Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Mengenali ACS: Cegah dan tangani dg cepat dan benar Mohammad Saifur Rohman, dr.SpJP, PhD.FICA Mengapa Penting? Jantung adalah organ yang sangat vital Menjamin pasokan kebutuhan seluruh organ tubuh Jantung memompa lebih dari 1 juta gallon pertahun Berhenti ----- Death Pertanda awal Kenali ! Terlambat Irreversible (?) Kegawatdarutan kardiak Cardiac arrest Acute coronary syndrome Cardiac dysrhythmias Acute pulmonary oedema Trauma – both blunt & penetrating Cardiogenic shock Aortic dissection Valve insufficiency Bgm Keluhan & Tanda ? Slide No. 3 Mengapa Harus Cepat? Serangan Jantung Proses adaptasi terhadap perubahan yang sangat cepat Kompensasi Dekompensasi Dapat di kenali dan diantisipasi serta dicegah Diperbaiki? Tidak!, Dicegah? Ya ! Prevalensi SKA Di Amerika : kejadian Infark miokard Akut (IMA) lebih 1 Juta/tahun 200,000 – 300,000 pasien IMA meninggal sebelum sampai RS Total : Warga negara Amerika mengalami IMA setiap 29 detik dan meninggal setiap menit. Indonesia ? Tahun 2008: PJN Harapan Kita 7 pasien SKA , 50-60% IMA !0% IMA < 40 thn Topol EJ. CV med 2009 Data PJN HK 2008 SKA DI RSSA MALANG AMI prevalence in Saiful Anwar General ApaHospital penyebab KEMATIAN? keterlambatan pasien 59 patients death cases among 356 patients datang ke RS Penanganan di RS The second deadliest diseases The mortality rate was 16,6% in 2010 Seeking care behaviour pattern Patient Saiful Anwar Hospital General Practitioner role Self Medication PHC Aterosklerosis SKA Atherogenesis Progression of Plaque toward rupture Progression of Plaque toward rupture Plaque Rupture Platelet aggregation in ruptured plaque Platelets aggregate at the site of rupture / erosion Lipid core Adventitia Weissberg, 1999 Thrombus formation Thrombus forms and extends into the lumen Thrombus Lipid core Adventitia Weissberg, 1999 Plaque Rupture Toward Occlusion Spektrum SKA Unstable Angina Pectoris : (EKG normal, Trop T/I (-)) Acute Non ST-Elevation Myocardial Infarction (NSTEMI) : (EKG normal/ST depresi/T inversi dan Trop T/I (+)) Acute ST-Elevation Myocardial Infarction (STEMI) : EKG ST elevasi dan Trop T/I(+) Bagaimana Diagnosa SKA ? Membedakan Nyeri dada: SKA? 1. Cardiac or non cardiac 2. Cardiac : Ischemic non Ischemic 3. Ischemic : Coronary non Coronary 4. Angina pektoris stabil atau SKA Nyeri (tidak enak) dada ….. ? Sifat :Berat/ tertindih (pressure, tightness, or heaviness, strangling, constricting, or compression), Panas (burning) ; Masuk angin, Sesak,”maag” Lokasi: Di dada kiri/tengah tidak bisa ditunjuk Penjalaran : ke bahu/lengan, leher, dagu, belakang,epigastrium Lama : 5-30’ Pencetus :aktifitas/stres/dingin Berkurang: Nitrat/Istirahat Tidak khas: Pingsan/kejang/tidak sadar/berdebar ESC guidelines for SAP 2006 ESC AMI ST elevation guidelines 2008 Angina Pectoris A syndrome resulting from myocardial ischemia Demand and supply imbalance Careful history taking; mode of onset, location, quality of pain, duration, precipitating factors, pattern of disappearance, risk factor, etc Angina Pectoris A syndrome resulting from myocardial ischemia Demand and supply imbalance Careful history taking; mode of onset, location, quality of pain, duration, precipitating factors, pattern of disappearance, risk factor, etc Hati-hati : Angina Equivalent Indigestion, belching, dyspnea DM, wanita, manula (post operative) Didapatkan 5% dari ACS 2% dipulangkan ternyata ACS Braunwalds Heart Disease 8th Ed 2008 DD Chest pain Ischemic Stenosis Aorta Regurgitasi Aorta Hypertrophic Cardiomyopathy Angina pada Hypertensi Hipertensi pulmonal berat 11th ed Hurst’s the heart 2005 DD Chest Pain Non Ischemic Diseksi Aorta Pericarditis Mitral valve prolaps 11th ed Hurst’s the heart 2005 DD Chest Pain Gastro intestinal Esophageal spasm/reflux/rupture Peptic Ulcer Neuromusculoskeletal Costochondritis Herpes zoster Chest wall pain dan tenderness etc 11th ed Hurst’s the heart 2005 DD chest pain Pulmonary Pulmonary emboli Pneumothorax Penumonia with pleural involvement Pleurisy Psychogenic Axiety/depression/cardiac psychosis etc 11th ed Hurst’s the heart 2005 Non Angina Pain Hanya terasa pada sebagian kecil dada kiri/kanan (bisa di tunjuk) Berkahir berjam jam sampai berhari hari. Biasanya tidak berkurang dengan nitrogliserin Mungkin dicetuskan