogen Plasmin
2-Antiplasmin
Fibrin
Fibrin
degradation
Product
Plasminogen Activator
Inhibitors (PA1, PA2, TAFI)
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SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
Streptokinase
Actylase (tPA)
Reteplase(r-PA)
Tenecteplase
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
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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
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Streptokinase (SK, Streptase)
Keuntungan : lebih baik pada anterior
MCI, age
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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)
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Complications of Acute MI
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Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm RV Infarct
Pericarditis
Mechanical Mural Thrombus
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Komplikasi awal :-aritmia
-disfungsi LV dan gagal jantung
-ruptur ventrikel
-regurgitasi mitral akut
-gagal fungsi RV
-syok kardiogenik
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Komplikasi akhir :
-trombosis mural dan emboli sistemik
-aneurisma LV
-DVT
-emboli paru
-sindrome Dressler
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Pemeriksaan awal pada Sindrom Koroner Akut
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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
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TERAPI INTERVENSI
PADA SINDROMAKORONER AKUT
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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
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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)
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Treatment Delayed is Treatment Denied
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Symptom
Recognition Call toMedical System EDCath LabPreHospital
Delay in Initiation of Reperfusion TherapyIncreasing Loss of Myocytes
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Options for Transport of Patients With STEMI and Initial
Reperfusion Treatment
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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
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Chest pain: focus on
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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
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Thank you
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