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Color Doppler Ultrasound in Fetal Echocardiography
RA
TV
SV
ab
LA
MV
22
cd
Fig. 22.21 Single ventricle (30th week of gest ation) with
a double-inlet left ventricle, a right ventricular outlet
chamber, VSD, and normal position of the great arteries.
a, b The right and left atria (RA, LA) drain respectively
through a tricuspid valve (TV) and mitral valve (MV) into
the single ventricle (SV).
c, d Doppler scan confirms the normal function of the tri-
cuspid valve (TV) and mitral valve (MV).
e Color Doppler shows blood flowing from the atria into
the ventricle. There is only partial mixing of the flows
within the single ventricle.
212
e
Fig. 22.21 f and g 컄
Ultrasound Examination of the Fetal Heart
Fig. 22.21 f, g The
aorta arises from the
single ventricle, which
has a left ventricular
morphology. The aor-
SVC
RA
TV
SV
fg
AA
PA
tic arch (AA) can be
identified. The pulmonary artery trunk (PA)
is imaged in cross sec-
tion. RA = right
atrium; TV = tricuspid
valve; SV = single ven-
tricle; SVC= superior
vena cava.
Anomalies of the Great Arteries (Fig. 22.22)
D(Dextro)-Transposition of the Great Arteries
(Fig. 22.22a–d)
Transposed position of the great arteries with:
– Atrioventricular concordance and ventriculoatrial discor-
dance
– An anterior, right-sided aorta arising from the right ventricle
– A posteriorly situated pulmonary artery arising from the left
ventricle
– A normal-appearing four-chamber view, but absence of a
centrally located aortic valve in the five-chamber view!
Color Doppler
Both great arteries leave the heart in a parallel arrangement;
they do not cross!
Combined with ventricular septal defect, rarely with pulmonary
stenosis or coarctation of the aorta.
L(Levo)-Transposition of the Great Arteries
(Fig. 22.22e–h)
There is ventricular inversion with atrioventricular and ventriculoatrial discordance:
– The right atrium is connected to a right-sided morphological
left ventricle, which empties into the pulmonary artery.
– The left atrium is connected to a left-sided morphological
right ventricle, which empties into the aorta.
Color Doppler
The ascending aorta is located anterior to the pulmonary artery
(the aorta arises from the right ventricle at a site anterior and to
the left of the pulmonary artery).
May be combined with ventricular septal defect and/or pulmonary stenosis.
Third-degree AV block is rarely present.
Common Truncus arteriosus (Fig. 22.23)
– Two ventricles of equal size.
Color Doppler
A common, large arterial trunk overrides the ventricular septal
defect.
The pulmonary artery arises posteriorly from the truncus arteriosus (with a common trunk or separate origin of both pulmonary
branches).
Frequently associated with CATCH 22 syndrome.
Tricuspid Valve Anomalies
➤
Tricuspid valve dysplasia (Figs. 22.24, 22.25)
– Valve leaflets are dysplastic, chordae are lengthened or
shortened.
➤
Ebstein anomaly
– Functional tricuspid valve plane is displaced into the right
ventricle.
– There is resultant arterialization of the right ventricular
inlet.
– Tricuspid valve is malformed and usually incompetent.
Both cardiac anomalies are highly variable in their degree.
Color Doppler
Tricuspid regurgitation with an enlarged right atrium.
Hypoplastic pulmonary artery trunk with reduced flow.
Right-sided inflow stasis with dilatation of the venae cavae and
hepatic veins.
Severe forms are usually associated with ascites, pleural effusion,
hydrops, lung hypoplasia, and intrauterine death.
The two forms are difficult to distinguish from each other an-
tenatally.
Specific Obstetric Problems
213
Associated with abnormalities of cardiac position.
Color Doppler Ultrasound in Fetal Echocardiography
Fig. 22.22 Transposition of the great arteries.
a, b D-transposition of the great arteries.
The pulmonary artery (PA) arises from the
posteriorly located left ventricle (LV).
LV
RV
PA
ab
LV
c, d D-transposition of the great arteries.
The aorta (A) arises from the anteriorly located right ventricle (RV).
e, f L-transposition of the great arteries
(36th week of gestation). The right atrium
(RA) drains into the left ventricle (LV), from
which the pulmonary artery arises.
g, h L-transposition of the great arteries. The
aorta (AAO) arises anteriorly from the right
ventricle (RV).
