Intrapartum Fetal Assessment and Therapy

Assessment of fetal well-being during labor and at the time of delivery is paramount to ensure optimal health of the mother and infant. Since its introduction in the 1960s, fetal surveillance during labor has been predominantly managed with continuous monitoring of fetal heart rate (FHR). Yet, despite more than a half-century of widespread application, debate remains about the clinical application—and value—of electronic cardiotocography (CTG) as well as the mechanisms by which FHR patterns occur. Understanding the interpretation of electronic FHR monitoring, its limitations, and the impact of the maternal condition is critical for intrapartum management as electronic FHR monitoring is the most common obstetric procedure.

FETAL RISK DURING LABOR

Continuous electronic FHR monitoring during labor was introduced to identify fetal asphyxia, with the expectation that timely intervention would prevent cerebral palsy (CP). A benefit attributed to electronic fetal monitoring is the near elimination of intrapartum fetal deaths, especially among preterm neonates. Importantly, data supporting these observations are from epidemiologic studies, which provide associations but do not necessarily establish causation. Additionally, widespread implementation of electronic fetal monitoring has been at the expense of increased operative interventions and a disappointing recognition that fetal neurologic injury and CP rates have remained essentially unchanged over decades ( Fig. 8.1 ).

A dual-axis graph presents trends in cesarean delivery types and live births with cerebral palsy from 1980 to 2009. — Fig 8.1

Animal models have been used to study the hypothesis that intrapartum events can have long-term neurologic sequelae. Fetal monkeys subjected to hypoxia in utero suffer neurologic injuries similar to those seen in children who presumably suffered asphyxia in utero . Complete asphyxia caused by total occlusion of the umbilical blood flow led to fetal arterial acidemia after approximately 8 minutes and neurologic injury following 10 minutes of occlusion. Work with rodent, rabbit, piglet, and sheep models has shown similar patterns of damage. Thus, fetal brain injury appears to be related to duration, frequency, and degree of cord occlusion.

In humans, a complex interplay of antepartum complications, suboptimal uterine perfusion, placental dysfunction, and intrapartum events can result in adverse neonatal outcome. Various methods for the identification of high-risk pregnancies have been published. High-risk pregnancies include, but are not limited to, pregnant individuals with (1) medical complications (e.g., hypertension, preeclampsia, diabetes mellitus, autoimmune disease, hemoglobinopathy); (2) fetal complications (e.g., fetal growth restriction, anomalies, preterm delivery, multiple gestation, hydrops fetalis); and (3) intrapartum complications (e.g., vaginal bleeding, maternal fever, meconium-stained amniotic fluid, oxytocin administration during labor). Owing to inadequate sensitivity, poor positive predictive values, and the inability to modify risk factor–related outcomes, the use of scoring systems has not been shown to improve pregnancy outcomes. In a study of term pregnancies with fetal asphyxia, 63% had no known risk factors.

Because of this, the magnitude of risk for intrapartum fetal neurologic injury is a matter of dispute with current data suggesting that it is unrealistic to expect detection of fetal asphyxia using FHR monitoring alone. In 2014, the American College of Obstetricians and Gynecologists (ACOG) Task Force on Neonatal Encephalopathy developed criteria for intrapartum events that may be contributory to neurologic injury ( Box 8.1 ). The Task Force concluded that 70% of fetal neurologic injuries result from events that occur before the onset of labor. Only 4% of cases of neonatal encephalopathy result solely from intrapartum hypoxia, an incidence of approximately 1.5/1000. The Task Force criteria are consistent with clinical findings in a case series of neurologically impaired infants with intrapartum compromise.

Box 8.1

Neonatal Encephalopathy and Association With Peripartum Events

Adapted from the American College of Obstetricians and Gynecologists. Executive summary: Neonatal encephalopathy and neurologic outcome, 2nd ed. Report of the American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy. Obstet Gynecol . 2014;123:896–901.