oleh debaran. ESC guidelines for SAP 2006 ESC AMI ST elevation guidelines 2008 Nyeri dada khas SKA Angina awitan baru derajat 3 menurut klasifikasi kanada kardiovaskuler group ( nyeri dada timbul pada aktifitas ringan sehari-hari) Angina saat istirahat > 20 menit Perburukan derajat angina menjadi derajat 3 dalam beberapa hari – 1 bln terakhir (Crescendo angina) Atypical Pemeriksaan Fisik Sadar-Koma TD: Hypertensi-Normal-Hypoptensi HR: Regular-irregular/ Bradycardia-Tachycardia pulseless RR: Tachypnea-apnea Cor: Regular-iregular, murmur, gallop Pulmo: Normal-Rales- wheezing Ext: dingin/hangat, edema+/-, etc. EKG Secepat mungkin – 10’ setelah pasien tiba Diulang apabila meragukan adanya kenaikan segmen ST (ST televasi) Bandingkan denga EKG sebelumnya Pasang monitor EKG EKG : Gambaran aktifitas listrik jantung EKG pada SKA EKG dapat menentukan adanya: Old/Recent/Acute infarction Pericarditis Arrhythmias Pembesaran jantung Gambaran EKG pada Iskemik/IMA UAP/Acute NSTEMI Acute NSTEMI Acute STEMI- Evolution Acute STEMI-Q wave Occluded artery Anterior STEMI ECG demonstrates large anterior infarction Inferior STEMI Proximal large RCA occlusion ST elevation in leads II, III, aVF, V5, and V6 with precordial ST depression Inferior STEMI Small inferior distal RCA occlusion ECG changes in leads II, III, and aVF EKG Gangguan Irama Infark baru atau lama Perikarditis Pembesaran jantung dll 1st degree 2nd degree Type 1 2nd degree Type II 3rd degree Ventricular Tachycardia (VT) Ventricular Tachycardia (V T) Unable to determine rhythm Regular ventricular rate (100-250) No P waves present QRS complex > 0.10 sec Ventricular Fibrillation (VF) Coarse Fine Peningkatan Enzym jantung Troponin T/Troponin I CKMB Chest x-ray CTR 62% Aorta elongation Po normal Cardiac Waist (+) Apex lat downward Congestion (+) Non Invasif Invasif Universal Definition of Myocardial Infarction Diagnosa AMI ditegakkan apabila min memenuhi 2 dari kriteria: Gejala Ischemic Perubahan EKG Kenaikan/penurunan Troponin T/I Stratifikasi Resiko High risk Intermediate risk Low risk Angina saat Istirahat Angina > 20 kurang dengan istirahat Angina dengan aktivitas ALO Riwayat CVD LBBB/RBBB baru Ada Q, ST depresi ENZYME (+) Sedikit meningkat ENZYM (-) MR ATAU S3 Baru, HYPOTENSI, BRADIKARDI, TAKIKARDI. VT Usia > 70 tahun ST DEPRESI> 0.5 T inversi EKG TETAP Prinsip Terapi Cepat (time responsif), obati penyebab buka sumbatan Terlambat: Fatal Monitor ketat tanda vital sejak awal Antisipasi dini tanda tanda perburukan dan komplikasi Terapi Awal SKA Atasi keadaan kegawat daruratan : asistol, apney, syock, lung edema, gagal jantung dll. Terapi reperfusi : PCI, Fibrinolitik, heparin Antiischemic Terapi komorbid; hipertensi, DM, dll Pentingnya Reperfusi Sumbatan total15-30 menit tanpa kolateral IMA Reperfusion selamatkan miorkard Kematian1 bulan: 25-30% 4-6% dengan reperfusi (PCI, fibrinolytic, antithombotic) ESC AMI ST elevation guidelines 2008 Kerusakan Miokard Irreversibel Miokard tidak mengalami regenerasi Terlambat/tidak dibuka Miokard mati Gagal Jantung rawat ulang biaya besar, kualitas hidup kurang baik Obat gagal Jantung hanya mencegah perburukan, tidak memperbaiki miokard yang mati/infark Alternatif terapi : Stem cell The time is muscle Terapi NSTEMI O2 Bed rest Pain killer Nitrate and anti-ischemia Antiplatelet : Aspirin, Clopidogrel Heparin HTN Hyperglicemia Treat the complication etc Terapi STEMI O2 Bed rest Pain killer Nitrate and anti-ischemia Antiplatelet : Aspirin, Clopidogrel Fibrinolytic time to neddle : 30 m/PCI HTN Hyperglicemia Treat the complication etc Fibrinolitik Manfaat bila onset < 12 jam, optimal bila onset < 3 jam Bila dikirim ke RS dengan PCI > 90 menit, fibrinolitik Konsep baru : Fibrinolitik di Ambulan menuju RS Perhatikan kontraindikasi fibrinolitik Awasi ketat komplikasi fibrinolitik seperti perdarahan, stroke, syok dll Perhatikan tanda tanda keberhasilan: nyeri hilang, ST elevasi turun >50%, Junctional VES(+), bila gagal rescue PCI Kontra Indikasi Absolut Any prior ICH Known structural cerebral vascular lesion (eg, AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed head or facial trauma within 3 months Kontra Indikasi Relatif History of chronic severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation (SBP greater than 180 mm Hg