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Syok HipovolemiaSyok Hipovolemia
Dr.Irfan Hamdani,Sp.An Dr.Irfan Hamdani,Sp.An Dept.Anestesiologi dan Terapi Intensif Dept.Anestesiologi dan Terapi Intensif
Fak.Kedokteran UMSU Fak.Kedokteran UMSU
Medan Medan
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SyokSyok
suatu kondisi dimana sistemsuatu kondisi dimana sistemkardiovaskular gagal dalamkardiovaskular gagal dalam
menghasilkan perfusi jaringanmenghasilkan perfusi jaringanyang adekuatyang adekuat
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Perfusi jaringan yang tidak adekuat akanPerfusi jaringan yang tidak adekuat akan
menghasilkan :menghasilkan :
• hipoksia celluler generalisatahipoksia celluler generalisata• gangguan berat metabolisme selulergangguan berat metabolisme seluler
•Kerusakan jaringanKerusakan jaringan
• gagal organgagal organ• kematiankematian
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Diagnosis SyokDiagnosis Syok
MAP < 60MAP < 60
Klinis :Klinis :terdapat gejalaterdapat gejala
dan tandadan tandahipoperfusihipoperfusi jaringan jaringan
IT IS NOT LOW BLOOD PRESSURE !!!
IT IS HYPOPERFUSION…..
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GangguanGangguan
PompaPompa
jantung jantung
Sistem sirkulasiSistem sirkulasi Volume Volume
Gangguan aliran keGangguan aliran ke Jaringan Jaringan
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CELLULARCELLULAR
OXYGENOXYGENSUPPLYSUPPLY
CELLULARCELLULAROXYGENOXYGEN
DEMANDDEMAND
Impaired tissue perfusion occurs when anImpaired tissue perfusion occurs when animbalance develops between cellular oxygenimbalance develops between cellular oxygen
supply and cellular oxygen demandsupply and cellular oxygen demand..
PATHOPHYSIOLOGY OFPATHOPHYSIOLOGY OFSHOCK SYNDROMESHOCK SYNDROME
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PATHOPHYSIOLOGY OFPATHOPHYSIOLOGY OFSHOCK SYNDROMESHOCK SYNDROME
Cells switch from aerobic to anaerobic metabolismCells switch from aerobic to anaerobic metabolism
lactic acid productionlactic acid production
Cell function ceases & swellsCell function ceases & swells
membrane becomes more permeablemembrane becomes more permeable
electrolytes & fluids seep in & out of cellelectrolytes & fluids seep in & out of cell
Na+/K+ pump impairedNa+/K+ pump impaired
mitochondria damagemitochondria damage
cell deathcell death
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COMPENSATORY MECHANISMS:COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Sympathetic Nervous System (SNS)-
Adrenal Response Adrenal Response
SNS - Neurohormonal responseSNS - Neurohormonal response
Stimulated by baroreceptorsStimulated by baroreceptorsIncreased heart rateIncreased heart rate
Increased contractilityIncreased contractility
Vasoconstriction (SVR-Afterload)Vasoconstriction (SVR-Afterload)
Increased PreloadIncreased Preload
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COMPENSATORY MECHANISMS:COMPENSATORY MECHANISMS:Sympathetic Nervous System (SNS)-Sympathetic Nervous System (SNS)-
Adrenal Response Adrenal Response
SNS - Hormonal:SNS - Hormonal: Renin-angiotensionRenin-angiotension
systemsystem Decrease renal perfusionDecrease renal perfusion
Releases renin angiotension IReleases renin angiotension I
Angiotension II potent vasoconstriction & Angiotension II potent vasoconstriction & Releases aldosterone adrenal cortexReleases aldosterone adrenal cortex
Sodium & water retentionSodium & water retention
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COMPENSATORY MECHANISMS:COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-AdrenalSympathetic Nervous System (SNS)-Adrenal
ResponseResponse
SNS - Hormonal: Antidiuretic HormoneSNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulatedOsmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary gland ADH released by Posterior pituitary gland
Vasopressor effect to increase BP Vasopressor effect to increase BP
Acts on renal tubules to retain water Acts on renal tubules to retain water
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COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS Sympathetic Nervous System (SNS)Sympathetic Nervous System (SNS)
Adrenal Response Adrenal Response
SNS - Hormonal:SNS - Hormonal: Adrenal Cortex Adrenal Cortex Anterior pituitary releases Anterior pituitary releases
adrenocorticotropic hormone (ACTH)adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cx to releaseStimulates adrenal Cx to release
glucorticoidsglucorticoids
Blood sugar increases to meet increasedBlood sugar increases to meet increased
metabolic needsmetabolic needs
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Failure of Compensatory ResponseFailure of Compensatory Response
Decreased blood flow to the tissues causesDecreased blood flow to the tissues causescellular hypoxiacellular hypoxia
Anaerobic metabolism begins Anaerobic metabolism beginsCell swelling, mitochondrial disruption,Cell swelling, mitochondrial disruption,
and eventual cell deathand eventual cell death
If Low Perfusion States persists:If Low Perfusion States persists:
IRREVERSIBLEIRREVERSIBLE DEATH IMMINENT!!DEATH IMMINENT!!
