TABLE 3 Nonreassuring and Ominous Patterns

NONREASSURING PATTERNS Fetal tachycardia Fetal bradycardia Saltatory (proceeding by leaps rather than by gradual transitions) (variability Variable decelerations associated with a nonreassuring pattern Late decelerations with preserved beat-to-beat variability

OMINOUS PATTERNS   Persistent late decelerations with loss of beat-to-beat variability Nonreassuring variable decelerations associated with loss of beat-to-beat variability Prolonged severe bradycardia Sinusoidal pattern (associated with hypoxia and severe fetal anemia, and has been reported in association with fetomaternal hemorrhage). Confirmed loss of beat-to-beat variability not associated with fetal quiescence, medications or severe prematurity

Interpreting FHR Patterns

A systematic approach is recommended when reading FHR recordings to avoid misinterpretation (Table 2). The FHR recordings may be interpreted as reassuring, nonreassuring or ominous, according to the pattern of the tracing. Reassuring patterns correlate well with a good fetal outcome, while nonreassuring patterns do not.
Evaluation of fetal well-being using fetal scalp stimulation, pH measurement, or both, is recommended for use in patients with nonreassuring patterns. Evaluation for immediate delivery is recommended for patients with ominous patterns. Table 3 lists examples of nonreassuring and ominous patterns. The FHR tracing should be interpreted only in the context of the clinical scenario, and any therapeutic intervention should consider the
 maternal condition as well as that of the fetus. For example, fetuses with intrauterine
growth restriction are unusually susceptible to the effect of hypoxemia, which tends
to progress rapidly.

A growing body of evidence suggests that, when properly interpreted, FHR
assessment may be equal or superior to measurement of fetal blood pH in the
 prediction of both good and bad fetal outcomes. Fetuses with a normal pH, i.e.,
greater than 7.25, respond with an acceleration of the fetal heart rate following fetal
scalp stimulation. Fetal scalp sampling for pH is recommended if there is no
acceleration with scalp stimulation.

A scalp pH less than 7.25 but greater than 7.20 is considered suspicious or
 borderline. Results in this range must also be interpreted in light of the FHR pattern
 and the progress of labor, and generally should be repeated after 15 to 30 minutes.
 A scalp pH of less than 7.20 is considered abnormal and generally is an indication for intervention, immediate delivery, or both.  A pH less than 7.20 should also be assumed
in the absence of an acceleration following fetal scalp stimulation when fetal scalp pH sampling is not available. Table 4 lists recommended emergency interventions for nonreassuring patterns. These interventions should also be considered for
ominous patterns while preparations for immediate delivery are initiated.

FHR Patterns

Baseline FHR

The FHR is controlled by the autonomic nervous system. The inhibitory influence
on the heart rate is conveyed by the vagus nerve, whereas excitatory influence is
conveyed by the sympathetic nervous system. Progressive vagal dominance
occurs as the fetus approaches term and, after birth, results in a gradual decrease
in the baseline FHR. Stimulation of the peripheral nerves of the fetus by its own
 activity (such as movement) or by uterine contractions causes acceleration of the FHR.

Baroreceptors influence the FHR through the vagus nerve in response to change
 in fetal blood pressure. Almost any stressful situation in the fetus evokes the
baroreceptor reflex, which elicits selective peripheral vasoconstriction and
 hypertension with a resultant bradycardia. Hypoxia, uterine contractions, fetal head compression and perhaps fetal grunting or defecation result in a similar response.

Chemoreceptors located in the aortic and carotid bodies respond to hypoxia,
excess carbon dioxide and acidosis, producing tachycardia and hypertension. The
 FHR is under constant and minute adjustment in response to the constant changes
in the fetal environment and external stimuli.

The normal FHR range is between 120 and 160 beats per minute (bpm). The baseline
rate is interpreted as changed if the alteration persists for more than 15 minutes.
 Prematurity, maternal anxiety and maternal fever may increase the baseline rate,
while fetal maturity decreases the baseline rate.

