心力衰竭课件

HeartFailure

XiaojuanBai

7yearsprogramofChinaMedicalUniversity教学心力衰竭Objective:1.Masteringclinicalmanifestation,diagnosisandmanagementofheartfailure2.Graspingcauses,pathophysiologyofheartfailure3.Understandingclassificationandinvestigationofheartfailure教学心力衰竭1.generalconcept

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

1)clinicalmanifestation2)investigation3)diagnosisanddifferentialdiagnosis4)management

Content教学心力衰竭教学心力衰竭

Heartfailureisanimprecisetermusedtodescribethestatethatdevelopswhentheheartcannotmaintainanadequatecardiacoutputorcandosoonlyattheexpenseofanelevatedfillingpressure.

Definition

教学心力衰竭

pulmonarycongestion,systemicvenouscongestion,tissueperfusiondeficiencyduetolowcardiacoutput.

ClinicalFeatures教学心力衰竭

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

heartfailure=cardiacinsuffiency.

HemodynamicFeatures教学心力衰竭Causesofheartfailure1.Reducedventricularcontractilitya.Cardiomyopathy,myocardialinfarction.b.Metabolicdysfunction教学心力衰竭

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.教学心力衰竭Precipitating/aggravatingfactors

myocardialischemiaorinfarctioninfectionarrhythmiapulmonaryembolismexertionpregnancyandparturitionanemiaintravenousfluidoverload,electrolytedisturbance,acid-baseimbalance教学心力衰竭Pathophysiology

1.Frank-Starling’sLawofthehearta.Thecardiacoutputisafunctionofthepreload,theafterload,andmyocardialcontractility.b.Preload:thevolumeandpressureofbloodintheventricleattheendofdiastole.c.Afterload:thearterialresistance.教学心力衰竭教学心力衰竭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教学心力衰竭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教学心力衰竭2.RAASinHeartFailure教学心力衰竭3.myocardiumimpairedandremodelinginitialmyocardiumimpairedventricularoverloadmyocardiuminfarctioninflammationdiseaseprogressheartfailurecomplicationdeathchamberenlargementmyocardialhypertrophyembryogenephenotypeextracellularmatrixchangesecondaryconductfactorsympatheticnervoussystemRAASendothelinsTNF-α,IL-6mechanicalstressoxidativestress教学心力衰竭4.Diastolicheartfailure

Heartfailuremaydevelopasaresultofpoorventricularfillingandhighfillingpressurecausedbyabnormalventricularrelaxation

教学心力衰竭顺应性↓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。容积教学心力衰竭sarcoplasmicreticulumintakeCa2+freeCa2+inmyocytedegradeslowlyb.InCHDwithobviousischemia,beforecontractilitydysfunction,haveoccurredrelaxationdysfunctionc.Inhypertrophyandhypertrophiccardiomyopathy,leftventricularend-diastolicfillingpressurepulmonaryhypertension,pulmonarycongestiondiastolicheartfailurerelaxationdysfunction教学心力衰竭

Typeofheartfailure

Heartfailurecanbedescribedorclassifiedinseveralways.

1.

Acuteandchronicheartfailure2.

Left,rightandbiventricularheartfailure3.

Highandlowoutputheartfailure4.

Diastolicandsystolicdysfunction5.Asymptomaticandcongestiveheartfailure教学心力衰竭Lowoutputheartfailure:

Clinicalmanifestationofabnormalperipheralcirculation:vasoconstrictioninsystem,cold,pale,extremitiescyanosis,inthelateperiod,outputperminutedecreaseandleadtodifferenceofpulsepressuredecrease,theabovemanifestationoccurinthemajorityofCHF.Highoutputheartfailure:Extremitieswarm,flush,differenceofpulsepressureincrease,seeninhyperthyroidism,anemia,pregnancy教学心力衰竭

Systolicdysfunction

Heartfailuremaydevelopasaresultofimpairedmyocardialcontraction.

DiastolicdysfunctionHeartfailurecanalsobeduetopoorventricularfillingpressurecausedbyabnormalventricularrelaxation,whichiscommonlyfoundinpatientswithleftventricularhypertrophy,hypertensionandischemicheartdisease.教学心力衰竭§1Chronicheartfailure

Definition

samemeaningascongestiveheartfailure教学心力衰竭

clinicalmanifestation

1.leftventricularheartfailure

mainlymanifestedwithpulmonarycongestionandreductionofcardiacoutput

Asymptom

1.dyspnea

1)breathlessness

2)paroxysmalnocturnaldyspnea:oftenwith

wheezesoundinbothlungcardiogenicasthma

教学心力衰竭3)Orthopnea:indecubitus,bloodvolumeflowtoheartincreaseelevatedend–diastolicfillingpressurepulmonaryvenousandcapillarypressureincreaseinterstitialpulmonaryedemapulmonarycompliancedecreaserespiratoryresistance