(a–d with kind permission of Dr. V. Fesslova,
Department of Pediatric Cardiology, Azienda
Ospedaliera, Instituti Clinici di Perfezionamento, Milan, Italy.)
RV
A
22
cd
RA
PA
LV
e
f
214
AAO
RV
gh
Ultrasound Examination of the Fetal Heart
a
Fig. 22.24 Tricuspid insufficiency (38th week of gestation). The fourchamber view shows a very mildly dilated right atrium (RA) with color
flow indicating mild to moderate tricuspid regurgitation (blue jet
across the tricuspid valve into the right atrium, directed toward the in-
teratrial septum). LA = left atrium; RV = right ventricle; LV = left ven-
tricle. The Doppler spectrum (right side of image) indicates a maximum systolic flow velocity of 3.67 m/s, corresponding to a pressure
gradient of 54 mmHg.
b
c
Fig. 22.23 Common truncus arteriosus (32nd week of gestation).
a B-mode cardiac scan demonstrates both ventricles and a large arte-
rial vessel. Both ventricles communicate through a large ventricular
septal defect straddled by an arterial trunk (AO). A pulmonary vessel is
not seen arising from the right ventricle. RV = right ventricle; LV= left
ventricle.
b Same situation as in a: color Doppler image of the common truncus
arteriosus.
c The pulmonary artery arises from the posterior part of the trunk just
above the valve plane.
Specific Obstetric Problems
Fig. 22.25 Tricuspid valve dysplasia with fetal hydrops (28th week of
gestation). Polyhydramnios, fetal pericardial effusion, and fetal cu-
taneous edema are present. The four-chamber view shows a greatly
enlarged right atrium (RA) with a dysplastic tricuspid valve. Otherwise
the right and lef t ventricles (RV, LV) are of normal size. There was
marked general enlargement of the heart leading to bilateral pulmonary hypoplasia, with severe postnatal breathing problems.
215
Color Doppler Ultrasound in Fetal Echocardiography
Heterotaxy Syndromes
These syndromes involve complex anomalies of the heart, vessels, and thoracoabdominal organs (synonym: Ivemark syndrome). Right atrial isomerism (asplenia syndrome) is distinguished from left atrial isomerism (polysplenia syndrome).
– Anomalous positions of the upper abdominal organs. The
liver is often centered in the abdomen, with the stomach on
the right side.
– Multiple small spleens (polysplenia) or absence of the spleen
(asplenia).
– Anomalous course of the inferior vena cava(on the same side
of the spine as the descending aorta) or duplication of the superior vena cava.
Color Doppler
Cardiac anomalies: single ventricle, common atrium, AV valve
anomalies, pulmonary stenosis or atresia, malposition of the
great arteries, anomalous pulmonary venous return, thirddegree AV block.
22
Affected infants show normal cerebral development postnatally, but often the cardiac anomalies cannot be fully corrected.
Cardiac Tumors
Rhabdomyomas. The most common tumors are rhabdomy-
omas, which are usually attached to the interior walls of the
heart (ventricular walls, interventricular septum, occasionally
the atrial walls) and are usually multiple. The tumors
frequently enlarge during the course of pregnancy. Hemodynamic complications depend on the size and location of the
rhabdomyomas (e.g., valvular obstruction). Af ter birth, the
tumors usually show a gradual reduction in size over a period
of several years. Bourneville–Pringle disease (tuberous sclero-
sis) is present as an underlying disorder in most cases
(Fig. 22.
Hemangiomas and teratomas. Rarely, hemangiomas can occur
in the pericardium and may cause pericardial effusion. Teratomas are also rare.
26).
Fig. 22.26 Cardiac
rhabdomyomas in
tuberous sclerosis
(34th week of gestation).
a, b Scan in the atrial
plane demonstrates a
tumor (Tu) 15.3 mm in
LA
Tu
a
b
RA
Tu
diameter (cursors in a)
located on the roof of
the right atrium (RA).
LA = left atrium.
c, d Scan in the
ventricular plane demonstrates three
tumors: one on the
subaortic left ventricular septum (8.6 mm in
diameter), one at the
right ventricular apex
(9.1 mm in diameter),
and a smaller tumor
located in the right
ventricular outflow
tract. LV = left ventricle; RV= right ventricle; AO= aorta.
