Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC ... · PDF fileProf. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI SR Negeri Tabing, Padang, Tahun 1957 SMPN Kuranji,

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

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.

1Harrison’s 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.

1Harrison’s 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 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

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


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

PATHOPHYSIOLOGY

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

DIAGNOSIS

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 (+)


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 (+)

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 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


Working diagnosis

Bio- chemistry

Risk Stratification

Management


Suspected ACS



Troponin, CKMB (+)

Risk: high / low




ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial ECG}

Troponin, CKMB (+)

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


Working diagnosis

Bio- chemistry

Risk Stratification

Management


Suspected ACS



Troponin, CKMB (+)

Risk: high / low




ECG


revascularization

Medical therapy,


Perform

ed in 10 min

{on serial ECG}

Troponin, CKMB (±)

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)

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


Working diagnosis

Bio- chemistry

Risk Stratification

Management


Suspected ACS



Troponin, CKMB (+)

Risk: high / low




ECG

Initial management,

±revascularization

Medical therapy,


Perform

ed in 10 min

{on serial ECG}

Troponin, CKMB (±)


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


Working diagnosis

Bio- chemistry

Risk Stratification

Management


Suspected ACS



Troponin, CKMB (+)

Risk: high / low




ECG


reperfusion

Medical therapy,


Perform

ed in 10 min

{on serial ECG}

Troponin, CKMB (±)

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



Working diagnosis

Bio- chemistry

Risk Stratification

Management


Suspected ACS



Troponin, CKMB (+)

Risk: high / low




ECG

Initial management,

±revascularization

Medical therapy,


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

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


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: 199–209.


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 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


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.


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


•Morfin: 2.5mg-5 mg IV pelan. Hati –hati pada : inferior MCI, asthma , bradikardia •Pethidin : 12.5-25 mg IV pelan

PAIN KILLER


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% bio-available/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

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


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

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


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

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


AGEN FIBRINOLITIK

• Streptokinase (SK)

• Actylase (tPA)

• Reteplase (r-PA)

• Tenecteplase (TNK-tPA)


Plasminogen Activators (t-PA, u-PA)

Skema sistem fibrinolitik

Plasminogen Plasmin

α2-Antiplasmin

Fibrin Fibrin degradation Product

Plasminogen Activator Inhibitors (PA1, PA2, TAFI)

Braunwald, A Textbook of Cardiovascular Medicine. 6th ed I.I. - ’09 / PDKI Pekanbaru

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)


Extension / Ischemia

Complications of Acute MI

Acute MI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical 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


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


TERAPI INTERVENSI PADA SINDROMA KORONER AKUT


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

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)



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


• 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



Chest pain: focus on

acute coronary syndromes

What doctor’s 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

Thank you


Prof. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC ... · PDF fileProf. Dr. dr. Idris Idham, SpJP (K), FIHA, FACC, FESC, FASCC, FSCAI SR Negeri Tabing, Padang, Tahun 1957 SMPN Kuranji,

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