The original goal among obstetric practice and basis for intrapartum fetal monitoring was the prevention of cerebral palsy (CP), hypoxic ischemic encephalopathy (HIE), neonatal encephalopathy, and perinatal death. Any of these morbidities and mortality of a term or near-term infant not only produces a wide array of long-term sequelae and disabilities, they are also a prominent cause of medicolegal claims against the health care system both in economic terms and in the length of time it takes to resolve them (1). Over five decades since its introduction, electronic fetal monitoring (EFM) became synonymous with intrapartum fetal monitoring and fetal heart rate (FHR) interpretation became the most common tool available for fetal surveillance. Although it is very sensitive for detecting a nonhypoxic fetus, it has repeatedly been shown to have a very poor predictive value for accurately identifying a hypoxic fetus or one that will develop CP (2). This may be partly related to a lack of standardized protocol for interpretation of FHR and high interobserver and intraobserver variability interpreting FHR tracings even in the presence of guidelines. Recent data indicate that compared to other peripartum causes, the incidence of CP secondary to intrapartum hypoxia is very low (2,3,4). There are very few tools available to predict a fetus at risk as insult may occur prior to the onset of labor, labor itself may not be tolerated, or the fetus is in an unhealthy environment that requires prompt delivery. Recently published new guidelines on standardizing the approach to the interpretation of FHR tracings and additional complementary tests to predict a fetus at risk for intrapartum hypoxia are the basis of current monitoring strategies and research discussed below.

The ideal goals of intrapartum fetal monitoring are to 1. assure fetal well-being and improve perinatal outcome; specifically by decreasing incidence of stillbirth and neonatal seizures and preventing injury to the fetal central nervous system and long-term neurologic impairments such as CP; 2. serve as a screening test to detect episodes, trends, and severity of hypoxia and metabolic acidemia, their effect on cardiac rhythm, variability, and depression which may also result in neurologic damage or fetal death; 3. identify and differentiate the fetus that is not affected by labor from the one that is negatively affected by labor but has enough reserve to tolerate it, and the fetus that lacks the reserve to compensate the insult of labor and can be harmed by it; 4. allow for timely interventions, such as prompt delivery, to avoid any morbidity and mortality in infants; and 5. minimize unnecessary obstetric interventions such as operative vaginal and cesarean deliveries. In conclusion, the ideal monitor should aim to reduce CP rates and fetal or neonatal deaths without increasing maternal morbidity and interventions. To this date, EFM has not been able to fulfill these objectives (5).

Intrapartum continuous EFM was introduced into obstetric practice in the 1960s for complicated pregnancies with the idea that it would prevent perinatal asphyxia and mortality (6). By 1978, almost 66% of all women in the United States were being monitored with EFM during labor, whether their pregnancy was complicated or not (7); and by 2002 over 85% of women in the United States underwent EFM during labor (8).

Although monitoring FHR is widely used and accepted, it has very poor interobserver and intraobserver reliability, uncertain efficacy, and a high false-positive rate (2).

According to ACOG’s task force on neonatal encephalopathy and cerebral palsy, neonatal encephalopathy is defined in term and near-term infants as “a constellation of findings to include a combination of abnormal consciousness, tone and reflexes, feeding, respiration, or seizures and can result from a myriad of conditions” (9,10,11). It is a clinical syndrome of disturbed neurologic function of the term and near-term infant in the early neonatal period, manifested by respiratory difficulties, depression of tone and reflexes, obtundation, and frequent seizures (10,12). The etiology is varied and can include multiple genetic and metabolic conditions that present with similar clinical signs (3). It is only called HIE if there is evidence that intrapartum asphyxia is the cause of the encephalopathy which resulted in neurologic depression or seizures. In order to define an acute intrapartum event sufficient to cause CP and intrapartum asphyxia, ACOG and the American Academy of Pediatrics Task Force on Neonatal Encephalopathy and Cerebral Palsy defined several criteria that must be met (Table 5-1) (13). While these criteria are still current as of writing of this chapter, revised criteria are expected and may be published by the time this textbook is published or shortly thereafter. It is important to note that over 75% of cases of neonatal encephalopathy have no clinical signs of intrapartum hypoxia (11).

Cerebral palsy (CP) is a static neurologic condition resulting from brain injury that mostly occurs before cerebral development is complete. It can occur during the prenatal, perinatal, or postnatal periods, during the time the brain is developing (14). It is described as an aberrant control of movement or posture that is nonprogressive and permanent, appearing in early life secondary to a defect or lesion in the immature brain (15). The onset occurs no later
than 1 year of age and the definite diagnosis is preferably reserved until the age of 4 and 5 (16). It affects 2/1,000 live-born children and its incidence has remained constant over the past 30 years.

