Acs Cardiovascular Emergency Jadi
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Transcript of 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
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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 and
Intervention (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
-
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 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.
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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 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.
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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 the organ(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
I.I. - 09 / PDKI Pekanbaru
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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 by movement, may be reproduced by localized pressure
Herpes zoster : sharp, burning, dermatomal distribution, 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
Gastrointestinal Esophageal reflux Esophageal rupture Gall bladder disease Peptic Ulcer Pancreatitis
Vascular Aortic dissection/aneurysm
Others Musculoskeletal Herpes zoster
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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
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Focus on:
Acute Coronary Syndromes
I.I. - 09 / PDKI Pekanbaru
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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
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PATHOPHYSIOLOGY
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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
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DIAGNOSIS
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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
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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 (+)
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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
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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 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 (+)
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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
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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 ()
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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)
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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
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
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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
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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 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
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High Risk
Sustained ventricular tachycardia
Syncope
LV systolic dysfunction (ejection fraction
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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 ()
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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 pump failure &/ malignant arrhythmia
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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
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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
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Algorithm in ACLS
I.I. - 09 / PDKI Pekanbaru
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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
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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
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ANTIPLATELET
ASPIRIN CLOPIDOGREL TICLOPIDINE
Gp IIb / IIIa inhibitor
I.I. - 09 / PDKI Pekanbaru
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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
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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
I.I. - 09 / PDKI Pekanbaru
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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
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
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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
I.I. - 09 / PDKI Pekanbaru
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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
I.I. - 09 / PDKI Pekanbaru
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Anti Ischemia
NITRAT
B BLOKER
ANTAGONIS KALSIUM
I.I. - 09 / PDKI Pekanbaru
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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
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
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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
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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
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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
I.I. - 09 / PDKI Pekanbaru
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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
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ANTITROMBOTIK DAN ANTIKOAGULAN
Heparin ( Unfractionated Heparin)
Low Molecular Weight Heparin
I.I. - 09 / PDKI Pekanbaru
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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
I.I. - 09 / PDKI Pekanbaru
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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
I.I. - 09 / PDKI Pekanbaru
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UFH
LMWH
I.I. - 09 / PDKI Pekanbaru
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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
I.I. - 09 / PDKI Pekanbaru
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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, 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
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TEHNIK INJEKSI LMWH SUBKUTAN
I.I. - 09 / PDKI Pekanbaru
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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
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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
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
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OBAT-OBATAN LAINNYA
Tranquilizer e,g diazepam 5mg bid
Stool softener
I.I. - 09 / PDKI Pekanbaru
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TERAPI FIBRINOLITIK
I.I. - 09 / PDKI Pekanbaru
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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 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
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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
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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
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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
I.I. - 09 / PDKI Pekanbaru
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AGEN FIBRINOLITIK
Streptokinase (SK)
Actylase (tPA)
Reteplase (r-PA)
Tenecteplase (TNK-tPA)
I.I. - 09 / PDKI Pekanbaru
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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)
Braunwald, A Textbook of Cardiovascular Medicine. 6th ed I.I. - 09 / PDKI Pekanbaru
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SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK
Streptokinase
Actylase (tPA)
Reteplase(r-PA)
Tenecteplase
(TNK-tPA)
Rendah
Tinggi
Sedang
Sangat tinggi
I.I. - 09 / PDKI Pekanbaru
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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 30 mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt berikutnya
I.I. - 09 / PDKI Pekanbaru
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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
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Extension / Ischemia
Complications of Acute MI
Acute MI
Arrhythmia
Heart Failure
Expansion / Aneurysm RV Infarct
Pericarditis
Mechanical Mural Thrombus
I.I. - 09 / PDKI Pekanbaru
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Komplikasi awal :
-aritmia
-disfungsi LV dan gagal jantung
-ruptur ventrikel
-regurgitasi mitral akut
-gagal fungsi RV
-syok kardiogenik
I.I. - 09 / PDKI Pekanbaru
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Komplikasi akhir :
-trombosis mural dan emboli sistemik
-aneurisma LV
-DVT
-emboli paru
-sindrome Dressler
I.I. - 09 / PDKI Pekanbaru
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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
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TERAPI INTERVENSI PADA SINDROMA KORONER AKUT
I.I. - 09 / PDKI Pekanbaru
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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)
I.I. - 09 / PDKI Pekanbaru
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I.I. - 09 / PDKI Pekanbaru
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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
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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
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I.I. - 09 / PDKI Pekanbaru
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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
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Thank you
I.I. - 09 / PDKI Pekanbaru