cusp

重度主动脉瓣狭窄（vereaorticstenosis，AS）病人手术的麻醉

【摘要】

目的：分析总结178例重度主动脉瓣狭窄病人外科手术的麻醉经验及住院期间转归。

方法：2000年1月至2006年12月，阜外心血管病医院实施的重度主动脉瓣狭窄

（AVA<1.0cm2，主动脉瓣跨瓣压差>60mmHg）手术治疗病人共178例，其中主动脉瓣置换

例，Ross手术例，主动脉瓣联合升主动脉置换（或成形）例，重度主动脉瓣狭窄合并冠

心病手术治疗

结果：全组无麻醉死亡，术中外科原因死亡1例，术后死亡2例

结论：麻醉处理应注意，麻醉诱导期至CPB开始前避免低血压，围术期心肌保护，重视心

脏复苏期灌注压维持及药物治疗，围术期一般不需大剂量正性肌力药、可应用受体阻滞药,

术后早期需维持较高的血压，积极治疗室性心律失常。

关键词

【Abstract】

重度主动脉瓣狭窄病人因长期左心室后负荷增高致左心室壁肥厚，围术期易发生心肌缺血，

一旦发生室颤，复苏成功率低。CPB术中恢复心肌灌注后常发生心脏复跳困难，是心血管

外科手术病人麻醉处理难点之一。本研究分析总结了178例重度主动脉瓣狭窄病人的麻醉处

理经验及住院期间病人转归。

1.资料与方法

年龄4916岁，体重6512Kg，CPB时间10037min，阻断时间7631min，停跳液

2102826ml，灌注次数2.31次，术前主动脉瓣压差9434mmHg，室间隔厚度142.7mm

术前左室舒张末内径497mm，EF64％9％，术后主动脉瓣压差2511mmHg,术后左室舒

张末内径467mm，EF60％7％。芬太尼诱导10.64.5ug/kg，总用量269ug/kg。气管拔管

时间13.48hICU时间4227h住院时间115d。

2.结果

3.讨论

1)围术期受体阻滞药的应用

2)围术期心肌保护

3)CPB中恢复心肌灌注后心脏的复苏

a)开放前温氧合血灌注心脏

b)受体阻滞药

c)可达龙＋肾上腺受体激动剂

d)

4)术后循环维持及正性肌力药应用问题

5)死亡病例讨论，由于左心室肥厚注意维持一定的血压，血容量，避免低血压导致心肌灌

注不足，心肌缺血，室颤。

Calcificdepositsinthebodiesofaorticcuspscaustiffness,restrain

normalmovement,andpreventadequatevalveopening(28).Ifthenormal

aorticvalveopeningareaof3–4cm2decreastoapproximately

one-fourthofthatarea,thestenosisbecomeshemodynamicallysignificant.

Mildaorticstenosisisprentwithavalveareaof1.5cm2;moderate

aorticstenosis,withavalveareabetween1.0and1.5cm2;vereaortic

stenosis,withavalveareaof1.0cm2orless;andcriticalaorticstenosis,

withavalveareaof0.7cm2orless(6).Findingsofourstudyindicate

forthefirsttime,toourknowledge,thatplanimetricmeasurementsof

theAVAbyusingretrospectivelyelectrocardiographicallygated

16–detectorrowCTallowaclassificationofaorticstenosisthatis

similartomeasurementsachievedwithestablishedroutine

–detectorrowCTfurthermore

providesmorphologicinformation,suchascuspcalcificationand

restrictionofcuspmovement,andallowsthedistinctionbetweenbicuspid

andtricuspidaorticvalves.

StructuralValveAbnormalitiesandSurgicalValveReplacement

Preoperativeknowledgeaboutaorticvalvemorphologiccharacteristics

andextentofaorticvalvecalcificationisdesirablewhenoneisplanning

surgicalvalvereplacement(19).Forexample,theprenceorabnceof

abicuspidaorticvalveposariskfactorforpostoperative

complicationsafteraorticvalveandaorticrootreplacement(29).

