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. 15
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. 15 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.
1
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 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 16; therefore, there is little rate
fluctuation before 28 weeks. Variability should be normal after 32 weeks. 17 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. 18 Decreased or
absent variability should generally be confirmed by fetal scalp electrode monitoring
when possible.
2
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
The combination of late or
used.3 Loss of variability may be uncomplicated
severe variable decelerations
and may be the result of fetal quiescence (rest-
with loss of variability is a
activity cycle or behavior state), in which case the
particularly ominous sign.
variability usually increases spontaneously within
30 to 40 minutes.19 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. 19
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. 19 Uncomplicated loss of
variability usually signifies no risk or a minimally increased risk of acidosis 19,20 or low
Apgar scores.21 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)19,20,22 and signifies that the infant will be
depressed at birth.21 The combination of late or severe variable decelerations with
loss of variability is particularly ominous.19 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 19; 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. 21 Although it is a
nonreassuring pattern, the saltatory pattern is usually not an indication for immediate
delivery.19
3
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.
4
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. 16 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. 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.4,11,17
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
5
acidosis. Bradycardia of this degree is common in post-date gestations and in
fetuses with occiput posterior or transverse presentations. 16 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.16 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.4,11,16 Causes of prolonged severe bradycardia are listed in Table 6. If
the cause cannot be identified and corrected, immediate delivery is recommended.
TABLE 6 TABLE 7
Causes of Severe Fetal Signs of Nonreassuring Variable
Bradycardia Decelerations that Indicate
Hypoxemia
Prolonged Epidural and
cord spinal Increased severity of the
compression anesthesia deceleration
Cord Maternal Late onset and gradual return
prolapse seizures phase
Tetanic Rapid Loss of "shoulders" on FHR
uterine descent recording
contractions Vigorous A blunt acceleration or
Paracervical vaginal "overshoot" after severe
block examination deceleration26 (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
6
stimulation.15 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. 15
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
7
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. 23
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
8
ominous. A pattern of persistent late decelerations is nonreassuring, and further
evaluation of the fetal pH is indicated.16 Persistent late decelerations associated with
decreased beat-to-beat variability is an ominous pattern 19 (Figure 7).
FIGURE 7. Late deceleration with loss of variability. This is an ominous pattern, and
immediate delivery is indicated.
9
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 membranes17 and decreased amniotic fluid
volume.24 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).
10
FIGURE 9. Severe variable deceleration with overshoot. However, variability is
preserved.
FIGURE 10. Late deceleration related to bigeminal contractions. Beat-to-beat variability
11
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.4,11,24 Variable decelerations are generally associated with a
favorable outcome.25 However, a persistent variable deceleration pattern, if not
corrected, may lead to acidosis and fetal distress 24 and therefore is nonreassuring.
Table 7 lists signs associated with variable decelerations indicating hypoxemia 4,11,26
(Figures 9 and 10). Nonreassuring variable decelerations associated with the loss of
beat-to-beat variability correlate substantially with fetal acidosis 4 and therefore
represent an ominous pattern.
12
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.24 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. 24 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).
13
