心力衰竭-英文版课件

Objective:1.Masteringclinicalmanifestation,diagnosisandmanagementofheartfailure2.Graspingcauses,pathophysiologyofheartfailure3.UnderstandingclassificationandinvestigationofheartfailureObjective:1.generalconcept

1)causesofheartfailure2)precipitating/aggravatingfactors3)pathophysiology4)typeofheartfailure2.chronicandacuteheartfailure

1)clinicalmanifestation2)investigation3)diagnosisanddifferentialdiagnosis4)management

Content

Content心力衰竭——英文版课件

Heartfailureisanimprecisetermusedtodescribethestatethatdevelopswhentheheartcannotmaintainanadequatecardiacoutputorcandosoonlyattheexpenseofanelevatedfillingpressure.

Definition

Definition

pulmonarycongestion,systemicvenouscongestion,tissueperfusiondeficiencyduetolowcardiacoutput.

ClinicalFeatures

ClinicalFeatures

leftventricularend-diastolicpressure>18mmHg,rightventricularend-diastolicpressure>10mmHg,

heartfailure=cardiacinsuffiency.

HemodynamicFeatures

HemodynamicFeaturesCausesofheartfailure1.Reducedventricularcontractilitya.Cardiomyopathy,myocardialinfarction.b.MetabolicdysfunctionCausesofheartfailure1.Redu

2.ventricularoverload

a.pressureoverload----hypertension,aorticstenosis,pulmonaryhypertension,pulmonaryvalvestenosis.

b.volumeoverload----mitralregurgitation,aorticregurgitation,atrialseptaldefect,ventricularsepalsdefect,hyperthyroidism,artery-venousfistula.

c.ventricularinflowobstruction----hypertrophy,mitralstenosis,tricuspidstenosis,restrictivecardiomyopathy,constrictivepericarditis.endocardialfibrosisandotherdisordersthatcauseastiffmyocardium.2.ventricularoverloadPrecipitating/aggravatingfactors

myocardialischemiaorinfarctioninfectionarrhythmiapulmonaryembolismexertionpregnancyandparturitionanemiaintravenousfluidoverload,electrolytedisturbance,acid-baseimbalancePrecipitating/aggravatingfaPathophysiology

1.Frank-Starling’sLawofthehearta.Thecardiacoutputisafunctionofthepreload,theafterload,andmyocardialcontractility.b.Preload:thevolumeandpressureofbloodintheventricleattheendofdiastole.c.Afterload:thearterialresistance.Pathophysiology

1.Frank-Starl心力衰竭——英文版课件1正常静息2正常活动3’心衰活动3心衰静息心肌收缩性BADC左室舒张末容量图3–2–1正常和心力衰竭时对机体活动时的代偿情况最大活动活动静息左室作功呼吸困难肺水肿E4静息致死性心肌受损1正常静息2正常活动3’心衰活动3心衰静息心肌收缩性心肌细胞死亡心力衰竭心肌细胞死亡++↑心肌能量消耗↑后负荷血管收缩↓心排血量神经体液兴奋RASSASInSP3循环↑心肌能量消耗↑胞浆Ca2+cAMPInSP3

心脏↓心肌松弛性↑变力效应+－—心律失常猝死图3–2–2肾素—血管紧张素和交感—肾上腺素能系统激活时对心脏代偿功能的影响2.RAASinHeartFailure心肌细胞死亡心力衰竭心肌细胞死亡++↑心肌能量消耗↑后负荷血2.RAASinHeartFailure2.RAASinHeartFailure3.myocardiumimpairedandremodelinginitialmyocardiumimpairedventricularoverloadmyocardiuminfarctioninflammationdiseaseprogressheartfailurecomplicationdeathchamberenlargementmyocardialhypertrophyembryogenephenotypeextracellularmatrixchangesecondaryconductfactorsympatheticnervoussystemRAASendothelinsTNF-α,IL-6mechanicalstressoxidativestress3.myocardiumimpairedandre4.Diastolicheartfailure

Heartfailuremaydevelopasaresultofpoorventricularfillingandhighfillingpressurecausedbyabnormalventricularrelaxation

