RESPONSI DOKTER INTERNSIP
NSTEMI + SVT + SYOK KARDIOGENIK K ARDIOGENIK
Disusun oleh : dr. Dian Wulandaru Sukmaning Pertiwi
Pembimbing: dr. Fani Suslina, Sp.JP, FIHA
Pendamping: dr. Erwin Era Prasetya
PROGRAM INTERNSIP DOKTER INDONESIA INSTALASI GAWAT DARURAT RSUD DR. R. KOESMA TUBAN 2016
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BAB I PENDAHULUAN
1.1 Latar Belakang NSTEMI atau non ST elevation myocardial infarction ialah salah satu diagnosis yang termasuk dalam sindrom koroner akut (SKA). SKA merupakan suatu masalah kardiovaskular yang utama karena menyebabkan angka perawatan rumah sakit dan angka kematian yang tinggi. Banyak kemajuan yang telah dicapai melalui penelitian dan oleh karenanya diperlukan pedoman tatalaksana sebagai rangkuman penelitian yang ada. Dibandingkan dengan STEMI, prevalensi NSTEMI dan unstable angina pectoris lebih tinggi, di mana pasien-pasien biasanya berusia lebih lanjut dan memiliki lebih banyak komorbiditas. Selain itu, mortalitas awal NSTEMI lebih rendah dibandingkan STEMI namun setelah 6 bulan, mortalitas keduanya berimbang dan secara jangka panjang, mortalitas NSTEMI lebih tinggi (PERKI, 2015). Major Adverse Cadiac Events ( MACE) ( MACE)
merupakan
suatu
kejadian
komplikasi
kardiovaskular selama fase perawatan, meliputi diantaranya kejadian gagal jantung kongestif, syok kardiogenik, aritmia dan kematian (Martalena et al ., ., 2013). Aritmia sering terjadi pada pasien infark miokard akut dan merupakan penyebab besar dari mortalitas pasien sebelum sampai di rumah sakit, salah satu bentuk aritmia yang paling umum adalah takikardia supraventrikel atau supraventricular tachycardia (SVT). SVT terjadi pada 1-3 per 100 orang. Dalam studi berbasis populasi, prevalensi SVT adalah 2,25 kasus per 1000 orang dengan kejadian 35 kasus per 100.000 orang/tahun (Lily, 2011). Syok kardiogenik merupakan penyebab kematian utama pada pasien rawat inap yang menderita infark miokardium. Syok kardiogenik ialah suatu keadaan gawat yang membutuhkan penanganan yang cepat dan tepat, bahkan dengan penanganan yang agresif karena terjadi pada lebih dari 10% pasien setelah infark miokard akut dengan mortalitas sebesar 70-80%. Walaupun akhir-akhir ini angka kematian dapat diturunkan sampai 56% (GUSTO), syok kardiogenik masih merupakan penyebab kematian yang terpenting pada pasien infark yang dirawat di rumah sakit (Lily, 2011; Kaligis, 2002).
1.2
Rumusan Masalah Bagaimana cara untuk menegakkan diagnosis dan penatalaksanaan NSTEMI?
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1.3
Tujuan
Mengetahui cara menegakkan diagnosa dan penatalaksanaan NSTEMI
Mengetahui cara menegakkan penatalaksanaan untuk SVT pada pasien NSTEMI
Mengetahui cara menegakkan penatalaksanaan untuk syok kardiogenik pada pasien NSTEMI
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BAB II TINJAUAN PUSTAKA
2.1 NSTEMI 2.1.1 Definsi NSTEMI (Non-ST-elevation Myocardial Infarct) termasuk dalam sindroma koroner akut (SKA). Sindroma Koroner Akut (SKA) adalah istilah operasional bagi spektrum kondisi yang kompatibel dengan iskemia dan atau infark miokard akut yang biasanya disebabkan oleh penurunan aliran pembuluh darah koroner jantung secara mendadak (PAPDI, 2009).
