Electronic Fetal Monitoring 9811573638, 9789811573637

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Electronic Fetal Monitoring Xiaohui Guo Editor

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Electronic Fetal Monitoring

Xiaohui Guo Editor

Electronic Fetal Monitoring

Editor Xiaohui Guo Department of Obestetrics Shenzhen People’s Hospital Shenzhen China

ISBN 978-981-15-7363-7    ISBN 978-981-15-7364-4 (eBook) https://doi.org/10.1007/978-981-15-7364-4 Jointly published with People’s Medical Publishing House, PR of China © People’s Medical Publishing House, PR of China 2021 This work is subject to copyright. All rights are reserved by the Publishers, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publishers, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publishers nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publishers remain neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore

Preface

Electronic fetal monitoring (EFM), which is a noninvasive means of evaluating fetal well-being, characterized by easy operation, low cost, and continuous monitoring, can reflect fetal well-being to some extent and thus is commonly used in clinical practice. It assists obstetric medical staff in detecting fetal ischemia-hypoxia or acidosis on a timely basis, but non-standard use of it may increase the probability of a cesarean section owing to “abnormal monitoring results.” Rational use of the EFM technology and normative interpretation of EFM patterns helps to detect fetal ischemia-hypoxia or acidosis more effectively, thereby suppressing the increase in the cesarean section rate caused by misinterpretations. In this book, the clinical application methods of EFM and precautions for use are described from multiple angles including the operation of EFM equipment, the basic definition and interpretation standards of patterns, the clinical analysis of prenatal and intrapartum cases, and the aversion of risks. Besides, the editorial board members’ years of clinical experience are summarized based on the latest clinical guidelines in the hope of providing obstetric medical staff with a concise, comprehensive, and practical book on EFM skills as a theoretical and practical basis for guidance on clinical decision-making. Starting with the basic knowledge of EFM, this book describes the clinical significance of pattern interpretation and monitoring results from the shallower to the deeper and analyzes typical cases in order to help obstetric medical staff easily master the clinical skills. Many clinical cases of physiological and pathological obstetrics are studied in the book, where clinical treatment procedures, clinical outcomes, and EFM patterns are summarized and analyzed comprehensively to offer the readers an accurate interpretation of the clinical significance of EFM patterns. There are also many clinical case pictures typeset as graphs in the book to provide readers with a more intuitive understanding of the EFM pattern interpretation methods. I would like to extend my heartfelt thanks to the editorial board members, who have made tremendous efforts for the publication of the book. With rich clinical experience, they have all offered good advice on guiding clinical decision-making about EFM in the book based on the latest literature and practical guidelines from home and abroad. I sincerely hope that every reader will make all comments on the book. You are welcome to send an email to [email protected] to point out mistakes so that we can correct all these errors in the second edition in order to better serve you.

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Contents

1 Assessment of Fetal Well-Being������������������������������������������������������   1 Zhaoxi Li and Xiaohui Guo 2 Management of EFM����������������������������������������������������������������������  19 Zhaoxi Li and Xiaohui Guo 3 Fundamental Electronic FHR Monitoring������������������������������������  39 Yinglan Wang, Wenqiong Sha, and Xiaohui Guo 4 Prenatal and Intrapartum EFM����������������������������������������������������  65 Wenqiong Sha and Xiaohui Guo 5 Abnormal Pregnancy���������������������������������������������������������������������� 119 Wei Shi and Xiaohui Guo 6 Pregnant Diseases���������������������������������������������������������������������������� 173 Li Lin and Xiaohui Guo 7 Fetal Acid-Base Balance������������������������������������������������������������������ 213 Xiurong Sun and Xiaohui Guo 8 Impact of Intrapartum Events on EFM���������������������������������������� 235 Xiaohui Guo 9 Fetal Arrhythmia������������������������������������������������������������������������������ 281 Jun Zhou and Xiaohui Guo

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Assessment of Fetal Well-Being Zhaoxi Li and Xiaohui Guo

There are several methods for assessing fetal well-being to learn about the developmental condition of the fetus within the uterus before childbirth. With the development of the society and the advancement of science, many fetal monitoring methods have been clinically applied, providing technical support for improving human reproductive quality.

1.1

Electronic Fetal Monitoring

Electronic fetal monitoring (EFM) dates back to the 1970s. Driven by the development of electronics, mechanical engineering and computer technology, in addition to the development of foundational medical technologies such as the Internet and cloud technology, fetal monitors are being produced in large quantities even as their size decreases. Network connectivity, data analysis, and storage techniques have vastly improved fetal monitor functionality, including signal reception, processing, and analysis in addition to intelligent monitor regulation, making it possible to monitor the fetal heart rate (FHR), uterine contraction curve, and pregnant women’s vital signs all simultaneously. Fetal monitoring grown in popularity, providing a comprehensive safety monitoring technology for pregnant women and Z. Li · X. Guo (*) Department of Obestetrics, Shenzhen People’s Hospital, Shenzhen, China

fetuses thanks to the use of an array of technologies like remote regulation, wireless probing, fetal heart tracking, information warning, wireless transmission and an intelligent analysis system of computer-assisted EFM.  At present, this technology is widely used for fetal monitoring before during labor and has become an important means for monitoring fetal safety while in the uterus. Moreover, it is used more and more widely at midwifery institutions, becoming a standard tool in maternity wards.

1.1.1 Basic Composition of Electronic Fetal Monitors The basic functions of an electronic fetal monitor fall into three parts: information collection, information processing, and information output. Some monitors also consist of an intelligent information processing and reporting system. 1. Information collection: The information collected is divided into three types: fetal information, uterine information, and other clinical information such as fetal movement information and fetal electrocardiogram (FECG). (a) Fetal Heartbeat (FHB): There are two methods to collect FHB. (i) Fetal Stethoscope: a fetal stethoscope, or fetoscope, is fixed to the pregnant woman’s abdominal wall where the FHB is loudest. Its specially made microphone can “pick

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up” FHB and send it to the main unit, where the sound is amplified and processed before being displayed on the screen in the form of a wave. Its simple structure and operation ensure that this device does not have any effect on the fetus, but it is susceptible to external sounds and uterine contractions. (ii) Doppler Ultrasound Monitoring: External Doppler ultrasound sensor utilizing the Doppler effect on ultrasound (probe frequency: 2  MHz) can be used to detect FHB.  The external Doppler ultrasound sensor utilizes the Doppler effect to transmit information collected about the heart, converting it into a doppler signal which is then processed and displayed in the form of sound and an on-screen wave. (b) Fetal Electrocardiogram (FECG): FECGs can be obtained in the following ways: (i) An abdominal electrode is affixed directly to the pregnant woman’s abdomen; or (ii) a fetal scalp electrode is usually fixed to the fetal scalp after the amniotic sac surrounding the fetus has been ruptured, either artificially or through natural means. This is used to clearly record the FECG, but the fetal scalp may be damaged and thus become infected. (c) Uterine Contraction: A pressure transducer is affixed directly against the pregnant woman’s abdominal wall. Information about uterine contractions is sent to the main unit through the pressure sensor and displayed simultaneously on the screen with the FHR curve; an intra-

Fig. 1.1  EFM patterns

uterine pressure sensor is sometimes adopted for intrauterine monitoring. 2. Information Processing: The information obtained above is processed in the main unit. FHR, FECG, and uterine contraction signals are then processed using a special method. The signal is then converted, and interference and false signals are removed, making the FHR and uterine contraction curves clearer and more accurate.A modern processor can also simultaneously process information from multiple channels and intelligently compare, analyze and store collected information, as well as automatically identify emergency signals, provide treatment advice and contact a doctor; in addition to performing an automatic remote transmission and receiving the processing results. 3. Information Output: The results processed in the main unit can be returned using multiple output methods. Common methods include single results (one machine for one pregnancy) and multiple results (multiple machines for multiple pregnancies) being displayed on the screen. The main display content includes the uterine contractions curve, FHR curve, and numerical values. A paper report (paper speed: 3 cm/min) can also be printed to analyze fetal heart rate monitor patterns (Fig. 1.1), making it possible to send the results to a remote doctor workstation or remote medical system. At present, a single machine can work independently while concurrently transmitting and sharing wired/wireless information to the central monitoring system, achieving the intelligent management and result analysis of multiple pregnancies, improving monitoring efficacy and level.

