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192
Intrapartum Fetal Heart Rate Changes and Doppler Sonography
which are associated with the appearance of reverse diastolic
flow with a significant transient reduction in fetal oxygen
supply. Time and again in recent years we have benefited from
the technical ability to make a gross assessment of fetal oxygen
supply in the delivery room.
Effect of Intrapartum FHR Decelerations on Quantitative Parameters of Umbilical Blood Flow
Fetal bradycardia. Within the physiological range of FHR (120–
160 bpm), the effects of heart rate on umbilical artery end-di-
astolic velocity waveforms with a normal impedance are not
clinically significant
with the length of diastole, fetal bradycardia of less than 100
bpm is associated with a significant prolongation of the compensatory diastolic flow described by Moll
end-diastolic frequency shift. Whereas direct resistance
changes during uterine contractions often radically alter the
umbilical artery waveform even before the FHR decelerates
(see above) and the heart-rate effect is “added on,” the presence of fetal bradycardia in cases where impedance is un-
21
changed by the uterine contraction has only an indirect effect
on the umbilical artery waveform. When the technique for
area-under-the-curve determination described above is used
for the quantitative assessment of the relative perfusion of the
umbilical arteries in these cases, we find that these areas have
major pathophysiological significance. For example, fetal
bradycardia in a normal umbilical arterial waveform (Fig.
21.
13a ) leads to an increase in the area under the waveform per
cardiac cycle. As a result, the decrease in perfusion caused by
the low heart rate is partially offset by blood still flowing at a
relatively high velocity during the prolonged diastolic phase.
This effect is barely evident in an abnormal umbilical
waveform (Fig. 21.
with absent diastolic flow (Fig. 21.
diastolic blood flow (Fig. 21.
would be theoretically increased due to the prolonged diastole,
and in extreme cases this would quicklycause the netquantitative blood flow to approach zero.
Fetal bradycardia in normal and abnormal umbilical
waveforms. We tested these theoretical considerations in
practice. In cases with intrapartum FHR decelerations with no
direct impedance changes, we measured the area integrals
under the waveform for a normal umbilical arterial flow spectrum, for reduced end-diastolic flow, for absent diastolic flow,
and for reverse diastolic flow in the umbilical artery. We found
that FHR deceleration occurring in a normal Doppler spectrum
was associated with a marked increase in the area under the
waveform relative to the length of the cardiac cycle (Figs. 21.
21.
11). This effect was much less pronounced when there was a
primary decrease in end-diastolic flow. With absent diastolic
flow, we observed no heart rate-dependent change in the area
integral under the waveform. It is particularly interesting
when FHR deceleration occurs in cases with negative diastolic
flow. While the systolic forward flow component remains unchanged during the deceleration, the diastolic reverse flow
component increases in proportion to the prolongation of dias-
5, 25, 36, 39, 52
13b ) and is imperceptible in a waveform
. But because the FHR correlates
37
and thus of the
13c ). In cases with reverse
13d ), the reverse flow volume
10,
a
b
c
d
Fig. 21.13 Waveform patterns in the fetal umbilical artery. Left
column: normal FHR. Right column: fetal bradycardia.
a With normal impedance.
b With primary increase in impedance.
c With absent end-diastolic flow.
d With reverse diastolic flow.
tole (Fig. 21.
14). Contrary to the conditions in a normal umbili-
cal artery waveform, the deceleration leads to a decrease in the
net blood flow per beat. If we calculate the area under the
waveform (in cm
2
per minute) for the situations described
above, which provides a relative measure of the amount of
blood perfusing the scanned vascular segment per minute, we
find a less steep reduction in the area under the normal
waveform during fetal bradycardia, a slightly steeper decline in
the initially abnormal umbilical waveform, a linear decline in
the waveform with absent diastolic flow, and an exponential
drop in relative blood flow per minute in the waveform showing reverse diastolic flow (Fig. 21.
15). The area in the reverse
flow channel at 60 bpm is equal to the area in the forward flow
channel during systole, resulting in a net blood flow of zero at
this FHR.
Practical implications. The markedly greater heart rate-de-
pendent decrease in quantitative blood flow per unit time in
abnormal umbilical arterial waveforms and the exponential
decline in waveforms with negative diastolic flow make it very
likely that these fetuses, already in jeopardy, are placed at considerable additional risk for hypoxia when decelerations occur
in the FHR. This helps us to understand the frequent clinical observation that some fetuses can develop a significant acid–base
Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
problem in the form of acute respiratory acidosis after just a
few FHR decelerations, while other fetuses continue to exhibit
normal acid–base values even after repeated decelerations.
Animal studies have also documented the heightened suscep-
tibility of growth-retarded fetuses to an additional hypoxic
2
stress
.
