ELECTRONIC FETAL MONITORING
OTHER INTRAPARTUM ASSESSMENT TECHNIQUES
FETAL DISTRESS
MECONIUM IN THE AMNIONIC FLUID
FETAL HEART RATE PATTERNS AND BRAIN DAMAGE
CURRENT RECOMMENDATIONS
INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVITY
Following earlier work by Hon (1958), continuous electronic fetal monitoring (EFM) was introduced into obstetrical practice in the late 1960s. No longer were intrapartum fetal surveillance and the suspicion of fetal distress based on periodic auscultation with a fetoscope. Instead, the continuous graph-paper portrayal of the fetal heart rate was potentially diagnostic in assessing pathophysiological events affecting the fetus. Indeed, there were great expectations: (1) that electronic fetal heart rate monitoring provided accurate information, (2) that the information was of value in diagnosing fetal distress, (3) that it would direct intervention to prevent fetal death or morbidity, and (4) that continuous electronic fetal heart rate monitoring was superior to intermittent methods.
When first introduced, electronic fetal heart rate monitoring was used primarily in complicated pregnancies, but gradually became used in most pregnancies. By 1978, it was estimated that nearly two thirds of American women were being monitored electronically during labor (Banta, 1979). Currently, more than 85 percent of all live births in the United States undergo electronic fetal monitoring (Ananth, 2013). Indeed, fetal monitoring has become the most prevalent obstetrical procedure in this country.
ELECTRONIC FETAL MONITORING
Internal (Direct) Electronic Monitoring
The fetus can be monitored electronically by direct or indirect methods. 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. Vaginal body fluids create a saline electrical bridge that completes the circuit and permits measurement of the voltage differences between the two poles. The two wires of the bipolar electrode are attached to a reference electrode on the maternal thigh to eliminate electrical interference. 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 most reliably detected.
FIGURE 24-1 Internal electronic fetal monitoring. A. Scalp electrode penetrates the fetal scalp by means of a coiled electrode. B. 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. The physiological event being counted, however, is not a mechanical event corresponding to a heartbeat but rather an electrical event.
FIGURE 24-2 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. Although the maternal electrocardiogram (ECG) signal is approximately five times stronger than the fetal ECG, its amplitude is diminished when it is recorded through the fetal scalp electrode. In a live fetus, this low maternal ECG signal is detected but masked by the fetal ECG. If the fetus is dead, the weaker maternal signal will be amplified and displayed as the “fetal” heart rate (Freeman, 2003). 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).
FIGURE 24-3 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.
FIGURE 24-4 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
Membrane rupture may be avoided by use of external detectors to monitor fetal heart action. External monitoring, however, does not provide the precision of fetal heart rate measurement afforded by internal monitoring (Nunes, 2014).
The fetal heart rate is detected through the maternal abdominal wall using the ultrasound Doppler principle (Fig. 24-5). 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, p. 209). 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 a belt. Care should be taken that maternal arterial pulsations are not confused with fetal cardiac motion (Neilson, 2008).
FIGURE 24-5 Ultrasound Doppler principle used externally to measure fetal heart motions. Pulsations of the maternal aorta also may be detected and erroneously counted. (Adapted from Klavan, 1977.)
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.
Fetal Heart Rate Patterns
It is now generally accepted that interpretation of fetal heart rate patterns can be problematic because of the lack of agreement on definitions and nomenclature (American College of Obstetricians and Gynecologists, 2013b). 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 authors cautioned that their results represented idealized circumstances that should not be considered reflective of routine clinical practice.
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 was repeated in 2008. The definitions proposed and shown in Table 24-1 as a result of this second workshop are used in this chapter. First, it is important to recognize that 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 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 (Fig. 24-6). Thus, pattern recognition can be considerably distorted depending on the scaling factors used.
TABLE 24-1. Electronic Fetal Monitoring Definitions
FIGURE 24-6 Fetal heart rate obtained by scalp electrode (upper panel) and recorded at 1 cm/min compared with that at 3 cm/min chart recorder paper speed. Concurrent uterine contractions are shown (lower panel).
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.
Rate
With increasing fetal maturation, the heart rate decreases. This continues postnatally such that the average rate is 90 bpm by age 8 (Behrman, 1992). Pillai and James (1990) longitudinally studied fetal heart rate characteristics in 43 normal pregnancies. The baseline fetal heart rate decreased an average of 24 bpm between 16 weeks and term, or approximately 1 beat/min 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 termed tachycardia. The average fetal heart rate is considered the result of tonic balance between acceleratorand decelerator influences on pacemaker cells. In this concept, the sympathetic system is the accelerator influence, and the parasympathetic system is the decelerator factor mediated via 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).
Bradycardia. In the third trimester, the normal mean baseline fetal heart rate has generally been accepted to range between 120 and 160 bpm. The lower normal limit is disputed internationally, with some investigators recommending 110 bpm (Manassiev, 1996). 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 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 24-7 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 also can cause fetal bradycardia. Sustained fetal bradycardia in the setting of severe pyelonephritis and maternal hypothermia also has been reported (Hankins, 1997). These infants apparently are not harmed by several hours of such bradycardia.
FIGURE 24-7 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.
Tachycardia. 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 increase baseline fetal heart rate. Such infections also have been observed to induce fetal tachycardia before overt maternal fever is diagnosed (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 (atropine) or sympathomimetic (terbutaline) drugs. The key feature to distinguish fetal compromise in association with tachycardia seems to be concomitant heart rate decelerations. Prompt relief of the compromising event, such as correction of maternal hypotension caused by epidural analgesia, can result in fetal recovery.
Wandering Baseline. 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.
Beat-to-Beat Variability
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 divided into 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. 24-8). 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. 24-9). The normal frequency of such waves is three to five cycles per minute (Freeman, 2003).
FIGURE 24-8 Schematic representation of short-term beat-to-beat variability measured by a fetal scalp electrode. t = time interval between successive fetal R waves. (Adapted from Klavan, 1977.)
FIGURE 24-9 Schematic representation of long-term beat-to-beat variability of the fetal heart rate ranging between 125 and 135 bpm. (Adapted from Klavan, 1977.)
It should be recognized that precise quantitative analysis of both short- and long-term variability presents a number of frustrating problems due to technical and scaling factors. For example, Parer and coworkers (1985) evaluated 22 mathematical formulas designed to quantify heart rate variability and found most to be unsatisfactory. Consequently, most clinical interpretation is based on visual analysis with subjective judgment of the smoothness or flatness of the baseline. According to Freeman and colleagues (2003), there is no current evidence that the distinction between short- and long-term variability has any 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 24-10 for quantification of variability. Normal beat-to-beat variability was accepted to be 6 to 25 bpm.
FIGURE 24-10 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 from National Institute of Child Health and Human Development Research Planning Workshop, 1997.)
Increased Variability. Several physiological and pathological processes can affect or interfere with beat-to-beat variability. Dawes and associates (1981) described increased variability during fetal breathing. In healthy infants, short-term variability is attributable to respiratory sinus arrhythmia (Divon, 1986). Fetal body movements also affect variability (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 and conversely, variability was increased during fetal activity. Fetal gender does not affect heart rate variability (Ogueh, 1998).
The baseline fetal heart rate becomes more physiologically fixed (less variable) as the rate increases. Conversely, there is more instability or variability of the baseline at lower heart rates. This phenomenon presumably reflects less cardiovascular physiological wandering as beat-to-beat intervals shorten due to increasing heart rate.
Decreased Variability. 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. They analyzed variability in the 20 minutes preceding delivery in 194 pregnancies. Decreased variability was defined as 5 or fewer bpm excursion of the baseline (see Fig. 24-10), whereas acceptable variability exceeded this range. Fetal scalp pH was measured 1119 times in these pregnancies, and mean values were found to be increasingly acidemic when decreased variability was added to progressively intense heart rate decelerations. For example, mean fetal scalp pH of approximately 7.10 was found when severe decelerations were combined with 5 bpm or less variability, compared with a pH of approximately 7.20 when greater variability was associated with similarly severe decelerations. Severe maternal acidemia also can cause decreased fetal beat-to-beat variability, as shown in Figure 24-11 in a mother with diabetic ketoacidosis.
FIGURE 24-11 A. External fetal heart recording showing lack of long-term variability at 31 weeks during maternal diabetic ketoacidosis (pH 7.09). B. Recovery of fetal long-term variability after correction of maternal acidemia.
The precise pathological mechanisms by which fetal hypoxemia results in diminished beat-to-beat variability are not totally understood. Interestingly, mild degrees of fetal hypoxemia have been reported actually to increasevariability, at least at the outset of the hypoxic episode (Murotsuki, 1997). According to Dawes (1985), it seems probable that the loss of variability is a result of metabolic acidemia that causes depression of the fetal brainstem or the heart itself. Thus, diminished beat-to-beat variability, when it reflects fetal compromise, likely reflects acidemia rather than hypoxia.
