laporan kasus stemi
DESCRIPTION
kardiologiTRANSCRIPT
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PRESENTED BY :FIKRI RIFA HAMDISUPERVISOR PEMBIM BING:PROF. DR. DR. ALI ASPAR M , SP.PD, SP. JP(K) , FIHA, FINASIM
CASE PRESENTATION: ST ELEVATION MIOCARD INFARK whole anterior onset >24 hours killip 4
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Patient identity
Name : Mr. H
Age : 57 years old
Registration no. : 566506
Room : CVCU
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History taking
Chief ComplainLeft chest painPresent illness historySuffered since 1 day agoThis pain was suddenly Described as intermittently compressed, through to the back,
pain accompanied with cold sweatingNo epigastric painNo DOE, PND and orthopneaHistory of smoking since 10 years ago with ± 10-12 cigarettes
per day
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History of Past Illness
History hospitalized with heart attack on July 2014 History of diabetes since 2 years ago and treated regularly History of hypertension denied No history of heart disease in the family
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PHYSICAL EXAMINATION
• Moderate illness/well-nourished/conscious (GCS 15: E4M6V5)General condition
• BP : 80/50 mmHg• HR : 100 x/minutes• RR : 24 x/minutes• T : 36.7 oC
Vital Signs
• Anemis (-) , icterus (-)Head
• JVP R + 2 cmH20Neck
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• I : symmetric R=L, normochest• P : mass (-), tenderness (-), VF R=L• P : sonor• A : breath sound : vesicular
additional sound : ronchi minimal at base of lung , wh -/-
Chest Examinatio
n
• I : ictus cordis not visible• P : ictus cordis not palpable• P : dull, Upper border 2nd ICS sinistra,
Right border 4th ICS linea parasternalis dextra, Left border 5th ICS linea axillaris anterior sinistra
• A : HS I/II pure, regular, murmur(-)
Cor
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Abdomen :• Inspection : flat and correspond with breathing
movement• Auscultation : peristaltic sound (+) , normal• Palpation : liver and spleen impalpable, epigastric
pain (-)• Percussion : tympani, ascites (-)Extremities:• Edema -/-
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PEMERIKSAAN HASIL NORMAL
WBC 15,4 x 103/mm3 4.0-10.0 x 103
RBC 5,71 x 106/mm3 4.0-6.0 x 106
HGB 18 gr/dL 12-16
HCT 52% 37-48
PLT 248 x 103/mm3 150-400 x 103
Ureum 63 10-50 mg/dl
Creatinin 1,4 0.5-1.2 mg/dl
SGOT 22 <35 U/L
SGPT 36 <45 U/L
Na 136 136-145 mmol/l
K 3,9 3.5-5.1 mmol/l
Cl 107 97-111 mmol/l
GDS 223 200 mg/dl
CK 753 L(<190U/L) P(<167U/L)
CK-MB 14,3 <25U/L
Troponin T <0,1 <0,05
Kolesterol total 108 200 mg/dl
Asam urat 6,8 L 3,4-7,0 ; P 2,4-5,7
HDL 18 L>55; P>65
LDL 69 <130 mg/dl
Trigliserida 158 200 mg/dl
7-3-2015
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Sinus rhytmHR : 110 bpmAxis : normoaxisPR-Interval : NormalP-Wave : NormalQRS Duration : 0,08 minuteST-segment : elevation on V1-V6
ConclusionSinus rhytm, normoaksis, whole anterior miokard infark
ELECTROCARDIOGRAPHY (7-3-2015)
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ECHOCARDIOGRAM
Disfunction systolik ventrikelEF 41%Left Ventricular HipertrophyMild hipokinetik anterior, anteroseptal and anterolateralCardiac valve :
Mitral : good function and movement Aorta : calsification Tricuspid: good function and movement Pulmonal : good function and movement
Conclude : Disfunction systolik and diastolik LV Left Ventricular Hipertrophy
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Risk Factor
Modified Risk Factor• Diabetes• Smoking
Non-modified risk factor:• Gender : male• 57 years old
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Diagnosis
ST Elevation Myocardial Infarction (STEMI) whole anterior onset >24 hours, Killip 4
DM type 2Syok Cardiogenic
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Treatment management
O2 2-4 lpm via nasal kanulIVFD NaCl 0.9% 500 ml/24 hoursAnti Platelet Aggregation:
Aspilet (loading dose 325 mg) maintenance 1x80 mg Clopidogrel (loading 600 mg) maintenance 1x75 mg
Anti Angina: Pethidine 12,5 mg/24 hours extra, maintenance 100mg/24 hours/drips
Anti Coagulant: Lovenox 0,6 cc/24 hours/SC
Simvastatin 20 mg/24 hours/oralDobutamin 5 mcg/ kgBB/minute/syringe pumpLaxadin syrup 15 ml/ 24 hours/ oralPrimary PCI
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PLANNING
Coronary angiography
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How to make the diagnosis?
