Acs Cardiovascular Emergency Jadi

Prof. Dr. dr.
Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI

Education

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
Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI
Staf senior, Dept. Kardiologi & Kedokteran Vaskular FKUI & Pusat Jantung Nasional Harapan Kita Chief cardiologist, RS Medika BSD Sekretaris Kolegium Pengurus Pusat Perhimpunan Dokter Spesialis Kardiovaskular (PP PERKI) 2008-sekarang Fellow of Indonesian Heart Association (FIHA) Fellow of American College of Cardiology (FACC) Fellow of European Society of Cardiology (FESC) Fellow of ASEAN Federation of Cardiology (FAsCC) Fellow of Society of Cardiovascular Angiography and Intervention (FSCAI) Head of Cardiovascular Devision Medika BSD Hospital
Cardiovascular Emergency : Focus On Acute Coronary Syndromes Roles of Primary Physicians
Idris Idham
RS MEDIKA BSD
Spectrum of CV Emergency
Congenital Heart Diseases Acute Coronary Syndrome : UAP, NSTEMI, STEMI Acute Lung Edema Acute Aortic Dissection Acute Limb Ischemia Deep Veins Thrombosis
Hypertensive Crisis : emergency, urgency Arrhythmia : AFRVR, SVT, VT, VF, TAVB Cardiomyopathy : PPCM, HCM, DCM.
CARDIOVASCULAR SPECIALIST COMPETENCY FRONTLINE DOCTORS
FROM PALPITATION TO CVD
Front-line medical practitioners

Play very important role in fighting cardiovascular diseases (CVD), the no.1 killer in Indonesia1 Front liners are doctors who first encounter the patient, including family physicians Patients will benefit from early diagnosis and prompt treatment Competent of recognizing important signs & symptoms of CVD, e.g. chest pain
1Dept.
of Health, RI. 2002.
Chest Pain
One of the most challenging symptoms1 Diagnosis ranges from benign esophageal reflux to fatal MCI
Failure to manage fatal conditions lead to complications including death Over management of low risk conditions causes unnecessary burden
Acute or escalating chronic chest discomfort is most challenging.

1Harrisons
principles of internal medicine: McGraw-Hill, 2005.
Evaluation Aim
To assess the general clinical condition of patient To determine the working diagnosis To initiate immediate management plan Should be performed rapidly yet accurately
General Clinical Assessment

Stratify patient : stable vs unstable condition; based on level of consciousness & vital signs. Stabilize the patient first! Secure ABC (airway, breathing, circulation)
Determining Working Diagnosis

Largely a clinical work, accurate anamnesis is the key. Characteristics of chest pain should be thoroughly explored:
Quality, duration, location, precipitating & relieving factors, other associated features.
Based on characteristics, determine the organ(s) or system(s) causing the pain.
Determining Working Diagnosis

Consider anatomical structure of thorax & adjacent abdominal organs ; each organ has typical characteristics Important : features may not always present ; several features may occur simultaneously
Anatomy of Thoracic Cavity
I.I. - 09 / PDKI Pekanbaru
Features of Major Causes of Chest Pain

Angina: sensation of pressure, tightness, squeezing, heaviness, burning ; located retrosternal, often radiate (detailed later) Aortic dissection : abrupt onset of tearing or ripping sensation, knife-like pain in anterior chest, often radiate to back Pleuritis : pleuritic pain, influenced by breathing ; accompanied by cough, fever.
1Harrisons
principles of internal medicine: McGraw-Hill, 2005.
Features of Major Causes of Chest Pain

Esophageal reflux : burning, substernal or epigastric pain, relieved by antacids Musculoskeletal : aching, worsened by movement, may be reproduced by localized pressure Herpes zoster : sharp, burning, dermatomal distribution, with vesicular rash
Differential Diagnosis of Chest Pain

Cardiac
ACS: infarct,angina MVP Aortic Stenosis Hypertrophic cardiomyopathy Pericarditis
Gastrointestinal
Esophageal reflux Esophageal rupture Gall bladder disease Peptic Ulcer Pancreatitis
Vascular
Aortic dissection/aneurysm
Lungs
Lung Emboli Pneumonia Pneumothorax Pleuritis
Others
Musculoskeletal Herpes zoster
General Approach for First liners

