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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5772_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Color Doppler Sonography in Gynecology and Obstetrics
- •Preface
- •Contributors
- •Contents
- •Physical and Technical Principles
- •Principles of Ultrasound Instrumentation
- •Analysis of B-Mode Information and Artifacts
- •Duplex and Color Doppler Sonography
- •Physical Principles of Motion Detection
- •Technical Principles and Equipment Settings
- •1 Physical and Technical Principles of Color Doppler Sonography
- •Historical Development
- •B-Mode Sonography
- •Physical Principles of Echo Production
- •Analysis of Doppler Information and Artifacts
- •New Technical Processes and Approaches
- •New Developments in Transducer Technology
- •New Techniques of Signal Acquisition and Processing
- •2 Safety Aspects of Doppler and Color Doppler Sonography
- •Mechanisms of Tissue Effects
- •Heating
- •Cavitation
- •Risk Assessment of Various Ultrasound Techniques
- •Duplex Sonography
- •Color Doppler
- •Power Doppler
- •Color Velocity Imaging (CVI)
- •Transvaginal Scanning
- •Ultrasound Contrast Agents
- •Exposure of Gas-Containing Tissues
- •Measures to Limit Risk
- •Recommendations
- •General Recommendations
- •Pulsed Doppler
- •Appendix: Statements on the Biological Safety of Diagnostic Ultrasound Fields
- •EFSUMB Statement on the Clinical Safety of Diagnostic Ultrasound
- •WFUMB Statement on Thermal Effects in Clinical Applications
- •3 Uterine Blood Flow in Fertile and Infertile Women
- •Uterine Blood Supply
- •Changes in Uterine Blood Flow during the Menstrual Cycle
- •Blood Flow Parameters in the Uterine Arteries
- •Uterine Blood Flow in InfertileWomen
- •Uterine Blood Flow and Fertilization Rate
- •Uterine Blood Flow in the Normal Cycle and during Ovarian Stimulation with Confirmed Ovulation
- •Endometrial Imaging
- •Conclusions
- •4 Uterine Causes of Infertility
- •Ultrasound Detection of Uterine Abnormalities
- •Congenital Anomalies
- •Endometrial Polyps
- •Submucous Leiomyomas
- •Adenomyosis
- •Endometritis
- •Asherman Syndrome
- •Ultrasound Detection of Endometrial Causes of Infertility
- •Effect of Endometrial Thickness and Morphology on Fertility
- •Effect of Age on Endometrial Function
- •Endometrial Peristalsis
- •Cervical Factor
- •Decline of Fertility in the Perimenopausal Period
- •Uterine Receptivity
- •Oocyte Quality
- •Ovarian Function
- •Effects of Estradiol and Progesterone on Vascular Resistance
- •Sympathetic Innervation of the Uterus
- •Estrogen Effect
- •Progesterone Effect
- •Effect of Age on Ovarian and Uterine Perfusion
- •Authors’ Study
- •Interpretation of the Results
- •Functional Evaluation of the Endometrium
- •Authors’ Studies
- •Patients and Methods
- •Examination Procedures
- •Results
- •Discussion of the Role of Doppler Examinations
- •Summary
- •Applications of Doppler Sonography in Reproductive Medicine
- •Assessment of Tubal Patency
- •Patients and Method
- •Examination Technique
- •Results
- •Discussion of the Value of the Test Procedures
- •Summary
- •8 Abnormalities of Corpus luteum Function
- •Morphology and Biochemistry of the Corpus luteum
- •Conventional Methods in the Diagnosis and Treatment of Luteal Phase Defect
- •Possible Causes of Luteal Phase Defect
- •Diagnosis of Luteal Phase Defect
- •Treatment of Luteal Phase Defect
- •Ultrasound and Doppler Sonography in the Detection of Luteal Phase Defect
- •LUF Syndrome
- •Blood Flow in the Corpus luteum during Early Pregnancy
- •Fallopian Tube Catheterization
- •Aspiration of Ovarian Cysts
- •Drainage of Cul-de-Sac Abscesses
- •Selective Reduction of Multiple Pregnancies
- •Techniques of Ultrasound Tubal Imaging
- •Hysterosonosalpingography
- •9 Interventional Ultrasound in Reproductive Medicine
- •Follicular Aspiration in Assisted Reproduction
- •Transabdominal Follicular Aspiration
- •Transurethral Follicular Aspiration
- •Transvaginal Follicular Aspiration
- •Embryo Transfer
- •Obstetric Ultrasound
- •Overview
- •Monitoring Folliculogenesis
- •Development of the Corpus luteum
- •Changes in Endometrial Blood Flow
- •Luteal Blood Flow in Normal and Abnormal Pregnancies
- •Trophoblastic Invasion and Development of the Placenta
- •Implantation
- •Development of the Intervillous Circulation
- •Classic Theory
- •Objections and Alternative Theories
- •Color Doppler Studies
- •Vascularization of the Yolk Sac and Vitelline Duct
- •Changes in Uterine Perfusion after Placentation
- •Uterine Arteries and Spiral Arteries
- •Embryonic and Fetal Circulation
- •Fetal Vessels
- •Summary
- •12 Color Doppler Sonography in Ectopic Pregnancy
- •Importance of Transvaginal Sonography and Serum hCG
- •Transvaginal Color Doppler Sonography
- •Diagnostic Efficiency
- •Author’s Studies
- •Assessment of the Method
- •Summary
- •Conditions of Intrauterine Life
- •Physical Principles
- •Anatomical and Physiological Principles
- •Adaptive Processes during Pregnancy
- •Technique of Transvaginal Pulsed Doppler Flowmetry
- •Authors’ Studies
- •Uterine Perfusion in a Normal Pregnancy
- •Uterine Perfusion in an Abnormal Pregnancy
- •Discussion
- •Uterine Perfusion in a Normal Pregnancy
- •Uterine Perfusion in an Abnormal Pregnancy
- •Uterine Perfusion on Medication or after Uterine Manipulation
- •Summary
- •Doppler Flowmetry of Maternal Vessels as a Screening Test?
