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This chapter should be cited as follows:
Valencia CM, Escobar MF, et al, Glob. libr. women's med.,
ISSN: 1756-2228; DOI 10.3843/GLOWM.415083

The Continuous Textbook of Women’s Medicine SeriesObstetrics Module

Volume 13

Obstetric emergencies

Volume Editor: Dr María Fernanda Escobar Vidarte, Fundación Valle del Lili, Cali, Colombia


Intrauterine Fetal Resuscitation

First published: January 2022

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By completing 4 multiple-choice questions (randomly selected) after studying this chapter readers can qualify for Continuing Professional Development awards from FIGO plus a Study Completion Certificate from GLOWM
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One of the most important causes of perinatal morbidity and mortality are the fetal complications related to labor and birth. Throughout history, several methods have been described and used for the assessment of fetal well-being in order to predict and avoid these complications. Since the electronic fetal monitoring (EFM) for fetal heart rate (FHR) was introduced for the first time in 1958 at Yale University,1 this has been the most used method for intrapartum fetal surveillance around the world.2

This chapter will briefly describe the pathophysiology of the nonreassuring fetal status, the method for the interpretation of fetal monitoring to achieve its diagnosis, and the strategies to prevent perinatal-associated morbidity and mortality, focusing on the actions aimed towards the recovery of fetal well-being (intrauterine fetal resuscitation).


A normal placental function is key for an adequate fetal oxygenation. The interactions between the uterus, placenta and the fetus have special characteristics that enhance this important function, working as protective mechanisms for fetal hypoxia. Some of them are as follows:

  • The uteroplacental unit has spiral arteries that lack self-regulation capacity (vasoconstriction and vasodilation), allowing a constant and adequate blood-flow volume to the intervillous space.
  • Oxygen (O2) and carbon dioxide (CO2) easily pass the membranes by simple diffusion, based on the gradient formed due to the normally low concentrations of O2 and high concentrations of CO2 of the fetus compared to the adult.
  • The fetal hemoglobin has a greater carrying capacity and affinity for O2, favoring the passage of oxygen from maternal to fetal circulation.
  • The fetal circulatory pattern allows a greater flow and oxygen supply to key organs (brain, heart, and adrenal), has a higher cardiac frequency and output, and also more capillaries per unit of tissue than adults.

The fetus is capable of maintaining the aerobic metabolism despite the transitory decreases of uterine blood flow that occurs in some circumstances. Indeed, the increase of frequency and/or intensity of uterine contractions, umbilical cord compression, maternal hypotension, compression of the aorto-cava by the uterus during supine position, or the use of drugs such as sympathomimetics can be associated to an important decrease of placental blood flow or reduction of the uteroplacental reserve. In some of these situations, the described protective mechanisms may fail and the fetoplacental unit could not be capable of maintaining the proper fetal pO2, changing from aerobic to an anaerobic metabolism with the subsequent production of lactic acid and the decrease of pH that produces changes in the FHR mediated by chemoreceptors that can be interpreted in the EFM tracing.

This is of vital importance when it comes to labor. During this process, the fetus is compressed along the birth canal during several hours, a period where the fetal skull receives considerable pressure and the fetus is partially deprived of oxygen. A reduction in the oxygen supply can be classified as follows: (1) hypoxemia, where there is a reduction in the oxygen supply of the fetal blood, but without compromising the cellular and organ functions; (2) hypoxia, where there is a reduction of the oxygen concentrations that conditions the development of an anaerobic metabolism in fetal peripheral tissues; and (3) asphyxia, where hypoxia extends to vital organs leading to a secondary metabolic acidosis.3

During labor, a decrease of placental blood flow and an increase in fetal concentrations of CO2 and bicarbonate tends to occur, leading to fetal hypercapnia. The conditions mentioned above lead to a respiratory acidosis as a phenomenon of initial appearance; however, if hypoxia is sustained over time, this will change to a fetal anaerobic metabolism, leading to inadequate lactate productions. The accumulation of lactate is associated with a depletion of the buffer system, originating a failure of the sodium-potassium ATPase pump. This develops a disruption in the ion exchange of the cell membrane, activating a chain of reactions that lead to cellular and organic fetal death.3

