Cabg Cad Rspad PDF

Update in Coronary a.
Disease
(CAD)
OVERVIEW
Skema TAUFIQ
jantung : Collection
pembuluh koroner & bilik jant
www.escardio.org/guidelines
Dr. TAUFIQ
RSPAD AW SpBTKV
1.CHEST PAIN
2.ANGINA PECTORIS
3.CAD (Coronary Artery Disease)
4.Stable Angina
5.Acut Coroner Syndrome (ACS)
6.UAP (Unstable Angina Pectoris)
7.AMI (Acut Myocard Infarc)
8.NSTEMI (Non ST Elevasi Myocard Infarc)
9.STEMI (ST Elevasi Myocard Infarc)
10.Cardiac Arrest , Suddent Death
Dr AW TAUFIQ, SpBTKV RSPAD
ACLS
modified by TAW
Asses responsiveness
Respon (+) Respon (-)
1. 0bservasi C all: - activated EMS (Emergency Respon System)

2. Tx sesuai indikasi - for defib
(di bawah ini): L ok
L isten Breath (-) 2 kali hembusan
F eel
(+)
PULSE
Positif Negatif
CPR
O2 (termasuk intubasi) 1 seri/1mnt=100x/mnt
I v line pola 15: 2 (unprotec airway)
-Chest pain M onitor (12 lead) 5: 1 (protected airway)
Klinis spt ASMA, ttp: -Elevasi ST
-Retraksi (-) -dg/tanpa BBB: Monitor
-Ronkhi basah s/d apec ARITMIA
-QRS > 12 VT
-Pucat, megap2,ala nasi lebar -Right=rsR di V1-V3 Non VT/VF VT pulse(-) Pulse (+)
-EKG variatif:-sinus taki -left = RR di V5-V6 Atau VF
-T bisa > 140/90 precordial thump
-PCO2 >> PO2 BRADIKARDI DC : 200-300-360
AMI PEA
N<50) (N=85 90) (<60) cardioversi
ASISTOLE
Serius:
-simptom:-nafas pendek TAKIKARDI (>100) Sirkulasi Persisten
- kesadaran turun Kembali VT pulseless
- chest pain 1. Serius spontan Atau VF
ACUTE LUNG OEDEM (ALO) STABIL
-sign:-T drop,pre/syock, simptom,sign
2. HR >150 Observasi
-congestive pulmo
-AMI,CHF AF PSVT VT
I0 or II0 tipe-1
www.escardio.org/guidelines A Fluter
TDK -II0type2
A-T-D-E-I YA TCP, iv pacing Dr AW TAUFIQ, SpBTKV RSPAD
-III0
KONSIL KEDOKTERAN
INDONESIA
STANDAR KOMPETENSI DOKTER
KONSIL KEDOKTERAN INDONESIA

Indonesian Medical Council
Jakarta 2006
TINGKAT KEMAMPUAN:
KASUS- A 1 2 3A 3B 4
KASUS- B 1 2 3A 3B 4
KASUS- C 1 2 3A 3B 4
KASUS- D 1 2 3A 3B 4
KASUS- E 1 2 3A 3B 4
Overview Ax,Px,Dx Ax,Px,Dx Ax,Px,Dx MANDIRI
Rujuk & Terapi-I Terapi-I
follow Rujuk- Rujuk- &
up elective CITO
TUNTAS
30% = 17 jt
WHO
USA INDONESIA
1,000 CILEGON
population 330.000.000 237.600.000
392.341
CAD (30 persentil) 9.900.000 7.128.000
11.770
IMA (6 persentil) PERSENTILE
1.980.000 CAD
1.425.600
2.354
mortality (30%) 594.000 427.680 785
pre hospital (15/30%) 3 118.8001 85.536 392
2
readmission 1 y (35/70%) 633.600 456.192 CAD 589
6
Cath/PCI 1.210.110 871.279 INFARK 1.177
30
CABG 356.730 256.846 MORTAL 392
Cath/PCI
CABG
www.escardio.org/guidelines Dr AW TAUFIQ, SpBTKV RSPAD