4.Diastolicheartfailure顺应性↓顺应性↑正常压力图3–2–4心室舒张末期压力和容积的关系舒张性心力衰竭时，心室顺应性降低，心室压力–容积曲线向左上方移位，即在任何特定的舒张末期压时，心室末期容量小于正常人。容积顺应性↓顺应性↑正常压力图3–2–4心室舒sarcoplasmicreticulumintakeCa2+freeCa2+inmyocytedegradeslowlyb.InCHDwithobviousischemia,beforecontractilitydysfunction,haveoccurredrelaxationdysfunctionc.Inhypertrophyandhypertrophiccardiomyopathy,leftventricularend-diastolicfillingpressurepulmonaryhypertension,pulmonarycongestiondiastolicheartfailurerelaxationdysfunctionsarcoplasmicreticulumintake

Typeofheartfailure

Heartfailurecanbedescribedorclassifiedinseveralways.

1.

Acuteandchronicheartfailure2.

Left,rightandbiventricularheartfailure3.

Highandlowoutputheartfailure4.

Diastolicandsystolicdysfunction5.AsymptomaticandcongestiveheartfailureTypeofheartfailure

HeartLowoutputheartfailure:

Clinicalmanifestationofabnormalperipheralcirculation:vasoconstrictioninsystem,cold,pale,extremitiescyanosis,inthelateperiod,outputperminutedecreaseandleadtodifferenceofpulsepressuredecrease,theabovemanifestationoccurinthemajorityofCHF.Highoutputheartfailure:Extremitieswarm,flush,differenceofpulsepressureincrease,seeninhyperthyroidism,anemia,pregnancy心力衰竭——英文版课件

Systolicdysfunction

Heartfailuremaydevelopasaresultofimpairedmyocardialcontraction.

DiastolicdysfunctionHeartfailurecanalsobeduetopoorventricularfillingpressurecausedbyabnormalventricularrelaxation,whichiscommonlyfoundinpatientswithleftventricularhypertrophy,hypertensionandischemicheartdisease.Systolicdysfunction§1Chronicheartfailure

Definition

samemeaningascongestiveheartfailure§1Chronicheartfailure

clinicalmanifestation

1.leftventricularheartfailure

mainlymanifestedwithpulmonarycongestionandreductionofcardiacoutput

Asymptom

1.dyspnea

1)breathlessness

2)paroxysmalnocturnaldyspnea:oftenwith

wheezesoundinbothlungcardiogenicasthma

clinicalmanifestation

1.lef3)Orthopnea:indecubitus,bloodvolumeflowtoheartincreaseelevatedend–diastolicfillingpressurepulmonaryvenousandcapillarypressureincreaseinterstitialpulmonaryedemapulmonarycompliancedecreaserespiratoryresistance

4)acutepulmonaryedema3)Orthopnea:indecubitus,bloo2.coughandhemoptysis

pink-tingedorbrownishsputum3.fatigueonexertion4.urinarysystemsymptom

inearlyperiod,nocturiaincreaseinlaterperiod,oliguria

2.coughandhemoptysisB.Sign1.generalsign

dyspneaafteractivity,alsocyanosis,jaundice,differenceofpulsepressuredecrease,SBpdecrease,rapidheartrate,peripheralvasoconstriction,extremitiescyanosis,cold,sinustachycardia.B.Sign2.Heartsigndiffuseandlaterallydisplacedapicalimpulsegallopinearlydiastolicperiod,accentuatedp2systolicmurmuratcardiacapexpulsesalternansoccurwhenleftventricularejectiveimpedanceincrease3.Lungsign

moistralesinthebaseoflung¼CHFpatientsoccurpleuralfluid2.Heartsign2.RightventricularFailure

systemiccirculationcongestionSymptom1)gastrointestinaltractsymptom:

anorexia,distention,nausea,vomiting,constipation2)kidneysymptom

kidneycongestionrenalfunctiondecrease3)hepaticregionpain:congestion,cardiaccirrhosis4)dyspnea

2.RightventricularFailureSign1.heartsign

heartdilatewhenrightheartfailureisobvious,strongimpulseoccurinthesystolicperiodattheleftsternalborder,obviousbeatoccurinfraxiphoiddiastolicgalloprelativetricupidincompetence2.hepaticcervicalreflux3.congestiveliverandtendernessoccurbeforeedema

