SKA Revisi

7/28/2019 SKA Revisi

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SINDROMA KORONER AKUT

PUSAT JANTUNG REGIONAL

REGIONAL CARDIVASCULAR CENTER

RS. DR. M DJAMIL, PADANG

Dr. MUHAMMAD SYUKRI, Sp JP

PUSAT

JANTUNG

Regional


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JANTUNG SEBAGAI POMPA

Kanan K


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Penyakit Kardiovaskuler :

Masalah Yang Berakibat Fatal

C V

Kanker

Peny.Infeksi &

parasit

Lain-lain

Kecelakaan

Peny.RespirasiNon infeksi

Infeksi Respirasi

Kondisi Ibu Hamil dan

Persalinan&

defisiensi

nutrisi

Survey Kesehatan Indonesia 2001

WHO World Health Report, 2001

Penyebab kematian

nomor I di dunia danIndonesia

30%


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Normal

Garis lemak Tumpukan

lemak

PenyempitanPlak pecah

Dan tersumbat

MCI

STROKE

Critical Leg

IschemiaGejala tersembunyi

MATI

Meningkat sesuai umur

Sakit dada

UAP

Proses penyempitan pembuluh darah

(Aterosklerosis)


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PATOFISOLOGI SKA


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ASA, Clopidogrel

Activated

platelets

GP IIb/IIIa Inhibitors

Adhesion1

Activation2

Aggregation3

Plaque

rupture

Peran Thrombosit pada ProsesAtherothrombosis

Cannon, Braunwald, Heart Disease. 2001;1232-1263

Fibrinogen

TxA2ADP

Platelets


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Peran Thrombosit pada ProsesAtherothrombosis


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AWASSERANGAN JANTUNG !!!


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SAKIT DADA


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1.Lifestyle

Diet

Smoking

Obesity

Physical inactivity

2. Blood Pressure

3. Plasma lipids

LDL-C

TG

HDL-C

3.Diabetes/ Insulin Resistance

4. Emerging Risk Factors :

- Plasma Homocysteine (tHcy)

-- Thrombogenic Factors

-- plasma fibrinogen

-- Plasminogen Activator Inhibitor (PAI-1)

-- Markers of Inflammation

5.Genetics

Family history

Faktor Risiko


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1. Gaya Hidup Diet

Obesitas Merokok fisik tidak aktif

2. Tekanan Darah3. Plasma lipid

LDL-C

TGHDL-C

Faktor lain lipid: Apoliproprotein

lipoprotein B (a)


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Gangguan metabolisme

Faktor risiko Batas NilaiKegemukan( Lingkaran Perut )

LakiWanita

>102 cm (>40 in)>88 cm (>35 in)

Trigliserida 150 mg/dLHDL-C

LakiWanita


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PREVENTIVE

PREVENTIVE

MAT

O S O


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FAKTOR RISIKO

SINDROMA KORONER AKUT


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Sindroma Koroner Akut

Suatu Spektrum Klinis peny. Jantung Koroner :

unstable angina

non-Q wave MI

Q-wave MI

Ditandai dengan adanya Plaque Ruptur sebagai

dasar Patofisiologi secara umum

5/98 MedSlides.com 17


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Unstable Angina - Definition

angina at rest (> 20 minutes)

new-onset (< 2 months) exertional angina(at least CCSC III in severity)

recent (< 2 months) acceleration of angina(increase in severity of at least one CCSCclass to at least CCSC class III)

angina saat istirahat (> 20menit)baru-onset (


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Unstable Angina precipitating factors

Inappropriate tachycardia anemia, fever, hypoxia,

tachyarrhythmias, thyrotoxicosis

High afterload

aortic valve stenosis, LVH

High preload high cardiac output, chamber

dilatation

Inotropic state

sympathomimetic drugs, cocaine

intoxication

inappropriate tachycardiaanemia, demam, hipoksia,tachyarrhythmias, tirotoksikosisTinggi afterload

katup aorta stenosis, LVHTinggi preloadtinggi jantung output, dilatasi chambeInotropic negarasimpatomimetik obat, intoksikasi koka


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Unstable Angina prognostic indicators

Presence of ST-T-wave changeswith pain

Hemodynamic deterioration

pulmonary edema, new mitralregurgitation,

3rd heart sound, hypotension

Other predictors

left ventricular dysfunction,extensive CAD, age, comorbidconditions (diabetes mellitus,

obstructive pulmonary disease,renal failure, malignancy)

Kehadiran perubahan ST-T-gelombang dengan rasa sakitHemodinamik kerusakan

pulmonary edema,regurgitasi mitral baru,3 suara jantung, hipotensiLain prediktordisfungsi ventrikel kiri, CADluas, usia, kondisikomorbiditas (diabetes

mellitus, penyakit paruobstruktif, gagal ginjal,keganasan)


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Unstable Angina pathogenesis

Plaque disruption

Acute thrombosis Vasoconstriction


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Non-Q-Wave MI clues to diagnosis

Prolonged chest pain

Associated symptoms fromthe autonomic nervoussystem

nausea, vomiting,diaphoresis

Persistent ST-segmentdepression after resolutionof chest pain

Berkepanjangan nyeri dadaAsosiasi gejala dari sistemsaraf otonom

mual, muntah, diaforesisPersistent ST-segmendepresi setelah resolusi nyeridada


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Unstable Angina Risk Stratification

Low Risk

new-onset exertional angina

minor chest pain duringexercise

pain relieved promptly bynitroglycerine

Management

can be managed safely as anoutpatient (assuming close

follow-up and rapidinvestigation)