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1.1.2 EFM Technology Advanced EFM technology has become the guarantee for achieving satisfactory monitoring results and the hallmark of professionalism. A wealth of clinical experience and consummate monitor operation skills can provide reliable EFM results for clinical obstetricians. 1. Predelivery Preparation: Examining the pregnant woman is the first step of fetal monitoring. The following aspects should be noted when examining: (a) Before the examination, the patient should be briefed on the purpose and methodology of the fetal monitoring technology, the key examination items, expected feelings, and duration, relieving her nervousness and stress so that she will understand and cooperate. The patient should be examined in a calm and relaxed state, or undergo examination after making a bowel movement when necessary. (b) The doctor should expose the patient’s abdomen to the air so as to identify the size of the fetus and the direction of the fetal head; then perform four-step palpation to determine the position of the fetal head and back, check whether the fetal head is already fixed, make clear whether there is too much or insufficient amniotic fluid, and feel the contraction of the uterine wall. If necessary, the doctor can perform EFM after ultrasonography. The ideal fetal heart signal should be easy to collect on the fetal back. (c) Doppler auscultation of the fetal heart helps to locate the site where the FHB is loudest and clearest, thus determining the placement location of the external Doppler ultrasound sensor. 2. Fixation of the External Doppler Ultrasound Sensor (a) The best position to detect FHB is the site of optimal fetal heart auscultation. This is generally located on the near end of the fetal back, and an external Doppler ultrasound sensor can be placed there to satis-

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factorily record an FHR signal. This is difficult to locate in a fetus whose back is unclear or retroverted, or when the fetus descends during labor, changing the location of the heart. Therefore, during intrapartum monitoring, the external Doppler ultrasound sensor should be continuously moved or held in the hand to collect the FHR signal. The best detection location of the fetal heart during operation is determined according to the optimal position of auscultation. If the FHB can be heard in several locations, attention should be paid to the optimal auscultation area, and placement location of the probe should be determined using an abdominal fetal examination. The external Doppler ultrasound sensor shall not be pressed with force or tilted to detect the fetal heart; when necessary, ultrasound can be used to determine the position of the fetal back and fetal heart. A Doppler ultrasound probe or transducer can be used to obtain a clear FHB and a satisfactory FHR curve; a lengthy observation should be performed before fixing the external Doppler ultrasound sensor. The external Doppler ultrasound sensor can be fixed the FHR wave is stable and non-fluctuating or fluctuating slightly. (b) Proper External Doppler Ultrasound Sensor Fixation: EFM routinely requires FHR recording. Proper fixation of the external Doppler ultrasound sensor (referring primarily to the Doppler probe) directly determines whether the monitoring work can be carried out smoothly. Proper fixation requires that (i) The abdominal belt must be wide and elastic to some extent, because the external Doppler ultrasound sensor easily falls off if it is too narrow and affects the patient’s physical activity if it is too wide. A certain amount of elasticity can keep the ­abdominal belt moderately tight, keeping the external Doppler ultrasound sensor stable while ensuring the patient does not feel constrained. (ii) The abdominal belt

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is fixed around the already determined location of the fetal heart, after which the external Doppler ultrasound sensor, covered with couplant, is slipped under the lower part of the abdominal belt. First, identify whether the sound is at its clearest and the curve is regular. If the sound is not clear or the curve is not regular, the external Doppler ultrasound sensor can be adjusted slightly to check whether the sound is being captured well. If the error remains, the external Doppler ultrasound sensor needs to be further adjusted. (iii) Try to find out a maximum range of adaptation for the fixation location of the fetal heart. When a non-stress test is being conducted, the external Doppler ultrasound sensor should be fixed to the dorsal side of the fetus as much as possible. If it is fixed to a lateral side of the fetal body, the fetal heart may deviate from the capture range of the external Doppler ultrasound sensor during FMs. Similarly, during intrapartum monitoring, the external Doppler ultrasound sensor shall not be fixed too high, rather it should be slightly lower so that the external Doppler ultrasound sensor can still maintain its capture range after fetal descent during uterine contractions. 3. Uterine Contraction Sensor (a) Pressure Transducer: The pressure transducer should be placed where the patient’s abdomen is in immediate contact with her uterine wall. When an examination is conducted during the second and third trimesters, the periumbilical region, such as the left side of the umbilical region or the position slightly higher than the right side of the umbilical region, is the best site. The pressure transducer shall not be placed in any uneven part of the maternal umbilical region, the lower uterine segment, or the abdomen of the fetus; if the pressure transducer is placed too high, the change in the pressure on the uterine wall cannot be truly sensed, and the curve will look irregular. When uterine contraction and fundus

descending disengage the pressure transducer from the uterine wall, the uterine contraction curve is inaccurate. The fixed abdominal belt must be wide and slightly elastic. The elastic segment should be removed while the pressure transducer is fixed. When the abdominal belt is fastened, be sure to maintain slight pressure and adjust the instrument until the pressure returns to zero. The abdominal belt should be moderately tight. If the abdominal belt is too tight, the patient may feel uncomfortable, but if it is too loose, the change in uterine contraction pressure cannot be described. (b) Internal Uterine Contraction Sensor: After membrane rupture, fill a catheter with normal saline and insert it 15–20 cm deep into the cervix, with the outer end connected to the pressure sensor. The operation must be strictly adhered to and standardized to prevent infection.

1.1.3 EFM Methods Monitoring methods can be divided into external EFM and internal EFM according to the monitoring routes, or into antepartum EFM and EFM according to the monitoring time. 1. External EFM: Monitoring is achieved using an external Doppler ultrasound sensor (a fetal stethoscope or ultrasound Doppler probe); an abdominal induction electrode and uterine contraction pressure sensor are placed on the body surface of the patient to collect information about the FHR and uterine contraction (Fig. 1.2). 2. Internal EFM: Direct electrocardiography is a method by which an electrode is implanted through the cervix and fixed onto the fetal scalp to collect FHR and ECG information. Monitoring is achieved using a pressure sensor placed directly in the uterine cavity to collect uterine contraction information. In clinical practice, external EFM or internal EFM can be performed depending on the

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induced FHR acceleration helps to more accurately predict the acid-base balance in the fetus, reducing non-reactive NST by 40% and shortening NST duration while still being able to detect fetal acidosis. (b) The contraction stress test (CST) can be performed after bleeding in late pregnancy, multiple pregnancy, hydramnion, or hypamnion, threatened preterm labor, premature rupture of the membrane (PROM), previous cesarean, and other relevant diseases have been ruled out. Uterine arterial blood flow is reduced Fig. 1.2  External EFM under the impact of contractional stress, thus inducing transient hypoxia in the actual conditions, or both methods can be fetus. Sub-hypoxia in a fetus will be proused together to get a high-quality signal and gressively aggravated under uterine conhelp clinicians monitor pregnant women more traction stimulation, inducing late easily and better analyze EFM patterns. deceleration. Uterine contractions can 3. Antepartum Monitoring: EFM performed at also cause compression of the umbilical the gestational age of 26–32 weeks to childcord, thereby inducing variable decelerabirth is known as antepartum fetal monitoring; tion. When non-reactive NST recurs durthis is aimed at learning about the living coning EFM and intrauterine fetal hypoxia dition of the fetus in the uterus and the stress may have already occurred, CST can be response of the fetus, as well as evaluating the conducted to further evaluate the intracondition of the fetus in the uterus. This also uterine fetal status. Research findings helps to predict fetal hypoxia and test the show that for pregnant women below age fetus’ ability to resist intrauterine hypoxia. 37, if EFM results show non-reactive The gold standard for judging sensitivity, NST, it is safe and effective to conduct accuracy, and specificity is whether neonatal CST for an evaluation without increasing asphyxia or acidosis occurs after childbirth. the risk of fetal death or obstetric compli (a) The non-stress test (NST) is the most cations. However, if NST patterns clearly common antepartum fetal heart monitorindicate that fetal hypoxia is already charing method, by which the oxygenation acterized by sinusoidal waves, it is best state of the fetus in utero, the reactivity of that CST not be conducted, lest that fetal the nervous system, and the response of hypoxia should be aggravated and emerthe fetal heart to fetal activities are evalugency treatment delayed. The uterus ated under episodic uterine contractions. should contract at least 3 times/10  min, The specific implementation method is as with each contraction lasting at least 40s. follows: Have the patient lie on her side or If the patient’s spontaneous uterine sit still. Monitoring duration is normally ­contractions meet the above conditions, 20 min. Because the fetus follows a sleep there is no need to induce uterine contraccycle, NST may need to be conducted for tions. If the above conditions are not met, 40 min or longer. Some studies show that the nipples can be stimulated or oxytocin sonic stimulation can cause a range of can be intravenously infused to induce physiological phenomena in the fetus such uterine contractions. as blinking, startle reflex, enhanced FMs, 4. Intrapartum Monitoring: EFM performed durand FHR acceleration. Sonic shock-­ ing the parturient period is known as intrapar-

