Cardiovascular Department
Case Report
Medical Faculty
August 2014
Hasanuddin University
EXTENSIVE ANTERIOR STEMI ONSET < 12 HOURS KILLIP II
Presented by : Juliarwon Putra C 111 09 284
Supervisor : Prof. dr. Peter Kabo, Ph.D, Sp.FK, Sp.JP (K), FIHA, FAsCC
PRESENTED FOR CLERKSHIP CARDIOVASCULAR DEPARTMENT MEDICAL FACULTY HASANUDDIN UNIVERSITY MAKASSAR 2014
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LEMBAR PENGESAHAN
Yang bertanda tangan dibawah ini menyatakan bahwa :
Nama
: Juliarwon Putra
NIM
: C 111 09 284
Judul Referat : EXTENSIVE ANTERIOR STEMI ONSET < 12 HOURS KILLIP II
Telah menyelesaikan tugas dalam rangka tugas kepaniteraan klinik pada Departemen Cardiovaskular Fakultas Kedokteran Universitas Hasanuddin.
Makassar,
Agustus 2014
Supervisor
Prof. dr. Peter Kabo, Ph.D, Sp.FK, Sp.JP (K), FIHA, FAsCC
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CASE REPORT
I.
PATIENT’S IDENTITY Medical Record
: 673070
Name
: Mr. J
Gender
: Male
Date of Birth / Age : 26-09-1951 / 62 years old old Date of Admission : 23-07-2014
II.
HISTORY TAKING Chief Complaint : Pain on left chest
Present disease history : Chest pain felt approximately 2 days ago and worsened since 9 hours prior to hospitalization. The pain was felt suddenly like being pressed and radiated to the back of the body, and lasted for more than 5 minutes. Cold sweat (+), nausea (+), vomiting (+). Syncope (-). Shortness of breath also felt during the pain. DOE (+). PND (-). Orthopneu (-). Cough (+) for ± 1 year. Defecation a nd urination is normal.
Risk Factor : Smoking (+) 1 pack / day. Alcoholism (-)
Past disease history : Diabetes mellitus (+) ± 20 years, not controlled. Hypertension (-). Stroke (-). History of tuberculosis treatment (-)
III.
PHYSICAL EXAMINATION •
General status : Moderate illness / under nutrition / consciousness GCS 15 (E4M6V5)
•
Vital sign Blood Pressure
: 100/60 mmHg
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•
Head and neck Examination Eye
: Conjunctiva anemic (-), Sclera icteric (-)
Lip
: Cyanosis (-)
Neck : No mass, no tenderness, JVP R +3 cmH2O •
Chest Examination Inspection
: Symetric left = right
Palpation
: No mass, no tenderness, focal phremitus left = right
Percussion : Sonor left = right, lung-liver lung-liver border on ICS VI right anterior Auscultation : Breath sound vesicular Additional sound : Ronchi
•
Wheezing -/-
Cardiac Examination Inspection
: Ictus cordis not visible
Palpation
: Ictus cordis not palpable
Percussion : Right heart border on right parasternal line, left heart border on two finger from left midclavicular line ICS VI Auscultation : Heart sound S I/II regular, no murmur •
Abdominal Examination Inspection
: Flat, follow breath movement
Auscultation : Peristaltic sound (+), normal Palpation
: No mass, no tenderness, liver and spleen not palpable
Percussion : Tympani (+) •
Extremity Examination Edema pretibial minimal
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IV.
ELECTROCARD OGRAPHY
Interpretation : Sinu Sinuss rhy rhyth thm, m, hea hea t rate 75 x/mnt Axis 45
O
Elevation of ST segmen on lead I, aVL, V1-V6
Conclusion : Sinus rh rhythm, no nor o axis Extensive anterior STEMI
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V.
CHEST X-RAY
Interpretation : Active tuberculosis minimal lession Dilatatio et elongatio aortae
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VI.
ECHOCARDIOGRAPHY
Conclusion : LV systolic and diastolic dysfunction
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VIII. DIAGNOSIS Extensive anterior STEMI onset < 12 jam KILLIP II DM Type II non-obese Suspect active tuberculosis
IX.
