PENATALAKSANAAN PASIEN DENGAN KELUHAN CHEST ( CARDIAC ) PAINWahyu Widjanarko

SUSPECTED CARDIAC PAIN :Clinical characteristics predictive of AMI in ED px with chest pain :

Description of pain Prob.MI (%)Pressure, tightness, crushing 24Burning, Indigestion 23Ache 13 Sharp, Stabbing 5Pleuritic 7Radiation 19Reproducibility 5 6Combination 0

HOW TO MANAGE Px with CHEST PAIN Suspected cardiac painECGNo ECG ST Normal ECG,CKMB,troponinIschaemic,CKMB/troponin ECG ST / LBBBAMI guidelineSuspected ACSConfirmid ACS

Normal ECG/CKMB/Troponin at 12 hrs consider DischargeAdmit CCU,ECG monitor,Aspirin/LMWH/-blockerStress testStable for 48 h,high risk features -Recurrent symptoms/ECG changes/other indication of high riskCoroner AngiographyRisk stratificationLow intermediate high

Discharge

Revascularisation/medical tx

ACUT CORONARY SYNDROME ( ACS ) DEFINISI : Segala bentuk gejala klinisyang sesuai dengan kondisi iskemia miokard akut

Patogenese dan Presentasi klinis sama, berbeda dalam derajat berat ringannya

ACUTE CORONARY SYNDROME

No ST Elevation ST ElevationUnstable AnginaNon-STEMINon-Q wave MIQ wave MIBraunwald et al. JACC 2000;36:970-1062

Iskemia Jantung Demand O2 meningkat pada:Exercise, makan, stress

Supply O2 berkurang akibat sumbatan (obstruksi) pembuluh darah jantung seperti pada: aterosklerosis vasokonstriksi (spasme) bekuan darah (thrombus)

Setelah lewat suatu batas waktu, jaringan iskemik akan mati (nekrosis), dan akhirnya digantikan oleh jaringan parut yang non-fungsional Infark Miokard

Tahapan Terbentuknya Aterosklerosis

Kerusakan endotelium pembuluh arteri

Trombosit/platelet melekat pada daerah yang rusak, diikuti proliferasi endotel, pembentukan kapsul fibrosis dan penumpukan kolesterol

Plak membesar, menutupi lumen arteri dan inti jaringan lemak bertambah besar

Oklusi sebagianPlak(inti kaya lemak,kapsul fibrosa)Plak pecah Kumpulan agregasi platelet, thrombosisOklusi sebagianOklusi komplitLysis and repairNo symptomsRapid progression of atherosclerosisUnstable anginaNon Q wave MIAngina,ECG changes,Troponin releaseQ wave MINon Q-wave MIAngina,ECG changes,Troponin releasetrombolisistrombosisCollateralsMonosit, macrofag, inflamasiPlak tidak stabil pada ACS

APTS/NSTEMI Diagnosa berdasarkan riwayat penyakit, EKG 12 lead, cardiac enzymes (CK, CK-MB, LDH) atau petanda lain di plasma (troponin I atau T)

1. Klinis sama: 1. Angina saat istirahat terus menerus > 15 mnt 2. Angina pertama kali (CCS class III ) 3. Angina yang meningkat ( makin lama, sering dan mudah tercetus )

2. EKG dan petanda biokimia kerusakan miokard berbeda

EKG : Segmen ST depresi ST elevasi transient spontan hilang dg atau tanpa nitrat Gelombang T inversi Riwayat infark miokard LBBB Perubahan yang tidak spesific Normal

ENZIM dan PETANDA JANTUNG : Conventional cardiac enzyms ( CK, CK-MB, LDH ) bisa normal atau meningkat Troponin T ( > 0,1 ug/l ) atau Troponin I ( > 0,4 ug/l ) merupakan petanda spesifik terjadinya kerusakan miokard High risk px Evaluasi troponin normal atau tidak terdeteksi dalam 12 jam Low risk px

