Internal (Direct) Electronic Monitoring
Direct fetal heart measurement is accomplished by attaching a bipolar spiral electrode directly to the fetus (Fig. 24-1). The wire electrode penetrates the fetal scalp, and the second pole is a metal wing on the electrode. The electrical fetal cardiac signal—P wave, QRS complex, and T wave—is amplified and fed into a cardiotachometer for heart rate calculation. The peak R-wave voltage is the portion of the fetal electrocardiogram (ECG) most reliably detected.
Internal electronic fetal monitoring. Schematic representation of a bipolar electrode attached to the fetal scalp for detection of fetal QRS complexes (F). Also shown is the maternal heart and corresponding electrical complex (M) that is detected.
An example of the method of fetal heart rate processing employed when a scalp electrode is used is shown in Figure 24-2. Time (t) in milliseconds between fetal R waves is fed into a cardiotachometer, where a new fetal heart rate is set with the arrival of each new R wave. As also shown in Figure 24-2, a premature atrial contraction is computed as a heart rate acceleration because the interval (t2) is shorter than the preceding one (t1). The phenomenon of continuous R-to-R wave fetal heart rate computation is known as beat-to-beat variability.
Schematic representation of fetal electrocardiographic signals used to compute continuing beat-to-beat heart rate with scalp electrodes. Time intervals (t1, t2, t3) in milliseconds between successive fetal R waves are used by a cardiotachometer to compute instantaneous fetal heart rate. ECG = electrocardiogram; PAC = premature atrial contraction.
Electrical cardiac complexes detected by the electrode include those generated by the mother. However, the amplitude of the maternal ECG signal is diminished when recorded through the fetal scalp electrode and is masked by the fetal ECG. Shown in Figure 24-3 are simultaneous recordings of maternal chest wall ECG signals and fetal scalp electrode ECG signals. This fetus is experiencing premature atrial contractions, which cause the cardiotachometer to rapidly and erratically seek new heart rates, resulting in the “spiking” shown in the standard fetal monitor tracing. Importantly, when the fetus is dead, the maternal R waves are still detected by the scalp electrode as the next best signal and are counted by the cardiotachometer (Fig. 24-4).
The top tracing shows standard fetal monitor tracing of heart rate using a fetal scalp electrode. Spiking of the fetal rate in the monitor tracing is due to premature atrial contractions. The second panel displays accompanying contractions. The bottom two tracings represent cardiac electrical complexes detected from fetal scalp and maternal chest wall electrodes. ECG = electrocardiogram; F = fetus; M = mother; PAC = fetal premature atrial contraction.
Placental abruption. In the upper panel, the fetal scalp electrode first detected the heart rate of the dying fetus. After fetal death, the maternal electrocardiogram complex is detected and recorded. The second panel displays an absence of uterine contractions.
External (Indirect) Electronic Monitoring
Although membrane rupture may be avoided, external monitoring does not provide the precision of fetal heart rate measurement afforded by internal monitoring (Nunes, 2014). In some women—for example, those who are obese—external monitoring may be difficult (Brocato, 2017).
With external monitoring, the fetal heart rate is detected through the maternal abdominal wall using the ultrasound Doppler principle. Ultrasound waves undergo a shift in frequency as they are reflected from moving fetal heart valves and from pulsatile blood ejected during systole (Chap. 10, Doppler). The unit consists of a transducer that emits ultrasound and a sensor to detect a shift in frequency of the reflected sound. The transducer is placed on the maternal abdomen at a site where fetal heart action is best detected. A coupling gel must be applied because air conducts ultrasound waves poorly. The device is held in position by an elastic belt. Correct positioning enhances differentiation of fetal cardiac motion from maternal arterial pulsations (Neilson, 2008).
Ultrasound Doppler signals are edited electronically before fetal heart rate data are printed onto monitor paper. Reflected ultrasound signals from moving fetal heart valves are analyzed through a microprocessor that compares incoming signals with the most recent previous signal. This process, called autocorrelation, is based on the premise that the fetal heart rate has regularity, whereas “noise” is random and without regularity. Several fetal heart motions must be deemed electronically acceptable by the microprocessor before the fetal heart rate is printed. Such electronic editing has greatly improved the tracing quality of the externally recorded fetal heart rate. Other features of current fetal monitors include the capability to monitor twin fetuses, monitor concurrent maternal heart rate, display the fetal ECG, and record maternal pulse oximetry values. Many fetal monitors are capable of interfacing with archival storage systems, which obviates maintaining actual paper tracings.
Technological advances now allow fetal heart rate monitoring from a remote, centralized location. Theoretically, the ability to monitor several patients simultaneously was hoped to improve neonatal outcomes. That said, only one study on centralized fetal monitoring has been reported. Anderson and colleagues (2011) measured the ability of 12 individuals to detect critical signals in fetal heart rate tracings on one, two, or four monitors. The results showed that detection accuracy declined as the number of displays increased.
