心力衰竭-英文版課件

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——英文版課件

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——英文版課件1正常靜息2正?；顒?dòng)3’心衰活動(dòng)3心衰靜息心肌收縮性BADC左室舒張末容量圖3–2–1正常和心力衰竭時(shí)對(duì)機(jī)體活動(dòng)時(shí)的代償情況最大活動(dòng)活動(dòng)靜息左室作功呼吸困難肺水腫E4靜息致死性心肌受損1正常靜息2正?；顒?dòng)3’心衰活動(dòng)3心衰靜息心肌收縮性心肌細(xì)胞死亡心力衰竭心肌細(xì)胞死亡++↑心肌能量消耗↑后負(fù)荷血管收縮↓心排血量神經(jīng)體液興奮RASSASInSP3循環(huán)↑心肌能量消耗↑胞漿Ca2+cAMPInSP3

心臟↓心肌松弛性↑變力效應(yīng)+－—心律失常猝死圖3–2–2腎素—血管緊張素和交感—腎上腺素能系統(tǒng)激活時(shí)對(duì)心臟代償功能的影響2.RAASinHeartFailure心肌細(xì)胞死亡心力衰竭心肌細(xì)胞死亡++↑心肌能量消耗↑后負(fù)荷血2.RAASinHeartFailure2.RAASinHeartFailure3.myocardiumimpairedandremodelinginitialmyocardiumimpairedventricularoverloadmyocardiuminfarctioninflammationdiseaseprogressheartfailurecomplicationdeathchamberenlargementmyocardialhypertrophyembryogenephenotypeextracellularmatrixchangesecondaryconductfactorsympatheticnervoussystemRAASendothelinsTNF-α,IL-6mechanicalstressoxidativestress3.myocardiumimpairedandre4.Diastolicheartfailure

Heartfailuremaydevelopasaresultofpoorventricularfillingandhighfillingpressurecausedbyabnormalventricularrelaxation

4.Diastolicheartfailure順應(yīng)性↓順應(yīng)性↑正常壓力圖3–2–4心室舒張末期壓力和容積的關(guān)系舒張性心力衰竭時(shí)，心室順應(yīng)性降低，心室壓力–容積曲線向左上方移位，即在任何特定的舒張末期壓時(shí)，心室末期容量小于正常人。容積順應(yīng)性↓順應(yīng)性↑正常壓力圖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——英文版課件

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

moistralesinthebaseoflung?CHFpatientsoccurpleuralfluid2.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參數(shù)正常值臨床意義中心靜脈壓（CVP）6~12cmH2O（0.59~1.18KPa）↑說(shuō)明血容量過(guò)多或右心衰竭肺動(dòng)脈壓（PAP）12~30/4~13mmHg（1.6~4.0/0.53~1.73KPa）↑說(shuō)明肺動(dòng)脈高壓、左心衰竭肺毛細(xì)血管楔嵌壓（PCWP）6~12mmHg（0.8~1.6KPa）↑說(shuō)明肺淤血、左心衰竭心搏量（SV）60~70ml↓可由于前負(fù)荷不足、心包填塞、心肌收縮力下降，心排阻力上升心搏指數(shù)（SI）41~51ml/m2同上心排血量（CO）5~6L/min↑可由于正性肌力藥物作用，↓說(shuō)明有心力衰竭心排指數(shù)（CI）2.6~4.0L/（min·m2）↓說(shuō)明收縮力減低或心力衰竭射血分?jǐn)?shù)（EF）0.5~0.6↓說(shuō)明心室收縮功能減低左室每搏作功（LVSW）60~123

左室每搏作功指數(shù)（LVSWI）50~62

體循環(huán)血管阻力（SVR）770~1500dynes·s/cm5↓見(jiàn)于缺血、血管擴(kuò)張劑，↑高血壓、血管活性藥物體循環(huán)血管阻力指數(shù)（SVRI）1970~2390dynes·s（cm5·m2）同上肺血管阻力（PVR）37~250dynes·s/cm5↑毛細(xì)血管前肺小動(dòng)脈收縮、肺栓塞、慢性肺疾病、肺間質(zhì)水腫、肺小血管阻塞性病變、二尖瓣狹窄肺血管阻力指數(shù)（PVRI）69~177dynes·s（cm5·m2）同上↑增高↓降低Invasivehomodynamicmonitoring參數(shù)正常值臨床意義中心靜脈壓（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利尿劑作用部位和機(jī)制劑量（mg/d）作用持續(xù)時(shí)間（h）排鉀類