216
Tu
AO
Tu
c
d
LV
RV
Tu
Fig. 22.27 Four-chamber view (30th week of gestation) shows a
rounded, echogenic structure in the papillary muscle of the mitral
valve. The feature pulsated with the valve movements and did not
cause mitral valve dysfunction. It disappeared during the first few
months of life.
Differential diagnosis. Differentiation is required from a harmless mitral valve anomaly,which appears as a rounded, hyperechoic structure in the papillary muscles that moves synchronously with the pulse and has an undetermined cause (described as the “tennis ball sign” or “golf ball sign”). It does not
interfere with mitral valve function (Fig. 22.
after birth. Today it is thought that this feature is associated
with a chromosome abnormality in approximately 1–2 % of fetuses.
27) and resolves
Ultrasound Examination of the Fetal Heart
Differential Diagnostic Considerations
Differential Diagnosis of Ventricular Hypoplasia
➤
Hypoplastic right ventricle:
– Tricuspid atresia
– Pulmonary atresia with an intact ventricular septum
Common feature: pulmonary trunk is often hypoplastic.
➤
Hypoplastic left ventricle:
– Hypoplastic left heart syndrome
– Aortic valve atresia, critical aortic stenosis
Common feature: hypoplastic ascending aorta.
Differential Diagnosis of Right Atrial and Right
Ventricular Dilatation
– Premature closure of the ductus arteriosus
– Premature closure of the foramen ovale
– Total anomalous pulmonary venous return
– Coarctation of the aorta
– Global heart failure (e.g., supraventricular tachycardia, fe-
tofetal transfusion syndrome)
Differential Diagnosis of an Enlarged Right Atrium
– Tricuspid valve dysplasia
– Ebstein anomaly
Common feature: tricuspid insufficiency.
Specific Obstetric Problems
Anomalies of Cardiac Position
Primary Anomalies of Cardiac Position
➤
Situs inversus of the thoracic organs: dextrocardia with the
cardiac apex pointing toward the right side.
➤
Complete situs inversus: situs inversus of the thoracic and
abdominal organs.
Both conditions may occur in isolation but are frequently combined with heart defects or with a heterotaxy syndrome.
➤
Ectopia cordis. In ectopia cordis, all or part of the heart is
displaced anterior to the sternum. It may be associated with
a chromosome abnormality, omphalocele, or an epigastric
hernia. A congenital heart defect is usually present.
➤
Thoracopagus. Twins conjoined in the sternal region have
very complex cardiac anomalies, often with symmetrical involvement of both hearts.
Secondary Anomalies of Cardiac Position
➤
Lung malformations. Lung hypoplasia, lung tumors, or cys-
tic adenomatoid malformation of one lung leads to displacement of the heart and mediastinum.
➤
Diaphragmatic hernia. A diaphragmatic hernia is often
present on the left side and is associated with cardiac and
mediastinal displacement into the right side of the chest.
➤
Diaphragmatic effusions. Copious, unilateral diaphrag-
matic effusions displace the heart toward the opposite side.
Differential Diagnosis of an Enlarged Left Atrium
– Severe valvular aortic stenosis
– Myocarditis, dilatative cardiomyopathy
Critical Postnatal Defects
Ductus-dependent defects. The following congenital heart de-
fects can lead to a critical hemodynamic situation in the newborn due to dependence on the ductus arteriosus. These cases
require early prostaglandin E
tervention or corrective surgery.
– Critical semilunar valvestenosis (aortic or pulmonary steno-
sis)
– Pulmonary atresia
– Tricuspid atresia
– Critical coarctation of the aorta, critical aortic valve stenosis
– Hypoplastic left heart syndrome
– Transposition of the great arteries
Decreased blood flow in the descending aorta caused by postnatal closure of the ductus arteriosus can lead to renal failure
with oliguria or anuria, necrotizingenterocolitis (decreased intestinal blood flow), and functional liver failure with
coagulopathy and protracted shock.
Decreased lung perfusion following ductal closure in the
presence of pulmonary or tricuspid valve atresia leads to a
hypoxic state that is not correctible by mechanical ventilation.
With a D-transposition of the great arteries, persistence of the
ductus arteriosus and foramen ovale is necessary for life.
therapy or prompt catheter in-
1
217
Color Doppler Ultrasound in Fetal Echocardiography
Defects dependent on an atrial septal defect. Infants with ASDdependent defects must undergo a balloon atrioseptostomy
(Rashkind maneuver) after birth. These are defects that involve
atresia of an AV or semilunar valve or a D-transposition of the
great arteries.