Fetal Heart Rate Patterns
The interpretation of fetal heart rate patterns can be problematic without definitions and nomenclature. In one example, Blackwell and colleagues (2011) asked three Maternal-Fetal Medicine specialists to independently interpret 154 fetal heart rate tracings. Interobserver agreement was poor for the most ominous tracings and moderate for less severe patterns. The National Institute of Child Health and Human Development (NICHD) Research Planning Workshop (1997) brought together investigators with expertise in the field to propose standardized, unambiguous definitions for interpretation of fetal heart rate patterns during labor. This workshop reconvened in 2008. The definitions proposed as a result of this second workshop are used in this chapter and have been adopted by the American College of Obstetricians and Gynecologists (2017a) (Table 24-1). Importantly, interpretation of electronic fetal heart rate data is based on the visual pattern of the heart rate as portrayed on chart recorder graph paper. Thus, the choice of vertical and horizontal scaling greatly affects the appearance of the fetal heart rate. Scaling factors recommended by the NICHD Workshop are 30 beats per minute (beats/min or bpm) per vertical cm (range, 30 to 240 bpm) and 3 cm/min chart recorder paper speed. Fetal heart rate variation is falsely displayed at the slower 1 cm/min paper speed compared with that of the smoother baseline recorded at 3 cm/min. Thus, pattern recognition can be considerably distorted depending on the scaling factors used.
TABLE 24-1Electronic Fetal Monitoring Definitions ||Download (.pdf) TABLE 24-1 Electronic Fetal Monitoring Definitions
|Pattern ||Definition |
|Baseline || |
The mean FHR rounded to increments of 5 bpm during a 10-min segment, excluding:
—Periodic or episodic changes
—Periods of marked FHR variability
—Segments of baseline that differ by more than 25 bpm
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 bpm
Tachycardia: FHR baselines is greater than 160 beats per minute
Bradycardia: FHR baseline is less than 110 beats per minute
|Baseline variability || |
|Acceleration || |
A visually apparent abrupt increase (onset to peak in less than 30 seconds) in the FHR
At 32 weeks of gestation and beyond, an acceleration has a peak of 15 bpm or more above baseline, with a duration of 15 sec or more but less than 2 minutes from onset to return
Before 32 weeks, an acceleration has a peak of 10 bpm or more above baseline, with a duration of 10 seconds or more but less than 2 minutes from onset to return
Prolonged acceleration lasts 2 minutes or more but less than 10 minutes in duration
If an acceleration lasts 10 minutes or longer, 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 of 30 seconds or more
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 the contraction
In most cases the onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending of the contraction, respectively
|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
|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 less than 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 or greater, lasting 15 seconds or greater, and less than 2 minutes in duration
When variable decelerations are associated with uterine contraction, their onset, depth, and duration commonly vary with successive uterine contractions
|Prolonged deceleration || |
Visually apparent decrease in the FHR below the baseline
Decrease in FHR from the baseline that is 15 beats per minute or more, and less than 2 minutes in duration
If a deceleration last 10 minutes or longer, it is a baseline change
|Sinusoidal pattern || |
Baseline Fetal Heart Activity
This refers to the modal characteristics that prevail apart from periodic accelerations or decelerations associated with uterine contractions. Descriptive characteristics of baseline fetal heart activity include rate, beat-to-beat variability, fetal arrhythmia, and distinct patterns such as sinusoidal or saltatory fetal heart rates.
With increasing fetal maturation, the heart rate decreases. This continues postnatally such that the average rate is 85 bpm by age 8 years (Tintinalli, 2016). Pillai and James (1990) reported that the baseline fetal heart rate declined an average of 24 bpm between 16 weeks’ gestation and term, or approximately 1 bpm per week. This normal gradual slowing of the fetal heart rate is thought to correspond to maturation of parasympathetic (vagal) heart control (Renou, 1969).
The baseline fetal heart rate is the approximate mean rate rounded to increments of 5 bpm during a 10-minute tracing segment. In any 10-minute window, the minimum interpretable baseline duration must be at least 2 minutes. If the baseline fetal heart rate is less than 110 bpm, it is termed bradycardia. If the baseline rate is greater than 160 bpm, it is called tachycardia. The average fetal heart rate is considered the result of tonic balance between accelerator and decelerator influences on pacemaker cells. In this concept, the sympathetic system is the accelerator influence, and the parasympathetic system is the decelerator factor mediated by vagal slowing of heart rate (Dawes, 1985). Heart rate also is under the control of arterial chemoreceptors such that both hypoxia and hypercapnia can modulate rate. More severe and prolonged hypoxia, with a rising blood lactate level and severe metabolic acidemia, induces a prolonged fall in heart rate (Thakor, 2009).
In the third trimester, the normal mean baseline fetal heart rate has generally been accepted to range between 120 and 160 bpm. But, pragmatically, a rate between 100 and 119 bpm, in the absence of other changes, usually is not considered to represent fetal compromise. Such low but potentially normal baseline heart rates also have been attributed to head compression from occiput posterior or transverse positions, particularly during second-stage labor (Young, 1976). Such mild bradycardias were observed in 2 percent of monitored pregnancies and averaged approximately 50 minutes in duration. Freeman and associates (2003) have concluded that bradycardia within the range of 80 to 120 bpm and with good variability is reassuring. Interpretation of rates less than 80 bpm is problematic, and such rates generally are considered nonreassuring.
