Clinical Management of Abnormal Fetal Heart Rate Patterns
The general premise of electronic fetal heart rate (FHR) monitoring is that when the FHR pattern is normal, it is essentially certain that the fetus at that point in time is neither hypoxic nor acidotic. The opposite is, however, often not the case; that is, when the FHR is abnormal, the fetus is often vigorous and not significantly acidotic at birth. The previously used term “fetal distress” was often inaccurate. As recommended by the ACOG Committee on Obstetric Practice in 2005, the nonspecific and imprecise term “fetal distress” should be replaced by “nonreassuring fetal status,” which is to say that all of the data available for assessing the fetus do not reassure the clinician (1). In addition, this should be followed by a further description of findings (e.g., types of FHR patterns, baseline changes, biophysical profile score). In addition, there is now an entirely new recommendation for nomenclature of FHR tracings (see Chapter 6).
There is no agreed definition of fetal distress because the term has various meanings for different people. Although not interchangeable, the terms fetal distress, fetal asphyxia, and asphyxial trauma are often freely substituted and erroneously equated. Such inconsistencies and inaccuracies create problems for caregivers, particularly in the increasingly litigious climate of our society. Dorland’s Medical Dictionary defines asphyxia as a “lack of oxygen and respired air resulting in impending or actual cessation of life.” Its Greek origin, “a stopping of the pulse,” gives the definition of birth asphyxia an imprecise meaning at best. In the past, asphyxia has been the assumed cause of depressed newborns with low Apgar scores. In the fetus, asphyxia refers to a lack of oxygen resulting in metabolic acidosis (2). Asphyxial trauma suggests cellular damage, particularly but not exclusively to the central nervous system (CNS), subsequent to some antepartum or intrapartum compromise. Neither fetal hypoxia nor asphyxia is necessarily associated with cellular death leading to fetal morbidity or mortality (3). Indeed, when recognized, the hope is that intervention significantly mitigates the risk of adverse outcomes. For any number of reasons, the correlation between an abnormal FHR and adverse outcome is poor.
The American College of Obstetricians and Gynecologists carefully reviewed the relationship between FHR patterns, Apgar scores, umbilical cord gases, newborn course, and subsequent outcome. Specific criteria to establish an acute intrapartum event being sufficient to cause cerebral palsy are as follows:
Evidence of metabolic acidosis in fetal umbilical artery blood at birth (pH <7.00 and base deficit >12 mmol/L)
Early onset of severe or moderate encephalopathy in infants born at or beyond 34 weeks’ gestation
Cerebral palsy of the spastic quadriplegic or dyskinetic type
Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infectious conditions, or genetic disorders (4)
Obtaining an umbilical artery blood gas assessment is critical in establishing this condition (5). We do not recommend routinely obtaining a blood specimen pH assessment on all deliveries as often (about 5% to 10%) an abnormal cord pH will be found in a baby with normal Apgar scores. These babies rarely have complications known to be correlated with acidosis or other problems in the newborn period. Hence we do not find that a cord pH is helpful in a newborn with normal Apgar scores. We do recommend obtaining a specimen of umbilical arterial blood for pH, pCO2, and base deficit in the following situations: unexpectedly depressed newborns; Category III FHR pattern immediately before delivery, especially when operative delivery has been performed for that indication; babies with anomalies or other situations where the baby is likely to go to the neonatal intensive care unit; and very premature infants (<32 weeks).
Ideally, the goal of FHR monitoring is to detect fetal hypoxia at its earliest stage and to attempt to prevent asphyxic damage resulting from prolonged and severe hypoxia. The
progression of normoxia to hypoxia to metabolic acidosis to asphyxic damage and ultimately death is believed to occur in that order (Fig. 8.1). When the FHR pattern suggests hypoxia, all measures short of operative delivery (hydration, position change, supplemental oxygen, decreasing/discontinuing oxytocin, etc.) should be used to try to reverse the situation. If the hypoxic pattern cannot be reversed, then the fetus should be delivered expeditious. Clinical judgment needs to be stressed since if birth occurs because the fetus is thought to be hypoxic but not acidotic, then far too many unnecessary operative deliveries will be done, for the majority of hypoxic babies do not become acidotic, are vigorous at birth, and have normal outcomes.