Risiko Rendahbaru-onset anginaexertionaldada nyeri ringan

selama latihansakit lega segera olehnitrogliserinManajemendapat dikelola denganaman sebagai rawatjalan (asumsi dekattindak investigasi-updan cepat


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Intermediate Risk

prolonged chest pain

diagnosis of rule-out MI

Management

observe in the ER or Chest PainUnit

monitor clinical status and ECG

obtain cardiac enzymes (troponinT or I) every 8 to 12 hours

Risiko Menengahberkepanjangan nyeri dadadiagnosis peraturan-out MI

Manajemenamati di ER atau Chest PainUnitmemonitor status klinis danEKGmemperoleh enzim jantung(troponin T atau aku) setiap8 sampai 12 jam


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High Risk

recurrent chest pain

ST-segment change

hemodynamic compromise

elevation in cardiac enzymes

Management

monitor in the Coronary CareUnit

Risiko Tinggiberulang nyeri dadaST-segmen perubahan

hemodinamik kompromielevasi dalam enzim jantungManajemenmonitor di Coronary Care Unit


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Risk Stratification by ECG

The risk of death or MI at 30 days isstrongly related to the ECG at thetime of chest pain.

ST depression 10%

T-wave inversion 5%

No ECG changes 1-2%

Risiko kematian atauMI di 30 hari sangatterkait dengan EKG

pada saat nyeri dada.ST depresi 10%T-gelombang inversi5%EKG Tidak adaperubahan 1-2%


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Unstable Angina Therapeutic Goals

Therapeutic Goals

Reduce myocardial ischemia

Control of symptoms Prevention of MI and death

Medical Management

Anti-ischemic therapy

Anti-thrombotic therapy

Terapi TujuanMengurangiiskemia miokardPengendalian

gejalaPencegahan MIdan kematianManajemen MedisAnti-iskemik terapiAnti-trombotikterapi


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Unstable Angina Medical Therapy

Anti-ischemic therapy nitrates, beta blockers,

calcium antagonists Anti-thrombotic therapy

Anti-platelet therapy aspirin, ticlopidine,

clopidogrel,GP IIb/IIIa inhibitors

Anti-coagulant therapy heparin, low molecular

weight heparin (LMWH),warfarin, hirudin, hirulog

Anti-iskemik terapinitrat, beta blocker, antagonis kalsiumAnti-trombotik terapiTerapi anti-trombositaspirin, Ticlopidine, clopidogrel, GP

IIb / IIIa inhibitorTerapi anti-koagulanheparin, heparin berat molekulrendah (LMWH), warfarin, hirudin,hirulog


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Unstable Angina Anti-ischemic Therapy

restrict activities

morphine

oxygen

nitroglycerine

pain relief, preventsilent ischemia, controlhypertension, improveventricular dysfunction

nitrate free periodrecommended after

the first 24-48 hours

membatasi kegiatanmorfinoksigennitrogliserinpenghilang rasa sakit, mencegah silent ischemiakontrol hipertensi, meningkatkan disfungsi

ventrikelperiode bebas nitrat direkomendasikan setelah24-48 jam pertama


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Unstable Angina Anti-ischemic Therapy

beta-blockers

lowering angina threshold

prevent ischemia and death after MI

particularly useful during highsympathetic tone

calcium antagonists

particularly the rate-limiting agents

nifedipine is not recommendedwithout concomitant -blockade

beta-blockermenurunkan ambang anginamencegah iskemia dan kematiansetelah MI

terutama berguna selama nadasimpatik tinggiantagonis kalsiumkhususnya tingkat-membatasi agenifedipin tidak dianjurkan tanpabersamaan-blokade


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Unstable Angina Anti-thrombotic Therapy

Thrombolytics are notindicated

lytic agents may stimulate

the thrombogenic processand result in paradoxicalaggravation of ischemiaand myocardial infarction

Circulation 1994; 89:1545-1556

Trombolitik tidak ditunjukkan"agen litik dapat merangsang proses

thrombogenic dan mengakibatkan kejengkelanparadoks iskemia dan infark miokard"


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Unstable Angina Anti-platelet Therapy

aspirinis the gold standard

irreversible inhibition of thecyclooxygenase pathway inplatelets, blocking formation ofthromboxane A2, and plateletaggregation

in AMI, ASA reduced the risk ofdeath by 20-25%

in UA, ASA reduced the risk offatal or nonfatal MI by 71%during the acute phase, 60% at 3months, and 52% at 2 years

bolus dose of 160-325 mg,

followed by maintenance dose of80-160 mg/d

aspirin adalah "standar emas"penghambatan ireversibel jalursiklooksigenase di trombosit,menghalangi pembentukantromboksan A2, dan agregasitrombositdi AMI, ASA mengurangi risikokematian sebanyak 20-25%di UA, ASA mengurangi risiko MIfatal atau nonfatal sebesar 71%selama fase akut, 60% pada 3bulan, dan 52% pada 2 tahun

bolus dosis 160-325 mg, diikutidengan dosis pemeliharaan 80-160mg / d


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Thienopyridines

ticlopidine (Ticlid;Hoffmann-La Roche)

clopidogrel (Plavix;Bristol-Myers Squibb)

block platelet aggregationinduced by ADP and thetransformation of GP IIb/IIIainto its high affinity state