Because the fetal oxygen supply declines significantly when
umbilical blood flow falls below 50% of the initial value
deceleration in the FHR should be considered a serious threat
to fetuses with reduced diastolic flow in the umbilical arteries
and especially to fetuses with absent or reversed umbilical diastolic flow. One clinical implication for cases with intrapartum decelerations is that “basic Doppler” of the umbilical arteries between contractions or on admission to the delivery
room can provide valuable information for estimating the
hypoxic risk to the fetus from FHR decelerations. Based on the
discoveries to date, spontaneous or induce d labor (oxytocin
test) should be avoided in fetuses that exhibit absent or reverse
flow. These contractions could trigger a potentially damaging
cascade of oxygen deprivation in the intervillous space and
FHR deceleration causing an exponential decline of blood flow
in the umbilical arteries, culminating in severe hypoxia.
19
,every
Specific Obstetric Problems
Fig. 21.14 Severely abnormal umbilical artery waveform with reverse
diastolic flow (top). Waveform from the same fetus during a decelera-
tion in the FHR (bottom).
8
7
/min)
3
6
5
4
3
2
Area under the waveform (cm
1
0
50 60 120100 110 130
70 80 90 140 150
Normal waveform
Abnormal waveform
Reverse diastolic flow
FHR (beats/min)
Fig. 21.15 Area under the umbilical artery waveform (flow volume/
min) as a function of the FHR. Top: normal waveform. Center: reduced
diastolic flow. Bottom: reverse diastolic flow.
Direct Effect of Intrapartum Fetal Hypoxia or Hypoxemia on Blood Flow Patterns in the Umbilical Arteries and Vein
Normal umbilical waveforms in acute hypoxemia. While the
effect of reduced umbilical perfusion on the fetal oxygen
supply is obvious, it is important to consider the direct effects
of fetal asphyxia on blood flow in the umbilical arteries. According to Jensen
proximately 35% reduction in umbilical blood flow, due mainly
to the decrease in FHR (Fig. 21.
level of the initial value has been found after brief, recurring
periods of asphyxia despite centralization of the fetal circulation, but with a normal FHR
can be induced in fetal sheep by restricting the oxygen supply
to the mother or by occluding the blood supply to the inter-
villous space. Umbilical blood flow remains unchanged in
these studies even when there are marked changes in the fetal
arterial oxygen partial pressure
unable to demonstrate acute fetal hypoxia or asphyxia in experimental animals
when we consider that the perfusion resistance in the fetal
placenta probably cannot change acutely due to the lack of a
nerve supply to the arterial resistance vessels of the placenta,
although it might be affected by the fetal epinephrine level.
The elevated fetal blood pressure in asphyxia
creased perfusion pressure, however, and could mask a hypothetical epinephrine effect. The clinical example in Fig. 21.
shows a normal umbilical artery waveform during acute fetal
asphyxia in the expulsion stage despite fetal respiratory acidosis and hypoxemia. A slight increase in the RI is not seen until
terminal bradycardia owing to the heart-rate effect described
above.
Abnormal Doppler indices associated with a chronic supply
deficit. The significant correlation between abnormal Doppler
22
, one minute of asphyxia leads to an ap-
11). Placental blood flow at the
22
. Acute or chronic hypoxic states
41
. Doppler velocimetry was
17,38, 45
. These results are not surprising
29
leads to an in-
16
193
Intrapartum Fetal Heart Rate Changes and Doppler Sonography
Fig. 21.16 Abnormal FHR
tracing in a patient admitted
at term with a fully dilated
cervix. A prolonged, Wshaped deceleration was recorded after amniotomy,
which yielded a greenish
amniotic fluid, and intrauterine resuscitation was
carried out. Preparations
were made for an emergency
cesarean section. Microblood test showed respiratory acidosis. Fetal asphyxia
cannot be detected by Doppler velocimetry of the umbilical arteries.
194
indices in the umbilical arteries and a poor fetal outcome in a
high-risk pregnancy does not contradict these f indings, as the
21
abnormal waveform in these cases reflects the chronic resistance increase in the fetoplacental circulation due to deficient formation or secondary occlusion of the vascular tree of
the fetal placenta
18
. This helps us to understand the studies
that found a poor correlation between the umbilical artery
Doppler findings obtained between contractions and the fetal
outcome
10, 43
. Besides the risks to the fetus that are incurred by
the delivery process itself, this is due mainly to the fact that the
prevalence of abnormal Doppler findings in term fetuses at
delivery is relatively small, since fetuses with an abnormal
umbilical artery flow pattern already manifest clinical abnormalities at an earlier time.
Late decelerations and an elevated S/D ratio. In cases with late
decelerations in the FHR, Brar et al.
