Fetal arrhythmias

Abstract

This chapter will describe the analysis of fetal cardiac rhythm, present a discussion of the pathophysiology of arrhythmias and their effect on the fetal circulatory system, and describe the latest methods for the diagnosis of tachyarrhythmias and a treatment algorithm of cardiac arrhythmias during fetal life. The normal fetal cardiac rhythm is characterized by a regular heart rate ranging between 100 and 160-180 beats/min with a normal 1:1 atrio-ventricular electromechanical relationship during each cardiac cycle. Fetal rhythm disturbances are diagnosed in at least 2% of pregnancies during routine ultrasound scanning and are common reasons for referral to a fetal cardiologist. Arrhythmias are most frequently due to multiple atrial premature contractions, of little clinical relevance in more than 90% of cases. About one in 200 fetuses with frequent atrial ectopy will develop supraventricular tachycardia, either in fetal life or in the newborn period; the risk of supraventricular tachycardia increases to about 10% when ectopy is re-entrant or complex. Fetal tachycardia occurs in approximately 0.5% of all pregnancies and is related to sinus tachycardia, atrial flutter and supraventricular tachycardia as the main aetiology. Appropriate management depends on accurate diagnosis and fetal echocardiography remains the main tool to diagnose and discern the mechanism of tachyarrhythmia, to study the impact on cardiac function, to exclude cardiac pathology, and to survey the fetal heart during anti-arrhythmic treatment. In addition to M-mode and flow Doppler, new ultrasounds techniques such as myocardial deformation imaging have become available. Infrequently, the tachyarrhythmias become sustained with a high risk for hydrops fetalis, neurological morbidity and fetal death. For the compromised fetus, the mortality rate ranges from 8% to 27% and the delivery of an immature, hydropic infant has equally unacceptable morbidity and mortality. In these cases there is a consensus treatment with drug therapy. The recognition of the type of tachyarrhythmia allows the choice of specific drug therapy and improves the chance for success. Approximately 75-85% of fetuses with sustained tachycardia and mild heart failure respond to transplacental antiarrhythmic therapy. To avoid the limits of placenta transfer of antiarrhythmic drugs when transplacental therapy fails, direct fetal therapy has been used. Sustained bradyarrhythmias relate to sinus bradycardia, atrial bigeminy or, from the most common cause, to complete atrio-ventricular block (CAB). CAB may present in fetuses with normal cardiac structure, and normally appears after 20 weeks of gestation in mothers with autoimmune conditions associated with high titres of anti-Ro/La autoantibodies that cross the placenta to cause immune-related inflammatory damage. Isolated fetal CAB has a significant mortality rate, particularly in association with fetal hydrops, poor ventricular function and low heart rates. CAB may be associated with either complex congenital heart malformations involving the atrio-ventricular junction of the heart; with worse outcome, typically left atrial isomerism; or corrected transposition of the great arteries. Treatment of a fetus with irreversible atrio-ventricular nodal damage is proposed, primarily to augment fetal cardiac output and to mitigate or prevent concomitant myocardial inflammation. Published studies have demonstrated a significant improved outcome with transmaternal dexamethasone and beta stimulation.