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CARDIOLOGYSYSTEM (ANATOMY, PHYSIOLOGY, PHARMACOLOGY) Punyaslok Mishra,Arjun AhluwaliaContent Overview 1. TheMediastinum 2. ThePericardium 3. TheHeartChambers 4. CoronaryCirculation 5. Innervationtotheheart 6. Clinicalrelevanceofcardiacanatomy 7. TheCardiacConductionSystem 8. CardiacOutput&controlofstrokevolume 9. ControlofBloodpressure 10. JVPTHE MEDIASTINUM 1. Themediastinumisthecentralcompartment ofthethoraciccavity,b/wthelungs 2. Themediastinum islinedbyapartofthe parietalpleura,formingthemediastinal pleura. 3. Themediastinumisborderedby:- A.Superiorthoracicaperture(superiorly) B.Diaphragm(inferiorly) C.Sternumandcostalcartilage(anteriorly) D.Bodyofthoracicvertebrae(posteriorly)THE MEDIASTINUM 1. Themediastinumcanbedividedintoa superiorandinferiorpartatthe manubriosternaljoint/sternalangle/angleof Louis(T4-T5) 2. TheInferiormediastinumcanbesubdivided intotheanterior,middleandposterior mediastinum 3. Thepericardium,heartandallrootsofit’s greatvesselsliewithinthemiddle mediastinumTHE PERICARDIUM 1. Thepericardiumisthefibroussacenclosing theheartandrootsofgreatvessels. 2. Itisdividedintotheouterfibrous pericardiumandtheinnerserous pericardium.Theserouspericardiumitselfis dividedintotheparietalpericardiumandthe visceralpericardium(epicardium) 3. Thepericardialspaceandfluidliesin betweentheparietalandvisceralserous pericardium.CARDIAC TAMPONADE 1. Therelativelyinextensiblefibrous pericardiumcancauseproblems whenthereisanaccumulationof fluid,knownaspericardial effusion,withinthepericardial cavity. 2. Therigidpericardiumcannot CLASSICTRIAD:- expand,andthustheheartis subjecttotheresultingincreased 1. lowbloodpressureinthearteries pressure.Thechamberscan 2. muffledheartsounds becomecompressed,thus compromisingcardiacoutput. 3. swollenorbulgingneckveins, calleddistendedveinsTHE HEART- BASICANATOMY 1. Theheartismadeofmuscles,bloodvessels andafibrousskeleton 2. Theheartismadeof4chambers-thetwo atriaandthetwoventricles 3. Whenbloodreturnstotheheart,itenters theatriaandispumpedintotheventricles. Bloodflowsfromtheleftventriclethrough theaortaandintothesystemiccirculation. Bloodalsoentersthepulmonarycirculation fromtherightventriclesthroughthe pulmonaryarteries.HEARTANATOMY- RIGHTATRIUM 1. Deoxygenatedbloodisreceivedbytheright atriumfromtheSVC,IVCandcoronaryveins 2. Deoxygenatedbloodflowsfromthis chamberintotherightventriclethroughan atrioventricularorificeguardedbya tricuspidvalve. 3. Theinteratrialseptumontherightwall containsasmallovalindentationcalledthe fossaovalis,Thisistheremnantofthe foramenovaleinthefetalheart,which allowsrighttoleftshuntingofbloodto bypassthelungs.Itclosesoncethenewborn takesitsfirstbreath.HEARTANATOMY- RIGHTVENTRICLES 1. Therightventriclereceivesdeoxygenated bloodfromtherightatrium 2. Thesurfaceoftheventriclescontain muscularelevationscalledtrabeculae carneae(ridges,bridgesandpapillary muscles) 3. Chordaetendineaearefibrouschords arisingfromthepapillarymusclesthat attachtothevalves(mostlybicuspid,but alsotricuspid),andpreventprolapseof valvesduringventricularsystole.HEARTANATOMY- LEFTATRIAAND VENTRICLE 1. Theleftatriumreceivesoxygenatedblood fromthefourpulmonaryveins,andpumpsit throughtheleftatrioventricularorifice (guardedbythemitralvalve)intotheleft ventricle. 