Definition of Neonatal Encephalopathy

Syndrome of disturbed neurologic function in the earliest days of life in an infant born at ≥35 weeks’ gestation

Neonatal signs consistent with an acute peripartum or intrapartum event :

1.
Apgar scores < 5 at 5 min and 10 min of life
2.
Evidence of metabolic acidosis in umbilical cord arterial blood obtained at delivery (pH < 7.00, base deficit > 12 mmol/L)
3.
Neuroimaging evidence of acute brain injury seen on brain magnetic resonance imaging or magnetic resonance spectroscopy consistent with hypoxemia-ischemia
4.
Presence of multisystem organ failure consistent with hypoxic-ischemic encephalopathy

Type and timing of contributing factors that are consistent with an acute peripartum or intrapartum event:

1.
Sentinel hypoxic or ischemic event occurring immediately before or during labor and delivery (e.g., uterine rupture, abruption, amniotic fluid embolus)
2.
Fetal heart rate monitor patterns consistent with an acute peripartum or intrapartum event
3.
Type and timing of brain injury pattern based on imaging studies consistent with an etiology of an acute peripartum or intrapartum event
4.
No evidence of other proximal or distal factors that could be contributing events

Developmental outcome is spastic quadriplegia or dyskinetic cerebral palsy .

Thus, as defined by the ACOG Task Force, neonatal encephalopathy is a clinically defined syndrome of disturbed neurologic function in the earliest days of life in an infant born at or beyond 35 weeks’ gestation, manifested by a subnormal level of consciousness, seizures, and often accompanied by difficulty with initiating and maintaining respiration and depression of tone and reflexes. Hypoxic-ischemic encephalopathy (HIE) or birth asphyxia accounts for some, but not all, cases of neonatal encephalopathy. For example, case series of sentinel events (e.g., uterine rupture, umbilical cord prolapse, placental abruption, amniotic fluid embolus) during labor have been associated with HIE in surviving infants.

With the current understanding of the pathophysiology of neonatal encephalopathy, and the contemporary technology used clinically, the extent to which obstetricians can prevent intrapartum injury remains unclear. Given these uncertainties, efforts to understand placental physiology and pathophysiology are central to efforts to support the health of the pregnant woman and her fetus, both antepartum and intrapartum. The fetus depends on the placenta for the diffusion of nutrients and for respiratory gas exchange. Many factors affect placental transfer, including concentration gradients, villus surface area, placental permeability, and placental metabolism (see Chapter 4 ). Maternal hypertensive disease, congenital anomalies, and intrauterine infection are examples of conditions that may impair placental transfer.

One of the most important determinants of placental function is uterine blood flow. A uterine contraction results in a transient decrease in uteroplacental blood flow. A placenta with borderline function before labor may be unable to support adequate gas exchange to prevent fetal asphyxia during labor. The healthy fetus may compensate for the effects of hypoxia during labor via (1) decreased oxygen consumption, (2) vasoconstriction of nonessential vascular beds, and (3) redistribution of blood flow to the vital organs (e.g., brain, heart, adrenal glands, placenta). Humoral responses (e.g., release of epinephrine from the adrenal medulla) may enhance fetal cardiac function during hypoxia. Prolonged or severe hypoxia overwhelms these compensatory mechanisms, resulting in fetal injury or death.

INTRAPARTUM FETAL ASSESSMENT

Electronic Fetal Heart Rate Monitoring

There is need for a sensitive yet specific method for the determination of fetal health during labor and delivery. Most contemporary methods include assessment of the FHR intermittently or continuously with Doppler ultrasonography. Alternatively, a fetal electrocardiography (ECG) electrode can be used. Experimental models have provided insight into FHR regulation. Both neuronal and humoral factors affect the intrinsic FHR. It has been proposed that parasympathetic outflow by means of the vagus nerve decreases the FHR, whereas sympathetic activity increases FHR and cardiac output. Baroreceptors respond to increased blood pressure and chemoreceptors respond to decreased Pa o ₂ and increased Pa co ₂ to modulate the FHR through the autonomic nervous system. Cerebral cortical activity and hypothalamic activity affect the FHR through their effects on integrative centers in the medulla oblongata ( Fig. 8.2 ).

