PENGENALAN GAWAT JANTUNG
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Prof. DR dr Zainal Musthafa SpJP, MSi, FS, FIHA
Dep.Jantung RSPAD-GS
FK. UPN “Veteran” Jakarta
PENGENALAN
KEGAWATAN JANTUNG
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GAWAT DARURAT JANTUNG
(GDJ)
TUJUAN UMUM :
1. Menyajikan suatu cara yg aman & terpercaya, penanggulangan GDJ
2. Memberi pengetahuan dasar untuk:
a. Evaluasi Px. GDJ dg Cepat & Tepat
b. Melakukan Resusitasi & Stabilisasi
c. Menentukan apakah kebutuhan Px. melebihi puan fasilitas
d. Mengatur sistem rujukan (Apa, Siapa, Kapan & Bgmn)
e. Menjamin penanganan Px. yg diberikan sudah optimal
1
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TUJUAN KHUSUS :
1. Mampu melakukan primary assesment
Gawat Darurat Jantung pd penderita :
a.l Asystole
Pulseless electrical activity (PEA)
Hipotensi (syok cardiogenik)
Ventrikel fibrilasi (VF)
Ventrikel takhikardia (VT)
Infark miokard akut (IMA)
Edema paru akut (EPA)
Takhikardia, Bradikardia
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2. Melakukan pembebasan airway dan memulai ventilasi
3. Melakukan RJP pada manikin
4. Melakukan intubasi pada manikin
5. Demontrasi penggunaan defibrilator
6. Pemantauan / Evaluasi EKG pada monitor
7. Demontrasi vena seksi
8. Demontrasi perikardiosintesis
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SEJARAH
Safar & Elam (1950) : Pernafasan mulut ke mulut
Kouwenhouven (1960) : Chest compression
Safar : Menggabungkan mm & cc
dikenal dg CPR & ECC
Para ahli sedunia merekomendasi
suatu cara / mekanisme / tehnik al :
Early Access,
Early CPR,
Early Defibrillation,
Early ACLS
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Penatalaksanaan
Acute Myocard Infark (AMI)
Pendahuluan
Difinisi
Penanganan AMI di Gadar
Penanganan 24 jam pertama
Penanganan ssd 24 jam
Persiapan pulang
Penatalaksanaan jangka panjang
Algorithma AMI
Zainal
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Zainal
DEFINISI
Ischemic yg berlangsung
lebih 20 menit
dan terjadi nekrosis miokard.
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Am J Cardiol 1997; 80: 17E-20E
• PATHOPHYSIOLOGY
OF ACS / CAD
• Common pathogenic
substrate : atherosclerotic
lesions THROMBUS
• STEMI :
• Fibrin and erythrocyte rich
(RED)
• Complete occlusion
• NSTEMI
• Platelet rich (WHITE)
• Subtotal / intermittent
occlusion
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Macam kegawatan jantung :
a. Infark miokard akut (IMA)
b. Ventrikel fibrilasi (VF)
c. Hipotensi (syok cardiogenik)
d. Asystole
e. Ventrikel takhikardia (VT)
f. Edema paru akut (EPA)
g. Pulseless electrical activity (PEA)
h. Takhikardia, Bradikardia
2
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Sebab Henti Jantung ?
1. Penyakit : Coroner, Arythmia
2. Kekurangan oksigen dari proses respirasi
3. Obat : digitalis, quinidin, adrenalin, antidepresan
4. Kecelakaan : listrik, tenggelam
5. Vagal reflek
6. Penekanan,penarikan/peregangan anus, bolamata
7. Anastesi
8. Tindakan Diagnostik, Terapi
9. Syok ( hipo, neuro, sepsis, anaf, cardio) dll
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Tehnik RJP ?
