llND\H|l|\N

SINDROM KLINIS
KEGAGALAN SISTEM SIRKULASI
KEBUTUHAN OKSIGEN
NUTRIEN JARINGAN
DEFISIENSI AKUT
DITINGKAT SEL
: SYO| l\D\ \N\|
|cuduun uu! dururu!

/ mcrb!d!!us mcr!u!!!us
% 8O h!pcvc!cm!k
/ . Svck kcmpcnsus! su!!! d! D c k
mun!cs!us! k!!n!s !uk ]c!us
( rc!cks s!mpu!!s Rcd!s!r!bus!
. sc!ck!! u! ducruh dur! crun
pcr!cr ncn- , , v!!u! kc ]un!un puru
) c!uk
: Tu]uun lr!mcr lcnc!c!uun Svck

- ( ) lrc!cud rcsus!!us! vc!umc

- |cn!ruk!!!!!us

- Rcs!s!cns! pudu s!s!cm!k

DllTNTST SYO|
DllTNTST SYO|

STNDROM |lTNTS \|Tl\T |lG\G\l\N STSTlM
: STR||l\ST |NT|| MlNC|||lT

v
Nutrisi
vOksigen
Pasokan
utilisasi
Metabolisme
Jaringan tubuh
Defisiensi 02 Seluler
l|NGST STSTlM STR||l\ST
l|NGST STSTlM STR||l\ST

Jantung
Pemu!u" Dara"
#$!ume Dara"

Curah jantung
&
adekuat
Aliran darah
Metabolisme
jaringan
Metab
olit
Eliminasi Di Organ
Pembuangan
llNG\T|R\N C|R\H J\NT|NG
llNG\T|R\N C|R\H J\NT|NG
D\N Tl|\N\N D\R\H
D\N Tl|\N\N D\R\H
PE!OAD CO"#AC#$!$#% A&#E!OAD
'EA# A#E S#O(E )O!*ME
CAD$AC O*#P*# S%S#EM$C )ASC*!A ES$S#A"CE
+!OOD PESS*E
llNG\NG||T\N O|STGlN
llNG\NG||T\N O|STGlN
Cardia, Out Put +lood flo-
O./gen
Deli0er/
+lood O
2
Content
'b Contentration
O
2
+ound to 'b
O
2
Dissol0ed in Plasma
|l\STlT|\ST SYO|
|l\STlT|\ST SYO|
MlN|R|T lTTOlOGT
MlN|R|T lTTOlOGT
v SYO| HTlO\OllMT|
v SYO| DTSTRTl|TTl
v SYO| |\RDTOGlNT|
v SYO| SllTT|
v SYO| OlSTR||TTl
ST\DT|M SYO|
ST\DT|M SYO|
: l\Sl T |OMllNS\ST
: l\Sl T |OMllNS\ST
Mckun!smc |cmpcnsus! Tubuh rc!cks!
s!mpu!!s

- Rcs!s!cns! s!s!cm!k

: ; , , HR ku!!! d!n!n pucu!

. , , cup rc!!! !cr!umbu! nud! !cmuh
. !ck nud! scmp!!

( ) Tckunun duruh N

- Tckunun D!us!c!!k

- Rcs!s!cns! pcmbu!uh duruh

: ( <), sp!unkn!k G!n]u! D!urcs!s Su!urun
( , ) ccrnu mun!uh !!cus

: ( ) l\Sl TT Dl|OMllNS\ST !
: ( ) l\Sl TT Dl|OMllNS\ST !
% Mckun!smc kcmpcnsus! uu!
- Mc!ubc!!smc unucrcb!k
- \sum !uk!u! us!dcs!s >>
!crbcn!uk usum kurbcnu!
!n!rusc!u!cr
- |cn!ruk!!!!!us c!c! ]un!un
- lcmpu Nu | sc!

Tn!cr!!us mcmbrun sc!

|crusukun sc!
: ( ) l\Sl TT Dl|OMllNS\ST ?
: ( ) l\Sl TT Dl|OMllNS\ST ?
\!!run duruh !umbu!

