Electronic fetal monitors continuously record the instantaneous fetal heart rate on the upper channel and uterine contractions on the lower channel. They do this by attaching, either externally (and non-invasively) or internally, to detect the fetal heart and each uterine contraction.

Labor is an inherently dangerous life event for a fetus and its mother. In the majority of cases, everything goes smoothly enough and ends happily. In a minority of cases, there are some problems. Electronic fetal monitoring is used to provide:
1. Minute-by-minute information on the status of the fetus
2. Accurate historical information on fetal status and the frequency/duration of contractions from earlier in labor.
3. Insight into the stresses on the fetus and its ability to tolerate those stresses.

Originally, electronic fetal monitoring was thought to be able to prevent such newborn problems as stillbirth, brain damage, and cerebral palsy. This hope proved to be overly optimistic.

Unfortunately, and contrary to earlier thinking, most of the problems that lead to stillbirth, brain damage, and cerebral palsy are not intrapartum problems, but have already occurred by the time a patient comes in to labor and delivery.

Nonetheless, electronic fetal monitoring has proved so useful in so many ways that it has become a prominent feature of intrapartum care, and indispensable for high risk patients.

Two forms of continuous electronic fetal heart monitoring are used, internal and external.
• Internal monitoring provides the most accurate information, but requires a scalp electrode be attached to the fetus, and a pressure-sensing catheter to be inserted inside the uterine cavity. Both of these require membranes be ruptured and both have small, but not inconsequential risks. For that reason, they are usually used only when the clinical circumstances justify the small increased risk of complication.
• External monitoring usually provides very good information about the timing of contractions and the fetal response. External monitoring consists of belts worn by the mother during labor that record the abdominal tension (indirectly recording a contraction), and the instantaneous fetal heart rate. External monitoring has the advantages of simplicity, safety, availability, and reasonable reliability under most general obstetrical circumstances. However, it is subject to more artifact than internal monitoring, may not detect subtle changes, and may not accurately record the information, particularly if the mother is overweight or active.

Uterine Blood Flow

Maternal blood flows to the uterus primarily through the uterine arteries. The arteries branch out, once they enter the uterus, and supply blood to the muscle cells of the myometrium, and through the wall to the intervillous space (IVS). Once the maternal blood reaches the IVS, it simply dumped into the space, where it drifts about until some is drained off through the maternal venous system. Unlike the highly controlled capillary circulation, there is little control over this process. The intervillus space is similar to a swimming pool, where fresh water is dumped in through a faucet (the maternal arterioles), while the drains in the bottom of the pool (maternal venous system) sucks up any available water that happens to be nearby.

The placenta floats on top of the IVS, with its chorionic villi dipping down into the pool. Across the villous membrane pass oxygen, carbon dioxide, nutrients and waste products. Some of this passage is active transport (eg, glucose), some facilitated (eg, because of pH gradient), and some is passive.

Many factors influence uterine blood flow delivery to the IVS, including:
• Maternal position (lateral, recumbant improves flow)
• Maternal exercise (decreases flow)
• Surface area of the placenta (placental abruption decreases flow)
• Hypotension or hypertension (both decrease flow)
• Uterine contractions (contractions reduce flow)

Once the maternal blood reaches the IVS, oxygen and nutrients must still must traverse the villous membrane. If thickened (as with edema or infection), then transvillous transport of materials will be impaired, at least to some degree.

Baseline Fetal Heart Rate

The baseline fetal heart rate is normally between 110 and 160 beats per minute. This seems to be the range that the normal, healthy fetus prefers to keep itself well-supplied with oxygen and nutrients. The heart can beat faster, but only at a cost of increased energy utilization that is normally not justified. The heart can beat slower, but if the bradycardia is prolonged, it can lead to progressive tissue oxygen debt.

Tachycardia

Tachycardia is the sustained elevation of fetal heart rate baseline above a 160 BPM. Tachycardia can be a normal response to some increased need for oxygen, for example:
• Increased fetal activity (everyone’s heart rate goes up when we exercise)
• Maternal fever (with an elevated body temperature, all enzyme systems speed up, increasing the need for oxygen on a metabolic basis)

It can also increase in the presence of more worrisome problems, including:
• Chorioamnionitis
• Maternal hypothyroidism
• Drugs (tocolytics, Vistaril, etc.)
• Fetal hypoxia
• Fetal anemia
• Fetal heart failure
• Fetal arrhythmias

Most tachycardias are not indicative of fetal jeopardy, particularly in the absence of any other FHR abnormalities.

