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Kiri
WHAT ARE THE STATISTIC FOR
“HEART ATTACKS” ?
Myocardial infarction is the leading cause of
death (COD) in industrialized countries.
Atherothrombosis* is the
Leading Cause of Death Worldwide1
Pulmonary Disease 6.3
Injuries 9
AIDS 9.7
Cancer 12.6
Atherothrombosis* 22.3
0 5 10 15 20 25 30
Causes of Mortality (%)
400
300
200
100
UA/NSTEMI† STEMI
Endothelial Dysfunction
From First From Third From Fourth
Decade Decade Decade
Plaque Atherosclerotic
WHY DOES THE THROMBUS FORM ?
Most of these complications arise because
of an event that interfered with endothelial
cell function.
Plaque Platelet,
Activation, Thrombus
Rupture Adhesion
and Formation
Aggregation
CAD
plaque
Atherosclerosis
Risk Factors
( DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc) Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
The cardiovascular continuum of events
Coronary
Thrombosis
Myocardial
Ischemia
CAD
Atherosclerosis
Risk Factors
(
DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc) Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
The cardiovascular continuum of events
ACS
Coronary
Thrombosis
Myocardial
Ischemia
CAD
Atherosclerosis
Risk Factors
(
DYSLIPIDEMIA , BP, DM,
Insulin Resistance, Platelets,
Fibrinogen, etc) Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
The cardiovascular continuum of events
ACS
Coronary
Thrombosis Arrhythmia and
Loss of Muscle
Myocardial
Ischemia Remodeling
Ventricular
CAD Dilatation
Atherosclerosis Congestive
Heart Failure
Risk Factors
(
DYSLIPIDEMIA , BP, DM, End-stage
Insulin Resistance, Platelets, Heart Disease
Fibrinogen, etc) Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
CAN YOU BE MORE SPESIFIC ABOUT
THE PATHOGENESIS OF
A THROMBIC OCCLUSION
thrombus plugs the lumen of the coronary
artery and blood flow stops
Exertion
BP, HR
Vasoconstriction
Vulnerable Plaque
Complete occlusion
STEMI
Paradigma lama :
Makin besar plak makin berat
obstruksi p darah koroner
iskemia makin berat
Paradigma baru :
Teori instabilitas plak ( ruptur plak )
Serangan Jantung ( Infark Myokard )
Infark Miokard
Pembuluh darah yang mengalami aterosklerosis & trombosis
Patofisiologi SKA
Perubahan yg tjd pd pembuluh darah koroner
Oleh karena penumpukan plak
Aterosklerosis
Iskemia
Perubahan Metabolisme
Manifestasi klinis
Repolarisasi listrik anaerob
Perubahan Metabolisme Manifestasi
Repolarisasi listrik anaerob Klinis
Troponin T CKMB
Evolusi akan
Menjadi Infark
CAN YOU DESCRIBE THE DIAGNOSTIC
OF “HEART ATTACKS”?
Spesific chest pain
ECG
CARDIAC ENZYME
3 Komponen dalam
mendiagnosa SKA
Keluhan sakit dada yg berupa
APTS/UAP
Myoglobin
Troponins (I&T)
Cardiac Biomarkers in STEMI
100
Multiples of the URL
50
Cardiac troponin-no reperfusion
20 Cardiac troponin-reperfusion
10 CKMB-no reperfusion
CKMB-reperfusion
5
2
Upper reference limit
1
0 1 2 3 4 5 6 7 8
Days After Onset of STEMI URL = 99th %tile of
Reference Control Group
Septal : V1-2
Anteroseptal: V1-3
Anterior : V1-5
Antero extensive: V1-6
Lateral : I – AVL
Inferior : II – III – AVF
Posterior : V8 – 9 / reciprox V1 - 3
Segmen ST
Diukur dari akhir QRS s/d awal gel T
Normal : Isoelektris
Non STEMI
STEMI
ST depresi dan perubahan gelombang T
Bentuk segmen ST :
Gelombang T hiperakut
kadang2 merupakan satu-satunya
perubahan EKG yang terlihat
Hyperacute T
Pathological Q
ST segment elevation
Anterior MI
Inferolateral MI with
reciprocating in I & AVL, V1
and V2
ECG : large anterior MI
SANDAPAN EKG
1. Lead I, aVL, V5, V6 Lateral = LCX
Atherosclerosis
Rupture
Thrombosis
Embolism Thrombosis Vasospasm
Obstruction
Non STEMI
STEMI
MANAGEMENT of ACS
Prehospital Chest Pain Evaluation
and Treatment
I IIa IIb III Prehospital EMS providers should administer 162 to 325 mg of aspirin
(chewed) to chest pain patients suspected of having STEMI unless
contraindicated or already taken by the patient. Although some trials
have used enteric-coated aspirin for initial dosing, more rapid buccal
absorption occurs with non–enteric-coated formulations.
I IIa IIb III It is reasonable for all 9-1-1 dispatchers to advise patients without a history
of aspirin allergy who have symptoms of STEMI to chew aspirin (162 to 325
mg) while awaiting arrival of prehospital EMS providers. Although some
trials have used enteric-coated aspirin for initial dosing, more rapid buccal
absorption occurs with non–enteric-coated formulations.
Imaging
Patients with STEMI should have a portable chest
I IIa IIb III
X-ray, but this should not delay implementation of
reperfusion therapy (unless a potential contraindication
is suspected, such as aortic dissection).
I IIa IIb III In patients with inferior STEMI, ECG leads should
also be obtained to screen for right ventricular
infarction.
Electrocardiogram
I IIa IIb III If the initial ECG is not diagnostic of STEMI, serial
ECGs or continuous ST-segment monitoring should
be performed in the patient who remains
symptomatic or if there is high clinical suspicion
for STEMI.
ED Evaluation of
Patients With ACS
Differential Diagnosis of STEMI: Other Noncardiac
Gastroesophageal reflux Cervical disc or neuropathic
(GERD) and spasm pain
Chest-wall pain Biliary or pancreatic pain
Pleurisy Somatization and
Peptic ulcer disease psychogenic pain disorder
Panic attack
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Other Cardiovascular and
Nonischemic
•Continous evaluation Anti ischemic therapy Access for suitability for reperfusion
•Serial cardiac markers • Thrombolysis
•Serial ECG • Primary PTCA
•Consider non invasive evaluation Initiate Anti-Ischemic therapy
•Consider alternative diagnosis