2.1.2 Patogenesis Non ST Elevation Myocardial Infarction (NSTEMI) dapat disebabkan oleh penurunan suplai oksigen dan atau peningkatan kebutuhan oksigen miokard yang diperberat oleh obstruksi koroner. Sebagian besar sindroma koroner akut (SKA) adalah manifestasi akut dari plak ateroma pembuluh darah koroner yang koyak atau ruptur. Ruptur plak ini sebelumnya telah menyebabkan
penyempitan
(stenosis)
minimal
dari
pembuluh
darah
koroner
yang
bersangkutan. Pada 70-80% pasien SKA terjadi pada pembuluh darah koroner yang mengalami stenosis <70%, sedangkan 60% lainnya pada pembuluh darah koroner yang mengalami stenosis sebesar 50% atau kurang. Pada plak yang tidak stabil ini biasanya terjadi perubahan komposisi plak (inti lipid besar sebesar >40% volume plak, densitas otot polos yang rendah, penipisan fibrous cap yang cap yang menutupi plak). Pada lokasi ruptur plak dapat dijumpai peningkatan aktivitas sel makrofag, sel mast dan limfosit T yang menunjukkan adanya proses inflamasi. Selsel ini akan mengeluarkan sitokin proinflamasi seperti TNF α dan IL -6 (Waly, 2010; Trisnohadi, 2006; Antono dalam PIT Penyakit Dalam, 2014). Terjadinya ruptur plak aterosklerosis akan diikuti oleh proses aktivasi, adhesi dan agregasi platelet serta aktivasi jalur koagulasi yang menyebabkan terbentuknya trombus yang kaya trombosit (white ( white thrombus). thrombus ). Setelah kontak dengan darah, faktor jaringan berinteraksi dengan faktor VIIa dan X untuk memulai kaskade koagulasi, terjadi konversi protrombin menjadi trombin, yang kemudian mengkonversi fibrinogen menjadi fibrin. Arteri koroner yang terlibat akan mengalami oklusi oleh trombus yang terdiri agregat trombosit dan fibrin. Dalam banyak kasus,
pembentukan
fisura
pada
plak
arterosklerotik
merupakan
suatu
patogenesis
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menyebabkan vasokonstriksi sehingga memperberat gangguan aliran darah koroner. Berkurangnya aliran darah koroner menyebabkan iskemia miokardium. Pasokan oksigen yang berhenti selama kurang-lebih 20 menit menyebabkan miokardium mengalami nekrosis (infark miokard). Pada NSTEMI biasanya terjadi oklusi trombus peristen >1 jam namun masih terdapat kolateral pada distal lokasi penyumbatan. (PERKI, 2015; Waly, 2010; Antono dalam PIT Penyakit Dalam, 2014). Obstruksi subtotal yang disertai vasokonstriksi yang dinamis dapat menyebabkan terjadinya iskemia dan nekrosis jaringan otot jantung (miokard). Akibat dari iskemia, selain nekrosis, adalah gangguan kontraktilitas miokardium karena proses hibernating dan stunning (setelah iskemia hilang), distritmia dan remodeling ventrikel (perubahan bentuk, ukuran dan fungsi ventrikel) (PERKI, 2015). Sebagian pasien SKA tidak mengalami ruptur plak seperti diterangkan di atas. Mereka mengalami SKA karena obstruksi dinamis akibat spasme lokal dari arteri koronaria epikardial (Angina Prinzmetal). Terjadinya vasokonstriksi juga mempunyai peran penting pada angina tak stabil. Di perkirakan ada disfungsi endotel dan bahan vasoaktif yang diproduksi oleh platelet berperan dalam perubahan dalam tonus pembuluh darah dan menyebabkan spasme. Penyempitan arteri koronaria, tanpa spasme maupun trombus, dapat diakibatkan oleh progresi plak atau restenosis setelah Intervensi Koroner Perkutan (IKP/PCI). Beberapa faktor ekstrinsik, seperti demam, anemia, tirotoksikosis, hipotensi, takikardia, dapat menjadi pencetus terjadinya SKA pada pasien yang telah mempunyai plak aterosklerosis (Trisnohadi, 2006; PERKI, 2015).
2.1.3 Faktor Risiko Terdapat dua jenis faktor risiko yang mempengaruhi terjadinya sindrom kroroner akut. Faktor risiko biologis adalah faktor risiko yang tidak dapat diubah yaitu: -
Umur : tua (≥65 tahun)
-
Jenis kelamin : prognosis NSTEMI pada pria sebanding dengan dengan wanita, kecuali pada usia tua prognosis NSTEMI lebih buruk pada pria.
-
Ras
-
Riwayat keluarga dengan penyakit jantung koroner sebelumnya.