Acute:jaundice,ALTincreaseLongterm:cardiaccirrhosisSign4.edema

occuraftercervicalfillingandliverlarge,istypicalsignofrightheartfailure.atfirstoccurinfoot,ankle,anteriortibia.Intheearlyperiod,edemaoccurinthemorning,worseintheevening,disappearaftersleeping.Inthelatetime,systemic,symmetric,pittingedemaIfcomplicatedwithmalnutritionorhepaticdysfunction,faceedemaoccur,prognosisispoor.5.pleuralfluidandascites

4.edema

3.biventricularheartfailure

haveclinicalmanifestationofleftandrightheartfailure.3.biventricularheartfailurConditionswithnormalsystolicfunctionanddecreaseddiastolicfunctioninclude:

(1)systemicarterialhypertension(2)myocarditis(3)hyretrophiccardiomyopathy(4)congestivecardiomyopathyConditionswithnormalsys

Inthesettingofleftventriculardysfunction,whichoffollowingneurohormonalfactorswouldbeactivated?(1)Norepinephrine(2)Endothelin(3)Arginievasopreein(4)Endothelial-derivedrelaxingfactorInthesettingofleftveInvestigation1.routineexamination

blood,urine,renalfunction,electrolyte,liverfunction2.ECGa.nospecificfindings.b.Abnormalitiesmayprovideetiologicalclue(ventricularhypertrophy,AMI,bundlebranchblock)c.V1ptf<-0.03mm/sleftatrialoverload

Investigation3.Echocardiography:evaluatingLVaswellasotherchamberdimensions,ejectionfraction,andwallmotionabnormality.a.M:obtaineddirectingastationaryultrasonographybeamatsomeportionoftheheart.b.Two-dimensionalEcho(2-DE):providesspatiallycorrectimagesofheartandhasbecomethedominantechocardiographicmodalityc.DopplerEcho:usingultrasonographytorecordtheflowofbloodwithinthecardiovascularsystem.3.Echocardiography:evaluating4.XrayaevaluationofchamberenlargementbpulmonaryvenouscongestionKerleyBlines:reflectchronicelevationofleftatrialpressureandrepresentchronicthickeningoftheinterlobularseptafromedema.venousbloodredistributiontotheupperlobes.Cpulmonaryvenouspressure>25-30mmHg(3.3-4KPa)interstitialedemaoccur.4.Xray参数正常值临床意义中心静脉压（CVP）6~12cmH2O（0.59~1.18KPa）↑说明血容量过多或右心衰竭肺动脉压（PAP）12~30/4~13mmHg（1.6~4.0/0.53~1.73KPa）↑说明肺动脉高压、左心衰竭肺毛细血管楔嵌压（PCWP）6~12mmHg（0.8~1.6KPa）↑说明肺淤血、左心衰竭心搏量（SV）60~70ml↓可由于前负荷不足、心包填塞、心肌收缩力下降，心排阻力上升心搏指数（SI）41~51ml/m2同上心排血量（CO）5~6L/min↑可由于正性肌力药物作用，↓说明有心力衰竭心排指数（CI）2.6~4.0L/（min·m2）↓说明收缩力减低或心力衰竭射血分数（EF）0.5~0.6↓说明心室收缩功能减低左室每搏作功（LVSW）60~123

左室每搏作功指数（LVSWI）50~62

体循环血管阻力（SVR）770~1500dynes·s/cm5↓见于缺血、血管扩张剂，↑高血压、血管活性药物体循环血管阻力指数（SVRI）1970~2390dynes·s（cm5·m2）同上肺血管阻力（PVR）37~250dynes·s/cm5↑毛细血管前肺小动脉收缩、肺栓塞、慢性肺疾病、肺间质水肿、肺小血管阻塞性病变、二尖瓣狭窄肺血管阻力指数（PVRI）69~177dynes·s（cm5·m2）同上↑增高↓降低Invasivehomodynamicmonitoring参数正常值临床意义中心静脉压（CVP）6~12cmH2ODiagnosisanddifferentialdiagnosis