The blood coming from the placenta goes through the umbilical vein towards the ductus venosus and the right atrium, from there to the left atrium through the foramen ovale, and finally to the left ventricle. At this point, blood content is ejected towards the aortic arch, neck and cranial vessels, and the descending aorta. The fetal heart is rich in baroreceptors and volume receptors capable of tracking pressure or blood volume changes from the mother. The aortic arch and the carotid bodies contain chemoreceptors that monitor oxygen content of the fetal blood. Therefore, the fetus is capable of producing a series of cardiovascular responses towards hypoxia when necessary.4 These changes occur because the fetal heart rate is regulated by the autonomous nervous system. Hypoxia activates both the sympathetic and the parasympathetic nervous systems, conditioning physiological changes later evident in the EFM tracing.

The adrenal sympathetic system involves the sympathetic nerves and the adrenal medulla. Compared to the adult, fetal circulatory catecholamines that come from the adrenal glands dominate the nervous effects. Therefore, alpha-adrenergic receptors regulate the degree of constriction in the peripheral vessels, while the beta-adrenergic receptors modify the cardiac function and various metabolic reactions such as glycolysis and lactate formation. Thus, through a hypoxic phenomenon with associated adrenal compromise, peripheral mechanisms that perpetuate cellular anaerobic production and that produce deterioration in the maintaining mechanisms of the peripheral vascular tone are responsible for fetal hypotension and bradycardia.3

In addition, the parasympathetic system supplies the sinoatrial and atrioventricular nodes by stimulating the vagus nerve. Thus, the acetylcholine stimulus through this can produce changes in the FHR, which is achieved through chemoreceptors located in the aortic and carotid arteries. These chemoreceptors detect changes in the circulating pO2, just as many other receptors detect variations in the pCO2 and hydrogen ions' concentrations in the medulla oblongata. Therefore, in the context of a hypoxic insult, the fetus reduces the oxygen supply to peripheral tissues, favoring parasympathetic stimuli towards the heart that translate into a non-reassuring cardiotocographic tracing.5


The purpose of FHR monitoring is to evaluate fetal oxygenation. Since FHR is influenced by chemoreceptors and baroreceptors, as well as the fetal autonomous nervous system (interaction between the sympathetic and the parasympathetic) and the cerebral cortex, decreased O2 concentrations in this important brain area, along with pH and blood pressure changes of the fetus, may cause abnormalities in different parameters of the FHR monitoring (baseline, variability, as well as presence or absence of accelerations and decelerations). In addition, some conditions or risk factors may have an impact in the interpretation of the EFM, such as maternal or fetal pathologies related to pregnancy, stage and progression of labor, use of some drugs, etc.

The intrapartum EFM has a low sensitivity but high specificity. In other words, it is a good test to identify non-hypoxic fetuses but has a low ability to recognize hypoxic fetuses. The positive predictive value of the FHR tracing for predicting cerebral palsy (CP) is only 0.14%. This means that among 1000 fetuses with a non-reassuring FHR monitoring, only one or two will develop CP. On the other hand, inter-observer variation, a false positive rate of up to 60%,6,7 and interpretation errors due to the absence of standardized guidelines, have been indicated as the main problems in intrapartum EFM failure to improve perinatal outcome.8

Due to the high intra- and inter-observer variability in the interpretation of EFM, the National Institute of Health of the United States (NIH), alongside with the American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal Fetal Medicine (SMFM), published a consensus in 20089 in order to review and update the definitions of the pattern classification of the FHR.

In this consensus, which has been widely adopted, the following definitions for the EFM interpretation were established (Table 1).


Definitions for the interpretation of the electronic fetal monitoring.



Uterine contractions

The frequency of uterine contractions is evaluated in a period of 10 min (average of a 30-min time window).

  • Normal: five or less contractions in 10 min.
  • Tachysystole: more than five contractions in 10 min.

Terms such as hyperstimulation and hypercontractility have been abandoned.