JAMA.2011;305(17):1769-1776. doi:10.1001/jama.2011.55
392,341 CILEGON
PENDUDUK: 392.341
CAD: 11.770
INSIDENSI CAD
INFARK: 2.354
Per Hari
MORTAL: 785
1 Pre RS: 392

3
2 Re admission: 589
CAD
6 PCI: 1.177
32 INFARK
MORTAL CABG: 392
Cath/PCI
CABG
CAD 1-VD
2-VD
3-VD
LM
Pembuntuan / penyumbatan
Pembuntuan / penyumbatan
Skema TAUFIQ Collection
jantung : pembuluh koroner & bilik jant
www.escardio.org/guidelines RSPAD
PATOFISIOLOGI
ATHEROSKLEROTIK
FAKTOR RESIKO:
Hiperlipidemia,
DM,
Hipertensi
Smoking ENDOTEL INJURY,
Toxins ggn:
Hemodinamic factor plaque erosion &
Immune reaction rupture
Microba,Viruses
1
3 6
2
4
5
PATOFISIOLOGI
Terbentuk plaqueflow dynamic & endothelial shear stress
plaque erosion & ruptureagregasi,cascade coagulation
thrombus Etc, endotel vasoconstriction occlusionACS Dr AW TAUFIQ, SpBTKV RSPAD
1
3 6
2
4
5
FAKTOR Hiperlipidemia, PATOFISIOLOGI
Terbentuk plaqueflow dynamic & endothelial shear stress Penyebab non plaque ACS:(10%)
RESIKO: DM,Hipertensi
Smoking plaque erosion & ruptureagregasi,cascade coagulation 1. Spasme a.coroner:
thrombus Etc, endotel vasoconstriction occlusionACS -Angina prinzmetal
Toxins
Culprit lesion: stenosis>70%, proximal, atherom rich macrofag,lipid -Cocain
Hemodinamic factor
near branch -Amfetamin
Immune reaction
2. Emboli: mis dr
Microba,Viruses Endotel Produksi:
Heparin sulfat, -valvular heart infeksi
Eicosanoid(prostasiclin) 3. Oklusi a.coroner:
thrombin activation, -Coroner vasculitis,Aodissect
ENDOTEL INJURY, ggn: platelet adesion -kawasaki,takayasu,marfan
plaque erosion&rupture Nitrous Oxide 4. Chest trauma
EDRF(epitel derivat relaxing factor) 1 5. Mistmath suplay-demand lain:
ADESI : Platelet, monosit
Plasminogen misal , hipertiroid,
-platelet (1)
Imbalance pro injury akut anemi ec GI bleeding
-monocytmacrofag 6
6. Hipertrofi ventrikel: LVOT
oxidized LDL, VLDL
subaortic Hipertrofi/IHSS, AS
lipid uptake by macrofag et all
7. Kongenital coroner anomali
Foam cells (2) of atheroma plaque
degeneratingextracellular lipid
imbalance influx-eflux (LDL vs HDL)
3
accumulation of cholesterol 2
in the plaque (3) Pro injuri:
-vasoactive(konstriksi):
Membrana elastica interna robek (4) endotelin,angiotensinII, 4
Cytokin dan serotonin, PDGF
Growth factor release (PDGF): -procoagulan:
migration & proliferation von wilebrand,PAI-1
smooth muscle cell(SMC)(5) -cytokine et all menarik monosit
-vasculer cell adesi molekul-1 5
extracellular matrix (6) :
-intercell adesi molekul-1
collagens, proteoglycans
(pd kondisi normal,isi:elastin,kolagen)
a.LDL LDL teroksidasi b.Oksigen free radical (LDL ter-oks & O2 free radical: inhibisi enzim NO-syntase)
-inhibisi:- platelet activationtromboxan A2 block
Oxidized LDL Inhibisi -platelet adesi
in Foam cell: -platelet agregasi
-Cytotoxic
-Pro Coagulant Nitric oxide syntase sulit terbentuk trombus
-Chemotaxtic: -vasodilatasi, via: blok platelet activation + thiolated.
macrofag, L - arginine (ctt: platelet activationrelease vasokonstrictor agen:
Nitric oxide
netrofil Tromboxan A2,dll)
cytocin Metaloproteinase (lisis kolagen cap) Dr AW TAUFIQ, SpBTKV RSPAD
Locus
minoris
Resistance,:
Junction:
cap endotel
Viscosity and Poiseuilles Law

