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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
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States.
88
Etiology
TheexactetiologyofPPCMremainsunclear.Thereisevidencetosupportviral,nutritional,and
autoimmunecontributors.Animalmodelandepidemiologicdatasuggestthatvasculardysfunctionand
toxicityincitedbytheperipartumhormonalenvironmentplaysacentralroleinPPCM.
89-91
RiskFactors
RiskfactorsthatpredisposeawomantoPPCMincludeadvancedmaternalage,multiparity,multiple
pregnancies,preeclampsia,andgestationalhypertension.ThereisahigherriskinAfrican-American
women,butthismaybeconfoundedbythehigherprevalenceofhypertensioninthispopulation.
DIAGNOSIS
ClinicalPresentation
Women with PPCM typically present with NYHA III and IV HF, although mild cases and sudden
cardiacarrestalsooccur.
Becausedyspneaonexertionandlowerextremityedemaarecommoninlatepregnancy,PPCMmaybe
difficult to recognize. Cough, orthopnea, and paroxysmal nocturnal dyspnea are warning signs that
PPCM may be present,as is the presence of a displaced apical impulse anda new MRmurmur on
examination.
DiagnosticTesting
ELECTROCARDIOGRAPHY
OnECG,LVhypertrophyisoftenpresent,asareST-T–waveabnormalities.
IMAGING
DiagnosisrequiresanechocardiogramwithanewlydepressedEFand/orLVdilatation.
TREATMENT
Medications
TherapyinthepostpartumpatientmirrorsGDMTforHFrEF.Mostagentsaresafeinlactation.Datafor
sacubitril/valsartanandivabradinearelacking.
During pregnancy, ACE/ARB/ARNI, MRA, and ivabradine should be avoided. β-Blockers, loop
diuretics,hydralazine/nitrates,anddigoxinaresafe.
Inpatientswiththromboembolism,lowmolecularweightheparinis required, followedbywarfarin
afterdelivery.
Outcome/Prognosis
TheprognosisinPPCMisbetterthanthatseeninotherformsofnonischemiccardiomyopathy.
The extent of ventricular recovery at 6 months after delivery can predict overall recovery, although
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continuedimprovementhasbeenseenupto2–3yearsafterdiagnosis.
SubsequentpregnanciesinpatientswithPPCMmaybeassociatedwithsignificantdeteriorationinLV
function andcanevenresultindeath,particularlyinwomenwhodo notrecovernormal LV function
after the first insult. Women who do not recover LV function should be encouraged to consider
foregoingfuturepregnancy.
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6
PericardialandValvularHeartDisease
PhillipM.King,NishathQuader
PericardialDisease
AcutePericarditis
Etiology
Idiopathic,neoplastic(chemotherapyandradiation),autoimmune,viral,tuberculosis,bacterial
(nontuberculous),uremia,post–cardiacsurgery,trauma,post–myocardialinfarction,drugs,dissecting
aorticaneurysm,hypothyroidism.
Pathophysiology
Thepericardiumis a fibroussacsurroundingtheheartconsistingoftwolayers: a thinviscerallayer
attachedtothemyocardiumandathickerparietallayer.
The pericardial space is normally filled with15–50 mL offluid, and thetwo layers slide smoothly
againsteachother,allowingfornormalexpansionandcontractionoftheheart.
Pericarditisoccurswhentheselayersareinflamed.
DIAGNOSIS
History
Theclinicalpresentationofacutepericarditiscanvarydependingontheunderlyingetiology.
Chest pain: typically sudden onset, anterior chest, sharp and pleuritic; improved by sitting up and
leaningforward,madeworsebyinspirationandlyingflat,radiationtoback,neckandshoulders,pain
alongthetrapeziusridge.
PhysicalExamination
Pericardialfrictionrub:highlyspecificforacutepericarditis.Describedasa“scratchy,grating,or
squeakingsound,”heardbestwiththediaphragmofthestethoscope.
DiagnosticTesting
Electrocardiogram (ECG): diffuse ST-segment elevation(usuallyinmore thanonecoronary artery
distribution)andPRdepression.
Transthoracicechocardiogram(TTE):mayobserveanassociatedpericardialeffusion.
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Othertests:completebloodcount,C-reactiveprotein,erythrocytesedimentationrate,bloodcultures(if
suspectinfection),thyroidfunction,cytology(ifsuspectingneoplasm).
TREATMENT
Treattheunderlyingcausewheneverpossible.
NSAIDs:ibuprofen,aspirin,ketorolac.
Colchicine: when added to conventional anti-inflammatory therapy, significantly reduces symptoms,
recurrencerates,andhospitalizations(COPEtrial).
1
Glucocorticoids: reserved for cases refractory to standard therapy or in the setting of uremia,
connectivetissuedisease,orimmune-mediatedpericarditis.Increasesriskofrecurrence.
ConstrictivePericarditis
Constrictivepericarditisisoftendifficulttodistinguishfromrestrictivecardiomyopathies.Multiple
imagingmodalities,invasivehemodynamictests,history,andphysicalexaminationareoftenneededto
confirmthediagnosis.
Etiology
Idiopathic,viralpericarditis(chronicorrecurrent),postcardiotomy,chestirradiation,autoimmune
connectivetissuedisorders,end-stagerenaldisease,uremia,malignancy(e.g.,breast,lung,lymphoma),
andtuberculosis(morecommoninendemiccountries).
Pathophysiology
Inthesettingofchronicinflammation,thepericardiallayersbecomethickened,scarred,andcalcified.
The pericardial space is obliterated, and the pericardium becomes noncompliant. This impairs
ventricularfillingandleadstoanequalizationofpressuresinallfourchambersandsubsequentheart
failuresymptoms.
