Since its inception, the primary objective of FHR monitoring has been to identify the fetus in distress so that measures might be taken in time to avert permanent fetal damage or death. However, a clear consensus regarding the definition of fetal distress has not been established. It has been described as “a condition in which fetal physiology is so altered as to make death or permanent injury a probability within a relatively short period of time” and is usually considered to denote disruption of normal fetal oxygenation, ranging from mild hypoxia to profound fetal asphyxia. The term hypoxia refers to the reduction of tissue oxygen supply below physiologic levels. Asphyxia, derived from the Greek word meaning “a stopping of the pulse,” implies a combination of hypoxia and metabolic acidosis. Historically, the clinical diagnosis of birth asphyxia has been based on findings such as meconium-stained amniotic fluid, abnormal FHR patterns, low Apgar scores, abnormal blood gases, and neonatal neurologic abnormalities. When present together, these findings are highly suggestive of a recent asphyxial insult. Isolated abnormalities, however, correlate poorly with birth-related asphyxia and subsequent neurologic impairment. In 2002, the American College of Obstetricians and Gynecologists Task Force on Neonatal Encephalopathy and Cerebral Palsy stated the criteria to define an acute intrapartum event sufficient to cause cerebral palsy (CP).

Essential criteria (must meet all four):

Criteria that collectively suggest an intrapartum timing (within close proximity to labor and delivery, e.g., 0–48 hours) but are nonspecific to asphyxial insults:

At the cellular level, asphyxia triggers a cascade of events, including membrane depolarization, disruption of energy metabolism, altered neurotransmission, ion shifts, protease activation, free radical production, and phospholipid degradation. Profound and prolonged asphyxia may result in cell death and, eventually, death of the organism. Sublethal asphyxia may lead to multiorgan system dysfunction. Severe asphyxial brain injury may lead to long-term neurodevelopmental impairment.

Cerebral palsy is a major disorder of neurodevelopment, defined as “a chronic disability, characterized by aberrant control of movement and posture, appearing early in life and not the result of recognized progressive disease.” It may be accompanied by mental retardation (41%), seizures (23%), or cortical visual impairment. The insult responsible for the development of CP may occur at any time during the prenatal, perinatal, or postnatal periods. Unlike other major neurodevelopmental disorders, the relationship between CP and abnormal or difficult birth has long been recognized, publicly dating back to a treatise presented by William John Little in 1862. In 1943, Windle demonstrated clinical and histopathologic evidence of neural damage in experimentally asphyxiated fetal guinea pigs. He later reported the effects of prolonged anoxia on fetal rhesus monkeys. Total anoxia for less than 8 minutes did not produce consistent injury, whereas anoxia for more than 10 minutes invariably resulted in neuropathology. There were no survivors beyond 20 to 25 minutes of anoxia. The pattern of injury produced by prolonged anoxia, however, did not correlate with the cerebral injury, mental retardation, and spasticity seen in CP. Later work demonstrated that prolonged partial asphyxia in monkeys produced acidosis, late FHR decelerations, and neuropathologic defects consistent with the findings in the common forms of CP. In addition to lesions in the thalamus and basal ganglia, prolonged partial asphyxia caused generalized cerebral necrosis or focal necrosis in the parasagittal regions and the border zones between the parietal and occipital lobes.

Although early studies created and fostered the assumption that birth-related asphyxia was the primary cause of CP, recent evidence challenges this assumption. In 1986, Nelson and Ellenberg reported a multivariate analysis of risk in 189 cases of CP. After accounting for major congenital malformations, low birth weight, microcephaly, and alternative explanations for the disorder, they were able to attribute only 9% of CP cases to birth asphyxia. Others have reached similar conclusions. Although birth asphyxia nearly tripled the odds of developing CP, only 8.2% of CP cases were potentially attributable to birth asphyxia.

As early as the 19th century, researchers using auscultation recognized that certain FHR patterns were associated with adverse perinatal outcome. The introduction of direct electronic fetal monitoring and fetal scalp blood sampling in the 1960s provided tools for evaluating the fetus. FHR decelerations have been found to be correlated with fetal acidosis. Fetuses with no decelerations, early decelerations, or mild variable decelerations had average scalp pH values greater than or equal to 7.29, whereas those with severe variable or late decelerations had pH values less than or equal to 7.15. In addition, FHR variability was found to be correlated with scalp pH values, as fetuses with normal FHR variability had higher scalp pH values than those with decreased variability. The absence of FHR accelerations was correlated with poor perinatal outcome, and the presence of FHR accelerations has been shown to predict normal scalp pH values. With the development of indirect monitoring techniques, the experience derived from direct intrapartum monitoring became applicable to the antepartum period, leading to the development of antepartum testing.

Antepartum fetal monitoring has the goal of identifying the fetus at risk, allowing sufficient time to intervene before permanent injury or death occur. Intrapartum fetal monitoring should be able to identify three groups of fetuses:

It is the third group that would most benefit from intervention.

Antepartum fetal monitoring typically is offered to patients at increased risk of fetal or neonatal morbidity/mortality. These include maternal medical complications, fetal conditions, and pregnancy complications. Overall, the studies supporting the methods of testing, the timing, and initiation are extremely varied; thus, absolute guidelines based on scientific evidence cannot be established. However, recommended gestational ages for initiation of testing, timing, and methods for specific maternal conditions and the supportive evidence can be found in Table 10.1.

Intrapartum fetal monitoring has remained controversial since its inception. The FHR may be evaluated by auscultation or by electronic monitoring. Auscultation is typically performed with a DeLee stethoscope or Doppler ultrasound. Electronic monitoring can be either performed externally or internally. External monitors use a Doppler device with computerized logic to interpret and count the signals. Internal monitoring uses a fetal electrode that records the fetal electrocardiogram (ECG). Well-controlled studies have shown the equivalence of intermittent auscultation to continuous fetal heart monitoring when
auscultation was performed at specific intervals with a 1:1 nurse-to-patient ratio. The intensity of monitoring is based on risk factors, with more intensive surveillance required for high-risk pregnancies.

Analysis of the fetal monitor strip requires a systematic approach. First, the FHR is analyzed with respect to (a) the baseline, (b) variability, and (c) periodic patterns, including FHR accelerations and decelerations (Table 10.2). Uterine activity is evaluated with attention to the frequency, duration, and strength of contractions as well as the baseline uterine tone between contractions.