Sedangkan faktor risiko kedua yakni faktor risiko yang dapat diubah, sehingga bila dikontrol dapat memperlambat proses aterogenik. Faktor risiko yang dmaksud antara lain:
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-
Merokok
Diagnosis SKA menjadi lebih kuat apabila pasien memiliki penyakit aterosklerosis non koroner (penyakit arteri perifer / karotis) dan atau riwayat memiliki PJK sebelumnya atas dasar pernah mengalami infark miokard, bedah pintas koroner, atau IKP (Intervensi Koroner Perkutan) (PERKI, 2015; Waly, 2010).
2.1.4 Diagnosis Pasien dengan kemungkinan tinggi SKA yang datang dengan nyeri dada kontinyu, dyspnea berat, sinkop/presinkop, atau palpitasi harus segera dirujuk ke instalasi gawat darurat (IGD) dan diangkut oleh layanan medis darurat bila tersedia. Pasien biasanya datang dengan keluhan utama nyeri dada khas angina pectoris (pada 50% pasien), hanya sebagian kecil pasien (20% sampai 30% pasien) SKA tidak menimbulkan nyeri dada. Silent IMA IMA ini terutama terjadi pada pasien dengan dibetes melitus dan hipertensi serta pada pasien usia lanjut (PAPDI, 2009; AHA, 2014; Waly, 2010). Berdasarkan anamnesis, pemeriksaan fisik, pemeriksaan elektrokardiogram (EKG), dan pemeriksaan marka jantung, Sindrom Koroner Akut dibagi menjadi: 1. Infark miokard dengan elevasi segmen ST (STEMI: ST segment elevation myocardial infarction) infarction) 2. Infark miokard dengan non elevasi segmen ST (NSTEMI: non ST segment elevation myocardial infarction) infarction ) 3. Angina Pektoris tidak stabil (UAP: unstable angina pectoris) pectoris ) Diagnosis NSTEMI dan angina pektoris tidak stabil ditegakkan jika terdapat keluhan angina pektoris akut tanpa elevasi segmen ST yang persisten di dua sadapan yang bersebelahan. Rekaman EKG saat presentasi dapat berupa depresi segmen ST, inversi gelombang T, gelombang T yang datar, gelombang T pseudo-normalizatio pseudo-normalization n, atau bahkan tanpa perubahan. Sedangkan Angina Pektoris tidak stabil dan NSTEMI dibedakan berdasarkan kejadian infark miokard yang ditandai dengan peningkatan marka jantung. Marka jantung yang lazim digunakan adalah Troponin I/T atau CK-MB. Bila hasil pemeriksaan biokimia marka jantung terjadi terjadi peningkatan peningkatan bermakna, bermakna, maka diagnosis diagnosis menjadi Infark Infark Miokard Akut Segmen Segmen ST Non Elevasi (Non (Non ST-Elevation Myocardial Infarction, Infarction , NSTEMI). Kemungkinan SKA dengan gambaran EKG nondiagnostik dan marka jantung normal perlu menjalani observasi di instalasi
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Tabel 3. Tingkat peluang SKA segmen ST non elevasi (dikutip dari Anderson JL, et al. J Am Coll Cardiol 2007;50:e1-157)
2.1.4.1 Anamnesa Menurut PERKI (2015), pasien biasanya datang dengan keluhan nyeri dada berupa: 1) Angina tipikal yang persisten selama lebih dari 20 menit. Dialami oleh sebagian besar pasien (80%). Keluhan angina tipikal berupa rasa tertekan/berat daerah retrosternal, menjalar ke lengan kiri, leher, rahang, area interskapular,
bahu,
atau
epigastrium.
Keluhan
ini
dapat
berlangsung
intermiten/beberapa menit atau persisten (>20 menit). Keluhan angina tipikal sering disertai keluhan penyerta seperti diaphoresis, mual/muntah, nyeri abdominal, sesak
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nafas saat beraktivitas. Nyeri di daerah penjalaran angina tipikal, rasa gangguan pencernaan (indigestion ( indigestion)) atau rasa lemah mendadak juga sering dikeluhkan pasien. Beberapa faktor yang menentukan bahwa keluhan tersebut presentasi dari SKA adalah sifat keluhan (nyeri >15 menit), riwayat PJK, jenis kelamin, umur, dan jumlah faktor risiko tradisional (PERKI, 2015; PAPDI, 2009; NHS, 2011). Selain itu juga terdapat nyeri dada non-kardiak yang presentasi klinisnya dapat menyerupai keluhan pada pasien iskemia miokard sehinggga dapat mengaburkan diagnosis. Nyeri yang dimaksud adalah sebagai berikut:
Nyeri pleuritik (nyeri tajam yang berhubungan dengan respirasi atau batuk)
Nyeri abdomen tengah atau bawah
Nyeri dada yang dapat dapat ditunjuk dengan satu jari, terutama di daerah apeks ventrikel kiri atau pertemuan kostokondral.