ThienopyridinesTiclopidine (Ticlid; Hoffmann-La Roche)clopidogrel (Plavix, Bristol-Myers Squibb)

blok agregasi platelet diinduksi oleh ADP dantransformasi GP IIb / IIIa ke negara afinitas

tinggi

GP IIb/IIIa Receptor


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GP IIb/IIIa Receptor

Final Pathway to Platelet Aggregation

Platelet activation andaggregation are early events inthe development of coronarythrombosis

GP IIb/IIIareceptors on activated

platelets undergo aconformational change allowingrecognition and binding offibrinogen

Fibrinogenacts like glue,bridging GP IIb/IIIa receptors on

adjacent platelets, leading toplatelet aggregation

Aktivasi dan agregasi trombosit adalahkejadian awal dalam perkembangan trombokoronerGP IIb / IIIa pada reseptor platelet diaktifka

mengalami perubahan konformasimemungkinkan pengakuan dan pengikatanfibrinogenFibrinogen "bertindak seperti lem",menjembatani GP IIb / IIIa reseptor padatrombosit yang berdekatan, menyebabkanplatelet agregasi


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GP IIb/IIIa inhibitors

abciximab (monoclonal antibody)

eptifibatide (peptidic inhibitor)

lamifiban and tirofiban (non-

peptides)

direct occupancy of the GP IIb/IIIareceptor by a monoclonal antibody orby synthetic compounds mimicking theRGDsequence for fibrinogen bindingprevents platelet aggregation

GP IIb / IIIa inhibitorabciximab (antibodi monoklonal)eptifibatide (inhibitor peptidic)lamifiban dan tirofiban (non-peptida)hunian langsung dari GP IIb / IIIa reseptor

oleh antibodi monoklonal atau dengan senyawsintetis meniru urutan RAK untuk mengikatfibrinogen mencegah agregasi trombosit

Unstable Angina


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Unstable Angina

Anti-coagulant Therapy

Heparin recommendation is based

on documented efficacy inmany trials of moderatesize

meta-analyses (1,2) of sixtrials showed a 33% riskreduction in MI and

death, but with a two foldincrease in major bleeding

titrate PTT to 2x the upperlimits of normal

1. Circulation 1994;89:81-882. JAMA 1996;276:811-815

Heparin

rekomendasi didasarkan pada keberhasilan ujicoba banyak didokumentasikan dalam ukuransedangmeta-analisis (1,2) dari enam percobaanmenunjukkan pengurangan risiko 33% di MI dankematian, tetapi dengan peningkatan dua kalilipat pendarahan utamatitrasi PTT untuk 2x atas batas normal

Unstable Angina


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g

Anti-coagulant Therapy

Low-molecular-weight heparinadvantages over heparin:

better bio-availability

higher ratio (3:1) of anti-Xa to

anti-IIa activity longer anti-Xa activity, avoid

rebound

induces less platelet activation

ease of use (subcutaneous - qdor bid)

no need for monitoring

Rendah-molekul-berat heparin keunggulandibandingkan dengan heparin:lebih baik bio-ketersediaantinggi rasio (3:1) anti-Xa untuk kegiatan anlagi anti-Xa aktivitas, menghindari rebound

menginduksi aktivasi platelet kurangkemudahan penggunaan (subkutan - qd atatawaran)tidak perlu untuk memantau

ST Elevation Myocardial Infarction


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Diagnosis Risk Stratification

Acute Therapy Reperfusion

Adjunctive

Complications

Pre-Discharge Management



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History Classic symptoms: intense,

oppressive chest pressureradiating to left arm

Other symptoms:

chest heaviness, burning radiation to jaw, neck,

shoulder, back, arms

nausea, vomiting diaphoresis dyspnea lightheadedness

Symptoms may be mild or subtle


Classic gejala: intens, tekanan dada menindasmenjalar ke lengan kiriGejala lainnya:dada berat, terbakarradiasi ke rahang, leher, bahu, punggung,lenganmual, muntahdiaforesis

nafas yg sulitringanGejala mungkin ringan atau halus



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Physical Examination Tachycardia or bradycardia

Extrasystoles

S3 or S4, mitralregurgitation murmur

Lung rales

Hypertension orhypotension

Pallor, distress


Takikardi atau bradikardiExtrasystolesS3 atau S4, murmur regurgitasi mitral

Rales paru-paruHipertensi atau hipotensiPucat, marabahaya



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ElectrocardiogramDefines location, extent, and prognosis of infarction

ST elevation diagnostic of coronary occlusion

Q-waves do NOT signify completed infarction

ST depression or T inversion: unlikely total coronary occlusion

ST elevation in RV4 for RV infarction

Observe up to 24 hrs for non-diagnostic ECG

Differentiate from early repolarization in V1-2


Mendefinisikan lokasi, luas, dan prognosi

infarkST diagnostik oklusi koroner elevasiQ-gelombang TIDAK menandakan selesainfarkST depresi atau inversi T: oklusi koronertotal mungkinST elevasi di RV4 untuk infark RV

Amati hingga 24 jam untuk ECG non-diagnostikBedakan dari awal repolarisasi V1-2ListenRead phonetically

ECG change in acute myocardial


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P

Q

R

S

T > 2 mm

normal ECG ECG indicating AMI

ECG change in acute myocardialinfarction

ST Elevation MI (STEMI )


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ST Elevation MI (STEMI )


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LOKASI INFARK


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LOKASI INFARK



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Echocardiography Not diagnostic, but supportive

Identify regional wall motion abnormalities

Absence of contralateral wall hyperkinesiasuggestsmultivessel disease or IRA recanalization