Basal heart rate

The average FHR in a period of 10 min, excluding the following:

  • Periodic or episodic changes.
  • Periods of marked FHR variability.
  • Baseline segments that differ by 25 heartbeats per min.
  • Baseline must be established for a minimum of 2 min in any period of time of 10 min.
  • Normal basal FHR: 110–160 heartbeats per min.
  • Tachycardia: basal FHR higher than 160 heartbeats per min.
  • Bradycardia: basal FHR lower than 110 heartbeats per min.

Baseline variability

Fluctuation of basal FHR that are irregular when it comes to amplitude and frequency.

  • Variability is visually quantified as the amplitude of peak to valley in heartbeats per min.
  • Absent: undetectable amplitude.
  • Minimum: detectable amplitude but 5 heartbeats per min or less.
  • Moderate (normal): amplitude range between 6–25 heartbeats per min.
  • Marked: amplitude range greater than 25 heartbeats per min.


  • A dramatic increase of FHR (start to peak in less than 30 min)
  • From 32 weeks of pregnancy onwards, acceleration has a peak of 15 heartbeats per min or more above the baseline, with duration of 15 s or more, but less than 2 min from its starting point.
  • Before 32 weeks of pregnancy, an acceleration has a peak of 10 heartbeats per min or more above the baseline, with a duration of 10 s or more but less than 2 min from its starting point.
  • Prolonged acceleration: duration of 2 min or more, but less than 10 min.
  • If an acceleration lasts 10 min or longer, that is a baseline change.

Early deceleration

  • Generally symmetrical gradual decrease of FHR with a return to the baseline associated to a uterine contraction.
  • A gradual decrease in FHR is defined as 30 s or more since the start until the nadir.
  • The decrease in fetal heart rate is calculated from the beginning until the nadir of the deceleration.
  • The nadir of the deceleration is produced at the same time as the peak of the contraction.
  • In most cases the start, the nadir and the recovery of the deceleration are coincident with the onset, peak, and end of the contraction, respectively.

Late deceleration

  • Generally symmetrical gradual decrease of FHR with a return to the baseline associated to a uterine contraction.
  • A gradual decrease in FHR is defines as 30 s or more since the start until the nadir.
  • The decrease in fetal heart rate is calculated from the beginning until the nadir of the deceleration.
  • The deceleration is delayed since the nadir of the deceleration happens after the contraction's peak.
  • In most cases the start, the nadir, and the recovery of the deceleration are coincident with the onset, peak, and end of the contraction, respectively.

Variable deceleration

  • Abrupt decrease of FHR.
  • An abrupt deceleration of FHR is defined as less than 30 s from the start to the deceleration nadir.
  • The decrease in fetal heart rate is calculated from the beginning until the nadir of the deceleration.
  • Fetal heart rate decrease if 15 heartbeats per min or more, with a duration of 15 s or more, and less than 2 min of duration.
  • When variable decelerations are associated to uterine contractions, its appearance, depth, and duration commonly vary with successive uterine contractions.

Prolonged deceleration

  • A decrease of FHR below baseline.
  • FHR decrease from the baseline that is 15 heartbeats per min or more, lasting 2 min or more, but with a duration of less than 10 min.
  • If a deceleration lasts 10 min or more, that is a baseline change.

Sinusoidal pattern

  • Visually apparent pattern, smooth, similar rippling sinusoidal wave in basal FHR with a cycle frequency of 3–5 per min that persists for 20 min or more.

FHR, fetal heart rate.

A moderate variability of the FHR is significantly associated (98%) with an umbilical pH >7.15 or an Apgar score >7 at 5 min. In contrast, minimal or undetectable variability in the presence of variable or late decelerations is the most consistent predictor of neonatal acidemia, although the association is only approximately 25%. Finally, there is a positive relationship between the degree of acidemia and the depth of decelerations or fetal bradycardia.10


There are several interpretation systems of FHR tracing used worldwide.11,12,13 In 2008, the NIH, ACOG, and the SMFM, agreed on a new classification of FHR, which established three categories: I, II, and III.9,14

  • Category I: it is considered normal or reassuring, and it is strongly predictive of a normal fetal acid-base status.
  • Category II: this type of tracing is not predictive of an abnormal fetal acid-base status, but still do not have enough evidence to be classified as category I or III.
  • Category III: they are considered non-reassuring and are associated more frequently to the abnormal fetal base acid status.