A common cause of diminished beat-to-beat variability is administration of analgesic drugs during labor (Chap. 25, p. 506). Various central nervous system depressant drugs can cause transient diminished beat-to-beat variability. Included are narcotics, barbiturates, phenothiazines, tranquilizers, and general anesthetics. Variability regularly diminishes within 5 to 10 minutes following intravenous meperidine administration, and the effects may last up to 60 minutes or longer depending on the dosage given (Petrie, 1993). Butorphanol given intravenously diminishes fetal heart rate reactivity (Schucker, 1996). In a study performed at Parkland Hospital, Hill and colleagues (2003) found that 5 bpm or less variability occurred in 30 percent of women given continuous intravenous meperidine compared with 7 percent in those given continuous labor epidural analgesia.
Magnesium sulfate, widely used in the United States for tocolysis as well as management of hypertensive women, has been arguably associated with diminished beat-to-beat variability. Hallak and associates (1999) randomly assigned 34 normal, nonlaboring women to standard magnesium sulfate infusion versus isotonic saline. Magnesium sulfate was associated with statistically decreased variability only in the third hour of the infusion. The average decrease in variability was deemed clinically insignificant, however, because the mean variability was 2.7 bpm in the third hour of magnesium infusion compared with 2.8 bpm at baseline. Magnesium sulfate also blunted the frequency of accelerations.
It is generally believed that 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. They observed that diminished variability (4.2 bpm or less) that was maintained for 1 hour was diagnostic of developing acidemia and imminent fetal death. By contrast, Samueloff and associates (1994) evaluated variability as a predictor of fetal outcome during labor in 2200 consecutive deliveries. They concluded that variability by itself could not be used as the only indicator of fetal well-being. Conversely, they also concluded 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 beats per minute).
In summary, beat-to-beat variability is affected by various pathological and physiological mechanisms. Variability has considerably different meaning depending on the clinical setting. The development of decreased variability in the absence of decelerations is unlikely to be due to 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 insult to the fetus that has resulted in neurological damage (Freeman, 2003).
Cardiac Arrhythmia
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. 24-12). Intermittent baseline bradycardia is frequently due to congenital heart block. As discussed in Chapter 59 (p. 1172), conduction defects, most commonly complete atrioventricular (AV) block, usually are found in association with maternal connective-tissue diseases. 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 electrocardiographic recorder. Because only a single lead is obtained, analysis and interpretation of rhythm and rate disturbances are severely limited.
FIGURE 24-12 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 infant was delivered spontaneously and had normal cardiac rhythm in the nursery.
Southall and associates (1980) studied antepartum 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 heart failure as evidenced by fetal hydrops. Many supra-ventricular arrhythmias disappear in the immediate neonatal period, although some are associated with structural cardiac defects (Api, 2008). Copel and coworkers (2000) used echocardiography to evaluate 614 fetuses referred for auscultated irregular heart rate without hydrops. Only 10 fetuses (2 percent) were found to have significant arrhythmias, and all but one of these infants survived.
Boldt and colleagues (2003) followed 292 consecutive fetuses diagnosed with a cardiac arrhythmia through birth and into childhood. Atrial extrasystoles were the most common arrhythmia (68 percent), followed by atrial tachycardias (12 percent), atrioventricular block (12 percent), sinus bradycardia (5 percent), and ventricular extrasystoles (2.5 percent). Chromosomal anomalies were found in 1.7 percent of the fetuses. Fetal hydrops developed in 11 percent, and 2 percent had intrauterine death. Fetal hydrops was a bad prognostic finding. Overall, 93 percent of the study population was alive at a median follow-up period of 5 years, and 3 percent—seven infants—had neurological handicaps. Of the infants with atrial extrasystoles, 97 percent lived, and none suffered neurological injury. Only 6 percent required postnatal cardiac medications. Lopriore and associates (2009) found low rates of death and long-term neurological impairment in fetuses with supraventricular tachycardia or atrial flutter. In contrast, higher mortality rates were noted in those with atrioventricular block.
Although most fetal arrhythmias are of little consequence during labor when there is no evidence of fetal hydrops, such arrhythmias impair interpretation of intrapartum heart rate tracings. Sonographic evaluation of fetal anatomy and echocardiography may be useful. Some clinicians use fetal scalp sampling as an adjunct. 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 associate with clear amnionic fluid, are managed conservatively. Freeman and colleagues (2003) have extensively reviewed interpretation of the fetal electrocardiogram during labor.
Sinusoidal Heart Rate
A true sinusoidal pattern such as that shown in panel 5 of Figure 24-10 may be observed with fetal intracranial hemorrhage, with severe fetal asphyxia, and with severe fetal anemia from Rh alloimmunization, fetomaternal hemorrhage, twin-twin transfusion syndrome, or vasa previa with bleeding (Modanlou, 2004). Insignificant sinusoidal patterns have been reported following administration of meperidine, morphine, alphaprodine, and butorphanol (Angel, 1984; Egley, 1991; Epstein, 1982). Shown in Figure 24-13 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.
FIGURE 24-13 Sinusoidal fetal heart rate pattern associated with maternal intravenous meperidine administration. Sine waves are occurring at a rate of 6 cycles per minute.
Modanlou and Freeman (1982), based on their extensive review, proposed adoption of a strict definition:
1. Stable baseline heart rate of 120 to 160 bpm with regular oscillations,
2. Amplitude of 5 to 15 bpm (rarely greater),
3. Long-term variability frequency of 2 to 5 cycles per minute,
4. Fixed or flat short-term variability,
5. Oscillation of the sinusoidal waveform above or below a baseline, and
6. Absent accelerations.
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 or more bpm to quantify fetal risk (Murphy, 1991; Neesham, 1993).
Some investigators 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 for up to 90 minutes in some cases and also in association with oxytocin or alphaprodine usage, or both.
The pathophysiology of sinusoidal patterns is unclear, in part due to various definitions. There seems to be general agreement that antepartum sine wave baseline undulation portends severe fetal anemia. Still, few 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) have proposed, based on studies in fetal lambs, that the sinusoidal fetal heart rate pattern is related to waves of arterial blood pressure, reflecting oscillations in the baroreceptor-chemoreceptor feedback mechanism for control of the circulation.
Periodic Fetal Heart Rate Changes
The periodic fetal heart rate refers to deviations from baseline that are temporally related to uterine contractions. Acceleration refers to an increase in fetal heart rate above baseline and deceleration to a decrease 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 in onset related to the corresponding uterine contraction. 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 1997 workshop proposed that decelerations be defined as recurrent if they occur with 50 percent or more 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 cause the pattern. In this system, early decelerations are termed head compression, late decelerations are termed uteroplacental insufficiency, and variable decelerations become cord compression patterns.
Accelerations
These are visually apparent abrupt increases—defined as onset of acceleration to a peak in less than 30 seconds—in the fetal heart rate baseline (American College of Obstetricians and Gynecologists, 2013b). At 32 weeks’ gestation and beyond, the acceleration has a peak of 15 bpm with a duration of 15 seconds or more but less than 2 minutes (see Table 24-1). Before 32 weeks, a peak of 10 bpm for 15 seconds to 2 minutes is considered normal. Prolonged acceleration was defined as 2 minutes or more but less than 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, and fetal stimulation during pelvic examination. Fetal scalp blood sampling and acoustic stimulation also incite fetal heart rate acceleration (Clark, 1982). Finally, accelerations can occur during labor without any apparent stimulus. Indeed, they are common in labor and are nearly always associated with fetal movement. These accelerations are virtually always reassuring and almost always confirm that the fetus is not acidemic at that time.
Accelerations seem to have the same physiological explanations as beat-to-beat variability in that they 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 accelerations during the first or last 30 minutes during labor, or both, was 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. There is an approximately 50-percent chance of acidemia in the fetus who fails to respond to stimulation in the presence of an otherwise nonreassuring pattern (Clark, 1984; Smith, 1986).
Early Deceleration
This consists of a gradual decrease and return to baseline associated with a contraction (Fig. 24-14). Such early deceleration was first described by Hon (1958), who observed that there was a heart rate drop with contractions and that this was related to cervical dilatation. He considered these findings to be physiological.
FIGURE 24-14 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.
Freeman and associates (2003) defined early decelerations as those generally seen in active labor between 4 and 7 cm dilatation. 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.
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 24-14 but also of those shown in Figure 24-15, 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.
FIGURE 24-15 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 24-14. Deceleration (B), however, is “variable” in appearance because of its jagged configuration and may alternatively represent cord occlusion.
