Andersons pediatric cardiology 231

Dexamethasone CardiacNLE

β-Agonists

CHB<50
beats/min

Immunoglobulin EFE;
incompleteAV
block

8mg/day
Notmeasured
for2
weeks,then
4mg/dayto
30weeks
and2
mg/dayto
birth
Afterbirth:
taper
motheroff
steroids
Newborn
(ifcarditis
orEFE),
prednisone
2
mg/kg/day
for2weeks

followedby
1
mg/kg/day
for4weeks
IVIG1
doseat
birth
Salbutamol Notmeasured
30–40
mg/dayin
3–4doses
Terbutaline:
10–30
mg/dayin
4–6doses
1g/kgIVq Notmeasured
2–3wk
(maximal
dose:70
g/dose)
Neonatal:
singledose
of1g/kg
IVand
prednisone
for6–8
weeks

0.3

nausea,vomiting,loss
oftaste,skinrash,
itching,drowsiness,
dizziness,headache
Adrenalgland
suppression,weight
gain,fluidretention,
hypertension,mood
changes,insomnia,
irritability,psychosis,
striae,diabetes,
impairedwound
healing,increased
susceptibilityto
infections

hypothyroidism
andgoiter

Oligohydramnios,
growth
restriction,
impairedwound
healing

0.5

Palpitations,tremor,
Neonatal
sweating,dyspnea,

hypoglycemia
hyperglycemia,chest
pain,nausea,
nervousness,dizziness,
arrhythmias

Variable

Headache,chestpain,
fever,chills,nausea,
malaise,anaphylaxis,
asepticmeningitis

Notreported

AF,Atrialflutter;AV,atrioventricular;CHB,completeheartblock;CHF,congestiveheartfailure;
EFE,endocardialfibroelastosis;F/Mratio,ratiooffetaltomaternalserumconcentrations;IV,
intravenous;IVIG,intravenousimmunoglobulin;LD,loadingdose;MD,maintenancedose;NLE,
neonatallupuserythematosus;SVT,supraventriculartachycardia;VT,ventriculartachycardia.


Digoxin.
Digoxin'sactionsincludeparasympatheticslowingofthesinusnode,
prolongationofAVnodalrefractoriness,andenhancedmyocardialcontractility.
MaternaldigoxinintakeleadstocharacteristicST-andT-segmentchangesonthe
ECG.Intheabsenceofhydrops,digoxiniswellabsorbedandtransferredtothe
fetus,reachingfetalserumconcentrationsthatareclosetothoseinmaternal
serumwithin3to5days.Fetalmyocardialdigoxinlevelsareoftenhigherthan
serumconcentrationsbecauseofenhanceduptakeofdrugbycardiactissue.
Therearenumerousknowndruginteractions,includingthosewithamiodarone

andflecainide,bothofwhichincreasethelevelofdigoxin.Noseriousdigoxinrelatedadverseeventshavebeenreportedinhealthywomen,butnausea,
anorexia,headache,visualdisturbances,anddizzinessareamongthemore
commonpatientcomplaints.5Digoxiniscontraindicatedinanymotherwith
ventricularpreexcitation(Wolff-Parkinson-Whitesyndrome),hypertrophic
cardiomyopathy,orhigh-degreeAVblock.
Flecainide.
FlecainideinhibitsslowNa+channels(classI)andβ-receptors(classII),which
prolongstheconductionandrefractorinessofallcardiactissues,includingthe
AVnodeandaccessorypathways.TheNa+channel–blockingeffectisuse
dependent,whichmeansthattheeffectincreasesastheheartrateincreases.
FlecainideprolongsthedurationofPR,QRS,andQTintervals.Theagentis
wellabsorbedandtransferredtothefetustoreachtherapeuticlevelswithin3
days.37Tominimizetheriskofproarrhythmia,theavoidanceofexcessiveQRS
prolongationisrecommendedaswellaskeepingthematernalflecainideserum
concentrations,ifmeasured,below1µg/mL.Therearenumerousinteractions
withotheragents,includingamiodarone,whichisalsometabolizedby
cytochromep450.Flecainideincreasesserumdigoxinlevelsbyapproximately
20%.Maternalcomplaintsincludeblurredvision,nausea,constipation,
dizziness,andheadache.Seriousmaternaleventshavenotbeenreported,but
thereisonecaseofunexplaineddemiseinuteromorethan2decadesagoofa
nonhydropicfetus.17Flecainideisnottobeusedinmotherswithcongestive
heartfailure,ventriculararrhythmias,ormajorCHD.38
Sotalol.
SotalolisbothaK+channelblocker(classIII)andaβ-blocker(classII),withβ-


blockadeasthemaineffectatdoseslessthan160mg/day.Thecombinedeffects
prolongthedurationofactionpotentialsandtissuerefractorinessthroughoutthe
heartanddecreasetheheartrate.39,40SotalolprolongsthematernalPRandQT
durationbutdoesnotaffectQRSintervals.Theagentiswellabsorbed,reaching

peakplasmaconcentrationswithin2to4hoursoforaladministration,andis
welltransferredacrosstheplacentatoreachafetalsteadystatesimilartothe
maternaldruglevel.22Sotalolisusuallywelltoleratedbymotherandfetus.
Symptomsrelatedtoβ-blockademayincludearterialhypotension,bradycardia,
worseningofasthmaorobstructivelungdisease,fatigue,depression,and
insomnia.Thereisonereportofanunexplainedfetaldeathintheabsenceof
fetalhydrops.21
Amiodarone.
AmiodaroneisapregnancyclassDagent,whichmeansthatthereisdefinite
evidenceoffetalriskwithitsuse.Thisagentthereforeshouldnotbeusedin
non–life-threateningsituationsorifsaferalternativesareavailable.Theduration
oftherapywithamiodaroneshouldalsobeminimized,withdiscontinuationonce
thearrhythmiaiscontrolledandhydropshasresolved.Thecompoundhas
multipleactions,includingblockageofK+channels(classIII),Na+channels
(classI),Ca2+channels(classIV),andβ-receptors(classII).Electrophysiologic
effectsincludeprolongationoftherefractorinessofcardiactissuesand,atfast
heartrates,slowingofconductionthroughtheHis-Purkinjesystemand
ventricularmyocardium.Amiodaronehasnonegativeeffectoncardiac
contractility.Thedrughasunusualpharmacokinetics,withabsorptionofthe
druggivenorallyrangingfromone-totwo-thirdsandplasmapeak
concentrationsreachedwithin3to7hoursofingestion.Amiodaroneis
metabolizedinthelivertodesethylamiodarone,whichalsohasantiarrhythmic
properties.Botharelipophilicandpreferentiallyaccumulateinfat,liver,lung,
skin,andmyocardium.Drugexcretionisslowandoccursviasheddingof
epithelialcellsoftheskinandgastrointestinaltract.Consequently,amiodarone's
effectsmaypersistforweeksfollowingcessationofthedrug.Amiodaroneand
desethylamiodronecrosstheplacentaonlyincompletely,whichexplainsthe
needforhighamiodaronedosestotreatfetalSVA.41Interferencewiththe
pharmacokineticsofotherdrugsiscommon,includingwithdigoxinand
flecainide.Amiodaronehasnumerouspossiblesideeffectsthataretypically

reversiblewithdosereductionorcessationoftreatment.Thyroiddysfunction