4)acutepulmonaryedema教学心力衰竭2.coughandhemoptysis

pink-tingedorbrownishsputum3.fatigueonexertion4.urinarysystemsymptom

inearlyperiod,nocturiaincreaseinlaterperiod,oliguria

教学心力衰竭B.Sign1.generalsign

dyspneaafteractivity,alsocyanosis,jaundice,differenceofpulsepressuredecrease,SBpdecrease,rapidheartrate,peripheralvasoconstriction,extremitiescyanosis,cold,sinustachycardia.教学心力衰竭2.Heartsigndiffuseandlaterallydisplacedapicalimpulsegallopinearlydiastolicperiod,accentuatedp2systolicmurmuratcardiacapexpulsesalternansoccurwhenleftventricularejectiveimpedanceincrease3.Lungsign

moistralesinthebaseoflung¼CHFpatientsoccurpleuralfluid教学心力衰竭2.RightventricularFailure

systemiccirculationcongestionSymptom1)gastrointestinaltractsymptom:

anorexia,distention,nausea,vomiting,constipation2)kidneysymptom

kidneycongestionrenalfunctiondecrease3)hepaticregionpain:congestion,cardiaccirrhosis4)dyspnea

教学心力衰竭Sign1.heartsign

heartdilatewhenrightheartfailureisobvious,strongimpulseoccurinthesystolicperiodattheleftsternalborder,obviousbeatoccurinfraxiphoiddiastolicgalloprelativetricupidincompetence2.hepaticcervicalreflux3.congestiveliverandtendernessoccurbeforeedema

Acute:jaundice,ALTincreaseLongterm:cardiaccirrhosis教学心力衰竭4.edema

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

教学心力衰竭

3.biventricularheartfailure

haveclinicalmanifestationofleftandrightheartfailure.教学心力衰竭Conditionswithnormalsystolicfunctionanddecreaseddiastolicfunctioninclude:

(1)systemicarterialhypertension(2)myocarditis(3)hyretrophiccardiomyopathy(4)congestivecardiomyopathy教学心力衰竭

Inthesettingofleftventriculardysfunction,whichoffollowingneurohormonalfactorswouldbeactivated?(1)Norepinephrine(2)Endothelin(3)Arginievasopreein(4)Endothelial-derivedrelaxingfactor教学心力衰竭Investigation1.routineexamination

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

教学心力衰竭3.Echocardiography:evaluatingLVaswellasotherchamberdimensions,ejectionfraction,andwallmotionabnormality.a.M:obtaineddirectingastationaryultrasonographybeamatsomeportionoftheheart.b.Two-dimensionalEcho(2-DE):providesspatiallycorrectimagesofheartandhasbecomethedominantechocardiographicmodalityc.DopplerEcho:usingultrasonographytorecordtheflowofbloodwithinthecardiovascularsystem.教学心力衰竭4.XrayaevaluationofchamberenlargementbpulmonaryvenouscongestionKerleyBlines:reflectchronicelevationofleftatrialpressureandrepresentchronicthickeningoftheinterlobularseptafromedema.venousbloodredistributiontotheupperlobes.Cpulmonaryvenouspressure>25-30mmHg(3.3-4KPa)interstitialedemaoccur.教学心力衰竭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教学心力衰竭Diagnosisanddifferentialdiagnosis

Clinicaldiagnosisinclude:

etiology(basiccauseandinducecause),pathoanatomy,pathophysiology,heartrhythmcardiacfunction教学心力衰竭NYHAclassificationⅠnoactivitylimit,dailyactivitydon'tleadtoinertia,dyspnea,palpitation.Ⅱslightactivitylimit,nosymptomatrest,dailyactivityleadtoinertia,dyspnea,palpitationoranginapectoris.Ⅲobviousactivitylimit,nosymptomatrest,dailyactivityleadtoinertia,dyspnea,palpitationoranginapectoris.Ⅳcannotdoanyactivity,havesymptomatrest.教学心力衰竭typeCI(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,severetypeForresterclassification教学心力衰竭KillipclassificationⅠnoheartfailuresymptom,nomoistrales,PCWPmayelevateⅡslighttomoderateheartfailure,<50%lungfieldmoistrales,S3gallop,persistsinustachycardia,xraymanifestationofpulmonarycongestionⅢsevereheartfailure,>50%lungfieldmoistrales,mayoccurlungedemaⅣcardiacshock,Bp<90mmHg,oliguria<20ml/h,skincold,cyanosis,tachypnea,rapidpulseVcardiogenicshockandpulmonaryedema教学心力衰竭Differentialdiagnosis1.LeftheartfailurePulmonary,cardiogenicdyspnea2.Rightheartfailureconstrictivepericarditisrenaledemahepaticcirrhosis教学心力衰竭Managementofheartfailure

