Andersons pediatric cardiology 371
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StrategiesforCooling
Surfacecoolingcanbeginwithinductionofanesthesia,whichpromoteslossof
heatandimpairsthermoregulatoryresponses.Areductionintemperatureto
35°Cisgenerallywelltolerated,andmayconferprotectionagainstischemiain
theperiodpriortobypassbymetabolicsuppressionandalterationofresponses
tocellularinjury.Furthercoolingonbypassistargetedbasedontheanticipated
levelofflowrequiredtocompletethesurgicalrepair.IfDHCAisanticipated,a
nasopharyngealtemperatureof18°Cisgenerallythetarget,withevidencefor
increasedcomplicationsatsignificantlyhigherandlowertemperatures.Active
coolingshouldbeaccompaniedbymeasuresoftheadequacyofuniformcerebral
cooling,forwhichmeasurementsofsurfacetemperatureareinadequate.227
Otherindicatorsincludejugularvenoussaturation,theelectroencephalogram,
andNIRS,fromwhichevidenceofmetabolicsuppressioncanbemoredirectly
ascertained.228–232Atleast20minutesofcoolingisassociatedwithimproved
outcomeifhypothermiccirculatoryarrestisutilized.233,234Ahigh-flowhardcoolingpumpstrategyisnecessarytoraisethejugularvenoussaturationabove
95%.182Measuresthatincreasecerebralbloodflow,suchasapH-statstrategy,
canimprovebraincoolingaspreviouslydiscussed.183
Recentevidence-basedreviewscitenoadvantagetohypothermiaineither
neurosurgeryoropenheartoperations.235,236Sincemanyoperationscanbe
completedwithoutsignificantinterruptioninflowofblood,thisfindingmaybe
unsurprising.237Thesemeta-analyticreviews,nonetheless,flyinthefaceof
overwhelminglaboratoryandclinicalevidenceofprotectionfromischemic
injurywithhypothermiainglobalischemia.238–242Becausethemetabolicbenefit
ofcoolingandhypothermiaislostduringrewarming,whichmaybe
superimposedonaperiodofreduceddeliveryofoxygen,agreaterriskof
ischemiatobothheartandcentralnervoussystemoccurswithrewarming.243
Giventhemultiplefactorsthatmaycauseunexpecteddisruptioninperfusionat
fullflow,someemergentinnature,mostcenterscontinuetousemildor
moderatehypothermiaasaprotectiveadjuncttoCPBwithoutplannedreduction
offloworcirculatoryarrest.237,244Whiletheoverallperioperativeinflammatory
response,althoughreducedduringhypothermia,doesnotseemtobealteredby
strategiesdependingontemperature,245moderatehypothermiaprobablyinduces
cellularadaptationsatthetranscriptionalandtranslationallevelthatresultin
survivalprogramming.246,247
Inpracticalterms,schemesforcoolingarerelativelystandardizedinmost
institutions.Thecomplexityofthedefecttobecorrectedorpalliateddictatesthe
strategyforthetemperatureusedduringbypass,albeitcompoundinganatomic
featuressuchasthepresenceofaortopulmonarycollateralarteriesmayinfluence
thestrategy.Typically,mildhypothermia,at37°Cto32°C,willbeemployedfor
simpledefectssuchasatrialandventricularseptaldefects.Moderate
hypothermia,between32°Cand28°C,isusedformorecomplexlesionssuchas
atrioventricularseptaldefectortetralogyofFallot.Deephypothermia,from
28°Cdownto18°C,isreservedforthemostcomplexlesionsrequiringaperiod
ofcirculatoryarrest,suchaspalliationofhypoplasiaoftheleftheart,repairof
interruptedaorticarchorcorrectionofdiscordantventriculoarterialconnections.
Whilethedescribedcoolingpracticeiscommon,somehavebegunusingwarm
CPBforeventhemostcomplexprocedures,coolingonlytoamildhypothermic
temperatureof34°C.248,249Apparentacutebenefitsofthisapproachinclude
decreasedCPBtimesandareductioninperioperativebleeding,butlonger-term
measuresofend-organpreservationincludingneurologicfunctionarenecessary.
