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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
2. Tx sesuai indikasi
(di bawah ini):

C all: - activated EMS (Emergency Respon System)


- for defib
L ok
L isten
Breath
(-)
2 kali hembusan
F eel
(+)

PULSE
Positif

Klinis spt ASMA, ttp:


-Retraksi (-)
-Ronkhi basah s/d apec
-Pucat, megap2,ala nasi lebar
-EKG variatif:-sinus taki
-T bisa > 140/90
-PCO2 >> PO2
N<50) (N=85 90)

-Chest pain
-Elevasi ST
-dg/tanpa BBB:
-QRS > 12
-Right=rsR di V1-V3
-left = RR di V5-V6

Negatif
CPR
1 seri/1mnt=100x/mnt
pola 15: 2 (unprotec airway)
5: 1 (protected airway)

O2 (termasuk intubasi)
I v line
M onitor (12 lead)

Monitor

ARITMIA

VT
VT pulse(-) Pulse (+)
Atau VF

Non VT/VF

precordial thump

AMI

BRADIKARDI
(<60)

DC : 200-300-360
cardioversi

PEA

ASISTOLE
Serius:
TAKIKARDI (>100)
-simptom:-nafas pendek
- kesadaran turun
1. Serius
- chest pain
ACUTE LUNG OEDEM (ALO)
STABIL
simptom,sign
-sign:-T drop,pre/syock,
2. HR >150
-congestive pulmo
-AMI,CHF
AF
PSVT
I0 or II0 tipe-1
A Fluter
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-II0type2
TDK
YA
TCP, iv pacing
A-T-D-E-I
-III0

Sirkulasi
Kembali
spontan

Persisten
VT pulseless
Atau VF

Observasi
VT
Dr AW TAUFIQ, SpBTKV RSPAD

KONSIL KEDOKTERAN
INDONESIA

STANDAR KOMPETENSI DOKTER


KONSIL KEDOKTERAN INDONESIA
Indonesian Medical Council
Jakarta 2006

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TINGKAT KEMAMPUAN:

KASUS- A

3A

3B

KASUS- B

3A

3B

KASUS- C

3A

3B

KASUS- D

3A

3B

KASUS- E

3A

3B

Ax,Px,Dx
Terapi-I
RujukCITO

MANDIRI

Overview

Ax,Px,Dx Ax,Px,Dx
Rujuk &
Terapi-I
follow
Rujukup
elective

&
TUNTAS

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Dr AW TAUFIQ, SpBTKV RSPAD

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30% = 17 jt

WHO

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Dr AW TAUFIQ, SpBTKV RSPAD

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Dr AW TAUFIQ, SpBTKV RSPAD

USA
population

INDONESIA

330.000.000

237.600.000

CAD (30 persentil)

9.900.000

7.128.000

IMA (6 persentil)

PERSENTILE
CAD
1.980.000
1.425.600

mortality (30%)

pre hospital (15/30%)


readmission 1 y (35/70%)

Cath/PCI
CABG

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JAMA.2011;305(17):1769-1776. doi:10.1001/jama.2011.55

1,000

CILEGON
392.341
11.770
2.354

594.000

427.680

785

3 118.8001

85.536

392

633.600

456.192

1.210.110
356.730

871.279

30

256.846

CAD
INFARK
MORTAL
Cath/PCI
CABG

Dr AW TAUFIQ, SpBTKV RSPAD

589
1.177
392

CILEGON

392,341

PENDUDUK: 392.341
CAD: 11.770

INSIDENSI CAD
Per Hari

6
32

CAD
INFARK
MORTAL
Cath/PCI
CABG

INFARK:

2.354

MORTAL:

785

Pre RS:

392

Re admission:

589

PCI:

1.177

CABG:

392

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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
Collection

Skema TAUFIQ
jantung : pembuluh koroner & bilik jant
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RSPAD
Dr AW TAUFIQ, SpBTKV RSPAD

PATOFISIOLOGI
ATHEROSKLEROTIK

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Dr AW TAUFIQ, SpBTKV RSPAD

FAKTOR RESIKO:
Hiperlipidemia,
DM,
Hipertensi
Smoking
Toxins
Hemodinamic factor
Immune reaction
Microba,Viruses

