Fetal Assessment during Labor

Early decelerations.

Early deceleration of the FHR is a visually apparent gradual (onset to lowest point 30 seconds or more) decrease in and return to the baseline FHR associated with UCs (Macones et al., 2008). Generally the onset, nadir, and recovery of the deceleration correspond to the beginning, peak, and end of the contraction (Fig. 11-10). For this reason, early decelerations are sometimes called the “mirror image” of a contraction.

Early decelerations are thought to be caused by transient fetal head compression and are considered a benign finding (Tucker et al., 2009). Early decelerations may also occur during vaginal examinations, as a result of fundal pressure, and during placement of the internal mode of fetal monitoring. When present, they usually occur during the first stage of labor when the cervix is dilated 4 to 7 cm but can also be seen during the second stage when the woman is pushing.

Because early decelerations are considered to be benign, interventions are not necessary. Early decelerations should be identified, however, so that they can be distinguished from late or variable decelerations, for which interventions are appropriate. Box 11-3 lists cause, clinical significance, and nursing interventions for early decelerations.

Late decelerations.

Late deceleration of the FHR is a visually apparent gradual (onset to lowest point 30 seconds or more) decrease in and return to baseline FHR associated with UCs (Macones et al., 2008). The deceleration begins after the contraction has started, and the lowest point of the deceleration occurs after the peak of the contraction. The deceleration usually does not return to baseline until after the contraction is over (Fig. 11-11).

Uteroplacental insufficiency causes late decelerations. Persistent and repetitive late decelerations indicate the presence of fetal hypoxemia stemming from insufficient placental perfusion during UCs. If recurrent or sustained, late decelerations can lead to metabolic acidemia (Tucker et al., 2009). They should be considered an ominous sign when they are uncorrectable, especially if they are associated with absent or minimal variability and tachycardia. Several factors can disrupt oxygen transfer to the fetus, including maternal hypotension, uterine tachysystole (e.g., more than five contractions in 10 minutes, averaged over a 30-minute window), preeclampsia, postdate or postterm pregnancy, amnionitis, small-for-gestational-age fetuses, maternal diabetes, placenta previa, abruptio placentae, conduction anesthetics, maternal cardiac disease, and maternal anemia. The clinical significance and nursing interventions are described in Box 11-4.

Variable decelerations.

Variable deceleration of the FHR is defined as a visually abrupt (onset to lowest point <30 seconds) decrease in FHR below the baseline. The decrease is at least 15 beats/min or more below the baseline, lasts at least 15 seconds, and returns to baseline in less than 2 minutes from the time of onset (Macones et al., 2008). Variable decelerations are not necessarily associated with UCs. Variable decelerations are caused by compression of the umbilical cord (Fig. 11-12).

The appearance of variable decelerations differs from those of early and late decelerations, which closely approximate the shape of the corresponding UC. Instead, variable decelerations often have a U, V, or W shape characterized by a rapid descent to and ascent from the nadir (lowest point) of the deceleration (see Fig. 11-12). Some variable decelerations are preceded and followed by brief accelerations of the FHR, known as “shoulders,” which is an appropriate compensatory response to compression of the umbilical cord.

Occasional variable decelerations have little clinical significance. Repetitive variable decelerations, on the other hand, indicate recurrent disruption in the fetus' oxygen supply. This disruption can result in hypoxemia and eventually metabolic acidemia (Tucker et al., 2009). Variable decelerations are most commonly found during the transition phase of first stage labor or the second stage of labor as a result of umbilical cord compression and stretching during fetal descent (Garite, 2007). Box 11-5 lists causes, clinical significance, and nursing interventions for variable decelerations.

Prolonged decelerations.

A prolonged deceleration is a visually apparent decrease (may be either gradual or abrupt) in FHR of at least 15 beats/min below the baseline and lasting more than 2 minutes but less than 10 minutes. A deceleration lasting more than 10 minutes is considered a baseline change (Macones et al., 2008) (Fig. 11-13).

Prolonged decelerations are caused by a disruption in the fetal oxygen supply. They usually begin as a reflex response to hypoxia. If the disruption continues, however, the fetal cardiac tissue itself will become hypoxic, resulting in direct myocardial depression of the FHR (Tucker et al., 2009). Prolonged decelerations may be caused by prolonged cord compression, profound uteroplacental insufficiency, or perhaps sustained head compression. The presence and degree of hypoxia present are thought to correlate with the depth and duration of the deceleration, how abruptly it returns to the baseline, how much variability is lost during the deceleration, and whether rebound tachycardia and loss of variability occur after the deceleration (Garite, 2007).

Significant stimuli that may result in prolonged decelerations are a prolapsed umbilical cord or other forms of prolonged cord compression, prolonged uterine tachysystole, hypotension after spinal or epidural anesthesia or analgesia, abruptio placentae, eclamptic seizure, and rapid descent through the birth canal. Other more benign causes of prolonged decelerations include pelvic examination, application of a spiral electrode, and sustained maternal Valsalva maneuver (Garite, 2007).