\rcus! Trcmbcs!!
lcmbcn!ukun Trcmbus
lcnduruhun
lc!cpusun Mcd!u!cr

\uscd!!u!us! \r!cr!u!

|cnu!kun lcrmcub!!!!us |up!!cr

\R
Fase dekompensasi
Perfusi jaringan indekuat disertai hipotensi

Kesadaran menurun krn perfusi ke otak

menurun

Hipotensi sebagai tanda terakhir dari syok

Untuk anak 1-10
th
: <0 mmHg !"umur#thn
$ %& mmHg
: l\Sl TTT TRl\lRSTlll
Kerusakan & Kematian Se!
Dis'ungsi sistem mu!ti $rgan
(a)angan '$stat E* Tinggi

+ He,ar- Jantung .

Tckunun duruh !uk

!crukur

Nud! !uk !crubu

|csudurun

Anuria

GMO
k'inis
llRJ\l\N\N l\TOlTSTOlOGT SYO|
llRJ\l\N\N l\TOlTSTOlOGT SYO|
Septic Shock Cardiogenic Shock
Hypovolemic Shock
Capillary Leak Mediators
Myocardial
Depression
Preload Vasodilatation Contractility
Cardiac Output
Blood Pressure
Sympathetic Discharge
Vasoconstriction,

H Contractility
!mproved Cardiac
output and "lood
pressure
COMP#$S%&#D
D#COMP#$S%&#D
Myocardial per'usion
Myocardial O
(

Consumption
Cardiac
Output
Mediator elease
Cell )unction
Cell Death Death o' Organism
&issue !schemia
Loss o' %uto
regulation o'
Microcirculation
COMP#$S%&#D
Vasoconstriction
H Contractility
(yok Hipo)o'emik
*tio'ogi: +iare, perdarahan, muntah, intake
tak adekuat, diuresis osmotik, 'uka bakar

'%PO
)O!
S'OC(
PE!OAD 1
A&#E!OAD 2
CO"#AC#$!$#%
" 3 2
(yok hipo)o'emik

Primar/ Assessment0 Fin)ing

A

B -akhipneu tanpa pe. /01

( -akhikardi

-ek2+rh 3# hipotensi dgn

tek2nadi sempit

3adi 'emah,ke4i' #tak teraba

Pengisian kapi'er 'ambat

ku'it dingin,pu4at

Kesadaran menurun

0'iguria

D Kesadaran menurun

+istributi)e (ho4k
Distributi0
e
sho,k
PE!OAD
" 3 2
CO"#AC#$!$#%
" 3 1
A&#E!OAD
)ariable
Findings of +istributi)e (ho4k
Primar/ Assessment Fin)ing
A Patent air5ay, un'ess un4on42
B -a4hypnea 5ithout ./01, e$4ept
4aused by pneumonia, 67+(, pu'm edema
( -a4hy4ardia, Hypotension 5ith 5ide
pu'se pressure"5arm sho4k& or narro5 p2pressure"4o'd
sho4k& or normotension8 1ounding perphera' pu'se,
+e'ayed 4ap2refi'', /arm9f'ush skin"5arm sho4k& or
pa'e skin"4o'd sho4k&: :hanges in menta' status8
o'iguria
D :hanges in menta' status

(epti4 (ho4k
PE!OAD
11
CO"#AC#
$4
!$#% 13 "
A&#E!OAD
)A$A+!E
:onsensus +efinitions and 4'ini4a'
:hara4teristi4 of Ped2(epsis
S/stemi1 In'!ammat$r/ Res,$nse
S/n)r$me + SIRS .
Se,sis
Se2ere Se,sis
Se,ti1 s"$1k
(;7(
:ore temp of <=>2?@: or <=A@:
-a4hy4ardia <%(+ abo)e norma' for age,
for 4hhi'dren <1 year brady4ardia <10
th

per4enti'e for age
Bean 77<%(+ abo)e norma' for age
Ceu4o4yte 4ount . or D for age or 10E
immature neutrophi's
" 6t 'east % of the F 4riteria &
(*P(;( :

(;7( in the presen4e of, or as a resu't of,

suspe4ted or pro)en infe4tion
(e)ere sepsis
(epsis p'us either 4ardio)as4u'ar
dysfun4tion or 67+(

0r
(epsis p'us % or more other organ fai'ures
7F as sign of organ dysfun4tion
in sepsis
Pa0%#Fi0% <=00 in absen4e of :H+ or
'ung disease
Pa:0% <A? mmHg or %0 mmHg abo)e
base'ine
Pro)en need Fi0% <?0E to maintain (a0%
<G%E
3eed none'e4ti)e BH "in)asi)e or
nonin)asi)e&
(epti4 sho4k
(epsis and