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Stages of ShockStages of Shock Initial stage -Initial stage - tissues are under perfused, decreased CO,tissues are under perfused, decreased CO,increased anaerobic metabolism, lactic acid is buildingincreased anaerobic metabolism, lactic acid is building
Compensatory stageCompensatory stage -- Reversible. SNS activated by lowReversible. SNS activated by lowCO, attempting to compensate for the decrease tissueCO, attempting to compensate for the decrease tissue
perfusion.perfusion. Progressive stage -Progressive stage -Failing compensatory mechanisms:Failing compensatory mechanisms:profound vasoconstriction from the SNSprofound vasoconstriction from the SNS
ISCHEMIA Lactic acid production is highISCHEMIA Lactic acid production is high
metabolic acidosismetabolic acidosis Irreversible or refractory stage -Irreversible or refractory stage -Cellular necrosis andCellular necrosis andMultiple Organ Dysfunction Syndrome may occurMultiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!DEATH IS IMMINENT!!!!
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Pathophysiology Systemic LevelPathophysiology Systemic Level
Net results of cellular shock:Net results of cellular shock: systemic lactic acidosissystemic lactic acidosis
decreased myocardial contractilitydecreased myocardial contractility
decreased vascular tonedecreased vascular tone
decrease blood pressure, preload, anddecrease blood pressure, preload, andcardiac outputcardiac output
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Clinical Presentation:Clinical Presentation:
Generalized ShockGeneralized Shock Vital signs Vital signs
HypotensiveHypotensive:(may be WNL or due to:(may be WNL or due to
compensatory mechanism)compensatory mechanism) < 90< 90mmHgmmHg
MAPMAP < 60 mmHg< 60 mmHg
Tachycardia Tachycardia:: Weak and Thready pulse Weak and Thready pulse Tachypneic Tachypneic-blow off CO2-blow off CO2 RRespiratory alkalosisespiratory alkalosis
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Mental status:Mental status: restless, irritable, apprehensiverestless, irritable, apprehensive unresponsive, painful stimuli onlyunresponsive, painful stimuli only
Decreased Urine outputDecreased Urine output
Clinical Presentation:Clinical Presentation:
Generalized ShockGeneralized Shock
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Shock SyndromesShock Syndromes
Hypovolemic ShockHypovolemic Shock
blood blood
VOLUME VOLUME
problemproblem
Cardiogenic ShockCardiogenic Shock blood bloodPUMPPUMP problemproblem
Distributive ShockDistributive Shock[septic;anaphylactic;neurogenic][septic;anaphylactic;neurogenic]
blood blood VESSEL VESSEL problemproblem
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Hypovolemic ShockHypovolemic Shock
Loss of circulating volume “Empty tank ”Loss of circulating volume “Empty tank ”
decrease tissue perfusiondecrease tissue perfusion general shockgeneral shock
responseresponse
ETIOLOGY:ETIOLOGY:
Internal or External fluid lossInternal or External fluid loss
Intracellular and extracellularIntracellular and extracellular
compartmentscompartmentsMost common causes:Most common causes:
HemmorhageHemmorhage
DehydrationDehydration
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Hypovolemic ShockHypovolemic Shock
External loss of fluidExternal loss of fluid
Fluid loss: DehydrationFluid loss: Dehydration Nausea & omiting, diarr!ea, massie diuresis,Nausea & omiting, diarr!ea, massie diuresis,
e"tensie #urnse"tensie #urns
Blood loss:Blood loss: trauma$ #lunt and penetratingtrauma$ #lunt and penetrating BLOOD YOU SEEBLOOD YOU SEE BLOOD YOUBLOOD YOU DON’TDON’T SEESEE
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Hypovolemic Shock:Hypovolemic Shock:
Internal fluid lossInternal fluid loss
Loss of Intravascular integrityLoss of Intravascular integrity
Increased capillary membraneIncreased capillary membranepermeabilitypermeability
Decreased Colloidal Osmotic PressureDecreased Colloidal Osmotic Pressure (third spacing(third spacing))
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Pathophysiology ofPathophysiology of
Hypovolemic ShockHypovolemic ShockDecreased intravascular volume leads to….Decreased intravascular volume leads to….Decreased venous return (Preload, RAP) leadsDecreased venous return (Preload, RAP) leads
to...to...
Decreased ventricular filling (Preload, PAWP)Decreased ventricular filling (Preload, PAWP)
leads to….leads to….