Figure 1. Reassuring pattern. Baseline fetal heart rate is 130 to 140 beats per minute (bpm), preserved beat-to-beat and long-term variability. Accelerations last for 15 or more seconds above baseline and peak at 15 or more bpm. (Small square=10 seconds; large square=one minute)

 

Figure 2. Saltatory (proceeding by leaps rather than by gradual transitions) pattern with wide variability. The oscillations of the fetal heart rate above and below the baseline exceed 25 bpm

FHR Variability

The FHR is under constant variation from the baseline (Figure 1). This variability
reflects a healthy nervous system, chemoreceptors, baroreceptors and cardiac responsiveness. Prematurity decreases variability; therefore, there is little rate
 fluctuation before 28 weeks. Variability should be normal after 32 weeks.  Fetal hypoxia, congenital heart anomalies and fetal tachycardia also cause decreased variability.
 Beat-to-beat or short-term variability is the oscillation of the FHR around the baseline in amplitude of 5 to 10 bpm. Long-term variability is a somewhat slower oscillation
in heart rate and has a frequency of three to 10 cycles per minute and an amplitude
 of 10 to 25 bpm. Clinically, loss of beat-to-beat variability is more significant than
loss of long-term variability and may be ominous. Decreased or absent variability
should generally be confirmed by fetal scalp electrode monitoring when possible.

Interpretation of the FHR variability from an external tracing appears to be more
reliable when a second-generation fetal monitor is used than when a first-generation
monitor is used. Loss of variability may be uncomplicated and may be the result of fetal

The combination of late or severe variable decelerations with loss of variability is a particularly ominous sign.

quiescence (rest-activity cycle or behavior state), in which case the variability usually increases spontaneously within 30 to 40 minutes. Uncomplicated loss of variability
may also be caused by central nervous system depressants such as morphine, diazepam (Valium) and magnesium sulfate; parasympatholytic agents such as atropine and
 hydroxyzine (Atarax); and centrally acting adrenergic agents such as
methyldopa (Aldomet), in clinical dosages.

Beta-adrenergic agonists used to inhibit labor, such as ritodrine (Yutopar) and
 terbutaline (Bricanyl), may cause a decrease in variability only if given at dosage
 levels sufficient to raise the fetal heart rate above 160 bpm.  Uncomplicated loss
of variability usually signifies no risk or a minimally increased risk of acidosis or low
 Apgar scores. Decreased FHR variability in combination with late or variable
deceleration patterns indicates an increased risk of fetal pre-acidosis (pH 7.20 to 7.25)
or  acidosis (pH less than 7.20) and signifies that the infant will be depressed
 at birth. The combination of late or severe variable decelerations with loss of variability
 is particularly ominous.  The occurrence of a late or worsening variable deceleration
 pattern in the presence of normal variability generally means that the fetal stress
is either of a mild degree or of recent origin; however, this pattern is considered nonreassuring.

Increased variability in the baseline FHR is present when the oscillations exceed
 25 bpm (Figure 2). This pattern is sometimes called a saltatory pattern and is usually
 caused by acute hypoxia or mechanical compression of the umbilical cord. This pattern is most often seen during the second stage of labor. The presence of a saltatory pattern, especially when paired with decelerations, should warn the physician to look for and try to correct possible causes of acute hypoxia and to be alert for signs that the hypoxia is progressing to acidosis.   Although it is a nonreassuring pattern, the saltatory pattern is usually not an indication for immediate delivery.

Figure 3. Fetal tachycardia with possible onset of decreased variability (right) during the second stage of labor. Fetal heart rate is 170 to 180 bpm. Mild variable decelerations are present.

 

Figure 4. Fetal tachycardia that is due to fetal tachyarrhythmia associated with congenital anomalies, in this case, ventricular septal defect. Fetal heart rate is 180 bpm. Notice the "spike" pattern of the fetal heart rate.

