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6/15/2016

HypovolemicShock:Background,Pathophysiology

HypovolemicShock
Author:PaulKolecki,MD,FACEPChiefEditor:BarryEBrenner,MD,PhD,FACEPmore...
Updated:Feb27,2014

Background
Hypovolemicshockreferstoamedicalorsurgicalconditioninwhichrapidfluidloss
resultsinmultipleorganfailureduetoinadequatecirculatingvolumeand
subsequentinadequateperfusion.Mostoften,hypovolemicshockissecondaryto
rapidbloodloss(hemorrhagicshock).
AcuteexternalbloodlosssecondarytopenetratingtraumaandsevereGIbleeding
disordersare2commoncausesofhemorrhagicshock.Hemorrhagicshockcanalso
resultfromsignificantacuteinternalbloodlossintothethoracicandabdominal
cavities.
Twocommoncausesofrapidinternalbloodlossaresolidorganinjuryandrupture
ofanabdominalaorticaneurysm.Hypovolemicshockcanresultfromsignificant
fluid(otherthanblood)loss.Twoexamplesofhypovolemicshocksecondarytofluid
lossincluderefractorygastroenteritisandextensiveburns.Theremainderofthis
articleconcentratesmainlyonhypovolemicshocksecondarytobloodlossandthe
controversiessurroundingthetreatmentofthiscondition.Thereaderisreferredto
otherarticlesfordiscussionsofthepathophysiologyandtreatmentforhypovolemic
shockresultingfromlossesoffluidotherthanblood.
Themanylifethreateninginjuriesexperiencedduringthewarsofthe1900shave
significantlyaffectedthedevelopmentoftheprinciplesofhemorrhagicshock
resuscitation.DuringWorldWarI,W.B.Cannonrecommendeddelayingfluid
resuscitationuntilthecauseofthehemorrhagicshockwasrepairedsurgically.
CrystalloidsandbloodwereusedextensivelyduringWorldWarIIforthetreatment
ofpatientsinunstableconditions.ExperiencefromtheKoreanandVietnamwars
revealedthatvolumeresuscitationandearlysurgicalinterventionwereparamount
forsurvivingtraumaticinjuriesresultinginhemorrhagicshock.Theseandother
principleshelpedinthedevelopmentofpresentguidelinesforthetreatmentof
traumatichemorrhagicshock.However,recentinvestigatorshavequestionedthese
guidelines,andtoday,controversiesexistconcerningtheoptimaltreatmentof
hemorrhagicshock.
Theprognosisisdependentonthedegreeofvolumeloss.
Forpatienteducationresources,seeFirstAidandInjuriesCenter,aswellasShock.

Pathophysiology
Thehumanbodyrespondstoacutehemorrhagebyactivatingthefollowingmajor
physiologicsystems:thehematologic,cardiovascular,renal,andneuroendocrine
systems.
Thehematologicsystemrespondstoanacuteseverebloodlossbyactivatingthe
coagulationcascadeandcontractingthebleedingvessels(bymeansoflocal
thromboxaneA 2release).Inaddition,plateletsareactivated(alsobymeansoflocal
thromboxaneA 2release)andformanimmatureclotonthebleedingsource.The
damagedvesselexposescollagen,whichsubsequentlycausesfibrindepositionand
stabilizationoftheclot.Approximately24hoursareneededforcompleteclot
fibrinationandmatureformation.
Thecardiovascularsysteminitiallyrespondstohypovolemicshockbyincreasingthe
heartrate,increasingmyocardialcontractility,andconstrictingperipheralblood
vessels.Thisresponseoccurssecondarytoanincreasedreleaseofnorepinephrine
anddecreasedbaselinevagaltone(regulatedbythebaroreceptorsinthecarotid
arch,aorticarch,leftatrium,andpulmonaryvessels).Thecardiovascularsystem
alsorespondsbyredistributingbloodtothebrain,heart,andkidneysandawayfrom
skin,muscle,andGItract.
Therenalsystemrespondstohemorrhagicshockbystimulatinganincreaseinrenin
secretionfromthejuxtaglomerularapparatus.Reninconvertsangiotensinogento
angiotensinI,whichsubsequentlyisconvertedtoangiotensinIIbythelungsand
liver.AngiotensinIIhas2maineffects,bothofwhichhelptoreversehemorrhagic
shock,vasoconstrictionofarteriolarsmoothmuscle,andstimulationofaldosterone
secretionbytheadrenalcortex.Aldosteroneisresponsibleforactivesodium
reabsorptionandsubsequentwaterconservation.
Theneuroendocrinesystemrespondstohemorrhagicshockbycausinganincrease
incirculatingantidiuretichormone(ADH).ADHisreleasedfromtheposterior
pituitaryglandinresponsetoadecreaseinBP(asdetectedbybaroreceptors)anda
decreaseinthesodiumconcentration(asdetectedbyosmoreceptors).ADH
indirectlyleadstoanincreasedreabsorptionofwaterandsalt(NaCl)bythedistal
tubule,thecollectingducts,andtheloopofHenle.

