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Case Studies: Fetal Arrhythmias




During the process of heart development, the primitive heart tube produces peristaltic waves of contractions, which suggest the presence of a cardiac pacemaker activity. The first morphological signs of sinus node development are present by 5 weeks of gestation. The heart rate is usually controlled by the sinoatrial (SA) nodal cells. These cells are capable of spontaneously depolarizing and thus acting as a pacemaker. The electrical impulse from the SA node is then propagated across the atria, the atrioventricular (AV) node, and the His-Purkinje system throughout the ventricles, allowing the sequential depolarization of the atrial and ventricular myocardium with each heartbeat. The cardiac mechanical actions, contraction of myocytes in systole, and relaxation in diastole are then orchestrated by rapid cyclic changes in their transmembrane action potentials and ion currents with each heartbeat. Following depolarization, the conducted impulse is prevented from immediately reactivating the conduction system and myocardium by refractoriness of the tissue that just has been activated. The heart must then await a new electrical impulse from the SA node to initiate the next heartbeat.

By 5– 6 weeks of gestation, the normal mean fetal heart rate (FHR) is 110 beats/min (bpm). With further growth and maturation of the conduction system, with the SA node serving as the primary cardiac pacemaker with its highest intrinsic rate of spontaneous depolarization, there is a subsequent increase in the rate to 170 bpm by 9–10 weeks of gestation. The rise in heart rate is followed by a decrease to 150 bpm by 14 weeks, likely as a consequence of increasing parasympathetic control and improved myocardial contractility. By 20 weeks the average FHR is 140 bpm with a gradual decrease to 130 bpm by term. In the healthy fetus, the heart rate is regular and usually remains between 110 and 180 bpm, and has a beat-to-beat variation of 5–15 bpm.

Fetal arrhythmias are typically classified into three groups: fetal tachyarrhythmias (fetal heart rate > beats/min [bpm]), fetal bradyarrhythmias (fetal heart rate < 100 bpm), and irregular cardiac rhythm. They are diagnosed in 1% to 3% of all pregnancies. Benign episodes of fetal bradycardia can occur during a second trimester screening scan, but they quickly recover to normal values, especially if maternal abdominal pressure of the ultrasound transducer is reduced. Note that mild tachycardia (>160?bpm) can transiently occur in normal fetuses. The following table outlines the classification of fetal dysrhythmias.




The majority of cases represent ectopic premature atrial contractions (PACs), also known as isolated extrasystoles, which are benign in most cases. In approximately 10% of pregnancies complicated by fetal arrhythmias the arrhythmia may be potentially life-threatening. In addition, some arrhythmias, bradyarrhythmias in particular, may be associated with structural heart disease. Thus, a fetal echocardiogram is warranted to assess the structural integrity of the fetal heart whenever there is concern for a fetal arrhythmia.


Motion mode imaging (M-mode) and pulsed-wave Doppler (PWD) echocardiography are the 2 ultrasound-based techniques used to assess fetal arrhythmias. M-mode detects motion of structures through time, and this provides very useful information regarding fetal arrhythmia assessment. With M-mode, the ultrasound beam (M-mode cursor or line) is usually placed to intersect both the atrium and ventricle, enabling atrial and ventricular wall movements to be recorded simultaneously (Fig. 1). Suboptimal fetal position and poor image quality may limit M-mode’s clinical utility. In addition, with M-mode, details about atrial and ventricular contractions, such as the onset and peak, are difficult to define, limiting its ability to measure atrioventricular (AV) time intervals.

In contrast to M-mode, which provides a representation of movement over time, PWD assesses blood flow over time. Pulsed-wave Doppler helps identify temporal cardiac events and allows for identification of various time intervals by its ability to acquire simultaneous signals from atrial and ventricular contractions (Fig. 2). Such information is important to obtain when classifying arrhythmias. Pulsed-wave Doppler is usually independent of fetal position and image quality, offering an advantage over M-mode. In PWD, the pulsed Doppler gate (i.e. sample volume) is placed across the mitral and aortic valves. Doppler waveforms are biphasic in shape for AV valves (mitral and tricuspid) and are uniphasic in shape for the semilunar (aortic and pulmonic) valves.