^{Fetal Tachycardia}

Fetal tachycardia is defined as a baseline heart rate greater than 160 bpm and is
considered a nonreassuring pattern (Figure 3). Tachycardia is considered mild
when the heart rate is 160 to 180 bpm and severe when greater than 180 bpm.
Tachycardia greater than 200 bpm is usually due to fetal tachyarrhythmia (Figure 4)
or congenital anomalies rather than hypoxia alone. Causes of fetal tachycardia
are listed in Table 5.

Persistent tachycardia greater than 180 bpm, especially when it occurs in conjunction
with maternal fever, suggests chorioamnionitis (inflammation of the fetal membranes) . Fetal tachycardia may be a sign of increased fetal stress when it persists for 10 minutes
or longer, but it is usually not associated with severe fetal distress unless decreased
variability or another abnormality is present.


^{Fetal Bradycardia}

Fetal bradycardia is defined as a baseline heart rate less than 120 bpm. Bradycardia
 in the range of 100 to 120 bpm with normal variability is not associated with fetal acidosis. Bradycardia of this degree is common in post-date gestations and in fetuses with occiput posterior or transverse presentations.  Bradycardia less than 100 bpm occurs in
fetuses with congenital heart abnormalities or myocardial conduction defects,
such as those occurring in conjunction with maternal collagen vascular disease.
Moderate bradycardia of 80 to 100 bpm is a nonreassuring pattern. Severe prolonged bradycardia of less than 80 bpm that lasts for three minutes or longer is an ominous
finding indicating severe hypoxia and is often a terminal event.  Causes of prolonged
 severe bradycardia are listed in Table 6.  If the cause cannot be identified and corrected,
immediate delivery is recommended.

TABLE 6 Causes of Fetal Bradycardia
Prolonged cord compression Cord prolapse Tetanic uterine contractions Paracervical block	Epidural and spinal anesthesia Maternal seizures Rapid descent Vigorous vaginal examination

TABLE 7   Signs of Nonreassuring Variable Decelerations That Indicate Hypoxemia

Increased severity of the deceleration Late onset and gradual return phase Loss of "shoulders" on FHR recording A blunt acceleration or "overshoot" after severe deceleration (Figure 9) Unexplained tachycardia Saltatory variability Late decelerations or late return to baseline (Figure 10) Decreased variability

FHR=fetal heart rate.

Periodic FHR Changes

Accelerations

Accelerations are transient increases in the FHR (Figure 1). They are usually associated
 with fetal movement, vaginal examinations, uterine contractions, umbilical vein
 compression, fetal scalp stimulation or even external acoustic (sounds) stimulation.
The presence of accelerations is considered a reassuring sign of fetal well-being. An acceleration pattern preceding or following a variable deceleration (the "shoulders"
of the deceleration) is seen only when the fetus is not hypoxic.  Accelerations are the
basis for the nonstress test (NST). The presence of at least two accelerations,
each lasting for 15 or more seconds above baseline and peaking at 15 or more
 bpm, in a 20-minute period is considered a reactive NST.

Early Decelerations

Early decelerations are caused by fetal head compression during uterine contraction, resulting in vagal stimulation and slowing of the heart rate. This type of deceleration
has a uniform shape, with a slow onset that coincides with the start of the contraction
and a slow return to the baseline that coincides with the end of the contraction.
Thus, it has the characteristic mirror image of the contraction (Figure 5). Although
 these decelerations are not associated with fetal distress and thus are reassuring,
 they must be carefully differentiated from the other, nonreassuring decelerations.

Figure 5. Early deceleration in a patient with an unremarkable course of labor. Notice that the onset and the return of the deceleration coincide with the start and the end of the contraction, giving the characteristic mirror image.

 

Figure 6. Nonreassuring pattern of late decelerations with preserved beat-to-beat variability. Note the onset at the peak of the uterine contractions and the return to baseline after the contraction has ended. The second uterine contraction is associated with a shallow and subtle late deceleration.

