INTRODUCTION — Interpretation of intrapartum electronic fetal heart rate (FHR) tracings has been hampered by interobserver and intraobserver variability, which historically has been high [1-3]. In 2008, the American College of Obstetricians and Gynecologists (ACOG), the Society for Maternal-Fetal Medicine (SMFM), and the United States National Institute of Child Health and Human Development (NICHD) convened a workshop to standardize definitions for and interpretation of electronic fetal monitoring (EFM), propose management guidelines, and develop research questions [4,5]. Major outputs from this workshop were clearer standards for FHR interpretation (table 1A) and a three-tier system for the categorization of intrapartum EFM (table 1B). This system has been widely adopted in the United States and elsewhere, and is the basis for this topic. The International Federation of Gynecology and Obstetrics (FIGO2015)  and others have published similar guidelines [7-10].
Intrapartum management of category I, II, and III FHR patterns will be discussed here. An overview of issues related to intrapartum FHR assessment is available separately. (See "Intrapartum fetal heart rate monitoring: Overview".)
CATEGORY I PATTERN: NORMAL — This pattern is considered normal because studies have demonstrated absence of fetal metabolic acidemia when the diagnostic criteria for a category I pattern are present [11-14].
Diagnostic criteria — A category I pattern (waveform 1) is defined by:
●Baseline rate of 110 to 160 beats per minute (bpm)
●Moderate FHR variability (ie, amplitude 6 to 25 bpm)
●Absence of late decelerations
●Absence of variable decelerations
Early decelerations and accelerations may be present or absent.
●Intervention – No resuscitative interventions are warranted since the fetus is presumed to be adequately oxygenated and nonacidemic.
•Electronic fetal monitoring (EFM) is generally performed continuously even in pregnancies with a category I pattern since the fetal status can change abruptly; however, if the maternal and fetal conditions appear stable, it is reasonable to interrupt monitoring of a category I pattern for up to 30 minutes to facilitate ambulation, bathing, position changes, or other activities for maternal comfort. It is also reasonable to switch to intermittent FHR monitoring in low-risk pregnancies (ie, those without risk factors that increase the risk for a complicated birth) as long as the category I pattern persists: The FHR is checked 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 . For patients with a category I pattern and pregnancy complications potentially associated with fetal hypoxemia where the risk of developing fetal acidosis is higher, continuous EFM is most practical as the EFM should be reviewed at least every 15 minutes in the first stage of labor and every five minutes during the second stage, based on expert opinion . (See "Intrapartum fetal heart rate monitoring: Overview".)
•Intermittent auscultation can be used in pregnancies that are not at high risk for adverse outcomes. However, intermittent auscultation only identifies changes in baseline rate and cannot measure variability or clearly identify FHR patterns. One reasonable approach to intermittent auscultation is to evaluate and record the FHR every 15 minutes in the active phase of the first stage of labor and every five minutes in the second stage. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Frequency and duration of monitoring'.)
CATEGORY III PATTERN: ABNORMAL — This pattern is considered abnormal because studies have demonstrated an increased risk for fetal hypoxic acidemia when the diagnostic criteria for a category III pattern are present [16,17]. Perinatal asphyxia has a range of outcomes, including normal, mild to severe neurological deficits, and death. (See "Etiology and pathogenesis of neonatal encephalopathy" and "Clinical features, diagnosis, and treatment of neonatal encephalopathy".)
Diagnostic criteria — A category III pattern is defined by:
●Absent baseline FHR variability (ie, amplitude undetectable) and any of the following:
•Recurrent late decelerations (waveform 2A and waveform 3)
•Recurrent variable decelerations (waveform 2B)
Recurrent decelerations are defined as occurring with at least 50 percent of uterine contractions in a 20-minute window [5,18]. Lack of interobserver agreement about absent versus minimal variability (ie, amplitude 0 to 5 bpm) is a common problem in clinical practice [3,19]. For this reason, management strategies for category III patterns tend to be the same whether variability is absent or minimal . (See "Intrapartum fetal heart rate monitoring: Overview".)
●A sinusoidal pattern (waveform 2C)
Management of nonsinusoidal category III pattern
●Perform scalp stimulation – Scalp stimulation should be attempted as it is a quick, minimally invasive, and informative maneuver to further evaluate the fetus. When scalp stimulation induces an acceleration, the probability of fetal pH <7.20 is less than 10 percent versus approximately 50 percent when no acceleration occurs in this setting [21-24]. The technique and evidence of efficacy are described separately. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'FHR response to stimulation'.)