A labeled diagram presents pathways involved in the regulation of fetal heart rate, connecting the brain and heart. — Fig 8.2

An electronic monitor simultaneously records the FHR and uterine contractions. Use of an electronic monitor allows determination of the baseline rate and patterns of the FHR and their relationship to uterine contractions. External or internal techniques allow continuous assessment of the FHR and uterine contractions ( Fig. 8.3 ). Doppler ultrasonography detects the changes in fetal ventricular wall motion and blood flow in major vessels during each cardiac cycle. The monitor calculates the FHR by measuring the intervals between fetal myocardial contractions. Alternatively, an ECG lead attached to the fetal scalp enables the cardiotachometer to calculate the FHR by measuring each successive R-R interval.

A medical diagram presents external and internal electronic fetal monitoring setups using sensors and recording devices. — Fig 8.3

The FHR tracing is typically superimposed over the uterine contraction pattern. Uterine contractions can be monitored externally with a tocodynamometer or internally with an intrauterine pressure catheter (IUPC). The tocodynamometer allows the determination of the approximate onset, duration, and offset of each uterine contraction. Normal uterine activity is defined as five or fewer contractions in 10 minutes, averaged over a 30-minute window. Tachysystole , applied to either spontaneous or induced labor, is defined as more than five contractions in 10 minutes, averaged over 30 minutes, and should be categorized by the presence or absence of FHR decelerations. The ACOG has recommended that the terms hyperstimulation and hypercontractility be abandoned.

An IUPC may be used to measure the relative strength, and the onset and offset, of each uterine contraction with greater precision than an external monitor. Such information may be used to distinguish among early, variable, and late FHR decelerations (see later). Additionally, the IUPC may be useful for obese parturients where the tocodynamometer lacks sensitivity.

The following features of the FHR pattern can be assessed: (1) baseline measurements, (2) variability (the extent to which the rate changes both instantaneously and over longer periods), (3) accelerations , and (4) decelerations , and their association with uterine contractions.

Baseline Fetal Heart Rate

A normal baseline FHR is defined as 110 to 160 beats per minute (bpm) and is determined by assessing the mean heart rate over a 10-minute period rounded to increments of 5 bpm. In general, term fetuses have a lower baseline FHR than preterm fetuses because of greater parasympathetic nervous system activity. Laboratory studies suggest that bradycardia (caused by increased vagal activity) is the initial fetal response to acute hypoxemia. After prolonged hypoxemia, the fetus may experience tachycardia as a result of catecholamine secretion and sympathetic nervous system activity. A baseline FHR < 110 bpm is termed bradycardia and a baseline FHR > 160 bpm is tachycardia .

Fetal bradycardia may be caused by congenital heart block, fetal central nervous system (CNS) injury, or fetal hypoxia. The most common cause of fetal tachycardia is maternal fever. Other causes include fetal cardiac arrhythmias and medications administered to the mother, such as beta-adrenergic receptor agonists (e.g., terbutaline for tocolysis). Epidural analgesia with local anesthetic agents (e.g., lidocaine, bupivacaine) can also lead to sympathetic blockade, maternal hypotension, transient uteroplacental insufficiency, and alterations in the FHR. Parenteral opioids also may affect the FHR. Lastly, FHR changes have been reported after an eclamptic seizure. In a retrospective study of FHR tracings associated with eclampsia at Parkland Hospital, 79% of fetuses demonstrated prolonged bradycardia, and half of the fetuses developed fetal tachycardia after recovery from the episode of bradycardia. The mean (± standard deviation) duration of bradycardia was 5.8 ± 3.0 minutes with a range of 2 to 15 minutes. FHR decelerations occurred, on average, 2.7 ± 1.6 minutes after the onset of the eclamptic seizure. Despite these periods of FHR decelerations associated with eclampsia, prioritization of maternal support and stabilization resulted in a favorable perinatal outcome without the need for immediate operative intervention in more than two-thirds of cases. Thus, an eclamptic seizure does not necessarily require immediate, emergent operative delivery for fetal indications.