Acid-BaseManagement
ThemanagementofbloodgasesduringCPBisintertwinedwiththatof
temperatureandhasbeenwidelyinvestigatedanddebated.Thecomplexity
ensuesbecausemetabolicrate,thesolubilityofgasesinblood,theionizationof
waterandthereforethepHofelectroneutrality,theionizationofintracellular
buffer,andtheaffinityofbothoxygenandcarbondioxideforhemoglobinareall
dependentontemperature.250TherearetwostrategiesforpHmanagement.A
pH-statstrategymaintainsnormallevelsofcarbondioxideandhydrogenions
whenmeasuredathypothermiaortemperaturecorrected.Analpha-statstrategy
maintainsnormalgastensionsandacid-basebalancewhenmeasuredat
normothermiaortemperatureuncorrected.Thealpha-statapproachisassociated
withminimalmetabolicsuppressionandrepresentsthephysiologicsituationin
homeothermswithtemperaturegradientsacrosspartsofthebodybutwith
thermoregulationmaintained.ThepH-statapproachisassociatedwithmetabolic
suppressionandmorecloselymimicsthemetabolicmilieuofhibernationwith
inductionofmetabolicsuppression.251
ThepHaffectstheratioofflowofbloodtometabolism.215Whilelevelsof
adenosinetriphosphateinthebrainaremaintainedduringalpha-stat
cooling,213,252withpH-statcoolingthereisevidenceofluxuryperfusion.At
temperaturesbelow30°Cbloodflowispressure-passiveoverawiderrangeof
metabolismwithover-perfusionevidencedbytheappearanceofedema.253The
increasedflowwithpH-statstrategyiswidelyutilizedtoincreaseuniformityof
cerebralcooling,oxygenation,204,213,254–258andmetabolicsuppression.212,250,258
ThereisevidenceofimprovedoutcomeinchildrensubjectedtoDHCA259–261or
low-flowbypasswhenusingthepH-statstrategy.262–264Evidencealsoexistsfor
improvedmyocardialfunctionwithpH-stattechniques.265TheeffectsofpHon
noncerebraltissuearealsoimportantindeterminingthedistributionofflowon
CPB.ApH-statstrategydirectsmorebloodtothebraininthepresenceof
aortopulmonarycollateralconnections.204ApproachesthatcombinepH-stat
strategyforcoolingwithalpha-statstrategyformaintenanceofhigh-flow
hypothermicperfusionmayrepresentacompromisebetweeninadequate
deliveryofoxygenandmetabolicsuppressionandover-perfusion–related
formationofedemaandpostacidoticincreasedcerebrovascularresistance.266,267
CerebralProtectionandAnesthesia
Suppressionofcerebralconsumptionofoxygenoccurswithbothvapor-and
barbiturate-basedanesthesiaandhypoxiatolerance,basedonlactateproduction,
isenhanced.268Thesuppressionofmetabolismbyanestheticvaporsis
accompaniedbymaintenanceofhighenergyphosphatesindicatingdesirable
energeticbalance.269Becausevaporagentsarealsocerebralvasodilators,the
ratioofcerebralflowtometabolismishigherwiththeseagentsandtheincrease
incerebralflowmaybemaintainedforhours.270–272Suppressionof
thermoregulatory273responsestohypothermiamaybeanimportantroleforthe
salutaryeffectoflower-stressanestheticstrategiesonsurvivalincomplex
repairs.274Inhibitionofpotassium–adenosinetriphosphate(K-ATP)channelsby
vaporsmayinducepreconditioning,reducereperfusioninjury,andreduce
apoptosisinischemicmodels.275–277Thevasodilatoryeffectsofvapor
anestheticscanbeexpectedtoimprovetheuniformityofcerebralcoolingand
warming.Withdrawalofanestheticvaporislikelytoinducecerebral
vasoconstrictioninafashionparalleltothevasodilationseenonacute
introduction.Becausetheneonatalbrainisparticularlyvulnerabletoapoptosis
viaexcitotoxicinjury,vaporanestheticsmightbeparticularly
indicated.276,278–281However,allanestheticagentswiththeexceptionof
dexmedetomidineandopioidshavebeenimplicatedinenhancedapoptotic
