Fetal Tachycardia

The normal fetal heart rate ranges from 110-180 beats per minute (bpm) and decreases with gestational age. Fetal tachycardia is defined as a fetal heart rate > 180 bpm.

Abnormalities in fetal heart rate and rhythm occur in 1% of pregnancies. The vast majority are due to benign, intermittent premature atrial contractions. However, 10% are significant arrhythmias that can lead to sustained bradycardia or tachycardia, with the potential for significant morbidity and mortality. The estimated prevalence of fetal tachycardia is 1 in 1,000-2,000 pregnancies (1-3).  

Echocardiography is an invaluable tool for the evaluation of fetal arrhythmia in general and tachycardia in particular, as cardiac electrical activity can be inferred from ultrasound’s temporal mapping of mechanical events. 

Various echocardiographic modalities can assess fetal rhythm. M-mode was one of the earliest modalities employed, and is performed by placing the cursor simultaneously through an atrial and ventricular wall. Indentations in each wall’s motion represents contraction, and ventricular and atrial rates can be compared, though exact intervals between atrial and ventricular contraction cannot be precisely measured (4).

Pulsed Doppler techniques use the timing of blood flow through a chamber or blood vessel to infer mechanical, and therefore electrical, activity. Doppler sampling at a location with closely related atrial and ventricular flow events permits analysis of timing of these flows to each other and within the cardiac cycle. The resulting pulsed Doppler tracing demonstrates the atrioventricular relationship, and the intervals between atrial systole (“A”) and ventricular systole (“V”) (5).  These tracings can be used to estimate the electrical PR interval, and can characterize RP intervals in the presence of tachycardia, which is helpful in delineating the types of tachycardia (see Differential Diagnosis).  In normal sinus rhythm, there is a short AV time and therefore a long VA time.

Three sample locations are typically used. 1) Mitral inflow (A) and left ventricular outflow (V), 2) Superior vena cava (A) and ascending aorta (V), and 3) Pulmonary vein (A) and pulmonary artery (V) (5,6).  The A wave of the mitral inflow represents the atrial contraction while the superior vena cava brief reversal in atrial systole identifies this event.  Atrial systolic flow in the pulmonary vein is usually antegrade, and delineating the beginning of the A wave can be more difficult.

Tissue Doppler imaging (TDI) is another ultrasound modality used to assess fetal rhythm though much less widely. It can measure the interval between atrial contraction and isovolumetric ventricular contraction and thus can also establish A and V relationships (7).

Sinus Tachycardia

When a fetus is noted to have sinus tachycardia, maternal factors such as infection, stress, thyrotoxicosis, and use of sympathomimetic agents such as beta-agonists should be explored as possible causes. Fetal distress, anemia, and infection can also lead to sinus tachycardia (2,8). Fetuses with sinus tachycardia should have heart rate variability, a long VA interval, and a 1:1 relationship between atrial and ventricular contractions. The fetal heart rate is usually less than 200 bpm. Treatment is directed towards the underlying cause of the tachycardia.

Short VA Supraventricular Tachycardia (SVT)

Short VA SVT is the most common type of fetal tachycardia, accounting for up to 60% of cases.  It typically starts with a premature atrial contraction that conducts through the AV node with retrograde conduction through an accessory electrical connection, thereby initiating a reentry circuit (9).  The accessory pathway can be within the AV node itself or another location between the atria and ventricles, though this cannot be distinguished prenatally.  They are collectively referred to as Atrioventricular reentry tachycardia (AVRT).  Heart rates range from 180-300 bpm, with 1:1 A:V conduction and a short VA interval. AVRT usually begins and terminates abruptly, and can be intermittent or sustained (present >50% of the time).        

Long VA SVT

Long VA SVT includes ectopic atrial tachycardia (EAT or AET) and permanent junctional reciprocating tachycardia (PJRT).  Like AVRT, PJRT is caused by an accessory pathway conduction retrograde from the ventricles to the atrium, but the accessory pathway conducts more slowly and tachycardia tends to be more incessant.  EAT is caused by an ectopic atrial focus of electrical activity with a faster rate than the sinus node.  Distinguishing between types of long VA SVT is very difficult prenatally.  Long VA SVT has similar ventricular rate ranges compared to Short VA SVT, although they tend towards the slower end.  EAT may have variable VA conduction whereas PJRT always has 1:1 conduction.  EAT may also have “warmup” and “cool down” periods with variability in the heart rate, a characteristic of automaticity.

Atrial Flutter

Atrial flutter is a subtype of SVT that accounts for roughly 30% of fetal tachycardias (10,11).  It is characterized by very fast atrial rates (300-600 beats per minute) with variable A-V conduction.  Ventricular rates range from normal to ~330 beats per minute).  It typically occurs later in gestation.

Ventricular Tachycardia

Ventricular tachycardia (VT), is caused by abnormal depolarization originating from the ventricles and is extremely rare in fetal life. VT can be caused by deficient myocardial oxygen supply or by myocardial inflammation, and is more often associated with myocardial anomalies such as myocarditis, cardiomyopathy, or intracardiac tumors (9). VT can also be associated with long QT syndrome, a disorder of cardiac repolarization that predisposes patients to ventricular arrhythmias. In all patients with both episodes of VT and bradycardia or heart block, long QT syndrome should be suspected. The hallmark of VT is VA dissociation, with more ventricular contractions than atrial contractions. Rarely, there can be a 1:1 relationship between atrial and ventricular contractions, making it difficult to distinguish from other tachyarrhythmias such as SVT. 

Fetuses with tachycardia should have a complete fetal echocardiogram, as approximately 10% of fetal tachycardias are associated with structural congenital heart disease. Certain tachyarrhythmias such as VT and PJRT can be secondary to cardiomyopathy, and VT can be associated with cardiac tumors such as rhabdomyomas or other anomalies such as cardiac aneurysms. It is critical to closely assess myocardial appearance and ventricular function.

Fetuses with any type of tachyarrhythmia must be closely monitored for hydrops fetalis which can develop as a consequence of significantly impaired cardiac output, poor ventricular filling, and elevated central venous pressures.

Observation with frequent fetal heart rate monitoring is a reasonable management strategy for fetal tachyarrhythmias that are intermittent (occurring <50% of the time), or if the heart rate is <200 beats per minute, though medications may also be considered depending on the combination of rate and frequency.  Principles of pharmacologic therapy include normalization of rhythm, normalization of fetal heart rate, prevention of fetal heart failure, and increasing duration of gestation to term wherever possible. For sustained tachyarrhythmias, the 2014 AHA guidelines recommend the following possible therapies (12):

Hydrops fetalis occurs in about half of all fetuses with tachyarrhythmias, and the overall rate of fetal demise is 9% in untreated cases (1,10). In fetuses who are initiated on transplacental drug therapy, rate or rhythm control is successfully achieved in 80-90% of patients (13).

50% of infants with fetal SVT will go on to develop postnatal SVT (14). Factors associated with increased incidence of postnatal SVT include ventricular dysfunction, sustained fetal SVT, earlier estimated gestational age at delivery, and lack of conversion to sinus rhythm during fetal life (14). Even if SVT recurs postnatally, the long term prognosis is quite favorable, and the majority of infants with prenatal SVT are off all antiarrhythmic medication by one year of age. Atrial flutter is associated with particularly good outcomes, as it almost never recurs once infants undergo electrical cardioversion postnatally.

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