Bradycardia

Bradycardia is the sustained depression of fetal heart rate baseline below 110. Most of these are caused by increased vagal tone, although congenital cardiac abnormalities can also be responsible.
Mild bradycardia (to 80 or 90 BPM) with retention of beat-to-beat variability is common during the second stage of labor and not of great concern so long as delivery occurs relatively soon. Moderate to severe bradycardia (below 80 BPM) with loss of beat-to-beat variability, particularly in association with late decelerations, is more troubling and may indicate fetal distress, requiring prompt resolution.

Variability

The normal fetal heart rate baseline is from 110 to 160 BPM and has “variability.” Variability means fluctuations in the fetal heart rate that are irregular in amplitude and frequency.
This variability is further classified by measuring the peak-to-trough distance, in beats per minute.

Absent Variability = No detectable fluctuations
Minimal Variability = Up to 5 BPM fluctuations
Moderate Variability = 6 to 25 BPM fluctuations
Marked Variability = Greater than 25 BPM fluctuations

Variability is normally controlled by the fetal brain through sympathetic and parasympathetic influences. Reduced variability occurs normally during fetal sleep and usually returns after 20 to 40 minutes.

Reduced variability may also occur:
• Following narcotic administration
• With fetal anomalies or injury
• With hypoxia and acidosis in combination with such FHR abnormalities as late decelerations, tachycardia, bradycardia, and severe variable decelerations.

Persistent or progressively reduced variability is not, by itself, a sign of fetal jeopardy. But in combination with other abnormalities may indicate fetal intolerance of labor.

Accelerations

An abrupt increase in fetal heart rate of at least 15 BPM and lasting at least 15 seconds is called an acceleration. These usually occur in response to fetal movement, and can sometimes be provoked by stimulating the fetal scalp during a pelvic examination, or by acoustically stimulating the fetus with a loud, obnoxious noise. The presence of fetal accelerations is a normal findings and indicates the fetus is tolerating the intrauterine environment well.

In pregnancies less than 32 weeks, the height and breadth of fetal accelerations may normally be a little less, at 10 BPM lasting at least 10 seconds.

If the acceleration lasts longer than 2 minutes, then it is classified as a prolonged acceleration. While unusual, it is of no clinical significance. Accelerations lasting longer than 10 minutes are considered a change in fetal heart rate baseline.

Sinusoidal Pattern

This is a smooth, sine-wave like pattern with a wave frequency of 3-5 per minute. By itself, this unusual pattern frequently has no significance, but in combination with a loss of variability is occasionally associated with fetal anemia.

Contraction Patterns

During latent phase labor (prior to 4 cm), contractions may occur every 3-5 minutes and may or may not be painful.

A normal contraction pattern in active labor shows contractions occurring about every 2-3 minutes and lasting about 60 seconds.
• If contractions are less often than every 2-3 minutes in the active phase, labor may progress more slowly, if at all. While less frequent contractions are the rule in latent phase labor (prior to 4 cm), they are the exception in active labor.

Coupling

Coupling means that two contractions occur one right after the other rather than the normal pattern. Usually, coupling is followed by a longer contraction-free interval. Tripling can also be seen where three contractions occur without any significant recovery time.
If labor is progressing normally, coupling can be ignored. But coupling is often associated with dysfunctional progress in labor. In these cases, coupling can be treated with:
• Rest
• Hydration
• Narcotics
• Epidural Anesthesia
• Oxytocin

Tachysystole

If contractions are persistently more often than 5 contractions in 10 minutes, this is called “tachysystole.” Tachysystole poses a problem for the fetus because it allows very little time for resupply of the fetus with oxygen and removal of waste products. For a normal fetus, tachysystole can usually be tolerated for a while, but if it goes on long enough, the fetus can be expected to become increasingly hypoxic and acidotic.

Tachysystole is most often caused by too much oxytocin stimulation. In these cases, the simplest solution is to reduce or stop the oxytocin to achieve a more normal and better tolerated labor pattern. Other causes of tachysystole include:
• Dehydration
• Placental abruption
• Pre-eclampsia
• Amnionitis

In cases of spontaneous tachysystole, increasing maternal hydration and placement in the lateral decubitus position may slow the contractions.

Effect of Contractions

The placenta floats on a lake of blood, called the intervillus space. This lake contains several hundred cc’s of maternal blood at full term. The blood is deposited in the lake by open maternal arteries, and is drained from the lake by open maternal veins. There is no capillary flow on the maternal side.

The placenta, floating on the lake, has finger-like projections, called villi that dip down into the lake. Fetal capillary circulation passes through these villi, and this is where gas, nutrient, and waste exchange between the mother and baby occurs.

During a uterine contraction, blood flow through the uterus slows, because the maternal vessels are being compressed by the myometrium. If the contraction is strong enough, all blood flow through it will stop.