TIP: During assessment for a possible fetal arrhythmia a key point is confirming the presence of 1:1 AV conduction. This simply means that every atrial beat is followed by an appropriately timed ventricular beat. The presence (or lack of) 1:1 AV conduction will help narrow down your differential diagnosis with regards to the specific fetal arrhythmia. Both M-mode and PWD may be used.


Supraventricular tachycardia (SVT) is the most common cause of fetal tachycardia, accounting for 66% to 90% of all cases. Atrial flutter is the second most common cause, responsible for 10% to 30% of cases. Other types of tachycardia include sinus tachycardia, atrial fibrillation, and ventricular tachycardia (VT). Structural congenital heart disease (CHD) is reported to occur in 1% to 5% of cases of fetal tachycardia.

Supraventricular tachycardia is usually due to an accessory pathway that exists between the atrium and ventricle, resulting in an AV reentry tachycardia. The fetal heart rate typically is around 220 to 240 bpm, with a 1:1 ratio of AV conduction (Fig. 3). There is no variation in either the atrial or ventricular rate. Approximately 90% of fetal SVT is due to a reentry circuit that is formed by an accessory pathway between the atrium and ventricle, which allows for retrograde conduction via fast reentry from the ventricle to the atrium.

In contrast to SVT, in sinus tachycardia, fetal heart rate variability is present. As seen with SVT, 1:1 AV conduction is present. Causes of sinus tachycardia include maternal fever, infection, fetal distress, and maternal use of drugs such as betamimetics.

Atrial flutter is defined by a rapid regular atrial rate of 300 to 600 bpm. In contrast to SVT, AV conduction is rarely 1:1, with variable degrees of AVB that result in a slower ventricular rate, typically around 220 to 240 bpm (Fig. 4). The AV conduction block is 2:1 in 80% of cases and 3:1 in the remainder of cases.



Figure 4. Atrial flutter with 2:1 AV block. The atrial rate is 414 bpm, and the ventricular rate is 207 bpm (A=atrial beat, V=ventricular beat).



Causes of bradycardias include sinus bradycardia, blocked PACs seen in atrial bigeminy, and AVB, of which the latter is the most important to identify. Transient episodes of sinus bradycardia may be common in the first and second trimester of pregnancy, and they are benign. Pressure on the maternal abdomen from the ultrasound probe can result in a transient bradycardia due to vagal stimulation.

In atrial bigeminy, every other atrial beat is premature and not conducted to the ventricle (i.e. blocked in the AV node), resulting in a slow ventricular rate, typically 70 to 80 bpm (Fig. 5). Usually, atrial bigeminy is benign and does not warrant treatment. However, for reassurance, increasing the frequency of fetal auscultation is prudent. In a small number of cases, a tachyarrhythmia may develop.

Atrioventricular block is associated with normal atrial activity and a disturbance of electrical conduction. Complete heart block (CAVB) occurs in up to 1 in 22,000 newborns, although the overall incidence of fetal heart block is unknown. In third-degree or complete AVB there is complete interruption of AV conduction so that the atria and ventricles beat independently. It is essential to distinguish the usually benign atrial bigeminy (i.e., blocked PACs) from the pathologic bradycardia due to AVB. In the former, the atrial rate is irregular, whereas the atrial rate is regular in AVB.  Up to 40% of CAVB cases are seen in fetuses with structural CHD, particularly left atrial isomerism (heterotaxy syndrome), and congenitally corrected transposition of the great arteries. If structural disease is not present, then most cases of CAVB are due to immune-mediated damage to the AV node, most commonly involving anti-Ro (SS-A) or anti-La (SS-B) antibodies. These are maternal immunoglobulin G antibodies that are present in the setting of maternal connective tissue disease (i.e., systemic lupus erythematosus or Sjogren syndrome). In the presence of anti-SSA/ SSB antibodies, the risk of CAVB is 1% to 2%. The recurrence risk ranges from 14% to 17%. When a fetus is at risk of developing CAVB, the mechanical PR interval is often assessed.


