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1994-07-14-18 Supraventricular tachycardia © Joffe
Supraventricular tachycardia

Gary M. Joffe, MD, Luis Izquierdo, MD, Anita Brown, RNC

Address correspondence to Gary M. Joffe, MD, Lovelace Medical Center, 5400 Gibson Blvd., S.E., Albuquerque, NM 87108-9980. Ph: 505-262-7752, Fax: 505-262-3571, ¶University of New Mexico Medical Center, 2211 Lomas Blvd., N.E., Albuquerque, NM 87131-5286

Synonyms: Atrial flutter, atrial fibrillation, ventricular tachycardia, and sinus tachycardia are tachyarrhythmias with different underlying electrophysiologic mechanisms.

Definition: Fetal cardiac rhythm disturbance characterized by sustained fetal heart rate between 220-260 beats per minute.

Prevalence: Four to fifteen percent of patients referred for audible fetal cardiac arrhythmia1.

Etiology: Caffeine, smoking, illicit drugs, fetal cardiac malformation and extracardiac malformation (diaphragmatic hernia) may contribute to frequent fetal premature atrial contractions which may progress to unrelenting tachyarrhythmia.

Pathogenesis: An extrasystole triggers a wave of depolarization that initiates a circular movement within the atrioventricular nodal tissue or between atrioventricular nodal tissue and an extranodal bypass tract resulting in reentrant tachycardia. Supraventricular tachycardia may result in cardiac failure, hydrops, and fetal demise. Supraventricular tachycardia results in shortened ventricular diastolic filling time in fetal ventricular cardiac tissue that may have less compliance than the adult counterpart. This fetal emergency may lead to congestive heart failure, hydrops, or fetal demise.

Associated anomalies: While supraventricular tachycardia is rarely associated with congenital cardiac anomalies (2%), atrial flutter and fibrillation have been associated with an increased incidence of pulmonary outflow obstruction, Ebstein malformation, and atrioventricular septal defect. Atrial fibrillation has been seen in association with congenital diaphragmatic hernia.

Prognosis: In utero therapy with antiarrhythmic medications has resulted in less than 10% perinatal mortality.

Management: Diagnosis of the type of arrhythmia, gestational age of the fetus, presence of hydrops fetalis, and presence of other anomalies guide the choice of antiarrhythmic agent and whether to treat in utero or ex-utero.

MESH Supraventricular tachycardia CDC 427 ICD9 427.000(*)


Fetal cardiac rhythm disturbances generally take the form of isolated extrasystoles that are of no consequence to the health of the gestation. Tachyarrhythmias, on the other hand, may result in fetal congestive heart failure and in utero fetal demise. The following case report describes the diagnosis and management of fetal supraventricular tachycardia. This will be followed by a discussion of underlying pathophysiology, diagnosis and management of this fetal emergency.

Case report

The patient is a 30-year-old G3P1011 with an estimated gestational age at initial evaluation of 25 weeks and 4 days. She was referred to the antenatal assessment unit at our institution secondary to an audible fetal tachycardia noted at her routine prenatal visit with her practitioner. Real-time ultrasound assessment revealed a singleton intrauterine pregnancy with marked fetal ascites and anasarca (fig. 1).

Figure 1: At 25 weeks 4 days, the liver and small bowel are surrounded by ascitic fluid.

The anatomical survey exclusive of the cardiac evaluation was completely within normal limits. The 4-chamber view of the heart did not demonstrate evidence of ventricular or atrial septal defect. All four valves were in their proper location, and the aorta and pulmonary artery arose normally from the left and right ventricles, respectively. The foramen ovale flap appeared to move to the left within the left atrium. The left atrium was moderately enlarged. Most significant was the finding on M-mode echocardiographic examination of supraventricular tachycardia with a rate of 270 beats per minute (fig. 2).

Figure 2: M-mode echocardiogram demonstrating supraventricular tachycardia with a 1:1 atrioventricular conduction. The M-mode cursor is directed through the enlarged left atrium (inferior portion of the inset) and the aortic valve (center). The time between vertical bars is 1 second.