– Pulmonary atresia with an intact ventricular septum
– Tricuspid atresia
– Mitral atresia, hypoplastic left heart syndrome
– D-transposition of the great arteries
– Total anomalous pulmonary venous return
All infants with congenital heart defects that are dependent on
a persistent ductus arteriosus or foramen ovale, and thus require immediate therapeutic intervention, should be delivered
at a center where the services of a pediatric cardiologist and
cardiac surgeon are available.
Management of Suspected Congenital Heart Disease
When a congenital heart defect is suspected, the pregnant
woman should be referred to a tertiary perinatal center where
22
(1) the heart defect and any associated extracardiac diseases or
genetic defects can be investigated and (2) appropriate family
counseling can be offered. Ideally, the patient should present at
20–21 weeks’ gestation to allow sufficient time for all necessary diagnostic tests. The same applies to the targeted exclusion of heart defects in high-risk pregnancies.
References
1 Allan LD, Crawford DC, Shita SK et al.: Familial recurrence of congenital
heart disease in a prospective series of mothers referred for fetal echocardiography. Amer. J. Cardiol. 58 (1986) 334
2 Bosi G, Scorrano M, Tosato G, Forini E, Chakrokh R and the Working
Party of the Italian Society of Ped. Cardiology: The Italian Multicentric
Study on Epidemiology of Congenital Heart Disease: First Step of the
Analysis. Cardiol. Young 9 (1999) 291
3 Boughman JA, Neill CA, Ferencz C, Loffredo CA: The genetics of con-
genital heart disease. In Ferencz C, Rubin JD, Loffredo CA, Magee C
(eds.): Perspectives in pediatric cardiology. Vol. 4. Epidemioloy of congenital heart disease: the Baltimore-Washington Infant Study 1981–
1989. Futura, Mount Kisco NY 1993
4 Buskens E, Grobbert D, Frohn-Muldet I, Wladimiroff J, Hess J: Aspects
of the aetiolgy of congenital heart disease. Eur. Heart J. 16 (1995) 584
5 Chinn A, Fitzsimmons J, Shepard TH, Fantel AG: Congenital heart dis-
ease among spontaneous abortuses and stillborn fetuses: prevalence
and associations. Teratology 40 (1989) 475
6 Copel J, Cullen M, Green J, Mahoney M, Hobbins J, Kleinman C: The
frequency of aneuploidy in prenatally diagnosed congenital heart disease: an indication for fetal karyotyping. Amer. J. Obstet. Gynecol. 158
(1988) 409
7 Gerlis LM: Cardiac malformations in spontaneous abortions. Int. J. Car-
diol. 7 (1985) 29
8 Hoffman JIE: Incidence of Congenital Heart Disease: I. Postnatal Inci-
dence. Ped. Cardiol. 16 (1995) 103
9 Mennicke K, Schwinger E: Genetische Aspekte kongenitaler fetaler
Herzerkrankungen. Gynäkologe 30 (1997) 181
10 Nora JJ, Nora AH: Maternal transmission of congenital heart diseases:
new recurrence risk figures and the questions of cytoplasmic inheritance and vulnerability to teratogens. Amer. J. Cardiol. 59 (1987) 459
11 Nora JJ, Nora AH: Update on counseling the family with a first-degree
relative with a congenital heart defect. Amer. J. Med. Genet. 29 (1988)
137
12 Paladini D, Calabro R, Palmieri S, Andrea T: Prenatal diagnosis of con-
genital heart disease and fetal karyotyping. Obstet. Gynecol. 81 (1993)
679
13 Rose V, Gold RJM, Lindsey G, Allen M: A possible increase in the inci-
dence of congenital heart defects among the offspring of affected
parents. J. Amer. Coll. Cardiol. 6 (1985) 376
14 Tennstedt C, Chaoui R, Körner H, Dietel M: Spectrum of congenital
heart defects and extracardiac malformations associated with chromosomal abnormalities: results of a seven year necropsy study. Heart
82 (1999) 34
15 Schwanitz G, Zerres K, Gembruch U, Bald R, Gamerdinger F, Hansmann
M: Prenatal detection of heart defects as an indication for chromosome analysis. Ann. Genet. 33 (1990) 79
16 Ursell PC, Byrne JM, Strobino BA: Significance of cardiac defects in the
developing fetus: a study of spontaneous abortuses. Circulation 72
(1985) 1232
17 VermilionRP: Basic Physical Principles. In Snider AR, Serwer GA, Ritter
SB (eds.): Echocardiography in Pediatric Heart Disease, 2
Year Book, St. Louis 1997
18 Whittemore R, Wells JA, Castellsague-Pique X, Holabird NB: Congeni-
tal heart defects in the progeny of affected mothers versus fathers.
