RyanPrince

Physiology

Mrs.Somer

April10,2015

CardiovascularStudyGuide

1.
Arteriesareequippedwithathickmusclelayertowithstandthepressurecausedbytheblood
asithitsthesurfaceofthearteriolewallsasitisejectedfromtheheart.Whileveinswiththin
musclelayersandonewayvalves,candistendwhenanincreasedamountofbloodenters
them.Sincetheyalsohaveonewayvalves,itensuresbloodflowsbacktotheheartwithout
backflush.Capillarieshavejustasinglelayerendotheliumandextensivebranchingsystemthat
allowsforefficientexchangeofgasandliquidmoleculesduetotheirthinstructureand
increasedsurfaceareatovolumeprovidedforbytheirextensivebranchingsystem.

2.
Cardiacoutputistheamountofbloodejectedintotheaortaperminute.Thiscanbe
calculatedbymultiplyingstrokevolumebypulserate.Forexample,ifapersonhasapulserate
of60beatsperminuteandastrokevolumeof80ml,theircardiacoutputwouldbe1.4litersper
minute.

4.
Apersonwithapositivebloodtypecanreceiveamatchingnegativebloodtypetransfusion
becauseofantigenstheyhaveonthesurfaceoftheirbloodcells.Anantigenisconsideredan
"antibodygenerator".Ifaforeignantigenistransfusedintoapatientsbody,itwillmake
antibodiestofightit.ButifthepatientwithA+bloodreceivesatransfusionfromsomeonewith
Ablood,althoughoneisnegativeandonepositive,theybothhavetheAantigenmakingthe
transfusionsafe.However,apatientwithamatchingnegativebloodtypecannotreceivea
transfusionfromsomeonewiththematchingpositivebloodtypebecauseofthemissing
antigensonthebloodcellssurface.Forexample,apersonwithabloodwouldbeunableto
haveasuccessfultransfusionwitha+becausetheydonthaveanyaantigensandonce
transfusedwouldgenerateantibodiestofightit.Obloodisconsideredauniversaldonor
becauseanyonecanreceiveanobloodtransfusionduetotheantigensitlacksonthesurface
ofitsbloodcells.Sincetherearenoantigensonthecellssurface,thebodywillnotgenerate
antibodiesagainsttheblood.Ontheotherhandpeoplewithab+bloodareconsidereduniversal
receiversbecausetheycanreceiveatransfusionfromanybloodtype.Thisisabletohappen
becauseab+bloodhasbothaandbantigensonthesurfaceofthebloodcells.Antibodieswill
notfightthesebloodcells,andwillkillthemselvesoff,resultinginasuccessfultransfusion.

5.
TheRHfactoristheadditionalsurfaceantigenonthebloodcell.Apersonwithapositive
bloodtypehasanadditionalRHsurfaceproteinontheirbloodcells,wheresomeonewitha

negativebloodtypelacksthisextraRHsurfaceprotein.Hemolyticdiseaseisadiseaseababy
cangetifthemotherhasanegativebloodtypeandthebabyhasapositivebloodtype.What
causesthisisthemothersRHantibodiescrossingtheplacentaandattackingthefetusblood
cellsdestroyingthemandmakingthemrupture.Thisresultsinhemolyticdisease.Ifanewborn
hashemolyticdisease,thebabywillbecloselymonitoredtolookforanemia,ischemia,and
blueingoftheskin.Ifseveresymptomsshowthebabysentiresystemwillneedtobeflushed
withplasma.NowbabiesbornwithRHmomsareconsideredtobesafeduetoaninjection
theycanreceiveduringpregnancythatwillshutdownthemothersRHantibodiesandprevent
themfrombeingmade.