Some causes of fetal bradycardia include congenital heart block and serious fetal compromise (Jaeggi, 2008; Larma, 2007). Figure 24-5 shows bradycardia in a fetus dying from placental abruption. Maternal hypothermia under general anesthesia for repair of a cerebral aneurysm or during maternal cardiopulmonary bypass for open-heart surgery can also cause fetal bradycardia. Sustained fetal bradycardia in the setting of severe pyelonephritis and maternal hypothermia also has been reported (Hankins, 1997). Involved fetuses apparently are not harmed by several hours of such bradycardia.
Fetal bradycardia measured with a scalp electrode (upper panel) in a pregnancy complicated by placental abruption and subsequent fetal death. Concurrent uterine contractions are shown in the lower panel.
Fetal tachycardia is defined as a baseline heart rate greater than 160 bpm. The most common explanation for fetal tachycardia is maternal fever from chorioamnionitis, although fever from any source can produce this. In some cases, fetal tachycardia may precede overt maternal fever (Gilstrap, 1987). Fetal tachycardia caused by maternal infection typically is not associated with fetal compromise unless there are associated periodic heart rate changes or fetal sepsis.
Other causes of fetal tachycardia include fetal compromise, cardiac arrhythmias, and maternal administration of parasympathetic inhibiting (atropine) or sympathomimetic (terbutaline) drugs. Prompt relief of the compromising event, such as correction of maternal hypotension caused by epidural analgesia, can result in fetal recovery. The key feature to distinguish fetal compromise in association with tachycardia seems to be concomitant heart rate decelerations.
This baseline rate is unsteady and “wanders” between 120 and 160 bpm (Freeman, 2003). This rare finding is suggestive of a neurologically abnormal fetus and may occur as a preterminal event. In contrast, changes of the normal baseline are common in labor and do not predict morbidity (Yang, 2017).
Baseline variability is an important index of cardiovascular function and appears to be regulated largely by the autonomic nervous system (Kozuma, 1997). That is, a sympathetic and parasympathetic “push and pull” mediated via the sinoatrial node produces moment-to-moment or beat-to-beat oscillation of the baseline heart rate. Such heart rate change is defined as baseline variability. Variability can be further analyzed over the short term and long term, although these terms have fallen out of use. Short-term variability reflects the instantaneous change in fetal heart rate from one beat—or R wave—to the next. This variability is a measure of the time interval between cardiac systoles (Fig. 24-6). Short-term variability can most reliably be determined to be normally present only when electrocardiac cycles are measured directly with a scalp electrode. Long-term variability is used to describe the oscillatory changes during 1 minute and result in the waviness of the baseline (Fig. 24-7). The normal frequency of such waves is three to five cycles per minute (Freeman, 2003).
Schematic representation of short-term beat-to-beat variability measured by a fetal scalp electrode. t = time interval between successive fetal R waves. (Adapted with permission from Klavan M, Laver AT, Boscola MA: Clinical concepts of fetal heart rate monitoring. Waltham, Hewlett-Packard, 1977.)
Schematic representation of long-term beat-to-beat variability of the fetal heart rate ranging between 125 and 135 bpm. (Adapted with permission from Klavan M, Laver AT, Boscola MA: Clinical concepts of fetal heart rate monitoring. Waltham, Hewlett-Packard, 1977.)
It should be recognized that precise quantitative analysis of both short- and long-term variability presents several frustrating problems due to technical and scaling factors (Parer, 1985). Thus, most clinical interpretation is based on visual analysis with subjective judgment of the smoothness or flatness of the baseline. According to Freeman and associates (2003), no evidence suggests that the distinction between short- and long-term variability has clinical relevance. Similarly, the NICHD Workshop (1997) did not recommend differentiating short- and long-term variability because in actual practice they are visually determined as a unit. The workshop panel defined baseline variability as those baseline fluctuations of two cycles per minute or greater. They recommended the criteria shown in Figure 24-8 for quantification of variability. Normal beat-to-beat variability was accepted to be 6 to 25 bpm.
Grades of baseline fetal heart rate variability shown in the following five panels. 1. Undetectable, absent variability. 2. Minimal variability, ≤5 bpm. 3. Moderate (normal) variability, 6 to 25 bpm. 4. Marked variability, >25 bpm. 5. Sinusoidal pattern. This differs from variability in that it has a smooth, sinelike pattern of regular fluctuation and is excluded in the definition of fetal heart rate variability. (Adapted with permission from National Institute of Child Health and Human Development Research Planning Workshop, 1997.)
Several physiological and pathological processes can affect beat-to-beat variability. Greater variability accompanies fetal breathing and body movements (Dawes, 1981; Van Geijn, 1980). Pillai and James (1990) reported increased baseline variability with advancing gestation. Up to 30 weeks, baseline characteristics were similar during both fetal rest and activity. After 30 weeks, fetal inactivity was associated with diminished baseline variability, but fetal activity enhanced it. Last, the baseline fetal heart rate becomes more physiologically fixed (less variable) as the rate rises. This phenomenon presumably reflects less cardiovascular physiological wandering as beat-to-beat intervals shorten with a higher heart rate.
