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Fetal arrhythmias

Fetal arrhythmias
Jami C Levine, MD
Mark E Alexander, MD
Section Editors:
Deborah Levine, MD
Louise Wilkins-Haug, MD, PhD
John K Triedman, MD
Deputy Editor:
Vanessa A Barss, MD, FACOG
Literature review current through: Dec 2022. | This topic last updated: May 11, 2022.

INTRODUCTION — The conduction system of the fetal heart is functionally mature by 16 weeks of gestation and normally produces a regular rhythm and rate between 110 and 160 beats per minute (bpm) for the remainder of the pregnancy [1]. Fetal arrhythmias are defined by deviations from these parameters. They complicate 1 to 2 percent of pregnancies and have the potential to compromise fetal health. A summary of the types and distribution of fetal arrhythmias in one large series is shown in the table (table 1). Accurate diagnosis of the mechanism and frequency is crucial to assess prognosis and need for medical intervention.

Issues related to fetal arrhythmias will be reviewed here. Diagnosis and management of arrhythmias in neonates and children are discussed separately. (See "Irregular heart rhythm (arrhythmias) in children" and "Identifying newborns with critical congenital heart disease", section on 'Physical examination'.)

SCREENING — Screening for fetal arrhythmias is already a routine component of prenatal care since determination of the fetal heart rate (FHR) is performed at each prenatal visit, and at least one fetal ultrasound examination is performed during pregnancy. All standard second- and third-trimester fetal ultrasound examinations should include a view of the four cardiac chambers and both ventricular outflow tracts and documentation of the FHR and rhythm (typically by M-mode). (See "Overview of ultrasound examination in obstetrics and gynecology", section on 'Obstetric sonography'.)

A simplified summary of fetal arrhythmias by rate, pattern, and echocardiography findings is shown in the table (table 2). Not all changes in FHR and rhythm noted during routine examinations are pathologic, but the distinction can be difficult without the assistance of specialized cardiac imaging. If obstetric examination (eg, auscultation of the FHR, cardiotocography, standard ultrasound examination) raises concern for a pathologic arrhythmia, then referral to a fetal cardiologist or other expert in fetal cardiac disorders is recommended for a comprehensive evaluation of cardiac structure and function. Although most fetal arrhythmias are isolated findings, some are associated with structural or functional heart disease. The frequency of structural or functional heart disease is approximately 10 percent in fetuses with tachycardia and approximately 50 percent in fetuses with bradycardia. (See "Congenital heart disease: Prenatal screening, diagnosis, and management".)

Selected pregnancies are at high risk for fetal arrhythmias and should undergo serial assessment of the FHR and rhythm by echocardiography, regardless of the findings on routine obstetric examination (auscultation, standard ultrasound examination). These include:

Pregnant patients with autoantibodies directed against Ro/SSA and La/SSB autoantigens, as these maternal antibodies can cross the placenta and lead to progressive abnormalities of fetal atrioventricular conduction, including complete heart block. These fetuses should be evaluated regularly during the second trimester for evidence of an evolving arrhythmia. Practices vary regionally, but most centers suggest assessment of FHR and mechanical PR interval by pulsed-wave (spectral) Doppler every two weeks between 18 and 26 weeks of gestation. Some clinicians monitor these fetuses weekly and until 28 weeks. Pregnant patients with higher levels of antibody may be at higher risk of an affected fetus. (See "Neonatal lupus: Epidemiology, pathogenesis, clinical manifestations, and diagnosis", section on 'Fetal surveillance for heart block'.)

Pregnant patients who have had a previous pregnancy with congenital heart block, regardless of their immune status. Evaluation is the same as described in the above bullet.

Pregnant patients carrying a fetus with congenital heart disease that includes L-looped ventricles. These fetuses can develop heart block at any time antepartum or intrapartum. Weekly evaluation of the heart rate by Doppler is advised. If Doppler suggests an irregular and/or slow heart rate, prompt referral to a fetal cardiology team is recommended.

MODALITIES FOR DIAGNOSTIC EVALUATION — When screening demonstrates an abnormal fetal heart rate (FHR) or worrisome rhythm and the patient is referred for further evaluation, the fetal cardiologist will choose the specific modality or combination of modalities needed. Options are described below.

Two-dimensional ultrasound – Two-dimensional ultrasound is used to diagnose the specific arrhythmia, evaluate cardiac anatomy and function, and look for signs of hydrops fetalis (defined as a collection of fluid in two body cavities [pleural, pericardial, ascites] or one body cavity plus anasarca; placental thickening and/or polyhydramnios may be present but are not part of the diagnostic criteria). Hydrops is an ominous sign that the arrhythmia has impaired the cardiovascular system by inhibiting ventricular filling and/or cardiac output.

(See "Congenital heart disease: Prenatal screening, diagnosis, and management".)

(See "Overview of ultrasound examination in obstetrics and gynecology".)

(See "Nonimmune hydrops fetalis", section on 'Cardiovascular abnormalities'.)

M-mode – M-mode ultrasonography is used to detect atrial and ventricular wall motion and/or the motion of the semilunar and atrioventricular valves (waveform 1). It has excellent temporal resolution, so it can be used to determine the relative timing of cardiac events, thus helping to characterize the arrhythmia.

Pulsed-wave Doppler – Pulsed-wave Doppler is used to evaluate the relationship of atrial contractions to ventricular contractions. This is done by placing the Doppler cursor over the left ventricular outflow tract so that the cursor is parallel to the direction of aortic flow. Once the cursor is lined up, the Doppler gate is widened so it can sample both left ventricular inflow and outflow at the same time. With this tracing, the sonologist can measure the PR interval and evaluate the timing of the atrial and ventricular contractions. The same technique can be used to gather similar timing data by evaluating the superior vena cava and ascending aortic flow simultaneously or the pulmonary artery and pulmonary venous flow simultaneously. (See "Echocardiography essentials: Physics and instrumentation".)

Pulsed-wave Doppler of the umbilical vein and artery flow can also be a diagnostic clue to an arrhythmia [2]. The waveform in the umbilical vessels may be abnormal in a fetus with an arrhythmia because of changes in intracardiac pressures or because of atrioventricular valve regurgitation caused by atrial-ventricular dyssynchrony and/or ventricular failure.

Cardiotocography – Standard electronic, continuous FHR monitoring is used to assess the FHR over long periods of time. However, aliasing at 240 bpm limits its ability to track the most rapid tachycardias and very transient arrhythmias (ie, the internal logic of the monitor may display a rate that is half that of the true rate). Despite these limitations, standard FHR monitoring is useful for sustained monitoring of fetuses with slower forms of supraventricular tachycardia (SVT; eg, atrial flutter) and to determine the proportion of time the fetus is in a normal versus abnormal rhythm. The primary benefit of this monitoring is to confirm or exclude the presence of periods of a normal heart rate pattern and to demonstrate abrupt shifts in rate.

Bedside Doppler – At rates faster than 200 to 220 bpm, the precise FHR cannot be clearly determined with this technique, but a semiquantitative judgment of "tachycardia" versus "normal" can be made and provides an inexpensive, readily accessible tool to inform additional testing. A plan of hourly/every other hour FHR determinations when the mother is awake and every three to four hours during the night can provide substantial information during a therapeutic trial.

Tissue Doppler echocardiography – Tissue Doppler echocardiography (TDE) permits an assessment of myocardial motion using Doppler ultrasound imaging, often with color coding. The technique uses frequency shifts of ultrasound waves to calculate myocardial velocity, similar to routine Doppler ultrasound assessment of blood flow, but its technological features focus on lower velocity frequency shifts. TDE makes it easier to identify the origin of the arrhythmia and can be quite helpful when other modalities are not diagnostic [3]. It is not always easy to analyze the data without specialized software; therefore, it is not widely available.

Fetal magnetocardiography – Magnetocardiography shifts the electrical signals into an evoked magnetic signal that can be processed to create a beat-to-beat magnetocardiogram that looks like a traditional electrocardiogram. Continuous recordings can be performed for relatively sustained periods and have permitted elegant demonstration of arrhythmia onset/offset and more direct observation of mechanisms. The equipment is not widely available and requires careful shielding and skilled technical support, so the technology remains investigational [4,5].