Other methods of fetal evaluation are either no longer widely available (fetal scalp blood sampling) or not useful (fetal electrocardiogram or pulse oximetry). These methods are reviewed separately. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Less common ancillary tests'.)
●Prepare for operative delivery – Preparations for operative delivery should be made while initiating resuscitative measures.
●Begin in utero resuscitation (table 2) – The following resuscitative measures are aimed at improving uteroplacental perfusion and fetal oxygenation. Multiple interventions are generally applied simultaneously. Data from randomized trials on the efficacy of in utero resuscitation are not available.
•Reposition the patient onto their left or right side to relieve any compression of the umbilical cord or maternal great vessels, which may improve utero-placental-fetal perfusion .
If lateral positioning is ineffective and the FHR tracing shows recurrent variable decelerations, a prolonged deceleration, or bradycardia, try a knee-chest or all fours position (figure 1) to relieve possible cord compression.
•Administer an intravenous (IV) fluid bolus (eg, 500 to 1000 mL of Lactated Ringer or normal saline solution). Although no randomized trials have evaluated the effect of IV fluid boluses alone on fetal heart abnormalities, an IV fluid bolus of a nonglucose containing crystalloid solution can improve uteroplacental blood flow and fetal oxygenation if the patient is hypovolemic from prolonged lack of oral or IV intake, vomiting, or sympathetic blockade, and thus may improve fetal oxygenation [25,26]. However, fluids should be administered cautiously in patients at increased risk of volume overload, such as patients with preeclampsia or heart disease and those who are receiving beta-adrenergic agonists for tocolysis.
Glucose-free solutions should be used because acute maternal glucose infusion can cause fetal hyperglycemia, metabolic acidosis, and neonatal hypoglycemia .
•Discontinue uterotonic drugs to improve utero-placental-fetal blood flow, which is reduced during contractions. Discontinuation of uterotonic drugs often provides adequate uterine relaxation to correct FHR abnormalities in patients receiving these drugs.
Patients not receiving uterotonic drugs can be told to stop pushing temporarily or to push with every other contraction or they can be given a tocolytic.
•Administer a tocolytic (eg, terbutaline 250 mcg subcutaneously) if the category III FHR pattern persists after discontinuation of uterotonic drugs or in the absence of their use, unless abruption is suspected. Tachysystole (defined as more than five contractions in 10 minutes, averaged over a 30-minute window ), prolonged contractions, or any contractile activity that exceeds the compensatory mechanism of the specific fetoplacental unit can reduce utero-placental-fetal blood flow. Uterine relaxation may improve blood flow and, in turn, fetal oxygenation. In a meta-analysis of acute tocolysis for intrapartum nonreassuring fetal status (four trials, 605 pregnancies with nonreassuring FHR tracings), compared with emergency cesarean birth, acute tocolysis improved neonatal acid-base status (reduced prevalence of base deficit >12 mmol/L: odds ratio [OR] 0.61, 95% CI 0.37-0.99) and reduced neonatal intensive care unit (NICU) admission (OR 0.42, 95% CI 0.22-0.78) despite an increased time-to-delivery interval (mean difference 17.62 minutes, 95% CI 15.66-19.58) . True maternal and neonatal benefits remain uncertain, given that the overall cesarean birth rate was similar for both groups and the improvement in neonatal acid-base status had a wide confidence interval approaching 1.0.
Uterine relaxation may also be induced with one or two doses of IV nitroglycerin (50 mcg). The onset of uterine relaxation occurs within 30 seconds to two minutes and lasts only a minute or two .
•Consult with the anesthesia team in patients who were recently given neuraxial drugs for labor pain. If maternal hypotension secondary to recent epidural dosing is identified, administering an alpha-adrenergic agonist (such as phenylephrine or ephedrine) and an IV fluid bolus is corrective and will improve utero-placental-fetal blood flow. These medications should be administered by someone with expertise in their dosing and side effects. Whether medication is indicated even in the absence of hypotension is an individualized decision as reduced placental perfusion from sympathetic blockade can occur without marked changes in maternal blood pressure.