progression of normoxia to hypoxia to metabolic acidosis to asphyxic damage and ultimately death is believed to occur in that order (Fig. 8.1). When the FHR pattern suggests hypoxia, all measures short of operative delivery (hydration, position change, supplemental oxygen, decreasing/discontinuing oxytocin, etc.) should be used to try to reverse the situation. If the hypoxic pattern cannot be reversed, then the fetus should be delivered expeditious. Clinical judgment needs to be stressed since if birth occurs because the fetus is thought to be hypoxic but not acidotic, then far too many unnecessary operative deliveries will be done, for the majority of hypoxic babies do not become acidotic, are vigorous at birth, and have normal outcomes.
 Figure 8.1. Model for declining fetal oxygenation with progressive development of hypoxia, metabolic acidosis, damage, and death. |
Normal FHR patterns include those with accelerations, normal baseline rate, and normal variability. Early decelerations and mild variable decelerations are associated with normal Apgar scores, no acidosis at birth, and normal perinatal outcome. Abnormal patterns include the more severe forms of variable deceleration, persistent late decelerations, prolonged decelerations, and various atypical or preterminal patterns. Such patterns are usually associated with normal Apgar scores, but low Apgar scores may accompany such patterns (6).
A most important concept that must be realized in evaluating and managing abnormal FHR patterns is the issue of the normal progression of these changes when they are due to hypoxia. For example, tachycardia can be a result of hypoxia (see Fig. 6.20), but only when there are associated decelerations suggestive of hypoxia. That is to say in the laboring patient, persistent late, moderate-to-severe variable, or prolonged decelerations are the first indicators of hypoxia and virtually always precede tachycardia if the increase in heart rate is due to hypoxia. Similarly, loss of variability or disappearance of accelerations will not be the first sign of hypoxia and does not require further evaluation or intervention unless associated decelerations suggest a progressive hypoxia. The only exception to this can be the fetus who has tachycardia, absent or decreased variability, and/or no accelerations when the monitor is first placed on the patient. In this situation, one cannot be sure that no hypoxic deceleration pattern preceded these findings.
LATE DECELERATIONS
ACOG Definition (2010)
Late 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 of 30 seconds or more.
The decrease in FHR is calculated from the onset to the nadir of the deceleration.
The deceleration 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 the contraction, respectively.
Late decelerations are found in association with uteroplacental insufficiency and imply some degree of fetal hypoxia (7). A decrease in pO2 detected by the fetal brain is the only trigger for late decelerations. In their mildest form, late decelerations are associated with normal or increased FHR variability. The pattern is characteristically described as uniform, appearing consistently from one contraction to the next. This rule is common once fetal hypoxia is established since in the early stages of developing fetal hypoxia, the pattern may be intermittent (Fig. 8.2). While it would seem prudent to take measures to optimize uterine blood flow at this stage, intermittent late decelerations with good or increased FHR variability require close watching and may not become any more severe. In this situation, the patient should be laboring in the lateral position, she should be well hydrated, oxytocin should be decreased or discontinued if contractions seem excessive, and she should be receiving oxygen (Fig. 8.3). If the late decelerations have occurred in association with decreased maternal blood pressure following conduction anesthesia or following the administration of an antihypertensive agent in a patient with hypertension, appropriate measures should be taken to restore blood pressure and placental perfusion (Table 8.1).
If persistent late decelerations develop despite maximizing uterine blood flow, the physician is obligated to be sure that a metabolic acidosis has not developed. The simplest and most straightforward way of ruling out acidosis is to look for spontaneous accelerations (Fig. 8.4) or, in their absence, attempt to elicit an acceleration with acoustic or scalp stimulation (Fig. 8.5A). In the presence of late decelerations, FHR accelerations, whether spontaneous or elicited, rule out acidosis. The absence of any acceleration is associated with an approximate 50% incidence of acidosis. When no acceleration is elicited, previous clinical alternatives included continuous fetal pulse oximetry monitoring (Fig. 8.5B) or intermittent scalp pH (Fig. 8.6). Unfortunately, fetal pulse oximetry monitoring is no longer available in this country,
and fetal scalp blood sampling is rarely performed. As long as the late decelerations persist and the pattern unchanged, efforts to rule out acidosis must be repeated at least every 30 minutes. The presence of repeated accelerations allows the clinician to follow such patterns as long as the labor is progressing satisfactorily.
and fetal scalp blood sampling is rarely performed. As long as the late decelerations persist and the pattern unchanged, efforts to rule out acidosis must be repeated at least every 30 minutes. The presence of repeated accelerations allows the clinician to follow such patterns as long as the labor is progressing satisfactorily.
