19 Fetal Arrhythmia

16 Pages·2006·0.43 MB·English

19
Fetal Arrhythmia
Elizabeth V. Saarel and Carlen Gomez
Clinical auscultation of fetal heart began in Beat-to-beatorshort-termvariabilityre-
the late 1800s, and the first reports of fetal fer to changes in FHR (cycle length) be-
arrhythmia detection were published in the tween successive cardiac impulses. Periodic
1930s. The detection, diagnosis, and treat- changesinFHRorlong-termvariabilityrefer
ment of fetal arrhythmias have evolved con- to changes in FHR between successive time
siderablybeyondtheseearlyobservations. intervals(secondstominutes).Adecreasein
heart rate variability may be a sign of fetal
distress. Heart rate variability is also mod-
FETALELECTROPHYSIOLOGY ulated by the parasympathetic nervous sys-
tem,andcanbeinhibitedbyatropine.Short-
NormalSinusFetalHeartRate and long-term heart rate variability tends to
bereducedorexaggeratedinaparallelfash-
Thesinusnode(SN),formedbythesev- ion,andthereisnoclearevidencethatdistin-
enthweekofgestation,generatesthenormal guishingbetweenthetwoentitiesisclinically
fetal rhythm. Important normal characteris- helpful.
tics of fetal heart rate (FHR) include base- AbaselineFHRlessthan120bpmaris-
linerate,beat-to-beatvariability,andperiodic ingfromtheSNwithnormalconductionhas
changes (transient decelerations or acceler- been defined as sinus bradycardia. A base-
ations). Baseline rate is significantly higher lineFHRgreaterthan160bpmgeneratedand
early in gestation than at term. At a nor- propagatedinanormalmannerhasbeende-
mal gestation of 20 weeks, the FHR is close fined as sinus tachycardia. As in infants and
to 160 bpm; by the mid-second trimester, children,sinusarrhythmia,evidencedbyheart
baseline FHR ranges from 120 to 160 bpm; ratevariability,isnormalinthefetus.
and at normal term, it is near 120 bpm. The
gradual decline in baseline FHR is modu-
latedbyanincreaseinparasympathetictone OVERVIEW:FETAL
withresultantprogressivevagalinfluenceon ARRHYTHMIA
the SN. If atropine is administered (to the
mother),FHRrevertstothehigherbaselineof Considerationoffetalarrhythmiaisusu-
160bpm. ally triggered by auscultation of an irregular
241
242 FETALARRHYTHMIA
heartrate,bradycardia,ortachycardiaduring familyandthehealthcareteam,andimproves
a prenatal visit. Abnormal FHR occurs in medicaloutcomes.
0.2%–2%ofpregnancies,with10%ofthese
havingsignificantarrhythmia.Oncethepos-
sibility of arrhythmia is raised, careful as- TECHNIQUESFORDIAGNOSIS
sessmentofoverallmaternalandfetalhealth OFFETALARRHYTHMIA
shouldbeperformed.Ifthearrhythmiaissus-
tained at a markedly fast or slow rate, or Electrocardiography
if it is associated with structural congenital
heart disease, fetal well-being may be com- Several non-invasive techniques are
promised. Indeed, a less common presenta- availableforfetalarrhythmiaanalysis.Incon-
tion of fetal arrhythmia is hydrops fetalis— trasttopostnatalevaluation,electrocardiogra-
generalized edema that represents an end- phyisnotpracticablefordiagnosis.Although
stage fetal response to significant stress and fetalelectrocardiogramscanberecordedfrom
insults.Moreover,severalmaternalconditions electrodes placed on the maternal abdomen,
areassociatedwithfetalarrhythmia,making signal detection is not reliable due to a low
maternal assessment essential in all cases of signal-to-noise ratio. Fetal cardiac electrical
abnormalFHR. activity is low in amplitude, on the order of
Whenafetalarrhythmiaissuspected,a about10µV,1/10ththeamplitudeofmaternal
detailed prenatal echocardiogram should be cardiacelectricalactivity.Inaddition,mater-
obtained in an experienced pediatric prena- nalabdominalwallmusculatureaddslowam-
talechocardiographicunit.Althoughreferral plitude noise to the electrocardiogram, often
patterns vary by institution, abnormal FHR obscuringfetalmyocardialelectricalactivity.
