Andersons pediatric cardiology 230
Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (87.15 KB, 3 trang )
ThreemanagementoptionscanbeconsiderediffetalSVAisdetected.Thefirst
isnottoattempttreatment.Thesecondoptionistoinstituteintrauterine
antiarrhythmictherapy,andthethirdistodeliverthefetusandoptforneonatal
care.Thedecisionofcareshouldbebasedonthegestationalageatpresentation;
arrhythmiacharacteristicsincludingthemechanism,rate,anddurationofthe
tachycardia;presenceanddegreeoffetalcompromise;maternalhealth;andthe
possiblerisksandbenefitsofthefetaltherapyversusthoseofanearlierdelivery
bycesareansection.
AVRTandAFcomplicatedbyfetalhydropsisassociatedwithaperinatal
mortalityof20%orhigher,evenwithactivetreatment.5,10Intheabsenceof
hydrops,thisriskrangesfrom0%to4%.3,5,10Antiarrhythmicdrugsexhibita
varietyofcardiacactionsthatcanbeusedeithertoterminateaSVAand,once
achieved,tomaintainanormalrhythmortoslowthetachycardiatoamore
normalrateiftheSVApersists.Oncethetachycardiaiscontrolled,fetalhydrops
typicallyresolveswithinafewdaystoseveralweeks.
Asageneralrule,thelikelihoodoffetalheartfailureincreasesif
AVRT―ratherthanAF,AET,orPJRT―isthearrhythmiamechanismandthe
tachycardiaisfast,incessant,anddetectedatayoungergestationalage.3,5Unless
thefetusisnearterm,therecentlypublishedAmericanHeartAssociation(AHA)
guidelines11recommendpharmacologictreatmenttoterminateorslowthe
tachycardiafor(1)incessantSVA(presentin>50%ofobservationtime)withor
withouthydropsandfor(2)intermittentSVA(in<50%oftime)inthepresence
ofcardiacdysfunctionorhydrops.Serialobservationwithoutpharmacologic
therapyisrecommendedforfetuseswithawell-toleratedintermittentSVAor
withanincessantSVTlessthan200beats/min,asfetalhydropswillonlyrarely
developundersuchcircumstances.Nonetheless,Simpsonetal.,reportingthe
outcomesofintermittentfetaltachyarrhythmiasovera12-yearperiodattheir
center,foundthatevenanintermittenttachycardiapatternmayhavedeleterious
hemodynamiceffectsonthefetus.12Of28fetuseswhohadanintermittentSVA,
14werehydropic,whichwasassociatedwithoneintrauterinedeath,two
neonataldeaths,andoneinfantdeath.Thearrhythmiarecurredpostnatallyin11
of23(48%)fetuses.Maternalantiarrhythmictherapymayalsobeindicatedfor
intermittentfetaltachyarrhythmias.AnotherreasontotreatSVAbeforebirthis
thatpermanentconversiontoanormalrhythmwillenableavaginaldeliveryby
allowingtheinterpretationofthefetalheartrateforsignsofdistressduring
labor.Withthisrationaleinmind,ourcenterisofferingtheoptionof
transplacentalantiarrhythmictreatmenttomostmotherswithafetalSVAunless
thetachycardiaisonlybriefand/ordetectednearterm.5Forfetuseswithbrief
SVA(<10%ofthetime),closemonitoringforsignsofprogressionisthe
preferredmanagementoption,astheSVAwilloftenresolvespontaneously.For
incessantfetalSVAthatisdetectedonlyatornearterm,deliveryusuallyby
cesareansectionwithpostnatalconversiontosinusrhythmistheusualchoice.
