Andersons pediatric cardiology 311

TransitioningCirculation
Theconditionoftheinfantatbirthisdependent,inpart,onintrauterinewellbeingandgrowth.Intrauterinegrowthretardationisthefailureofthefetusor
infanttoachievehisorherpredeterminedgeneticpotential.Typically,the
preterminfantislessthanthethirdcentileforweight,length,andhead
circumference.Theconsequencestothedevelopingheartincludecardiac
hypertrophy,abnormaldiastolicperformance,andimpairedvascular
relaxation.11–13Dopplerinterrogationoffetalandneonatalmitralvalvar
velocitiesrevealedlowerEwaveamplitudecomparedwithnormalmaturemitral
Epeaks.14,15Impairedearlyleftventricularfillingmayrelatetoadiminished
abilitytorelaxandhighermuscularstiffness.Theimplicationsmayinclude
impairedmyocardialperformance,hypertension,andhypotension.Poor
glycemiccontrolduringpregnancy,particularlyinthesettingofmaternal
diabetes,isaknownriskfactorforstructuralheartdiseaseandhypertrophic
cardiomyopathy.16–18Inseverecases,wherethereisplacentalmalfunction
leadingtoretardationofgrowth,thesamevascularandmyocardialdysfunction
mayoccurasdescribedpreviously.


PhysiologyofthePostnatalTransition
Thepreterminfantundergoesdramaticcardiorespiratorychangesatbirth,which
coincidewithimprovedlungcomplianceandterminationoftheplacental
circulation.Thesecriticaladaptivechanges:

▪Includeincreasedpulmonarybloodflow,to
approximately20timesfetallevels
▪Occurinpartduetotheexposureofthepulmonary
vascularbedtohigheralveolarconcentrationsof
oxygenthantherelativelyhypoxicintrauterine
environment.Othermetabolicallyactivesubstances,
suchasmetabolitesofprostaglandin,bradykinins,or
histamine,mayplaysomerolethroughinducing

pulmonaryvasodilation.
▪Includealterationinflowthroughfetalchannels
suchasthearterialductandovalforamen,whichmay
lastformanydays.Themajorchangeinflowthrough
fetalchannelsiseitheradirectresultofincreased
flowtothelungsorimprovedsystemicarterial
tensionsofoxygen.Increasedleftatrialpressure
secondarytoimprovedpulmonaryvenousreturn
causesdisplacementoftheflapoftheovalforamen
overtherimsofthefossa,thusabolishinganyrightto-leftatrialflow.Thepatternofflowthroughthe
arterialductissignificantlyalteredaslung
complianceimprovesandpulmonaryvascular


resistancedecreases.Anincreaseinsystemicvascular
resistancealsooccursoncethecompliantplacentais
removedfromthesystemiccircuit,andasaresultof
systemicvasoresponsivenesstoincreasedtensionsof
oxygen.Thiswillalsocontributetoincreased
transductalflow.Thearchitectureofthearterialduct
priortotermdifferssuchthatductaltoneisless
responsivetooxygen,thusdelayingclosureand
potentiallycontributingtoexcessiveflowtothelungs
andcompromisedsystemicflow.Theadministration
ofsurfactantcanaltertransductalflowsignificantly
throughreducedpulmonaryvascularresistance.There
isevidenceoffunctionalclosureby6hoursinsome
immaturepatients,althoughthisisrare.19Changesin
transductalflowmayhaveamajorimpactonendorganperfusion;inparticular,therelationshipof
augmentedcardiacoutputoncerebralreperfusion

hemodynamicsandintraventricularhemorrhageis
subjecttorecentinvestigation.20
▪Includeimprovedleftandrightventricularoutputs
tomeetthemetabolicneedsofimmatureneonatewith
insufficientthermoregulatorymechanismsand
increasedworkofbreathing.Thetransitionfromright
toleftventriculardominanceoccursoverhoursandis
secondarytoincreasedleftatrialpreloadandleft
ventricularafterload.Intotal,thereisathreefold
increaseinleftventricularoutput,whichisnecessary