Category I FHR tracings are strongly predictive of normal fetal acid-base status at the time of observation. Category I FHR tracings may be monitored in a routine manner, and no specific action is required.

Category II FHR tracings are not predictive of abnormal fetal acid-base status, yet presently there is not adequate evidence to classify these as Category I or Category III. Category II FHR tracings require evaluation and continued surveillance and reevaluation, taking into account the entire associated clinical circumstances. In some circumstances, either ancillary tests to ensure fetal well-being or intrauterine resuscitative measures may be used with Category II tracings.

Category III tracings are associated with abnormal fetal acidbase status at the time of observation. Category III FHR tracings require prompt evaluation. Depending on the clinical situation, efforts to expeditiously resolve the abnormal FHR pattern may include but are not limited to provision of
maternal oxygen, change in maternal position, discontinuation of labor stimulation, treatment of maternal hypotension, and treatment of tachysystole with FHR changes. If a Category III tracing does not resolve with these measures, delivery should be undertaken. We attempt to follow these new guidelines for nomenclature in this edition of this book.

Fetal tachycardia is defined as a baseline heart rate in excess of 160 BPM. Factors associated with or causing tachycardia are listed in Table 6.1. Because tachycardias represent increased sympathetic and/or decreased parasympathetic autonomic tone, they are generally associated with a loss of variability (Fig. 6.1). Most fetal tachycardias do not reflect a hypoxic fetus, particularly when present in a term gestation. In a preterm
fetus or when seen in a term pregnancy without an obvious explanation (e.g., maternal fever), close evaluation is critical.

Bradycardia is a baseline FHR of <110 BPM Bradycardia, within the range of 80 to 110 BPM with moderate variability generally indicates good oxygenation without acidemia (Fig. 6.2). Slowing of the baseline heart rate is most likely in response to an increased vagal tone (3). Fetal bradycardia that is first noted at the initiation of monitoring may be difficult to distinguish from a prolonged deceleration. Generally, prolonged decelerations are associated with loss of variability and their rate fluctuates up and down rather than remaining consistent, unless rates below 70 BPM are seen.

Actual baseline FHRs of <70 BPM are generally seen without variability and may represent congenital heart block (Fig. 6.3). Persistent bradycardia from complete atrioventricular dissociation should alert the clinician to the possible diagnosis of maternal connective tissue disease, most often systemic lupus erythematosus, which results in fetal heart block and bradycardia consequent to transplacental passage of maternal antibodies that have an affinity for fetal cardiac conduction fibers (4) (see Chapter 4). Structural cardiac defects and cytomegalovirus infections are also potential etiologies of congenital heart block. To reliably establish that fetal cardiac activity is present and that the persistent bradycardia is due to fetal heart block, confirmation with realtime ultrasound is necessary. Ultrasound allows for a further advantage in that cardiac structure can be carefully evaluated as well (see Chapter 7). However, ultrasound is really only an option in the antepartum period because it may not be possible to take the time required to make this evaluation in labor where either a bradycadia or prolonged deceleration may require urgent operative intervention. When the diagnosis of complete fetal heart block is made antenatally, the problem then becomes how to monitor the fetus in labor because the normal alterations in FHR in response to hypoxrmia and other central nervous system (CNS) input cannot be transmitted to the ventricles. Thus, in this situation, the FHR cannot be used as a way to monitor for fetal hypoxemia and to rule out acidemia. Three options are reasonable in this situation. Intermittent scalp pH is theoretically an option, but the need for repeating the test every 30 minutes makes this option unrealistic except in very rapid labors. In the past, an elective cesarean section was often undertaken, simply because there had been no other way to monitor the fetus. Although no longer available in the United States, fetal pulse oximetry has
provided a logical option, and limited data suggest that this is a safe and effective way of monitoring patients whose fetal arrhythmia prevents adequate FHR monitoring (5).

Bradycardia with moderate variability may occur in the second stage and is not indicative of abnormal fetal acidbase status. Other, more rare causes of fetal bradycardia are maternal hypothermia, prolonged hypoglycemia, betablocker therapy, and fetal panhypopituitarism with brainstem injury (6). Persistent bradycardia requires careful evaluation to ensure that it is not the maternal heart rate being recorded in the presence of a fetal demise or secondary to signal ambiguity. Real-time ultrasound can establish the correct diagnosis and thus avoid unnecessary and potentially dangerous therapy in the presence of an already dead fetus. Maternal heart rate can also be recorded from the Doppler transducer and in the rare situation where the fetus is dead the MHR may be recorded from the scalp electrode (see Chapter 4).

