Protocols for High-Risk Pregnancies. Группа авторов
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Table 6.3 AIUM recommended components of detailed fetal echocardiographic exam
Gray‐scale imaging Four‐chamber view including pulmonary veinsLeft ventricular outflow tractRight ventricular outflow tractBranch pulmonary artery bifurcationThree‐vessel view (including view with PA bifurcation and more superior view with ductal arch)Short‐axis views (“low” for ventricles, “high” for outflow tracts)Long‐axis view (if clinically relevant)Aortic archDuctal archSuperior (SVC) and inferior vena cava (IVC) Color Doppler sonography Systemic veins (including superior and inferior vena cava and ductus venosus)Pulmonary veins (at least two, one right vein and one left vein)Atrial septum and foramen ovaleAtrioventricular valvesVentricular septumSemilunar valvesDuctal archAortic arch Pulsed Doppler sonography Right and left atrioventricular valvesRight and left semilunar valvesPulmonary veins (at least two; one right vein and one left vein)Ductus venosusSuspected structural or flow abnormality on color Doppler sonography Heart rate and rhythm assessmentCardiac biometry (z‐scores recommended) Aortic and pulmonary valve annulus in systole (absolute size with comparison of left‐ to right‐sided valves)Tricuspid and mitral valve annulus in diastole (absolute size with comparison of left‐ to right‐sided valves) Optional biometry Right and left ventricular lengthsAortic arch and isthmus diameter measurements from the sagittal arch view or three vessels and trachea view with comparison of aortic isthmus to ductus arteriosusMain pulmonary artery and ductus arteriosus measurementsEnd‐diastolic ventricular diameter just inferior to the atrioventricular valve leaflets in the short or long axis viewThickness of the ventricular free walls and interventricular septum in diastole just inferior to the atrioventricular valvesAdditional measurements if clinically relevant, including:systolic ventricular dimensions (short or long axis views)transverse atrial dimensionsbranch pulmonary artery diametersCardiac function assessment (if clinically relevant) Fractional shorteningVentricular strainMyocardial performance index |
Management
When a cardiac anomaly is found, a full detailed fetal scan to detect any other extracardiac anomalies is mandatory. Many fetal syndromes include cardiac anomalies, and accurate counseling requires complete enumeration of associated anomalies. Fetal karyotype testing should be offered to the parents, as chromosome abnormalities are seen in a large segment of fetuses with congenital heart disease. Additional testing for a microdeletion of chromosome 22q11 can be helpful in fetuses with conotruncal malformations (e.g., tetralogy of Fallot, truncus arteriosus). As for all fetal anomalies, microarray testing for microdeletions and microduplications has also become routine. In selected cases specific gene sequencing or even whole exome or genome sequencing is indicated.
Overall survival once a cardiac lesion is found depends on the nature of the cardiac problem, the presence of extracardiac anomalies, the karyotype, and the presence of fetal hydrops. Fetal hydrops in association with structural heart disease is virtually universally fatal. Aneuploid fetuses may have dismal prognoses even in the absence of heart disease; for example, fetal trisomy 18 may make repairing even a straightforward ventricular septal defect inadvisable.
Lesions that can be repaired into a biventricular heart carry a better long‐term prognosis than those that result in a univentricular heart. In general, infants known to have congenital heart disease prenatally do better than those whose cardiac defects are only found after birth.
Fetal arrhythmias
Diagnosis and management
The largest group of fetal arrhythmias are intermittent and due to atrial, junctional or ventricular extrasystoles. They carry a small risk of co‐existent structural abnormality. A greater risk exists of an unrecognized tachyarrhythmia, or the development of a tachyarrhythmia later in gestation. Atrial extrasystoles predispose the fetus to development of reentrant atrial tachycardia, which can lead to fetal hydrops. We recommend weekly auscultation of the fetal heart, along with avoidance of caffeine or other sympathomimetics, until resolution of the arrhythmia.
Fetal tachycardias represent a management challenge, because determination of the precise electrophysiological cause of the arrhythmia is essential to any rational management strategy, but fetal electrocardiography is not yet clinically practical in the presence of intact membranes. The differential diagnoses of fetal tachycardias include reentrant atrial tachycardia, atrial flutter, and ventricular tachycardia. The treatment of these disorders differs significantly, and appropriate medications for one may be contraindicated for another. The correct diagnosis, which should be based on combinations of M‐mode, Doppler and color Doppler–M‐mode imaging, is essential to appropriate therapy.
If there is a fetal bradycardia, the first step is to determine if there is a regular or an irregular atrial rate. If the atrial rate is regular and slow, that is, below 100 beats per minute, there may be sinus bradycardia, which should prompt a complete evaluation of fetal well‐being. The most common clinically important fetal bradycardia results from complete heart block, which will demonstrate a normal regular atrial rate with a slower ventricular rate whose beats do not occur in conjunction with atrial beats. In structurally normal hearts this is usually caused by maternal antibodies associated with lupus erythematosus and Sjögren syndrome, termed SSA/Ro and SSB/La. A smaller group of patients, without maternal antibodies, may present with congenital complete heart block in a setting of complex congenital heart disease involving the central fibrous body of the heart (e.g., left atrial isomerism, corrected transposition of the great arteries). In these patients, the prognosis is directly related to the complexity of the heart disease and the association with congestive heart failure.
A more benign cause of fetal bradycardia, which may be mistaken for 2:1 heart block, is blocked atrial bigeminy. In such cases the atrial