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INTRODUCTION
Acute coronary syndromes (ACS) is a term for situations where the blood supplied to the heart muscle is suddenly blocked.
• described as a group of conditions resulting from acute myocardial ischemia (insufficient blood flow to heart muscle)
• ranging from unstable angina (increasing, unpredictable chest pain) to myocardial infarction (heart attack).
Myocardial infarction (MI) rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium.
This usually results from plaque rupture with thrombus formation in a coronary vessels, resulting in an acute reduction of blood supply to a portion of the myocardium.
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• Occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis.
• In most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures, or ulcerates.
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Diagnosis Of ACS
At least 2 of the following (WHO criteria):
Ischemic symptoms
Diagnostic ECG changes
Serum cardiac marker elevations
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Diagnosis Of ACS
At least 2 of the following
Ischemic symptoms
Diagnostic ECG changes
Serum cardiac marker
elevations
• Prolonged chest pain (usually >20 minutes) – constricting, crushing, squeezing
• Usually retrosternal location, radiating to left chest, left arm; can be epigastric
• Dyspnea• Diaphoresis• Palpitations
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Diagnosis Of ACS
At least 2 of the
following
Ischemic symptoms
Diagnostic ECG
changes
Serum cardiac marker
elevations
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ECG evolution for MI
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Diagnosis Of ACS
At least 2 of the following
Ischemic symptoms
Diagnostic ECG changes
Serum cardiac marker
elevations
Troponin T
CK-MB
CK
Myoglobin
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DIAGNOSIS
No
Yes
YesNo
Acute Myocardial Infarction( Q-wave, non-Q wave )
NSTEMI(No ST-Segment
Elevation Myocardial Infarction)
Unstable Angina
Signs of myocardial ischemia
ST segmen elevation?
Biochemical cardiac markers?
ECG
Lab
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Unstable Angina
• Non-occlusive thrombus• Non-specific on ECG• Normal cardiac enzyme markers
NSTEMI
• Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis
• ST depression +/-• T wave inversion on ECG• Elevated cardiac enzyme markers
STEMI
• Complete thrombus occlusion• ST elevation on ECG• Elevated cardiac enzyme markers• Symptoms more severe
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INFARCT LOCATION
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Class Description Mortality Rate (%)
I no clinical signs of heart failure
6
II rales or crackles in the lungs, an S3, and elevated jugular venous pressure
17
III acute pulmonary edema 30 - 40IV cardiogenic shock or
hypotension (systolic BP < 90 mmHg), and evidence of peripheral vasoconstriction
60 – 80
KILLIP CLASSIFICATION
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Relieve painHemodynam
ic stabilization
Myocardial reperfusion
Prevent the complication
GOAL OF TREATMENT
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COMPLICATIONS
Ventricular dysfunction
Hemodynamic
disturbances
Cardiogenic shock Arrhythmia
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Thank you