Figure 5. M-mode imaging demonstrating fetal bradycardia due to atrial bigeminy. In this case, every atrial beat (A) is conducted to the ventricle where there is a ventricular beat (V). Each atrial beat is followed by a premature beat (AE). The ventricular rate is 84 bpm.


The PR INTERVAL: What It Is and How Is It Measured

The PR interval is the time it takes for the electrical impulse to travel from the SA node to the bundle of His. It represents the onset of the atrial contraction (i.e. atrial systole) to the onset of the ventricular systole (i.e. ventricular systole), and the normal measurements is 120-150 milliseconds. On an electrocardiogram it corresponds to the electrical P and QRS waves. Since both atrial and ventricular contractions need to be assessed, the location for PR interval assessment requires both left ventricular inflow, which corresponds to atrial systole, and left ventricular outflow, which corresponds to ventricular systole. PWD of the mitral valve is an ideal location to assess the PR interval, as the spectral display provides information on both left ventricular inflow and outflow. The reason both inflow and outflow can be assessed is that the mitral valve and aortic valves reside close to each other, thus interrogation of the mitral valve will also provide information about the aortic valve. Figure 6 indicates the location of where to place the Doppler gate to assess both left ventricular inflow and outflow.



When interrogating the mitral valve with PWD, a biphasic waveform is obtained. The first peak of is known as the E-wave, which corresponds to peak opening of the valve during early ventricular filling in diastole. The second peak in the biphasic waveform is known as the A-wave, which corresponds to the atrial contraction, also known as the atrial ‘‘kick’’ (i.e. active ventricular filling). In the fetus, in contrast to postnatal life, the velocity of the A-wave is higher than that of the E-wave. This is thought to be due to increased cardiac muscle stiffness during fetal life.  The mechanical PR interval is measured from the onset of the A-wave to the onset of ventricular systole. Figure 7 illustrates these principles.




Irregular rhythm is the most common reason for referral and the most common fetal arrhythmia. Most fetuses with irregular fetal heart rhythm are found to have PACs, also known as isolated atrial extrasystoles. These premature beats may or may not be conducted to the ventricle (Fig. 8). Rarely, premature beats originate in the ventricle (premature ventricular contractions [PVCs]). Most PAC’s and PVC’s are benign and resolve spontaneously, and they are not associated with fetal distress. However, in 2% to 3% of cases, there may be progression to tachycardia (typically SVT, al- though atrial flutter is possible), which may occur in the setting of multiple blocked PACs (as noted above in atrial bigeminy). Extra systoles do not warrant de- livery, although if they persist during labor, then fetal monitoring may prove difficult with standard fetal heart rate monitoring. For reassurance, an increased frequency of fetal auscultation is reasonable.





Abuhamad A, Chaoui R. Fetal arrhythmias. In: Abuhamad A, Chaoui R, eds. A Practical Guide to Fetal Echocardiography. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:351-365.

Bravo-Valenzuela NJ, Rocha, LA, Machado LM, Araujo Junior, E. Fetal cardiac arrhythmias: Current evidence. Ann Pediatr Cardiol 2018;11:148–163.

Carvalho JS. Best Pract Res Clin Obstet Gynaecol 2019;58:28-41. 

Hornberger LK, Sahn DJ. Rhythm Abnormalities of the Fetus. Heart 2007;93:1294-1300.

Jaeggi E, Ohman A. Fetal and Neonatal Arrhythmias. Clin Perinatol 2016;43:99–112.

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