Version May 2024
INTRODUCTION — Normal human labor is characterized by regular uterine contractions, which cause repeated intermittent reductions of blood flow to the intervillous spaces resulting in repeated transient interruptions of fetal oxygenation. Contractions may also compress the umbilical cord and fetal head. Most fetuses tolerate this process well because of placental reserve and effective compensatory mechanisms, but some do not because of preexisting uteroplacental insufficiency and/or intrapartum factors. The fetal heart rate (FHR) pattern helps to distinguish the former from the latter as it is an indirect marker of fetal cardiac and central nervous system responses to changes in blood pressure, blood gases, and acid-base status. (See "Nonstress test and contraction stress test", section on 'Physiologic basis of fetal heart rate changes'.)
The rationale for intrapartum FHR monitoring is that identification of FHR changes potentially associated with inadequate fetal oxygenation, such as changes in baseline rate, frequent decelerations, and/or absent/minimal variability, may enable timely intervention to reduce the likelihood of hypoxic injury or death. In addition, accurate identification of appropriately oxygenated fetuses may prevent unnecessary intervention. Although virtually all obstetric societies advise monitoring the FHR during labor, the benefit of this intervention has not been conclusively demonstrated, and this position is largely based upon expert opinion and medicolegal precedent.
The procedure for intrapartum FHR monitoring, physiology behind FHR accelerations and decelerations, classification of FHR tracings, and use of ancillary tests to evaluate the fetus will be discussed here. Intrapartum management of category I, II, and III FHR tracing is reviewed separately (see "Intrapartum category I, II, and III fetal heart rate tracings: Management"). Antepartum FHR monitoring (nonstress test, contraction stress test) is also reviewed separately. (See "Nonstress test and contraction stress test".)
DOES INTRAPARTUM FHR MONITORING IMPROVE OUTCOME? — Although some evidence suggests that intrapartum FHR monitoring is associated with a reduction in intrapartum death [1], a reduction in long-term neurologic impairment has not been proven. All available data are derived from trials comparing techniques (eg, continuous electronic monitoring with intermittent auscultation). No randomized trials have compared intrapartum FHR monitoring with no intrapartum FHR monitoring.
For both low- and high-risk pregnancies, continuous electronic FHR monitoring is not clearly superior to intermittent auscultation with respect to preventing death or poor long-term neurologic outcome and has a high false-positive rate [2,3]. The lack of superiority has been attributed, at least in part, to intra- and interobserver variability in interpretation of continuous electronic FHR tracings [4].
Evidence:
●Meta-analysis – A 2017 meta-analysis that compared continuous electronic FHR monitoring with intermittent auscultation (13 randomized trials, >37,000 low- and high-risk pregnancies) reported the following major findings [2]:
•No statistically significant differences between techniques were noted for the following newborn/childhood outcomes:
-Acidemia (measured in cord blood) (relative risk [RR] 0.92, 95% CI 0.27-3.11)
-Apgar score <4 at five minutes (RR 1.80, 95% CI 0.71-4.59)
-Neonatal intensive care unit admission (RR 1.01, 95% CI 0.86-1.18)
-Hypoxic-ischemic encephalopathy (RR 0.46, 95% CI 0.04-5.03)
-Perinatal mortality (RR 0.86, 95% CI 0.59-1.24)
-Neurodevelopmental impairment at ≥12 months of age (RR 3.88, 95% CI 0.83-18.2)
-Cerebral palsy (RR 1.75, 95% CI 0.84-3.63)
•Although use of continuous electronic FHR monitoring resulted in fewer neonatal seizures (RR 0.50, 95% CI 0.31-0.80), there were no differences in long-term neurologic outcomes [2,5].
•Continuous electronic FHR monitoring resulted in:
-More operative vaginal births for abnormal FHR patterns or acidosis (RR 2.54, 95% CI 1.95-3.31)
-Fewer spontaneous vaginal births (RR 0.91, 95% CI 0.86-0.96)
-More cesarean births for abnormal FHR patterns or acidosis (RR 2.38, 95% CI 1.89-3.01)
-More operative vaginal and cesarean births overall (RR 1.15 and 1.63, respectively). Data for low-risk and high-risk subgroups, preterm pregnancies, and high-quality trials were consistent with these overall results.
It is important to note that all seven trials published after 1980 (including the only trial with several thousand patients) found no significant increase in the rate of cesarean birth for patients monitored continuously compared with those monitored by intermittent auscultation, in contrast to the four small trials published before 1980, which found significantly higher rates of cesarean birth with continuous monitoring [2].
It is also important to note that a statistical reduction in the perinatal death rate is difficult to demonstrate because death is a rare outcome. Even the pooled results from multiple randomized trials lacked sufficient power to permit a definitive conclusion in the 2017 meta-analysis [2]. However, a previous meta-analysis that specifically evaluated perinatal deaths attributed to fetal hypoxia in low- and high-risk pregnancies concluded that this outcome was significantly less common in continuously monitored patients than those monitored with intermittent auscultation (7/9398 versus 17/9163; 0.7 versus 1.8 per 1000; odds ratio 0.41, 95% CI 0.17-0.98; nine trials) [1].
A statistical reduction in the incidence of cerebral palsy with continuous intrapartum FHR monitoring is also difficult to prove for several reasons. Many cases of cerebral palsy are due to antepartum, rather than intrapartum, events. In such cases, intrapartum interventions are unlikely to change the course of the disease [6]. In addition, most FHR abnormalities are not associated with fetal acidemia or hypoxemia, and most fetal acidemia and hypoxemia does not result in neurologic disability. In fact, one study calculated that 99.8 percent of "abnormal" FHR tracings are not associated with the later development of cerebral palsy, yielding a positive predictive value that is equal to, or lower than, the prevalence of cerebral palsy in the general population [6]. Another potentially confounding factor is that a preexisting fetal neurologic disorder may be the cause, rather than the result, of an intrapartum FHR abnormality [7]. In many cases, the interventions that are undertaken in the setting of abnormal FHR tracings may alter the natural history of fetal oxygen deprivation, potentially decoupling FHR abnormalities from hypoxic neurologic sequelae such as cerebral palsy. Lastly, the degree of fetal oxygen deprivation that leads to long-term neurologic injury is close to that causing fetal death; thus, many severely depressed term fetuses may either survive intact or die, rather than survive with disability [8].
●Network meta-analysis – A 2021 network meta-analysis (33 trials, >118,000 participants) evaluated multiple forms of intrapartum fetal monitoring, including intermittent auscultation and cardiotocography with and without computer-aided decision support, fetal scalp lactate assessment, fetal scalp pH analysis, fetal pulse oximetry, and fetal ST segment analysis (STAN) [3]. Major findings were:
•No method of intrapartum fetal monitoring increased or decreased the overall cesarean birth rate.
•Compared with other forms of intrapartum fetal monitoring, intermittent auscultation neither reduced nor increased adverse neonatal outcomes, including low Apgar scores, neonatal acidemia, neonatal intensive care unit admissions, or perinatal deaths. Intermittent auscultation was associated with fewer emergency cesarean births overall and fewer emergency cesarean births for fetal distress.