This classification provides the concepts needed for decision making (Table 2). It is important to note that the FHR interpretation may vary over time during birth and, therefore, the tracing provides an estimate of the fetal acid-base status at the time of observation.


Interpretation of the fetal heart rate monitoring by the NIH.



Category I

  • Baseline of 110–160 heartbeats per min.
  • Variability: moderate.
  • Accelerations: present or absent.
  • Early decelerations: present or absent.
  • Variable or late decelerations: absent.

Category II

This category includes all of those that cannot be included in categories I and III.


  • Bradycardia with presence of variability.
  • Tachycardia.

Baseline variability:

  • Baseline minimal variability.
  • Absence of baseline variability without recurrent decelerations.
  • Baseline marked variability.


  • Absence of induced accelerations after fetal stimulation.

Periodic or episodic decelerations:

  • Recurrent variable decelerations* alongside minimal or moderate baseline variability.
  • Prolonged deceleration for more than 2 min but less than 10 min.
  • Recurrent late decelerations* with moderate baseline variability.
  • Variable deceleration with slow return to baseline, anterior or posterior shoulder.

Category III

Traces of category III include any of the following:

Absent or minimal variability in the baseline with any of the following characteristics:

  • Recurrent late decelerations*.
  • Recurrent variable decelerations*.
  • Bradycardia.

Sinusoidal pattern.

*Recurrent decelerations: those that occur within half or more of the traced contractions. *Intermittent decelerations: those that occur within less than half of the traced contractions.

The International Federation of Gynecology and Obstetrics (FIGO) did the same in 2015, after publishing an update of its intrapartum EFM interpretation guide.15 Using the same basic elements of interpretation, this guide also classifies fetal monitoring into three types: normal, suspected, and pathological (Table 3), considered easier for interpretation than other guidelines.16 Category I or normal monitoring confirms fetal well-being, is a powerful predictor of normal fetal acid-base status, and does not require any specific intervention. Category II or suspicious monitoring corresponds to approximately 80% of intrapartum monitoring. In this case, the risk of fetal hypoxemia/acidemia is between 10–30%, which is a poor predictor of fetal acid-base status abnormality. Finally, a category III or pathological monitoring is a strong predictor of an abnormal fetal acid-base status at the time of assessment. It is estimated that, in this scenario, more than 50% of fetuses will have hypoxemia/acidemia.17


FIGO fetal heart rate monitoring interpretation.





110–160 bpm.

Loss of at least one characteristic of normality, but without the pathological characteristics.

<100 bpm.


5–25 bpm.

Loss of at least one characteristic of normality, but without the pathological characteristics.

Reduced variability, increased variability or sinusoidal pattern.


No recurrent decelerations.

Loss of at least one characteristic of normality, but without the pathological characteristics.

Recurrent deceleration of more than >30 min or 20 min with reduced variability or a prolonged deceleration longer than 5 min.


Fetus without hypoxia or acidosis.

Fetus with little chance of hypoxia/acidosis.

Fetus with high chance of hypoxia/acidosis.

Clinical management

No intervention needed to improve fetal oxygenation status.

Identify and correct reversible causes strict monitoring and/or another method for fetal oxygenation evaluation.

Take immediate action to correct reversible causes, use different methods to evaluate fetal oxygenation. If this is not possible, unobstructed birth.

bpm, beats per minute.


A normal tracing must be managed as established by the routine follow-up of patients in labor. The recommendation for maternal surveillance with a normal FHR monitoring determined at the beginning of labor depends on the clinical state and the classification of the maternal and fetal risks. During the first phase of labor, the EFM tracing must be evaluated every 30 min, and every 15 min during the second phase of labor.18,19

Some of the suspicious tracings and all of the pathological tracings are considered non-reassuring fetal states. Identification of the causes of a non-reassuring fetal state is key to determine if those causes can be modified or not. For example, fetal sleep cycles are associated to a physiological decrease of the variability, resulting in a suspicious tracing that can be easily reverted to a normal tracing with fetal vibroacoustic stimulation.