Nyeri dada yang diakibatkan oleh gerakan tubuh atau palpasi
Nyeri dada dengan durasi beberapa detik
Nyeri dada yang menjalar ke ekstremitas bawah bawah (PERKI, 2015).
2.1.4.2 Pemeriksaan Fisik Hasil pemeriksaan fisik yang ditemukan pada penderita NSTEMI bervarias mulai dari normal
atau
ditemukan
diaphoresis,
akral
pucat
dan
dingin,
takikardia,
sampai
didapatkannya suara jantung empat (S 4). Regurgitasi katup mitral akut, suara jantung tiga (S3), ronkhi basah halus dan hipotensi hendaknya selalu diperiksa untuk mengidentifikasi komplikasi iskemia. Pericardial friction rub karena perikarditis, kekuatan nadi tidak seimbang dan regurgitasi katup aorta akibat diseksi aorta, pneumotoraks, nyeri pleuritik disertai suara napas yang tidak seimbang perlu dipertimbangkan dalam memikirkan diagnosis banding
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Tabel 1. Klasifikasi Nyeri Dada Berdasarkan Pemeriksaan Klinis Dikutip dari NHS, 2011
2.1.4.3 Pemeriksaan Elektrokardiogram (EKG) Semua pasien dengan keluhan nyeri dada atau keluhan lain yang mengarah kepada iskemia harus menjalani pemeriksaan EKG 12 sadapan dalam waktu 10 menit kedatangan di ruang gawat darurat. EKG pada SNTEMI tidak menunjukkan adanya elevasi segmen ST yang
persisten,
kecuali
pada
pasien-pasien
dengan
infark
miokardium
posterior.
Pemeriksaan EKG jantung kanan (sadapan V3R dan V4R) serta EKG jantung posterior (sadapan V7-V9) harus dilakukan pada semua pasien dengan perubahan EKG yang mengarah kepada infark dinding inferior. Selain itu, pemeriksaan sadapan V3R-V4R juga dapat mendeteksi terjadinya infark ventrikel kanan pada pasie dengan infark dinding inferior. Pemeriksaan EKG jantung posterior juga sebaiknya direkam pada semua pasien angina
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Semua perubahan EKG yang tidak sesuai dengan kriteria EKG yang diagnostik dikategorikan sebagai perubahan EKG yang nondiagnostik (Wijaya, IP dalam Naskah PIT Penyakit Dalam, 2014; PERKI, 2015). Penilaian ST elevasi dilakukan pada J point dan ditemukan pada 2 sadapan yang bersebelahan. Pada sadapan V1-V3 nilai ambang untuk diagnostik beragam, bergantung pada usia dan jenis kelamin. Nilai ambang elevasi segmen ST di sadapan V1-V3 pada pria usia ≥40 tahun adalah ≥0,2 mV, pada pria usia <40 tahun adalah ≥0,25 mV. Sedangkan pada perempuan nilai ambang elevasi segmen ST di lead V1-V3, tanpa memandang usia, adalah ≥0,15 mV. Bagi pria dan wanita, nilai ambang elevasi segmen ST di sadapan V3R dan V4R adalah ≥0,05 mV, kecuali pria usia <30 tahun nilai ambang ≥0,1 mV dianggap lebih tepat. Nilai ambang di sadapan V7- V9 adalah ≥0,5 mV (PERKI, 2015). Abnormalitas Abnormalitas gambaran EKG dan peningkatan peningkatan troponin darah harus disesuaikan dengan kondisi klinis dalam penegakkan diagnosis SKA, karena sensitivitas pemeriksaan EKG dalam mendiagnosis SKA, baik tunggal maupun serial, hanya 40-60% saja. Pemeriksaan EKG serial harus dilakukan tiap 15-30 menit dalam 1 jam pertama untuk dengan EKG awal nondiagnostik atau normal dengan keluhan menetap. Pemeriksaan EKG juga sebaiknya sebaiknya diulang setiap keluhan angina timbul kembali. Hasil EKG normal dapat terjadi pada oklusi artreri koroner kanan atau arteri sirkumfleksa kiri. Jika EKG serial tetap menunjukkan gambaran nondiagnostik sementara keluhan angina sangat sugestif SKA, maka pasien dipantau selama 12-24 jam. EKG diulang tiap 6 jam dan setiap terjadi angina berulang (AHA, 2014; Wijaya, IP dalam Naskah PIT Penyakit Dalam, 2014; PERKI, 2015).