氫氯噻嗪（hydrochlorothiozide）遠(yuǎn)曲小管：抑制NaCl共轉(zhuǎn)運(yùn)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轉(zhuǎn)運(yùn)20~1000口服/靜注4~6丁脲酸（bumetanide）同上0.5~20口服4~6潴鉀類

氨體舒通（spironolactone集合管：醛固酮拮抗劑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利尿劑作用部位和機(jī)制劑量（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藥物機(jī)制前負(fù)荷后負(fù)荷常用劑量作用時(shí)間開(kāi)始高峰持續(xù)硝酸鹽血管擴(kuò)張劑

硝酸甘油NO供者++++0.2~10μg/（kg·min）iv5~6mg經(jīng)皮2min5~15min<30min二硝酸異山梨醇酯++++10~60mgpotid15~20min1h4h10~20mg舌下5min15~30min3h2~7mg/hiv3~5min2h3h硝普鈉++++++0.1~0.3μg/（kg·min）iv幾乎立即

停藥2~15min消失交感神經(jīng)阻滯劑

酚妥拉明非選擇性α–腎上腺素能激動(dòng)劑++++0.5~1.0mg/miniv15~20min

3~4h哌唑嗪α1–腎上腺素能受體拮抗劑+++++1~6mgpotid30min1~3h6h腎素–血管緊張素系統(tǒng)拮抗劑

卡托普利抑制由ACE引起的腎系統(tǒng)性生成和組織生成血管緊張素Ⅱ；降低緩激肽的代謝++++6.25~50mgpoq8h15~30min1~2h4~6h依那普利++++5~10mgpobid2h4~6h24h賴諾普利++++2.5~20mgpoq12~24h

6~8h12h雷米普利++++1.25~5mgpoqd1~2h3~6h24h蘆沙坦阻斷血管緊張素Ⅱ（AT1受體）++++25~50mgpoq12h

5~6h24h藥物機(jī)制前負(fù)荷后負(fù)荷常用劑量作用時(shí)間開(kāi)始高峰持續(xù)硝酸鹽血管擴(kuò)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——英文版課件

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——英文版課件1正常靜息2正?；顒?dòng)3’心衰活動(dòng)3心衰靜息心肌收縮性BADC左室舒張末容量圖3–2–1正常和心力衰竭時(shí)對(duì)機(jī)體活動(dòng)時(shí)的代償情況最大活動(dòng)活動(dòng)靜息左室作功呼吸困難肺水腫E4靜息致死性心肌受損1正常靜息2正?；顒?dòng)3’心衰活動(dòng)3心衰靜息心肌收縮性心肌細(xì)胞死亡心力衰竭心肌細(xì)胞死亡++↑心肌能量消耗↑后負(fù)荷血管收縮↓心排血量神經(jīng)體液興奮RASSASInSP3循環(huán)↑心肌能量消耗↑胞漿Ca2+cAMPInSP3

心臟↓心肌松弛性↑變力效應(yīng)+－—心律失常猝死圖3–2–2腎素—血管緊張素和交感—腎上腺素能系統(tǒng)激活時(shí)對(duì)心臟代償功能的影響2.RAASinHeartFailure心肌細(xì)胞死亡心力衰竭心肌細(xì)胞死亡++↑心肌能量消耗↑后負(fù)荷血2.RAASinHeartFailure2.RAASinHeartFailure3.myocardiumimpairedandremodelinginitialmyocardiumimpairedventricularoverloadmyocardiuminfarctioninflammationdiseaseprogressheartfailurecomplicationdeathchamberenlargementmyocardialhypertrophyembryogenephenotypeextracellularmatrixchangesecondaryconductfactorsympatheticnervoussystemRAASendothelinsTNF-α,IL-6mechanicalstressoxidativestress3.myocardiumimpairedandre4.Diastolicheartfailure

Heartfailuremaydevelopasaresultofpoorventricularfillingandhighfillingpressurecausedbyabnormalventricularrelaxation

4.Diastolicheartfailure順應(yīng)性↓順應(yīng)性↑正常壓力圖3–2–4心室舒張末期壓力和容積的關(guān)系舒張性心力衰竭時(shí)，心室順應(yīng)性降低，心室壓力–容積曲線向左上方移位，即在任何特定的舒張末期壓時(shí)，心室末期容量小于正常人。容積順應(yīng)性↓順應(yīng)性↑正常壓力圖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