Targetted anamnesis and thorough physical exams Consider most likely diagnoses
If more than one, consider the worst one
Closely monitor vital signs Administer essential first-line drugs Refer to higher facility if required, after patient is reasonably stabilized
Focus on:
Acute Coronary Syndromes
DEFINITION
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.
PATHOPHYSIOLOGY
Atherosclerosis Timeline
Foam Cells Fatty Streak Intermediate Atheroma Lesion Fibrous Plaque Complicated Lesion/Rupture
Endothelial Dysfunction
From first decade From third decade From fourth decade
Smooth muscle and collagen
Growth mainly by lipid accumulation
Thrombosis, hematoma
Stary HC et al. Circulation 1995;92:1355-1374.
DIAGNOSIS
Presentation (Clinical, Initial ECG)
Working diagnosis
Time
ST-Seg Elevation Myocardial Infarction
Non-STSeg Elevation Acute Coronary Syndr
Evolution of ECG & Biomarkers

Final diagnosis
Biomarker (+)
Biomarker (-)
ST-Seg Elevation MCI
Non-ST-segElevation MCI
Unstable Angina
National Heart Foundation Australia &The Cardiac Society of Australia and New Zealand, MJA 2006
Algorithm in Acute Coronary Syndrome

Admission Working diagnosis ECG CHEST PAIN Suspected ACS Persistent ST elevation Troponin, CKMB (+) No persistent ST elevation Troponin, CKMB (+)
Performed in 10 min
{on serial ECG}

- ACS unlikely - NSTEMI - STEMI
Biochemistry
Risk Stratification Management Secondary prevention
Risk: high / low Initial management, revascularization Medical therapy, coronary angiography
Modified from ESC 2007
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 <=1 of the typical angina characteristics

Diamond GA. J Am Coll Cardiol 1983;1:574
UA/NSTEMI THREE PRINCIPAL PRESENTATIONS

Rest Angina* Angina occurring at rest and prolonged, usually > 20 minutes
New-onset angina of at least CCS Class III severity 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
New-onset Angina
Increasing Angina

Admission Working diagnosis ECG CHEST PAIN Suspected ACS Persistent ST elevation Troponin, CKMB (+) No persistent ST elevation Troponin, CKMB (+)
Performed in 10 min
{on serial ECG}

Biochemistry
ECG pattern Ischemia : ST , tall T, inverted T Injury : ST Infarction : pathologic Q

EVOLVING ECG A. Normal ECG B. Tall or peaked T waves C. ST D. & E. ST with inverted T waves F. Abnormal Q

Admission Working diagnosis ECG CHEST PAIN
Performed in 10 min
Suspected ACS Persistent ST elevation Troponin, CKMB (+) No persistent ST elevation Troponin, CKMB ()
{on serial ECG}

Biochemistry
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)
Biomarkers
Multiple of the AMI cutoff limit
Early release myoglobin of CKMB isoform Cardiac troponin after classical myocardial infarction
50 20 10 5 2
CK-MB after myocardial infarction

Cardiac troponin after microinfarction
1 0 1 2 3 4 5 6 7 8
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

Performed in 10 min
{on serial ECG}

Biochemistry
Risk: high / low

Initial management, revascularization Medical therapy, coronary angiography
High Risk
Repetitive or prolonged (> 10 minutes) pain Elevated level of cardiac biomarker (troponin or creatine kinase-MB isoenzyme); Persistent or dynamic ST depression 0.5 mm or new T-wave inversion Transient ST-segment elevation (0.5 mm) in more than two contiguous leads Haemodynamic compromise
Guideline ACS 2006 National Heart Foundation Australia
High Risk
Sustained ventricular tachycardia Syncope LV systolic dysfunction (ejection fraction <40%); Prior PCI or CABG within 6 months or prior Diabetes Chronic kidney disease (estimated GFR< 60 mL/min)
Guideline ACS 2006 National Heart Foundation Australia

Performed in 10 min
{on serial ECG}

Biochemistry
Risk: high / low Initial management, reperfusion Medical therapy, coronary angiography
Initial Management
Monitor and support ABCs Check vital signs, including O2 saturation Establish IV access Administer
Oxygen 4L/min Aspirin 160-325 mg chewed Clopidogrel loading dose 300 mg ISDN 5 mg sublingual, nitroglycerine iv if necessary Morphine if pain not relieved with NTG
Caution: hemodynamic instability due to pump failure &/ malignant arrhythmia
Anticoagulation & Reperfusion

Heparin administration (LMWH or UFH) Reperfusion in STEMI
Fibrinolysis or primary percutaneous coronary intervention (PCI). GPs should be trained to give fibrinolytic Assess onset (12 hours) and contraindication (bleeding, etc) Door to needle time: 30 min Door to balloon time: 90 min
Fibrinolytic Absolute Contraindication