Clinicaldiagnosisinclude:

etiology(basiccauseandinducecause),pathoanatomy,pathophysiology,heartrhythmcardiacfunctionDiagnosisanddifferentialdiNYHAclassificationⅠnoactivitylimit,dailyactivitydon'tleadtoinertia,dyspnea,palpitation.Ⅱslightactivitylimit,nosymptomatrest,dailyactivityleadtoinertia,dyspnea,palpitationoranginapectoris.Ⅲobviousactivitylimit,nosymptomatrest,dailyactivityleadtoinertia,dyspnea,palpitationoranginapectoris.Ⅳcannotdoanyactivity,havesymptomatrest.NYHAclassificationtypeCI(L/min·m2）PCWP（mmHg）ClinicalmanifestationⅠ≥2.2≤18（2.4）Noperipheralperfusiondeficiencyandpulmonarycongestion,nosymptomandsignofheartfailureⅡ≥2.2＞18（2.4）Noperipheralperfusiondeficiency,pulmonarycongestion,noobviousclinicalmanifestationⅢ＜2.2≤18（2.4）peripheralperfusiondeficiency,nopulmonarycongestion,seeninrightventricularinfarctionandbloodvolumedeficiencyⅣ＜2.2＞18（2.4）peripheralperfusiondeficiencyandpulmonarycongestion,severetypeForresterclassificationtypePCWPClinicalmanifestationKillipclassificationⅠnoheartfailuresymptom,nomoistrales,PCWPmayelevateⅡslighttomoderateheartfailure,<50%lungfieldmoistrales,S3gallop,persistsinustachycardia,xraymanifestationofpulmonarycongestionⅢsevereheartfailure,>50%lungfieldmoistrales,mayoccurlungedemaⅣcardiacshock,Bp<90mmHg,oliguria<20ml/h,skincold,cyanosis,tachypnea,rapidpulseVcardiogenicshockandpulmonaryedemaKillipclassificationⅠnoheaDifferentialdiagnosis1.LeftheartfailurePulmonary,cardiogenicdyspnea2.RightheartfailureconstrictivepericarditisrenaledemahepaticcirrhosisDifferentialdiagnosisManagementofheartfailure

1.Etiologictreatmentbasiccause,precipitatingcauses.2.Reductionofventricularoverloada.restandsedativeagentb.salt-intakecontrolnormaladultintake3-6gsaltperdayⅠ0heartfailure:2gsalt/perdayⅡ0heartfailure:1gsalt/perdayⅢ0heartfailure:0.4gsalt/perdayManagementofheartfailurec.waterintakecontrolmaynotlimitwaterintakestrictly,intakewater1.5-2.0Lperdayinsevereheartfailure,waterretention,seralalbumindecrease,dilutivehyponatremia,notonlylimitsaltintake,butalsocontrolwaterintakec.waterintakecontrold.diuretics利尿剂作用部位和机制剂量（mg/d）作用持续时间（h）排钾类

氢氯噻嗪（hydrochlorothiozide）远曲小管：抑制NaCl共转运25~100口服12~18美托拉宗（metolazone）同上5~20口服12~24氯噻酮（chlorothalidone同上25~100口服24~72呋噻米（furosemide）Henle襻上升支：抑制Na-K-2Cl转运20~1000口服/静注4~6丁脲酸（bumetanide）同上0.5~20口服4~6潴钾类

氨体舒通（spironolactone集合管：醛固酮拮抗剂25~100口服24~96氨苯喋啶（triamterene）集合管：抑制Na重吸收100~300口服12~16阿米洛利（amiloride）同上5~20口服12~18d.diuretics利尿剂作用部位和机制剂量（mg/d）作Rbinedmedication

K-sparingdiureticsiscontradictedinrenaldysfunction

3.intermissionaltherapy4.PayattentiontowaterandelectrolytedisturbanceReasonableapplicationofdiur

Differentialofdeficitsodiumanddilutedhyponatremiadeficitsodiumhyponatremia

occurredafterusingmanydiuretics.feature:postohypotension,oliguria,highurinegravity,shouldintakesaltdilutedhyponatremia

alsocalledrefractoryheartfailure,hyponatremiaofhighbloodvolume,shouldlimitwater-intakeDifferentialofdeficitsodiu

e.Vasodilatordrugs

Indication

1.Leftend-diastolicfillingpressure>18mmHg,pulmonarycongestion2.clinicalmanifestationofperipheralcirculatoryperfusiondeficiencyCI<2.2L/min.m23.valveinsufficiency,ventricularseptaldefectpulmonaryhypertension,valveregurgitationwithcardiacdysfunctionIfbloodvolumedeficiency,shouldfluidreplacementatfirst,thenusevasodilatordrugs.