The administration of opioids intrathecally may induce a tetanic uterine contraction leading to transient fetal bradycardia . As discussed above, uterine hypertonus may be reversed with one or two doses of IV nitroglycerin (50 mcg). The onset of uterine relaxation occurs within 30 seconds to two minutes and lasts only a minute or two . (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension' and "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Fetal bradycardia'.)
•Role of amnioinfusion – Amnioinfusion is generally not indicated with category III patterns. If considered, it should only be used for a category III pattern with recurrent variable decelerations and delivery should be undertaken promptly if the decelerations do not rapidly diminish or resolve. (See "Amnioinfusion".)
•Role of maternal oxygen supplementation – Maternal oxygen supplementation is appropriate when treating maternal hypoxemia. It has no role in fetal resuscitation in parturients with normal respiratory function. (See 'Interventions of no or uncertain benefit' below.)
●Assess results and act
•If fetal stimulation and/or in utero resuscitation promptly leads to resolution of the category III tracing, then continue maternal and fetal monitoring as appropriate for the FHR pattern (category I or II).
•If scalp stimulation does not result in a FHR acceleration and the FHR tracing does not improve after resuscitative measures, then delivery should be expedited since a 10-minute period of a category III pattern, particularly with a large total area of deceleration, is associated with acidemia . However, the time from this decision to delivery should consider the health of both mother and fetus: there may be circumstances (eg, difficult maternal airway, maternal coagulopathy, severe obesity) when safe delivery cannot be performed expeditiously.
It is also important to consider the probable underlying cause(s) of the category III pattern, as urgent delivery is necessary in some acute settings, such as uterine rupture, visible cord prolapse, or severe abruption, but may be delayed in less urgent settings to treat maternal acute illness, such as sepsis, trauma, or diabetic ketoacidosis. Physician judgment plays an important role in assessing the probable cause of the category III pattern, choosing the appropriate interventions for the specific patient setting, assessing the response to those interventions, and timing of cesarean or assisted vaginal birth if the category III pattern persists.
Interventions of no or uncertain benefit
●Supplemental oxygen for nonhypoxemic parturients – In a nonhypoxemic mother, the underlying causes of fetal hypoxemia need to be addressed (eg, maternal hypotension or hypovolemia, cord compression, tachysystole, abruption) because maternal oxygen administration will not correct fetal acidemia .
In a 2021 meta-analysis of 16 randomized trials comparing oxygen supplementation versus room air for intrauterine resuscitation (n = 1078 oxygen, n = 974 room air), oxygen supplementation resulted in no clinically relevant improvement in umbilical artery (UA) pH or other neonatal outcomes (eg, Apgar scores, neonatal intensive care unit [NICU] admissions) . The trials included patients with singleton, nonanomalous pregnancies in labor or patients undergoing scheduled cesarean birth.
When stratified for the presence or absence of labor, oxygen administration in patients undergoing scheduled cesarean increased UA partial pressure of oxygen (PaO2; weighted mean difference [WMD] 2.12 mmHg, 95% CI 0.09-4.15 mmHg) and reduced the incidence of UA pH less than 7.2 (relative risk [RR] 0.63, 95% CI 0.43-0.90); these changes were not noted among those in labor (PaO2: WMD 3.60 mmHg, 95% CI -0.30 to 7.49 mmHg; UA pH <7.2, RR 1.34, 95% CI 0.58-3.11). A limitation of the analysis was that it did not specifically assess use of oxygen for management of abnormal FHR tracings. If maternal hyperoxemia is achieved, a therapeutic effect on recurrent late decelerations due to impaired placenta-to-fetus oxygen delivery is plausible; however, data from underpowered randomized trials have not shown a statistically significant improvement .
Management of sinusoidal category III pattern — True sinusoidal FHR patterns are exceedingly rare and thus intervention has not been studied systematically.
●The pattern has been associated with severe fetal anemia, some opioids (eg, meperidine, alphaprodine [Nisentil], butorphanol, nalbuphine hydrochloride), and hypoxia with acidosis . (See "Spontaneous massive fetomaternal hemorrhage", section on 'Clinical presentation'.)
●Delivery is generally indicated if resuscitative measures do not improve the pattern. However, if the pregnancy (including the intrapartum course) was uncomplicated, the sinusoidal appears to be related to recent administration of an opioid, and the FHR pattern was normal until administration, then the pattern may be transient and unrelated to fetal hypoxia/acidosis. Sinusoidal pattern has observed 19 minutes after alphaprodine administration and lasting 60 minutes .
