正常心脏的生理

正常心脏的生理 Cardiovasculardisorders an1.drider{)ll_0s…1thIhterm1…IbnChsoftheposterior fn[erve~tncu… 1he10%oflndividualslnwhommoslofbothventridesand theseptumaresuppliedbytllelPtI……arIe…resaidto jlaveleftcardiacdemll_anceThere】sl1O0rc0?aIrc0_T1l__?lilt11】a 11011Lle【wee?lherighIandleltcor0ndrysys[emsN0tethatthe corons~r~riesm1anddistrihulethebloodduringdlaslolewhen thecardiacii1uscle】axell1L1}l1PvascLI1arresistalice1s^1I lOWeSI Thev…ii0flhec1a…I1I】variableth…therteriesDrainage 【"t.1leftal?rightventriclesstansw1ththegreatcardiacveini1 theanteriorinterventdculargraove【FigureItlsssIothelefl In【l1e…In0rAVgroovew?rP【ICo?(=ls?1P【eftn…【lidIvein and…ItufinfileposteriorAVgrooveis1oinedbytheoblique veiiiofthelegatrium.theposteriorventricul~ve[/iand,nnaiIy heddlecardiacveinwhichIies?theu0srJrinleFvenlncl lagrooveanddraiilsIgeJeftal】-lrighlver?riclespostedorIyThe oonfluence0ftheseveinsisthe3cmlongCOl'O//aFysillus;lying 1ntheposted0rAV~[ooveJuslbeforethecoronaslntise}llerS ?erightalriunltolheleftofthePn1ryofth111fefforvPnacava1t i5tl~HafIVloinedthesmallcdrdiacveinw}lichdraillstheright d[rlllnlandrightventricleThesl~ld?cardiacv…IInT1T】i?drans direedyi?nI】1erightlril…1ACaLlplLcIerh,rcajicveins dralnl}1PaItteriGras【)e"【,ltherightvnIncledndrightatr】Hm beloJecrossingthedghtfI)n?】aartelonlrtherishtdtr]tlm lnadditl0Il2030%ofaIIdrdiilageI5lnthevenac?rdisminimae lThehesial1veinwhlchdraiudirecllyill[OthechanlbetsIhe heartmostly0ntherightside Physiologyofthenormal heart MecganicaIevenb AftermePwaveolIhECC.aI1dn】nckl1nEwithatrialsystole …appearinjnandrightatrialpr~suretracingsandlhe iugtIrve110LIsptlIsPAtriaI…acll0nillcre~sesVeilIricularli}} inbyaboul10%The0nsiofvP…trlu】arc0l11racl?c'"Iirides w1U1thepeak0ftileR…P0fthECGandIhempid1ncredse iiii【1l?…ricurPFeSStlr~closesIhem1traIandtl"icuspidvves 1hisproducesthefirsthearls【)undWhenvPntricuIrpressurc5 DavidE,Wllck~n…ConsultGn$PhysicianandHead吖lhe c0fd…【u}口r6ene{tLaboratoryattheUniversi(y0fNewSouthwnles andthPrinceo,WolesHospita1.Srdhey,AustroliaHequald#omthe Uni~iz~0fSydney,andhasworkedinL#~donUKondSanf…s? USA.HiscuF…chinters"hlcludegenetic?ntnbut}Onsto cordio~culurd~easeConBIc~ofinle[est:n0ne 20(37TheMedf0?nePub5hn口C…Lid 一一蒸薹 一 ? 一一一 Vol7NO1Jan,2007 sourc~JunquBiraLcCamero』K~lleVR0Histology9thed 51am~ord-Appletonandtangel99Bwilh~eFm]ssion PceedIh【】…iiIhpu【iii…ryrtervl1d.1?fla1lIoLIlflOW vaIyesopenandvntricul…Iect】0n?ows^sthestrengthof ventricnlarcomracbondecinestheao~icand口"ImonaryvaIve5 closecoincidingw】thdieendolth0r…eofIbeECGandthe d~cmti~I,0thn01…utTacings^^Ilccl0lslighlly precedespulmonaryclosure,resu}ti噜inthetwocompo[1e]lts0T ll1esec0J1dl'ea"sou AIhirdheartSOUl】,i0…ddhlgwith?1subsequenlperiod0f earlyrapMdiaslolicfiLlilisalsousuallyaudibleinchildrenand youngadults ThebloodvoItlmii1]lOFTn~Ia《{1IItsisI)OtlI5Iif【haeli/~tocdf 4Slj0twbich15li[Fes…re『卜fleartandILlngsilheCelltI l_1l】"VOIumThepulmonaryarteries.capilla?esandvell1s