e.Vasodilatordrugs药物机制前负荷后负荷常用剂量作用时间开始高峰持续硝酸盐血管扩张剂

硝酸甘油NO供者++++0.2~10μg/（kg·min）iv5~6mg经皮2min5~15min<30min二硝酸异山梨醇酯++++10~60mgpotid15~20min1h4h10~20mg舌下5min15~30min3h2~7mg/hiv3~5min2h3h硝普钠++++++0.1~0.3μg/（kg·min）iv几乎立即

停药2~15min消失交感神经阻滞剂

酚妥拉明非选择性α–肾上腺素能激动剂++++0.5~1.0mg/miniv15~20min

3~4h哌唑嗪α1–肾上腺素能受体拮抗剂+++++1~6mgpotid30min1~3h6h肾素–血管紧张素系统拮抗剂

卡托普利抑制由ACE引起的肾系统性生成和组织生成血管紧张素Ⅱ；降低缓激肽的代谢++++6.25~50mgpoq8h15~30min1~2h4~6h依那普利++++5~10mgpobid2h4~6h24h赖诺普利++++2.5~20mgpoq12~24h

6~8h12h雷米普利++++1.25~5mgpoqd1~2h3~6h24h芦沙坦阻断血管紧张素Ⅱ（AT1受体）++++25~50mgpoq12h

5~6h24h药物机制前负荷后负荷常用剂量作用时间开始高峰持续硝酸盐血管扩ACE-I

ContradictionSevererenaldysfunction,renalarterystenosis,obviousmitralandaorticstenosisAmericanandEuropeanguideline:thatallheartfailurepatientsincludingasymptomaticfailure,exceptpatientsthathavecontradictionorcannottolerateACE-I,shoulduseACE-I,andforthelongtermtherapy.ACE-I3.increasecardiacoutputa.DigitalisPharmacology

increasemyocardialcontractileforceInhibitNa+-K+ATPaseNa+-Ca2+changeintracellularCa2+increasecontractilityincrease

increase

cardiacoutput

RenalflowincreaseSASactivitydecreaseperipheralvasodilateperipheralresistancedecrease

3.increasecardiacoutputRAASactivitydecrease

Reductionofwaterandsaltretentionduetoaldosteronedecrease

ProlongatrioventricularconductionHighlyeffectiveinthetreatmentofatrialfibrillationinadditiontoslowingventricularresponse,itmayconventtherhythmtonormalsinusmechanism.RAASactivitydecreaseUsecarefullyHypertrophiccardiomyopathyMitralstenosiswithsinusrhythmPericardiumconstrictionPulmonaryheartdiseaseHighdegreeAVBAMIin24hUsecarefullyDigitalistoxicityInducecauseHypokalemiaHypomagnemiaHypercalcemiaAcidintoxicationHypoxiaRenaldysfunctionSeveremyocardiallesionHypothyroidismDigitalistoxicityClinicalmanifestationofdigitalisSystemictoxiceffects:

Gastrointestinaltractsymptom:nausea,vomiting,anorexia,diarrhea,confusion,amblyopiaCardiacsymptom:arrhythmiaProlongedPRintervalandAVconduction.IncreasetheautomaticityofPurkinjefibersandenhancereentry,resultinginextrasystoles,ventricularfibrillation.ClinicalmanifestationofdigiTreatmentStoppingusingdigitalisUsepotassium,magnesiumifserumKislow.Rapidarrhythmia:lidocarineordipheninesodium,1-4mg/minusuallydon'tcardioversionSlowlyarrhythmiaatropine0.5-1mg.Treatment

b.Otherinotropicagent1.-adrenocepteragonistsDopamine1-5ug/Kg.minactivatedopaminereceptor,renalflowincrease>10ug/Kg.minactivateα-receptor,vasoconstrictDobutamine2-7.5ug/Kg.min

b.Otherinotropicagent2.PhosphodiesteraseinhibitorInhibitcAMPdegradeincreaseintracellularcAMPCa2+increase

cardiaccontractionincrease

AmrinoneMilrione

3.AldosteroneantagonistProtectaldosteroneescape.2.Phosphodiesteraseinhibito4.-adrenocepterantagonists