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ENDOTEL INJURY,
ggn:
plaque erosion &
rupture

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

3 6
2
4

5
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Dr AW TAUFIQ, SpBTKV RSPAD

PATOFISIOLOGI
FAKTOR Hiperlipidemia,
Terbentuk plaqueflow dynamic & endothelial shear stress
RESIKO: DM,Hipertensi
plaque erosion & ruptureagregasi,cascade coagulation
Smoking
thrombus Etc, endotel vasoconstriction occlusionACS
Toxins
Culprit lesion: stenosis>70%, proximal, atherom rich macrofag,lipid
Hemodinamic factor
near branch
Immune reaction
Microba,Viruses Endotel Produksi:
Heparin sulfat,
Eicosanoid(prostasiclin)
thrombin activation,
ENDOTEL INJURY, ggn:
platelet adesion
plaque erosion&rupture
Nitrous Oxide
EDRF(epitel derivat relaxing factor)
ADESI : Platelet, monosit
Plasminogen
-platelet (1)
Imbalance pro injury
6
-monocytmacrofag

Penyebab non plaque ACS:(10%)


1. Spasme a.coroner:
-Angina prinzmetal
-Cocain
-Amfetamin
2. Emboli: mis dr
-valvular heart infeksi
3. Oklusi a.coroner:
-Coroner vasculitis,Aodissect
-kawasaki,takayasu,marfan
4. Chest trauma
5. Mistmath suplay-demand lain:
misal , hipertiroid,
akut anemi ec GI bleeding
6. Hipertrofi ventrikel: LVOT
subaortic Hipertrofi/IHSS, AS
7. Kongenital coroner anomali

oxidized LDL, VLDL


lipid uptake by macrofag et all
Foam cells (2) of atheroma plaque
degeneratingextracellular lipid
imbalance influx-eflux (LDL vs HDL)
3
accumulation of cholesterol
2
Pro
injuri:
in the plaque (3)
-vasoactive(konstriksi):
4
Membrana elastica interna robek (4) endotelin,angiotensinII,
Cytokin dan
serotonin, PDGF
Growth factor release (PDGF):
-procoagulan:
migration & proliferation
von wilebrand,PAI-1
-cytokine
et all menarik monosit
smooth muscle cell(SMC)(5)
5
-vasculer cell adesi molekul-1
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
Oxidized LDL
in Foam cell:
-Cytotoxic
Nitric oxide syntase
-Pro Coagulant
-Chemotaxtic:
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macrofag,
L - arginine
Nitric oxide
netrofil
Metaloproteinase
(lisis
kolagen cap)
cytocin

-inhibisi:- platelet activationtromboxan A2 block


-platelet adesi
-platelet agregasi
sulit terbentuk trombus
-vasodilatasi, via: blok platelet activation + thiolated.
(ctt: platelet activationrelease vasokonstrictor agen:
Tromboxan A2,dll)

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=50%:angina effort
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
AP

UnStable
AP
(UAP)

AMI

NSTEMI
(energy loss P turun 4x tiap r turun)
P1-P2 = V . 8 L n = Q . 8 L n
r2
phi r4

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


atherom: rich macrofag&lipid
stenosis=50%:angina effort
stenosis=90% angina at rest

STEMI

CAD
ACS

INFARK

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Dr AW TAUFIQ, SpBTKV RSPAD

Atherosclerosis Timeline
Foam
Cells

Fatty
Streak

Intermediate
Atheroma
Lesion

Fibrous Complicated
Plaque Lesion/Rupture

Endothelial dysfunction

From first decade

From third decade

Growth mainly by lipid accumulation

From fourth decade


Smooth muscle
and collagen

Thrombosis,
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
-numerous inflamatory cell
Activated
Inflamatory cell

Dissolution
Fibrous cap

Release: metalloproteinase
(collagenase)

Plaque disruption

-agregasi
-cascade coagulasi
-vasokonstriksi

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

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thrombin

Release substance:
Promote vasoconstriction
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

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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)

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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
on going myocardial ischemia or injury

(+)

K+

Na+

Na-KATP

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
on going myocardial ischemia or injury

(+)

K+

Na+

Na-KATP

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
ggn electrical,
Skema
jantung
: Collection
pembuluh koroner & bilik jant
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3. ggn RSPAD
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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Dr AW TAUFIQ, SpBTKV RSPAD

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

VISCERAL
(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

KILLIP CLASSIFICATION:

Exm. Statifikasi resiko:


(TIMI, Killip,GRACE)

Class

Description

1
2
3

Absence of rales over the lung fields and absence of S3.


