Infark Miokard dengan Elevasi ST

EPIDEMIOLOGI• Coronary artery disease is the leading cause of morbidity and

mortality in Western society and is worldwide epidemic.

• In 2001, iscemic heart disease was responsible for 11,8 percent of

all deaths (5,7 million) in low income countries and 17,3 percent

(1,36 million) of all deaths in high income countries.

• Approximately 850.000 Americans suffer for an acute myocardial

infarction (AMI) per year, one third of this are caused by an acute

ST segmen elevation myocardial infarction(STEMI).

• The incidence of AMI has declined over the past two decades from

244 per 100.000 population in 1975 to 184 per 100.000 population

in 1995.

• The in-hospital mortality rate also declined from 18 percent in 1975

to 12 percent in 1995.

Etiology

• Penyebab tersering : trombosis

• Penyebab yang jarang : emboli arteri koroner,

kelainan kongenital, dll.

• Ada beberapa faktor yang mempengaruhi

terjadinya penyakit jantung koroner : dapat

dimodifikasi dan tidak dapat dimodifikasi.

Faktor yang mempengaruhi

Tidak dapat dimodifikasi

• Usia, jenis kelamin

• Suku bangsa dan

warna kulit

• Genetika

Dapat dimodifikasi

• Hipertensi

• Hiperlipidemia

• Merokok

• Diabetes melitus

• Kegemukan, kurang gerak

• Konsumsi kontrasepsi oral

Patofisiologi • Iscemia miocard terjadi ketika suplay oksigen tidak

sebanding dengan kebutuhannya.

• Hal ini dapat disebabkan karena adanya oklusi arteri

koroner yang dicetuskan oleh trombus.

• Oclusi tersebut menyebabkan aliran darah, suplay oksigen

berkurang.

• Mencetuskan terjadinya glikolisis anaerob

• Berkurangnya kontraktilitas dari otot jantung

• Infark terjadi jika oklusi berlangsung lama dan berat.

• Luasnya infark tergantung dari lamanya aclusi terjadi.

Patofisiologi

Symptoms

• Classic symptoms AMI is precordial or retrosternal

discomfort that is commonly described as pressure,

crushing, aching, or burning sensation.

• Radiation of discomfort to the neck, back, or arms

frequently occurs and the pain usually persistent

• Nausea, diaphoresis, generalized weakness, and fear of

impending death.some patient particulary elderly, may

also present with syncope, unexplained nausea and

vomiting, acute confusition, agitation, or palpitation.

Physical Examination

• Patients can appear anxious and unconfortable

• With substansial left ventricular (LV) dysfunction at presentation may

have tachycardia, pulmonary rales, tachypnea, and a thirrd heart sound.

• The presence of a mitral regurgitant murmur suggest ischemic

dysfunction of the mitral valve apparatus, rupture, or ventriculare

remodelling

• In patients with right ventricular infarction, increased jugular venous

pressure, Kussmaul sign (rise in jugular venous pressure with inpiration)

and right ventricular third sound may be prsent.

• Extensive left ventricular dysfunction, shock is indicated by hypotension,

diaphoresis, cool skin and extremities, pallor, oliguria, and possible

confusion.

Help full test

• Electrocardiogram

• Labarotory studies

- Myoglobin

- CK-MB

- Troponins

Initial theraphy in the emergency department

• Oxygen : low flow oxygen theraphy delivered by nasal

canula should be routinely given during the first 24 to

48 hours and perhaps several days after acute

myocardial infarction in most patients.

• Aspirin : initial dose 160-325 mg, dosis lanjutan 75-325

mg/ hari. Bagi yang alergi aspirin, diberikan clopidogrel.

• β blockers: pemberian β blocker pada pasien dengan

hemodinamik yang tidak stabil harus ditunda dulu

smpai kondisinya stabil.

• Analgesia: morfin IV bolus 1-2 mg, max: 10-15 mg.

