Diagnosis And Management Of

Shock
Shock
Always a symptom of primary cause
Inadequate blood flow to meet tissue oxygen demand
May be associated with hypotension
Associated with signs of hypoperfusion: mental status change, oliguria, acidosis
Definisi
Gangguan dari perfusi jaringan yang terjadi akibat adanya ketidakseimbangan
antara suplai oksigen ke sel dengan kebutuhan oksigen dari sel tersebut
!emua jenis shock mengakibatkan gangguan pada perfusi jaringan yang selanjutnya
berkembang menjadi gagal sirkulasi akut atau disebut juga sindroma shock
Its not Low Blood Pressure!!
Its Hypoperfusion!!
Shock Categories
Cardiogenic Decreased contractility
Increased filling pressures, decreased LV stroke work, decreased cardiac
output
Increased systemic vascular resistance compensatory
Hypovolemic Decreased cardiac output
Decreased filling pressures
Compensatory increase in systemic vascular resistance
Distributive Normal or increased cardiac output
Low systemic vascular resistance
Low to normal filling pressures
Sepsis, anapyla!is, neurogenic, and acute adrenal insufficiency
"bstructive Decreased cardiac output
Increased systemic vascular resistance
Variable filling pressures dependent on etiology
Cardiac tamponade, tension pneumotora!, massive pulmonary embolus
C#$DI"%&NIC SH"C' (#N#%&(&N)
*+ "reat arrhythmias
,+ #iastolic dysfunction may require increased filling pressures
-+ $asodilators if not hypotensi%e
.+ Inotrope administration
/+ $asopressor agent needed if hypotension present to raise aortic diastolic
pressure
0+ &onsultation for mechanical assist de%ice
1+ 'reload and afterload reduction to impro%e hypoxemia if blood pressure
adequate
H23"V"L&(IC SH"C' (#N#%&(&N)
*+ $olume resuscitation : crystalloid, colloid
,+ Initial crystalloid choices
a (actated )inger*s solution
b +ormal saline ,high chloride may produce hyperchloremic acidosis-
KAN-182 Mira Yulianti (01-107)
-+ Match fluid gi%en to fluid lost : .lood, crystalloid, colloid
DIS)$I45)IV& SH"C' (#N#%&(&N)
*+ )estore intra%ascular %olume
,+ /ypotension despite %olume therapy : Inotropes and0or %asopressors
-+ $asopressors for MA' 1 23 mm /g
.+ Adjuncti%e inter%entions dependent on etiology
"4S)$5C)IV& SH"C' (#N#%&(&N)
*+ )elie%e obstruction
a 'ericardiocentesis
b "ube thoracostomy
c "reat pulmonary embolus
,+ "emporary benefit from fluid or inotrope administration
Fluid Therapy
*+ &rystalloids : (actated )inger*s solution, +ormal saline
,+ &olloids : /etastarch, Albumin, Gelatins
-+ 'acked red blood cells
.+ Infuse to physiologic endpoints
/+ &orrect hypotension first
0+ #ecrease heart rate
1+ &orrect hypoperfusion abnormalities
6+ Monitor for deterioration of oxygenation
Inotropic/Vasopressor Agents
*+ Dopamine
(ow dose ,456 g0kg0min- 7 mild inotrope plus renal effect
Intermediate dose ,8593 g0kg0min- 7 inotropic effect
/igh dose , :93 g0kg0min- 7 %asoconstriction
&hronotropic effect
,+ Dobutamine
;543 g0kg0min
Inotropic and %ariable chronotropic effects
#ecrease in systemic %ascular resistance
-+ Norepineprine
33; g0kg0min and titrate to effect
Inotropic and %asopressor effects
'otent %asopressor at high doses
.+ &pineprine
.oth and actions for inotropic and %asopressor effects
39 g0kg0min and titrate
Increases myocardial <4 consumption
Therapeutic Goals in Shock
*+ Increase <4 deli%ery
,+ <ptimi=e <4 content of blood
-+ Impro%e cardiac output and blood pressure
.+ Match systemic <4 needs with <4 deli%ery
/+ )e%erse0pre%ent organ hypoperfusion
Pediatric Considerations
.' not good indication of hypoperfusion
&apillary refill, extremity temperature better signs of poor systemic
perfusion
KAN-182 Mira Yulianti (01-107)
>pinephrine preferable to norepinephrine due to more chronotropic benefit
?luid boluses of 43 m(0kg titrated to .' or total 23 m(0kg, before
inotropes or %asopressors
+eonates consider congenital obstructi%e left heart syndrome as cause
of obstructi%e shock
<liguria
14 yrs old, urine %olume 14 m(0kg0hr
<lder children, urine %olume 1 9 m(0kg0hr
Ho !uch Fluid To Gi"e #
*+ Some measure of intravascular filling
a 'ressure ,&$' or 'A<'-
,+ Some assessment of risk of pulmonary oedema and capillary leak
a 'ulmonary gas exchange ,'a<4:?i<4-
b )equirement for positi%e pressure ,'>>'-
c &hest @5ray
-+ Some assessment of response to treatment
a &hanges in acid base balance, lactate
b Measurement of cardiac output
$hat do you need to kno hen you resuscitate patients in Shock #
Arterial blood pressure
Arine output
!ystemic acid7base balance ,p/, !.>, lactate-
!ome clinical assessment of tissue perfusion
Bwarm and well perfusedC or Bcold and shut downC
!ome measurement of global blood flow and tissue perfusion
&ardiac output or cardiac index
Arterial oxygen deli%ery, oxygen uptake index
Mixed %enous saturation and '%<4
KAN-182 Mira Yulianti (01-107)
Cardiogenic Sock
35(3
7
H&#$)
3ipe 7
Vascular
Volume 7 4lood
4lood 3ressure
Cardiac "utput !
SV$
"bstructive
Sock
Inotropes 8Dop, Dob, #dr, #mr9 Vasopreesor 8N&, 3&, #dr,
Dop9
$elease
tamponade, etc
Hypovolemic
Sock
:luid
s
Distributive
Sock
Patofisiologi %espons Tu&uh Terhadap Shock
)espons +euroendokrin
)espons /emodinamik
)espons Metabolik
$&S3"N N&5$"&ND"'$IN
$&S3"N H&("DIN#(I' mekanisme untuk memperbaiki keseimbangan kardiovaskular
)edistribusi aliran darah
'eningkatan &ardiac <utput
Memperbaiki $olume Intra%askular
KAN-182 Mira Yulianti (01-107)
:&#$
Stimulation of Limbic #rea of 4rain
increased
Hypotalamic, adrenomedullary, adrenocortical
activity
N&5$"&ND"C$IN& $&S3"NS
#drenal
Corte!
Cortisol
$elease
$enal
$enin $elease
3ituitary %land
#C)H, #DH, %H release
#drenal %land
&pineprine, N& release
#ngiotensin
II
#drenal corte!
#ldosterone
$elease
H23"V"L&(I
#
L"SS ": )"NIC INHI4I)I"N
": C&N)$#L #ND
S2(3#)H&)IC N&$V"5S
S2S)&(
#orta;Carotids
Hig pressure baroreceptors
Decreased $enal
3erfusion
$ atrium
Low pressure Stretc
$eceptors