:ardio)as4u'ar dysfun4tion despite

administration of isotoni4 i) bo'uses < F0
m'#kg in 1 hour
:ardio)as4u'ar dysfun4tion
Hypotension "(1P <?
th
per4enti'e for age or (1P
<%(+ be'o5 norma' for age or

3eed for )asoa4ti)e drug to maintain 1P in

norma' range or

-5o of the fo''o5ing 4hara4teristi4 of inadeIuate

organ perfusion:

;nadeIuate organ perfusion

Une$p'ained metabo'i4 a4idosis: base
defi4it < ?meI#'
;n4rease arteria' 'a4tate < t5i4e the upper
'imit of norma'
0'iguria: Urine output02? m'#kg#hour
Pro'onged 4ap refi'': < ? se4ond
:or to periphera' temp gap < =@:
SEP#$C
S'OC(
PE!OAD
DECEASE
CO"#AC#$!$#%
" 3 DECEASED
A&#E!OAD
)A$A+!E
. TTT SYO| |\RDTOGlNT|
. TTT SYO| |\RDTOGlNT|

: l!!c!c!
luscu lcduh lcnvuk!! Jun!un luuun
M!ckurd!!!s
/ Tnurk Tskcm!k Jun!un
/ |urd!cm!cpu!! lr!mcr Sckundcr
, H!pc!!kcm!u Gunuun Mc!ubc!!k
, \s!ks!u Scps!s
CAD$O5E"$
C
S'OC(
PE!OAD
)A$A+!E
CO"#AC#$!$#%
DECEASED
A&#E!OAD
$"CEASED
Ml|\NTSMl SYO| |\RDTOGlNT|
Ml|\NTSMl SYO| |\RDTOGlNT|
Cardiogeni,
Sho,k
Contra,tilit/
CO
+P
Metaboli, a,idosis6 h/7o.ia6
M/o,ardial de7ressant fa,tor
Com7ensator/ me,h8
Afterload
S)
SYO| |\RDTOGlNT|
SYO| |\RDTOGlNT|
Curd!uc \cn!r!cu!ur lcrcrmuncc
: luc!cr Dc!crm!nun!

. u lrckucns! dun Trumu Jun!un

. b lrc!cud dun \!cr!cud

. c |cn!ruk!!!!!us M!ckurd
|cmpcnsus! Tubuh Sc! lcrpc!uu!!n
Cvc!c

Svck lrcrcs!
Mcmburuk
Findings of :ardiogeni4 (ho4k
Primary 6ssessment Finding
6
1 -a4hypnea8 /01.
: -a4hy4ardia8 3#'o5 1P 5ith
a narro5 pu'se pressure8 5eak or absent of
periphera' pu'se8 3 and then 5eak 4entra'
pu'ses8+e'ayed 4ap refi'' 5ith 4oo' e$tremities8
(igns of :HF8 4yanosis":H+#pu'm2edema&8
*nd-organ Fun4tion " :o'd, pa'e skin, o'iguria&
+ :hanges of menta' status