Circulation 78 (Suppl. II) (1988) 396 (abstract)
nd
ed. Mosby-
218
23 Use of Color Doppler in Echocardiography
U. Gembruch
Importance of Color Doppler Echocardiography in Prenatal Diagnosis
The introduction of color Doppler echocardiography (synonym: two-dimensional Doppler echocardiography) can be
considered a milestone in the prenatal diagnosis of heart defects and disturbances of cardiac function. While it is true that
most fetal heart defects can be diagnosed in the second and
third trimesters by two-dimensional imaging with a modern
high-resolution ultrasound scanner (two-dimensional echocardiography),the ability to simultaneously display blood flow
can greatly facilitate the diagnosis of complex cardiac anomalies. Color-flow imaging can also supply essential information
on the hemodynamics of specific heart defects, which can vary
greatly with the degree and severity of the defect. Moreover,
prognostic evaluations can be made antenatally by analyzing
the changes in intracardiac blood flow.
Examination of the Normal Heart
Equipment Settings
There is no need to explore the physical aspects of color Doppler sonography in this chapter. One essential aspect of fetal
echocardiography is using the correct equipment settings.
Pulse repetition frequency. Because color Doppler sonography
is itself a pulsed Doppler technique, aliasing will occur when
the sampled blood flow exceeds the selected velocity range,
i.e., when the detected Doppler shift frequencies exceed the
Nyquist limit. Given the high blood flow velocities that occur in
the fetal heart, it is best to use a relatively initial high pulse repetition frequency (PRF) setting in fetal echocardiography. On
the other hand, some flows in and around the fetal heart will
require a low PRF setting, such as pulmonary venous flow, flow
across the foramen ovale, and also diastolic ventricular inflow
and systolic outflow into the two great arteries when an unfavorable insonation angle is used. The PRF setting is considered optimal when the imaged blood flow completely fills
the associated vessel or cardiac chamber with no aliasing.
Toachieve the highest possible spatial and temporal resolution of intracardiac blood flow, the ROI (region of interest) box
should be set to display color flow in the smallest possible area.
This is necessary to ensure a high line density and frame rate.
The wall filters in fetal echocardiography are generally set
higher than in the Doppler scanning of peripheral vessels. The
persistence is set relatively low due to the desired high frame
rate.
Some heart defects cannot even be diagnosed without the
aid of color Doppler imaging. This is particularly true when
fetal echocardiography is performed during the first and early
second trimesters, when the flow image is useful and sometimes essential for locating the desired cardiac scan planes.
This chapter deals primarily with the situations and
anomalies in which color Doppler echocardiography provides
an essential adjunct to two-dimensional echocardiography.
Further information on color Doppler echocardiography and
its role in fetal echocardiography can be found in many current
articles and textbooks
Variance mode. An essential step in the initial color setup is to
select the variance mode. When this mode is selected, increasing variance (bandwidth) of the velocities and Doppler
shift frequencies about the mean velocity or Doppler shift
frequency in the selected sample volume causes more and
more green pixels to be added to the basic flow color. When
the flow is directed toward the transducer, red becomes increasingly yellow; when the flow is away from the transducer,
blue becomes increasing turquoise. The variance mode setting is a rapid way to detect disturbed or turbulent blood flow
in the heart such as that caused by valve stenosis, valve re-
gurgitation, or intracardiac shunts. For this reason, the variance mode is preferred over the velocity mode in fetal echocardiography. The latter mode, which is standard in obstetric
Doppler, displays higher Doppler shift frequencies in brighter
shades of color. This is less important in fetal echocardiography because, based on the Doppler equation, the encoded
colors do not reflect the flow velocities but are always influenced by velocity and insonation angle. For this reason, absolute velocity measurements in the heart are always performed with a spectral Doppler system, generally pulsed
Doppler, making an effort to keep the insonation angle in the
range 0–10⬚ or 170–180⬚. Angle correction should not be used
for intracardiac flow studies. Based on the cosine function of
the insonation angle in the Doppler equation, angle correction
at very low angles is unnecessary while at higher angles it
leads to gross errors in the estimation of blood flow velocities.
