Andersons pediatric cardiology 590

mustberemovedtomaintainarterialcarbondioxidelevelswithinthenormal
range.Thiscausesasignificantriseinproductionofcarbondioxideoutof
proportiontotheriseinconsumptionofoxygen,resultingintherespiratory
exchangeratioincreasingtogreaterthan1.0.Theratioinadultsatpeakexercise
maybeashighas1.2to1.4butisoftenlowerinchildren.6,7,10–12
Theincreaseinproductionofcarbondioxideassociatedwiththebufferingof
lacticacidallowsformeasurementofanoninvasivesurrogateofthelactate
threshold.Thissurrogate,knownastheventilatoryanaerobicthreshold,is
definedasthepointwhereproductionofcarbondioxide,andminuteventilation,
begintoriseoutofproportiontotheconsumptionofoxygen.Likethelactate
threshold,theventilatoryanaerobicthresholdoccursatapproximately50%to
60%ofthemaximalconsumptionofoxygen.Itmaybesignificantlyloweror
higherindeconditionedorhighlytrainedathletes,respectively.Likemaximal
consumptionofoxygen,theventilatoryanaerobicthresholdisaphysiologic
limitandhasbeenusedasamarkerofaerobicfitness.Unlikemaximal
consumptionofoxygen,theventilatoryanaerobicthresholdhasthevirtueof
beingeffortindependent,isalevelofexercisethatcanbesustainedovera
prolongedperiodoftime,andiseasilyaffectedbytrainingorsedentary
behavior.Unfortunately,theventilatoryanaerobicthresholdcanbeespecially
difficulttomeasureaccuratelyinsmallerchildren,whotendtohaveerratic
patternsofbreathing.6,10–13


HeartandLungasServiceOrgans
Aspreviouslymentioned,consumptionofoxygenrisesinnearlinearresponseto
increasingworkrate.TheconsumptioncanbederivedfromtheFickequationas
follows:

WhereVOisconsumption,Qiscardiacoutput,anda−vO2diffisthedifference
incontentofoxygenisarterialandmixedvenousblood.Qisdefinedas:

whereSVisstrokevolumeandHRisheartrate.Rearrangingtheequations,
VOcanbecalculatedas:

Thereforetheriseinconsumptionofoxygenduringexerciseisdependenton
theincreasesinstrokevolumeandheartrate,andwideningofthedifferencein
thecontentofoxygeninarterialandmixedvenousblood.Duringstrenuous
exercise,cardiacoutputmayriseasmuchasfivefoldoverrestinglevels.5,14–17
Bothstrokevolumeandheartratecontributetothisincrease,buttherelative
contributionsofeacharedifferent.5Atrest,strokevolumeisapproximately60%
ofitsmaximalvalue.Attheonsetofexercise,acombinationofincreased
venousreturnandsympathetictonecausesstrokevolumetoincrease.This
occursasconsequenceoftwomechanisms.First,increasedpreloadstretchesthe
myocyteandincreasestension,resultinginchangesintheFrank-Starlingforces.
Second,theincreaseinsympathetictoneresultsinanincreaseintheinotropic
stateofthemyocardium.Thisincreaseininotropyimprovestheactivetension
developedforanygivenpreload,thusfurtheraugmentingstrokevolume.Most
oftheincreaseinstrokevolumetakesplaceatlessthan30%to40%ofthe


maximalconsumptionofoxygen(Fig.23.4).Athigherheartrates,diastolic
fillingtimeisdecreased,whichlimitsanyfurtheraugmentationinstrokevolume
irrespectiveofanyincreaseintheinotropicstate.Therefore,athigherheartrates
andnaturallyathigherworkloads,therelativecontributionofstrokevolumeto
theoverallincreaseincardiacoutputissmall.

FIG.23.4 Relationshipofheartrateandstrokevolumetoincreasing
consumptionofoxygenduringcycleergometryin23maleandfemale
subjects.Notethatstrokevolumereachesitsmaximalvalueat
approximately30%to40%ofthemaximaluptakeofoxygen.Heartrate
continuestoriseinalinearfashionthroughoutexercise.(FromAstrandP,

RodahlK.TheMuscleandItsContraction.TextbookofWorkPhysiology,
PhysiologicalBasesofExercise.3rded.McGraw-Hill;1986:12–53.)

Itshouldbenotedthatcardiacoutputresponsetoexercisevariesquite
strikinglywithposition.Thepatterndescribedearlierappliestouprightexercise.
Thereisevenlessstrokevolumeaugmentationwhenexerciseisperformedin
thesupinepositionbecausepreloadhasalreadybeenredistributedfromthe
lowerextremitiestocentralcirculationatrestwithoutfurthereffectduetothe
musclepump.Strokevolumeandcardiacoutputatbothrestandpeakexercise
arehigherduringsupineexercise,whereasheartrateishigherduringupright