CANDIDATES FOR INTRAPARTUM FETAL MONITORING — Any patient with a pregnancy in which detection of an FHR abnormality would prompt intervention (maternal maneuvers to improve fetal oxygenation and/or operative delivery) is a candidate for intrapartum fetal monitoring.
Some degree of FHR monitoring during labor has become routine in the United States, even though the clinical benefit has not been established conclusively (see 'Does intrapartum FHR monitoring improve outcome?' above). It is unlikely that this practice will be abandoned in the near future because most patients and clinicians are reassured by normal FHR monitoring results, and most believe that detection of an FHR abnormality and prompt intervention is likely to be beneficial.
Intermittent versus continuous monitoring
●Low- or average-risk pregnancies – Some major national organizations endorse monitoring low-risk pregnancies intermittently using a Doppler device or fetal stethoscope (eg, Pinard or DeLee stethoscope); however, this is relatively uncommon in the United States because it provides limited information about FHR variability, accelerations, or decelerations and requires one-to-one nursing care, which is costly and impractical for most maternity units. The possible increase in operative birth associated with continuous electronic FHR monitoring usually is considered a reasonable trade-off for a possible reduction in risk of adverse fetal/neonatal outcome and the reduction in personnel costs. (See 'Does intrapartum FHR monitoring improve outcome?' above.)
American College of Obstetricians and Gynecologists (ACOG) guidelines state that either continuous electronic FHR monitoring or intermittent auscultation is acceptable in uncomplicated patients [9].
●High-risk pregnancies – There is consensus that high-risk pregnancies should be monitored continuously during labor. A high-risk pregnancy can be defined as one with antepartum or intrapartum complications that may lead to maternal or fetal compromise (eg, previous cesarean birth, preeclampsia, growth restriction, diabetes mellitus requiring medication for glucose control, abruption or unexplained vaginal bleeding, chorioamnionitis or sepsis, meconium-stained amniotic fluid, postterm pregnancy).
PROCEDURE
Choice of equipment — External FHR monitoring is as reliable as internal FHR monitoring in most cases [10]. However, internal FHR monitoring is preferable when the externally derived tracing is difficult to obtain or interpret because of poor technical quality. This may result from a number of conditions, including early gestational age, maternal habitus, frequent maternal or fetal movement, uterine myomata, polyhydramnios, or multiple gestation
External electronic monitoring — Noninvasive external FHR monitoring can be performed continuously or for variable periods of time with a Doppler ultrasound device on the maternal abdomen. This device detects the motion of the fetal heart and uses this information to create a complex wave form. The computer then detects the peaks of successive waves to calculate a mechanical R wave-to-R wave (RR) interval. To minimize artifact caused by the inherent variation in the Doppler ultrasound signal, the computer calculates the FHR by averaging several consecutive RR intervals. This technology, called autocorrelation, reduces signal variation. The FHR tracing derived from Doppler ultrasound using the autocorrelation technique closely resembles that derived from a fetal electrocardiogram (ECG), although baseline variability may be more apparent with the Doppler technique. An alternative technology (eg, Monica AN24) uses several electrodes placed on the maternal abdomen to detect the electrical fetal RR interval. Wireless monitors enable FHR monitoring while the patient is ambulating [11].
Intermittent auscultation — A Pinard or DeLee fetal stethoscope (figure 1) (also called a fetoscope) or a Doppler device may be used for intermittent auscultation. A systematic review concluded that available evidence is limited and inadequate to make a strong recommendation for choosing one device versus another [12].
Internal electronic monitoring — A fetal ECG can be obtained by placing a bipolar spiral electrode into the fetal scalp transcervically; a second reference electrode is placed on the maternal thigh to eliminate electrical interference from maternal cardiac activity. A computer calculates the FHR based on the RR interval (waveform 1). Artifact is minimal so the signal is clear and provides accurate measurement of the variability between successive heartbeats without the need for autocorrelation.
Application of artificial intelligence computer programs to fetal ECG signal processing has led to development of devices to overcome the limitations of FHR pattern interpretation by human observers [13,14]. This has been made possible by technical improvements in signal acquisition and processing, and by algorithms for pattern interpretation based on standardization of visual pattern analysis and correlation with fetal scalp blood and umbilical artery pH determinations. As an example, the STAN monitor analyzes the fetal T wave and ST segment. However, this technology has not been widely adopted in the United States and remains investigational. (See 'ST analysis' below.)
Frequency and duration of monitoring
Electronic FHR monitoring — Upon admission to the labor unit, the standard of care in most hospitals in the United States is to assess the FHR for a minimum of 20 to 30 minutes, along with uterine activity and maternal vital signs. The goal is to identify fetuses who have or are at increased risk for abnormal intrapartum FHR patterns and who might benefit from continuous rather than intermittent intrapartum FHR monitoring [15]. This initial assessment and additional assessments during labor may also inform decisions regarding the use of uterine stimulants, such as oxytocin or prostaglandins. However, a systematic review of randomized trials found that, in low-risk pregnancies, this "labor admission test" did not reliably predict fetal ability to tolerate labor over time and did not reduce neonatal morbidity compared with intermittent auscultation of the FHR [16]. There were insufficient data to draw conclusions about the value of the labor admission test in patients with high-risk pregnancies.
In the United States, a common practice in low-risk pregnancies with a normal initial FHR pattern is to monitor the FHR continuously when possible (ie, patient is not ambulating, bathing, moving around, etc) and review the FHR at least every 30 minutes in the active phase of the first stage of labor and at least every 15 minutes in the second stage [9]. High-risk pregnancies are monitored continuously, and the FHR is usually reviewed at least every 15 minutes in the active phase of the first stage of labor and at least every 5 minutes in the second stage.
The interpretation of the FHR should be documented in the intrapartum record. (See 'NICHD classification of FHR patterns' below.)
Intermittent auscultation — As discussed above, intrapartum intermittent auscultation is used relatively infrequently in the United States. (See 'Candidates for intrapartum fetal monitoring' above.)
No trials have compared protocols for performing intermittent auscultation [12]. If used in low-risk pregnancies, a common approach is to listen to the FHR for ≥60 seconds and record the rate during and immediately after a uterine contraction at least every 30 minutes during the active phase of the first stage of labor and at least every 15 minutes during the second stage [17]. If risk factors for fetal compromise are present, the FHR is determined, evaluated, and recorded preferably before, during, and after a uterine contraction at least every 15 minutes during the active phase of the first stage of labor and at least every 5 minutes during the second stage.
The American College of Nurse-Midwives considers abnormal findings to be any of the following: irregular rhythm, decrease in FHR below the baseline, tachycardia, or bradycardia [18]. An increase in the baseline fetal heart rate by ≥20 beats/minute from the start of labor is also concerning [19].