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tum monitoring. EFM is performed during the parturient period in order to assess whether fetal hypoxia is occurring in the delivery process and to timely detect fetuses with hypoxia to ensure that appropriate intervention measures are adopted before the injury occurs. When fetal hypoxemia is predicted, intrauterine resuscitation and timely, effective pregnancy termination can be performed to relieve fetal hypoxemia, acidosis, and cell injuries, thus improving fetal prognosis. Poor fetal outcomes caused by hypoxia and acidosis can thus be prevented. Hypoxic ischemic encephalopathy (HIE) is a short-term dysfunction of the nervous system caused by hypoxia and acidosis. Spastic or dyskinetic cerebral palsy is a long-term complication of the nervous system. Metrypercinesia and/or compression of the umbilical cord are the main causes of intrapartum fetal hypoxia. Other rare intrapartum complications, such as mechanical trauma, maternal disorders, hysterauxesis-­ induced compression, rupture of vasa previa, or fetomaternal hemorrhage may also affect the oxygen supply to the fetus. (a) Intermittent EFM: Guidelines recommend conducting intermittent EFM for low-risk pregnant women, i.e., conducting EFM intermittently and recording data. (b) Continuous EFM: This means conducting EFM throughout labor. Continuous EFM needs to be conducted when intermittent EFM detects something abnormal or when high-risk factors are present, such as antenatal maternal factors, which include: Pregnancy induced hypertension (PIH), pregnancy associated with diabetes, antenatal hemorrhage, heart disease, severe anemia, hyperthyroidism, vascular diseases, kidney diseases; antenatal fetal factors: fetal growth restriction (FGR), preterm birth, hypamnion, wave velocity anomaly of umbilical artery anomaly by Doppler, maternal-fetal blood group incompatibility, multiple pregnancy, breech position. Intrapartum maternal factors include vaginal bleeding, intra-

uterine infection; parturient factors: cesarean section history, over-long-term PROM, child delivery expedition, labor induction, uterine hypertonia. Fetal factors include anomaly suggested by FHR auscultation, meconium-staining amniotic fluid, prolonged pregnancy. EFM is conducted during the perinatal period with the primary aim of recording and analyzing the baseline FHR, baseline variability, acceleration, deceleration, and uterine contraction. The specific content is explained in detail in the relevant chapter below.

1.2

Other Monitoring Methods

1.2.1 FHR Auscultation Fetal heart auscultation was developed in the early nineteenth century when Swiss surgeon Francois Mayor used this method to collect FHB through a pregnant woman’s abdomen. Laennec, a professor at the Paris College, France, invented a wooden drum-type FHB stethoscope (Fig. 1.3). With the popularization of clinical applications and electronic technologies since the 1960s, the Doppler FHB stethoscope is commonly used in

Fig. 1.3  Wooden drum-type FHB stethoscope

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Fig. 1.4  Doppler FHB stethoscope

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The fetal head should be located first during auscultation, after which the fetal back should be located. The pregnant woman’s abdominal wall, which is against the fetal back, is the best position for auscultation. In the case of occipital presentation, FHB can be clearly heard at the bottom left or right of the pregnant woman’s umbilicus; in the case of breech presentation, FHB can be clearly heard at the top left or right of the pregnant woman’s umbilicus; in the case of shoulder presentation, FHB can be clearly heard around the pregnant woman’s umbilicus or on one side of the umbilicus. If the pregnant woman is overweight or her abdominal wall is tense or uterus is sensitive, it will be difficult to locate the fetus, which can be located according to the relative position of the fetal heart and head.

(III) Doppler Detection In the 1960s, the Doppler ultrasound method began to be used to detect FHB. Different Doppler auscultation devices have been developed with the continuous development and improvement of science and technology. There are now a variety of compact Doppler auscultation instruments to choose from which are easy to operate. Both doctors and patients can use such instruments to monitor fetal heart activity; in addition to directly detecting the fetal heart, the FHR can also be detected by measuring the blood flow of the umbilical cord. Moreover, the FHR per second is automatically counted and displayed. In addition, the Doppler auscultation device’s amplification instrument can be used to amplify FHB, which greatly promote self-monitoring and can be ­performed by the patient herself or her family members. At the earliest, the Doppler auscultation device can detect FHB within 7–8  weeks after (I) Auscultation by Stethoscope cessation of menstruation. It is generally recogFHB can be heard from a wooden bell-type FHB nized that FHB can be clearly heard within stethoscope, a frontal FHB stethoscope (Delee-­ 12 weeks after cessation of menstruation. In the Hillis stethoscope), or a common stethoscope. first trimester of pregnancy, FHB is a single, Both the wooden bell-type FHB stethoscope and high-pitched sound, with rhythmic double sounds frontal FHB stethoscope are for fetuses only, appearing later. Owing to the directional sensitivcharacterized by their clear positioning and sound ity of ultrasonic waves, patience and multiple transmission. Common stethoscopes are popular, positions may to be used during monitoring. easy to operate, and conducive to self-­monitoring. Low-pitched sounds of different lengths caused clinical practice due to its portability and high precision (Fig. 1.4). FHR auscultation and counting are the most basic clinical obstetrical EFM techniques. A normal FHB is a double sound. The first and second sounds are very close to each other, similar to the “ticking” sound of a clock. They are fast and periodic. Before the gestational age of 24 weeks, FHB can be clearly heard right below the umbilicus or slightly tilted to the left or the right; after the gestational age of 24 weeks, the position of FHB is related to the position of the fetus in the uterine cavity. Regardless of the position of the fetus, FHB can always be heard most clearly on the fetal back. When FHB is heard for fetal monitoring; uterine souffles, the pregnant woman’s abdominal aorta sounds, and sounds of FMs should be excluded.

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by fetal activities can be detected at the gestational age of 10  weeks. Two different types of FHB are detected in different positions with a frequency difference greater than ten times/min may suggest twin gestation.

1.2.2 FM Monitoring FMs are movements made by a fetus touching the uterine wall in the uterine cavity. The pregnant woman can feel the fetus move between the gestational ages of 18 weeks to 20 weeks. Movements include leg kicks, hand stretches, or direct striking of the uterine cavity. FM is a sign of good fetal conditions. As early as the 1940s, it was believed that the presence or absence of FMs had a direct relationship with fetal well-being. FMs can be felt from the gestational age of 18 weeks to 20 weeks. FM becomes obvious from the gestational age of 24  weeks to 28  weeks. FMs become increasingly periodic and obvious from the gestational age 30  weeks to 32  weeks, with the daily number of FMs becoming countable. After the gestational age of 36 weeks, the number of FMs decreases by 20%–30% due to a smaller uterine space, head engagement, or other factors. The fetus’ “biological clock,” i.e., the sleep cycle, also becomes an important determinant. Usually, the fetus is least active in the morning, becoming more active in the afternoon and most active between 18:00-22:00. However, some scholars hold that there are two peaks of FM during the day, one at 17:00–9:00, the other from 23:00 to early morning. (I) Factors Influencing Fetal Movements The pregnant woman’s movements, postures, and emotions, as well as strong light, loud noises or the abdomen being touched may cause changes in FM. FMs are more frequent when the pregnant woman lies down, and less so when the pregnant woman sits up, with the least being when she stands. There will be fewer FMs when the pregnant woman is engaged in strenuous exercise, such as running or swimming and more when she is resting. In addition, there will be more FMs if the fetus is discomforted while the pregnant

