Tata laksana SKA.ppt

7/27/2019 Tata laksana SKA.ppt

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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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74

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
http://www.hellasfm.us/uploads/quit-smoking.jpg


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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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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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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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TEXT

http://www.health-first.org/hospitals_services/heart_institute/heart_assoc/images/anticoag.gif


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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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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

CHANGED

TEXT


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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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TEXT

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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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

CHANGED

TEXT

NEW

REC


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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

CHANGED

TEXT



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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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TERIMA

KASIH

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