pleno a blok 15 23 jan 15 stemi

7/23/2019 Pleno a Blok 15 23 Jan 15 Stemi

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Oleh

Dr.Liniyanti D.Oswari.MNS.MSc.

PLENO A BLOK 15

23 February 2015


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Mr.T, 56 years old, a becak driver, comes to MH Hospitalbecause he has been having epigastric pain since eight

hours ago while he was working. The pain radiated to hislower jaw, and it felt like burning. He was unconcious forthree minutes. He also complained shortness of breath,sweating, and nauseous. He has history of hypertension.He is a heavy smoker.

Physical Exam:

yspnea, height!"6# cm, body weight! 55 kg, $M%!&'.()

$*! "5#+"## mmHg, H! 5- bpm regular. *! 5- bpm,regular, eual. ! &) /+min.

*allor, diaphoresis, 01* 253&4 cmH&, mue heart sounds,basal rales 234, liver! not palpable, ankle edema 234


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Laboratory Results:Hemoglobin! ") g+dl, 7$8 ! 9.-##+mm(, i: count !

#+&+5+65+&&+6, ; "(#mg+dl4

H? &5 mg= 2 normal @ )5 mg+dl48A BC8 )'( D+?, 2(-E"') units+? for men and 96E")#

units+? for women.

8A M$ '& D+?, 2 Bormal ! #3( ng+ml atau "# 3"( D+?4

Troponin %! #,( ng+ml. 2normal! >#." ng+ml4

FCARDIAC MARKERS.Troponin %, # 3 #." ng+ml 2onset! )36 hrs, peak! "&3&) hrs, return to normal! )3' days4.

Troponin T, # 3 #.& ng+ml 2onset! (3) hrs, peak! "#3&) hrs


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Additional Exam:

Chest X-ray c!r C"# $ 50%& b!!t-sha'e(.Lun)s br!nch!*ascular 'attern is n!r+al.

,C sinus rhyth+& n!r+al ais&

/# 5 b'+& re)ular& # inter*al 0&22 sec& 'ath!l!)ic wa*eS" ele*ati!n at lea( 44& 444& aF an( S"(e'ressi!n at lea( 1& 2& 3

Hypothesis:

Mr. "& 56 years !l(& su77ere( 7r!+ S",M4 in7eri!r wall


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Learning Objeti!es:". Memahami anatomi dan siologi jantung dan pembuluh

darahnya.&. Memahami patogenesis aterosklerosis(. Memahami faktor risiko penyakit jantung koroner). Memahami patosiologi sindrom koroner akut dan

penyulitnya

5. Memahami interpretasi hasil pemeriksaan sik6. Memahami interpretasi hasil pemeriksaan laboratorium'. Mengetahui pemeriksaan penunjang diagnostik sindrom

koroner akut-. Memahami kriteria diagnosis sindorom koroner akut

9. Memahami tatalaksana holistik sindrom koroner akuttermasuk pencegahan sekunder

"#. Memahami komplikasi sindrom koroner akut danrencana tatalaksananya


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"ynthesis

isk Iactors 2Male, Middle age,islipidemia, *revious history ofhypertension, Heavy smoker4 disfungsi endotel aterosklerosis

precipitating factor 2working4 coronary plaue rupture thrombosistotal coronary occlusion


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Ctherosclerosis

Figure 233-5: The atherosclerotic process. A. Artery depicting early fatty streakdevelopment. B. 1, LDL becomes oxidized ithin the arterial s!bendothelial space. ",

#irc!lating monocytes are recr!ited to the s!bendothelial space by chemoattractants

incl!ding oxidized LDL. $, These monocytes !ndergo differentiation, becoming

macrophages, hich are scavenger cells that recognize and acc!m!late oxidized LDL. %,

The lipid&laden macrophages then become foam cells, hich cl!ster !nder the endothelial

lining to form a b!lge into the artery. ', This b!lge is called a fatty streak and is the first

overt sign of atherosclerotic change. #. #ross&section of an artery ith an atherosclerotic

lesion ith a narroed l!men.