CATEGORY II PATTERN (INDETERMINATE) — This pattern is of uncertain clinical significance because the potential for development of fetal acidosis varies widely across the different types of category II patterns. The American College of Obstetricians and Gynecologists (ACOG) considers category II tracings as indeterminate as they comprise a diverse spectrum of FHR patterns that require evaluation, ongoing surveillance, initiation of appropriate corrective measures, and reevaluation . The Society of Obstetricians and Gynaecologists of Canada classifies these tracings as "atypical" .
Diagnostic criteria — Category II FHR patterns include all FHR patterns that are not classified as category I (normal) or category III (abnormal) (table 1B). (See 'Category I pattern: Normal' above and 'Category III pattern: Abnormal' above.).
●Perform scalp stimulation – As discussed above, scalp stimulation should be attempted as it is a quick, minimally invasive, and informative maneuver to further evaluate the fetus. When scalp stimulation induces an acceleration, the probability of fetal pH <7.20 is less than 10 percent versus approximately 50 percent when no acceleration occurs in this setting [21-24,39-41]. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'FHR response to stimulation'.)
Other methods of fetal evaluation are either no longer widely available (fetal scalp blood sampling) or not useful (fetal electrocardiogram or pulse oximetry). These methods are reviewed separately. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Less common ancillary tests'.)
●Assess variability – Moderate variability (ie, amplitude 6 to 25 bpm) is strongly associated (98 percent) with absence of fetal acidosis [39,42-44]. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Fetal scalp blood sampling'.)
●Evaluate for factors that may reduce fetal oxygenation – Clinical scenarios associated with intrapartum fetal compromise include abruption, uterine rupture from a trial of labor after a previous cesarean birth, fetal growth restriction, preeclampsia with severe features, and severe fetal anemia.
●Initiate one or more of resuscitative measures, as described above. (See 'General approach' above.)
●Frequently reassess, taking into account the stage and progress of labor, to determine whether to perform an operative intervention and the urgency of the intervention. Continued surveillance and frequent reassessment are indicated until the pattern resolves to category I or progresses to category III, which develops when fetal compensatory mechanisms fail to maintain adequate cerebral and tissue oxygenation, leading to fetal acidosis. Expeditious delivery of these fetuses is indicated. Timely and effective intervention before acidemia becomes severe may prevent perinatal morbidity or mortality . (See 'Category III pattern: Abnormal' above.)
However, there are virtually no data to inform decision-making as to how long to monitor a fetus with a persistent category II tracing despite use of standard resuscitative measures.
Because of the wide spectrum and significance of category II patterns, various decision aids have been created to help with their identification, interpretation, and management, but these systems have not been well-validated. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Use of decision/interpretation aids and algorithms'.)
Approach to selected category II patterns
Late decelerations without loss of variability — Recurrent late decelerations are a reflex central nervous system (CNS) response to fetal hypoxia and acidemia, as well as direct myocardial depression and humoral factors . (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Late deceleration'.)
●Identify the potential source – Recurrent late decelerations may occur in the following settings:
•Placental disorders associated with placental insufficiency
•The general approach is described above (see 'General approach' above). Assessment of FHR variability and accelerations is important, given the low predictive value of late decelerations alone for fetal acidosis and poor neonatal outcome [47-49]. Moderate variability is strongly associated (98 percent) with an umbilical pH >7.15  and spontaneous or elicited FHR accelerations are strongly associated with pH >7.2 [21-24]. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'FHR response to stimulation'.)
•The duration of time for which it is safe to closely monitor a category II tracing with late decelerations associated with moderate variability and/or accelerations depends on the specific clinical scenario, particularly whether the potential source is reversible or can be ameliorated with resuscitative maneuvers.
Fetal tachycardia — Fetal tachycardia is defined as a baseline FHR greater than 160 bpm for at least 10 minutes.
●Identify the potential source – Causes of fetal tachycardia include:
•Medications (eg, beta-agonists, atropine, cocaine)
•Elevated maternal catecholamine levels
•The general approach is described above. (See 'General approach' above.)