 Figure 8.2. Intermittent late decelerations in early labor. Note lack of accelerations. |
The discussion thus far has concerned the management of late deceleration in association with good variability. An FHR pattern of persistent late decelerations with complete absence of variability is much more ominous and almost always associated with fetal acidosis (Fig. 8.7). When encountered in either the antepartum or intrapartum period, our approach is to discontinue uterine stimulation and expedite delivery. This is most often via cesarean section since these patients are unable to tolerate labor without continuing to experience persistent late decelerations (8).
A common cause of late decelerations is excessive stimulation of contractions. Frequently, discontinuation of oxytocin results in improvement of the FHR (Fig. 8.8). The careful reinstitution of oxytocin at a lower rate often results in continued labor progress without continued late decelerations.
Another clinical situation that arises not infrequently is when late decelerations are persistent but when the oxytocin is discontinued, the decelerations resolve. Yet, without augmentation, the labor is inadequate. Following some period of time, the oxytocin is restarted, and late decelerations appear again. The clinician may choose to monitor the fetus closely and allow labor to continue as long as there is no evidence of acidosis. Alternatively, the choice may be to deliver the fetus expeditiously. This has been termed fetal intolerance to labor and has become a common indication for cesarean delivery for patients in labor.
 Figure 8.3. Late decelerations corrected by turning patient on her side. |
TABLE 8.1 Medical management of late deceleration | |||||||||||||||||||||
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VARIABLE DECELERATIONS ACOG
Definition (2010)
Variable deceleration
Visually apparent abrupt decrease in FHR
An abrupt FHR decrease is defined as from the onset of the deceleration to the beginning of the FHR nadir of <30 seconds.
The decrease in FHR is calculated from the onset to the nadir of the deceleration.
The decrease in FHR is 15 beats per minute (BPM) or greater, lasting 15 seconds or greater, and <2 minutes in duration.
When variable decelerations are associated with uterine contractions, their onset, depth, and duration commonly vary with successive uterine contractions.
Variable decelerations are most frequently the result of umbilical cord compression. It is the most common periodic change observed in laboring patients. The pattern is characterized by abrupt decreases in FHR to levels as low as 50 BPM. The pattern varies from one moment to the next and may be influenced by such simple things as maternal position changes. While the pattern is the most profound appearing of the periodic FHR changes, the vast majority of the time it cannot be considered nonreassuring, because, unless the cord occlusion is frequent, prolonged, and severe, there is no increased risk of low Apgar scores, fetal metabolic acidosis, or other significant neonatal morbidity. The problem with variable decelerations is that they may suddenly become severe. Variable decelerations are less predictable than late decelerations, which tend to follow a slowly deteriorating course, allowing their development to be watched over time. Also, because variable decelerations can change from one contraction to the next, it is hard to know what to expect in the near future. This makes the management of this pattern especially difficult, particularly when working in a setting without the capability to move rapidly to operative delivery.
We have found that it is much easier to define the limits of reassuring variable decelerations than it is to give absolute criteria for when variable deceleration represents sufficient evidence of hypoxia to demand operative intervention. The following four criteria may be used as a guide to the limits of reassuring variable deceleration (Fig. 8.9):
The FHR decelerations last no more than 40 to 60 seconds on a repetitive basis.
The return of the FHR to the baseline is abrupt. There is no persistent “late component” manifested by a slow return or a late deceleration after the return.
The baseline FHR is not increasing.
The FHR variability is not decreasing.
