Richard A. Bashore, Brian J. Koos
Fetal surveillance during labor is an essential element of good obstetric care. On the basis of antepartum maternal history, physical examination, and laboratory data, 20% to 30% of pregnancies may be designated high risk, and 50% of perinatal morbidity and mortality occurs in this group. However, the remaining 50% occurs in pregnancies that are considered to be normal at the onset of labor.
Methods of Monitoring Fetal Heart Rate
AUSCULTATION OF FETAL HEART RATE
The time-honored technique of evaluating the fetus during labor has been auscultation of the fetal heart. Optimally, auscultation of the fetal heart is performed every 15 minutes after a uterine contraction during the first stage of labor, and at least every 5 minutes in the second stage of labor. Some studies have suggested that intermittent auscultation of the fetal heart is comparable to continuous electronic monitoring in terms of neonatal outcome, if performed at the intervals stated above with a 1:1 patient-to-nurse ratio.
CONTINUOUS ELECTRONIC FETAL MONITORING
Electronic fetal monitoring (EFM) during labor was developed to detect fetal heart rate (FHR) patterns that were frequently associated with delivery of infants in a depressed condition. It was reasoned that early recognition of changes in heart rate patterns that may be associated with such fetal conditions as hypoxia and umbilical cord compression would serve as a warning to enable the physician to intervene and prevent fetal death in utero or irreversible brain injury.
EFM allows continuous reporting of the FHR and uterine contractions (FHR-UC) by means of a monitor that prints results on a two-channel strip chart recorder. Uterine contractions result in a reduction in blood flow to the placenta, which can cause decreased fetal oxygenation and corresponding alterations in the FHR. The FHR-UC record can be obtained using external transducers that are placed on the maternal abdomen. This technique is used in early labor. Internal monitoring is carried out by placing a spiral electrode onto the fetal scalp to monitor heart rate and placing a plastic catheter transcervically into the amniotic cavity to monitor uterine contractions (Figure 9-1). To carry out this technique, the fetal membranes must be ruptured, and the cervix must be dilated to at least 2 cm.
FIGURE 9-1 Technique for continuous electronic monitoring of fetal heart rate and pressure of uterine contractions.
Internal monitoring gives better FHR tracings because the rate is computed from the sharply defined R-wave peaks of the fetal electrocardiogram, whereas with the external technique, the rate is computed from the less precisely defined first heart sound obtained with an ultrasonic transducer. The internal uterine catheter allows precise measurement of the intensity of the contractions in millimeters of mercury, whereas the external tocotransducer measures only frequency and duration, not intensity.
In the clinical setting, internal and external techniques are often combined by using a scalp electrode for precise heart rate recording and the external tocotransducer for contractions. This approach minimizes possible side effects from invasive internal monitoring.
Etiology of Hypoxia, Acidosis, and Fetal Heart Rate Changes
The developing fetus presents a paradox. Its arterial blood oxygen tension is only 25 ± 5 mm Hg compared with adult values of about 100 mm Hg. The rate of oxygen consumption, however, is twice that of the adult per unit weight, and its oxygen reserve is only enough to meet its metabolic needs for 1 to 2 minutes. Blood flow from the maternal circulation, which supplies the fetus with oxygen through placental exchange of respiratory gases, is momentarily interrupted during a contraction. A normal fetus can withstand the temporary reduction in blood flow to the placenta without suffering from hypoxia because sufficient oxygen exchange occurs during the interval between contractions.
Under normal circumstances, the FHR is determined by the atrial pacemaker. Modulation of the rate occurs physiologically through innervation of the heart by the vagus (decelerator) and sympathetic (accelerator) nerves. A fetus whose oxygen supply is marginal cannot tolerate the stress of contractions and will become hypoxic. Under hypoxic conditions, chemoreceptors and baroreceptors in the peripheral arterial circulation of the fetus influence the FHR by giving rise to contraction-related or periodic FHR changes. Hypoxia, when sufficiently severe, will also result in anaerobic metabolism, resulting in the accumulation of pyruvic and lactic acid and causing fetal acidosis. The degree of fetal acidosis can be measured by sampling blood from the presenting part. The pH of fetal scalp blood normally varies between 7.25 and 7.30. Values below 7.20 are considered to be abnormal but not necessarily indicative of fetal compromise. Clinical and experimental data indicate that fetal death occurs when 50% or more of the transplacental oxygen exchange is interrupted.