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Cm 0 M;d. "999J"#'J&5)3&6"Myocardial %nfarction in Koung

8igarette


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PATHOPHYSIOLOGY OF MYOCARDIAL

INFARCTION

THE PATHOPHYSIOLOGY OF A!TE ORO"ARYTHE PATHOPHYSIOLOGY OF A!TE ORO"ARY

SY"#RO$ES A"# %IO$AR&ERS RELEASE# I"TOSY"#RO$ES A"# %IO$AR&ERS RELEASE# I"TO

%LOO#%LOO# Continuum of AMI riskContinuum of AMI risk

Plaque rupture C-reactive proteinPlaque rupture C-reactive protein

Intracoronary thrombus P.selectin, fibrinopeptide AIntracoronary thrombus P.selectin, fibrinopeptide A

educed blood flo! Myocardial perfusion ima"in"educed blood flo! Myocardial perfusion ima"in"

Myocardial ischemia Ischemia-modified albuminMyocardial ischemia Ischemia-modified albumin

Myocardial necrosis #roponin, myo"lobin, C$-M%Myocardial necrosis #roponin, myo"lobin, C$-M% &I'(')I%*' +AMA'&I'(')I%*' +AMA'

.nstable

an"ina

.nstable

an"ina

MyocardialInfarcti

on

MyocardialInfarction

Asymptomatic

Asymptom

atic

Acute coronary syndromes are due to an acute or sub acute primary reduction ofmyocardial oxygen supply provoked by disruption of an atherosclerotic plaque associated

with inflammation, thrombosis, vasoconstriction and microembolization.

Finite process. (!"# h for necrosis to develop$.


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Plaque disruption or erosion

#hrombus formation !ith or !ithout embolisation

Acute cardiac

ischaemia/o )# se"ment elevation )# se"ment elevation

'levated markers of

myocardial necrosis

)# se"ment elevation

myocardial infarction

&0 !aves usually present

Markers of myocardial

necrosis not elevated

'levated markers

of myocardial

necrosis

nstable an"ina /on-)# se"ment elevation

myocardial infarction

&0 !aves usually absent

Acute coronary syndromes

%pectrum of acute coronary syndromes according to electrocardiography and biochemical

markers of myocardial necrosis (troponin &, troponin ' and creatine kinase )$, in patients

presenting with acute cardiac chest pain

Grech,BMJ 7/6/2003 326 , 259-261

PAT

HOPHYS

IOLOGY

OF

MYOC

ARDIAL

INFARCTION


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BIOCHEMICAL CARDIAC MARKERS

WHAT ARE CARDIAC MARKERS?WHAT ARE CARDIAC MARKERS?

?ocated in the myocardiumeleased in cardiac injuryMyocardial infarctionBon3L3wave infarctionDnstable angina pectoristher conditions a:ecting cardiac

muscle

2trauma, cardiac surgery, myocarditisetc.4

8an be measured in blood samples


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TIME LINE OF MARKERS OF

MYOCARDIAC DAMAGE & FUNCTION

'()*

'(+*

'(,*

'(-*

'((*

***

**)

ASTi/

A$I

&i/

A$I

Electro0horesis 1or & a/2

L#

& 3$%

$yo4lobi/assay

RIA 1orA"P

&5$%massassay

cT/Tassay

RIA 1or%"P a/20roA"P

cT/lassay

RIA 1or0ro%"P

POT 1or myo4lobi/&5$%6 cT/I

Immu/oassay 1or0ro%"PI$A

Ge/etic$ar7ers

Timeli/e history o1 assay metho2s 1or mar7ers o1 car2iac tissue 2ama4ea/2 myocar2ial 1u/ctio/.

AST: as0artate ami/otra/s1erase A"P: atrial /atriuretic 0e0ti2e

&: creati/e 7i/ase %"P: brai/ /atriuretic 0e0ti2e

L#: lactate 2ehyy2ro4e/ase POT: 0oi/t5o15care testi/4

Time 9years


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BIOCHEMICAL MARKERS IN

MYOCARDIAL ISCHAEMIA / NECROSIS

IN:IN:

8A3M$ 2mass48A3M$ 2mass4c.Troponins 2% or T4c.Troponins 2% or T4MyoglobinMyoglobin

OUT:OUT:

C


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&I"ETIS OF AR#IA $AR&ERSAFTER A$I

MA$' +'#'C#I1/ P'A$ +I)APP'AA/C'

yoglobin * + ! h # + h -! h

/") mass 0 + *- h *- + *1 h - + 0 days

&otal / ! + 1 h *- + 02 h 0 + ! days

c&n& ! + *- h *- + !1 h 3 + *3 days

c&n' ! + *- h *- + -! h 3 + days

These values represent averages.

