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Fetal Surveillance during Labor


Clinical Keys for this Chapter

  • ▪

    The most important principle of both fetal and maternal surveillance during labor is that childbirth is a normal process, and the majority of laboring women and their fetuses will have a safe journey. Obstetricians must be aware of each patient's past history and be prepared to monitor the journey based upon maternal and fetal needs during the labor process.

  • ▪

    Simple auscultation of the fetal heart rate in accordance with specific guidelines is acceptable to assess the health of the fetus. Continuous fetal heart rate and uterine activity monitoring have the advantage of providing continuous electronic records throughout the labor process but may not always be necessary.

  • ▪

    The pathophysiology of abnormal fetal heart rate patterns is complex, and both clinical and research findings suggest that hypoxia, acidosis, and inflammation form a triad of mixed metabolic dysregulation that may increase the risk of early (during delivery) and late (during childhood) physical and mental abnormalities.

  • ▪

    To improve our understanding of the assessment of abnormal and potentially pathologic heart rate patterns, the National Institutes of Health (NIH) has developed a three-tier fetal heart rate interpretation system (normal, intermediate, and abnormal). This is designed to improve the recognition of risk for poor fetal outcomes and to allow implementation of strategies for effective intervention.

  • ▪

    Abnormal fetal heart rate tracings associated with hypoxia, acidosis, and inflammation have five characteristics: (1) absent base line variability, (2) recurrent late decelerations, (3) recurrent variable decelerations, (4) bradycardia, and (5) sinusoidal patterns.

Effective fetal surveillance during labor is an essential element of good obstetric care. On the basis of the antepartum maternal history, physical examination, and laboratory data, 20-30% of pregnancies may be designated high risk, and 50% of perinatal morbidity and mortality occurs in this group. The remaining 50% of morbidity and mortality occurs in pregnancies that are considered to be normal at the onset of labor. Although fetal heart rate (FHR) monitoring by auscultation or continuous electronic fetal monitoring (EFM) provides useful information that improves the management of labor and reduces perinatal morbidity and mortality, evidence about its complete adequacy for fetal surveillance is conflicting.

The pathogenesis of abnormal FHR patterns is complex and remains poorly understood. In the past, it was felt that hypoxia was the main cause of abnormal FHR patterns and that continuous EFM and fetal scalp sampling would reliably identify those fetuses at greatest risk. However, a decrease in the incidence of cerebral palsy, one of the most serious complications associated with pregnancy and childbirth, has not occurred with increased monitoring.

This chapter provides the current concepts and recognized standards for appropriate fetal surveillance during labor.

Methods of Monitoring Fetal Heart Rate

Auscultation of the Fetal Heart Rate

The time-honored technique for evaluating the fetus during labor has been auscultation of the FHR. The first step in deciding on the optimal method (auscultation or continuous EFM) is to determine whether a patient has any risk factors. Auscultation of the fetal heart is performed by listening from the beginning of one contraction to the beginning of the next contraction. For low-risk patients, a competent nurse should listen every 30 minutes during the first stage of labor and at least every 15 minutes in the second stage of labor. For high-risk patients, the FHR should be assessed every 15 minutes during the first stage of labor and every 5 minutes during the second stage. Some studies have suggested that intermittent auscultation of the fetal heart is comparable to continuous electronic monitoring, in terms of neonatal outcome, if performed at the intervals stated above with a 1 : 1 patient-to-nurse ratio.

Continuous Electronic Fetal Heart Rate Monitoring

EFM during labor was developed to detect FHR patterns frequently associated with delivery of infants in a depressed condition. It was reasoned that early recognition of changes in FHR patterns that are associated with hypoxia and umbilical cord compression would serve as a warning that would enable a physician to intervene and prevent fetal death or irreversible brain injury.

Pathophysiology of Abnormal Fetal Heart Rate Patterns

The focus of EFM has been on the recognition that hypoxia leads to a greater risk of acidosis, which can be identified by fetal scalp blood sampling during labor and cord blood gas analysis at delivery. Today, the cause of abnormal FHR patterns is thought to be more complex and probably related to a combination of hypoxia, acidosis, and inflammation that subjects all physiologic systems (brain, heart, placenta, blood vessels, and the fetal adrenal gland) to multisystem dysregulation and is associated with a complex array of FHR perturbations. These changes in heart rate are difficult to interpret without better ways to define the most optimal biomarkers that identify the fetus at highest risk. Important maternal and fetal biomarkers of current research interest are inflammatory markers (such as C-reactive protein) and vitamin D deficiency.