or DBP greater than 110 mm Hg)† History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks) Recent (within 2 to 4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agents Pregnancy Active peptic ulcer Current use of anticoagulants: the higher the INR, the higher the risk of bleeding Treatment of STEMI Percutaneous Coronary Intervention •Primary PCI : Pasien langsung di lakukan tindakan reperfusi dengan membuka sumbatan di arteri koroner tanpa dilakukan fibrinilotik terlebih dahulu •Rescue PCI : Dilakukan PCI setelah gagal dengan terapi fibrinolitik •Facilitated PCI : Pasien dilakukan fibrinolitik terlebih dahulu meskipun sudah ada rencana PCI •Urgent PCI: As soon as possible •Early PCI : Dalam waktu 24 jam pertama Early/urgent PCI: Resiko tinggi, hemodinamik tidak stabil, aritmia maligna, angina (+) dgn terapi, EF <40%,Gagal jantung, Riwayat PCI, CABG dl 6 bl Tim PCI Target 1. Time to balloon : 90 m 2. Yang dibuka hanya Culprit lesion (pembuluh darah tersumbat yang menyebabkan IMA kali ini) saja 3. Aliran darah yang diintervensi kembali lancar Primary PCI Case A 53 yo man reffered from a private hospital for primary PCI A typical chest after exercise 2 hr prior to admission ECG send by fax PCI appointment via phone Patient directly transfer red to cath lab Komplikasi MI Mechanical Electrical Ischemia Embolic Inflammation Komplikasi Mekanik Ventricular Septal Rupture Mitral Regurgitation Cardiac free wall rupture Large ventricular aneurysms LV pump failure and cardiogenic shock Dynamic LVOT obstruction RV failure Gagal Jantung (Kriteria Framingham) Major Acute pulmonary edema PND or orthopnea Crackles S3 gallop HJR/Increased JVP Cardiomegaly Wt loss >4.5 kg 5d into Rx Minor Night cough Tachycardia >120 Pleural effusion Hepatomegaly Ankle edema Vital capacity decrease >1/3 from max *Two major or one major and two minor* Komplikasi Elektrik SA Dysfunction Atrial Fibrillation First-Second degree AV block Total AV Block Left Bundle Branch Block Right Bundle Branch Block Ventricular Tachycardia Ventricular Fibrillation Komplikasi Ischemik Perluasan Infark Angina Post-infark Komplikasi Emboli Systemic embolism ; stroke, limb ischemia, renal infarction, intestinal ischemia Komplikasi Inflamasi Early Pericarditis Late Pericarditis (Dresslers syndrome) Primary PCI Case CASE 2 CABG Failed PCI with persistent pain or hemodynamic instability in patients with coronary anatomy suitable for surgery. Persistent or recurrent ischemia refractory to medical therapy in patients who have coronary anatomy suitable for surgery, have a significant area of myocardium at risk, and are not candidates for PCI or fibrinolytic therapy. At the time of surgical repair of postinfarction ventricular septal rupture (VSR) or mitral valve insufficiency. CABG Cardiogenic shock in patients less than 75 years old with ST elevation, LBBB, or posterior MI who develop shock within 36 hours of STEMI, have severe multivessel or left main disease, and are suitable for revascularization that can be performed within 18 hours of shock Life-threatening ventricular arrhythmias in the presence of greater than or equal to 50% left mainstenosis and/or triple-vessel disease. Tips Obat anti ischemik atau anti nyeri segera di berikan Anti platelet dan heparin dimasukkan secepatnya setelah diagnosis ACS-NSTEMI ditegakkan, jangan di tunda Turunkan kebutuhan/kerja jantung dengan berikan rasa nyaman dan aman pasien dan bed rest total Setengah duduk pada pasien dengan gagal jantung Pikirkan immediate/urgent PCI pada pasien resiko tinggi/hemodinamik tidak stabil/nyeri berkepanjangn/aritmia maligna dll Yang sering di lupakan….. Edukasi pasien mengenai : Mengapa bisa sampai sakit….. Pola hidup Kepatuhan untuk merubah pola hidup Faktor resiko di kendalikan, rokok, HT, dll Kepatuhan minum obat Mencegah serangan jantung berikutnya dengan…..merubah pola hidup, atur pola makan, olah raga teratur dan terukur Reperfusi adalah awal dimulainya hidup baru …agar koroner tetap terbuka Simpulan Tegakkan diagnosa dengan cepat dan tepat Terapi dengan cepat dan tepat : Reperfusi Monitor ketat Cegah komplikasi Edukasi untuk prevensi dan rehabilitasi …..…….Kerja keras di awal…… Pesan Penting Tambah ilmu…..3X ..amalkan… Semoga menjadi ilmu yang bermanfaat Pengabdian dengan ilmu dan ikhlas