Dilakukan 3 tahap : (A.B.C – D.E.F----G.H.I )
1. Pertolongn dasar (Basic Life Support / BLS)
A. Airway kontrol
B. Breathing Support
C. Circulation Support
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2. Pertolongn Lanjut ( Advanced life Support / ALS)
D. Drug & Fluid
E. Elektrokardiography
F. Fibrilation treadment
3. Pertolongn Jangka Panjang (PLS)
G. Gauging : Monitor / evaluasi RJP,
penentuan penyebab dasar, tindakan lanjut / stop
H. Human mentation, penentuan kerusakan otak
I. intensive Care, perawatan jangka lama.
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CVD is a leading cause of death
Source: CDC/NCHS and the American Heart Association
World Health Organization 2002.
0
100
200
300
400
500
600
Dea
ths
(th
ou
san
ds)
Men
Women
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Penyakit Cardiovasculer
• Penyakit yang berhubungan dengan kesehatan
JANTUNG dan PEMBULUH DARAH
– Penyakit Jantung Koroner (PJK)
– Stroke
– Peripheral Vascular Disease (PVD)
• Angka kejadian tinggi
• Hiperkolesterolemia (Kolesterol tinggi) adalah penyebab utama (40%)1,2
• 80% pasien meninggal mendadak & 50%nya tanpa gejala sebelumnya3
1. Betteridge DJ; Lipids: Current Perspectives. Special Patients Groups. Martin Dunitz Ltd. 1996:2
2. Nagard M, Libby P, Falk E, et al. From Vulnerable plaque to Vulnerable A Call for New Definities and Risk Assesment Strategies: Part 1. Circulation. 2003; 106: 1654-1672
3. Myerburg RJ, Interian A, Mitrani RM, et al. Frequency of Sudden Cardiac Death and Profiles of Risk. Am J Cardiol. 1997; 80(68): 10F-19F
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Why should Vascular be treated?
• ischaemia
• myocardial infarction
• cardiac hypertrophy
• congestive heart failure
• stroke
• TIA (transient ischaemic attack)
• PRIND (prolonged, reversible,
ischaemic, neurological deficit)
• nephrosclerosis
• atrophy of nephrons
• renal failure
• retinopathy
• lesions
• swelling of optic disc
• blindness
Vaskuler
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PEMBULUH DARAH
ARTERI
• Jantung seluruh tubuh
• Dinding tebal & berototsupaya tahan terhadaptekanan tinggi
VENA
• Seluruh tubuh jantung
• Dinding tipis & tidakberlapis otot
Kolesterol yang tidak terkontrol dapat menyebabkan sumbatan pada pembuluh darah
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Risk Factors for
Cardiovascular Disease
• Modifiable– Smoking– Dyslipidaemia
• raised LDL cholesterol• low HDL cholesterol• raised triglycerides
– Raised blood pressure– Diabetes mellitus– Obesity– Dietary factors– Thrombogenic factors– Lack of exercise– Excess alcohol consumption
• Non-modifiable– Personal history of
CHD– Family history of
CHD– Age – Gender
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Classic Manifestations of Atherothrombosis
Unstable angina
(UA)
Non-ST elevated
MIStroke/TIA
Peripheral Arterial
Disease (PAD)
Common underlying
atherothrombosis
Atherothrombotic event
(MI, stroke, vascular death)
Plaque rupture Platelet activation
and aggregation
Thrombus formation
Acute Coronary Syndrome (ACS)
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Atherogenesis and Atherothrombosis: A Progressive Process
NormalFatty
StreakFibrousPlaque
Athero-scleroticPlaque
PlaqueRupture/Fissure &
Thrombosis
Myocardial
Infarction
Ischemic
Stroke
Critical
Leg
IschemiaClinically Silent
Cardiovascular Death
Increasing Age
Angina
Transient Ischemic Attack
Claudication/PAD
3
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ACSCoronary
Thrombosis
Myocardial
Ischemia
PJK
Atherosclerosis
Risk Factors
( Dyslipidemia, HT, DM, Insulin
Resistance, Platelets, Fibrinogen,
etc)Adapted from
Dzau et al. Am Heart J. 1991;121:1244-1263
Arrhythmia and
Loss of Muscle
Remodeling
Ventricular
Dilatation
Congestive
Heart Failure
End-stage Heart
Disease
Primary prevention
Secondary prevention Stroke
The Cardiovascular Continuum of Events
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Aggregation
of platelets into a
thrombus
Platelets
Endothelial cells
Platelets adhering to subendothelial space
Platelet thrombus
Normal platelets
in flowing blood
Platelets adhering to
damaged endothelium
and undergoing activation
Platelet Adhesion and Activation
Subendothelial space
Adapted from: Ferguson JJ. The Physiology of Normal Platelet Function. In: Ferguson JJ,
Chronos N, Harrington RA (Eds). Antiplatelet Therapy in Clinical Practice. London: Martin
Dunitz; 2000: pp.15–35.
