Laporan Kasus STEMI

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Transcript of Laporan Kasus STEMI

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

Patient identity

Name : Mr. H

Age : 57 years old

Registration no. : 566506

Room : CVCU

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

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

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

• 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

Abdomen :• Inspection : flat and correspond with breathing

movement• Auscultation : peristaltic sound (+) , normal• Palpation : liver and spleen impalpable, epigastric

pain (-)• Percussion : tympani, ascites (-)Extremities:• Edema -/-

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

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)

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

Risk Factor

Modified Risk Factor• Diabetes• Smoking

Non-modified risk factor:• Gender : male• 57 years old

Diagnosis

ST Elevation Myocardial Infarction (STEMI) whole anterior onset >24 hours, Killip 4

DM type 2Syok Cardiogenic

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

PLANNING

Coronary angiography

How to make the diagnosis?

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.

• 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.

Diagnosis Of ACS

At least 2 of the following (WHO criteria):

Ischemic symptoms

Diagnostic ECG changes

Serum cardiac marker elevations

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

Diagnosis Of ACS

At least 2 of the

following

Ischemic symptoms

Diagnostic ECG

changes

Serum cardiac marker

elevations

ECG evolution for MI

Diagnosis Of ACS

At least 2 of the following

Ischemic symptoms

Diagnostic ECG changes

Serum cardiac marker

elevations

Troponin T

CK-MB

CK

Myoglobin

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

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

INFARCT LOCATION

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

Relieve painHemodynam

ic stabilization

Myocardial reperfusion

Prevent the complication

GOAL OF TREATMENT

COMPLICATIONS

Ventricular dysfunction

Hemodynamic

disturbances

Cardiogenic shock Arrhythmia

Thank you