)ranscapillary $efill 3ase

*+ Decreased capillary pressure caused by ypotension
,+ Sympatetic increase in precapillary arteriolar constriction

Decrease capillary ydrostatic pressure promotes passage of fluid from interstitium to intravascular space
3lasma 3rotein $estitution 3ase
Increased plasma osmolarity due to mainly epatic release of glucose, pyruvate, amino acids, etc+

Increased interstitial osmolarity

Increased interstitial volume and pressure

)ranscapillary movement of albumin into intravascular space

KAN-182 Mira Yulianti (01-107)
$edistribusi #liran Dara
$&S3"N
H&("DIN#(I'
H23")&NSI"N
Stimulasi
Neuroendokrin
4lood :low 3rotected
Heart
4rain
#drenal;3ituitary %land
4lood :low Decreased
Skin
(uscle
Splancnic Circulation
Limited to *6< beats;min before decreased
C" due to decreased diastolic filling time
C#$DI#C "5)35) 7 Heart $ate ! Stroke Volume
Sypatetic n+ System
Catecolamine
release
Increased contractility Increased &DV via =
Venoconstriction,
#rteriolar constriction,
$enal reabsorbtion
(&(3&$4#I'I V"L5(& D#$#H
HAEMODYNAMIC RESPONSES
Venoconstriction
Sympatetic n+ system8SNS9
Catecolamines 8C#9
#ngiotensin II 8#)II9
#DH
Reduced venous
capacitance
#rteriolar constriction
SNS, C#, #)II, #DH
Decreasedcapillary 3
:luidsift frominterstitiuminto vascular
compartment
Increased distal tubular
reabsorption
#ldosterone, #DH
Increased pro!imal tubular
reabsorption
SNS, C#, #)II
Increasedmyocardial contractility
SNS, C#
Restoration of
blood volume
Increased
ventricular filling
3
Increased ventricular
e>ection fraction
SV
CO
P
Increased eart rate
SNS, C#
Increased SV$ due to
arteriolar construction
SNS, C#, #)II, #DH
SVR
$&S3"N (&)#4"LI'
/yperglikemia
Mobilisasi lemak
Databolisme0pemecahan protein
'eningkatan sintesis urea
'eningkatan asam amino aromatik
'enurunan sintesis reactan fase akut
'eningkatan osmolalitas ekstrasel
RESPON ME!AO"I# RESPON ME!AO"I#
4reakdown of
skeletal muscle
into a+a+
Conversion of
a+a+ to glucose
$elease of=
Catecolamines
Cortisol
%lucagon
%rowt ormone
Impaired periperal
glucose uptake
HYPER$"YCEMIA HYPER$"YCEMIA
%lycogen
breakdown
Decreased 4lood Volume