While severe variable decelerations, increasing baseline heart rate, and loss of variability in the face of progressive variable decelerations are reasonably reliable indicators of progressively severe cord compression and developing hypoxia, this may not be the case with a slow return to baseline. As described in the chapter on the physiology of FHR patterns, there may be two and possibly three potential causes of a slow return to baseline. First, progressively severe cord compression may result in sufficient residual fetal hypoxia as to result in this pattern (see Fig. 6.21). The other primary mechanism is a combination of late and variable decelerations caused by two different mechanisms: cord compression and placental insufficiency. Finally, there maybe a third, more benign cause, perhaps due to slower than usual release of the cord compression. In a recent review of variable decelerations with slow return to baseline in patients who were also being monitored with pulse oximetry, we found that when these patterns were preceded by severe variable or persistent late decelerations, there was indeed an increased likelihood of significant hypoxia. However, when such patterns were preceded by neither, there was no more likelihood of hypoxia than in patients with mild variable decelerations (9).
 Figure 8.4. Persistent late decelerations. Note the presence of a spontaneous acceleration at panel 27595 (arrow). The presence of the acceleration virtually eliminates, at this point in time, any likelihood of a metabolic acidosis. |
 Figure 8.5. A, B: Both cases illustrate persistent late decelerations. In A, the clinician is reassured of the absence of a metabolic acidosis with an acceleration following acoustic stimulation. In B, reassurance is attained using fetal pulse oximetry, which reveals a continuous fetal oxygen saturation above 30%. |
 Figure 8.6. Late decelerations with good variability are seen in the upper panel. The lower panel is 1½ hours later, showing a continuation of late deceleration with good variability. The pH taken at this time was 7.08, suggesting that earlier intervention might have been advisable. |
 Figure 8.7. Late deceleration with poor variability. (From Paul R, Freeman R: Selected records of intrapartum fetal monitoring with self instruction. USC Publishers, Los Angeles, 1971, with permission.) |
 Figure 8.8. Late deceleration due to oxytocin and corrected by stopping the oxytocin infusion when it says “Pit off” in section 114634. (From Paul R, Freeman R: Selected records of intrapartum fetal monitoring with self instruction. USC Publishers, Los Angeles, 1971, with permission.) |
 Figure 8.9. Reassuring variable decelerations. |
When criteria for nonreassuring variable decelerations are met and the pattern persists, the ability to effect immediate delivery is crucial. Increasing baseline, loss of variability, and/or delayed return to baseline can evolve in a short time with variable decelerations (Figs. 8.10 and 8.11). Similar to late decelerations, when variable decelerations meet any of the previous criteria as a nonreassuring pattern, one must either be reassured of the absence of acidosis, using the presence of spontaneous or elicited accelerations or move expeditiously to delivery.
It is useful from a management perspective to categorize variable decelerations based on their most likely cause (Table 8.2). Variable decelerations due to oligohydramnios usually appear relatively early in labor, and these are best reversed using amnioinfusion. Probably the most common cause of variable decelerations are nuchal cords. Nuchal cords probably cause decelerations, not due to compression, but due to the cord tightening, becoming stretched as the fetus descends into the pelvis. Because in most labors, the rapid phase of descent usually begins between 8 and 10 cm of dilation, it is common for nuchal cords to manifest variable decelerations at this stage (Fig. 8.12). These patterns are not likely to benefit from amnioinfusion or maternal repositioning. If the pattern becomes nonreassuring, the patient will often benefit by having her push less frequently, giving the fetus more time to recover from the cord compression between contractions (Fig. 8.13). A rare cause of variable or prolonged deceleration is umbilical cord prolapse. When significant variable or prolonged decelerations suddenly appear, this etiology should be considered and a pelvic examination performed immediately because cord prolapse virtually always requires elevation of the presenting part and immediate cesarean section. Finally, there is a group in which no good treatment other than repositioning may help relieve the cord compression. This group includes cord entanglement other than nuchal cords, such as around a fetal extremity or body, a true knot in the cord, or a short cord. The presentation of these may occur at any time during labor (Fig. 8.14).