Late Deceleration
The fetal heart rate response to uterine contractions can be an index of either uterine perfusion or placental function. A late deceleration is a smooth, gradual, symmetrical decrease in fetal heart rate beginning at or after the contraction peak and returning to baseline only after the contraction has ended. A gradual decrease is defined as 30 seconds or more from the onset of the deceleration to the nadir. In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively (Fig. 24-16). 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.
FIGURE 24-16 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.
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 phase was predictive of the fetal Po2 but not fetal pH. The lower the fetal Po2 before contractions, the shorter the lag phase to onset of late decelerations. This lag period reflected the time necessary for the fetal Po2 to fall below a critical level necessary to stimulate arterial chemoreceptors, which mediated decelerations.
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.
Numerous clinical circumstances can result in late decelerations. Generally, any process that causes maternal hypotension, excessive uterine activity, or placental dysfunction can induce late decelerations. The two most common causes are hypotension from epidural analgesia and uterine hyperactivity caused by oxytocin stimulation. Maternal diseases such as hypertension, diabetes, and collagen-vascular disorders can cause chronic placental dysfunction. Placental abruption can cause acute late decelerations (Fig. 24-17).
FIGURE 24-17 Late decelerations due to uteroplacental insufficiency resulting from placental abruption. Immediate cesarean delivery was performed. Umbilical artery pH was 7.05 and the Po2 was 11 mm Hg.
Variable Deceleration
The most common deceleration patterns encountered during labor are variable decelerations attributed to umbilical cord occlusion. Melchior and Bernard (1985) identified variable decelerations in 40 percent of more than 7000 monitor tracings when labor had progressed to 5 cm dilatation and in 83 percent by the end of the first stage of labor. Variable deceleration is defined as an abrupt decrease 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. 24-18).
FIGURE 24-18 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 decelerations measure ≥ 15 bpm for ≥ 15 seconds and have an onset-to-nadir phase of < 30 seconds. Total duration is < 2 minutes.
Very early in the development of electronic monitoring, Hon (1959) tested the effects of umbilical cord compression on fetal heart rate (Fig. 24-19). Similar complete occlusion of the umbilical cord in experimental animals produces abrupt, jagged-appearing deceleration of the fetal heart rate (Fig. 24-20). Concomitantly, fetal aortic pressure increases. Itskovitz and colleagues (1983) observed that variable decelerations in fetal lambs occurred only after umbilical blood flow was reduced by at least 50 percent.
FIGURE 24-19 A. The effects of 25-second cord compression compared with those of 40 seconds in panel (B). (Redrawn from Hon, 1959, with permission.)
FIGURE 24-20 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 from Künzel, 1985, with permission.)
Two types of variable decelerations are shown in Figure 24-21. The deceleration denoted by “A” is very much like that seen with complete umbilical cord occlusion in experimental animals (see Fig. 24-20). 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 acceleration represents the same events occurring in reverse (Fig. 24-22).
FIGURE 24-21 Varying (variable) fetal heart rate decelerations. Deceleration (B) exhibits “shoulders” of acceleration compared with deceleration (A). (Adapted from Künzel, 1985, with permission.)
FIGURE 24-22 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 from Lee, 1975.)
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 decrease 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 occlusion 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 (2013a), recurrent variable decelerations with minimal to moderate 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. 24-23) was first described by Hammacher and colleagues (1968) and linked to umbilical cord complications during labor. 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 (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).
FIGURE 24-23 Saltatory baseline fetal heart rate showing rapidly recurring couplets of acceleration combined with deceleration.
Prolonged Deceleration
This pattern, which is shown in Figure 24-24, is defined as an isolated deceleration greater than 15 bpm lasting 2 minutes or longer 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 common causes include cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension.
FIGURE 24-24 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 prolonged deceleration of the fetal heart rate. For example, Eberle and coworkers (1998) reported that prolonged decelerations occurred in 4 percent of normal parturients given either epidural or intrathecal labor analgesia. 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 even maternal Valsalva maneuver.
The placenta is very 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 rightfully 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. Melchior and Bernard (1985) reported that only 1.4 percent of more than 7000 deliveries lacked decelerations during second-stage labor. Both cord compression and fetal head compression have been implicated as causes of decelerations and baseline bradycardia during second-stage labor. The high incidence of such patterns minimized their potential significance during the early development and interpretation of electronic monitoring. For example, Boehm (1975) described profound, prolonged fetal heart rate deceleration in the 10 minutes preceding vaginal delivery of 18 healthy infants. However, Herbert and Boehm (1981) later reported another 18 pregnancies with similar prolonged second-stage decelerations. There was one stillbirth and one neonatal death. 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 and found that as the total number of decelerations to < 70 bpm increased, the 5-minute Apgar score decreased. Put another way, the longer a fetus was exposed to variable decelerations, the lower the Apgar score was at 5 minutes.
Picquard and coworkers (1988) analyzed heart rate patterns during second-stage labor in 234 women in an attempt to identify specific patterns to diagnose fetal compromise. Loss of beat-to-beat variability and baseline fetal heart rate < 90 bpm were predictive of fetal acidemia. Krebs and associates (1981) also found that persistent or progressive baseline bradycardia and baseline tachycardia were associated with low 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 second-stage decelerations, is associated with increased but not inevitable fetal compromise (Fig. 24-25).
FIGURE 24-25 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, and continuous monitoring is used only if fetal heart rate abnormalities are subsequently identified. Mires and coworkers (2001) randomly assigned 3752 low-risk women in spontaneous labor at admission either to auscultation of the fetal heart or to 20 minutes of electronic fetal monitoring. Use of admission electronic fetal monitoring did not improve infant outcome. Moreover, its use resulted in increased interventions, including operative delivery. Impey and associates (2003) performed a similar study in 8588 low-risk women and also found no improvement in infant outcome. More than half of the women enrolled in these studies, whether they received admission electronic monitoring or auscultation, eventually required continuous monitoring for diagnosed abnormalities in the fetal heart rate.
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. The American College of Obstetricians and Gynecologists (2010) has concluded that data are insufficient to determine the value of fetal monitoring under these circumstances.
Centralized Monitoring
Technological advances have made it possible to observe fetal heart rate monitors from a remote, centralized location. Such intrapartum monitoring equipment has become common in American labor and delivery units. The rationale behind centralized monitoring is that the ability to monitor several patients simultaneously would lead to better outcomes. What is the evidence that this rationale is correct? To our knowledge, 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.
OTHER INTRAPARTUM ASSESSMENT TECHNIQUES
Fetal Scalp Blood Sampling
According to the American College of Obstetricians and Gynecologists (2009), measurements of the pH in capillary scalp blood may help to identify the fetus in serious distress. That said, it also emphasized that neither normal nor abnormal scalp pH results have been shown to be predictive of infant outcome. The College also indicated that the procedure is now used uncommonly and is not even available at some hospitals.
For completion, an illuminated endoscope is inserted through the dilated cervix after membrane rupture so as to press firmly against the fetal scalp (Fig. 24-26). The skin is wiped clean with a cotton swab and coated with a silicone gel to cause the blood to accumulate as discrete globules. An incision is made through the skin to a depth of 2 mm with a special blade on a long handle. As a drop of blood forms on the surface, it is immediately collected into a heparinized glass capillary tube. The pH of the blood is measured promptly.
FIGURE 24-26 The technique of fetal scalp sampling using an amnioscope. The end of the endoscope is displaced from the fetal vertex approximately 2 cm to show the disposable blade against the fetal scalp before incision. (Adapted from Hamilton, 1974.)
The pH of fetal capillary scalp blood is usually lower than that of umbilical venous blood and approaches that of umbilical arterial blood. Zalar and Quilligan (1979) recommended a protocol to try to confirm fetal distress. If the pH is > 7.25, labor is observed, and if between 7.20 and 7.25, the pH measurement is repeated within 30 minutes. If the pH is < 7.20, another scalp blood sample is collected immediately, and the mother is taken to an operating room and prepared for surgery. Delivery is performed promptly if the low pH is confirmed. Otherwise, labor is allowed to continue, and scalp blood samples are repeated periodically.
The only benefits reported for scalp pH testing are fewer cesarean deliveries for fetal distress (Young, 1980b). Goodwin and coworkers (1994), however, in a study of 112,000 deliveries, showed a decrease in the scalp pH sampling rate. The rate dropped from approximately 1.8 percent in the mid-1980s to 0.03 percent by 1992 but with no increased delivery rate for fetal distress. They concluded that scalp pH sampling was unnecessary. Kruger and colleagues (1999) have advocated the use of fetal scalp blood lactate concentration as an adjunct to pH. Wiberg-Itzel and associates (2008) randomized 1496 fetuses to scalp blood pH analysis and 1496 to scalp blood lactate analysis. They found either to be equivalent in predicting fetal acidemia. The advantage of lactate measurement was that a smaller amount of blood was needed, which led to a lower procedural failure rate compared with scalp sampling for pH.