2. Theleftventriclereceivesoxygenatedblood fromtheleftatrium,andpumpsitthrough theaorticorifice(guardedbytheaortic valve)intotheaorta.TETRALOGY OF FALLOT 1. TetralogyofFallotisacyanoticcongenitalheart disease,comprisingfourabnormalitiesasaresultof asingledevelopmentdefect. 2. ABNORMALITIES a. Ventricularseptaldefect b. Overridingaorta(thisiswheretheaortaispositioned directlyovertheVSD) c. Pulmonaryvalvestenosis d. RightventricularhypertrophyCoronary Circulation - Coronaryarteries-supplytheheart;comefromtheascendingaorta,superior totheaorticsemilunarvalves - TWOMAJORONES:RightCoronaryandLeftCoronary - Rightcoronary-O:rightaorticsinus,C:RauricleandPul.trunk,E:Coronary Sulcus(aroundthecruxoftheheart) - LeftCoronary:O:Leftaorticsinus,C:LAuricleandPulTrunkRight CoronaryArtery - Rightcoronary-O:rightaorticsinus,C:RauricleandPul. trunk,E:CoronarySulcus(aroundthecruxoftheheart) - Branches: SANodalArtery AVNodalBranch PosteriorDescending RightMarginal Supplies: RA,RVentricle,Post.⅓ ofinterventricularseptum,SA&AVnodesLeft CoronaryArtery - LeftCoronary:O:Leftaorticsinus,C:LAuricleandPul Trunk - Branches: Circumflexartery LeftMarginal Ant.Interventricular/LAD Diagonal - Supplies:LA,LV,Ant⅔ofinterventricularsep tumThe RCA and Heart Dominance - RightDominantHeart=90%;Posteriordescendingarisesastheterminal branchofRCABUTinfewcasesLCXsuppliesPDA=LeftDominant - Whydoesthismatter? - ImplicationsinMI,CoronaryArteryBypassGraft- “This study demonstrated that patients with a left dominant system were associated with increased risk of cardiac mortality, heart failure, nonfatal myocardial infarction, and revascularization, shortly after primary PCI either during hospital stay or at 3 months follow-up after STEMI.” -Value of three-dimensional echocardiography study of left ventricle function correlated to coronary arterial dominance in predicting the outcome of primary percutaneous coronary intervention (Hanboly et al.)The CardiacVeins AnteriorCardiacVeins GreatCardiacVeins(G)[RunswithLAD]-O:Apexofheart, Ascendsintoant.Interventriculargroove,curvesontopost heartandenlarges->coronarysinus MiddleCardiacVeins(M)[runswithPosteriorDescending] SmallCardiacVeins (S)[runswiththerightmarginalartery] G,M,S->CoronarySinus->RightAtrium AntCardiacVein->directlyintotheR.AInnervation to the Heart ● Maincontrol->MedullaOblongata ● a)Upperpartofthemedullaoblongata= cardioacceleratory/pressorcentre ● b)Lowerpart=cardioinhibitory/depressorcentre ● a+b=cardioregulatorycentre ● Sympatheticnervoussystemactsonthesinoatrialnode, speedingupthedepolarisationrate,andtherefore increasingtheheartrate;“flightorfight” ● Parasympathetic system = reverse function; “rest and digest” ● The sympathetic fibres arise from the superior, middle, and inferior cervical ganglia ● The parasympathetic fibres originate in the medulla oblongata, innervate the heart via vagus nerve ● Both join in the cardiac plexusInnervation to the heart - referred pain ● T2,T3,andT4=intercostalnerves. ● Sensorycomponentofthesympatheticsupplyto theheartpassestothesamesensoryrootasthe above. ● Hencefeelingabandofpainacrossthechest whenhavingaheartattack. ● T1isdraggedintotheupperlimb,hencethe referredpaininthearmduringaheartattack. Thepainismoreusuallyfeltintheleftarm(since theheartismoretotheleftthantheright) ● Butalsopossibletogetrightarmpain duringa heartattack.The Cardiac Conduction System Action potential beings from the SA node, propagated