Decreased stroke volume (HR, Preload, &Decreased stroke volume (HR, Preload, &
Afterload) leads to ….. Afterload) leads to …..Decreased CO leads to...(CompensatoryDecreased CO leads to...(Compensatory
mechanisms)mechanisms)
Inadequate tissue perfusion!!!!Inadequate tissue perfusion!!!!
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Assessment & Management Assessment & Management
S/S vary depending on severity of fluid loss:S/S vary depending on severity of fluid loss: 15%[750ml]-15%[750ml]- compensatory mechanismcompensatory mechanismmaintains COmaintains CO
15-30% [750-1500ml15-30% [750-1500ml- Hypoxemia, decreased- Hypoxemia, decreasedBP & UOPBP & UOP
30-40% [1500-2000ml]30-40% [1500-2000ml] -Impaired-Impairedcompensation & profound shock along withcompensation & profound shock along with
severe acidosissevere acidosis 40-50%40-50% - refactory stage:- refactory stage:
loss of volume= deathloss of volume= death
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Clinical PresentationClinical Presentation
Hypovolemic ShockHypovolemic Shock Tachycardia and tachypnea Tachycardia and tachypnea
Weak, thready pulses Weak, thready pulses
HypotensionHypotension
Skin cool & clammySkin cool & clammy
Mental status changesMental status changesDecreased urine output: dark &Decreased urine output: dark &
concentratedconcentrated
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Hemodynamic ChangesHemodynamic ChangesCorrelate with volume lossCorrelate with volume loss
Low COLow CODecreased RAP ( Preload)Decreased RAP ( Preload)
Decreased PAD, PAWPDecreased PAD, PAWP
Increased SVR (Afterload)Increased SVR (Afterload)
Hypovolemic Shock:Hypovolemic Shock:
l h kH l iSh k
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Initial ManagementInitial Management
Management goal:Management goal:Restore circulating volume, tissue perfusion,Restore circulating volume, tissue perfusion,& correct cause& correct cause::
Early Recognition- Do not relay on BP! (30%Early Recognition- Do not relay on BP! (30%fluid loss)fluid loss)
Control hemorrhageControl hemorrhage
Restore circulating volumeRestore circulating volume Optimize oxygen deliveryOptimize oxygen delivery Vasoconstrictor if BP still low after volume Vasoconstrictor if BP still low after volume
loadingloading
Hypovolemic ShockHypovolemic Shock
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Restore circulating volumeRestore circulating volume
HemorrhageHemorrhage
DehydrationDehydration
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ISFISF IVFIVF ICFICF
Physiologic principlesPhysiologic principles
of fluid managementof fluid management
PerdarahanPerdarahan
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PRE-LO!PRE-LO! CO"#RC#ILI#$CO"#RC#ILI#$ F#ER-LO!F#ER-LO!
S#RO%E VOL&'ES#RO%E VOL&'E (ER#-R#E(ER#-R#E
CR!IC OPCR!IC OP S$S#E'ICS$S#E'IC
VSC&LRVSC&LR
RESIS#"CERESIS#"CE
)LOO!)LOO!
PRESS&REPRESS&RE
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Oxygen TransportOxygen Transport
CaOCaO22 = (SaO= (SaO22 x Hb x 1.34) + (PaO x Hb x 1.34) + (PaO22 x 0.003) x 0.003)
DODO22 = CO x CaO= CO x CaO22
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PERDARAHANPERDARAHAN
HILANG VOLUMEHILANG VOLUME
HILANG ERITROSITHILANG ERITROSIT
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THE FLUIDSTHE FLUIDS
CRYSTALLOIDCRYSTALLOID
HYPERTONIC FLUIDHYPERTONIC FLUIDNATURAL COLLOIDNATURAL COLLOID
ARTIFICIAL COLLOID ARTIFICIAL COLLOID
BLOOD, COMPONENTBLOOD, COMPONENT
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TOTAL BODY WATER : 60% TOTAL BODY WEIGHT TOTAL BODY WATER : 60% TOTAL BODY WEIGHT
*+ L*+ L
IS
+, kg+, kg
LL
ISFISF IVFIVF ICFICF
*L*L ./ L./ L
Physiologic principlesPhysiologic principles
of fluid managementof fluid management
PhysiologicprinciplesPhysiologicprinciples
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IS
LL
ISFISF IVFIVF ICFICF
*L*L ./ L./ L.01,ml.01,ml .1, ml.1, ml
Physiologic principlesPhysiologic principlesof fluid managementof fluid management
EDEMAEDEMA
3LD5W
PhysiologicprinciplesPhysiologicprinciples
