The fetal heart: A practical sonographic approach

The fetal heart: A practical sonographic approach

The Fetal Heart: A Practical Sonographic Approach R o y a S o h a e y and W i l l i a m J. Z w i e b e l Structural abnormalities of the heart are a ...

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The Fetal Heart: A Practical Sonographic Approach R o y a S o h a e y and W i l l i a m J. Z w i e b e l

Structural abnormalities of the heart are a fairly common problem, affecting more than 8 of 1,000 newborns annually in the United States. Therefore, sonographic detection of these anomalies in utero is important. It is possible to detect a high percentage of fetal cardiac anomalies through proper sonographic examination using three central views of the heart: (1) the four-chamber view; (2) the aortic outflow tract view; and (3) the pulmonary output tract view. Although average sonologists may not be able to provide a precise diagnosis for a cardiac abnormality, they are able to recognize such abnormalities in a high percentage of cases by using these three views and by answering the following questions: (1) Is the heart in a normal position? (2) Is the heart size normal? (3) Are the ventricles equa ! in size? (4) Is there a septal defect? (5) Are the atrioventricular valves in a normal position? and (6) Is there any abnormality of the endocardium, myocardium, or pericardium? This article presents a practical approach to the detection of fetal cardiac anomalies using the four-chamber and outflow tract views. Examples of normal anatomy and cardiac pathology are provided as well as a listing of differential diagnoses that should be reviewed when certain abnormalities are visualized. Copyright © 1996 by W.B. Saunders Company

ETAL CARDIAC evaluation is challenging

to most sonographers and sonologists. CarF diovascular anomalies are not rare, and struc-

tural abnormalities of the heart and great vessels occur in more than 8 of 1,000 live births. 1,2 Congenital heart defects (CHDs) are the most common severe congenital anomalies seen in neonates) The reported incidence of CHDs in fetuses is 0.8% to 2.4%. 4 The risk of a CHD increases to 4% if there has been a sibling with a CHD and to 12% if a parent had a CHD. s In this article, cardiac embryology, fetal circulation, and routine sonographic cardiac evaluation are reviewed. The examination of the normal heart and the pitfalls of cardiac sonography also are discussed. EMBRYOLOGY

The cardiovascular system is the first system to function in an embryo. Heart development begins at 18 to 19 days postfertilization. From the embryonic "cardiogenic area," two thinwalled tubes form and eventually fuse to become the endocardial tube. With the development of the "C-shaped" embryo, the heart comes to lie ventrally to the foregut and caudally to the oral pharyngeal membrane. The single tubular heart elongates and develops alternating areas of dilatation and constriction. The superior dilatation, the bulbus cordis, eventually becomes the aorta and pulmonary artery. The atrial constriction is initially caudal to the ventricular bulge, but at 22 to 24 days, the heart bends, and the atria come to lie superiorly to the ventricles. The four chambers of the heart form between

the 4th and 7th week. The centrally located endocardial cushion plays a key role in the formation of the atrial septum, ventricular septum, and valves. 6 The embryology of the atrial septum is complicated and is demonstrated in schematic form (Fig 1). Partition of the ventricles first occurs when the intraventricular septum grows cranially from the cardiac apex. The muscular portion of the intraventricular septum forms before the more cranial, membranous portion, which is derived from the endocardial cushion. The intraventricular foramen closes near the end of the 7th week of gestation. Therefore, the normal fetal heart, as seen with ultrasound, always demonstrates an intact ventricular septum, whereas the atrial septum normally contains a patent foramen ovale. The great vessels are derived from the fetal branchial arches during the 4th week. A total of six pairs of aortic arches are present initially, but only certain arches contribute to the cardiovascular system. The final disposition of the aortic arches is outlined in Table 1.6 Fetal Circulation Because prenatal life is aquatic, the prenatal circulation differs vastly from the postnatal circulation. The unique characteristics of fetal

From the Department of Radiology, University of Utah School of Medicine, Salt Lake City, UT. Address reprint requests to Roya Sohaey, MD, Department of Radiology, University of Utah School of Medicine, 50 N Medical Dr, Salt Lake City, UT84132. Copyright © 1996 by W.B. Saunders Company 0887-2171/96/1701-000355.00/0

