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PEMBIMBING DR. ANDIKA SITEPU SP.JP DR. ALI NAFIAH NASUTION SP.JP
Definition
A Spectrum of clinical syndromes due to sudden, significantly compromised coronary circulation. ACS: Q wave Acute MCI (STEMI) Non-Q wave Acute MCI(NSTEMI) Unstable Angina Pectoris (UAP) These conditions were the further stages of stable angina pectoris.
Pathogenesis
Mostly caused by coronary atherosclerosis Ruptured atherosclerosis plaqueFormation of thrombus which occludes blood vessel. The degree of blood vessel occlusion determines the degree of damage to Myocardium.
Risk Factors
Unmodified Risk factors: 1. Age 2. Sex
3. Race
4. Genetics (Family History)
CAD
plaque
Atherosclerosis
Risk Factors ( , BP, DM, DYSLIPIDEMIA Insulin Resistance, Platelets, Fibrinogen, etc)
CAD Atherosclerosis
Risk Factors ( DYSLIPIDEMIA, BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)
ACS
Coronary Thrombosis Myocardial Ischemia
CAD Atherosclerosis
Risk Factors ( DYSLIPIDEMIA, BP, DM, Insulin Resistance, Platelets, Fibrinogen, etc)
DIAGNOSIS
HISTORY
PRODROMAL SYMPTOMS History very valuable to establish D/. Prodoma : chest discomfort unstable angina 1/3 symptoms for 1 4 wks 20% symptoms for < 24 hrs Malaise, exhaustion NATURE OF PAIN Most patients severe prolonged, 30 minutes - hours Constricting, crushing, oppressing, compressing heavy weight or squeezing in chest Choking, vise-like, heavy pain or stabbing, knife-like, boring or burning discomfort Location : retrosternal, spreading frequently to both sides of the chest with predilection to the left side Often pain radiates down ulnar aspect of left arm, producing tingling sensation in left wrist, hand and fingers
NATURE OF PAIN SOME INSTANCES : pain begins in epigastrium, and simulates abdominal disorder Sometimes pain radiates to shoulders, upper extremities, neck, jaw and interscapular region favoring the left side
Elderly : no chest pain but acute left ventricular failure and chest tightness or marked weakness or syncope
Pain arises from nerve endings in ischemic or injured, but not necrotic, myocardium OTHER SYMPTOMS 50% nausea or vomiting in transmural infarcts Occasionally diarrhea, profound weakness, dizziness, palpitation, cold perspiration, sense of impending doom Occasionally : cerebral embolism or systemic arterial embolism
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Clinical Classification of Angina Typical angina (definite) substernal chest discomfort with a characteristic quality and duration provoked by exertion or emotional stress relieved by rest or nitroglycerin Atypical angina (probable) meets 2 of the above characteristics
PHYSICAL EXAMINATION
GENERAL APPEARANCE Anxious, considerable distress, restless, fist on chest (Levine sign) LV failure & sympathetic stimulation : cold perspiration, pallor, dyspnea, cough with frothy pink or blood-streaked sputum. Shock : cool, clammy skin, facial pallor, cyanosis, confusion or disorientation HEART RATE Variable depending on underlying rhythm and degree or ventr. failure Most commonly, HR 100 110/min; > 95% patients : VPBs within first 4 hours
BLOOD PRESSURE Majority normotensive, but syst. BP may decline and diast. BP may rise Half of pts with inferior MI parasympathetic stimulation : hypotension, bradycardia or both (Bezold Jarisch reflex) half of pts with anterior MI, sympathetic excess : hypertension, tachycardia or both TEMPERATURE AND RESPIRATION Most pts with extensive MI fever within 24-48 hrs, fever resolves by 4th or 5th hari Respiration due to anxiety and pain, in LV failure : resp. rate correlates with degree of heart failure
WORKUP
Electrocardiogram
Q-wave Acute Miocard Infarction (STEMI) : Elevated ST segment 1 mm at 2 (extremities leads) Or 2 mm at 2 (Precordial leads which represents the same area or close by)
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ST Segment depression or inverted T wave(1mm) at 2 or more closely positioned lead. ST segment changes from ST depression at the moment of symptom to normal ST segment when symptom is relieved -> UAP
ACS
