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. There is no scientific evidence that has identified the most effective method, including frequency or duration of fetal surveillance, that ensures optimum results.
ELECTRONIC FETAL HEART RATE MONITORING
With internal monitoring the fetal heart rate may be measured by attaching a bipolar spiral electrode directly to the fetus. The electrical fetal cardiac signal is amplified and fed into a cardiotachometer. Time intervals between successive fetal R waves are used by the cardiotachometer to compute an instantaneous fetal heart rate.
The necessity for membrane rupture and uterine invasion may be avoided by use of external (indirect) electronic monitors to measure fetal heart action and uterine activity. However, external monitoring does not provide the precision of fetal heart measurement or the quantification of uterine pressure afforded by internal monitoring. The fetal heart rate is detected through the maternal abdominal wall using the ultrasound Doppler principle. Ultrasonic waves undergo a shift in frequency as they are reflected from moving fetal heart valves and from pulsatile blood ejected during systole. Care should be taken that maternal aortic pulsations are not confused with fetal cardiac motion.
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. In 1997, the National Institute of Child Health and Human Development Fetal Monitoring Workshop brought together investigators with expertise in the field to propose standardized, unambiguous definitions for interpretation of fetal heart rate patterns during labor (Table 13-1). The definitions proposed as a result of this workshop will be used in this chapter. It is important to recognize that interpretation of electronic fetal heart rate data is based upon 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 (bpm) per vertical centimeter (range, 30 to 240 bpm) and 3 cm/min chart recorder paper speed (see Figure 13-1).
TABLE 13-1. The National Institute of Child Health and Human Development Research Planning Workshop Definitions of Fetal Heart Rate Patterns
FIGURE 13-1 Fetal heart rate obtained by scalp electrode (upper panel) and recorded at 1 cm/min compared with that of 3 cm/min chart recorder paper speed. Concurrent uterine contractions are shown in the (lower panel).
Baseline Fetal Heart Activity
Baseline fetal heart activity 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 the sinusoidal fetal heart rate.
With increasing fetal maturation, the heart rate decreases. The baseline fetal heart rate decreases an average of 24 bpm between 16 weeks and term, or approximately 1 bpm/wk. It is postulated that this normal gradual slowing of the fetal heart rate corresponds to maturation of parasympathetic (vagal) heart control.
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 to be the result of tonic balance between accelerator and decelerator influences on pacemaker cells. Heart rate is also under the control of arterial chemoreceptors such that both hypoxia and hypercapnia can modulate rate.
Baseline variability is an important index of cardiovascular function and appears to be regulated largely by sympathetic and parasympathetic control of the sinoatrial node. Short-term variability reflects the instantaneous change in fetal heart rate from one beat (or R wave) to the next. It 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 that occur during the course of 1 minute and result in the waviness of the baseline. The normal frequency of such waves is 3 to 5 cycles/min. The criteria shown in Figure 13-2 are recommended for quantification of baseline variability. It is important to remember that diminished beat-to-beat variability (5 bpm or less) can be an ominous sign indicating a seriously compromised fetus. In fact, it is generally believed that reduced baseline heart rate variability is the single most reliable sign of fetal compromise.
FIGURE 13-2 Panels 1–4: Grades of baseline fetal heart rate variability–irregular fluctuations in the baseline of two cycles per minute or greater. 1. Undetectable, absent variability. 2. Minimal variability, ≤5 beats/min. 3. Moderate (normal) variability, 6 to 25 beats/min. 4. Marked variability, >25 beats/min. Panel 5: Sinusoidal pattern. The sinusoidal pattern 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: Electronic fetal heart rate monitoring: Research guidelines for integration. Am J Obstet Gynecol 177:1385, 1997.)
Sinusoidal Heart Rates
A true sinusoidal pattern such as that shown in panel 5 of Figure 13-2 may be observed with serious fetal anemia, whether from D-isoimmunization, ruptured vasa previa, fetomaternal hemorrhage, or twin-to-twin transfusion. Insignificant sinusoidal patterns have been reported following administration of meperidine, morphine, alphaprodine, and butorphanol.
Periodic Fetal Heart Rate Changes
Periodic fetal heart rate changes are deviations from baseline related to uterine contractions. Such deviations are termed accelerations or decelerations.
