NSTEMI (NON ST ELEVATION MYOCARDIAL

INFARCTION)

BY:ST. HARDIYANTI . S . MAL IK

C111 10 257

SUPERVISOR :D R . A B D U L H A K I M A L K AT I R I , S P. J P, F I H A

PATIENT IDENTITY

Name : Mr. M Age : 67 years old MR : 699300 Day of Admission : Januari 30, 2015

HISTORY TAKINGChief Complaint : chest painGuided Anamnesis :Chest pain occurred since 6 days before patient is admitted to the hospital. The pain especially felt in the left side of the chest and it is radiated to the back, left arm, and lower jaw. The patient feel a pressed-like sensation on his chest. Pain occurred more than 20 minutes, continously. Pain is not affected by activities or exercise and it is not relief by resting. There is no dyspneau, epigastric pain, vomiting, or nausea.

POST MEDICAL HISTORY

History of hospitalized in RS Masamba for two days with the same complaint but the patient forget the medication that given to him

History of DM (-)History of hypertension (-)History of dyslipidemia is unknown

PERSONAL HISTORY

History of smoking cigarettes (+), since 25 years ago, 1 pack/2 days

GENERAL STATESBW : 62 kgBH : 165 cmBMI : 22,7 kg/m2 (normal)Moderate illness / well nourished / conscious

Vital Sign Blood pressure : 130/80 mmHg Pulse rate: 92x/min Respiratory rate : 24x/min Temperature : 36,50 C

PHYSICAL EXAMINATIONHead and Neck ExaminationsEye : anemia (-), icteric (-)Lip : cyanosis (-)Neck : JVP R+2 cmH2OChest ExaminationInspection : symmetric between left and right chestPalpation : no mass, no tendernessPercussion : sonor left = right chest, lung-liver border in right ICS 4Auscultation : respiratory sound : vesicular; additional sound : ronchii -/- , wheezing -/-

Heart ExaminationInspection : heart apex is not visible Palpation : heart apex is not palpable Percussion : dull

Upper heart border in left ICS IIRight heart border in ICS IV right

parasternal line Left heart border in ICS V left

midclavicular lineAuscultation: Heart sounds : S I/II regular, murmur (-)Abdomen ExaminationInspection : flat, follows respiratory motionAuscultation : peristaltic sound (+), normalPalpation : no mass, no tenderness, liver and spleen are not palpable Percussion : tympani (+)Extremities ExaminationWarm akralEdema -/-

LABORATORY FINDINGS

TEST RESULT NORMAL VALUESWBC 8,6 x 103 /mm3 4,0 – 10,0 x 103 /mm3

RBC 4,68 x 106 /mm3 4,0 – 6,0 x 103 /mm3 Hb 13,8 gr/dl 12,0 – 16,0 gr/dlHct 39,9% 37,0 – 47,0%Plt 156 x 103 /mm3 150 – 400 x 103 /mm3

Ureum 30 mg/dl 10 - 50 mg/dlCreatinin 0,9 mg/dl M(<1,3); F(<1,1) mg/dl

Random Blood Glucose 137 mg/dl 140 mg/dl

CK 157 U/l M(<190); F(<167) U/lCK-MB 27,3 U/l < 25 U/l

Troponin T 1,6 ng/ml < 0,05 ng/ml

SGOT 65 mg/dl < 38 U/lSGPT 66 mg/dl < 41 U/l

Uric Acid 4,4 mg/dl M(3,4-7,0); F(2,4-5,7) mg/dl

Natrium 141 mmol/l 135 – 145 mmol/lKalium 4,3 mmol/l 3,5 – 5,1 mmol/lClorida 103 mmol/l 97 – 111 mmol/l

ELECTROCARDIOGRAPHY

ST Segment : ST-depressed on lead I, aVL, V3, V4, V5T wave : T inverted on lead I, aVL, V3, V4, V5, V6

INTERPRETATION

Rhythm : Sinus rhythmHeart rate : 70 bpmRegularity : regulerAxis : normoaxisP wave : normalPR interval : 0,08 sQRS complex : QS on lead V2

duration 0,12 sST Segment : ST-depressed on lead I, aVL, V3, V4, V5

T wave : T inverted on lead I, aVL, V3, V4, V5, V6

Conclusion : sinus rhythm, HR 70 bpm, normoaxis, anterolateral + high lateral wall ischemia