Maternal mean arterial pressure (MAP) is around 85 mm Hg. The pressure on the inside of the uterus (at rest) is around 10 mm Hg. The pressure within the uterine muscle (intramyometrial pressure or IMP) is usually about 2-3 times that of the intra-amniotic pressure. Because of these pressures, blood flows from the high pressure uterine arteries, through the intramyometrial spiral arteries (and past the medium pressure intramyometrial zone) and into the low pressure intravillous space. From the IVS, blood is drained out through the even lower pressure venous system and returned to the mother’s circulation.

During a contraction, the intramyometrial pressures rise with the increased muscle tone. As the compressive pressure rises, blood flow through the spiral arteries diminishes (less pressure gradient to drive the blood through them), and then stops when the IMP equals the MAP. The IMP usually equals the MAP when the amniotic fluid pressure is around 40 mm Hg. (Remember that the intramyometrial pressure is 2-3 time that of the amniotic fluid pressure). As the contraction eases up, blood flow through the spiral arteries resumes and by the end of the contraction, blood flow is back to normal.
Thus, with each contraction of any significance, there is initially reduced blood flow to the intervillous space, then a cessastion of blood flow, followed by a gradual resumption of blood flow.
On one level, you could imagine the danger of the fetal oxygen supply being interrupted by each uterine contraction. On another level is the realization that for a normal fetus, this interruption is nearly trivial (similar to holding your breath for 5 seconds). But if the contractions are coming too frequently (with very little time between contractions for the fetus to resupply), or if the fetus already has a significant problem, then contractions can pose a threat.

Periodic Heart Rate Changes

These heart rate changes are recurring throughout labor. They are typically associated in some way with uterine contractions. There are three basic recognized types:
• Early Decelerations
• Late Decelerations
• Variable Decelerations

Each has its own features and clinical significance. In addition, a fetus may demonstrate combined decelerations (for example, a severe variable deceleration with a late deceleration component.)

Early Decelerations

Early decelerations are periodic slowing of the fetal heartbeat, gradual in onset and recovery, and synchronized exactly with the contractions. These dips are rarely more than 20 or 30 BPM below the baseline, but last at least 30 seconds from onset to nadir.
These innocent changes are thought to be due, in many cases, to fetal head compression within the birth canal.

Sometimes, patients demonstrating early decelerations will later develop variable decelerations.

Late decelerations

Late decelerations are repetitive, gradual slowings of the fetal heartbeat toward the end of the contraction cycle. From onset to nadir, they last at least 30 seconds, and have a gradual recovery to the baseline. They are felt to represent some degree of utero-placental insufficiency.

All blood flow in and out of the IVS stops briefly during a contraction. A normal fetus with normal reserve (oxygen in its bloodstream, in the blood of the placenta, and in the intravillous space) will probably not notice the tiny drop in total oxygen availability during these contractions. But a fetus who has used up its reserve, or cannot maintain its reserve will, over the course of the contraction, develop some degree of hypoxia, hypercarbia and acidosis. This otherwise normal fetus will respond by slowing its heart rate, to conserve energy. The fetal heart is the largest consumer of oxygen in the fetus and if the rate can be slowed, the fetus will survive longer on less oxygen.

After the contraction passes and fresh blood resupplies the intervillous space, the hypoxia, hypercarbia and acidosis is eased and the fetal heart rate returns to normal.

Clinically, the development of late decelerations is a worrisome sign that the fetus has very little reserve. Techniques that may be used to correct this problem include:
• Changing maternal position to improve uterine blood flow
• IV hydration to increase maternal blood volume, presumably leading to increased uterine blood flow
• Administering oxygen to the mother to try to get some additional oxygen through to the fetus. Of the three standard treatments, oxygen administration is the least useful, since the maternal hemoglobin oxygen saturation is likely already 99%. The effect of breathing additional oxygen will probably have minimal effect on the oxygen saturation.
• Decreasing or discontinuing oxytocin infusion to slow down or stop contractions that are provoking the decelerations.
• Tocolytic drugs to slow down or stop contractions that are provoking the decelerations.

If the late decelerations are persistent and non-remediable, this is considered “fetal distress,” “fetal intolerance of labor,” or a “non-reassuring fetal heart rate pattern.” Such patients should be delivered promptly to avoid fetal injury or death. Sometimes cesarean section is required to achieve prompt delivery.
If persistent and not correctable, they represent a threat to fetal well-being.

Variable Decelerations

Variable decelerations are variable in onset, duration and depth. They may occur with contractions or between contractions. They are at least 15 BPM in depth and last at least 15 seconds, but not longer than 2 minutes. Their onset to nadir is less than 30 seconds.
Typically, variable decelerations have an abrupt onset and rapid recovery (in contrast to other types of decelerations which gradually slow and gradually recover.