Heart Biomarker
BIOMARKER TIME OF ELEVATION PEAK NORMALIZED
CK-MB
3 12 hours
24 hours
48 72 days
(cTn)T
3 12 hours
24 hours
5 10 days
(cTn)I
3 12 hours
12 hour s 2 days
5 14 days
ACS
Coronary Thrombosi s Myocardial Ischemia Arrhythmia and Loss of Muscle Remodeling
CAD Atherosclerosi s Risk Factors ( , BP, DM, DYSLIPIDEMIA Insulin Resistance, Platelets, Fibrinogen, etc)
ACS
ACS ALGORITHM
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Time from onset of symptoms 12 hours - Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) - ACE-I/ARB within 24 h of symptom onset) - Statin - High risk: early invasive strategy - Continue ASA, heparin, ACE-I, statin ST-depression or dynamic T-wave inversion strongly suspicious for injury Normal or nondiagnostic changes in ST-segment or Twaves Develops high or intermediate risk criteria or troponin-positive Monitored bed in ED Develops high or intermediate risk criteria or troponin-positive
Start adjunctive treatment 12 hrs Admit to monitored bed Assess risk status
study
Portable chest x-ray ( 30 minutes)
Chest discomfort suggestive of ischemia Immediate ED assessment and immediate ED general treatment Review initial 12 lead ECG ST elevation or new or presumably new LBBB strongly suspicious for injury Start adjunctive treatment Time from onset of symptoms 12 hours - Reperfusion strategy: PCI (90 min) or fibrinolysis (30 min) - ACE-I/ARB within 24 h of symptom onset) - Statin - High risk: early invasive strategy - Continue ASA, heparin, ACE-I, statin ST-depression or dynamic T-wave inversion strongly suspicious for injury Normal or nondiagnostic changes in ST-segment or Twaves Develops high or intermediate risk criteria or troponin-positive Monitored bed in ED Develops high or intermediate risk criteria or troponin-positive
Start adjunctive treatment 12 hrs Admit to monitored bed Assess risk status
Adjunctive Therapy
Heparin (UFH/LMWH)
-Adrenoreceptor blockers
Clopidogrel
From: 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2013;61(4):e78-e140. doi:10.1016/j.jacc.2012.11.019
Figure Legend:
Reperfusion therapy for patients with STEMI. The bold arrows and boxes are the preferred strategies. Performance of PCI is dictated by an anatomically appropriate culprit stenosis. *Patients with cardiogenic shock or severe heart failure initially seen at a nonPCIcapable hospital should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset (Class I, LOE: B). Angiography and revascularization should not be performed within the first 2 to 3 hou rs after administration of fibrinolytic therapy. CABG indicates coronary artery bypass graft; DIDO, door-indoor-out; FMC, first medical contact; LOE, Level of Evidence; MI, myocardial PCI, percutaneous coronary intervention; and STEMI, ST-elevation Date of download: Copyrightinfarction; The American College of Cardiology. myocardial infarction. 6/3/2013 All rights reserved.
RISK STRATIFICATION
HIGH-RISK PATIENT
Repetitive or prolonged (> 10 minutes) pain Elevated level of cardiac biomarker (troponin or creatine kinase-MB isoenzyme); Persistent or dynamic ST depression 0.5 mm or new T-wave inversion Transient ST-segment elevation (0.5 mm) in more than two contiguous leads Haemodynamic compromise Sustained ventricular tachycardia Syncope LV systolic dysfunction (ejection fraction <40%); Prior PCI or CABG within 6 months or prior Diabetes Chronic kidney disease (estimated GFR< 60 mL/min)
Guideline ACS 2006 National Heart Foundation Australia
Outpatient Care
Medication to relieve symptoms and prevent Aspirin Beta-blocker ACE inhibitor
KILLIP CLASSIFICATION
Stage I- No heart failure. No clinical signs of cardiac
decompensation; Stage II- Heart failure. Diagnostic criteria include rales, S3 gallop and pulmonary hypertension. Pulmonary congestion with wet rales in the lower half of the lung fields; Stage III- Severe heart failure. Frank pulmonary oedema with rales troughout the lung fields; Stage IV- Cardiogenic shock. Signs include hypotension (SBP <= 90 mmHg), and evidence of peripheral vasoconstriction such as oliguria, cyanosis, and diapohoresis.