In 1861–1862 William J. Little, an orthopedic surgeon, proposed the hypothesis that cerebral palsy was primarily caused by prematurity, birth trauma, and asphyxia neonatorum (3,17). This hypothesis was accepted as soon as it was proposed, without any significant scientific evidence to confirm it, and it was not challenged for many years. Although many people continue to believe this original hypothesis about the etiology of CP, there is substantial evidence that 70% to 80% of cerebral palsy cases in term and preterm infants arise during pregnancy due to antenatal factors long before the onset of labor (15,18,19,20,21,22). Birth complications including asphyxia account for only about 8% to 28% of the cases of CP (3,12,15,23). Only 24% of all term children with CP had a history of neonatal encephalopathy, which means 76% had a normal intrapartum and newborn course. Among the children that survived moderate to severe neonatal encephalopathy at term, the overall rate of those who developed CP was 13%, and the rate was higher in the group that presented with neonatal seizures (18,24). It is now believed that as few as 4% of moderate and severe neonatal encephalopathy cases which are attributable to hypoxia incurred solely during the intrapartum period, explaining the estimated low overall incidence of neonatal encephalopathy due to intrapartum hypoxia (1.6 per 10,000 births) (25).

FHR analysis and its variability are the primary means by which the fetus is evaluated for adequacy of oxygenation. Variability of FHR results from the interaction of the sympathetic and parasympathetic autonomic nervous system. The fetal brain is known to modulate the heart rate through a series of interactions between the sympathetic and parasympathetic systems; as a result, if the fetal brain is hypoxic, FHR changes would reflect the insult. FHR variability is believed to represent an intact neurologic pathway that includes the fetal cerebral cortex, midbrain, vagus nerve, and cardiac conduction system. It has prognostic importance clinically, and valuable empiric interpretations can be made according to its presence or absence. A fetus with unexplained minimal or absent FHR variability and no periodic changes can fall into one of several categories: (a) quiet sleep state; (b) idiopathic reduced FHR variability with no obvious explanation but without evidence of asphyxia or central nervous system compromise; (c) centrally acting drugs given to the mother, for example, opioids; (d) congenital neurologic abnormality due to either a developmental CNS defect or an in utero infection or asphyxic event (26); (e) abnormal cardiac conduction system, for example, complete heart block; or (f) deep asphyxia with inability of the heart to manifest periodic changes (27). Severely growth restricted fetuses can also have minimal FHR variability without any demonstrable asphyxia. It is important to consider that a fetus with an abnormal cardiac conduction system, anencephaly, or other congenital neurologic deficit may present with minimal or absent variability. In the case of congenital neurologic impairment, this FHR pattern may actually represent asphyxia that occurred during the antepartum period (11).

Sympathetic outflow in the fetus is thought to be relatively tonic. The vagus nerve, hence the vagal tone, is responsible for FHR variability, and blocking it with atropine results in disappearance of this variability (28). Modulation in vagal tone occurs in response to changes in blood pressure detected by baroreceptors in the aortic arch and to changes detected in chemoreceptors on the carotid bodies detecting oxygen and carbon dioxide fluctuations. The sympathetic influence is tonic and helps improve pumping activity in the heart during intermittent stressful situations by increasing the FHR. As with the vagal tone, the sympathetic tone influence increases during fetal hypoxia.

The term asphyxia is defined experimentally as impaired respiratory gas exchange accompanied by the development of metabolic acidosis. In the clinical setting, it is a continuum of oxygen deficit. One side of this spectrum includes transient or intermittent hypoxemia, which if repeated, continued, or prolonged may progressively lead to hypercarbia, metabolic acidemia, and acidosis especially in a fetus with already reduced reserve (29,30,31,32). During periods of asphyxia, fetal response can vary from physiologic compensatory mechanisms to asphyxia damage.

Alpha adrenergic activity alters the distribution of blood flow to specific organs during hypoxia causing vasoconstriction to certain vascular beds such as the intestines, liver, and lung, hence improving perfusion to vital organs such as the brain, heart, adrenals, and placenta (33,34). It is known that hypoxia in the fetus causes bradycardia with hypertension (35). Umbilical blood flow is unaffected by acute moderate hypoxia but is decreased by severe hypoxia. Umbilical blood flow is also affected by the administration of catecholamines and acute cord occlusion.

Brief reduction of intervillous blood flow during uterine contractions and temporary cord occlusion causing transient hypoxemia is common during labor. During these periods there is hyperemia-induced redistribution of blood flow favoring the heart, brain, and adrenal glands (33,36). These transient events decrease the arterial and venous oxygen concentration gradient across the myocardial and cerebral circulation but increase the respective blood flow,
thus maintaining constant oxygen consumption in the heart and brain (33,37,38,39). This compensation is achieved by reducing blood flow to other vascular beds thereby inducing anaerobic metabolism.

During repetitive hypoxic events, the fetus develops metabolic acidosis from accumulation of lactic acid which is often an end result of vasoconstriction and anaerobic oxidation in certain vascular beds. Increase in carbon dioxide tension superimposes a respiratory component to this acidosis (40). These compensating mechanisms allow the fetus to survive moderately long periods of limited oxygen supply (up to 30 minutes) without affecting vital organs like the brain and heart (38,39).

