Laporan Kasus Kardiovaskuler (Fransiska_C11107156)

CASE REPORT (SEPTEMBER 20th, 2011)

Presented by:Fransiska C. Subeno (C11107156)

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

PATIENT’S IDENTITY

Name : Mr. AAge : 52 years oldRegister no. : 47 82 46Date 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 yearsHistory 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 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 : 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 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 onset > 12 hours, Killip I

MANAGEMENT

O2 4-6 L/minuteBed rest with mobilizationCardiac dietIVFD NaCl 0,9% 10 gtt per minuteAspirin (Aspilet) 160 mg (loading dose),

then continued once daily on the next dayClopidogrel (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 0-0-1Bisoprolol 2,5 mg once dailyCaptopril 6,25 mg three times dailyLaxadyn syr. once dailyAlprazolam 0,5 mg 0-0-1The patient must be catheterized

PLANNING

Enter the patient to CVCUMonitoring ECG everydayChest X-RayEchocardiographyCoronary Angiography

ECHOCARDIOGRAPHY

Interpretation

Conclusion:Systolic and dyastolic dysfunction of

left ventricle e.c. Coronary Artery Disease

Left Ventricle HypertrophyEF 36%

DISCUSSIONACUTE CORONARY SYNDROME

(ST SEGMENT ELEVATIONMYOCARDIAL INFARCTION)

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: Harrison’s

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

Acute myocardial infarction (AMI) is an 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

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…

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 segment elevation?

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 T-wave

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 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)1

o β-blockero Calcium channel blocker (CCB)o ACE-Inhibitor

Reperfusion of the myocard1

o Thrombolytic

KILLIP CLASSIFICATION

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 - 40

IV cardiogenic shock or hypotension (systolic BP < 90 mmHg), and evidence of peripheral vasoconstriction

60 – 80

THANK YOU