1. What every clinician should know
Clinical features and incidence
Fetal tachycardia is defined as a heart rate greater than 160-180 beats per minute (bpm). This rapid rate may have a regular or irregular rhythm which may be intermittent or sustained. A sustained fetal tachyarrhythmia is uncommon, affecting fewer than 1% of all pregnancies.
There are a number of maternal conditions that increase the likelihood of tachycardia in the fetus. Hyperthyroidism secondary to thyroid stimulating antibodies, fever associated with systemic infections and substance abuse may result in an increase in the fetal heart rate above the normal range. Beta-agonists used in the treatment of asthma or for tocolysis can cross the placenta and cause a fetal tachycardia. Fetal tachycardia also can be the presenting sign of intrauterine infection and chorioamnionitis and associated with metabolic derangements in the fetus.
In addition to extrinsic factors, congenital heart disease predisposes the fetus to the development of a tachyarrhythmia. Ectopic beats, even in the presence of a normal fetal heart, increase the probability of a fetus developing a sustained tachyarrhythmia.
2. Diagnosis and differential diagnosis
A. Establishing the diagnosis
The diagnosis of fetal tachycardia is usually made during office auscultation or at the time of an ultrasound scan. A fetal heart rate of over 160-180 bpm requires a thorough maternal history and examination, screening for potential precipitating factors. A history of leakage of fluid per vagina or uterine tenderness on palpation may indicate intrauterine infection. Fetal tachycardia in labor may indicate the presence of chorioamnionitis or the development of metabolic acidemia. Thyroid function tests, CBC with differential, samples for culture and sensitivity, and a urine toxicology screen may be indicated.
A comprehensive fetal anatomic survey with particular attention to the screening views of the heart should be performed. A significant tachyarrhythmia can lead to the development of hydrops so an assessment for pericardial, pleural, ascitic and subcutaneous fluid is indicated. (Figure 1) Amniotic fluid volume should also be quantified, as oligohydramnios may indicate membrane rupture while polyhydramnios is often associated with congestive heart failure secondary to a sustained tachyarrhythmia.
A detailed fetal echocardiogram is also warranted to firmly establish the rate and rhythm, confirm normal cardiac anatomy and assess any hemodynamic consequences related to the tachycardia. In addition to standard two-dimensional imaging and color flow mapping, M-mode and pulsed Doppler are critical for the characterization of a fetal arrhythmia.
B. Differential diagnosis
While the diagnosis of a fetal tachycardia is simple, establishing the nature of the tachycardia often requires further evaluation and consultation with an expert in fetal echocardiography such as a maternal-fetal medicine specialist, radiologist or pediatric cardiologist. Fetal sinus tachycardia is most commonly seen in cases related to maternal conditions, such as Graves’ disease or infection, or secondary to drug use. The fetal heart rate is usually less than 200 bpm and tends to resolve once the precipitating condition is corrected or exposure eliminated. In this type of tachycardia, there is 1-to-1, atrial-to-ventricular conduction with origin from the sinus node.
In contrast, extra beats are triggered by ectopic foci in the wall of the heart and result in an irregular rhythm of the fetal heart rate. Premature atrial contractions (PACs) and premature ventricular contractions (PVCs) affect 1-2% of all pregnancies and are responsible for over 90% of arrhythmias detected in utero, with atrial extrasystoles being most common. (Figure 2 and Figure 3) Ectopic beats occur earlier than expected and may be followed by a ventricular contraction. The subsequent atrial contraction tends to be delayed due to a compensatory pause.
In some cases, the ectopic beats can couple to sinus beats leading to atrial bigeminy or trigeminy. (Figure 4 and Figure 5) These extra beats are believed to be secondary to immaturity of the fetal conduction system and tend to resolve spontaneously with advancing gestational age. As a result, in the absence of underlying cardiac malformations or tumors stimulating these foci, extrasystoles are considered benign, well tolerated and generally do not require any in utero treatment. (Figure 6 and Figure 7) However, in 2-3% of cases, progression to a clinically significant arrhythmia occurs.
Tachyarrhythmias, such as supraventricular tachycardia, atrial flutter and atrial fibrillation, are usually intrinsic to the fetus with the potential to adversely impact fetal well-being. Overall, these serious tachyarrhythmias comprise less than 10% of arrhythmias detected prenatally. The most common tachyarrhythmia is supraventricular tachycardia (SVT), representing up to 5% of all fetal arrhythmias. Both pulsed Doppler and M-mode echocardiography can be used to recognize SVT which tends to have an atrial rate of 220 to 240 bpm with 1-to-1 atrioventricular conduction. (Figure 8)
This rapid atrial reactivation occurs as a result of a fast-conducting, accessory pathway that permits reentry of electrical activity from the ventricle to atrium. SVT may be sustained or intermittent in response to frequent atrial extrasystoles. Congenital heart disease is found In up to 5% of SVT cases and hydrops fetalis in 30-50%.