When asphyxia becomes severe and fetal acidemia ensues, the protective mechanisms become overwhelmed, and vasoconstriction becomes severe and extensive. At this point, oxygen delivery and consumption by all organs is decreased, even in the organs previously favored. Fetal bradycardia mostly accompanied by hypotension is marked at this point, and in a short period of time death can occur. It is thought that hypoxic organ damage occurs during this period of physiologic decompensation (41).

During labor, there are four major mechanisms by which a fetus can have decreased oxygen delivery: (a) inadequate uterine blood flow (UBF) to the intervillous space, (b) interruption of umbilical blood flow, (c) decrease in maternal oxygen tension, and (d) fetal pathology.

UBF is one of the major determinants of oxygen exchange across the placenta. Reducing UBF beyond a certain level will result in inadequate fetal oxygen uptake. This reduction may occur acutely, for example, in cases of abruptio placenta or hypotension following spinal anesthesia; chronically, as in cases of pregnancy-induced hypertension; or intermittently, during maternal hypotension secondary to supine positioning.

Once oxygen has been transported from the maternal to the fetal side of the placenta, the adequacy of umbilical blood flow will determine its availability to the fetus. When umbilical cord occlusion occurs, it results in fetal hypertension, which initiates a vagal response with subsequent bradycardia. If the occlusion is intermittent in an otherwise healthy fetus, the FHR will intermittently decrease as evidence of a variable deceleration.

A decrease in maternal oxygen tension is a rare cause of fetal asphyxia during the intrapartum period. It can be caused during maternal apnea, pulmonary edema, amniotic fluid embolism, venous air embolism, or severe asthma. Another rare cause of asphyxia or hypoxemia is abnormal fetal pathology with either increased metabolic rate (e.g., pyrexia) or with decreased oxygen carrying capacity (e.g., anemia from Rh sensitization). These fetuses and the preterm fetus can be less tolerant of the decreased oxygen delivery during uterine contractions in labor and may develop metabolic acidosis sooner.

Since the 1970s EFM became widely available and its use disseminated rapidly. Interpretations of FHR tracings were empirical and with time the tracings that were considered abnormal were the ones where a depressed baby was delivered. Believing that intrapartum asphyxia was the main cause of CP, proponents of EFM hoped that by using this monitor fetuses at risk of asphyxia would be recognized easily and delivered promptly, therefore reducing the rate of CP. Studies have shown that the use of EFM has neither decreased the rate of CP nor proven to be a precise tool for predicting either fetal metabolic acidosis or HIE (42,43). In fact, relevant clinical trials argue that EFM as it exists today, does not decrease neonatal morbidity or mortality related to intrapartum acidosis or hypoxia, but rather increases the risks to mothers and babies of having additional surgical or instrumental deliveries (44).

Even though EFM has not been able to prove substantial benefits to both mother and fetus, it is still the commonest obstetric procedure performed in the United States, used in about 85% of all births in 2002 (45).

The most commonly used monitors for fetal well-being during labor consist of three complementary techniques:

In addition to these techniques, during labor the use of the ultrasound to verify FHR and fetal movements can be used and some mothers and care givers still use intermittent auscultation of the FHR with a Doppler monitor or fetoscope during labor to assess the fetus. Other complementary techniques used to assess the fetus include the use of ultrasound for a biophysical profile (BPP) and newer techniques such as fetal ECG monitoring using fetal ST segment analysis and fetal oximetry monitoring. Some of these techniques require validation and are currently undergoing clinical trials to confirm their utility.

The use of FHR monitoring is not without risks. The increase in operative deliveries and cesarean deliveries is not negligible and imposes risks for the mother and the fetus (46,47). There are also infectious complications associated with invasive fetal monitoring that include endometritis, chorioamnionitis, and direct fetal infections. The use of an IUPC has been associated with uterine perforation, placental laceration, abruption, placental vessel perforation, cord entanglement, and possible amniotic fluid embolism (48,49). Monitoring has also been blamed for affecting women’s and partners’ experience of labor, changing the interaction with healthcare practitioners, and has been considered by some patients intrusive and dehumanizing during a natural event of labor and delivery.

The EFM device has two components: one for the FHR and one for uterine contractions. The FHR can be recorded directly or indirectly. The indirect method can be used throughout pregnancy and has no contraindications. This indirect method utilizes ultrasound waves (approximately 2.5 MHz) originating from a transducer, that reflect from the moving structures of the heart and return to the transducer and are interpreted as electrical signals (Fig. 5-1). The direct method utilizes an ECG electrode placed subcutaneously on the fetus that detects the electrical impulses originating in the fetal heart, the R wave of the fetal ECG complex is detected and amplified and the interval between two complexes is used to calculate the FHR. This direct method requires the cervix to be at least 1 cm dilated, rupture of the fetal membranes, and the insertion of a probe into the fetal scalp, which carries a small risk of infection, and should only be used when the benefit of it outweighs the risk.