DIAGNOSIS
History
Theclinicalpresentationofconstrictivepericarditisisinsidious,withgradualdevelopmentoffatigue,
exerciseintolerance,andvenouscongestion.
PhysicalExamination
Features of right-sided heartfailure: lower extremity edema,hepatomegaly,ascites, elevatedjugular
venouspressure(JVP).
Othercharacteristicsigns
Kussmaulsign:paradoxicalincreaseinJVPwithinspirationorlackofappropriatedecreaseinJVP
withinspiration.
Pericardialknock:early,loud,high-pitchedS3.
DiagnosticTesting
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TTE
First-linediagnostictest.
Ventricularsystolicfunctioncanbedeceptively“normal.”
Featuressuggestiveofconstrictivepericarditisincludethefollowing:
Increasedpericardialthickness/tetheringofthepericardiumtothemyocardium.
Dilated,incompressibleinferiorvenacava(IVC).
Septalbounce(exaggeratedseptalmotion).
Inspiratoryvariationinmitralflowvelocitycurves.
Expiratorydiastolicflowreversalinhepaticveins.
Preserved(orincreased)tissueDopplervelocitiesofthemitralannulus.
Bluntedsuperiorvenacavaflow.
Cardiaccatheterization:allowsforsimultaneousmeasurementofrightventricularandleftventricular
pressures.
CardiacCTandMRI
Provideexcellentvisualizationofpericardialanatomy(thicknessandcalcification).
AnMRIandgatedCTcanshowevidenceofventricularinterdependence(septalbounce).
Canprovideotheranatomicinformationthatmaybehelpfulinmakingthediagnosisofconstriction
(i.e.,engorgementofIVCandhepaticveins)anditsetiology(i.e.,lymphnodes,tumors).
TREATMENT
Limitedroleformedicaltherapy:diuretics,low-sodiumdiet.
Patients with constriction often have a resting sinus tachycardia. Because of limited stroke volume
(SV),theyaremoredependentonheartrateforadequatecardiacoutput(CO).Avoideffortstoslow
downtheheartrate.
Surgicalpericardiectomy istheonly definitivetreatment forconstrictive pericarditis. Operative
mortalityis5%–15%;moreadvancedheartfailuresymptomsconferhigheroperativerisk.
CardiacTamponade
Cardiactamponadeisaclinicaldiagnosisandisconsideredamedicalemergency.Imagingisusedto
confirmthepresenceofapericardialeffusion;however,itshouldnotbesolelyreliedontomakethe
diagnosisoftamponade.
Etiology
Proceduralcomplications,infection,neoplasms,oridiopathicpericarditis,postcardiotomy,autoimmune
connectivetissuedisorders,uremia,trauma,radiation,myocardialinfarction(subacute),drugs
(hydralazine,procainamide,isoniazid,phenytoin,minoxidil),hypothyroidism
Pathophysiology
Fluidaccumulationinthepericardial space increasespericardial pressure.Thepressure dependson
theamountoffluid,therateofaccumulation,andthecomplianceofthepericardium.
Tamponadedevelops when thepressureinthe pericardial space is sufficiently high tointerfere with
adequatecardiacfilling,resultinginadecreaseinCO.
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DIAGNOSIS
History
ThediagnosisofcardiactamponadeshouldbesuspectedinpatientswithelevatedJVP,hypotension,
anddistantheartsounds(Beck’striad).
Symptomscanincludedyspnea,fatigue,anxiety,presyncope,chestdiscomfort,abdominalfullness,and
lethargy.
PhysicalExamination
Pulsusparadoxus refers toanabnormallylarge decrease in systolic blood pressure, SV, and pulse
waveamplitudewithinspiration.
Anormalfallinpressureislessthan10mmHg.Adecreaseinsystolicpressure>10mmHgisone
ofthephysicalexaminationfindingsintamponade.
Patientsarealsofrequentlytachycardicandhypotensive.
DiagnosticTesting
Remember:Cardiactamponadeisaclinicaldiagnosisthatcanbemadebasedonhistory,physical
examination,andvitalsigns(bloodpressure,pulsusparadoxus)alone.
ECG: low voltage (more likely with larger pericardial effusions), sinus tachycardia, electrical
alternans(specificbutnotsensitive).
TTE
First-linediagnostictesttoevaluatethehemodynamicsignificanceofpericardialeffusion.
Featuressuggestiveofahemodynamicallysignificantpericardialeffusion:
Dilated,incompressibleIVC.
Significant respiratory variation of tricuspid and mitral inflow velocities (>25% mitral, >40%
tricuspid).
Earlydiastoliccollapseoftherightventricleandsystoliccollapseoftherightatrium.
TREATMENT
Limited role for medical therapyto treat cardiac tamponade. Goal is to maintain adequate filling
pressureswithIVfluids.Avoiddiuretics,nitrates,andanyotherpreload-reducingmedications.Avoid
effortstoslow downsinustachycardia: itcompensates for a reduced SVtotrytomaintainadequate
CO.
Percutaneous pericardiocentesis with echocardiographic guidance can be a relatively safe and
effectivewaytodrainthepericardialfluid;theapproachshouldbeguidedbylocationofthefluidand
isusuallyeasiestwhentheeffusionisinanteriorlocation.
Creationofapericardialwindowispreferredforrecurringeffusions,loculatedeffusions,orthosenot
safelyaccessiblepercutaneously.
ValvularHeartDisease
The2020AmericanHeartAssociation/AmericanCollegeofCardiology(AHA/ACC)Guidelines
describedifferentstagesintheprogressionofvalvularheartdisease(VHD).
2
StageA(atrisk):patientswithriskfactorsfordevelopmentofVHD.
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