While SVT is the most likely intrinsic cause of fetal tachycardia, atrial flutter and atrial fibrillation are other possibilities. The distinction often is made using M-mode echocardiography to demonstrate the characteristic saw-tooth appearance of atrial contractions in cases of flutter or the irregularly irregular appearance of atrial activity in fibrillation. In SVT the atrial and ventricular rates are the same; in atrial flutter and fibrillation, these rates are different depending on the degree of atrioventricular block.
There tends to be no relationship between atrial and ventricular activity in atrial fibrillation due to blocked conduction, and in atrial flutter there can be 2-1, 3-1, or even 4-1 conduction with atrial rates over 300-400 bpm. Atrial flutter and fibrillation are relatively uncommon, and ventricular tachyarrhythmias exceedingly rare when compared to fetal SVT.
Extrinsic causes of fetal tachycardia should be identified and treated appropriately. Sinus tachycardia secondary to maternal hyperthyroidism can be managed with antithyroid medications such as methimazole. Antibiotics are necessary for maternal systemic infections and acetaminophen can be used short-term to reduce maternal fever and subsequently to normalize the fetal heart rate. Any drugs that may precipitate a sinus tachycardia should also be discontinued. Unfortunately, intrauterine infection with chorioamnionitis is an indication for evacuation of the delivery, which may result in a termination of pregnancy or preterm delivery rather than a term birth.
Although PACs and PVCs can trigger the onset of SVT, they are benign without significant sequelae in the majority of cases. A fetal echocardiogram should be obtained when these extra beats are detected to exclude associated heart anomalies and to confirm the diagnosis. Smoking, alcohol, and ingestion of caffeine-containing products should be eliminated. Serial surveillance with office auscultation or ultrasound examination every 1-2 weeks is recommended in these cases until no further extrasystoles are detected. If a fetal tachycardia is discovered on follow-up assessments, repeat fetal echocardiography and consultation with pediatric cardiology is advised.
Unlike extrasystoles, fetal tachyarrhythmias may require intervention depending on gestational age, coexisting congenital heart disease and risk for hemodynamic compromise. This risk depends on the fetal heart rate, the type of tachyarrhythmia, and whether it is intermittent or sustained. The presence of hydrops indicates that the tachyarrhythmia is not well tolerated and that medical therapy or delivery should be considered based on gestational age. When major heart defects are also present and the prognosis is poor, expectant management may be desired by the patient and her family
In the absence of hemodynamic compromise and hydrops, expectant management may also be reasonable for cases of intermittent SVT. For SVT that occurs less than 50% of the time over a 24-hour period of observation, spontaneous resolution is common over a period of days to weeks. However, frequent reassessments are necessary to exclude conversion to a sustained SVT so many patients and practitioners elect to proceed with medical therapy if remote from term. In utero conversion to normal sinus rhythm involves the administration of antiarrhythmic agents to the mother.
Digoxin is the most commonly used drug for fetal SVT, administered to the mother at a dose of 0.25 mg every 8 hours orally to reach maternal plasma levels of 0.8-2 ng/ml. Despite the safety of digoxin, consultation with adult cardiology is recommended when prescribing antiarrhythmic agents to pregnant women. A thorough baseline cardiac evaluation including an electrocardiogram is warranted for comparison to subsequent testing after the initiation of medial therapy. This is even more important when proarrhythmic drugs such as flecanide or procainamide are used. Flecanide is often used as the second-line agent if digoxin fails to result in cardioversion.
Even in the absence of achieving sinus rhythm, decreasing the fetal heart rate below 200 bpm lowers the risk of hemodynamic compromise. In cases of hydrops, the transplacental transfer of digoxin is decreased so flecanide is often used as first-line therapy. Sotalol is another commonly used second-line agent in the treatment of fetal tachyarrhythmias. Overall, the administration of antiarrhythmic drugs to the mother results in successful cardioversion in 80-90% of cases.
However, this is reduced to 65-75% in cases of hydrops and even when normal sinus rhythm is restored, it takes weeks for the hydrops to resolve. Similar treatment approaches are used for atrial flutter and fibrillation but the goal is often just to control the rate as these tachyarrhythmias are much more difficult to convert to sinus rhythm.
Regardless of whether the cause of the tachycardia is extrinsic or intrinsic to the fetus, persistent fetal tachycardia during the intrapartum period limits the ability to monitor the fetal response to labor to ensure fetal well-being. New-onset fetal tachycardia in labor may indicate intrauterine infection or fetal acidemia, so prompt evaluation, judicious interventions and timely delivery is indicated.
Unresolved maternal conditions causing fetal sinus tachycardia or unsuccessfully treated fetal tachyarrhythmias will almost certainly require cesarean delivery unless nonintervention is planned due to a coexisting cardiac malformation. A trial of labor with vaginal delivery can be considered in cases with spontaneous or medically-induced conversion to normal sinus rhythm. Regardless of the planned mode of delivery, neonatologists and pediatric cardiologists experienced in the management of tachyarrhythmias should be available for the immediate evaluation of the newborn.
