Cardiac Arrhythmias in the Human Fetus

Abstract

Fetal cardiac arrhythmias have been recognized with increasing frequency during the past several years. Most fetal arrythmias are intermittent extrasystoles, often presenting as irregular pauses of rhythm. These are significant only when they occur with appropriate timing to initiate sustained tachycardia, mediated by anatomic bypass pathways. The most common important fetal arrhythmias are: 1) supraventricular tachycardias, and 2) severe bradyarrhythmias, associated with complete heart block. Symptomatic fetal tachycardias are usually supraventricular in origin, and may be associated with the developmet of hydrops fetalis. These patients may respond to antiarrhythmic drug therapy, administered via maternal ingestion or via direct fetal injection. Such therapy should be offered with careful fetal and maternal monitoring, and must be based on a logical, sequential analysis of the electrical mechanism underlying the arrhythmia, and an appreciation of the pharmacology and pharmacokinetics of the maternal, placental fetal system. Bradycardia from complete heart block may either be associated with complex congential heart malformations involving the atrioventricular junction of the heart, or may present in fetuses with normal cardiac structure, in mothers with autoimmune conditions associated with high titres of anti-SS-A or anti-SS-B antibody, which cross the placenta to cause immune-related inflammatory damage to the fetal atroventricular node. This paper reviews experience with the analysis of fetal caridac rhythm, a detailed discussion of the pathophysiology of arrhythmias and their effect on the fetal circulatory system, and offers a logical framework for the construction of treatment algorithms for fetuses at risk for circulatory compromise from fetal arrhythmias.

Transport of digoxin-loaded Polymeric Nanoparticles Across BeWo cells, an In Vitro Model of Human Placental Trophoblast

“…Transplacental transfer of digoxin to the fetus is limited because digoxin is a substrate for the efflux transporter P-gp, which is highly expressed in human placenta [8], and is also expressed in BeWo cells [9]. Therefore, higher and more frequent doses of digoxin are required during pregnancy to maintain therapeutic concentrations [10]. Prenatal digoxin therapy can lead to undesirable side effects for the mother, because the majority of the dose remains in the maternal circulation [11].…”

First‐Line Antiarrhythmic Transplacental Treatment for Fetal Tachyarrhythmia: A Systematic Review and Meta‐Analysis

“…The majority of fetal arrhythmias are benign intermittent premature atrial contractions that require no intervention 1, 2, 3. Sustained fetal tachyarrhythmias (FTs) are less common, ≈1 in 1000 pregnancies, but are associated with significant morbidity and mortality 4.…”

“…This may result in fetal hemodynamic compromise and development of nonimmune hydrops fetalis that can lead to fetal demise. Hydrops fetalis occurs in about half of these cases, with fetal demise occurring in 9% of untreated FT cases 2, 5, 6…”

Relationship between Deceleration Areas in the Second Stage of Labor and Neonatal Acidemia

“…Although CTG is highly reliable for fetal hypoxia identification [14], its predicting value could be enhanced by combining it with fetal electrocardiography (FECG) which records the electrical activity of the fetal heart [15]. Indeed, beside FHR evaluation, FECG allows to have additional information on fetal well-being based on FECG signal morphology, such as ST-segment [16][17][18][19][20]. However, FECG may increase risk of infection when the electrode is directly placed on the fetal scalp [21] or may require significant signal-processing to reduce noise when the electrode in placed on the mother's abdomen [22,23].…”