PLANNING Check laboratory FPG, FPG 2PP, HbA1C, Lipid profile Sputum Examination ECG control Coronary angiography
X.
TREATMENT Oxygenation O2 2-4 Lpm via nasal canule Fluid NaCl 0.9% 500 cc/24 hours/IV Antiplatelet Aspirin 160 mg/24 hours/oral (loading dose) Antiplatelet Clopidogrel 300 mg/24 hours/oral (loading dose) Anticoagulan Enoxaparin 0.6 cc/12 hours/SC ACE Inhibitor Captopril 6.25 mg/8 hours/oral Oral hypolipidemic agent Simvastatin 40 mg/24 hours/oral Vasodilator Isosorbid dinitrat long acting 10 mg/8 hours/oral Diuretic Furosemide 20 mg/8 hours/oral Anxiolytic Alprazolam 0.5 mg/24 hours/oral Laxantive Laxadyn syrup 10 cc/24 hours/oral
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DISCUSSION
I.
PENDAHULUAN Acute coronary syndrome diklasifikasikan berdasarkan ada atau
tidak adanya ST elevasi. ST elevasi biasanya menggambarkan sumbatan akut pada arteri koroner oleh trombus. Terapi yang paling efekstif antara lain adalah rekanalisasi arteri yang tersumbat secepat mungkin dengan percutaneous coronary intervention (PCI) atau dengan terapi thrombolitik. (1)
. Di seluruh dunia, coronary artery disease (CAD) merupakan penyebab
kematian tersering. Lebih dari 7 juta orang meninggal setiap tahunnya karena CAD, terhitung sekitar 12.8% dari semua kematian. Setiap 6 pria dan 7 wanita di Eropa akan meninggal karena i nfark myocard.
(2)
STEMI yang merupakan singkatan dari ST Elevated myocardial infarction merupakan sebuah tipe serangan jantung. Infark myocard
(serangan jantung) terjadi ketika sebuah arteri koroner terblok parsial oleh bekuan darah, yang menyebabkan beberapa otot jantung yang disuplai oleh arteri tersebut mengalami infark (mati). STEMI merupakan bagian dari kelompok kelainan pada jantung yang disebut sebagai acute coronary syndromes yang terdiri atas angina pektoris tak stabil, IMA tanpa elevasi
segmen ST, dan IMA dengan elevasi ST .
(3-5)
Insidens STEMI telah menurun
selama 20 tahun terakhir. Mortalitas di rumah sakit akibat acute coronary syndrome telah menurun dari sekitar 20% menjadi sekitar 5%, karena
perbaikan terapi dan cepatnya didapatkan terapi yang efektif.
(4)
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masih dapat diubah sehingga berpotensi dapat memperlambat proses aterogenik, antara lain kadar serum lipid, hipertensi, merokok, gangguan toleransi glukosa, dan diet yang tinggi lemak jenuh, kolesterol, serta kalori. (6)
Mekanisme utama terjadinya acute coronary syndrome adalah proses thrombosis akut akibat rupturnya plak aterosklerosis yang menyebabkan sumbatan mendadak aliran darah koroner. Penyebab non-aterosklerotik lainnya
seperti
arteritis,
trauma,
diseksi,
thromboemboli,
kongenital, kokain, serta komplikasi tindakan kateterisasi jantung.
kelainan (7)
Kejadian infark myocard diawali dengan terbentuknya aterosklerosis yang kemudian ruptur dan menyumbat pembuluh darah. Penyakit aterosklerosis ditandai dengan pembentukan bertahap fatty plaque di dalam dinding arteri. Lama-kelamaan plak ini terus tumbuh ke dalam lumen, sehingga diameter lumen menyempit. Penyempitan lumen mengganggu aliran darah ke distal dari tempat penyumbatan pe nyumbatan terjadi.
