低血压对器官灌注及预后的影响存在异质性：一项叙述性综述

845

BritishJournalofAnaesthesia,127(6):845_861(2021)

doi:10.1016/j.bja.2021.06.048

AdvanceAccessPublicationDate:12August2021ReviewArticle

CARDIOVASCULAR

Heterogeneousimpactofhypotensiononorganperfusionandoutcomes:anarrativereview

LingzhongMeng*

DepartmentofAnesthesiology,YaleUniversitySchoolofMedicine,NewHaven,CT,USAE-mail:

lingzhong.meng@

Summary

Arterialbloodpressureisthedrivingforcefororganperfusion.Althoughhypotensioniscommoninacutecare,thereisalackofacceptedcriteriaforitsdefinition.Mostpractitionersregardhypotensionasundesirableeveninsituationsthatposenoimmediatethreattolife,buthypotensiondoesnotalwaysleadtounfavourableoutcomesbasedonexperienceandevidence.Thuseffortsareneededtobetterunderstandthecauses,consequences,andtreatmentsofhypotension.Thisnarrativereviewfocusesontheheterogeneousunderlyingpathophysiologicalbasesofhypotensionandtheir

impactonorganperfusionandpatientoutcomes.Weproposetheiso-pressurecurvewithhypotensionandhypertensionzonesasawaytovisualizechangesinbloodpressure.Wealsoproposeahaemodynamicpyramidandapressur-

e_output_resistancetriangletofacilitateunderstandingofwhyhypotensioncanhavedifferentpathophysiological

mechanismsandend-organeffects.Weemphasisethathypotensiondoesnotalwaysleadtoorganhypoperfusion;tothecontrary,hypotensionmaypreserveorevenincreaseorganperfusiondependingontherelativechangesinperfusionpressureandregionalvascularresistanceandthestatusofbloodpressureautoregulation.EvidencefromRCTsdoesnotsupportthenotionthatahigherarterialbloodpressuretargetalwaysleadstoimprovedoutcomes.Managementofbloodpressureisnotaboutmaintainingaprespecifiedvalue,butratherinvolvesensuringorganperfusionwithoutundue

stressonthecardiovascularsystem.

Keywords:autoregulation;bloodpressure;hypotension;organperfusion;outcome;pathophysiology;perfusion

Editor’skeypoints

.Hypotensionhasheterogenousunderlyingpatho-physiologicalcausesandorgan-specificeffectsontissueperfusion.

.Hypotensiondoesnotalwaysleadtoorganhypo-perfusion;infact,itmaynotaffectormayevenin-creaseorganperfusion.

.TheoverallevidencefromRCTsdoesnotsupportthenotionthatahigherbloodpressuretargetalwaysleadstoimprovedpatientoutcomes.

ArterialBPisperhapsthemostcommonlymeasuredhaemo-dynamicvariable.Itcanincreaseordecreaseacutelytopro-ducehypertensionorhypotension,respectively.Althoughthetermshypertensionandhypotensionhavelongbeeninuse,

widelyacceptedcriteriadefiningtheminacutecare,includingintheperioperative,intensivecare,andemergencysettings,havenotbeenestablished.Thisisexemplifiedbythefactthatalthoughthediagnosticcriteriaforchronichypertensionaredefinedinchroniccare,

1

,

2

althoughdiagnosticcriteriahaverecentlybeenrevised,

3

similarclearlydefinedcriteriaforacutehypertensioninacutecaredonotexist(butseeSesslerandcolleagues

4

forrecenteffortstoestablishsuchcriteria).Thisreviewfocusesonthediscussionofacutehypotension,whichisamorefrequentoccurrencethanacutehypertensioninacutecare.

Hypotensioncurrentlylackswidelyacceptedcriteriafordiagnosisinacutecare.

5

,

6

Acohortstudyshowedthatboththethresholdusedtodefinehypotensionandthemethodchosentoquantifyhypotensionaffecttheassociationbe-tweenintraoperativehypotensionandoutcomes.

7

Thisfindingsuggeststhatintraoperativehypotensionstudies

Received:7April2021;Accepted:25June2021

©2021BritishJournalofAnaesthesia.PublishedbyElsevierLtd.Allrightsreserved.