Scalp Stimulation
Clark and coworkers (1984) have suggested that scalp stimulation is an alternative to scalp blood sampling. This proposal was based on the observation that heart rate acceleration in response to pinching of the scalp with an Allis clamp just before obtaining blood was invariably associated with a normal pH. Conversely, failure to provoke acceleration was not uniformly predictive of fetal acidemia. Later, Elimian and associates (1997) reported that of 58 cases in which the fetal heart rate accelerated ≥ 10 bpm after 15 seconds of gentle digital stroking of the scalp, 100 percent had a scalp pH of ≥ 7.20. Without an acceleration, however, only 30 percent had a scalp pH < 7.20.
Vibroacoustic Stimulation
Fetal heart rate acceleration in response to vibroacoustic stimulation has been recommended as a substitute for scalp sampling (Edersheim, 1987). The technique uses an electronic artificial larynx placed approximately 1 cm from or directly onto the maternal abdomen (Chap. 17, p. 341). Response to vibroacoustic stimulation is considered normal if a fetal heart rate acceleration of at least 15 bpm for at least 15 seconds occurs within 15 seconds after the stimulation and with prolonged fetal movements (Sherer, 1994). Lin and colleagues (2001) prospectively studied vibroacoustic stimulation in 113 women in labor with either moderate to severe variable or late fetal heart rate decelerations. They concluded that this technique is an effective predictor of fetal acidosis in the setting of variable decelerations. The predictability for fetal acidosis, however, is limited in the setting of late decelerations. Other investigators have reported that although vibroacoustic stimulation in second-stage labor is associated with fetal heart rate reactivity, the quality of the response did not predict neonatal outcome or enhance labor management (Anyaegbunam, 1994).
Skupski and coworkers (2002) performed a metaanalysis of reports on intrapartum fetal stimulation tests published between 1966 and 2000. Four types of fetal stimulation were analyzed and included scalp puncture for pH testing, Allis clamp pinching of the fetal scalp, vibroacoustic stimulation, and digital stroking of the scalp. Results were similar for all four methods. These investigators concluded that intrapartum stimulation tests were useful to exclude fetal acidemia. They cautioned, however, that these tests are “less than perfect.”
Fetal Pulse Oximetry
Using technology similar to that of adult pulse oximetry, instrumentation has been developed that may allow assessment of fetal oxyhemoglobin saturation once membranes are ruptured. A unique padlike sensor such as shown in Figure 24-27 is inserted through the cervix and positioned against the fetal face, where it is held in place by the uterine wall. A transabdominal fetal pulse oximeter has also been described in a preliminary study (Vintzileos, 2005). As reviewed by Yam and coworkers (2000), the transcervical device has been used extensively by many investigators. It has been reported to reliably register fetal oxygen saturation in 70 to 95 percent of women throughout 50 to 88 percent of their labors. The lower limit for normal fetal oxygen saturation is generally considered to be 30 percent by investigators (Gorenberg, 2003; Stiller, 2002). As shown in Figure 24-28, however, fetal oxygen saturation normally varies greatly when measured in umbilical artery blood (Arikan, 2000). Bloom and associates (1999) reported that brief, transient fetal oxygen saturations below 30 percent were common during labor because such values were observed in 53 percent of fetuses with normal outcomes. Saturation values below 30 percent, however, when persistent for 2 minutes or longer, were associated with an increased risk of potential fetal compromise.
FIGURE 24-27 Schematic diagram of fetal pulse oximeter sensor placement.
FIGURE 24-28 Frequency distribution of umbilical artery oxygen saturation values in 1281 vigorous newborn infants. Dotted line indicates normal distribution. (Redrawn from Arikan, 2000, with permission.)
Garite and colleagues (2000) randomly assigned 1010 women with term pregnancies and in whom predefined abnormal fetal heart rate patterns developed. Patients received either conventional fetal monitoring alone or fetal monitoring plus continuous fetal pulse oximetry. Cesarean delivery for fetal distress was performed when pulse oximetry values remained < 30 percent for the entire interval between two contractions or when the fetal heart rate patterns met predefined guidelines. The use of fetal pulse oximetry significantly reduced the cesarean delivery rate for nonreassuring fetal status from 10.2 to 4.5 percent. Alternatively, the cesarean delivery rate for dystocia increased significantly from 9 to 19 percent when pulse oximetry was used. There were no neonatal benefits or adverse effects associated with fetal pulse oximetry. Based on these observations, in 2000, the Obstetrics and Gynecology Devices Panel of the Medical Devices Advisory Committee of the Food and Drug Administration (FDA) (2012) approved marketing of the Nellcor N-400 Fetal Oxygen Monitoring System.
Since then, another three randomized trials of fetal pulse oximetry have been reported. Of these, Klauser and colleagues (2005) randomly assigned 360 women with nonreassuring fetal heart rate patterns to standard fetal monitoring plus fetal pulse oximetry or to standard monitoring alone and found no benefits for oximetry. East and coworkers (2006) randomized 600 women with nonreassuring fetal heart rate patterns to standard monitoring either alone or with added fetal pulse oximetry. These investigators reported that addition of oximetry significantly reduced cesarean delivery rates for a nonreassuring fetal heart rate pattern. They further reported, however, that neonatal outcomes were not different between the study groups. Also, Bloom and associates (2006) reported the largest trial, which was performed by the Maternal-Fetal Units Network. A total of 5341 women in labor at term underwent placement of the fetal oximetry sensor, but the information was randomly withheld from care providers. Unlike the earlier studies, participants were not required to have nonreassuring fetal heart rate patterns. Sensor application was generally successful and fetal oxygen saturation values were registered 75 percent of the time. Knowledge of fetal oxygen saturation did not change the cesarean delivery rates in the overall population or in the subgroup of 2168 women who had nonreassuring fetal heart rate patterns. Moreover, neonatal outcomes were not improved by knowledge of fetal oxygen saturation status. Because of these findings, in 2005, the manufacturer discontinued sale of the fetal oximeter system in the United States.
Fetal Electrocardiography
As fetal hypoxia worsens, there are changes in the T-wave and in the ST segment of the fetal ECG. Because of this, several investigators have assessed the value of analyzing these parameters as an adjunct to conventional fetal monitoring. The technique requires internal fetal heart monitoring and special equipment to process the fetal ECG. The rationale behind this technology is based on the observation that the mature fetus exposed to hypoxemia develops an elevated ST segment with a progressive rise in T-wave height that can be expressed as a T:QRS ratio (Fig. 24-29). It is postulated that increasing T:QRS ratios reflect fetal cardiac ability to adapt to hypoxia and appears before neurological damage. Worsening hypoxia results in an increasingly negative ST-segment deflection such that it appears as a biphasic waveform (Fig. 24-30). In 2005, the manufacturer—Neoventa Medical—received FDA (2012) approval for their ST analysis program—the STAN system.
FIGURE 24-29 A. ST segment changes in normal and hypoxic conditions. B. Generation of T:QRS ratios. (Redrawn from Devoe, 2006, with permission.)
FIGURE 24-30 Biphasic ST-segment waveform with progressive fetal hypoxia. (Adapted from Devoe, 2006.)
There have been a few studies of ST-segment changes with fetal monitoring. Westgate and coworkers (1993) conducted a randomized trial of 2400 pregnancies. Infant outcomes were not improved compared with those in whom conventional fetal monitoring alone was used. There was, however, a reduction in the cesarean delivery rate for fetal distress. In another randomized trial of 4966 Swedish women, Amer-Wåhlin and colleagues (2001, 2007) found that the addition of ST-segment analysis to conventional fetal monitoring significantly reduced cesarean delivery rates for fetal distress and metabolic acidemia in umbilical artery blood. Subsequently, Doria and associates (2007) introduced STAN as a clinical practice in a London hospital and reported no changes in the incidence of operative delivery or neonatal encephalopathy. Most recently, Becker and colleagues (2012) performed a metaanalysis of five randomized trials comprising 15,352 patients and found that use of ST-segment analysis did not reduce the rates of cesarean delivery or fetal metabolic acidemia at birth.
It must be considered that ST-segment abnormalities might occur late in the course of fetal compromise. Neilson (2013) reviewed the Cochrane Database to assess fetal ECG analysis during labor. There were 16,295 women in which such monitoring was performed. He concluded that fetal ST-segment waveform analysis was perhaps useful in preventing fetal acidosis and neonatal encephalopathy when standard fetal heart rate monitoring suggested abnormal patterns. Although no randomized trials have yet been performed in the United States, the Maternal-Fetal Medicine Units Network has one in progress.