• Nitrat : nitrogliserin IV 5-10 µg/min

• Heparin

- unfractionated : inisial bolus 60 U/kg (4000 U

maximum) followed by 12 U/kg/h (max 1000 U/h).

- LMWH IV initial loading dose 30 mg followed 1

mg/kg subcutaneus dose every 12 hours for

patients younger than 75 years of age.

• Direct thrombin inhibitors : diberkan jika heparin

menginduksi trombositopenia. (bolus 00,25

mg/kg followed infusion of 0,5 mg/kg/h for first 12

hours and 0,25 mg/kg/h for the subsequent 36

hours).

• Factor Xa inhibitors :

Reperfusion strategies

• The main goal of STEMI management is rapid

reperfusion to establish coronary blood flow to

ischemic myocardium.

• There are 3 main reperfusion strategies:

thrombolytic theraphy, primary PCI, and

thrombolytic-facilated primary PCI.

Thrombolytic Therapy

• Thrombolytic Therapy is most effective when given within 3 hours from onset of chest pain.

• Absolute contraindications :- any prior intracranial hemoorage- known structural cerebral vascular lesion- known intracranial neoplasma- ischemic stroke within the past 3 months (except for acute stroke within 3 months)- suspected aortic dissection- active bleeding or bleeding diathesis (excluding mensis)- significant closed-head or facial trauma within 3 months

• Relative contraindications

o history of chronic, severe, poorly controled

hypertension

o systolic pressure >180 mmHg or diastolic < 110

mmHg

o history of prior ischemic stroke >3 months previously,

dementia, or known intracranial pathology not

covered in absolute contraindication

o recent (within 2 to 4 weeks) internal bleeding

o noncompressible vascular puncture

o pregnancy

o Active peptic ulcer

o Current use anticoagulant : the higher the

international ratio, the higher the risk of bleeding

o For streptokinase / anistreplase : prior exposure

(more than 5 days previously) or prior allergic

reaction to theese agents.

Primary PCI

• Should be performed as quickly as possible with a

goal of a medical contact –to-ballon or door to

ballon interval of within 90 minutes.

Thrombolytic –Facilitated PCI

• Pretreatment with thrombolytic inSTEMI patients

as a bridge to immediate PCI.

• This pretreatment has been proposed as a

method to initiate earlier reperfution and reduce

ischemic time and infarct size in patients who

experience a delay before the onset of PCI

Adjuvant antiplatelet theraphy

• Clopidogrel

- older than 75 years of age, 75 mg without

loading dose

- in patients 75 years of age or younger, 300 mg

loading dose followed by 75 mg daily.

• Glycoprotein II b/III a inhibitors

Komplikasi

• Disfungsi ventrikel

• Gangguan hemodinamik

• Syok kardiogenik

• Infark ventrikel kanan

• Aritmia

• Ekstrasistol ventrikel

• Ruptur muskulus papilaris, rupture septum

ventrikel, rupture dinding ventrikel

Prognosis

Klasifikasi Killip

Kelas Definisi Mortalitas (%)

I Tak ada tanda gagal jantung kongestif

6

II +S3 dan/atau ada ronkhi basah 17

III Edema paru 30-40

IV Syok kardiogenik 60-80

Unstable angina and non ST segment elevation MIC

• Causes of unstable angina and non-Q wave MI

1. Nonobstructive thrombus on pre-existing plaque

2. Dynamic obstruction (coronary artery spasm or

vasoconstrivtion)

3. Progressive mechanical obstruction

4. Inflammation an/or infection

5. Secondary unstble angina

• Noncardiac events can cause a mismatch in

myocardial oxygen demand and supply:

o Increased myocardial oxygen demand (fever,

thyrotoxicosis)

o Reduced myocardial oxygen delivery (anemia,

hipoxemia)

o Reduced coronary blood flow (arrhytmia,

hypotension).

Presenting symptoms and signs

• The caracter of the angina is the same as that

encoutered in chronic stable angina, but is

ussually more severe and of longer duration, may

occur at rest, or may presipitated by less exertion

than previously.

