See discussions, stats, and author profiles for this publication at: [Link]

net/publication/227037193

Fetal Monitoring

Chapter · March 2010

DOI: 10.1007/978-0-387-88602-2_11

CITATIONS READS
0 578

3 authors, including:

Bhavani Shankar Kodali Scott Segal

Partners HealthCare Wake Forest School of Medicine
120 PUBLICATIONS   1,269 CITATIONS    170 PUBLICATIONS   2,063 CITATIONS   

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Intrapartum fever View project

Obstetric anesthesia View project

All content following this page was uploaded by Scott Segal on 10 June 2014.

The user has requested enhancement of the downloaded file.

 10
Fetal Monitoring
䉲

Fetal Heart Rate Monitoring

Baseline Heart Rate
Baseline Variability
Fetal Heart Rate Pattern (Periodic Changes)
Early Decelerations
Variable Decelerations
Late Decelerations
Biophysical Profile
Nonstress Test
Contraction Stress Test or Oxytocin Challenge Test
Assessment of Fetal Maturity

One of the most important goals for the anesthesiologist caring

for a pregnant women should be to maintain the uteropla-
cental unit and fetus in optimal condition. Hence, an adequate
knowledge of uterine activity and fetal monitoring is impor-
tant. Different devices are used for the intrapartum assessment
of uterine activity as well as fetal well-being.
Assessment of uterine activity is important in predicting the
normal progress of labor and also fetal well-being.1 Parame-
ters related to uterine activity are (1) baseline uterine tone and
amplitude, (2) duration of contractions, and (3) the interval
between contractions. Normal baseline tone varies between 8
and 20mmHg and increases to between 25 and 75mmHg
during contractions. However, the peak pressure can rise to
130mmHg with bearing-down efforts in the second stage of
labor. A contraction can last from 30 to 90 seconds, and
the interval between contractions normally varies from 2 to 3
minutes. A tocodynamometer can measure the parameters
of uterine activity when placed on the abdominal wall.2
118 FETAL MONITORING

However, one of the major limitations of external tocody-

namometry is the possible reception of inaccurate data from
improper positioning of the instrument on the abdominal wall.
Internal monitoring is more accurate and reliable, and it mea-
sures both amniotic fluid and intrauterine pressure.3 The pre-
requisites of internal monitoring include (1) engagement of the
presenting part, (2) adequate cervical dilatation, and (3) rup-
tured membranes. Internal measurement of uterine activity is
commonly used in high-risk cases (e.g., diabetes, postmatu-
rity) as well as in parturients receiving epidural analgesia for
the relief of labor pain.

Fetal Heart Rate Monitoring

The baseline heart rate, beat-to-beat variability (short and long
term), and the fetal heart rate pattern (periodic changes) are
the most important variables that should be followed in
recording the fetal heart rate.

Baseline Heart Rate

The normal baseline fetal heart rate varies between 120 and
160 beats per minute (BPM), and it is modulated by parasym-
pathetic and sympathetic nerve activity (Fig. 10-1).
Fetal tachycardia is diagnosed when the baseline escalates
above 160 BPM. The major causes of fetal tachycardia are:
1. Fetal hypoxia due to any cause
2. Maternal fever, most often associated with infection
3. Maternal administration of sympathomimetic drugs, e.g.,
ephedrine, b-mimetic drugs for tocolysis (terbutaline),
epinephrine
4. Maternal administration of parasympatholytic drugs, e.g.,
atropine, phenothiazines
5. Maternal hyperthyroidism
6. Fetal anemia
7. Fetal tachyarrythmias
Fetal bradycardia is defined as a fetal heart rate less than
100 BPM. The following are major causes:
1. Fetal head compression or umbilical cord compression
 FETAL MONITORING 119

240

210

180

150

120

90

60

30
49051
*17110
100
MEDS MEDS
DL DL
EFF
80 EFF
STA STA
ROM
60 ROM
PH PH
O2
40 O2
PULSE PULSE
TEMP
20 TEMP
B/P B/P
0

Figure 10-1. Normal fetal heart rate pattern.

2. Maternal administration of parasympathomimetic drugs,

e.g., neostigmine
3. Maternal administration of b-blockers, e.g., propranolol
4. Prolonged fetal hypoxia for any reason
5. Fetal congenital heart block
6. Combined spinal epidural technique, especially in parturi-
ents with decreased ureteroplacental blood flow.