0bstru4ti)e (ho4k
:ardia4 tamponade
-ension pneumothora$
+u4ta' J dependent 4ongenita' heart 'esions
Bassi)e pu'monary embo'ism
:ardia4 tamponade
Buff'ed or diminished heart sound
Pu'sus parado$us"de4rease in systo'i4 1P
by more than 10 mmHg during
inspiration
+istended ne4k )ein
N$te0 ("i!)ren '$!!$3ing 1ar)ia1
surger/- D& n)istinguis"a!e 'r$m
1ar)i$geni1 s"$1k- E1"$0 im,$rtant
-ension pneumothora$
Patients 5ith 4hest trauma, or any intubated 4hi'd
5ho deteorates sudden'y during PPH
Hyperresonan4e on the affe4ted side
+iminished breath sounds on the affe4ted side
+istended ne4k )ein
-ra4hea' de)iation to5ards 4ontra'atera' side
7apid deteoration in perfusion and rapi 4hange
from ta4hy4ardia to bradi4ardia
Pat"$genesis an) Pat"$,"/si$!$g/ $' Se,sis
Ne3 ($n1e,t a$ut SIRS- SEPSIS- (ARS- MARS
Pro-
inflammatory
response
Anti-
inflammatory
response
Systemic Reaction:
SIRS (pro-
inflammatory)
CARS (anti-
inflammatory)
MARS (mixed)
Systemic spillover of
pro-inflammatory
mediators
Systemic spillover of
anti-inflammatory
mediators
Initial insult
(bacteria viral traumatic t!c mal)
Cardiovascular
Compromise
s!oc"
SIRS pre-
dominates
#omeostasis
CARS and
SIRS
balanced
Apoptosis
(cell deat!)
$eat! %it!
minimal
inflammation
&r'an
dysfunction
SIRS
Pre-
dominated
Suppression
of t!e
immune
system
CARS
pre-
dominated
SllSTS D\N G\NGG|\N |O\G|l\ST SllSTS D\N G\NGG|\N |O\G|l\ST
Scps!s
Tn!ummu!crv
cv!ck!ncs
- Tl G - TNl
T!ssuc uc!cr
Mcd!u!cd
uc!!vu!!cn c
ccuu!u!!cn
Tnh!b!!!cn c
phvs!c!c!cu!
un!!ccuu!un!
pu!huvs
Dcprcss!cn
c
!br!nc!vs!s
duc !c h!h
!cvc!s c
- l\T !
lnhunccd !br!n
crmu!!cn
Tmpu!rcd !br!n
rcmcvu!
M!crcvuscu!ur
!hrcmbcs!s
- CYTO|TNl MlDT\TlD l\THOGlNlTTC - CYTO|TNl MlDT\TlD l\THOGlNlTTC
l\TH"\YS c MTCRO\\SC|l\R THROMlOSTS l\TH"\YS c MTCRO\\SC|l\R THROMlOSTS
!n SllSTS !n SllSTS
Scps!s
\c!!vu!!cn c
ccuu!u!!cn
"!dcsprcud
!br!n
Dcpcs!!!cn
Ccnsump!!cn
c p!u!c!c!s
und c!c!!!n
uc!cr
M!crcvuscu!ur
!hrcmbcs!s
l!ccd!n
( ) scvcrc
M\NTllST\ST |lTNTS SYO| SllTT|
M\NTllST\ST |lTNTS SYO| SllTT|
v STADIUM KOMPENSASI

% Resistensi #asku!er

% (ura" Jantung

% Tak"ikar)ia

% Ekstermitas Hangat

% Di2resis N$rma!
v STADIUM DEKOMPENSASI

% #$!ume Intra2asku!er

% De,resi Mi$kar)

% Eksterna! Dingin

% Ge!isa"- Anuria- Distres Res,irasi

% Resistensi #asku!er

% (ura" Jantung
v STADIUM IRE#ERSIBEL

% GMO

Mcs! Ccmmcn lu!hccns !n Ch!!dhccd luc!cr!u! Mcs! Ccmmcn lu!hccns !n Ch!!dhccd luc!cr!u!
Scps!s Scps!s
%ge *roup Pathogens %ntimicro"ial
+Pending culture,
!nitial dose
+mg-kg,
. / 0 months *roup B Strept1 #ntero"acteriaceae
Staph1 %ureus
Listeria meningtides
%mpiciline 2
*entamicin
Ce'ota3ime
4.
(14
45.
0 / (6 months H1 in'luen7ae, Strept1 Pneumoniae
S1 aureus, $eisseria meningtidis
*roup B Streptococcus
Ce'ota3ime
%mpiciline 2
Chlorampenicol
4.
4.
(4
8 (6 months S1 Pneumoniae
H1 !n'luen7ae
S1 %ureus
$1 Meningtidis
Ce'ota3ime
Ce'ria3one
%mpiciline 2
Chlorampenicol
4.
4.
4.
(4
!mmuno
compromised
S1 aureus, Proteus
Pseudomonas
#ntero"acteriaceae
Vancomycin 2
Ce'ta7idime 2
&icarcillin
(4
4.
94
llN\T\l\|S\N\\N SYO|
llN\T\l\|S\N\\N SYO|

1. 2.
Oksigenasi
CaO
2

SaO
2
9: ; <00 =
Sistem
:1V
a8Preload
> resusitasi 0olume ?
b8Atasi Disritmia
,8(oreksi keseimbangan
asam 4 basa
Jalan nafas Oksigen