Fetal oxygenation can be impaired at different anatomic locations within the uteroplacental-fetal circulatory loop. For example, impairment of oxygen transportation to the intervillous space may occur as a result of maternal hypertension or anemia; oxygen diffusion may be impaired in the placenta because of infarction or abruption; or the oxygen content in the fetal blood may be impaired because of hemolytic anemia in Rh-isoimmunization. Figure 9-2 summarizes the clinical conditions that may be associated with fetal distress during labor.
FIGURE 9-2 Clinical conditions associated with fetal distress in labor.
FETAL HEART RATE PATTERNS
The assessment of the FHR depends on an evaluation of the baseline pattern and the periodic changes related to uterine contractions.
This requires determination of the rate (in beats per minute) and the variability. Normal and abnormal rates are listed in Table 9-1. Baseline variability can be divided into short-term and long-term intervals. These are described as follows:
1. Short-term or beat-to-beat variability. This reflects the interval between either successive fetal electrocardiogram signals or mechanical events of the cardiac cycle. Normal short-term variability fluctuates between 5 and 25 beats/minute. Variability below 5 beats/minute is considered to be potentially abnormal. When associated with decelerations, a variability of less than 5 beats/minute usually indicates severe fetal distress.
2. Long-term variability. These fluctuations may be described in terms of the frequency and amplitude of change in the baseline rate. The normal long-term variability is 3 to 10 cycles per minute.Variability is physiologically decreased during the state of quiet sleep of the fetus, which usually lasts for about 25 minutes until transition occurs to another state.
TABLE 9-1 BASELINE FETAL HEART RATES
Periodic Fetal Heart Rate Changes
These are changes in baseline FHR related to uterine contractions. The responses to uterine contractions may be categorized as follows:
1. No change. The FHR maintains the same characteristics as in the preceding baseline FHR.
2. Acceleration. The FHR increases in response to uterine contractions. This is a normal response.
3. Deceleration. The FHR decreases in response to uterine contractions. Decelerations may be early, late, variable, or mixed. All except early decelerations are abnormal.
Types of Patterns
EARLY DECELERATION (HEAD COMPRESSION)
This pattern usually has an onset, maximum fall, and recovery that are coincident with the onset, peak, and end of the uterine contraction (Figure 9-3). The nadir of the FHR coincides with the peak of the contraction. This pattern is seen when engagement of the fetal head has occurred. Early decelerations are not thought to be associated with fetal distress. The pressure on the fetal head leads to increased intracranial pressure that elicits a vagal response similar to the Valsalva maneuver in the adult. The vagal reflex can be abolished by the administration of atropine, but this approach is not used clinically.
FIGURE 9-3 Early deceleration on electronic fetal monitoring tracing. Note that the deceleration starts and ends with the uterine contraction. Good beat-to-beat variability is demonstrated.
LATE DECELERATION (UTEROPLACENTAL INSUFFICIENCY)
This pattern has an onset, maximal decrease, and recovery that are shifted to the right in relation to the contraction (Figure 9-4). The severity of late decelerations is graded by the magnitude of the decrease in FHR at the nadir of the deceleration (Table 9-2). Fetal hypoxia and acidosis are usually more pronounced with severe decelerations. Severe repetitive late decelerations usually indicate fetal metabolic acidosis, low arterial pH, and increased base deficit values. The partial pressure of carbon dioxide (PCO2) in the fetal blood is usually in the normal range, and the fetal blood oxygen partial pressure (PO2) is only slightly below normal because of the Bohr effect—the shift to the left of the oxygen dissociation curve caused by the acidosis.
FIGURE 9-4 Late decelerations on electronic fetal monitoring tracing as would be recorded with a severely distressed fetus. Note the fetal tachycardia, decreased beat-to-beat heart rate variability, and the late decelerations (upper panel). Uterine contractions are recorded in the lower panel.
TABLE 9-2 PRINCIPLES OF GRADING LATE AND VARIABLE DECELERATIONS
VARIABLE DECELERATION (CORD COMPRESSION)
This pattern has a variable time of onset and a variable form and may be nonrepetitive. Variable decelerations are caused by umbilical cord compression. Partial or complete compression of the cord causes a sudden increase in blood pressure in the central circulation of the fetus. The bradycardia is mediated by baroreceptors and is a reflex resulting in a rapid drop in heart rate and, depending upon duration, quickly returns to baseline. This reflex can be abolished or ameliorated by atropine (e.g., chemical vagotomy), although this approach is not used clinically. Fetal blood gases indicate respiratory acidosis with a low pH and high CO2. When cord compression has been prolonged, hypoxia is also present, showing a picture of combined respiratory and metabolic acidosis in fetal blood gases.