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woman is sitting or standing. Sedatives, anesthetics, ethanol, and nicotine can easily enter the fetal body through the placenta. These inhibit the fetal central nervous system, thus decreasing the number of FMs. Abstaining from such chemicals will usually correct the movements. Ultrasound, abdomen touch, strong light and loud noises can all increase the number of FMs. Pathologic pregnancy, such as pre-eclampsia, placental dysfunction, and prolonged pregnancy, feature a decrease in the number of FMs owing to fetal hypoxia and even distress. In addition, FGR, gestational diabetes, Rh hemolysis disease, hydramnion, and fetal malformation may also decrease the number of FMs or even make FMs disappear. (II) Common FM Counting Methods The pregnant woman usually begins to feel the fetus stretch their arms, kick their legs or strike the uterine wall by the 18th to 20th weeks. At the gestational age of 29  weeks to 38  weeks, FM becomes the most common. FM becomes much fewer before delivery. As such it is recommended for women to start counting FM themselves by the 28th to 43rd weeks. Anybody position can be adopted while doing so. Considering the great difference in FM strength and frequency from individual to individual, the pregnant woman is suggested to count FM according to her personal perception, recording their regularity. Different methods of counting FM have been developed since FM monitoring was proposed decades ago. The two major methods worldwide are: 1. The Sadovsky Counting Method: This method calculates the number of FMs within a fixed period of time; with the patient speeding 1 h each morning, noon, and evening in doing so. The sum of these counts is then multiplied by 4 to obtain a 12-h FM number. According to researchers, less than 3 FMs within an hour may suggest decreased FM. 2. “Counting-to-Ten method”: This method requires the patient to count the number of FMs once a day until the number reaches 10, then record how long it takes to reach that number. Usually, it is required that the pregnant woman should count FMs during periods

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of high frequency. Less than 10 FMs within 12  h is considered a warning value. If the number of FMs in the first 12 h is less than 10, the number should be considered as the warning value; however subsequent 12-h clinical monitoring can bring a burden to the pregnant woman. The difference in FM frequency within a 12-h period can be anywhere between 4–1400 times, with the number generally lying between 30 and 100 times. Therefore, every pregnant woman has her own FM frequency. On average, it takes 21 min to count to 10 FMs during periods of high frequency, with the time rarely exceeding 2 h. As such, some scholars have revised the warning value to less than 10 times within 2 h.

1.2.3 Ultrasonography of Fetus and Appendages in the Third Trimester of Pregnancy (I) Ultrasonography of Fetus in the Third Trimester of Pregnancy Third trimester ultrasonography is mainly used to evaluate fetal growth and development and identify any possible fetal structural abnormalities. Third trimester ultrasonography is primarily aimed at further, timely evaluation of first and second trimester ultrasonography of the fetus. In addition to evaluating fetal growth and examining the fetal body’s surface and internal structural development, ultrasonography helps to evaluate the maturity of fetal organs, estimate fetal viability after birth, learn about the fetal posture in the uterine cavity and reveal presentation. (II) Ultrasonography of Fetal Appendages During the Third Trimester of Pregnancy 1. Amniotic Fluid: Ultrasonic testing of the amniotic fluid volume is already widely used for antepartum monitoring. It is generally believed that the amniotic fluid volume is related to the perinatal fetus outcome. The determination of the amniotic fluid index (AFI) and amniotic fluid volume (AMV) is already commonly applied in clinical practice. Because AFI has four quadrants, it can correct

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measurement errors and subjective factors to a certain extent. Therefore, due to its higher detection accuracy and sensitivity compared to other methods, the AFI method is a satisfactory index for routine antenatal monitoring. The AFI is a reliable index during fetal monitoring. 2. Placenta: Ultrasonography helps to determine the position, size, shape, and grade of the placenta. Placental abnormalities during the third trimester, e.g., placenta previa have a great impact on the pregnant woman and the fetus. The more severe the placenta previa is, the earlier vaginal bleeding is likely to occur and the more serious the bleeding will be. Repeated vaginal bleeding may cause patient anemia and even shock, fetal hypoxia, distress, and even intrauterine death. The placenta grade already trends to be mature during the third trimester, but hypertension, pre-­ eclampsia, and chronic kidney diseases may advance placenta grading; gestational diabetes and maternal-fetal blood group incompatibility may delay placenta grading. Third trimester placenta ultrasonography plays an important role in assessing intrauterine fetal safety. 3. Umbilical Cord: Ultrasonography cannot accurately measure the length of the umbilical cord, but it can accurately judge cord entanglement, cord bleeding, and abnormal umbilical cord insertion. Third trimester ultrasound monitoring is of great significance for clinical management and delivery timing and mode selection.

1.2.4 Ultrasonic Doppler Examination of Pregnant Uterus and Fetus The essential function of the pregnant uterus is for the breeding of an embryo and fetus, for which ultrasonic Doppler examination is an important antepartum monitoring method. The pregnant uterus and fetal development can be comprehensively evaluated by dynamically

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observing the growth and development, anatomical structure, and hemodynamics of the embryo and fetus during the entire pregnant period using the Doppler ultrasound examination technique. Not only can the morphologic structure of the embryo and fetus be displayed, but the intrauterine fetal behavior state and hemodynamic changes can also be displayed, thus making it possible to timely and reliably evaluate the developmental and physiological status of the embryo and fetus throughout the entire pregnancy, in addition to fetal-placental circulation and placental-­uterine circulation.

1.2.5 Fetal Biophysical Profile (BPP) Fetal BPP was a method presented by Manning et  al. in the 1980s to monitor high-risk fetuses using ultrasound. This is referred to as the Manning 5-item scoring method and includes the following 5 items: FM (FM), fetal breathing movement (FBM), non-stress test (NST), fetal toning (FT), and amniotic fluid volume (AFV). 10 points on the test is full marks; 8–10 points are normal, while 6 points is equivocal; below 6 points suggests fetal hypoxia while 4 points or below is abnormal. Abnormal results indicate the risk of intrauterine fetal infection, fetal hypoxia, and intrauterine fetal distress. Further, if hypamnion is present, i.e., the vertical depth of the largest dark region of amniotic fluid is less than 2 cm, then the next step of evaluation must be conducted. Later, Vintzileos et al. improved upon the Manning scoring method by adding a placenta grade item (P) to it, forming Vintzileos’ 6-item scoring method. Full marks for this method is 12 points.

1.2.6 Fetal Holter Examination Fetal Holter examination is an emerging fetal monitoring method that uses the abdominal FECG technique and a fetal Holter monitor. Cordless monitoring can be conducted to obtain up to 24  h of FHR, maternal heart rate, uterine myoelectricity, and maternal activity. The method

can not only monitor intrauterine fetal conditions accurately and effectively, but also avoids interference caused by the maternal heartbeat. Studies have shown that the fetal Holter examination method can detect relevant indications of the fetal central nervous system and autonomic neuromodulation system, thus identifying fetal distress and providing effective evidence for clinical diagnosis.

1.2.7 Umbilical Artery Determination The umbilical artery is one of three blood vessels contained in the umbilical cord. In the process of mammalian embryo development, two arteries transfer fetal metabolic waste and metabolites, including carbon dioxide and malnourished blood, through the placenta to the pregnant woman’s body. The umbilical vein transports maternal oxygen and nutrient-rich blood into the fetus through the placenta and umbilical cord. Venous blood is contained inside the fetus. Fetal umbilical blood flow detection (Table 1.1) is a method by which a noninvasive detection is conducted of fetal umbilical arterial hemodynamics, it reflects the characteristics of fetoplacental circulation resistance. Vascular resistance in blood circulation can be directly reflected by continuously monitoring fetal umbilical artery using the ultrasonic Doppler instrument, and observing the ratio (S/D) of the highest blood flow velocity (S) during the umbilical artery systole to the blood flow velocity (D) during the diastole, the pulsatility index (PI) and resistance index (RI). The change in umbilical blood flow can well reflect the functionality of the placenta. Under normal pregnancy conditions, the fetal heart function strengthens and the heart rate decreases slightly as the fetus develops. Moreover, the placenta gradually grows, vascular resistance decreases gradually, umbilical arterial blood flow S/D value declines gradually, and the S/D value is less than 3 at term pregnancy. The umbilical artery S/D value does not decline in the case of intrauterine fetal growth retardation, poor placental circulation, placental

Gestational weeks 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40

PI The 5th Cases percentile 61 1.13 102 1.06 214 1.0 116 0.98 80 0.98 81 0.83 90 0.81 83 0.83 106 0.78 129 0.76 101 0.77 100 0.72 107 0.7 101 0.7 100 0.67 118 0.61 103 0.63 104 0.64 101 0.56 105 0.56 111 0.57

The 50th percentile 1.39 1.29 1.27 1.21 1.22 1.1 1.1 1.06 1.01 0.98 0.98 0.92 0.95 0.91 0.85 0.84 0.83 0.81 0.81 0.82 0.8

The 95th percentile 1.64 1.5 1.52 1.53 1.6 1.5 1.44 1.41 1.23 1.26 1.23 1.19 1.25 1.2 1.15 1.11 1.12 1.09 1.13 1.05 1.05