Fetal Heart Rate Variability

FHR variability is the fluctuation in the baseline FHR that is irregular in amplitude and frequency. Variability is usually quantified as the amplitude of peak-to-trough heart rate in beats per minute. Box 8.2 describes the variation of recorded findings. Baseline variability is defined as the irregular fluctuations in the baseline excluding accelerations and decelerations. FHR variability increases over the course of gestation. A representative FHR is shown in Fig. 8.4 .

Box 8.2

Definitions for Baseline Variability Based on Peak-to-Trough Amplitude

From American College of Obstetricians and Gynecologists. Practice Bulletin No. 106: Intrapartum fetal heart rate monitoring: nomenclature, interpretation, and general management principles (reaffirmed 2025). Obstet Gynecol. 2009;114:192–202.

Baseline Variability

•
Fluctuations in the baseline fetal heart rate that are irregular in amplitude and frequency
•
Variability is visually quantitated as the amplitude of peak-to-trough in beats per minute
- •
  Absent: amplitude range undetectable
- •
  Minimal: amplitude rage detectable but 5 beats per minute or fewer
- •
  Moderate (normal): amplitude range 6–25 beats per minute
- •
  Marked: amplitude > 25 beats per minute

A fetal monitoring tracing shows fetal heart rate and uterine contractions with repeated variable decelerations. — Fig 8.4

The presence of normal FHR variability reflects the presence of normal, intact pathways from and within the fetal cerebral cortex, midbrain, vagus nerve, and cardiac conduction system (see Fig. 8.2 ). Variability is greatly influenced by the parasympathetic tone. Maternal administration of atropine, which readily crosses the placenta, can eliminate some variability. In humans, the sympathetic nervous system appears to have a lesser role in influencing variability. Maternal administration of the beta-adrenergic receptor antagonist propranolol has little effect on FHR variability.

During hypoxemia, fetal myocardial and cerebral blood flow increase to maintain oxygen delivery. With severe hypoxemia, however, fetal blood flow cannot increase sufficiently to maintain oxygen delivery. The decompensation of cerebral blood flow and oxygen delivery results in a loss of FHR variability. The absence of variability in an anencephalic fetus also suggests that the presence of FHR variability reflects the integrity of the CNS. In animal models, perfusion of the CNS with calcium results in depolarization of electroencephalographic activity, which abolishes FHR variability.

Clinically, the presence of normal FHR variability predicts early neonatal health, as defined by an Apgar score of greater than 7 at 5 minutes. In a case series of monitored fetal deaths, no fetus had normal variability immediately before demise. However, in a cohort of 500 deliveries, the presence or absence of variability was not associated with neonatal acidosis. The differential diagnosis of decreased variability includes fetal hypoxia, fetal sleep state, fetal neurologic abnormality, and decreased CNS activity that results from exposure to drugs, such as opioids. Decreased FHR variability is observed following acute maternal meperidine administration and long-term administration of buprenorphine. Magnesium sulfate, commonly used for fetal neuroprotection and eclampsia prevention, decreases FHR variability but without adverse neonatal effects.

Accelerations

Accelerations are abrupt changes—onset-to-peak in 30 seconds—in the FHR from baseline. Beyond 32 weeks’ gestation, an acceleration is defined by a peak of at least 15 bpm above baseline and lasting at least 15 seconds. Before 32 weeks’ gestation, a peak of 10 bpm above the baseline, lasting at least 10 seconds, is required. While an acceleration that extends for 2 minutes is considered prolonged, at 10 minutes it is considered a baseline change. During the antepartum period, the heart rate of the healthy fetus accelerates in response to fetal movement. Antepartum FHR accelerations signal fetal health, and their presence indicates a reactive nonstress test. Intrapartum accelerations most commonly preclude the existence of significant fetal metabolic acidosis. The absence of accelerations, however, does not necessarily suggest fetal compromise unless other nonreassuring findings are present.

Decelerations

Decelerations include early, late, or variable decelerations. Early decelerations occur simultaneously with uterine contractions. The onset and offset of each deceleration coincide with the onset and offset of the uterine contraction (see Fig. 8.4 ). In animal models, head compression can precipitate early decelerations. In humans, early decelerations are believed to result from reflex vagal activity. Early decelerations are considered benign and not associated with fetal acidemia.