Assessment of uterine activity — Interpretation of intrapartum monitoring should include assessment of measures of uterine activity in context, and this assessment should be incorporated routinely into FHR management decisions. In the United States, the National Institute of Child Health and Human Development (NICHD) has identified several essential components of uterine activity, including uterine contraction frequency, contraction intensity, contraction duration, resting time between contractions, and resting tone between contractions [20]. Normal uterine contraction frequency was defined as five or fewer contractions in 10 minutes, averaged over 30 minutes. Contraction frequency above this limit was termed tachysystole.
Normal ranges for the other components of uterine activity are addressed elsewhere. (See "Labor: Overview of normal and abnormal progression".).
PHYSIOLOGIC SIGNIFICANCE OF SELECTED FHR CHARACTERISTICS
Baseline FHR — A normal baseline FHR is 110 to 160 bpm (table 1) and reflects lack of pathology related to factors that regulate FHR. These factors include 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), which are discussed in detail separately. (See "Nonstress test and contraction stress test", section on 'Physiologic basis of fetal heart rate changes'.)
Baseline bradycardia may be related to maternal beta blocker therapy, hypothermia, hypoglycemia, hypothyroidism, or fetal heart block or interruption of fetal oxygenation.
Baseline tachycardia may be related to maternal fever, infection, medications, hyperthyroidism, elevated catecholamines, fetal anemia, arrhythmia, or interruption of fetal oxygenation.
Variability — FHR variability is the result of integrated activity between the sympathetic and parasympathetic branches of the autonomic nervous system. Moderate baseline variability reflects adequate oxygenation of the central nervous system and reliably predicts the absence of damaging degrees of hypoxia-induced metabolic acidemia at the time it is observed (table 1) [20-22]. However, the converse is not true: Minimal or absent variability alone is a poor predictor of fetal metabolic acidemia or hypoxic injury at the time it is observed [20]. Other conditions potentially associated with minimal or absent variability include normal cyclic variation, fetal sleep cycle, fetal arrhythmia, extremely preterm fetus, fetal cardiac anomaly, preexisting fetal neurologic injury, or fetal effects of maternally administered medications.
Most of the literature regarding decreased variability does not differentiate between absent variability (amplitude range undetectable) and minimal variability (amplitude range detectable but ≤5 bpm). Therefore, it is not possible to make definitive conclusions about the clinical significance of absent versus minimal variability. Variability is generally present at ≥24 weeks of gestation and may increase as pregnancy progresses, but not to a degree that can be accurately measured by conventional Doppler-based cardiotocography and applied clinically [23,24]. The National Institute of Child Health and Human Development (NICHD) guideline for classification of FHR patterns does not provide gestational-age specific definitions of variability because no clinical data support using different criteria at earlier versus later gestational ages, in contrast to accelerations where criteria vary before and after 32 weeks [20,25].
The significance of markedly increased variability is unclear. It may be a normal variant or an exaggerated autonomic response to transient or sustained interruption of fetal oxygenation. It has been observed in the early stages of intrapartum fetal hypoxemia and before birth in some acidotic newborns [26,27].
Accelerations — FHR accelerations are frequently associated with fetal movement, possibly as a result of stimulation of peripheral proprioceptors, increased catecholamine release, and autonomic stimulation of the heart. As with moderate baseline variability, FHR accelerations reliably predict the absence of damaging degrees of fetal hypoxia and fetal metabolic acidemia at the time they are observed [20,22]. (See 'FHR response to stimulation' below.)
However, the converse is not true. The absence of accelerations is a poor predictor of fetal metabolic acidemia or hypoxic injury [20]. Other conditions potentially associated with the absence of accelerations include normal cyclic variation, fetal sleep cycle, arrhythmia, medications, extreme prematurity, congenital anomalies, fetal anemia, and preexisting neurologic injury.
The definition of an acceleration varies by gestational age (table 1). Before 32 weeks, accelerations are defined by a ≥10 bpm rise above baseline lasting for ≥10 seconds and at ≥32 weeks they are defined by a ≥15 bpm rise above baseline lasting for ≥15 seconds. This distinction was introduced in the 1997 National Institute of Child Health and Human Development (NICHD) guideline for classification of FHR patterns and has been carried forward since that time [20,25], although the scientific evidence supporting the gestational age-related distinction is extremely limited [28,29].
Decelerations unrelated to fetal oxygenation
Early deceleration — An early deceleration (table 1) likely represents an autonomic response to changes in intracranial pressure and/or cerebral blood flow caused by intrapartum compression of the fetal head during a uterine contraction and maternal expulsive efforts, although the precise physiologic mechanism is not known. Early decelerations are clinically benign: They are not associated with an interruption of fetal oxygenation, metabolic acidemia, or hypoxic-ischemic neurologic injury. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category I pattern: Normal'.)
Decelerations related to interruption of fetal oxygenation
Late deceleration — In most cases, a late deceleration is a reflex fetal response to transient hypoxemia during a uterine contraction (table 1 and waveform 2 and waveform 3 and waveform 4 and waveform 5 and waveform 6) [30]. When uterine contractions compress maternal blood vessels traversing the uterine wall, maternal perfusion of the intervillous space is reduced; myometrial diastolic blood flow may cease temporarily when intrauterine pressure exceeds 35 mmHg [31,32]. Reduced delivery of oxygenated blood to the intervillous space due to strong, excessively frequent, and/or prolonged contractions can reduce diffusion of oxygen into the fetal capillary blood in the chorionic villi, leading to a decline in fetal PO2. The fetus can compensate for reductions in oxygen delivery by the high oxygen affinity of fetal red cells (high hemoglobin F) and the high oxygen-carrying capacity of fetal blood (high hemoglobin level) [33].
When fetal PO2 falls below the normal range (approximately 15 to 25 mmHg in the umbilical artery), chemoreceptors initiate an autonomic reflex response. Initially, sympathetic outflow causes peripheral vasoconstriction, shunting oxygenated blood flow away from non-vital vascular beds and toward vital organs such as the brain, heart and adrenal glands. The resulting increase in fetal blood pressure is detected by baroreceptors, which trigger a parasympathetic reflex and slow the heart rate, reduce cardiac output, and return blood pressure to normal. After the contraction, fetal oxygenation is restored, autonomic reflexes subside, and the FHR gradually returns to baseline. This combined sympathetic-parasympathetic reflex response to transient interruption of fetal oxygenation has been confirmed in animal studies [30,34-42]. Interruption of the oxygen pathway to the fetus can occur at multiple maternal levels in addition to uterine contractions, such as the lungs (eg, maternal hypoxemia), heart (eg, poor cardiac output) or vasculature (eg, hypotension).
Rarely, fetal oxygenation is interrupted sufficiently to result in both severe hypoxemia and metabolic acidemia and, in turn, direct myocardial depression and late decelerations [30]. Late decelerations related to severe hypoxemia, metabolic acidemia, and myocardial depression increase the risk of adverse neonatal outcome. Late decelerations resulting from a reflex response to transient hypoxemia can be distinguished from more concerning late decelerations by the presence of moderate baseline variability or accelerations, which reliably exclude the presence of damaging degrees of hypoxia-induced metabolic acidemia [20-22]. Recurrent late decelerations with absent/minimal variability and no accelerations require prompt attention [20-22,30]. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category III pattern: Abnormal' and "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Late decelerations without loss of variability'.)