ForPermissions,pleaseemail:

permissions@

846■L.Meng

basedondifferentmethodologiesarenotcomparableand

thatitischallengingtoapplythereportedresultsinclinicalpractice.Althoughhypotensiondoesnotalwaysappeartobehazardousbasedonbothclinicalexperienceandavailableevidence,mostpractitionersstillregarditasundesirable,eveninsituationsthatposenoimmediatethreattolife.Thisincongruityimpliesthatwemayneedtoreflectonthefundamentalsofhypotension,includingitsunderlyingpathophysiologyandcriticalimpact.Clarificationofthesefundamentalsmayimproveourunderstandingofacutehy-potensioninacutecare.

Hypotensionandoutcomesbasedoncohortstudies

Mostcohortstudiesshowaconsistentassociationbetweenacutehypotensionandunfavourableoutcomesinacutecare.

8

,

9

Forexamplecohortstudiesperformedinnoncardiacnon-neurologicsurgicalpatientsshowanassociationbe-tweenperioperativehypotensionandunfavourableout-comes,namelymortality,

10

_

25

all-causemorbidity,

26

acutekidneyinjury,

27

_

32

myocardialinjury,

11

,

19

,

27

,

29

,

30

,

33

_

39

4025,39,4142

congestiveheartfailure,stroke,cognitivedecline,

delirium,

43

poorliver

8

andkidney

44

graftfunction,andpost-oesophagectomyleak.

45

However,thereareexceptionsinwhichnoassociationbetweenhypotensionandunfav-ourableoutcomeswasfoundfornoncardiacnon-neurologicsurgicalpatients.

46

_

50

Similarly,mostcohortstudiesper-formedincardiacsurgicalpatientsinvolvingcardiopulmo-narybypassshowanassociationbetweenperioperativehypotensionandincreasedmortality,

51

,

52

majormorbidity,

52

watershedstroke,

53

earlycognitivedysfunction,

54

post-5556_58

operativedelirium,andacutekidneyinjury.However,thereareexceptionsinthispatientpopulationaswell:onestudyfailedtoassociatehypotensionwithpostoperativedelirium,

59

andthreestudiesfailedtoassociatehypotension

60_62

withacutekidneyinjury.

Theresultsofthesecohortstudiesshouldbeinterpretedinlightoftheirinherentlimitations.Thefirstlimitationisrelatedtothevarietyofthresholdsusedtodefinehypoten-sionandthemethodschosentoquantifytheaccumulativeeffectsofhypotension(i.e.theexposure).

5

,

7

Thevarietyinexposuredefinitionsaffectstheresultsoftheassociationbetweenintraoperativehypotensionandoutcomes.

7

More-over,thebaselineBPusedinretrospectivestudiesmightbeunreliableasBPhasacircadianfluctuation

63

andalsotendstobehigherinclinical/hospitalsettings(whitecoathyper-tension).

64

Thesecondlimitationisrelatedtothedefinitionofoutcomes.Theoutcomes,definedretrospectively,werenotpre-specified,leadingtovariationsinthetiming,criteria,validity,relevance,andavailabilityofthedifferentoutcomemeasures.Thethirdlimitationisrelatedtoconfoundercontrol.Hypotensionhasdifferentunderlyingpathophysio-logicalcausesandeffectsonorganperfusion(seebelow),andorganperfusion,notthebloodpressureperse,de-terminesoutcomesrelevanttohaemodynamics.Cohortstudiesinvestigatingintraoperativehypotensiondonotnormallyconsiderflow/perfusion-relatedinformation(owingtothelackofroutinemeasurement);therefore,thesestudiescouldbeconfoundedbythisunmeasuredyetcriticalinformation.Howhypotensionistreatedcouldalso

confoundcohortstudiesbecausedifferenttreatments,althoughtheymayallincreaseBP,mayhavedifferentef-fectsonorganperfusionandothervariables.

65

Hypotensionandoutcomesbasedonrandomisedcontrolledtrials

Amongstudiesinvestigatingtherelationshipbetweenhypo-tensionandoutcomes,thereisaconspicuousdiscrepancybetweenevidencebasedoncohortstudiesandevidencebasedonRCTs.Althoughanabundanceofcohortstudieshavesug-gestedanassociationbetweenperioperativehypotensionandunfavourableoutcomes,

4

RCTshavefailedtodemonstrateconsistentlyimprovedoutcomesfrommaintainingahigherBP(

Table1

).

