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Cholid Tri TjahjonoLab Kardiologi dan Kedokteran Vaskular
Fakultas Kedokteran
Univ ersitas Brawijaya
Tata laksana
Sindroma Koroner Akut
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Definisi Sindroma Koroner Akut Acute coronary syndrome (ACS) describes the continuum
of myocardial ischemia that ranges from unstable anginaat one end of the spectrum to nonST segment elevationmyocardial infarction (MI) at the other end.
Unstable angina is distinguished from stable angina by the
new onset or worsening of symptoms in the previous 60days or by the development of post-MI angina 24 hours ormore after the onset of MI.
When the clinical picture of unstable angina isaccompanied by elevated markers of myocardial injury,
such as troponins or cardiac isoenzymes, nonSTsegment elevation MI is diagnosed.
The distinction between nonST segment elevation MI andMI with ST segment elevation is clinically importantbecause acute recanalization therapy is critical for
improving the outcome in ST elevation MI but is lessurgent in nonST segment elevation MI.
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Definition
Myocardial infarction (MI) is myocardial necrosiscaused by ischemia.
Practically, MI can be diagnosed and evaluated
by clinical, electrocardiographic, biochemical,
radiologic, and pathologic methods.
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ACUTE CORONARY SYNDROME
No ST Elevation ST Elevation
Unstable Angina NQMI QwMI
Myocardial
Infarction
NSTEMI
SINDROMA KORONER AKUT
spektrum sindrom klinis yang mencakup angina tak stabil
sampai ke non ST elevasi MI dan ST elevasi MI
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Mengapa SKA harus SEGERA
ditangani?
Mortalitas dan morbiditas tinggi , 40 %kematian terjadi sebelum sampai di rumah sakit
( HARUS SEGERA DIRUJUK!!)
Setidaknya 250.000 kematian sehubunganinfark miokard terjadi dalam 1 jam setelah onsetgejala dan sebelum terapi dimulai (USA)
Dalam 2 minggu setelah diagnosa, Infarkmiokard terjadi pada 12% pasien dengan U.A.
Dalam SATU tahun hampirsetengah kematianterjadi pada 4 minggu pertama setelahdiagnosa.
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Angina Stabil
Angina Tidak stabil
Infark Miokard Akut Gagal Jantung
Kematian
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Atherogenesis and Atherothrombosis:A Progressive Process
NormalFatty
StreakFibrousPlaque
Athero-scleroticPlaque
PlaqueRupture/Fissure &
Thrombosis
Myocardial
Infarction
Ischemic
Stroke
Critical
Leg
IschemiaClinically Silent
Cardiovascular Death
Increasing Age
Angina
Transient Ischemic Attack
Claudication/PAD
3
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Different Stage of Atherosclerosis Development
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Pathway to Thrombosis
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Faktor risiko Penyakit Jantung
Koroner
Merokok,berapapun jumlahnya Kadar kolesterol total dan LDL yg
tinggi Hipertensi Diabetes mellitus Usia lanjut
Faktor risiko ini sifatnya independen dan aditif, semakinbanyak memiliki Faktor risiko semakin besar risiko menderita PJK
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Faktor predisposisi
faktor yang memperbesar risiko PJK akibat faktorrisiko yang kausal
1.Obesitas (BMI >25 Kg/m2)
2.Obesitas abdominal (lingkar pinggang >94cm(pria)-
>80cm(wanita); waist-hip ratio>0,9(pria) dan>0,8 (wanita)
3.Sedentary
4.Riwayat keluarga terkena PJK usia muda (pria:
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Faktor risiko kondisional:Berhubungan dengan peningkatan risiko
PJK
1.Kadar trigliserida yang tinggi
2.Homosistein serum yang tinggi3.Lp(a) yang tinggi
4.Faktor protrombotik (mis;fibrinogen)
5.Penanda inflamasi (mis CRP)
Pedoman tata laksana SKA denganST elevasi , PERKI 2004
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KELUHAN UTAMA:
Sakit dada atau nyeri ulu hati yang berat, asalnya non-
traumatik, dengan ciri-ciri tipikal iskemia miokard atauinfark:
Dada bgn tengah/substernal rasa tertekan atau sakit
seperti diremas
Rasa sesak, berat/tertimpa beban , mencengkeram,terbakar,sakit
Penjalaran ke leher, rahang, bahu, punggung atau 1
atau ke 2 lenganDisertai sesak
Disertai mual dan/atau muntah