(8)
Faktor-faktor seperti usia, genetik, diet, merokok, diabetes mellitus tipe II, hipertensi, reactive oxygen species, dan inflamasi menyebabkan disfungsi dan aktivasi endotelial. Pemaparan terhadap faktor-faktor di atas menimbulkan injury bagi sel endotel. Akibat disfungsi endotel, sel-sel tidak dapat lagi memproduksi molekul-molekul vasoaktif seperti nitric oxide, yang bekerja sebagai vasodilator, anti-thrombotik dan anti-proliferasi. Sebaliknya, disfungsi endotel justru meningkatkan produksi vasokonstriktor, endotelin-1, dan angiotensin II yang berperan dalam migrasi dan
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III.
DIAGNOSIS Diagnosis infark myocard bergantung kepada hasil anamnesis dan pemeriksaan fisis, pengukuran marker biokimia kerusakan otot jantung (khususnya Troponin), dan hasil pemeriksaan EKG.
(10)
Dari anamnesis,
diagnosis infark myocard biasanya didasarkan pada riwayat nyeri dada selama 20 menit atau lebih di daerah substernal, tidak hilang dengan istirahat dan tidak berespon terhadap nitrogliserin. Ciri khas lain adalah nyeri yang menjalar ke leher, rahang bawah, atau tangan kiri. Nyerinya tidak berat. Beberapa pasien datang dengan gejala yang lebih ringan, seperti mual/muntah, sesak nafas, kelelahan, palpitasi, atau pingsan.
(2, 7)
Pasien juga
sering mengalami keringat malam. Pada sebagian kecil pasien (20% sampai 30%) IMA tidak menimbulkan nyeri dada. Silent AMI ini terutama terjadi pada pasien dengan diabetes mellitus dan hipertensi serta pada pasien berusia lanjut.
(5, 11)
Dari pemeriksaan fisis, didapatkan pasien tampak cemas dan tidak bisa beristirahat (gelisah) dengan ekstremitas pucat disertai keringat dingin. Kombinasi nyeri dada substernal > 30 menit dan banyak keringat merupakan kecurigaan kuat adanya STEMI.
(5)
Pemeriksaan laboratorium harus dilakukan sebagai bagian dalam tatalaksana pasien STEMI tetapi tidak boleh menghambat implementasi terapi reperfusi. Pemeriksaan penanda kerusakan jantung yang dianjurkan adalah creatinin kinase (CK)MB dan Troponin T atau I yang merupakan biomarker pilihan karena sensitifitas dan spesifitas yang tinggi untuk
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•
Segmen ST kembali ke baseline
•
Gelombang T menjadi inverted Lead EKG yang menunjukkan perubahan tipikal dari infark myocard
tergantung dari bagian jantung yang mengalami gangguan.
(10)
ST elevasi pada infark myocard akut yang diukur dari J point harus ditemukan pada 2 lead yang sama dan harus 40 tahun,
≥ 0.2
≥ 0.25
mV pada pria berusia <
mV pada pria berusia > 40 tahun, atau
wanita di lead V2-V3 dan/atau ≥ 0.1 mV pada lead lainnya.
Tabel 1 – Penentuan Lokasi Infark Myocard
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≥ 0.15
mV pada
(2)
(7)
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dianggap sebagai penanda iskemik yang masih terus berlangsung. ST elevasi persisten juga sering diikuti oleh gelombang T inverted persisten.
(1)
Diagnosis STEMI yang cepat merupakan kunci keberhasilan terapi. Monitoring EKG harus dimulai secepat mungkin pada pasien yang dicurigai menderita
STEMI
membahayakan jiwa.
untuk (2)
mendeteksi
adanya
aritmia
yang
dapat
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V.
•
Myocarditis
•
Kardiomyopati hipertrofi
•
Gatroesophageal reflux (GERD).
•
Serangan panik
•
Somatisasi dan gangguan psikogenik
TERAPI Tujuan utama penatalaksanaan IMA adalah mendiagnosis secara cepat, menghilangkan nyeri dada, menilai dan mengimplementasikan strategi reperfusi yang mungkin dilakukan, memberi antithrombotik dan anti platelet, serta memberi obat penunjang. Terdapat beberapa pedoman (guideline) penatalaksanaan STEMI yaitu dari ACC/AHA dan ESC, tetapi perlu disesuaikan dengan kondisi sarana / fasilitas di masing-masing tempat dan kemampuan ahli yang ada.