co11tainahcniI?9IiIres.df1LlaEll75?Iar【nthepudnona6' …PIIrIsAboul06】iresofbloodarP【nlhel_earIIheIeftve" frl口|_8rll?1…dt?asI(icvolL…cEDVjcIIstiluIsabouII40l11l gleStlokevo1tl~le{SV1abou【90…IIlLI…Peje~liOllfrac1io11{SV/ EDV1abou【70JforeacbventricleThPilori~aJresling…Il10r …【IrIi1lI『1rlILlgrealvessels{lileastlredw0hreference l【]Ihezeropress[fiearbitrartlysdI…1belowIheslern.Ing】 wilhIbepadentrubent)dsbownii1Figure2 CardiacOtllpt]IIstr0kevo【LIn1e×heartrgle)isrelatedlobodysize and1sexpressedi『'Iitres/milI1te,Tnh0dvsurlace,~rea(rilecardi,~c iIidex1Tbei11e~nCaldiacindexunderrelaxedmsthlgcon(1iilOils 351iIre~/mi1me/mvalue~beio~2andabove5ilres/minute/m drabnornTdIIiIiorlllaIsubi~tstiledrl~ovenousdIfferencefor oxygena【rPs【isnlainlainedwiIhinii~rrowlitllils54Sill】/…re). vaILies0f5ml/iIPl1_rn0r…ways1nor]llal?ilia}"pul lnongl~orsystemicvascul~l0slstaI1cethedifierencebetweenIhe ITle~tlj11n1)wI】'l011IlOWI)re,skisiI1nlIl_IIgdividedbyIheIlowin 1itres/m?niiIbroughIhc'resp~'Ovecirculadlms1llnrmsubiects. 1idsflowlstbecardiacoutputStrokewoikisusuallycs[Jmatedas fileproductofstrokevolumeandmeaI1electionpre~stlreNl LVworkHisabouIb/m/mhmte Fouressenlialfac【0determinetheperformanceoftheheart. …?l】usre{urllfpreload) .0I】Ifltlwresis(aIlC~faflerload) 'Imlimpicsleorcc)[11mc?1llv ?l_anmIe Mecba~isnlsthatal[erthesefotlrdetermhlanmoduIjcardi8c perTonnaIc Venousretur~.preloadandtheF~nR5tarUng~tionship Therelali~.sh【"Ilelwee.enddiasll~licfibrelengdla.dI'riJ1 c(,m…dollsdescribed…Llc口P1【1…lvb5mnkandglarlitlg andisshowninFigur3WhentheVe~l[iclecollll'aC[sagainsl ac~]11~[a11[pressulethedegle(1fretchoIIhenlusclefibresin Right~lrium RighlvBntT【1e Pulmonarya… Lealfiumfdirec[of1ndlre[1 口uImonarycapillarywedge) Leftventr~c SystoR~DTessu (mmH时(mmH(mmH NnaD口I1cab Notapplkable Cardiovasculardisorders7.NO.1Jan.2007 diastoleresultingfromvariationsinvenousreturndetermines contractionstrengthandworkoutput.Thenumberofactiveforce' generatingsitesineachfibreincreasesasitlengthenssothat, withinlimits,forceofcontractionandstrokeworkarepositively relatedtoend.diastolicfibrelength.Forclinicalpurposes,itis convenienttoequatevenousreturnwiththepreloadbecause,as itchangesfrombeattobeat,venousreturnadjuststhestrength ofthesubsequentventricular(andatria1)contractionbyvarying theforcestretchingtherelaxedcardiacmuscleandalteringend— diastolicfibrelength. Thecontractileresponseoftheheartatanyparticulartime dependson: ?theintrinsicstateofthemuscle ?theprevailingneurohumoralstate(increasedsympatheticout— flowproducesamoreforcefulcontractionatanyend—diastolic fibrelengthandshiftsthecurveupwardsandtotheleft) .extrinsicinotropicinfluences(drugswithapositiveinotropic effectshiftthecurveupwardsandtotheleft,whereasmyo— cardialdepressantsshiftthecurvedownwardsandtotheright — Figure3). Ou讯owresistance(afterload) Thepressuresthattheventriclesmustdeveloptoopenthepulmo— naryandaorticvalvesaredeterminedlargelybythepulmonary andsystemicvascularresistances.Theseresistances(togetherwith