A common cause of diminished beat-to-beat variability is administration of analgesic drugs during labor (Chap. 25, Analgesia and Sedation During Labor). Various central nervous system depressant drugs can cause transient diminished beat-to-beat variability. Included are narcotics, barbiturates, phenothiazines, tranquilizers, and general anesthetics. Corticosteroids also dampen variability (Knaven, 2017). As one specific example, variability regularly diminishes within 5 to 10 minutes following intravenous meperidine administration, and the effects may last up to 60 minutes or longer (Hill, 2003; Petrie, 1993). Butorphanol given intravenously has similar effects (Schucker, 1996). And, chronically administered buprenorphine suppresses fetal heart rate and movement (Jansson, 2017).
Magnesium sulfate, widely used in the United States for tocolysis or management of hypertensive gravidas, is associated with diminished beat-to-beat variability. In a study of nearly 250 term gestations, magnesium sulfate administration led to decreased variability but without evidence of adverse neonatal effects (Duffy, 2012). Others have echoed these findings (Hallak, 1999; Lin, 1988). With magnesium sulfate tocolysis of preterm labor, variability was also diminished in most reviewed studies (Nensi, 2014; Verdurmen, 2017).
Of greatest concern, diminished beat-to-beat variability can be an ominous sign indicating a seriously compromised fetus. Paul and coworkers (1975) reported that loss of variability in combination with decelerations was associated with fetal acidemia. Decreased variability was defined as an excursion of the baseline of ≤5 bpm (see Fig. 24-8). Severe maternal acidemia can also lower fetal beat-to-beat variability, for example, in a mother with diabetic ketoacidosis.
According to Dawes (1985), metabolic acidemia that causes depression of the fetal brainstem or the heart itself creates the loss of variability. Thus, diminished beat-to-beat variability, when it reflects fetal compromise, likely reflects acidemia rather than hypoxia. Indeed, mild degrees of fetal hypoxemia have been reported actually to enhance variability, at least initially (Murotsuki, 1997).
Reduced baseline heart rate variability is the single most reliable sign of fetal compromise. Smith and coworkers (1988) performed a computerized analysis of beat-to-beat variability in growth-restricted fetuses before labor. Diminished variability (≤4.2 bpm) maintained for 1 hour was diagnostic of developing acidemia and imminent fetal death. In contrast, Samueloff and associates (1994) evaluated variability in 2200 consecutive deliveries and concluded that variability by itself could not be used as the only indicator of fetal well-being. They also warned that good variability should not be interpreted as necessarily reassuring. Blackwell and associates (2011) found that even experts often disagreed as to whether variability was absent or minimal (≤5 bpm).
In sum, beat-to-beat variability is affected by fetal physiology, and its meaning differs depending on the clinical setting. Decreased variability in the absence of decelerations is unlikely to reflect fetal hypoxia (Davidson, 1992). A persistently flat fetal heart rate baseline—absent variability—within the normal baseline rate range and without decelerations may reflect a previous fetal insult that has resulted in neurological damage (Freeman, 2003).
When fetal cardiac arrhythmias are first suspected using electronic monitoring, findings can include baseline bradycardia, tachycardia, or most commonly in our experience, abrupt baseline spiking (Fig. 24-9). An arrhythmia can only be documented, practically speaking, when scalp electrodes are used. Some fetal monitors can be adapted to output the scalp electrode signals into an ECG recorder. Because only a single lead is obtained, analysis and interpretation of rhythm and rate disturbances are severely limited.
Internal fetal monitoring at term demonstrated occasional abrupt beat-to-beat fetal heart rate spiking due to erratic extrasystoles shown in the corresponding fetal electrocardiogram. The normal newborn was delivered spontaneously and had normal cardiac rhythm in the nursery.
Southall and associates (1980) studied fetal cardiac rate and rhythm disturbances in 934 normal pregnancies between 30 and 40 weeks. Arrhythmias, episodes of bradycardia <100 bpm, or tachycardia >180 bpm were encountered in 3 percent. Most supraventricular arrhythmias are of little significance during labor unless there is coexistent fetal heart failure as evidenced by hydrops. Many supraventricular arrhythmias disappear in the immediate neonatal period, although some are associated with structural cardiac defects (Api, 2008). Intermittent baseline bradycardia is frequently due to congenital heart block. Conduction defects, most often complete atrioventricular (AV) block, usually are found in association with maternal connective tissue diseases (Chap. 59, Perinatal Mortality and Morbidity). Antepartum evaluation of the fetus with an identified arrhythmia and potential treatment options are discussed in Chapter 16 (Tachyarrhythmias).
Most fetal arrhythmias without comorbid fetal hydrops are inconsequential during labor, but they may hinder interpretation of fetal heart rate tracings. Sonographic evaluation of fetal anatomy and echocardiography can be useful. Generally, in the absence of fetal hydrops, neonatal outcome is not measurably improved by pregnancy intervention. At Parkland Hospital, intrapartum fetal cardiac arrhythmias, especially those associated with clear amnionic fluid, are typically managed conservatively.