Care Management 

Care of the woman receiving EFM in labor begins with evaluation of the EFM equipment. The nurse must ensure that the monitor is recording FHR and UA accurately and that the tracing is interpretable. If external monitoring is not adequate, changing to a fetal spiral electrode or IUPC may be necessary. A checklist for fetal monitoring equipment can be used to evaluate the equipment functions (Box 11-6).

After ensuring that the monitor is recording properly, the FHR and UA tracings are evaluated regularly throughout labor. Guidelines for Perinatal Care published jointly by the American Academy of Pediatrics (AAP) and ACOG (2007) recommends that the FHR tracing be evaluated at least every 30 minutes during the first stage of labor and every 15 minutes during the second stage of labor in low risk women. If risk factors are present, then the FHR tracing should be evaluated more frequently, every 15 minutes in the first stage of labor and every 5 minutes in the second stage of labor.

Based on assessment findings the nurse identifies relevant nursing diagnoses and expected outcomes of care, implements appropriate interventions, and evaluates the care provided (see Nursing Process box). Assessing FHR and UA patterns, implementing independent nursing interventions, documenting observations and actions according to the established standard of care, and reporting abnormal patterns to the primary care provider (e.g., physician, certified nurse-midwife) are the responsibilities of the nurse providing care to women in labor.

Fetal scalp stimulation and vibroacoustic stimulation.

Several research studies undertaken in the 1980s found that a FHR acceleration in response to digital or vibroacoustic stimulation was highly predictive of a normal scalp blood pH. The two methods of fetal stimulation currently used most often in clinical practice are scalp stimulation (using digital pressure during a vaginal examination) and vibroacoustic stimulation (using an artificial larynx or fetal acoustic stimulation device on the maternal abdomen over the fetal head for 1 to 5 seconds). The desired result of both methods of stimulation is an acceleration in the FHR of at least 15 beats/min for at least 15 seconds (Tucker et al., 2009). A FHR acceleration indicates the absence of metabolic acidemia. If the fetus does not respond to stimulation with an acceleration, fetal compromise is not necessarily indicated; however, further evaluation of fetal well-being is needed. Fetal stimulation should be performed at times when the FHR is at baseline. Neither fetal scalp stimulation nor vibroacoustic stimulation should be instituted if FHR decelerations or bradycardia is present (Tucker et al.).

Umbilical cord acid-base determination.

In assessing the immediate condition of the newborn after birth, a sample of cord blood is a useful adjunct to the Apgar score. The procedure is generally performed by withdrawing blood from both the umbilical artery and the umbilical vein. Both samples are then tested for pH, carbon dioxide pressure (PCO₂), oxygen pressure (PO₂), and base deficit or base excess (Garite, 2007; Tucker et al., 2009). Umbilical arterial values reflect fetal condition, whereas umbilical vein values indicate placental function (Tucker et al.).

ACOG (2006a) suggests obtaining cord blood values in the following clinical situations: cesarean birth for fetal compromise, low 5-minute Apgar score, severe intrauterine growth restriction, abnormal FHR tracing, maternal thyroid disease, intrapartum fever, and multifetal gestation. Normal umbilical artery and vein cord blood values are listed in Table 11-4. Normal findings preclude the presence of acidemia at, or immediately before, birth (Tucker et al., 2009). If acidemia is present (e.g., pH <7.20), then the type of acidemia is determined (respiratory, metabolic, or mixed) by analyzing the blood gas values (Table 11-5) (Tucker et al.).

Fetal scalp blood sampling.

Sampling of the fetal scalp blood for pH determination was first described in the 1960s and performed extensively in the 1970s. The procedure is performed by obtaining a sample of fetal scalp blood through the dilated cervix after the membranes have ruptured. Its use is limited by many factors, including the requirement for cervical dilation and membrane rupture, technical difficulty of the procedure, need for repetitive pH determinations, and uncertainty regarding interpretation and application of results. This procedure is now seldom used in the United States but remains a common practice in other countries (Tucker et al., 2009).

Fetal pulse oximetry.

Fetal pulse oximetry or continuous monitoring of fetal oxygen saturation levels is a method of fetal assessment that indirectly measures the oxygen saturation of hemoglobin in fetal blood. An intrauterine sensor placed in contact with the fetal cheek or temple area provides a continuous estimation of fetal oxygen saturation. Fetal pulse oximetry was approved for clinical use by the U.S. Food and Drug Administration in May 2000. The hope was that this technology would help to interpret nonreassuring FHR patterns more accurately and perhaps decrease the number of cesarean births performed for nonreassuring FHR tracings (Garite, 2007). Several studies, however, found that although fetal pulse oximetry did decrease the incidence of cesarean births for fetal indications, it had no consistent impact on overall cesarean birth rates or newborn outcomes. Therefore, fetal pulse oximetry has not been proven to be a clinically useful test for determining fetal status (ACOG, 2009). Because the manufacturer no longer distributes the sensors, the product has in effect been taken off the market (Tucker et al., 2009).