aninertialcomponentdependentonthemassofbloodwithinthe vessels,thecompliance(stiffness)ofthevesselsandthepulsatile natureoftheflow1constitutetheimpedancetoventricularout— flow.Thisistheloadagainstwhichtheventriclecontracts(the afterload1.Itbecomesappliedtothemuscleonlyaftertheventricle hasbeguntodeveloptension. Ventricutarvotumeandaftertoad Ventricularvolumehasamajoreffectonafterload.Becausepres— surerepresentsforceperunitarea,theforceactingradiallyonthe innersurfaceofthewholeventricleatanytimeduringsystoleis theproductofintraventricularpressureandventricularsurface areaatthattime.AnincreaseinLVdiameterfrom5cmfnormal1 t0,forexample,10cmwouldresultinaboutafourfoldincreasein theforceopposingejectionforthesameintracavitysystolicpres' sure.Toovercomethatforce,theventriclemustdevelopgreatly increasedwalltension.,^,aIltensiondevelopedduringsystoleis themajordeterminantofmyocardialoxygenconsumption,sothe contractionismuchlessefficientinthelargerheartforthesame strokevolumeandejectionpressurefstrokework1. EDVisinfluencedbypreload,afterload,circulatingblood volume,theinotropicstateoftheventricle,heartrateandneuro— humoraIinfluences.Forexample.itissmallerintheerectposition thaninthehorizontalpositionbecauseofreducedvenousreturn. andwithamoderateincreaseinheartratebecauseofanassoci? atedpositiveinotropiceftect.Itisdifficulttomeasureaccurately changesincontractilityinthehumanheart,despitethenumber ofdifferentapproachesexplored.However,peakrateofchange ofintraventricularpressure(peakdp/dt)isauseful,andeasyto measure,indexofchangeincontractility,providedthatpreload, afterloadandheartrateremainconstant. Thenatriureticpeptidesandtherenin—angiotensinsystemare importantcontributorstotheregulationofventricularvolumeand ofafterload.Thenatriureticpeptides,atrialnatriureticpeptideand MEDICINEINTERNATIONAL 3 Leftventricularend-diastolicfibreIengthandleft ventricularstrokework End-diastolicfibrelength TherelationshipbetweenIeftventricularend?diastolicfibrelength andIeftventricularstrokeworkexhibitsdisplacementupwards andtotheIeftwithincreasedcontractility.anddownwardsandto therightwithdecreasedcontractiIity.SimilarbutnotidenticaI curvesareobtainedbyplottingIef【ventricularstrokeworkasa measureoftheforceofcontractionagainstventricuIar end.diastolicpressureorvolume.Similarfunctioncurvesare obtainedfr0mbothventriclesandbothatria. B?typenatriureticpeptide,arereleasedfromsecretorygranulesin atrialmusclefatrialnatriureticpeptide)andventricularmuscle(B— typenatriureticpeptide).2Theyarereleasedbyvolumeincreases inthesechambersandmediatecorrectivesaltandwaterexcretion bythekidneys,thuscontributingtoareductioninpreloadand afterload. Therenin—angiotensinsystemiSalsoofmajorimportancein theregulationofcirculatingbloodvolumeandthemaintenanceof normalbloodpressure.Increasedactivationofthesystemincreases aldosteroneproduction,whichpromotesreabsorptionofsodium bythekidneyandexpansionofthecirculatingbloodvolume. IncreasesinangiotensinII,apotentvas0c0nstrict0Lincreases