Dr. Bambang pamungkas, Sp.

JP,
FIHA
 Pangkat : letkol CKM nrp 33822
Jabatan : Kadep Peny Dalam, jantuing dan Paru
Tempat/tgl lahir :
Purworejo, 25 Pebruari 1961

Pendidikan :
Dokter FK Unibraw Malang 1988
Dokter spesialis FK Unair Surabaya 2003
Pekerjaan :
Dokter YONIF 743 Kupang 1989 1993
Denkesyah/RST Wirasakti Kupang 1993
-1996
Ditkesad 1997 2003
RST M Ridwan Maureksa Jakarta 2003
RST Dr. Soedjono Magelang 2003 -
 STEMI is a clinical syndrome defined by characteristic symptoms of
myocardial ischemia in association with persistent electrocardiographic
(ECG) ST elevation and subsequent release of biomarkers of myocardial
necrosis.

Diagnostic ST elevation in the absence of left ventricular (LV) hypertrophy or left bundle-
branch block (LBBB)
at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in
leads V2V3 and/or of 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.
New or presumably new LBBB..!
ST depression in 2 precordial leads (V1V4) may indicate transmural posterior injury;
multilead ST depression with coexistent ST elevation in lead aVR has been described in
patients with left main or proximal left anterior descending artery occlusion.
hyperacute T-wave changes may be observed in the very early phase of STEMI, before
the development of ST elevation.
Transthoracic echocardiography may provide evidence of focal wall motion abnormalities.
Cardiac troponin is the preferred biomarker for diagnosis of MI.
 the independent predictors of early death from STEMI
include
age,
Killip class,
time to reperfusion,
cardiac arrest,
tachycardia,
hypotension,
anterior infarct location,
prior infarction,
diabetes mellitus,
smoking status,
renal function, and
biomarker findings
 crushing
crushing chest
chest pain 11 22 jam
pain jam hrs
hrs diketahui
diketahui
1/3 patients
1/3 patients with
with MI
MI experience
experience symptoms
symptoms other
other
than chest
than chest pain.
pain.
 CSS Definisi
Kelas I Angina timbul saat aktivitas berat

Kelas II Angina timbul dengan aktivitas sehari-hari

Kelas III Angina timbul dengan aktivitas lebih ringan

dari aktivitas sehari-hari

Kelas IV Angina timbul bahkan saat istirahat

 Rasa sakit / nyeri dada sentral / retrosentral
yang dapat menyebar
Gelisah dan takut
Berkeringat dingin dan lemas
Kulit sianotik dengan akral teraba dingin
Denyut nadi cepat, isi nadi kecil dan lambat
Auskultasi suara jantung melemah,
S3 dan S4
Presentasi Kejadian di
Indonesia
MAYOR MINOR
TIDAK DAPAT DIMODIFIKASI Obesity/kegemukan
Umur Kurang gerak/Sedentary
lifestyle
Riwayat keluarga PJK usia < 55Stress psikologis
Laki-laki Type a personality
Postmenopause (wanita) Gout
Kulit putih Hiperurikemia
DAPAT DIMODIFIKASI Kontrasepsi oral
Hipertensi Gangguan toleransi glukose
HiperKholesterolemia Infeksi/inflammasi
Diabetes mellitus Homosistein
Merokok

Kombinasi faktor resiko menambah dan mungkin bersinergi meningkatkan

resiko PJK
 Plak tidak stabil

Plak srabil

Lawrence GS
Atherogenesis and Atherothrombosis:
A Progressive Process
Plaque Myocardial
Athero- Rupture/
Fatty Fibrous sclerotic Fissure & Infarction
Normal Streak Plaque Plaque Thrombosis

Ischemic
Stroke

Critical
Leg
Angina
Ischemia
Clinically Silent
Transient Ischemic Attack
Claudication/PAD Cardiovascular Death
Increasing Age
TERAPI REPERFUSI TERAPI LAINNYA
Terapi Percutaneus o Anti-platelet : aspirin,
Coronary clopidogrel, prasugrel,
Interventions (PCI) ticagrelor
o Anti-koagulan :
Terapi Fibrinolitik UFH/LMWH, nitrat,
(tissue o penyekat beta, ACEI,
plasminogen ARB
activator, o Statin
streptokinase,
tenekteplase,
o Nitrat : isdn, ntg
reteplase) o Co morbid/risk factor
o komplikasi
 TIME IS MUSCLE

REVASKULARISA
SI
TIMI SCORE
SECONDARY PROGNOSIS QOL
PREVENTION
KLASIFIKASI/
the independent predictors of early death from RISK
BORG
NTpro
STEMI include age, Killip class, time to reperfusion,
Cardiac arrest, tachycardia, hypotension, anterior STRATIFICATION

BNP
infarct location, prior infarction, diabetes mellitus,
smoking status, renal function, and biomarker find
ings.

