1. The document reports a case of a 53-year-old female patient presenting with chest discomfort.
2. Physical examination, laboratory tests, electrocardiography and echocardiography revealed ST elevation myocardial infarction of the inferior wall occurring less than 12 hours ago.
3. The patient was diagnosed with ST elevation myocardial infarction of the inferior wall onset less than 12 hours ago and treated with antiplatelet therapy, statins, anticoagulants, and supplements.
1. The document reports a case of a 53-year-old female patient presenting with chest discomfort.
2. Physical examination, laboratory tests, electrocardiography and echocardiography revealed ST elevation myocardial infarction of the inferior wall occurring less than 12 hours ago.
3. The patient was diagnosed with ST elevation myocardial infarction of the inferior wall onset less than 12 hours ago and treated with antiplatelet therapy, statins, anticoagulants, and supplements.
1. The document reports a case of a 53-year-old female patient presenting with chest discomfort.
2. Physical examination, laboratory tests, electrocardiography and echocardiography revealed ST elevation myocardial infarction of the inferior wall occurring less than 12 hours ago.
3. The patient was diagnosed with ST elevation myocardial infarction of the inferior wall onset less than 12 hours ago and treated with antiplatelet therapy, statins, anticoagulants, and supplements.
1. The document reports a case of a 53-year-old female patient presenting with chest discomfort.
2. Physical examination, laboratory tests, electrocardiography and echocardiography revealed ST elevation myocardial infarction of the inferior wall occurring less than 12 hours ago.
3. The patient was diagnosed with ST elevation myocardial infarction of the inferior wall onset less than 12 hours ago and treated with antiplatelet therapy, statins, anticoagulants, and supplements.
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CASE
REPORT ST Elevation Miokard Infark Nancy Dwi Puspita (C014182113)
Pembimbing : Prof. dr. Peter Kabo, Ph. D, Sp. FK, Sp. JP(K), FIHA, FAsCC CASE REPORT ST Elevation Miokard Infark PATIENT’S IDENTITY Name : Tn. E
Age : 53 Tahun
Gender : Female
Address : Enrekang
Occupation : Civil Servant
Religion : Moeslim
MR : 00875554
Admitted on : March, 2nd 2019
HISTORY TAKING Chief Complaint : Chest Discomfort
Recent Disease History :
Feeling chest discomfort about +/-30 minutes before admitted to the hospital. It can be localized by the patient. It was aggravated by heavy activity. Chest discomfort felt like tenderness, and intermitten. It complained heavy enough and distrub patient activity. There were history of diaphoresis, shortness of breath, nausea and vomitting. There were no history of fever, and cough. HISTORY TAKING Past Disease History • There was no history of hipertension • There was no history of diabetes melitus • There was history of dislipidemia
Family History There was no family history of cardiovascular disease
Risk Factor • Un-modifable : Age, Gender • Modifable : Smoking +/- 7 years ago, high consumed of fatty food PHYSICAL EXAMINATION General Apparance • Moderate illness/Adequate Nutrition/Compos mentis • Weight : 72 kg • Height : 160 cm • BMI : 28,1 kg/m2 (Obes I) • GCS : E4M6V5
2 INR 1,04 -- 3 APTT 25,9 22,0-30,0 Second LABORATORY RESULT No Examination Result Reference Unit Blood Chemistry 1 Glucose 156 140 mg/dl 2 Uric acid 3,8 P (2.4-5.7); L (3.4-7.0) mg/dl Lipid Profile
1 Total Cholesterol 257 200 mg/dl
2 HDL 40 L (> 55), P (> 65) mg/dl 3 LDL 156 < 130 mg/dl 4 Trygliceride 182 200 mg/dl Kidney Function
1 Ureum 19 10-50 mg/dl
2 Creatinin 0,71 L (<1,3); P( <1,1) mg/dl Liver Function
1 SGOT 192 <38 U/L
2 SGPT 70 <41 U/L LABORATORY RESULT No Examination Result Reference Unit
Immunoserology
1 Troponin I 18208,8 Laki-laki 17 – 50 ng/l Perempuan : 8 - 29
QRS Rate : 77 bpm QRS Complex : Normal Regularity : Regular ST Segment : Elevasi on II, III, avF Axis : Normal axis T-wave : Normal P-wave : Normal, duration 0.08 seconds ECHOCARDIOGRAPHY
Decreased left ventricle systolic function EF 43% BIPLANE
Dilated left atrium
Concentric left ventricular hypertrophy
Segmental hypokinetic
Moderate mitral regurgitation
Moderate ventricle diastolic dysfunction
DIAGNOSIS ST Elevasi Infark Miokard Inferior Onset <12 jam Killip 1
• Antikoagulan : Arixtra 2,5mg /24 Jam / Subkutaneous
• Hepar Supplement : Maxiliv 1 tab/ 24 Jam / Oral
DISCUSSION ST ELEVATION INFARK MIOKARD DEFINITION Acute Coronary Syndrome (ACS) is a condition caused by disrupted atherosclerotic plaque with platelet aggregation and thus created intracoronary thrombosis. Thrombosis will become an occlusion either severe/complete or partial occlusion and this flow disturbance will lead to the imbalance between oxygen demand and supply on myocardia and myocardium will be damaged.