A normal post-operative course is expected for those requiring a cesarean delivery and normal postpartum course for those having a vaginal birth. Any antiarrhythmic agent administered to the mother can be discontinued. Bonding and breastfeeding may be delayed if the baby requires lengthy observation in the neonatal intensive care unit and prolonged hospitalization. Overall, a normal postpartum course is expected.
A. Complications as a consequence of the condition
The major risks of fetal tachycardia are hemodynamic compromise, development of hydrops and intrauterine fetal death. The best strategy to avoid these complications is to identify and treat maternal conditions causing fetal sinus tachycardia and to deliver term pregnancies or medically manage preterm pregnancies with fetal tachyarrhythmias that have features associated with a poor prognosis. Fetal tachycardia due to intrauterine infection or fetal acidemia may be associated with adverse outcomes such as neonatal asphyxia, hypoxic-ischemic encephalopathy and cerebral palsy.
B. Complications as a consequence of management
Both maternal and fetal adverse effects have been reported secondary to the administration of antiarrhythmic agents in pregnancy. While prolongation of the PR interval can convert the fetus with SVT into sinus rhythm, the same effect can be detrimental to a healthy mother. Proarrhythmic drugs can result in life-threatening arrhythmias in the mother and cases of sudden death in the fetus. Careful drug selection in consultation with pediatric and adult cardiologists and close follow-up of both patients are required for optimal management of fetal tachyarrhythmias requiring maternal medical therapy.
5. Prognosis and outcome
A. Maternal and fetal/neonatal outcomes
The outcome of pregnancies complicated by fetal tachycardia is related to the underlying cause of the arrhythmia. PACs and PVCs are benign and the prognosis is excellent. In cases where these extrasystoles result in SVT and in utero medical therapy is successful, a favorable outcome is also expected. The majority of these infants are treated with antiarrhythmic agents for 12 months and about 80% will not require any intervention beyond that first year.
In those with a sustained tachyarrhythmia, antiarrhythmic drugs or ablation of accessory pathways in cases of SVT may be required. In these cases, the prognosis remains good but is more guarded if there is coexisting structural heart defects. Fetal tachycardia related to chorioamnionitis or metabolic acidemia also tends to have a favorable outcome but may be associated with permanent neurologic injury related to the inciting condition.
B. Impact on long term health
In general, fetal tachyarrhythmias have no lasting impact on a woman’s well-being apart from an increased risk for cesarean delivery and its implications on future health. If a chronic condition such as Graves’ disease or substance abuse precipitated a fetal tachycardia, appropriate referral and treatment is required to optimize long-term prognosis. Loss of a pregnancy from intrauterine infection or birth of a preterm infant due to membrane rupture and chorioamnionitis may complicate a patient’s physical and mental health. Neurological impairment or complications of prematurity in survivors can also have psychological consequences on parental well-being. However, in the majority of cases of fetal tachycardia a favorable maternal outcome is anticipated.
6. What is the evidence for specific management and treatment recommendations
Cuneo, BF. “Treatment of fetal tachycardia”. Heart Rhythm. vol. 5. 2008. pp. 1216-8. (Review of the treatment options for fetal tachycardia.)
Lopriore, E, Aziz, MI, Nagel, HT, Blom, NA, Rozendaal, L. “Long-term neurodevelopmental outcome after fetal arrhythmia”. Am J Obstet Gynecol. vol. 201. 2009. pp. 46.e1-5. (One of few studies looking at neurodevelopment outcomes of tachyarrhythmias.)
Kleinman, CS, Nehgme, RA. “Cardiac arrhythmias in the human fetus”. Pediatr Cardiol. vol. 25. 2004. pp. 234-51. (Wonderful review by the "father" of fetal echocardiography, the late Charlie Kleinman.)
Matta, MJ, Cuneo, BF. “Doppler echocardiography for managing fetal cardiac arrhythmia”. Clin Obstet Gynecol. vol. 53. 2010. pp. 899-914. (Reviews the diagnosis and treatment of fetal dysrhythmias.)
Rasiah, SV, Ewer, AK, Miller, P, Kilby, MD. “Prenatal diagnosis, managment and outcome of fetal dysrhythmia: a tertiary fetal medicine centre experience over an eight-year period”. Fetal Diagn Ther. vol. 30. 2011. pp. 122-7. (Experience of a single referral center.)
Simpson, JM. “Fetal arrhythmias”. Ultrasound Obstet Gynecol. vol. 27. 2006. pp. 599-606. (Another good review of fetal dysrhythmias.)
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?”. Pacin Clin Electrophysiol. vol. 31. 2008. pp. S54-7. (Discussion of treatment approach of fetal tachycardia.)
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- Fetal Tachycardia
- 1. What every clinician should know
- 2. Diagnosis and differential diagnosis
- 3. Management
- 4. Complications
- 5. Prognosis and outcome
- 6. What is the evidence for specific management and treatment recommendations