Fetal electrocardiography – Obtaining the fetal electrocardiogram signal is complicated by fetal motion, low voltage, background noise, and the inclusion of the maternal electrocardiogram signal during the examination [6,7]. Vernix caseosa can attenuate the fetal electrocardiogram signal because of its electric insulating properties. Thus, the technique requires time and expertise to ensure good-quality signals [8]. For all of these reasons, this is a technique that is not widely available outside of research environments.



Irregular rhythms due to intermittently blocked beats tend to be very well tolerated and rarely cause symptoms or progress to serious disease of the conduction system.

Isolated ectopic beats are generally benign (regardless of the chamber of origin) as they are rarely associated with congenital heart disease and tend to subside without intervention. It is important to note, however, that ectopic beats can be a cause of concern if there is also a substrate for reentrant tachycardia, in which case the ectopic beats can precipitate a tachycardic rhythm.

Persistent ectopy or ectopy of ventricular origin is of greater concern, although determining the chamber of origin for the ectopic beats can be difficult.

Irregular rhythms due to conduction abnormalities (eg, second-degree heart block) are of much more concern and should prompt cardiac evaluation/consultation with a fetal cardiologist. The distinction can be difficult to make, particularly when ectopy is frequent and blocked beats are present such that the heart rate varies quite a bit.

The following guidelines can help identify fetuses at lower versus higher risk for symptomatic arrhythmia:

Lower risk irregular rhythms (<3 to 5 beats ectopy/minute and fetal heart rate [FHR] <160 bpm)

Differential diagnosis:

Isolated premature atrial complex (PAC; also referred to as premature atrial beat, premature supraventricular complex, or premature supraventricular beat) with 1:1 conduction or with blocked conduction. These are by far the most common fetal arrhythmias (table 1).

Isolated premature ventricular or junctional contractions.

Intermittent conduction due to type II heart block.

Intermittent ventricular or junctional escape beats due to sinus node dysfunction.


Since most of these fetuses do not have significant structural heart disease, a standard ultrasound examination by a sonologist with experience in assessment of cardiac function and structure is generally sufficient. The examination should include assessment of the four chambers and outflow tracts and evaluation for hydrops. If this examination is abnormal, we suggest referral to a fetal cardiologist for a specialized evaluation of cardiac function and anatomy. (See "Congenital heart disease: Prenatal screening, diagnosis, and management".)

If the standard ultrasound is normal, we generally advise evaluating the FHR one week after ectopy is identified for approximately five minutes with either an electronic FHR monitor, Doppler device, or echocardiography to detect irregularity. If ectopy is still noted, we suggest reevaluation weekly by the obstetric provider to exclude intermittent sustained tachycardia [8]. Ectopy will often resolve within a few weeks, at which point routine obstetric visit schedules can be resumed.

The mother should be instructed to call if they note decreased fetal activity, as this may be a sign of cardiovascular compromise from fetal tachycardia. (See "Decreased fetal movement: Diagnosis, evaluation, and management".)

Some consultants recommend evaluating the mother for thyroid disease and advising them to decrease consumption of stimulants such as caffeine; however, no studies have established that thyroid disease or stimulant use contributes to the development of fetal PAC. We feel these interventions are unnecessary unless clinically indicated because of maternal symptoms.

Higher risk irregular rhythms (>3 to 5 beats ectopy/minute, heart rate <110 or >160 bpm, bigeminy or trigeminy, ectopy that persists for more than two weeks)

Differential diagnosis:

Nonsustained supraventricular tachycardia

Nonsustained ventricular tachycardia

Alternating bradycardia and tachycardia (most likely secondary to long QT syndrome)


The American Heart Association (AHA) suggests a baseline fetal echocardiogram/cardiac evaluation for detailed assessment of cardiac structure and function and to determine the mechanism of the arrhythmia [8].

Plans for further evaluation/treatment will be based on the evaluation by the cardiologist. In general, if no other abnormalities are identified, AHA guidelines suggest weekly assessment of FHR and rhythm (we suggest five minutes of continuous monitoring with any modality) and sonography to detect evolving hydrops fetalis.

The mother should be instructed to call if they note decreased fetal activity, as this may be a sign of cardiovascular compromise from fetal tachycardia. (See "Decreased fetal movement: Diagnosis, evaluation, and management".)



Fetal tachyarrhythmias are defined by fetal heart rate (FHR) >160 bpm.

Five to 10 percent of fetuses with a tachyarrhythmia have congenital heart disease. Any anatomic abnormality may be present, although there is an increased incidence of Ebstein anomaly and other causes of atrial enlargement (atrioventricular canal, hypoplastic left heart syndrome, intracardiac tumors). (See "Clinical manifestations and diagnosis of Ebstein anomaly" and "Cytomegalovirus infection in pregnancy".)

Differential diagnosis includes:

Sinus tachycardia

Supraventricular tachycardia (SVT):

-Typical 1:1 reentrant tachycardia, most frequently atrioventricular reciprocating tachycardia mediated by an accessory pathway and including Wolff-Parkinson-White syndrome, but at times caused by atrioventricular nodal reentry tachycardia.

-Atrial flutter, which typically has 2:1 conduction with atrial rates of 400 to 440 bpm and ventricular rates of 200 to 220 bpm.

-Automatic mechanisms (eg, ectopic atrial tachycardia, junctional ectopic tachycardia, and atrial fibrillation).

Ventricular tachycardia

Sinus tachycardia (160 to 200 bpm)

Diagnosis – Sinus tachycardia is characterized by [9]:

Atrial rates of 160 to 200 bpm

1:1 atrioventricular conduction

Normal duration of the atrioventricular interval

At least some heart rate variability


Short bursts of sinus tachycardia (typically up to 200 bpm) associated with fetal movement are normal in late pregnancy and do not require cardiac evaluation [10].

Prolonged sinus tachycardia requires maternal and fetal evaluation as it may be a marker of early fetal hypoxia, elevated maternal catecholamine levels due to anxiety or pain, maternal fever or thyrotoxicosis, intra-amniotic infection, fetal anemia, or maternal medications (typically beta-adrenergic or vagolytic drugs, but sometimes antihistamines with anticholinergic activity [eg, diphenhydramine, dimenhydrinate [11]]) [12].

A complete maternal history and physical examination should be performed. Maternal laboratory testing, a nonstress test or biophysical profile, fetal ultrasound examination, and/or Doppler measurement of fetal middle cerebral arterial peak systolic velocity are obtained when clinically appropriate. Management depends on the underlying cause. In the absence of fetal anemia, these cases are not typically associated with development of hydrops.

The sustained monitoring possible with cardiotocography is particularly helpful in looking at the pattern of heart range changes at these rates. Abrupt shifts in rate (from 200 to 150 bpm or from 160 to 80 bpm, as examples) suggest a primary arrhythmia as opposed to the typical patterns (eg, early, late, and variable decelerations) recognized by all obstetricians.

If obstetric evaluation does not reveal an underlying cause, referral to a fetal cardiologist is suggested to evaluate ventricular function and to exclude rare causes of slow SVT, such as ectopic atrial tachycardia. If any evidence for ventricular dysfunction is identified, maternal treatment should be considered to reduce the risk of development of hydrops. (See 'Supraventricular tachycardia' below.)

Although uncommon, benign sinus tachycardia in the fetus has also been described. This should be a diagnosis of exclusion.

Supraventricular tachycardia


Supraventricular tachycardia (SVT) is the most common fetal tachycardia, accounting for up to 90 percent of cases [13].


SVT is characterized by a regular rate that is typically between 220 and 260 bpm but rarely may be as high as 300 bpm. The rate can be sustained for hours or days but more commonly is intermittent.

Mechanism – The most common mechanism for fetal SVT is a reentrant tachycardia, and the most common type is atrioventricular reentrant tachycardia [5]. It is generally believed to be initiated by a critically timed spontaneous premature atrial complex (PAC) and terminated by spontaneous block. The PAC causes delayed antegrade conduction through the atrioventricular node with subsequent retrograde conduction through the accessory connection, thus initiating orthodromic reciprocating tachycardia.