Seminarsin Ultrasound, CT, andMRI, Vo117, No 1 (February), 1996: pp 15-33

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SOHAEY AND ZWIEBEL Septum Primum

circulation are demonstrated in schematic form in Figure 2 and by ultrasound in Figures 3 and 4. Note in particular that the foramen ovale and ductus arteriosus shunt blood from the pulmonary circulation to the systemic circulation. At birth, aeration of the lungs leads to a decrease in pulmonary vascular resistance and

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Foramen Ovale Open Fig 1, Atrial septal embryology, e (A) Initially, the septum primum develops and begins to elongate. The right and left atria communicate through the foramen primum (arrow). (B) Perforations develop in the septum primum, creating the foramen secundum (arrow) and the foramen primum closes. (C) Concurrently, the septum secundum elongates (upper limb and lower limb) parallel to the septum primum. At this stage, the foramen secundum becomes the foramen ovale, which is seen routinely with ultrasound. (D) In its final form, the foramen ovale is composed of the septum secundum superiorly and the septum primum inferiorly. The foramen ovale valve opens from the right atrium into the left atrium. Table 1. Branchial Arch Derivatives Branchial Arch Pair

FinalAnatomy Portion of maxillary arteries Foramina in stapes of the ears Proximal: Common carotid arteries Distal: Internal carotid arteries Right: Proximal right subclavian artery Left: Part of aortic arch No derivatives Right: Proximal right pulmonary artery Left: Proximal left pulmonary artery, Ductus arteriosus

Fig 2, Fetal circulation. Oxygenated blood from the placenta enters the fetus through the umbilical vein. Half of the blood passes through the hepatic sinusoids. The remainder bypasses the liver, through the ductus venosus, and goes into the inferior vena cava. The oxygenated blood enters the right atrium and mixes with deoxygenated blood from the fetal lower limbs, abdomen, and pelvis. The majority of the blood is directed from the right atrium through the foramen oval e and into the left atrium where it mixes with a small amount of deoxygenated blood returning from the fetal lungs via the pulmonary veins. The blood passes through the mitral valve, into the left ventricle (LV), and into the ascending aorta. A small stream of oxygenated blood reaches the right ventricle and is pumped into the pulmonary trunk, and most of this passes through the ductus arteriosus into the aorta. Pulmonary vascular resistance is high, resulting in low pulmonary blood flow. Not more than 10% of the blood reaches the fetal lungs, yet this is enough for oxygenating the tissue. Most of the blood in the descending aorta passes into the umbilical arteries and returns to the placenta, whereas a small amount circulates through the lower part of the body. 6

THE FETAL HEART

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Fig 3. Ultrasound of the fetal circulation. A sagittal image demonstrates the ductus venosus (black arrow) and the aortic arch (white arrow), The great vessels arise from the aortic arch (open arrow).

an increase in left atrial pressure, which closes the foramen ovale. The ductus arteriosus (between the pulmonary artery and aorta) usually remains patent for a few days but eventually constricts. Initially, the closure of this vessel and the foramen ovale is a functional change, but closure later becomes anatomic as endothelial and fibrous tissues proliferate. 6 Routine Cardiac Examination

The recommended screening test for the fetal heart is the four-chamber view. v The fourchamber heart view can be obtained in 95% of fetuses between 18 and 40 weeks s,9 on transverse sonograms of the chest. While obtaining this view, the sonographer should note the

cardiac axis by drawing an imaginary line through the intraventricular septum and a second imaginary line through the spine and sternum (Fig 5). The angle subtended by these lines is the cardiac axis, which usually is 45 degrees to the left of midline (range 22 to 75 degrees). 1° The right ventricle of the properly oriented heart contacts the anterior chest wall. To properly assess cardiac position, the sonographer must know the fetal position; otherwise, there is no way of knowing which are the right and left sides of the fetus. However, for a quick frame of reference, the sonographer can glance below the heart and confirm that the cardiac apex is on the same side of the fetus as the gastric fundus, which usually is on the left.

Fig 4. Ductal arch. The ductus arteriosus connects the pulmonary artery with the descending aorta, and forms the "'ductal arch" (black arrow). Notice the difference in configuration between the aortic arch (Fig 3) and the ductal arch.

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SOHAEY AND ZWIEBEL

Fig 5. Normal heart. (A} Normal four-chamber view. (B) Normal cardiac axis. The line drawn from the spine to the sternum forms a 45-degree angle with the line drawn through the intraventricular septum.