Other pertinent obstetrical history was that of a negative indirect Coombs titer. There was no maternal or family history of cardiac disease, and the patient did not consume excessive amounts of caffeine. The patient was admitted for administration of antiarrhythmic therapy. She was started on a regimen of Digoxin, with a loading dose of 0.5 mg followed by 0.25 mg every 6 hours. Despite maternal serum digoxin levels that were in the therapeutic range, the fetus demonstrated conversion to a normal sinus rhythm for only short periods of time. After 4 days of digoxin therapy, Sotalol 120 mg was added to the regimen. This was followed by resolution of the tachyarrhythmia on day two of the dual medication regimen. There was no evidence of any recurrence of the supraventricular tachycardia for the remainder of the pregnancy. Fetal ascites was absent two weeks after re-establishment of sinus rhythm (fig. 3,4). Induction was carried out at 38 weeks of gestation, and the patient successfully delivered a 2838g male infant with APGARs of 9 and 9 at 1 and 5 minutes, respectively. After a 3-day period of neonatal cardiac monitoring, the patient and her baby were discharged in stable condition. The neonate is healthy six weeks after delivery with no evidence of cardiac rhythm disturbance.

Figure 3: The M-mode cursor is directed through the enlarged left atrium after re-establishment of the sinusal rhythm of 180 beats per minute.
Figure 4: Resoluation of the ascites, three weeks after resumption of the normal sinusal rhythm.



In a series of 984 patients referred for evaluation of audible fetal arrhythmias, the number of fetuses demonstrating supraventricular tachycardia was 47 (4.8%)2. In the same series, of the 878 patients who originally had the echocardiographic diagnosis of isolated extrasystoles, three returned later in gestation with supraventricular tachycardia and hydrops fetalis (0.3%).

Etiology and pathogenesis

There are three forms of abnormal conduction which may result in supraventricular tachycardia, defined as incessant fetal tachycardia with rates between 220-260 beats per minute. The first form is that of atrioventricular nodal reentrant tachycardia, in which two pathways with differing conduction velocities and refractory periods are located within the atrioventricular node. An extrasystole generates an electrical wavefront of depolarization that arrives at the atrioventricular node (fig. 5). The "fast tract" pathway within the atrioventricular node is refractory to the arriving wave of depolarization; the "slow tract" has recovered sufficiently from its prior depolarization to depolarize again with the arrival of the extrasystolic wavefront. However, the His-Purkinje system is still refractory from the prior "normal" depolarization. At precisely the right time, the "fast tract" within the atrioventricular node becomes repolarized and accepts the wavefront from the "slow tract" and depolarizes in a retrograde fashion, re-entering atrial tissue. Depolarization occurs through the fastest conduction pathway available, and so this "circular movement" predominates over the slower impulses generated by the sinoatrial node.

In atrioventricular reentrant tachycardia, the same "circular movement" is established, but the "fast tract" limb of the pathway occurs outside of the atrioventricular node (fig. 6). This pathway directly connects the atria and ventricular myocardium and is known as the Wolff-Parkinson-White syndrome. The final mechanism for supraventricular tachycardia is that of automatic atrial tachycardia resulting from a discreet pacemaker within the atrium outside of the sinoatrial node. Atrial flutter and fibrillation, characterized by rates of 400-460 beats per minute in the fetus, result from "circular pathways" within the atria themselves rather than in atrioventricular nodal or atria-ventricular connecting pathways2.

Figure 5: Three causes of supraventricular tachycardia: atrial flutter (left), ectopic atrial tachycardia (middle) and circular electrical dipolarization within atrioventricular node (right). The atria respond to the fastest wavefront of depolarization (bottom panel). The aberrant pathway has a faster rate of depolarization than pathways from sinoatrial node.
Figure 6: Wolff-Parkinson-White syndrome demonstrating circular electrical depolarization through the atrioventricular node and an aberrant conduction pathway directly linking atria and ventricles.


The diagnosis of supraventricular tachycardia is established using M-mode echocardiography, which may demonstrate paroxysms of atrial tachycardia in the range of 220-260 beats per minute, often following an extrasystole. M-mode echocardiography uses a sampling line placed across atrial and ventricular walls and times electromechanical events in the fetal cardiac cycle. Atrial flutter and fibrillation are characterized by much faster rates, and often with varying degrees of atrioventricular block. Abrupt onset and arrest of tachycardia can often be seen.

Associated anomalies

Supraventricular tachycardia is rarely associated with intra- or extracardiac anomalies, in contrast to those fetuses with atrial flutter or fibrillation. Intracardiac anomalies include Ebstein malformation, atrioventricular septal defect and pulmonary outflow obstruction. Congenital diaphragmatic hernia has also been associated with fetal atrial fibrillation.

Differential diagnosis

The differential diagnosis for supraventricular tachycardia includes atrial flutter, atrial fibrillation, ventricular tachycardia, and sinus tachycardia. Sinus tachycardia is established with a baseline fetal heart rate between 160 and 220 beats per minute. Maternal infection and thyroid dysfunction should be ruled out in these patients.