KOMPLIKASI AKUT KOMPLIKASI KRONIS

KILLIP/FORRESTER/GRAC AHA
E -NYHA
Circulation. 2005;111(15):20132014, and Circulation. 2007;115(15):e411].
Circulation. 2004;110(9):e116e118, e124, e127.
Reperfusion therapy for patients with STEMI.
The bold arrows and boxes are the preferred strategies.

WRITING COMMITTEE MEMBERS* et al. Circulation

2013;127:e362-e425
Copyright American Heart Association
 The recommendation an early revascularisation strategy for shock patients up
to 48 hours post-index MI and up to 18 hours post-shock.
early consideration of IABP placement for patients with cardiogenic shock who
are candidates for an aggressive strategy
Grade Definisi
0 Menunjukkan oklusi total (complete occlusion) pada
arteri yang terkena infark
1 Menunjukkan penetrasi sebagian materi kontras
melewati titik obstruksi tetapi tanpa perfusi vaskular
distal
2 Menunjukkan perfusi pembuluh yang mengalami
infark ke arah distal tetapi dengan aliran yang
melambat dibandingkan aliran arteri normal
3 Menunjukkan perfusi penuh pembuluh yang
mengalami infark dengan aliran normal
 If patients with STEMI have cardiogenic shock, they should be transported to a facility
capable of cardiac catheterization and rapid revascularization (PCI and coronary artery
bypass graft surgery).
Patients with contraindications to fibrinolysis should be immediately transported to
such a facility, or transferred within 30 minutes.
Rescue PCI after failed thrombolysis is still appropriate
as evidenced by shock, severe CHF or pulmonary edema (Killip class III or
greater), or hemodynamically compromising ventricular arrhythmias.
Rescue PCI is reasonable in patients who have less than 50 percent resolution of
ST-segment elevation 90 minutes after initiation of fibrinolytic therapy and a
moderately large area of myocardium at risk.

use intravenous beta blocker therapy in the acute setting to manage hypertension
NSAIDs (nonselective and cyclooxygenase-2 [COX-2] selective agents) increased risk
of mortality, reinfarction, hypertension, heart failure, and myocardial rupture
there is a significant association between arrival at the ED by ambulance and earlier
delivery of reperfusion therapy. Any regional medical system must seek to enable rapid
recognition and timely reperfusion of patients with STEMI.
 DANAMI-2 (Danish Multicenter Randomized Study on Thrombolytic Therapy Versus Acute Coronary
Angioplasty in Acute Myocardial Infarction) showed that a reperfusion strategy involving the
transfer of patients with STEMI from a non PCI-capable hospital to a PCI-capable hospital for
primary PCI was superior to the use of fibrinolysis at the referring hospital,
Shorter system delays were associated with a reduced mortality rate for both fibrinolysis- and
primary PCI treated patients the average first door-to-device time delay was approximately 110
minutes
Fibrinolytic therapy, in the absence of contraindications to its use, should be administered within 30
minutes of first door arrival when this 120-minute time goal cannot be met.

Because patients with STEMI may first present with cardiac arrest, regional systems also should
emphasize early access to care (recognition of the problem and bystander activation of EMS), rapid
dispatch, bystander cardiopulmonary resuscitation (CPR), defibrillation when indicated, advanced
cardiac life support, and an organized approach to postresuscitation care.

The time delay from symptom onset to treatment can be shortened by administration of
prehospital fibrinolytic therapy by a trained EMS unit either with a physician on board or with a
hospital-based physician the CAPTIM (Comparaison de l'Angioplastie Primaire et de la
Thrombolyse) trial within 2 hours of symptom onset showed a significantly lower 5-year mortality
rate for patients treated with prehospital fibrinolysis than for patients managed with primary PCI
(p=0.04)
 Contraindication ?