Once cardiac situs and orientation are confirmed, intracardiac anatomy can be assessed. The right (RV) and left ventricles (LV) tend to be the same size (RV:LV ratio of 1:1), 11 and it is not necessary to measure the ventricles routinely if they are symmetrical. Figure 6 is a standardized list of ventricular measurements related to biparietal diameter that may be used in cases that appear abnormal, u Such a table is particularly beneficial in determining whether a ventricle is large or small, in cases of asymmetry. An intact ventricular septum should be seen at all times. If the ventricular septum appears interrupted, care should be taken to determine that this interruption is not an artifact from

echo "drop out," which occurs if the image is aligned parallel to the long axis of the septum. In such cases, a change of transducer angle (perpendicular to the septum) usually shows that the septum is intact (Fig 7). The RV contains a prominent muscular band called the "moderator band" near the apex (Fig 8). In certain image planes, this band of muscle may artifactually cause the R V to appear small. The LV may contain an echogenic focus within its lumen, that probably represents the papillary muscle2 2 This and other "bright spots" in the heart are described elsewhere. The atria also should be symmetric in size, and the foramen ovale should be seen routinely

THE FETAL HEART

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(Fig 9). The flap or "valve" covering the foramen ovale extends into the left atrium because the route of fetal blood flow is from right to left. The foramen ovale valve is a complex threedimensional structure 13 that can have a variety of appearances that are discussed in the pitfalls section of this report. The tricuspid valve is located between the right atrium and the RV, and the mitral valve is located between the left atrium and LV. The "valve ring," at which the tricuspid valve attaches to the ventricular wall, is positioned slightly inferiorly to the mitral valve ring (Fig 1 0 ) . 14 The motion of the mitral and tricuspid valves should be coordinated and regular. The normal elements of the four-chamber view are summarized in Table 2. Most cardiac anomalies can be identified with the fourchamber view, although the efficacy of this view for detecting CHDs is debatable. Some authors quote 96% sensitivity for CHD, 8 whereas others report only 63% sensitivity.15 Therefore, many centers routinely obtain ventricular outflow tract images, in addition to the four-chamber view, in order to show additional normal anatomy, including the connection of the ventricles with the great vessels. Although obtaining views of the outflow tracts is more challenging than the four-chamber view, the output tracts can be examined routinely with practice. To visualize

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the aortic outflow tract, begin with the fourchamber view and rotate the transducer a quarter turn (either clockwise or counterclockwise, depending on fetal position). The left atrium will disappear from view and the left ventricular outflow tract will appear in its place, as shown in Fig 11. A long axis of the pulmonary artery (Fig 12) is achieved by returning to the four-chamber view and then rotating the transducer sharply in the direction opposite to that used for the aortic view while angling the image toward the fetal head. The pulmonary artery always is anterior to the aortic root, as seen in the pulmonary outflow tract view, and the patent ductus arteriosus extends posteriorly toward the aorta. This connection forms the so-called "ductal arch" shown in Figure 4. If the pulmonary artery is not clearly anterior to the aorta, then transposition of the great vessels should be suspected. The diameter of the aortic root and pulmonary artery are similar. The graphs shown in Figure 13 can be used if measurements are needed in cases of apparent abnormalities. 16 These reference diameters are particularly useful in deciding which output tract is normal and which is reduced or enlarged in size. In a recent study, 83% of fetuses with cardiac anomalies were identified prenatally when both the four-chamber and outflow tract views were used. How-

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SOHAEY AND ZWIEBEL

Fig 7. Pseudoventricular septal defect. (A) The ventricular septurn appears interrupted because the sound beam is parallel to the thin membranous portion of the septum. (B) A change in the angle of the beam shows an intact ventricular septum.

ever, only 63% of anomalies were recognized with the four-chamber view used alone. 15 The Abnormal Four-Chamber View

McGahan 17has described a six-step approach to the four-chamber view that helps identify the vast majority of cardiac defects. The approach asks six questions with respect to the abnormalappearing heart: 1. Is the heart in a normal position? Overall, an abnormal cardiac axis is associated with a 50% to 81% fetal mortality rate. 1° As noted previously, the heart axis should be 45 degrees

to the left midline, and the anterior aspect of the heart (RV) should touch the anterior chest wall (Fig 5). Dextrocardia is defined as malposition of the cardiac apex toward the right. This position can either be caused by inversion of the normal ventricular relationship (right for left) or simple rotation of the heart (dextroversion). The moderator band (Fig 8) may help to differentiate between these types of dextrocardia by identifying the anatomic right ventricle. Levoversion is defined as a cardiac axis that is more to the left than normal. Mesocardia is a midline-appearing

Fig 8. Moderator band. The right ventricle contains a moderator band (black arrow) near the apex. This band identifies the ventricle as the anatomic right ventricle.