PROGNOSIS
STATUS PASIEN
No : 00.55.87.56 Tanggal : 16 Mei 2013 Nama pasien: Saiman
Umur
: 73th/ 10 bln/4 hr Seks : LK Pekerjaan: Wiraswasta Alamat : Jl. Aek Raso Kec. Torgamba Agama: Islam Tlp: Hp: -
Keluhan utama: Nyeri dada Anamnesis: Hal ini dialami os 3 hari yang lalu (Senin, 13/5,
sekitar pukul 9 pagi) saat os jalan pagi. Nyeri dada dirasakan os seperti terhimpit benda berat. Penjalaran (+) ke bahu dan punggung. Durasi > 30 menit, disertai mual (+), keringat dingin (+), muntah (-). Nyeri dada yang seperti ini merupakan pertama kali dirasakan os. Sesak nafas (-), DOE (+), PND (-), OP (-), kaki bengkak (-). Riwayat nyeri dada sebenarnya telah dirasakan os 1 tahun ini, bersifat hilang timbul. Nyeri dada terutama dirasakan os bila beraktifitas berat, durasi 5-10 menit, menghilang dengan beristirahat. Oleh karena keluhan nyeri dada tersebut, os lalu dibawa keluarga ke RSUD Rantau Prapat dan dirawat oleh SpPD selama 3 hari.
Prapat, os telah diberikan obat 4 tablet yang dimakan sekaligus dan 2 tablet kunyah, serta dapat obat suntikan di perut sebanyak 2 kali. Kemudian os dirujuk ke RSHAM untuk penanganan selanjutnya. Riwayat hipertensi dan DM disangkal os. Os adalah pasien baru RSHAM, saat di IGD keluhan nyeri dada sudah berkurang. Riwayat merokok (+) 2 bungkus perhari selama >50 tahun.
merokok Riwayat Penyakit Terdahulu: Riwayat obat: Clopidrogel, Fasorbid, Fluxum, tanapres s, Alovastatin, Ranitidin, Aspilet.
STATUS PRESENS
Status presens: KU: Nyeri dada.
Kesadaran: CM
TD: 90/70
mmHg Pols:94 x/i, irreguler RR: 24 x/i Suhu: 36,5C Sianosis : (-) Ortopnu: (+) Dispnu: (-) Ikterus: (-) Edema (-) pucat (-) BB: 50 kg TB: 158 cm IMT : BB/(TB)2 = 50/(1.58)2 = 20.08 (normoweight)
PEMERIKSAAN FISIK
Pemeriksaan Fisik: Kepala : sklera ikterik (-/-) konjungtiva palpebra inferior
anemis (-/-) Leher: TVJ : R+3 cmH2O Dinding toraks: Inspeksi : simetris fusiformis Palpasi : stem fremitus kanan = kiri, kesan normal Perkusi : sonor pada kedua lapangan paru Batas jantung : Atas : ICS III sinistra Kanan : Linea parasternalis dextra Kiri : 1 cm lateral LMCS
Murmur : (-) , Tipe : (-). Paru : suara pernafasan vesikuler suara tambahan : ronki (+) wheezing (-/-) Abdomen: Palpasi Hepar/Lien : tidak teraba Bising Usus (+) Asites (-) Ekstremitas: akral hangat edema (-)
SINUS RHYTM, QRS RATE 96X/MNT, QRS AXIS (N), GEL. P (N), PR INTERVAL 0,16, QRS DURATION 0,08, Q PATOLOGIS DI II, III, AVF, ST DEPRESI DI I, AVL, V2-V6. LVH (-), VES (-), AES (-), (ECG POST: Q PATH DENGAN ST ELEVASI V8 V9/EKG KANAN: ST ELEVASI V3R-V4R.) KESAN EKG: SR + STEMI INFEROPOSTERIOR + RV INFARK
Interpretasi Foto Thorax: CTR 55%, segmen aorta dilatasi, segmen Po normal,
