What is the most likely cause for early decelerations in the fetal heart rate (fhr) pattern?

Fetal Heart Rate Tracing

FHR monitoring is most commonly accomplished with a surface Doppler ultrasound transducer (external monitoring), but it may be necessary to apply a fetal scalp electrode to obtain accurate continuous FHR monitoring (internal monitoring). For internal monitoring, a peak or threshold voltage of the fetal R wave from the scalp electrode is used to measure FHR. Of note, a fetal scalp electrode can be placed only if the cervix is minimally dilated and the membranes are ruptured. The FHR pattern changes in response to fetal asphyxia from activation of peripheral and central chemoreceptors and baroreceptors.76 It also shows changes as a result of various fetal brain metabolic changes that occur with asphyxia.76 These changes in the FHR produce specific patterns and characteristics that provide an evaluation of the fetal state.

The FHR tracing is used as a nonspecific reflection of fetal acidosis. It should be interpreted over a time course in relation to the clinical context and other known maternal and fetal comorbidities, because multiple factors other than fetal acidosis can influence the FHR tracing.Box 62.1 defines FHR baseline, variability, and accelerations. A normal baseline FHR ranges from 110 to 160 bpm. FHR variability are fluctuations in the baseline FHR that are irregular in frequency and amplitude. Normal FHR variability predicts early neonatal health and a fetal central nervous system that is normally interacting with the fetal heart. Accelerations are abrupt changes in the FHR above baseline and are defined by gestational age of the fetus.

Fig. 62.3 details FHR tracing deceleration characteristics. Late decelerations are a result of uteroplacental insufficiency causing relative fetal brain hypoxia during a contraction. The resulting sympathetic outflow elevates the fetal blood pressure and activates the fetal baroreceptors and an associated slowing in the FHR. A second type of late deceleration is from myocardial depression in the presence of increasing hypoxia.77 Therefore late decelerations are considered worrisome. On the other hand, early decelerations are considered benign and tend to mirror the uterine contraction and are believed to be in response to vagal stimuli, which are often the result of fetal head compression. Variable decelerations are associated with umbilical cord compression. A sinusoidal FHR pattern is associated with fetal anemia and is considered ominous.78 In general, minimal-to-undetectable FHR variability in the presence of variable or late decelerations is associated with fetal acidosis.79 Prolonged decelerations (<70 beats/min for >60 seconds) are associated with fetal acidemia and are extremely ominous, particularly with the absence of variability.80

Tachycardia

The fetal heart rate baseline evaluation must also take gestational age into account, as with fetal heart rate reactivity. Vagal activity has a greater influence on fetal heart rate at baseline as gestation advances; thus baseline fetal heart rate will decrease from an average of 155 beats/min at 20 weeks to 145 beats/min at 30 weeks. The most common etiology of fetal tachycardia is maternal-fetal fever secondary to maternal-fetal infection such as chorioamnionitis. Other causes include chronic hy­poxemia, maternal hyperthyroidism, and fetal tachyarrhythmia. Fetal heart rates above 200 beats/min, and certainly above 220 beats/min, should increase the index of suspicion of fetal tachyarrhythmia and lead to further fetal cardiac evaluation with a targeted fetal echocardiogram. For fetal heart rates between 160 and 180 beats/min, the presence or absence of baseline variability is an important indicator of fetal acid-base status. Fetal acidosis is more likely if baseline variability is absent.69

Management of Non–Category I FHR Patterns During Labor

The evaluation of a category II or III pattern begins with a search for an underlying etiology that would itself require immediate delivery. For example, an acute change in the FHR pattern with prolonged deceleration (Fig. 12.10) could have occurred secondary to umbilical cord prolapse, placental abruption, or uterine rupture. In the absence of such events, one should search for a remediable cause of the concerning FHR tracing. Uterine perfusion is very sensitive to maternal blood pressure, and even relative redistributions of maternal blood flow, such as can occur after the initiation of regional anesthesia, can impact the FHR pattern. Abnormal FHR patterns may also result from contractions that are too frequent in timing to allow for recovery between them. The occurrence of uterine contractions more frequently than 5 in 10 minutes, averaged over 30 minutes, is generally referred to as tachysystole (Fig. 12.11) and can occur as a consequence of labor induction agents. When the tachysystole is resolved, either by discontinuing or decreasing an oxytocin infusion or administering a tocolytic, the fetal status typically improves. Maternal position in labor can affect the FHR tracing, because the supine position decreases uterine blood flow and placental perfusion. Repositioning a patient to the lateral recumbent position can improve a concerning FHR pattern with no other intervention. Supplemental oxygen therapy for the mother should also be administered. When recurrent variable decelerations are present, amnioinfusion, in which fluid is infused into the uterine cavity, has been shown to decrease the rate of variable decelerations and cesarean delivery for nonreassuring fetal status.10 When faced with a concerning FHR tracing with no clear secondary cause and which persists despite attempts at conservative management, some options do exist for additional reassurance, because many of these fetuses will still have a normal acid-base status secondary to the imprecision of continuous FHR monitoring. An acceleration in FHR after vibroacoustic stimulation or fetal scalp stimulation with a digital examination provides reliable reassurance of a normal fetal pH and allows labor to continue. Blood sampling from the fetal scalp can be used to assess the fetal pH or lactate directly, although this is invasive and uncommonly performed in contemporary practice.