RI The 5th percentile 0.68 0.69 0.67 0.66 0.64 0.59 0.57 0.58 0.55 0.55 0.56 0.52 0.51 0.51 0.49 0.45 0.47 0.45 0.43 0.43 0.44 The 50th percentile 0.8 0.77 0.76 0.74 0.73 0.69 0.69 0.68 0.66 0.65 0.64 0.63 0.63 0.62 0.59 0.59 0.58 0.58 0.57 0.57 0.56

Table 1.1  Reference values of various umbilical arterial resistance indexes in different gestational weeks The 95th percentile 0.85 0.84 0.83 0.84 0.81 0.79 0.81 0.78 0.74 0.75 0.72 0.73 0.72 0.71 0.71 0.68 0.69 0.69 0.68 0.68 0.65

S/D The 5th percentile 3.16 3.15 3.0 2.9 2.71 2.45 2.33 2.4 2.19 2.26 2.22 2.12 1.97 2.02 1.96 1.86 1.89 1.96 1.77 1.78 1.78 The 50th percentile 4.91 4.3 4.14 3.9 3.73 3.19 3.2 3.08 2.9 2.86 2.79 2.68 2.65 2.58 2.42 2.42 2.4 2.33 2.33 2.34 2.28

The 95th percentile 6.63 5.89 6.11 6.17 5.37 4.84 4.74 4.17 3.93 3.83 3.63 3.7 3.6 3.46 3.39 3.14 3.12 3.12 3.14 3.07 2.88

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growth retardation, and non-reduced vascular resistance. Clinically, the S/D value does not decline regularly or increases indirectly suggests fetal dysplasia. The umbilical vessels are very sensitive to changes in the concentration of oxygen and carbon dioxide in the blood. Fetal breathing may squeeze the umbilical cord, causing temporary frequency instability, possibly making the measured value slightly higher for a short time. Umbilical blood flow may also be affected by thick subcutaneous fat of the pregnant woman and the depth of the fetal umbilical cord. Results can thus be unclear, affecting the measurement of umbilical blood flow data, leading to an increase in the S/D value. When the umbilical cord is under pressure, umbilical blood flow resistance may increase, and so may the measured value of S/D.  In this case, the S/D value is variable and reversible. In some cases, as the umbilical blood flow S/D value increases, the placental blood flow resistance rises. This is not because of placental insufficiency or any abnormalities in the pregnant woman or fetus and may be caused by something wrong with the details of the detection technology or the fetus moving during detection. If there are no other high-risk factors that can be repeatedly monitored, there will be a good perinatal fetus outcome in these cases. However, perinatal mortality significantly increases when the diastolic flow is absent or even reversed during the fetal umbilical arterial diastole. If diastolic reverse flow occurs or is absent during the umbilical arterial diastole in the second and third trimesters of pregnancy, the fetus must be carefully monitored while adopting other monitoring methods, such as fetal middle cerebral artery monitoring and ductus venosus Doppler. Termination of pregnancy is recommended if this occurs around the period of full-­ term pregnancy. As a noninvasive examination technique, umbilical artery Doppler monitoring is already widely used as intrapartum detection of FGR, gestational hypertension, fetal anemia and fetal distress. Studies prove that abnormal umbilical artery is commonly associated with gestational hypertension, positive thyroid antibodies,

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antiphospholipid syndrome and fetal malformation. The umbilical artery in a normally developing fetus flows quickly during diastole. In a growth-restricted fetus, blood flow velocity decreases during the umbilical arterial diastole while the S/D value increases. The increase in the S/D value is correlated to the fetal prognosis: An S/D value 3.0 at level 2 usually will not lead to acute fetal distress, timely intervention measures should be taken to prevent the disease from worsening; An S/D value > 4.0 at level 3 leads to poor perinatal fetal prognosis. The umbilical vascular resistance index can show abnormalities about 2 weeks in advance of abnormalities revealed by EFM. It is a simple and easily repeatable monitoring method, but attention should be paid to false positives and measurement location. When necessary, monitoring should be repeated. A reasonable therapeutic schedule and clinical treatment method should also be developed based on medical history, high-­ risk factors and other monitoring results.

1.2.8 M  easurement of Fetal Middle Cerebral Artery Color Doppler Flow Imaging (CDFI) technology is used to display the fetal cerebral Willis’ circle and measure the Middle Cerebral Artery (MCA), End Diastolic Velocity (EDV), Peak Systolic Velocity (PSV), peak Systolic Velocity/end Diastolic Velocity (S/D), Pulsatility Index (PI) and Resistance Index (RI). The Fetal MCA measurement method (Table  1.2) is a noninvasive technique that can be used to explore intrauterine fetal conditions. It is already widely used in obstetrical clinical practice. Values of MCA-PI  1.55MOM represents severe anemia. It has been used for the diagnosis of twin-to-twin transfusion syndrome (TTTS). The blood donor’s MCA-­ PSV ≥ 1.5MOM is an important basis for the certain diagnosis of fetal anemia. Usually, the receptor’s MCA-PSV   1.27MOM has a sensitivity of 63.33% to the prediction of severe fetal thalassemia, with a specificity of 75.18%.

1.2.9 Ductus Venosus Doppler As one of the three arteriovenous communication branches in the fetal body, the ductus venosus (DV) is connected to the umbilical vein and inferior vena cava and plays a vital role in fetal growth and development. The DV frequency spectrum

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consists of “two peaks and one valley,” of which the first peak is the ventricular systolic peak, i.e., the S peak; and the second peak is the ventricular diastolic peak, i.e., the D peak; the valley is the atrial contraction valley, i.e., the A valley, also known as a wave. Of them, the S peak boasts the highest flow velocity while the A valley boasts the lowest flow velocity. The S/D value of DV has a close correlation to fetal hypoxemia. When the A valley descends significantly and diastolic flow is intermittently or even continuously absent or reversed, this probably suggests that there is no compensatory reaction to fetal hypoxia, and proper heart function has significantly deteriorated. This is all the more so when the spectrum shows multiple veins, as such timely intervention measures must be taken.

1.2.10 Umbilical Artery pH Analysis Since the actual oxygen concentration in tissues cannot be measured directly in clinical practice, fetal histanoxia can only be assessed using metabolic acidosis. Determination of neonatal umbilical blood or the blood gas and lactic acid level in neonatal blood within several minutes after birth is considered to be currently the only objective, quantitative method for confirming whether hypoxia and acidosis have occurred before delivery. Lots of studies have been conducted both at home and abroad on the standard value of umbilical artery for the diagnosis of neonatal asphyxia. Most foreign scholars tend to take an umbilical artery pH < 7.0 as the highest risk factor for poor prognosis of neonatal asphyxia. If asphyxiated and hypoxic newborns have to be treated with cardiopulmonary resuscitation (CPR), e.g., umbilical artery pH < 7.0, 83.3%, 83.3% of them will have a poor prognosis; if umbilical artery pH is >7.0, 10.8% will have a poor prognosis. The specificity of the diagnosis of neonatal asphyxia is 92%, the sensitivity is 86%, and the positive predictive value is 89%. The highest risk factor for neonatal asphyxia was changed to an umbilical artery pH < 6.7 and base excess less than −12  mmol/L in Nelson Textbook of Pediatrics (19th edition).

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Multi-center clinical studies in China show that the clinically corrected value of the umbilical artery pH of neonatal asphyxia follows a normal distribution range of 7.0–7.2; base excess follows a distribution range of −10 to −18  mmol/L.  As such, the blood gas indexes for the diagnosis of neonatal asphyxia can be flexibly controlled within the above range. The specificity of the diagnosis of neonatal asphyxia at pH < 7.15 is 69.9%, with a sensitivity of 96.1%; the specificity of the diagnosis of neonatal asphyxia at pH  25 bpm). The normal range is 110–160 beats/min. The baseline must be a graph that lasts for more than 2 min in any 10 min, which can be discontinuous. The baseline can be determined by reference to the FHR of the previous 10 min. A baseline of lower than 110 bpm is known as bradycardia; one of higher than 160 bpm is tachycardia. The definition of the baseline is simple and clear, but clinically it is often difficult to confirm. If the baseline cannot be determined, it is less likely to determine whether there is accelerating or decelerating of FHR.  Therefore, sometimes it is necessary to make a judgment by referring to the earlier monitoring results or extending the monitoring time, as shown in Fig. 3.2.