3. STRATIFIKASI RESIKO :Resiko tinggi : - Usia > 65 th - Nyeri saat istirahat > 15 - Perubahan segmen ST dinamis - ST depresi transient - Angina tdk stabil paska infark - Comorbid : DM - Troponin T/I - Fungsi Vki - Aritmia mayor

PenatalaksanaanPengobatan darurat / immediate treatment:Oksigen, morfin, nitrogliserinMenghilangkan nyeri, mencegah terjadinya MI dan kematian akibat perluasan thrombus

Reperfusi segera:Thrombolitic agents (aspirin, heparin)Mechanical reperfusion (PCI, CABG)

PenatalaksanaanANTI ISKEMIKMengoptimalisasi keseimbangan antara kebutuhan dan supply oksigen pada miokardiumANTI TROMBOTIKMengatasi proses perjalanan penyakit yakni pada pembentukan trombus

Antiiskemik Beta blockerTerapi tunggal pada unstable angina, kombinasi dengan nitrat untuk mencegah recurrent iskemiaMengurangi kebutuhan oksigen, menurunkan HR dan tekanan darahKontraindikasi pada jenis angina vasospastik

Antiiskemik - Calcium channel blockerBaik untuk vasodilator pada angina

Tidak ada bukti manfaatnya pada pencegahan infark miokard.

Memberikan hasil yang baik dalam jangka pendek pada episode iskemik.

Antiiskemik - Nitrat

VasodilatorMengurangi konsumsi oksigenEfektif menurunkan jumlah episode iskemiaSediaan sublingual, spray, IV (dosis disesuaikan dengan gejala klinis dan EKG)

Jenis Antitrombotik Obat anti platelet/antitrombosis aspirin, clopidogrel / ticlopidine, anti Gp IIb/IIIaMencegah haemostasis primer

Antikoagulanheparin, LMWHMencegah perluasan trombus

TrombolitikstreptokinaseMenghancurkan trombus

Antitrombotik pada Unstable Angina

AspirinHeparinLMWH

AspirinAgregasi platelet = titik awal pembentukan trombusMenghambat enzim platelet (cyclooxygenase) , mengganggu sintesa aktivator platelet (thromboxane A2)Dosis: 75mg/hari 325 mg q.i.d.Unstable angina akut diberikan secepat mungkin, dosis awal 150-325 mg

Heparin (UFH)

Mencegah pembentukan dan perluasan trombus (anti Xa dan IIa)

Manfaatnya sulit dibuktikan dari studi klinis.

Keunggulan Potensial LMWHBioavailabilitas total dengan pemberian per SK Waktu paruh panjang Tidak ada ikatan endotelInteraksi dengan platelet minimalIkatan protein plasma minimalSensitivitas terhadap PF4 rendahPemberian per SKlebih mudah penggunaannyaEfek antikoagulan stabil dan dapat diprediksi

Lebih aman tanpa kontrol biologis

Studi klinis penggunaan LMWHpada ACSFRISCDalteparin dibanding plasebo (1996)FRISC IIDalteparin dibanding plasebo (1999)

FRICDalteparin dibanding UFH (1996)

ESSENCEEnoxaparin dibanding UFH (1997)TIMI 11BEnoxaparin dibanding UFH (1998)

FRAXISNadroparin dibanding UFH (1998)

STEMI Dx 2 dari 3 kriteria ( WHO ) : 1. Nyeri dada iskemi yang khas2. Evolusi EKG ( serial )3. Peningkatan yang diikuti penurunan kadar enzim-2 jantung (CK-MB dan Troponin secara serial)

Strategi dan penanganan dini Early open artery dengan terapi reperfusi : TROMBOLITIK atau PTCA PRIMER

2. Penanganan di ICVCU : Tindakan Umum : - Bed rest - Monitoring Farmakoterapi : - Oksigen 2 4 l/mnt - Aspirin - - blocker - Nitrat - ACEI

*Aterosklerosis adalah patologi dasar yang berhubungan dengan ACS dan penyakit utama arteri koroner.Ruptur plag mengaktivasi jalur ekstrinsik pada mekanisme pembekuan darah.Fibrin dihubungkan pada stabilisasi pembekuan darah platelet berhenti yang segera membentuk mengikuti luka endotelialBersama-sama : platelet, fibrin, dan sel darah merah membentuk trombus intra-koroner yang berperan pada UA / non-Q-wave MI (NQMI) dan AMI

**9b- Beta-blockers

These are effective in both symptomatic and prophylactic treatment of myocardial infarction.