66

_

73

Assessingthisbodyofevidenceinsurgicalpa-tientsislimitedby:(1)differentsurgeries,(2)differentBPtar-getsanddifferentBP-relatedinterventions,(3)differentoutcomemeasures,and(4)differentflow/perfusion(includingpumpflowduringcardiopulmonarybypass).Inpatientswithsepticshockrequiringresuscitation,therewasnosignificantdifferenceinmortalitybetweenstrategiestargetingahigher(80_85mmHg)orlower(65_70mmHg)MAP.

74

Incriticallyillolderpatientswithvasodilatoryhypotension,therewasnosignificantdifferenceinmortalitybetweenpermissivehypo-tension(targetinganMAPof60__65mmHg)andusualcare(targetingahigherBP).

75

Theseinconsistentfindings,albeitlikelytohavemultifactorialcauses,suggestthatwemayneedanimprovedapproachtowardunderstandinghypotension,includingitsdefinition,pathophysiology,andeffectsonorganperfusionandpatientoutcomes,inacutecare.Inotherwords,BPmanagementisnotassimpleasmerelytargetingapre-specifiedBPvalue.

Natureofbloodpressure

UnderstandingthenatureofBPhelpstoclarifywhenandwhyhypotensionisworrisome.BPistheforceexertedbythecirculatingbloodthatpropelsbloodthroughthetissuesandorgans,thatisorganperfusion,especiallytothebrainbecauseitisatahigherlevelrelativetotheheartinsittingorstandingindividuals.HigherBPisrequiredfortheincreasedheightdifferencebetweenthebrainandheart,asillustratedbytheremarkablydifferentbaselineBPbetweenstandinggiraffesandhumans(systolicBP,~300vs~120mmHg).

76

Hypotensionhasdifferentunderlyingpathophysiologicalmechanisms

Arterialbloodpressureistheresultofmultiplehaemody-namicelements(

Fig.1

).

77

Therefore,hypotensionisnotal-waysequivalentbecauseitcanhavedifferentunderlyingpathophysiologicalmechanismsasaresultofdifferentcom-binationsofchangesinrelevantfactors.Thevarietyofpo-tentialunderlyingpathophysiologicalmechanismsbasedonthehaemodynamicpyramidframeworkispresentedin

Figure1

.However,weuseasimplerpressure_output__resist-ancetriangleframeworkthatregardsBPastheproductofcardiacoutput(CO)andsystemicvascularresistance(SVR)(

Fig.2

a).

BPisdeterminedprimarilybystrokevolume(orCO)andSVRatagivenfillingpressure,forexamplecentralvenous

Heterogeneousimpactofhypotension■847

Table1RCTscomparingahigherBPtargetwithalowerBPtargetinperioperativecare.*Earlytermination.CABG,coronaryarterybypassgrafting;CPB,cardiopulmonarybypass;DWI,diffusion-weighedmagneticresonanceimaging.

Year(Authors)SurgeryPatients

(n)

HigherBPtargetLowerBPtargetOutcomesConclusion

Noncardiacsurgery

1999(Williams-

Russo

andcolleagues)

73

2016(Carrickandcolleagues)

66

,*

2017(Futierandcolleagues)

67

Cardiacsurgery1995(Goldandcolleagues)

68

2007(Charlsonandcolleagues)

70

2011(Siepeandcolleagues)

69

2014(Azauand colleagues)

71

2018(Vedelandcolleagues)