Three principal presentations of unstable angina

Rest angina Angina occuring at rest ang prolonged, usually>20 min

New onset angina New onset of angina of at least CCS claa III severity

Increasing angina Previously diagnosed angina that has become distrinctly more frequent, longer in duration, or lower in threshold.

Helpful test

• Electrocardiography : ST segmen depression

(>0,5 mm), inverted T waves

• Biochemical markers

- troponin I atau T: terdeteksi setelah 6 jam post

injury, bertahan sampai 2 minggu. Troponin I

lebih akurat pada renal insufisiensi.

- CKMB

• Cardiac catheterization

Jenis Nyeri dada EKG Enzim jantung

UAP •Angina pd wkt ist atau akrifitas ringan• Crescendo angina• Dpt hilang dgn nitrat

• Depresi segmen ST• Inversi gel T• Tdk ada gel Q

Tidak meningkat

NSTEMI • Lbh brt dan lama (>30 mnt)• Tdk hilang dgn nitrat•Mungkin diperlukan opiat

• Depresi segmen ST• Inversi gel T dalam Meningkat min 2x dr nilai

BAN

STEMI • Lbh lama dan brt (>30 mnt)• Tdk hilang dgn nitrat • Mungkin diperlukan opiat

•Hiperakut T•Elevasi segmen ST > 0,1mV pd 2 atau lbh sadapan ekstr. >0,2mV pd prekordial•Gel Q•Inversi gel T

Meningkat min 2x dr nilai BAN

Differential Diagnosis

• Musculoskeletal chest pain

• Gastrointestinal discomnfort (GERD, peptic ulcer disease,

biliary or pancreatic disease, esophageal spasm)

• Cardiac non ischemic pain (valvular heart disease,

hypertrophic cardiomyopathy, pulmonary hypertension,

pericarditis)

• Pulmonary discomfort (pulmonary embolus,

pneumothorax, pneumonia, COPD exacerbation).

• Anxiety

Complications

• 5-10% patients with UA die , 10-20% have

nonfatal MI with 30 days.

• ¼ patients with NSTEMI, Q wave MI develops,

with the reminder having non-Q wave MI.

• Arrhytmia

• Congestive heart failure

• Cardiogenic shock

Theraphy

• Bedrest

• Analgesic : morfin sulfat

• Anti-ischemic agents:

o Nitrates => vasodilator, mengurangi preload dan afterload.

jika gejala terus berlanjut setelah pemberian nitrogliserin

sublingual 3x dalam 10 menit => nitrogliserin IV 10mcg/

menit dan dinaikkan setiap 3- 5 menit sampai ischemia

teratasi atau terjadi penurunan tekanan darah(sistol <110

mmHg)

o β blocker => < kontraktilitas miocard, < tekanan

sistolik, sinus node rate, kecepatan konduksi

AV=> mengurangi kebutuhan oksigen otot

jantung.

o Calcium channel blocker : vasodilatasi,

<kontraktilitas miocard, av block, and sinus node

slowing.

• Antiplatelet theraphy

o Aspirin : 75-325 mg/hari

o Thienopyridines, ticlopidine, clopidogrel => inhibit

ADP-induced platelet agregation. Dose 75 mg

dailyfor 1 month and ideally up to a year in

patients treated medically, 1 month and ideally up

to a year in patients treated with a bare metal

stent, and for at least a year if treated with a drug-

eluting stend in addition to aspirin.

o Glycoprotein II b/III a inhibitors : abxicmab

• Antithrombin agents

o Unfractionated heparin

o Low molecular weight heparin

• Direct thrombin inhibitors : hirudin, bivalirudin

(subtitusi unfractionated haparin in patients with

UA undergoing PCI).

• Factor Xa inhibitors (fondaparinux) :

supplemented with unfractionated heparin

• Coronary revascularization

Pencegahan

Olahraga

Berhenti merokok

Pengontrolan tekanan darah & gaya hidup

Diet