When is a fetus heart fully formed

Evaluation for Fetal Congestive Heart Failure

Fetal CHF may be related to extracardiac disease (e.g., anemia, cerebral arteriovenous fistula, twin-twin transfusion syndrome) or to fetal heart disease (Box 25.4). Some of the most severe forms of CHD (e.g., HLHS, TOF with pulmonary atresia and ductal-dependent pulmonary blood flow) do not typically generate fetal CHF. Rather, fetal heart disease that causes CHF almost invariably includes one or more of the following123,143,144: sustained tachycardia or bradycardia (e.g., supraventricular tachycardia [SVT], complete heart block), myocardial dysfunction (e.g., dilated cardiomyopathy), valvar regurgitation (e.g., Ebstein anomaly of the tricuspid valve, TOF with absent pulmonary valve), or restrictive flow across the foramen ovale or ductus arteriosus.142 The fetus with absence of a valve (e.g., tricuspid atresia) or absence of a ventricle (e.g., HLHS) generally does better prenatally than one with a poorly functioning valve or ventricle.

Unlike the postnatal diagnosis of CHF, which relies more on clinical signs (tachycardia, tachypnea, hepatomegaly, rales, and peripheral edema) than on radiographic or echocardiographic findings, the prenatal diagnosis of CHF relies exclusively on sonographic findings.103,123,143,144 The sonographic findings associated with fetal CHF from any cause include (1) dilated, poorly squeezing ventricle with systolic and diastolic dysfunction; (2) cardiomegaly; (3) pericardial effusion; (4) tricuspid regurgitation; and (5) increased atrial flow reversal in the systemic veins (Box 25.5). More detailed cardiac and peripheral Doppler evaluation may also be performed.103,123,144-146 Severe forms of CHF lead to hydrops (seeFig. 25.1) and cardiac pulsations in the free-floating umbilical vein. The diagnosis of fetal CHF or hydrops should prompt further evaluation for clues to the etiology, as well as serial follow-up studies, because of the potential for progression of disease and even fetal demise.

Development

The fetal heart develops from the splanchnic mesoderm and in its earliest and most rudimentary form is represented by two tubes which subsequently fuse and then canalize. Repeated rotations and septations then occur, which ultimately result in a four-chamber organ. The myocardium increases by cell division until birth and subsequent growth is due to cell hypertrophy. A fetal heart beat can be detected by 22 days, and by 8 weeks of gestation some degree of neurogenic regulation occurs as a result of innervation by the sympathetic and parasympathetic nervous systems. However, the fetal myocardium, in general, shows immaturity of structure, function and sympathetic innervation relative to the adult heart.

The fetal heart has a limited capacity to increase its output as it normally operates at the top of its cardiac function curve. An increase in fetal heart rate can increase the cardiac output, albeit modestly, but bradycardia can significantly compromise its function.

Fetal Heart and Vascular System

The four-chamber view of the heart has been established as an important part of the routine fetal anatomic survey. However, as this view became incorporated into the routine survey, many examiners noted that outflow tract abnormalities were being missed. This occurs because many outflow tract abnormalities do not affect the appearance of the four-chamber view. The practice parameters adopted by the American Institute of Ultrasound in Medicine, American College of Radiology, and American College of Obstetricians and Gynecologists in 2013 suggested that there is a benefit in incorporating the right and left ventricular outflow tracts into the fetal survey to detect more cardiac anomalies.

Obtaining these views requires freehand sweeping of the transducer in a plane transverse and parallel to the four-chamber view of the heart. This can be difficult, and small deviations in transducer position will alter the displayed anatomy. TUI is a method of simultaneously displaying multiple sequential cardiac images with the ability to rotate the image in any plane desired. It can be thought of as being analogous to computed tomography imaging. TUI images can be displayed with either static or gated cardiac motion64 (spatiotemporal image correlation [STIC]) volume acquisitions. A major benefit of TUI is the ability to evaluate the heart either in real time (i.e., at the time of scanning) or offline at a later time, using the data acquired during scanning. DeVore and Polanko demonstrated that TUI decreases the time spent evaluating cardiac anatomy.65 Other techniques such as color Doppler, power Doppler, high-definition Doppler, B-flow, and various rendering techniques were used by Gindes and coworkers to assess 81 fetuses with cardiac anomalies and were found to make a major contribution in classifying cardiac anomalies from volume data.66 Turan and Yagel and their colleagues also reviewed the benefits of these various techniques in assessing cardiac anomalies.67,68

Gonçalves and coauthors described a method for examining the fetal heart using 4D US and STIC, a method allowing acquisition of a fetal heart volume and its visualization as a 4D cine sequence.69 Only one satisfactory volume data set needs to be obtained. Acquisition is performed with an automated slow sweep, and frames are sequentially acquired at a rapid rate. This method also is valuable for 3D surface rendering of structures such as cardiac valves. STIC allows the entire volume of the heart to be evaluated; it is useful for diagnosis and for teaching (Fig. 20.10). The STIC technology allows for the heart to be rotated using the cursor dot in any plane. For example, in transposition of the great vessels (Fig. 20.11), the bifurcation of the pulmonary artery can be seen in one plane and its relationship to the left ventricle (i.e., abnormal outlet) can be seen in another plane.

Fetal Life

The fetal heart and circulation rely on the maintenance of a parallel pulmonary and systemic circuit, with flow exchange between the anatomical right and left atrium at the patent foramen ovale (from right to left) and across the arterial duct (from pulmonary to systemic). While interruption of either of these ‘shunts’ results in developmental consequences for the heart and great vessels (http://www.medindia.net/animation/patent-ductus-arteriosus.asp), they do not result in pump failure in and of themselves. For the heart to fail, other disturbances must be severe enough and prolonged enough to result in excessive chamber filling and eventually compromise myocardial function. Common conditions, which have this effect, are listed in Table 2, along with the mechanism of this disturbance.

Table 2. Common abnormalities resulting in fetal heart failure

Fetal abnormalityMechanismPhenotypeNotesFetal tachycardiaAtrioventricular reentry, atrial flutter, or ectopic atrial tachycardia most commonDilated ventricles, poor systolic function, pericardial effusion, and hydrops fetalisMedical therapy of mother with antiarrhythmic drugs is effective in 50%Fetal bradycardiaSinus node dysfunction or congenital atrioventricular blockTypically dilated ventricles with effusion and extreme bradycardia (< 60 bpm). LV endocardial fibroelastosis also describedWell described due to maternal autoantibodies (anti-Ro or Anti-La) in maternal SLE. Maternal corticosteroid therapy may prevent progressionFetal tricuspid valve diseaseEbstein’s anomaly of the TV with regurgitation and functional atresia of the PVMassive dilation of the atrialized right ventricle (RV) and compression of the other chambersSevere cases may lead to intrauterine fetal demiseIncreased cardiac output demandsFetal anemia (typically antibody-mediated), AV malformations, and TTTS (occurs in 20% of monochorionic twin pregnancies)In TTTS, the recipient twin has RV chamber dilation, hypertrophy, and hydrops fetalis. The donor twin is typically SGA and anemic and may also have poor cardiac functionFetoscopic laser ablation of vessels communicating between the two placentas is the treatment of choicePrimary fetal cardiomyopathyEither hypertrophic or nonhypertrophic phenotypesCommonly in association with chromosomal abnormalitiesHigh rate of fetal demise. No effective treatment of primary cardiomyopathies in utero