Kuliah Shock Cardiogenic

7/26/2019 Kuliah Shock Cardiogenic

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SHOCK CARDIOGENIC

Bag. Anestesiologi dan Therapy Intensive Care

Fakultas Kedokteran Universitas Islam Sumatera Utara

20!

Fir


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DEFINISI

IT IS NOTLOW BLOODPRESSURE!!!

IT ISHYPOPERFUSION..

Gangguan dari perfusi jaringan yangterjadi akibat adanya

ketidakseimbangan antara suplaioksigen ke sel dengan kebutuhan

oksigen dari sel tersebut.

Semua jenis shock mengakibatkan

gangguan pada perfusi jaringan yangselanjutnya berkembang menjadigagal sirkulasi akut atau disebut juga

sindroma shock


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Shock adalah kondisi saat tansot o$DO%& d#li'#( O%) k# *ain"an "a"al +#+

k#-,t,han +#ta-olik di *ain"an t#s#-,


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Always a symptom of primary caus

Inad!uat "lood #ow to mt tissu o$y%n dm

&ay " associatd wit' 'ypotnsion

Associatd wit' si%ns of 'ypoprfusion( mntal stc'an%, oli%uria, acidosis

S'oc)


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*+-+*

Type of shock

Hypovolemic

Cardiogenic

Distributive [vasomotordysfunction]

. High or normalresistance

. Low resistance

Obstructive

Primary mechanism

Volume loss

ump failure

!"panded venous capacitance[pooling]# CO normal or low

$rteriovenous shuntingCO normal or high!"tracardiac obstruction ofmain channel of blood flow

Clinical causes

!"ogenous %lood loss due to hemorrhage lasma loss due to burn# inflammation &luid and electrolyte loss due to vomit ing# dehydration# osmolal diuresis [diabetes]

!ndogenous !"travasation due to inflammation# trauma

sna'e venom# pheochromocytoma

(yocardial infarctionHeart failure

$rrhythmia)ntracardiac obstruction

Hypodynamic septic shoc' due to gram*neg+pinal shoc'# ,arcotic over dose# barbitura

neumonia# peritonitis# abscess# reactive h

Vena caval obstruction# pericarditis [cardiacpulmonary embolism# aorta dissecting aneu

Classification of shoc' states

-eil# (H et al Card iovascular +ystem failu

emergency medicine. +chwart/. 01 [ed] -%


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*+-+*

Hemorrhagic

Sign & Symptoms

allor# fainting+'in clammy# cold

6achycardia

Oliguria

Collapse

Laboratory

Hct, Hb

Cardiogenic

Sign & Symptoms

allor# fainting+'in clammy# cold

$rrhythmias

Oliguria

Collapse

Laboratory

Cardiac en/ymes

!C0

Traumatic

Sign & Symptoms

History 7 hysicalevidence of in8ury

Oliguria

6achycardia

Collapse

Laboratory

9*1ays# C6*scan

PathophysiologyDirect in8ury to organ

Therapy

2. 1epair in8ury

:. &luids

;. %lood

Pathophysiology %lood volume

Therapy

2. &luids

:. %lood

;. Control %leeding

Pathophysiology Cardiac output

Therapy

2. $ntiarrhythmic

:. Vasopressors

;. Vasodilators

Septic

Sign & Sympt

&ever# chills+'in warm

6achycardia

Oliguria

$ltered mental

CollapseLaboratory

[


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*+-+*

A./ production + lactic acidosis

Sur0i0al + dlaydmor"idity + mortality

Intr0ntion + sta"ili1ation

Cllular functionimpaird

Continud 0olum loss

&m"ran porosity

&o0mnt of#uid from

intra0ascular tointrstitial

spacs

2yso1ymal

la)a%

Cllular autodi%st

Irr0rsi"l s'oc)

intr0ntion

DEA.HNo3 intr0ntion

Cllular 'ypo$ia +anaro"ic

mta"olism

/A.HO/H4SIO, CON.5N


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*+-+*

/RE62OAD CON.RAC.I2I.4 AF.ER62OA

S.ROKE 7O28&E HEAR.6RA.E

CARDIAC O8./8. .O.A2

/ERI/HERA2RESIS.ANCE

92OOD /RESS8RE


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/RDI/ OUTPUT

Cardiac output : stok# 'ol,+# 0 h#at at#

Stro) 0olum #load& contactilit( ; a1t#load

2#no,s #t,n


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/RDI/ OUTPUT

Fank3Stalin" #lationshi "twn t'0ntricularnd6diastolic prssur


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*+-+*

DO?

: CAO?

@ CO

7O? : CAO?6C7O?B @ CO

CAO? : SAO? @ H9 @ 3

C7O?: S7O?@ H9 @ 3

SHOCK, DO? 7O?