5
found that Doppler
velocimetry of the umbilical arteries could detect an elevated
S/D ratio in fetuses that developed signs of hypoxemia during
the delivery. These measurements were obtained between
contractions, however, and our experience indicates that the
S/D ratio is not affected during late decelerations, aside from
heart-rate effects. This was confirmed in a study by Damron et
8
al.
, who recorded umbilical artery waveforms between and
also during contractions. Fetuses with late decelerations were
found to have a higher S/D ratio than fetuses with a normal
heart rate in measurements performed between contractions.
Measurements at the height of contractions yielded indices
that corresponded to the values between contractions.
Umbilical vein pulsations. Ninety percent of the fetuses with
late decelerations showed umbilical vein pulsations during
contractions, signifying a possible short-term overload of the
right heart. In cases with a normal intrapartum FHR, the
authors found constant, undisturbed blood flow in the umbilical vein, which is consistent with the earlier results of other
authors
12, 16, 44
. The umbilical vein recording in Fig. 21.17 also
shows that the acute hypoxic response of the fetus can be
clearly recognized in the flow pattern of the venous system.
Fig. 21.17 Blood flow pattern of the umbilical vein during terminal
bradycardia before delivery of the fetus in Fig. 21.16.
Intrapartum Blood Flow Patterns in the Fetal
Aorta
With a normal intrapartum FHR, uterine contractions do not
have an appreciable effect on the Doppler waveforms of the
fetal aorta
flow velocities due to a heart-rate effect
umbilical cord can induce reverse diastolic flow in the fetal
aorta of experimental animals
firmed by other authors in animal studies using isolated com-
12
. Decelerations lead to a decrease in end-diastolic
33
. These results have been con-
13
. Occlusion of the
Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
pression of the umbilical vein17and correspond to the findings
in the umbilical arteries on occlusion of the umbilical vein. It is
reasonable to conclude that acute fetal hypoxia does not have a
direct effect on the waveform of the fetal aorta. On the other
hand, a redistribution of the fetal cardiac output in favor of
cerebral perfusion could have an indirect effect on the fetal
aortic waveform, as acute animal experiments have demonstrated
22, 23
.
Quantitative blood flow measurements. Quantitative
measurements of blood flow in the fetal aorta showed no significant change in volume flow during labor
12
. Other authors
measured a slightly significant increase in quantitative flow
from 200 to 245 (ml/min)/kg between contractions
32
. The reliability of these quantitative measurements is uncertain,
however, since the determination of aortic diameters involves
considerable errors
31
that become exponentially large in calcu-
lations.
Intrapartum Blood Flow Patterns in Fetal
Cerebral Vessels
Compression of the fetal head. Animal studies have demon-
strated a reduction of cerebral blood flow in response to fetal
head compression as a cause of decelerations in the FHR
fetal anterior, middle, and posterior cerebral arteries and the
internal and common carotid arteries are accessible to Doppler
velocimetry
54
. Transducer pressure on the fetal head is sufficient to lower end-diastolic flow velocities in cerebral vessels,
and strong transducer pressure can even cause reverse diastolic flow in the middle cerebral artery (MCA)
changes in the internal carotid artery flow pattern have been
demonstrated in oligohydramnios
46
.
30
48
. Similar
. The
Table 21.3 Doppler measurements of cerebral perfusion during
labor
Authors n Flow pattern during dilation stage (DS)
Fendel et al.
14
(1990)
Maesel et al.
34
(1990)
Our results 8 No waveform change during contractions
DS = dilation stage; COD = cervical os diameter; FHR = fetal heart rate
7 Early DS: S/D ratio slightly increased
Late DS: S/D ratio markedly increased
Breech presentation: S/D ratio not affected
15 No waveform change during contractions
(COD 4 –9 cm, membranes ruptured)
with a normal FHR (COD 2 –9 cm), absent
diastolic flow during early deceleration
Early and late dilation stage. Only a few studies on intrapartum
measurements have been published to date. With a normal
FHR, the blood flow pattern of the MCA is apparently unchanged during uterine contractions
34
. Other authors14found a
slightly increased S/D ratio in the internal carotid artery during
the early dilation stage of labor. But as the fetal head descends
during the late dilation stage, the S/D ratio rises from 3.5 to 5.5
during contractions, reflecting the increased resistance to
cerebral perfusion with increasing head compression. Our own
studies (Table 21.
3) have shown no effect on the MCA
waveforms with a normal FHR. In the presence of decelerations, which may be synchronous or delayed in relation to
uterine contractions, the absence of diastolic flow in the MCA
may well be an expression of fetal head compression
(Fig. 21.
18). Thus, Doppler has confirmed the concept of a re-
duction in cerebral blood flow by fetal skull compression as the
cause of these relatively early-onset decelerations during
labor.
Specific Obstetric Problems
Fig. 21.18 Absent diastolic flow in the middle
cerebral artery (MCA)
during labor as an expression of fetal head compression with typical early
decelerations in the FHR.