prompts roughly 25% of prenatal cardiol-
ogy referrals. In addition to the evaluation Magnetocardiography
ofthefetalcardiacanatomyandfunctionby
echocardiogram during these visits, it is im- Amagnetocardiogramrecordsthemag-
portanttoobtainathoroughmaternalandfam- neticfieldgeneratedbycardiacelectricalac-
ilyhistory.Asmanyas50%offetuseswithar- tivity.Thistechniquehasbeenappliedtothe
rhythmia(particularlythosewithheartblock) fetus for the last decade. There have been
haveassociatedstructuralcardiacmalforma- multiplereportsfromseveralinstitutionsde-
tions. scribingmagnetocardiogramsthatdetailfetal
Optimal patient evaluation and treat- cardiac electrical activity, including P-wave
mentrequiresateammedicalapproach.The and QRS inscription, similar to a postna-
team should consist of obstetricians, peri- talelectrocardiogram.Magnetocardiographic
natologists, pediatric cardiologists with fetal equipment is complex and large, requires
echocardiographic expertise, social workers, shieldinganddedicatedspace,isveryexpen-
and nurses that work closely with pediatric sive, and is not yet commercially available;
electrophysiologists to care for affected fe- widespreaduseisnotavailable.Fetalmagne-
tuses. Other relevant ad hoc members may tocardiography would undoubtedly become
includeneonatologists,anesthesiologists,ge- morewidespreadiftechnicalrefinementsde-
neticists, and endocrinologists. If significant creasedcostandincreasedaccessibility.
structuralheartdiseaseisidentified,pediatric
cardiothoracic surgeons should be alerted Echocardiography
near term. A team approach streamlines pa-
tient care, allows more accurate prognos- Because of limited access to the elec-
tication, improves communication between trocardiographic forces of the fetal heart,
FETALARRHYTHMIA 243
FIGURE1.M-modeechocardiogramfromafetusinsinusrhythm.Upperimagedemonstratesbeampositionthrough
theatriumandventricle.Smallarrowsmarkatrialcontractions,andarrowheadsmarkventricularseptalmotion.Note
1:1ratioofatrialtoventricularcontractions.
echocardiography is the current method for diastoleasrepresentationofatrialandventric-
the diagnosis of fetal arrhythmias. Evalua- ular motion. An apical four-chamber image
tion for arrhythmia begins by examining the of the fetal heart is obtained, and the pulsed
timing and association of atrial and ventric- Doppler cursor is positioned with the gate
ular wall motion. This is best accomplished spanningthemitralinflowaswellastheaortic
through the use of M-mode and Doppler outflow(Figure2).
echocardiography. Doppler tissue color M-mode imaging
M-modeechocardiographydisplaysmo- mayaidinthediagnosisoffetalarrhythmias
tionofthecardiactissuewithrespecttotime. whenstandardM-modeandDopplerechocar-
An M-mode tracing of the fetal heart cham- diography are indeterminate. Gated pulsed
bers is obtained by placing the cursor line DopplermaybeusedtomeasurefetalPRin-
acrossboththeatrialandventricularwallssi- tervals. In addition, new techniques includ-
multaneously (Figure 1). The display shows ing tissue velocity imaging, with creation of
movement of both chamber walls with time, a “fetal kinetocardiogram,” as well as strain
reflectingatrialandventricularsystole. rate imaging, have recently been described.