P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4
P = potensial energi (dyne/cm2)
V = mean flow velocity (cm/detik) = Q/phi r2
L = jarak (cm)
n = koefisien viskositas (poise =dyne.detik/cm2)
Q = flow (cm3/detik)
r = jari jari
(energy loss P turun 4x tiap r turun)
Culprit lesion= stenosis>70%,proximal,near branch,
atherom: rich macrofag&lipid
www.escardio.org/guidelines stenosis=50%:angina effort
stenosis=90% angina at rest Dr AW TAUFIQ, SpBTKV RSPAD
Jean Louis Marie Poiseuille
Viscosity and Poiseuilles Law
P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4
P = potensial energi (dyne/cm2)
V = mean flow velocity (cm/detik) = Q/phi r2
L = jarak (cm)
n = koefisien viskositas (poise =dyne.detik/cm2)
Q = flow (cm3/detik)
r = jari jari
(energy loss P turun 4x tiap r turun)
Culprit lesion= stenosis>70%,proximal,near branch,

stenosis=50%:angina effort
stenosis=90% angina at rest
Stable UnStable AMI
AP AP
(UAP)
NSTEMI STEMI
(energy loss P turun 4x tiap r turun) CAD
P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4
Culprit lesion= stenosis>70%,proximal,near branch, ACS
stenosis=50%:angina effort INFARK
stenosis=90% angina at rest
Atherosclerosis Timeline
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture
Endothelial dysfunction
From first decade From third decade From fourth decade

Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen haematoma
Adapted from Stary HC et al. Circulation 1999;92:1355-1374.

SPEKTRUM: ChestPain-Stable Angina-Unstable Angina (UAP)-Infark
A.Chronic Stable Angina (demand ischemi)
plaque aterosklerosis masih stabil.
lumen coroner menyempit (50% stenosis?), masih cukup suplay,
ttp saat demand J(exercise, stress, eat)transitory imbalance suplay demand
iskemisymptom (+).
saat demand Kimbalance suplay demand (-)symptom (-)
[tdk ada perub dlm frek dan beratnya serangan]/durasi 5-15mnt.(Umumnya 1-5)
menghentikan aktivitas dan atau NTG akan menghilangkan symtom.
B.Plaque membesar,tdk stabil/rapuh/dinding plaque robek,ruptur
thrombogenic surface agregasi platelet/trombi .
Coroner vasospasme dan atau agregasi platelet/trombi: akut
coroner flow turun atau sama sekali tak adaacut reduction O2 suplay
suplay ischemibiasanya bersamaan demandk
acut coroner sindrome(ACS):
sumbatan total>6jam=irreversible necrose
flow dynamic & endothelial shear stress
Vulnerable plaque:
-large lipid pool
-thin-fibrous cap Plaque disruption
-numerous inflamatory cell
-agregasi
Activated Dissolution -cascade coagulasi
Inflamatory cell Fibrous cap -vasokonstriksi
Release: metalloproteinase
(collagenase) THROMBOSIS
ACS
Resistensi coroner,ditentukan oleh:
1.Epicard coroner vessel=conductive vessel=5%
2.Small coroner/arteriol=resisten vessel=95% case
Plaque disruption
Sub endotel exposure:

Vessel wall collagen
Local agregates:
Thromboxan, ADP
Platelet agregation
thrombin Release substance:

www.escardio.org/guidelines Promote vasoconstriction
P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4
Atherosclerosis
CAD
Angina pectoris
ACS
Unstable angina Myocardial infarction
NSTEMI STEMI
CORONARY ARTERY DISEASE (CAD):
Key word: 1. chest pain
2. angina, angina pectoris,
ankhone pectus =strangling chest
CAD: Stable angina & ACS
A. Stable Angina .
B. Acute Coronar syndrome (ACS

:
a spectrum continuum representing
on going myocardial ischemia or injury
1. Unstable Angina Pectoris (UAP)

2. Miokard Infark: - a. Non ST Elevasi Miokard Infark (NSTEMI)
- b. ST Elevasi Miokard Infark (STEMI)
A. Stable Angina . INJURY:

Sel miokard (++)
(+)
B. Acute Coronar syndrome (ACS):

a spectrum continuum representing K+
on going myocardial ischemia or injury Na-K-

ATP
Na+

2. Miokard Infark: -a. Non ST Elevasi Miokard Infark (NSTEMI)
-b. ST Elevasi Miokard Infark (STEMI)
A. Stable Angina . INJURY:

Sel miokard (++)
(+)

a spectrum continuum representing K+
on going myocardial ischemia or injury Na-K-

ATP
Na+

Imbalance suplay demand myocard ischemia an aerob

tjd gangguan:
1. ggn metabolik,
2.TAUFIQ
Skema ggn electrical,
jantung : Collection
pembuluh koroner & bilik jant
www.escardio.org/guidelines 3. ggn RSPAD
mekanik
SYMPTOMS & SIGNS?
( GEJALA-GEJALA & TANDA-TANDA .. ? )
SymptomS & SignS:
(25% silent)(intense &unremitting for30-60)
-chest pain:
-dispneu,whezing
-palpitasi, takikardi, sinkope
-dizziness, weakness, diaphoresis,anxiety
-nausea,abdomen pain-vomitus
-cough
-hiccup
-simptom yg berhub FR
Onset sering pd pagi / menjelang pagi / dini hari

angina decubitus
-asimptomatik
chest pain: P-QRST=Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)
To Talamus
Skin
www.escardio.org/guidelines VISCERAL
Dr AW TAUFIQ, SpBTKV RSPAD (Heart)
Klinis CAD: broad spectrum:
-Asymptomatic state (subclinical phase)
-Stable angina pectoris
-Unstable angina (ie/yaitu: ACS)
-Acute MI
-Chronic ischemic cardiomyopathy
-Congestive heart failure
-Sudden cardiac arrest
P-QRS
Symptom & Sign:(25% silent)(intense &unremitting for30-60)
-chest pain: P-QRST=Pain-Quality-Radiation-Severity-Timing
radiate: jaw,arm (trtm kiri),neck,back,epigastrium
(EXCLUDE: Nyeri up mandible,belowepigast,<1mnt (bbrp dt)
-dispneu(buktikhas adanya poor ventricular compliance),whezing
-palpitasi, takikardi, sinkope -cough
-dizziness, weakness, diaphoresis,anxiety -asimptomatik
-nausea,abdomen pain-vomitus (trtm infark inferior & posterior)
-simptom yg berhub FR hiccup: iritasi frenic, diafragma
Onset sering pd pagi krn: naiknya katekolamin induce-platelet