There are reversible causes that can be associated to a suspicious tracing, such as maternal hypotension, tachysystole, or cord compression by oligohydramnios; these can be corrected with certain intrauterine resuscitation maneuvers that will be described below. When irreversible causes are identified in normal or suspicious tracings such as a cord prolapse, placental abruption, or uterine rupture, the most appropriate management is the immediate and safest delivery of the fetus.

Suspicious tracings require assessment, continuous surveillance, and initiation of intrauterine resuscitation maneuvers in cases where a subsequent re-evaluation is indicated. Given the wide spectrum of abnormal patterns of FHR in suspicious tracings, the presence of accelerations (spontaneous or digitally stimulated) or the presence of moderate variability can be highly suggestive of a normal fetal acid-base status, leading to continuous surveillance and a more conservative management.18 When there are no accelerations or the variability in the baseline is minimal or absent, a suspicious FHR monitoring will require the assessment of the cause and the use of intrauterine resuscitation maneuvers if the cause is unknown or reversible.18

A pathological tracing is always considered abnormal and implies a high risk for fetal acidemia. The management of a pathological tracing involves the use of intrauterine resuscitation maneuvers and an expedited birth if they are ineffective. Therefore, while these maneuvers are being conducted, the operative room should be prepared for a prompt vaginal delivery or an emergency cesarean section.

During labor, there are some special situations that must be considered in order to maintain optimal recording and interpretation conditions for the intrapartum EFM. Frequent artifacts and loss of focus determine that obese patients are monitored about 10% less than normal-weight patients, a difference that may be of risk in situations of deterioration of the fetal-placental unit. This sometimes requires invasive monitoring by inserting a cephalic electrode into the fetal scalp to obtain a better-quality signal.20 In relation to the interpretation of fetal monitoring, prematurity is a major problem since 60% of monitoring in premature fetuses are classified as suspicious, and 55–70% of fetuses have variable heart rate decelerations. All these elements combine to give greater complexity in the evaluation of monitoring during labor in preterm fetuses.21,22 In addition, the use of medications such as opiates, corticosteroids, and especially magnesium sulfate (used to prevent maternal seizures in the context of pre-eclampsia), have an effect on the variability and accelerations that requires a differential diagnosis with the effects of hypoxia that, in some situations, may be difficult to perform.14


Intrauterine fetal resuscitation interventions are aimed to facilitate and improve fetal oxygenation through different mechanisms, decreasing the risk for a hypoxic state and fetal acidosis.23 In order to understand the mechanisms proposed to achieve an effective resuscitation process, it is important to know how oxygen delivery to the placenta is determined by uterine blood flow and maternal oxygen content:

  • Uterine blood flow = uterine perfusion pressure/uterine vascular resistance.
  • Maternal oxygen content = (1.34 × Hb × %SatO2) + 0.03 × pO2.

Uterine perfusion pressure (uterine arterial pressure – uterine venous pressure) is affected during the third trimester because of compression of the abdominal aorta and inferior vena cava by the uterus. This effect appears to be more pronounced in supine position and is exacerbated if systemic hypotension is present. Uterine vascular resistance is influenced by a series of intrinsic and extrinsic vascular factors. During labor, uterine contractions may cause a temporary interruption of the blood flow to the intervillous space, causing periods of transitory fetal hypoxia. Therefore, if contractions are frequent or last for a long time, the interruption of blood flow increases and may exacerbate the fetal hypoxia and acidemia. Other intrinsic vascular factors such as blood viscosity and vascular tone may play a role in uterine vascular resistance. For example, pre-eclampsia is associated to an abnormal physiological transformation of the spiral arteries that increases vascular resistance by endogenous factors.24,25,26,27 Maternal oxygen saturation improves around 2 to 3% when oxygen is administered. This effect is achieved with rather modest increases in FiO2 (0.3% or more), since most healthy women during pregnancy and also during labor show high contents of O2 and high SatO2.