Late decelerations are delayed in timing with the nadir occurring after the peak of the contraction. In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively. Animal studies suggest that late decelerations represent a response to hypoxemia. The delayed onset of the deceleration reflects the time needed for the chemoreceptors to detect decreased oxygen tension and mediate the change in FHR by means of the vagus nerve. Late decelerations may also result from decompensation of the myocardial circulation and myocardial failure. Clinical and animal studies suggest that late decelerations may be an overly sensitive indication of fetal asphyxia. However, the combination of late decelerations and decreased or absent FHR variability is an ominous signal of fetal compromise.

Variable decelerations vary in depth, shape, and duration. They often are abrupt in onset and offset. These are the most frequent decelerations identified during labor and are reported to occur in more than 80% of patients during the first stage of labor. Variable decelerations result from baroreceptor- or chemoreceptor-mediated vagal activity or possible transient hypoxemia. Experimental models and clinical studies suggest that umbilical cord occlusion, either partial or complete, results in variable decelerations. During the second stage of labor, variable decelerations may result from compression of the fetal head. In this situation, dural stimulation leads to increased vagal discharge. The healthy fetus can typically tolerate mild to moderate variable decelerations without decompensation. With prolonged, severe variable decelerations (<60 bpm) or persistent fetal bradycardia, it is difficult for the fetus to maintain cardiac output and umbilical blood flow. Recurrent variable decelerations with minimal to moderate variability are indeterminant, whereas those with absent variability are deemed abnormal.

Sinusoidal and saltatory patterns are two unusual FHR tracing patterns that may indicate fetal compromise. The sinusoidal FHR pattern is a regular, smooth, wavelike pattern that may signal fetal anemia. Occasionally, maternal administration of an opioid, such as butorphanol, can lead to a sinusoidal FHR pattern. The saltatory pattern consists of excessive swings in variability (>25 bpm) and may signal the occurrence of acute fetal hypoxia; there is a weak association between this pattern and low Apgar scores.

Limitations of Electronic Fetal Heart Rate Monitoring

Despite laboratory and early clinical data suggesting that FHR monitoring accurately reflects fetal health, controversy exists regarding the ability of this assessment tool to improve fetal and neonatal outcomes. It remains unclear why prospective studies have not confirmed greater benefit of the use of continuous electronic FHR monitoring during labor; the intensity of intrapartum assessment and care may play a role. In prospective trials, pregnant women were randomly assigned to receive intermittent FHR auscultation or continuous electronic FHR monitoring, but all patients were monitored by dedicated nursing staff who provided intensive intrapartum care. By contrast, the historical cohort studies compared patients who received continuous electronic FHR monitoring and intensive intrapartum care with patients who had intermittent FHR auscultation with nonintensive nursing care. At Parkland Hospital, alternating months of universal electronic FHR monitoring and selective FHR monitoring were compared over 3 years in more than 17,000 patients. No significant differences were noted in perinatal outcomes; however, the period of universal monitoring was associated with a significantly increased rate of cesarean delivery. There are no published studies that have randomly assigned a group of patients to not receive FHR monitoring, and the practice of continuous electronic FHR monitoring has been widely adopted as standard practice in most labor units in the United States.

Consistent with the results of the prospective trials, the ACOG endorses the use of either intermittent auscultation or continuous electronic FHR monitoring during labor. In high-risk patients, the ACOG guidelines recommend that the obstetrician or nurse review the electronic FHR tracing every 15 minutes during the first stage of labor and every 5 minutes during the second stage. For low-risk patients, the intervals may be lengthened to 30 minutes for the first stage and 15 minutes for the second stage. The optimal interval for intermittent FHR monitoring has not been studied, but the intervals of 15 to 30 minutes in the active phase and every 5 minutes in the second stage have some indirect support. Adherence to these standards for intermittent auscultation may be difficult to achieve in the clinical setting; in one study, this standard was met for only 3% of parturients. A systematic review and metaanalysis compared intermittent use of handheld Doppler CTG to an obstetric stethoscope or fetoscope (nonelectronic device) and demonstrated no improvement in neonatal outcome but an increase in operative delivery.