The severity of variable decelerations is graded by their duration (see Table 9-2). When the FHR falls below 80 beats/minute during the nadir of the deceleration, there is usually a loss of the P wave in the fetal electrocardiogram, indicating a nodal rhythm or a second-degree heart block.
COMBINED OR MIXED PATTERNS
These patterns may be difficult to define and may exhibit characteristics of any of the aforementioned patterns.
DECREASED BEAT-TO-BEAT VARIABILITY
A flat baseline can be the result of several conditions: fetal acidosis, quiet sleep state, or maternal sedation with drugs.
Strategies for Intervention
A normal FHR pattern on the electronic monitor indicates a greater than 95% probability of fetal well-being. Abnormal patterns, or nonreassuring patterns, may occur in the absence of fetal distress. The false-positive rate (i.e., good Apgar scores and normal fetal acid-base status in the presence of abnormal FHR patterns) is as high as 80%. Therefore, electronic fetal monitoring is a screening rather than a diagnostic technique. Failure to appreciate this limitation may lead to inappropriate intervention and contribute to a high rate of cesarean deliveries.
Strategies for intervention always depend on the clinical circumstances. When abnormal FHR patterns are seen, the first step should be a search for the underlying cause. When the cause is identified, such as maternal hypotension, steps should be taken to correct the problem. In general, a term-sized fetus tolerates ominous fetal heart patterns better than a preterm fetus. A fetus with additional risk factors, such as intrauterine infection from chorioamnionitis, may deteriorate sooner than a fetus in a normal parturient. Other considerations in the management of fetal distress include the maternal condition and the stage of labor.
The most frequently encountered abnormal FHR pattern is that of variable decelerations. A change in maternal position to the right or left side generally relieves fetal pressure on the cord and abolishes the decelerations. One hundred percent oxygen should be given by face mask to the mother. If the pattern is persistent, placing the mother in the Trendelenburg position or elevating the presenting part by vaginal examination may be tried. If an oxytocic infusion is running, it should be discontinued. A tocolytic agent such as terbutaline may also be used to diminish uterine activity.
Variable decelerations of severe degree are most frequently seen during the second stage of labor, with the patient pushing during uterine contractions. Amnioinfusion, which is the replacement of amniotic fluid with normal saline infused through a transcervical intrauterine pressure catheter, has been reported to decrease both the frequency and severity of variable decelerations. Amnioinfusion results in reduced cesarean deliveries for fetal distress and fewer low Apgar scores at birth without apparent maternal or fetal distress. The use of a double-lumen uterine catheter is recommended because it allows a continuous infusion while simultaneously measuring uterine tone to guard against overdistention from excessive fluid accumulation.
If cervical dilation and station permit, the safest intervention for compression of the umbilical cord is assisted vaginal delivery. Cesarean delivery is indicated for severe, repetitive decelerations and an FHR tracing indicative of developing acidosis. Another circumstance that may require intervention is a prolonged deceleration. This condition occurs when the FHR falls to 60 to 90 beats/minute for more than 2 minutes.
NONREACTIVE FETAL HEART RATE TRACING
A nonreactive tracing with loss of FHR accelerations and lack of beat-to-beat variability needs further evaluation because it may be associated with fetal acidosis. By placing an artificial larynx with 120 dB of sound on the maternal abdomen in the vicinity of the vertex, acoustic stimulation can be used to try to induce FHR accelerations. A response of greater than 15 beats/minute lasting at least 15 seconds always ensures the absence of fetal acidosis. Conversely, the likelihood of acidosis in the fetus who fails to respond to such stimulation is about 50%.
Late decelerations of the FHR are most commonly seen in pregnancies associated with uteroplacental insufficiency. The following steps should be taken in rapid succession:
1. Change the maternal position from supine to left or right lateral. The supine hypotension syndrome is caused by compression of the vena cava and aorta by the heavy uterus, leading to lowering of maternal cardiac output and underperfusion of the placenta. In addition, the weight of the term uterus can compress the internal and external iliac vessels, resulting in poor perfusion of the uterus and fetal bradycardia. When this occurs, the femoral pulse cannot be palpated on the affected side. This is called the Posiero effect.
2. Give oxygen by face mask. This can increase fetal PO2 by 5 mm Hg.
3. Stop any oxytocic infusion to exclude uterine hyperstimulation
4. Inject intravenously a bolus of a tocolytic drug (e.g., magnesium sulfate, 2.0 g, or terbutaline, 0.25 mg) to relieve uterine tetany.
5. Monitor maternal blood pressure to exclude hypotensive episodes that can occur as a consequence of epidural analgesia.