Rales over 50% or less of the lung fields or the presence of an S3.
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
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

No heart failure. No clinical signs of cardiac decompensation

Heart failure. Diagnostic criteria include rales, S3 gallop and venous hypertension.

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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Dr AW TAUFIQ, SpBTKV RSPAD

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
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

Limit of Normal

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
Septum

Epicardial Coronary Artery


Lateral Wall of LV

Inferior Wall of LV

Positive Electrode
VAT

QRS
interval

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Dr AW TAUFIQ, SpBTKV RSPAD

INJURY
INJURY:

Prolonged ischemia
Represented by ST elevation

referred to as an injury pattern

Transmural injury ST elevasi

(++)

Sel miokard

(+)

K+

Na+

Na-KATP

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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Dr AW TAUFIQ, SpBTKV RSPAD

Kecepatan rekaman : 25 mm/dt 1 mm=1/25 dt = 0.04 dt


Kekuatan voltase : 10 mm = 1 mV
5 mm
- 90
0,2 dt

VAT

- 30

0,1 mV
PR
segment

ST
segment

point
PR
interval

QRS
interval

ST
interval

+ 120

QT
interval

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


infarction
6

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

TREATMENT:
10 menit Pertama

Sudah Suspect kuat: AMI


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

Nilai segera (dlm < 10 mnt I):


-vital sign, sat., iv line, EKG 12 lead
-perdalam anamnesis & pem.fisik
fokus ke indikasi-KI trombolitik:
-lab:troponin, CK-CKMB, elek,CBC
koag (door to lab result < 30 mnt)
-Ro thorax (<30 mnt, sdh dapat)
KI thrombolitik:Mutlak:
-post stroke hemoragi atau
unknown,onset kapanpun
-poststroke infark dlm6bln
-post ops:berat;intracranial
serius head trauma<3mgg
-tumor intra cranial
-dissecsi aorta
-kelainan hemostasi
-GI bleeding dlm 1 bln
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Terapi Umum segera (MONA):


-Oksigen kanul 4 ltr/mnt (sat>90%)
-Aspirin 160 325 mg PO
-NTG SL/spray(dptdiulang/5 mnt,3x
-Morfin iv10mg, (4-8mg/5-15 mnt)
(bila nyeri tak membaik dg NTG3x)
maintenance: 20 ugr/kg/jam
KI relatif thrombolitik:
-usia > 80 th
-hipertensi tak terkontrol:
EKG LVH, T>180/110 meski sdh di
th/ nitrat SL; sudah aspirin kunyah &
morfin 5 mg iv(1/2 Amp)utk nyerinya.
-sedang th/ antikoagulan dg INR > 1,5
-syock kardiogenik
-pericarditis
-kehamilan
-th/ laser retina

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

Hasil EKG 12 lead, sadapan Pertama


TREATMENT:
10 menit Kedua

10 menit II
Keputusan: primerPCI
thrombolitik,
atau lainnya

Target: door to needle/drug = 30 mnt


door to balon= 90 mnt. >120mnt: + =4:0

Elevasi ST dan atau LBBB baru

Mulai th/:
-NTG iv(KI:S<90,bradi/taki,RV AMI)
-Heparin iv
-bradiatropin
-ACE inhibitor,ARB
b blocker iv
-HMG CoA reductase inhibitor
(terapi statin)

Onset serangan
sd sekarang

> 12 jam

-ST depress(0.5mm),
T inverted suspect iskemi
-Resiko tinggi UAP/NSTEMI

-EKG tak khas


-resiko sedang/rendah:
UAP/STEMI

-aspirin 160-325 mg qd (clopidogrel bila SE)


-glikoprot. IIb/IIIa reseptor inhibitor
-heparin (utk UAP,NSTEMI: pakai LMWH) Memenuhi kriteria
UAP baru
-NTG iv
YA
-b blocker(bila nyeri berlanjut &
atau
Tx Ca chanel blok, bila KI bblocker)
Troponin positif

Tentukan status klinis

??
Klinis tdk stabil

Tidak

stabil

< 12 jam
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-Observasi di EMG+monitor
-enzim serial (8-12 jam kmd)
-monitor EKG/ST
-2DE/radionuklid
Dr AW TAUFIQ, SpBTKV RSPAD

Onset serangan
sd sekarang

> 12 jam

Memenuhi kriteria UAP baru


atau Troponin positif

??