 Figure 8.10. Variable deceleration with a rising baseline and slow return to baseline. This is an abnormal pattern. |
 Figure 8.11. Variable deceleration with tachycardia and loss of fetal heart rate variability. This pattern is concerning. (From Paul R. Petrie R: Fetal intensive care current concepts. USC Publishers, Los Angeles, 1973, with permission.) |
TABLE 8.2 Management classification of variable declarations | ||||||||||||||||||||||||||||||||
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 Figure 8.12. The new onset of variable decelerations occurring late in labor often heralds the transition to the second stage of labor. As seen in this patient, shortly after the appearance of the first deep variable deceleration, she begins spontaneously pushing and is found to be completely dilated. |
 Figure 8.13. This patient is having rather severe variable decelerations in the second state of labor. Note that the depth and duration of the deceleration diminishes when the patient is not pushing. This is an effective method to allow additional recovery when significant variable decelerations are occurring in the second stage of labor. |
Generally speaking, persistent and uncorrectable non-reassuring variable decelerations in early labor are best managed with delivery. On the other hand, during the second stage of labor, it is very common to see variable decelerations with maternal pushing. With continued pushing, these decelerations may appear to be concerning (Fig. 8.15). However, if progress is being made with descent of the presenting part, and the baseline heart rate level and variability remain unchanged, it is better to allow labor to progress than to attempt a difficult midpelvic delivery. It is common to see variable decelerations lasting more than a minute at 2- to 3-minute intervals during the second stage of labor. Other than position change and attempting to have the mother not push with each contraction, we continue to monitor and allow labor to continue as long as the baseline rate is not increasing and baseline variability is present.
The clinical guideline for management of patients with variable decelerations is, then, to be reassured if the pattern does not exceed the previously stated criteria for nonreas-suring variable decelerations and to treat the patient expectantly. If these criteria are exceeded, the general rule is that the closer one estimates vaginal delivery to be, the higher
will be the threshold for intervention (Table 8.3). With the introduction of both prophylactic and therapeutic amnioinfusion, the frequency of variable decelerations should be decreased, often making management decisions much easier. Variable decelerations are responsible for most unnecessary cesarean sections performed when the physician is not experienced with fetal monitoring, and they must have been a major reason for operative intervention when only auscultatory FHR monitoring was available.
will be the threshold for intervention (Table 8.3). With the introduction of both prophylactic and therapeutic amnioinfusion, the frequency of variable decelerations should be decreased, often making management decisions much easier. Variable decelerations are responsible for most unnecessary cesarean sections performed when the physician is not experienced with fetal monitoring, and they must have been a major reason for operative intervention when only auscultatory FHR monitoring was available.
 Figure 8.14. These variable decelerations are typical of “unusual cords.” Their frequency, depth, duration, and shape are inconsistent, and they do not bear a regular relationship to contractions. At delivery the umbilical cord was noted to be quite short (11 in). |
 Figure 8.15. Variable deceleration of progressive severity occurring at the end of the second stage of labor. |
TABLE 8.3 Medical management of severe variable decelerations | ||||||
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PROLONGED DECELERATIONS
ACOG Definition (2010)
Prolonged deceleration
Visually apparent decrease in the FHR below the baseline
Decrease in FHR from the baseline that is 15 BPM or more, lasting 2 minutes or more but <10 minutes in duration
If a deceleration lasts 10 minutes or longer, it is a baseline change.
Prolonged decelerations lasting several minutes and occurring as more or less isolated events will be observed either in association with identifiable causes or without apparent etiology. If there is no known cause, prolonged decelerations may represent umbilical cord compression of a severe degree or may represent a catastrophic event such as placental abruption, uterine rupture, or bleeding from vasa previa. The following is a list of potential causes of prolonged decelerations that may be identified and managed during the intrapartum period:
Hypertonic or prolonged contractions (spontaneous or oxytocin-induced) (Fig. 8.16)
Vaginal examination (Fig. 8.17)
Application of internal fetal scalp electrode
Fetal scalp blood sampling
Prolapsed umbilical cord (Fig. 8.18)
Figure 8.16. The upper panel demonstrates a tetanic contraction with severe prolonged fetal heart rate (FHR) deceleration after institution of oxytocin. The lower panel represents a tetanic contraction with a severe prolonged FHR deceleration after intravenous dimenhydrinate (Dramamine). (From Paul R, Freeman R: Selected records of intrapartum fetal monitoring with self instruction. USC Publishers, Los Angeles, 1971, with permission.)
Figure 8.17. A prolonged deceleration associated with a vaginal examination.
Maternal seizure
Epidural or spinal block (Fig. 8.19)
Supine hypotension
Fetal CNS anomalies
Prolonged umbilical cord compression, often associated with rapid descent of the fetus
Maternal respiratory arrest (high spinal, intravenous [IV] narcotic) or cardiac decompensation
Uterine rupture (Fig. 8.20)
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