Fetal resuscitation maneuvers could be considered basic and specific. Basic maneuvers are the ones that should be implemented in all patients with suspicious FHR tracings since most of them will need resuscitation:

  • Maternal position: most patients during labor are in a supine decubitus position, which favors compression of the aorta and inferior vena cava. The change in maternal position from supine decubitus to left (or sometimes right) aims to decompress these large vessels in order to increase the venous return to the maternal heart, improving the cardiac output and the blood flow to the placenta.28 In special cases, such as a cord prolapse, the knee-to-thorax position is used.
  • Hydration with intravenous crystalloids: because fetal oxygenation is highly dependent on placental perfusion, and optimal intravascular volume is required to keep it normal. It has been demonstrated that the maternal administration of 1000cc of intravenous crystalloids increases fetal oxygen saturation in about 14% in non-hypoxic fetuses vs. 10% after administration of 500cc volume.29 Therefore, it is expected that the impact of maternal administration of high crystalloid volumes in hypoxic fetuses is greater. The rapid administration of 1000cc intravenous crystalloid bolus is a measure that must be applied whether there is, or no, maternal arterial hypotension and it may be contraindicated in special cases such as patients with pre-eclampsia or with cardiac diseases. However, this intervention is not necessarily associated to an increase in maternal blood pressure. This process allows an increase of maternal cardiac output, decreases the blood viscosity, and also acts like a temporary tocolytic effect in response to increased uterine blood flow and placental perfusion.30
  • Discontinuation or decrease of uterotonic agents: during induction of labor or delivery, uterotonic agents such as intravenous oxytocin or intravaginal prostaglandins are commonly used. In cases where an EFM suggests a non-reassuring fetal state with the concomitant use of uterotonic agents, with or without the development of tachysystole, the decrease of the infusion dose or discontinuation of oxytocin, the withdrawal of pessaries, or the remains of prostaglandins from the vagina (without performing any kind of cleaning) must be part of the management. In a prospective study31 involving 14,398 women undergoing oxytocin administration for birth induction, a decrease of oxytocin infusion velocity in certain suspicious tracings was associated to a significantly lower rate of admission to the neonatal intensive care unit (3.8% vs. 5.2%, p = 0.01) and an Apgar score lower than 7 at 1 and 5 min, respectively (4.9% vs. 6.4%, p = 0.01; 0.6% vs. 1.1%, p = 0.04). However, these actions do not achieve an immediate effect, allowing a reduction of only 48% of the contractions within 45 min.32 Therefore, for some cases, the adjuvant use of tocolytic agents is recommended as described below.
  • Oxygen administration: normal fetal saturation is approximately 40% to 60%. It has been demonstrated that maternal administration of high oxygen concentrations (FiO2 of 60% in 10–15 l per min) with devices such as a mask with reservoir bag, increase the oxygen saturation in hypoxic fetuses approximately from 26% to 37%.29,33 Nevertheless, there is some concern about the possible deleterious effects of oxygen-free radicals in the fetus and the newborn secondary to a prolonged use of high oxygen concentrations.34

In the past 50 years, various studies have looked at the effects of maternal hyperoxygenation on fetal oxygenation and well-being.35 In fact, several studies have shown an increase in maternal pO2 concentrations related to the increase of fetal SaO2 concentrations. However, these studies have been performed in uncompromised fetuses.36,37,38 Only few non-randomized studies with low statistical power have been performed in stressed fetuses33,39,40,41 and have found some improvement in fetal cardiotocographic patterns. On the other hand, a systematic review published by the Cochrane Database including two studies42,43 about prophylactic oxygen administration during labor demonstrated that abnormal cord blood pH values (<7.2) were significantly more common in the prophylactic oxygenation group than in the control group (RR 3.51, 95% CI 1.34 to 9.19), with no other significant differences between the groups. The authors concluded that there is not enough evidence to support the use of prophylactic oxygen therapy during labor, nor to evaluate its effectiveness for fetal distress.44 In addition, there are controversial results regarding the effect of the oxygen administration duration, proposing its use only for short periods of time (15 to 30 min).32