TlR\lT C\TR\N l\D\ SYO|
TlR\lT C\TR\N l\D\ SYO|

%:S#S V#$% +;. detik,< &ak "erhasil !O

:!S&%LO!D dan atau :OLO!D

0. / =. ml - kg B1B +>50. menit,

diulang ( / = kali

S?O: S#P&!: >. / 0.. ml - kg B1B

+dalam > @am pertama,

&H# 0
st
CO$S#$SAS CO$)##$C#

on CCM 0;;9

+S?O: S#P&!:,

a1 :oloid terapi inisial, dilan@utkan

koloid-kristaloid

"1 Dipandu B respons klinis,per'usi, peri'es, tvs,

tekanan sistem,M%P
\!cr!!mc Tcrup! Cu!run ludu Svck \!cr!!mc Tcrup! Cu!run ludu Svck
Suspected shock
Hypovolemia, Hypoper'usion, &achycardia
0. / =. mL Cryst-Colloid - kg - > /
0. min
$ormotensive
Hypotensive
!n Sepsis B
%nti"iotics,
!munotheraphy
!n %naphylaksis B
Catekolamin,
steroid,
antihistamin
Arine 8 0 ml-kg-hr
0.5(. mL
crys or
coll-kg-0.
min
%nuria
Arine C 0 ml-kg-hr
Arine output C 0 ml-kg-hr
eevaluated 0. mL D1tal-kg 0. mL D1tal-kg 0./(. mL D1tal-kg
eevaluated 0. mL D1tal-kg 0. mL D1tal-kg 0.5(. mL D1tal-kg
!mproved
eevaluated
!mproved
eevaluated
Hypotensive, urine C 0 mL-kg-hr
CVP C 0. mmHg CVP,
Cardiac status,
chest D5ay,
#chocardiography
CVP 8 0. mmHg
%'terload reduction,
inotropic support,
consider pulmonary
0.5(. mL D1tal-kg
eevaluated
Ear!/ G$a! Dire1te)
Ear!/ G$a! Dire1te)
T"era,/ ,a)a S/$k Se,tik
T"era,/ ,a)a S/$k Se,tik
*ar'y aggressi)e f'uid therapy ":rysta'oid or
4o''oid& n U w t n
ours o m ss on
V sopr ssors notrop
ru s w n r s st n
to lu t r p
n po nts oo
p r p r l p r us on
on ousn ss
p ll r l n
t m < rm
tr m t s
uls pr ssur !
or :HP >-1% mmHg,
ur s s ml ()40% <
0E
6dmission to P;:U 5hen stabi'iKed
Supplemental oxy'en
endotrac!eal intubation and
mec!anical ventilation
Central venous and
arterial
cat!eteri(ation
Sedation paralysis
(if intubated) or bot!
)oals
ac!ieve
d
Scv&*
MAP
C+P
#ospital admission
,--* mm#'
. /0 and 1 23 mm#'
. 435
6es
7o
Crystalloid
Colloid
8 , mm#'
+asoactive a'ents
8 /0 mm#'
9 23 mm#'
:ransfusion of red cells
until !ematocrit . ;35
Inotropic a'ents
8 435
Pr$t$1$! '$r Ear!/
G$a!%Dire1te)
T"era,/
F!ui) T"era,/
in Se,sis an) Se,ti1 S"$1k
Type of
Type of
Fluid
Fluid
Colloid
Colloid
Crystalloi
Crystalloi
d
d
Volume
Volume
60 100
60 100
ml/kg
ml/kg
(6 hours)
(6 hours)
CO , estore !"
CO , estore !"


#OF
#OF
$notro7i,
)aso7ressor

+S?O: :%D!O*#$!:, B
)luid Chalenge hati / hati B
a1 memper"aiki kontraktilitas @antung
"1 dipantau ketat dengan &VS
lck vc!umc !nus ! l kc!c!d pudu
lck vc!umc !nus ! l kc!c!d pudu
( ) kcmpur!cmcn !ubuh O k
( ) kcmpur!cmcn !ubuh O k
Larutan Vol1 Plasma Vol1 !nters !1!ntrasel
%l"umin 4E 0... 5 5
Hemacel 9.. =.. 5
*ela'undin 0... 5 5
Plasma'usin 0... 5 5
De3tran 6. 0>.. +5(>., +5=6.,
De3tran 9. 0=.. +50=., +509.,
#3pa'usin 0... 5 5
H%#S steril >E 0... 5 5
H%#S steri0.E 064. +564., 5
\DRlN\l TNS|llTSTlNST
\DRlN\l TNS|llTSTlNST
l\D\ SYO|
l\D\ SYO|

