Fetal Surveillance during Labor

Published on 10/03/2015 by admin

Last modified 10/03/2015

Print this page

This article have been viewed 3322 times

Chapter 9 Fetal Surveillance during Labor

Fetal surveillance during labor is an essential element of good obstetric care. On the basis of antepartum maternal history, physical examination, and laboratory data, 20% to 30% of pregnancies may be designated high risk, and 50% of perinatal morbidity and mortality occurs in this group. However, the remaining 50% occurs in pregnancies that are considered to be normal at the onset of labor.

Methods of Monitoring Fetal Heart Rate

AUSCULTATION OF FETAL HEART RATE

The time-honored technique of evaluating the fetus during labor has been auscultation of the fetal heart. Optimally, auscultation of the fetal heart is performed every 15 minutes after a uterine contraction during the first stage of labor, and at least every 5 minutes in the second stage of labor. Some studies have suggested that intermittent auscultation of the fetal heart is comparable to continuous electronic monitoring in terms of neonatal outcome, if performed at the intervals stated above with a 1:1 patient-to-nurse ratio.

CONTINUOUS ELECTRONIC FETAL MONITORING

Electronic fetal monitoring (EFM) during labor was developed to detect fetal heart rate (FHR) patterns that were frequently associated with delivery of infants in a depressed condition. It was reasoned that early recognition of changes in heart rate patterns that may be associated with such fetal conditions as hypoxia and umbilical cord compression would serve as a warning to enable the physician to intervene and prevent fetal death in utero or irreversible brain injury.

EFM allows continuous reporting of the FHR and uterine contractions (FHR-UC) by means of a monitor that prints results on a two-channel strip chart recorder. Uterine contractions result in a reduction in blood flow to the placenta, which can cause decreased fetal oxygenation and corresponding alterations in the FHR. The FHR-UC record can be obtained using external transducers that are placed on the maternal abdomen. This technique is used in early labor. Internal monitoring is carried out by placing a spiral electrode onto the fetal scalp to monitor heart rate and placing a plastic catheter transcervically into the amniotic cavity to monitor uterine contractions (Figure 9-1). To carry out this technique, the fetal membranes must be ruptured, and the cervix must be dilated to at least 2 cm.

FIGURE 9-1 Technique for continuous electronic monitoring of fetal heart rate and pressure of uterine contractions.

Internal monitoring gives better FHR tracings because the rate is computed from the sharply defined R-wave peaks of the fetal electrocardiogram, whereas with the external technique, the rate is computed from the less precisely defined first heart sound obtained with an ultrasonic transducer. The internal uterine catheter allows precise measurement of the intensity of the contractions in millimeters of mercury, whereas the external tocotransducer measures only frequency and duration, not intensity.

In the clinical setting, internal and external techniques are often combined by using a scalp electrode for precise heart rate recording and the external tocotransducer for contractions. This approach minimizes possible side effects from invasive internal monitoring.

Etiology of Hypoxia, Acidosis, and Fetal Heart Rate Changes

The developing fetus presents a paradox. Its arterial blood oxygen tension is only 25 ± 5 mm Hg compared with adult values of about 100 mm Hg. The rate of oxygen consumption, however, is twice that of the adult per unit weight, and its oxygen reserve is only enough to meet its metabolic needs for 1 to 2 minutes. Blood flow from the maternal circulation, which supplies the fetus with oxygen through placental exchange of respiratory gases, is momentarily interrupted during a contraction. A normal fetus can withstand the temporary reduction in blood flow to the placenta without suffering from hypoxia because sufficient oxygen exchange occurs during the interval between contractions.

Under normal circumstances, the FHR is determined by the atrial pacemaker. Modulation of the rate occurs physiologically through innervation of the heart by the vagus (decelerator) and sympathetic (accelerator) nerves. A fetus whose oxygen supply is marginal cannot tolerate the stress of contractions and will become hypoxic. Under hypoxic conditions, chemoreceptors and baroreceptors in the peripheral arterial circulation of the fetus influence the FHR by giving rise to contraction-related or periodic FHR changes. Hypoxia, when sufficiently severe, will also result in anaerobic metabolism, resulting in the accumulation of pyruvic and lactic acid and causing fetal acidosis. The degree of fetal acidosis can be measured by sampling blood from the presenting part. The pH of fetal scalp blood normally varies between 7.25 and 7.30. Values below 7.20 are considered to be abnormal but not necessarily indicative of fetal compromise. Clinical and experimental data indicate that fetal death occurs when 50% or more of the transplacental oxygen exchange is interrupted.

Fetal oxygenation can be impaired at different anatomic locations within the uteroplacental-fetal circulatory loop. For example, impairment of oxygen transportation to the intervillous space may occur as a result of maternal hypertension or anemia; oxygen diffusion may be impaired in the placenta because of infarction or abruption; or the oxygen content in the fetal blood may be impaired because of hemolytic anemia in Rh-isoimmunization. Figure 9-2 summarizes the clinical conditions that may be associated with fetal distress during labor.

FIGURE 9-2 Clinical conditions associated with fetal distress in labor.

FETAL HEART RATE PATTERNS

The assessment of the FHR depends on an evaluation of the baseline pattern and the periodic changes related to uterine contractions.

Baseline Assessment

This requires determination of the rate (in beats per minute) and the variability. Normal and abnormal rates are listed in Table 9-1. Baseline variability can be divided into short-term and long-term intervals. These are described as follows:

1. Short-term or beat-to-beat variability. This reflects the interval between either successive fetal electrocardiogram signals or mechanical events of the cardiac cycle. Normal short-term variability fluctuates between 5 and 25 beats/minute. Variability below 5 beats/minute is considered to be potentially abnormal. When associated with decelerations, a variability of less than 5 beats/minute usually indicates severe fetal distress.

2. Long-term variability. These fluctuations may be described in terms of the frequency and amplitude of change in the baseline rate. The normal long-term variability is 3 to 10 cycles per minute. Variability is physiologically decreased during the state of quiet sleep of the fetus, which usually lasts for about 25 minutes until transition occurs to another state.

TABLE 9-1 BASELINE FETAL HEART RATES

Rate	Beats/Minute
Normal	120-160
Abnormal
Tachycardia	>160
Bradycardia	<120

Periodic Fetal Heart Rate Changes

These are changes in baseline FHR related to uterine contractions. The responses to uterine contractions may be categorized as follows:

1. No change. The FHR maintains the same characteristics as in the preceding baseline FHR.

2. Acceleration. The FHR increases in response to uterine contractions. This is a normal response.

3. Deceleration. The FHR decreases in response to uterine contractions. Decelerations may be early, late, variable, or mixed. All except early decelerations are abnormal.

This pattern usually has an onset, maximum fall, and recovery that are coincident with the onset, peak, and end of the uterine contraction (Figure 9-3). The nadir of the FHR coincides with the peak of the contraction. This pattern is seen when engagement of the fetal head has occurred. Early decelerations are not thought to be associated with fetal distress. The pressure on the fetal head leads to increased intracranial pressure that elicits a vagal response similar to the Valsalva maneuver in the adult. The vagal reflex can be abolished by the administration of atropine, but this approach is not used clinically.