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Update in Coronary a.

Disease
(CAD)
OVERVIEW

Skema TAUFIQ
jantung : Collection
pembuluh koroner & bilik jant
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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
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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
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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

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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

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30% = 17 jt

WHO

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Dr AW TAUFIQ, SpBTKV RSPAD
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

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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

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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
CAD 1-VD
2-VD
3-VD
LM

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Dr AW TAUFIQ, SpBTKV RSPAD
Pembuntuan / penyumbatan
Pembuntuan / penyumbatan
Skema TAUFIQ Collection
jantung : pembuluh koroner & bilik jant
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Dr AW TAUFIQ, SpBTKV RSPAD
PATOFISIOLOGI
ATHEROSKLEROTIK

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Dr AW TAUFIQ, SpBTKV RSPAD
FAKTOR RESIKO:
Hiperlipidemia,
DM,
Hipertensi
Smoking ENDOTEL INJURY,
Toxins ggn:
Hemodinamic factor plaque erosion &
Immune reaction rupture
Microba,Viruses

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1
3 6
2
4
5
PATOFISIOLOGI
Terbentuk plaqueflow dynamic & endothelial shear stress
plaque erosion & ruptureagregasi,cascade coagulation
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thrombus Etc, endotel vasoconstriction occlusionACS Dr AW TAUFIQ, SpBTKV RSPAD
1
3 6
2
4
5
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Dr AW TAUFIQ, SpBTKV RSPAD
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.
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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
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stenosis=90% angina at rest Dr AW TAUFIQ, SpBTKV RSPAD
Jean Louis Marie Poiseuille

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Dr AW TAUFIQ, SpBTKV RSPAD
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
stenosis=50%:angina effort
stenosis=90% angina at rest

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Dr AW TAUFIQ, SpBTKV RSPAD
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
atherom: rich macrofag&lipid
stenosis=50%:angina effort INFARK
stenosis=90% angina at rest

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Dr AW TAUFIQ, SpBTKV RSPAD
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.


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Dr AW TAUFIQ, SpBTKV RSPAD
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

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Dr AW TAUFIQ, SpBTKV RSPAD
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:


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Dr AW TAUFIQ, SpBTKV RSPAD
P1-P2 = V . 8 L n = Q . 8 L n
r2 phi r4

Atherosclerosis

CAD

Angina pectoris

ACS

Unstable angina Myocardial infarction

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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)

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Dr AW TAUFIQ, SpBTKV RSPAD
CORONARY ARTERY DISEASE (CAD):
Key word: 1. chest pain
2. angina, angina pectoris,
ankhone pectus =strangling chest

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+

1. Unstable Angina Pectoris (UAP)


2. Miokard Infark: -a. Non ST Elevasi Miokard Infark (NSTEMI)
-b. ST Elevasi Miokard Infark (STEMI)

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Dr AW TAUFIQ, SpBTKV RSPAD
CORONARY ARTERY DISEASE (CAD):
Key word: 1. chest pain
2. angina, angina pectoris,
ankhone pectus =strangling chest

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+

1. Unstable Angina Pectoris (UAP)


2. Miokard Infark: -a. Non ST Elevasi Miokard Infark (NSTEMI)
-b. ST Elevasi Miokard Infark (STEMI)

Imbalance suplay demand myocard ischemia an aerob


tjd gangguan:
1. ggn metabolik,
2.TAUFIQ
Skema ggn electrical,
jantung : Collection
pembuluh koroner & bilik jant
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mekanik
Dr AW TAUFIQ, SpBTKV RSPAD
SYMPTOMS & SIGNS?
( GEJALA-GEJALA & TANDA-TANDA .. ? )

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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

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chest pain: P-QRST=Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)

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Dr AW TAUFIQ, SpBTKV RSPAD
To Talamus

Skin

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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
(tightness-squeezing-pressure)
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
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Dr AW TAUFIQ, SpBTKV RSPAD
STRATIFIKASI?
PROGNOSA ?

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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.)

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Ex.: Dx, UAP FCCS II
Dr AW TAUFIQ, SpBTKV RSPAD
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.

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Dr AW TAUFIQ, SpBTKV RSPAD
LABORATORIUM?

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CORONARY ARTERY DISEASE (CAD):
Key word: 1. chest pain
2. angina, angina pectoris,
ankhone pectus =strangling chest

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)

UAP atau NSTEMI atau kah STEMI ?


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CK
CK-MB
TROP-T
TROP-I

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Dr AW TAUFIQ, SpBTKV RSPAD
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 (+/-)
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-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?

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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

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Dr AW TAUFIQ, SpBTKV RSPAD
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

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Ischemia
Dr AW TAUFIQ, SpBTKV RSPAD
ECG has important rule in ACS

Transmural infarction Subendocardial infarction

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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
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Dr AW TAUFIQ, SpBTKV RSPAD Sequence of changes seen during evolution of myocardial
6 infarction V
TREATMENT?

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TREATMENT:
10 Menit Pertama

MONA

10 Menit Kedua

10 Menit Ketiga

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Dr AW TAUFIQ, SpBTKV RSPAD
Sudah Suspect kuat: AMI
TREATMENT: chest pain: P-QRST
10 menit Pertama Pain-Quality-Radiation-Severity-Timing
(tightness-squeezing-pressure)

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
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Hasil EKG 12 lead, sadapan Pertama
Dr AW TAUFIQ, SpBTKV RSPAD
10 Menit Pertama

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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
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
Dr AW TAUFIQ, SpBTKV RSPAD
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

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Dr AW TAUFIQ, SpBTKV RSPAD Treatmil, Etc
Revaskularisasi:
PCI atau CABG???

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Dr AW TAUFIQ, SpBTKV RSPAD
Operasi CABG :
BYPASS
koroner Coronary Artery
Bypass Graft

Sambungan / bypass
pemb.darah dari kaki

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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
Instalasi
Diagnostik PCI :
Invasif
Kardiologik Percutaneous
(Kateterisasi/ Coronary
cathlab)
Intervention

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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
PTCA
Percutaneus
Transluminal
Coronary
Angioplasty D.E.S : Drug Eluted Stent

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Dr AW TAUFIQ, SpBTKV RSPAD
Revaskularisasi:

PCI Versus CABG???

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Dr AW TAUFIQ, SpBTKV RSPAD
E B M?
Evident Base Medicine

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CAD 1-VD
2-VD
3-VD
LM
PTCA versus CABG
pada pasien dengan Multivessel Disease

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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
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Dr AW TAUFIQ, SpBTKV RSPAD
Menghilangkan PENDERITAAN
Meningkatkan KUALITAS HIDUP

SELANJUTNYA..
Memperpanjang USIA, serahkan pd-NYA

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Dr AW TAUFIQ, SpBTKV RSPAD
TAUFIQ Collection
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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