These errors result from the fact that blood flow in the central
4–6, 8–11, 14, 28, 31
.
Specific Obstetric Problems
219
Use of Color Doppler in Echocardiography
portion of the heart or great arteries may not move parallel to
the vessel wall.
Imaging jets. In imaging flow jets through stenotic or regurgitant valves and intracardiac shunts, absolute velocities can be
measured only if the beam angle is close to 0⬚ or 180⬚ in relation
to the jet. Angle corrections are not used for these measurements because they lead to extreme overestimation of the jet
velocity due to the eddies that form in the parajet. Due to the
high Doppler shift frequencies, it is often necessary to use continuous-waveDoppler so that flow can be sampled without aliasing. Also, when the velocity mode is used instead of variance
mapping, a turbulent jet may not produce an abnormal color
Doppler flow pattern because the encoded mean velocities
may fall within the normal range due to the tremendous variance of Doppler shift frequencies in the jet area. This is the
main reason why variancemapping is always preferred in color
Doppler echocardiography over the velocity mapping traditionally used in obstetrics.
Examination Technique
23
Screening. Color Doppler echocardiography permits rapid
screening of the fetal heart for abnormal blood flow patterns.
When color-flow abnormalities are found, they should always
be confirmed with spectral Doppler, as this is the only technique that can positively distinguish aliasing from turbulence.
In cases with unfavorable access angles to the fetal heart and in
early echocardiography, color Doppler is helpful in quickly locating the veins and arteries leading to and away from the
heart. It provides a natural adjunct to two-dimensional echocardiography, in which a 90⬚ insonation angle is best for defining cardiac structures and vessels, as opposed to the parallel
angle (0⬚ or 180⬚) that is best for visualizing blood flow in
Doppler echocardiography.
Procedure. Doppler echocardiography follows a standard segmental protocol that starts by imaging the visceral situs, the
descending aorta, and the inferior vena cava. Next the
visceroatrial, atrioventricular, and ventriculoarterial connections are defined along with the blood flow patterns in those
areas. The PRF should be continually adjusted at this stage to
obtain an optimum flow image that is not distorted by aliasing.
For example, a low PRF is generally necessary to define pulmonary venous inflow into the left atrium, while a relatively high
PRF is better for def ining the origin of the great arteries from
the two ventricles. A relatively low PRF is nee ded to demonstrate the brachiocephalic vessels arising from the aortic arch,
which generally have an unfavorable angle relative to the
transducer.
ventricular flow across the tricuspid and mitral valves; ventriculoarterial flow across the pulmonary and aortic valves; the
two pulmonary arteries, the ductus arteriosus, and the aortic
arch with the origins of the brachiocephalic vessels; interatrial
blood flow across the foramen ovale; and the venous flow in
the coronary sinus, which travels from left to right along the
posterior cardiac wall facing the diaphragm
hand, the coronary arteries arising from the aortic sinus can be
visualized in the normal fetus only under extremely favorable
examination conditions (advanced gestational age, or a fetus
lying dorsoanterior with the aortic root close to the transducer,
allowing the use of relatively high frequencies) or in cases of
myocardial hypoxia with extreme dilatation and increased
perfusion of the coronary vascular bed (Fig. 23.
occur in chronic and acute hypoxemic states
Differentiation of abnormal flow patterns. Aliasing can occur
even with normal blood flow patterns and velocities, depending on the transducer frequencies that are used (when the
transducer frequency is doubled, the same blood flow velocities produce twice the Doppler frequency shift). Aliasing is
most pronounced in the great arteries and especially in the
ductus arteriosus, where the highest flow velocities normally
occur. Thus, when abnormal blood flow patterns are detected
in the area of the semilunar valves and ductus arteriosus, spectral Doppler analysis of flow velocity waveformsshould be performed to differentiate between aliasing and disturbed blood
flow due to pathological obstructions. This points to another
advantage of color Doppler echocardiography: areas with abnormal flow patterns can be quickly located with color Doppler
and then interrogated by selective positioning of the pulsed
Doppler sample volume or the CW (continuous-wave) Doppler
sampling beam. This application of color Doppler is also useful
in studies of normal and abnormal hemodynamics, as it permits very accurate positioning of the pulsed Doppler sample
volume, thereby increasing the precision of absolute velocity
measurements compared with conventional duplex Doppler
echocardiography.