2.1.4.4 Pemeriksaan Laboratorium Pemeriksaan laboratorium utama untuk mendiagnosis SKA adalah pemeriksaan
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jam. Spesifitas Spesifitas mioglobin dalam mendiagnosis mendiagnosis SKA paling paling rendah rendah dibandingkan dibandingkan CK-MB dan Troponin I/T. Pemeriksaan yang disarankan adalah pemeriksaan kadar troponin (I dan atau T) dalam kurun 3 sampai 6 jam setelah onset gejala pada semua pasien yang hadir dengan gejala SKA konsisten untuk mengidentifikasi rising and/or fall pattern. pattern . Jika onset gejala tidak jelas, waktu pasien datang dengan presentasi klinis SKA dianggap sebagai onset (AHA, 2014; Wijaya, IP dalam Naskah PIT Penyakit Dalam, 2014). Pemeriksaan kadar troponin tambahan harus diperoleh di luar 6 jam setelah onset gejala pada pasien dengan kadar troponin yang normal pada pasien dengan kadar troponin normal pada pemeriksaan serial namun memiliki kecurigaan SKA sedang atau tinggi berdasarkan klinis dan EKG. Evaluasi troponin dilakukan tiap 3-4 hari pada pasien dengan infark miokard (Ml) sebagai indeks ukuran infark dan dinamika nekrosis. Pada pasien
dengan infark miokard akut, peningkatan awal troponin pada daerah perifer terjadi setelah 3-4 jam dan dapat menetap sampai 2 minggu (Trisnohadi, 2006; AHA, 2014). 2014). Pasien dengan kemungkinan SKA yang hasil EKG serial dan serum troponinnya dalam batas normal hendaknya diperiksakan EKG saat treadmill,
stress myocardial
perfusion imaging imaging atau stress atau stress echocardiography saat saat MRS atau dalam kurun 72 jam setelah KRS. Pasien-pasien tersebut juga dirikan obat rawat jalan berupa aspirin, nitrogliserin kerja cepat, dan medikamentosa lain (misalkan golongan penyekat beta) dalam dosis harian, dengan disertai edukasi aktivitas fisik yang sesuai serta jadwal follow up selanjutnya up selanjutnya (NHS, 2011; AHA, 2014). Pemeriksaan laboratorium tambahan yang diperlukan adalah profil lipid, menurut the National Cholesterol Education Program Adult Treatment Panel Panel III dan guideline terapi ACC/AHA tahun 2007 profil lipid diperiksakan dalam 24 jam setelah onset SKA. Beberapa pasien dengan keadaan klinis tertentu mungkin membutuhkan pemeriksaan laboratorium
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bagi pasien tersangka SKA. Ekokardiografi Multislice Cardiac CT (MSCT) (MSCT) dapat digunakan untuk menyingkirkan PJK sebagai penyebab nyeri pada pasien dengan kemungkinan PJK rendah hingga menengah dan jika pemeriksaan troponin dan EKG tidak meyakinkan (PERKI, 2015).
2.1.5 Diagnosis Banding Pasien dengan kardiomiopati hipertrofik atau penyakit katup jantung (stenosis dan regurgitasi katup aorta) dapat mengeluh nyeri dada disertai perubahan EKG dan peningkatan marka jantung menyerupai yang terjadi pada pasien NSTEMI. Miokarditis dan perikarditis dapat menimbulkan keluhan nyeri dada, perubahan EKG, peningkatan marka jantung, dan gangguan gerak dinding jantung. Stroke dapat disertai dengan perubahan EKG, peningkatan marka jantung, dan dan gangguan gangguan gerak gerak dinding jantung. jantung. Diagnosis Diagnosis banding banding non kardiak kardiak yang mengancam mengancam jiwa dan selalu harus disingkirkan adalah emboli paru dan diseksi aorta. Pemeriksaan Pemeriksaan tambahan
dengan
ekokardiografi
dapat
membantu
menyingkirkan
kardiomiopati hipertrofik, stenosis aorta atau diseksi aorta (PERKI, 2015).