EFM allows continuous reporting of the FHR, uterine contractions, maternal heart rate, and blood pressure (FHR-UC-MHR-MBP) by means of a monitor that prints results on a two-channel strip chart recorder that can be stored as part of an electronic record. Uterine contractions result in a reduction in blood flow to the placenta, which can cause an interruption in fetal oxygenation and lead to corresponding alterations in the FHR. The “FHR-UC-MHR-MBP” record can be obtained using external transducers that are placed on the maternal abdomen and arm. It is important that external palpation of the uterus is carried out to determine the intensity of contractions with this method. This technique is used in early labor.

Internal monitoring is carried out by placing a spiral electrode onto the fetal scalp to monitor heart rate and inserting a plastic catheter transcervically into the amniotic cavity to monitor uterine contractions ( Figure 9-1 ). To carry out this technique, the fetal membranes must be ruptured and the cervix must be dilated to at least 2 cm. Caution must be exercised when the decision to rupture the membranes is made, and it should be performed only when more exact information is needed to monitor a mother or fetus at risk.

FIGURE 9-1, Technique for internal continuous electronic monitoring of both fetal and maternal heart rates, as well as the pressure and frequency of uterine contractions. External monitoring of uterine contractions provides information only about the frequency of contractions.

Internal monitoring gives better FHR tracings because the rate is computed from the sharply defined R-wave peaks of the fetal electrocardiogram, whereas with the external technique, the rate is computed from the less precisely defined first heart sound obtained with an ultrasonic transducer. However, fetal scalp electrodes should be placed only when the benefit outweighs the risk, and fetal scalp electrodes should always be placed with care. For example, patients with specific infections (HIV and hepatitis B) should not have a scalp electrode placed. In addition, when placing a scalp electrode, the presenting part of the fetus must be ascertained to avoid placing the electrode on the face or external genitals if the fetus is presenting as a breech.

The internal uterine catheter allows precise measurement of the intensity of the contractions in millimeters of mercury, whereas the external tocodynamometer measures only frequency and duration, not intensity. The strength of uterine contractions, however, can easily be assessed by abdominal palpation by a trained observer (a nurse or physician).

In the clinical setting, internal and external techniques are often combined by using a scalp electrode for precise heart rate recording and the external tocodynamometer for contractions. This approach minimizes possible side effects from invasive internal monitoring.

Etiology of Hypoxia, Acidosis, and Fetal Heart Rate Changes

The developing fetus presents a paradox. Its arterial blood oxygen tension is only 25 ± 5 mm Hg, as compared with adult values of about 100 mm Hg. The rate of oxygen consumption, however, is twice that of the adult per unit weight, and its oxygen reserve is only enough to meet its metabolic needs for 1 to 2 minutes. Blood flow from the maternal circulation, which supplies the fetus with oxygen through placental exchange of respiratory gases, is momentarily interrupted during a contraction. A normal fetus can withstand the temporary reduction in blood flow to the placenta without developing hypoxia because sufficient oxygen exchange occurs during the interval between contractions.

Under normal circumstances, the FHR is determined by the atrial pacemaker. Modulation of the rate occurs physiologically through innervation of the heart by the vagus (decelerator) and sympathetic (accelerator) nerves. A fetus whose oxygen supply is marginal cannot tolerate the stress of contractions and will become hypoxic. Under hypoxic conditions, chemoreceptors and baroreceptors in the peripheral arterial circulation of the fetus influence the FHR by giving rise to contraction-related or periodic FHR changes. Hypoxia, when sufficiently severe, will also result in anaerobic metabolism, resulting in the accumulation of pyruvic and lactic acid and causing fetal acidosis. The degree of fetal acidosis can be measured by sampling blood from the presenting part. The normal fetal scalp blood pH varies between 7.25 and 7.30. Values below 7.20 are considered to be abnormal (fetal acidosis) but not necessarily indicative of fetal compromise.

The fetal oxygenation pathway can be interrupted at different locations within the uteroplacental-fetal circulatory loop. For example, impairment of oxygen transportation to the intervillous space may occur as a result of maternal hypertension or anemia; oxygen diffusion may be impaired in the placenta because of infarction or abruption; or the oxygen content in the fetal blood may be impaired because of hemolytic anemia in rhesus (Rh)-isoimmunization. Figure 9-2 summarizes the clinical conditions that may be associated with fetal distress during labor.

FIGURE 9-2, Clinical conditions associated with fetal distress in labor.

It is unrealistic to believe that hypoxia and acidosis are the only markers that determine the ultimate outcome of the fetus and neonate. Other markers of inflammation and the immune system must also play a role. Current research is focused on vitamin D deficiency and inflammatory markers such as interleukin-6 and C-reactive protein.

Fetal Heart Rate Patterns

The assessment of the FHR depends on an evaluation of the baseline pattern and the periodic changes related to uterine contractions. Table 9-1 gives a comprehensive list of FHR patterns and definitions based upon a workshop sponsored by the National Institute of Child Health and Human Development in 2008.