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Fig. 3.2 (a) The baseline is clear, 135 bpm; (b) the FHR fluctuates at 160–170 bpm most of the time, so it is difficult to judge the baseline by reading pattern b only; by referring to the previous patterns, the part of pattern b where the FHR is faster can be judged as prolonged accel-

eration while the arrow points to the baseline, not deceleration. This pattern is mostly related to excessively active FMs, and the continuous black FM indication block also suggests frequent FMs

2. Abnormal Baseline (a) Fetal Bradycardia: Refers to baseline of FHR < 110 beats/min, duration ≥10 min In the past, it was believed that the normal baseline in the third trimester of pregnancy was 120–160  bpm, but the lower limit of the baseline was controversial. The currently recognized lower limit of a normal FHR is 110 bpm. Fetal hypoxia is not usually considered if the baseline is equal to 110–119 bpm without other FHR abnormality. Some researchers believe that if the baseline variability is normal, it is also safe when the baseline fluctuates from 80 to 120 bpm, but a baseline lower than 80  bpm is abnormal. According to NICE’s 2017 recommendations for the clinical pathway of intrapartum fetal monitoring, there is not necessarily a fetal abnormality when the baseline is lower

than 110 bpm and uncombined with other abnormal patterns or high-risk factors. However, most normal baselines should fluctuate between 110 and 160 bpm, and an FHR lower than 110  bpm is uncommon. It is necessary to check whether the FHR pattern has been misinterpreted when this occurs or makes a comprehensive assessment of the fetus through alternative methods (Fig. 3.3). Causes of Fetal Bradycardia: (i) After the beginning of the 40th gestational week, vagus nerve tension increases significantly, causing a decrease in the baseline. (ii) Umbilical cord compression. In the case of acute hypoxemia and ­umbilical cord compression, the FHR drops significantly from the normal level to bradycardia. (iii) Congenital fetal heart malformation. A fetus with congenital heart disease may

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Fig. 3.3 Bradycardia. After the gestational age of 39  weeks, B-ultrasonography suggests single atrial malformation in the fetus and the pregnant woman requires

the pregnancy to continue. Electronic FHR monitoring suggests fetal bradycardia, and the FHR is lower than the maternal heart rate

suffer from cardiac conduction system dysplasia as well, with symptoms including atrioventricular conduction block and decreased FHR. A baseline below 80 bpm and an absence of variability may be suggestive of a congenital heart block. A low FHR caused by a complete heart block suggests the pregnant woman may be suffering from a connective tissue disease such as systemic lupus erythematosus (SLE) or abnormal development of fetal heart structure, as shown in Fig.  3.3. Persistent fetal bradycardia can be diagnosed in combination with ultrasonic cardiogram. (iv) Some medications, such as

benzodiazepines or high-dose β receptor blocker taken by a patient with preeclampsia, affect the sympathetic nervous system from regulating the FHR, causing fetal bradycardia. (v) Severe fetal complications, such as placental abruption, uterine rupture, umbilical cord prolapse, late-term fetal distress, severe hypoxemia, decompensated fetal tolerance to hypoxia, and fetal bradycardia, are all signs of fetal jeopardy. (vi) Fetal bradycardia may occur when the maternal body temperature is too low during aneurysm repair under general anesthesia or the extrinsic cycle of cardiac surgery.

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(b) Fetal Tachycardia: Refers to baseline >160 min, duration ≥10 min Causes of fetal tachycardia: (i) Fetal hypoxia. In some cases, fetal tachycardia is a manifestation of fetal hypoxia. However, fetal hypoxia is generally accompanied by minimal or absent baseline variability or deceleration. Tachycardia with normal baseline variability does not indicate fetal jeopardy. In some cases, fetal tachycardia occasionally occurs after recovering from fetal hypoxia. For example, if the FHR rises after a great deceleration, this may be caused by the release of catecholamine from the sympathetic nervous system during fetal hypoxia. This phenomenon is known as an “overshoot”. (ii) Maternal fever is one of the most common causes of fetal tachycardia (Fig. 3.4). Maternal fever caused for various reasons can increase the baseline. The FHR increases 10–15  bpm on average for every 1 °C increase in maternal body temperature. Fetal tachycardia caused by a maternal infection is generally uncorrelated to complications unless fetal infection and sepsis occur. The pregnant woman may have an infection-­ unrelated fever before labor, especially when epidural anesthesia is performed or the labor is prolonged or the mother feels nervous or has had a dystocia. (iii) Chorioamnionitis. When this occurs, the fetus needs more oxy-

Fig. 3.4  It is a FHR pattern of DCDA in a woman at the gestational age of 34th weeks and suffering from PROM. The pregnant woman has a fever, her body tem-

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gen. The FHR will increase to improve systemic oxygen delivery. Chorioamnionitis can increase the baseline prior to the rise in maternal body temperature. (iv) Excessive FMs or fetal irritation. There are many causes of excessive FMs, such as insufficient maternal sleep, hypoglycemia, fatigue, environmental stimuli, and emotional excitement. An increase in the FHR caused by FMs is a normal fetal response. Frequent FMs lasting for a prolonged period of time may be an early manifestation of fetal hypoxia. Over-­ frequent FM occurrence with a prolonged acceleration lasting ≥10  min should be grounds for considering a change in baseline and not an acceleration of FM. (v) Some drugs, such as the β adrenergic agonist ritodrine, which is used to treat preterm labor, and drugs used in the maternal body that affect the sympathetic nervous system and parasympathetic nervous system, such as atropine and adrenaline, as shown Fig.  3.5. (vi) Extremely preterm labor. This is due to the immature development of the parasympathetic nervous system. (vii) Fetal arrhythmia. (viii) There are obvious causes of maternal-fetal hypoxemia. FHR acceleration may be induced by hemorrhagic shock caused by various maternal factors, including obstetric factors such as placenta previa and placental abruption, and non-obstetric ­factors

perature has risen to 38.7 °C, and the baseline of the two fetuses exceeds 160 bpm. The results of the pathological placental examination suggest chorioamnionitis

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Fig. 3.5  A woman pregnant for 33 weeks and suffering from antenatal hemorrhage and partial placenta praevia. Ritodrine (Anpo) is being injected intravenously to inhibit

uterine contractions. Both maternal heart rate and FHR are high, and the baseline is fluctuating from 170 to 180 bpm

such as gastrointestinal bleeding and traumainduced hemorrhagic shock, hypoalimentation caused by maternal vomiting or other reasons, low blood circulation volume and fall of blood pressure in the maternal body, decrease in placental blood perfusion, decrease of fetal oxygen concentration, more frequent sympathetic nervous activities, and release of adrenalin and norepinephrine from the fetal adrenal gland. Fetal tachycardia is the initial response to fetal hypoxemia. (ix) Other causes of tachycardia include maternal stress and anxiety, use of epidural anesthesia, maternal hyperthyroidism, fetal complications, and fetal anemia. The key characteristic of tachycardia associated with fetal hypoxia or acidosis that it is accompanied with FHR deceleration. Quickly eliminating factors affecting the FHR, such as correcting the maternal hypotension caused by epidural anesthesia, can restore the baseline to its normal range. It should be noted that even if fetal tachycardia is not caused by fetal hypoxia, if it fails to return to normal after a prolonged period, fetal compromise may occur. (c) Baseline Wandering or Instability: The baseline drifts within the range of 110–160 bpm, meaning it is unstable. This rare phenomenon may suggest abnormal development of the fetal nervous system. However, there are

very few literature reports on this kind of FHR change (Fig. 3.6). (II) Baseline Variability Baseline variability refers to a light cyclical fluctuation of FHR, i.e., the FHR fluctuates up and down around a fixed level within a certain period of time. Baseline variability is divided into long-­ term variability and short-term variability. Long-­ term variability (LTV): Refers to a waveform generated when the baseline fluctuates up and down macroscopically within 1  min. Variability can be calculated by analyzing the 1-min variation range of the electronic FHR monitoring pattern. In other words, it is equal to the difference between the fastest heart rate and the slowest heart rate. For example, if the fastest heart rate is 155  bpm (beats per minute) while the slowest heart rate is 145 bpm within 1 min, the variability is 10 bpm. Short-term variability (STV): Refers to the difference between each FHR and the next FHR, i.e., the time interval between two systoles. The baseline variability can be described with two indexes: amplitude and frequency. Amplitude refers to the swing scope of the waveform, expressed in bpm. Frequency refers to the number of fluctuations within 1  min visible to the naked eye, expressed in cpm (cycles per minute). The moderate variability amplitude is 6–25 bpm; the moderate variability frequency is 3–5 cpm. The FHR fluctuates around a certain level under the control of the fetal central nervous sys-