through the atrial myocytes, which have intercalated discs -> action potential to moves freely across both atria The impulse then travels to the AV node (in the interatrial septum) Conduction is delayed at the AV node for 0.1 seconds before continuing on towards the bundle of His; time delay allows for ventricular filling to take place Depolarisation then continues through the bundle of His (which subdivides into left and right bundle branches) and then through Purkinje fibres to the ventricular muscle, which provokes contraction.CARDIAC CONTRACTION 3. Myosinheadscanbindtoactinoncecalcium 1. Anactionpotentialisstartedby hasbeencoupledtotroponin-C,and pacemakercellsintheSAandAV tropomyosinhasundergonea nodesandiscarriedacrosstheheart conformationalshift.Themyosinhead bygapjunctions. releasesADPandinorganicphosphateto allowforthepowerstroke.Thiscausesthe actintobepulled,whichcontractsthe 2. Aninfluxofcalciumionsintothe muscle,whilethemyosinheadpivotsand sarcoplasmistheresultoftheaction bends. potentialtravellingalongthe T-tubulesbetweensarcomeres. 4. Themyosinheadthenconnectstoafresh Throughreceptors,calciumentersthe ATPmolecule,forcingittoseparatefromthe sarcoplasmandbindstocardiac troponin-C,whichdisplaces actin.Afterthis,thecyclemightstartover tropomyosinfromtheactinbinding andmorecontractionscanhappen. site,exposingit,andstarting cross-bridgebinding.CARDIAC CONTRACTIONCardiac output CO=H.R.*StrokeVolume StrokeVolume=EndDiastolicVolume-Endsystolicvolume EDV=VentricularVolumeattheendoffillingindiastole ESV=Ventricularvolumeattheendofsystoliccontraction StrokeVolume=Volumeofbloodpumpedbyeachventricleperbeat EjectionFraction=%bloodpumpedoutbyeachventricleperbeatCardiac Output - Factors affecting stroke volume 3factorsthatregulateit-preload,afterload,and contractility Preload=force that stretches the cardiac muscle prior to contraction; Essentially more in = more out Afterload = the pressure/load on the cardiac muscle, which the heart must overcome to eject blood during ventricular contraction Contractility refers to the force of myocardial contractility, measured by EFBlood Pressure Regulation ● BP=C.OxTPR ● Controlledthroughstretchreceptors (Baroreceptors)inthecarotidsinusandaorticarch ● TransmitinfoviaVagus(X)&Glossopharyngeal (afferent)nervestothebrain(medullarycardiacand vasomotorareas) ● Afferentssynapseinthemedulla ● Dependingonthesituation,differentchangesare facilitatedinthesympatheticandvagaloutflow.The RAAS system for BP regulation Scenario:Fallinarterialpressure Reninisreleasedfromjuxtaglomerularcellsofthekidney ConvertsAngiotensinogentoAT1 ACE(inlungs)convertsAT1toAT2 AT2=vasoconstriction&secretionofADHfromadrenals(Increased waterreabsorption)=increaseinB.V.=increaseinB.P [secretionofaldosterone&TubularNa+,Cl-reabsorption+K+ excretion]=increasedwaterretention=IncreaseinB.V.=increasein B.P. ViceversaforriseinArterialpressureJVP 1. Jugularvenouspressure(JVP)providesan indirectmeasureofcentralvenous pressure.Thisispossiblebecausethe internaljugularvein(IJV)connectstothe rightatriumwithoutanyintervening valves,resultinginacontinuouscolumnof blood. 2. AssessmentoftheJVPcanprovideinsight intothepatient’sfluidstatusandcentral venouspressure.Ifapatientis hypervolaemictheJVPwillappearraised duetoincreasedvenouspressurewithin therightatriumcausingahigherthan normalcolumnofbloodwithintheIJV.