Streptase : 1,5 unit

diluted in NS/D5 100 cc
give 30-60 mnt.
Reteplase
Alteplase : 0,75 mg/kg
BB in 30 mnt,
0,5mg/kgBB in 6 hr

Bleeding
Allergy
Hypotension
Arrhythmia
 Aritmia Perikarditis
AV Block
Aneurisma ventrikel
Atrial Flutter (AFL)

Atrial Fibrillation (AF)

Tromboembolisme
Takikardia Ventrikel (VT) Regurgitasi mitral akut
Fibrilasi Ventrikel (VF)

Gagal Jantung
Acute Lung Oedem (ALO)
Syok Kardiogenik
Sudden Cardiac Arrest (SCA)
Myocardial Rupture
AVB 1

AVB II
TYPE 1

AVB II
TYPE 2

AVB III/
TOTAL
Class 1 No rales, no 3rd heart sound
Class 2 Rales in <12 lung field or presence of
a 3rd heart sound
Class 3 Rales in >12 lung fieldpulmonary
edema
Class 4 Cardiogenic shockdetermined
clinically
Stage Keterangan
- Distensi dan keterlibatan pembuluh darah kecil di paru akibat peningkatan tekanan di
atrium kiri dapat memperbaiki pertukaran udara di paru dan meningkatkan kemampuan
difusi gas karbon dioksida.
Stage I
- Akan terjadi sesak nafas saat melakukan aktifitas fisik, dan disertai ronki inspirasi akibat
terbukanya saluran pernafasan yang tertutup.

- Edema interstisial diakibatkan peningkatan cairan pada daerah interstisial yg longgar

dengan jaringan perivaskular dari pembuluh darah besar, hal ini akan mengakibatkan
hilangnya gambaran paru yang normal secara radiografik dari petanda vascular paru,
hilangnya demarkasi dari bayangan hilus paru dan penebalan septa interlobular (garis
Kerley B).
Stage II - Akan terjadi kompetisi untuk memperebutkan tempat antara pembuluh darah, saluran
nafas dan peningkatan jumlah cairan di interstisium yang longgar tsb dan akan terjadi
pengisian di lumen saluran nafas yang kecil yang menimbulkan reflex bronkokonstriksi.
- Ketidakseimbangan antara ventilasi dan perfusi hipoksemia

- Proses pertukaran gas sudah menjadi abnormal, dengan hipoksemia yang berat dan
seringkali bahkan menjadi hipokapnea.
- Alveolar yang sudah terisi cairan terjadi akibat saluran nafas yang besar terisi cairan
Stage III
berbusa dan mengandung darah.
- Kapasitas vital dan volume paru semakin berkurang di bawah normal.
 Klasifikasi gagal jantung
ACC/AHA
Stadium A
Memiliki resiko tinggi untuk berkembang
menjadi gagal jantung. Tidak terdapat
gangguan structural atau fungsional jantung,
tidak terdapat tanda atau gejala
Stadium B
Telah terbentuk penyakit struktur jantung
yang berhubungan dengan perkembangan
gagal jantung, tidak terdapat tanda atau
gejala.
Stadium C
Gagal jantung yang simptomatik
berhubungan dengan penyakit structural
jantung yang mendasari
Stadium D
Penyakit jantung structural lanjut serta gejala Tidak dapat melakukan aktifitas
gagal jantung yang sangat bermakna saat
istirahat walaupun sudah mendapat terapi
medis maksimal (refrakter)
Klasifikasi fungsional
NYHA
Kelas I
Tidak terdapat batasan dalam
melakukan aktifitas fisik. Aktifitas
fisik sehari-hari tidak menimbulkan
kelelahan, palpitasi atau sesak
napas.
Kelas II
Terdapat batasan aktifitas ringan.
Tidak terdapat keluhan saat
istirahat, namun aktifitas fisik
sehari-hari menimbulkan
kelelahan, palpitasi atau sesak
nafas.
Kelas III
Terdapat batasan aktifitas
bermakna. Tidak terdapat keluhan
saat istirahat, tetapi aktifitas fisik
ringan menyebabkan kelelahan,
palpitasi atau sesak
Kelas IV
fisik tanpa keluhan. Terdapat
gejala saat istirahat. Keluhan
meningkat saat melakukan
aktifitas
 KRITERIA
FRAMINGHAM