Several hypotheses to account for the apparent failure of intrapartum FHR monitoring to reduce the incidence of CP have been proposed and include the following:

•
A large proportion of asphyxial damage begins before the onset of labor;
•
Catastrophic, “sentinel” events (e.g., cord prolapse, placental abruption, uterine rupture) may not allow sufficient time for intervention before neurologic damage occurs;
•
A larger proportion of very-low-birthweight infants survive and thus contribute to the number with CP;
•
Infection is associated with abnormal FHR patterns and the subsequent development of CP, and it is unclear if early intervention offers any benefit in such cases;
•
The amount of asphyxia required to cause permanent neurologic damage approximates the amount that causes fetal death, leaving a narrow window for intervention. The number of children in whom CP develops from intrapartum asphyxia is probably small.

Limitations of FHR monitoring include a poor positive predictive value in distinguishing between abnormal FHR tracings and abnormal outcomes. Because of this imprecision, the ACOG recommended that abnormal FHR tracings be described with the term nonreassuring fetal status rather than fetal distress or birth asphyxia . In one population-based, case-control study of children with CP, FHR tracings were retrospectively reviewed. While a markedly higher incidence of abnormal FHR tracings was found in children with CP than in controls, there was a 99.8% false-positive rate of abnormal tracings. Later case-control studies have yielded similar results. A 2017 metaanalysis of 13 trials, including 37,000 patients, found continuous CTG fetal monitoring reduced rates of neonatal seizures but found no clear differences in CP, infant mortality, or other standard measures of neonatal well-being. However, continuous CTG was associated with an increase in cesarean and operative vaginal births.

While poor specificity of electronic fetal monitoring is a documented concern, inadequate sensitivity is also an issue. A 2017 report noted that 20% of fetuses born with acidemia do not have an abnormal FHR tracing even with expert retrospective evaluation. A case-control study of infants with HIE showed that FHR monitoring the hour before delivery was poorly predictive of neurologic injury. Further limitations of continuous FHR monitoring include: (1) poor intraobserver and interobserver agreement despite the use of trained observers, especially when FHR patterns are observed; (2) the required continual presence of a nurse or physician to assess the FHR tracing; (3) the inconvenience to the patient (e.g., confinement to bed and the application of monitor belts or a scalp electrode); and (4) the need to maintain the FHR tracings as legal documents.

Despite little evidence for its efficacy, obstetricians rely on electronic FHR monitoring for the following three reasons: (1) professional obstetric organizations (e.g., ACOG) advise some form of monitoring during labor, (2) electronic FHR monitoring is logistically easier and less expensive than one-on-one nursing care during labor, and (3) individual (often anecdotal) experiences cause “many obstetricians [to] believe that in their own hands FHR monitoring is … efficacious.”

In 2008, the National Institute of Child Health and Human Development sponsored a workshop that resulted in the publication of updated definitions, interpretation, and research guidelines for intrapartum electronic FHR monitoring. The published report proposed a three-tier system for the categorization of FHR patterns ( Box 8.3 ). The ACOG has adopted this system with suggested options for management.

•
Category I (normal): Strongly predictive of normal fetal acid-base status at the time of observation.
•
Category II (indeterminate): Not predictive of abnormal fetal acid-base status, but without adequate evidence to classify as normal or abnormal.
•
Category III (abnormal): Predictive of abnormal fetal acid-base status at the time of observation and thus requiring prompt evaluation ( Box 8.4 ).
Box 8.4

Logistical Considerations in Preparation for Operative Delivery in the Setting of Category III Tracing

From American College of Obstetricians and Gynecologists. Practice Bulletin No. 116: Management of intrapartum fetal heart rate tracings (reaffirmed 2025). Obstet Gynecol. 2010;116:1232–1240.
- •
  Obtain informed consent (verbal or written as feasible)
- •
  Assemble surgical team (surgeon, scrub technician, and anesthesia personnel)
- •
  Assess patient transit time and location for operative delivery
- •
  Ensure intravenous access
- •
  Review status of laboratory tests (e.g., complete blood type and screen) and assess need for, and availability of, blood products
- •
  Assess need for preoperative placement of indwelling Foley catheter
- •
  Assemble personnel for neonatal resuscitation

Box 8.3

Three-Tiered Fetal Heart Rate (FHR) Interpretation System

Modified from Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring. Obstet Gynecol . 2008;112:661–666.