Many factors influence the quality of Tissue velocity and strain rate imaging may
the M-mode tracing. First, alignment with significantly enhance current fetal echocar-
bothheartchamberscanbechallenging,and diographicdiagnosticcapabilities.
several different probe positions and angles In addition to determination of the
should be attempted to optimize the tracing. arrhythmia mechanism, echocardiographic
Second, a clearer tracing will be obtained evaluationofthefetusshouldincorporateas-
where chamber walls have the greatest ex- sessmentforanyhemodynamicandanatomic
cursion with contraction, such as the atrial abnormality. Both tachyarrhythmias and
appendage,orlateralventricularwall. bradyarrhythmiascancauseheartfailure,and
Dopplerechocardiographyutilizesspec- ultimately hydrops fetalis. Complete evalua-
tral blood flow patterns during systole and tionforfetalheartfailureincludesassessment
244 FETALARRHYTHMIA
FIGURE2.Dopplerechocardiogramfromfetusinsinusrhythm.Upperimagedemonstratesbeampositioninthe
ventricle.Note1:1relationshipofnormalmitralinflow(E-andA-wavesabovebaseline)andnormalaorticoutflow
(belowbaseline).
of heart size, ventricular systolic function, SPECIFICFETALARRHYTHMIAS
atrioventricular valve incompetence, venous
Doppler patterns (increased reversal with Extrasystole
atrialcontraction)includingumbilicalvenous
Doppler (Figure 3), and documentation of Extrasystoles account for 60% to 90%
the presence and size of pleural, pericardial, of fetal arrhythmia. Ectopic beats may arise
andabdominaleffusions.Alloftheseindices in the atria, junctional tissue, or ventri-
needtobereassessedforprogressionbyserial cle. Supraventricular ectopy (SVE) is most
echocardiographicstudiesalongwithongoing common. Ventricular ectopy (VE) com-
obstetricalevaluationoffetalwellbeing. prises fewer than 10% of fetal extrasystole.
FIGURE3.PulsedspectralDopplertracingfromtheumbilicalveininafetuswithhydropsfetalis.Upperpanel
demonstratesgatepositionintheumbilicalvein.Arrows(lowerpanel)indicatepulsationswithatrialsystole,consistent
withhighatrialpressure.
FETALARRHYTHMIA 245
Frequencyofectopicbeatsinthenormalfe- or quadrigeminy. Diagnosis can be made
tus has not been well established; however, withacombinationofDopplerandM-mode
therateofextrasystolesinhealthypremature echocardiography.WithM-mode,simultane-
infants is 20% to 30%, with a slightly lower ous atrial and ventricular recording is per-
frequencyinterminfants. formed,demonstratinganormalsequenceof
Ectopic beats present as an irregular A-V contractions and an early atrial beat.
FHR.Asinolderpatients,veryearlySVEre- The atrial beat after the premature contrac-
sults in blocked atrioventricular conduction, tion demonstrates an incomplete compen-
eithercompleteorpartial(intheformofbun- satorypause.
dle branch block with aberrant depolariza- Dopplersamplingatthejunctionofthe
tion).Hence,SVEcanpresentasbradycardia. mitralinflowandleftventricularoutflowtract
Themajorityoffetuseswithprematurebeats displays E- and A-waves (early, rapid ven-
arehealthy,andtheectopyresolvesovertime. tricular filling followed by atrial contraction
Although the vast majority of fetuses with active ventricular filling) and ventric-
withextrasystoleshaveastructurallynormal ular systole (with semilunar valve outflow).
heart, SVE and VE can be associated with SVE will cause early active ventricular fill-
anatomiccongenitalheartdisease,cardiactu- ing (A-wave), obscuring part of the early
mors, and fetal genetic abnormalities such ventricularfilling(E-wave)tracingwithsub-
as Trisomy 18. In addition, SVE precedes sequent early ventricular systole (Figure 4).
supraventricular tachycardia (SVT) in 15%. In cases of fully blocked SVE, no ventric-
Thus,allfetuseswithprematurebeatsshould ular systole will follow the premature atrial
bemonitoreduntildelivery,oruntilresolution contraction. The post-extrasystolic contrac-
oftheectopyhasbeensustained. tion will demonstrate a prolonged filling
(diastolic) time interval. An additional
Doppler finding is flow reversal in the IVC
SupraventricularEctopy
duringearlyatrialcontraction.
