SHOCKHistorical

AspectsTheconceptofshockhasevolvedoverthecenturiesfromtheearliestdescriptioninantiquityoftraumaticwoundsand

hemorrhage.Hippocraticfacies(460~380B.C.):tourniguet.

BloodlettingGalen(A.D.130~200):erroneousknowledgeofanatomy.LigationofbleedingvesselsVesalius.WilliamHarvey(16centuries):anatomyandcirculationofthecardiovascularsystemAFrenchmilitarysurgeon:theuseofsimple

bandagesThomasLatta:in1831.infusionofintravenousfluidsintohypo-volemicpatientsinflictedwithcholeracausedclinical

improvent.Pathogenesis:a.vasomotorexhaustion:neurogenic

theoryb.traumatictoxemia:cannon.Bay(WorldWar

I)c.hypovolemia:Keith,Blalock(experimentson

dogs)d.fat

embolism;e.acidosisf.adrenal

dysfunctionPathogenesis:resuscitation,individualargandysfunction,cellularderangements(Korean,Vietnamconflict).Shocklung.ARDSmolecularbiology,inflammatory

mediator,metabolicsupport,oxygendelivery,organischemia,sepsis.II. Definitionof shockAsyndromeresultsfrominadequateperfusionoftissuesalterationsincellularmetabolism,cellulardysfunctionandcellularinjury,MODSduetotissuehyperfusion,

hypoxia.Oxygendelivery;oxygendebt;oxygendemandexceedstheoxygen

supply.III. Cause, classificationof shock1. hypovolemic

shock1)hemorrhagiclosses:trauma,gastrointestinalbleedingruptured

aneurysm.2)plasmavolumelosses:extravascularfluidsequestration,pancreatitis,burns,bowelobstruction.2. cardiogenic

shockdinminishedcardiac

outputintrinsic

causeextrinsic

causemyocardial

infarctioncardiacrhythm

disturbances.Tensionpneumothoraxpericardial

tamponade3. neurogenic

shockfailureofthesympatheticnervoussystemtomaintainnormalvascular

tone.Spinalcordinjury,severeheadinjury.Spinalanesthesia4. vasogenicendogenousorexogenousvaso-active

mediatorssystemicinflammatoryresponse

syndrome(SIRS)sepsis(infectious)noninfectiousAnaphylacticHypoadrenaltraumaticIV. Pathophysiology of shockImpairedtissue

perfusionTissue

hypoxiaAnaerobicmetabolismAcidosisCellular

dysfunctionSIRS/

SepsisMultipleorgandysfunction

syndromeInflammatoryMediatorsCirculatoryredistributionIschemia/ReperfusionPathophysiology:RoleofhypoxiaAnaerobicmetabolismand

acidosisHyperlactatemiaCirculatoryredistributionImpairmentofgut

perfusionAnaerobicmetabolismandacidosisGlucoseGlycogenlactatePyruvateAcetyl

CoACitricAcidcyclecytosolmitochondriaAerobicglycolysisAnaerobicglycolysisCirculatory redistributionVaso-constrictive

factors:Catechol,angiotensinII,vasopressin,endothelin,thromboxanA2Vaso-dilatory:Nitricoxide,prostaglandinE2,prostacyclin,interleukin-2,

bradykinin.Impairmentofgut

perfusion:Subsequentbacterialortoxin

translocationSystemicinflammatoryresponse,

MODSI. baroreceptorsVasomotorcenter(medulla)Sympatheticneural

outputIncreasedsystemicvascular

resistanceIncreasedvenousreturntothe

heartArteriolarvasoconstriction(cutaneoustissue.Skeletalmuscle.Renalandsplanchnicvascularbeds)II. adrenal

medullary output↑tachycardia, enhancedcardiac

contractilityIII. Antidiuretichormone(posterior

pituitary)VasoconstrictionWater reabsorption in the

distaltubule

of the

kidneyIV. rennin(kidney)AngiotensinI(liver)AngiotensinII

(lungs)vasoconstrictoraldosterone(adrenalcortex)→reabsorptionofsodiumV.microcirculatory

autoregulationMediator

of shockand

sepsisEndotoxinComplement

fragmentsEicosanoidsLeukotrienes,Prostaglandins,

ThrobomxanesCytokines:TNF-a; CSF,Interleukins(IL1,IL2,IL6);GCSF,GM-CSF;