72

Hipsurgeryunder

epiduralanaesthesia

Laparotomyor

thoracotomyfortraumaMajorabdominalsurgery

CABGwithCPB

CABGwithCPB

CABGwithCPB

CardiacsurgerywithCPB

CardiacsurgerywithCPB

235

168

292

248

412

92

300

197

MAP=55__70mmHg

MAP=65mmHg

SBP=90__110%ofrestingvalue

MAP=80__100mmHgduringCPB

MAPtarget=80mmHgduringCPB

MAP=80__90mmHgduringCPB

MAP=75__85mmHgduringCPB

MAP=70__80mmHgduringCPB

MAP=45__55mmHg

MAP=50mmHg

SBP>80mmHgor60%ofresting

value

MAP=50__60mmHgduringCPB

MAPtarget=pre-bypasslevel

duringCPB

MAP=60__70mmHgduringCPB

MAP=50__60mmHgduringCPB

MAP=40__50mmHgduringCPB

Cognitive,cardiacandrenal

complications

30daymortality

Acompositeofsystemicinflammatoryresponsesyndromeandorgan

dysfunctionbyday7aftersurgery

Mortality,cardiac,

neurologic,andcognitivecomplications,and

changesinqualityoflife

Mortality,major

neurologicorcardiac

complications,cognitive

complicationsordeteriorationinfunctionalstatus

Earlypostoperative

cognitivedysfunctionanddelirium

Acutekidneyinjury

CerebralinfarctsdetectedbyDWI

Nodifference

Nodifference

AhigherBPtargetisbeneficial

AhigherMAPduringCPBisbeneficial

Nodifference

AhigherMAPduringCPBisbeneficial

Nodifference

Nodifference

848■L.Meng

pressure(CVP);therelationshipamongthesevariablesisgovernedbytheequationCO×SVR=(MAP_CVP)×80(

Fig.3

).

80

ThusBPcanbethesamefordifferentCOandSVRvaluesaslongastheCO-SVRproductsarethesame.ForaconstantCO-SVRproduct,thecurveformedbydifferentCOandSVRpairs(withdifferentvalues)isreferredtohereastheiso-pressurecurve(

Fig.3

).Theareasbelowandabovetheiso-pressurecurvearereferredtoasthehypotensionandhyper-tensionzones,respectively(

Fig.3

).Theconceptsoftheiso-pressurecurveandthehypotensionandhypertensionzonesareexplainedin

Figure3

.HypotensionhasthefollowingfiveexclusiveunderlyingpathophysiologicalmechanismsbasedondifferentchangesinCOandSVR(

Figs2and3

):

●SVRdecreaseswhereasCOremainsstable(

Fig.2

b).

●SVRdecreaseswhereasCOincreases,buttheeffectoftheSVRdecreaseexceedstheeffectoftheCOincrease(

Fig.2

c).

●COdecreaseswhereasSVRremainsstable(

Fig.2

d).

●COdecreaseswhereasSVRincreases,buttheeffectoftheCOdecreasesurpassestheeffectoftheSVRincrease(

Fig.2

e).

●BothCOandSVRdecrease(

Fig.2

f).

Althougheachofthesemechanismsleadstohypotension,theyhavedifferentimpactsonorganperfusion,asdiscussedinthefollowingsection.

ThissimplifiedapproachshouldnotdistractourattentionfromthecausesofchangesinCOandSVRastheythemselveshavedifferentdeterminants(

Fig.1

).COistheproductofHRandstrokevolume(SV),withSVdependentonpreload,myocardialcontractility,andafterload.SVRisdeterminedbythevascularradius,vascularlength,andbloodviscosity.Clinically,interventionssuchastheadministrationofvaso-pressors,

65

beta-adrenergicantagonists,

81

andcalciumchan-

8283

nelblockersandtheuseofpacemakers,canleadtochangesinthesehaemodynamicaspects,andthereforeBPchanges.

Supply-demandbalance

Echocardiography

Coupling

Tissue

metabolism

Pulsepressurevariation

StrokevolumevariationSystolicpressurevariation Plethvariabilityindex CorrectedflowtimeCentralvenouspressure