Similarly,extensivevalvecalcificationisassociatedwithahigher

prevalenceofsurgicaldifficulties;placementandfixationofthevalve

prosthesisintotheannulus,aswellasinrtionofthecoronaryarteries,

afteraorticrootreplacementarecomplicatedbyverecalcification

(30).Furthermore,preoperativequantificationofvalvecalcificationin

patientswhoareundergoingaorticvalvereplacementallowsprediction

ofpostoperativeconductiondefects(31).Ourresultsweresimilartothe

resultsofapreviousstudy(18)withfour–detectorrowCT,forwewere

abletoaccuratelydepictmorphologicabnormalitiesoftheaorticvalve

withsimilarresultswhenwecomparedresultsachievedwithCTand

tion,theuof20reformationsin5%stepsof

theR-Rintervalenableddynamicaorticvalveimagingthroughoutthe

cardiaccycleandallowedacorrectestimationofcuspmotionrestriction,

whichreprentsthemajorpathophysiologiccontributortoaortic

stenosis(32).

ClassificationofAorticStenosis

Determinationofverityofaorticstenosisiscrucial,andmany

laboratorytestsareavailable;however,exactclassificationremains

difficultbecauallmethodshavelimitationspeculiartothetechniques

(1,5,6,11–13,33,34).

Previously,directplanimetryoftheAVAbyusingmagneticresonance(MR)

imagingwasdemonstratedtobefeasible,andresultswiththattechnique

andresultswithechocardiographyandventriculographywithacatheter

(7,8)ultsofourstudyaresimilarto

thoreportedwithMRimaginganddemonstratethatthereisasignificant

correlationbetweenplanimetricAVAmeasurementswithmulti–detector

rmore,the

associationbetweenplanimetrywithCTandtransvalvularpressure

gradientswasmoderateandindicatedareductionoftheAVAwith

increasingtransvalvularpressuregradients.

Whenweassdtheplanimetricallymeasuredorificearea,apotential

flawmighthaveoccurredinthatwithpoorleftventricularsystolic

functionandlowstrokevolume,thepressurenecessarytoopenthecusps

tothefullextentmaynothavebeengeneratedand,hence,mayhaveled

toanunderestimationoftheAVA(7).Ontheotherhand,rearchersin

astudy(35)withTEEsimultaneouslycomparedtheplanimetricmeasurement

oftheAVAwiththecalculatedAVAinpatientswithaorticstenosisand

demonstratedthatchangesoftransvalvularbloodflowdidnotresultin

significantalterationsofplanimetricAVAmeasurements.

AnotherlimitationofplanimetricAVAmeasurementscouldarifromthe

factthatthecontinuityequationisudtodeterminetheeffectivearea,

whereasplanimetryisudtomeasuretheanatomicarea;thelatteris

suppodtobelargerthantheformer(12).Thiscouldexplaintheslight

overestimationinregardtoAVAmeasurementswithCTandTEEcomparedwith

measurementswithTTE,asalsohasbeenobrvedinourstudy;however,

thedifferenceswerenotsignificant.

AorticValveCalcificationandStenosis

Recently,investigatorsinalargecomprehensivestudy(19)examinedthe

hemodynamiccorrelates,thediagnosticvalue,andtheoutcome

implicationsofquantitativeaorticvalvecalcificationmeasurementsin

100patientswithaorticstenosisandfoundthiscorrelationtobe

nvestigatorsconcludedthatthegradeofaorticvalve

calcificationandthatofstenosisprovidecomplementaryinformation.

Moreover,thevalvecalcificationscorewasanindependentpredictorof

survivaland,thus,providedimportantoutcomeinformation(19).This

findingsupportstheideathatvalvecalcificationisassociatedwitha

50%increaintheriskofdeathfromcardiovasculardia,evenin

theabnceofleftventricularoutflowtractobstruction(36).Oneof

theimplicationsofourinvestigationforapplicationinfurtherimaging

studiesinpatientswithaorticstenosisisthattheextentofaorticvalve

calcificationshouldnotbetakenasadirectmarkeroftheverityof

aorticstenosis,ashasbeenpreviouslysuggested(15–18),butthat

aorticvalvecalcificationshouldbeparatelyquantifiedinaddition

toverityofaorticstenosis.