Clinical findings

Early echocardiographic signs of hemodynamic compromise include biatrial enlargement and atrioventricular valve regurgitation.

Later findings include cardiomegaly and decreased systolic function, ultimately resulting in nonimmune hydrops fetalis.


The mortality rate of hydropic fetuses with SVT is over 50 percent, which is far higher than in cases without evidence of significant heart failure.

Individual series report that maternal therapy results in cardioversion in 65 to 95 percent of cases within 48 hours to one week of initiating therapy [14]. With effective therapy and conversion to sinus or low burdens of nonsustained atrial tachycardia, the mortality rates are quite low. However, even with therapy, larger case series report occasional fetal deaths. When initial efforts at in utero therapy are ineffective, the subsequent options, complicated in utero therapy or delivery, are each associated with morbidity and mortality of hydropic preterm fetuses/neonates. The highly selected nature of these challenging cases makes numeric estimates of risk challenging.

Management – The goal in managing fetuses with SVT is not necessarily to stop the SVT but to slow the rate enough to allow for a good cardiac output. Even if the abnormal rhythm persists, a slower rate should prevent the development of hydrops or, if already present, may permit resolution of hydrops.

Management of SVT should be individualized to take into account the specific maternal and fetal factors of each case. These decisions should be made with input from both the obstetric and fetal cardiac providers. When available, a pediatric electrophysiologist should be an integral part of the management team. In our institution, the electrophysiologist is typically the main decision maker with regard to treatment and the frequency of follow-up needed. Often, the adult electrophysiology team will be assisting in maternal monitoring. All providers need to understand the challenges of enhanced renal drug clearance in pregnancy, specific short- and medium-term goals of therapy, and the sometimes shifting social realities of extended care of pregnant patients.

Multiple case series have reported a variety of approaches that lead to the successful management of fetal SVT; however, no controlled therapeutic trials have been performed that allow for a complete understanding of when a specific option may be a best choice. Options for management include observation alone, delivery and postnatal management, in utero therapy via maternal administration of drugs, and in utero therapy via direct fetal injection.

Our general approach is discussed below. An overall summary of the approach to treatment is shown in the table (table 3).

Influence of gestational age — Gestational age affects the overall approach to decision making regarding transplacental therapy.

≥37 weeks – For the fetus ≥37 weeks (ie, term), the primary decision revolves around where and how to deliver the newborn.

There is rarely a reason to pursue transplacental drug therapy for the term fetus. Hydrops can be the exception. (See 'Persistent SVT (any rate) at presentation and hydrops fetalis' below.)

Local assessment should specifically focus on measures of fetal and maternal well-being other than the heart rate in preparing to determine the timing and location of delivery.

Coordination with the regional fetal cardiac team and their affiliated maternal fetal medicine providers may permit in utero transfer, which keeps the mother and newborn together; may decrease the chances of cesarean birth; and may offer the neonate more options for treatment of tachycardia.

30 to 36 weeks

Given the established morbidity of preterm delivery, a focused effort at transplacental drug therapy is reasonable.

The risks of Mirror syndrome and preeclampsia are likely increased and could be an indication for delivery if they develop. (See "Preeclampsia: Antepartum management and timing of delivery".)

<30 weeks

With increasing prematurity, the risks of delivery and postnatal management rise and increase our motivation to pursue transplacental therapy.

When initial transplacental therapy fails, a sequential approach to therapy appears to have a high overall success rate.

Carefully monitored use of higher drug doses, combination therapy, and accepting the risks of amiodarone may be warranted to avoid delivery of a hydropic preterm neonate.

SVT with rates between 200 and 220 bpm at presentation and no hydrops

Refer to a fetal cardiologist for accurate diagnosis and assessment of cardiac function and structure.

FHRs of 200 to 220 bpm are unlikely to cause hemodynamic consequences and may not warrant immediate intervention or hospitalization. If function is good and fetal well-being does not appear to be compromised, then we follow the fetus with frequent checks of heart rate and ventricular function, which typically include weekly evaluation by the cardiologist in addition to two FHR checks per week by the obstetric provider.

This is a heart rate range for which standard weekly or twice weekly antepartum fetal monitoring tests (eg, biophysical profiles, nonstress tests) can provide useful data.

In addition, the importance of daily maternal monitoring of fetal movement is emphasized as a means of daily fetal assessment in outpatients.

SVT with persistent rate >220 bpm at presentation and no hydrops

Refer to a fetal cardiologist for evaluation of fetal cardiac function, anatomy, and mechanism of SVT. If structural anomalies are present, the postnatal management and prognosis of these anomalies need to be taken into account when deciding about the timing of delivery and/or the aggressiveness of maternal therapy. These decisions should be made on a case-by-case basis with a team approach that includes the obstetric providers and the fetal cardiologists.

Maternal assessment:

Medical history (especially cardiac history).

Medication history.


Blood pressure.

Laboratory tests (serum electrolytes, tests of renal and hepatic function, urine protein, platelet count).

Note: The incidence of maternal thyroid disease was increased in one series of 28 fetuses with SVT (21 versus 3 percent in controls), in contrast to fetal-isolated PAC [15]. Thyroid function studies may be warranted as a routine component of maternal assessment and are always appropriate if the mother has symptoms of thyroid disease.

Local practice may prefer a formal cardiology consult to evaluate the mother.

FHRs >220 bpm are likely to progress to hydrops, but progression depends more on the duration of SVT than the rate. If SVT is confirmed by the cardiologist, admit the mother to the hospital for FHR monitoring for 24 hours to assess the amount of time that the fetus is tachycardic.

If SVT is present >50 percent of the time, then maternal treatment is typically initiated. Because maternal therapy is less successful once hydrops has developed, we tend to treat fetuses <37 weeks with persistent tachycardia unless there are maternal contraindications. Even if they have no evidence for hydrops, the risk of developing hydrops is significant, and therapeutic effect is faster and greater before hydrops develops.

As discussed above, if the pregnancy is at term (≥37 weeks), then delivery with postnatal treatment of arrhythmia should be considered. This decision needs to be made on a case-by-case basis with an experienced pediatric cardiology team. (See 'Influence of gestational age' above.)

If SVT is present <25 percent of the time, we suggest weekly FHR determination, ultrasound evaluation for hydrops fetalis, and reevaluation by the fetal cardiologist. SVT at this rate is usually well tolerated and does not warrant intervention. If it persists at a low rate and the fetus remains well, the frequency of visits can be reduced.

If SVT is present between 25 and 50 percent of the time, we suggest twice-weekly FHR determination and ultrasound evaluation for hydrops fetalis and weekly reevaluation by the fetal cardiologist. After a few weeks, surveillance can be decreased if there are no signs of progression.

Persistent SVT (any rate) at presentation and hydrops fetalis

We begin treatment of hydropic fetuses, regardless of the amount of time the fetus is in SVT.

If the fetus is ≥37 weeks of gestation, we consider a short trial of an effective agent (eg, flecainide, sotalol, or digoxin) for 48 to 72 hours, administered with the aggressive dosing typically needed in the pregnant patient to obtain adequate fetal drug levels rather than delivery. If this attempt to slow the FHR is ineffective, we proceed with delivery (see 'Digoxin' below and 'Flecainide, sotalol' below). Some groups would advocate use of amiodarone in this setting, but the pharmacokinetics of that agent necessitate a longer commitment to the drug trial, so we typically do not use this as first-line therapy. Amiodarone has a median time to arrhythmia control of approximately one week, hence limiting its efficacy in this setting.

If the fetus is <37 weeks, maternal therapy should be initiated in the sequence described below. The combination of hydrops and preterm birth is associated with very high morbidity and mortality, so we always advocate maternal treatment as opposed to delivery followed by newborn therapy [16]. (See 'Choice of drug' below.)

Preeclampsia or Mirror syndrome places the mother at risk of severe sequelae and of toxicity from drug therapy (digoxin, flecainide, sotalol). If present, the maternal status must be considered and may be an indication for delivery before all options for fetal therapy have been implemented. (See "Preeclampsia: Antepartum management and timing of delivery".)