IFN-rNeuroendocrine

mediators:catechols,cortisol,

glucagonsV. diagosisandmanagement ofshock:General

approachKeepSaO2>

90%Optimizecardiac

indexOptimize

HbsupplysupplementalO2mechanicalventilation,ifnecessaryMayneedearlyhemodynamic

monitoring11-13g/dlAssessvolume

status(preload)PCWP<15volume

expansionPCWP>15considervolumeifPCWP<18diuresesif

PCWP>18Reassesstokeep:PCWP15-18

mmHgMAP60-80

mmHgSvO2

>65-70%Deliveryindependent

O2consumptionGoals

metTreatincitingcauseofshockcontrolinflammatoryresponsenutritional

supportGoalsnotmetInotropicsupport(bagonism)DobutamineDopamineEpinephrine注：此圖表太大，一個(gè)幻燈頁面不能全部顯示ConsidervasodilatorsNitroglyceninNitroprussideConsidera

agonistNorepinephrineEpinephrineNeosynephrinePlusDopamineGoals

met Goalsnot

metReassessTreatincitingcauseof shockcontrolinflammatoryresponse

nutritionalsupport注：此圖表太大，一個(gè)幻燈頁面不能全部顯示SPECIFIC

SHOCKSYNDROMESicalsignsandsymptomsofhemorrhagicshockbasedonseverityof

blulating

blood Pulse

rate Systolic

pressure Pulse

pressuressfor70kg

male)Capillary RespirationsrefillCentralnervoussystemUrine

outputl)0-1500ml)00-2000ml)ml)normal>100>120>140nonpalpablenormalnormalweak

decreasedmarked

decreasednormaldecreaseddecreasedmarkeddecreasednormaldelayeddelayedabsentNormalMildtachypneaMarked

tachypneaMarked

tachypneanormalanxiousconfusedlathargicnormal20-30ml/hr20ml/hrnegligible注：此圖表太大，一個(gè)幻燈頁面不能全部顯示Traumatic

shockHypovolemicshockwith1.largervolumelosses2.greaterfluidsequestrationintheextravascularcompartments3.moreintenseactivationofinflammatorymediatorsdevelopmentof

SIRS4.microcirculatoryderangements5.MODSfrequently

occurTraumatic

shocktreatment1.excessivefluid

requirements2.mechanical

ventilation3.pulmonaryarterycatheter

monitoring4.cardiovascularsupportShockAssociatedwithSIRS,Sepsis, and

MODSSIRS:twoormoreof

following1.temperaturegreaterthan38℃

orlessthan36℃2.heartrategreaterthan90beatsper

minute3.respiratoryrategreaterthan20breathsperminuteorPaCO2lessthan

32mmHg4.whitebloodcellcountgreaterthan12,000percumm,lessthan4000percummorgreaterthan10%band

formsVII.Diagnosisofhypovolemicshock1.clinical

history;2.physical

findings;3.bloodtests.4.characteristic

hemodynamics1.lowrightandleftsidedfillingpressures(lowcentralvenouspressure,low

PCWP)2.decreasedcardiacoutput,decreasedSvO23.increasedsystemicvascular

resistanceVIII.

TreatmentPatientsairway;adequateventilation,

oxygenationFluid

replacement isotonicelectrolyte

solutionsCrystalloid---Ringer’slactate

solutionBloodtransfusion---type-specifictypeOpackedredbloodcellsGuide

treatmentIfabsentmonitorthecentralvenous

pressurePlaceapulmonaryarterycatheterThen:urinaryoutputrateof0.5to1.0

ml/kg/hourThepneumaticanti-shockgarmentColloidsolution;hyper-tonic

saline(controversy)SEPSISSepsis:

thepresenceofSIRSinassociationwithculture-proveninfectionSepticshock:

sepsiswithhypotensiondespiteadequatefluidresuscitation,alongwiththepresenceofmanifestationsofhypoperfusion,including,butnotlimitedto,lacticacidosis,oliguria,oranacutealterationinmental

status.Mutipleorgandysfunctionsyndrome

(MODS):

thepresenceofalteredorganfunctioninanacutelyillpatientsuchthathomeostasiscannotbemaintainedwithout

intervention.Mortality rate

26%SIRS→SepsisMortalityrate:

7%→16%4%Sepsis→SepticshockMortalityrate:

7%→46%MODSmortalityrangefrom20%to100%dependingonthenumberoffailedorgansseverityofillnessscoring

systemsMODSPrimaryMODSIschemicReperfussiondirect

insultSecondaryMODS(two-hitmodel)exaggerateduncontrolled

systemicinflammatoryresponseclinical

features:fever,tachycardia,hypotension,oliguria(obtundation,coma)alteredmentalstatus.Leukocytosisorleukopeniaincreasedordecreasedsystemicvascularresistance.Positivemicrobial

culturesgram-negative

bacteriaescherichiacoli,klebsiellapseudomonasstaphylococcusstreptococcusspices,fungal,viral,protozoalpneumonia,gastrointestinalperforationbiliarytractinfection,urinarytractinfectionburn

woundsTheTwo-hitTheoryof

MODSFirstHit1°MODSDeathRecoverySystemicInflammatoryresponseSecondHitAmplifiedSystemicInflammationresponse2

°MODSRecoveryDeath1. Pulmonary failure

ARDSMortalityexceeds50%ventilationperfusionabnormalitiespulmonaryedemahypoxemiadecreasedfunctionalresidual

capacitydecreasedinfiltratesonchest

X-rays2. Gastroint