 

Late Decelerations

Late decelerations are associated with uteroplacental insufficiency and are provoked by uterine contractions. Any decrease in uterine blood flow or placental dysfunction can cause late decelerations. Maternal hypotension and uterine hyperstimulation may decrease uterine blood flow. Postdate gestation, preeclampsia, chronic hypertension and diabetes mellitus are among the causes of placental dysfunction. Other maternal conditions such as acidosis and hypovolemia associated with diabetic ketoacidosis may lead to a decrease in uterine blood flow, late decelerations and decreased baseline variability.

A late deceleration is a symmetric fall in the fetal heart rate, beginning at or after the
 peak of the uterine contraction and returning to baseline only after the contraction
has ended (Figure 6). The descent and return are gradual and smooth. Regardless of the depth of the deceleration, all late decelerations are considered potentially ominous.
A pattern of persistent late decelerations is nonreassuring, and further evaluation
of the fetal pH is indicated. Persistent late decelerations associated with
decreased beat-to-beat variability is an ominous pattern^.  (Figure 7).

 

Figure 7. Late deceleration with loss of variability. This is an ominous pattern, and immediate delivery is indicated.

 

Figure 8. Variable deceleration with pre- and post-accelerations ("shoulders"). Fetal heart rate is 150 to 160 beats per minute, and beat-to-beat variability is preserved.

^{Variable Decelerations}

Variable decelerations are shown by an acute fall in the FHR with a rapid downslope
and a variable recovery phase. They are characteristically variable in duration, intensity
and timing. They resemble the letter "U," "V" or "W" and may not bear a constant
 relationship to uterine contractions. They are the most commonly encountered patterns during labor and occur frequently in patients who have experienced premature rupture of membranes and decreased amniotic fluid volume. Variable decelerations are caused by compression of the umbilical cord. Pressure on the cord initially occludes the umbilical vein, which results in an acceleration (the shoulder of the deceleration) and indicates a healthy response. This is followed by occlusion of the umbilical artery, which results in the sharp downslope. Finally, the recovery phase is due to the relief of the compression and the sharp return to the baseline, which may be followed by another healthy brief acceleration or shoulder (Figure 8).

Figure 9. Severe variable deceleration with overshoot. However, variability is preserved.

Figure 10. Late deceleration related to bigeminal contractions. Beat-to-beat variability is preserved. Note the prolonged contraction pattern with elevated uterine tone between the peaks of the contractions, causing hyperstimulation and uteroplacental insufficiency. Management should include treatment of the uterine hyperstimulation. This deceleration pattern also may be interpreted as a variable deceleration with late return to the baseline based on the early onset of the deceleration in relation to the uterine contraction, the presence of an acceleration before the deceleration (the "shoulder") and the relatively sharp descent of the deceleration. However, late decelerations and variable decelerations with late return have the same clinical significance and represent nonreassuring patterns. This tracing probably represents cord compression and uteroplacental insufficiency.

Variable decelerations may be classified according to their depth and duration as mild,
 when the depth is above 80 bpm and the duration is less than 30 seconds; moderate,
when the depth is between 70 and 80 bpm and the duration is between 30 and 60 seconds; and severe, when the depth is below 70 bpm and the duration is longer than 60 seconds.  Variable decelerations are generally associated with a favorable outcome.  However, a persistent variable deceleration pattern, if not corrected, may lead to acidosis and fetal distress and therefore is nonreassuring. Table 7 lists signs associated with variable decelerations indicating hypoxemia (Figures 9 and 10). Nonreassuring variable decelerations associated with the loss of beat-to-beat variability correlate substantially with fetal acidosis and therefore represent an ominous pattern.

A.  B. Figure 11. (A) Pseudosinusoidal pattern. Note the decreased regularity and the preserved beat-to-beat variability, compared  with a true sinusoidal pattern (B).