- •Applications of Color Doppler Sonography during Pregnancy
- •Technique of Transvaginal Doppler Sonography
- •Normal Development of Uterine Artery Doppler Spectra
- •Normal Values in Early Pregnancy
- •Early Doppler Examination of Uteroplacental Blood Flow in Abnormal Pregnancy
- •Patients
- •Results
- •Discussion
- •Summary
- •Establishing Normal Curves
- •Methodology
- •Defining the Normal Population
- •Plotting Quantile Curves
- •Results
- •Discussion
- •16 Venous Doppler Sonography
- •Historical Development
- •Physiology
- •Umbilical Vein
- •Ductus venosus
- •Inferior Vena Cava
- •Hepatic Veins
- •Clinical Applications
- •Intrauterine Growth Retardation Due to Chronic Placental Insufficiency
- •Growth Discordance in Multiple Pregnancy
- •Hydrops fetalis
- •Conclusion
- •Other Diseases
- •Specific Obstetric Problems
- •Importance of Nuchal Cord
- •Color Doppler Study on the Diagnosis of Nuchal Cord
- •Examination Technique
- •Results
- •Importance of Nuchal Cord Diagnosis in the Biophysical (ABCD) Profile
- •Role of Doppler Sonography in NC
- •Summary
- •18 Chronic Placental Insufficiency
- •Definitions
- •Definition and Incidence of Chronic Placental Insufficiency
- •Intrauterine Growth Retardation
- •Diagnosis of Chronic Placental Insufficiency
- •Diagnostic Systems
- •Indications for Doppler Sonography
- •Clinical Management of Chronic Placental Insufficiency Suspected from Doppler Findings
- •Antenatal Fetal Heart Rate Monitoring
- •Pathological Changes in Organ Systems
- •Biophysical Profile
- •Summary
- •Identifying Cases with IUGR
- •Obstetric Management
- •Surveillance of Compromised Fetuses
- •Absent End-Diastolic Flow (AEDF) and Reverse Flow
- •Absent End-Diastolic Flow in the Umbilical Artery and/or Fetal Aorta
- •Reverse Flow in the Umbilical Artery and/or Fetal Aorta
- •Clinical Results of AEDF or Reverse Flow in the Umbilical Artery and/or Fetal Aorta
- •Significance of Severely Abnormal Doppler Findings
- •Summary
- •20 Fetal Doppler Findings in Late Pregnancy
- •Physiological Findings in Late Pregnancy
- •Aorta: Quantitative Analysis
- •Aorta: Qualitative Analysis
- •Cerebral Arteries
- •Renal Arteries
- •Femoral Arteries
- •Changes in Findings at Term and in Postterm Pregnancies
- •Term Effect
- •Circulatory Balance
- •Summary
- •Pathophysiology and Technical Problems
- •Changes in Uterine ArteryWaveforms during Labor
- •Our Results
- •Discussion of Uterine Doppler Changes during Labor
- •IntrapartumWaveform Changes in Umbilical and Intrafetal Vessels
- •Umbilical Cord Doppler during Labor
- •Effect of Intrapartum FHR Decelerations on Quantitative Parameters of Umbilical Blood Flow
- •Direct Effect of Intrapartum Fetal Hypoxia or Hypoxemia on Blood Flow Patterns in the Umbilical Arteries and Vein
- •Summary
- •22 Color Doppler Ultrasound in Fetal Echocardiography
- •Congenital Heart Disease—Incidence and Risk Factors
- •General Introductory Remarks on Color Doppler Sonography of the Fetal Heart
- •Special Features of Fetal Echocardiography
- •Ultrasound Examination of the Fetal Heart
- •Normal Findings
- •Management of Suspected Congenital Heart Disease
- •23 Use of Color Doppler in Echocardiography
- •Importance of Color Doppler Echocardiography in Prenatal Diagnosis
- •Examination of the Normal Heart
- •Equipment Settings
- •Examination Technique
- •Cardiac Valve Regurgitation
- •Functional Physiological Tricuspid Regurgitation
- •Pathological Tricuspid Regurgitation
- •Tricuspid and Mitral Valve Regurgitation
- •Semiquantification of AV Valve Regurgitation
- •Anomalies of Visceroatrial Blood Flow
- •Anomalies of Atrioventricular Blood Flow
- •Anomalies of Ventriculoarterial Blood Flow
- •Anomalies of Blood Flow through the Cardiac Septa
- •Color Doppler Sonography in Fetal Arrhythmias
- •Summary
- •Structure of the Human Placenta
- •Weight and Dimensions
- •Early Development of the Human Placenta
- •Structure of the Villous Tree
- •Microstructure of the Terminal Villus
- •Maturation of the Placenta
- •Vascular Architecture of the Villous Tree
- •Regulation of Villous Blood Flow
- •Concept of the Placentone
- •Morphology and Physiological Transformation of the Maternal Basal-Plate Vessels
- •Placental Insufficiency
- •Definition and Etiology of Placental Insufficiency
- •Placental Compensatory Mechanisms
- •Classification of Placental Insufficiency by its Progression
- •Morphological Counterparts of Latent or Overt Placental Insufficiency
- •Clinical Aspects of Placental Insufficiency
- •Pathophysiological Aspects of Placental Insufficiency
- •Pathomorphological Aspects of Placental Insufficiency
- •Validation of Doppler Findings by Placental Histology
- •Resistance Index of the Umbilical Arteries