Tentukan status klinis

Klinis tdk stabil


< 12 jam
Hipotensi, syock kardiogenik:
echo: disfunction:
1. miokard sd ruptur
2. valvular

REPERFUSI: ideal<6jam
-angiografi angioplasty
-PCI (angioplasty + stent)
primer atau rescue PCI

Rawat CICU
Stabilisasi Hemodinamik:
Fluid, inotrop, IABP

Coroner-angiografi
Sesuai utk revaskularisasi?

stabil

Tidak

-Observasi di EMG+monitor
-enzim serial (8-12 jam kmd)
-monitor EKG/ST
-2DE/radionuklid

Pasien resiko tinggi:


-angina menetap
-iskemia berulang
-fungsi LV turun
-perub. EKG: luas
-riwayat IMA,PCI,CABG

YA

Ada bukti:
-iskemi / infark?
TDK

CABG

Revaskularisasi:
PCI atau CABG

Rawat CICU:
-enzim serial
-EKG serial
-2DE/nuklir

BLPL
(BoLehPuLang)
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

CABG :

Operasi
BYPASS
koroner

Coronary Artery
Bypass Graft

Sambungan / bypass
pemb.darah dari kaki

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Bedah Pintas Koroner


Dr AW TAUFIQ, SpBTKV RSPAD

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Dr AW TAUFIQ, SpBTKV RSPAD

PCI :

Instalasi
Diagnostik
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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PTCA versus CABG

CAD 1-VD
2-VD
3-VD
LM

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

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TAUFIQ Collection
RSPAD
TAUFIQ Collection

STUNNING MIOKARD:
Prolong depression contractile function
after a reversible episode of ischemia
(miocyte remain viable, but depressed contractile)

Analisa hasil rekaman perfusi:TC99M


-Fix defec
- partial
-mild
-Area necrosis,scar,
reversible rvsble
-EF < 30%
defect
defect
-hipokinetik,dll
Vertical long axis:

Horizontal long axis:


Apex
(LAD,
RCA)

HIBERNATION:
Chronic ischemia with contractile dysfunction
Short axis:

Infark coagulation necrosismyocardial fibrosis,


contraction-band necrosis, myocytolysis
(no evidence of damage respon to: apoptosis or inflamation)
SUPLAY:
Septum
Apex
LAD:anterior LV, apex, 2/3 septal anterior
(LAD)
(LAD,
Cx :lateral & posterior LV
Septum
Lateral
RCA)
Lateral RCA: RV, 1/3 septal posterior, inferior(diafragma surface) LV
(LAD)
Wall
wall
Inferior wall
(infero-posterior surface)
(Cx)
(Cx)
(RCA)
PDA: posterior wall LV
Inferior wall
(RCA)
bila PDA (yg suplay 1/3 post septal) mendapat suplay
dari Cx =left dominan
dari RCA right dominan AV node
(90% pasien, 10% AV node dari Cx)
Kelainan tampak
Perubahan
Lokasi
Tempat
left
coronerbundle hisLBLAF+LPF blok
di lead
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
cab acut marginal : suplay RV
V1-4
Inferior
anteroseptal
a. septalis
blok RCA=sinus bradi;AV blok;AMI:RV,inferopostr
Anterior wall
(LAD)

Anterior wall

V4-6, I, aVL

Inferior

anterolateral

Cx

I, aVL, V5-6

II, III, aVF

Lateral wall

Cx

II, III, aVF

I, aVL, V1-6

Inferior wall

RCA

V8, V9, V4R,V3R

V1, V2-3
Posterior wall
(depresi ST,
R tinggi) R/S>1
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-RCA tikungan s/d


a. Desc posterior
-ujung Cx

SA node: 60%RCA,40%Cx
AV node: 90%RCA,10%Cx
Septal branch,LPF,LAF:
100% dari left coroner