10 Intrapartum Care and Fetal Surveillance Carolina Ghia, Luciana Prozzillo and Gustavo F. Leguizamón In the last 50 years different techniques have been developed to assess fetal health during labor. From intermittent auscultation to the most recent invasive techniques, the objective of these methods is to detect fetal stress early, so that complications, such as intrapartum fetal hypoxia leading to cognitive impairment, cerebral palsy, or even fetal death, can be prevented. Persistent intrapartum hypoxia, which complicates about 1% of all labors, can lead to severe acidemia, which in turn may compromise those vital tissues requiring strict oxygen levels, such as in the renal, cardiovascular, and central nervous systems. The latter is the most vulnerable to oxygen deprivation and is, therefore, frequently involved in long-term sequelae. Thus, an ideal method of intrapartum fetal surveillance should be able to differentiate between transient hypoxia without metabolic acidosis and pathologic hypoxia leading to acidosis and tissue damage. This is of utmost importance, since it allows accurate intervention and prevention of long-term sequelae without increasing unnecessary cesarean sections. In other words, it requires a method with a high degree of sensitivity and a low false-positive rate. Since alterations in maternal blood pressure, heart rate, and uterine contractions have direct effects on fetal oxygenation, maternal vital signs should be monitored during labor, especially in the event of a non-reassuring fetal pattern. Fetal heart rate and its variations is a good parameter of fetal response to labor events. In particular, knowledge of normal and abnormal patterns will allow both detection of fetal distress and accurate intervention. Other methods of measuring metabolic status, such as fetal blood sampling, pulse oximetry, and lactate measurement, have been developed in order to complement fetal assessment. These methods are discussed in detail in this chapter. Acceleration: This describes a short-term rise in fetal heart rate of greater than 15 beats per minute (bpm) that lasts for more than 15 seconds. Acidemia: This condition arises from increased hydrogen content in the blood. Acidosis: This term describes a state of increased hydrogen content in the tissues. Respiratory acidosis: The accumulation of CO2 leads to respiratory acidosis. When the umbilical cord is compressed, CO2 rapidly accumulates in the fetal blood. Metabolic acidosis: During the peak of uterine contraction, intramyometrial pressure exceeds uterine arterial pressure and therefore, the blood flow decreases, leaving the fetus in a transient state of hypoperfusion. In the event of basal inadequate oxygen delivery to the fetus, this transitory lack of perfusion leads to fetal hypoxia, which can result in metabolic acidosis. Asphyxia: This is a state of hypoxia with metabolic acidosis. Deceleration: This describes a fall in the fetal heart rate of greater than 15 bpm that lasts for more than 15 seconds (but less than 10 minutes). Hypoxemia: This condition occurs following decreased oxygen concentration in the blood. Hypoxia: This term describes decreased oxygen concentration in the tissues. The normal fetal heart rate at term varies between 110 and 160 bpm. This is measured by a cardiotachometer during intrapartum fetal monitoring and is defined as the baseline heart rate, which is much higher in the second trimester and declines thereafter with increasing gestational age. This decline in baseline heart rate is a good indicator of development of the vagal tone. A heart rate above 160 bpm that persists for more than 10 minutes (a shorter period could represent a transient acceleration) is referred to as tachycardia. Among the most frequent causes of tachycardia are maternal fever (as seen in chorioamnionitis), the use of drugs that elevate heart rate (e. g., ritodrine), fetal anemia, and fetal arrhythmias. However, if tachycardia is persistent, it can also indicate fetal hypoxia. A heart rate of less than 110 bpm that persists for more than 10 minutes (as distinct from transient deceleration) is known as bradycardia. Some fetuses have normal baselines of 100–105 bpm. However, in most cases, it indicates some metabolic alteration (e. g., maternal hypothermia or hypoglycemia), use of drugs that diminish heart rate (e. g., magnesium sulfate), or cardiac abnormalities (e. g., heart block, umbilical cord occlusion). The difference in heart rate from beat to beat, which is registered by a device known as a cardiotachometer as a trace moving over and under the baseline, is known as variability (Fig. 10.1). Normal variability ranges from 5 bpm to 25 bpm, and is an indicator of a well-functioning fetal brain. However, heart rate variability increases with gestational age, reaching a stable pattern at approximately 28 weeks of gestation. Variations between fetuses are also observed. Decreased variability is defined as less than 5 bpm for longer than 80 minutes (Fig. 10.2). It may reflect different physiological conditions, including fetal sleep and prematurity, or may be secondary to drugs such as narcotics, barbiturates, tranquilizers, phenotiazines, and general anesthetics. Among the pathologic causes of decreased heart rate variability are maternal hypoglycemia, reduced fetal oxygenation and acidosis, major anomalies of the fetal central nervous system, chorioamnionitis, and fetal heart block. Heart rate accelerations are usually a response to fetal movement or external stimulations, such as uterine contractions (Fig. 10.3). Their spontaneous presence indicates absence of hypoxia, especially in the context of normal baseline and variability. The presence of provoked accelerations, even in a context of non-reassuring fetal heart rate, rules out a pH lower than 7.20 on scalp sampling. The absence of accelerations should be interpreted in the context of other variables. In general, if the fetal heart rate pattern is non-reassuring with no accelerations, approximately half of such fetuses will be acidotic. On the other hand, the lack of accelerations in an otherwise reassuring pattern is generally not associated with an increased fetal risk of hypoxia. Decelerations are classifed in three groups, according to their location regarding uterine contractions:
Definitions
Fetal Heart Rate: Normal and Pathologic Patterns
Variability
Transient Accelerations
Transient Decelerations