- •End-Diastolic Blood Flow Velocities in the Umbilical Arteries
- •Clinical and Diagnostic Value of Doppler Sonography of the Umbilical Arteries
- •Gynecological Ultrasound
- •Classification of Uterine Anomalies
- •Diagnosis and Complications of Septate Uterus
- •Ultrasound in the Diagnosis and Treatment of Septate Uterus—Authors’ Results
- •Patients and Methods
- •Results
- •New Thoughts on Old Problems
- •Changes in the Normal Endometrium during the Menstrual Cycle
- •Changes in Endometrial Blood Flow during the Menstrual Cycle
- •Submucous Leiomyomas
- •Endometrial Polyps
- •Endometrial Hyperplasia
- •Adenomyosis
- •Endometritis
- •Incomplete Abortion
- •Decidua
- •Examination Technique, Anatomy, and Physiology
- •Leiomyomas (Fibroids)
- •Vascularization of Leiomyomas
- •Management of Uterine Leiomyomas and the Importance of Color Doppler Sonography
- •Medical Treatment with GnRH Agonists
- •Surgical Treatment
- •Vascular Diseases in the Lesser Pelvis (Varicose Veins or Arteriovenous Malformations)
- •Incidence of Endometrial Carcinoma
- •Diagnostic Investigation of Suspicious Endometrial Findings
- •Color Doppler Sonography
- •Examination of the Uterine Artery
- •Experience at the Department of Obstetrics and Gynecology, Homburg University Hospital, Saar
- •Patients and Methods
- •Visualization and Morphology of the Vessels
- •Resistance Indices of Endometrial Vessels
- •Effect of Menopausal Status and Hormone Use
- •Effect of Histopathological Parameters, with Reference to Prognostic Factors
- •Subendometrial and Myometrial Vessels
- •Summary
- •30 Malignant Uterine Tumors
- •Endometrial Carcinoma
- •Incidence
- •Risk Factors
- •Target Group for Screening
- •Screening: Dream or Reality?
- •Authors’ Experience
- •Review of the Literature
- •Uterine Sarcoma
- •Authors’ Experience
- •Cervical Carcinoma
- •Conclusion
- •Treatment of Cervical Carcinoma
- •Assessing Treatment Response with Pulsed Color Doppler Sonography
- •Authors’ Studies
- •Discussion
- •Summary
- •Appearance of Normal Ovaries by B-Mode and Color Doppler Ultrasound
- •Specific Adnexal Masses
- •Cystic and Cystic-Solid Ovarian Masses
- •Solid Ovarian Masses
- •Conclusions
- •33 Malignant Adnexal Tumors
- •Color Doppler Sonography of Adnexal Malignancies
- •Review of the Literature
- •Neoangiogenesis
- •Detecting Blood Vessels and Defining their Location
- •Vascular Patterns
- •Pulsed Doppler Waveforms
- •Vascular Impedance
- •Blood Flow Velocities
- •Stages of Malignant Tumors
- •False-Positive Results
- •Conclusions
- •Contribution of Transvaginal Color Doppler Sonography
- •Three-Dimensional Imaging
- •Three-Dimensional Imaging of Vascular Patterns
- •Display Modes for Three-Dimensional Vascular Images
- •Ultrasound Technology in Tumor Diagnosis
- •Problems in the Interpretation of 3D Power Doppler Data
- •Current Methods for Evaluating Vascular Geometry and Function
- •Technique for Evaluating Vascular Geometry
- •Example of 3D Power-Mode Imaging of Benign and Malignant Gynecological Tumors
- •Advances in Tumor Therapy
- •Summary
- •Future Outlook
- •35 Ovarian Cancer Screening
- •Incidence and Five-Year Survival Rates of Ovarian Cancer
- •Requirements of a Screening Program
- •Definition
- •Screening Methods
- •Screening Parameters
- •Possible Screening Tests
- •Bimanual Pelvic Examination
- •Cul-de-sacWashings and Radiological Studies
- •Tumor Marker
- •Ultrasound
- •Who Should be Screened?
- •Age Distribution
- •Family History
- •Conclusion
- •Other Risk Factors
- •Historical Development
- •Blood Flow Detection
- •Number of Tumor Vessels
- •Resistance Index
- •Absolute Velocities
- •Doppler Waveform
- •Comparison of “Mirror Image Areas”
- •Conceptual Misunderstandings in the Interpretation of Doppler Measurements
- •Evolution of Breast Cancer Diagnosis
- •Continuous-Wave Doppler
- •Pulsed Doppler Techniques
- •Color Doppler
- •Equipment Settings
- •Examination Technique
- •Blood Flow Analysis
- •Study Results
- •Discussion
- •Conclusions
- •Flow Resistance in Malignant Breast Tumors
- •Authors’ Studies
- •Patients and Methods
- •Results and Discussion
- •Summary
- •Menopausal Status and Benign–Malignant Tumor Discrimination
- •Authors’ Studies
- •Patients and Methods
- •Results
- •Discussion
- •Summary
- •Applications of Color Doppler Sonography in Breast Cancer
- •Authors’ Studies
- •Methods
- •Results
- •Discussion
- •Conclusion
- •Index

Intrapartum Fetal Heart Rate Changes and
21
The surveillance of high-risk pregnancies with Doppler ultrasound is concerned with chronic or at most subacute changes
of blood flow in the uterofetoplacental system. Fetal and
uterine waveforms are recorded when the fetus is at rest and
the uterus is not contracting.