Intrapartum Doppler Velocimetry
Doppler analysis of the umbilical artery has been studied as another potential adjunct to conventional fetal monitoring. Further described in Chapter 10 (p. 219), abnormal Doppler waveforms may signify pathological umbilical-placental vessel resistance. From their review, Farrell and associates (1999) concluded that this technique was a poor predictor of adverse perinatal outcomes. They concluded that Doppler velocimetry had little if any role in fetal surveillance during labor.
FETAL DISTRESS
The terms fetal distress and birth asphyxia are too broad and vague to be applied with any precision to clinical situations (American College of Obstetricians and Gynecologists, 2005). Uncertainty regarding the diagnosis based on interpretation of fetal heart rate patterns has given rise to descriptions such as reassuring or nonreassuring. The term “reassuring” suggests a restoration of confidence by a particular pattern, whereas “nonreassuring” suggests inability to remove doubt. These patterns during labor are dynamic—they can rapidly change from reassuring to nonreassuring and vice versa. In this situation, obstetricians experience surges of both confidence and doubt. Put another way, most diagnoses of fetal distress using heart rate patterns occur when obstetricians lose confidence or cannot assuage doubts about fetal condition. These assessments are subjective clinical judgments that are inevitably subject to imperfection and must be recognized as such.
Pathophysiology
Why is the diagnosis of fetal distress based on heart rate patterns so tenuous? One explanation is that these patterns are more a reflection of fetal physiology than of pathology. Physiological control of heart rate includes various interconnected mechanisms that depend on blood flow and oxygenation. Moreover, the activity of these control mechanisms is influenced by the preexisting state of fetal oxygenation, for example, as seen with chronic placental insufficiency. Importantly, the fetus is tethered by an umbilical cord, whereby blood flow is constantly in jeopardy. Moreover, normal labor is a process of increasing acidemia (Rogers, 1998). Thus, normal labor is a process of repeated fetal hypoxic events resulting inevitably in acidemia. Put another way, and assuming that “asphyxia” can be defined as hypoxia leading to acidemia, normal parturition is an asphyxiating event for the fetus.
Diagnosis
Because of the above uncertainties, it follows that identification of “fetal distress” based on fetal heart rate patterns is imprecise and controversial. It is well known that experts in interpretation of these patterns often disagree with each other. In fact, Parer (1997), a strong advocate of electronic fetal heart rate monitoring and an organizer of the 1997 NICHD fetal monitoring workshop, lightheartedly compared the experts in attendance to marine iguanas of the Galapagos Islands, to wit: “all on the same beach but facing different directions and spitting at one another constantly!”
Ayres-de-Campos and colleagues (1999) investigated interobserver agreement of fetal heart rate pattern interpretation and found that agreement—or conversely, disagreement—was related to whether the pattern was normal, suspicious, or pathological. Specifically, experts agreed on 62 percent of normal patterns, 42 percent of suspicious patterns, and only 25 percent of pathological patterns. Keith and coworkers (1995) asked each of 17 experts to review 50 tracings on two occasions, at least 1 month apart. Approximately 20 percent changed their own interpretations, and approximately 25 percent did not agree with the interpretations of their colleagues. And although Murphy and associates (2003) concluded that at least part of the interpretation problem is due to a lack of formalized education in American training programs, this is obviously only a small modifier. Put another way, how can the teacher enlighten the student if the teacher is uncertain?
National Institutes of Health Workshops Three-Tier Classification System
The NICHD (1997) held a succession of workshops in 1995 and 1996 to develop standardized and unambiguous definitions of fetal heart rate (FHR) tracings and published recommendations for interpreting these patterns. In 2008, a second workshop was convened to reevaluate the 1997 recommendations and to clarify terminology (see Table 24-1)(Macones, 2008). A major result was the recommendation of a three-tier system for classification of FHR patterns (Table 24-2). The American College of Obstetricians and Gynecologists (2013b) subsequently recommended use of this tiered system.
TABLE 24-2. Three-Tier Fetal Heart Rate Interpretation System
A few studies have been done to assess the three-tiered system. Jackson and coworkers (2011) studied 48,444 women in labor and found that category I (normal FHR) patterns were observed during labor in 99.5 percent of tracings. Category II (indeterminate FHR) patterns were found in 84.1 percent of tracings, and category III (abnormal FHR) patterns were seen in 0.1 percent (54 women). Most—84 percent of women—had a mix of categories during labor. Cahill and colleagues (2012) retrospectively studied the incidence of umbilical cord acidemia (pH ≤ 7.10) correlated with fetal heart rate characteristics during the 30 minutes preceding delivery. None of the three categories demonstrated a significant association with cord blood acidemia. The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics (2014) concluded that a category I or II tracing with a 5-minute Apgar score > 7 or normal arterial blood acid-base values was not consistent with an acute hypoxic-ischemic event.
Sholapurkar (2012) also challenged the validity of the three-tier system because most abnormal fetal heart rate patterns fall into the indeterminate category II, that is, one for which no definite management recommendations can be made. It was further suggested that this resulted from most fetal heart rate decelerations being inappropriately classified as variable decelerations due to cord compression.
Parer and King (2010) compared the current situation in the United States with that of other countries in which a consensus on classification and management has been reached by a number of professional societies. Some of these include the Royal College of Obstetricians and Gynecologists, the Society of Obstetricians and Gynecologists of Canada, the Royal Australian and New Zealand College of Obstetricians and Gynecologists, and the Japan Society of Obstetrics and Gynecology. Parer and King (2010) further comment that the NICHD three-tier system is inadequate because category II—indeterminate FHR—consists of a “vast heterogenous mixture of patterns” that prevents development of a management strategy. Parer and Ikeda (2007) had previously proposed a color-coded five-tier system for both FHR interpretation and management. There have been two reports comparing the five-tier and three-tier systems. Bannerman and associates (2011) found that the two systems were similar in fetal heart rate interpretations for tracings that were either very normal or very abnormal. Coletta and coworkers (2012) found that the five-tier system had better sensitivity than the three-tier system. It is apparent that, after 50 years of continuous electronic fetal heart rate monitoring use, there is not a consensus on interpretation and management recommendations for FHR patterns (Parer, 2011).
Meconium in the Amnionic Fluid
Obstetrical teaching throughout the past century has included the concept that meconium passage is a potential warning of fetal asphyxia. In 1903, J. Whitridge Williams observed and attributed meconium passage to “relaxation of the sphincter ani muscle induced by faulty aeration of the (fetal) blood.” Even so, obstetricians have also long realized that the detection of meconium during labor is problematic in the prediction of fetal distress or asphyxia. In their review, Katz and Bowes (1992) emphasized the prognostic uncertainty of meconium by referring to the topic as a “murky subject.” Indeed, although 12 to 22 percent of labors are complicated by meconium, only a few are linked to infant mortality. In an investigation from Parkland Hospital, meconium was found to be a “low-risk” obstetrical hazard because the perinatal mortality rate attributable to meconium was 1 death per 1000 live births (Nathan, 1994).
Three theories have been suggested to explain fetal passage of meconium and in part may explain the tenuous connection between its detection and infant mortality. First, the pathological explanation proposes that fetuses pass meconium in response to hypoxia and that meconium therefore signals fetal compromise (Walker, 1953). Second, the physiological explanation is that in utero passage of meconium represents normal gastrointestinal tract maturation under neural control (Mathews, 1979). A final theory posits that meconium passage follows vagal stimulation from common but transient umbilical cord entrapment with resultant increased bowel peristalsis (Hon, 1961). Thus, meconium release may represent physiological processes.
Ramin and associates (1996) studied almost 8000 pregnancies with meconium-stained amnionic fluid delivered at Parkland Hospital. Meconium aspiration syndrome was significantly associated with fetal acidemia at birth. Other significant correlates of aspiration included cesarean delivery, forceps to expedite delivery, intrapartum heart rate abnormalities, depressed Apgar scores, and need for assisted ventilation at delivery. Analysis of the type of fetal acidemia based on umbilical blood gases suggested that the fetal compromise associated with meconium aspiration syndrome was an acute event. This is because most acidemic fetuses had abnormally increased Pco2 values rather than a pure metabolic acidemia.
Dawes and coworkers (1972) observed that such hypercarbia in fetal lambs induces gasping and resultant increased amnionic fluid inhalation. Jovanovic and Nguyen (1989) observed that meconium gasped into the fetal lungs caused aspiration syndrome only in asphyxiated animals. Ramin and colleagues (1996) hypothesized that the pathophysiology of meconium aspiration syndrome includes, but is not limited to, fetal hypercarbia, which stimulates fetal respiration leading to aspiration of meconium into the alveoli. Lung parenchymal injury is secondary to acidemia-induced alveolar cell damage. In this pathophysiological scenario, meconium in amnionic fluid is a fetal environmental hazard rather than a marker of preexistent compromise. This proposed pathophysiological sequence is not all-inclusive, because it does not account for approximately half of the cases of meconium aspiration syndrome in which the fetus was not acidemic at birth.