Category I tracings include all of the following:

•
Baseline rate: 110–160 beats per minute (bpm)
•
Baseline FHR variability: moderate
•
Accelerations: present or absent
•
Late or variable decelerations: absent
•
Early decelerations: present or absent

Category II tracings include:

•
All tracings not categorized as Category I or Category III
•
Baseline FHR
- •
  Bradycardia not accompanied by absent baseline variability
- •
  Tachycardia
•
Baseline FHR variability
- •
  Minimal baseline variability
- •
  Absent baseline variability not accompanied by recurrent decelerations
- •
  Marked baseline variability
•
Accelerations
- •
  Absence of induced accelerations after fetal stimulation
•
Periodic or episodic decelerations
- •
  Recurrent variable decelerations accompanied by minimal or moderate variability
- •
  Prolonged deceleration ≥ 2 min but <10 min
- •
  Recurrent late decelerations with moderate baseline variability
- •
  Variable decelerations with other characteristics such as slow return to baseline, overshoots, or shoulders
Category III tracings include either:
•
Absent baseline FHR variability and any of the following:
- •
  Recurrent late decelerations
- •
  Recurrent variable decelerations
- •
  Bradycardia
•
Sinusoidal pattern

In a large population review, at any one time, 78% of tracings were Category I, 22% of tracings were Category II, and 0.004% of the tracings were Category III. Whereas only 0.2% of Category I tracings were associated with low Apgar scores and neonatal intensive care unit (NICU) admissions, this increased to 0.7% with Category II tracings, suggesting a greater association with increased short-term morbidity. A 2023 systematic review and metaanalysis evaluating the three-tier classification system concluded that the three-tiered interpretation system provides an approximate but imprecise measurement of neonatal prognosis. Although the incidence of an Apgar score < 7 at 5 minutes and umbilical artery pH < 7.00 increased significantly with increasing FHR tracing category, approximately 98% of newborns with Category II tracings did not have adverse outcomes. Notably, of the 671 articles reviewed, only 3 publications met inclusion criteria.

Several other classification systems have been developed. For example, a five-tier FHR pattern interpretation system has been developed based on the Federal Homeland Security Classification of Risk in US airports (green = low risk, red = severe risk of acidemia, and/or evolution to a more serious pattern). In a small retrospective study, the five-tier classification system performed better than the three-tier classification system in characterizing fetuses with acidemia who required subsequent admission to the NICU and respiratory support. That said, this classification system is more complex, and in most US birthing facilities, the three-tier system is utilized as it is currently endorsed by national organizations. Indeed, national organizations now have developed educational programs and clinical practicums for FHR monitoring using the three-tier system in obstetric practice. Evidence for the impact of such training on neonatal and maternal outcomes is limited and requires further study.

Methods for Improving the Efficacy of Electronic Fetal Heart Rate Monitoring

Several technologies have been employed to enhance the value of electronic FHR monitoring. To facilitate continual FHR assessment, many labor and delivery units transmit the tracings from the bedside to the nurses’ station, referred to as “centralized” monitoring. Presumably, this practice facilitates a more rapid response to worrisome FHR tracings. Electronic archiving allows for the electronic storage and retrieval of FHR tracings and eliminates the need for long-term storage of the paper record. Storage, either using an electronic record or a paper FHR tracing, is necessary as a component of the medical record. While commercially available programs with sound or light alerts have been developed, randomized controlled trials have not shown improvement over visual interpretation of tracings. In fact, it is possible that intrapartum maternal overmonitoring can negatively impact care by generating alarm fatigue. This has prompted some centers to explore risk-based alarm systems to reduce such fatigue.

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Oct 18, 2026 | Posted by Editorial Team in ANESTHESIA | Comments Off

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Intrapartum Fetal Assessment and Therapy

FETAL RISK DURING LABOR

Definition of Neonatal Encephalopathy