Kriteria Mayor Kriteria Minor

Paroxysmal nocturnal
Edema ekstremitas
dyspnoe (PND)
Distensi vena leher
Batuk malam hari
Ronki paru
Dyspnea on effort
Kardiomegali Hepatomegali
Edema paru akut Efusi pleura
S3 gallop Penurunan
Peninggian JVP kapasitas vital 1/3
Refluks hepatojugular dari normal
 Tanda klinis : hipoperfusi, CHF, edema paru akut, panyakit dasar yang paling mungkin

Edema paru akut Hipovolemia Low output : syok kardiogenik Aritmia

Pemberian :
Furosemid iv 0,5-10 mg/kg
Morfin iv 2-4 mg
Oksigen bila diperlukan
Nitrogliserin SL, kemudian 10-20 mcg/menit bila TDS >100 mmHg
Dopamin 5-15 mcg/kg/menit iv bila TDS 70-100 mmHg dan tanda/
gejala syok (+)
Dobutamin 2-20 mcg/kg/menit iv bila TDS 70-100 mmHg dan tanda/
gejala syok (-)

Periksa tekanan
darah
Diberikan ACE-I golongan
TDS >100 mmHg dan tidak kurang dari kerja pendek,
30 mmHg dibawah TDS sebelumnya misal : Captopril 6,25 mg
Syok Kardiogenik didefinisikan sebagai tekanan
darah sistolik <90 mmHg selama >1 jam dimana:
Tidak responsif dengan pemberian cairan saja
Sekunder terhadap disfungsi jantung
Berkaitan dengan tanda- tanda hipoperfusi atau
indeks kardiak <2,2 L/menit/m2 dan tekanan baji
kapiler paru >18 mmHg.
Langkah 1: Tindakan resusitasi segera

Langkah 2: Menentukan secara dini anatomi koroner

IABP
Langkah 3 : Melakukan revaskularisasi dini

CABG
 Tanda klinis : hipoperfusi, CHF, edema paru akut, panyakit dasar yang paling mungkin

Edema paru akut Hipovolemia Low output : syok kardiogenik Aritmia

Periksa tekanan darah

TDS > 100 mmHg TDS 70-100 mmHg dan TDS 70-100 mmHg dan TDS <70dan
tanda/gejala syok (-) tanda/gejala syok (+) tanda/gejala syok (+)

Nitrogliserin Dobutamin Dopamin Norepinefrin

10-20 mcg/menit IV 2-20 mcg/kg/menit 5-15 mcg/kg/menit 0,5-30 mcg/menit IV
IV IV
MYOCARDIAL
RUPTURE
 For the 6-min walk test (6 MWT) performed
at baseline and 24 weeks, patients received
standardised instructions to walk as far as
possible in 6 min on a 33-m course.
Prior to and immediately on completion of
the 6 MWT, symptoms were assessed by
means of the 10- point Borg scale rating of
perceived exertion (Borg RPE)
 delay in seeking treatment
1) inappropriate reasoning that symptoms will be self-limited or are not serious
2) attribution of symptoms to other preexisting conditions
3) fear of embarrassment should symptoms turn out to be a false alarm
4) reluctance to trouble others unless really sick
5) preconceived stereotypes of who is at risk for a heart attack, an especially common trait among
women
6) lack of knowledge of the importance of rapid action, the benefits of calling EMS or 9-1-1, and the
availability of reperfusion therapies
7) attempted self-treatment with prescription and/or nonprescription medications
THE DISEASE PROGRESS

Remodelling Ventricular Dilation /

Cognitive Dysfunction

Myocardial Congestive
Infarction & Stroke Macro- Heart Failure /
Micro- proteinuria Secondary Stroke
PAD
albuminuria
DE
Nephrotic End-Stage
Atherosclerosis Heart Disease /
Proteinuria
and LVH Endothelial Brain Damage &
Dysfunction Dementia

End-Stage
Risk factors Renal Disease Cardio /
Diabetes Cerebrovascular
Hypertension Death

Adapted from Dzau, Braunwald. Am Heart J 1991;121:12441263