As previously stated, in addition to the worsening of possible fetal acidemia, another emerging concern related to the use of maternal hyperoxygenation is the deleterious effect of oxygen-free radicals in the fetus.35 These types of markers have been recognized among the general population after the administration of high amounts of oxygen, as well as in fetuses with an EFR suggestive of hypoxia. In fact, it is known that oxygen-free radicals are produced physiologically at high concentrations in the presence of different maternal and fetal conditions such as pre-eclampsia, diabetes mellitus, smoking, fetal growth restriction, and fetal distress.35 Despite what is known regarding the production of oxygen-free radicals and their maternal and fetal effect, its production after oxygen administration has not been investigated properly when trying to improve a non-reassuring fetal status. It has been proposed that most neonatal oxygen-guided resuscitation can lead to an increased neonatal morbidity and mortality by developing bronchopulmonary and retinopathy disease. However, fetal pO2 concentrations after maternal hyperoxygenation will never reach those administered directly to the neonate.45 Although the possibility of an abnormal fetal and/or neonatal condition related to this maternal oxygenation process has not been clearly identified, the use of high oxygen-inspired fractions in the absence of tissue hypoxia may cause some harmful effects in the mother as a result of an oxidative stress process. This condition can be characterized by mucous inflammation, hypoperfusion, and pneumonitis, as well as cerebral vasoconstriction.35 Based on the abovementioned, it is important to acknowledge the use of oxygen therapy as an in utero fetal resuscitation maneuver. Currently, its use is recommended only in fetuses with signs of fetal distress, such as in pathological tracings (or category III) or suspicious tracings (category II) that show prolonged or late recurrent decelerations, variable decelerations of poor prognosis, bradycardia, or minimal or absent variability 30–60 min.17,46 In comparison, the Royal College of Obstetricians and Gynecologists clearly states that its use should be restricted to cases of maternal hypoxia, until further evidence is obtained.35

  • Tocolysis: the use of tocolytic agents must be considered in order to improve a non-reassuring FHR tracing secondary to tachysystole, although the management of a tachysystole depends of its origin. If a tachysystole is originated from spontaneous labor and there is a reassuring tracing, then no additional interventions are required. However, if it is associated to an abnormal FHR monitoring (suspicious or pathological) and there is no response to basic intrauterine resuscitation maneuvers, the use of tocolytic agents must be considered.18 On the other hand, if the tachysystole is secondary to the use of oxytocin or prostaglandins for labor induction, and it is related to a reassuring tracing, a reduction and/or discontinuation of uterotonics should be the first line of treatment. If it is related to an abnormal tracing, the use of tocolytics should be considered alongside with uterotonic discontinuation and basic fetal resuscitation maneuvers.18

The drugs most frequently used for this purpose are subcutaneous terbutaline or intravenous fenoterol. However, due to the secondary effect of this tocolytic agent, other drugs such as nitroglycerin have been introduced, demonstrating the same effect for intrauterine resuscitation of terbutaline or fenoterol, but with less maternal adverse effects.47 An intravenous bolus of 100 to 200 mcg of nitroglycerin is used for this purpose.

  • Management of maternal hypotension: in cases of documented maternal hypotension, the first step is to modify the maternal position in order to decompress the aorta and inferior vena cava to improve venous return to the heart, along with the administration of an intravenous crystalloid bolus. If the maternal systolic blood pressure remains below 100 mmHg, it is recommended to use vasopressor drugs such as phenylephrine or ephedrine to normalize the blood pressure. If hypotension is related to the use of neuraxial analgesia, the anesthesiologists must be informed.48

Despite some evidence that favors the use of phenylephrine as the best option when using vasopressors in obstetrics,49 the guidelines of the United Kingdom National Institute for Health and Care Excellence (NICE)50 and others51,52,53 proposed that both agents are similarly effective as vasopressors in pregnancy. The American Society of Anesthesiology indicates that, even if both are acceptable for their use, phenylephrine should be preferred since a better outcome in the fetal and neonatal acid-base status has been demonstrated in comparison to ephedrine.54 Similarly, the Canadian guidelines55 propose the use of phenylephrine rather than ephedrine as a first-line drug for the management of maternal hypotension.