Prematureatrialandjunctionaldepolar- The fetal PR interval can be measured
izations occur most often as single beats, usingagatedpulsedDopplertechnique.Pre-
but can present with bigeminy, trigeminy, matureatrialcontractionsshoulddemonstrate
FIGURE4.DopplerechocardiogramfromafetuswithSVE.Thelargearrowmarkstheprematureatrialcontraction.
Thefirstsmallarrow(lowerpanel)marksthediminishedaorticoutflowvolumewiththeSVE,andthesecondsmall
arrowshowstheincreasedaorticoutflowvolumeduringthepost-extrasystoliccontraction.Notetheprolongeddiastolic
timeintervalfollowingtheSVE.
246 FETALARRHYTHMIA
FIGURE5.PulsedspectralDopplerthroughthemitralinflowandaorticoutflowinanormalfetus,demonstrating
mechanicalPRintervalmeasurement.E-andA-wavecomponentsofmitralinflowareabovethebaseline,whereas
theaorticoutflowsignalisbelowthebaseline.CalipersmeasurefromthebeginningoftheA-wave(lineA)tothe
beginningoftheaorticoutflowsignal(lineB).
anormal(Figure5)orprolongedPRinterval ultrasound demonstrates a characteristic AV
(ifslowconductionoccurs). valveinflowpatternwithdecreaseddiastolic
The prognosis is favorable for the ma- antegradeflow.Markedretrogradeflowinthe
jority of fetuses with SVE. In addition to IVCisseenduringatrialcontraction.
the conditions mentioned earlier, fetal SVE Inadditiontotheconditionsmentioned
can be associated with maternal drug use or previously,VEhasbeenassociatedwithfetal
hyperthyroidism.Forfetuseswithassociated myocarditis, cardiomyopathy, long QT syn-
maternal disease, structural congenital heart drome,andcompleteAVblockwithaslowes-
disease, tumors, or sustained tachyarrhyth- caperate.Prematureventricularcontractions
mias,theprognosiscorrelateswiththeasso- also occur in healthy fetuses, for whom the
ciatedcondition.Notreatmentisindicatedfor prognosisisexcellent.Prognosisisdependent
isolatedfetalSVE. ontheassociatedcondition.Notreatmentof
isolatedprematureventricularcontractionsis
indicated.
VentricularEctopy
M-modeechocardiographymaydemon- Tachyarrhythmias
strate subtle distortion of normal ventricular
contraction due to aberrant muscle depolar- Most cases of elevated FHR are due to
ization (Figure 6). Also, a complete atrial sinus tachycardia. SVT, atrial flutter, atrial
compensatory pause is seen after most pre- fibrillation,andventriculartachycardia(VT)
mature ventricular depolarizations. Doppler are less common. In one large single-center
FETALARRHYTHMIA 247
FIGURE6.M-moderecordingfroma36-weekfetuswithitsbacktowardthetransducerpresentinganinvertedviewof
theheart.Prematureaorticvalveopening(largearrow)canbeclearlyseentobefollowedbyatrialwallcontractionbut
withnovariationinP-Pinterval(A-waveinterval),givingacompensatorypause(smallarrow,allowingdiagnosisof
ventricularprematurebeat).LA=leftatrium;Ao=aorta;RVOT=rightventricularoutflowtract(5MHztransducer).