Disertai berkeringat
Sakit perut yg tdk dpt dijelaskan, sendawa, nyeri uluhati
Start ECG
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KEADAAN YANG DAPAT
MENIMBULKAN SAKIT DADA
Kardiak : SKA: Infark,angina
MVP (mitral valveprolaps)
Stenosis Aorta Kardiomiopati
hipertropi
Perikarditis
Paru :
Emboli Paru Pneumonia
Pneumothorax
Pleuritis
Gastrointestinal :
Reflux esofagus
Ruptur esofagus
Penyakit kel empedu
Ulkus peptikumPankreatitis
Vaskuler
Diseksi Aorta /aneurisma
Lain-lain:
Musculoskeletal
Herpes zoster
ACC/AHA Guideline of STEMI 2004
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NYERI KARDIAK :
Tidak berhubungan dengangerakan respirasi dan batukTidak berhubungan denganposisi dan gerakan tubuh
Tidak berhubungan dengankondisi lain seperti herpeszoster, trauma, dll
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ANGINA PEKTORIS
Sifat & kualitas
LokasiPenjalaranDurasi
Gejala dan tanda klinis yangmenyertainya
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Angina Pektoris Stabil ( Stable Angina
Pectoris)
ANGINA PEKTORIS STABIL, ditandai nyeri dada
atau rasa tidak enak sewaktu adanya beban
(aktivitas, beban mental) dimana kebutuhanmiokardium tidak dapat dipenuhi dengan
suplai yang cukup.
Angina Stabil dapat diprediksi dan dapat hilang atau
berkurang dengan istirahat dan nitrogliserin.
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Angina Pektoris Tak Stabil (Unstable
angina )3 Penampilan klinis tersering:
Angina saat istirahat, terus menerus 20 menit atau
lebih Angina pertama kali setidaknya CCS kelas III dari
Canadian Cardio-vascular Society Classification(CCSC)
Angina yang meningkat, angina makin lama makinsering,makin lama atau makin mudah tercetus.
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Anatomi Koroner dan EKG 12 sandapan
Sandapan V1 dan V2 menghadap septal area ventrikel kiri
Sandapan V3 dan V4 menghadap dinding anterior ventrikel kiri
Sandapan V5 dan V6 ( ditambah I dan avL ) menghadap
dinding lateral ventrikel kiri
Sandapan II, III dan avF menghadap dinding inferior ventrikel kiri
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Mid LAD occlusion
after the first septal
perforator (arrow)ECG : large anterior MI
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Occlusion of diagonal
branch ( arrow)
ST elevation in I and aVL
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ECG demonstrates large anterior infarction
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Proximal large RCA occlusion
ST elevation in leads II, III, aVF, V5, and V6
with precordial ST depression
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Small inferior distal RCA occlusion
ECG changes in leads II, III, and aVF
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Early repolarization
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Unstable angina
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Subendocardial ischemia.
Anterolateral ST-segment depression
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Acute anteroseptal myocardial infarction.
Hyperacute T-wave changes are noted
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Acute anterolateral myocardial infarction
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High lateral infarction
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Lateral myocardial infarction
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Inferior myocardial infarction
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Acute inferoposterior myocardial infarction
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Right bundle branch block
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Pemeriksaan awal pada Sindrom Koroner Akut
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SAKIT DADAMasuk RS
Diagnosis
Kerja
ECG
Bio-
chemistry
Stratifikasi
risiko
Pengobatan
Pencegahan
sekunder
Curiga Sindrom Koroner Akut
Elevasi ST
menetap
Tanpa Elevasi
ST menetap
Normal atau
Tdk dpt ditentukan
Troponin
(CKMB)
Troponin ECG
Troponin
2 X negative
Risiko tinggi Risiko rendah
Pemeriksaan awal pada Sindrom Koroner Akut
Mungkin bukan SKA
SINDROMA KORONER AKUTP N i D d
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SINDROMA KORONER AKUTAspirin 160 / 320mg mg dikunyah dan Nitrat s.l.