OXYGEN TRANSPORT


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CARDIOGENIC SHOCK

Dcrasd contractility

Incrasd llin% prssurs, dcrasd 27 stro) wor),

dcrasd cardiac output Incrasd systmic

0ascular rsistanc compnsatory


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PATOFISIOLOGI DARI RESPONTUBUH TERHADAP SHOCK

Respon Neuroendokrin

Respon Hemodinamik

Respon e!a"o#ik


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H$PO%OLEIA

R a!rium#o&'pressure s!re!()

re(ep!ors

Aor!a*(aro!idsHi+)'pressure

"arore(ep!ors

LOSS OF TONICINHIBITION OFCENTRAL ANDS$PATHETIC

NER%OUS S$STES

Rena#Renin re#ease

Pi!ui!ar, +#andACTH- ADH and GH re#eas

Adrena# +#and .medu##a/Epinep)rine*norepinep)rin

re#ease

Adrena# (or!e0Cor!iso# re#ease

Adrena# (or!e0A#dos!erone re#ease

An+io!ensin II

De(reased rena#per1usion

FEARS!imu#a!ion o1 #im"i(

area o1 "rain

Increased2),po!)a#ami(-

adrenomedu##ar,adreno(or!i(a# a(!i3i!,

Neuroendo(rine Respons


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RESPON HEODINAIKMekanisme untuk memperbaiki keseimbangan

kardiovaskular

Redis!ri"usi a#iran dara)

Penin+ka!an 4(ardia( ou!pu!5

emper"aiki 3o#ume in!ra3asku#ar


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STIULASI NEUROENDOKRIN

H$POTENSION

BLOOD FLO6 PROTECTEDHear!Brain

Adrena#*pi!ui!ar, +#and

BLOOD FLO6 DECREASEDSkin

us(#eSp#an()ni( (ir(u#a!ion

RESPON HEODiNAiKREDISTRIBUSI ALIRAN DARA


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CARDIAC OUTPUT 7 HR 8 S%

S,mpa!)e!i( n9 s,s!emCa!e()o#amine

re#ease

In(rease ED% 3ia!enoconstriction

Arteriolar constrictionRenal reabsorption

In(reased(on!ra(!i#i!,

Limi!ed !o :;< "ea!s*min"e1ore de(reased CO due !o

de(reased dias!o#i( 1i##in+!ime


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Trans(api##ar, re1i## p)ase"# Decreased capillar$ pressure caused b$ %$potension

S$mpat%etic increase in precapillar$ arteriolar constriction

Decrease capillar$ %$drostatic pressure promotes passage o' ''rom interstitium to intravascular space

P#asma pro!ein res!i!u!ion p)aseIncreased plasma osmolarit$ due to mainl$ %epatic release o

glucose( p$ruvate( amino acids( etc#

Increased interstitial osmolarit$

Increased interstitial volume and pressure

Transcapillar$ movement o' albumin into intravascular spac


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HAEOD$NAIC RESPONSES%eno(ons!ri(!ion

S$mpat%etic n# s$stem )SNS*+atec%olamines )+A*Angiotensin II )ATII*

AD

Redu(ed 3enous(apa(i!an(e

Ar!erio#ar (ons!ri(!ionSNS( +A( ATII( AD

De(reased (api##ar, P

F#uid s)i1! 1rom in!ers!i!ium in!o3as(u#ar (ompar!men!

In(reased dis!a# !u"u#arrea"sorp!ion

A#dos!erone- ADH

In(reased pro0ima# !u"u#arrea"sorp!ion

SNS- CA- ATII

In(reased m,o(ardia#(on!ra(!i#i!,

SNS- CA

Res!ora!ion o1"#ood 3o#ume

In(reased

3en!ri(u#ar1i##in+ P

In(reased 3en!ri(u#are=e(!ion 1ra(!ion

S%

CO

BPIn(reased )ear! ra!e

SNS- CA

In(reased S%R due !oar!erio#ar (ons!ru(!ion

SNS- CA- ATII- ADH

S%R


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RESPON ETABOLIK

H,per+#ikemia

o"i#isasi #emak

Ka!a"o#isme*peme(a)an Pro!ein,eningkatan sintesis urea,eningkatan asam amino aromatik

Penurunan sin!esis rea(!an 1ase aku!

Penin+ka!an osmo#a#i!as eks!rase#


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RESPON ETABOLIK

Breakdo&n o1ske#e!a# mus(#e

in!o a9a9

Con3ersiono1 a9a9 !o+#u(ose

Re#ease o12Ca!e()o#aminesCor!iso#G#u(a+onGro&!) )ormone

Impairedperip)era#

+#u(ose up!ake

H$PERGL$CEIA

G#,(o+en

"reakdo&n


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EFEK SHOCK PADA TINGKATAN SEL

H$PO8IA

LO6'FLO6-

POOR PERFUSION

ANAEROBIC

ETABOLIS

ACIDOSIS

DECREASED CELLULARENERG$ EFFICIENC$


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CELL EBRANE FAILURE2

DIRECTEndoto-in+omplement

INDIRECT.ailure to maintain normal Na/( 0/or +a&/gradientDecreased o-idative p%osp%or$lation