•The evaluation of fetal tachycardia should include assessment for maternal infection or abruption and a review of maternal medications. Appropriate treatment should be initiated if the underlying cause can be identified and treated (eg, acetaminophen for reduction of fever and antibiotics for treatment of intraamniotic infection). Delivery is indicated if acidemia or placental abruption is suspected. Tachycardia due to chorioamnionitis is generally not an indication for delivery unless decelerations or category III pattern is present, or if the patient is remote from delivery and the tachycardia does not resolve with maternal hydration and antipyretic therapy. (See "Acute placental abruption: Management and long-term prognosis" and "Intraamniotic infection (clinical chorioamnionitis)", section on 'Delivery'.)
Isolated fetal tachycardia less than 200 bpm has not been strongly associated with fetal acidemia [50-53]. Rarely, fetal tachycardia can be due to a fetal tachyarrhythmia, such as atrial flutter or supraventricular tachycardia. These tachyarrhythmias are characterized by a very high FHR, often in excess of 200 bpm, and may lead to hydrops fetalis. (See "Fetal arrhythmias", section on 'Tachyarrhythmias'.)
Variable decelerations without loss of variability or accelerations — Variable decelerations occur when the umbilical cord is compressed. (See "Intrapartum fetal heart rate monitoring: Overview", section on 'Variable deceleration'.)
●Identify the potential source
•Umbilical cord prolapse
•Nuchal cord, knot in cord
•Intermittent variable decelerations (associated with <50 percent of contractions) are frequently observed intrapartum and usually associated with moderate variability and/or accelerations. They do not typically result in adverse consequences, presumably because transient cord compression is well tolerated by the fetus . Thus, they do not require intervention.
•Metabolic acidosis or mixed metabolic and respiratory acidosis can develop with increasing duration, depth, and frequency of variable decelerations . Therefore, recurrent variable decelerations (>50 percent of contractions) require close surveillance for loss of variability and accelerations, which signify a category III pattern. (See 'Category III pattern: Abnormal' above.)
-A vaginal examination is performed to assess for cord prolapse.
-One or more in utero resuscitation measures are initiated, with the major focus to resolve cord compression. Change of maternal position is a reasonable first treatment option . (See 'General approach' above.)
-Amnioinfusion is a reasonable second-line option. In a meta-analysis of randomized trials comparing amnioinfusion with no amnioinfusion in patients with potential cord compression because of oligohydramnios or suspected cord compression because of variable FHR decelerations, amnioinfusion resulted in a 50 to 60 percent reduction in FHR abnormalities compared with controls . There was a reduction in the number of cesarean births performed because of FHR abnormalities (risk ratio [RR] 0.46, 95% CI 0.31-0.68) and improvement in several neonatal outcomes, including a trend toward fewer neonates with umbilical artery (UA) pH <7.2 (RR 0.58, 95% CI 0.29-1.14). However, more research is needed to confirm the findings since longer-term measures of fetal/neonatal outcome were not assessed, the diagnosis of fetal distress in the trials was not stringent, and the value in specific clinical situations, such as FHR decelerations, oligohydramnios, or prelabor rupture of membranes was not evaluated. Patients with low preamnioinfusion amniotic fluid volume are most likely to experience resolution of variable decelerations with amnioinfusion. In patients with a high amniotic fluid volume (amniotic fluid index >12 cm) and variable decelerations, a nuchal cord or umbilical cord knot is a more likely cause of the variable pattern than reduced amniotic fluid, so amnioinfusion is less likely to be beneficial . (See "Amnioinfusion".)
-Delivery is indicated if a category III pattern develops. (See 'Category III pattern: Abnormal' above.)
Loss of variability without decelerations — FHR variability results from oscillatory input by the parasympathetic nervous system.
●Identify the potential source – The new onset of minimal variability (amplitude 0 to 5 bpm) may occur for several reasons, including [59-61]:
•Fetal sleep cycle – These cycles generally last approximately 20 minutes, but may persist for as long as one hour. When the fetal sleep cycles are over, moderate variability should return.
•CNS depressants – The most common medications that decrease variability are opioids and magnesium sulfate. The effect of maternal opioids on FHR variability generally lasts no more than two hours.
Long-standing loss of variability can be related to congenital or acquired anomalies of the CNS or heart, or to very preterm gestation [62-64]. Antenatal corticosteroid administration has been associated with a decrease in variability on days 2 and 3 after administration [65-69].
•If the FHR pattern had been normal and there are no decelerations, a reasonable approach to the assessment and management of new-onset minimal fetal variability is to make a presumptive diagnosis of a fetal sleep cycle or the effect of recently administered maternal medications and continue routine intrapartum care.