Decreased C"

Cellular ypoperfusion and ypo!ia

KAN-182 Mira Yulianti (01-107)

#naerobic %lycolisis
3yruvat converted to lactic acid

(&)#4"LIC #SCID"SIS
$elease of Catecolamines, Cortisol, %lucagon

Lipolysis

Increase in 3lasma :ree :atty #cids

'fek Shock Pada tingkatan Sel
Low?:low, 3oor 3erfusion Hypo!ia #naerobic metabolism #scidosis Decrease Cellular &nergy
&fficiency
%lucose breakdown+ 8#9 Stage one, glycolysis, is anaerobic
8does not re@uire o!ygen9+ It yields pyruvic acid, wit to!ic by?
products suc as lactic acid, and very little energy+ 849 Stage
two is aerobic 8re@uires o!ygen9+ In a process called te 'rebs
or citric acid cycle, pyruvic acid is degraded into carbon dio!ide
and water, wic produces a muc iger yield of energy+
KAN-182 Mira Yulianti (01-107)
CE"" MEMRANE %AI"&RE'
DI$&C)
&ndoto!in
Complement
INDI$&C)
:ailure to maintain normal Na
A
, '
A
or Ca
,A
gradient
Decreased o!idative posporylation
OSMO!IC
$RADIEN!
Bater entry
into cell
C&LL5L#$
&D&(#
I(3#I$&D
IN)$#C&LL5L#$
(&)#4"LIS(
C
E
"
"
D
E
A
!
H
Na
A
entry
into cell
E%E# SHOC# PADA !IN$#A!AN SE"
'fek Shock Pada Tingkatan (rgan
Didney : Oliguric renal failure, High output renal failure
(i%er : Liver failure
GI tract : Failure of intestinal barrier (sepsis, bleeding)
(ung : Capillary leak associated with or caused by sepsis and infection
">+!I<+ '+>AM<"/<)A@
Prinsip %esusitasi
*+ Mempertahankan %entilasi
,+ Meningkatkan perfusi
-+ "erapi penyebab
KAN-182 Mira Yulianti (01-107)
MAIN!AIN (EN!I"A!ION MAIN!AIN (EN!I"A!ION
Increased o)*+en
demand
H*perventilation
Respirator* failure
Respirator* acidosis, let-ar+*.coma, -*po)ia
&specially in=
Sepsis
Hypovolemia
)rauma
Respirator* fati+ue
Diversi blood flo/ from vital or+an
Or+an in0ur*
)$&#)(&N) ": $&S3I$#)"$2 :#IL5$&
Hypovolemia 84lood Loss9

Decreased C"

Decreased "!ygen Delivery, Increased "!ygen $e@uirement

(etabolic ascidosis, ypo!emia tacypnea

)$&#)(&N) = 3rimary $esuscitation, "!ygen, (ecanical ventilation if needed
!REA!MEN! CONCEP! O% SHOC#
ENHANCIN$ PER%&SION 1 O2Y$EN DE"I(ERY
O)*+en deliver*1DO
3
4 HR 2 S( 2 Hb 2 S5
3
2 6789 : Hb 2 paO
3
Cardiac
output
Arterial O
3
content
%luids
!ransfuse Partiall*
dependent on
%IO
3
and
pulmonar*
status
Inotropes
DO
3
4 CO ) CaO
3
Su))ary
!hock is an altered state of tissue perfusion se%ere enough to induce
derangements in normal cellular function
+euroendocrine, hemodynamic and metabolic changes work together to restore
perfusion
!hock has many causes and often may be diagnosed using simple clinical
indicators
"reatment of shock is primarily focused on restoring tissue perfusion and oxygen
deli%ery while eliminating the cause
KAN-182 Mira Yulianti (01-107)