Fig 9. Normal atria and foramen ovale. The atria are symmetric in size, and the normal foramen ovale (arrowheads) bows into the left atrium because the flow of blood is from the right atrium into the left atrium.

Fig 10. Tricuspid valve position. The normal tricuspid valve (short arrow) is attached slightly more toward the cardiac apex than the mitral valve (long arrow).

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SOHAEY AND ZWlEBEL Table 2. Characteristics of the Normal Four-Chamber View of the Heart Cardiac axis is to the left (45 degrees) Cardiac apex and stomach are on the same side RV contacts the anterior chest wall RV is identified by the moderator band RV: LV size is 1:1 Right atrium: left atrium size is 1:1 Ventricular septum is intact Foramen ovale flap moves from right to left Tricuspid valve is slightly inferior to the mitral valve

heart that is often associated with midline anatomic defects and may be associated with transposition of the great vessels. The heart may be intrinsically normal by ultrasound but displaced from its normal position, in which case a thoracic mass or diaphragmatic hernia should be sought diligently (Fig 14). The most common cause of cardiac malposition is a diaphragmatic hernia, 1° which is discussed in an accompanying article on the fetal chest.

Fig 11. Left ventricular outflow tract. A normal aorta (calipers) is seen attached to the left ventricle,

Fig 12. Right ventricular outflow tract. The pulmonary artery (long arrow} is anterior to the aorta (short arrow). The three aortic valve leaflets are visible within the aorta.

THE FETAL HEART

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The heart also may be located outside of the chest (ectopia cordis), and this is a fatal anomaly. 18 If ectopia cordis is associated with a large upper abdominal omphalocele, then an anomaly complex called the pentalogy of Cantrel should be suspected (Fig 15). This fatal anomaly complex consists of an omphalocele (midline abdominal wall defect), a sternal cleft, a dia-

Fig 14. Diaphragmatic hernia. The heart is displaced into the right chest by a left-sided diaphragmatic hernia, The fluid-filled stomach fundus is seen in the chest (arrow),

phragmatic hernia, and a variety of cardiovascular malformations. ]9 2. Is the heart size normal? Cardiac size can be assessed by comparing the cardiac circumference with the chest circumference on the standard four-chamber view. 2° An abnormal cardiothoracic ratio may result from cardiomegaly, pulmonary hypoplasia, or a combination of

Fig 15. Ectopia cordis. The heart (arrow) is clearly outside of the confines of the thoracic cage. This fetus also had an omphalocele and was diagnosed with pentalogy of Cantrel.

Fig 16. Hypoplastic left heart. The LV and left atrium are much smaller than the RV and right atrium in this case of severe hypoplastic left heart,

Fig 17. Hypoplastic aorta. A less severe case of hypoplastic left heart is shown with a smaller than expected aortic diameter (calipers).

THE FETAL HEART

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Fig 18. Atrial septal defect. There is a complete absence of septal tissue between the right and left atria. The ventricular septurn is intact.

both. Comparison with standard tables should help differentiate between an abnormally small chest and an abnormally enlarged heart. (A table of normal thoracic circumference measurements is presented in the fetal chest article in this issue.) Overall, the fetal heart, as seen on the four-chamber view, should not take up more than 50% of the area of the thorax. A full discussion of the small thorax and its usual

cause, pulmonary hypoplasia, is included in the fetal chest article. 3. Are the ventricles equal in size? As stated previously, the RV and LV should be equal in size throughout pregnancy. If the LV is smaller than expected, the fetus may have one of a variety of hypoplastic left heart syndromes21 (Fig 16), or the small LV may be a secondary sign of coarctation of the aorta. = A hypoplastic

Fig 19. Endocardial cushion defect, A complete atrioventricular septal defect (arrow) is seen in this fetus with trisomy 21,

Fig 20, Ventricular septal defect. An oblique image showing only the ventricles demonstrates a moderate-sized membranous ventricular septal defect (arrow),

Fig 21, Tetralogy of Fallot. The aorta (arrow) overrides a ventricular septal defect,

Fig 22. Ebstein anomaly. The tricuspid valve is displaced inferiorly (arrow) and the right atrium is enlarged,

Fig 23. Rhabdomyoma, This echogenic left ventricular mass (arrow) proved to be a rhabdomyoma.