An acceleration is a visually apparent abrupt increase in the fetal heart rate baseline. 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. Finally, accelerations can occur during labor without any apparent stimulus. Indeed, accelerations are common in labor and 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. The absence of accelerations during labor, however, is not necessarily an unfavorable sign unless coincidental with other nonreassuring changes.
Early deceleration of the fetal heart rate is a gradual decrease and return to baseline associated with a contraction (Figure 13-3). The slope of the fetal heart rate change is gradual (defined as onset of deceleration to nadir lasting at least 30 seconds), resulting in a curvilinear and symmetrical waveform. Typically, early decelerations are a result of fetal head compression, which probably causes vagal nerve activation due to dural stimulation. Early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores.
FIGURE 13-3 Features of early fetal heart rate deceleration. Characteristics include gradual decrease 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 onset of the deceleration. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)
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 peak of the contraction and returning to baseline only after the contraction has ended. In most cases the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively (Figure 13-4). The magnitude of late decelerations is rarely more than 30 to 40 bpm below baseline and typically not more than 10 to 20 bpm in intensity.
FIGURE 13-4 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. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)
A large number of 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 due to oxytocin stimulation. Maternal diseases such as hypertension, diabetes, and collagen-vascular disorders can cause chronic placental dysfunction. Placental abruption can cause acute and severe late decelerations.
The most common deceleration patterns encountered during labor are variable decelerations attributed to umbilical cord occlusion. Variable deceleration of the fetal heart rate is defined as a visually apparent abrupt decrease (onset of deceleration to nadir lasting less than 30 seconds) in rate. The onset of deceleration commonly varies (hence “variable”) with successive contractions (Figure 13-5). The duration of deceleration is less than 2 minutes. Significant variable decelerations have been defined as those decreasing to less than 70 bpm and lasting more than 60 seconds.
FIGURE 13-5 Features of variable fetal heart rate decelerations. Characteristics include abrupt decrease in the heart rate with onset commonly varying with successive contractions. The decelerations measure ≤15 beats/min for 15 seconds or longer with an onset-to-nadir phase of less than 30 seconds. Total duration is less than 2 minutes. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)
These are defined as isolated decelerations lasting 2 minutes or longer, but less than 10 minutes from onset to return to baseline (Figure 13-6). Some of the more common causes include cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension.
FIGURE 13-6 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. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)
Epidural, spinal, or paracervical analgesia are frequent causes of prolonged deceleration of the fetal heart rate. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia due to 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.
Second-Stage Labor Fetal Heart Rate Patterns
Decelerations are virtually ubiquitous during the second stage of labor. Both cord compression and fetal head compression have been implicated as causing decelerations and baseline bradycardia during second-stage labor. A consequence of the high incidence of such patterns is difficulty identifying true fetal jeopardy. That said, an 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.
OTHER INTRAPARTUM ASSESSMENT TECHNIQUES
Fetal Scalp Blood Sampling
Measurement of the pH in capillary scalp blood may help identify the fetus in serious distress (Figure 13-7). If the pH is greater than 7.25, labor is observed. If the pH is between 7.20 and 7.25, the pH measurement is repeated within 30 minutes. If the pH is less than 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. Perhaps in part due to the cumbersome nature of the procedure, fetal scalp sampling is uncommonly used.
FIGURE 13-7 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. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010. Adapted from Hamilton LA Jr, McKeown MJ: Biochemical and electronic monitoring of the fetus. In Wynn RM (ed). Obstetrics and Gynecology Annual. 1973. New York: Appleton-Century-Crofts; 1974.)
Acceleration of the heart rate in response to stimulation has been associated with a normal scalp blood pH. Conversely, failure to provoke acceleration is not uniformly predictive of fetal acidemia.
This technique involves use of an electronic artificial larynx placed a centimeter or so from, or directly onto, the maternal abdomen. 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 with prolonged fetal movements.
Fetal Pulse Oximetry
Using technology similar to that of adult pulse oximetry, instrumentation has been developed that allows measurement of fetal oxyhemoglobin saturation once the membranes are ruptured. The device was designed to be used in labors complicated by a nonreassuring fetal heart rate pattern in order to improve the reliability of the assessment of fetal well-being. Current evidence from randomized, multicentered trials, however, suggests that use of the device is not associated with a reduction in the rate of cesarean delivery or improvement in neonatal outcome.