195
Intrapartum Fetal Heart Rate Changes and Doppler Sonography
Summary
196
Doppler velocimetry during labor, as opposed to measurements in the resting fetus and uterus, can detect waveform
changes in uterine and fetal vascular regions that occur in a
matter of seconds.
Uterine arteries. Contraction of the uterine muscles leads to a
dramatic rise of impedance in the uterine arteries, with a
corresponding reduction in quantitative blood flow. The extent
of these changes depends on the strength of the uterine contractions and does not show a reliable correlation with external tocometry in the contraction stress test. With a preexisting
abnormal uterine artery waveform in a patient with pregnancy-induced hypertension, Doppler velocimetry during a
uterine contraction shows forward-directed systolic flow but
reverse diastolic flow.
Umbilical arteries. In examinations of the umbilical and intrafetal vessels, direct mechanical effects due to compression
are distinguished from heart-rate- and/or hypoxia-related factors that can alter the flow patterns. In cases with a normal
21
FHR, uterine contractions do not alter the blood flow pattern in
the umbilical arteries. In cases with umbilical cord compression during labor, Doppler can demonstrate an arrest of umbilical perfusion caused by bidirectional movement of the blood
column due to occlusion of the umbilical vessels. If decelerations due to a different cause occur during labor, the heart rateinduced waveform changes in deceleration with a normal initial flow pattern lead only to a slight reduction of mean blood
flow velocity in the umbilical arteries owing to the relatively
high diastolic flow velocities. This ensures that a volume flow
of approximately 70% of the initial value is maintained even if
the FHR falls below 60 bpm. But in cases with primarily abnormal waveforms and especially with preexisting reverse diastolic flow in the umbilical arteries, a deceleration in the FHR
will cause a significantly sharper or even exponential fall of
relative volume flow in the umbilical circulation. Thus, intrapartum FHR decelerations in fetuses with initially abnormal
umbilical artery waveforms are considered to be a much less
favorable prognostic sign. Decelerations should be avoided,
therefore, in fetuses with absent or reverse diastolic flow.
Based on available results, labor induction and challenge tests
that may induce decelerations in the FHR are contraindicated
in these cases.
Fetal hypoxemia. Fetal hypoxemia does not directly affect the
umbilical artery waveforms during labor. However, if umbilical
vein pulsations occur during a deceleration or during a uterine
contraction, this appears to be an unfavorable prognostic sign.
Fetal aorta. Uterine contractions with a normal FHR do not
alter the blood flow patterns in the fetal aorta. When decelerations occur, the changes are similar to those seen in the umbilical arteries. No representative studies have been published on
this subject, however, due to the technical difficulties of scanning the fetal aorta during labor.
Cerebral vessels. The rise of intrauterine pressure during labor
does not affect the velocity waveforms of the cerebral vessels.
However, the mounting external pressure on the descending
fetal head during labor leads to a decrease in diastolic flow
velocities as an expression of the increased intracranial pressure.
References
1 Abitbol MM, Monheit AG, Rochelson BL, Stern W, Blyakher L, Saraf V:
The use of an indwelling Doppler probe to study acute changes in
umbilical artery waveforms in the fetal sheep. Amer.J. Obstet. Gynecol.
161 (1989) 1324–1331
2 Block BSB, Llanos AJ, Creasy RK: Responses of the growth-retarded
fetus to acute hypoxemia. Amer. J. Obstet. Gynecol. 148 (1984) 878–
885
3 Borell V, Fernström I, Ohlson L, Wiquist N: Influence of uterine con-
tractions on the uteroplacental blood flow at term. Amer. J. Gynecol.
Obstet. 93 (1965) 44–57
4 Brar HS, Platt LD, DeVore GR, Horenstein J, Medearis AL: Qualitative
assessment of maternal uterine and fetal umbilical artery blood flow
and resistance in laboring patients by Doppler velocimetry. Amer. J.
Obstet. Gynecol. 158 (1988) 952 –956
5 Brar HS, Platt LD, Paul RH: Fetal umbilical blood flow velocity
waveforms using Doppler ultrasonography in patients with late
decelerations. Obstet. Gynecol. 73 (1989) 363–366
6 Campbell S, Diaz-Recasens J, Griffin DR, Cohen-Overbeek TE, Pearce
JM, Willson K: New Doppler technique for assessing uteroplacental
blood flow. Lancet i (1983) 675–677
7 Cruz AC, Frentzen BH, Gomez KJ, Allen G, Tyson-Thomas M: Continu-
ous-wave Doppler ultrasound and decreased amniotic fluid volume in
pregnant women with intact or ruptured membranes. Amer. J. Obstet.