ReprintedfromClinicalCardiology1985;8:1–10withpermissionfromClinicalCardiologyPublishingCompany,Inc,
Mahwah,NJ07430USA.
retrospectivereport,SVTandatrialflutterto- gated-Dopplerultrasound,shouldbeconstant
getheraccountedfor12%offetalarrhythmia andofnormalduration.
diagnoses. Fetal sinus tachycardia is due to an un-
derlyingfetalormaternalabnormalitysuchas
SinusTachycardia drugexposure,hyperthyroidism,myocarditis,
infection, hypoxia, or other causes of fetal
Fetalsinusratesrarelyexceed210bpm, distress.Treatmentisdirectedattheprimary
whereasfetalSVTrarelyfallsbelow200bpm. causeofsinustachycardia.
In sinus tachycardia, fetal M-mode echocar-
diography shows synchronous atrioventric- SupraventricularTachycardia
ular contractions. Sinus arrhythmia with
varyingcyclelengthsmaybepresent.Certain Fetal supraventricular tachycardia
tachyarrhythmiasthattendtowardlongerand (SVT) can be sustained or intermittent.
more variable cycle lengths, such as persis- Typicalratesare240–250bpm,witharange
tentjunctionalreciprocatingtachycardiaand from 200 to 320 bpm. Detection is most
ectopicatrialtachycardia,aredifficulttodif- common after 15 weeks gestation, although
ferentiate from sinus tachycardia using cur- earlier presentation has been reported. Fetal
rentultrasounddiagnostictechniques. toleranceofSVTdependsonthedurationand
Insinustachycardia,Dopplertracingof rate of arrhythmia; intermittent and slower
atrioventricular valve inflow often demon- (≤260 bpm) rhythms are less malignant.
stratesamalgamationoftheE-andA-waves. Mechanisms of SVT in the fetus are similar
ThemechanicalPRinterval,asmeasuredby tothoseinneonates(Figure7).
248 FETALARRHYTHMIA
FIGURE7.M-modeechocardiogramfromafetuswithsupraventriculartachycardia.Arrowheadsindicateatrial
contractions,andlargearrowsindicateventricularcontractions.Notethe1:1relationshipofatrialandventricular
contractions.Thecalipersmeasure243msbetweensuccessiveventricularcontractions,indicatingaheartrateof
approximately250bpm.
Atrioventricularreentrytachycardia,uti- by gated-Doppler, the PR interval will be
lizing an accessory connection between the constantinreentrytachyarrhythmias.
atria and ventricles, is most common when Treatmentispredicatedontheeffectof
examined post partum. AV node reentry the tachyarrhythmia on fetal well being. If
tachycardia, ectopic atrial foci, persistent SVT is intermittent, slow, and late in preg-
junctional reciprocating tachycardias, and nancy,fetalhealthisusuallynotjeopardized.
junctional tachycardias are less common. Insuchpatients,prognosisisgenerallyexcel-
Althoughanabruptonsetandterminationof lent, and no treatment is indicated. If tachy-
the tachycardia, if observed during the fe- cardia is sustained at fast rates (>260 bpm),
tal echocardiogram, would support the di- prenatal demise may be as high as 25%. It
agnosis of a reentry tachycardia, it is not isthereforeimportanttofrequently(every3–
possible to distinguish with certainty be- 5 days) assess all fetal patients with SVT.
tweentheseentitiesusingcurrentultrasound Moreover,mothersshouldbeeducatedtolook
techniques. forsymptomsoffetaldistress.Bothobstetri-
Diagnosis of SVT is consistent with an ciansandcardiologistsshouldfollowpatients.
M-mode tracing through the atria and ven- Of note, patients with structural congenital
tricle showing sequential 1:1 contractions at heartdiseaseareatgreaterriskfortachycar-
retrogradetimeintervalsof80–120ms.Simi- diaassociatedcomplications.Twooftheearli-
larly,Dopplerultrasoundofventricularinflow estsignsoffetalcompromiseareexaggerated
and outflow demonstrates sequential atrial umbilicalvenousorinferiorvenacavaflowre-
and ventricular contractions. If measurable versal (greater than 30%) and cardiomegaly.