2.1.6 Stratifikasi Risiko
diagnosis
banding
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A. Skor TIMI Dalam menentukan skor TIMI untuk pasien NSTEMI ada beberapa hal yang perlu digali, yaitu: 1. Usia > 65 tahun 2. Tiga atau lebih faktor risiko penyakit jantung koroner (PJK) : hipertensi, merokok, DM, dislipidemia, riwayat PJK dalam keluarga 3. Angiogram sebelumnya menunjukkan terdapat stenosis >50% 4. Penggunaan aspirin dalam 7 hari terakhir 5. Setidaknya dua episode nyeri nyeri saat istirahat dalam 24 jam terakhir 6. Peningkatan marka jantung (CK, troponin) 7. Deviasi segmen ST > 1 mm saat tiba Masing-masing kriteria mendapatkan 1 poin. Stratifikasi TIMI telah divalidasi untuk prediksi kematian 30 hari dan 1 tahun pada berbagai spektrum SKA termasuk Angina pektoris tidak stabil dan NSTEMI.Poin skor TIMI adalah sebagai berikut:
Tabel. Stratifikasi Risiko Berdasarkan Skor TIMI (Dikutip dari PERKI, 2015)
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Tabel. Skor GRACE (Dikutip dari PERKI, 2015) I Usia
II Skor
(dalam tahun) <40
Denyut Jantung
V Skor
(kali/menit) 0
Gagal Jantung Berdasarkan
Skor
Klasifikasi Killip
<70
0
I
0
40-49
18
70-89
7
II
21
50-59
36
90-109
13
III
43
60-69
55
110-149
23
IV
64
70-79
73
150-199
36
80
91
>200
46 VI: Henti jantung saat tiba di RS
43
VII: Peningkatan marka jantung
15
VII: Deviasi Segmen ST
30
III Tekanan Darah
IV Skor
Sistolik (mmHg)
Kreatinin
Skor
(μmol/L)*
<80
63
0-34
2
80-99
58
35-70
5
100-119
47
71-105
8
120-139
37
106-140
11
140-159
26
141-176
14
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diikutsertakan sebagai prediktor, namun tetap berpengaruh melalui perhitungan klirens kreatinin. Skor CRUSADE yang tinggi dikaitkan dengan kemungkinan perdarahan yang lebih tinggi (PERKI, 2015).
Tabel. Skor CRUSADE (Dikutip dari PERKI, 2015) I Hematokrit Awal
II Skor
(dalam %)
Klirens
Skor Skor
V : Jenis Kelamin
kreatinin,
Laki-laki
0
mL/menit
Perempuan
8
<31
9
≤15
39
VI: Tanda gagal jantung saat
31-33,9
7
>15-30
35
datang
34-36,9
3
>30-60
28
Tidak
0
37-39.9
2
>60-90
17
Ya
7
≥40
0
>90-120
7
>120
0
VII: Riwayat penyakit vaskular sebelumnya Tidak
0
Ya
6
VIII: Diabetes
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Tabel. Stratifikasi Risiko Perdarahan Berdasarkan Skor CRUSADE (DIkutip dari PERKI, 2015)
D. LVEF Left ventricle ejection fraction atau biasa disingkat LVEF merupakan gambaran fungsi sistolik dari ventrikel kiri yang diukur saat pemeriksaan ekokardiografi. Fungsi sistolik dari ventrikel kiri ini mempengaruhi prognosis pasien jantung koroner, termasuk NSTEMI. Nilai normal LVEF adalah >60% (dengan range range berkisar antara 50-70%), LVEF ≤40% merupakan bukti penurunan fungsi jantung atau kardiomiopati. Nilai LVEF sebesar 41-49 merupakan borderline, borderline , angka ini menunujukkan seseorang sedang mengalami proses ke a rah gagal jantung maupun merupakan indikasi terjadi kerusakan struktural jantung akibat infark sebelumnya (Hamm et al, 2011).