Many FHR tracings will remain indeterminate without either a reversible cause or additional reassurance from scalp stimulation or pH measurement. Management of these cases is complicated and depends upon the exact clinical circumstances, including the stage and progress of labor. Because of this common scenario there has been longstanding interest in technological advancements to provide additional information regarding the fetal status. The two areas of greatest promise had been the fetal pulse oximetry and ST segment analysis. Unfortunately, neither of these technologies has demonstrated a reduction in cesarean delivery or neonatal outcomes in large clinical trials. Specifically, a randomized trial of ST segment analysis in 11,108 subjects was published in 2015 and demonstrated no differences in either composite neonatal morbidity or cesarean delivery between open and masked monitoring.2

Physiology

Baseline FHR is regulated by intrinsic cardiac pacemakers (sinoatrial node, atrioventricular node), cardiac conduction pathways, autonomic innervation (sympathetic, parasympathetic), intrinsic humoral factors (catecholamines), extrinsic factors (medications), and local factors (calcium, potassium). Sympathetic innervation and plasma catecholamines increase baseline FHR, whereas parasympathetic innervation reduces the baseline rate. Autonomic input regulates the FHR in response to fluctuations in the partial pressure of oxygen (PO2), partial pressure of carbon dioxide (PCO2), and blood pressure detected by chemoreceptors and baroreceptors located in the aortic arch and carotid arteries. A normal FHR baseline of 110 to 160 beats/min is consistent with normal neurologic regulation of the FHR. Fetal tachycardia is defined as a baseline rate above 160 beats/min for at least 10 minutes. Conditions potentially associated with fetal tachycardia are summarized in Box 15-5.

Fetal bradycardia is defined as a baseline rate below 110 beats/min for at least 10 minutes. Box 15-6 summarizes conditions associated with fetal bradycardia.

Fetal Heart Rate Analysis

The traditional NST is a visually analyzed record of the FHR baseline, variability, and episodic changes. Normal FHR characteristics are determined by gestational age, maturational and functional status of central regulatory centers, and oxygen tension. A “reactive” NST exhibits two 15-beat accelerations above the baseline maintained for 15 seconds in a 30-minute monitoring period. When the NST is analyzed as part of the five-component BPP reactivity criteria that account for gestational age are applied (see later).Irrespective of the context, a “reactive” NST indicates absence of fetal acidemia at the moment of the FHR recording. Many growth-restricted fetuses with a normal heart rate tracing can have low-normal pO2 values, but acidemia is virtually excluded by a reactive NST. Heart rate reactivity also correlates highly with a fetus not in immediate danger of intrauterine demise. Nonreactive NST results, on the other hand, are often falsely positive and require further evaluation. The development of repetitive decelerations may reflect fetal hypoxemia or cord compression as a result of the development of oligohydramnios and have been associated with a high perinatal mortality rate.58

The CST is an additional option for testing placental respiratory reserve.59 Positive CST results have been reported in 30% of pregnancies complicated by proven growth restriction.In one study, 30% of growth-restricted infants had nonreactive NST results and 40% had positive CST results.60Ninety-two percent of FGR infants with a nonreactive positive pattern exhibited perinatal morbidity. However, some investigators have reported a 25% to 50% false-positive rate with the CST. A possible role for the CST may be evaluation of placental reserve prior to induction in FGR fetuses in whom induction of labor is planned, especially in the setting of absent/reversed end-diastolic flow or oligohydramnios.