IMA &ischaemiaIMA &ischaemia fe! minutesfe! minutes 2 3 h2 3 h 4 hours4 hours


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%IOHE$IAL $AR&ERS I" A$I:RELEASE6 PEA& A"# #!RATIO" OF

ELE;ATIO"


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REATI"E &I"ASE

"OR$AL ;AL!ES:"OR$AL ;AL!ES:

4ary according to +

agesex

race

physical condition

muscle mass

PATHOLOGIAL I"REASES:

yocardial infarction or in5ury

%keletal muscle in5ury or disease6ypothyroidism

' in5ections

7eneralised convulsions

erebral in5ury

alignant hyperpyrexia

8rolonged hypothermia


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REATI"E &I"ASE: &5$%

&5$% is the most car2iac5s0eci8c & isoe/ car2iac

muscleI/ /ormal 0o0ulatio/ &5$% ? +@ Tot &

Se/siti=e mar7er ith ra0i2 rise > 1all$ore s0eci8c tha/ Tot & but has limitatio/sBGol2 sta/2ar2C biochemical mar7er 1or D

2eca2esBThere is /o 0lace 1or measureme/t o1 &5$% by

electro0horetic or immu/oi/hibitio/ metho2s i/the 'stce/tury laboratoryC Jacobs, Lab Test Handbook 5thEd 2001,157

O/ly &5$%massshoul2 be measure2


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&5$%massRELATI;E I"#E

@RI

= % P 28A3M$mass+ Tot 8A activity4 / "##

%ncreased % suggests myocardial originBot absolute E lack of 8A3M$massassay

standardisation and tissue variability

% @ ( E 6 = with Tot 8A activity elevated

2preferably @ &/ D limit4 suggestsmyocardial necrosis


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"E GE"ERATIO" AR#IA$AR&ERS

$yo4lobi/8urrently earliest marker?ike total 8A it is by no

means cardio3specic

Tro0o/i/sAinetics comparable

with total 8A and 8A3M$8ardio3specic


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$YOGLO%I" $b

?ow M7 protein


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AR#IA TROPO"I"S


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TH; T*B%B ;OD?CTK8M*?;S


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TROPO"I" S!$$ARY

egulatory comple/ of striated musclecontraction

;arly release e/ cytosolic pool

*rolonged release due degradation ofmyolaments

istinct skeletal Q myocardial muscleforms

High specicity for myocardial injury


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LA%ORATORY O"SI#ERATIO"S I"THE HOIE OF AR#IA $AR&ERS

%nstrumentation should allow rapid Q reliable measurement ofTroponin, Myoglobin Q 8A3M$massOood Troponin tests should be heparinate 2plasma4

compatible. *lasma specimens preferred for cardiac markersto improve turn3around time of results

8hoice of Troponin cut3o: level!Ior our Tn% assay we use a cut3o: of #.#6 ng+m?, based on EThe 99thpercentile cut3o: 2#.#) ng+m?4

CBThe level at which the analytic precision of the method is

within "# = 2#.#6 ng+m?4Ior our TnT assay we use a cut3o: #." ng+m? 2within "#=

precision4To achieve comparability with the less sensitive 8A3M$

method, a Tn% cut3o: of #.) ng+m? would have to be used


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TROPO"I" A"# $I#IAG"OSIS

IschemicIschemic DiscomfortDiscomfort

(o )T *levation(o )T *levation )T *levation)T *levation

UnstableUnstable

anginaangina

Myocardial InfarctionMyocardial Infarction

Ac!te #oronary )yndromesAc!te #oronary )yndromes

#ardiac +arkers #linical ,tility#ardiac +arkers #linical ,tility

(on -&(on -&

.ave +/.ave +/-&.ave-&.ave

+/+/

()T*+/

0Diagnosis

0 1rognosis

)T*+/

01rognosis

0 2eperf!sion

()T*+/ )T*+/

It !s est!"ated that abo#t $0% o& 'at!ents (ho ')esent (!th chest 'a!n (!tho#t ST*se+"ent ee-at!on and (o#d othe)(!se be d!a+nosed asha-!n+ #nstabe an+!na beca#se o& a ack o& CK*M. ee-at!on act#a/ha-e STEMI (hen assessed (!th ca)d!ac*s'ec!c t)o'on!n assa/s