Variable deceleration — A variable deceleration reflects a fetal autonomic reflex response to transient mechanical compression of the umbilical cord (table 1 and waveform 7 and waveform 8) [38,43-51]. Initially, compression of the umbilical cord occludes the thin-walled, compliant umbilical vein, decreasing fetal venous return and triggering a baroreceptor-mediated reflex rise in FHR (sometimes referred to as a "shoulder"). Further compression occludes the umbilical arteries, causing an abrupt increase in fetal peripheral resistance and blood pressure. Baroreceptors detect the abrupt rise in blood pressure, triggering an increase in parasympathetic outflow and an abrupt decrease in heart rate. As the cord is decompressed, this sequence of events occurs in reverse.
Cord compression with or without other sources of interrupted fetal oxygenation may result in recurrent variable decelerations with absent/minimal variability and no accelerations. These decelerations often become deeper and last longer over time (reaching a nadir >60 bpm below baseline or <60 bpm and lasting longer than 60 seconds is concerning [21,52]). In such cases, prompt attention is required because ongoing hypoxic injury cannot be excluded by the tracing alone [20-22]. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category III pattern: Abnormal' and "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Variable decelerations without loss of variability or accelerations'.)
Classification of variable decelerations as mild, moderate, or severe does not correlate with outcome and is not recommended by the National Institute of Child Health and Human Development [20]. Similarly, the clinical significance of "atypical" features of variable decelerations is unclear (atypical features include a slow return of the FHR to baseline after the end of the contraction [sometimes called a "variable with a late component"], biphasic decelerations, tachycardia after the variable deceleration [sometimes referred to as "overshoot"], accelerations preceding and/or following the variable deceleration [sometimes called "shoulders"], or reduction in post-deceleration baseline) [20]. Terms such as "variable with a late component," "shoulders," "overshoots," "Hon pattern," and "conversion pattern" have been used in some descriptive reports to identify FHR patterns that have not been demonstrated to impact fetal condition or neonatal outcome in appropriately controlled studies. Such terms are not included in standard fetal monitoring terminology. In the absence of appropriate scientific confirmation of clinical significance, the use of such terms should be avoided.
Prolonged deceleration — A prolonged deceleration reflects a fall in FHR by ≥15 bpm, lasting ≥2 but <10 minutes (table 1) [20,25]. It is caused by the same physiologic mechanisms responsible for late or variable decelerations, but interruption of fetal oxygenation occurs for a longer period of time. As discussed above, absent/minimal variability and no accelerations require prompt attention because ongoing hypoxic injury cannot be excluded by the FHR tracing alone.
If the fall in FHR lasts ≥10 minutes, it is defined as a baseline change [20]. A baseline change with absent/minimal variability and no accelerations requires prompt attention because ongoing hypoxic injury cannot be excluded. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category III pattern: Abnormal' and "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Fetal bradycardia/prolonged deceleration without loss of variability'.)
Sinusoidal pattern — The sinusoidal pattern is rare. It is defined as a smooth, sine wave-like undulating pattern in FHR baseline with a cycle frequency of three to five cycles per minute of regular amplitude of 5 to 15 bpm that persists for at least 20 minutes (table 1 and waveform 9). The sinusoidal pattern was historically associated with severe fetal anemia, although the pathophysiologic mechanism has not been definitively proven [53-55]. Variations of the pattern have been described in association with administration of opioids. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Management of sinusoidal category III pattern'.)
NICHD CLASSIFICATION OF FHR PATTERNS — Interpretation of an FHR tracing includes several components:
●Qualitative and quantitative descriptions of baseline rate and variability
●Presence/absence of accelerations, decelerations, or sinusoidal pattern
●Changes or trends of the FHR over time
●Assessment of uterine activity
Standard definitions of FHR baseline, variability, accelerations, decelerations, and sinusoidal pattern (table 1) were proposed by the National Institute of Child Health and Human Development (NICHD) in 1997 and reaffirmed in 2008 [20,25]. They are used clinically throughout the United States, and have been endorsed by American College of Obstetricians and Gynecologists (ACOG) [9]. The International Federation of Gynecology and Obstetrics (FIGO) published a similar consensus guideline in 2015 (FIGO2015) (table 2), which is used in many countries [56].
In 2008, the NICHD also introduced a three-tier FHR classification system (table 3), in which category I represents a normal tracing (predictive of normal fetal acid-base status at the time of observation), category II represents an indeterminate tracing, and category III represents an abnormal tracing (associated with an increased risk of abnormal fetal acid-base status at the time of observation) [20]. Some evidence suggests that neonatal outcomes can be improved with use of this standardized approach to pattern recognition coupled with a standardized package of therapeutic interventions (table 4) [57]. These patterns are described below briefly and elsewhere in more detail along with management recommendations. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management".)
Category I FHR pattern — A category I pattern is normal: it indicates minimal likelihood of significant metabolic acidemia and ongoing fetal hypoxic injury at that point in time. The fetal status and FHR pattern may remain stable over time, or the fetal status may change, resulting in a category II or category III pattern.
A category I pattern has all of the following components (table 3 and waveform 10) [20]:
●A baseline FHR of 110 to 160 bpm
●Moderate FHR variability (6 to 25 bpm)
●Absence of late, variable, or prolonged FHR decelerations
●Early decelerations may or may not be present (waveform 11)
●Accelerations may or may not be present
Category I patterns were observed at some point during labor in over 99 percent of tracings in one large study [58].
Category III FHR pattern — A category III pattern is abnormal: it is associated with an increased likelihood of severe hypoxia and metabolic acidemia at that point in time.
A category III tracing has at least one of the following components (table 3) [20]:
●Absent variability with recurrent late decelerations (waveform 2 and waveform 3)
●Absent variability with recurrent variable decelerations (waveform 7)
●Absent variability with bradycardia
●A sinusoidal pattern (waveform 9)
Late decelerations and variable decelerations are considered recurrent when they occur with at least 50 percent of uterine contractions in a 20-minute window [20,25].
Category III patterns were observed at some point in 0.1 percent of tracings in one large study [58].
Prompt evaluation, expeditious use of conservative measures to improve fetal oxygenation, and/or expeditious delivery are indicated when a category III pattern is observed because fetal/neonatal morbidity or mortality may occur if the pattern persists. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category III pattern: Abnormal'.)
However, category III patterns may also be caused by conditions unrelated to hypoxemia. (See 'Pitfalls in attributing category II and category III patterns to fetal hypoxia' below.)
Category II FHR pattern — Category II FHR patterns include all FHR patterns that are not classified as category I (normal) or category III (abnormal) (table 3). Because category II tracings may remain stable for a prolonged period of time, have variable prognostic significance based on the specific components, and are common (observed at some point in 84 percent of tracings [58]), pregnancies with this pattern are the most difficult to evaluate and manage. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Category II pattern (Indeterminate)'.)
