in which a premature atrial beat follows closely after a normal atrial beat with no ventricular response to the premature beat. This arrhythmia has no significance beyond that of isolated atrial extrasystoles.
Follow‐up
The fetus with congenital heart disease should be carefully followed by ultrasound up to delivery. Structural lesions may evolve prenatally even as they do postnatally. It is particularly important to evaluate areas of potential obstruction, and the relationships of the great arteries to the ventricles. Fetuses with significant arrhythmias (including reentrant tachycardias, atrial flutter, and complete heart block) should also be followed at a center with experience in the prenatal medical management of fetal arrhythmias, by a team that includes perinatologists, pediatric cardiologists, and adult electrophysiologists. Delivery need not be by cesarean except in the presence of selected fetal arrhythmias that do not permit adequate fetal heart rate monitoring. For fetuses with lesions that are expected to render the neonate dependent on ductus arteriosus patency for systemic or pulmonary perfusion, prostaglandin E1 should be available in the nursery at the time of delivery to keep the ductus open.
Suggested reading
1 American Institute of Ultrasound in Medicine. AIUM Practice Guideline for the Performance of Obstetric Ultrasound Examinations. www.aium.org/resources/guidelines/obstetric.pdf
2 American Institute of Ultrasound in Medicine. AIUM Practice Parameter for the Performance of Fetal Echocardiography. https://doi.org/10.1002/jum.15188
3 Bahtiyar MO, Dulay AT, Weeks BP, Friedman AH, Copel JA. Prenatal course of isolated muscular ventricular septal defects diagnosed only by color Doppler sonography: single‐institution experience. J Ultrasound Med 2008; 27:715–20.
4 Copel JA, Liang RI, Demasio K, Ozeren S, Kleinman CS. The clinical significance of the irregular fetal heart rhythm. Am J Obstet Gynecol 2000; 182:813–17.
5 Copel JA, Tan AS, Kleinman CS. Does a prenatal diagnosis of congenital heart disease alter short‐term outcome? Ultrasound Obstet Gynecol 1997; 10:237–41.
6 Donofrio MT, Moon‐Grady AJ, Hornberger LK, et al. Diagnosis and treatment of fetal cardiac disease: a scientific statement. Am Heart Assoc Circ 2014; 129:2183–242.
7 Kleinman CS, Copel JA. Electrophysiological principles and fetal antiarrhythmic therapy. Ultrasound Obstet Gynecol 1991; 4:286–97.
8 Miller A, Riehle‐Colarusso T, Alverson MS, et al. Congenital heart defects and major structural noncardiac anomalies, Atlanta, Georgia, 1968 to 2005. J Pediatr 2011; 159:70–8.
9 Pierpont ME, Brueckner M, Chung WK, et al. Genetic basis for congenital heart disease: revisited. A scientific statement from the American Heart Association. Circulation 2018: 138:e653–e711.
10 Silverman NH, Kleinman CS, Rudolph AM, et al. Fetal atrioventricular valve insufficiency associated with nonimmune hydrops: a two‐dimensional echocardiographic and pulsed Doppler study. Circulation 1985; 72:825–32.
11 Todros T, Faggiano F, Chiappa E, Gaglioti P, Mitola B, Sciarrone A. Accuracy of routine ultrasonography in screening heart disease prenatally. Gruppo piemontese for prenatal screening of congenital heart disease. Prenatal Diag 1997; 17:901–6.
PROTOCOL 7 Clinical Use of Doppler
Henry L. Galan
Department of Obstetrics and Gynecology, Division of Maternal‐Fetal Medicine, University of Colorado School of Medicine, Colorado Fetal Care Center, Aurora, CO, USA
Overview
Doppler ultrasound depends upon the ability of a pulsed ultrasound beam to be changed in frequency when encountering moving objects such as red blood cells (RBC). The change in frequency (Doppler shift) between the emitted reflected beams is proportional to the velocity of the RBC and dependent on the angle between the ultrasound beam and the vessel. Pulsed‐wave Doppler velocimetry provides a flow velocity waveform from which information can be obtained to determine three basic characteristics of blood flow that are useful in obstetrics: velocity, resistance indices, and volume blood flow. Doppler velocimetry is applied in a broad number of clinical circumstances in high‐risk pregnancies including diagnostic fetal echocardiography, fetal growth restriction (FGR), fetal anemia, adverse pregnancy outcome assessment, twin‐twin transfusion syndrome (TTTS), twin anemia polycythemia sequence (TAPS), and preterm labor (ductus arteriosus assessment for indomethacin tocolysis). Pulsed‐wave Doppler velocimetry is also used to evaluate the ductus venosus (DV) in first‐trimester risk assessment for Down syndrome but is not discussed in this protocol.
Pathophysiology
Normal fetal circulation
The umbilical vein is a conduit vessel bringing oxygen and nutrient‐rich blood from the placenta to the fetus. The umbilical vein enters the umbilicus, courses anteriorly along the abdominal wall prior to entering the liver, and becomes the hepatic portion of the umbilical vein. The umbilical vein eventually becomes the portal vein, but first gives off the left inferior and superior portal veins, the DV, and finally the right portal vein. Approximately 50% of umbilical vein blood is directed into the DV and then to an area under the diaphragm referred to as the subdiaphragmatic vestibulum. The subdiaphragmatic vestibulum also receives blood from the inferior vena cava and blood exiting the liver via the right, middle, and left hepatic veins.
The process of preferential streaming begins in the subdiaphragmatic vestibulum with blood from the DV and the left and middle hepatic veins preferentially shunted across the foramen ovale into the left atrium and left ventricle so that the heart and head receive the most oxygenated and nutrient‐rich blood. In contrast, blood coming from the inferior vena cava and right hepatic vein are preferentially streamed into the right atrium and right ventricle. Then, after exiting through the pulmonary artery, this blood is shunted to the descending aorta via the ductus arteriosus. Blood leaves the fetus via two umbilical arteries arising from the hypogastric arteries which course around the lateral aspects of the bladder in an anterior and cephalad direction, exiting the umbilicus, returning oxygen‐reduced blood and waste products back to the placenta.
There are three primary fetal circulatory shunts that require closure after delivery for normal newborn cardiopulmonary transition to occur and for the subsequent adult circulation to be established. As mentioned above, the DV shunts blood from the umbilical vein toward the heart. The ductus arteriosus shunts approximately 90% of the blood in the main pulmonary artery to the descending aorta, leaving only 10% of pulmonary artery blood to reach the fetal lungs. The third shunt is the foramen ovale, which is maintained in a patent state in utero to allow the process of preferential streaming to occur from the right atrium to the left. Failure of any one of these shunts to close properly may result in adverse cardiopulmonary transition in the newborn.
Fetal growth restriction
Fetuses that fail to reach their genetically determined growth potential due to uteroplacental dysfunction may develop abnormal resistance to blood flow in the placenta. This abnormal resistance is due to numerous placental vascular abnormalities (poor villous capillarization, reduced number and branching of stem arteries, luminal reduction, and wall hypertrophy), which can be detected with Doppler velocimetry in the umbilical artery located upstream from the placenta.