^{Sinusoidal Pattern}

The true sinusoidal pattern is rare but ominous and is associated with high rates
 of fetal morbidity and mortality. It is a regular, smooth, undulating form typical of a
 sine wave that occurs with a frequency of two to five cycles per minute and an amplitude range of five to 15 bpm. It is also characterized by a stable baseline heart rate
of 120 to 160 bpm and absent beat-to-beat variability. It indicates severe fetal anemia,
 as occurs in cases of Rh disease or severe hypoxia. It should be differentiated
 from the "pseudosinusoidal" pattern (Figure 11a), which is a benign, uniform long-term variability pattern. A pseudosinusoidal pattern shows less regularity in the shape
and amplitude of the variability waves and the presence of beat-to-beat variability,
compared with the true sinusoidal pattern (Figure 11b).

SOURCE:  Sweha, Amir MD., Hacker, Trevor MD., and Nuovo, Jim MD.   American Family
Physician published by the Academy of American Family Physicians. 
A systematic approach to the interpretation of electronic fetal heart rate monitoring
is critical to ensure appropriate patient management.  May 1, 1999.   p. 2485.
 

About The Authors

Amir Sweha, M.D.

is residency director and medical director at the family practice residency program
 at Mercy Healthcare Sacramento and assistant clinical professor at the University of California, Davis, School of Medicine. He completed medical school at AIN Shams
 University in Cairo, Egypt, and completed a residency in family practice and a faculty development fellowship at the University of California, Davis, School of Medicine.

Trevor W. Hacker, M.D.

is associate medical director of the family practice residency program at
 Mercy Healthcare Sacramento and assistant clinical professor at the University
of California, Davis, School of Medicine. A graduate of the UCLA School of Medicine, he completed a residency in family practice at the Shasta-Cascade Family Practice
Residency Program in Redding, Calif., and completed a faculty development fellowship
at the University of California, San Francisco, School of Medicine.

Jim Nuovo, M.D.

is residency director of the University of California, Davis, Family Practice
 Residency Program. Dr. Nuovo received his medical degree from the University
 of Vermont College of Medicine, Burlington, and completed a residency in family
 practice at Madigan Army Medical Center, Tacoma, Wash.

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Non-Stress Test (NST)

The NST is another way of externally monitoring the baby. The NST can be done
as early as the 27th week of pregnancy, and it measures the FHR accelerations with
normal movement. For this test, the patient will sit with knees and back partially
elevated with a cushion under the right hip, which moves the uterus to the left.

The same monitors described above are placed on the abdomen to measure the
ability of the uterus to contract and the FHR. If there is no activity after 30-40 minutes,
the mother will be given something to drink or a small meal which may stimulate fetal
activity.  Other interventions that might encourage fetal movement include the use of fetal
acoustic stimulation (sending sounds to the fetus) and gently placing her hands
on her abdomen and moving the fetus.

Contraction Stress Test (CST)

The CST is a final method of externally monitoring the fetus. This test measures the
ability of the placenta to adequately oxygenate the fetus under pressure (contractions).

For this test, the mother will sit with knees and back partially elevated with a cushion under
 the right hip, which moves the uterus to the left. The same monitors described above
 are placed on her abdomen to measure uterine contractility and FHR. If contractions
are not occurring spontaneously, either a medication (called Oxytocin) will be given intravenously, or nipple stimulation will be used to induce contractions.

If oxytocin is administered, it is called the oxytocin challenge test (OCT). Oxytocin is administered through an IV until three uterine contractions are observed, lasting
40 to 60 seconds, over a 10-minute period.

A test involving nipple stimulation is called the nipple stimulation contractions
 stress test. Every effort will be taken to ensure patient privacy, but the nurse will be
with the patient through the entire procedure.

After being positioned as described above, the patient  will rub the palm of her hand
across one nipple through her garments for 2 to 3 minutes. After a 5-minute rest,
the nipple stimulation should continue until 40 minutes have elapsed, or 3 contractions
have occurred, lasting more than 40 seconds, within a 10-minute period. If a uterine contraction starts, the patient should stop the nipple stimulation.

Source:  http://www.nlm.nih.gov/medlineplus/ency/article/003405.htm
 

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