Fig 24. Normal pericardial fluid, A small amount of pericardial fluid (arrow) can normally be seen and usually measures less than 2 mm in "thickness."

Fig 25. Pericardial effusion. This monochorionic twin fetus involved with twin-twin transfusion developed this pericardial effusion (arrow) and subsequently developed hydrops fetalis.

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Fig 26. Pericardial teratoma. (A) Normal four-chamber view of the heart at 16 weeks. (B) Six weeks later, there is a large chest mass with cystic and solid components (arrow) that displaces the heart (open arrow). This mass proved to be a pericardial teratoma at autopsy.

aorta is almost always seen in association with a hypoplastic LV (Fig 17). Alternatively, if the RV is small, the fetus may have a hypoplastic right heart, which is a more complex anomaly. Hypoplastic right heart can be associated with pulmonary artery atresia in company with an intact ventricular septum, or tricuspid atresia with associated ventricular septal defect. 17,23 Alternatively, either the right heart or left heart may be atretic and the fetus may have a single ventricle. 24 4. Is there a septal defect? The normal atrial septum contains the foramen ovale and its valve. If the valve is not seen within the left

atrium, then an atrial septal defect may be present, but sonographic confirmation of such a defect is difficult (Fig 18). It is easier to confirm the integrity of the ventricular septum, which should also appear intact on the four-chamber view. Complete atrioventricular septal defect (endocardial cushion defect) is almost always detected with the four-chamber view (Fig 19). s Fetuses with this defect are at an increased risk for chromosome abnormalities, commonly trisomy 21. 25,26 Large ventricular septal defects (VSDs) may be detected with ultrasound (Fig 20); however, small- and even moderate-sized VSDs can be overlooked, s,27 VSDs are often

THE FETAL HEART Table 3. Cardiovascular Chamber Abnormalities: Differential Considerations Large RV Ventricular failure (Fig 31) Cardiomyopathy Aortic interruption or coarctation Total anomalous pulmonary venous return Small RV Hypoplastic right heart Ebstein's anomaly Single ventricle Small L V Hypopiastic left heart Single ventricle Aortic coarctation Large right atrium Ebstein's anomaly Tricuspid dysplasia with regurgitation Pulmonary stenosis Small aorta Hypoplastic left heart Supravalvular aortic stenosis Aortic atresia Aortic coarctation or interruption Small pulmonary artery Pulmonary stenosis Pulmonary atresia Tetralogy of Fallot Incorrect great vessel orientation Transposition Tetralogy of Fallot mruncus arteriosus Double outlet RV

associated with complex cardiac abnormalities, such as tetralogy of Fallot (Fig 21), and the initial detection of a VSD necessitates a more careful examination of the fetal heart. 5. Are the atrioventricular valves in a normal position? The tricuspid valve normally is located slightly inferior to the mitral valve (Fig 10) .14 Tricuspid valve malformations occur more commonly than mitral valve malformations and usually are heralded by dilatation of the right atrium. Displacement of the septal leaflet of the tricuspid valve into the RV suggests Ebstein's anomaly (Fig 22). In this condition, the RV is small functionally and the tricuspid valve is insufficient. The result is massive right atrial dilatation, as seen on the four-chamber view. 8 Right atrial dilation can also result from tricuspid dysplasia and regurgitation; however, in these cases, the tricuspid valve attachment is not displaced inferiorly. ~4 6. Is there any abnormality of the endocardium, myocardium, or pericardium? Increased thick-

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ness and abnormal echogenicity of the endocardium may be caused by a cardiomyopathy, such as endocardial fibroelastosis. Sonographically, a large heart is seen that contracts poorly and has diffusely thickened and echogenic endocardium. 28 Focally increased echogenicity within the ventricles may be caused by a tumor, the most common being rhabdomyoma (Fig 23). Tuberous sclerosis should be suspected when multiple rhabdomyomas are seen. 29,3° Focal echogenic areas can occur normally in the ventricles and are discussed in the section on normal variants of the fetal heart. A small amount of fluid within the pericardial sac also can be a normal finding (Fig 24). Pericardial effusions appear as an anechoic region separating the two layers of the pericardium. A pericardial fluid collection measuring greater than 2 mm in width is probably abnormal (Fig 25). 31 Depending on the cause for the fluid collection,

