ACUTE CORONARY SYNDROME

Pathophysiologic and Diagnostic

 Serangan Jantung…
Sering didengar … dibaca…
Apa serangan Jantung Itu ?
Bagaimana mendiagnosis nya ?
Bagaimana menolong / mengatasinya?
Respon terhadap nyeri dada ?
Letak Jantung JANTUNG SEBAGAI POMPA
Pembuluh Darah Koroner

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

Infectious Disease 19.3

Atherothrombosis* 22.3

0 5 10 15 20 25 30
Causes of Mortality (%)

* Atherothrombosis defined as ischemic heart disease and cerebrovascular disease.

WHO. The World Health Report 2001. Geneva; 2001.
CVD is a leading cause of death
600 Men
500 Women
Deaths (thousands)

400

300

200

100

Source: CDC/NCHS and the American Heart Association

World Health Organization 2002.
Hospitalizations in the U.S. Due to Acute
Coronary Syndromes (ACS)
Acute Coronary
Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million .33 million

Admissions per year
Admissions per year
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171.
*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
 1.5 million cases annually in the USA, and
1/3 of these will die.

 Of those that die, half will do so before

reaching the hospital.
 DEFINISI
Penyakit Jantung Koroner
adalah penyakit akibat penyempitan atau penyumbatan
pembuluh darah koroner akibat adanya endapan lemak (
kolesterol, trigliserida) sehingga mengakibatkan suplai darah
ke jantung terganggu dan memicu serangan jantung.
 CAN YOU DESCRIBE THE
PATHOGENESIS OF A HEART ATTACKS ?
 There is a sudden total thrombotic occlusion of a major
extramural coronary artery in an individual who had no
previous clinical coronary artery disease.
What is Atherothrombosis?
 Atherothrombosis is characterized by a sudden
(unpredictable) atherosclerotic plaque disruption
(rupture or erosion) leading to platelet activation and
thrombus formation

Plaque rupture1 Plaque erosion2

1
14
 Atherosclerosis Timeline
Complicated
Foam Fatty Intermediate Fibrous Lesion/
Cells Streak Lesion Atheroma Plaque Rupture

Endothelial Dysfunction
From First From Third From Fourth
Decade Decade Decade

Adapted from Pepine CJ. Am J Cardiol. 1998;82(suppl 104).

 Clinical Manifestation of
Arterial Thrombosis

Plaque Atherosclerotic
WHY DOES THE THROMBUS FORM ?
 Most of these complications arise because
of an event that interfered with endothelial
cell function.

 Once a thrombus forms, the body’s

fibrinolytic system attacks it slowly.
 Common Underlying
Atherothrombotic Disease Process

Plaque Platelet,
Activation, Thrombus
Rupture Adhesion
and Formation
Aggregation

Atherothrombotic Events (MI, Stroke, or CV Death)

Majerus PW and Tollefsen D., Goodman and Gilman’s 10th ed 2001
 The cardiovascular continuum of events

Ischemia = oxygen supply

and demand imbalance
Myocardial
Ischemia22

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

 Muscle that was perfused by that vessel

becomes ischemic, and rapidly loses
function.

 The cells in this condition might die if

circumstances do not improve
 Pathogenesis of
Acute Coronary Syndrome
Platelet aggregation Incomplete occlusion
Thrombus Distal embolization
formation
Vasospasm
UAP
Plaque rupture
(55-80%)
NSTEMI

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 )

kematian sebagian otot jantung disebabkan

oleh terhentinya pasokan darah akibat
tersumbatnya satu / lebih pembuluh koroner
oleh gumpalan darah (trombus).

KENALI GEJALA / TANDA SERANGAN JANTUNG

Serangan jantung sering kali terjadi antara
pukul 4 - 10 pagi, karena:

jumlah adrenalin lebih tinggi dikeluarkan oleh

kelenjar adrenal

dpt menyebabkan pecahnya lesi aterosklerosis

> 90% penderita serangan jantung, sumbatan
akibat bekuan darah
karena adanya plak aterosklerosis yang pecah.
 menghambat / memblokir aliran darah yg
memperdarahi otot jantung dibagian distal
setelah sumbatan  sel-sel akan mati

Infark Miokard
Pembuluh darah yang mengalami aterosklerosis & trombosis
Patofisiologi SKA
Perubahan yg tjd pd pembuluh darah koroner
Oleh karena penumpukan plak

Aterosklerosis

Gangguan pasokan darah koroner ke miokard

Area miokard kekurangan pasokan darah

Iskemia

Perubahan Metabolisme
Manifestasi klinis
Repolarisasi listrik anaerob
 Perubahan Metabolisme Manifestasi
Repolarisasi listrik anaerob Klinis