Pitfalls in attributing category II and category III patterns to fetal hypoxia — Category II and category III patterns can be related to a number of conditions other than hypoxia:
●Normal cyclical variation – FHR tracings in labor can move between category I and category II with variable frequency. Episodes of moderate variability often alternate with episodes of minimal variability. Normal cyclic variation should be considered when interpreting the FHR tracing.
●Fetal sleep cycle – Fetal quiet sleep is associated with decreased variability and reduced frequency of accelerations, as well as decreased fetal movement. Quiet sleep cycles may last up to 40 minutes [59].
●Technical factors – Technical factors include a faulty leg plate, electrode, or monitor; setting the recording rate at 1 cm/min instead of the standard 3 cm/min; and the computer algorithm used by the monitor, which may double very slow FHRs and halve fast rates (>240 bpm).
●Maternal heart rate artifact – Maternal artifact refers to an electronic fetal monitor record that shows the maternal, rather than the fetal, heart rate [60]. It may occur in several scenarios, which can be detected if the clinician is aware of the phenomenon, and evaluates suspicious tracings. Evaluation for maternal artifact involves using more reliable methods for documenting the maternal heart rate (eg, checking the radial pulse, applying a pulse oximetry or electrocardiographic [ECG] monitor) and FHR (eg, ultrasound of fetal heart, internal scalp electrode).
•If the fetus is not alive, an internal fetal scalp electrode may detect the maternal ECG and record the maternal heart rate instead of the FHR [61].
•The external Doppler device may record the maternal heart rate from a nearby artery (eg, uterine artery), even if the fetus is alive. When the mother is tachycardic, the maternal heart rate pattern can appear deceptively similar to a normal FHR pattern, including normal-appearing baseline rate and variability. In a prospective study, nearly 10 percent of parturients had a heart rate ≥120 bpm and nearly 20 percent had a heart rate ≥110 bpm in the second stage of labor [62].
•If the maternal heart rate is recorded, maternal heart rate accelerations during uterine contractions can be mistaken for FHR accelerations [63-65]. Heart rate accelerations that coincide with uterine contractions should prompt further evaluation to exclude this phenomenon, especially during maternal pushing in the second stage.
•The external Doppler device can alternate between recording the fetal and the maternal heart rate. When switching from one to the other, the tracing will not necessarily show visual discontinuity; therefore, visual continuity does not reliably exclude this phenomenon. Some newer electronic monitors will alert the user to "signal coincidence" or "signal ambiguity" when the monitor's computer logic determines that the maternal heart rate derived from a maternal ECG or pulse oximetry transducer is the same as the presumed FHR derived from the Doppler transducer (or scalp electrode).
Suspected signal coincidence or ambiguity should prompt further evaluation to confirm the source of the heart rate signal, since the maternal heart rate is not informative of fetal condition. If there is any question, other methods should be employed as needed, including ultrasound of the fetal heart, palpation of the maternal pulse, fetal scalp electrode, or maternal pulse oximetry.
●Drug effects – Transplacental passage of maternal medication can affect the FHR. For example, opioids and magnesium sulfate can decrease variability, butorphanol can cause a sinusoidal pattern, and beta-blockers and atropine can increase FHR [9].
●Maternal fever – Maternal fever is associated with increased baseline FHR and decreased variability.
●Fetal cardiac arrhythmias – Electronic FHR monitoring patterns may suggest the presence of a fetal arrhythmia, which may be benign or may seriously affect cardiac function. Other sonographic and non-sonographic modalities are needed to make a definitive diagnosis and treatment plan. (See "Fetal arrhythmias".)
The following are clues that an arrhythmia is present; however, any FHR less than 110 bpm requires thorough evaluation before it can be attributed to a benign condition.
•Sharp downward spikes that nadir at approximately half of the baseline rate suggest dropped beats.
•A sharp upward spike followed immediately by a downward spike suggests a premature beat with a compensatory pause.
•A persistent or intermittent baseline rate that is approximately half of the normal rate may be due to 2:1 heart block.
•A baseline rate less than 110 bpm but higher than half of the normal rate suggests sinus bradycardia. Structural cardiac abnormalities may be associated with bradyarrhythmias, such as complete heart block.
•An FHR >240 bpm suggests a tachyarrhythmia; however, because the upper limit of the FHR graph on standard paper is 240 bpm, the monitor may not record any heart rate or it may record half of the FHR.
●Preexisting fetal neurologic injury – Abnormal FHR patterns observed from the moment monitoring is initiated have been attributed to antepartum neurologic injury, such as stroke. The most commonly described pattern is a persistent nonreactive heart rate and a persistent fixed baseline with minimal or absent variability [7,66].
However, normal intrapartum FHR monitoring does not exclude the possibility of antepartum neurologic injury since antepartum injury does not always manifest in the intrapartum FHR tracing [67].
Studies of infants with congenital brain lesions suggest that damage to the medulla oblongata and midbrain may be responsible for the loss of FHR variability [68].
CLINICAL APPROACH TO FHR MONITORING AND EVALUATION OF ABNORMAL PATTERNS — To improve neonatal outcome, it is crucial that clinicians correctly define and interpret FHR tracings, communicate effectively with other labor and delivery providers when the pattern is not normal, and initiate appropriate and timely interventions [57].
Key principles — Key principles when monitoring the FHR pattern include:
●Confirm that the monitor is recording the FHR and uterine activity adequately to permit appropriately-informed management decisions. Ensure that the maternal heart rate is not being recorded. (See 'Pitfalls in attributing category II and category III patterns to fetal hypoxia' above.)
●Assess uterine activity along with baseline FHR, variability, accelerations, decelerations, and sinusoidal pattern, and place the tracing in a category (I, II, or III).
●If the tracing is category I and the patient is low-risk, initiate routine intrapartum fetal surveillance.
●If the tracing is not category I, evaluate the integrity of the fetal oxygen pathway (maternal lungs, heart, and vasculature, as well as the uterus, placenta, and umbilical cord).
Attempt to correct the problem, if possible, by initiating measures to improve fetal oxygenation, such as maternal position changes, intravenous fluid bolus, correcting hypotension, stopping or reducing uterine stimulants, administering a uterine relaxant, amnioinfusion, and/or modifying maternal pushing efforts. If the mother is hypoxemic, provide supplemental oxygen.
Also employ ancillary tests to further assess the fetal condition. (See 'Useful ancillary tests for intrapartum fetal evaluation' below.)
The management of category II and III tracings is summarized in the table (table 4) and discussed in detail separately. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management".)
●Assess how the FHR pattern is evolving. Deepening decelerations, increasing frequency and longer duration of decelerations, decreasing variability to minimal or undetectable, and change in baseline (usually tachycardia) are signs that acidosis may be developing. In fetuses with initially normal FHR tracings, newborn acidosis has been observed when decelerations in combination with decreasing FHR variability develops and persists over approximately one hour [69].
●If the FHR pattern does not improve within a reasonable period of time, begin planning for the possible need for rapid delivery. This may include availability of an operating room and specialized equipment, notification of anesthesia and pediatrics, consent forms, and laboratory tests.