A true sinusoidal pattern such as that shown in panel 5 of Figure 24-8 can be observed with fetal intracranial hemorrhage, with severe fetal asphyxia, and with severe fetal anemia. The last may stem from anti-D alloimmunization, fetomaternal hemorrhage, twin-twin transfusion syndrome, fetal parvoviral infection, or vasa previa with bleeding. Insignificant sinusoidal patterns have been reported following administration of meperidine, morphine, alphaprodine, and butorphanol (Angel, 1984; Egley, 1991; Epstein, 1982). Shown in Figure 24-10 is a sinusoidal pattern seen with maternal meperidine administration. An important characteristic of this pattern when due to narcotics is the sine frequency of 6 cycles per minute. A sinusoidal pattern also has been described with chorioamnionitis, fetal distress, and umbilical cord occlusion (Murphy, 1991). Young (1980a) and Johnson (1981) with their coworkers concluded that intrapartum sinusoidal fetal heart patterns were not generally associated with fetal compromise. Thus, management is usually dictated by the clinical setting. Modanlou and Freeman (1982), based on their extensive review, proposed adoption of a strict definition:
Sinusoidal fetal heart rate pattern associated with maternal intravenous meperidine administration. Sine waves are occurring at a rate of 6 cycles per minute.
Stable baseline heart rate of 120 to 160 bpm with regular oscillations
Amplitude of 5 to 15 bpm (rarely greater)
Long-term variability frequency of 2 to 5 cycles per minute
Fixed or flat short-term variability
Oscillation of the sinusoidal waveform above or below a baseline
Although these criteria were selected to define a sinusoidal pattern that is most likely ominous, they observed that the pattern associated with alphaprodine is indistinguishable. Other investigators have proposed a classification of sinusoidal heart rate patterns into mild—amplitude 5 to 15 bpm, intermediate—16 to 24 bpm, and major—≥25 bpm to quantify fetal risk (Murphy, 1991; Neesham, 1993).
Some have defined intrapartum sine wavelike baseline variation with periods of acceleration as pseudosinusoidal. Murphy and colleagues (1991) reported that pseudosinusoidal patterns were seen in 15 percent of monitored labors. Mild pseudosinusoidal patterns were associated with use of meperidine and epidural analgesia. Intermediate pseudosinusoidal patterns were linked to fetal sucking or transient episodes of fetal hypoxia caused by umbilical cord compression. Egley and associates (1991) reported that 4 percent of fetuses demonstrated sinusoidal patterns transiently during normal labor. These authors observed patterns persisting for up to 90 minutes in some cases.
The pathophysiology of sinusoidal patterns is unclear, in part due to various definitions. There seems to be general agreement that antepartum sine wave baseline undulations portend severe fetal anemia. Still, few anti-D alloimmunized fetuses develop this pattern (Nicolaides, 1989). The sinusoidal pattern has been reported to develop or disappear after fetal transfusion (Del Valle, 1992; Lowe, 1984). Ikeda and associates (1999) proposed that the pattern is related to waves of arterial blood pressure, reflecting oscillations in the baroreceptor-chemoreceptor feedback mechanism.
Periodic Fetal Heart Rate Changes
These refer to deviations from baseline that are temporally related to uterine contractions. Acceleration refers to a rise in fetal heart rate above baseline, and deceleration is a drop below the baseline rate. The nomenclature most commonly used in the United States is based on the timing of the deceleration in relation to contractions—thus, early, late, or variable. The waveform of these decelerations is also significant for pattern recognition. In early and late decelerations, the slope of fetal heart rate change is gradual, resulting in a curvilinear and uniform or symmetrical waveform. With variable decelerations, the slope of fetal heart rate change is abrupt and erratic, giving the waveform a jagged appearance. The NICHD Workshop (1997) proposed that decelerations be defined as recurrent if they accompanied ≥50 percent of contractions in any 20-minute period.
Another system now used less often to describe decelerations is based on the pathophysiological events considered most likely to underlie the pattern. In this system, early decelerations are termed head compression, late decelerations are termed uteroplacental insufficiency, and variable decelerations are cord compression patterns.
These are abrupt heart rate increases above the fetal heart rate baseline and defined by an onset-to-peak rise within 30 seconds (American College of Obstetricians and Gynecologists, 2017a). At 32 weeks’ gestation and beyond, an acceleration has a peak ≥15 bpm above baseline. Its duration is ≥15 sec but <2 minutes from onset to baseline return (see Table 24-1). Before 32 weeks, a peak ≥10 bpm for 10 seconds to 2 minutes is considered normal. Prolonged acceleration is defined as ≥2 minutes but <10 minutes.
According to Freeman and coworkers (2003), accelerations most often occur antepartum, in early labor, and in association with variable decelerations. Proposed mechanisms for intrapartum accelerations include fetal movement, stimulation by uterine contractions, umbilical cord occlusion, fetal stimulation during pelvic examination, scalp blood sampling, and acoustic stimulation. Accelerations are common during labor. These are virtually always reassuring and almost always confirm that the fetus is not acidemic at that time.