dan naiknya plasminogen activator inhibitor-1 (PAI-1)
(katekolamin juga naik pd: anxiety, pain),
angina decubitus:tidur malamvenous return naik
demand meningkatangina
STRATIFIKASI?
PROGNOSA ?
Canadian Cardiovascular Society Grading System for effort related angina,
Functional Class Canadian Society (FCCS I-IV)
Grade I - Angina with strenuous, rapid, or prolonged exertion
(Ordinary physical activity such as climbing stairs
does not provoke angina.)
Grade II -Slight limitation of ordinary activity (Angina
occurs with postprandial, uphill, or rapid walking;
when walking more than 2 blocks of level ground
or climbing more than 1 flight of stairs; during
emotional stress; or in the early hours after
awakening.) (1 block = 100-250 m)
Grade III -Marked limitation of ordinary activity (Angina
occurs with walking 1-2 blocks or climbing a flight
of stairs at a normal pace.)
Grade IV-Inability to carry on any physical activity without
discomfort (Rest pain occurs.)
Ex.: Dx, UAP FCCS II
Exm. Statifikasi resiko:
KILLIP CLASSIFICATION: (TIMI, Killip,GRACE)
Class Description
1 Absence of rales over the lung fields and absence of S3.
2 Rales over 50% or less of the lung fields or the presence of an S3.
3 Rales over more than 50% of the lung fields.
Cardiogenic shock. Hypotension (a systolic blood pressure of less than 90 mmHg for at least 30 minutes or the need for
supportive measures to maintain a systolic blood pressure of greater than or equal to 90 mmHg), end-organ hypoperfusion
(cool extremities or a urine output of less than 30 ml/h, and a heart rate of greater than or equal to
4
60 beats per minute). The hemodynamic criteria are a cardiac index of no more than 2.2 l/min per
square meter of body-surface area and a pulmonary-capillary wedge pressure of at least 15 mmHg.
Class Description
1 No heart failure. No clinical signs of cardiac decompensation

2 Heart failure. Diagnostic criteria include rales, S3 gallop and venous hypertension.
3 Severe heart failure. Frank pulmonary edema.
Cardiogenic shock. Signs include hypotension (systolic pressure < 90 mm Hg) and evidence of peripheral
4 vasoconstriction such as oliguria, cyanosis and diaphoresis. Heart failure, often with pulmonary edema, has also been
present in the majority of these patients.
KILLIP > 2 = POOR PROGNOSIS

From ACC Key Data Elements and Definitions for Measuring the Clinical Management and Outcomes of Patients With Acute Coronary Syndromes. JACC Vol. 38, No. 7, 2001.
From T. Killip III and J.T. Kimball, Treatment of myocardial infarction in a coronary care unit: A two year experience with 250 patients, Am J Cardiol 20 (4) (1967), pp. 457464.
LABORATORIUM?
A. Stable Angina .

a spectrum continuum representing
on going myocardial ischemia or injury

UAP atau NSTEMI atau kah STEMI ?

CK
CK-MB
TROP-T
TROP-I
Definisi infark miokard:
Irreversible necrosis of
heart muscle
secondary to prolong ischemia
Cut of point: serial per 6-8j ULN: Upper Limit of Normal
Trop-I : >4 (0,4 ngr/ml)
or >10%: CV, or percentile99
T: >1 (0,1 ng/ml)
CV= coeficient of variation=
= % variation in assay result
CKMB:>52 , atau
CKMB >10% CK
Troponin I & T: marker lain:- myoglobin, CRP, IL-6,serum Amiloid-A