ST Segment Non ST Segment Metabolisme

Elevasi Infark Elevasi Infark Anaerob Nyeri
Miokard Miokard

Pelepasan Enzim Asam Laktat

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

 Perubahan EKG, STEMI atau Non

STEMI dengan atau tanpa Q
patologik

 Peningkatan Enzim jantung

WHAT ARE THE CLINICAL SIGNS AND
SYMPTOMS OF A HEART ATTACK ?
Dr H.A.M. HANF
SMF P. DALAM
 Gejala Serangan Jantung
 Nyeri dada khas
Lokasi :
Dibelakang tulang dada, Dada sebelah kiri
Kualitas:
seperti ditekan/ditindih benda berat,
dibakar, diremas, ditusuk, diiris, tercekik
Penjalaran:
Leher, Rahang bawah, Bahu,Punggung,
pergelangan s/d jari-jari, Ulu hati.
Gejala penyerta:
Rasa sukar hirup/ sesak napas
Keringat dingin, Pucat
Dimana Rasa Nyeri Dirasakan??
 WHAT IS “ECG APPEARANCE “
IN ACUTE CORONARY SYNDROME ?
Segmen ST, diukur dari akhir QRS s/d awal
gel T
 Normal : Isoelektris

 Kepentingan : Elevasi Pada injuri/infark akut

Depresi Pada iskemia

Non STEMI STEMI

 Creatine Kinase ©

 Lactic Dehydrogenase (LDH)

 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

Alpert et al. J Am Coll Cardiol 2000;36:959.

Wu et al. Clin Chem 1999;45:1104.
NILAI RUJUKAN TROP-T

 ) Negatif < 0,05

 ) Low < 0,05 – 0,1
 ) MCI 0,1 – 0,2
 ) Massive MCI >2
iccu
Diagnosa pasti PJK
CT scan p.d. koroner (MSCT)
Kateterisasi jantung (CAG)
Kateterisasi Jantung
Balloon Angioplasty
Pemasangan stent
Pemasangan stent
Operasi bedah pintas koroner (CABG)
LOKASI

 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

 Kepentingan : Elevasi Pada injuri/infark akut

 Depresi Pada iskemia

Non STEMI
STEMI
 ST depresi dan perubahan gelombang T

• ST depresi dianggap bermakna bila > 1 mm di bawah garis dasar PT di titik J

• Titik J didefinisikan sebagai akhir kompleks QRS dan permulaan segmen ST

Bentuk segmen ST :

• up-sloping ( tidak spesifik )

• horizontal ( lebih spesifik untuk iskemia )
• down-sloping ( paling terpercaya untuk iskemia )

Perubahan gelombang T pada

iskemia kurang begitu spesifik

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

Mid LAD occlusion

after the first septal
perforator (arrow)
 Proximal large RCA occlusion

ST elevation in leads II, III, aVF, V5, and V6

with precordial ST depression
Small inferior distal RCA occlusion

ECG changes in leads II, III, and aVF

Unstable angina
Subendocardial ischemia.
Anterolateral ST-segment depression
Acute anteroseptal myocardial infarction.
Hyperacute T-wave changes are noted
Acute anterolateral myocardial infarction
Lateral myocardial infarction
Inferior myocardial infarction
Inferior myocardial infarction.
Inferior Q waves with T-wave inversions
Acute inferoposterior myocardial infarction
NON-STEMI / UAP
Bila Penderita Sadar :
1. Kendurkan Pakaian dari
leher s/d pinggang
2. Pastikan tidak kedinginan,
Bilka kedinginan Tutup
dengan selimut.
3. Jangan memberi apapun
melalui mulut.
4. Jangan memindah
-mindahkan.
5. Temani untuk
menenangkan penderita.
6. Segera ke dokter terdekat.
 Bila Penderita Tidak Sadar :

1. Letakkan penderita ditempat datar. Angkat kepala penderita

pada tengkuknya dan tekan pada dahinya.
2. Dorong dagunya naik turun.
 Bila Penderita Tidak Sadar (2):

1. Periksa pernapasan dengan mendekatkan telinga anda pada

Mulut penderita , sambil memperhatikan gerak pada dadanya.
2. Bila ada makanan atau gigi palsu pada penderita, Bersihkan;
dengan memiringkan penderita lebih dahulu.
 Bila Penderita Tidak Sadar (3) :

 Bila pernapasan tampak lancar : Posisi Recovery

untuk menjaga agar jalan napas tetap bebas.
Bila Napas Berhenti : Berikan Ventilasi :
Dari Mulut ke Mulut
16 –18 x/menit

Cek Nadi Karotis

Untuk tentukan
Denyut Jantung
 Psn Nyeri Dada SINDROM KORONER AKUT
Rwyat nyeri dada Aspirin 300 mg dikunyah dan Nitrat s.l.
khas
EKG 12 sandapan*
Petanda biokimia

•EKG Non diagnostik •Perubahan ST/T Elevasi seg

•Petanda biokimia (-) •Petanda biokimia (+)
ST
•Nyeri dada (-) •Nyeri dada menetap