Strokevolumechange(fluidchallenge)

viscosity

Pulmonarycapillarywedgepressure

PreloadContractilityAfterload

LV

diastolictime

Organ

perfusion

Autoregulation

Blood

pressure

Regional

vascularresistance

Vascular

radius

Poiseuille’sLaw

8μLResistance=4

πRR,VascularradiusL,Vascularlengthμ,Bloodviscosity

Cardiac

output

Systemic

vascularresistance

Vascular

length

Heart

rate

Stroke

volume

Blood

Baroreflex

Venous

return

Pulmonarycirculation

Atrial

contraction

Mitralvalvestatus

LV

compliance

lntravascularvolume

Aorticvalvestatus

Fig1.Haemodynamicpyramid.Venousbloodmustreturntotheheartandflowthroughtherightheart,pulmonaryvasculature,leftatrium,andmitralvalvetocreatethepreloadoftheleftventricle.Themagnitudeofleftventriclepreloadisalsodependentonatrialcontraction,mitralvalvestatus,aorticvalvestatus(e.g.aorticvalveregurgitationleadingtoaugmentedpreload),andthecomplianceanddiastolictimeoftheleftventricle.Themagnitudeofstrokevolumeisdependentonpreload,myocardialcontractility,andafterload.Bloodpressureisdependentoncardiacoutputandsystemicvascularresistance(SVR),whereascardiacoutputistheproductofstrokevolumeandheartrate.AfterloadandSVRarerelated.SVRisproportionaltothevascularlengthandbloodviscosityandinverselyproportionaltovascularradiustothefourthpower,arelationshipdescribedbytheHagen_Poiseuilleequation.Organperfusionisdependentonbloodpressure(orperfusionpressure)andregionalvascularresistance(RVR).TherelationshipbetweenorganperfusionpressureandRVRisgovernedbypressureautoregulation.Thematchbetweenorganperfusionandtissuemetabolicactivitydeterminesperfusionadequacyandisoneofthepremisesoforganwell-being.Adequateorganperfusionistheprimarygoalofhaemodynamicmanagement.Baroreflexexertsitseffectsprimarilyonthevascularradius,heartrate,andmyocardialcontractility.Bloodpressure(highlightedinredfonts)andheartratearealwaysmonitoredinacutecare.Themodernhaemodynamicmonitorenablestheassessmentofstrokevolumeandthuscardiacoutputorindex.Tissueoximetrybasedonnear-infraredspectroscopyenablesassessingthebalancebetweentissueoxygenconsumptionandsupply.Avarietyofmeansandparametersassessespreload.Modernhaemodynamicmanagementhasavarietyofapproacheswithlikelydifferenteffectivenessdependingontheoutcomesofinterest.77__79LV,leftventricle.

Heterogeneousimpactofhypotension■849

BPKCO*SVR

ΔP

PerfusionK

RVR

BPKCO*SVR

BP(↓)KCO(↑)*SVR(↓↓)

Perfusion(↑)KR(()

BP(↓)KCO(↑)*SVR(↓↓)

BP(↓)KCO(–)*SVR(↓)

BP(↓)KCO(↓)*SVR(–)

BP(↓)KCO(↓↓)*SVR(↑)

BP(↓↓)KCO(↓)*SVR(↑)

Perfusion(–)K

Perfusion(↓)K

Perfusion(↓↓)K

Perfusion(↓)K(↓)(–)

BP(↓)KCO(–)*SVR(↓)

BP(↓)KCO(↓)*SVR(–)

BP(↓)KCO(↓↓)*SVR(↑)

BP(↓↓)KCO(↓)*SVR(↓)

=CO*distribution

Pressure-output-resistance

triangle

Organperfusion

Perfusion

CO

VR

BP

=CO(↑)*distribution(–)

HypotensioniscausedbySVRdecreasewithlessincreaseinCO;

Organ

perfusion

(↑)

Perfusion(↑)

VR

(↓↓)

CO

(↑)

BP

(↓)

c

BP

(↓)

CO

(-)

VR

(↓)

BP

(↓)

BP

(↓)

BP

(↓↓)

CO

(↓)

VR

(-)

CO

(↓↓)

VR

(↑)

CO

(↓)

VR

(↓)

a

b

Organ

perfusion

(-)

Perfusion(–)

=CO(–)*distribution(–)

HypotensioniscausedbySVR

decreasewithoutchangesinCO;

OrganperfusionremainsstableOrganperfusionincreases

def

Organ

perfusion

(↓)

Perfusion(↓)

=CO(↓)*distribution(–)

HypotensioniscausedbyCO

decreasewithoutchangesinSVR;

Organperfusiondecreases

Organ

perfusion

(↓)

Perfusion(↓)

=CO(↓)*distribution(–)

Hypotensioniscausedby

decreasesinbothCOandSVR;