DIAGNOSIS OF FETAL DISTRESS
Identification of fetal distress based upon fetal heart rate patterns is imprecise and controversial. Experts in interpretation of these patterns often disagree with each other. The interpretation system recommended in 2008 by the National Institute of Child Health and Development is shown in Table 13-2.
TABLE 13-2. Three-Tier Fetal Heart Interpretation System Recommended by the 2008 NICHD Workshop on Electronic Fetal Monitoring
Clinical management for nonreassuring fetal heart rate patterns consists of correcting the potential fetal insult, if possible. Management measures for nonreassuring fetal heart rate patterns are shown in Table 13-3.
TABLE 13-3. Initial Evaluation and Treatment of Nonreassuring Fetal Heart Rate Patterns
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 for this action is that inhibition of uterine contractions might improve fetal oxygenation, thus achieving in-utero resuscitation.
Given that variable fetal heart rate decelerations are associated with cord compression in the setting of decreased amnionic fluid, replenishment of fluid with saline, or amnioinfusion, has been developed as a potential treatment for variable decelerations attributed to cord entrapment. Amnioinfusion has also been used prophylactically in cases of known oligohydramnios as well as in attempts to dilute thick meconium. Many different amnioinfusion protocols have been developed, but most include a 500- to 800-mL bolus of warmed normal saline followed by a continuous infusion of approximately 3 mL per hour. The results of clinical studies of amnioinfusion have been mixed and complications such as uterine hypertonus, infection, and uterine rupture have been reported.
MECONIUM IN THE AMNIONIC FLUID
Obstetrical teaching for more than a century has included the concept that meconium passage is a potential warning of fetal asphyxia. Obstetricians, however, have also long realized that the detection of meconium during labor is problematic in the prediction of fetal distress or asphyxia. Indeed, although 12 to 22 percent of human labors are complicated by meconium, few such labors are linked to infant mortality.
Three theories have been suggested to explain fetal passage of meconium and may, in part, explain the tenuous connection between the detection of meconium and infant mortality. The pathological explanation proposes that fetuses pass meconium in response to hypoxia, and that meconium therefore signals fetal compromise. Alternatively, in-utero passage of meconium may represent normal gastrointestinal tract maturation under neural control. Third, meconium passage could also follow vagal stimulation from common but transient umbilical cord entrapment and resultant increased peristalsis. Thus, fetal release of meconium may also represent physiological processes.
The aspiration of some amnionic fluid before birth is most likely a physiological event also. Unfortunately, this normal process can result in the inhalation of meconium-stained fluid, which, in some cases, may lead to subsequent respiratory distress and hypoxia. In spite of the fact that meconium staining of the amnionic fluid is quite common, meconium aspiration syndrome is quite rare. Meconium aspiration syndrome is associated with fetal acidemia at birth.
FETAL HEART RATE PATTERNS AND BRAIN DAMAGE
In humans, the contribution of intrapartum events to subsequent neurological handicaps has been greatly overestimated. From the evidence to date, the following conclusions can be drawn regarding intrapartum brain injury in humans: (1) There is not a single unique fetal heart rate pattern that is associated with fetal neurological injury; (2) the majority of term infants with neonatal encephalopathy due to fetal acidemia are associated with events beyond the control of the obstetrician; (3) for brain damage to occur, the fetus must be exposed to more than a brief period of hypoxia; and (4) the metabolic acidemia necessary to produce neurological injury must be profound.
INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVITY
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. Intrauterine pressure catheters are also available that have the pressure sensor in the catheter tip, which obviates the need for the fluid column.
Uterine contractions can also be measured by a displacement transducer in which the transducer button (“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 does not give an accurate measure of intensity.
Patterns of Uterine Activity
Uterine contractility is commonly expressed in terms of Montevideo units. 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 (Figure 13-8).
FIGURE 13-8 Calculation of Montevideo units. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010.)
For further reading in Williams Obstetrics, 23rd ed.,
see Chapter 18, “Intrapartum Assessment.”