DETERMINANTSANDCONTROLOFCARDIACOUTPUT

Assessingmyocardialperformance:theoverallfunctionofthecardiovascularsystemistodeliver
oxygenandmetabolicsubstratestothetothetissuesandtoremovetheproductsofmetabolism.It
performsthesefunctionsbypumpingblood;thereforemostassessmentsofmyocardialperformanceare
basedonhowwelltheheartcanpumpblood.Measuringpumpeffectivenessisusuallybythevolume
ofbloodpumpedperunittime.Thisisdonebymeasuringthecardiacoutput(CO)measuredinlitres
perminute.Toenablecomparisonitissometimesdividedbybodysurfacearea,thisisthecardiac
index(CI).
CardiacOutputistheproductofStrokeVolume(SV)andHeartRate(HR).
Strokevolumeisdeterminedbythreefactors:preload,afterloadandcontractility.

Preloadistheinitialfibrelength.Preloadistheloadonmyocardialfibresjustpriortocontraction.It
canbeusedtorefineourunderstandingofmyocardialperformancebeyondjustCOorCI.Ifaheartcan
pump5litresfromalowpreloadthenitisusuallyconsideredtobeperformingbetterthanaheartrequiring
morepreload.Asstatedabovepreloadistheinitalfibrelengthofasarcomere,thishoweverisnotpossible
tomeasureinanintactheart.Thereforevolumeandpressureareusedassurrogatemarkersofpreload.The
mostcommonlyusedisthevolumeofbloodintheleftventricleattheendofdiastole(LVEDV)whichis
representedonthepressurevolumeloopatthebottomright.Volumesareoftendifficulttoestimateminute
tominutewithoutmonitoringsuchasanECHO.Pressureisalsousedbutitisproblematicbecauseof
complianceasaconfounder.Leftatrialpressurewillequalventricularpressureattheendofdiastole
(LVEDP)(whensarcomeresarestretchedpriortocontraction).Leftatrialpressurecanbeestimatedusing
aswanganzcatheterandmeasuringpulmonaryarteryocculsionpressure(PAOP)ontherightsideofthe
circulationbecauseitisalowresistancecircuit,thearteryisoccludedandtheyareatthesamehorizontal
level.Ifthereismitralstenosishoweverthenthiswillbeinaccurate.FinallytheCVPandrightatrial
pressuremaybeusedasindicesoftherightventriclepreload.Thismaysometimesalsocorrelatetoleft
sidedfilingpressuresalthoughthisisnotalwaysthecase.

Afterloadisthetension,whichneedstobegeneratedincardiacmusclebeforeshorteningwilloccur.
Againthisisunabletobemeasuredintheintactheartandthenearestestimationisinstantaeouswall
tension.Thereareseveralsurrogatemarkers.Initssimplesttermsafterloadisthoughtofastheimpedence
toflowfromtheventricleduringsystole.Assuchmeanarterialpressuremaybeusedasanestimate.More
accuratestillittoconsidertherelationshipbetweenmeanpressureandmeanflowrepresentedbysystemic
vascularresistance(orPVRontheright).Againhoweverthisisinaccuratebecausetheflowgeneratedby
theheartisnotcontinuousbutintermittantandpulsitile.Usingapressurevolumeloopafterloadis
representedbytheendsystolicpressureconnectedtotheLVEDVpoint.

MyocardialContractilityisdefinedastheintrinsicabilityofthemyocardialfibretoshorten
independentofpreloadandafterload.Brandisdefinesthisasthefactorthatisresponsibleforchangesin
myocardialperformancethatisnotduetochangesinheartrate,preloadandafterload.Theintracellular
mechanismthatisresponsibleforallfactors,whichincreasecontractility,isincreasedintracellular
calcium.Measurementofcontractilityisdifficult.dp/dtmaxrefersthethemaximumrateofchangein
pressureintheleftventricleduringisovolumetriccontraction.Amoreforcefulcontractionwouldbe
associatedwithagreaterriseinpressureandforthisreasonthisisoftenusedasamarkerofcontractility.