Assess LV function, prior infarcts

More sensitive than ECG for RV infarctionTidak diagnostik, tetapi mendukungMengidentifikasi kelainan gerakan dindingregionalTidak adanya dinding hyperkinesia kontralateralmenunjukkan penyakit multivessel ataurekanalisasi IRAMenilai LV fungsi, infark sebelumnyaLebih sensitif dari EKG untuk infark RV



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Differential DiagnosisIschemic Heart Disease

angina, aortic stenosis, hypertrophic CMP

Nonischemic Cardiovascular Disease

pericarditis, aortic dissection

Gastrointestinal

esophageal spasm, gastritis, PUD,

pancreatitis, cholecystitis

Pulmonary

pulmonary embolism, pneumothorax,

pleurisy

Penyakit Jantung Iskemikangina, stenosis aorta, CMP hipertropiNonischemic Penyakit Kardiovaskularperikarditis, diseksi aortaGastrointestinal

kejang esofagus, gastritis, PUD, pankreatitis,kolesistitisParuemboli paru, pneumotoraks, radang selaputdada

Management of Acute MI


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Diagnosis

Risk Stratification


Adjunctive

Complications Pre-Discharge Management

DiagnosaStratifikasi RisikoTerapi akutReperfusiAdjunctiveKomplikasiPra-Discharge Manajemen

Acute MI - Risk Stratification


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ECG Classification - GUSTO I Outcome

Category Occlusion Site ECG 1-YearMortality

1. Prox LAD before septal ST V1-6, I, aVL 25.6%fasicular or BBB

2. Mid LAD before diagonal ST V1-6, I, aVL 12.4%

3. Distal LAD beyond diagonal ST V1-4 or 10.2%Diagonal in diagonal ST I, aVL, V5-6

4. Moderate-to- proximal RCA ST II, III, aVF and 8.4%large inferior or LCX V1, V3R, V4R or(post, lat, RV) V5-6 or

R > S V1-25. Small inferior distal RCA or ST II, III, aVF only 6.7%

LCX branch

Kategori Occlusion Situs ECG 1-Tahun


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g

Kematian

1. Prox LAD sebelum septum ST V1-6, aku, aVL 25,6%

fasicular atau BBB

2. LAD Mid sebelum diagonal ST V1-6, aku, aVL 12,4%3. LAD distal luar diagonal ST V1-4 atau 10,2%

Diagonal di ST diagonal saya, aVL, V5-6

4. Moderat-untuk-proksimal RCA ST II, III, aVF dan 8,4%

besar inferior atau LCX V1, V3R, V4R atau

(pos, lat, RV) V5-6 atau

R> S V1-25. Kecil distal RCA inferior atau ST II, III, aVF hanya 6,7%

LCX cabang



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Ejection Fraction

Gottlieb et al. Am J Cardiol 1992;69:977-984

707030302020 4040 5050 6060

50%50%

40%40%

30%30%

20%20%

00

10%10%

Ejection Fraction (%)Ejection Fraction (%)

Mortality (2-Year)



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Hemodynamic Subgroups - Killip Class

GISSI-1 (%)

Killip Definition Incidence Control LyticClass Mortality Mortality

I No CHF 71 7.3 5.9

II S3 gallop or 23 19.9 16.1basilar rales

III Pulmonary edema 4 39.0 33.0(rales >1/2 up)

IV Cardiogenic shock 2 70.1 69.9



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Diagnosis

Risk Stratification


Adjunctive Complications


DiagnosaStratifikasi RisikoTerapi akutReperfusiAdjunctiveKomplikasiPra-Discharge Manajemen

PENANGANAN ACS DI RUMAH SAKIT

PENANGANAN SKA DI RUMAH SAKIT


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45 % 75 %

Pasien dilakukan penanganan secara NON STENT / Non PCI

TUJUAN UTAMA

STRATEGI PENGOBATAN

Thrombolysis in Acute MI


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Uncontrolled HTN (BP > 180/110) on presentation

History prior CVA beyond 1 yr

Anticoagulant Rx with INR > 2-3; bleeding diathesis

Recent trauma (within 2-4 wks)

Noncompressible vascular punctures

Recent internal bleeding (within 2-4 wks)

Pregnancy

Active peptic ulcer

Prior exposure (5 day - 2 yr) for SK or APSAC

yRelative Contraindications


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Hipertensi yang tidak terkontrol (BP> 180/110)

presentasiSebelum CVA luar 1 Sejarah thAntikoagulan Rx dengan INR 2-3>; diatesisperdarahanRecent trauma (dalam waktu 2-4 wks)Noncompressible vaskular tusukanRecent perdarahan internal (dalam waktu 2-4

wks)KehamilanUlkus peptik aktifSebelum paparan (5 hari - 2 tahun) untuk SKatau APSAC

Thrombolysis in Acute MI


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Absolute Contraindications

Previous hemorrhagic stroke

CVA within previous yr

Intracranial neoplasia or AVM

Active internal bleeding (not menses)

Suspected aortic dissection

Sebelumnya hemorrhagic strokeCVA dalam tahun sebelumnyaNeoplasia atau AVM intrakranialPendarahan internal aktif (tidak menDiduga diseksi aortaListen

Read phonetically

Myocardial Reperfusion


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The Original Paradigm

Re-establishInfarct Vessel

Patency

Limit InfarctSize

Mortality

Thrombolytic: Placebo-Control


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Streptokinase GISSI 495/4865 623/4878 23% 6

ISAM 50/842 61/868 16% 18

ISIS-2 471/5350 648/5360 30% 5

APSAC AIMS 32/502 61/502 50% 16

t-PA ASSET 182/2516 245/2495 28% 9

Overall: any thrombolytic 1230/14075 1623/14103 27% 3

Patients < 6 hours 8.7% 11.6%

OddsAgent Trial Name Deaths/Patients Odds Ratio Reduction

Active Control (& 95% Cl) ( s.d.)