  • Amnioinfusion: the infusion of crystalloids in the amniotic cavity has been proposed in cases of non-reassuring FHR tracings with recurrent variable decelerations that suggest umbilical cord compression by oligohydramnios. Although there is limited evidence regarding an improvement of short- or long-term neonatal results, amnioinfusion has proven to decrease the recurrence of variable decelerations as well as the rate of cesarean deliveries.56


The acceptable period of time between the decision of an emergency cesarean section and delivery of the fetus within the framework of a pathological FHR tracing has not been established. Historically, an arbitrary standard of 30 min between decision of performing the cesarean section and the incision has been established;19 however, scientific evidence to support such a threshold is insufficient.

Table 4 displays a proposal of a classification for emergency cesarean section adopted from the original classification proposed by Lucas et al.57 in 2000, which is based on the assessment of maternal and/or fetal compromise and its implication in the decision-to-birth time according to the threat to life of one or both.


Standards for urgent cesarean section prioritization.




Decision–birth time

With fetal or maternal compromise.

With immediate threat to the fetus or the mother's life.



Without immediate threat to the fetus or the mother's life.


15 to 75 min.

Without fetal or maternal compromise.

Rapid birth required.


As soon as possible depending on room availability. Categories 1 and 2 should be given priority before category 4.

Schedule in the moment that suits the mother or the institution.



Neonatal encephalopathy is clinically defined as the alteration of the neurological function during the first days of life of a newborn older than 35 weeks of gestational age. This abnormal neurological function is manifested by an abnormal level of consciousness or seizures, that are usually related to the difficulty to start and maintain breathing, tone depression, and reflexes, it can be secondary to a hypoxic event – acute ischemic peripartum or intrapartum.

Within the different criteria to establish the neonatal encephalopathy because we can find the fetal acidemia defines as a pH greater than 7.0 or a base deficit greater than or equal to 12 mmol/l in a sample of cord gases taken from the umbilical artery at the time of birth.58

From the above originates the importance of the practice of sampling cord gases at the moment of birth in the cases in which there is an increased risk of this kind of ischemic hypoxic event such as urgent cesarean section regardless of the Apgar score at birth, cesarean section with general anesthesia, labor or cesarean section with a depressed newborn without apparent cause, a newborn with obstetric trauma evidence, intrauterine growth restriction, chorioamnionitis, congenital malformations, or maternal comorbidity among others. The decision to take samples of cord gases must be taken by any of the professionals responsible for the fetal or newborn care during labor or birth (obstetrician, anesthesiologist, and neonatologist).


Labor and birth can be a susceptible moment for the loss of fetal well-being with the consequent detriment of neonatal results. Electronic fetal monitoring is the most used method for intrapartum fetal surveillance worldwide and, even if it has low sensitivity as a diagnostic test, it remains the primary tool for fetal evaluation. The interpretation method of the traces of fetal heart rate has evolved over time and is still far from perfect; it provides guidelines for clinical management in the cases of suspected fetal well-being loss.


  • The intrapartum EFM has a low sensitivity but high specificity, which means that it is a good test to identify non-hypoxic fetuses but has a low capability to recognize hypoxic fetuses.
  • Clear definitions for the EFM interpretation are key to reduce the high intra- and inter-observer variability in its interpretation.
  • A normal monitoring is a powerful predictor of normal fetal acid-base status. In a case of suspicious monitoring, the risk of fetal hypoxemia/acidemia is between 10–30%, being a poor predictor of fetal acid-base status abnormality.
  • Intrauterine fetal resuscitation interventions are intended to facilitate and improve fetal oxygenation, reducing the risk for a hypoxic state and fetal acidosis.
  • Change in maternal position, management of maternal hypotension, hydration with intravenous crystalloids, discontinuation of uterotonic agents and tocolysis are the most important interventions for intrauterine fetal resuscitation.
  • A pathological monitoring is a strong predictor of an abnormal fetal acid-base status at the time of assessment, since >50% of fetuses will have hypoxemia/acidemia. Therefore, reversible causes might be corrected. If this is not possible, an immediate delivery should be performed.


The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.



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