A very different situation exists when Doppler waveforms
are recorded during labor, especially when scanning is done in
cases with intrapartum fetal heart rate changes. Here it is important to consider the entirely different conditions of uterine
Doppler Sonography
E. Weiss
Pathophysiology and Technical Problems
21
Causes of FHR decelerations. Uterine contractions lead to an
acute reduction of uterine blood flow, causing a decreased maternal oxygen supply in the intervillous space
acute interruption of fetoplacentalblood flowcan occur as a result of umbilical cord compression during labor, especially if
the membranes have ruptured
causes a rise of intracranial pressure, which in turn alters the
blood flow patterns of intracranial arteries
shows accelerations in response to these acute intrapartum
events. It is more common to observe decelerations, which
cannot always be referred to a specific pathophysiological
28
cause
nostic significance is disputed
corresponding prolongation of the fetal cardiac cycle, leads
basically to a lengthening of diastole with a consequent
decrease in the maximum end-diastolic frequency shift in the
Doppler waveforms
tolerated by patients, making it a useful study for investigating
the pathophysiological mechanisms that underlie FHR alterations. It may also allow for a more accurate prognostic assessment in some cases and can help to determine whether acute
fetal asphyxia, with its dramatic effects on fetal hemodynamics
and/or maternal vessels.
. Even when a causal diagnosis is attempted, its prog-
53
.
Intrapartum Doppler velocimetry is noninvasive and is well
21, 23, 29, 30
, leads to altered blood flow patterns in the fetal
26
. Compression of the fetal head
15, 27
. A slowing of the FHR, with a
3
. Similarly, an
48
. The FHR rarely
blood flow that exist during and between uterine contractions.
In the umbilical cord and intrafetal vessels, direct mechanical
effects due to vascular compression must be distinguished
from other causes of acute impedance changes.
This chapter explores the diagnostic capabilities of intrapartum Doppler sonography based on personal results with
uterine waveforms recorded during labor and with umbilical
waveforms recorded during decelerations in the fetal heart
rate (FHR) at delivery.
Technical problems. To date, only a few authors have performed intrapartum Doppler velocimetry examinations even
though such studies are of extraordinary help in understanding pathophysiological mechanisms during delivery. This is
most likely due to the formidable technical problems that arise
when Doppler velocimetry is attempted during labor.The most
significant problems and obstacles are listed below.
➤
Uterine contractions during the dilation stage lead to
changes in maternal circulatory parameters.
➤
Maternal respiratory excursions, especially at the height of
contractions, hamper the continuous recording of Doppler
signals.
➤
The amniotic fluid volume is usually reduced at term or may
be absent due to amniotomy, greatlyincreasing the difficulty
of examining the fetal vessels with Doppler ultrasound.
➤
Uterine contractions alter the position of the transducer, the
maternal abdominal wall, and the fetus, often resulting in
loss of signal.
➤
The deeply engaged fetal head makes it difficult to record
Doppler waveforms from intracranial vessels with an
abdominal transducer.
➤
At present, on-line analysis of Doppler waveforms correlated
with the FHR trace is practically impossible or requires very
costly, nonroutine protocols.
182

Changes in Uterine Artery Waveforms during Labor
Method of measurement. When the ascending branch of the
uterine artery has been identifie d with color Doppler
(Fig. 21.
with pulsed Doppler during spontaneous or induced uterine
contractions (Fig. 21.
achieved during a contraction can be quantified by measuring
the area under the uterine artery waveform. When the angle
between the vessel and Doppler beam is kept constant, the
area under the waveform is proportional to uterine perfusion,
assuming that the low flow velocities contributing to the spectrum are uniformly distributed and can thus be disregarded
when determining a relative change in perfusion. If the area integral between contractions is taken as the initial value, then
the relative reduction in blood flow can be stated for each individual contraction. An additional angle-independent
measure of uterine impedance is the resiatnce index (RI) of the
scanned uterine artery, which is easily determined.
1), the frequency spectra are continuously recorded
2). The reduction of uterine perfusion
Our Results
Reduction in uterine blood flow during contractions. A total of
68 uterine contractions in 16 pregnancies were studied during
oxytocin-induced contractions. Within limits, the results of
these “Doppler-controlled” contraction stress tests are also applicable to the intrapartum situation. The area under the induced uterine waveforms showed a considerable variability of
flow reduction during contractions, with values ranging from
14% to 85 % of the initial value (median 54 ⫾ 20 %), despite
comparable tocodynamometry (TKD) traces. The example in
Fig. 21.
is particularly evident with a positive contraction stress test,
where the continuous uterine arterial waveform indicates the
degree of uterine flow reduction during the contraction and
also explains the decrease in hypoxic FHR decelerations occurring at contractions 2, 3, and 4. Contraction 5, which is especially prominent in the TKD trace, appears to have the least
impact on uterine perfusion and does not induce a late deceleration in this example. We cannot offer a satisfactory explanation for the absence of FHR decelerations at contraction 1
despite synchronous uterine velocimetry.
Changes in Uterine Artery Waveforms during Labor
3 shows inadequate quantification by external TKD. This
Specific Obstetric Problems
Fig. 21.1 Color-flow image of the ascending branch of the right
uterine artery at its apparent “crossover” with the iliac artery.