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6/15/2016

HypovolemicShock:Background,Pathophysiology

Thepathophysiologyofhypovolemicshockismuchmoreinvolvedthanwhatwas
justlisted.Toexplorethepathophysiologyinmoredetail,referencesforfurther
readingareprovidedinthebibliography.Theseintricatemechanismslistaboveare
effectiveinmaintainingvitalorganperfusioninseverebloodloss.Withoutfluidand
bloodresuscitationand/orcorrectionoftheunderlyingpathologycausingthe
hemorrhage,cardiacperfusioneventuallydiminishes,andmultipleorganfailure
soonfollows.
ClinicalPresentation

ContributorInformationandDisclosures
Author
PaulKolecki,MD,FACEPAssociateProfessor,DepartmentofEmergencyMedicine,DirectorofUndergraduate
EmergencyMedicineStudentEducation,ThomasJeffersonUniversityHospital,JeffersonMedicalCollegeof
ThomasJeffersonUniversityConsultant,PhiladelphiaPoisonControlCenter
PaulKolecki,MD,FACEPisamemberofthefollowingmedicalsocieties:AlphaOmegaAlpha,American
CollegeofEmergencyPhysicians
Disclosure:Nothingtodisclose.
Coauthor(s)
CarlRMenckhoff,MD,FACEPAssociateProfessor,DepartmentofEmergencyMedicine,MedicalCollegeof
GeorgiaMedicalDirectorandChairman,MedicalCenterofLewisvilleEducationDirectorandUltrasound
Director,QuestcarePartners
CarlRMenckhoff,MD,FACEPisamemberofthefollowingmedicalsocieties:AmericanCollegeofEmergency
Physicians
Disclosure:Nothingtodisclose.
SpecialtyEditorBoard
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedicalCenterCollege
ofPharmacyEditorinChief,MedscapeDrugReference
Disclosure:ReceivedsalaryfromMedscapeforemployment.for:Medscape.
AAntoineKazzi,MDDeputyChiefofStaff,AmericanUniversityofBeirutMedicalCenterAssociateProfessor,
DepartmentofEmergencyMedicine,AmericanUniversityofBeirut,Lebanon
AAntoineKazzi,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofEmergencyMedicine
Disclosure:Nothingtodisclose.
ChiefEditor
BarryEBrenner,MD,PhD,FACEPProfessorofEmergencyMedicine,ProfessorofInternalMedicine,Program
DirectorforEmergencyMedicine,CaseMedicalCenter,UniversityHospitals,CaseWesternReserveUniversity
SchoolofMedicine
BarryEBrenner,MD,PhD,FACEPisamemberofthefollowingmedicalsocieties:AlphaOmegaAlpha,
AmericanHeartAssociation,AmericanThoracicSociety,ArkansasMedicalSociety,NewYorkAcademyof
Medicine,NewYorkAcademyofSciences,SocietyforAcademicEmergencyMedicine,AmericanAcademyof
EmergencyMedicine,AmericanCollegeofChestPhysicians,AmericanCollegeofEmergencyPhysicians,
AmericanCollegeofPhysicians
Disclosure:Nothingtodisclose.
AdditionalContributors
DanielJDire,MD,FACEP,FAAP,FAAEMClinicalProfessor,DepartmentofEmergencyMedicine,Universityof
TexasMedicalSchoolatHoustonClinicalProfessor,DepartmentofPediatrics,UniversityofTexasHealth
SciencesCenterSanAntonio
DanielJDire,MD,FACEP,FAAP,FAAEMisamemberofthefollowingmedicalsocieties:AmericanAcademy
ofClinicalToxicology,AmericanAcademyofPediatrics,AmericanAcademyofEmergencyMedicine,American
CollegeofEmergencyPhysicians,AssociationofMilitarySurgeonsoftheUS
Disclosure:Nothingtodisclose.

References
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2009Feb.174(2):1068.[Medline].
3.GhafariMH,MoosavizadehSA,MoharariRS,KhashayarP.Hypertonicsaline5%vs.lactatedringerfor
resuscitatingpatientsinhemorrhagicshock.MiddleEastJAnesthesiol.2008Oct.19(6):133747.
[Medline].
4.ReinhartK,PernerA,SprungCL,JaeschkeR,SchortgenF,JohanGroeneveldAB,etal.Consensus
statementoftheESICMtaskforceoncolloidvolumetherapyincriticallyillpatients.IntensiveCareMed.
2012Mar.38(3):36883.[Medline].
5.ZinkKA,SambasivanCN,HolcombJB,ChisholmG,SchreiberMA.Ahighratioofplasmaandplateletsto
packedredbloodcellsinthefirst6hoursofmassivetransfusionimprovesoutcomesinalargemulticenter

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