Lytic better Lytic worse

0.0 0.5 1.0 1.5 2.

Meta-Analysis

Thrombolysis for Acute MI


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00

1010

2020

3030

4040

00 66 1212 1818 2424

Absolute Mortality Reduction per 1000 PatientsAbsolute Mortality Reduction per 1000 Patients

Time from Symptom Onset to Randomization (h)Time from Symptom Onset to Randomization (h)

Time to Therapy and Mortality ReductionPooled Analysis of Randomized Trials

Fibrinolytic Therapy Trialists. Lancet 1994;343:311.


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Primary PCITreatment ofchoice for Acute M


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TATALAKSANA INFARK MYOCARDIAL AKUT


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Thrombololytic PRIMARY PTCA


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APA itu EBM ?


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ESC Guidelines for the treatment of ST segment elevationMI


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Class

evidence

Level

evidence

Primary PCI preferred treatment ifperformed by experienced

team


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STENTING ( CINCIN )


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Aspirin in Acute MI

ISIS 2


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ISIS-2

ISIS-2 Collaborative Group, Lancet 1988;2:349.

PlaceboPlacebo ASAASA SKSK SK + ASASK + ASA

00

55

1010

1515

2020 35 Day Mortality (%)35 Day Mortality (%)

13.213.2

10.710.7 10.410.488

4300 43004295 4292

Aspirin in Acute MI

Recommendations


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Recommendations

Indicated in ALL patients with acute MI,

except for true aspirin allergy (notintolerance)

Initiate orally with chewable compound, at

least 160 mg stat

some data suggest first dose shouldbe

650 mg to achieve full antiplatelet

effect

Continue 325 mg per day indefinitely

Diindikasikan pada pasienSEMUA dengan MI akut, kecualiuntuk alergi aspirin benar (tidakintoleransi)Memulai secara lisan dengansenyawa kunyah, setidaknya 160mg statbeberapa data yang

menyarankan dosis pertamaharus 650 mg untuk mencapaiefek antiplatelet penuhLanjutkan 325 mg per hari tanpabatas

GUIDELINE PENANGANAN PASIENACS NON STENT


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BAGAIMANA GUIDELINES MENURUT ESC & ACC-AHA

NEW ACLS - ACS ALGORITHM


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NEW ACLS ACS ALGORITHM

ACC / AHA

Update 2007

Nyeri dada (kecurigaan ischemia)

ACC/AHA ACLS ACS Algorithm2006

1


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Diagnosa, penatalaksanaan dan persiapan/pre hospital oleh EMS :

- Monitor, support ABC. Persiapan untuk CPR dan defibrilasi

- Berikan oksigen, aspirin, nitroglycerin dan morphine bila dibutuhkan

- Jika tersedia, periksa ECG 12 lead, jika terdapat ST-Elevasi :

Hubungi rumah sakit yang dituju dengan DX pasien

Mulai membuat fibrinolytic checklist

- RS yang dituju harus menyaiapkanMobilize Hospital Resourcesuntuk

merespon pasien STEMI

Diagnosa cepat oleh Emergency Departemen Penatalaksanaan umum cepat oleh E.D( 90%- Anamnese singkat, terarah, pemeriksaan fisik -Nitroglycerin SL atau spray atau IV- Periksa awal level cardiac marker, elektrolit -Aspirin 160 samapai 325 mg (jika tidakDan faal hemostatis diberikan oleh EMS)

- Periksa Rontgen dada (


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( / ) g

Mulai terapi tambahan sesuai indikasi.Jangan menunda reperfusi

-Clopidogrel--adrenergic reseptor blockers-Heparin (UFH or LMWH)

Mulai terapi tambahan sesuai indikasi

-Clopidogrel-Nitroglycerin--adrenergic reseptor blockers-Heparin (UFH or LMWH)-Glycoprotein IIb/IIIa inhibitor

Berlanjut memenuhi kriteria sedang atautinggi (tabel 3,4)atau troponin positive?

Onset gejala < 12 jamOpname di ruangan dgn monitoring bed

Tentukan status resiko

Pertimbangkan opname di ED chestpaint unit atau monitored bed di EDLanjutkan dengan :Serial cardiac marker (termasuktroponin)Ulang ECG, monitor segmen STPertimbangan stress test

Strategi reperfusi:Terapi ditetapkan berdasarkankeadaan pasien dan center criteriaMenyadari tujuan terapi reperfusi:Door-to-balloon inflation (PCI) = 90mntDoor-to-needle (fibrinolysis) = 30mntLanjutkan dengan terapi:

ACE inhibitor/angiotensi receptorblocker (ARB) 24 jam dari onsetHMG CoA reductase inhibitor (statin

therapy)

Pasien High-risk:Refractory ischemic chest painRecurrent/persistent ST deviation

Ventricular tachycardiaHemodynamic tachycardiaSigns of pump failureStrategi invasive awal termasukkateterisasi & revaskularisasi penderitaIMA dgn syok dlm 48 jamLanjutkan pemberian ASA, heparin &terapi lain sesuai indikasi:

ACE inhibitor / ARBHMG CoA reductase inhibitor (statintherapy)Tidak pada resiko tinggi: penentuanpenggolongan resiko dari cardiology