Gynecol. 159 (1988) 708–714
8 Damron DP, Chaffin DG, Anderson CF, Reed KL: Changes in umbilical
arterial and venous blood flow velocity waveforms during late decelerations of the fetal heart rate. Obstet. Gynecol. 84 (1994) 1038–1040
9 Fairlie FM, Lang GD, Sheldon CD: Umbilical artery flow velocity
waveforms in labour. Brit. J. Obstet. Gynaecol. 96 (1989) 151–157
10 Feinkind L, Abulafia O, Delke I, Feldmann J, Minkoff H: Screening with
Doppler velocimetry in labor. Amer. J. Obstet. Gynecol. 161 (1989)765–
770
11 Fendel H, Fendel M, Pauen H, Liedtke B, Schonlau H, Warnking R: Dop-
pleruntersuchungen des arteriellen uterinen Flows während der Wehentätigkeit. Z. Geburtsh. u. Perinat. 188 (1984) 64–67
12 Fendel H, Fettweis P, Billet P et al.: Doppleruntersuchungen des ar-
teriellen utero-feto-plazentaren Blutflusses vor und während der Geburt. Z. Geburtsh. u. Perinat. 191 (1987) 121–129
13 Fendel H, Sohn Ch: Dopplersonographie in der Geburtshilfe. Springer,
Berlin 1989
14 Fendel H, Funk A, Jörn H, Gans A: ZerebralerBlutfluß unter der Geburt.
Z. Geburtsh. u. Perinat. 194 (1990) 272–274
15 Fischer WM: Kardiotokographie. Thieme, Suttgart 1981
16 Fleischer A, Anyaegbunam AA, Schulman H, Farmakides G, Randolph
G: Uterine and umbilical artery velocimetry during normal labor.
Amer. J. Obstet. Gynecol. 157 (1987) 40–43
17 Fouron JC, Teyssier G, Maroto E, Lessard M, Marquette G: Diastolic
circulatory dynamics in the presence of elevated placental resistance
and retrograde diastolic flow in the umbilical artery: A doppler echographic study in lambs. Amer. J. Obstet. Gynecol. 164 (1991) 195–203
18 Hitschold T, Weiss E, Beck T, Müntefering H, Berle P: Beeinflußt die
Vaskularisation der Placenta fetalis die enddiastolischen Blutflußgeschwindigkeiten in den Nabelarterien? Geburtshilfe Frauenheilkd.
50 (1990) 623–627
References
19 Itskovitz J, LaGamma EF, Rudolph AM: The effect of reducing umbilical
blood flow on fetal oxygenation. Amer. J. Obstet. Gynecol. 145 (1983)
813–818
20 Janbu T, Koss KS, Nesheim B-I, Wesche J: Blood velocities in the uterine
artery in humans during labour. Acta. Physiol. Scand. 124 (1985) 153–
161
21 Jensen A, Hohmann M, Künzel W: Redistribution of fetal circulation
during repeated asphyxia in sheep: effects on skin blood flow, transcutaneous PO2, and plasma catecholamines. J. Dev. Physiol. 9 (1987)
41–45
22 Jensen A: Das Schocksyndrom des Feten. Med. Welt 38 (1987) 1072–
1083
23 Jensen A, Hohmann M, Künzel W: Dynamic changes in organ blood
flow and oxygen consumption during acute asphyxia in fetal sheep. J.
Dev. Physiol. 9 (1987) 543–559
24 Kirkinen P, Jouppila P, Huch R, Huch A: Blood flow velocity waveforms
at late pregnancy and during labor. Arch. Gynecol. Obstet. 244 (1988)
19–23
25 Kofinas AD, Espeland M, Swain M, Penry M, Nelson LH: Correcting
umbilical artery flow velocity waveforms for fetal heart rate is unnecessary. Amer. J. Obstet. Gynecol. 160 (1989) 704–707
26 Künzel W, Mann LI, Bhakthavathsalan A, Airomlooi J, Liu M: The effect
of umbilical vein occlusion on fetal oxygenation, cardiovascular parameters, and fetal electroencephalogramm. Amer. J. Obstet. Gynecol.
128 (1977) 201–208
27 Künzel W, Kurz CS, Kastendieck E: Die Variabilität der fetalen Herz-
frequenzreaktion auf die Reduktion der uterinen Durchblutung. Z. Geburtsh. u. Perinat. 185 (1981) 343–350
28 Künzel W, Hohmann M: Interpretation der fetalen Herzfrequenz
währendder Schwangerschaftund Geburt. Gynäkologe 17 (1984)255–
261
29 Künzel W: Das fetale Schocksyndrom. Z. Geburth. u. Perinat. 190
(1986) 177–184
30 Künzel W: Überwachung des Feten während der Geburt. In Wulf KH,
Schmidt-Matthiesen H (eds.): Klinik der Frauenheilkunde und Geburtshilfe. Bd 7/I. Urban & Schwarzenberg, München 1990, 91–134
31 Künzel W,Jovanovic V, Grüßner S: Der Blutfluß in der Venaund Arteria
umbilicalis während der Schwangerschaft. Geburtshilfe Frauenheilkd.