FrankStarlingmechanismstatesthatthestrengthofcardiaccontractionisdependentontheinitial
fibrelength.IncreasedfibrelengthalterscardiacperformancemainlybychangingtheCa2+sensitivityof
themyofilamentsand,inpartbychangingthenumberofmyofilamentcrossbridgesthatcaninteract.

Beyondanoptimalfibrelength,contractionisactuallyimpaired.Fromapracticalperspectivethisis
importantbecauseincreasesinenddiastolicvolumecauseanincreaseinventricularfibrelength,which
producesanincreaseindevelopedtension.Thisisveryimportantbecauseitmatchescardiacoutputto
venousreturnthisensuresaprecisematchingoftheoutputsoftherightandleftventricles.Positive
iontropyincreasesCa2+sensitivityandthereforeresultsinanincreaseinCOforanylevelofrightatrial
pressureorLVEDV.Negativeiontropydoestheopposite.TheFrankStarlingmechanismisbest
representedbyafamilyofsocalledventricularfunctioncurveswhichmaptheCO(orignoretheHRand
justusetheSV)ontheordinate(yaxis)andtheenddiastolicatrialpressureorLVEDV.Fromleftshift
impliesimprovedinotropy,rightshiftnegativeinotropy.

MyocardialoxygenconsumptionTheheartisanaerobicorganandcannottolerate(exceptforbrief
periods)oxygendebt.AtrestMVO2isabout79mls/100g/min(whichequatestoabout21to27mls
O2/minfora300gheart).Anunderstandingofmyocardialoxygenconsumption(MVO2)hasboth
physiologicalandclinicalrelevance(especiallyinthesettingofischaemia).Clinicalstudieshaveshown
thatthethreemajordeterminantsofMVO2areMyocardialWallTension,ContractilityandHeartRate.
Minordeterminantsincludeelectricaldepolarisation,directmetaboliceffectofcatecholamines,basal
metabolicactivityandexternalwork.Thisexplainswhypatientswithmitralregurgrarelydevelop
ischaemia(decreasedwalltension)whybetablockadeisveryeffectiveinangina(decreasedheartrate)and
whyanginaisrareindilatedcardiomyopathy(decreasedcontractility).Furtherstudieshaveshownaclose
relationshipbetweentheareaunderthesystolicportionoftheLVPressureTimecurvewithMVO2and
thisisknownasthetensiontimeindex.

VascularFunctionCurvesIftheentirecirculationwasbroughttoastandstill(egasystole)thenthere
wouldbearesidualpressureinthevascularsystemduetoadegreeofoverfilling.Thisisthemean
systemicpressure(whichismeasuredintherightatria)whencardiacoutputiszeroandissaidtobe8
mmHgthisisalsoknownasthemeansystemicfillingpressureMSFP.Eitherincreasedvolumeor
resistancemayalterthemeansystemicpressure.PeterKamidentifiesthenormalpointtobyRAPof
0mmHgandCOof5l/min.Thevascularfunctioncurveintersectstheyaxisatthepointwheredecreasing
theRAPnolongerincreasesvascularreturnduetostarlingresistorforcesintheextracardiacvessels.
IncreasingresistancealtersthesteepnessofthecurvebutnottheMSFP.Increasingtheloadshiftsthe
curvebutnotthesteepness.

CardiacandVascularFunctioncurvesintegrateditispossibletooverlaythenormalFrankStarling
curveshownaboveandthevascularfunctioncurveusingRAPasasurrogateforpreload.Thisisimportant
becauseitgivestheequilibriumpointwhichmatchesvenousreturntocardiacoutput.Itwillalsoallow
youtoppredictthechangesthatoccurwithincreasedcontractility,increasedfluidvolumeandchangesin
peripheralresistance.