Partial Occlusion : Unstable Angina Pectoris
(UAP) and non-ST segment elevation myocardial infraction (NSTEMI) Total Occlusion : ST- segment elevation myocardial infraction (STEMI) EPIDEMIOLOGY
. However, reported incidence in United States is decreasing from 133 per 100.000 in 1999 to 50 per 100.000 in 2008,
In the whole world, ischemia heart disease STEMI is relatively common in younger has become the single common cause of people and occurring more in men than death with its frequency that keeps women (ESC, 2017). increasing. STEMI in Europe is approximately 43 to 144 per 100.000 per year. RISK FACTOR Modifiable : Unmodifiable :
• Dyslipidemia • Age
• Smoking • Gender
• Hypertension • Family History
• DM • Genetic
• Less physical activity PATHOPHYSIOLOGY
ACS is the manifestation of torn or ruptured atheroma
plaque of coronary vessel DIAGNOSIS Acute Coronary Syndrome is diagnosed when 2/3 criteria is found :
1. Chest pain ±20 minutes or didn't relieve
with sublingual nitrate
2. Electrocardiography changes (EKG)
3. Elevated heart biomarker
DIAGNOSIS Anamnesis The most important complain was CAD and radiated pain to the neck, jaw, or left hand. It's also important to ask about risk factors.
Physical Examination To identify the trigger factors, complication, and morbidity of ischemia, and to exclude differential diagnosis DIAGNOSIS ECG Done in 10 minutes since patient was admitted to the hospital with chest pain that lead to ischemia. Assessment of ECG from ST segment elevation. Suspect infarct if ECG with new LBBB/suspect also accompanied by ST segment elevation ≥1 mm on positive QRS complex and lead with positive QRS complex and ST segment depression ≥ 1 mm in lead V3-V6 DIAGNOSIS Heart Enzym Examination Creatinine kinase – MB (CK-MB) or Troponin T/I are heart myosite necrosis marker and becomes the biomarker to diagnose myocardial infarction Laboratorium Laboratorium data, that needs to be collected in emergency unit besides heart biomarker, are hematology routine test, gds, electrolyte status, blood coagulation, kidney function test, and lipid fraction.
Chest X-Ray To determine differential diagnosis, identify complication and comorbidity. Unstable Angina NSTEMI STEMI
Occluding thrombus Complete thrombus
sufficient to cause occlusion Non occlusive tissue damage & mild thrombus myocardial necrosis ST elevations on Non specific ECG ST depression +/- ECG T wave inversion on Elevated cardiac ECG enzymes Normal cardiac enzymes Elevated cardiac More severe enzymes symptoms KILLIP CLASSIFICATION MANAGEMENT Fixing the chest pain and fearness Stabilizing the hemodinamic (blood pressure and perpheral pulse control) Reperfusion of the myocard INITIAL TREATMENT • Bed rest • Oxygen (2-4 lpm) • Anti platelet therapy : Aspirin 160-320mg chewed immediately and 80-160 mg continued indefinitely. Clopidogrel 300-600mg loading dose and 75mg daily continued for at least 14 days and up to 12 months. • Nitroglycerin : 0.4 mg SL tablets every 3-5 min up to 3 times; if effect is not sustained, can continue with an IV drip of 50mg in 250mL Dextrose 5%. • Morphine 2-5mg iv (can be administered again in 5-30 minutes later) • Fibrinolytic therapy: Streptokinase 1.5 million units in 100 mL dextrose 5% or NaCl 0,9% finished in 30 – 60 minutes Actilyse : 15 mg bolus iv 0.75mg/kg weight body in 30 minutes and 0,5 mg/kg weight body in 60 minutes • Anticoagulation therapy: Low Molecular Weight Heparins (Fluxum) 0.4cc/sc for up to 8 days post-MI. Unfractionated heparin • Anti Hypertension Drugs • Lipid Lowering Agents PROGNOSIS Clinical Manifestation Aside from various typical signs such as age, diabetes mellitus, kidney failure and other comorbidity, prognosis also can be predicted from clinical presentation when the patient was admitted to the hospital. The presence of symptoms at rest will give a worse prognosis. Besides that, a continuous pain or often accompanied by tachycardia, hypotension, and heart failure also markers of increased risk and need prompt diagnosis and treatment. COMPLICATION THANK YOU