Choice of drug — Transplacental therapy is the mainstay of management, unless there is some unusual contraindication to medicating the mother. Many medications have the potential to break SVT; they differ in their side effects and their ability to cross the placenta. In general, they all have a lower success rate in fetuses with hydrops, likely due to lower transplacental transfer and because some cardiac decompensation has already occurred. There are no standards for drug dosing or the need for loading doses. Drug dosing is empiric and depends on maternal, as well as fetal, factors. To date, there are no trials that show that one drug is more successful than another, so which drug to start with should depend on the conditions of the mother and fetus as well as the preference and experience of the cardiologist.

First-line therapy – Most antiarrhythmic drugs are initiated with inpatient maternal monitoring, including daily electrocardiograms. For therapies other than digoxin (eg, sotalol, flecainide, amiodarone), continuous cardiac monitoring is the standard practice in the United States for patients undergoing medical cardioversion and a reasonable approach in pregnancy. We occasionally make an exception for a healthy mother with a nonhydropic fetus, particularly with clearly intermittent SVT or slow SVT. In this scenario, we sometimes slowly initiate digoxin orally as an outpatient.

Digoxin has a long history of being the drug of first choice, but more recent experience has challenged that recommendation. Given its safety, rapid oral absorption, ease of monitoring serum levels, and a reasonable response, we believe that a trial of oral digoxin remains reasonable as first-line therapy for the nonhydropic fetus with either self-terminating SVT or sustained SVT. A literature review found that termination of atrial flutter/SVT before birth occurred in 51 percent of fetuses (115 of 226) treated with digoxin as first-line therapy [17]. The most successful contemporary experience with digoxin targeted drug levels at >2 ng/mL [18]. Direct fetal therapy (intramuscular or intraperitoneal) is feasible, though rarely used by the authors.

Contemporary data suggest good effects with sotalol or flecainide, as well. In a meta-analysis of 21 studies of transplacental treatment of fetal tachycardia, both flecainide and sotalol were more effective than digoxin for conversion of any fetal tachycardia to sinus rhythm, and the difference in efficacy was greatest in hydropic fetuses [19]. Fetal demise has been reported in patients receiving these drugs; details are sparse, and death could have been due to the arrhythmia, not the treatment. The higher success rates of sotalol or flecainide therapy have motivated rapid transition to these drugs for treatment of sustained arrhythmias. Practically, it takes approximately 24 to 48 hours of monitoring to evaluate whether most tachycardias are sustained.

Second-line therapy – If the fetal condition is not improving or is deteriorating despite adequate maternal digoxin levels (1 to 2 ng/mL), other medications should be considered. There are no clear guidelines about how long to wait before moving to a second-line therapy. In general, the more compromised the fetus, the more likely we are to try a second drug if there has been no improvement in 48 to 72 hours.

Which second-line drug to use will depend on individual maternal and fetal factors. Some specialists advocate adding the second drug, while others suggest discontinuing digoxin when starting the second drug. Our approach depends on several factors, including whether there was a partial response to relatively high doses of digoxin. (See 'Flecainide, sotalol' below.)

Flecainide, sotalol, and amiodarone are popular second-line therapies [16-18,20-31]. Different institutions have published single-center data looking at their experience with second-line therapies in hydropic fetuses, including sotalol, flecainide, and amiodarone. Because none of these drugs have been evaluated in randomized trials, there are no strong data favoring one drug or drug combination over another. All of the treatments appear to be safe for the mother, although careful monitoring for maternal toxicity is important.

Flecainide reliably slows the rate of SVT, likely by slowing retrograde conduction [18]. In a meta-analysis including over 500 patients, digoxin had a lower rate of SVT termination compared with flecainide (odds ratio [OR] 0.77, 95% CI 0.61-0.99), particularly with coincident hydrops [32]. At the author's institutions, 68 percent of the patients with sustained arrhythmias treated with advanced therapies were treated with drugs other than digoxin [33]. These analyses illustrate both practice variation and the recognition that, as in postnatal arrhythmias, there is not a simple single approach to management of these patients.

Amiodarone has been reported to be very successful for fetuses with refractory tachycardia, all of whom failed digoxin and most of whom had persistent arrhythmia despite a trial of flecainide and/or sotalol [20,26]. However, amiodarone has a long half-life and has been associated with neonatal hypothyroidism [34-36]. Time to conversion can be prolonged, with a mean of six days. Given its use in refractory cases, a second agent is often added. Expert consultation is critical when considering use of amiodarone.

Dosing — Digoxin, flecainide, and sotalol are all renally cleared, and pregnancy is associated with enhanced renal clearance of medications. For this reason, we initiate these agents in three divided doses rather than the typical twice-daily dosing that would be used in nonpregnant adults.


Initial dosing

Presuming normal maternal renal function, a reasonable oral digoxin loading dose for rapid loading is 1 to 2 mg, which can be given in three doses: 0.5 mg, 0.25 mg, and 0.25 mg over 18 to 24 hours, followed by a digoxin level. Additional doses are given if the digoxin level is low. Our target level is 1 to 2 ng/mL. After this target is achieved, it may take an additional 24 hours before fetal serum levels reach a steady state, so a 48- to 72-hour period of observation to assess the fetal response to maximum maternal therapy is reasonable. The upper end of the range for observation time is most appropriate for the nonhydropic fetus with self-terminating tachycardia. Once the target (therapeutic) maternal serum level is achieved, the risk of maternal toxicity from additional dose increases likely outweighs any fetal benefits of supratherapeutic maternal digoxin levels. (See "Treatment with digoxin: Initial dosing, monitoring, and dose modification", section on 'Rapid digoxin loading'.)

When the fetus is hydropic, it is less likely to respond at standard therapeutic levels, so higher doses of digoxin may be given, but there is substantial practice variation on this issue [26,37]. Some groups advocate serum levels of 2 to 3 ng/mL, which presumes tolerating maternal electrocardiographic changes and other potential symptoms of low-grade digoxin toxicity, but may be more effective than the traditional dosing level [18].

Maintenance dose

The maternal maintenance dose is determined by titrating to the fetal response, which might take several days. Close inpatient maternal monitoring is mandatory to avoid maternal toxicity (gastrointestinal and central nervous system disturbances, arrhythmias including PAC and atrioventricular block). Daily electrocardiograms to monitor for PR prolongation and T-wave changes are required when rapid loading is performed; continuous cardiac monitoring is not usually done. With slower or nonsustained SVT, a slower outpatient course of drug initiation and maintenance is appropriate.

Maintenance dosing usually needs to be higher in pregnant individuals than in nonpregnant individuals, often ranging from 0.5 to 0.75 mg daily given in three divided doses, because of increases in blood volume and glomerular filtration rates associated with pregnancy. Digoxin levels can be obtained rapidly in most facilities, which permits relatively timely dose adjustments. If sustained SVT control and stable maternal electrocardiograms and serum levels are achieved, then decreasing dosing frequency to twice daily is reasonable.

Other routes of digoxin administration — Direct fetal intramuscular injection of digoxin is another approach that has been used to achieve more rapid therapeutic fetal drug levels, particularly in the hydropic fetus [38]. Fetal intramuscular therapy can be combined with maternal/transplacental therapy. Drug treatment in this setting is beyond the scope of this topic. We do not advise direct umbilical artery or vein digoxin injection because of the increased risk of fetal mortality, which may be procedure related, due to the poor underlying cardiovascular condition in these cases, or a combination of these factors.

Maternal intravenous dosing has been described, but use is limited. Oral administration is convenient because most obstetric clinicians and obstetric units can manage it as well as fetal and uterine monitoring, whereas intravenous administration would require transferring the patient to a cardiac intensive care unit, where fetal and uterine monitoring is more challenging.

Flecainide, sotalol — Flecainide (50 mg, 100 mg, and 150 mg tablets; pregnancy class C) and sotalol (80 mg, 120 mg, and 160 mg tablets; pregnancy class B) are similar; both are cleared by the kidney. While twice-daily dosing is typical in nonpregnant patients, three-times-daily dosing is appropriate during pregnancy, given enhanced renal clearance. There is no intravenous formulation of flecainide in the United States. Intravenous sotalol is available, but there are no data on use in fetal arrhythmias.