Thus, it was concluded that the high incidence of meconium observed in the amnionic fluid during labor often represents fetal passage of gastrointestinal contents in conjunction with normal physiological processes. Although normal, such meconium becomes an environmental hazard when fetal acidemia supervenes. Importantly, such acidemia occurs acutely, and therefore meconium aspiration is unpredictable and likely unpreventable. Moreover, Greenwood and colleagues (2003) showed that clear amnionic fluid was also a poor predictor. In a prospective study of 8394 women with clear amnionic fluid, they found that clear fluid was an unreliable sign of fetal well-being.
Growing evidence indicates that many infants with meconium aspiration syndrome have suffered chronic hypoxia before birth (Ghidini, 2001). Blackwell and associates (2001) found that 60 percent of infants diagnosed with meconium aspiration syndrome had umbilical artery blood pH ≥ 7.20, implying that the syndrome was unrelated to the neonatal condition at delivery. Similarly, markers of chronic hypoxia, such as fetal erythropoietin levels and nucleated red blood cell counts in newborn infants, suggest that chronic hypoxia is involved in many meconium aspiration syndrome cases (Dollberg, 2001; Jazayeri, 2000).
In the recent past, routine obstetrical management of a newborn with meconium-stained amnionic fluid included intrapartum suctioning of the oropharynx and nasopharynx. Guidelines from the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, however, recommend that such infants no longer routinely receive intrapartum suctioning because it does not prevent meconium aspiration syndrome (Perlman, 2010). As discussed in Chapter 32 (p. 626), if the infant is depressed, the trachea is intubated, and meconium suctioned from beneath the glottis. If the newborn is vigorous, defined as having strong respiratory efforts, good muscle tone, and a heart rate > 100 bpm, then tracheal suction is not necessary and may injure the vocal cords.
Management Options
The principal management options for significantly variable fetal heart rate patterns consist of correcting any fetal insult, if possible. Measures suggested by the American College of Obstetricians and Gynecologists (2013b,c) are listed in Table 24-3. Moving the mother to the lateral position, correcting maternal hypotension caused by regional analgesia, and discontinuing oxytocin serve to improve uteroplacental perfusion. Examination is done to exclude prolapsed cord or impending delivery. Simpson and James (2005) assessed benefits of three maneuvers in 52 women with fetal oxygen saturation sensors already in place. They used intravenous hydration—500 to 1000 mL of lactated Ringer solution given over 20 minutes; lateral versus supine position; and using a nonrebreathing mask that administered supplemental oxygen at 10 L/min. Each of these maneuvers significantly increased fetal oxygen saturation levels, although the increments were small.
TABLE 24-3. Some Resuscitative Measures for Category II or Category III Tracings
Tocolysis
A single intravenous or subcutaneous injection of 0.25 mg of terbutaline sulfate given to relax the uterus has been described as a temporizing maneuver in the management of nonreassuring fetal heart rate patterns during labor. The rationale is that inhibition of uterine contractions might improve fetal oxygenation, thus achieving in utero resuscitation. Cook and Spinnato (1994) described their experience during 10 years with terbutaline tocolysis for fetal resuscitation in 368 pregnancies. Such resuscitation improved fetal scalp blood pH values, although all fetuses underwent cesarean delivery. These investigators concluded that although the studies were small and rarely randomized, most reported favorable results with terbutaline tocolysis for nonreassuring patterns. Small intravenous doses of nitroglycerin—60 to 180 μg—also have been reported to be beneficial (Mercier, 1997). The American College of Obstetricians and Gynecologists (2013b) has concluded that there is insufficient evidence to recommend tocolysis for non-reassuring fetal heart rate patterns.
Amnioinfusion
Gabbe and coworkers (1976) showed in monkeys that removal of amnionic fluid produced variable decelerations and that replenishment of fluid with saline relieved the decelerations. Miyazaki and Taylor (1983) infused saline through an intrauterine pressure catheter in laboring women who had either variable decelerations or prolonged decelerations attributed to cord entrapment. Such therapy improved the heart rate pattern in half of the women studied. Later, Miyazaki and Nevarez (1985) randomly assigned 96 nulliparous women in labor with cord compression patterns and found that those who were treated with amnioinfusion required cesarean delivery for fetal distress less often.
Based on many of these early reports, transvaginal amnioinfusion has been extended into three clinical areas. These include: (1) treatment of variable or prolonged decelerations, (2) prophylaxis for women with oligohydramnios, as with prolonged ruptured membranes, and (3) attempts to dilute or wash out thick meconium (Chap. 33, p. 638).
Many different amnioinfusion protocols have been reported, but most include a 500- to 800-mL bolus of warmed normal saline followed by a continuous infusion of approximately 3 mL per minute (Owen, 1990; Pressman, 1996). In another study, Rinehart and colleagues (2000) randomly gave a 500-mL bolus of normal saline at room temperature alone or 500-mL bolus plus continuous infusion of 3 mL per minute. Their study included 65 women with variable decelerations, and the investigators found neither method to be superior. Wenstrom and associates (1995) surveyed use of amnioinfusion in teaching hospitals in the United States. The procedure was used in 96 percent of the 186 centers surveyed, and it was estimated that 3 to 4 percent of all women delivered at these centers received such infusion. Potential complications of amnioinfusion are summarized in Table 24-4.
TABLE 24-4. Complications Associated with Amnioinfusion from a Survey of 186 Obstetrical Units
Prophylactic Amnioinfusion for Variable Decelerations. Hofmeyr and Lawrie (2012) used the Cochrane Database to specifically analyze the effects of amnioinfusion in the management of fetal heart rate patterns associated with umbilical cord compression. Nineteen suitable studies were identified, most with fewer than 200 participants. It was concluded that amnioinfusion appeared to be useful in reducing the occurrence of variable decelerations, improving neonatal outcome, and reducing cesarean delivery rates. The American College of Obstetricians and Gynecologists (2013a) recommends consideration of amnioinfusion with persistent variable decelerations.
Prophylactic Amnioinfusion for Oligohydramnios. Amnioinfusion in women with oligohydramnios has been used prophylactically to avoid intrapartum fetal heart rate patterns from cord occlusion. Nageotte and coworkers (1991) found that this resulted in significantly decreased frequency and severity of variable decelerations in labor. However, the cesarean delivery rate or condition of term infants was not improved. In a randomized investigation, Macri and colleagues (1992) studied prophylactic amnioinfusion in 170 term and postterm pregnancies complicated by both thick meconium and oligohydramnios. Amnioinfusion significantly reduced cesarean delivery rates for fetal distress and meconium aspiration syndrome. In contrast, Ogundipe and associates (1994) randomly assigned 116 term pregnancies with an amnionic fluid index < 5 cm to receive prophylactic amnioinfusion or standard obstetrical care. There were no significant differences in overall cesarean delivery rates, delivery rates for fetal distress, or umbilical cord acid-base studies.
Amnioinfusion for Meconium-Stained Amnionic Fluid. Pierce and associates (2000) summarized the results of 13 prospective trials of intrapartum amnioinfusion in 1924 women with moderate to thick meconium-stained fluid. Infants born to women treated by amnioinfusion were significantly less likely to have meconium below the vocal cords and were less likely to develop meconium aspiration syndrome than infants born to women not undergoing amnioinfusion. The cesarean delivery rate was also lower in the amnioinfusion group. Similar results were reported by Rathore and coworkers (2002). In contrast, several investigators were not supportive of amnioinfusion for meconium staining. For example, Usta and associates (1995) reported that amnioinfusion was not feasible in half of women with moderate or thick meconium who were randomized to this treatment. These investigators were unable to demonstrate any improvement in neonatal outcomes. Spong and coworkers (1994) also concluded that although prophylactic amnioinfusion did dilute meconium, it did not improve perinatal outcome. Last, Fraser and colleagues (2005) randomized amnioinfusion in 1998 women with thick meconium staining of the amnionic fluid in labor and found no benefits. Because of these findings, the American College of Obstetricians and Gynecologists (2012a, 2013c) does not recommend amnioinfusion to dilute meconium-stained amnionic fluid. According to Xu and coworkers (2007), in areas lacking continuous monitoring, amnioinfusion may be used to lower the incidence of meconium aspiration syndrome.