Berlanjut memenuhi kriteria resikotinggi atau sedang (tabel 3,4)

atautroponin-positive

Jika tidak ada ischemia atau infare,

maka dapat pulang denganrencana kontrol

10

11

12

6

7

8

14

15

16

17

ACC/AHA 2007 Guidelines Updateuntuk UA / NSTEMI

Rekomendasi untuk Antiplatelet dan Anticoagulant 1


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6/29/2013

Low Risk ACSHigh Risk ACSIntermediate Risk ACS

Early Conservative ManagementAspirin* (Class IA)

Clopidogrel# (Class IA)LMWH (enoxaparin)/UFH (Class IA)

Early Invasive ManagementAspirin* (Class IA)

Clopidogrel (Class IA)LMWH (enoxaparin)/UFH (Class IA)

* Or Clopidogrel if contraindicated (IA)#

For at least 1 month (IA) and for up to 9 months (IB)Gibler, WG, et al. Circul. 2005; 111: 2699-2710

ESC Guidelines 2007

ASA ( Klas 1 A )


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Direkomendasikan pada semua pasien NSTE-ACS bila tidak ada kontra

indikasi, dengan initial LD 160-325 (non enteric) dan dosis pemeliharaan 100 mg untuk jangka panjang

CLOPIDOGREL ( Klas 1A )

Untuk semua pasien ACS, SEGERA berikan Clopidogrel 300mg LD,

dilanjutkan dengan 75mg/ hari, Clopidogrel harus dilanjutkan hingga 12

bulan, kecuali ada resiko tinggi perdarahan.

Untuk pasien yang kontra indikasi terhadap ASA, Clopidogrel harus

digunakan sebagai penggantinya ( 1B )

1. Clopidogrel di indikasikan pada pasien dengan UA, NSTEMI, dan STEMI da

LEARNING FROM GUIDELINES


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g g

diberikan bersama ASA. Clopidogrel diberikan tunggal jika ASA

kontraindikasi.

2. Efek yang cepat dan memberikan perlindungan yang lebih besar jika

pemberian clopidogrel therapy dimulai dengan loading dose 300-mg. dosis

3. Clopidogrel direkomendasikan sebagai antiplatelet Class 1 untuk

penanganan ACS baik STEMI maupun NON STEMI. ( ACC-AHA / ESC /

AUSSIE )

Acute MI

Heparin


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Heparin

Intravenous heparin recommended with t-PA(intial bolus 5000 U, infusion 1000 U/hr, adjust forweight < 50 kg)

No clear data for benefit with streptokinase and

increased bleeding

Discontinue after 24 hrs, except for:

atrial fibrillation recurrent ischemia

anteroapical MI for CVA prophylaxis


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Heparin intravena direkomendasikan dengan t-PA(bolus awal 5000 U, infus 1000 U / jam,menyesuaikan berat 50 kg


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ACE Inhibitors in Acute MI

Pooled Analysis of Randomized Trials


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Mortality Odds Ratio & 95% CI

0 1

Hennekens et al. NEJM 1996;335:1660.

Study N

DuringMI

Agent

ISIS-4 58,050Captopril

GISSI-3 19,394Lisinopril

CONSEN II 6,090Enalaprilat

SAVE 2,231Captopril

AIRE 2,006RamiprilPostMI

Control BetterRx Better

TRACE 1,749Trandolapril

Adjunctive Therapy for Acute MI

Calcium Channel Antagonists


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Agent Ca+2Ant ControN

15.0%Nifedipine 13.0%1358

Odds Ratio & 95% CI

0 1 2More MortalityLess Mortality

10.8%Verapamil 13.3%1775

13.5%Diltiazem 13.5%2466

12.4%Verapamil/Diltiazem

13.4%4241

13.0%Pooled 13.3%5599

Held et al, in Topol: Text Int Cardiol 2nd Ed 1993, p.52.

Management of Acute MI Diagnosis


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Risk Stratification


Adjunctive

Complications Pre-Discharge

Management

Diagnosa

Stratifikasi RisikoTerapi akutReperfusiAdjunctiveKomplikasiPra-Discharge Manajemen

Complications of Acute MI


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Extension / Ischemia

Acute MI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical Mural Thrombus

Acute MI - Recurrent Infarction / Ischemia

Pathophysiology


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In distribution of infarct vessel: IRA reperfusion, then reocclusion

thrombus propogation, branch occlusion

distal embolization

reduced coronary perfusion pressure with severe residual

IRA stenosis reduced collateral flow from stenosed artery

At a distance:

reduced collateral flow from IRA

new coronary thrombus (hypercoagulable state)

reduced systemic perfusion pressure increased myocardial oxygen consumption


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Dalam distribusi kapal infark:IRA reperfusi, maka reocclusion

trombus penjalaran, oklusi cabangembolisasi distalmengurangi tekanan perfusi koroner denganstenosis IRA berat sisamengurangi jaminan mengalir dari arteristenosed

Di kejauhan:mengurangi jaminan mengalir dari IRAbaru koroner trombus (negara hiperkoagulasi)mengurangi tekanan perfusi sistemikpeningkatan konsumsi oksigen miokard

Acute MI - Complications

Recurrent Ischemia / Infarction


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Prevention:

Aspirin

Beta blockers

ACE inhibitors with low LVEF

? heparin with fibrin-specific lytics (reocclusion)

Treatment:

Pharmacologic (beta blockers, nitrates)

IABP

Urgent revascularization Repeat lytics (antibodies to SK)


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Pencegahan:

AspirinBeta blockersACE inhibitor dengan LVEF rendah? heparin dengan lytics fibrin-spesifik(reocclusion)Pengobatan:

Farmakologis (beta blockers, nitrat)IABPMendesak revaskularisasiUlangi lytics (antibodi terhadap SK)

Acute MI - CHF and Shock

Pathophysiology


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Extensive (or multiple) LV infarction(s) - systolic dysfunction Impaired relaxation, compliance due to infarction or ischemia -

diastolic dysfunction

Extensive RV infarction or ischemia

VSD or acute severe MR

Tamponade (w/ or w/o free wall rupture)

Others

e.g. critical valve stenosis or regurgitation, toxic-metabolic,

sepsis, beta- or Ca+2-blocker overdose, pulmonary embolism,bowel ischemia

Luas (atau beberapa) LV infark (s) - disfungsi sistolik

Gangguan relaksasi, kepatuhan karena infark atau iskemia -

disfungsi diastolik


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g

RV luas infark atau iskemia

VSD atau MR berat akut

Tamponade (w / atau w / pecah dinding o gratis)

Lain-lain

misalnya katup stenosis atau regurgitasi kritis, racun-

metabolik, sepsis, overdosis beta-blocker atau Ca +2-,emboli paru, iskemia usus

Acute MI - CHF and Shock

Hemodynamic Subsets


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Subset PCWP CI Clinical Setting(mm Hg) (l/min)

1 < 18 > 2.2 asymptomatic

2 > 18 > 2.2 pulmonary congestion

3 < 18 < 2.2 RV failure,hypovolemia, or

profound venodilation

4 > 18 < 2.2 severe LV dysfxn

cardiogenic shock

Forrester JS et al. NEJM 1976;295:1356 and 1404.

Acute MI - Cardiogenic Shock

Outcome with PTCAPooled Analysis of 22 Retrospective Studies


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Pooled Analysis of 22 Retrospective Studies

Historical controlmortality ~ 80%

Total 646 pts

PTCA success rate= 76%

TotalTotal

SuccessfulPTCA

Successful

PTCA UnsuccessfulPTCA

Unsuccessful

PTCA

00

2020

4040

6060

8080

100100Mortality (%)Mortality (%)

4545

3333

8181

Hochman, Gersh in Topol, Text Cardiovasc Med 1998, p. 461.

Acute MI - Mechanical Complications

Free Wall Rupture


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Less frequent (1-3.4%), but earlier, with thrombolysis

Uncontained sudden EMD or asystole

Pseudoaneurysm transient hypotension, EMD,bradycardia, repetitive emesis, restlessness

Echocardiogram usually diagnostic

Surgical repair - may require pericardiocentesis for

uncontained rupture


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Kurang sering (1-3,4%), tetapi sebelumnya,dengan trombolisisTidak mengandung EMD mendadak atau adadetak jantungPseudoaneurysm hipotensi transien, EMD,bradikardia, emesis berulang, kegelisahanEchocardiogram biasanya diagnostik

Perbaikan bedah - mungkin memerlukanpericardiocentesis untuk pecah tidakmengandung


Interventricular Septal Rupture


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Incidence 1-3% of transmural MIs

Acute shock, pulmonary edema, right heart failure, new loud

pan-systolic murmur (thrill in 50%)

Diagnose with echocardiogram or O2 saturation step-up

Medical stabilization and IABP for CHF, shock

Early surgical repair for decompensated pts; mortality highest in

pts with inferior MI and complex ruptures involving RV (~70%),

lowest for apical ruptures (~30%)

Small asymptomatic VSDs may not require repair


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Infarct ExpansionPotensi konsekuensi:


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Potential consequences: LV aneurysm +/- mural

thrombus +/- embolization

adverse LV remodeling and CHF

ventricular rupture ventricular arrhythmias

Prevention:

ACE inhibitors

? nitrates

the open artery

LV aneurisma + / - mural

trombus + / - embolisasimerugikan LV remodelingdan CHFventrikel pecahventrikel aritmiaPencegahan:ACE inhibitor

? nitratyang "arteri terbuka"


Acute Mitral Regurgitation Transient MR common in early MI (20-40%)


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Transient MR common in early MI (20 40%)

Associated with advanced age, prior MI,

infarct extension, recurrent chest pain, CHF,

female gender

Persistent MR, even mild, associated with

increased long-term mortality post-MI

May be due to papillary muscle or chordal

rupture or to geometric changes (dilation) of

ventricle and annulus Most common with inferior MI (single blood

supply to posteromedial papillary muscle) -

MI often small

Transien umum MR di MI awal (20-40%)

Terkait dengan usia lanjut, sebelum MI, perluasan infark, nyedada berulang, CHF, jenis kelamin perempuanPersistent MR, bahkan ringan, berhubungan denganpeningkatan jangka panjang pasca kematian-MIMungkin karena otot papiler atau pecah chordal atauperubahan geometrik (dilation) ventrikel dan anulus

Paling umum dengan inferior MI (suplai darah tunggal untukposteromedial otot papiler) - MI seringkali kecil

Acute Mitral Regurgitation

Diagnosis and Management

harsh, short systolic murmur - may be

muffled keras murmur sistolik pendek - mungkin


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muffled

sudden CHF +/- hypotension or shock 2-7

days post MI

echocardiography (surface or TEE) usually

diagnostic - mobile papillary muscle head or

flail MV leaflet

LV function often normal or hyperkinetic

sudden hemodynamic deterioration common

stabilize medically, IABP, then surgical repair surgical mortality high if shock is present

role of surgery in MR not due to rupture less

clear

keras, murmur sistolik pendek - mungkinteredammendadak CHF + / - hipotensi ataushock 2-7 hari pasca MIechocardiography (permukaan atau TEE)biasanya diagnostik - mobile otot kepalapapiler atau memukul MV leafletLV fungsi sering normal atau

hyperkineticmendadak kerusakan hemodinamikumummenstabilkan medis, IABP, maka bedahperbaikanbedah kematian tinggi jika shock hadirperan operasi dalam MR tidak akibat

pecahnya kurang jelas


Right Ventricular InfarctionA i t d ith l i f i l RCA


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Associated with occlusion of proximal RCA