51 (1991) 513–522
32 Lindblad A, Bernow J, Marsál K: Obstetric analgesia and fetal blood
flow during labour. Brit. J. Obstet. Gynaecol. 94 (1987) 306–311
33 Lingman G, Marsál K, Rosén K-G, Kjellmer I: Blood flow measurements
in exteriozized lamb fetuses during asphyxia. In Jung H, Fendel H
(eds.): Doppler technics in obstetrics. Thieme, Stutgart 1986, 36–40
34 Maesel A, Lingman G, Marsál K: Cerebral blood flow during labor in
human fetus. Acta. Obstet. Gynecol. Scand. 69 (1990) 493–495
35 Mansouri H, Gagnon R, Hunse C: Relationship between fetal heart rate
and umbilical blood flow velocity in term human fetuses during labor.
Amer. J. Obstet. Gynecol. 160 (1989) 1007–1012
36 Mires G, Dempster J, Patel NB, Crawford JW: The effect of fetal heart
rate on umbilical artery flow velocity waveforms. Brit. J. Obstet.
Gynaecol. 94 (1987) 665–669
37 Moll W: Strömungsgeschwindigkeit und Doppler-Shift in fetalen und
maternen Gefäßen. Gynäkologe 25 (1992) 278–28
38 Morrow RJ, Adamson SL, Bull SB, Ritchie JWK: Hypoxic acidemia, hy-
perviscosity, and maternal hypertension do not affect the umbilical
arterial velocity waveform in fetal sheep. Amer. J. Obstet. Gynecol. 163
(1990) 1313–1320
39 Newnham J, Patterson L, James I, Reid S: The effect of heart rate on
Doppler flow velocity systolic/diastolic ratios in umbilical and uteroplacental arterial waveforms. Early Hum. Dev. 21 (1990) 21–29
40 Olofsson P, Thuring-Jönsson A, Marsál K: Uterine and umbilical circu-
lation during the oxytocin challenge test. Ultrasound Obstet. Gynecol.
8 (1996) 247–251
41 Peeters LLH, Sheldon RE, Jones MD, Makowski EL, Meschia G: Blood
flow to fetal organs as a function of arterial oxygen content. Amer. J.
Obstet. Gynecol. 135 (1979) 637–646
42 Rosenkrantz TS, Oh W: Cerebral blood flow in infants with poly-
cythemia and hyperviscosity: Effect of partial exchange transfusion
with plasmanate. J. Pediatr. 101 (1982) 94–98
43 Sarno AP, Ahn MO, Brar HS, Phelan JP, Platt LD: Intrapartum Doppler
velocimetry, amniotic fluid volume, and fetal heart rate as predictors
of subsequent fetal distress. Amer. J. Obstet. Gynecol. 161 (1989) 1508–
1514
44 Stuart B, Drumm J, FitzGerald DE, Duignan NM: Fetal blood velocity
waveforms in uncomplicated labour. Brit. J. Obstet. Gynaecol. 88
(1981) 865–869
45 van Huisseling H, Hasaart THM, Ruissen CJ, Muijsers GJJ, de Haan J:
Umbilical artery flow velocity waveformsduring acute hypoxemiaand
the relationship with hemodynamic changes in the fetal lamb. Amer.J.
Obstet. Gynecol. 161 (1989) 1061–1064
46 van den Wijngaard JAGW, Wladimiroff J W, Reuss A, Stewart PA: Oligo-
hydramnios and fetal cerebral blood flow. Brit. J. Obstet. Gynaecol. 95
(1988) 1309–1311
47 Vetter K: Dopplersonographie in der Schwangerschaft. Ed. Medizin
VCH, Weinheim 1991
48 Vyas S, Campbell S, Bower S: Maternal abdominal pressure alters fetal
cerebral blood flow. Brit. J. Obstet. Gynaecol. 97 (1990) 740–747
49 Weiss E, Hundemer H-P, Berle P: Dopplersonographische Untersu-
chung der Art. umbilicalis: Abhängigkeit von der fetalen Herzfrequenz. In Dudenhausen JW, Saling E (eds.): Perinatale Medizin. Bd
XII. Thieme, Stuttgart 1988, 170 –171
50 Weiss E, Hitschold T, Berle P: Untersuchungen zur Reduktion der
umbilikalen Durchblutung bei Feten mit variablen Dezelerationen der
Herzfrequenz mittels Dopplersonographie der Nabelarterie. Z. Geburtsh. u. Perinat. 193 (1989) 60–67
51 Weiss E, Hitschold T, Berle P: Umbilical artery blood flow velocity
waveforms during variable decelerations of the fetal heart rate. Amer.