Sotalol and flecainide can be proarrhythmic in certain settings, so it is important to have an accurate diagnosis of the arrhythmia and to monitor both the fetus and the mother carefully.

Initial dosing

An initial dose of sotalol 80 mg orally three times per day or flecainide 100 mg orally three times per day or 100 mg, 50 mg, 100 mg orally over one day (ie, 250 to 300 mg per day) is reasonable. The target flecainide level is >250 mcg/L and <1000 mcg/L; maternal toxicity should be avoided and is seen as drug levels approach 1000 mcg/L [24,39]. Sotalol levels are available clinically, though there is no published experience with them. Like flecainide levels, they generally require 48 to 72 hours for completion.

There is significant practice variation as to whether first-line digoxin therapy is continued or discontinued if second-line therapy with flecainide or sotalol therapy is begun. There is also practice variation as to whether digoxin is added as a second-line drug when first-line trials of flecainide or sotalol therapy are unsuccessful. Specific medical factors that can influence that decision include anticipated need for combination therapy in a fetus with hydrops; the presence or absence of a partial response to relatively high doses of the initial medication; and maternal medical conditions that can affect drug choice, such as asthma, which may be exacerbated by sotalol. Another issue is that flecainide increases serum digoxin levels; therefore, adding it as a second drug in a patient already on digoxin requires both digoxin dose adjustment and repeated monitoring.

Maternal monitoring

Local practice patterns will dictate the location of care. The authors generally initiate sotalol and flecainide on the antepartum or labor floors. Cardiac telemetry units are ideal for monitoring the drug side effects but are inexperienced in monitoring fetal well-being and other antepartum issues. Antepartum units, which have obstetric and fetal monitoring expertise, may have limited experience with maternal cardiac issues.

With use of either flecainide or sotalol, the mother is monitored with continuous cardiac monitoring for 48 hours or for the first five to six doses and with daily electrocardiograms. Daily electrocardiograms are obtained to look for QT prolongation (corrected QT interval [QTc] >480 milliseconds suggests toxicity) and QRS prolongation (QRS duration >120 milliseconds suggests toxicity). (See "Major side effects of class I antiarrhythmic drugs", section on 'Flecainide' and "Clinical uses of sotalol", section on 'Cardiac toxicity'.)

Fetal monitoring

The frequency of fetal monitoring will depend on the relative health of the fetus; there are no data suggesting how often the fetus should be evaluated. In sicker fetuses, we typically keep the mother in the hospital and monitor the FHR continuously or at least every hour.

Amiodarone — While there has been concern about delayed placental transport in hydropic fetuses, a strategy of initial loading to a total of 12 to 13 grams over a week has been reported to lead to conversion to sinus rhythm at a mean of six days [20]. Maternal thyroid function needs to be monitored and dysfunction treated, as clinically appropriate. There is not an established practice for direct fetal thyroid monitoring. Amiodarone has a long half-life and has been associated with neonatal hypothyroidism [34-36]. (See "Amiodarone: Clinical uses" and "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring" and "Amiodarone and thyroid dysfunction".)

Other rarely used drugs

While verapamil has also been used in the past, it is contraindicated in newborns and not recommended because of concerns about cardiovascular collapse in fetuses and infants [27].

Oral procainamide and quinidine are no longer readily available; the anticipated maternal risks of quinidine are higher than with the alternative drugs. Therefore, these drugs are rarely used for fetal SVT.

There are no substantive data on the use of pure beta blockers such as propranolol for fetal arrhythmia control.

Direct fetal administration of adenosine can be performed, but there is minimal experience with this. If the arrhythmia may spontaneously terminate, there is no logic in a short-acting cardioversion approach.

Follow-up after rate control

Once SVT is controlled, close outpatient monitoring typically includes:

Daily fetal kick counts.

Prenatal visits to check the FHR two or three times per week.

Weekly nonstress tests or biophysical profile scores to assess fetal well-being, although the usefulness of these tests in this setting has not been established in randomized trials.

Evaluation by a fetal cardiologist every two to three weeks.

Maternal electrocardiograms and serum drug levels every one to two weeks. In contrast to digoxin levels, both flecainide and sotalol levels typically require a minimum of two to three business days for results to return from the laboratory.

Preeclampsia may develop even in the absence of Mirror syndrome and is routinely screened for at each prenatal visit. If laboratory studies performed for evaluation of severity of preeclampsia show evidence of renal insufficiency, all drugs except amiodarone should be discontinued or their doses decreased.

Drug taper

After several weeks of controlled sinus rhythm or as the fetus approaches term, an attempt to taper medications (sotalol in particular) can help limit neonatal side effects.

For mothers on sotalol, lowering the dose in the days before delivery may limit neonatal hypoglycemia and other neonatal effects of beta blockade.

Because digoxin and flecainide have less serious neonatal effects and amiodarone has a prolonged half-life, tapering these drugs before delivery has limited benefits.

Refractory cases — Fetuses at a gestational age compatible with ex utero survival and unresponsive to in utero treatment may be best served by delivery for further evaluation and direct therapy of the neonate [16]. Decisions about delivery should be made after consultation with a neonatologist and pediatric cardiologist; consultation with an experienced center may permit delay in delivery and limit the consequences of prematurity [40].

Atrial flutter — Atrial flutter is less common than SVT and tends to occur in the third trimester [41]. Postnatal experience with atrial flutter suggests that nearly 20 percent of affected fetuses will also have SVT [42].


Atrial flutter is characterized by extremely fast, regular atrial rates (400 to 500 bpm) with a slower, but regular, ventricular rate (very fixed ventricular rates of 200 to 220 bpm without spontaneous terminations).

Typically, there is 2:1, 3:1, or 4:1 atrioventricular block, producing a ventricular rate that may be tachycardic but may also be within the normal range. On echocardiogram, atrial dilation is often present, particularly if flutter is sustained.

Atrial flutter with 3:1 or 4:1 block may not be recognized on routine FHR assessment since the ventricular rate may be normal. However, in flutter, the ventricular rate is usually fixed and does not change with fetal activity; thus, evaluation of FHR that reveals no variation in rate with fetal movement should raise concern that atrial flutter may be present.


There are no data from randomized trials to guide therapy of fetal atrial flutter. Treatment plans are typically based on institutional experience and data from small series and case reports.

Atrial flutter can be treated with digoxin to slow the ventricular response rate or with flecainide, sotalol, or amiodarone to restore normal sinus rhythm [22,25,31,43,44]. (See 'Dosing' above.)

A literature review found that termination of atrial flutter/SVT before birth occurred in 51 percent of fetuses (115 of 226) treated with digoxin as first-line therapy, in 64 percent (45 of 70) of those treated with flecainide initially, and in 66 percent (23 of 35) of those treated with sotalol initially [17].

Other tachyarrhythmias

Atrial fibrillation – Atrial fibrillation is exceptionally rare in the fetus, and in the absence of significant atrioventricular valve disease, an alternative explanation should be considered [43]. The physiology may be very rapid ectopic atrial tachycardia with fibrillatory conduction, which cannot be determined with fetal echocardiography.

Ventricular tachycardia and fibrillation – Ventricular tachycardia and fibrillation are rarely diagnosed in the fetus. By definition, ventricular rates are over 200 bpm. M-mode will show complete dissociation of atrial and ventricular contraction with an atrial rate that is slower than the ventricular rate. Ventricular tachycardia is usually paroxysmal and may be associated with myocarditis, complete heart block, or congenital long QT syndrome [45]. The prognosis depends on the underlying mechanism.

The rarity of fetal ventricular tachycardia means that there is no consensus about optimal therapy; expectant management of stable fetuses has been described with spontaneous resolution of the arrhythmia [46]. Successful treatment with intravenous magnesium sulfate, oral propranolol, or amiodarone has also been described [45].



Diagnosis – Fetal bradycardia is defined as an intermittent or persistent fetal heart rate (FHR) <110 bpm [1].

Differential diagnosis includes:

Sinus bradycardia – Brief episodes of sinus bradycardia with rates of 100 to 110 bpm are common and physiologic, especially in the second trimester fetus (sometimes due to transient fetal head or umbilical cord compression).

Blocked ectopic beats.