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Adapted from: Kuwahara M et al. Arterioscler Thromb Vasc Biol 2002; 22: 329–34.
Platelet Aggregation
FIRM, BUT REVERSIBLEADHESION
IRREVERSIBLEADHESION
Scanning electron micrograph
of discoid, dormant platelets
Activated, aggregating platelets
illustrating fibrin strands
Flowingdisc-shaped
platelet
Rollingball-shaped
platelet
Hemisphere-shapedplatelet
Spreadingplatelet
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Plaque Disruption Leading to
Atherothrombosis Formation
Adapted from: Falk E et al. Circulation 1995; 92: 657–71.
Macrophage Tissue factor
Fibrin
Aggregated platelets
BLOOD
FLOW
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VIDEO
ATHEROTROMBOSIS
atheroslerosis terbaru.flv
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Lokasi nyeri
Rasa nyeri
Radiasi
Lama nyeri
Progresifitas
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Diagnosis Banding
•Pleuritis
•Emboli paru, pneumonia
•Prolaps katup mitral
•Sakit muskuloskeletal
•Gangguan gastrointestinal
•Deseksi Aorta
•Herpes, dll
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Penyebaran nyeri
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Gradasi beratnya angina pectoris
( Canadian Cardiovascular Sosciety )
1. Aktifitas sehari-hari tidak menimbulkan angina,
angina baru timbul pada aktifitas berat, tergesa-gesa,
2. Aktifitas sehari-hari terganggu sedikit.
Angina timbul waktu berjalan atau naik tangga dengan
cepat, berjalan lebih dari 2 blok ( 400 m )
3. Aktifitas sehari-hari sangat terganggu.
4. Tidak mampu melakukan aktifitas apapun tanpa angina
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Kriteria Diagnosis
1. Nyeri dada khas infark atau
ekuivalen lebih dari 20 menit,
tidak hilang dengan pemberian nitrat
2. Gambaran EKG dan evolusinya yang khas IMA
a) Pada STEMI ditandai oleh elevasi 2 mm
di precordial lead atau 1 mm di extremity lead
atau new BBB,
semua perubahan terjadi minimal pada
dua lead yang berhubungan
b) Pada non STEMI EKG bisa normal atau
berubah tapi tidak memenuhi kriteria STEMI
3. Gambaran laboratorium : peningkatan enzim
( CK MB, Troponin T, dll )
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Kelainan EKG pada SKA
– ST depresi, tanpa T inverted
– ST elevasi saat Nyeri dada
– Tidak ada Q wave
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CAD & PTCA
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1. Umum : Pengendalian faktor-faktor risiko
Menghindari faktor-faktor pencetus
2. Khusus : Pemberian obat-obat yang dititrasi
sesuai dengan kebutuhan
Antiplatelet, Antikoagolan,
Antithrombitik/thrombolitik
Coroner delator
Penyekat beta, Pencahar, Penenang
CCB, Hipolipid, ACE-inh / ARB,
Antasida, dll
Terapi di rs (Gadar, ICU, Ruangan)
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Penanganan di Gadar
• PD : Angina pectoris
• EKG : Normal (ischemi, injury, necrosis)
• Lab : Enzym CPK/CKMB (troponin)
• Tx : Oksigen 3-6 L / menit
IV. line (NaCL 0,9% )
Koroner delator (Nitrat)
Antiplatelet (Aspirin)
Trombolitik (Streptase)