3
. On the other
1), which may
2, 19
.
220
Structures visualized. Besides the blood flow in the inferior and
superior vena cava and pulmonary veins (with practice,
patience, and the proper transducer, all four pulmonary veins
can be identified as earlyas the 13th week of gestation), the following are easily defined with color Doppler ultrasound: atrio-
Fig. 23.1 Origin of the right coronary artery from the aortic sinus
(AO) in a severely growth-retarded fetus (29 weeks + 5 days).
Cardiac Valve Regurgitation
Functional Physiological Tricuspid Regurgitation
Owing to the specific features of the fetal circulation, regurgitation through the atrioventricular (AV) valves most commonly involves the tricuspid valve apparatus. The right heart
dominance and higher ventricular afterloads, along with the
structural peculiarities of the tricuspid valve apparatus, explain why functional tricuspid valve regurgitation occurs in
6–7% of all fetuses
tion is almost unknown. This “physiological” tricuspid regurgitation is transient, is generally confined to early and mid-systole, has a maximum velocity no higher than 2 m/s, and produces a relatively small color-flow jet within the atrium.
Rarely, there are also cases in which transient, physiological
tricuspid regurgitation is holosystolic, occupies more of the
atrial area, and reaches velocities higher than 2 m/s.
Pulmonary valve regurgitation is rare, with an incidence of
approximately 0.5 %
21, 27
, while functional mitral valve regurgita-
30
, and aortic regurgitation is much rarer
Cardiac Valve Regurgitation
still. The observation that both tricuspid regurgitation and pulmonary valve regurgitation occur during periods of fetal
breathing indicates that the degree of distention and afterload
are factors that affect functional valve regurgitation.
Pathological Tricuspid Regurgitation
Cardiac valve malformations. Severe tricuspid regurgitation
occurs as a result of tricuspid valve malformations due to dysplasia (Fig. 23.
gurgitation can lead to massive dilatation of the fetal right
atrium and in some cases to venous pressure elevation culminating in fetal hydrops (see Anomalies of Atrioventricular
Blood Flow).
Stretching of the valve ring. Stretching of the tricuspid valve
ring leads to secondary functional tricuspid regurgitation that
is no longer within the normal range. The stretching can result
from volume overload of the ventricle and/or pressure loads
due to outflow tract obstruction. For example, relatively mild
forms of tricuspid regurgitation result from flow obstructions
in the left heart that cause volume loading of the right ventricle. They also result from volume overloads due to arterio-
venous shunts. Outflow tract obstructions such as constriction
of the ductus arteriosus, which is usually drug-induced
rarely occurs spontaneously
tion with an intact interventricular septum or in absent-pulmonary-valve syndrome can lead secondarily to tricuspid
valve regurgitation.
2) and in the setting of Ebstein anomaly. This re-
27
23
, and severe pulmonary obstruc-
and
Specific Obstetric Problems
a
b
Fig. 23.2 Severe, holosystolic tricuspid regurgitation in a fetus with
tricuspid valve dysplasia and pulmonary atresia (33 weeks + 4 days).
a Color Doppler shows a long regurgitant jet covering a large area
within the dilated right atrium.
b Spectral analysis with continuous-wave Doppler shows that the regurgitation is holosystolic with a peak velocity of 3.09 m/s.
Tricuspid and Mitral Valve Regurgitation
Myocardial diseases and tachyarrhythmias. Besides a volume
overload that distends the valve ring, AV valve regurgitation
may also be caused by myocardial dysfunction due to an infectious disease (myocarditis) or cardiomyopathy or by a rise of
ventricular pressure with secondary papillary muscle dysfunction due to local hypoxia. AV valve regurgitation in fetal tachyarrhythmias most commonly results from a tachycardia-induced “cardiomyopathy” that develops above a critical heart
rate due to myocardial hypoxemia (Fig. 23.
cardial perfusion takes place in diastole, as the extravascular
wall pressure is much lower in this phase than during systole.
But the length of diastole is greatly shortened when tachyarrhythmia is present. The final stage of severe myocardial
hypoxia is marked by AV valve regurgitation on both the right
and left sides of the heart
1
.
Fetofetal transfusion syndrome. In this syndrome the elevated
preload and afterload in the recipient twin lead initially to tricuspid valve regurgitation and, in the advanced stage, to mitral
valve regurgitation.
3)
16, 25
. Most myo-
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