Reduction in uterine blood flow during premature labor. An
unphysiological reduction in uterine blood flow may occur
during labor as well as during prenatal contractions. The following example shows a case in which premature contractions
occurred at exactly 31 weeks’ gestation (Fig.21.
contractions were recorded by external TKD. The patient did
not perceive the contractions as painful (hemodynamically
stable, semilateral position), but the uterine artery waveforms
showed a massive, bilateral decrease in blood flow velocities
with reverse diastolic flow that practically canceled out the
forward flow. As a result of this, an abnormally high reduction
of blood flow in the uterine bed occurred during uterine contractions, evoking a hypoxic response in the FHR. After tocolytic therapy, the eutrophic fetus was delivered at 32 weeks 4
Fig. 21.2 Blood flow
pattern of the ascending
branch of the uterine
artery with oxytocin-induced contractions at 37
weeks.
4). The uterine
183

Intrapartum Fetal Heart Rate Changes and Doppler Sonography
Fig. 21.3 Synchronous
displays of the uterine
artery RI, the FHR in
beats/min, uterine contractions recorded by external tocodynamometry,
and relative uterine blood
flow in the examined vessel, given as a percentage
of the area integral under
the waveform in relation
to the value measured
between contractions
during the oxytocin stress
test. Gestational age 38
weeks + 2 days, possible
placental insufficiency.
21
Fig. 21.4 Doppler
waveform recorded continuously from the ascending branch of the
uterine artery during a
uterine contraction in
premature labor (31
weeks).
184
days by cesarean section due to a breech presentation with increasing cervical dilation. The placenta showed no histomorphological abnormalities (H. Müntefering, personal communication), and the acid–base balance in the umbilical cord
blood was normal.
Physiological and unphysiological reduction in uterine blood
flow. The typical uterine waveform recorded continuously
during a contraction under physiological conditions is com-
pared in Fig. 21.
5 with an unphysiological response recorded
during premature labor and with the response in a patient with
pregnancy-induced hypertension and a preexisting abnormal
uterine blood flow pattern. We see that in the physiological
case, the maximum systolic and diastolic flow velocities are
initially reduced to an equal degree until the height of the contraction, at which point we observe a massive shift in the RI
(Fig. 21.
5a). With an unphysiological flow reduction during
premature labor, the strong decrease in systolic flow velocities

Changes in Uterine Artery Waveforms during Labor
Fig. 21.5 Uterine artery
waveforms.
a Physiological response of
continuously recorded
uterine waveforms to an
oxytocin-induced contrac-
tion.
b Unphysiological response of uterine
waveforms in premature
labor.
a
b
c Response of uterine
waveforms in a patient with
pregnancy-induced hyper-
tension and a preexisting
early diastolic notch.
c
is accompanied by holosystolic reverse flow (Fig. 21.5b). An entirely different pattern is seen when there is preexisting pregnancy-induced hypertension and an early diastolic notch in the
uterine artery waveform (Fig. 21.
5c ). While the uterine con-
traction has almost no effect on maximum systolic velocities,
end-diastolic reverse flow occurs at the height of the contraction, and the waveform pattern is similar to that of the external
iliac artery. The relative reduction in blood flow, calculated as
the area under the waveform, is approximately 50–60 % of the
initial value in the physiological case and in pregnancy-induced hypertension. The initial level is assumed to be different
in both cases, however.
Discussion of Uterine Doppler Changes during Labor
Marked reduction of diastolic flow. The first Doppler measure-
ment of blood flow in the arcuate arteries was described in
6
1983
. The first uterine artery waveforms recorded during
11, 13
labor
to approximately 40% of the initial value for a maximum intrauterine pressureof approximately 60 mmHg. The maximum
systolic flow velocity decreased by only 25%, while the detectable diastolic flow velocities were absent or very low
This can be explained by the markedly reduced perfusion pressure of uterine blood flow at the height of the contraction. The
perfusion pressure during systole is approximately
60–70 mmHg when the intrauterine pressure is 50–60 mmHg
(systolic perfusion pressure = maternal systolic blood pressure
minus the intrauterine pressure minus the maternal central
showed a reduction in the mean blood flow velocity
Specific Obstetric Problems
110
100
90
80
70
60
50
40
30
Relative area under the waveform (%)
20
10
0
20 30 40 50 7060 80
10
0
Fig. 21.5d Relative reduction in blood flow determined for cases
a–c (calculated as the relative area under the uterine waveforms).
venous pressure). In diastole, a perfusion pressure is no longer
present when the intrauterine pressure exceeds the maternal
13
arterial diastolic blood pressure (disregarding the maternal
.
central venous pressure of 3–8 mmHg). Fendel et al.
definite correlation between the diastolic reduction of Doppler
flow and the strength of the uterine contraction, with diastolic
flow dropping to zero when the intrauterine pressure is
80 mmHg or higher. Systolic flow can still be demonstrated up
to an intrauterine pressure of 130 mmHg
c
a
b
Time (s)
12
showed a
185
12
.

Intrapartum Fetal Heart Rate Changes and Doppler Sonography
Table 21.1 Doppler measurements of uteroplacental perfusion during labor and in the dilation stage
Authors n UP RM COD Flow
parameters
Brar et al. (1988)
Janbu et al. (1985)
Fendel et al. (1984)
Fendel et al. (1987)
Fendel et al. (1989)
Fleischer et al. (1987)
Our results (CST) 16 Ext – 1–2 TAMV Uterine artery Reduction to 54 % ⫾ 20 % of initial value
UP = uterine pressure; RM = rupture of membranes; COD = cervical os diameter,Int= internal pressure measurement; Ext = external pressure measurement;
TASAV = time-averaged spatial average velocity over one cardiac cycle; TAMV =time-averaged maximum velocity over one cardiac cycle; CST = contraction stress
21
test.