As with beat-to-beat variability, accelerations represent intact neurohormonal cardiovascular control mechanisms linked to fetal behavioral states. Krebs and colleagues (1982) analyzed electronic heart rate tracings in nearly 2000 fetuses and found sporadic accelerations during labor in 99.8 percent. Fetal heart rate accelerations during the first or last 30 minutes during labor, or both, were a favorable sign for fetal well-being. The absence of such accelerations during labor, however, is not necessarily an unfavorable sign unless coincidental with other nonreassuring changes. The chance of acidemia in the fetus that fails to respond to stimulation in the presence of an otherwise nonreassuring pattern approximates 50 percent (Clark, 1984; Smith, 1986).
This physiological response shows a gradual fetal heart rate decline and then return to baseline associated with a contraction (Fig. 24-11). Freeman and associates (2003) defined early decelerations as those generally seen in active labor between 4 and 7 cm cervical dilation. In their definition, the degree of deceleration is generally proportional to the contraction strength and rarely falls below 100 to 110 bpm or 20 to 30 bpm below baseline. Such decelerations are common during active labor and not associated with tachycardia, loss of variability, or other fetal heart rate changes. Importantly, early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores.
Features of early fetal heart rate deceleration. Characteristics include a gradual decline in the heart rate with both onset and recovery coincident with the onset and recovery of the contraction. The nadir of the deceleration is 30 seconds or more after the deceleration onset.
Head compression probably causes vagal nerve activation as a result of dural stimulation, and this mediates the heart rate deceleration (Paul, 1964). Ball and Parer (1992) concluded that fetal head compression is a likely cause not only of the deceleration shown in Figure 24-11 but also of those shown in Figure 24-12, which typically occur during second-stage labor. Indeed, they observed that head compression is the likely cause of many variable decelerations classically attributed to cord compression.
Two different fetal heart rate patterns during second-stage labor that are likely both due to head compression (upper panel). Maternal pushing efforts (lower panel) correspond to the spikes with uterine contractions. Fetal heart rate deceleration (C) is consistent with the pattern of head compression shown in Figure 24-11. Deceleration (B), however, is “variable” in appearance because of its jagged configuration and may alternatively represent cord occlusion.
The fetal heart rate response to uterine contractions can reflect uterine perfusion or placental function. A late deceleration is a smooth, gradual, symmetrical decline in fetal heart rate beginning at or after the contraction peak and returning to baseline only after the contraction has ended. This deceleration reaches its nadir within 30 seconds of its onset. In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively (Fig. 24-13). The magnitude of late decelerations is seldom more than 30 to 40 bpm below baseline and typically not more than 10 to 20 bpm. Late decelerations usually are not accompanied by accelerations. Myers and associates (1973) studied monkeys in which they compromised uteroplacental perfusion by lowering maternal aortic blood pressure. The interval or lag from the contraction onset until the late deceleration onset was directly related to basal fetal oxygenation. They demonstrated that the length of the lag was predictive of the fetal Po2 but not fetal pH. The lower the fetal Po2 before contractions, the shorter the lag to the onset of late decelerations. This lag reflected the time necessary for the fetal Po2 to fall below a critical level necessary to stimulate arterial chemoreceptors, which mediated the decelerations.
Features of late fetal heart rate deceleration. Characteristics include gradual decline in the heart rate with the contraction nadir, and recovery occurring after the end of the contraction. The nadir of the deceleration occurs 30 seconds or more after the onset of the deceleration.
Murata and coworkers (1982) also showed that a late deceleration was the first fetal heart rate consequence of uteroplacental-induced hypoxia. During the course of progressive hypoxia that led to death over 2 to 13 days, monkey fetuses invariably exhibited late decelerations before development of acidemia. Variability of the baseline heart rate disappeared as acidemia developed.
Generally, any process that produces maternal hypotension, excessive uterine activity, or placental dysfunction can induce late decelerations. The two most common sources are hypotension from epidural analgesia and uterine hyperactivity from oxytocin stimulation. Maternal diseases such as hypertension, diabetes, and collagen vascular disorders can cause chronic placental dysfunction. Placental abruption can produce acute late decelerations.
The most frequent deceleration patterns encountered during labor are variable decelerations attributed to umbilical cord occlusion. In a study of more than 7000 monitor tracings, variable decelerations were identified in 40 percent when labor had progressed to 5 cm dilation and in 83 percent by the end of first-stage labor (Melchior, 1985). A variable deceleration is defined as an abrupt drop in the fetal heart rate beginning with the onset of the contraction and reaching a nadir in less than 30 seconds. The decrease must last between 15 seconds and 2 minutes and must be ≥15 bpm in amplitude. The onset of deceleration typically varies with successive contractions (Fig. 24-14).
Features of variable fetal heart rate decelerations. Characteristics include an abrupt decline in the heart rate, and onset that commonly varies with successive contractions. The deceleration measures ≥15 bpm for ≥15 seconds and has an onset-to-nadir phase of <30 seconds. Total duration is <2 minutes.