6. Notify personnel that operative delivery may be necessary.
When late decelerations persist for more than 30 minutes despite these resuscitative efforts and the FHR pattern suggests developing acidosis, operative delivery is indicated.
As a baseline change, tachycardia is not a very reliable sign of fetal distress. In general, fetal tachycardia occurs to improve placental circulation when the fetus is stressed. Brief periods of tachycardia (15 to 30 minutes) are usually associated with excessive oxytocic augmentation of labor, after which the heart rate returns to baseline when the augmentation is discontinued. Prolonged periods of tachycardia are usually associated with elevated maternal temperature or an intrauterine infection, which should be ruled out. The fetal tachycardia improves perfusion of the placenta to allow a greater exchange of excess heat to the mother’s circulation (placenta acts as a radiator). The acid-base status is usually normal.
The presence of meconium in the amniotic fluid may be a sign of fetal distress. Classification of meconium into early and late passage facilitates a clearer understanding of its importance.
Early passage occurs any time before rupture of the membranes and is classified as light or heavy, based on its color and viscosity. Light meconium is lightly stained yellow or greenish amniotic fluid. Heavy meconium is dark green or black and is usually thick and tenacious. Light passage is not associated with poor outcome. Heavy passage is associated with lower 1- and 5-minute Apgar scores and is associated with the risk for meconium aspiration.
Late passage usually occurs during the second stage of labor, after clear amniotic fluid has been noted earlier. Late passage, which is most often heavy, is usually associated with some event (e.g., umbilical cord compression or uterine hypertonus) late in labor that causes fetal distress.
A decrease in meconium-related respiratory complications in the infants of patients who receive amnioinfusion has been reported, presumably as a result of the dilutional effect of the infused fluid. A common technique is to infuse a bolus of up to 800 mL of normal saline at a rate of 10 to 15 mL/minute over a period of 50 to 80 minutes through an intrauterine catheter. This is followed by a maintenance dose of 3 mL/minute until delivery. Overdistention of the uterine cavity can be avoided by maintaining the baseline uterine tone in the normal range and at less than 20 mm Hg.
Fetal Blood Sampling
Fetal scalp blood sampling for pH determination has been used when clinical parameters, such as heavy meconium, are present or when FHR patterns are suggestive of acidosis, but is not the standard of practice in many centers. Fetal scalp pH correctly predicts neonatal outcome in 82% of cases as determined by the Apgar score. The false-positive rate is about 8% and the false-negative rate about 10%. Blood is obtained from the fetus by placing an amnioscope transvaginally against the fetal skull (Figure 9-5). Cervical mucus is removed with cotton swabs. Silicone grease is applied to the skull for blood bead formation. A 2 × 2-mm lancet is used for a stab incision, and a drop of blood is aspirated into a long heparinized capillary tube.
FIGURE 9-5 Technique of fetal scalp blood sampling with an amnioscope still used in many centers. After making a small stab incision in the fetal scalp, the blood is drawn off through a long capillary tube.
UMBILICAL CORD BLOOD SAMPLING
The Apgar scoring system has been classically used to assess the newborn condition. Over time, however, the Apgar score has come to be used inappropriately to define asphyxia, which is a misapplication, because many other conditions (e.g., prematurity, maternal drug administration) can result in low scores that are not reflective of asphyxia. Asphyxia implies hypoxia of sufficient degree to cause metabolic acidosis. Thus, the Apgar score alone cannot be used to define asphyxia. A more appropriate tool for defining this condition is assessment of the fetal and neonatal acid-base status. Normal ranges for these indices are given in Table 9-3. One reasonable protocol for umbilical cord blood pH and blood gas analysis is as follows:
1. Doubly clamp a segment of umbilical cord immediately after birth in all preterm deliveries and in term deliveries in which fetal distress is suspected and in cases in which the 1- or 5-minute APGAR score is low (<7).
2. If a specimen cannot be obtained from the umbilical artery, obtain a specimen from an artery on the chorionic surface of the placenta.
TABLE 9-3 NORMAL RANGES FOR FETAL SCALP AND CORD BLOOD INDICES
Ultrasonic Doppler velocimetry, for blood flow measurements in umbilical and fetal blood vessels, and percutaneous umbilical blood sampling (PUBS) have been used antepartum, but are generally not feasible methods for labor management.
Newborn cerebral dysfunction, manifested as seizures and attributable to true birth asphyxia, does not seem to occur unless the Apgar score at 5 minutes is 3 or less, the umbilical artery blood pH is less than 7, and resuscitation is necessary at birth. The later onset of cerebral palsy can occur without these abnormalities and may be attributed to untoward events occurring earlier in the pregnancy or intrapartum infection in which various cytokines can affect the fetal brain. The impact of lesser degrees of asphyxia, as measured by the Apgar score and acid-base status at birth, requires further study. Figure 9-6 is an algorithm for the management of abnormal heart rate tracings during fetal monitoring.