Marked intraobserver and interobserver variability of visual FHR analysis has been identified as a potential factor affecting the prediction of fetal status. Currently, traditional FHR parameters and short- and long-term variation of the heart rate in milliseconds, length of episodes with low and high variation, and the rate of signal loss can be assessed by computerized analysis. The objective assessment of these variables circumvents the issue of observer variability, and a direct correlation between FHR variation and pO2 in the umbilical vein as assessed at cordocentesis prior to the onset of labor has been documented. UsingcCTG, documentation of a mean minute variation less than 3.5 ms has been reported to predict a UA cord pH less than 7.20 with greater than 90% sensitivity. In addition, FHR variation usually decreases gradually in the weeks that precede the appearance of late decelerations and fetal hypoxemia and is therefore the most useful computerized FHR parameter for longitudinal assessment in FGR. As with the traditional NST, gestational age, time of day, and the presence of fetal rest-activity cycles also need to be taken into account in the interpretation of computerized results. Wide normal ranges are apparent for FHR patterns and their variations, but the individual fetus shows a certain intrafetal consistency throughout gestation. For monitoring of trends, each fetus should therefore serve as its own control, using recordings of standardized duration and appropriate reference ranges.

Monitoring the Fetus during Surgery

Fetal heart rate (FHR) and uterine contraction monitoring are frequent dilemmas in nonobstetric surgery. The usual problems are logistic and medical. The proposed site of surgery may interfere with monitoring. Vaginal ultrasound probes have been used when the abdominal wall cannot be used. The issue of who will perform and evaluate the fetal tracing is also a common problem. Most anesthesiologists are either uncomfortable in this role or do not wish to have their attention diverted from the mother. In most hospitals, a labor and delivery room nurse stays with the patient to interpret the FHR and uterine contraction tracing in the operating room (OR) and into the recovery period. Commonly, these skilled personnel are in scarce supply so there can be considerable production pressure to reduce, or in some cases omit, the monitoring altogether.

The principal goals of monitoring are to identify fetal compromise and preterm labor. Both these goals are problematic. Electronic FHR monitoring has been used by obstetricians for many years to assess fetal well-being in labor. The use of electronic FHR monitoring has not been shown to be superior to intermittent auscultation in fetal assessment.8,9 Nevertheless, FHR monitoring combined with the current medicolegal climate is the major reason for the increase in cesarean delivery rate in the United States and other countries. It is estimated that the false-positive rate for performing a cesarean section to prevent a case of cerebral palsy using electronic FHR monitoring is 99.8%.10 With this in mind, is it reasonable to ignore FHR monitoring for nonobstetric surgery? Not necessarily. It is often incorrectly argued that FHR monitoring is unnecessary or cumbersome in a given patient because “we wouldn't do a cesarean section anyway” if an FHR abnormality was detected either because the surgery was impractical or because the fetus was previable. However, although immediate cesarean section may not be useful or practical, there are many possible therapeutic options short of cesarean delivery that can be employed. Changes in patient position, maternal cardiovascular manipulations to improve placental blood flow, and increasing fetal oxygenation via increasing maternal oxygenation (via manipulating ventilation or hemoglobin concentration) may have a salutary effect on the fetus. The detection of uterine contractions could lead the anesthesiologist to deepening anesthetic depth, thus decreasing uterine tone and improving the uteroplacental circulation for the fetus. Alternatively, FHR monitoring may be useful in defining the limits of manipulations that can be safely employed. For example, permissive hypoventilation, hemodilution, or hypotension might be required, and the FHR serves as a rough guide for threshold values that are permissible. No absolute agreed-on values exist in these circumstances. Rather than expressing “threshold values” in terms of fetal health, most clinicians prefer terms such as “lack of nonreassuring FHR abnormalities.” Such carefully worded phrases reflect the reality of the poor predictive value of FHR analysis and the medicolegal environment in the United States and elsewhere.

The reliability of FHR monitoring is gestational age–dependent. It is often possible as early as 18 weeks of gestation but generally only reliable after 22 weeks.11,12 The kinds of surgery amenable to monitoring are generally nonabdominal cases, but, as mentioned, vaginal ultrasound has been used even in these situations. The interpretation of the FHR trace requires knowledge of the effects of anesthetic agents. Except under situations of very light sedation, most narcotics and general anesthetics decrease or obliterate long- and short-term FHR variability,11 hence one is left interpreting changes in baseline FHR. Thus, tachycardia (greater than 160 beats/min), bradycardia (less than 100 beats/min), or decelerations in conjunction with uterine contractions are the main diagnostic criteria remaining under general anesthetics. The question as to how long one should measure FHR following surgery is also controversial. The most common monitoring period is 12 to 24 hours, but again data are lacking.