In the 2008 NICHD update on nomenclature, FHR variability was classified as follows:

In determining the immediate fetal status, the most important single FHR characteristic is variability. Moderate variability (6 to 25 BPM peak to trough) is a reflection of intact neurologic modulation of the FHR and of intact or normal cardiac responsiveness. The two components are short-term and long-term variability (LTV) (Fig. 6.4). Shortterm variability (STV) is the beat-to-beat irregularity caused by the normal variance in intervals between consecutive cardiac cycles. It is a consequence of the constant “push-pull” effect of sympathetic and parasympathetic nervous system input. LTV is the waviness of the FHR tracing, generally at a frequency of 3 to 5 cycles per minute. With older EFM systems, using external Doppler, FHR variability could not be accurately determined because Doppler monitoring can artifactually increase FHR variability due to the imprecision of the signal. With newer Doppler signal processing systems, however, variability can be accurately assessed. Although there is utility in distinguishing between LTV and STV in research settings because mathematical quantification of these two types are different, there is no current evidence that the distinction between the two has any clinical relevance. Perhaps the single exception to this is the sinusoidal tracing that is absent short term but uniformly increased LTV. Increased variability has been shown in animals to be a sign of mild hypoxia (7). However, when FHR variability is moderate or increased, fetal pH is usually normal.

As gestation advances and the fetal autonomic nervous system matures, the baseline FHR decreases and both STV and LTV increases. This is thought to reflect an increase in vagal control of cardiovascular reflexes. Decreased variability may be seen with prematurity, fetal sleep cycles or anything that causes fetal CNS depression. Fetal hypoxemia with acidemia is the most worrisome cause; however, any condition that depresses the CNS can also decrease variability (Table 6.2). In labor it is critical to carefully review the strip for the presence or absence of late, variable, or prolonged decelerations when decreased variability is seen. It is highly unlikely that minimal or absent variability reflects CNS depression due to metabolic acidemia unless there are decelerations indicating ongoing hypoxemia. The exception to this rule may occur in the fetus who presents in labor with a absent variability without decelerations, as one cannot rule out an hypoxic insult prior to the initiation of electronic monitoring. Especially in the absence of significant decelerations, other causes of CNS depression should be considered. Certain drugs may be responsible (Table 6.3), particularly drugs that depress the CNS (Fig. 6.5) and drugs with autonomic blocking effects. Parasympathetic blocking drugs
decrease variability while increasing baseline heart rate. Sympatholytic drugs (e.g., beta-adrenergic blockers) also decrease variability but decrease baseline heart rate.

Baseline heart rate variability is also associated with fetal wakefulness. When the fetus is sleeping, there may be decreased variability (Fig. 6.6). Usually the variability will spontaneously return to its previous level after a reasonable time, although the duration of fetal sleep states in labor is not as consistent as in the antepartum period. Stimulation of the fetus by manipulation of the uterus or noise may arouse the fetus and cause the variability to return or result in a FHR acceleration, both of which reliably predict the absence of abnormal fetal academia. The new onset of loss of variability in the absence of periodic FHR decelerations with contractions is not a sign of fetal hypoxia.

From an intrapartum monitoring perspective, the most ominous cause of decreased variability is fetal hypoxemia where FHR decelerations precede the loss of variability. In the presence of heart rate patterns, such as persistent late decelerations, loss of variability is associated with a high incidence of fetal acidosis and low Apgar scores (8) (Fig. 6.7), particularly in the case of preterm infants (9). A most difficult heart rate pattern to interpret is absent variability seen in the fetus with a normal baseline heart rate and no decelerations. This may represent a previous insult to the fetus that has since been corrected but has resulted in persistent neurologic damage. Also, this pattern may be seen in fetuses with significant congenital anomalies, especially of the central nervous and cardiac systems. Extreme prematurity is associated with decreased variability and nonreactive FHR patterns. Finally, these patterns can be idiopathic and occur in a subsequently vigorous and healthy neonate (10). Table 6.3 lists the causes of decreased variability.