Hon (1959) tested the effects of umbilical cord compression on fetal heart rate (Fig. 24-15). In experimental animals, complete occlusion of the umbilical cord produces abrupt, jagged-appearing deceleration of the fetal heart rate (Fig. 24-16). Concomitantly, fetal aortic pressure rises. Itskovitz and colleagues (1983) observed that variable decelerations in fetal lambs occurred only after umbilical blood flow was reduced by at least 50 percent.
A. The effects of 25-second cord compression compared with those of 40 seconds in panel (B). (Redrawn with permission from Hon EH: The fetal heart rate patterns preceding death in utero, Am J Obstet Gynecol. 1959 Jul;78(1):47–56.)
Total umbilical cord occlusion (arrow) in the sheep fetus is accompanied by an increase in fetal aortic blood pressure. Blood pressure changes in the umbilical vessels are also shown. (Redrawn with permission from Künzel W: Fetal heart rate alterations in partial and total cord occlusion. In Künzel W (ed): Fetal Heart Rate Monitoring: Clinical Practice and Pathophysiology. Berlin, Springer, 1985.)
Two types of variable decelerations are shown in Figure 24-17. The deceleration denoted by “A” is very much like that seen with complete umbilical cord occlusion in experimental animals (see Fig. 24-16). Deceleration “B,” however, has a different configuration because of the “shoulders” of acceleration before and after the deceleration component. Lee and coworkers (1975) proposed that this form of variable deceleration was caused by differing degrees of partial cord occlusion. In this physiological scheme, occlusion of only the vein reduces fetal blood return, thereby triggering a baroreceptor-mediated acceleration. With increasing intrauterine pressure and subsequent complete cord occlusion, fetal systemic hypertension develops due to obstruction of umbilical artery flow. This stimulates a baroreceptor-mediated deceleration. Presumably, the aftercoming shoulder of the acceleration represents the same events occurring in reverse (Fig. 24-18).
Varying (variable) fetal heart rate decelerations. Deceleration (B) exhibits “shoulders” of acceleration compared with deceleration (A).
Schematic representation of the fetal heart rate effects with partial and complete umbilical cord occlusion. Uterine pressures generated early in a contraction cause cord compression predominantly of the thin-walled umbilical vein. The resulting decrease in fetal cardiac output leads to an initial compensatory rise in fetal heart rate. As cord compression intensifies, umbilical arteries are then also compressed. The resulting rise in fetal systolic blood pressure leads to a vagal-mediated fetal heart rate deceleration. As the contraction abates and compression is relieved first on the umbilical arteries, elevated fetal systolic blood pressures drop and the deceleration resolves. A final increase in fetal heart rate is seen as a result of persistent umbilical vein occlusion. With completion of the uterine contraction and cord compression, the fetal heart rate returns to baseline. BP = blood pressure. (Adapted with permission from Lee CV, DiLaretto PC, Lane JM: A study of fetal heart rate acceleration patterns, Obstet Gynecol. 1975 Feb;45(2):142–146.)
Ball and Parer (1992) concluded that variable decelerations are mediated vagally and that the vagal response may be due to chemoreceptor or baroreceptor activity or both. Partial or complete cord occlusion produces an increase in afterload (baroreceptor) and a drop in fetal arterial oxygen content (chemoreceptor). These both result in vagal activity leading to deceleration. In fetal monkeys, the baroreceptor reflexes appear to operate during the first 15 to 20 seconds of umbilical cord occlusion followed by decline in Po2 at approximately 30 seconds, which then serves as a chemoreceptor stimulus (Mueller-Heubach, 1982).
Thus, variable decelerations represent fetal heart rate reflexes that reflect either blood pressure changes due to interruption of umbilical flow or changes in oxygenation. It is likely that most fetuses have experienced brief but recurrent periods of hypoxia due to umbilical cord compression during gestation. The frequency and inevitability of cord occlusions undoubtedly have provided the fetus with these physiological mechanisms as a means of coping. The great dilemma for the obstetrician in managing variable fetal heart rate decelerations is determining when variable decelerations are pathological. According to the American College of Obstetricians and Gynecologists (2017a), recurrent variable decelerations with minimal-to-moderate beat-to-beat variability are indeterminate, whereas those with absent variability are abnormal.
Other fetal heart rate patterns have been associated with umbilical cord compression. Saltatory baseline heart rate (Fig. 24-19) was first linked to umbilical cord complications during labor (Hammacher, 1968). The pattern consists of rapidly recurring couplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate. We also observed a relationship between cord occlusion and the saltatory pattern in postterm pregnancies (Leveno, 1984). In the absence of other fetal heart rate findings, these do not signal fetal compromise. Lambda is a pattern involving an acceleration followed by a variable deceleration with no acceleration at the end of the deceleration. This pattern typically is seen in early labor and is not ominous (Freeman, 2003). This lambda pattern may result from mild cord compression or stretch. Overshoot is a variable deceleration followed by acceleration. The clinical significance of this pattern is controversial (Westgate, 2001).