●Determine whether operative intervention (cesarean or operative vaginal birth) is needed and the urgency of this intervention. Consider individual characteristics of the facility, staff, mother, fetus, and labor, and make an informed estimate of the time needed to accomplish delivery in the event of a sudden change in maternal or fetal condition.
Useful ancillary tests for intrapartum fetal evaluation
FHR response to stimulation — An FHR acceleration rising ≥15 bpm above baseline lasting for ≥15 seconds almost always assures the absence of fetal acidemia [70,71]. Before 32 weeks of gestation, accelerations with a rise of ≥10 bpm and a duration of ≥10 seconds almost always assure the absence of fetal acidemia [20].
In the absence of spontaneous FHR accelerations, the fetal scalp stimulation maneuver is easy to perform, inexpensive, and readily available. The examiner uses the first and second fingers to rub the fetal scalp for approximately 15 to 30 seconds during a vaginal examination. As early studies of the efficacy of scalp stimulation used a gentle pinch with an atraumatic (Allis) clamp as the fetal stimulus, digital stimulation should be sufficiently firm to approximate this level of stimulation. Fetal vibroacoustic stimulation to the maternal abdominal wall overlying the uterus is another effective method of fetal stimulation [72]. If an internal electrode has not been applied, fetal scalp puncture during application of the electrode is also effective. Regardless of the technique used, stimulation should be performed when the FHR is at its baseline rate because performance during a deceleration is unlikely to terminate the deceleration and is not predictive of fetal acid-base status.
When accelerations are induced in this setting, the fetal pH is >7.20 in over 90 percent of cases, and when no accelerations occur, pH is <7.20 in approximately 50 percent of cases [72-76]. Accelerations elicited by fetal scalp stimulation have the same ability to exclude on-going hypoxic injury as spontaneous accelerations [20].
A meta-analysis of observational studies that assessed performance of various stimulation tests (vibroacoustic stimulation, digital scalp stimulation, fetal scalp puncture, Allis clamp scalp stimulation) for the prediction of intrapartum fetal acidemia found them to be similarly effective and more useful for predicting the absence, rather than the presence, of acidemia [74]. For digital stimulation, the pooled likelihood ratio (LR) for acidemia with a negative test (ie, acceleration elicited) was 0.06 (95% CI 0.01-0.31), and the pooled LR of acidemia with a positive test (ie, no acceleration) was 15 (95% CI 3-76). Data from adequately powered randomized trials are not available. (See "Evaluating diagnostic tests", section on 'What are the positive and negative likelihood ratios?'.)
In resource-limited and nonobstetric settings where a change in FHR in response to acoustic stimulation cannot be assessed electronically, maternal perception of sound-provoked fetal movement appears to be predictive of fetal well-being [77-81].
Less common ancillary tests
ST analysis — Use of ST analysis does not appear to result in meaningful improvements in pregnancy outcome.
The STAN S31 fetal heart monitor, monitors the fetal electrocardiogram (ECG) during labor. Use of this device is based on the principle that fetal hypoxemia can result in elevation or depression of the ST segment. The monitor's software automatically identifies and analyzes changes in the T wave and the ST segment of the fetal ECG, which is obtained via a spiral electrode attached to the fetal scalp. The analysis is displayed in the lower section of the monitor's screen as a series of data points ("T/QRS crosses") and event markers. A visual alert ("ST event") appears when ST changes occur. Studies have reported the STAN computerized interpretation of FHR monitoring system has 38 to 90 percent sensitivity and 83 to 100 percent specificity for detecting fetal acidemia [82-84].
Clinicians who choose to use ST analysis should be trained and credentialed in its use and interpretation. The STAN S31 fetal heart monitor has been approved by the US Food and Drug Administration as an adjunct to assessment of abnormal FHR tracings in pregnancies over 36 weeks of gestation, in labor, with vertex presentation and ruptured fetal membranes. It is not indicated for monitoring initiated in the second stage of labor, since there may not be sufficient time to establish the baseline fetal ECG data required for automatic ST event signals. Transcutaneous Electrical Nerve Stimulation (TENS) for analgesia during labor is another contraindication because TENS may interfere with acquisition of the fetal ECG signal.
Three meta-analyses concluded use of ST analysis did not result in meaningful improvements in pregnancy outcome [85-87]. As an example, in a 2016 meta-analysis including seven randomized trials with a total of over 27,000 pregnancies, intrapartum fetal ECG analysis (PR to RR interval, ST segment) did not improve any neonatal outcome or decrease cesarean birth rates compared with continuous electronic FHR monitoring alone, but fewer fetal scalp sampling procedures were performed [87]. The largest randomized trial in the review assigned over 11,000 patients to "open" or "masked" monitoring with fetal ST-segment analysis and reported no significant between-group differences in the rate of cesarean birth, any operative birth, or the primary composite outcome (stillbirth, neonatal death, 5-minute Apgar score ≤3, cord artery pH ≤7.05 and base deficit in extracellular fluid ≥12, intubation in the delivery room, seizures, neonatal encephalopathy) [72,84].
These conclusions have been challenged in an editorial in which the authors asserted that, while the meta-analyses of ST analysis did not confirm a significant reduction in perinatal death, neonatal seizures, or neonatal encephalopathy, these outcomes are so uncommon that it is unlikely a study sufficiently large to prove no benefit statistically will ever be performed [88]. They also argued that reductions in the rates of fetal blood sampling, operative vaginal birth, and metabolic acidemia are clinically relevant, despite the lack of reduction in more patient-important neonatal outcomes.
Fetal scalp blood sampling — Fetal scalp blood sampling is an intrapartum procedure intended to assess the presence and degree of fetal acidemia by analyzing fetal capillary blood. An amnioscope with a light source is used to expose the fetal scalp, which is cleansed of blood, mucous, and amniotic fluid. The scalp is smeared with silicone gel so that a droplet of blood forms when the scalp is punctured with a 2-mm blade. The blood is collected in long, heparinized capillary tubes. The test requires that the cervix is dilated at least 2 to 3 cm, can be difficult to perform, and can be uncomfortable for the parturient. It is contraindicated when the mother is known to have a serious transmissible infection, such as HIV or hepatitis, and in fetuses at increased risk of a bleeding diathesis. Rare complications described in case reports include infection, hemorrhage, and leakage of cerebrospinal fluid [89-91].
Both pH and lactate measurements require the same laboratory facilities for microsample analysis. Less blood is needed for measurement of lactate than pH, otherwise one test does not clearly perform better than the other [92]. Intrapartum fetal scalp blood sampling to measure pH (and base excess/deficit) or lactate has not been clearly proven to reduce emergency cesarean deliveries or operative vaginal births or to improve long-term perinatal outcome [93-95]. For this reason and many others, including quality control issues, cost, patient discomfort, sample failure rates up to 10 percent, and unavailability of sampling kits, fetal scalp blood sampling is performed only rarely in the United States and elsewhere. (See "Umbilical cord blood acid-base analysis at delivery".)
