Resuscitation of the neonate starts during labor. Any compromise of the uteroplacental circulation readilyproduces fetal asphyxia. Intrauterine asphyxia during labor is the most common cause of neonatal depression. Fetal monitoring throughout labor is helpful in identifying which babies may be at risk, detecting fetal distress, and evaluating the effect of acute interventions. These include correcting mater-nal hypotension with fluids or vasopressors, supple-mental oxygen, and decreasing uterine contraction (stopping oxytocin or administering tocolytics). Some studies suggest that the normal fetus can compensate for up to 45 min of relative hypoxia, a period termed fetal stress; the latter is associated with a marked redis-tribution of blood flow primarily to the heart, brain, and adrenal glands. With time, however, progressive lactic acidosis and asphyxia produce increasing fetal distress that necessitates immediate delivery.
Monitoring of fetal heart rate (FHR) is presently the most useful technique in assessing fetal well-being, although alone it has a 35–50% false-positive rate of predicting fetal compromise. Because of this, the term fetal distress in the context of FHR monitoring has been largely replaced with nonreassuring FHR. Correct interpretation of heart rate patterns is cru-cial. Three parameters are evaluated: baseline heart rate, baseline variability, and the relationship to uter-ine contractions (deceleration patterns). Monitoring of heart rate is most accurate when fetal scalp elec-trodes are used, but this may require rupture of the membranes and is not without complications (eg, amnionitis or fetal injury).
The mature fetus normally has a baseline heart rate of 110–160 beats/min. An increased baseline heart rate may be due to prematurity, mild fetal hypoxia, chorio-amnionitis, maternal fever, maternally administered drugs (anticholinergics or β agonists), or, rarely, hyperthyroidism. A decreased baseline heart rate may be due to a postterm pregnancy, fetal heart block, or fetal asphyxia.
The healthy mature fetus normally displays a base-line beat-to-beat (R wave to R wave) variability that can be classified as minimal (<5 beats/min), mod-erate (6–25 beats/min), or marked (>25 beats/min). Baseline variability, which is best assessed with scalp electrodes, has become an important sign of fetal well-being and represents a normally functioning autonomic system. Sustained decreased baseline variability is a prominent sign of fetal asphyxia. Central nervous system depressants (opioids, bar-biturates, volatile anesthetics, benzodiazepines, or magnesium sulfate) and parasympatholytics (atro-pine) also decrease baseline variability, as do pre-maturity, fetal arrhythmias, and anencephaly. A sinusoidal pattern that resembles a smooth sine wave is associated with fetal depression (hypoxia, drugs, and anemia secondary to Rh isoimmunization).
Accelerations of FHR are defined as increases of 15 beats/min or more lasting for more than 15 s. Periodic accelerations in FHR reflect normal oxy-genation and are usually related to fetal movements and to responses to uterine pressure. Such accel-erations are generally considered reassuring. By 32 weeks, fetuses display periodic increases in base-line heart rate that are associated with fetal move-ments. Normal fetuses have 15–40 accelerations/h. The mechanism is thought to involve increases in catecholamine secretion with decreases in vagal tone. Accelerations diminish with fetal sleep, some drugs (opioids, magnesium, and atropine), as well as fetal hypoxia. Accelerations to fetal scalp or vibro-acoustic stimulation are considered a reassuring sign of fetal well-being. The absence of both baseline variability and accelerations is nonreassuring and may be an important sign of fetal compromise.
Early deceleration (usually 10–40 beats/min) (Figure 41–4A) is thought to be a vagal response
to compression of the fetal head or stretching of the neck during uterine contractions. The heart rate forms a smooth mirror image of the contraction. Early decelerations are generally not associated with fetal distress and occur during descent of the head.
Late decelerations (Figure 41–4B) are associated with fetal compromise and are characterized by a decrease in heart rate at or following the peak of uterine contractions. Late decelerations may be subtle (as few as 5 beats/min). They are thought to represent decreased arterial oxygen tension on atrial chemoreceptors. Late decelerations with nor-mal variability may be observed following acute insults (maternal hypotension or hypoxemia) and are usually reversible with treatment. Late decelera-tions with decreased variability are associated with prolonged asphyxia and may be an indication for fetal scalp sampling (see Other Monitoring section). Complete abolition of variability in this set-ting is an ominous sign signifying severe decompen-sation and the need for immediate delivery.
The most common type of decelerations are variable (Figure 41–4C). These decelerations are variable in onset, duration, and magnitude (often >30 beats/ min). They are typically abrupt in onset and are thought to be related to umbilical cord compression and acute intermittent decreases in umbilical blood flow. Variable decelerations are typically associated with fetal asphyxia when fetal heart rate declines to less than 60 beats/min, last more than 60 s, or occur in a pattern that persists for more than 30 min.
Other less commonly used monitors include fetal scalp pH measurements, scalp lactate concentration, fetal pulse oximetry, and fetal ST-segment analysis. Clinical experience is limited with all except fetal scalp pH measurements. Unfortunately the latter is associated with a small but significant incidence of false negatives and false positives. Fetal blood can be obtained and analyzed via a small scalp puncture once the membranes are ruptured. A fetal scalp pH higher than 7.20 is usually associated with a vigor-ous neonate, whereas a pH less than 7.20 is often, but not always, associated with a depressed neonate and necessitates prompt (typically operative) delivery. Because of wide overlap, fetal blood sampling can be interpreted correctly only in conjunction with heart rate monitoring.
Treatment of intrauterine fetal asphyxia is aimed at preventing fetal demise or permanent neurological damage. All interventions are directed at restoring an adequate uteroplacental circulation. Aortocaval compression, maternal hypoxemia or hypoten-sion, or excessive uterine activity (during oxytocin infusions) must be corrected. Changes in maternal position, supplemental oxygen, and intravenous ephedrine or fluid, or adjustments in an oxytocin infusion often correct the problem. Failure to relieve fetal stress, as well as progressive fetal acidosis and asphyxia, necessitate immediate delivery.
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