4
20
11
12
13
27 Int + ? S/D ratio Uterine artery Up to 60 torr, inverse correlation
19 Ext ⫾ ? TASAV Radial arteries 40–100% reduction
10 Int + ? TASAV Uterine artery 58% reduction
7 Int + ? TASAV Uterine artery 43 % reduction
? Int + ? TASAV Uterine artery Absent diastolic flow at 100 mmHg or
16
12 Int + ? S/D ratio Uterine artery Absent diastolic flow at 36 mmHg or
Vessel Velocimetry
between S/D ratio and intrauterine
pressure
Uterine artery 37% reduction
Ascending uterine
artery
Vaginal artery 100% increase
60% reduction
higher
higher
(68 contractions, range 14–85%)
186
Compression of the radial arteries. The Doppler studies of
uterine blood flow during labor that have been published to
date are summarized in Table 21.
ings reported by Fendel et al.
1. The data confirm the find-
11
. Janbu et al.20recorded transvaginal velocity waveforms from the main branch, ascending
branch, and vaginal branch of the uterine artery. The patterns
in the ascending branch and main trunk of the uterine artery
were the same, showing an approximately 60 % reduction of
mean blood flow velocity during labor. The blood flow in the
radial arteries, however, appeared to show a much greater
decrease due to the course of the vessels in the myometrium.
Compression of the radial arteries should be seen as the essential cause of the increased resistance in the uteroplacental bed
during uterine contractions. Apparently the mean blood flow
velocity in the vaginal branch of the uterine artery is subsequently increased during labor
20
due to the increased perfusion pressure in that vascular bed, which itself does not undergo mechanical compression. Brar et al.
4
found an inverse
correlation between intrauterine pressure during labor and
the ratio of the maximum systolic and end-diastolic velocities
(S/D ratio) in the examined arteries, with absent diastolic flow
occurring when the intrauterine pressure reaches 60 mmHg.
Omitting the contraction stress test. Our own studies were
performed during induced uterine contractions. We found that
the reduction in mean uterine blood flow velocity corresponded to the reductions measured during spontaneous
labor. Our studies confirmed the principle of a transient reduction in uterine blood flow, and thus of the oxygen supply in the
intervillous space, that underlies the contraction stress test. It
is also clear, however, that the inability to quantify the findings
by external TKD is responsible for the poor sensitivity and the
high percentage of false-positive findings. Moreover, the improvementof FHR monitoring by the assessment of fetal move-
ments as well as intrafetal arterial and venous Doppler sampling can provide an accurate picture of fetal and placental
condition, suggesting that the contraction stress test is unnecessary in cases with a suspicious FHR and could actually increase the risk of fetal deterioration in cases with abnormal
hemodynamic f indings by Doppler ultrasound. In postterm
pregnancies as well, we have abandoned the oxytocin stress
test at our center due to its poor sensitivity and specificity in
favor of a differentiated induction strategy with prostaglandins.
Indication for tocolysis. Uterine artery velocimetry during nor-
mal or premature labor can detect an unphysiological impedance increase in cases with suspected uterine hyperactivity, providing an indication for tocolysis. Systolic blood flow is
present up to an intrauterine pressure of approximately
130mmHg under physiological conditions
12
and guarantees a
certain minimum blood flow to the intervillous space.
Findings in pregnancy-induced hypertension. The results in
patients with pregnancy-induced hypertension (PIH) and a
preexisting early diastolic notch in the uterine artery
waveform represent isolated cases that are certainly not representative. They demonstrate, however, that diastolic flow disappears in these cases when there is an increase in uterine
tone, and that a reflected resonance wave appears in early diastole due to the high peripheral resistance. The blood supply to
the intervillous space during contractions is partially maintained almost entirely by the unchanged systolic flow velocities, apparently as a result of the raised perfusion pressure due
to maternal hypertension. These findings and considerations
should caution against the indiscriminate use of antihypertensive medical therapy in patients with PIH. In cases with a
preexisting abnormal uterine waveform, Doppler scanning

Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
shows a greater rise of impedance during labor compared with
the physiological situation, indicating a greaterdanger to these
fetuses. Olofsson et al.
40
found a significantly greater rise of
uterine artery flow resistance in cases with a positive oxytocin
challenge test than in OCT-negative cases. The authors suggest
that continued susceptibility to vasopressor stimuli in the
uterine resistance vessels based on impaired trophoblastic in-
vasion may be the cause.
Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
Even more interesting than the effect of labor on uterine artery
waveforms is its effect on umbilical and intrafetal waveforms,
owing to the potential interactions between mechanical and
hypoxic factors. Some of the relationships and interactions are
so complex that they allow for different interpretations of the
observed phenomena. The material is organized below by subheads in order to make the diverse flow changes easier to understand.
Umbilical Cord Doppler during Labor
No change in blood flow velocities during the dilation stage of
labor. When the fetal membranes are intact and an adequate
amniotic fluid volume is present, the uterus can be regarded as
a hollow sphere
sure in both the umbilical vein and the umbilical arteries rises
in response to uterine contractions. As a result, there is no
change of perfusion pressure in the placental vascular tree. To a
degree, this is also true after rupture of the membranes has occurred, since the fetal head seals off most of the cervical orifice
during labor. At the same time, direct mechanical compression
of the umbilical cord is much more frequent after the membranes have ruptured
velocimetry of the umbilical arteries during spontaneous labor
in 1981
44
velocity waveforms of the umbilical arteries were not altered
by uterine contractions during the dilation stage, nor were
they affected by artificial rupture of the membranes or the infusion of oxytocin. Several other authors confirmed these results in subsequent years (Table 21.
this with a case from our files. The slight changes in end-diastolic flow velocities are caused entirely by fluctuations of the
FHR and the associated change in the length of diastole.
