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Syok Hypovolemik-IH FK UMSU2012

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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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    2020

    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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    4343

      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


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