Fetal Heart Rate Patterns and Brain Damage
Attempts to correlate fetal heart rate patterns with brain damage have been based primarily on studies of infants identified as a result of medicolegal actions. Phelan and Ahn (1994) reported that among 48 fetuses later found to be neurologically impaired, a persistent nonreactive fetal heart rate tracing was already present at the time of admission in 70 percent. They concluded that fetal neurological injury occurred predominately before arrival to the hospital. When they looked retrospectively at heart rate patterns in 209 brain-damaged infants, they concluded that there was not a single unique pattern associated with fetal neurological injury (Ahn, 1996). Graham and associates (2006) reviewed the world literature published between 1966 and 2006 on the effect of fetal heart rate monitoring to prevent perinatal brain injury and found no benefit.
Experimental Evidence
Fetal heart rate patterns necessary for perinatal brain damage have been studied in experimental animals. Myers (1972) described the effects of complete and partial asphyxia in rhesus monkeys in studies of brain damage due to perinatal asphyxia. Complete asphyxia was produced by total occlusion of umbilical blood flow that led to prolonged deceleration (Fig. 24-31). Fetal arterial pH did not drop to 7.0 until approximately 8 minutes after complete cessation of oxygenation and umbilical flow. At least 10 minutes of such prolonged deceleration was required before there was evidence of brain damage in surviving fetuses.
FIGURE 24-31 Prolonged deceleration in a rhesus monkey shown with blood pressure and biochemical changes during total occlusion of umbilical cord blood flow. (Adapted from Myers, 1972.)
Myers (1972) also produced partial asphyxia in rhesus monkeys by impeding maternal aortic blood flow. This resulted in late decelerations due to uterine and placental hypoperfusion. He observed that several hours of these late decelerations did not damage the fetal brain unless the pH fell below 7.0. Indeed, Adamsons and Myers (1977) reported subsequently that late decelerations were a marker of partial asphyxia long before brain damage occurred.
The most common fetal heart rate pattern during labor—due to umbilical cord occlusion—requires considerable time to significantly affect the fetus in experimental animals. Clapp and colleagues (1988) partially occluded the umbilical cord for 1 minute every 3 minutes in fetal sheep. Rocha and associates (2004) totally occluded the umbilical cord for 90 seconds every 30 minutes for 3 to 5 hours a day for 4 days without producing necrotic brain cell injury. Results from such studies suggest that the effects of umbilical cord entrapment depend on the degree of occlusion—partial versus total, the duration of individual occlusions, and the frequency of such occlusions.
Human Evidence
The contribution of intrapartum events to subsequent neurological handicaps has been greatly overestimated, as discussed in further detail in Chapter 33 (p. 638). It is clear that for brain damage to occur, the fetus must be exposed to much more than a brief period of hypoxia. Moreover, the hypoxia must cause profound, just barely sublethal metabolic acidemia. Because of this, the American College of Obstetricians and Gynecologists (2012b) recommends umbilical cord blood gases be obtained whenever there is cesarean delivery for fetal compromise, a low 5-minute Apgar score, severe fetal-growth restriction, an abnormal fetal heart rate tracing, maternal thyroid disease, or multifetal gestation (Chap. 32, p. 628). Fetal heart rate patterns consistent with these sublethal conditions are fortunately rare.
Benefits of Electronic Fetal Heart Rate Monitoring
There are several fallacious assumptions behind expectations of improved perinatal outcome with electronic monitoring. One assumption is that fetal distress is a slowly developing phenomenon and that electronic monitoring permits early detection of the compromised fetus. This assumption is illogical—that is, how can all fetuses die slowly? Another presumption is that all fetal damage develops in the hospital. Within the past 20 years, attention has been focused on the reality that most damaged fetuses suffered insults before arrival at labor units. The very term fetal monitor implies that this inanimate technology in some fashion “monitors.” The assumption is made that if a dead or damaged infant is delivered, the tracing strip must provide some clue, because this device was monitoring fetal condition. All of these assumptions led to great expectations and fostered the belief that all neonatal deaths or injuries were preventable.
By the end of the 1970s, questions regarding the efficacy, safety, and costs of electronic monitoring were being voiced from the Office of Technology Assessment, the United States Congress, and the Centers for Disease Control and Prevention. Banta and Thacker (2002) reviewed 25 years of the controversy on the benefits, or lack thereof, of electronic fetal monitoring. Using the Cochrane Database, Alfirevic and colleagues (2013) reviewed 13 randomized trials involving more than 37,000 women. They concluded that electronic fetal monitoring increased the rate of cesarean and operative vaginal deliveries but produced no declines in rates of perinatal mortality, neonatal seizures, or cerebral palsy. Grimes and Peipert (2010) wrote a Current Commentary on electronic fetal monitoring in Obstetrics & Gynecology. They summarized that such monitoring, although it has been used in 85 percent of the almost 4 million annual births in the United States, has failed as a public health screening program. They noted that the positive predictive value of electronic fetal monitoring for fetal death in labor or cerebral palsy is near zero—meaning that “almost every positive test result is wrong.”
There have been two recent attempts to study the epidemiological effects of electronic fetal monitoring in the United States, each using national vital statistics of births linked to infant deaths. Chen and coworkers (2011) used 2004 data on 1,732,211 singleton live births, 89 percent of which underwent electronic fetal monitoring. They reported that monitoring increased operative delivery rates but decreased early neonatal mortality rates. This benefit was gestational age dependent, however, and the highest impact was seen in preterm fetuses. Most recently, Ananth and colleagues (2013) reported a similar but larger epidemiological study using United States birth certificate data linked with infant death certificate data. They studied 57,983,286 nonanomalous singleton livebirths born between 1990 and 2004. The temporal increase in fetal monitoring use between 1990 and 2004 was associated with a decline in neonatal mortality rates, especially in preterm gestations. In an accompanying editorial, Resnik (2013) cautioned that an epidemiological association between fetal monitoring and reduced neonatal death does not establish causation. He suggested that the limitations of the study by Ananth “should make the reader skeptical of the findings.” He opined that the electronic fetal monitoring debate “goes on … and on … and on.” And it does indeed.
Parkland Hospital Experience: Selective versus Universal Monitoring
In July 1982, an investigation began at Parkland Hospital to ascertain whether all women in labor should undergo electronic monitoring (Leveno, 1986). In alternating months, universal electronic monitoring was rotated with selective heart rate monitoring, which was the prevailing practice. During the 3-year investigation, 17,410 labors were managed using universal electronic monitoring, and these outcomes were compared with a similar-sized cohort of women selectively monitored electronically. No significant differences were found in any perinatal outcomes. There was a small but significant increase in the cesarean delivery rate for fetal distress associated with universal monitoring. Thus, increased application of electronic monitoring at Parkland Hospital did not improve perinatal results, but it slightly increased the frequency of cesarean delivery for fetal distress.
Current Recommendations
The methods most commonly used for intrapartum fetal heart rate monitoring include auscultation with a fetal stethoscope or a Doppler ultrasound device, or continuous electronic monitoring of the heart rate and uterine contractions. No scientific evidence has identified the most effective method, including the frequency or duration of fetal surveillance that ensures optimum results. Summarized in Table 24-5 are the recommendations of the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2012). Intermittent auscultation or continuous electronic monitoring is considered an acceptable method of intrapartum surveillance in both low- and high-risk pregnancies. The recommended interval between checking the heart rate, however, is longer in the uncomplicated pregnancy. When auscultation is used, it is recommended that it be performed after a contraction and for 60 seconds. It also is recommended that a 1-to-1 nurse–patient ratio be used if auscultation is employed. The position taken by the American College of Obstetricians and Gynecologists (2013b) in their Practice Bulletin, however, is somewhat different. While acknowledging that the available data do not show a clear benefit for the use of electronic monitoring over intermittent auscultation, the committee recommends limiting use of auscultation to low-risk pregnancies and further recommends recording the fetal heart rate every 15 minutes in active first stage labor and every 5 minutes in the second stage.
TABLE 24-5. Guidelines for Methods of Intrapartum Fetal Heart Rate Monitoring
INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVITY
Analysis of electronically measured uterine activity permits some generalities concerning the relationship of certain contraction patterns to labor outcome. There is considerable normal variation, however, and caution must be exercised before judging true labor or its absence solely from a monitor tracing. Uterine muscle efficiency to effect delivery varies greatly. To use an analogy, 100-meter sprinters all have the same muscle groups yet cross the finish line at different times.
Internal Uterine Pressure Monitoring
Amnionic fluid pressure is measured between and during contractions by a fluid-filled plastic catheter with its distal tip located above the presenting part (Fig. 24-32). The catheter is connected to a strain-gauge pressure sensor adjusted to the same level as the catheter tip in the uterus. The amplified electrical signal produced in the strain gauge by variation in pressure within the fluid system is recorded on a calibrated moving paper strip simultaneously with the fetal heart rate recording (see Fig. 24-6). Intrauterine pressure catheters are now available that have the pressure sensor in the catheter tip, which obviates the need for the fluid column.