•EKG tdk Observasi

berubah •EKG serial
Evaluasi utk
•Petanda(-) •Ulang petanda
6-12 jam stlh
reperfusi
•Nyeri dada(-)
onset nyeri dada* Rawat Terapi
Pulang • Nitrat
•Perubahan seg ST • ASA
Risiko rendah Risko tinggi •Petanda (+) APTS/NSTEMI •Clopidogrel
Periksa di Periksa •Nyeri dada •UFH/LMWH
Rawat jalan segera •(+/- Antagonis
menetap
Receptor GPIIb/IIIa
 Pengobatan Cepat pada
SKA
 Oksigenisasi 2-3 l/mnt dg kanul
 Aspirin 160 – 300 mg dikunyah 
diberikan pada semua pasien SKA
 Nitrogliserin (SL) 5 mg, jika sakit dada
tetap berlanjut dapat diulang setiap 5
menit sampai 3 kali pemberian ”
tidak boleh diberikan pada pasien
dengan hipotensi”.
 Pengobatan cepat pada
SKA

 Morphine, dg dosis 2-4 mg IV

Untuk mengurangi kecemasan dan
kegelisahan, sakit karena iskemia,
meningkatkan venous capacitance.
Efek Samping : Mual, bradikardi,
depresi pernafasan
 Menentukan Lokasi Infark
Sandapan EKG
Menentukan Lokasi Infark

 SANDAPAN EKG
1. Lead I, aVL, V5, V6  Lateral = LCX

2. Lead II, III, aVF  Inferior = RCA

3. Lead V1, V2, V3, V4  Anterior = LAD

Acute Coronary Syndrome

 ST-segment elevation MI (STEMI)

 Non ST-segment elevation MI (NSTEMI)
 Unstable Angina
ACS Physiology

Atherosclerosis
Rupture

Local Effects Distal Effects

Thrombosis
Embolism Thrombosis Vasospasm

Obstruction

Large vessel Injury Microvascular Injury

 Segmen ST
Diukur dari akhir QRS s/d awal gel T
 Normal : Isoelektris

 Kepentingan : Elevasi Pada injuri/infark akut

 Depresi Pada iskemia

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).

Imaging studies such as a high quality portable chest

I IIa IIb III
X-ray, transthoracic and/or transesophageal
echocardiography, and a contrast chest CT scan or an
MRI scan should be used for differentiating STEMI from
aortic dissection in patients for whom this distinction is
initially unclear.
Laboratory Examinations

Laboratory examinations should be performed as part of the

I IIa IIb III
management of ACS patients, but should not delay the
implementation of reperfusion therapy.

 Serum biomarkers for cardiac damage

 Complete blood count (CBC) with platelets
 International normalized ratio (INR)
 Activated partial thromboplastin time (aPTT)
 Electrolytes and magnesium
 Blood urea nitrogen (BUN)
 Creatinine
 Glucose
 Complete lipid profile
 Electrocardiogram

I IIa IIb III

Show 12-lead ECG results to emergency physician
within 10 minutes of ED arrival in all patients with
chest discomfort (or anginal equivalent) or other
symptoms of STEMI.

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

Pericarditis LV hypertrophy with strain

Atypical angina Brugada syndrome
Early repolarization
Wolff-Parkinson-White Myocarditis
syndrome Hyperkalemia
Deeply inverted T-waves Bundle-branch blocks
suggestive of a central
nervous system lesion Vasospastic angina
or apical hypertrophic Hypertrophic
cardiomyopathy cardiomyopathy
 ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Life-Threatening
Aortic dissection Tension pneumothorax
Pulmonary embolus Boerhaave syndrome
Perforating ulcer (esophageal rupture with
mediastinitis)
 ED Evaluation of
Patients With ACS
Brief Physical Examination in the ED
1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and gallops
6. Presence or absence of stroke
7. Presence or absence of pulses
8. Presence or absence of systemic hypoperfusion (cool,
clammy, pale, ashen)
 Chest pain consistent with coronary ischemia
Within 10 minutes
•Initial evaluation 12 leads ECG
•Establish IV access Establish continous ECG monitoring
•Blood for baseline cardiac marker Aspirin 160-325 mg

Therapeautic Diagnostic tracking according to

12-leads ECG result

Normal ECG ECG suggestive of Ischemia- ST-Elevation or New LBBB

T-wave inversion
ST-depression

•Continous evaluation
•Serial cardiac markers
•Serial ECG
•Consider non invasive evaluation
•Consider alternative diagnosis
Anti ischemic therapy Access for suitability for reperfusion
• Thrombolysis
• Primary PTCA
Initiate Anti-Ischemic therapy

Initiate Thrombolisis Primary PTCA

No Evidence of MI MI or
Or Ischemia Demonstrable Ischemia

Discharge Admit to ICCU

Acute Coronary Syndrome

 ST-segment elevation MI (STEMI)

 Non ST-segment elevation MI (NSTEMI)
 Unstable Angina