FETALARRHYTHMIA 249
Othersignsoffetaldistressincludedecreased setting of fetal distress. Maternal flecainide
ventricular systolic function, atrioventricu- by mouth in cases where premature delivery
lar valve regurgitation, and hydrops fetalis of the fetus is too high a risk may be help-
(pericardialeffusion,pleuraleffusion,ascites, ful.Cardioversionwithflecainideisgenerally
and/orskinedema).Ominoussignsofdistress achieved within 3 to 4 days. Sotalol appears
includedecreasedfetalmovementandabnor- to be effective for atrial flutter, but probably
malumbilicalarterypulsations. shouldbeavoidedforSVT.Successwiththe
Fetal treatment options include early combination of digoxin with amiodarone or
delivery, transplacental (maternal) pharma- the combination of digoxin with verapamil
cotherapy,ordirectfetalpharmacotherapy.In hasbeendescribed.
addition,thereisonereportoffetalSVTcon- Atrial flutter (intra-atrial reentry tachy-
versionusingtransabdominalumbilicalcord cardia)isresponsibleforapproximatelyone-
compression. Although not described in hu- third of non-sinus fetal tachyarrhythmias.
mans, there has been a single report of SVT Atrial rates vary from 400 to 550 bpm. As
conversion using transesophageal pacing in in postnatal patients, ventricular response is
fetal sheep. Labor induction is the treatment variable, but rates are greater than 200 bpm
ofchoicefortermandnear-termpregnancies inamajorityofuntreatedfetuses.Variations
with sustained fetal tachycardia or evidence inatrioventricularconductionfrequentlylead
offetalcompromise. toanirregularFHR.Whenconductioniscon-
Althoughcontroversyexists,itisgener- sistent,thereisgreaterelevationoftheFHR;
ally agreed upon that transplacental digoxin 2:1 atrioventricular block is most common.
shouldbethefirst-linetreatmentofchoicein Although atrial flutter is usually sustained,
pre-termpregnancieswithsustainedtachycar- paroxysmalcasesdooccur.
dia or fetal compromise (Table 1). Digoxin The diagnosis of prenatal atrial flutter
treatmentissafeandofteneffective.Thedrug is confirmed by characteristic echocardio-
can be administered to the mother in oral or graphic findings. M-mode tracings through
IVformatrelativelyhighmaternaldoses(up the atria and ventricle demonstrate regular,
to1mgqdbymouth)inordertoachievean fastatrialcontractionswithvariableatrioven-
adequateleveloffetaldrug.SVTcessationis tricularblock,andthuslessfrequentventric-
achieved in approximately three-quarters of ulardepolarizations (Figure8).Atrialrateis
cases with maternal oral therapy. If conver- calculated after measurement of the time in-
sion has not been achieved after two weeks terval between successive atrial contractions
of therapy, a second antiarrhythmic agent (themechanicalP-Pinterval).Similarly,ven-
may be added; flecainide, along with other tricular rate is calculated after measurement
drug choices are reasonable (Table1). Other of the time interval between successive ven-
medications with reported efficacy include tricularcontractions(themechanicalR-Rin-
procainamide, verapamil, quinidine, amio- terval). Using this information, the degree
darone,orsotalol.Therehasbeennodefinitive of atrioventricular block can be determined.
large,randomizedpublishedstudycomparing Doppler echocardiography of ventricular in-
fetalantiarrhythmicagents. floworoutflowcanalsobeusedtocalculate
In the case of significant fetal distress theventricularresponserate.