Fetal pulse oximetry — Although intuitively a promising technique for fetal evaluation, fetal pulse oximetry has not been useful clinically.
Data from human and animal studies suggest that fetal arterial oxygen saturation (SaO2 by blood gas co-oximetry) >30 percent is usually associated with pH >7.13 [82,96]. In humans, the mean fetal oxygen saturation (SpO2 by fetal pulse oximetry) during the first and second stages of labor is 59±10 percent and 53±10 percent, respectively [83,97]. In the setting of an abnormal FHR pattern, fetal SpO2 <30 percent for greater than 10 minutes has been associated with an increased risk of fetal acidemia [84,85,98-101].
However, in a meta-analysis of randomized trials comparing the outcome of pregnancies in which both fetal pulse oximetry and cardiotocography results were available for intrapartum clinical management with the outcome of controls in which only cardiotocography results were available (7 trials, 8013 participants), fetal pulse oximetry had no statistical effect on the overall rate of cesarean birth or the rate of maternal or neonatal outcomes evaluated; the rates were similar in both groups [76,102].
Use of decision/interpretation aids and algorithms — Although recognition and management of category I and III tracings is relatively straightforward, the potential for development of progressive fetal hypoxia, metabolic acidosis, and metabolic acidemia varies widely across the different types of category II tracings. In part for this reason, investigators have proposed various algorithmic approaches to recognition, interpretation, and management of FHR tracings beyond category I. These approaches have had some success in achieving earlier recognition of tracings associated with metabolic acidemia [103]. However, their ability to improve neonatal outcome and/or reduce unnecessary interventions remains unproven, thus a change in the standard clinical approach described above is not warranted [104,105].
The following are examples of some decision/interpretation aids:
●A five-tier FHR classification system has been proposed to identify fetuses at risk of developing acidosis [106-108]. The system focuses on baseline FHR, variability, and decelerations to stratify the risk of evolution to acidemia. Depending on risk level, the system suggests different interventions, such as conservative measures or delivery. The five-tier has not been validated in a large prospective or randomized trial and no data are available to indicate that it improves neonatal outcome or reduces operative intervention.
●An online risk assessment calculator is available for management of category II tracings [109]. It takes into account factors such as labor stage (latent or active first stage or second stage), labor progress (normal or abnormal), assessment of variability (presence/absence of moderate variability or accelerations), and assessment of decelerations (frequency and duration of recurrent decelerations). Based on information entered by the clinician, the calculator suggests observation or delivery. The algorithm on which the calculator is based has been reported to facilitate earlier recognition of some, but not all, FHR tracings associated with metabolic acidemia without increasing the rate of operative intervention [21,103]. The performance of the calculator has not been assessed in a clinical trial.
●Artificial intelligence has also been used for interpretation of FHR tracings, but meta-analyses have concluded that it did not improve neonatal outcomes compared with usual clinical assessment of FHR tracings, and inter-rater reliability between experts and computer systems was moderate at best [110,111]. The analyses were dominated by two randomized trials (FM-ALERT [104] and INFANT [105]), which evaluated the use of continuous intrapartum FHR monitoring with computerized interpretation and real-time alerts. Neither trial reported a benefit in any maternal or neonatal outcome compared with usual care (intrapartum fetal monitoring with clinician interpretation).
The larger INFANT trial included over 47,000 pregnancies at or near term and followed offspring to two years of age [105]. Compared with usual care, the intervention did not increase recognition of abnormal FHR patterns, did not increase the rate of spontaneous vaginal birth, and did not improve neonatal outcome (composite or individual endpoints such as pH <7.05, metabolic acidosis, seizures, neonatal encephalopathy, hospital stay). Developmental assessment at age two years was similar for both groups.
●In 2018, one group described a standardized algorithm for the management of category II FHR tracings with recurrent "significant" FHR decelerations, defined as late decelerations, prolonged decelerations, or variable decelerations lasting at least 60 seconds and reaching a nadir of ≤60 bpm or at least 60 bpm below baseline [112]. Six hospitals in a large health system participated in a cohort study comparing maternal and neonatal outcomes before and after the introduction of the algorithm. Fetal monitor tracings that demonstrated moderate (or marked) variability and significant decelerations with >50 percent of contractions for 30 minutes were managed as follows:
•If cervical dilation was <4 cm and recurrent decelerations did not resolve with conservative corrective measures, delivery was accomplished.
•If cervical dilation was ≥4 cm, labor was permitted to continue only if progress was normal (first stage: cervical dilation ≥1 cm/hour; second stage: descent with pushing, total duration ≤90 minutes).
•Delivery was indicated if criteria for normal labor progress were not met or if the FHR tracing demonstrated a persistent pattern of minimal-absent variability.
Nearly 98 percent of screened patients were managed according to the algorithm. After its introduction, the rate of primary cesarean birth fell from 19.8 to 18.3 percent, low 5-minute Apgar scores fell from 2.3 to 1.7 percent, and a composite of severe newborn complications fell from 1.6 to 1.2 percent (all statistically significant differences).
If the results of this study can be replicated in other clinical settings, the approach may provide valuable guidance in the management of some of the most difficult category II FHR tracings. In the meantime, it seems reasonable to consider adopting more conservative expectations for normal labor progress, such as those described in this study, in a subset of patients with significant recurrent decelerations or minimal-absent variability that persists despite appropriate conservative corrective measures.
INVESTIGATIONAL PREVENTIVE THERAPY — Sildenafil citrate has marked vasodilatory effects on the pelvic and pulmonary circulations. It has been hypothesized that, if given prophylactically in early labor, its favorable effects on uteroplacental and fetal blood flow [113,114] may reduce the frequency of intrapartum fetal distress and, in turn, emergency cesarean or operative vaginal birth for this indication.
In a trial that randomly assigned 300 pregnant patients at term in early labor to receive sildenafil (50 mg orally every eight hours to a maximum of three doses) or placebo, sildenafil reduced the frequency of strictly defined pathologic FHR patterns by 43 percent (25.3 versus 44.7 percent, relative risk [RR] 0.57, 95% CI 0.41-0.79) [115]. Importantly, sildenafil was associated with a 51 percent reduction in emergency operative births (18 versus 36.7 percent, RR 0.49, 95% CI 0.33-0.73), without an increase in adverse neonatal outcomes (20.7 versus 21.3 percent, RR 0.97, 95% CI 0.62-1.50). Maternal side effects were mild and self-limited, and there was no increase in postpartum bleeding. The findings of this trial are promising; however, larger trials are needed to confirm the safety and efficacy of sildenafil in this setting before it can be routinely recommended as part of the management of pathologic FHR patterns.
CONTROVERSIAL THEORIES — There is clear consensus that normal intrapartum FHR monitoring, when accompanied by normal Apgar scores, normal umbilical artery blood gas results, or both, is inconsistent with an acute intrapartum hypoxic-ischemic event sufficient to cause hypoxic-ischemic encephalopathy (HIE) and cerebral palsy (CP) [22,116]. Intrapartum hypoxic injury that is sufficient to cause CP requires significant interruption of fetal oxygenation, usually manifested by significant neonatal metabolic acidemia (reflected by low umbilical artery pH and elevated base deficit), immediate newborn depression (usually reflected by low Apgar scores), and moderate-severe neonatal encephalopathy. (See "Etiology and pathogenesis of neonatal encephalopathy".)