naik dlm 312 j dr onset pain, peak 24-48 j, N 5-14 hari. - LDH (onset dlm 24 jam, peak 3-6 hr, durasi 8-12 hr)
(tjd perub kadar naik > 0,2 ng/ml setelah 2 jam). Trop.T>0,03 - NT-pro BNP (naik pd kenaikan LVEDP/wall stress)
CK-MB(creatine kinase-miocardband)):sensitif hh,spesifiki (N-Terminal pro Brain Natriuretic Peptide).
- kadar enzim naik dlm 3 s/d 12 j onset pain (umumnya 6-9 j) Low level bila < 80 pgr/mL
- peak dlm 24 j, baseline 48 72 j kmd.
- (tjd perub kadar naik >1,5 ng/ml)
- Normal: CKMB = 3 6 % dari total CK
-Non ST Elevation Miocard Infarc (NSTEMI):
ST depress, T change (+/-)
-ST Elevasi Miocard Infarc (STEMI):- Q wave dan Non Q wave
hati-hati: NSTEMI pun (meski kecil insidensi):dpt tjd Q wave Dr AW TAUFIQ, SpBTKV RSPAD
E K G?
ECG: Normal-Ischemia-Injury-Infarct Recognition
Well Perfused Myocardium Epicardial Coronary Artery
Lateral Wall of LV
Septum
Inferior Wall of LV
Positive Electrode
VAT
QRS
interval
INJURY
INJURY:
(++)
Prolonged ischemia
Sel miokard
(+)
Represented by ST elevation
K+
Na-K-
ATP
Na+
referred to as an injury pattern
Transmural injury ST elevasi
Injury
Usually results in infarct
may or may not develop
Thrombus
Q wave
ISCHEMIA Subendocard transmural
INJURY
Ischemia
ECG has important rule in ACS
Transmural infarction Subendocardial infarction
VAT Kecepatan rekaman : 25 mm/dt 1 mm=1/25 dt = 0.04 dt
Kekuatan voltase : 10 mm = 1 mV
5 mm
0,2 dt - 90
0,1 mV - 30
PR
segment ST
segment
0
J
point
ST
+ 120
PR
interval QRS interval
interval
QT
interval
N ST depressST elevas
V1
Pola Strain:
ST depress
T inverted
Dr AW TAUFIQ, SpBTKV RSPAD Sequence of changes seen during evolution of myocardial
6 infarction V
TREATMENT?
TREATMENT:
10 Menit Pertama
MONA
10 Menit Kedua
10 Menit Ketiga
Sudah Suspect kuat: AMI
TREATMENT: chest pain: P-QRST
10 menit Pertama Pain-Quality-Radiation-Severity-Timing
Nilai segera (dlm < 10 mnt I): Terapi Umum segera (MONA):
-vital sign, sat., iv line, EKG 12 lead -Oksigen kanul 4 ltr/mnt (sat>90%)
-perdalam anamnesis & pem.fisik -Aspirin 160 325 mg PO
fokus ke indikasi-KI trombolitik: -NTG SL/spray(dptdiulang/5 mnt,3x
-lab:troponin, CK-CKMB, elek,CBC -Morfin iv10mg, (4-8mg/5-15 mnt)
koag (door to lab result < 30 mnt) (bila nyeri tak membaik dg NTG3x)
-Ro thorax (<30 mnt, sdh dapat) maintenance: 20 ugr/kg/jam
KI thrombolitik:Mutlak: KI relatif thrombolitik:
-post stroke hemoragi atau -usia > 80 th
unknown,onset kapanpun -hipertensi tak terkontrol:
-poststroke infark dlm6bln EKG LVH, T>180/110 meski sdh di
-post ops:berat;intracranial th/ nitrat SL; sudah aspirin kunyah &
morfin 5 mg iv(1/2 Amp)utk nyerinya.
serius head trauma<3mgg
-sedang th/ antikoagulan dg INR > 1,5
-tumor intra cranial -syock kardiogenik
-dissecsi aorta -pericarditis -kehamilan
-kelainan hemostasi -th/ laser retina
-GI bleeding dlm 1 bln
Hasil EKG 12 lead, sadapan Pertama
10 Menit Pertama
TREATMENT: Hasil EKG 12 lead, sadapan Pertama 10 menit II
Keputusan: primerPCI
10 menit Kedua thrombolitik,
atau lainnya
Target: door to needle/drug = 30 mnt
door to balon= 90 mnt. >120mnt: + =4:0
Elevasi ST dan atau LBBB baru -ST depress(0.5mm), -EKG tak khas
T inverted suspect iskemi -resiko sedang/rendah:
-Resiko tinggi UAP/NSTEMI UAP/STEMI
Mulai th/:
-NTG iv(KI:S<90,bradi/taki,RV AMI) -aspirin 160-325 mg qd (clopidogrel bila SE)
-Heparin iv -bradiatropin -glikoprot. IIb/IIIa reseptor inhibitor
-ACE inhibitor,ARB -heparin (utk UAP,NSTEMI: pakai LMWH) Memenuhi kriteria
b blocker iv -NTG iv YA
UAP baru
-HMG CoA reductase inhibitor -b blocker(bila nyeri berlanjut & atau
(terapi statin) Tx Ca chanel blok, bila KI bblocker) Troponin positif
> 12 jam ?? Tidak