Recentclinictrialshaveshown,whengiveninverysmalldosesundercarefullymonitoredconditions,theycanincreaseejectionfraction,improvesymptomsandreducethefrequencyofhospitalizationinpatientwithchronicheartfailure..Relievetoxiationofcatecholamine.OnthebaseofusingACE-I,diuretics,digitalis,usingbloker..GiveninverysmallincrementaldosesBisoprool1.25mgmetoprolol6.25mg4.-adrenocepterantagonists5.diastolicheartfailuretreatment

treatprimarydiseaserelaxmyocardiumrevertmyocardialhypertrophydecreasepreloadcontroltachycardiacalciumchannelblocker,andblockercanbeuseful.5.diastolicheartfailuretrea6.Refractoryheartfailure1)Havetheetiologyandprecipitatingcausesbeenestablished?2)Aredrugdoseoptimal?3)Isthepatientadheringtoanadequatelow-saltdiet?4)Needanothercardiactransplantation.

6.Refractoryheartfailure7.AcutepulmonaryedemaEmergencytreatment1)position:Don'tkeeppatientinasupineposition2)Maintainoxygenation:highconcentrationsofO2shouldbegivenbymaskornasalcannula.3)Morphinesulfate3-5mgIVor5-10mgIMcanreduceagitation,reducetransientarterialandvenousdilation,decreasetherespiratoryrate,slowtheheartrate,andreducerespiratoryandcardiacwork.7.Acutepulmonaryedema4)Intravenousadministrationofarapidlyactigdiuretic,eg.(furosemide40mgIV)canbeinitiateapromptdiuresisin15to20min.5)RotatingtourniquetsareeffectivewithBpcuffappliedto3limbs,inflatedmidwaybetweendiastolicandsystolicpressure,deflatedandrotated10to20min.6)Vasodilatordrugs7)Digitalis8)Aminophylline9)others4)Intravenousadministrationo

Pathophysiologicconsequencesofamyocardialinfarctioninclude:(1)increasedsystolicloadduetotheakineticsegment(2)decreasedejectionfractionthatapproximatestheamountofmuscleloss.(3)hypertrophyofnoninfarctedmyocardium.(4)decreasedend-diastoicvolumePathophysiologicconsequence

Supportiveevidencethatleft-sidedfailureispresentincludesallthefollowingEXCEPT:A.abnormallyelevatedfillingpressuresasdetectedbyrightheartcatheterizationB.acardiacindexof3.5liters/min/m2C.areductioninmaximumoxygenconsumptiondeterminednoninvasivelybyexerciseD.thepresenceofpulmonaryralesonphysicalexaminationE.lowleftventricularejectionfractionatrestonechocardiographySupportiveevidencethatObjective:1.Masteringclinicalmanifestation,diagnosisandmanagementofheartfailure2.Graspingcauses,pathophysiologyofheartfailure3.UnderstandingclassificationandinvestigationofheartfailureObjective:1.generalconcept

1)causesofheartfailure2)precipitating/aggravatingfactors3)pathophysiology4)typeofheartfailure2.chronicandacuteheartfailure

1)clinicalmanifestation2)investigation3)diagnosisanddifferentialdiagnosis4)management

Content

Content心力衰竭——英文版课件

Heartfailureisanimprecisetermusedtodescribethestatethatdevelopswhentheheartcannotmaintainanadequatecardiacoutputorcandosoonlyattheexpenseofanelevatedfillingpressure.

Definition

Definition

pulmonarycongestion,systemicvenouscongestion,tissueperfusiondeficiencyduetolowcardiacoutput.

ClinicalFeatures

ClinicalFeatures

leftventricularend-diastolicpressure>18mmHg,rightventricularend-diastolicpressure>10mmHg,

heartfailure=cardiacinsuffiency.