Heart-rate effect. Only a few authors to date have described
Doppler velocimetry of the umbilical arteries during intrapartum decelerations of the FHR in human patients. Fairlie
that unspecified decelerations in the FHR during uterine contractions were associated with a marked decrease in end-diastolic blood flow velocities. Kirkinen
variable decelerations in the FHR and absent end-diastolic flow
during the decelerations. The flow velocity waveforms were almost unchanged, however, suggesting that a heart-rate effect
may have been involved. This effect is caused by the lengthening of diastole that occurs when the FHR is slowed. It results in
a protracted fall of diastolic flow velocities to a lower end-diastolic value, with a corresponding change in Doppler indices.
Various authors have described the relationship between enddiastolic flow velocity and the fetal heart rate
30
. In this model, proposed by Künzel, the pres-
30
. Stuart et al. reported on Doppler
. When the FHR was normal, it was found that the
2). Figure 21.6 illustrates
9
found
24
described a case with
35, 36, 49
.
Table 21.2 Doppler measurements of fetoplacental perfusion during
labor
Authors n Umbilical artery waveforms
Stuart et al.
44
(1981)
Fendel et al.
12
(1987)
Fleischer et al.
16
(1987)
Brar et al. (1988)
Kirkinen et al.
24
(1988)
Fairlie et al.
9
(1989)
Weiss et al. (1989,
50, 51
199 1)
Cruz et al. (1988)
Sarno et al.
43
(1989)
Feinkind et al.
10
(1989)
FHR = fetal heart rate.
10 No change in waveforms during con-
15/7 No change in waveforms during con-
12 No change in waveforms during con-
4
27 No change in waveforms during con-
? Absent diastolic flow during decelera-
43 Heart-rate effect during decelerations
8 Variable decelerations in FHR
7
71 Rupture of fetal membranes had no
109 No relationship between intrapartum
273 No relationship between P
Our Results
Simultaneous recording of Doppler waveforms and the FHR. A
total of 130decelerations of the FHR were studied in eight term
fetuses with ruptured membranes and variable decelerations
by simultaneous Doppler measurement of umbilical artery
flow and internal FHR monitoring. The pregnant women were
between 38 weeks + 1 day and 40 weeks + 6 days’ gestation,
and the fetuses were eutrophic. Typical, repetitive variable FHR
decelerations were recorded in all cases. Fetal-scalp blood gas
analysis, done before Doppler velocimetry, was normal in
seven cases and preacidotic in one case. The umbilical artery RI
between contractions was within the normal range of our
physiological reference curves in all the fetuses.
Technical problems. The technical problems in Doppler
velocimetry were related to an absence of amniotic fluid and
increased maternal respiratory excursions during labor, which
often caused the selected fetal umbilical artery to move out of
traction
No effect from amniotomy or oxy-
tocin
traction
traction
traction
tions
with no significant waveform change
Reverse diastolic flow in 6 fetuses,
heart-rate effect in 2 fetuses
effect on S/D ratio (measured be-
tween contractions)
asphyxia and S/D ratio (measured be-
tween contractions)
,P
,O
O
CO
2
2
saturation, and velocity waveforms
(measured between contractions)
Specific Obstetric Problems
2
187

Intrapartum Fetal Heart Rate Changes and Doppler Sonography
Fig. 21.6 Flow velocity waveforms recorded from
an umbilical artery during labor (cervical dilation
5 cm), with mild fetal tachycardia.
188
21
the Doppler sample volume. In 45 contractions the signals
were lost for more than 10 seconds per contraction, and in 50
contractions they were lost for 5–10 seconds per contraction.
Thirty-five contractions wererecorded with a signal loss of less
than 5 seconds, and 22 with no signal loss at all. At least two recordings with losses of less than 5 seconds could be obtained
for each case. The Doppler waveforms were recorded on videotape and analyzed later.
Analysis. The video recordings were digitized, and the area integral under the Doppler envelope curve was determined with
special PC analytical software. For exact synchronization of the
flow patterns and FHR traces, the duration of each cardiac cycle
was measured in the flow spectra to calculate the beat-to-beat
heart rate. The FHR curve was then plotted with a graphic program and expanded according to the paper feed rate of the
Doppler traces (4 cm/s). In this way the FHR tracing could be
synchronized with the waveforms.
Reverse diastolic flow. Although typical umbilical cord decelerations were present in the FHR traces based on the criteria of
Fischer
served in the umbilical arteries. The waveforms in two fetuses
showed only a heart-rate effect consisting of a prolonged decline of diastolic flow velocities in bradycardia (Fig. 21.
slope of the diastolic velocity decline was not significantly altered, however, so no change was found in the impedance parameter (RI) when the measurement was adjusted for heart
rate. By contrast, the umbilical artery waveforms in six fetuses
changed dramatically during the decelerations, showing a reversal of diastolic flow (Fig. 21.
15
, two distinctly different waveform changes were ob-
7b). This finding cannot be ex-
7a). The
plained by the decrease in FHR or by changes in the beam–vessel angle. The reverse diastolic flow pattern in these cases
correlates with an acute rise of impedance in the fetoplacental
circulation caused by the occlusion of umbilical blood flow.
When Abitbol et al.
1
and Fouron et al.17experimentally occluded the umbilical veins in fetal sheep, they observed Doppler patterns of reverse diastolic flow in the umbilical arteries
like those we observed during human labor
50, 51
.
Delayed appearance of deceleration. We related the timing of
the drop in the FHR and the appearance of absent end-diastolic
flow in the umbilical arteries using the complicated method
outlined above (detailed description in reference 50). The synchronous display in Fig. 21.