bloodpressureandsmoothcellproliferation;hence.theclinical relevanceofangiotensin—?convertingenzymeinhibitorandangi?? otensinreceptorblockingdrugtherapy,andaldosteroneinhibition, inthetreatmentofhypertensionandofcardiacfailure. Coronarybloodflowandmyocardialoxygensupply Coronarybloodflowaccountsforabout4%ofthecardiacoutput. Theheartextractsmostf70%1oftheoxygencarriedinthecoro. narycirculation;thearteriovenousdifferenceforoxygenacross theheartisabout110ml/litre,whereasthatforthewholebody isonlyabout40ml/litreunderrestingconditions.Increasesin myocardialoxygenrequirementsaremetlargelybyincreasesin coronarybloodflow,whichmayincreasefivefoldorsixfoldduring @2007TheMedicinePublishinoComoanvLtd 【uo;】|暑cou邑芒.事里2 CardiovasculardisordersV01.7.N0.1Jan.2007 becomesslower,cardiacoutputismaintainedbyincreasedEDV andstrokevolume,theheartrateresponsetoastandardsubmaxi— malworkloadisreduced.systemicbloodflowismoreeffectively distributedawayfromvisceralandskincirculationstoworking muscles,andoxygenextractionfromperfusingbloodisimproved. Rhythmicexercise(e.g.running)andisometricexercise(e.g. weight—lifting)havedifferentphysiologicaleffects.Bloodpressure risesdisprOpOrtiOnatelyduringthelatter;themechanismsare partlyreflexandpartlymechanicalfromthecontractingmuscles. Isometricexercisetrainingisnotrecommendedforcardiacpatients, becauseoftheassociatedincreasedafterload. Regularexercisemayalsopartlypreventthenowwel1..docu.. mentedendothelialdysfunctionassociatedwithageing.Anage— relateddecreaseintheavailabilityofnitricoxidehasbeenestab— lished.resultingfromreducedactivityoftheL—arginine—nitdcoxide pathwayintheendothelium,butregularexerciseimprovesnitric oxideavailability.Regularexercisealsoreducesbloodpressurein normotensiveandmildlyhypertensiveindividuals,andmodula— tionofcatecholaminereleasebychangesinendogenousopioid peptidesecretionmaybeapossiblecontributingmechanism.Of theotherdiverseexercise—inducedhormonalchanges.reduced glucose—stimulatedinsulinreleaseisofparticularclinicalrelevance inindividualswithtype2diabetes.? REFERENCES 1WilckenDEL.Clinicalphysiologyofthenormalheart.In:WarreUDA, CoxTM.FirthJDefa1..eds.Oxfordtextbookofmedicine.Vo1.2.4th ed.Oxford:OxfordUniversityPress.2003:820—8. 2RademakerMRichardsM.Cardiacnatriureticpeptidesforcardiac health.CIinSci2005;108:23—36. 3StruthersAD.MacDonaldTM.Reviewofaldosteroneandangiotensin II-inducedtargetorgandamageandprevention.Cl0rdiovascRes 2004;61:663-70. 4BlackHR.Evolvingroleofaldosteroneblockersaloneandin combinationwithangiotensin—convertingenzymeinhibitorsor angiotensinIIreceptorblockersinhypertensionmanagement: AreviewofmechanisticandclinicaIdata.AmHeartJ2004;147: 564-72. FURTH,RREADII_6 BraunwaldE.ZipesDRLibbyRAtextboakofcardiovascularmedicine. 