FIGURE 24-32 Placement of an intrauterine pressure catheter to monitor contractions and their pressures. A. The white catheter, contained within the blue introducer, is inserted into the birth canal and placed along one side of the fetal head. B. The catheter is then gently advanced into the uterus, and the introducer is withdrawn.
External Monitoring
Uterine contractions can be measured by a displacement transducer in which the transducer button, or “plunger,” is held against the abdominal wall. As the uterus contracts, the button moves in proportion to the strength of the contraction. This movement is converted into a measurable electrical signal that indicates the relative intensity of the contraction. It has generally been accepted to not give an accurate measure of intensity. Bakker and associates (2010) performed a randomized trial comparing internal versus external monitoring of uterine contractions in 1456 women. The two methods were equivalent in terms of operative deliveries and neonatal outcomes.
Patterns of Uterine Activity
Caldeyro-Barcia and Poseiro (1960), from Montevideo, Uruguay, were pioneers who have done much to elucidate the patterns of spontaneous uterine activity throughout pregnancy. Contractile waves of uterine activity were usually measured using intraamnionic pressure catheters. But early in their studies, as many as four simultaneous intramyometrial microballoons were also used to record uterine pressure. These investigators also introduced the concept of Montevideo units to define uterine activity (Chap. 23, p. 458). By this definition, uterine performance is the product of the intensity—increased uterine pressure above baseline tone—of a contraction in mm Hg multiplied by contraction frequency per 10 minutes. For example, three contractions in 10 minutes, each of 50 mm Hg intensity, would equal 150 Montevideo units.
During the first 30 weeks of pregnancy, uterine activity is comparatively quiescent. Contractions are seldom greater than 20 mm Hg, and these have been equated with those first described in 1872 by John Braxton Hicks. Uterine activity increases gradually after 30 weeks, and it is noteworthy that these Braxton Hicks contractions also increase in intensity and frequency. Further increases in uterine activity are typical of the last weeks of pregnancy, termed prelabor. During this phase, the cervix ripens (Chap. 21, p. 410).
According to Caldeyro-Barcia and Poseiro (1960), clinical labor usually commences when uterine activity reaches values between 80 and 120 Montevideo units. This translates into approximately three contractions of 40 mm Hg every 10 minutes. Importantly, there is no clear-cut division between prelabor and labor, but rather a gradual and progressive transition.
During first-stage labor, uterine contractions increase progressively in intensity from approximately 25 mm Hg at commencement of labor to 50 mm Hg at the end. At the same time, frequency increases from three to five contractions per 10 minutes, and uterine baseline tone from 8 to 12 mm Hg. Uterine activity further increases during second-stage labor, aided by maternal pushing. Indeed, contractions of 80 to 100 mm Hg are typical and occur as frequently as five to six per 10 minutes. Interestingly, the duration of uterine contractions—60 to 80 seconds—does not increase appreciably from early active labor through the second stage (Bakker, 2007; Pontonnier, 1975). Presumably, this duration constancy serves fetal respiratory gas exchange. During a uterine contraction, as the intrauterine pressure exceeds that of the intervillous space, respiratory gas exchange is halted. This leads to functional fetal “breath holding,” which has a 60- to 80-second limit that remains relatively constant.
Caldeyro-Barcia and Poseiro (1960) also observed empirically that uterine contractions are clinically palpable only after their intensity exceeds 10 mm Hg. Moreover, until the intensity of contractions reaches 40 mm Hg, the uterine wall can readily be depressed by the finger. At greater intensity, the uterine wall then becomes so hard that it resists easy depression. Uterine contractions usually are not associated with pain until their intensity exceeds 15 mm Hg, presumably because this is the minimum pressure required for distending the lower uterine segment and cervix. It follows that Braxton Hicks contractions exceeding 15 mm Hg may be perceived as uncomfortable because distention of the uterus, cervix, and birth canal is generally thought to produce discomfort.
Hendricks (1968) observed that “the clinician makes great demands upon the uterus.” The uterus is expected to remain well relaxed during pregnancy, to contract effectively but intermittently during labor, and then to remain in a state of almost constant contraction for several hours postpartum. Figure 24-33 demonstrates an example of normal uterine activity during labor. Uterine activity progressively and gradually increases from prelabor through late labor. Interestingly, as shown in Figure 24-33, uterine contractions after birth are identical to those resulting in delivery of the infant. It is therefore not surprising that the uterus that performs poorly before delivery is also prone to atony and puerperal hemorrhage.
FIGURE 24-33 Intrauterine pressure recorded through a single catheter. A. Prelabor. B. Early labor. C. Active labor. D. Late labor. E. Spontaneous activity ½ hour postpartum. F. Spontaneous activity 2½ hours postpartum. (Redrawn from Hendricks, 1968, with permission.)
Origin and Propagation of Contractions
The uterus has not been studied extensively in terms of its nonhormonal physiological mechanisms of function. The normal contractile wave of labor originates near the uterine end of one of the fallopian tubes. Thus, these areas act as “pacemakers” (Fig. 24-34). The right pacemaker usually predominates over the left and starts most contractile waves. Contractions spread from the pacemaker area throughout the uterus at 2 cm/sec, depolarizing the whole organ within 15 seconds. This depolarization wave propagates downward toward the cervix. Intensity is greatest in the fundus, and it diminishes in the lower uterus. This phenomenon is thought to reflect reductions in myometrial thickness from the fundus to the cervix. Presumably, this descending gradient of pressure serves to direct fetal descent toward the cervix and to efface the cervix. Importantly, all parts of the uterus are synchronized and reach their peak pressure almost simultaneously, giving rise to the curvilinear waveform shown in Figure 24-34. Young and Zhang (2004) have shown that the initiation of each contraction is triggered by a tissue-level bioelectric event.
FIGURE 24-34 Schematic representation of the normal contractile wave of labor. Large uterus on the left shows the four points at which intramyometrial pressure was recorded with microballoons. Four corresponding pressure tracings are shown in relation to each other by shading on the small uteri at top. (Adapted from Caldeyro-Barcia, 1960.)
The pacemaker theory also serves to explain the varying intensity of adjacent coupled contractions shown in panels A and B of Figure 24-33. Such coupling was termed incoordination by Caldeyro-Barcia and Poseiro (1960). A contractile wave begins in one cornual-region pacemaker, but does not synchronously depolarize the entire uterus. As a result, another contraction begins in the contralateral pacemaker and produces the second contractile wave of the couplet. These small contractions alternating with larger ones appear to be typical of early labor. Indeed, labor may progress with such uterine activity, albeit at a slower pace. These authors also observed that labor would progress slowly if regular contractions were hypotonic—that is, contractions with intensity less than 25 mm Hg or frequency less than 2 per 10 minutes.
Hauth and coworkers (1986) quantified uterine contraction pressures in 109 women at term who received oxytocin for labor induction or augmentation. Most of these women achieved 200 to 225 Montevideo units, and 40 percent had up to 300 units to effect delivery. The authors suggested that these levels of uterine activity should be sought before consideration of cesarean delivery for presumed dystocia.
New Terminology for Uterine Contractions
This has been recommended by the American College of Obstetricians and Gynecologists (2013b), for the description and quantification of uterine contractions. Normal uterine activity is defined as five or fewer contractions in 10 minutes, averaged over a 30-minute window. Tachysystole was defined as more than five contractions in 10 minutes, averaged over 30 minutes. Tachysystole can be applied to spontaneous or induced labor (Chap. 26, p. 527). The term hyperstimulation was abandoned. Stewart and associates (2012) prospectively studied uterine tachysystole in 584 women undergoing labor induction with misoprostol at Parkland Hospital. There was no association of adverse infant outcomes with increasing number of contractions per 10 minutes or per 30 minutes. Six or more contractions in 10 minutes, however, were significantly associated with fetal heart rate decelerations.
Complications of Electronic Fetal Monitoring
Electrodes for fetal heart rate evaluation and catheters for uterine contraction measurement are both associated with infrequent but potentially serious complications. Rarely, an intrauterine pressure catheter during placement may lacerate a fetal vessel in the placenta. Also with insertion, placental and possibly uterine perforation can cause hemorrhage, serious morbidity, and spurious recordings that have resulted in inappropriate management. Severe cord compression has been described from entanglement with the pressure catheter. Injury to the fetal scalp or breech by a heart rate electrode is rarely severe. However, application at some other site—such as the eye in face presentations—can be serious.
Both the fetus and the mother may be at increased risk of infection from internal monitoring (Faro, 1990). Scalp wounds from the electrode may become infected, and subsequent cranial osteomyelitis has been reported (Brook, 2005; Eggink, 2004; McGregor, 1989). The American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2012) have recommended that certain maternal infections, including human immunodeficiency virus (HIV), herpes simplex virus, and hepatitis B and C virus, are relative contraindications to internal fetal monitoring.
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