TABLE 9-1
Electronic Fetal Monitoring Definitions
From Macones A, Hankins GDV, Spong CY, et al: The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet Gynecol 112:661–666, 2008.
Pattern Definition
Baseline

  • The mean FHR rounded to increments of 5 excluding:

    • Periodic or episodic changes

    • Periods of marked FHR variability

    • Segments of baseline that differ by more than 25 beats/min

  • The baseline must be for a minimum of 2 min in any 10-min segment, or the baseline for that time period is indeterminate; in this case, one may refer to the prior 10-min window for determination of baseline

  • Normal FHR baseline: 110-160 beats/min

  • Tachycardia: FHR baseline is >160 beats/min

  • Bradycardia: FHR baseline is <110 beats/min

Baseline variability

  • Fluctuations in the baseline FHR that are irregular in amplitude and frequency

  • Variability is visually quantitated as the amplitude or peak-to-trough in beats per minute

    • Absent: amplitude range undetectable

    • Minimal: amplitude range detectable, but ≤5 beats/min

    • Moderate (normal): amplitude range 6-25 beats/min

    • Marked: amplitude range >25 beats/min

Acceleration

  • A visually apparent abrupt increase (onset to peak in <30 sec) in the FHR

  • At 32 weeks' gestation and beyond, an acceleration has a peak ≥15 beats/min above baseline, with a duration of 15 sec to 2 min from onset to return

  • Before 32 weeks' gestation, an acceleration has a peak ≥10 beats/min above baseline, with a duration of ≥10 sec but <2 min from onset to return

  • Prolonged acceleration lasts ≥2 min but <10 min in duration

  • If an acceleration lasts ≥10 min, it is a baseline change

Early deceleration

  • Visually apparent, usually symmetrical, gradual decrease and return of the FHR associated with a uterine contraction

  • A gradual FHR decrease is defined as from the onset to the FHR nadir or ≥30 sec

  • The decrease in FHR is calculated from the onset to the nadir of the deceleration

  • The nadir of the deceleration occurs at the same time as the peak of contraction

  • In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively

Late deceleration

  • Visually apparent, usually symmetrical, gradual decrease and return of the FHR associated with uterine contraction

  • A gradual FHR decrease is defined as one of ≥30 sec from the onset to the FHR nadir

  • The decrease in FHR is calculated from the onset to the nadir of the deceleration

  • The decrease is delayed in timing, with the nadir of the deceleration 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 contraction, respectively

Variable deceleration

  • Visually apparent abrupt decrease in FHR

  • An abrupt FHR decrease is defined as one of <30 sec from the onset of the deceleration to the beginning of the FHR nadir

  • The decrease in FHR is calculated from the onset to the nadir of the deceleration

  • The decrease in FHR is ≥15 beats/min, lasting ≥15 sec and <2 min in duration

  • When variable decelerations are associated with uterine contractions, their onset, depth, and duration commonly vary with successive uterine contractions

Prolonged deceleration

  • Visually apparent decrease in the FHR below the baseline

  • Decrease in the FHR from baseline that is ≥15 beats/min, lasting ≥2 min but <10 min in duration

  • If a deceleration lasts ≥10 min, it is a baseline change

Sinusoidal pattern Visually apparent, smooth, sine wave–like, undulating pattern in FHR baseline with a cycle frequency of 3-5 per min that persists for ≥20 min
FHR, Fetal heart rate.

Baseline Assessment

Baseline assessment of FHR requires the determination of the rate (in beats/min) and the variability. Normal and abnormal rates are listed in Table 9-1 . Normal FHR baseline is from 110 to 160 beats/min; tachycardia is a baseline greater than 160 beats/min, and bradycardia is less than 110 beats/min. Baseline variability can be divided into short- and long-term intervals. These are described in the subsections below.

  • 1

    Short-term or beat-to-beat variability. This reflects the interval between either successive fetal electrocardiographic signals or mechanical events of the cardiac cycle. Normal short-term variability fluctuates between 6 and 25 beats/min. Variability below 5 beats/min is considered to be potentially abnormal. When associated with decelerations, a variability of less than 5 beats/min usually indicates severe fetal distress.

  • 2

    Long-term variability. These fluctuations may be described in terms of the frequency and amplitude of change in the baseline rate. The normal long-term variability is 3 to 10 cycles per minute. Variability is physiologically decreased during the state of quiet sleep of the fetus, which usually lasts for about 25 minutes until transition occurs to another state. Changes in the long-term variability in prolonged and difficult labors may be a sign of an accumulated risk of metabolic dysregulation.

  • 3

    Decreased beat-to-beat variability. A prolonged flat baseline is the result of fetal acidosis.

Periodic Fetal Heart Rate Changes

Periodic FHR changes are changes in baseline FHR related to uterine contractions. The responses to uterine contractions may be categorized as follows:

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