Saltatory baseline fetal heart rate showing rapidly recurring couplets of acceleration combined with deceleration.
This pattern, which is shown in Figure 24-20, is defined as an isolated deceleration ≥15 bpm that lasts ≥2 minutes but <10 minutes from onset to return to baseline. Prolonged decelerations are difficult to interpret because they are seen in many different clinical situations. Some of the more frequent causes are cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension.
Prolonged fetal heart rate deceleration due to uterine hyperactivity. Approximately 3 minutes of the tracing are shown, but the fetal heart rate returned to normal after uterine hypertonus resolved. Vaginal delivery later ensued.
Epidural, spinal, or paracervical analgesia may induce a prolonged deceleration (Eberle, 1998). Hill and associates (2003) observed prolonged deceleration in 1 percent of women given epidural analgesia during labor at Parkland Hospital. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia from any cause, placental abruption, umbilical cord knots or prolapse, maternal seizures including eclampsia and epilepsy, application of a fetal scalp electrode, impending birth, or maternal Valsalva maneuver. In one example, Ambia and colleagues (2017) described prolonged decelerations lasting 2 to 10 minutes following an eclamptic seizure.
The placenta is effective in resuscitating the fetus if the original insult does not recur immediately. Occasionally, such self-limited prolonged decelerations are followed by loss of beat-to-beat variability, baseline tachycardia, and even a period of late decelerations, all of which resolve as the fetus recovers. Freeman and colleagues (2003) emphasize that the fetus may die during prolonged decelerations. Thus, management of prolonged decelerations can be extremely tenuous. Management of isolated prolonged decelerations is based on bedside clinical judgment, which inevitably will sometimes be imperfect given the unpredictability of these decelerations.
Fetal Heart Rate Patterns During Second-Stage Labor
Decelerations are virtually ubiquitous during the second stage of labor. In one study, only 1.4 percent of more than 7000 deliveries lacked decelerations during second-stage labor (Melchior, 1985). Both cord and fetal head compressions have been implicated as causes of decelerations and baseline bradycardia in this stage. Profound, prolonged fetal heart rate deceleration in the 10 minutes preceding vaginal delivery has been described (Boehm, 1975). And, similar prolonged second-stage decelerations were associated with a stillbirth and neonatal death (Herbert, 1981). These experiences attest to the unpredictability of the fetal heart rate during second-stage labor.
Spong and associates (1998) analyzed the characteristics of second-stage variable fetal heart rate decelerations in 250 deliveries. They found that as the total number of decelerations <70 bpm increased, the 5-minute Apgar score decreased. Of other patterns in second-stage labor, Picquard and coworkers (1988) reported that loss of beat-to-beat variability and baseline fetal heart rate <90 bpm predicted fetal acidemia. Krebs and associates (1981) also found that persistent or progressive baseline bradycardia or baseline tachycardia was associated with lower Apgar scores. Gull and colleagues (1996) observed that abrupt fetal heart rate deceleration to <100 bpm associated with loss of beat-to-beat variability for 4 minutes or longer was predictive of fetal acidemia. Thus, abnormal baseline heart rate—either bradycardia or tachycardia, absent beat-to-beat variability, or both—in the presence of deep second-stage decelerations is associated with a greater risk for fetal compromise (Fig. 24-21).
Cord-compression fetal heart rate decelerations in second-stage labor associated with tachycardia and loss of variability. The umbilical cord arterial pH was 6.9.
Admission Fetal Monitoring in Low-Risk Pregnancies
With this approach, women with low-risk pregnancies are monitored for a short time on admission for labor. In one study, 3752 low-risk women in spontaneous labor at admission were randomly assigned either to auscultation of the fetal heart or to 20 minutes of electronic fetal monitoring (Mires, 2001). Use of admission electronic fetal monitoring did not improve neonatal outcome. Moreover, its use resulted in a greater number of interventions, including operative delivery. A similar study echoed these neonatal outcomes (Impey, 2003). More than half of the women enrolled in these studies eventually required continuous monitoring. A review by Devane and associates (2017) found that admission fetal monitoring programs for low-risk pregnancy are associated with a higher risk for cesarean delivery. Somewhat related, with the increasing rate of scheduled cesarean deliveries in the United States, clinicians and hospitals must decide whether fetal monitoring is required before the procedure in low-risk women.
Fetal heart rate pattern interpretations are subjective. Thus, the potential for computer assistance to enhance the precision of identifying abnormal patterns appeared promising. The INFANT Collaborative Group (2017) studied whether the addition of computer-based decision-support software for interpretation of fetal heart rate patterns lowered the number of poor neonatal outcomes. In this trial, 23,515 women were randomized to computer-assisted interpretation compared with 23,055 women in a conventional clinical interpretation arm. Perinatal outcomes such as intrapartum stillbirth, early neonatal death, and neonatal encephalopathy were not improved by computer assistance. Cesarean delivery rates were similar in both groups. Moreover, a 2-year follow-up of a subset of the surviving children showed no differences in their neurological development.