Cardiac ectopy, composed of premature atrial (PACs) and ventricular contractions (PVCs), represents the most common fetal arrhythmia. Occurring in 1% to 2% of normal pregnancies,¹ fetal ectopy is typically benign and short-lived²,³ with increasing incidence and frequency as gestation progresses.⁴ Conversion to atrial tachyarrhythmia occurs rarely with PACs, in only ˜0.5%, though increased risk is present in fetuses with atrial bigeminy or trigeminy and blocked PACs.⁵,⁶ Atrioventricular reentrant tachycardia (AVRT; see Part 3, Chapter 2) is the most common tachyarrhythmia associated with PACs. AVRT is precipitated by a PAC and terminated by a blocked PAC; therefore, presence of atrial bigeminy, trigeminy, or blocked PACs suggests the potential presence of a reentrant pathway. The risk of developing ventricular tachycardia in the setting of PVCs in an otherwise normal fetal heart is unknown.

A baseline echocardiogram is recommended for the fetus with frequent ectopy to define the arrhythmia, assess heart function, and exclude significant structural heart disease.⁷ The incidence of concomitant congenital heart disease is low at 0.3% (similar to baseline risk) though higher prevalence has been noted in some studies.⁸ 1° and 2° atrioventricular (AV) block may also be present in 1% to 2% of these fetuses. Though most ectopy is isolated, occasional secondary causes include myocarditis, atrial septal aneurysm, or cardiac tumors. The fetus should be closely monitored if myocarditis is suspected or tumors diagnosed, since ventricular tachycardia can occur.

PACs are common, are present in 51% of healthy newborns,⁹ and compromise 43% of fetal arrhythmias.¹⁰ Occurring as early as 15 weeks, PACs increase in frequency in the last trimester when they are observed in 1% to 3% of pregnancies.¹ PACs typically originate in the atria from an automatic focus. Compared with a sinus beat, during a PAC, the atrial activation occurs early and the interval between the
atrial contraction before the PAC and the next normal atrial contraction is longer than the interval during normal sinus rhythm (FIG. 3.1.1A and B).¹¹ Premature atrial impulses can be conducted or blocked, or a combination of the two, depending on the refractoriness of the AV node (FIG. 3.1.2). They have a typical appearance on M-mode and spectral Doppler (FIG. 3.1.3). The etiology of PACs remains speculative, but some have suggested a prominent aneurysm of septum primum or redundancy of the foramen flap¹,⁸,¹² may be causative; intracardiac tumors, for example, rhabdomyomas as seen in tuberous sclerosis, and congenital heart disease are also associated with PACs. In the setting of aneurysmal septum primum, fetal ectopy should resolve as the foramen ovale closes within the first few days of life.

The effects of atrial ectopy are reflected in the fetal venous system. There is exaggerated retrograde A-wave flow all the way to the ductus venosus (FIG. 3.1.4A and B). The irregular ventricular contractions secondary to PACs can be seen in the umbilical artery. The velocity arterial flow during PACs is higher than that of PVCs (FIG. 3.1.4C and D).

Blocked PACs occur when the AV node is refractory at the time of premature impulse arrival, such that the atrial impulse does not conduct to the ventricle and hence does not produce a ventricular contraction (FIG. 3.1.5A). The rhythm during blocked PACs can be irregular or regular. If every other atrial beat is a PAC that is not conducted, the rhythm is very regular, and referred to as blocked atrial bigeminy (BAB) (FIG 3.1.5B). BAB can be confused with 2° or 3° AV block because both
result in ventricular bradycardia. Distinguishing BAB from AV block relies on the timing of atrial events. In BAB, the interval between the sinus beat (a) and the premature beat (a′) is shorter and the interval between the premature beat (a′) and subsequent sinus beat (a) is longer because a′ is premature. In contrast, the intervals between the conducted (a) and nonconducted atrial beats (a′) in AV block are constant (FIG. 3.1.6A). In other words, the a-a′ and a′-a intervals are the same and the atrial rate constants in AV block, including 2° AV block with 2:1 conduction (Part 3: Chapter 5) (FIG. 3.1.6B).

Another way to distinguish BAB from 2° AV block is by examining the isovolumic contraction time (IVCT), which is shorter in BAB than in 2° AV block with 2:1 conduction (FIG. 3.1.7).¹³ Fetal magnetocardiography confirms that the interval between the sinus atrial beat (a) and the PAC (a′) is much shorter in BAB, compared to 2° AV block with 2:1 conduction (FIG. 3.1.8).¹⁴ Distinguishing between the two rhythms is important since 2° AV block carries a more guarded prognosis and may represent evolving anti-Ro/SSA-mediated AV block or long QT syndrome (LQTS). On the other hand, BAB is almost always benign and usually resolves spontaneously.¹