Second-degree or third-degree (complete) heart block – A persistent ventricular rate <60 bpm is usually associated with complete heart block, while rates between 60 and 80 bpm can be due to nonconducted bigeminy or second- or third-degree block. It is possible for fetuses to tolerate heart rates in the 70 to 90 bpm range over a long period of time, but there is some risk for development of cardiac dysfunction.

Long QT syndrome.

Sinus bradycardia


Sinus bradycardia refers to an FHR <110 bpm in which the atria and ventricles are beating at the same rate. The electrical impulse originates in the sinus node and is normally conducted. Sustained sinus bradycardia may be associated with structural cardiac anomalies, heterotaxy, or long QT syndrome [47-49].

Differential diagnosis

Structural heart disease – Bradycardia is sometimes seen in fetuses with heterotaxy syndrome. In this scenario, the bradycardia is thought to be due to a primary abnormality of the sinus node. The associated structural heart disease may be quite mild (eg, interrupted inferior vena cava) or can be very complex (single ventricle). (See "Heterotaxy (isomerism of the atrial appendages): Anatomy, clinical features, and diagnosis" and "Heterotaxy (isomerism of the atrial appendages): Management and outcome".)

Long QT syndrome – The primary fetal presentations are low FHR and, in more severe cases, functional 2:1 atrioventricular block [50]. Fetuses carrying pathogenic variants associated with long QT syndrome may have persistent mild bradycardia at rates of 100 to 110 bpm [50]. There is a very high likelihood that a parent is affected, but the parental phenotype can be mild.

Long QT syndrome can be a cause of ventricular arrhythmia and death in children and adults. A number of reports suggest that approximately 10 percent of sudden infant death syndrome can be attributed to long QT syndrome, frequently with de novo pathogenic variants. An increased frequency of pathogenic variants associated with the long QT phenotype has been noted in stillbirths. In one study of 91 stillbirths, three had clearly pathogenic variants associated with the syndrome, and eight had potentially pathogenic variants [51]. If a specific pathogenic variant associated with long QT syndrome is present in one parent, testing the fetus for that variant should be considered. (See "Congenital long QT syndrome: Pathophysiology and genetics".)

Noncardiac conditions – In the setting of antepartum or intrapartum maternal or pregnancy complications, new-onset sinus bradycardia can be secondary to maternal hypotension, maternal seizures, paracervical block anesthesia, or impaired fetal oxygenation, which can result from conditions including, but not limited to, placental abruption, uterine rupture, prolapsed umbilical cord, fetal hemorrhage, and fetal hypotension. Under these circumstances, a poor outcome may result if the cause of the fetal distress cannot be corrected.

On the other hand, maternal hypothermia can result in fetal bradycardia that is a normal physiologic response and corrects with rewarming [52]. The baseline heart rate may be sustained at <100 bpm, but variability is normal and accelerations consistent with gestational age often occur. Several cases of fetal bradycardia related to maternal temperatures of 33 to 36°C have been reported in the literature. Maternal conditions included urosepsis, hypoglycemia, and drug or cold weather exposure. Fetal bradycardia during cardiopulmonary bypass can be due to maternal hypothermia and/or hypoperfusion [53].


Standard ultrasound examination to exclude major heart disease and hydrops fetalis.

Biophysical profile to assess fetal well-being. The nonstress test is likely to be nonreactive with sustained bradycardias, but variability may be normal.

Maternal laboratory testing for anti-Ro/SSA and anti-La/SSB antibodies.

Management – If the standard ultrasound examination is normal:

Intermittent bradycardia <110 bpm

-Perform FHR checks weekly for a few weeks to make sure that the bradycardia is not becoming sustained. Reassessment for hydrops and referral to a fetal cardiologist are indicated if the intermittent bradycardia persists.

Sustained bradycardia <110 bpm

-In consultation with the maternal cardiologist, discontinue any maternal medications that could be impacting corrected QT interval (QTc).

-Refer to a fetal cardiologist for definitive diagnosis of the arrhythmia, evaluation of conduction intervals, as well as full evaluation of cardiac structure and function.

Heart block

Blocked ectopic beats — Blocked ectopic beats can lead to sustained low heart rates, particularly in the case of bigeminy or trigeminy, but rarely cause the fetus any harm. When premature atrial complexes (PACs) occur in bigeminy (or trigeminy) and are consistently blocked, the rhythm will be regular but slow (65 to 90 bpm). Typically, this is a benign and transient arrhythmia, but it can mimic the auscultatory findings of complete heart block or 2:1 atrioventricular block. Recurrent, abrupt shifts from heart rates of approximately 60 to 80 bpm to 120 to 160 bpm suggest blocked PAC during the bradycardic periods. It is important to distinguish blocked ectopic beats from complete heart block, as the prognosis and fetal surveillance are quite different. The distinction can be made by assessing the atrial rhythm; in complete heart block, the atrial rhythm should be regular, whereas in atrial ectopy with blocked beats, the atrial rhythm will be irregular. Furthermore, abrupt shifts to 2:1 block at physiologic rates are exceptionally rare in heart block but common in patterns of blocked atrial bigeminy with ectopic atrial beats.

We suggest weekly obstetric evaluation to determine the FHR as long as atrial ectopy persists. Routine prenatal care can be resumed after ectopy resolves.

Second-degree heart block — Second-degree heart block is uncommon in the fetus and is often a sign that the atrioventricular conduction system is damaged. Maternal blood should be sampled for anti-Ro/SSA and anti-La/SSB antibodies.

Progression to complete heart block is a common outcome in this setting; therefore, referral to cardiology for diagnosis and discussion of medical intervention is indicated. In second-degree atrioventricular block, there is often an irregular rhythm at a slow rate with lengthening of the mechanical PR interval from one beat to the next.

Complete (third-degree) heart block — In third-degree block, there is complete dissociation of the atrial and ventricular rates because of absence of atrioventricular conduction. The atrial rate is typically normal, and the ventricular rate is typically between 50 and 80 bpm but can be lower or higher. The rate may slow as the pregnancy progresses, so regular evaluation of heart rate and ventricular function is important. As the rate slows, cardiomegaly and occasionally ventricular dysfunction develop.

Fifty percent of fetuses with complete heart block will have congenital heart disease [54]. While any type of heart disease can be present, the most common lesions are L-transposition of the great arteries, other heart diseases with L-looped ventricles, and certain types of heterotaxy, particularly those associated with polysplenia [54-56]. Other causes of complete heart block include exposure to maternal autoantibodies and myocarditis. The risk of fetal/neonatal death is particularly high in fetuses with heart block associated with structural heart disease, endocardial fibroelastosis, or hydrops fetalis [55-60].

When a fetus with a structurally normal heart is diagnosed with heart block, maternal blood should be sampled for anti-Ro/SSA and anti-La/SSB antibodies. Anti-Ro antibodies are thought to induce fetal myocarditis and destruction of the conducting fibers in the fetal, but not maternal, heart. It is rare to see heart block from this type of exposure before 18 weeks or after 28 weeks. The hearts of fetuses exposed to these antibodies have normal morphology but may develop endocardial fibroelastosis and, rarely, dilated cardiomyopathy [58,61]. Screening for and management of complete heart block, including in utero interventions and planning for delivery, are discussed in detail separately. Prompt referral to a fetal arrhythmia specialist is recommended as there is a possibility of reversing or mitigating the block. (See "Pregnancy in women with systemic lupus erythematosus", section on 'Maternal-fetal monitoring' and "Neonatal lupus: Epidemiology, pathogenesis, clinical manifestations, and diagnosis" and "Neonatal lupus: Management and outcomes".)

MANAGEMENT OF LABOR AND DELIVERY — The fetus with an arrhythmia can undergo labor and be delivered vaginally as long as fetal well-being can be monitored in some way. Fetuses with intermittent arrhythmias may display a normal fetal heart rate (FHR) pattern frequently enough to allow the clinician to be reassured of fetal well-being. If fetal well-being cannot be evaluated adequately, then cesarean delivery is the best option.