Beta-blockers are known to be moderate vasoconstrictors : they must therefore be systematically associated with a nitrate and preference should be given to cardioselective agents.

They are contra-indicated in vasospastic angina.

*10c- calcium-channel blockers

There is no evidence that calcium-channel blockers alone are of benefit in the prevention of myocardial infarction.

However, in the short term, they do give good results in the treatment of symptomatic or non-symptomatic ischemic episodes.

In cases where there is cause to suspect a vasospastic element, the association of calcium-channel blockers is quite justified.

*8a- organic nitrates

Nitrates are vasodilators which reduce oxygen consumption.They are widely used (based on empirical findings) and are extremely effective for reducing the number of ischemic episodes during the first few hours after initiation of intravenous treatment.

They are used in moderate doses to start (1 mg per hour in continuous infusion) which are thereafter increased by progressive stages according to the clinical response.

*3Reminder :Antithrombotics include 3 classes of drugs :- antiplatelet drugs (aspirin, Ticlid[ticlopidine], ReoPro)- anticoagulants (unfractionated heparin, LMWH, Antivitamin K)- thrombolytics (streptokinase, Actilyse)

*1Antithromboticsin unstable angina

A. AspirinLewis, Cairns, RISC Studies

B. Unfractionated heparinThroux, RISC, ATACS Studies

C - Low Molecular Weight Heparins1. Potential advantages of LMWH2. Clinical studiesFraxiparin : Garfinkel StudyFragmin : FRISC, FRIC StudiesLovenox : TIMI 11A, ESSENCE Studies

*5A. Aspirin

Platelet aggregation on a ruptured atherosclerotic plaque is the starting point for the formation of an intracoronary thrombus.Antiplatelet drugs are consequently an essential element in the treatment of unstable angina.Sufficient evidence exists to prove their efficacy. The advantages of aspirin have been demonstrated in all the studies in this field, regardless of the duration of observation and the dosage used. (see Table : Lewis, Cairns, RISC Studies).

Globally :aspirin reduces by half the occurence of myocardial infarction and cardiac death.The doses of aspirin generally administered are between 100 and 350 mg per day, but lower doses have also been assessed (75 mg). Other antiplatelet drugs, such as ticlopidine (TICLID) have also been proved to be effective and can be used in patients unable to tolerate aspirin. Potent new antiplatelet drugs, fibrinogen platelet receptor inhibitors (anti GP IIb/IIIa) are currently being evaluated in the treatment of unstable angina.

*7B. Unfractionated heparin

Standard or unfractionated heparin inhibits the production of thrombin (anti Xa action) and also neutralises its effects (anti IIa action).Its essential role is that of preventing the extension of thrombi, without dissolving any already formed thrombi.Its use in the treatment of unstable angina is therefore rational, even though its efficacy has been difficult to demonstrate in clinical trials.

*14C - Low Molecular Weight Heparins

1. Potential advantages of LMWH

The efficacy of low molecular weight heparins has been widely demonstrated to be at least equal to that of unfractionated heparin for the prophylaxis and treatment of venous thrombosis. They have evident advantages in terms of convenience and simplicity of use.

However, studies aiming at evaluating the use of low molecular weight heparins in arterial pathology are relatively limited. Nevertheless, they ought to be considered "a priori" to be at least as effective as unfractionated heparin in the treatment of arterial thrombosis and immediate prevention of their recurrence.Compared with unfractionated heparin, they present potential advantages which can be of major importance in the acute phase of arterial accidents, coronary episodes in particular.

In these situations, rapid onset of effective anticoagulation is essential.

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