Andersons pediatric cardiology 202
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FIG.7.11 Distributionofbloodflowandoxygensaturationsacrossthe
normallate-gestationhumanfetalcirculationbyphasecontrastmagnetic
resonanceimagingandmagneticresonanceoximetry.Thecolorcoding
indicatestheoxygensaturationsandnumbersindicatevesselflowsasa
percentageofthecombinedventricularoutput(left)andinmL/min/kgof
fetalweight(right).AAo,Ascendingaorta;CVO2,centralvenousoxygen
saturation;DA,ductusarteriosus;DAo,descendingaorta;FO,foramen
ovale;IVC,inferiorvenacava;LA,leftatrium;LV,leftventricle;MPA,main
pulmonaryartery;PBF,pulmonarybloodflow;RA,rightatrium;RV,right
ventricle;SVC,superiorvenacava;UA,umbilicalartery;UV,umbilicalvein.
HumanFetalCirculatoryAdaptationto
Hypoxia
Fetalcirculatoryadaptionstoacuteandchronichypoxiahavebeenstudied
extensivelyinthefetalsheepandhuman.2Theacuteresponseischaracterized
byredistributionofcirculationresultingfromdifferentialchangesinthe
systemic,cerebral,andpulmonaryvascularresistance.Someofthemechanisms
involvedincludeareductionincerebralvasculartoneinresponsetoneuronal
productionofadenosine.Carotidchemoreceptorsinitiallyinducebradycardiavia
vagalstimulation,whilecatecholaminereleasefromtheadrenalglandsresultsin
reboundtachycardiaandperipheralvasoconstriction.Thepulmonarycirculation
becomesmorevasoconstrictedthroughreductionsinendothelialnitricoxide
production.Theseopposingchangesindownstreamresistanceinthepresenceof
openshuntsbetweenthesystemicandpulmonarycirculationsallowsfor
dramaticredistributionofbloodflow,whichresultsinpreferentialperfusionof
thebrain,heart,andadrenalglandsattheexpenseoftheskinand
musculoskeletalsystem,abdominalviscera,andespeciallythelungs.Theability
ofthefetustomaintaincerebraloxygendeliverydespitesignificantacute
hypoxemiahasledtotheterm“brain-sparingphysiology,”andtheasymmetric
growthwithrelativesparingoftheheadseeninfetalgrowthrestrictionresulting
fromplacentalinsufficiencyislikelytobepartlyduetothesecirculatory
adaptations.However,inchronichypoxemiaadegreeofnormalizationof
circulatorydistributionisseen.16Thisislikelypossiblethroughsecondary
endocrine,metabolic,circulatory,andbehavioralmechanisms,whichleadtothe
downregulationofthefetalrequirementforoxygenandothermetabolic
substrates.However,thesesecondaryadaptationsresultindownstreameffects
onfetalgrowthanddevelopment,whichcanhavelastingeffects.Increasedrates
ofhypertension,obesity,diabetes,cardiovasculardisease,and
neurodevelopmentalproblemshaveallbeenassociatedwithfetalgrowth
restriction.17
Inlate-onsetfetalgrowthrestriction,MRIrevealsdramaticreductionsin
oxygensaturationthroughoutthecirculationassociatedwithredistributionofthe
fetalcirculationinkeepingwithbrain-sparing,withincreasesinSVCflowand
ductusarteriosusflow,andreductionsinpulmonaryandumbilicalbloodflow.12
Reductionsinumbilicaloxygencontentandflowresultinaprofounddropin
fetaloxygendelivery,evenwhenoxygendeliveryisindexedtofetalweight.
Fetaladaptationincludesareductioninoxygenconsumptionandanincreasein
oxygenextraction,whilethecirculatoryredistributionresultsinconsiderably
milderreductionincerebraloxygendelivery.Ofnote,thedistributionofthefetal
circulationisnormalinaboutone-thirdofcasesoflateonsetfetalgrowth
restriction.Thisisinkeepingwiththeverystableplacentalinsufficiencyseenin
thecarunclectomymodelofovinefetalgrowthrestriction.16