Variable decelerations are thought to represent a vagal response to some degree of umbilical cord compression. If the umbilical cord is only slightly compressed, this will obstruct the umbilical vein (low pressure system) which returns re-oxygenated blood to the fetal heart. The initial normal fetal response to this is a slight increase in fetal heart rate to compensate for the lack of blood return and the slowly diminishing oxygen supplies. If this slight increase in FHR is followed by a major drop in FHR, this phenomenon is called a “shoulder.”

As pressure on the umbilical cord increases, the high-pressure umbilical arteries become occluded. When this happens, there is an immediate rise in fetal blood pressure. 30% of the fetal cardiac output goes to the placenta and if that flow is blocked, the fetus will rapidly develop significant hypertension. The normal fetus will respond to this hypertension by immediately slowing the heart down by sending a signal through the vagus nerve. When the umbilical cord obstruction is released, the vagal response disappears and the fetal heart returns to normal.

If a mild degree of cord compression continues (enough to continue to obstruct the umbilical veins for a while), then another “shoulder” may appear at the end of the deceleration.

If the variable deceleration lasts long enough to cause hypoxia, there may be a more gradual rise back to the baseline and some “overshoot.” Overshoot means the heart rate goes higher than the baseline for a while, to compensate for the mild degree of hypoxia and acidosis that has occurred during that deceleration. If you exercise vigorously for a minute, your muscle tissues will acquire some degree of oxygen debt and a mild degree of local acidosis. When you sit down and rest, your heart rate will be higher than before you started exercising, but will return to normal as you resupply your muscles with oxygen and remove the local waste products. The fetus responds in a similar fashion.

Variable decelerations, unlike late decelerations, are not caused by hypoxia, although if severe enough, frequent enough and persistent enough, can ultimately lead to some degree of fetal acidosis.
The interventions to effectively treat variable decelerations may include:
• Changing maternal position to improve uterine blood flow
• IV hydration to increase maternal blood volume, presumably leading to increased uterine blood flow
• Administering oxygen to the mother to try to get some additional oxygen through to the fetus. Of the three standard treatments, oxygen administration is the least useful, since the maternal hemoglobin oxygen saturation is likely already 99%. The effect of breathing additional oxygen will probably have minimal effect on the oxygen saturation.
• Amnioinfusion to improve oligohydramnios
• Decreasing or discontinuing oxytocin infusion to slow down or stop contractions that are provoking the decelerations.
• Tocolytic drugs to slow down or stop contractions that are provoking the decelerations.
• Digital elevation of the fetal head out of the maternal pelvis to ease pressure on the umbilical cord.

Occasional mild or moderate variable decelerations are common and not considered threatening. They are seen in the majority of laboring patients at some time or other. They are more common in the second stage of labor.

Mild variable decelerations do not dip below 70 BPM and last less than 30 seconds.

Severe variable decelerations dip below 60 BPM for at least 60 seconds (“60 x 60”). If persistent and not correctable by simple means, they can be threatening to fetal well-being. Like persistent, non-remediable late decelerations, fetuses demonstrating persistent, non-remediable severe variable decelerations should be delivered promptly, preferably vaginally, but by cesarean section if necessary.

Prolonged decelerations

Prolonged decelerations last more than 2 minutes and occur in isolation. Causes include maternal supine hypotension, epidural anesthesia, paracervical block, tetanic contractions, and umbilical cord prolapse.

Some of these are largely self-correcting, such as the deceleration following paracervical block, while others (maternal supine hypotension) respond to simple measures such as repositioning.
Other causes (such as umbilical cord prolapse) require prompt intervention to avoid or reduce the risk of fetal injury.

EFM Categories

In 2008, the National Institute of Child Health and Human Development issued a statement with recommended categories for describing EFM tracings.
• Category I means normal, with a baseline between 110 and 160, moderate variability, and no late or variable decelerations.
• Category II means not Category I or III, and is indeterminate in its significance.
• Category III means abnormal, with absent variability, accompanied by bradycardia, or variable decelerations, or late decelerations, or a sinusoidal pattern.

Describing a Tracing

In communicating the pattern seen on an electronic fetal monitor tracing, it is useful to use a systematic approach, primarily to avoid omitting important information. I recommend you use this 4-step approach.
1. Contractions. Start with the contraction pattern. In this example, I would say, “There are regular uterine contractions every 2-3 minutes, lasting 60 seconds.”
2. Baseline. Next, provide the baseline fetal heart rate and variability. In this case, I would say, “The baseline fetal heart rate is 140 BPM and has moderate variability.”
3. Decel/Accel. Next, describe accelerations and decelerations. In this tracing, I would say, “There are multiple fetal accelerations greater than 15 x 15, and no decelerations.
4. Category. Last, Categorize the tracing as Category I, II, or III. “This is a Category I tracing.”