Analgesik (Morphin)
dll
Zainal
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Penanganan 24 jam pertama
• Istirahat total (ICU/ICCU)
• Monitor EKG
• IV. line
• Oksigen
• Serial enzym CPK/CKMB tiap 6 jam
• Thorax foto
• Lab darah u/ faktor risiko
• Tx : Konservative (obat-obatan)
Pertimbangkan (PTCA, CABG )
Zainal
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Penanganan sesudah 24 jam
• Tx : Heparinisasi, Aspirin, LMH
Nitrat
Ca. antagonis
Beta bloker
Antagonis ACE
Hipolipid
ACE-inh, ARB
• Mobilisasi bertahap
• 2 X 24 jam keadaan stabil dapat pindah
ke ruangan perawatan
Zainal
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Penatalaksanaan jangka panjang
* Tx: Aspirin
Nitrat
Ca. antagonis
Beta bloker
Antagonis ACE, ARB
Hipolipid
ACE-Inh, ARB
* Hindari faktor resiko
(Diet, olah-raga dll)
* Rehabilitasi.
Zainal
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Penyulit yang mungkin timbul
Aritmia
Gagal Jantung
Syok Cardiogenik
Infark miokard akut
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Penanganan komplikasi
1. Aritmia
Gx.
PD.
EKG.
Tx. Sesuaikan type aritmianya al :
(Bradicardia, Blok, VT, VF dll)
Zainal
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Zainal
2. Dekompensasi
Gx.
PD.
Tx * Kurangi load cairan
* Inotropik positif
* Vasodelotor
* PTCA / CABG
(sesauaikan patofisiologinya)
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3. Syok kardiogenik
Gx.
PD.
Tx * Loading cairan cukup !
* Inotropik positif
* Vasokontraksi perifer
* IABP
* Kateterisasi / PTCA / CABG
(sesauaikan patofisiologinya)
Zainal
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4. Pertimbangkan Pacemaker
apabila ada :
a. Sinus bradikardia, tidak respon thd obat .
b. 20 AV block tipe Mobitz II.
c. 30 AV block.
d. Bilateral BBB.
e. BBB yang baru.
f. BBB dg 10 AV block.
Zainal
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5. Pertimbangkan CABG
apabila :
a. PTCA gagal
b. Persistent iskhemia
c. Cardiogenik shock
d. Gangguan mekanik (VSD)
Zainal
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Persiapan ambulatoir
(pulang)
• Penyuluhan ttg PJK thd keluarga
• Treadmill test
Zainal
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TERIMA KASIH
Zainal
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Zainal
Kasus 1
Infark myocard acut
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Zainal
Man , age 65
Clinical AMI
onset 7 hours
Coronary risk factors
Hypertension, dyslipidemia
BP 220/120
Persistent ST elevation
Elevated CKMB 259
PRIMARY ANGIOPLASTY
PRE ANGIOPLASTY
BALLOON INFLATION
POST ANGIOPLASTY
CASE
ILLUSTRATION
Acute STEMI,
Hypertension grade III
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Zainal
Kasus 2
Acut coronary syndrome
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Zainal
Man, age 49
Progressive angina for 3 days
2 coronary risk factors :
DM & hypertension
Persistent ST depression
1mm, no elevated CKMB
ACS,UAP,TIMI risk score 1
UFH, Aspirin, Nitrate,
Betabloker
Coronary angiography &
angioplasty on day 7
PRE ANGIOPLASTY
BALLOON INFLATION
POST ANGIOPLASTY