•It is also prudent to attempt to induce accelerations with scalp stimulation, as the presence of accelerations is strong evidence of the absence of fetal acidemia at that time . Clinicians should have a plan for cases in which no acceleration occurs after scalp stimulation. In general, if the tracing does not improve, delivery is indicated.
•A maternal fluid bolus and repositioning are appropriate adjunctive measures (table 2), especially in settings in which a benign etiology is less certain, such as coexistent pregnancy complications associated with uteroplacental insufficiency. (See 'General approach' above.)
Fetal bradycardia/prolonged deceleration without loss of variability — Fetal bradycardia (below 110 bpm) and a prolonged deceleration (table 1A) are approached similarly, since the distinction between these two entities is based primarily on the number of minutes of the decrease in FHR.
●Identify the potential cause – The causes of prolonged deceleration or fetal bradycardia include:
•Rapid fetal descent
•Treatment of fetal bradycardia or prolonged deceleration is aimed at the cause. Evaluation should include assessment of maternal blood pressure and contraction frequency and strength, and physical examination for evidence of rapid fetal descent, cord prolapse, abruption, or uterine rupture. (See "Umbilical cord prolapse" and "Uterine rupture: Unscarred uterus" and "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences" and "Uterine rupture: After previous cesarean birth".)
•Delivery is indicated if resuscitative measures to correct the underlying cause are not possible or fail to resolve the bradycardia. In one study of 5388 term, singleton pregnancies at full dilation with a nonanomalous fetus in cephalic presentation, a terminal deceleration occurred in 951 (17.7 percent) and 12 (1.3 percent) had umbilical cord gas arterial pH <7.10 . Of the 31 who had terminal bradycardia (FHR <110 bpm for ≥10 minutes before delivery), four had an umbilical cord gas arterial pH ≤7.10. Although infants with terminal bradycardia were at increased risk of acidemia, the positive predictive value was only 12.9 percent. The authors also noted a positive association between increasing duration of a terminal deceleration beyond two minutes and decreasing pH (pH decreased by 0.042 for every additional two minutes after the first two minutes).
•Delivery is also indicated for development of a category III tracing.
•If the FHR returns to a normal baseline rate and variability and accelerations are present, fetal acidemia is unlikely.
PREVALENCE OF CATEGORY I, II, AND III PATTERNS DURING LABOR — Most parturients have a category I pattern for most of the intrapartum period, although the prevalence of category I patterns decreases and the prevalence of both category II and III patterns increases near delivery. For example, in a study of the intrapartum FHR characteristics of over 48,000 patients in labor with a singleton, nonanomalous fetus at term in 10 hospitals:
●At some point during labor:
•Category I patterns were present in over 99 percent of tracings
•Category II patterns were present in 84 percent of tracings
•Category III patterns were present in 0.1 percent of tracings
●Over the course of labor:
•Category I patterns were present 78 percent of the time
•Category II patterns were present 22 percent of the time
•Category III patterns were present 0.004 percent of the time
●In the two hours before delivery:
•Category I were present in 61 percent of tracings
•Category II tracings were present in 39 percent of tracings
•Category III tracings were present in 0.006 percent
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
●Three-tier system of classification – The three-tier system for the categorization of intrapartum fetal heart rate (FHR) tracings (table 1A-B) is a useful means of approaching management (table 3). (See 'Introduction' above.)
•Category I tracings – Category I tracings (waveform 1) are normal and not associated with fetal metabolic acidemia at the time of observation. Low-risk patients with category I tracings may be followed intermittently, with reapplication of the monitor and reassessment of the tracing at least every 30 minutes in the first stage of labor and every 15 minutes in the second stage. High-risk patients (ie, those with risk factors that increase the risk for a complicated birth) are typically monitored continuously because of a greater potential for change to a category II or III pattern and practicality. (See 'Category I pattern: Normal' above.)
•Category III tracings – Category III tracings (waveform 2A-C) are abnormal and associated with an increased risk of fetal hypoxic acidemia. Patients with category III tracings should be prepared for delivery while initiating resuscitative measures (table 2). If there is no improvement in the tracing after resuscitative measures and scalp stimulation does not result in FHR acceleration, delivery should be accomplished expeditiously, but ensuring maternal safety. (See 'Category III pattern: Abnormal' above.)