OSOTICGRADIENT

6a!er en!r,in!o (e##

CELLULAREDEA

IPAIREDINTRACELLULAR

ETABOLIS

CELL

DEATH

Na>en!r,in!o (e##

EFEK SHOCK PADA TINGKATAN SEL


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Kidne,

1liguric renal 'ailureig% output renal 'ailure

Li3erLiver 'ailure

GI !ra(! .ailure o' intestinal barrier )sepsis( bleeding*

Lun++apillar$ leak associated 2it% or caused b$ sepsis andin'ection

EFEK SHOCK PADA TINGKATANORGAN


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PRINSIP RESUSITASI

emper!a)ankan 3en!i#asi

enin+ka!kan per1usi

Terapi pen,e"a"


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AINTAIN %ENTILATIONIn(reased o0,+en

demand

H,per3en!i#a!ion

Respira!or, 1ai#ureRespira!or, a(idosis- #e!)ar+,'(oma- ),po0ia

Espe(ia##, in2

SepsisH,po3o#emia

Trauma

Respira!or, 1a!i+ueDi3ersi "#ood 1#o& 1rom

3i!a# or+an

Or+an in=ur,


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H,po3o#emia ."#ood #oss/

De(reased CO

De(reased o0,+en de#i3er,- in(reasedo0,+en re?uiremen!

e!a"o#i( a(idosis- ),po0emia!a(),pnea

TREATENT2Primar, resus(i!a!ion

O0,+ene()ani(a# 3en!i#a!ion i1 needed

TREATENT OF RESPIRATOR$ FAILURE


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TREATENT CONCEPT OF SHOCK

ENHANCING PERFUSION * O8$GEN DELI%ER$

O0,+en de#i3er,*DO@7HR 8 S%8 H" 8 S H" 8 paO@

Cardia(ou!pu!

Ar!eria# O@(on!en!

F#uids Trans1use Par!ia##,dependen! on

FIO@andpu#monar,

s!a!us

Ino!ropes

DO@7 CO0 CaO@


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.HERA/E8.IC GOA2S IN SHOCK

Incras O? dli0ry

Optimi1 O? contnt of "lood

Impro0 cardiac output and"lood prssur

&atc' systmic O? nds wit' O? dli0ry

R0rs+pr0nt or%an 'ypoprfusion


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CARDIOGENIC SHOCK&ANAGE&EN.

.rat arr'yt'mias

Diastolic dysfunction mayr!uir incrasd llin%prssurs

7asodilators if not 'ypotnsi0 Inotrop administration


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CARDIOGENIC SHOCK&ANAGE&EN.

7asoprssor a%nt ndd if'ypotnsion prsnt to raisaortic diastolic prssur

Consultation for mc'anicalassist d0ic

/rload and aftrload rductionto impro0 'ypo$mia if "loodprssur ad!uat


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F28ID .HERA/4

Crystalloids 2actatd Rin%r5s solution

Normal salin

Colloids Htastarc'

Al"umin

Glatins

/ac)d rd "lood clls

Infus to p'ysiolo%ic ndpoints

F28ID .HERA/4


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F28ID .HERA/4

Corrct 'ypotnsion rst Dcras 'art rat

Corrct 'ypoprfusion a"normalitis

&onitor for dtrioration of o$y%nation

INO.RO/IC + 7ASO/RESSOR AGEN.S


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Dopamin 2ow dos


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INO.RO/IC AGEN.S

Do"utamin

J6? %+)%+min

Inotropic and 0aria"l c'ronotropiccts

Dcras in systmic 0ascularrsistanc


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INO.RO/IC + 7ASO/RESSORAGEN.S

Norpinp'rin

3J %+)%+min and titrat toct

Inotropic and 0asoprssor

cts /otnt 0asoprssor at 'i%'

doss


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Epinp'rin

9ot' and actions for inotropicand 0asoprssor cts

3 %+)%+min and titrat

Incrass myocardial O?

consumption

HO &8CH F28ID .O GI7EL


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HO &8CH F28ID .O GI7EL

Som masur of intra0ascular llin% /rssur


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HA. DO 4O8 NEED .O KNO HEN4O8 RES8SCI.A.E A /A.IEN. IN

SHOCKL

Artrial "lood prssur 8rin output Systmic acid>"as "alanc


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+ardiac 1utput - S!R

Pipe3!ascularPump 7

eart

%o#ume3

Blood

$povolemic

S%ock

+ardiogenic

S%ockDistributive

S%ock

Inotropes

)Dob(Dop(Adr(Amr*!asopressor ) NE(,E(Adr(Dop*

.luids

1bstructive

S%ock

Release

tamponade(etcBlood ,ressure


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SUAR$ S)o(k is an a#!ered s!a!e o1 !issue per1usion se3er

!o indu(e deran+emen!s in norma# (e##u#ar 1un(!io

Neuroendo(rine- )emod,nami( and me!a"o#i( ()a!o+e!)er !o res!ore per1usion

S)o(k )as man, (auses and o1!en ma, "e dia+nossimp#e (#ini(a# indi(a!ors

Trea!men! o1 s)o(k is primari#, 1o(used on res!oriper1usion and o0,+en de#i3er, &)i#e e#imina!in+ !)

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Kuliah Shock Cardiogenic