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Tabel . Kriteria Stratifikasi Risiko Tinggi untuk Strategi Invasif (Dikutip dari PERKI, 2015)
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2.1.7 Tatalaksana Terapi NSTEMI/UA ditujukan untuk mengatasi thrombus intra arteri yang terlibat, serta mengembalikan keseimbangan suplai dan kebutuhan oksigen miokard. Pasien dengan skor risiko sangat tinggi paling baik dilakukan intervensi agresif (PAPDI, 2009). Berikut ini adalah rekomendasi tatalaksana pasien dengan NSTEMI: A. Penanganan Penanganan Non Farmakologis Farmakologis 1. Oksigenisasi Oksigen tambahan diberikan pada semua pasien NSTEMI dengan SpO 2 arteri <90% (menurut AHA (2014)) atau SpO 2 arteri <94% (menurut NHS (2011)), distresss respirasi, atau dengan risiko tinggi hipoksemia. Target SpO 2 yang dianjurkan adalah 94-98%. Untuk
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Tabel. Jenis dan Dosis Nitrat untuk Pasien SKA (DIkutip dari PERKI, 2015)
2. Penyekat beta ( beta blocker ) Terapi dengan golongan penyekat beta oral diberikan dalam 24 jam pertama dengan
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3. Calcium channel blockers (CCB) blockers (CCB) Calcium channel blockers blockers (CCB) atau antagonis kanal kalsium banyak digunakan dalam terapi angina dan memiliki lebih sedikit efek samping serius di bandingkan dengan
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Tabel. Jenis dan Dosis CCB untuk Pasien SKA (DIkutip dari PERKI, 2015)
Terapi anti antiagregasi trombosit (anti platelet) Terapi antiplatelet dan terapi antikoagulan diberikan secara bersamaan dan merupakan strategi terapi antitrombotik. Terapi anti platelet antara lain:
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ini akan meningkatkan aliran darah ke otak dan dengan demikian akan menurunkan jejas iskemik (PERKI, 2015). 2. Penghambat reseptor P2Y12 Penghambat reseptor P2Y12 terdiri dari dua golongan, yeitu thienopyridine (clopidogrel
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ticagrelor seharusnya tidak ditunda pada pasien SKA dengan riwayat stroke iskemik atau TIA. Berdasarkan penelitian subanalisis dari PLATO tahun 2009, penggunaan ticagrelor bersama daspirin pada pasien STEMI dan NSTEMI selama 1 tahun menurunkan secara signifikan angka kematian akibat kardiovaskular, infark miokard atau stroke, dibandingkan
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permukaan asing dan antar trombosit, sehingga terjadi agregasi trombosit (Tjay, 2005). Berbagai macam penelitian menunjukkan penggunaan penghambat reseptor glikoprotein (GP) IIb/IIIa berperan penting pada pasien-pasien UA/NSTEMI yang menjalani IKP. Jenis obat yang dapat digunakan ada tiga, yaitu abciximab, eptifibatide, dan tirofiban. Abciximab
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Pemberian heparin dilakukan secara intravena dengan dosis loading 60 IU/kg (maksimal 4000 IU), pemberian awal 12 IU/kg/jam (maksimal 1000 IU/jam) kemudian disesuaikan dengan kadar aPTT, diberikan selama 48 jam atau sampai dilakukan PCI. Target aPTT adalah 1,5 2,5 kali nilai aPTT normal atau pada tingkat optimal yaitu 50-70
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3. Fondaparinux Obat ini bekerja dengan menghambat secara selektif antithrombin-mediated factor Xa, Xa, yaitu dengan menghambat pembentukan trombin tanpa menganggu molekul trombin yang sudah ada. Fondaparinux adalah pilihan utama agen antitrombolitik (menggantikan
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BAB V PENUTUP
5.1
Kesimpulan 1. Diagnosis NSTEMI, SVT dan syok kardiogenik pada kasus ini didasarkan atas anamnesis, pemeriksaan fisik dan pemeriksaan penunjang. 2. Penatalaksanaan NSTEMI pada pasien ini sesuai dengan teori, yaitu dengan menjaga airway dan breathing stabil, memberikan medikamentosa sesuai strategi terapi antiiskemia, anti platelet, antikoagulan ditambah pengontrolan kadar lipid, glukosa darah, dan penambahan ACE-inhibitor sebagai pencegahan remodeling jantung. 3. Penatalaksanaan SVT pada pasien ini sesuai dengan teori, yaitu melakukan maneuver vagal, kardioversi tersinkronisasi, serta pemberian medikamentosa berupa amiodarone. 4. Penatalaksanaan syok kardiogenik pada pasien ini sesuai dengan teori, yaitu dengan pemberian dobutamine.