•Category II tracings – The potential for development of fetal acidosis varies widely across the different types of category II tracings. Patients with these tracings should be evaluated for factors that may reduce fetal oxygenation, taking into account associated clinical circumstances (eg, abruption, fetal growth restriction, trial of labor after cesarean, stage of labor, decelerations/bradycardia). An attempt at in utero resuscitation rather than operative delivery is usually appropriate (table 2), with frequent reassessment to determine whether operative delivery should be performed. Moderate variability or FHR accelerations generally excludes hypoxic injury at that time and warrants continued surveillance, as long as labor progress is normal and no condition associated with rapid fetal compromise (eg, abruption, uterine rupture) is present. (See 'Category II pattern (Indeterminate)' above.)
3 : Intrapartum nonreassuring fetal heart rate tracing and prediction of adverse outcomes: interobserver variability.
4 : The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines.
5 : Electronic fetal heart rate monitoring: research guidelines for interpretation. National Institute of Child Health and Human Development Research Planning Workshop.
14 : Electronic fetal heart rate monitoring: early neonatal outcomes associated with normal rate, fetal stress, and fetal distress.
15 : ACOG Practice Bulletin No. 106: Intrapartum fetal heart rate monitoring: nomenclature, interpretation, and general management principles.
16 : ACOG Practice Bulletin No. 106: Intrapartum fetal heart rate monitoring: nomenclature, interpretation, and general management principles.
17 : An evaluation of fetal heart rate characteristics associated with neonatal encephalopathy: a case-control study.
18 : The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines.
19 : Interobserver and intraobserver reliability of the NICHD 3-Tier Fetal Heart Rate Interpretation System.
20 : Intrapartum management of category II fetal heart rate tracings: towards standardization of care.
24 : Intrapartum assessment of fetal well-being: a comparison of fetal acoustic stimulation with acid-base determinations.
25 : Efficacy of intrauterine resuscitation techniques in improving fetal oxygen status during labor.
27 : A prospective randomized trial of two solutions for intrapartum amnioinfusion: effects on fetal electrolytes, osmolality, and acid-base status.
28 : Acute tocolysis for intrapartum nonreassuring fetal status: how often does it prevent cesarean delivery? A systematic review and meta-analysis of randomized controlled trials.
29 : Intravenous nitroglycerin to relieve intrapartum fetal distress related to uterine hyperactivity: a prospective observational study.
30 : Uterine hyperactivity after intrathecal injection of fentanyl for analgesia during labor: a cause of fetal bradycardia?
31 : A prospective cohort study of fetal heart rate monitoring: deceleration area is predictive of fetal acidemia.
33 : Maternal Oxygen Supplementation Compared With Room Air for Intrauterine Resuscitation: A Systematic Review and Meta-analysis.
43 : Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis.
46 : The intrapartum deceleration in center stage: a physiologic approach to the interpretation of fetal heart rate changes in labor.
48 : Intrapartum electronic fetal heart rate monitoring and the identification of metabolic acidosis and hypoxic-ischemic encephalopathy.
49 : Clinical fetal monitoring. VII. The evaluation and significance of intrapartum baseline FHR variability.
50 : Umbilical artery blood acid-base analysis and fetal heart rate baseline in the second stage of labor.
53 : Intrapartum fetal heart rate monitoring. V. Fetal heart rate patterns in the second stage of labor.
54 : A multicenter controlled trial of fetal pulse oximetry in the intrapartum management of nonreassuring fetal heart rate patterns.
55 : Measures of acidosis with repetitive umbilical cord occlusions leading to fetal asphyxia in the near-term ovine fetus.
59 : Comparison of the effects of meperidine and nalbuphine on intrapartum fetal heart rate tracings.
61 : The effect of magnesium sulfate on fetal heart rate parameters: A randomized, placebo-controlled trial.
65 : Immediate and delayed effects of antenatal corticosteroids on fetal heart rate: a randomized trial that compares betamethasone acetate and phosphate, betamethasone phosphate, and dexamethasone.
66 : Antenatal corticosteroid therapy and fetal behaviour: a randomised study of the effects of betamethasone and dexamethasone.
67 : Effect of dexamethasone and betamethasone on fetal heart rate variability in preterm labour: a randomised study.
68 : The effect of betamethasone and dexamethasone on fetal heart rate patterns and biophysical activities. A prospective randomized trial.
69 : Effect of betamethasone administration on fetal heart rate tracing: a blinded longitudinal study.
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