Although sustained tachycardia, particularly supraventricular tachycardia, is rarely life-threatening during delivery, it is important to try to convert the rhythm as soon as possible after delivery. Optimally, if sustained tachycardia is present, either cardiac or pediatric specialists with experience in taking care of newborn arrhythmias should be available at the time of delivery to help with diagnosis and therapeutic decision making.

For mildly bradycardic fetuses, delivery is typically uneventful, and the heart rate is adequate to support cardiac output. In a small percentage of cases, the heart rate can drop dramatically after birth, resulting in poor cardiac output. Even in those newborns whose heart rates do not change much, cardiac output can be insufficient to support systemic perfusion once the low resistance placenta is gone. It is important that an experienced clinician with expertise in treating/pacing newborns with symptomatic bradycardia is available at the time of delivery. In fetuses with significant congenital heart disease or ventricular dysfunction, all of these concerns are amplified.

Transferring the mother to a comprehensive center for delivery may be preferable to emergency local delivery, as the in utero environment is generally more favorable to the fetus with any arrhythmia. When delivery occurs, having a full neonatal cardiac care team available immediately minimizes the time to effective therapy for the newborn and provides the parents close contact with the neonatal/pediatric intensive care unit, which can facilitate ongoing care. (See "Irregular heart rhythm (arrhythmias) in children".)


Overview – The fetal conduction system is functionally mature by 16 weeks of gestation and normally produces a regular rhythm and rate between 110 and 160 beats per minute (bpm). Fetal arrhythmias are defined by deviations from these parameters. They complicate 1 to 2 percent of pregnancies and have the potential to compromise fetal health. (See 'Introduction' above.)

A simplified summary of fetal arrhythmias by rate, pattern, and echocardiography findings is shown in the table (table 2). (See 'Screening' above.)

Screening – Assessment of the fetal heart rate (FHR) at each prenatal visit and viewing the four cardiac chambers and ventricular outflow tracts on standard ultrasound examinations are routine components of prenatal care and sufficient for screening most pregnancies for fetal arrhythmias.

Pregnancies at high risk for fetal arrhythmias (eg, autoantibodies directed against Ro/SSA and La/SSB autoantigens, previous pregnancy with congenital heart block, a fetus with congenital heart disease that includes L-looped ventricles) should undergo more intensive screening using serial echocardiography. (See 'Screening' above.)

Irregular rhythms – Irregular rhythms due to intermittently blocked beats tend to be well tolerated and rarely progress to serious arrhythmias. Premature atrial complexes (PACs; also referred to as premature atrial beats, premature supraventricular complexes, or premature supraventricular beats) are the most common cause of an irregular rhythm and are generally benign. Ectopy that is of ventricular origin, persistent, >3 to 5 beats ectopy/minute, or associated with FHR <120 or >160 bpm is of greatest concern. (See 'Irregular rhythms' above.)


Sinus tachycardia – Short bursts of sinus tachycardia (typically up to 200 bpm) associated with fetal movement are normal. Prolonged sinus tachycardia requires maternal and fetal evaluation as it may be a marker for a variety of maternal and fetal disorders. (See 'Sinus tachycardia (160 to 200 bpm)' above.)

Supraventricular tachycardia – Supraventricular tachycardia (SVT) is the most common fetal tachycardia. Referral to a fetal cardiologist is indicated for accurate diagnosis and assessment of rhythm, cardiac function, and cardiac structure. Our general approach to management of SVT is shown in the table (table 3). In general, an FHR of 200 to 220 bpm is unlikely to cause hemodynamic consequences and thus does not automatically warrant intervention. For fetuses with SVT >220 bpm >50 percent of the time or hydrops, transplacental treatment is usually warranted. We suggest digoxin as the first-line drug rather than flecainide or sotalol (Grade 2C). If the fetal condition does not improve despite adequate maternal digoxin levels (1 to 2 ng/mL), other medications (eg, flecainide, sotalol, amiodarone) are considered in addition to or as a replacement for digoxin, depending on the clinical scenario. (See 'Supraventricular tachycardia' above.)

Bradycardias – A slow FHR may be due to sinus bradycardia, blocked ectopic beats, long QT syndrome, second-degree heart block, or complete (third-degree) heart block. Standard ultrasound examination is indicated to exclude major heart disease and hydrops fetalis. Maternal laboratory testing for anti-Ro/SSA and anti-La/SSB antibodies is also performed. Management depends on the arrhythmia. (See 'Bradyarrhythmias' above.)

Labor and delivery – The fetus with a sustained arrhythmia can undergo labor and be delivered vaginally as long as fetal well-being can be monitored in some way. Appropriate support personnel from pediatrics, neonatology, and/or cardiology should be available at the delivery. (See 'Management of labor and delivery' above.)

