Andersons pediatric cardiology 374
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improvedwiththisapproach,351,355arandomizedoutcometrialislacking.356
Therelationshipbetweenhemodynamics,oxygendelivery,andoutcomesin
neonatesundergoingarchreconstructionusingα-adrenergicblockadehasbeen
recentlyreviewed.357
ControlofGlucose
Evidenceforabeneficialeffectofglycemiccontrolinpediatriccardiacsurgery
isdistinctlylacking.Theneonatalbrainandheartarepoorlytolerantof
hypoglycemia,whichhasbeenrelatedtoseizureactivityandpooroutcomeina
largeretrospectivestudyofintraoperativeglycemicpatternsandneurologic
outcome.358Incontrasttofindingsinadults,posthypoxicsupplementationof
glucosemayreduceneurologicinjuryinthedevelopingbrain.359Insulinhas
antioxidative,antiapoptoticprosurvivalcellprogrammingeffectsindependentof
itsglycemiceffects.333,360Becausedeficiencyofinsulinisrareininfantsand
children,theroleforexogenousinsulinisnotyetestablished.
Ultrafiltration
MUFisatechniquetoremoveexcessivewaterfromthebodyafterrestorationof
thenativecirculationbutbeforeremovalofthecannulasusedforbypass.361,362
Asanincrementalstrategyinadults,MUFreducesmorbidityandpostoperative
useofresources.363Inchildren,benefitsincludeimprovedhemodynamics,
pulmonarymechanics,andcerebralmetabolism.266,364–367Someoftheseeffects
maybeachievedbyotherstrategiestoreducethedeleteriouseffectsofbypassrelatedhemodilutionandactivationofbloodproducts,includingconventional
ultrafiltrationandstrategiesforreductionoftheprime.368–370Thedirecteffectof
MUFoninflammatorymediatorsandonultimateclinicaloutcomeis
uncertain.363,364Extremereductioninthevolumeofprimevolume
miniaturizationofthecircuitmayeventuallyreplaceultrafiltration.371Itislikely
thatacombinationofultrafiltrationandincrementalalterationsincomponentsof
thecircuittoimprovebiocompatibilitycanalsoimproveoutcomes.183,364MUF
hasbeenestablishedasaclass1Arecommendationasacomponentofblood
conservationstrategies.372
Preconditioning
Ischemicpreconditioning,orinductionoftolerancetoprolongedischemiaby
briefexposuretoischemia,hasbeenobservedinthemyocardium,brain,liver,
kidney,intestine,andskeletalmuscle,andprobablyisafeatureofall
mammaliancells.373Theeffectwasfirstdescribedbytheobservationofreduced
sizeofinfarctsafter40minutesofcoronaryarterialocclusionifprecededby
cyclesof5minutesofocclusion.374Theearlyprotectivewindowoccurswithin
minutes,andfadeswithinafewhours.Alatersecondwindowofprotection,or
delayedpreconditioning,opensabout24hoursaftersomepreconditioning
stimuluses.373,375,376
Earlyprotectiveresponsestosublethalischemiainducealterationintheflow
ofbloodandmetabolism.Withinhours,signalingsystemsinvolvinghypoxiainduciblefactorsandheatshockproteinsconferresistancetoapoptotic
transformation.377Featuresofthischaracteristicresponsecanbeinducedby
hypoxia-ischemia,hyperthermia,hypothermia,hypoglycemia,arangeofdrugs
includingK-ATPchannelblockers,erythromycin,volatileanesthetics,opioids,
acetylsalicylicacid,glutamate,anderythropoietin,thelatterhavingreceived
muchattentioninrecentclinicaltrials.378,379Themediatorsofthisresponse
favoringsurvivalcanbereleasedremotelyfromthetargetorgan,andimproved
myocardialfunctionhasbeendemonstratedinhumansafterminimalischemia
inducedbyatourniquetplacedontheleg.380Inductionofacommonsignaling
pathwayforsurvivalofcells,asopposedtoapoptosis,hasbeensuggestedasthe
underlyingmechanismforthesefindings.381,382
ConsiderationsattheEndofBypass
AlteredCerebralFlowofBloodandMetabolism
Theincreasedrelativeflowofbloodtothebraininducedbyhypothermiacan
resultinapostoperativeincreaseincerebrovascularresistanceandcerebral
edema,althoughresponsivenesstocarbondioxideismaintained.383–386Someof
thisimpairedflowmaybeduetomicrovascularocclusionandcanbe
amelioratedbytreatmentsthatreduceaggregationandadhesionofplatelets,
suchasdonorsofnitricoxide,antagonistsofthromboxane,andantiplatelet
drugs.387–390MUFalsoseemstoimprovecerebralbloodflowandmetabolism,
presumablybyreductionofinflammatorymediators.266
Hypothermiccirculatoryarrestresultsinbothlossofautoregulationand
delayedreflow,withaprolongedsuppressionofflowofbloodanduptakeof
oxygen.214,391,392Thisdelayedrecoveryofcerebralmetabolismmayexacerbate
theneurologicinjuryrelatedtocirculatoryarrest.193Suppressionofmetabolism
duringhypothermiccirculatoryarrestusingapH-statstrategy254and
maintenanceofahigherpostoperativehematocrit393can,inpiglets,partially
amelioratethismetabolicderangementoccurringaftercirculatoryarrest.
Postoperativearterialhypoxemiaexacerbatesthearrest-relatedinjury394and
maintenanceofdeliveryofoxygentothebrainwithmechanicalassistancemay
bepreferabletoinadequatepostoperativedelivery.198,395Wehavedemonstrated
that,followinghypothermiccirculatoryarrestinneonates,inadequate
postoperativeeconomyforoxygenisrelatedtopoorlateneurodevelopmental
outcomeandpostoperativehypercapniaisprotectiveinthissetting.235
Continuouscerebralperfusiondoesnoteliminatetheriskofpostoperative
cerebraldesaturation334,396andtheinteractionbetweenintraoperative
managementandpostoperativeflowsofbloodremainscomplex.
Postconditioning
Ischemicpostconditioningdescribesmodificationofinjurybyinterventions
appliedjustatthetimeofreperfusion,andwasfirstobservedwithintermittent
reperfusion.397Thismaybeaformofmodifiedreperfusion,andhasbeen
observedwithavarietyofagents,includingerythropoietin,insulin,and
isoflurane,whicharecommonlyadministeredintheoperatingroomaroundthe
timeofCPBandotherischemicchallenges.373,398,399Whilehypothermiaand
volatileanestheticsamplifytheprotectionaffordedbypreconditioningfor
toleranceofprolongedischemia,postconditioningseemstohavelimitedeffect
afterprolongedischemia.400–402Remotepostconditioninghasbeendescribedvia
briefocclusionoflegorkidneyperfusionjustatthetimeofreperfusionof
myocardium,yieldingareductioninthesizeofinfarcts48to72hours
later.378,403Whiletheapplicationofthesetechniquesmayseemsimpleand
associatedwithminimalrisk,theclinicalutilityremainstobeelucidated.
Inadvertentconditioningmayresultfromaspectsofstimulationsprovidingpreandpostconditioningcommonlypresentthroughouttheoperativeperiod.The
techniqueofintermittentreperfusionduringprolongedhypothermiccirculatory
arrest308maybeaparadigmforbothpreconditioningandpostconditioning.An
acidoticperfusionmilieuatthebeginningofreperfusionmaynotonlyenhance
flowbutmayalsobeimportantinpromotingischemicpostconditioningand