Psn Nyeri Dada
Rwyat nyeri dada
khas
EKG 12 sandapan
Petanda biokimia
EKG Non diagnostik
Petanda biokimia (-)
Nyeri dada (-)
Perubahan ST/T
Petanda biokimia (+)
Nyeri dada menetap
Elevasi seg
ST
Evaluasi utk
reperfusi
APTS/NSTEMI
Observasi
EKG serial
Ulang petanda
6-12 jam stlh
onset nyeri dada*
EKG tdk
berubah
Petanda(-)
Nyeri dada(-)
Perubahan seg ST
Petanda (+)
Nyeri dada
menetap
Pulang
*
Risiko rendah
Periksa di
Rawat jalan
Risko tinggi
Periksa
segera
Rawat Terapi
Nitrat
ASA
Clopidogrel
UFH/LMWH
(+/- Antagonis
Receptor GPIIb/IIIa
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Pasien dengan tanda dan gejala klinis SKA
EKG 12 sadapan
ST Elevasi = STEMI
> 0.1 mV pd > 2 sadapan ekstrimitas yang bersebelahan
dan/atau > 0,2 mV pd > 2 sadapan prekordial yang
bersebelahan atau LBBB baru (yang dianggap baru) EKG Abnormal lainnya (Bukan ST elevasi)atau
EKG normal
High Risk (Risiko Tinggi)
-Perubahan EKG yang dinamis meliputi ST depresi
- hemodinamik
-irama yang tidak stabil (aritmia malignan)- diabetes melitus
= Non STEMI, jika nilai troponin positif (T atau I)
Low Risk (Risiko rendah)
Tidak ada tanda-tanda high risk
= UAP , jika nilai troponin negatif
ALGORITMA DIAGNOSIS SKA ACC/AHA
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SAKIT DADA ISKEMIK
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Nilai dan tatalaksana segera ( 8-12 jam ?
RevaskularisasiPTCACABG
ICCU :
Terapi sesuai indikasiSerum serialEKG serialEcho/radionuklir
Boleh
Rawat jalan
& kontrol
teratur
Ya
> 12 jam
< 12 jam
Atau alternatifekuivalen
YaTdk
TdkYa
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TERAPI PADA SINDROMA KORONER AKUT
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PERAWATAN DI RUMAH SAKIT
1.Pain k i l ler (morf in )
2.Suplemen O23.Terapi anti iskemia
Nitrat
Beta Bloker
CCB
4.Antiplatelet dan antikoagulan
Aspirin,Ticlopidine, Clopidogrel
Heparin atau Low Molecular Weight Heparin
Tranquil izer
5.Fibrinolisis ( pada infark miokard dengan elevasi ST)6. Revaskularisasi koroner
Tata laksana pasca perawatan di rumah sakit
MO
N
A
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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 dalampemakaian secara IV
Berkaitan dengan kejadian perdarahan yang kecil,namun bukan perdarahan besar
Stimulasi trombosit kurang dari UFH dan jarang
menimbulkan HIT (Heparin inducedthrombocytopenia)
Penghematan biaya perawatan (dari studi ESSENCE)
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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
1X2.5 mg/hari
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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 MI
with heparin : anterior MI
tPA
15 mg IV bolus kemudian 0.75 mg/Kg selama 30mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt
berikutnya
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Secondary Prevention and Long Term Management
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y g g
Status of tobacco use should be asked at
every visit.
Every tobacco user and family member who
smoke should be advised to quit at every visit.
The tobacco users willingness to quit shouldbe assessed.
The tobacco user should be assisted by
counseling and developing a plan for quitting.
Follow-up, referral to special programs, or
pharmacotherapy (including nicotinereplacement and pharmacological rx) should
be arranged.
Exposure to environmental tobacco smoke at
home and work should be avoided.
Smoking
2007Goal:Complete
cessation.
No exposure toenvironmental
tobacco smoke.
Goals Class I Recommendations
NEW
NEW
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Secondary Prevention and Long Term Management
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78
If TG are 150 mg per dL or HDL-C < 40 mg per dL, weightmanagement, physical activity, and smoking cessation should be
emphasized.
If TGs are 200 to 499 mg per dL, nonHDL-C target should be less than
130 mg per dL.
If TGs are 200 to 499 mg/dL, nonHDL-C target is < 130 mg/dL. (ClassI; LOE: B); further reduction of nonHDL-C to < 100 mg dL is reasonable.
(Class IIa; LOE: B)
Therapeutic options to reduce nonHDL-C include:
More intense LDL-C-lowering rx is indicated
Niacin (after LDL-C-lowering rx) can be beneficial (Class IIa; LOE B)
Fibrate therapy (after LDL-C-lowering rx) can be beneficial (Class IIa;LOE B)
If TG are 500 mg/dL, therapeutic options indicated
and useful to prevent pancreatitis are fibrate or niacin
before LDL-lowering rx; and treat LDL-C to goal after TG-
lowering rx. Achieving nonHDL-C < 130 mg/dL is recommended.