WORKING DIAGNOSIS

NON ST ELEVATION MYOCARDIAL INFARCTION

(NSTEMI)

MANAGEMENT AND THERAPY

O2 3 lpm via nasal kanulIVFD NaCl 0,9% 500cc/24 jamIsosorbid dinitrat 5 mg/sublingual Aspilet (anti platelets) loading 160 mg Clopidogrel (anti platelets) loading 300 mgFarsorbid 3 x 10 mgArixtra (anti koagulan) 2,5mg/24 jam/subkutanSimvastatin (anti cholestrol) 20 mg 0-0-1Laxadine syrup 0-0-2 cthAlprazolam (anti anxietas) 0,5 mg 0-0-1

Discussion

DEFINITION Acute myocardial infarction (AMI) is an

irreversible necrosis of heart muscle due to prolonged ischemia, which is suddenly happened.

Imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

DEFINITIONNon ST Elevation Myocardial Infarction (NSTEMI) is a syndrome characterized by chest pain resulting from an imbalance between O2 supply & demand, and is most commonly caused by the inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial O2 consumption.

Risk factor

Modifiable• Smoking• Hypertension• Obesity• Diabetes Mellitus• Dyslipidemia• Low HDL < 40• Elevated LDL / TG

Non-modifiable• Gender and age:• - male after age 45 y.o• - ♀ after age 55 y.o

• Family History• in first degree • relative > 55 y.o for • male/ 65 y.o for ♀

PATHOPHYSIOLOGY

American Heart Association: http://watchlearnlive.heart.org

American Heart Association: http://watchlearnlive.heart.org

American Heart Association: http://watchlearnlive.heart.org

American Heart Association: http://watchlearnlive.heart.org

American Heart Association: http://watchlearnlive.heart.org

American Heart Association: http://watchlearnlive.heart.org

DIAGNOSIS

WHO Diagnostic Criteria:• Clinical history of ischemic type

chest pain lasting >20 minutes.• Changes in serial ECG tracings.• Rise and fall of serum cardiac

biomarkers such as creatinine kinase-MB fraction and troponin.

Oxford Handbook of Clinical Medicine 6th Edition

CLINICAL FEATURES• Deep and visceral chest pain > 20 minutes, similar to

discomfort of angina pectoris but commonly occurs at rest, more severe, and lasts longer.

• Feels “squeezing," "griplike," "pressurelike," "suffocating" and "heavy”; or just "discomfort" but not pain.

• Location in substernal, retrosternal area, radiated to neck, jaw, shoulder, or ulnar side of the arm

• It is often accompanied by weakness, sweating, nausea, vomiting, anxiety.

• Not relieved with rest or nitrat.

ECG FOR AMI

Hyperacute T waveThe earliest signs of AMI are subtle and include increased T wave amplitude over the affected area.T waves become more prominent, symmetrical, and pointed(“hyperacute”). It most evident in the anterior chest leads

ST segment Elevation In two or more anatomically contiguous leads. Usually evident within hours of the onset of symptoms.

Pathological Q wavesEvidence of myocardial necrosis

BIOMARKERS

Biochemical marker for detection of myocardial necrosisNormal value First rise

after AMIPeak after AMI

Return to normal

CK-MB < 5.0 ng/ml 4 h 24 h 72 hMyoglobin < 82 ng/ml 2 h 6-8 h 24 hTroponin T Negatif 4 h 24 - 48 h 5 – 21 daysTroponin I Detection

Limit = 0.5 ng/mlAbnormal > 2.0 ng/mlBorderline - Not detected

3-4 h 24 – 36 h 5 – 14 days

MANAGEMENT

Fixing the chest pain and fearnesso Bed resto Diet o O2 2-4 lpmo Nitrat sublingual/oral/IVo Antiplatelet : aspirin and clopidogrelo Morfin/ petidine

Stabilizing the hemodynamic (blood pressure and pheripheral pulse control)o β-blockero Calcium chanel blocker (CCB)o ACE-Inhibitor

Reperfusion of the myocardo Thrombolitic

MANAGEMENT

KILLIP CLASSIFICATION

Class Description Mortality Rate (%)I no clinical signs of heart

failure6

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

Thank you