orrapid,sustainedSVT,whereprompttreat- Cardiac lesions reported in association
mentisessential,digoxincanbegivendirectly with fetal atrial flutter include atrial septal
tothefetusthroughumbilicalvein,intramus- defect, Ebstein’s malformation of the tricus-
cular,orintraperitonealadministration;how- pid valve, atrioventricular septal defect with
ever, the later two routes are unreliable due atrioventricularvalvarregurgitationandatri-
to unpredictable drug absorption. Umbilical oventricular block, right ventricular outflow
cordocentesiscarriesasignificantriskinthe tractobstructionwithtricuspidregurgitation,
250 FETALARRHYTHMIA
Maternal/FetalAdverseEffects TachycardiacommonlyrecursrequiringadditionalagentMaternalorfetalhypothyroidism(common);bradycardia(common);IUGR;prematuredelivery;hepatotoxicityMaternaloverdose;heartblock;arrhythmiainduction Dizziness;headache;paraesthesias;tremors;visualdisturbances;nausea;vomiting;flushing;possibleneonatalconjugatedhyperbilirubinemiaorneonatalprolongedQTHypotension;asystole;seizures;respiratoryarrest Atrialandventriculararrhythmias;bradycardia;hypotension;confusion;dizziness;nervousness;tremor;ataxia;numbnessoffingersortoes;weakness;blurredvision;tinnitus;nausea;hepatotoxicityHypotension;nausea;vomiting;blooddyscrasias;lupus-likesyndrome;rash;confusion;prolongedQT Idiosyncraticreaction(prolonged>.QRS002sec);prolongedQT;torsadesdepointes;nausea;vomiting;diarrhea;hypotension;tinnitus;confusion;blooddyscrasias;rash;heartblockMyocardialdepression;arrhythmiainduction;torsadesdepointesMyocardialdepression;bradycardia;heartblock;hepatotoxicity
VT No Yes No Yes Yes Yes Yes Yes 1Yes Yes
AFL No No 1Yes No No No Yes No 2Yes Yes
SVT Yes Yes 1Yes 2Yes No No Yes Yes No Yes
MaximumDosage 0.2mg/kg 800mgQDmaint. PO:0.25mgBIDmaint.IV:1.0mgQDmaint. Totaldailydosenottoexceed600mg;maternalbloodlevelnottoexceed1mg/L 3–5mg/kgwithinfirsthour Max1200mg/d;maternalbloodlevelnottoexceed2mg/L IV:6mg/minPO:500mgq3hrs;plasmalevels4–10mg/L PO:600mgq4–6hrsIV:0.5mg/kg/min<(infuse10mg/min) 320mgBID Maygivesecond10mgdoseafter30min.
a
ofFetalTachyarrhythmi StartingDosage 0.1mg/kg ×800–1200mgQD8–14dload;then200–400mgQDmaint. PO:0.25–1.5mgload,then0.125BIDmaint.IV:1–2mgload(mayrepeat),then0.5mgQDmaint.Startat100mgBID,advanceto200mgBID-TID 1mg/kgloadover2min,may×repeatin10–15min2(alternate20–50mg/kg/min)200mgPOq8hrs;therapeuticlevel0.5–2mg/L IV:100mgloadover2min.,then1–6mg/minPO:1gloadthen200–500mgq3–6hrsPO:Testdose200mg;800–1000mgload,then200mgq4–6hrsmaint.IV:0.3mg/kg/min<(infuse10mg/min) 80mgBID 5–10mgover3–5min.(alternate0.005mg/kg/min) present
DrugsforTreatment RouteofAdministration FetalIV MaternalPO(FetalIV;FetalIM;FetalIP) MaternalPO;MaternalIV(FetalIV;FetalIM;FetalIP) MaternalPO MaternalIV MaternalPO MaternalIV;MaternalPO MaternalPO(sulfateform);MaternalIV(gluconateform) MaternalPO MaternalIV first-lineagentsecond-lineagentmecautionifhydropsfetalisis
TABLE1. Drug Adenosine Amiodarone Digoxin Flecainide Lidocaine Mexiletine Procainamide Quinidine ∗Sotalol Verapamil 1Recommended2Recommended∗Usewithextre