7thed.Philadelphia:Saunders.2005. (Detaileddiscussianofcardiovascularphysiologyinhealthand disease.) GanongWF.ReWewofmedicalphysiology.21sted.NewYork:McGraw Hill.2003. clear,up'to'dateaccountafcardiovascularphysiology.) JonesNL.KillianKJ.ExerciseIimitationinhealthanddisease.NEnglJ 朋ed2000;243:632-41. goodreviewofexercisetes咖9.) MEDIClNEINTERNAT10NAL Biochemistryand physiologyofcardiacmuscle JLayland AMShah Thesynchronouscontractionofcardiacmyocytesduringventricu— larsystolegeneratesthepowerrequiredtopumpbloodoutofthe heart.Conversely,myocyterelaxationandthepassiveproperties oftheventriclesduringdiastole(dependentlargelyontheproper— tiesoftheextracellularmatrix1determinethefillingoftheheart betweenbeats.Severalinteractingregulatoryprocessesoperateto ensurethatcardiacperformanceisfinelytunedtomatchcircula— tOryrequirements.Thiscontributionprovidesanoverviewofthe mechanismsthatregulatecardiaccontractility,dysfunctionof whichisimplicatedindiseasestatessuchasheartfailure. Structureofcardiacmuscle Thesarcolemmalmembraneofcardiacmyocyteshasinvaginations thatfcIrmanextensiveT-tubulenetwork.regionsofwhichliein closeappositionwiththesarcoplasmicreticulum.Thesarcoplasmic reticulumisthemajorintracellularstoreofcalcium.thecentral regulatorofcardiaccontractility.Thefundamentalcontractile unit,thesarcomere,isformedfromcontractilemyofibrils,which compriseinterdigitatin只thinfilaments(actinandassociated ?AlterationsinthepropertiesoftheSRcalcium-release channelsinheartfailuremayrenderthemfunctionally 'leaky'andmaycontdbutetoreducedcalciumloadand decreasedcontractility ?Reactiveoxygenspeciesmaydirectlymodulate E-CcouplingandcOntributetocontractiledefectsin hypertrophyandheartfailure.Theclinicalbenefitsof antioxidanttherapiesarecurrentlyunderinvestigation ?Modulationofmyofilamentpropertiescansignificantly contributetoalteredcontractilityinhumanheartfailure ILoylandP~oisaPost-doctorolResearchFellowatKing'sCollegeLondon. UK.Herresearchinterestistheintrecellularmechanismsresponsiblefor contractileeffectsofinterventionsoncardiacmuscle.Conflictsofinterest: none. AMShahFRCPFMEdS~IisBHFProfessorofCardiologyandConsultant CardiologistatKing'sCollegeHospital,London,UK.Hisresearchinterest isendothelialregulationofcardiovascularnction.Conflictsofinterest: none. @2007TheMedicinePublishinaComoanvLtd 国际内科逼塞查!:Z:筻51 由左冠状动脉供血,称之为左冠优势型.右冠状动脉 系统和左冠状动脉系统之间的侧支交通较少.应注意 的是,冠状动脉的灌注是在舒张期当心肌松弛并且血 管阻力最低时进行的. 心脏的静脉回流 心脏静脉的变异性要比动脉明显.左右心室的回 流起始于位于前室间沟内的心大静脉(图3).它左 行至前房室沟,在该处收集左缘静脉的血液;当其走 行于后房室沟内时,与左心房斜静脉,室后静脉汇 合.最终心中静脉也参与其中,该静脉位于后室间沟 内,引流左心室和右心室后部的血液.上述这些静脉 的汇合处形成一3cm长的冠状静脉窦,位于后房室沟 内.在冠状窦进入右心房前(下腔静脉人口左侧), 通常还有心小静脉汇人冠状窦.心小静脉引流右心房 和右心室的血液.心小静脉有时直接汇人右心房.两 支心前静脉在跨过右冠状动脉之前引流右心室和右心 房前面的血液进入右心房.此外,心脏静脉回流血液 的约20%,30%由心最小静脉(底比斯静脉)引流, 直接汇人邻近心腔内,多数为右心腔. (陈益和译程康安校) 7.心包包绕并保护着心脏,同时也提供 了足够的潜在空间保证心腔的充盈和排空.外 层心包为坚韧的纤维性心包,与主动脉,肺动 脉干,上腔静脉的外膜以及横膈的中心腱相连 汇合.(是非题) 8.关于心脏解剖结构下列描述错误的是: (单选题) A由于左室壁要比右室壁厚得多,所以 室间隔突向右侧 B下腔静脉在第八胸椎水平穿过横膈后 立即汇入右心房 C右冠状动脉自发出后,在右心耳与肺 动脉干之间前行,首先到达右前房室沟 D心脏动脉的变异性要比静脉明显 正常心脏的生理 DavidELWilcken? MEDICINE,2006,34(5):165,169 功能发挥正常的心脏可提供足够的氧合血,其中 包含有营养物质,代谢物质和激素,以满足机体每时 每刻代谢的需要,并保持稳定的内环境.心脏的两个 基本特征为收缩性和节律性.在上述调节过程中,神 经系统和神经体液作用调整着静脉回流,外周阻力,?