Fig 27. Papillary muscle. An echogenic focus within the lumen of the left ventricle represents a normal papillary muscle (arrow),

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Fig 28. Rib end. An echogenic focus adjacent to the RV myocardium (arrow) proved to be the end of a rib on oblique imaging.

pericardial effusions can be transient or lethal. 32 When a pericardial effusion is identified, further clinical evaluation is indicated because the effusion may be a clue to systemic disorders that may lead to fetal hydrops. 17 Intrapericardial teratomas are rare masses that have been diagnosed prenatally (Fig 26). 33 A n y abnormality observed on the fourchamber view that cannot be explained easily

Fig 29. Redundant foramen ovale flap. The anatomy of the foramen ovale is complex, and a normal flap may appear circular (arrow).

Fig 30. Normal myocardium. The peripheral rim of the myocardium may appear hypoechoic (arrowheads) compared with the inner portion of the myocardium. This should not be confused with a pericardial effusion.

THE FETAL HEART

should be investigated with a complete fetal echocardiogram performed and interpreted by a sonologist with experience in fetal cardiac examination. The authors have found that for difficult cardiac examinations, the correct identification of CHD occurred most frequently when the investigator with the most experience performed the examination at a scheduled time that was different from the initial obstetrical examination.34 A detailed discussion of fetal echocardiography is beyond the scope of this work, but a

Fig 31. Heart failure in the donor twin with twin-twin transfusion. (A) The right atrium (RA) and RV are larger than the left atrium (LA) and LV and a pericardial effusion is present, Enddiastolic ventricular measurements showed that the LV w a s normal in size and the right heart was enlarged. (B) Doppler examination of the umbilical cord in the compromised twin showed reversal of diastolic flow. This twin was in heart failure and died 5 days after this examination despite reduction amniocentesis of the polyhydramnios twin,

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guideline to differential diagnosis is listed in Table 3.

Normal Variants and Pitfalls Occasionally, normal structures associated with the fetal heart or chest may mimic pathology, and familiarity with these normal variants and pitfalls is helpful. 35 Echogenic loci are sometimes seen within the lumen of the ventricles (Fig 27). These foci are probably of no clinical significance and most likely represent normal papillary muscle or

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chordae tendineae. Up to 20% of normal fetuses may have an echogenic focus within the LV. 12 An anterior rib end or part of the sternum can produce an echogenic focus located in or at the periphery of the ventricular myocardium (Fig 28). This echogenic focus should not be mistaken for a tumor or myocardial calcification. By changing the plane of imaging, the focus may readily be identified as a rib or the sternum. 35 A ventricular septal defect may be wrongly identified if the ultrasound beam is parallel to the membranous portion of the septum (Fig 7). Because the membranous portion is very thin, it may not reflect ultrasound sufficiently for visualization when viewed "on end." When a VSD is suspected, therefore, the sonographer should confirm its presence by demonstrating the defect in orthogonal planes. As described previously, the foramen ovale is a complex three-dimensional structure that can have a variety of appearances. The redundant flap can appear circular and mimic an atrial septal aneurysm or the aortic root (Fig 29). 13 The flap should always project into the left atrium.

Although a small amount of pericardial fluid can be seen in normal second and third trimester fetuses (Fig 24), pericardial fluid measuring greater than 2 mm is abnormal (Fig 25). 31 A pitfall leading to overdiagnosis of pericardial effusion is the peripheral hypoechoic part of the myocardium (Fig 30). This hypoechoic rim measures 0.6 to 6.0 mm and can be observed in 94% of fetal hearts when sought diligently. 36 The hypoechoic layer most likely results from differences in orientation of muscle fibers within the ventricle. The longitudinal fibers are closer to the ventricular lumen, whereas the relatively circular fibers are located peripherally. The latter most likely cause the hypoechoic appearance observed with ultrasound. 36 A final diagnostic pitfall relates to misinterpretation of cardiac chamber size discrepancies. For instance, in Figure 31, it appears at first glance that the left atrium and LV are small. In fact, the right atrium and RV are dilated, and the left chambers are normal in size. Misinterpretation of such discrepancies can be avoided by measuring the chambers and referring the measurements to standard tables such as those presented in this report.

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