Nonstress test and cardiotocography

Fetal heart rate (FHR) characteristics are normally controlled through parasympathetic innervation, in which the vagus nerve innervates both the sinoatrial and atrioventricular nodes. This tonic influence results in decreased rates of firing, thereby controlling the FHR. The vagus nerve also transmits impulses that result in FHR variability. When a fetus is exposed to prolonged periods of uteroplacental insufficiency, a noradrenergic response through the fetal adrenals occurs. This supersedes vagal influence, leading to both fetal tachycardia and decreased variability. If this continues, there is ultimately myocardial depression that manifests as late decelerations. Thus, in theory, instituting nonstress tests (NSTs) should identify fetuses at risk for adverse perinatal outcome. This is supported by observational studies demonstrating lower stillbirths in pregnancies with reactive NSTs than in those with nonreactive NSTs in addition to a lower stillbirth rate when NSTs are increased from once to twice per week.160,161

However, a recent Cochrane Database review found that no clear evidence exists that antenatal cardiotocography (CTG) improves perinatal outcome in the general population.162 In pregnancies complicated by impaired fetal growth, there is also insufficient data to determine whether there was any one surveillance regimen that would decrease risks for adverse pregnancy outcome.163 Despite this evidence, however, NSTs and CTGs remain a mainstay of management of FGR, with the rationale that nonreactive and abnormal tracings have been associated with hypoxemia and acidemia.164

Factors Influencing the Nonstress Test Result

Fetal heart rate is modified by autonomic activity and may show reduction or absence of reactivity in the presence of hypoxia, neurologic depression, maternal drug ingestion, or acidosis. Fetal behavioral state influences the cardiac reactivity. The human fetus commonly exhibits periods of lowered activity referred to as “sleep cycles.” These periods may produce a decrease or absence of reactivity on an NST. The sleep cycles rarely last more than 20 minutes and may be discounted by observing the fetus for up to 40 minutes.

Adjustments must be made for monitoring of the fetus remote from term (Lagrew, 1987). Between 24 and 32 weeks, the fetus may show accelerations of lesser amplitude that are of shorter duration, reduced reactivity (Druzin et al, 1985; Lavin et al, 1984), and spontaneous low-amplitude decelerations with movement (Sorokin et al, 1982), which do not carry the same ominous portent as in later gestations.

21 What methods are used to evaluate fetal well-being during labor?

Measurement of FHR and uterine activity is important. The baseline (FHR) is measured between contractions and is normally 110 to 160 beats/min. Fetal tachycardia (>160) may indicate fever, hypoxia, use of β-sympathomimetic agents, maternal hyperthyroidism, or fetal hypovolemia. Fetal bradycardia (<110) may be caused by hypoxia, complete heart block, β-blockers, local anesthetics, or hypothermia. The beat-to-beat variability is thought to represent an intact neurologic pathway in the fetus. Increased variability is seen with uterine contractions and maternal activity. Decreased variability can be seen with central nervous system depression, hypoxia, acidosis, sleep, narcotic use, vagal blockade, and magnesium therapy for preeclampsia. Absence of beat-to-beat variability, especially in the presence of FHR decelerations or bradycardia, is a particular concern for fetal acidosis.

Beat-to-Beat Variability

Normal fetal heart rate exhibits fluctuations of approximately 6 to 25 beats/minute (see Fig. 17.11).216,235,236 This beat-to-beat variability reflects the modulation of heart rate by autonomic, particularly parasympathetic, input and especially depends on inputs from cerebral cortex, diencephalon, and upper brain stem to the cardiac centers in the medulla and then to the vagus nerve.191,200,216,237-239 Of the autonomic input, parasympathetic influences are more important than sympathetic influences.216,240-242 The presence of normal beat-to-beat variability is considered the best single assessment of fetal well-being.191,216,231,239 Indeed, the presence of normal variability is a reassuring finding in the presence of the mild variable decelerations common in the second stage of labor.191 Loss of or diminished beat-to-beat variability may be observed not only with significant fetal hypoxia but also with prematurity, fetal sleep, drugs (e.g., sedative-hypnotics, narcotic-analgesics, benzodiazepines, atropine, and local anesthetics), congenital malformations (e.g., anencephaly), and intrauterine, a ntepartum cerebral destruction.a The loss of beat-to-beat variability coupled with variable or late decelerations (see subsequent sections) significantly enhances the likelihood that the fetus is undergoing significant hypoxia.191,200,216,231,239 The importance of careful longitudinal assessment of heart rate variability has been suggested.234 Ample documentation has shown the association between decreased fetal heart rate variability and decelerations, fetal acidosis, intrauterine fetal death, and low Apgar scores.191,216,239,240