HASIL LABORATORIUM
Hematologi Hb 15.60 gr% (Ti) RBC 5.22 x 106 /mm3 WBC 14.22 x 103/mm3 PLT 91 x 103/mm3 Ht 44,40 % (Ti) MCHC 35,10 % RDW 14,40 % Kimia Klinik pH 7,451 pO2 181,2 mmHg (Ti) HCO3 15.6 mmol/L (Tu) CO2 16.3 mmol/L (Tu) BE -6,0 mmol/L (Tu) SO2 99,6%
Ginjal
Kreatinin: 1.42 mg/dl Ureum: 110 mg/dL Elektrolit Natrium : 121 mEq/L Kalium : 4,2 mEq/L Klorida : 107 mEq/L
Diagnosa Kerja : STEMI inferoposterior Fungsional : STEMI inferoposterior onset 3 hari KILLIP II TIMI Risk Score 7/14 Anatomi : Arteri Koroner Etiologi : Atherosklerosis
Differensial Diagnosa : - STEMI Inferoposterior onset 3 hari KILLIP II TIMI Risk Score 7/14 -NSTEMI -UAP
Pengobatan: Bed Rest O2 4L/i IVFD NaCl 0,9 % 10 gtt/I (mikro) Inj UFH 600 IU/hour Aspilet 1x80 mg Plavix 1x75 mg ISDN 5mg (k/p) Simvastatin 1x40 mg Laxadin 1x1CI
Rencana Pemeriksaan Lanjutan: KGDN/ 2JPP, HbA1c Faal Hemostasis Lipid profile Echocardiography Angiography coroner Prognosis : Dubia ad bonam
FOLLOW UP PASIEN
FOLLOW UP.docx
FOLLOW UP (16 Mei 2013 30 Mei 2013)
Kesimpulan
Pembentukan thrombus di daerah plak akan mempersempit oklusi,dan gangguan aliran darah menyebabkan ketidakseimbangan yang nyata antara pemasukan oksigen dan kebutuhan oksigen. Bentuk ACS merupakan hasil yang bergantung dari derajat obstruksi koroner dan berhubungan dengan iskemia. Oklusi thrombus parsial menyebabkan sindrom unstable angina (UAP) dan non-ST Elevation Myocardial Infarction (NSTEMI). Jika thrombus menyumbat arteri koroner secara komplit, maka menyebabkan iskemik yang lebih parah dan nekrosis yang lebih banyak, dikenal sebagai ST Elevation Myocardial Infarction (STEMI).
RV infark dengan gejala klinis nyeri dada dirasakan os seperti terhimpit benda berat. Penjalaran (+) ke bahu dan punggung. Durasi > 30 menit, disertai mual (+), keringat dingin (+). Dari interpretasi EKG terlihat kesan SR + STEMI inferoposterior + RV infark. Pasien juga telah mendapat penatalaksaanaan awal dengan ace inhibitor, anti platelet, dan antikoagulan. Pada pasien ini di berikan terapi berupa Bed Rest semi fowler, O2 4L/i, IVFD NaCl 0,9 % 10 gtt/I (mikro), Inj UFH 600 IU/hour , Aspilet 1x80 mg, Plavix 1x75 mg, ISDN 5mg (k/p), Simvastatin 1x40 mg dan Laxadin 1x1ci.
TERIMA KASIH
PDKI 2009 ..\Downloads\Documents\acs-cardiovascular-emergency-jadi.pdf AHA/ACC 2013 ..\Downloads\Documents\Circulation-2013-O-Gara-529-55.pdf ECS 2012 STEMI ..\Downloads\Documents\Guidelines_AMI_STEMI.pdf NSTEMI ..\Downloads\Documents\Guidelines-NSTE-ACS-FT.pdf Ppt ..\Downloads\Documents\Figure.ppt(aha) ..\Downloads\Documents\Slide_Set_AMI_STEMI.ppt(ecs) ..\Downloads\Documents\guidelines_ACS_NSTE_Slides-2011.ppt(ecs)