J. Obstet. Gynecol.164 (1991) 534–540
52 Weiss E: Die Blutflußmessung in der Schwangerschaft. Bedeutung der
Dopplersonographie in der klinischen Anwendung. Habilitationsschrift, Johannes Gutenberg Universität Mainz 1993
53 Weiss E: Fetale Herzfrequenz und Dopplersonographie. Gynäkologe
27 (1994) 146–150
54 Wladimiroff JW, Tonge HM, Stewart PA: Doppler ultrasound assess-
ment of cerebral blood flow in the human fetus. Brit. J. Obstet. Gynaecol. 93 (1986) 471–475
Specific Obstetric Problems
197
22 Color Doppler Ultrasound in Fetal Echocardiography
A. Lindinger
Congenital Heart Disease—Incidence and Risk Factors
Congenital heart disease has a reported incidence of
0.4–0.8%
unknown but is believed to be multifactorial. A genetic defect
can be demonstrated in approximately 5–10% of cases. Teratogenic agents can be identified in a small percentage of cases
➤
In approximately two-thirds (35–99%) of cases where a fetal
chromosome abnormality exists.
➤
In approximately 25% of cases with extracardiac anomalies.
➤
In fetuses with a structural cardiac malformation, a chromo-
22
some abnormality is present in approximately 30% of cases
and an extracardiac anomaly in 50%
Heart defects account for a very high percentage of fetal deaths
in the early stage of pregnancy. This percentage declines with
advancing gestation (Table 22.
ties and genetic defects with the most important associated
cardiac anomalies and their incidences.
fetal findings that are commonly associated with congenital
heart disease and thus warrant an examination of the fetal
heart.
congenital heart disease is between 2 % and 20%, depending on
the degree of the relationship and the number of affected relatives (Table 22.
volve left ventricular outflow tract obstruction such as severe
2, 3, 8
. The etiology of most congenital heart defects is
It is estimated that a cardiac anomaly is present:
6, 12, 14, 15
5, 7,16
1)
.
Table 22.
Table 22.
The risk of recurrence in patients with a family history of
There is a high risk of recurrence for heart defects that in-
2 lists the most frequent chromosome abnormali-
3 lists the maternal diseases and risk factors and
1, 10, 11, 13, 18
4)
.
.
4, 9
Table 22.1 Percentage of fetal deaths due to heart defects atvarious
gestational ages. (After reference 7)
Gestational age Percentage of fetal deaths
due to heart disease
.
⬍ 10th week of gestation 40
Weeks 11–15 18
Weeks 16–20 8
Weeks 21–25 7
aortic stenosis and especially hypoplastic left heart syndrome,
for which recurrence rates up to 20% have been reported
Thus, a fetal ultrasound examination should be recommended in the 20th or 21st week of gestation in patients with a
positive family history of congenital anomalies, patients with
maternal metabolic diseases, patients on chronic medication,
and patients with pregnancy complications that involve one of
the known risk factors.
10, 18
.
198
Table 22.2 Types and incidences of cardiac anomalies in the setting of chromosome abnormalities and genetic defects
Chromosome abnormality/genetic defect Cardiac disease Incidence (%)
Down syndrome (trisomy 21) Complete AV septal defect, tetralogy of Fallot 40
Pätau syndrome (trisomy 13) Atrial or ventricular septal defect, patent ductus arteriosus 90
Edwards syndrome (trisomy 18) Conotruncal defects 100
CATCH 22 (microdeletion 22q11) Conotruncal defects 90
Marfan syndrome (defect in fibrillin-1 gene,
chromosome 15q21.1)
Williams–Beuren syndrome (deletion at 7q11.23) Supravalvular aortic stenosis, peripheral pulmonary stenosis 100
Bourneville–Pringle disease, tuberous sclerosis
(9q34, 16p13.3)
Turner syndrome (45 XO) Coarctation of the aorta 30
Dilatation of aortic root and ascending aorta, mitral valve
prolapse
Multiple cardiac rhabdomyomas 50
90
General Introductory Remarks on Color Doppler Sonography of the Fetal Heart
Table 22.3 Maternal and fetal risk factors and diseases that are an
indication for ultrasound evaluation of the fetal heart
Maternal risk factor Incidence
(%)
Infections (e.g., rubella)
Alcohol abuse
Metabolic disorders:
Poorly controlled diabetes mellitus
PKU: phenylalanine level ⬎ 15mg/dl
Medications: hydantoin, lithium, thalidomide, sex
hormones, retinoids
Polyhydramnios/oligohydramnios
Fetal risk factors
Extracardiac anomalies
Single umbilical artery
Fetal arrhythmias:
Supraventricular extrasystoles
Supraventricular tachycardia
Third-degree AV block
Fetal effusions, hydrops
Intrauterine growth retardation
Monochorionic twins
up to 70
30–50
3
15
2–10
10/20
2–50
1–2
1–2
5–10
40
10–20
10
2
Table 22.4 Risk of recurrence for congenital heart disease in patients
with a positive family history
Affected relatives Recurrence risk (%)
One affected sibling
Two affected siblings
Affected father or mother
2–4
6–12
4–15
Specific Obstetric Problems
General Introductory Remarks on Color Doppler Sonography of the Fetal Heart
The preselected velocity range of the Doppler spectrum
Indications for Color Doppler
Sonography—Advantages and Limitations
In most cases a structurally normal fetal heart can be adequately examined with B-mode and Doppler ultrasound. The
use of color Doppler sonography is advantageous for the rapid
localization of extracardiac structures (e.g., the aortic arch) and
for evaluating the function of the cardiac valves. In the presence of a heart defect, color Doppler alwaysprovides a valuable
adjunct by color-encoding the direction of blood flow (e.g., in
cases with valvular insufficiency or reversed flow in the ductus
arteriosus) and the velocity of the flow (e.g., turbulence).