ClinicalInvestigation1:
AfterreviewingthepatientsMRIresults,wewereabletoseetheheartwasenlargedanda
coronaryarterywasblocked.Thisiscausingthepatienttosufferfrombothatherosclerosisand
hypertension.Atherosclerosisisaconditionwherethearterialwallsthickencausedbyabuildup
offattysubstancesandplaquebuildupinsidethearterialwalls.Hypertensionisaconditionin
whichapatienthashighbloodpressure,likethismanwithabloodpressureof140/90.Thisis
abovetheaverageof120/80.Ifhypertensiongoesuntreatedfora1015yearperiod,itcanlead
toextensivearterialwalldamage.Thiswillcausethearterialwallstotear,followedbythem
beingrepairedwithplaque,onlynarrowingthearteriesevenfurther.Thispatientsobesityhas
contributedtohiscurrentcondition.Duetohispoordietand/orlackofexercise,thereisan
excessiveamountofplaquebuildupinhisarterialwalls,causinghishearttoworkharderto
pushhisbloodthroughthesenarrowedarteriesandaroundthebody,leadingtohypertension.
Alsothepatient'sheavysmokinghascontributedtohisstate.Nicotine,achemicalincigarettes,
hastorntheinnerwallsofhisarteriesandhisbodytryingtorepairthesetearsbybuildingup
plaqueoverthetearstoformascablikestructure.Sadlythishasonlycausedhisarteriesto
becomemorenarrow,calledatherosclerosis.Thispatientisalsointroubleofgettingangina
pectoris,ischemia,andmyocardialinfarctionduetohispoorhealth.Anginapectorisoccurs
whenthemyocardiumisnotreceivingenoughoxygen,resultinginextremechestpain.Heisat
riskforthisbecausehehasexcessiveplaqueinhisarterieswhichcoulddelayoxygenated
bloodfromreachingthemyocardium.Thispatientsexcessiveplaquebuildupcouldalsoleadto
ischemia,oradecreaseinbloodflow,thatwillstarvecellsofoxygenaroundhisbody.Finally
myocardialinfarctionoccurswhenthereisadecreaseinbloodflowtothemyocardiumthatwill
suffocatethecellsresultinginaheartattack,whereasthispatient'snarrowedarterialwallsmay
causethisduetotheinsufficientbloodflow.Themyocardiumisthemuscleoftheheartand
receivesbloodfromthecoronaryarteries.Becausethispatienthasablockedcoronaryartery,
themyocardiumcouldsuffocate,sufferingischemia,andresultinaheartattack.Topreventthis
fromhappening,thispatientneedsaCABG,orcoronaryarterybypassgraftsurgery.This
surgerywillcallforaveininthepatientslegtoberemovedandunderanesthesiawillreplace
thecoronaryarterythatisblocked.Thepatientwillnowhavealikenewcoronaryarterythat
willbeabletoproperlynourishtheheartandpreventaheartattack.
ClinicalInvestigation2:
Duetothispatientsabnormallylowheartrate,fatigue,andinabilitytomaintainanormalactivity
level,thereisaproblemintheintrinsicconductivesystemoftheheart.Thesinoatrialnodeis

thepacemakerfortheheart.Depolarizationbeginsatthisnodeandcontinuesacrossthe
surfaceoftheheart.IftheSAnodeisdamaged,itwillcausethehearttobeatoutofrhythm.
Thisresultsinadelayeddepolarizationthatwillleadtoadecreasedheartrate.WhentheEKG,
themeasurementofelectricalflowacrosstheheart,wastakentheheartratewasslowduetoa
faultySAnode.Thisisconditionisknownasbradycardia,orslowedheartrate.Anaverage
heartrateisbetween60100beatsperminute.Duetothepatientsheartrateunder60bpm,
theyaresufferingfrombradycardia.Symptomsofthisconditionincludefatigueandlackof
energywhichcanexplainourpatientsfatigueandinabilitytoperformnormalactivities.
Bradycardialeftuntreatedisdangerousbecausethedelayeddepolarizationandheartrate
causesadecreasedbloodflowintissuesalloverthebody,leadingtostarvationofthetissues,
alsoknownasischemia.Untreatedbradycardiawillleadtoischemia,whichcouldthen
potentiallyleadtomyocardialinfarctionoraheartattack.Tofixourpatientsbradycardia,a
pacemakermustbeinstalledtomimictheSAnodesjobbecauseitisdamaged.Afterthis
deviceisinstalledthepatientwillhaveanormalheartrhythmandrateduetoanormal
depolarizationoftheheart.

ClinicalInvestigation3:
Whensomeonehassufferedfromrheumaticfever,therehasbeenanexcessivestrainonthe
ventricularwallswithintheheartwhichcausesthemtostretchandbecomeflabby.Stretched
ventricularwallsresultinapoolinginbloodatthebaseoftheheart.Rheumaticfeveriscaused
byuntreatedstreptococcusa,commoninthirdworldcountries,andcausesdamagetoour
heartsvalves.Whenthesevalvesaredamageditcausesbloodtobackflushbackinthe
oppositedirectiontheyaresupposedtogothroughthevalves.Resultinginbloodpoolinginthe
ventriclesatthebottomoftheheart.Thedoctorheardabnormalheartsounds,alsoknownas
murmurs.Thesoundthedoctorheardisfromnotallofthebloodbeingpushedthroughthe
valves.Ifthereisbackflushingintheatria,theconditionisextreme.Thismeansthebloodis
poorlyoxygenatedwhichcouldeventuallystarvethetissuesaroundthebody,whichcould
causetheseverefatigueourpatientisexperiencing.Thepoolingintheatriaiscausedbymitral
stenosis,oranarrowingofthemitralvalve.Mitralstenosiscausesthemitralvalvetonot
properlycloseandispartiallyopenduringventricularcontraction,causingbloodtobackflush
intotheatria.Thisbackflushisthesoundthedoctorheardandwhatiscausingourpatienttobe
bedriddenbecauseofherfatigue.Tosolveourpatientsproblemshemustgetamitralvalve
replacementinordertokeepbloodfrombackflushingandprovidingtheirbodywithoxygenrich
blood.