SllTT|
SllTT|

KORTIKOSTEROID

Pada syok septik, bila refrakter thdp

dopamin/adrenalin/nor-adrenalin
munkin ter!adi I"S#$ISIE"SI %DRE"%&
'ydro(ortisone )*m +bolus,,
dilan!utkan --. m/k/// .0 !am1 )-2 hari

TlR\lT S|lORTTl
TlR\lT S|lORTTl
v
Substitusi faktor koaulasi +pada
'emodilusi/PI3, 4

- $resh $ro5en Plasma

- 6yropre(ipitate
v
Tranfusi 3asif setiap ) 7 8 unit P6 ditambah .
unit $$P
v
$ibrinoen 9 -** m/dl +tak respons terhadap
$$P, 4 - 6yro pre(ipitate 0 unit/-* k //
v
Konsentrat trombosit diberikan 4

Trombositopeni berat 9 :*;*** denan

perdarahan atau tindakan in<asif 4 - Konsentrat
Trombosit

TM|NOTlR\lT
TM|NOTlR\lT
Tranfusi tukar pada sepsis 4

- memperbaiki oksienasi !antun

- meneluarkan mediator dan endotokin

Immunolobulin +I;=, pada sepsis
'emofiltrasi dan Plasmafiltrasi 4
meneluarkan endotoksin, mediator


menurani respons inflamasi sistemik
+SIRS,
l|NGST ORG\N
l|NGST ORG\N
. \ : l\R|

Sup!u! Oks!cn udckuu!

- / . Tn!ubus! pcmusunun \ mckun!k d!n! pudu

svck

scp!!k

- , lcmbcr!un cu!run rcsus!!us! b!!u !cr!u!u

/ bunvuk

urcs! rcs!kc !!n! cdcmu puru

. l : OT\|

- , H!ndur! h!pcks!u h!pc!!kcm!u

- ( ) H!ndur! h!pcrkupncu dcnun vcn!!!u!cr

- : lcr!uhunkun pcrus! scrcbru!

. u vc!umc !n!ruvusku!ur

. b CO

. / c Hb !ckunun duruh udckuu!

- , - lcmun!uuun kudur Nu scrum kcrcks! hu!!

hu!!
( ) l|NGST ORG\N !un]u!un
( ) l|NGST ORG\N !un]u!un
. C / STR||l\ST Sll\N|HNT| S\l|R\N ClRN\

- , , Rcsus!!us! vc!umc cp!!mu!!su! CO

!ckunun duruh

- ( / ) |crcks! h!pc!cns! vuscprcscr !nc!rcp!k

- N|TRTST lNTlR\l DTNT

. D GTNJ\l

- , , Rcsus!!us! vc!umc cp!!mu!!sus! CO

!ckunun duruh

- |crcks! h!pc!cns!

- |crcks! h!pcks!u dun uncm!u bcru!