HemodynamicFeatures

HemodynamicFeaturesCausesofheartfailure1.Reducedventricularcontractilitya.Cardiomyopathy,myocardialinfarction.b.MetabolicdysfunctionCausesofheartfailure1.Redu

2.ventricularoverload

a.pressureoverload----hypertension,aorticstenosis,pulmonaryhypertension,pulmonaryvalvestenosis.

b.volumeoverload----mitralregurgitation,aorticregurgitation,atrialseptaldefect,ventricularsepalsdefect,hyperthyroidism,artery-venousfistula.

c.ventricularinflowobstruction----hypertrophy,mitralstenosis,tricuspidstenosis,restrictivecardiomyopathy,constrictivepericarditis.endocardialfibrosisandotherdisordersthatcauseastiffmyocardium.2.ventricularoverloadPrecipitating/aggravatingfactors

myocardialischemiaorinfarctioninfectionarrhythmiapulmonaryembolismexertionpregnancyandparturitionanemiaintravenousfluidoverload,electrolytedisturbance,acid-baseimbalancePrecipitating/aggravatingfaPathophysiology

1.Frank-Starling’sLawofthehearta.Thecardiacoutputisafunctionofthepreload,theafterload,andmyocardialcontractility.b.Preload:thevolumeandpressureofbloodintheventricleattheendofdiastole.c.Afterload:thearterialresistance.Pathophysiology

1.Frank-Starl心力衰竭——英文版课件1正常静息2正常活动3’心衰活动3心衰静息心肌收缩性BADC左室舒张末容量图3–2–1正常和心力衰竭时对机体活动时的代偿情况最大活动活动静息左室作功呼吸困难肺水肿E4静息致死性心肌受损1正常静息2正常活动3’心衰活动3心衰静息心肌收缩性心肌细胞死亡心力衰竭心肌细胞死亡++↑心肌能量消耗↑后负荷血管收缩↓心排血量神经体液兴奋RASSASInSP3循环↑心肌能量消耗↑胞浆Ca2+cAMPInSP3

心脏↓心肌松弛性↑变力效应+－—心律失常猝死图3–2–2肾素—血管紧张素和交感—肾上腺素能系统激活时对心脏代偿功能的影响2.RAASinHeartFailure心肌细胞死亡心力衰竭心肌细胞死亡++↑心肌能量消耗↑后负荷血2.RAASinHeartFailure2.RAASinHeartFailure3.myocardiumimpairedandremodelinginitialmyocardiumimpairedventricularoverloadmyocardiuminfarctioninflammationdiseaseprogressheartfailurecomplicationdeathchamberenlargementmyocardialhypertrophyembryogenephenotypeextracellularmatrixchangesecondaryconductfactorsympatheticnervoussystemRAASendothelinsTNF-α,IL-6mechanicalstressoxidativestress3.myocardiumimpairedandre4.Diastolicheartfailure

Heartfailuremaydevelopasaresultofpoorventricularfillingandhighfillingpressurecausedbyabnormalventricularrelaxation

4.Diastolicheartfailure顺应性↓顺应性↑正常压力图3–2–4心室舒张末期压力和容积的关系舒张性心力衰竭时，心室顺应性降低，心室压力–容积曲线向左上方移位，即在任何特定的舒张末期压时，心室末期容量小于正常人。容积顺应性↓顺应性↑正常压力图3–2–4心室舒sarcoplasmicreticulumintakeCa2+freeCa2+inmyocytedegradeslowlyb.InCHDwithobviousischemia,beforecontractilitydysfunction,haveoccurredrelaxationdysfunctionc.Inhypertrophyandhypertrophiccardiomyopathy,leftventricularend-diastolicfillingpressurepulmonaryhypertension,pulmonarycongestiondiastolicheartfailurerelaxationdysfunctionsarcoplasmicreticulumintake

Typeofheartfailure

Heartfailurecanbedescribedorclassifiedinseveralways.

1.

Acuteandchronicheartfailure2.

Left,rightandbiventricularheartfailure3.

Highandlowoutputheartfailure4.

Diastolicandsystolicdysfunction5.AsymptomaticandcongestiveheartfailureTypeofheartfailure

HeartLowoutputheartfailure:

Clinicalmanifestationofabnormalperipheralcirculation:vasoconstrictioninsystem,cold,pale,extremitiescyanosis,inthelateperiod,outputperminutedecreaseandleadtodifferenceof