The two most common tachyarrhythmias are supraventricular tachycardia (ST) and atrial lutter. SVT is characterized by an abrupt increase in the fetal heart rate to 180 to 300 bpm with 1: 1 atrioventricular concordance. he typical range is 200 to 240 bpm. ST may develop secondary to an ectopic focus or to an accessory atrioventricular pathway leading to a reentrant tachycardia. Atrial lutter is characterized by a much higher atrial rate, generally 300 to 500 bpm, with varying degrees of atrioventricular block. As a result, the ventricular rate in a fetus with atrial flutter may range from below normal to approximately 250 bpm (Fig. 16-1). In contrast, fetal sinus tachycardia typically presents with a gradual heart rate rise to a rate that is only slightly above normal. With this, readily discernible causes may be maternal fever or hyperthyroidism, or rarely, fetal anemia or infection.
If a fetal tachyarrhythmia is identified, it is important to determine whether it is sustained-deined as present for at least 50 percent of the time. It may be necessary to monitor the fetal heart rate for 12 to 24 hours upon initial detection, and then periodically to reassess (Srinivasan, 2008). Unsustained or intermittent tachyarrhythmias generally do not require treatment, provided that fetal surveillance is reassuring.
Sustained fetal tachyarrhythmia with ventricular rates exceeding 200 bpm impairs ventricular illing to a degree that the risk for hydrops is significant. With atrial flutter, lack of coordinated atrioventricular contractions may further compound this risk. Maternal administration of antiarrhythmic agents that cross the placenta may convert the rhythm to normal or lower the baseline heart rate to forestall heart failure. Therapy may require dosages at the upper end of the therapeutic adult range. Thus, a maternal electrocardiogram is obtained before and during therapy.
Antiarrhythmic medications most commonly used include digoxin, sotalol (Betapace), flecainide (Tambocor), and procainamide (Pronestyl). heir selection depends on the type of tachyarrhythmia as well as provider familiarity and experience with the drug. Traditionally, digoxin has been the initial preferred treatment, although it may poorly transfer to the fetus after hydrops has developed. Many centers now use lecainide or sotalol as first-line therapy Gaeggi, 2011; Shah, 2012). In many cases, additional agents are needed, particularly if hydrops has developed. SVT is generally more likely than atrial flutter to convert to a normal rhythm. With either arrhythmia, however, the overall neonatal survival rate now exceeds 90 percent (Ekman-Joelsson, 2015; Jaeggi, 2011; van der Heijden, 2013).
FIGURE 16-1 Atrial flutter. In this M-mode image at 28 weeks' gestation, calipers mark the ventricular rate, which is approximately 225 bpm. There are two atrial beats (A) for each ventricular beat (), such that the atrial rate is approximately 450 bpm with 2:1 atrioventricular block.
The most common etiology of pronounced fetal bradycardia is congenital heart block. Approximately 50 percent of cases occur in the setting of a structural cardiac abnormality involving the conduction system. hese include heterotaxy, in particular ltatrial isomerism; endocardial cushion deect; and less commonly corrected transposition of the great vessels (Srinivasan, 2008). he prognosis of heart block secondary to a structural cardiac anomaly is extremely poor, and fetal loss rates exceed 80 percent (Glatz, 2008; Strasburger, 2010).