8 shows that when end-diastolic
flow disappears, the flow changes can be detected approximately 6–8 seconds prior to the FHR deceleration. This finding
is consistent with the effects of umbilical vein occlusion in experimental animals
26
. This time delay was evident in all cases
with absent end-diastolic umbilical flow, although the range of
variation was from 4 to 10 seconds. Figure 21.
8 also shows that
the FHR deceleration may still be present at a point where almost normal diastolic flow velocities reappear in the umbilical
arteries.
Relative perfusion of the fetal placenta with reverse diastolic
flow. To obtain a measure of the actual flow reduction in cases
with absent end-diastolic umbilical flow and umbilical cord
decelerations, we determined the area under the umbilical
artery waveforms for each individual cardiac cycle and compared it with the average area in the interval between contractions (mean value of 10 waveforms before the next contrac-

Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
Fig. 21.7 Umbilical artery
velocity waveforms recorded
before and during variable
decelerations in the FHR.
a Heart-rate effect associated with fetal bradycardia. Measurement of the
end-diastolic flow velocity
after an interval corresponding to the cardiac cycle
Specific Obstetric Problems
ab
Fig. 21.8 Synchronous display of continuously
recorded Doppler waveforms and FHR traces
during the appearance of absent end-diastolic flow.
189

Intrapartum Fetal Heart Rate Changes and Doppler Sonography
tion). This procedure assumes a constant beam–vessel angle as
well as a uniform distribution of all flow velocities over the
vessel cross section (ideal laminar flow with a parabolic profile) in determining the area integral under the waveform. This
type of flow is essentially present in fetal vessels when a normal hematocrit is assumed
close correlation with actual volume-flow changes in areaunder-the-waveform determinations
change in beam–vessel angle cannot be completely ruled out,
but it cannot account for the occurrence of reverse diastolic
flow. Also, repeat measurements taken at different umbilical
cord sites in the same fetus showed almost identical flow
changes, and so this error is considered slight. When the relative perfusion of the fetal placenta is calculated by determining
the relative flow velocity (Fig. 21.
complete cessation of fetoplacental perfusion during the
deceleration with absent end-diastolic flow in the umbilical
artery.
47
. Other authors have described a
42
. The possibility of a
9), we find an almost
160
140
Heart rate
(beats/min)
120
100
80
60
100
80
( ) per min
60
0 102030405060s
Relative perfusion of the fetal placenta with a heart-rate effect.
When the same calculation is performed during a deceleration
and shows only a heart-rate effect on the umbilical artery
waveforms (Fig. 21.
21
10), we observe a decrease in the relative
flow per minute, which paralleled the deceleration in the FHR
(Fig. 21.
11). But the fall in FHR from approximately 135 to 70
bpm causes only a 30% decrease in relative blood flow, because
an increase in the area under the waveform due to the prolonged cardiac cycle in bradycardia represents an increased
stroke volume. It may be assumed, then, that in cases that
show a heart-rate effect only, the fetal blood volume that is
40
( ) per cardiac cycle
Relative blood flow (%)
20
0
Fig. 21.9 FHR trace (top) and relative blood flow (bottom) during
FHR deceleration with reverse diastolic flow in the umbilical artery.
The area integral under the waveform in relation to the mean area integral between contractions was used as a measure of relative blood
flow.
Fig. 21.10 Synchronous display of continuously recorded Doppler waveforms
and FHR traces, with a heartrate effect on the fetal
umbilical artery waveform.
190

Intrapartum Waveform Changes in Umbilical and Intrafetal Vessels
140
120
100
Heart rate (beats/min)
80
60
0
140
120
100
80
Relative blood flow (%)
60
10
20 30
per cardiac cycle per min
40
50
60
sec
Fig. 21.11 FHR trace (top) and relative perfusion of the scanned
umbilical artery (bottom) during the deceleration in Fig. 21.10, with a
heart-rate effect on the velocity waveforms. Calculated as in Fig. 21.9.
delivered into the placenta per heartbeat is increased and partially compensates for the loss of perfusion due to bradycardia.
Different reverse flow patterns. In cases with acute reverse diastolic flow during the deceleration, we were able to identify
different types of reverse flow pattern (Fig.21.
12). The early di-
astolic form with brief reverse flow, occurring in some cases
during the previous flow phase, can be interpreted in terms of
the double-expansion-chamber (“windkessel”) model of
37
Moll
as resonant flow in the presence of an extremely high
resistance located just past the sampling site and may well reflect an occlusion of the umbilical artery. According to this
model, holodiastolic reverse flow that tends to increase at the
end of diastole would be interpreted as compensatory flow
from the peripheral expansion chamber (i.e., the placenta) in
the presence of an umbilical vein occlusion. The question
whether an occlusion of the umbilical vein alone or of both the
umbilical vein and artery underlies the cases with acute diastolic reverse flow is of minor importance in terms of placental
perfusion. In both cases the result is a cessation of fetoplacental
perfusion, as there is only an ineffectual to-and-fro movement
of the fetal blood column in the umbilical arteries.
Clinical evaluation of variable decelerations. Since animal experiments have shown that the oxygen supply to the fetus remains almost constant when umbilical blood flow is reduced
to approximately 50% of normal but that the fetal oxygen
supply declines exponentially when umbilical flow is reduced
below 50%, intrapartum Doppler velocimetry is a valuable tool
in the clinical evaluation of variable decelerations in the FHR,
Specific Obstetric Problems
Fig. 21.12 Early diastolic resonant
flow and holodiastolic reverse flow
during a variable deceleration in the
FHR.
191
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