- H!ndur! cbu!- cbu!un ncrc!cks!k

T\T\l\|S\N\ SYO| |\RDTOGlNT|

T\T\l\|S\N\ SYO| |\RDTOGlNT|
Oks!cnus! \dckuu!
|crcks! GGN \sum lusu dun l!ck!rc!!!
|urun! Rusu Suk!! dun \ns!c!us
\!us! D!sr!!m!u Jun!un
: |c!cb!hun lrc!cud D!urc!!ku
: |cn!ruk!!!!!us l!u!d Chu!!cnc
/ (") Scsuu! C\l lO\l Obu! Tnc!rcp!k
( ) : lcbun \!cr!cud S\R \uscd!!u!cr
|crcks! lcnvcbub lr!mcr
Ccmmcn!v |scd Curd!cvuscu!ur Drus !n Shcck Ccmmcn!v |scd Curd!cvuscu!ur Drus !n Shcck
Svndrcmcs Svndrcmcs
Drug D$se
+ ug&kg&min .
($mment
Inotropioc agents
N$re,"rine
+ % a)renergi1 .
4*45 6 7*4 F$r ,r$'$un) "/,$tensi$n n$t res,$n)ing
t$ '!ui) $r $t"er in$tr$,i1 )rugs
E,"ine,"rine
+ % an) % a)renergi1 .
4*45 6 7*4 D$se re!ate) res,$nse- "ig"er )$ses 1ause
2as$1$nstri1ti$n* Use'u! in maintaining (O
an) BP in,atients unres,$nsi2e t$
)$,amine $r )eutamine
Is$,r$teren$!
+ % a)renergi1 .
4*45 6 4*5 In)i1ate) in ra)/1ar)ia unres,$nsi2e t$
atr$,ine i' in1rease in "eart rate is n$t
e81essi2e- ma/ e "e!,'u! in rea1ti2e
,u!m$nar/ "/,ertensi$n
D$,amine
+ % an) %
)$,aminergi1 .
7 6 94 (ar)i$2as1u!ar e''e1ts are 1$m,!e8 an)
)$se re!ate)* L$3 )$se in'usi$n 1an rest$re
1ar)i$2as1u!ar stai!it/ an) im,r$2e rena!
'un1ti$n
#( ) Ccmmcn!v |scd Curd!cvuscu!ur !un]u!un #( ) Ccmmcn!v |scd Curd!cvuscu!ur !un]u!un
Drug D$se
+ ug&kg&min .
($mment
D$utamine
+ % an) % a)renergi1 .
7 6 94 P$siti2e in$tr$,i1 e''e1t 3it" minima!
1"anges in "eart rate $r s/stemi1 2as1u!ar
resistan1e
Amrin$ne 7 6 74 Initia! $!us in'usi$n ma/ e re:uire)*
Limite) )ata a2ai!a!e in 1"i!)ren
Vasodilators
Nitr$,russi)e 4*445 6 ; Ba!an1e) arteria! an) 2en$us )i!at$r*
Ma/ resu!t in t"i$1/anate $r 1/ani)e
t$8i1it/
P"ent$!amine 7 6 94 (auses )i!atati$n $' arteria! an) 2enus
e)s* In)ire1t in$tr$,i1 e''e1t ma/ 1ause
1$m,ensat$r/ ta1"/1ar)ia
Nitr$g!i1erine 4*5 6 94 #enus )i!at$r* D$se n$t 3e!! esta!is"e)
'$r in'ants an) 1"i!)ren
MONTTORTNG
MONTTORTNG
- S!u!c c Ccns!cusncss G!usc Ccmu Scu!c
Rcsp!ru!crv Ru!c und Churuc!cr
: Curd!cvuscu!ur lurumc!crs

. u Sk!n und Ccrc Tcmpcru!urc D!crcncc

. b lu!sc Ru!c und \c!umc

. c l!ccd lrcssurc

. d Cup!!!urv lcrus!cn T!mc

. c Ccn!ru! \cncus lrcssurc Shcu!d lc

Mcn!!crcd !n

lu!!cn! "hcrc Thcrc Hus lccn lccr

Rcspcnsc

Tc l!u!d Thcrupv Or "!!h ls!ub!!shcd

Shcck
|r!nurv Ou!pu!- , |r!nc lu Or lrccrub!v
; - / Cu!hc!cr Ou!pu! Shcu!d lc ! ? m! k lcdv
"c!h!
lu!sc Ox!mc!rv
SvcO?
|lY lOTNTS TN M\N\GlMlNT
|lY lOTNTS TN M\N\GlMlNT

emem"er BP and pulse are unrelia"le indicators in

early septic shock

Look 'or minor degrees o' mental impairment

+an3iety,restlessness,

Do not delay treatment, try to prevent the onset o'

hypotension, meta"olic acidosis, and hypo3ia

*ive adeFuate 'luids early in treatment, especially

colloids

Do not use inotropic agents until the patients has

received adeFuate 'luid therapy

Monitor "lood glucose, gases, and PH, and treat

appropriately
/ RTNG|\S\N |lSTMl|l\N
/ RTNG|\S\N |lSTMl|l\N
Syok merupakan keadaan a>at darurat, serin ditemukan
pada anak
3orbiditas dan mortalitas syok masih tini
Syok hipo<olemik, palin serin ter!adi pada anak
+?*@,, sisanya syok kardioenik
Dianosis syok dini sulit, tetapi pentin diketahui melalui
pemahaman patofisioloi syok +stadium kompensasi,
dekompensasi dan ire<ersibel,

Penelolaan syok bertu!uan meninkatkan DO

.
melalui pe
6O yaitu 4

-; 3emperbaiki prabeban denan resusitasi <olume

.; 3e kontraktilitas !antun dan

:; 3e S=R
Denan pemahaman patofisioloi, dianosis dini dan
memperhatikan Akey manaementA syok, diharapkan
dapat me mortalitas syok