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Fig. 3.6  This figure shows a case of baseline instability (arrow) that occurs during labor. Placental pathological testing suggests chorioamnionitis; the newborn is diagnosed with pneumonia (caused by a viral infection); MRI suggests mild ventriculomegaly. Baseline wandering or

instability is not a common phenomenon. Currently, experts at home and abroad have different interpretations of this pattern. Some other experts argue that a downward-­ moving FHR pattern can be interpreted as FHR deceleration (triangle)

tem. Anatomically, a normal fetal brain, autonomic nervous system and cardiac oxygenation and good baseline variability are signs of the absence of fetal metabolic acidosis or central nervous system damage. When fetal hypoxia or acidosis occurs, the excitability of the central nervous system decreases or disappears, resulting in a reduction or disappearance of STV.  The lower the STV value is, the more likely fetal hypoxia or acidosis is to occur. Both the NICHD Electronic FHR Monitoring Conference 2008 and the Expert Consensus on Electronic FHR Monitoring 2015 by the Perinatal medicine branch of the Chinese Medical Association propose to divide baseline variability into 4 levels: (i) Absent variability, which means that the amplitude of baseline variability cannot be detected by the device; (ii) Minimal variability, which means that the amplitude of baseline variability can be detected, but it is less than 5 bpm. This is also known as reduced variability or decreased baseline variability; (iii) Normal (moderate) variability, which means that the amplitude of baseline variability is greater than 6  bpm and less than or equal to 25  bpm; (iv) Marked variability, which means that the amplitude of baseline variability is greater than 25 bpm

(Fig. 3.7). However, the 2008 guidelines do not contain a clear definition of baseline variability frequency. The 2007 edition points out that the normal baseline should fluctuate twice or more per minute. 1. Absent variability or minimal variability: Absent baseline variability is caused by an abnormal FHR regulatory mechanism of the sympathetic nerve and vagus nerve. Placental infarction, placental abruption, and velamentous placenta are important causes of baseline variability disappearance. Umbilical cord factors cannot be ignored, either. Decreased or absent baseline variability indicates that the regulation of the fetal central nervous system is inhibited due to hypoxia. This can be caused by the following: (i) Fetal hypoxia or acidosis; (ii) Fetal immaturity or fetal nervous system damage or dysfunction; (iii) The fetus is in deep sleep; (iv) the mother is anesthetized and sedated; (v) fetal tachycardia. The most common reduction of baseline variability is the transient reduced or absent beat to beat variability caused by high-dose central nervous system depressant while an analgesic is used during labor. Common drugs affecting

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Fig. 3.7 (a) For absent baseline variability, the FHR curve is smooth; (b) For minimal variability, baseline variability is visible, but the amplitude does not exceed

5 bpm; (c) Normal baseline variability; (d) Marked baseline variability (arrow)

Fig. 3.8  Effects of diazepam on baseline variability. (a) After the use of diazepam during labor, minimal baseline variability occurs; (b) 40 min later, normal baseline variability occurs, accompanied with normal FMs

the baseline variability include anesthetics, barbitones, phenothiazine, sedatives, and general anesthetics, as shown in Fig.  3.8. Absent baseline variability usually occurs 5–10  min after intravenous administration, and lasts for 60 min or longer, depending primarily on the dosage. Butorphanol, administered intravenously, can make the baseline variability disappear. After the exclusion of reduced or minimal variability caused by sedative use or fetal sleep,

reduced or minimal baseline variability may suggest intrauterine fetal hypoxia or acidosis, or fetal brain damage, or fetal congenital defects and intrauterine infection, as well as a poor prognosis. Disappearing baseline variability with FHR deceleration is often related to fetal acidosis (Fig. 3.9). According to research findings by Paul and his colleagues, when the reduced baseline variability is accompanied with slow FHR deceleration, the pH value of the fetal scalp blood is low; when the reduced variability is accompanied with significant FHR deceleration, the pH value

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Fig. 3.9  A case of a primipara. This patient was hospitalized due to PROM 6d past 38 gestational weeks and went into spontaneous labor under continuous electronic FHR monitoring; when the cervix was dilated to 7 cm, minimal baseline variability occurred and continued, no acceleration. As monitoring continued, the FHR decelerated sharply multiple times, after which the cervix was dilated to 8 cm, presentation +1; the pregnancy was then terminated by performing a cesarean section, delivering a living infant. Level-I meconium-stained amniotic fluid, no cord around neck or body, no abnormality seen on after birth surface, umbilical artery pH 7.039, base excess

(BE)-8 mmol/L; after birth the newborn was transferred to the department of pediatrics for monitoring and treatment. According to radial arterial blood pH 7.284 and BE-8  mmol/L, the newborn was diagnosed with mild asphyxia and acidosis, pathologic jaundice, and subarachnoid hemorrhage. The baseline variability caused by fetal acidosis was accompanied with multiple times of strenuous FHR deceleration. (a) Baseline variability was reduced and became almost absent, no FHR acceleration, and the cervix was dilated to 7 cm; (b) Drastic FHR deceleration occurred many times, and the lowest FHR value was 60 bpm (arrow)

of the fetal scalp blood is around 7.1; however, when baseline variability is greater than 5  bpm and accompanied with the same FHR deceleration, the pH value is around 7.2. Severe maternal acidosis can also reduce baseline variability. For example, in patients with diabetic ketoacidosis, the baseline variability can return to normal after the acidosis is corrected. The detailed pathophysiologic mechanism by which fetal hypoxia causes absent baseline variability remains unknown. Mild fetal hypoxia may slightly increase baseline variability, especially during the early stages of hypoxia. A disappearing baseline variability may suggest fetal brainstem or cardiac depression caused by metabolic acidosis. Thus, a disappearing baseline variability is more likely to suggest fetal acidosis than hypoxia. Zhu Caihong et  al. conducted a study using 40 cases of reduced or absent baseline variability as the observation group and 40 patients

with normal fetal monitoring as the control group. The results show that the most common related factors in the observation group are nuchal cord (57.5%), long and thin cord around neck (25%), battledore placenta (17.5%), presentation of the umbilical cord (12.5%), placental abruption and velamentous placenta (7.5%, respectively), accompanied with level-II or above meconium-stained amniotic fluid (37.5%). In the observation group, the cesarean section rate is 85%, the severe neonatal asphyxia rate is 7.5% and the death rate is 0; in the control group, the cesarean section rate is 22.5%, the neonatal asphyxia rate is 0 and the death rate is 0; Chen Suqin et al.’s research conclusion is similar to the above. The study data of 150 cases shows that in the observation group, the cesarean section rate is 77.3% and the neonatal asphyxia rate is 8%; in the control group, the cesarean section rate is 20% and the neonatal asphyxia rate is 0%.

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2. Marked Variability: Refers to an amplitude fluctuation of >25 bpm The significance of increased baseline variability: (i) With the increase of gestational months, the central nervous system and the autonomic nervous system gradually grow into maturity, with an increase in short variability; (ii) Stimulation from FMs and uterine contractions may lead to a transient increase in variability, and the increase will then slow down; (iii) Part of the fetal body or the umbilical vein is compressed temporarily, with variability probably increasing; (iv) In the case of acute fetal hypoxia, there is initially a transient increase in the baseline variability as the parasympathetic nervous system is stimulated. Baseline variability is one of the most important indexes used for intrauterine fetal safety assessment during electronic FHR monitoring. This can even reflect fetal prognosis more accurately than FHR deceleration. When reduced baseline variability occurs independently and is not accompanied with an FHR deceleration, fetal hypoxia may not necessarily be suggested, however, it is necessary to actively look for etiological factors, observe carefully and exclude the influence of uterine contraction inhibitors such as sedatives and magnesium sulfate or fetal sleep cycle on the fetus. After the exclusion of the above factors, non-parturient persistent FHR variability reduction or disappearance may be due to fetal hypoxia, acidosis, and central nervous system dysfunction caused by placental factors, umbilical cord factors, or fetal factors. Fetal distress can then be confirmed or excluded based on the pregnant woman’s medical history and ultrasound examination results and oxytocin challenge test (when necessary. A reduced baseline variability occurring and continuing during labor, especially when the FHR is decelerated, is likely suggestive of intrauterine fetal hypoxia, and timely treatment is recommended. (III) Fetal Arrhythmia Arrhythmia refers to the abnormality of any of the heart rhythm origin, heartbeat, frequency and