(12)
Tatalaksana awal di ruang emergensi (10 menit pertama setelah pasien
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oksigen juga harus diberikan kepada pasien tanpa sesak nafas atau gagal jantung masih belum jelas. Monitoring saturasi oksigen dapat sangat membantu untuk memutuskan apakah pasien membutuhkan bantuan oksigen atau ventilator. Semua pasien STEMI tanpa komplikasi dapat diberikan oksigen selama 6 jam pertama.
(2, 13)
Mengurangi nyeri sangat penting karena nyeri berhubungan dengan aktivasi simpatik yang menyebabkan vasokonstriksi dan peningkatan beban kerja jantung. Titrasi opioid IV (seperti morfin) merupakan obat yang paling sering digunakan. Morfin dapat diberikan dengan dosis 2-4 mg dan dapat diulang dengan interval 5-15 menit sampai dosis total 20 mg. Tidak boleh diberikan dalam bentuk injeksi IM. Efek sampingnya dapat berupa mual dan muntah, hipotensi dengan bradikardi, dan depresi pernafasan. Obat antiemetik dapat diberikan bersamaan dengan opioid untuk mengurangi mual.
(2, 13)
Percutaneous Coronary Intervention
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utamanya adalah merestorasi patensi arteri koroner dengan cepat. Terdapat beberapa macam obat fibrinolitik antara lain tissue plasminogen activator (tPA), streptokinase, tenekteplase (TNK), reteplase (rPA), yang bekerja dengan memicu konversi plasminogen menjadi plasmin yang akan melisiskan trombus fibrin.
(14)
Fibrinolitik dianggap berhasil jika terdapat resolusi nyeri dada dan penurunan elevasi segmen ST > 50% dalam 90 menit pemberian fibrinolitik. Fibrinolitik tidak menunjukkan hasil pada graft vena, sehingga pada pasien pasca CABG yang datang dengan IMA, cara reperfusi yang lebih disukai adalah PCI.
(14)
(7, 14)
Kontraindikasi terapi fibrinolitik : A. Kontraindikasi absolut
1. Setiap riwayat perdarahan intraserebral 2. Terdapat lesi vaskular serebral struktural (contoh : malformasi AV) 3. Terdapat neoplasma ganas intrakranial
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6. Pungsi vaskular yang tak terkompresi te rkompresi 7. Untuk streptase / anisreplase : riwayat penggunaan > 5 hari sebelumnya atau reaksi alergi sebelumnya terhadap obat ini 8. Kehamilan 9. Ulkus peptikum aktif
Obat fibrinolitik : 1) Streptokinase : Merupakan fibrinolitik non-spesifik fibrin. Pasien yang pernah terpajan dengan SK tidak boleh diberikan pajanan selanjutnya
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VI.
PROGNOSIS Mortalitas rata-rata STEMI adalah sebesar 30%, dengan 25 hingga 30% dari pasien yang meninggal tersebut meninggal sebelum sampai di rumah sakit (umumnya karena fibrilasi ventrikel).
Tabel 2 – Klasifikasi KILLIP (18)
(18)
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DAFTAR PUSTAKA 1.
Pie´rard LA. ST elevation after myocardial infarction: what does it mean? Heart Journal. November 2007;93(11):1329–30.
2.
Steg PG, James SK, Atar D, Badano LP, Blo¨mstrom-Lundqvist Blo¨mstrom-Lundqvist C, Borger MA, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation . European Heart Journal. 24 August 2012;33(20):2569-619. 2012;33(20):2569-619.
3.
STEMI - ST Segment Elevation Myocardial Infarction [Internet]. 2014 [cited 29 July 2014]. Available from:
http://heartdisease.about.com/od/heartattack/g/STEMI.htm.. http://heartdisease.about.com/od/heartattack/g/STEMI.htm 4.
NICE. Myocardial infarction with ST-segment elevation : The acute
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15.
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