Lipidmanagement:
(TG 200 mg/dL
or greater)
Primary goal:
NonHDL-C
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Goals Class I Recommendations
It is useful to assess body mass index and/or waistcircumference on each visit and consistently
encourage weight maintenance/reduction through an
appropriate balance of physical activity, caloric
intake, and formal behavioral programs when
indicated to maintain/achieve a body mass index
between 18.5 and 24.9 kg/m2.
The initial goal of weight loss therapy should be to
reduce body weight by approximately 10% from
baseline. With success, further weight loss can be
attempted if indicated through further assessment.
If waist circumference (measured horizontally at the iliac
crest) is 35 inches (102 cm) in women and 40
inches (89 cm) in men, it is useful to initiate lifestyle
changes and consider treatment strategies for
metabolic syndrome as indicated.
Weightmanagement:
Goal:
BMI 18.5 to 24.9
kg/m2
Waist
circumference:
Women: < 35 in.
(102 cm)
Men: < 40 in. (89
cm)
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Goals Class I Recommendations
For all post-PCI STEMI stented patients
without aspirin resistance, allergy, or increased
risk of bleeding, aspirin 162 to 325 mg dailyshould be given for at least 1 month after bare-
metal stent implantation, 3 months after
sirolimus-eluting stent implantation, and 6
months after paclitaxel-eluting stent
implantation, after which long-term aspirin use
should be continued indefinitely at a dose of 75
to 162 mg daily.
Antiplatelet
agents/
anticoagulants:
Aspirin
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Goals Recommendations
In patients where the physician is
concerned about the risk of bleeding lower-
dose 75 to 162 mg of aspirin is reasonable
during the initial period after stent
implantation. (Class IIa; LOE: C)
Antiplatelet
agents/
anticoagulants:
Aspirin
NEW
REC
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Goals Class I Recommendations
For all post-PCI patients who receive a drug-eluting
stent (DES), clopidogrel 75 mg daily should be
given for at least 12 months if patients are not athigh risk of bleeding.
For post-PCI patients receiving a bare metal stent
(BMS), clopidogrel should be given for a minimum
of 1 month and ideally up to 12 months (unless thepatient is at increased risk of bleeding; then it
should be given for a minimum of 2 weeks).
Antiplatelet
agents/
anticoagulants:
Clopidogrel
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NSAIDs with increasing degrees of relative COX-2
selectivity may be considered for pain relief only forsituations where intolerable discomfort persists
despite attempts at stepped care therapy with
acetaminophen, small doses of narcotics,
nonacetylated salicylates, or non-selective
NSAIDs. In all cases, the lowest effective doses
should be used for the shortest possible time.
NSAIDs with increasing degrees of relative COX-2
selectivity should not be administered to STEMI
patients with chronic musculoskeletal discomfort
when therapy with acetaminophen, small doses ofnarcotics, non-acetylated salicylates, or non-
selective NSAIDs provides acceptable levels of
pain relief.
Antiplatelet
agents: NSAIDs
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NEWREC
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Goals Class I Recommendations
ACE inhibitors should be started and continued indefinitely in
all patients recovering from STEMI with LVEF 40% and for
those with hypertension, diabetes, or chronic kidney
disease, unless contraindicated.
ACE inhibitors should be started and continued indefinitely inpatients recovering from STEMI who are not lower risk
(lower risk defined as those with normal LVEF in whom
cardiovascular risk factors are well controlled and
revascularization has been performed), unless
contraindicated.
Among lower risk patients recovering from STEMI (i.e., those
with normal LVEF in whom cardiovascular risk factors are
well controlled and revascularization has been performed)
use of ACE inhibitors is reasonable. (Class IIa; LOE: B)
Renin-
Angiotensin-
Aldosterone
System
Blockers:ACE
Inhibitors
NEW
REC
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Goals Class I Recommendations
Use of aldosterone blockade in post-STEMI
patients without significant renal dysfunction or
hyperkalemia is recommended in patients whoare already receiving therapeutic doses of an
ACE inhibitor and beta blocker, have an LVEF
of 40% and have either diabetes or HF.
Renin-
Angiotensin-
Aldosterone
System
Blockers:Aldosterone
Blockade
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Goals Class I Recommendations
It is beneficial to start and continue beta-
blocker therapy indefinitely in all patients
who have had MI, acute coronarysyndrome, or left ventricular dysfunction
with or without HF symptoms, unless
contraindicated.
Beta-
Blockers
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7/27/2019 Tata laksana SKA.ppt
96/96
TERIMA
KASIH