MostprenatallytreatednewbornswithAVRT,AET,orPJRTwillreceive
antiarrhythmicdrugtherapyduringthefirstyearoflife,whereasAFisexpected
nottorecurafterconversionatbirth.9
Pharmacotherapy
TransplacentalfetaltreatmentforSVAwasfirstattemptedwithdigoxin13–15and
procainamide,16respectively,almost40yearsago.Todaytreatmentis
predominantlyinitiatedeitherwithdigoxin,flecainide,orsotalol,5,6,9,10,17–32
whereascombinationsofantiarrhythmicagents5,33and/oramiodarone34,35are
mainlyreservedfortherapy-resistantand/orpoorlytoleratedtachycardia.Direct
fetaldrugtreatmentwithamiodarone,digoxin,orbothisusedtotreatlifethreateningconditions.19,36Becauseofthepotentialriskofhazardous
proarrhythmia,eachantiarrhythmictreatmentotherthandigoxinshould
probablybestartedinaninpatientsettingtoallowserialmonitoringofthe
maternalelectrocardiogram(ECG)aswellasthefetaleffects.Toexcludeunsafe
maternalconditions,suchaslong-QTsyndrome(LQTS)forclassIIIagentsor
ventricularpreexcitationfordigoxin,thepregnantmothershouldundergoa
detailedmedicalassessmentincludinga12-leadECG,testingofherserum
electrolytes,andperhapsanechocardiogramtoconfirmnormalcardiacfindings
priortotheadministrationofanymedication.Thyroidfunctionshouldbe
checkediffetalhyperthyroidismissuspectedoriftreatmentwithamiodaroneis
considered.Aclearunderstandingofthedrugdosages,pharmacokinetics,and
actionsisessentialifthetachycardiaistobetreatedefficientlyandsafely.The
riskofadversedrugreactionsmaybefurtherreducedbyrestrictingtreatment
wheneverpossibletoasingleagentandbyavoidingexcessivedosages,toxic
concentrations,orpotentiallyhazardouscombinationsifadditional
pharmacologictreatmentisrequired.
Table9.1listsclinicalusageinformationofthemainantiarrhythmicagentsto
treatfetalSVA;thesearediscussedinturn.
Table9.1
PrenatallyUsedCardiovascularDrugs:TreatmentIndications,Drug
Dosages,andPossibleAdverseEffects
MainFetal
Therapeutic
UsualDosages
F/MRatio
Indications
Concentrations
SVT,AF,CHF
LD:0.5mg
1–2.0
0.8–1
q12hover2
ng/mL
↓in
days
1.3–2.6
hydrops
MD:
nmol/L
0.375–0.75
mg/day
Fetal/Newborn
Risks
Notreported
Flecainide
SVT,AF,VT
200–400
mg/dayin2–3
doses
<1µg/mL
Proarrhythmia,
negativeinotropy
Sotalol
AF,SVT,VT
160–480
mg/dayin2–3
doses
Notmeasured
Amiodarone
SVT,VT
Lidocaine
VT
MaternalEffects,
Risks,andSymptoms
Dose-dependent
effectsandnarrow
therapeuticrange:
nausea,dizziness,
anorexia,disturbed
vision,fatigue,sinus
bradycardia,first
degreeblock
0.7–0.9
QRSprolongation,
proarrhythmia,
negativeinotropy,
blurredvision,nausea,
paresthesia,headache
0.7–2.9
Dose-dependent
effects:bradycardia,
fatigue,hypotension,
headache,nausea,
dizziness,
proarrhythmia
0.1–0.3
Dose-dependent
↓in
effects:QThydrops
prolongation,
bradycardia,
thrombocytopenia,
rash
Notexpectedwith
short-termuse:
lungfibrosis,
thyroid
dysfunction,
hepatitis;corneal
microdeposits,
neuropathy,
myopathy
0.5–0.7
Drowsiness,
numbness,minor
adverseneural
reactions
0.9–1.3
Bradycardia,AV
block,fatigue,
hypotension,
bronchospasm,cold
extremities
1.9
Agranulocytosis,
Growth
restriction,
bradycardia,
hypoglycemia,
respiratory
depression
Riskof
Drug
Digoxin
Propranolol
LD:1.6–
1–2.5µg/mL
2.4g/day
for2–7
days
MD:0.2–
0.4g/day
Direct:2.5–
5mg/kg
fetalweight
IVslowly
over10
min
LD:1–1.5
mg/kgIV
followedby
infusionof1–4
mg/min
Thyrotoxicosis 60–120mgin
2–3doses
1.5–5
µg/mL
toxic>9
µg/mL
Notmeasured
Propylthiouracil Thyrotoxicosis 50–200mg/day Notmeasured
Proarrhythmia,
bradycardia
Proarrhythmia,
bradycardia,
transientthyroid
dysfunction,
growth
restriction,
bradycardia
Centralnervous
system
depressionathigh
serumlevels