1.Etiologictreatmentbasiccause,precipitatingcauses.2.Reductionofventricularoverloada.restandsedativeagentb.salt-intakecontrolnormaladultintake3-6gsaltperdayⅠ0heartfailure:2gsalt/perdayⅡ0heartfailure:1gsalt/perdayⅢ0heartfailure:0.4gsalt/perday教学心力衰竭c.waterintakecontrolmaynotlimitwaterintakestrictly,intakewater1.5-2.0Lperdayinsevereheartfailure,waterretention,seralalbumindecrease,dilutivehyponatremia,notonlylimitsaltintake,butalsocontrolwaterintake教学心力衰竭d.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12~18教学心力衰竭Reasonableapplicationofdiuretics1.strictlyfollowingindication2.combinedmedication

K-sparingdiureticsiscontradictedinrenaldysfunction

3.intermissionaltherapy4.Payattentiontowaterandelectrolytedisturbance教学心力衰竭

Differentialofdeficitsodiumanddilutedhyponatremiadeficitsodiumhyponatremia

occurredafterusingmanydiuretics.feature:postohypotension,oliguria,highurinegravity,shouldintakesaltdilutedhyponatremia

alsocalledrefractoryheartfailure,hyponatremiaofhighbloodvolume,shouldlimitwater-intake教学心力衰竭

e.Vasodilatordrugs

Indication

1.Leftend-diastolicfillingpressure>18mmHg,pulmonarycongestion2.clinicalmanifestationofperipheralcirculatoryperfusiondeficiencyCI<2.2L/min.m23.valveinsufficiency,ventricularseptaldefectpulmonaryhypertension,valveregurgitationwithcardiacdysfunctionIfbloodvolumedeficiency,shouldfluidreplacementatfirst,thenusevasodilatordrugs.教学心力衰竭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教学心力衰竭ACE-I

ContradictionSevererenaldysfunction,renalarterystenosis,obviousmitralandaorticstenosisAmericanandEuropeanguideline:thatallheartfailurepatientsincludingasymptomaticfailure,exceptpatientsthathavecontradictionorcannottolerateACE-I,shoulduseACE-I,andforthelongtermtherapy.教学心力衰竭3.increasecardiacoutputa.DigitalisPharmacology

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

increase

cardiacoutput

RenalflowincreaseSASactivitydecreaseperipheralvasodilateperipheralresistancedecrease

教学心力衰竭RAASactivitydecrease

Reductionofwaterandsaltretentionduetoaldosteronedecrease

ProlongatrioventricularconductionHighlyeffectiveinthetreatmentofatrialfibrillationinadditiontoslowingventricularresponse,itmayconventtherhythmtonormalsinusmechanism.教学心力衰竭UsecarefullyHypertrophiccardiomyopathyMitralstenosiswithsinusrhythmPericardiumconstrictionPulmonaryheartdiseaseHighdegreeAVBAMIin24h教学心力衰竭DigitalistoxicityInducecauseHypokalemiaHypomagnemiaHypercalcemiaAcidintoxicationHypoxiaRenaldysfunctionSeveremyocardiallesionHypothyroidism教学心力衰竭ClinicalmanifestationofdigitalisSystemictoxiceffects:

Gastrointestinaltractsymptom:nausea,vomiting,anorexia,diarrhea,confusion,amblyopiaCardiacsymptom:arrhythmiaProlongedPRintervalandAVconduction.IncreasetheautomaticityofPurkinjefibersandenhancereentry,resultinginextrasystoles,ventricularfibrillation.教学心力衰竭TreatmentStoppingusingdigitalisUsepotassium,magnesiumifserumKislow.Rapidarrhythmia:lidocarineordipheninesodium,1-4mg/minusuallydon'tcardioversionSlowlyarrhythmiaatropine0.5-1mg.教学心力衰竭

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

教学心力衰竭2.PhosphodiesteraseinhibitorInhibitcAMPdegradeincreaseintracellularcAMPCa2+increase

cardiaccontractionincrease

AmrinoneMilrione

3.AldosteroneantagonistProtectaldosteroneescape.教学心力衰竭4.-adrenocepterantagonists

Recentclinictrialshaveshown,whengiveninverysmalldosesundercarefullymonitoredconditions,theycanincreaseejectionfraction,improvesymptomsandreducethefrequencyofhospitalizationinpatientwithchronicheartfailure..Relievetoxiationofcatecholamine.OnthebaseofusingACE-I,diuretics,digitalis,usingbloker..Giveninverysmallincremen