Classic triad by hypotension, JVP, clear lungsspecific but insensitive

Kussmauls sign, JVP > 8 cm H2O sensitive andspecific

EKG: ST in RV4

Echo: RV dilation and hypokinesia

PA catheter: RA >10 mm, RA/PCWP ratio > 0.8

Terkait dengan oklusi proksimal

RCAClassic triad oleh hipotensi, JVP, paru-paru yang jelas khusus,

namun tidak sensitifKussmaul's sign, JVP> 8 cmH2O sensitif dan spesifikEKG: ST di RV4Echo: RV pelebaran danhypokinesiaKateter PA: RA> 10 mm, RA /rasio PCWP> 0,8ListenRead phonetically

Acute MI - RV Infarction

Management


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Extensive irreversibleinfarction is unusual -

transient ischemic dysfunction with long-

term recovery common

Marked by sensitivity to preload reduction

(nitrates, diuretics, morphine), bradycardia,

AV block

Fluid volume infusion for hypotension and

low

cardiac output

PCWP elevation may occur due to septal

shift

Dobutamine if fluids RA and PCWPwithout improved BP and CI

nfark Ekstensif ireversibel tidak biasa -

disfungsi iskemik transient denganpemulihan jangka panjang umumDitandai dengan kepekaan terhadappengurangan preload (nitrat, diuretik,morfin), bradikardia, AV blokVolume cairan infus untuk hipotensidan output jantung yang rendahElevasi PCWP dapat terjadi karenapergeseran septalDobutamine jika cairan RA dan PCWPtanpa BP ditingkatkan dan CI

Acute MI - Arrhythmias

Ventricular Tachycardia or Fibrillation

Prognosis of VT or VF in first 48 hoursPrognosis VT atau VF dalam 48 jampertama kontroversial


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Prognosis of VT or VF in first 48 hours

controversial

MILIS - no increased in-hospital mortality

GISSI - increased in-hospital mortality

No increased mortality after hospital

discharge

VT or VF after first 48 hours associated with

poorer long-term prognosis

Acute management - K+ replacement,

antiarrhythmic therapy (lidocaine, procainamide,

or amiodarone) if stable, electrical shock if

unstable

Long term management - pharmacologic

therapy of unclear benefit, ICD may be

beneficial

pertama kontroversial

MILIS - tidak meningkat kematiandi rumah sakitGISSI - peningkatan mortalitas dirumah sakitTidak ada kematian meningkatsetelah dikeluarkan dari rumah sakitVT atau VF setelah 48 jam pertama

berhubungan dengan prognosisjangka panjang miskinAkut manajemen - K + pengganti,terapi antiarrhythmic (lidocaine,procainamide, atau amiodarone)jika stabil shock, listrik jika tidak

stabilManajemen jangka panjang -farmakologi terapi manfaat jelas,ICD mungkin beRMANFAAT


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Acute MI - Antiarrhythmic Agents

Pooled Analysis of Randomized Trials

St d NA t


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0.1 1

NEJM 1996;335:1660. Lancet 1997;349:667 and 675.

Study N

ClassI

Agent

CAST 1,498Enc / Flec

CAST II 1,325Moricizine

EMIAT 1,486Amiodarone

CAMIAT 1,202AmiodaroneClassIII

Control BetterRx Better

SWORD 3,121d-Sotalol

Julian et al 1,456l-Sotalol

Acute MI - Arrhythmias

Indications for Permanent Pacing


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persistent complete (third-degree) AV block

persistent sinus node dysfunction - symptomaticbradycardia

intermittent second-degree Mobitz II or third-degreeAV block

second-degree Mobitz II or third-degree AV blockwith new bundle branch block

PERSISTENT lengkap(tingkat tiga) AV blokgigih disfungsi sinus node -bradikardia simptomatikintermiten tingkat duaMobitz II atau blok AV

derajat ketigatingkat dua Mobitz II atautingkat tiga blok AVdengan blok cabangbundel baru


Diagnosis

Risk Stratification DiagnosaStratifikasi Risiko


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Adjunctive

Complications

Pre-DischargeManagement

Stratifikasi Risiko

Terapi akutReperfusiAdjunctiveKomplikasiPra-Discharge Manajemen

Acute MI



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Risk stratification

Catheterization andrevascularization strategy

Electrophysiologic evaluationfor VT or VF

Lifestyle modification: diet,exercise, tobacco

Pharmacologic therapy

Stratifikasi risikoKateterisasi danstrategi revaskularisasiElektropsikologievaluasi untuk VT atau

VFModifikasi gaya hidup:diet, olahraga,tembakauTerapi farmakologis

Acute MI Management

Pharmacologic Therapy on Hospital Discharge


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Aspirin indefinitely (ticlopidine orclopidogrel for aspirin allergy orintolerance)

Beta blockers for at least 2-3 years

ACE inhibitors for CHF, LVEF


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STENTING ( CINCIN )


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OPERASI BYPASS KORONER


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OSAMA BIN LADEN


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Documents

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