Contrary to this consensus, one group has proposed that the standard markers of intrapartum fetal hypoxia described above need not be present to establish that an intrapartum event was the cause of later neurologic impairment and that impairment can be due to the effects of mechanical forces of labor on the fetal head [117]. Although mechanical forces of labor cause pressure on the fetal head, injury by this hypothetical mechanism has no scientific basis: It has never been reported, and a systematic review concluded that fetal intracranial pressure is well protected from extracranial forces and available data do not support intrapartum extracranial pressure as a cause of fetal brain injury [118].
Another group has proposed a risk-scoring system, dubbed the "Fetal Reserve Index (FRI)," for interpretation and management of FHR patterns [119-121]. The FRI is a weighted calculation of eight risk categories, including 10 maternal risk factors (eg, chronic debilitating disease, short stature), 9 obstetric risk factors (eg, placental abruption, malpresentation), and 12 fetal risk factors (eg, meconium passage, chorioamnionitis). Their criteria for abnormal FHR patterns and uterine activity are defined differently from standard National Institute of Child Health and Human Development and international definitions. This system has never been validated; furthermore, the authors' lack of standard criteria for diagnosing cases of HIE, lack of appropriate controls, and multiple obvious sources of potential bias preclude reasonably founded conclusions regarding safety or utility of the FRI.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Labor".)
SUMMARY AND RECOMMENDATIONS
●Goal – Normal human labor is characterized by regular uterine contractions and repeated episodes of transient interruption of fetal oxygenation. Most fetuses tolerate this process well, but some do not. The primary goal of intrapartum fetal heart rate (FHR) monitoring is to assess the adequacy of fetal oxygenation during labor so that timely intervention can be undertaken when appropriate to reduce the likelihood of neurologic injury or death. Another important goal is accurate identification of appropriately oxygenated fetuses so that unnecessary intervention can be avoided. There is evidence that intrapartum fetal monitoring is associated with a reduction in intrapartum death. However, conclusive evidence of a reduction in long-term neurologic impairment is lacking. (See 'Does intrapartum FHR monitoring improve outcome?' above and 'Clinical approach to FHR monitoring and evaluation of abnormal patterns' above.)
●Candidates
•Medicolegal precedent in the United States mandates some form of intrapartum FHR monitoring. For most high-risk pregnancies, continuous electronic FHR monitoring is recommended. For low-risk pregnancies, either intermittent or continuous electronic FHR monitoring is reasonable, but frequent intermittent monitoring can be cumbersome and difficult for many institutional nursing services to achieve. (See 'Candidates for intrapartum fetal monitoring' above.)
•Intrapartum FHR monitoring is usually not performed when detection of an FHR abnormality would not prompt any intervention (eg, conservative maneuvers to improve fetal oxygenation and/or cesarean birth). For example, pregnancies at a gestational age below the limit of viability and pregnancies in which the fetus has an untreatable anomaly lethal in the newborn. (See 'Candidates for intrapartum fetal monitoring' above.)
●Continuous versus intermittent – Two commonly used modalities for intrapartum FHR monitoring are continuous electronic FHR monitoring and intermittent auscultation. Neither test has been proven to be superior, provided that intermittent auscultation is performed as prescribed in randomized trials. (See 'Does intrapartum FHR monitoring improve outcome?' above.)
●Definitions and classification
•Standardized FHR definitions proposed by the National Institute of Child Health and Human Development (NICHD) and endorsed by the American College of Obstetricians and Gynecologists (ACOG) are summarized in the table (table 1). (See 'NICHD classification of FHR patterns' above.)
•The three-tier system of FHR classification proposed by the NICHD is summarized in the table (table 3). General concepts of intrapartum FHR management are summarized in the table (table 4). Use of this standardized approach to pattern recognition coupled with a standardized package of therapeutic interventions may improve neonatal outcome. (See 'NICHD classification of FHR patterns' above and "Intrapartum category I, II, and III fetal heart rate tracings: Management".)
•Interpretation of intrapartum monitoring should include assessment of measures of uterine activity in context, and this assessment should be incorporated routinely into FHR management decisions. In the United States, the NICHD has identified several essential components of uterine activity, including uterine contraction frequency, contraction intensity, contraction duration, resting time between contractions, and resting tone between contractions. Normal uterine contraction frequency was defined as five or fewer contractions in 10 minutes, averaged over 30 minutes. Contraction frequency above this limit was termed tachysystole. (See 'Assessment of uterine activity' above.)
●Interpretation and evaluation – Key principles for evaluation of the FHR tracing and management of FHR patterns include (see 'Key principles' above):
•Confirm that the monitor is correctly recording the FHR and uterine activity. Make sure that the recorded heart rate is not maternal.
•Assess uterine activity and classify the tracing in a category (I, II or III).
•If the tracing is category I and the patient is low-risk, initiate routine intrapartum fetal surveillance. Moderate baseline variability and/or FHR accelerations reflect the oxygenation of the central nervous system and reliably predict the absence of ongoing hypoxic injury and metabolic acidemia at the time it is observed. (See 'Variability' above and 'Accelerations' above.)
•If the tracing is not category I, evaluate the fetal oxygenation pathway. Attempt to correct oxygenation problems, if appropriate. Remember that the appearance of the FHR tracing can be affected by factors other than fetal oxygenation (eg, fetal sleep and arrhythmias, maternal artifact and medications). (See 'Pitfalls in attributing category II and category III patterns to fetal hypoxia' above.)
•The management of category II and III tracings is summarized in the table (table 4) and discussed in detail separately. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management".) In the absence of spontaneous FHR accelerations, fetal scalp stimulation resulting in a FHR acceleration rising ≥15 bpm above baseline lasting for ≥15 seconds almost always assures the absence of fetal acidemia. (See 'Useful ancillary tests for intrapartum fetal evaluation' above.)
•If the FHR pattern does not improve within a reasonable period of time, begin planning for the possible need for rapid delivery.
●Predictive value
•Electronic fetal monitoring has a very high false-positive rate for predicting adverse neurologic outcomes. However, the false-negative rate of electronic fetal monitoring is very low. Fetal monitoring is not a diagnostic test for fetal injury; it is a screening test for interrupted fetal oxygenation. A normal FHR tracing identifies a fetus with a very low risk of hypoxic intrapartum injury. An abnormal FHR tracing signals the need for further evaluation of fetal oxygen status. (See 'Does intrapartum FHR monitoring improve outcome?' above.)
•Contemporary evidence does not confirm earlier assumptions that electronic FHR monitoring is associated independently with a significant increase in the rate of cesarean birth. (See 'Does intrapartum FHR monitoring improve outcome?' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Bruce K Young, MD, who contributed to an earlier version of this topic review.
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