CASE REPORT, SEPTEMBER 2011

Presented by:Fransiska C. Subeno (C11107156)

Supervisor:dr. Abdul Hakim Alkatiri, Sp.JP, FIHA

STEMI Extensive Anterior Wall

PATIENT’S IDENTITY

Name : Mr. AAge : 52 years oldRegister no. : 47 82 46Date of admission : September, 4th 2011

HISTORY TAKING

Chief complaint : Chest pain

It has been felt since four hours before admitted to the hospital. The history of chest pain had been felt since two days ago, lost and appeared, but since 08.30 a.m. on the day he was admitted, it was felt continuously, sometimes he felt like strangulated. Cold sweat (+) everytime he had a chest pain, dyspnea (-), nausea (-), vomitting (-)

Defecation and urination are normal

History of Past Illness

History of chest pain (-)History of hypertension (-)History of Diabetes Mellitus (-)History of dyslipidemia (-)Family history of heart disease (-)History of smoking (+) about 1-2

packs a day for about 20 years.

Risk Factors

MODIFIABLE :• Hypertension (-) • Diabetes mellitus

(-)• Dyslipidemia (-)• Smoking (+)• Obesity (-)

NON-MODIFIABLE• Gender : man• Age : 52 years old • Personal history of CAD

(-)• Family history of CAD

(-)

PHYSICAL EXAMINATION

• General Status :

moderate-illness/well-nourished/composmentis

• Vital Sign :

BP = 130/90 mmHg

Pulse = 85 bpm, regular

RR = 22 bpm

Temperature = afebris

Regional Status

Head Examination Eyes : anemic -/-, icterus -/- Lip : cyanosis (-) Neck : lymphadenopathy (-), JVP R-1 cmH2O supineChest Examination Inspection : symmetric R=L, normochest Palpation : mass (-), tenderness (-), VF R=L Percussion : sonor Auscultation : vesicular breath sound, no additional

sound

Cardiac Examination Inspection : IC wasn’t visible Palpation : IC wasn’t palpable Percussion : normal heart size

Upper border : left 2nd ICS Lower border : left 5th ICS Right border : right parasternalis line Left border : left medioclavicular line

Auscultation : Regular of I/II heart sound, murmur (-)

Regional Status

Regional Status

Abdominal Examination Inspection : convecs and following breath movement Auscultation : peristaltic sound (+) , normal Palpation : liver and spleen unpalpable Percussion : tympani, ascites (-)

Extremities Oedema : pretibial -/- ; dorsum pedis -/- Cold extremities (-)

ELECTROCARDIOGRAPHY(4th September 2011 at emergency unit)

Interpretation

Sinus Rhythm, heart rate 76 bpmLeft Axis DeviationPathological Q wave at V1-V4Elevation of ST segment at I, aVL, V1-V5Normal T wave

Conclusion:ST elevation myocardial infarction on extensive anterior wall

LABORATORY FINDINGS

Haematological Routine

Examination

• WBC = 12,50. 103

• RBC = 4,94. 106

• HGB = 16,1• HCT = 46,3• PLT = 290. 103

Chemical Blood Examination and Cardiac enzymes

• GDS = 108• GOT/GPT =

31/37• CK = 222• CKMB = no

reagen• Trop-T = 0,13

WORKING DIAGNOSE

ST Elevation Myocardial Infarction extensive anterior wall

MANAGEMENT

O2 4-6 L/minuteIVFD NaCl 0,9% 10 drips per minuteAspirin (Aspilet) 180 mg (loading dose), then

continued once daily on the next dayClopidogrel (Plavix) 300 mg (loading dose), then

continued once daily on the next dayNitrat (Farsorbid) 5 mg (SL), then continued with

Farsorbid via SPNa Fondaparinux (Arixtra) 2,5 mg/24 hours/SCSimvastatin 20 mg 0-0-1Captopril 12,5 mg three times dailyLaxadyn syr. twice dailyThe patient must be catheterized

PLANNING

Enter the patient to CVCUMonitoring ECG everydayEchocardiographyCoronary Angiography

ECHOCARDIOGRAPHY

Interpretation

Conclusion:Systolic and dyastolic dysfunction of

left ventricle e.c. Coronary Artery Disease

Left Ventricle HypertrophyEF 36%

DISCUSSION

ST ELEVATIONMYOCARDIAL INFARCTION

INTRODUCTION

Acute myocardial infarction (AMI) is an irreversible necrosis of heart muscle due to prolonged ischemia, which is suddenly happened.

Acute myocardial infarction (AMI) is one of the most common diagnoses in hospitalized patients in industrialized countries.

PATHOPHYSIOLOGY

STEMI generally 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 and when condition favor thrombogenesis.

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 like “heavy”, “squeezing”, “crushing”, “burning sensation”

Involves the central portion of chest and/or the epigastrium, radiates to the arm, abdomen, back, lower jaw, and neck.

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

Not relieve with rest or nitrat

HOW TO DIAGNOSE…

No

Yes

Yes

No

Acute Myocardial Infarction

NSTEMI( Non ST-Elevation

Myocardial Infarction )

Unstable Angina

Signs of myocardial ischemia

↑ Biochemical cardiac markers ?

ECG

Lab

ST segmen elevation?

ADDITIONAL EXAMINATION (1)

Electrocardiogram It is begun with depression of ST-segment and

inverted of T-wave Then it is changed to elevation of ST-segment and

absence of R-wave until the presence of Q-wave

ADDITIONAL EXAMINATION (2)

Serum cardiac biomarkers Certain proteins are released from necrotic heart

muscle after STEMI Cardiac Troponin (cTnT and cTnI) are not normally

detectable in the blood of healthy individuals but may increase after STEMI to levels >20 times higher than the upper reference limit

Other serum cardiac biomarkers are Creatine phosphokinase (CK) and the MB isoenzyme of CK

MANAGEMENT

Fixing the chest pain and fearnesso Bed resto Dieto O2 2-4 lpm via nasal prongs or face masko Sublingual/oral/IV nitroglycerineo Antiplatelet: aspirin and clopidogrelo Morfin/petidineo Diazepam 2-5mg/8 hour

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

Reperfusion of the myocardo Thrombolytic

THANK YOU