The limitations of color Doppler ultrasound are based on
technical factors and are a particularly important consideration in fetal cardiac examinations. As in Doppler velocimetry,
blood flow is optimally depicted only when the ultrasound
beam is roughly parallel to the flow, i.e., when the beam axis
forms an angle less than 20⬚ relative to the flow direction (20⬚ is
the maximum permissible angle for the Doppler sampling of
blood flow in the heart or an adjacent vessel; there is no need
for angle correction within this range
17
).
should be matched to the velocities of the sampled blood flow,
and the color intensity should be finely adjusted. This will
eliminate the majority of false-positive and false-negative artifacts in color Doppler imaging (e.g., extraluminal “color
bleed”).
Special Features of Fetal Echocardiography
Limits are generally imposed by scanning at greaterdepths and
by the frequent need for image magnification. These limitations result in low signal amplitudes with decreased lateral
and depth resolution and low frame rates. Image formation can
be optimized under these conditions by using the smallest
possible sector angle.
199
Color Doppler Ultrasound in Fetal Echocardiography
Ultrasound Examination of the Fetal Heart
Normal Findings
The procedure for ultrasound examination of the fetal heart
consists of the following components, which are illustrated in
Figs. 22.
1– 22.11.
Septum primum
RV
RA
LA
LV
Pulmonary veins
S
D
22
Moderator band
ab c
Fig. 22.1 Fetal heart in a transverse scan through the thorax.
a, b The descending aorta (DAO) appears anterior to the spine (S). In
front of the descending aorta are the left atrium (LA) and left ventricle
(LV). The cardiac apex points toward the left side. The four-chamber
view demonstrates bothatria (RA, LA) and both ventricles(RV, LV). The
right ventricle is distinguished morphologically by a transverse muscle
bundle at the apex (the moderator band) and abuts the right chest
wall. The site of entry of the pulmonary veins into the left atrium can
be identified. The septumprimum flap is deflected into theleft atrium.
c Color Doppler image in the same plane as a shows blood, encoded
in blue, flowing from the atria into the ventricles.
a b
200
Fig. 22.2 Four-chamber view with color Doppler image of blood
flowing from both atria into the ventricles. The Doppler spectra across
the tricuspid valve(TV) and mitral valve (MV) show the typicaldiastolic
flow pattern that occurs across the AV valves: the flow velocity during
the e-wave (early diastolic inflow) is slower than during the a-wave
(late diastolic inflow through atrial contraction).
a Tricuspid valve.
b Mitral valve.
Ultrasound Examination of the Fetal Heart
ab
Fig. 22.4 Upper left: four-chamber view demonstrating the sites of
entry of the right and left pulmonary veins into the left atrium (LA).
The sample volume has been placed in the right pulmonary vein.
Upper right: color Doppler image of the entry of the right pulmonary
vein and blood flow from the right atrium (RA) into the left atrium and
from there into the left ventricle (LV). RV =right ventricle. Below: typical Doppler spectrum of pulmonary venous flow with a brief dip during
atrial contraction (앖).
Fig. 22.3 The scan plane is tilted from
the four-chamber view (a) to the fivechamber view (b) by anterior angulation
of the transducer. This brings the left ven-
tricle (LV) and the base of the aortic valve
(AAo) into view. RA = right atrium,
LA = left atrium, RV = right ventricle.
Specific Obstetric Problems
a
Fig. 22.5 Four-chamber view demonstrating the foramen ovale.
a The septum primum flap is deflected into the left atrium (LA).
b Color Doppler image of blood flow from the right atrium (RA) into
the left atrium (LA), with a typical Doppler spectrum. RV = right ventricle, LV =left ventricle.
201
b