  1. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet Gynecol 2008; 112:661.
  2. Indik JH, Chen V, Reed KL. Association of umbilical venous with inferior vena cava blood flow velocities. Obstet Gynecol 1991; 77:551.
  3. Rein AJ, O'Donnell C, Geva T, et al. Use of tissue velocity imaging in the diagnosis of fetal cardiac arrhythmias. Circulation 2002; 106:1827.
  4. Zhao H, Chen M, Van Veen BD, et al. Simultaneous fetal magnetocardiography and ultrasound/Doppler imaging. IEEE Trans Biomed Eng 2007; 54:1167.
  5. Wakai RT, Strasburger JF, Li Z, et al. Magnetocardiographic rhythm patterns at initiation and termination of fetal supraventricular tachycardia. Circulation 2003; 107:307.
  6. Taylor MJ, Smith MJ, Thomas M, et al. Non-invasive fetal electrocardiography in singleton and multiple pregnancies. BJOG 2003; 110:668.
  7. Behar JA, Bonnemains L, Shulgin V, et al. Noninvasive fetal electrocardiography for the detection of fetal arrhythmias. Prenat Diagn 2019; 39:178.
  8. Donofrio MT, Moon-Grady AJ, Hornberger LK, et al. Diagnosis and treatment of fetal cardiac disease: a scientific statement from the American Heart Association. Circulation 2014; 129:2183.
  9. Jaeggi ET, Nii M. Fetal brady- and tachyarrhythmias: new and accepted diagnostic and treatment methods. Semin Fetal Neonatal Med 2005; 10:504.
  10. Allan LD. Fetal arrhythmias. In: Fetal and Neonatal Cardiology, Long WA (Ed), WB Saunders, 1989. p.180.
  11. Abernathy A, Alsina L, Greer J, Egerman R. Transient Fetal Tachycardia After Intravenous Diphenhydramine Administration. Obstet Gynecol 2017; 130:374.
  12. Shenker L. Fetal cardiac arrhythmias. Obstet Gynecol Surv 1979; 34:561.
  13. van Engelen AD, Weijtens O, Brenner JI, et al. Management outcome and follow-up of fetal tachycardia. J Am Coll Cardiol 1994; 24:1371.
  14. Simpson LL. Fetal supraventricular tachycardias: diagnosis and management. Semin Perinatol 2000; 24:360.
  15. Johnson JA, Williams P, Lu Z, et al. Fetuses of Mothers with Thyroid Disease May Be at Higher Risk of Developing Supraventricular Tachycardia. Am J Perinatol 2015; 32:1240.
  16. van den Heuvel F, Bink-Boelkens MT, du Marchie Sarvaas GJ, Berger RM. Drug management of fetal tachyarrhythmias: are we ready for a systematic and evidence-based approach? Pacing Clin Electrophysiol 2008; 31 Suppl 1:S54.
  17. Jaeggi E, Tulzer G. Pharmacological and interventional fetal cardiovascular treatment. In: Paediatric Cardiology, 3rd ed, Anderson RH, Baker EJ, Redington A, et al (Eds), Elsevier, Philadelphia 2009. p.199.
  18. Jaeggi ET, Carvalho JS, De Groot E, et al. Comparison of transplacental treatment of fetal supraventricular tachyarrhythmias with digoxin, flecainide, and sotalol: results of a nonrandomized multicenter study. Circulation 2011; 124:1747.
  19. Hill GD, Kovach JR, Saudek DE, et al. Transplacental treatment of fetal tachycardia: A systematic review and meta-analysis. Prenat Diagn 2017; 37:1076.
  20. Strasburger JF, Cuneo BF, Michon MM, et al. Amiodarone therapy for drug-refractory fetal tachycardia. Circulation 2004; 109:375.
  21. Frohn-Mulder IM, Stewart PA, Witsenburg M, et al. The efficacy of flecainide versus digoxin in the management of fetal supraventricular tachycardia. Prenat Diagn 1995; 15:1297.
  22. Oudijk MA, Michon MM, Kleinman CS, et al. Sotalol in the treatment of fetal dysrhythmias. Circulation 2000; 101:2721.
  23. Shah A, Moon-Grady A, Bhogal N, et al. Effectiveness of sotalol as first-line therapy for fetal supraventricular tachyarrhythmias. Am J Cardiol 2012; 109:1614.
  24. Vigneswaran TV, Callaghan N, Andrews RE, et al. Correlation of maternal flecainide concentrations and therapeutic effect in fetal supraventricular tachycardia. Heart Rhythm 2014; 11:2047.
  25. van der Heijden LB, Oudijk MA, Manten GT, et al. Sotalol as first-line treatment for fetal tachycardia and neonatal follow-up. Ultrasound Obstet Gynecol 2013; 42:285.
  26. Jouannic JM, Delahaye S, Fermont L, et al. Fetal supraventricular tachycardia: a role for amiodarone as second-line therapy? Prenat Diagn 2003; 23:152.
  27. Oudijk MA, Ruskamp JM, Ambachtsheer BE, et al. Drug treatment of fetal tachycardias. Paediatr Drugs 2002; 4:49.
  28. Etheridge SP, Craig JE, Compton SJ. Amiodarone is safe and highly effective therapy for supraventricular tachycardia in infants. Am Heart J 2001; 141:105.
  29. Strizek B, Berg C, Gottschalk I, et al. High-dose flecainide is the most effective treatment of fetal supraventricular tachycardia. Heart Rhythm 2016; 13:1283.
  30. Sridharan S, Sullivan I, Tomek V, et al. Flecainide versus digoxin for fetal supraventricular tachycardia: Comparison of two drug treatment protocols. Heart Rhythm 2016; 13:1913.
  31. Oudijk MA, Ruskamp JM, Ververs FF, et al. Treatment of fetal tachycardia with sotalol: transplacental pharmacokinetics and pharmacodynamics. J Am Coll Cardiol 2003; 42:765.
  32. Alsaied T, Baskar S, Fares M, et al. First-Line Antiarrhythmic Transplacental Treatment for Fetal Tachyarrhythmia: A Systematic Review and Meta-Analysis. J Am Heart Assoc 2017; 6.
  33. O'Leary ET, Alexander ME, Bezzerides VJ, et al. Low mortality in fetal supraventricular tachycardia: Outcomes in a 30-year single-institution experience. J Cardiovasc Electrophysiol 2020; 31:1105.
  34. Grosso S, Berardi R, Cioni M, Morgese G. Transient neonatal hypothyroidism after gestational exposure to amiodarone: a follow-up of two cases. J Endocrinol Invest 1998; 21:699.
  35. Matsumura LK, Born D, Kunii IS, et al. Outcome of thyroid function in newborns from mothers treated with amiodarone. Thyroid 1992; 2:279.
  36. Lomenick JP, Jackson WA, Backeljauw PF. Amiodarone-induced neonatal hypothyroidism: a unique form of transient early-onset hypothyroidism. J Perinatol 2004; 24:397.
  37. Ebenroth ES, Cordes TM, Darragh RK. Second-line treatment of fetal supraventricular tachycardia using flecainide acetate. Pediatr Cardiol 2001; 22:483.
  38. Parilla BV, Strasburger JF, Socol ML. Fetal supraventricular tachycardia complicated by hydrops fetalis: a role for direct fetal intramuscular therapy. Am J Perinatol 1996; 13:483.
  39. Cuneo BF, Benson DW. Use of maternal flecainide concentration in management of fetal supraventricular tachycardia: a step in the right direction. Heart Rhythm 2014; 11:2054.
  40. Naheed ZJ, Strasburger JF, Deal BJ, et al. Fetal tachycardia: mechanisms and predictors of hydrops fetalis. J Am Coll Cardiol 1996; 27:1736.
  41. Moodley S, Sanatani S, Potts JE, Sandor GG. Postnatal outcome in patients with fetal tachycardia. Pediatr Cardiol 2013; 34:81.
  42. Texter KM, Kertesz NJ, Friedman RA, Fenrich AL Jr. Atrial flutter in infants. J Am Coll Cardiol 2006; 48:1040.
  43. Krapp M, Kohl T, Simpson JM, et al. Review of diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia. Heart 2003; 89:913.
  44. Lisowski LA, Verheijen PM, Benatar AA, et al. Atrial flutter in the perinatal age group: diagnosis, management and outcome. J Am Coll Cardiol 2000; 35:771.
  45. Strasburger JF. Prenatal diagnosis of fetal arrhythmias. Clin Perinatol 2005; 32:891.
  46. Simpson JM, Maxwell D, Rosenthal E, Gill H. Fetal ventricular tachycardia secondary to long QT syndrome treated with maternal intravenous magnesium: case report and review of the literature. Ultrasound Obstet Gynecol 2009; 34:475.
  47. Boldt T, Eronen M, Andersson S. Long-term outcome in fetuses with cardiac arrhythmias. Obstet Gynecol 2003; 102:1372.
  48. Horigome H, Nagashima M, Sumitomo N, et al. Clinical characteristics and genetic background of congenital long-QT syndrome diagnosed in fetal, neonatal, and infantile life: a nationwide questionnaire survey in Japan. Circ Arrhythm Electrophysiol 2010; 3:10.
  49. Copel JA, Liang RI, Demasio K, et al. The clinical significance of the irregular fetal heart rhythm. Am J Obstet Gynecol 2000; 182:813.
  50. Mitchell JL, Cuneo BF, Etheridge SP, et al. Fetal heart rate predictors of long QT syndrome. Circulation 2012; 126:2688.
  51. Crotti L, Tester DJ, White WM, et al. Long QT syndrome-associated mutations in intrauterine fetal death. JAMA 2013; 309:1473.
  52. Spires BP, Towers CV. Fetal Bradycardia in Response to Maternal Hypothermia. Obstet Gynecol 2020; 135:1454.
  53. Kapoor MC. Cardiopulmonary bypass in pregnancy. Ann Card Anaesth 2014; 17:33.
  54. Lopes LM, Tavares GM, Damiano AP, et al. Perinatal outcome of fetal atrioventricular block: one-hundred-sixteen cases from a single institution. Circulation 2008; 118:1268.
  55. Jaeggi ET, Hornberger LK, Smallhorn JF, Fouron JC. Prenatal diagnosis of complete atrioventricular block associated with structural heart disease: combined experience of two tertiary care centers and review of the literature. Ultrasound Obstet Gynecol 2005; 26:16.
  56. Maeno Y, Himeno W, Saito A, et al. Clinical course of fetal congenital atrioventricular block in the Japanese population: a multicentre experience. Heart 2005; 91:1075.
  57. Jaeggi ET, Hamilton RM, Silverman ED, et al. Outcome of children with fetal, neonatal or childhood diagnosis of isolated congenital atrioventricular block. A single institution's experience of 30 years. J Am Coll Cardiol 2002; 39:130.
  58. Izmirly PM, Saxena A, Kim MY, et al. Maternal and fetal factors associated with mortality and morbidity in a multi-racial/ethnic registry of anti-SSA/Ro-associated cardiac neonatal lupus. Circulation 2011; 124:1927.
  59. Kuleva M, Le Bidois J, Decaudin A, et al. Clinical course and outcome of antenatally detected atrioventricular block: experience of a single tertiary centre and review of the literature. Prenat Diagn 2015; 35:354.
  60. Escobar-Diaz MC, Tworetzky W, Friedman K, et al. Perinatal outcome in fetuses with heterotaxy syndrome and atrioventricular block or bradycardia. Pediatr Cardiol 2014; 35:906.
  61. Nield LE, Silverman ED, Taylor GP, et al. Maternal anti-Ro and anti-La antibody-associated endocardial fibroelastosis. Circulation 2002; 105:843.
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