FromJ!"" an# "irc$la%ion 2002


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PRE#ITIO" OFRIS&PROG"OSIS

(on )T *levation /schemic Discomfort

Troponin

3admission and 4&1" hrs5

Troponin

(egative

Troponin

ositive

NSTEMI -

High Risk

Low risk

Other disease?

Troponin can be used to eRciently categorise patients intohi4h a/2 lo ris7groups for appropriate management

pathways.!#a&%e# 'rom !""/!H! G$i#eline (a%e 'or %he Mana)emen% o' &a%ien%* +i%h (! an# M. 2002

G!I#ELI"ES: !SE OF AR#IA


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G!I#ELI"ES: !SE OF AR#IA$AR&ERS I" PATIE"TS ITH HEST

PAI"

$b6 &5$%$b6 &5$%massmass6 Tro0o/i/6 Tro0o/i/ POSITI;EPOSITI;EA$IA$I

$b$b O"LYO"LY POSITI;EPOSITI;E

Possible early i/1arctio/ or s7eletal musclePossible early i/1arctio/ or s7eletal musclei/Juryi/Jury

epeat markers2B$ importance of Mb is as a "e4ati=e Pre2ictor"e4ati=e Pre2ictor4

$b K &5$%$b K &5$% POSITI;EPOSITI;EProbable early i/1arctio/Probable early i/1arctio/epeat markersC rising 8A3M$ or increased 8A3M$mass % CM%


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G!I#ELI"ES: !SE OF AR#IA $AR&ERSI" PATIE"TS ITH HEST PAI"

T/IT/I ??*.*+ /4mL OR T/T*.*+ /4mL OR T/T ??*.* /4mL*.* /4mLo/ to s0ecime/s M + hours a0arto/ to s0ecime/s M + hours a0art!/stable A/4i/a!/stable A/4i/a

Tro0o/i/ I M *.*+ OR T/T M *.' /4mLTro0o/i/ I M *.*+ OR T/T M *.' /4mL2TnT levels @ #.#( and2TnT levels @ #.#( and >>#." ng+m? are euivocal and#." ng+m? are euivocal and

should be repeated4should be repeated4N Hi4h ris7 ASA$I or /o/5ischaemic myocar2ialN Hi4h ris7 ASA$I or /o/5ischaemic myocar2ial

2ama4e2ama4edepending on clinical cardiac ischaemia

These patients reuire follow3up

Tro0o/i/ I M *. /4mLTro0o/i/ I M *. /4mLBBtra2itio/alC A$Itra2itio/alC A$I


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8oronary Ctherosclerosis denganThrombosis

2*enebalan pembuluh darah 0antung dgsumbatan4


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7olesterol

".


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Aolesterol hanya dijumpai pada *roduk hewani.$entuk cincin


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C8


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6ospitalizations in the .). D!e to Ac!te

#oronary )yndromes 3A#)5

Ccute 8oronary


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Oeneral Therapy


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Oeneral Therapy

MBCMorphine 2 53"5 min 8?C


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*reventive ! ;ducation

8hange ?ifestyle33


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Aoleste rol termasuk mencegah *0A Q


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Aolesterol termasuk mencegah *0A Q


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iet

". ?emak yang dimakan dikurangi sampai "&3") g+hari.&.Menjadi vegetaris ! Tidak mengkonsumsi produk

hewani 2aging, ikan,ayam, telur4 ! $anyak makan

sayuran 2(3) penukar4 dan buah3buahan 2(3 6 penu

kar dan produk kedelai 2 Tahu, tempe, susu kedele4 setiap kali makan.

(.Tidak menambahkan Minyak , margarine apalagi

WbutterX dalam makanan.

pleno a blok 15 23 jan 15 stemi

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