Hemorrhagic stroke, or stroke of unknown origin Ischemic stroke in preceding 6 months Central nervous system trauma or neoplasm Recent major trauma/surgery/head injury (within preceding 3 weeks) Gastro-intestinal bleeding within the last month Known bleeding disorder Aortic dissection Non-compressible punctures (e.g liver biopsy, lumbar puncture)
ESC Guidelines of STEMI, 2008
Algorithm in ACLS

Performed in 10 min
{on serial ECG}

Biochemistry
Risk Stratification
Management
Secondary prevention
Secondary Prevention Strategy

A Aspirin and Anticoagulants
B
C D
Beta blockers and Blood Pressure

Cholesterol and Cigarettes Diet and Diabetes
E
F
Education and Exercise

Fun and Faith
Invasive Strategy
As secondary prevention Early catheterization (before discharge): for patients with moderate-high risk not receiving primary percutaneous coronary intervention Later catheterization: for low risk patients
Summary
Acute Coronary Syndrome as one of potentially fatal cardiovascular emergency should be recognized immediately Early diagnosis and prompt treatment should be managed to overcome good results and avoid myocardial damage (Time is muscle)
Thank You
OKSIGEN
Pemberian suplemen O2 diberikan pada pasien dengan desaturasi O2 (SaO2 <90%) Suplemen O2 mungkin membatasi injury miokard atau bahkan mengurangi elevasi ST Pemberian suplemen O2 rutin > 6 jam pertama pd kasus tanpa komplikasi, belum terdapat landasan ilmiah yang kuat.
ACC/AHA Guideline of STEMI 2004

ANTIPLATELET
ASPIRIN CLOPIDOGREL TICLOPIDINE Gp IIb / IIIa inhibitor
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)
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 Clopidogrel and ASA1

CLOPIDOGREL C
ADP ADP
GPllb/llla
(Fibrinogen receptor)
Activation
Collagen thrombin TXA 2
ASA ASA
TXA COX (cyclo-oxygenase) ADP (adenosine diphosphate) TXA2 (thromboxane A2)
1. Schafer AI. Am J Med 1996; 101: 199209.
COX
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
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
Anti Ischemia
NITRAT B BLOKER ANTAGONIS KALSIUM
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
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
Beta-bloker
Metoprolol Metoprolol Atenolol Propranolol oral Bisoprolol Carvedilol IV oral oral
oral 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
Antagonis kalsium
Pd UAP atau NSTEMI bila ada indikasi kontra Bbloker Tidak ada bukti manfaatnya pada pencegahan infark miokard. Memberikan hasil yang baik dalam jangka pendek pada episode iskemik.
Antagonis kalsium
Diltiazem 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
Verapamil
PAIN KILLER
Morfin: 2.5mg-5 mg IV pelan. Hati hati pada : inferior MCI, asthma , bradikardia Pethidin : 12.5-25 mg IV pelan
ANTITROMBOTIK DAN ANTIKOAGULAN

Heparin ( Unfractionated Heparin) Low Molecular Weight Heparin
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
Low Molecular Weight Heparin

Depolimerasi dari UFH standar dengan berat molekul lebih kecil dari pada UFH SQ injections/ 90% bioavailable/predictable Anti-Xa: Anti-thrombin 2-4:1 FDA menyetujui pemakaian enoxaparin/ dalteparin untuk SKA
UFH
LMWH
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
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

TEHNIK INJEKSI LMWH SUBKUTAN
DOSIS YANG DIREKOMENDASIKAN

UFH
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
LMWH 1mg/kg, SC , bid Enoxaparine 0,1 ml/10 kg , SC , bid Nadroparine 2.5 mg Fondaparinux
ACC/AHA 2007 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 hospital
+ Clopidogrel
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 1. Braunwald E et al. American College of Cardiology (ACC) and the American Heart Association (AHA) 6/12/2011 Guidelines, USA: ACC/AHA; 2007.
OBAT-OBATAN LAINNYA
Tranquilizer e,g diazepam 5mg bid Stool softener
TERAPI FIBRINOLITIK
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
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

Fibrinolitik :indikasi kontra relatif

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
ACC/AHA guideline of STEMI 2004
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
AGEN FIBRINOLITIK
Streptokinase (SK) Actylase (tPA) Reteplase (r-PA) Tenecteplase (TNK-tPA)
Skema sistem fibrinolitik

Plasminogen Activators (t-PA, u-PA) Plasminogen Activator Inhibitors (PA1, PA2, TAFI)
Plasminogen
2-Antiplasmin
Plasmin
Fibrin
Fibrin degradation Product

