CASE REPORT (SEPTEMBER 20th, 2011)

Presented by: Fransiska C. Subeno (C11107156)

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

PATIENTS IDENTITY

Name : Mr. A Age : 52 years old Register no. : 47 82 46 Date of admission : September 4th, 2011 Time of admission : 11.00 a.m.

HISTORY TAKING
Chief complaint : Chest pain
It had been felt since two days ago, suddenly and

uncontinuously. It had been worsen since a day before he was admitted to the hospital (at 08.30 p.m., September 3rd, 2011). The chest pain was felt more frequent, sometimes he felt like strangulated. He had sweat during the chest pain. There were no dyspnea, nausea, and vomiting.

Defecation and urination were 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 History of asthma (-)

Risk Factors

MODIFIABLE : Smoking (+) Hypertension (-) Diabetes mellitus (-) Dyslipidemia (-) 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 supine Chest Examination Inspection : symmetric R=L, normochest Palpation : mass (-), tenderness (-), VF R=L Percussion : sonor Auscultation : vesicular breath sound, no additional sound

Regional Status
Cardiac Examination Inspection : IC wasnt visible Palpation : IC wasnt 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
Abdominal Examination Inspection : convex 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 bpm

Left Axis Deviation

Pathological Q wave at V1-V4 Elevation of ST segment at I, aVL, V1-V5

Normal 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 onset > 12 hours, Killip I

MANAGEMENT
O2 4-6 L/minute

Bed rest with mobilization

Cardiac diet IVFD NaCl 0,9% 10 gtt per minute

Aspirin (Aspilet) 160 mg (loading dose), then

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

MANAGEMENT
Nitrat (Farsorbid) 5 mg (SL), then continued with

Farsorbid via SP Na Fondaparinux (Arixtra) 2,5 mg/24 hours/SC Simvastatin 20 mg 0-0-1 Bisoprolol 2,5 mg once daily Captopril 6,25 mg three times daily Laxadyn syr. once daily Alprazolam 0,5 mg 0-0-1 The patient must be catheterized

PLANNING
Enter the patient to CVCU

Monitoring ECG everyday

Chest X-Ray Echocardiography

Coronary Angiography

ECHOCARDIOGRAPHY

Interpretation
Conclusion:
Systolic

and dyastolic dysfunction of left ventricle e.c. Coronary Artery Disease Left Ventricle Hypertrophy EF 36%

References: 1. Kabo P. Penyakit jantung koroner. Dalam: Bagaimana menggunakan obat-obat kardiovaskular secara rasional. Jakarta: Balai Penerbit FKUI; 2010. 2. Fauci et al. ST-segment elevation myocardial infarction. In: Harrisons Principles of Internal Medicine 17th edition. New York: The McGraw-Hill Companies; 2008. Chapter 239. 3. Brashers VL. Ischemic Heart Disease. In: Clinical application of pathophysiology 3rd ed : An evidence-based approach. United State of America: Elsevier Inc; 2002. p. 38.

INTRODUCTION
irreversible necrosis of heart muscle due to prolonged ischemia, which is suddenly happened.1 Acute myocardial infarction (AMI) is one of the most common diagnoses in hospitalized patients in industrialized countries.2
Acute myocardial infarction (AMI) is an

Picture 1. Acute Coronary Syndrome (from 2nd reference)

PATHOPHYSIOLOGY
STEMI

generally occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis.1 In most cases, infarction occurs when an atherosclerotic plaque fissures, ruptures, or ulcerates and when condition favor thrombogenesis.2

RISK FACTORS
Modifiable: Hypertension Diabetes Mellitus Dyslipidemia Smoking Obesity Non-modifiable: Gender: male Age >45 years old Personal history of Coronary Artery Disease Family history of Coronary Artery Disease

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.2 Feels like heavy, squeezing, crushing, burning sensation.2 Involves the central portion of chest and/or the epigastrium, radiates to the arm, abdomen, back, lower jaw, and neck.2 It is often accompanied by weakness, sweating, nausea, vomiting, anxiety.2 Not relieved by rest or nitrat.1

HOW TO DIAGNOSE
Signs of myocardial ischemia ECG ST segment elevation?
No Yes Acute Myocardial Infarction

Lab
Yes
NSTEMI ( Non ST-Elevation Myocardial Infarction )

Biochemical cardiac markers ?

No

Unstable Angina
Diagram 1. Flowchart to diagnose acute coronary syndrome (from 3rd reference)

ADDITIONAL EXAMINATION (1)

Electrocardiogram2 It is begun with depression of ST-segment and inverted of Twave Then it is changed to elevation of ST-segment and absence of R-wave until the presence of Q-wave

Picture 2. Severe ischemia on anterior wall of myocardium (from 2nd reference)

ADDITIONAL EXAMINATION (2)

Serum cardiac biomarkers2 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 fearness1 o Bed rest o Diet o O2 2-4 lpm via nasal prongs or face mask o Sublingual/oral/IV nitroglycerine o Antiplatelet: aspirin and clopidogrel o Morfin/petidine o Diazepam 2-5mg/8 hour Stabilizing the hemodynamic (blood pressure and peripheral pulse

control)1 o -blocker o Calcium channel blocker (CCB) o ACE-Inhibitor Reperfusion of the myocard1 o Thrombolytic

KILLIP CLASSIFICATION
Class I II Description no clinical signs of heart failure rales or crackles in the lungs, an S3, and elevated jugular venous pressure acute pulmonary edema cardiogenic shock or hypotension (systolic BP < 90 mmHg), and evidence of peripheral vasoconstriction Mortality Rate (%) 6 17

III IV

30 - 40 60 80