Onset serangan Tentukan status klinis
sd sekarang
Klinis tdk stabil stabil
< 12 jam
-Observasi di EMG+monitor
-enzim serial (8-12 jam kmd)
-monitor EKG/ST
www.escardio.org/guidelines -2DE/radionuklid
Memenuhi kriteria UAP baru
atau Troponin positif
> 12 jam ??
Onset serangan Tentukan status klinis
sd sekarang Tidak
Klinis tdk stabil stabil
< 12 jam -Observasi di EMG+monitor
Hipotensi, syock kardiogenik: -enzim serial (8-12 jam kmd)
-monitor EKG/ST
echo: disfunction:
-2DE/radionuklid
1. miokard sd ruptur
2. valvular
Pasien resiko tinggi:
-angina menetap
REPERFUSI: ideal<6jam
-iskemia berulang
-angiografi angioplasty Rawat CICU
-fungsi LV turun
-PCI (angioplasty + stent) Stabilisasi Hemodinamik: -perub. EKG: luas
primer atau rescue PCI Fluid, inotrop, IABP -riwayat IMA,PCI,CABG
Coroner-angiografi Ada bukti:

Sesuai utk revaskularisasi? YA -iskemi / infark?
TDK
Rawat CICU:
CABG Revaskularisasi: -enzim serial
BLPL
(BoLehPuLang)
-EKG serial
PCI atau CABG -2DE/nuklir
Follow up
Dr AW TAUFIQ, SpBTKV RSPAD Treatmil, Etc
Revaskularisasi:
PCI atau CABG???
Operasi CABG :
BYPASS
koroner Coronary Artery
Bypass Graft
Sambungan / bypass
pemb.darah dari kaki
www.escardio.org/guidelines Bedah Pintas Koroner

Instalasi
Diagnostik PCI :
Invasif
Kardiologik Percutaneous
(Kateterisasi/ Coronary
cathlab)
Intervention
PTCA
Percutaneus
Transluminal
Coronary
Angioplasty D.E.S : Drug Eluted Stent
Revaskularisasi:
PCI Versus CABG???
E B M?
Evident Base Medicine
CAD 1-VD
2-VD
3-VD
LM
PTCA versus CABG
pada pasien dengan Multivessel Disease
Menghilangkan PENDERITAAN
Meningkatkan KUALITAS HIDUP
SELANJUTNYA..
Memperpanjang USIA, serahkan pd-NYA
TAUFIQ Collection
RSPAD
TAUFIQ Collection
Analisa hasil rekaman perfusi:TC99M STUNNING MIOKARD:
Prolong depression contractile function
-Fix defec - partial -mild after a reversible episode of ischemia
-Area necrosis,scar, reversible rvsble (miocyte remain viable, but depressed contractile)
-EF < 30% defect defect
-hipokinetik,dll HIBERNATION:
Chronic ischemia with contractile dysfunction
Vertical long axis: Horizontal long axis: Short axis:
Infark coagulation necrosismyocardial fibrosis,
Apex Anterior wall
Anterior wall contraction-band necrosis, myocytolysis
(LAD,
(LAD) (no evidence of damage respon to: apoptosis or inflamation)
RCA)
Apex Septum SUPLAY:
(LAD, (LAD) LAD:anterior LV, apex, 2/3 septal anterior
RCA) Septum Lateral Cx :lateral & posterior LV
Lateral RCA: RV, 1/3 septal posterior, inferior(diafragma surface) LV
(LAD) Wall
Inferior wall wall (infero-posterior surface)
(Cx)
(RCA) Inferior wall
(Cx) PDA: posterior wall LV
(RCA) bila PDA (yg suplay 1/3 post septal) mendapat suplay
dari Cx =left dominan
dari RCA right dominan AV node
Kelainan tampak Perubahan Lokasi Tempat (90% pasien, 10% AV node dari Cx)
di lead left coronerbundle hisLBLAF+LPF blok
resiprocal infark sumbatan
2/3 pasien: cab ke-1 RCA ke conus arteri
conus arteriosus(RVOT)
I, aVL, V1-6 inferior Ekstensif anterior LAD 60% pasien: SA node dari RCA (40% dari Cx)
cab anterior RCA : suplay free wall RV
V1-4 Inferior anteroseptal a. septalis cab acut marginal : suplay RV
blok RCA=sinus bradi;AV blok;AMI:RV,inferopostr
V4-6, I, aVL Inferior anterolateral Cx
I, aVL, V5-6 II, III, aVF Lateral wall Cx