Braunwald, A Textbook of Cardiovascular Medicine. 6th ed
SPESIFISITI FIBRIN BERBAGAI AGEN FIBRINOLITIK Streptokinase Actylase (tPA) Reteplase(r-PA) Tenecteplase (TNK-tPA) Rendah Tinggi Sedang Sangat tinggi
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
Streptokinase (SK, Streptase)

Keuntungan : lebih baik pada anterior MCI, age <75; lebih murah Komplikasi: antigenic, perdarahan intraserebral pada studi GUSTO 0.6% Trials: GISSI-1, ISIS-2 (88)
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
Extension / Ischemia
Arrhythmia Pericarditis
Expansion / Aneurysm
Acute MI
RV Infarct
Mechanical
Heart Failure
Mural Thrombus
Komplikasi awal :
-aritmia -disfungsi LV dan gagal jantung -ruptur ventrikel -regurgitasi mitral akut -gagal fungsi RV -syok kardiogenik
Komplikasi akhir :
-trombosis mural dan emboli sistemik -aneurisma LV -DVT -emboli paru -sindrome Dressler
Pemeriksaan awal pada Sindrom Koroner Akut

Masuk RS
SAKIT DADA Curiga Sindrom Koroner Akut Elevasi ST menetap Troponin (CKMB) Tanpa Elevasi ST menetap Troponin Normal atau Tdk dpt ditentukan ECG Troponin 2 X negative
Mungkin bukan SKA
Diagnosis Kerja ECG
Biochemistry
Stratifikasi risiko Pengobatan Pencegahan sekunder
Risiko tinggi Risiko rendah
Esc/EHJ 2002
TERAPI INTERVENSI PADA SINDROMA KORONER AKUT
Angioplasty
Keberhasilan Primer Kematian Infark Miokard Operasi By-pass darura : : : : 85 - 95 % 0.3 - 1.3 % 1.6 - 6.3 % 1 -7% : 30 - 40 % : 15-20% : almost 0%
Stenosis lebih lanjut sblm era stent era stent Drug eluting stent
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)
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
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 PCI or CABG
Noninvasive Risk Stratification

Rescue Ischemia driven Late Hospital Care and Secondary Prevention
Primary PCI
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
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Acs Cardiovascular Emergency Jadi

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Prof. Dr. dr.

Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI

Cardiovascular Emergency : Focus On Acute Coronary Syndromes Roles of Primary Physicians

CARDIOVASCULAR SPECIALIST COMPETENCY FRONTLINE DOCTORS

FROM PALPITATION TO CVD

Front-line medical practitioners

of Health, RI. 2002.

Acute or escalating chronic chest discomfort is most challenging.

principles of internal medicine: McGraw-Hill, 2005.

General Clinical Assessment

Determining Working Diagnosis

Based on characteristics, determine the organ(s) or system(s) causing the pain.

Determining Working Diagnosis

Anatomy of Thoracic Cavity

I.I. - 09 / PDKI Pekanbaru

Features of Major Causes of Chest Pain

principles of internal medicine: McGraw-Hill, 2005.

Features of Major Causes of Chest Pain

Differential Diagnosis of Chest Pain

General Approach for First liners

Acute Coronary Syndromes

I.I. - 09 / PDKI Pekanbaru

Topol EJ, ed. Textbook of cardiovascular medicine 2007.

Growth mainly by lipid accumulation

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

Presentation (Clinical, Initial ECG)

ST-Seg Elevation Myocardial Infarction

Non-STSeg Elevation Acute Coronary Syndr

Evolution of ECG & Biomarkers

ST-Seg Elevation MCI

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Modified from ESC 2007

Clinical Classification of Angina

Noncardiac chest pain meets <=1 of the typical angina characteristics

UA/NSTEMI THREE PRINCIPAL PRESENTATIONS

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Modified from ESC 2007

ECG pattern Ischemia : ST , tall T, inverted T Injury : ST Infarction : pathologic Q

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Modified from ESC 2007

CK-MB after myocardial infarction

Day after onset of AMI

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Risk: high / low

Modified from ESC 2007

Guideline ACS 2006 National Heart Foundation Australia

Guideline ACS 2006 National Heart Foundation Australia

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Modified from ESC 2007

Caution: hemodynamic instability due to pump failure &/ malignant arrhythmia

Anticoagulation & Reperfusion

Fibrinolytic Absolute Contraindication

I.I. - 09 / PDKI Pekanbaru

Algorithm in Acute Coronary Syndrome

{on serial ECG}

Modified from ESC 2007

Secondary Prevention Strategy

Beta blockers and Blood Pressure

Education and Exercise