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rhythm, and impulse conduction; it is an irregular FHR unrelated to uterine contractions, or a heart rate outside the normal range (a regular FHR beyond 110–160  bpm). Fetal arrhythmia is mainly detected by comprehensive means, including FHR auscultation, electronic FHR monitoring, fetal echocardiography, and fetal electrocardiogram. Routine antenatal examinations show that 0.03%–1% of fetuses have arrhythmia, with occurrences differing from region to region. Fetal arrhythmia is generally divided into fetal tachycardia, fetal bradycardia, and irregular fetal heart rhythm. Fetal bradycardia refers to an FHR that is consistently below 110 bpm. Fetal tachycardia refers to an FHR that is consistently above 160 bpm. 1. Fetal Tachycardia: Fetal tachycardia is divided into nodal tachycardia, ventricular tachycardia, supraventricular tachycardia, atrial tachycardia, atrial flutter, and auricular fibrillation. Fetal atrial flutters are generally the cause of fetal congestive heart failure, edema, and death. If fetal ventricular tachycardia is accompanied with cardiac structural abnormality and heart failure, the newborn will have a poor prognosis. Fetal nodal tachycardia with a normal heart structure is more common in clinical practice. This type of tachycardia may be related to the mother’s mental state, maternal fever, infection, medication, environmental factors, and episodic uterine contractions in the second and third trimesters of pregnancy. 2. Fetal Bradycardia: Fetal bradycardia includes sinus bradycardia and atrioventricular blockages. Structural heart abnormality is the main cause of fetal bradycardia. The causes of fetal bradycardia include atrioventricular septal defects, transposition of the great arteries, mitral atresia, single ventricle, and pulmonary stenosis. Fetal bradycardia may also be caused by polyhydramnios, fetal hydrops, hydrocephalus, etc. 3. Irregular Heart Rhythm: Irregular heart rhythm in most fetuses is atrial extrasystole. Atrial extrasystole is the most common type of fetal arrhythmia. The fetal heart structure is

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normal in most cases, and the atrial extrasystole naturally disappears within a few days of birth. Fetal ventricular extrasystole is far less common than atrial extrasystoles, and occurs sporadically in most cases while occurring frequently in a very few cases; however, its duration is short. Fetal ventricular extrasystole is accompanied with fetal cardiac structural abnormality in very few cases. However, it is usually difficult for electronic FHR monitoring to detect extrasystole, while fetal echocardiography or fetal electrocardiogram are conducive to detection.

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(IV) Sinusoidal Pattern A sinusoid is a relatively rare pattern. The typical sinusoidal curve reported by Modanlou et al. in

1982 is characterized by the disappearance of STV and smooth and consistent baseline in the absence of FMs. The definition of the sinusoidal curve in the 2008NICHD Guidelines for Electronic FHR Monitoring: The special pattern of the baseline is smooth and fluctuates up and down like a sinusoidal pattern. The duration is greater than or equal to 20 min; in the expert consensus on the application of electronic FHR monitoring issued by the Chinese Society of Perinatal Medicine of Chinese Medical Association in 2015, this is defined as an obviously visible and smooth pattern like sinusoidal waves. The LTV is 3–5 cycles per minute and lasts ≥20 min. The sinusoidal pattern usually contains a section of the FHR pattern with disappearing variability, often accompanied with late deceleration, absent STV, periodic, homogeneous LTV and absent FHR acceleration (Fig. 3.10). There is currently no clear definition of the duration and meaning of a sinusoid. Some scholars argue that sinusoidal pattern falls into benign/ pseudo-sinusoidal pattern and pathological sinusoidal pattern. Some researchers have analyzed intrapartum sinusoidal pattern, with the curves showing baseline variability with periodic acceleration. Such a pattern is known as a pseudo-­ sinusoidal pattern, which can be seen in 15% of parturients under electronic FHR monitoring. The pseudo-sinusoidal pattern is related to the

Fig. 3.10  Sinusoidal pattern. (a) A pseudo-sinusoidal pattern. Torsion of the umbilical cord was seen during delivery; (b) A pathological sinusoidal pattern. The pregnant woman suffered from preeclampsia accompanied

with lower abdominal pain and vaginal bleeding during the 32nd gestational week. She underwent a cesarean section for terminating pregnancy, and placental abruption was seen during the operation

Owing to the immature fetal cardiac conduction system, imperfect physiological functionality, and unstable autonomic nerve functionality, a fetus is more susceptible to arrhythmia. The occurrence mechanism of fetal tachycardia remains unknown. Immature atrial rhythm occurs during the atrial relative refractory period, inducing one or more repetitive reactions. Inhomogeneous conduction forms reentry, possibly causing atrial flutter and auricular fibrillation. In addition, the increased myocardial stress and alternative pathway occurrence rate may also be related to atrial fluttering.

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use of pethidine or analgesia during labor, and 10 bpm at the baseline level and 10s but 2 min may also have something to do with fetal swalin duration. At and after the gestational age of lowing, finger sucking or transient fetal hypoxia, 32 weeks, acceleration is greater than or equal torsion, or compression of the umbilical cord. to 15  bpm at the baseline level and15s but Pathological sinusoidal pattern may occur in the 2  min is greater than or equal to. Prolonged presence of fetal anemia, especially Rh blood acceleration: Refers to that FHR acceleration type incompatibility-induced isoimmune hemois 2 min but 10 min in duration. If acceleration lysis, twin-to-twin transfusion syndrome, fetolasts10min or more, a change in the baseline maternal hemorrhage, and acute fetal blood loss should be considered. from vasa previa; severe fetal hypoxia or acidosis 2 . Mechanism of FHR Acceleration: FHR acceland chorioamnionitis may also cause pathologieration is due to FMs, uterine contractions, cal sinusoidal pattern. compression of the umbilical cord, and fetal The pathophysiological formation mechanism irritation from sounds and vaginal examinaof FHR sinusoidal patterns remains unclear. It tion (Fig. 3.11). Stimulation from fetal scalp may be related to the fluctuation of arterial blood blood sampling also causes FHR acceleration. pressure and reflect how the baroreceptor-­ The emergence of FHR acceleration suggests chemoreceptor feedback mechanism controls that the fetal nervous system regulates the carand regulates the circulatory system. Some diovascular system normally. FHR acceleraresearchers argue that ischemia and hypoxia distion has something to do with fetal activities, rupt the mechanism by which the nervous system and the fetus may suffer from absent FHR regulates the fetal heart, making the FHR pattern acceleration during sleep. If the FHR is accellook like a sinusoidal pattern. Animal experimenerated within 30 min, it suggests that the fetus tal studies suggest that the sinusoidal pattern is is in good condition, and it can be confirmed related to the level of arginine vasopressin in that fetal acidosis does not occur. It is not necplasma. The level of arginine vasopressin in essarily detrimental if the FHR is not accelerplasma rises after bleeding or acidosis, possibly ated during labor unless the FHR pattern is exerting a direct or indirect effect on the transport accompanied with other abnormal pattern of calcium ions at sinoatrial nodes, causing dyschanges. regulation of the FHR. (II) FHR Deceleration FHR deceleration refers to a temporary slowing 3.1.2 Periodic Changes in FHR down of the FHR.  This is divided into early deceleration, late deceleration, and variable Periodic FHR change refers to deviations from deceleration according to the relationship baseline that are temporal. This is usually related between occurrence time and uterine contracto uterine contractions and primarily includes tions. From a clinical perspective, the deceleraFHR acceleration and FHR deceleration. tion pattern can be divided into two types Acceleration refers to the FHR increase rising according to the occurrence period of FHR decelover the baseline level; deceleration refers to the eration: one in nonstress test (NST) and one in FHR declining below the baseline level. labor. Deceleration patterns in NSTs do not occur frequently, the occurrence rate of which, which is (I) FHR Acceleration reported differently in literature, is 1.3%–10.0%. 1. Definition: Refers to a sudden significant The deceleration pattern mainly involves variable increase in the baseline, to them in less than deceleration and prolonged deceleration. It is 30s; the time from the initial acceleration of very common to see a deceleration pattern in the FHR till return to the baseline level is known electronic FHR monitoring throughout labor, as acceleration time. In the first 32 gestational particularly the second stage. According to the weeks, acceleration is greater than or equal to definition proposed in the expert consensus

3  Fundamental Electronic FHR Monitoring

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Fig. 3.11 (a) Typical FHR acceleration; (b) prolonged FHR acceleration, with acceleration lasting over 2 min

issued by the Chinese Society of Perinatal Medicine of Chinese Medical Association in 2015, if ≥50% uterine contractions are accompanied with deceleration during a 20-min observation, this is known as recurrent deceleration; if