Abstract
Fetal distress refers to what is appropriately called nonreassuring fetal heart rate tracing, or more recently, Category III fetal heart rate tracing. It is an indication that fetal asphyxia may be occurring and requires prompt intervention. Anesthetic management of patients with Category III fetal heart rate tracing is dependent on the mode of delivery anticipated, the urgency of that delivery, the patient’s medical condition, and the anesthetic indications and contraindications for that patient. For cesarean delivery the choice between extending an existing epidural, administering spinal anesthesia, or inducing a general anesthetic requires prompt assessment and must consider these factors while deciding the safest care for the mother and the baby. Anesthetic options and their relative benefits are discussed.
Keywords
cesarean delivery, fetal distress, neuraxial anesthesia, nonreassuring fetal heart rate, obstetric anesthesia
Case Synopsis
A 38-year-old, 120-kg primigravida with poorly controlled type 2 diabetes presents at 35 weeks’ gestation with ruptured membranes and a temperature of 38.5°C. The decision is made to induce labor. During labor the obstetrician declares that the electronic fetal heart rate monitor indicates fetal distress ( Fig. 56.1 ) and urgent cesarean delivery is required.
Acknowledgment
The author wishes to thank Dr. Brenda Bucklin for her contribution to the previous edition of this chapter.
Problem Analysis
Definition
Fetal distress is an imprecise term that has been used progressively less in the medical record since the American College of Obstetricians and Gynecologists (ACOG) published a committee opinion in 1998 that suggested replacing the term fetal distress with nonreassuring fetal heart rate tracing. Despite the ominous implications associated with the term fetal distress, it was frequently associated with delivery of an infant in good condition. In accordance with the ACOG recommendations, the medical record usually describes nonreassuring fetal heart rate (FHR) tracing with additional descriptions of the findings such as fetal bradycardia, repetitive late or variable decelerations, or loss of variability. Nonetheless, the term fetal distress is still often used when communicating patient condition and carries the implication of great urgency. When called to help with the treatment of fetal distress, part of the initial communication with the obstetrician should be to get clarification of the maternal and fetal condition and the true urgency of delivery because these will largely determine the anesthetic options.
Recognition
One of the great challenges to obstetricians managing patients in labor is deciding when the risk of injury to the mother or child is greater by continuing in labor than it would be by proceeding to an operative delivery. The obstetrician has a limited number of tools for assessing the condition of the fetus and predicting the future course of labor. Electronic FHR monitoring is the primary means of assessing fetal oxygenation because it is usually simple, continuous in real time, minimally invasive or noninvasive, and widely available. It is a monitor of the fetus’ own measurement and response to oxygenation and perfusion, which makes it at the same time both richly informative and subject to many confounders. Factors that alter the fetal central nervous system and autonomic responses, such as drugs (e.g., opioids, anesthetics, sympathetic or parasympathetic modulators such as β-agonists or atropine), neurologic abnormalities (e.g., anencephaly), or conditions that alter the measured response such as fetal cardiac arrhythmias are examples of influences that will make interpretation of the FHR more complicated. On the other hand, decades of widespread use and interpretation have produced a large library of observed FHR patterns and associated fetal outcomes that make it the most useful and trusted primary monitor of fetal well-being in labor.
Other measures of fetal well-being, such as the presence or absence of meconium in the amniotic fluid; the FHR response to acoustic or scalp stimulation; measurement of plasma pH in a blood sample obtained from a fetal scalp; and umbilical artery Doppler velocimetry looking for evidence of reduced, absent, or reversed umbilical artery diastolic blood flow can all be used to add information about fetal status, but none has the utility or value of FHR monitoring.
FHR monitoring is based on the premise that increasing degrees of hypoxia or asphyxia produce characteristic changes in the FHR pattern. Regulation of the FHR involves mechanisms that are still incompletely understood. At its most basic level, input from baroreceptors and chemoreceptors for oxygen and carbon dioxide are processed through brainstem nuclei and centers in the hypothalamus and cerebral cortex to produce sympathetic, parasympathetic, and humoral signals that modulate heart rate.
Electronic FHR monitors record the FHR and uterine contractions. The baseline FHR and changes in the heart rate can be analyzed in relation to uterine contractions. The main features of the FHR pattern that are measured ( Box 56.1 ) include baseline heart rate, heart rate variability, accelerations, and decelerations (three types: early, late, and variable). In 2008 a three-tier system for FHR tracing interpretation was introduced in the United States to standardize the overall interpretation and communication of FHR tracings ( Box 56.2 ). Tracings are rated Category I (Normal), Category II (Indeterminate), or Category III (Abnormal) based on the features observed in the tracing and their prognostic value.
Baseline
A normal baseline FHR is defined as 110 to 160 beats per minute. Changes from that range suggest increased vagal or sympathetic tone.
Variability
Fetal heart rate variability is the fluctuation in the FHR. Previously, FHR variability was categorized as short term (beat to beat) and long term (over the course of 1 minute), but this distinction has been abandoned. The presence of normal FHR variability reflects normally functioning pathways in the fetal cerebral cortex, midbrain, vagus nerve, and cardiac conduction system.
Accelerations
Abrupt changes in the FHR ≥15 beats per minute above the baseline, lasting ≥15 seconds.
Antepartum FHR accelerations are a response to fetal movement and viewed as a sign of fetal well-being; their presence indicates a reactive nonstress test.
Intrapartum FHR accelerations indicate no significant fetal metabolic acidemia.
Decelerations
Early Deceleration
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Visually apparent, usually symmetric, gradual decrease and return of the FHR associated with a uterine contraction.
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A gradual FHR decrease is defined as one from the onset to the FHR nadir of ≥30 seconds.
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The decrease in FHR is calculated from the onset to the nadir of the deceleration.
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The nadir of the deceleration occurs at the same time as the peak of the contraction.
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In most cases the onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending of the contraction, respectively.
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Probably due to reflex vagal responses to mild hypoxia.
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Not considered to be ominous.
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Variable Deceleration
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Visually apparent abrupt decrease in FHR.
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An abrupt FHR decrease is defined as from the onset of the deceleration to the beginning of the FHR nadir of <30 seconds. The decrease in FHR is calculated from the onset to the nadir of the deceleration.
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The decrease in FHR is ≥15 beats per minute, lasting ≥15 seconds, and <2 minutes in duration.
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When variable decelerations are associated with uterine contractions, their onset, depth, and duration commonly vary with successive uterine contractions.
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Probably vagal responses to baroreceptor or chemoreceptor signals triggered by such things as cord compression or head compression in the second stage of labor.
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Mild to moderate (≥80 beats per minute) variable decelerations are usually well tolerated, but prolonged severe (<60 beats per minute) decelerations may lead to fetal compromise.
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Late Deceleration
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Visually apparent usually symmetric gradual decrease and return of the FHR associated with a uterine contraction.
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A gradual FHR decrease is defined as from the onset to the FHR nadir of ≥30 seconds.
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The decrease in FHR is calculated from the onset to the nadir of the deceleration.
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The deceleration is delayed in timing, with the nadir of the deceleration occurring after the peak of the contraction.
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In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively.
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Probably a response to hypoxemia but may also be a reflection of myocardial failure.
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Possibly oversensitive as an indicator of fetal asphyxia, but in combination with decreased or absent FHR variability it is a reliable signal of fetal compromise.
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FHR, Fetal heart rate.
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