The management of the fetus with a normal anatomical survey and supraventricular tachycardia is dependent upon the gestational age at diagnosis, and the presence or absence of hydrops fetalis. In the non-hydropic fetus in whom fetal lung maturity can be demonstrated, delivery with evaluation and treatment of the neonate should be considered. At earlier gestational ages, treatment ideally should be directed at the exact underlying electrophysiologic aberration responsible for the arrhythmia. Unfortunately, this is exceedingly difficult to define for the fetus. Therefore, pharmacologic agents are prescribed on the basis of the arrhythmia itself, rather than on the precise knowledge of the location of the abnormal conduction pathway(s). For example, if digoxin therapy results in atrioventricular nodal block without resolution of the arrhythmia, then atrioventricular nodal reentrant tachycardia and atrioventricular reentrant tachycardia have been ruled out in an indirect fashion2.

Given the above limits of diagnosis, digoxin remains the drug of first choice for the treatment of supraventricular tachycardia. Digoxin at therapeutic levels terminates "circular movements" within reentrant circuits by prolonging the refractory phase so that the aberrant wave of excitation reaches depolarized tissue. There is debate as to the effective levels of digoxin reaching the cardiac conduction system of the hydropic fetus3,4, but larger series of patients have demonstrated resolution of supraventricular tachycardia in a significant number of these cases2. Second line medications such as sotalol hydrochloride7, which was given to the patient described above, depress atrioventricular nodal conduction, produce an increase in the duration of the action potential and lengthen the effective and absolute refractory periods5. Sotalol prolongs action potential duration, lengthens the refractory period, prolongs the cycle length of tachycardia, and prevents it from deteriorating into fibrillation7.


Combined series of patients with supraventricular tachycardia which were treated in utero suggest a perinatal mortality rate of 5% (3/56)2,6. The prognosis for atrial flutter and atrial fibrillation is not as good, suggesting greater difficulty in controlling the arrhythmia, and a higher incidence of intra- and extracardiac anomalies. Given the observations of the cited investigators, perhaps a reasonable management approach to the fetus with supraventricular tachycardia is to determine whether hydrops fetalis is in evidence. If not present, then a trial of transplacental therapy with digoxin may be started and further medications and more invasive therapies reserved for refractory arrhythmia. For the fetus with supraventricular tachycardia and fetal hydrops, perhaps early direct intervention either in the form of fetal intramuscular injection of digoxin3,4 or umbilical venous administration of adenosine2, will result in a rapid break in the arrhythmia. Adenosime is generally administered as a rapid intrvenous bolus at a dosage of 100 to 200 mg/kg of estimated dry body weight8. The extremely short half life means that it must be delivered by betal umbilical vein rather than maternal I.V. route. This may then be combined with maternal administration of digoxin for arrhythmia prophylaxis.

In summary, the diagnosis of fetal arrhythmia can be made using M-mode echocardiography, but presently it is not possible to completely identify its precise electropathophysiologic mechanism. In retrospect, given the degree of fetal compromise at presentation of the patient described above, soon after initiation of maternal digoxin therapy, direct fetal therapy might have been considered to break the arrhythmia. Recognition and aggressive transplacental and direct treatment of fetal supraventricular tachycardia have led to significantly improved prognosis for those who manifest this disease.


1. Schmidt KG, Silverman NH. The fetus with a cardiac malformation. In Harrison M, Golbus M, Filly R (eds): The unborn patient. Second Edition. Philadelphia W.B. Saunders Company, 1991.

2. Kleinman CS, Copel JA. Fetal cardiac arrhythmias: diagnosis and therapy. Eighth International Fetal Cardiology Symposium. March 11-12, 1994, Atlanta, Georgia.

3. Weiner CP, Thompson MI. Direct treatment of fetal supraventricular tachycardia after failed transplacental therapy. Am J Obstet Gyn 158;570-573 March 1988.

4. Hallak M, Neerhof MG, Perry R, et al.: Fetal supraventricular tachycardia and hydrops fetalis: combined intensive, direct, and transplacental therapy. OB/Gyn Vol. 78.No.3, Sept 1991.

5. Camm AJ, Paul V. Sotalol for paroxysmal supraventricular tachycardias. Am J Cardiol 65:67A-83A, 1990.

6. Smith MBH, Colford D, Human MA. Perinatal supraventricular tachycardia. Can J Cardiol 8:565-568, 1992.

7. Singh BN: Historical development of the concept of controlling cardiac arrhythmias by lenghtening repolarization: particular reference to Sotalol. Am J Cardiol 65:3A-36A, 1990.

8. Kleinman CS, Copel JA. Fetal Cardiac Arrhythmias: Diagnosis and Therapy. Maternal Fetal Medicine 3rd Edition p:339, 1994.

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