Organperfusiondecreases

Organperfusion

(↓↓)

Perfusion(↓↓)

=CO(↓↓)*distribution(–)

HypotensioniscausedbyCO

decreasewithlessincreaseinSVR;

Organperfusiondecreases

Fig2.Thepressure_output_resistancetriangle.Organperfusionisinthecentreofthetriangle.Thisdiagramisbasedonthefollowingpremises:(1)changesinsystemicvascularresistance(determinantofbloodpressure)andregionalvascularresistance(determinantoforganperfusion)areconcordant,and(2)theshareofcardiacoutputamongvariousorgansremainsstable.Bloodpressureisproportionaltocardiacoutputandsystemicvascularresistance.Organperfusionisproportionaltoperfusionpressureandinverselyproportionaltoregionalvascularresistance;itisalsoapercentageshareofcardiacoutput(a).Hypotensioncanbecausedbyadecreaseinsystemicvascularresistance(closeredcircleandredarrow),andinthiscase,organperfusionremainsstablebecauseoftheproportionaldecreasesinbloodpressureandregionalvascularresistance(b).Hypotensioncanbecausedbyasignificantdecreaseinsystemicvascularresistance(closedredcircleandredarrow),althoughthereisalesserdegreeofincreaseincardiacoutput(closedbluecircle).Inthiscase,organperfusionisincreasedbecauseofthelesserdecreaseinbloodpressurethanthedecreaseinregionalvascularresistance(c).Hypotensioncanbecausedbyadecreaseincardiacoutput(closedredcircleandredarrow),andinthiscase,organperfusionisdecreasedbecauseofdecreasedperfusionpressureinthefaceofanunchangedregionalvascularresistance(d).Hypotensioncanbecausedbyasignificantdecreaseincardiacoutput(closedredcircleandredarrow),althoughthereisalesserdegreeofincreaseinsystemicvascularresistance(closedbluecircle).Inthiscase,organperfusionhasasignificantdecreasebecauseofdecreasedperfusionpressureinthefaceofanincreasedregionalvascularresistance(e).Hypotensioncanbecausedbysimultaneousdecreasesincardiacoutputandsystemicvascularresistance(closedredcirclesandredarrows).Inthiscase,organperfusionisdecreasedbecauseofthemoresignificantdecreaseinperfusionpressurethanthedecreaseinregionalvascularresistance(f).CO,cardiacoutput;VR,vascularresistancewhichcanbeeitherSVR(systemicvascularresistance)orRVR(regionalvascularresistance)dependingonthecontext;ΔP,perfusionpressure

850■L.Meng

Organ-specificimpactofhypotensiononperfusion

Hypotension,althoughusuallyleadingtodecreasedperfusionpressure,doesnotalwaysleadtoorganhypoperfusionbecauseorganperfusionisdeterminedbytheperfusionpressuredividedbytheregionalvascularresistance(RVR).BasedonPoiseuille’slaw,RVRisdeterminedbythevascularradius,vascularlength,andbloodviscosity,althoughthevascularlengthrarelychangesclinically.Multiplefactorscanchangethevascularradiusorvasomotortone,forexampleage,atherosclerosis,bloodpressure,hypercapnia,andvaso-activedrugs(tonameafew),andthusleadtoRVRchanges.Thechangeinvasomotortonesecondarytoachangeinperfusionpressureismediatedbythemyogenicmechanismandisthefoundationofthepressure-dependent

autoregulationoforganbloodflow(

Fig.4

).DependingontherelativedirectionandmagnitudeofchangesinRVRascomparedwithperfusionpressure,hypotensioncanhavethefollowingthreeeffectsonorganperfusion:

●OrganperfusionremainsstableiftheeffectsofthedecreasesinperfusionpressureandRVRarecomparable,ascenarioinwhichtheunderlyingpathophysiologyofhypotensionisanSVRdecreasewithoutchangesinCO(

Fig.2

b).Thisimpactisconsistentwiththeconventionalconceptofpressureautoregulation,asdiscussedinthefollowingsection.