SA node: 60%RCA,40%Cx
II, III, aVF I, aVL, V1-6 Inferior wall RCA AV node: 90%RCA,10%Cx
V8, V9, V4R,V3R V1, V2-3 Posterior wall -RCA tikungan s/d Septal branch,LPF,LAF:
100% dari left coroner
(depresi ST, a. Desc posterior
R tinggi) R/S>1
www.escardio.org/guidelines -ujung Cx

Cabg Cad Rspad PDF

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Cabg Cad Rspad PDF

Uploaded by

Copyright:

Available Formats

Update in Coronary a.

1. 0bservasi C all: - activated EMS (Emergency Respon System)

STANDAR KOMPETENSI DOKTER

KONSIL KEDOKTERAN INDONESIA

www.escardio.org/guidelines Dr AW TAUFIQ, SpBTKV RSPAD

1 Pre RS: 392

Viscosity and Poiseuilles Law

(energy loss P turun 4x tiap r turun)

Culprit lesion= stenosis>70%,proximal,near branch,

From first decade From third decade From fourth decade

Adapted from Stary HC et al. Circulation 1999;92:1355-1374.

saat demand Kimbalance suplay demand (-)symptom (-)

Sub endotel exposure:

thrombin Release substance:

Unstable angina Myocardial infarction

ankhone pectus =strangling chest

CAD: Stable angina & ACS

B. Acute Coronar syndrome (ACS

1. Unstable Angina Pectoris (UAP)

A. Stable Angina . INJURY:

B. Acute Coronar syndrome (ACS):

on going myocardial ischemia or injury Na-K-

1. Unstable Angina Pectoris (UAP)

A. Stable Angina . INJURY:

B. Acute Coronar syndrome (ACS):

on going myocardial ischemia or injury Na-K-

1. Unstable Angina Pectoris (UAP)

Imbalance suplay demand myocard ischemia an aerob

Onset sering pd pagi / menjelang pagi / dini hari

Onset sering pd pagi krn: naiknya katekolamin induce-platelet

1 No heart failure. No clinical signs of cardiac decompensation

3 Severe heart failure. Frank pulmonary edema.

KILLIP > 2 = POOR PROGNOSIS

B. Acute Coronar syndrome (ACS):

1. Unstable Angina Pectoris (UAP)

UAP atau NSTEMI atau kah STEMI ?

Troponin I & T: marker lain:- myoglobin, CRP, IL-6,serum Amiloid-A

Well Perfused Myocardium Epicardial Coronary Artery

ISCHEMIA Subendocard transmural

Transmural infarction Subendocardial infarction

> 12 jam ?? Tidak

Coroner-angiografi Ada bukti:

www.escardio.org/guidelines Bedah Pintas Koroner

PCI Versus CABG???

I, aVL, V5-6 II, III, aVF Lateral wall Cx

You might also like