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RYSTALLO!DRYSTALLO!D
RL, RA,RL, RA,
NaCl 0.9%NaCl 0.9%
IS
LL
ISFISF IVFIVF ICFICF
*L*L ./ L./ L..1,ml..1,ml 01, ml01, ml
Physiologic principlesPhysiologic principlesof fluid managementof fluid management
EDEMAEDEMA
3L
Require large volumeRequire large volume
CheaperCheaper
Fewer adverse side effectsFewer adverse side effects
But…………But…………
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IS
LL
ISFISF IVFIVF ICFICF
*L*L ./ L./ L2L2L
Physiologic principlesPhysiologic principles
of fluid managementof fluid management
Albumin-5% Albumin-5%1 L1 Lexpensiveexpensive
Physiologic principlesPhysiologic principles
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IS
LL
ISFISF IVFIVF ICFICF
*L*L ./ L./ L2L2L
Physiologic principlesPhysiologic principles
of fluid managementof fluid management
HES-6%, 200/0.5HES-6%, 200/0.51 L1 L
•More rapidly correctMore rapidly correcthypovolemiahypovolemia
•Maintain intravascularMaintain intravascular
oncotic pressureoncotic pressure
•More expensive thanMore expensive thancrystalloidcrystalloid
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ISISFISF IVFIVF ICFICF
*L*L ./ L./ L
Physiologic principlesPhysiologic principles
of fluid managementof fluid management
LL
7.5%-Hypertonic Saline7.5%-Hypertonic Saline+ Dextran+ Dextran500 ml500 ml
625 ml625 ml
EDEMAEDEMA
Subjected to recentintensive investigation
Resuscitate rapidly,reduced volume of fluid
Reduce cerebral edema
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!lass I!lass I !lass II!lass II !lass III!lass III !lass I"!lass I"
#lood$%oss&ml'#lood$%oss&ml' $(750$(750 750$1500750$1500 1500$20001500$2000 (2000(2000
#lood$loss &)#"'#lood$loss &)#"' $(15)$(15) 15$30)15$30) 30$40)30$40) (40)(40)
*ulse$+ate &-min.'*ulse$+ate &-min.' /100/100 (100(100 (120(120 (140(140
#lood$*ressure#lood$*ressure ormalormal ormalormal ecreasedecreased ecreasedecreased
*ulse$*ressure*ulse$*ressure or orincreasedincreased
ecreasedecreased ecreasedecreased ecreasedecreased
+espiratory +ate+espiratory +ate 14$2014$20 20$3020$30 30$3530$35 (35(35
rine out$put &ml-our'rine out$put &ml-our' (30(30 20$3020$30 5$155$15 eliibleeliible
ental status-!Sental status-!S SlitlySlitlyaniousanious
idly aniousidly anious nious and nious andconusedconused
!onused and!onused andletaricletaric
Estimated Fluid and )lood LossesEstimated Fluid and )lood Losses
)ased on Patient3s Initial Presentation)ased on Patient3s Initial Presentation
#" 70 ml-#" 70 ml-
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Oxygen TransportOxygen Transport
CaOCaO22 = (SaO= (SaO22 x Hb x 1.34) + (PaO x Hb x 1.34) + (PaO22 x 0.003) x 0.003)
DODO22 = CO x CaO= CO x CaO22
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PRE-LO!PRE-LO! CO"#RC#ILI#$CO"#RC#ILI#$ F#ER-LO!F#ER-LO!
S#RO%E VOL&'ES#RO%E VOL&'E (ER#-R#E(ER#-R#E
CR!IC OPCR!IC OP S$S#E'ICS$S#E'IC
VSC&LRVSC&LR
RESIS#"CERESIS#"CE
)LOO!)LOO!
PRESS&REPRESS&RE
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Pola ker4a penangananPola ker4a penanganan
shock perdarahanshock perdarahan
*enderita datan*enderita datan
denan perdaraandenan perdaraan
*asan inus :arum*asan inus :arum
aliber besar ;16
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LU!D REPLAE"ENT
LU!D REPLAE"ENT
# : $ Rule
: $ Rule
lass !lass ! rystalloidrystalloid
lass !!lass !! rystalloidrystalloid %% olloid &olloid &
lass !!!lass !!! rystalloidrystalloid
%%olloidolloid' Blood' Bloodlass !(lass !( rystalloidrystalloid
%%olloidolloid' Blood' Blood
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1000 ml berdarah
3000 ml kristalloid
(RL, RA, NaCl 0.9%)
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"ana)e*ent
ana)e*ent
selan+utnya
elan+utnya
+apid response,+apid response,perdaraan /20)perdaraan /20)
>ransient response,>ransient response,
perdaraan 20$40) #"perdaraan 20$40) #"
onoin lossonoin loss
resusitasi td ade?atresusitasi td ade?at
+%, a!l 0.9),+%, a!l 0.9), @olloid@olloid, ara A, ara A
inimal, no responseinimal, no response>indaan beda seera>indaan beda seera
>ransusi dara>ransusi dara