●Organperfusionincreasesiftheeffectoftheperfusionpres-suredecreaseislessthanthatoftheRVRdecrease,ascenarioinwhichhypotensionissecondarytoanSVRdecreaseaccompaniedbyalesserdegreeofCOincrease(

Fig.2

c),asexemplifiedbytheuseofcertaincalciumchannelblockers.

82

SVR(mmHgminL–1)

Hypertensionzone

*CO↑

*SVR↑

*CO↑

*SVR(–)

*CO↑

*SVR↓CO↑>SVR↓

Iso-pressurecurve

*CO↓

*SVR↑CO↓>SVR↑

A

*CO↓

*SVR(–)

*CO↓

*SVR↓

3000

2500

2000

1500

1000

500

0

*CO(–)

*SVR↑

B

*CO(–)

*SVR↓

02.54567.51012.51517.520

*CO↓

*SVR↑CO↓<SVR↑

*CO↑

*SVR↓CO↑<SVR↓

HypotensionZone

CO(Lmin–1)

Fig3.Hypotensionandhypertensionzonesdividedbytheiso-pressurecurve.TheabscissaindicatesCO,andtheordinateindicatesSVR.Thefollowingequationgovernstherelationshipamongdifferentsystemichaemodynamicvariables:COXSVR¼(MAP_CVP)X80.Theblackcurveistheiso-pressurecurve;foragivenpairofCOandSVRvalues,aslongastheCO_SVRproductequalsthedifferenceofMAPandCVPtimes80,thepointdeterminedbytheCO_SVRpairfallsontheiso-pressurecurve.Inthiscase,weassumeMAPis85mmHgandtheCVPis5mmHgtoexemplifytheconcept;thepointrepresentingaCOof5Lmin__1andanSVRof1280mmHgminL__1fallsontheblackiso-pressurecurvebecausetheCO-SVRproductequalstheMAP_CVPdifferencetimes80.Theleftlowerpurpleareaiscalledthehypo-tensionzonebecauseanypointinthisarea,nomatterwhatCOandSVRvaluesitpresents,leadstoasmallerMAP_CVPdifferencethantheMAP-CVPdifferencedictatingtheiso-pressurecurve.Forexample,pointA,determinedbyaCOof4Lmin__1andanSVRof1100mmHgminL__1,correspondstoaMAP_CVPdifferenceofapproximately55mmHg;ifassumingCVPequals5mmHg,MAPis60mmHginthisexample.ThecombinationsofdifferentCOandSVRchangesrepresentdifferentunderlyingpathophysiologiesofhypotension.Therightupperblueareaiscalledthehypertensionzonebecauseanypointinthisarea,nomatterwhatCOandSVRvaluesitrepresents,leadstoalargerMAP_CVPdifferencethantheMAP_CVPdifferencedictatingtheiso-pressurecurve.Forexample,pointB,determinedbyaCOof6Lmin__1andanSVRof1400mmHgminL__1,correspondstoaMAP_CVPdifferenceofapproximately105mmHg;ifassumingCVPequals5mmHg,theMAPis110mmHginthisexample.ThecombinationsofdifferentCOandSVRchangesrepresentdifferentunderlyingpathophysiologiesofhypertensionCO,cardiacoutput;SVR,systemicvascularresistance;CVP,centralvenouspressure

..

Heterogeneousimpactofhypotension■851

●Organperfusiondecreasesifperfusionpressuredecreasesin

thefaceofoneofthefollowingchangesinRVR:(1)anun-changedRVR_thatisascenarioinwhichtheunderlyingpathophysiologyofhypotensionisaCOdecreasewithoutchangesinSVR(

Fig.2

d);(2)anincreasedRVR_thatisascenarioinwhichhypotensionissecondarytoaCOdecreaseaccompaniedbyalesserdegreeofSVRincrease(

Fig.2

e);or(3)adecreasedRVR,withthedegreeoftheRVRdecreaselessthanthatoftheperfusionpressuredecrease_ascenarioinwhichhypotensionissecondarytoadecreaseinbothCOandSVR(

Fig.2

f).

Theoverarchingmessageisthathypotensiondoesnotinevitablyleadtoadecreaseinorganperfusion;instead,itsimpactonorganperfusionisdependentonthedirectionofthechangeinRVR(

i.e.no

change,increase,ordecrease)and,whenRVRdecreases,ontherel