FIGURE 9-6 Algorithm for the management of an abnormal heart tracing during fetal monitoring.
Complications of Fetal Monitoring
The introduction of a catheter into the uterine cavity and application of a scalp electrode may cause a slight increase in the incidence of maternal infection, but length of labor, rupture of the membranes, and the number of vaginal examinations are of much greater importance in this regard. The incidence of fetal scalp abscesses and soft tissue injuries from electrode applications is less than 5%. Scalp abscesses are managed by opening the intradermal vesicle to allow drainage. Always consider herpes simplex virus as a cause of the lesion in patients with a history of recurrent vaginal or labial herpes. These small abscesses heal without the need for antibiotic therapy. Spread of the infection into adjacent tissues is rare.
The incidence of scalp abscesses from microblood sampling is less frequent than infection from electrode application. After fetal scalp blood sampling, a cotton swab should always be applied throughout the next uterine contraction and the puncture site inspected for hemostasis during the second contraction. If these precautions are followed, hemorrhage does not occur with scalp blood sampling.
Controversies about Fetal Monitoring in the Diagnosis and Treatment of Fetal Distress
After more than 35 years of routine use of electronic monitoring for assessing FHR in labor, there is still no conclusive evidence of its advantage in long-term fetal outcome. In 12 prospective, randomized, controlled trials involving more than 55,000 infants worldwide, EFM appears to have little documented benefit over intermittent auscultation with respect to perinatal mortality and long-term neurologic outcome. The increase in the rate of cesarean deliveries in the United States and elsewhere during recent decades has not been reflected in a decrease in the incidence of cerebral palsy.
The prevalence of intrapartum fetal asphyxia is of the order of 2%. Most of these children have no evidence of brain damage.
When the decision has been made to monitor the FHR, the particular method used can be left to the woman and her obstetrician. Both intermittent and continuous monitoring of the heart rate are regarded as acceptable by the American College of Obstetricians and Gynecologists. Either method will have a similar outcome in terms of the overall incidence of long-term neurologic damage, including cerebral palsy. Intrapartum events appear to play only a small part in the overall incidence of this disorder. Newer methods must be introduced to determine the actual prenatal event, or unrecognized intrapartum event (e.g., chorioamnionitis), that leads to cerebral palsy.
Despite the “intensive obstetrics” of the past 30 years, with increasing attention directed to prenatal care, reduction of birth trauma, and greater use of cesarean birth for high-risk deliveries, the frequency of cerebral palsy has remained unchanged at about 2 cases per 1000 term infants. There is a pressing need to inform the public, as well as the medical profession, that cerebral palsy is probably not caused by events during labor, and that the cause in most cases remains unknown.
The current technical approaches to fetal assessment are likely to remain. There are many common conditions in obstetrics in which evaluation of uterine contractility is of primary interest to the physician, with FHR being of secondary significance. Among the indications for contraction measurements are arrest disorders of labor. In patients who undergo induction of labor for maternal or fetal reasons, the contraction response to oxytocic stimulation can be quantified in Montevideo units, which many physicians prefer to palpation of the uterus.
Until new concepts for monitoring are validated, the type of fetal monitoring needs to take into consideration the wishes of the informed patient, the capabilities of the nursing service to carry out monitoring, and the requirements of the physician managing the labor.
American College of Obstetricians and Gynecologists. ACOG Practice Bulletin. Intrapartum Fetal Heart Rate Monitoring. Obstet Gynecol. 2005;106:1453-1461.
Liston R., Sawchuck D., Young D. Society of Obstetricians and Gynecologists of Canada: British Columbia Perinatal Health Program. Fetal health surveillance guideline: Antenatal and intrapartum consensus. [Erratum in: J Obstet Gynaecol Can 29:909, 2007.]. J Obstet Gynaecol Can. 2007;29:S3-S56.
Olagundoye V., Black R., Mackenzie I.Z. Impact of the severity of fetal distress on decision-to-delivery intervals for assisted vaginal delivery. J Obstet Gynaecol. 2008;28:51-55.
Parer J.T., Ideda T. A framework for standardized management of intrapartum fetal heart rate patterns. Am J Obstet Gynecol. 197, 2007. 26e1–26e6
Wilson R.D. Fetal health surveillance guideline: Antenatal and intrapartum consensus. J Obstet Gynaecol Can. 2007;29:912.