Baseline Variability
Baseline variability is generally recognized as the single
most important parameter for the recognition of intrauterine
fetal well-being. Baseline variability is due to a constant battle
between the fetal sympathetic (increasing the heart rate) and
parasympathetic systems (decreasing the heart rate). The pres-
ence of good baseline variability is an indicator of intact
central nervous system as well as normal cardiac functions.
120 FETAL MONITORING

Baseline variability has been classified into (1) short-term vari-

ability, representing a beat-to-beat difference of 5 to 15 beats,
and (2) long-term variability, which generally shows a fre-
quency of 3 to 5 cycles per minute. Fetal heart rate variabil-
ity can be a very accurate indicator if it is used by direct fetal
electrocardiogram monitoring. Short-term variability is more
important in predicting fetal well-being. Various factors that
can affect this are as follows (Fig. 10-2):
1. Maternal administration of narcotic drugs, e.g., meperidine
(Demerol), morphine, alphaprodine (Nisentil), or butor-
phanol, which work by depressing the fetal central nervous
system
2. Maternally administered sedatives and hypnotics, e.g.,
barbiturates, diazepam, phenothiazines, or promethazine
(Phenergan), which also affect the fetal central nervous
system

240

210

180

150

120

90

60

30

100

75

50

25

Figure 10-2. Decreased variability of the fetal heart rate.

 FETAL MONITORING 121

3. Maternally administered parasympatholytic drugs, e.g.,

atropine or phenothiazines
4. The use of inhalational anesthetics
5. Fetal sleep cycle
6. Extreme prematurity
7. Fetal tachycardia

Fetal Heart Rate Pattern (Periodic Changes)

Periodic changes are defined as transient accelerations or
decelerations of short duration of the fetal heart rate followed
by a return to baseline levels. There are three categories of
decelerations: early, variable, and late.

Early Decelerations
Characteristics of early decelerations (Fig.10-3) are as
follows:
1. Uniform. U-shaped deceleration
2. Slow onset and slow return to baseline
3. Exact mirror image of uterine contractions in duration
4. Acceleration of the fetal heart not preceding the onset of a
contraction or following the end of a contraction
5. Fetal heart rate usually not falling below 20 to 30 BPM
6. Good beat-to-beat variability
Two mechanisms for early deceleration that have been
suggested are (1) fetal head compression with increased
intracranial pressure (Fig. 10-4) and (2) increased volume
of blood entering the fetal circulation during contractions,
thus triggering the baroceptor reflex activity. Both of these
mechanisms are vagally mediated and can be prevented by
atropine.4

Variable Decelerations
This is the most common of all fetal heart rate patterns
(Fig. 10-5), and the characteristics of this pattern are a
follows:
1. Variability in duration
2. Variability in shape and size
3. Variability in time
240 240
122

210 210

180 180

150 150

120 120

90 90
FETAL MONITORING

60 60

30 30
84550 84551
*19120
100 100
MEDS MEDS
DL DL
80 EFF
80 EFF
STA STA
60 ROM
60 ROM
PH PH
40 O2
40 O2
PULSE PULSE
20 TEMP
20 TEMP
B/P B/P
0 0

Figure 10-3. Early decelerations.

 FETAL MONITORING 123

Pressure on fetal head

Alteration in cerebral blood flow

Central vagal stimulation

Blocked by atropine

FHR deceleration

Figure 10-4. Mechanism of early decelerations (FHR = fetal

heart rate). (Adapted from Freeman RK, Garite TS: Fetal Heart
Rate Monitoring. Baltimore, Williams & Wilkins, 1981.)

This is probably caused by compression of the umbilical

cord against the fetal body parts, e.g., head, neck, or shoul-
der. Because the maximum pressure on the cord is generated
at the time of uterine contractions, the pattern coincides
with uterine contraction. These decelerations are usually
very abrupt in relation to both the onset and the return to
baseline levels. Depending upon the magnitude of the
decrease in the fetal heart rate, the variable decelerations have
been further subdivided into (1) mild (duration less than 30
seconds and deceleration not below 80 BPM), (2) moderate
(regardless of the duration, the fetal heart rate is less than
80 BPM), and (3) severe (duration greater than 60 seconds and
a fetal heart rate less than 70 BPM). Occasionally, variable
decelerations can change to late decelerations or severe fetal
bradycardia.
240 240
124

210 210

180 180

150 150

120 120

90 90
FETAL MONITORING

60 60

30 30
98715 98716
*09100
100 100
MEDS
DL
80 EFF
80
STA
60 ROM
60
PH
40 O2
40
PULSE
20 TEMP
20
B/P
0 0

Figure 10-5. Variable decelerations.

 FETAL MONITORING 125

Late Decelerations
Definitely a sign of uteroplacental insufficiency, late decel-
erations (Fig. 10-6) are characterized by the following:
1. The onset of deceleration usually starts 30 seconds or more
after the onset of uterine contraction.
2. The peak of the deceleration arrives long after uterine
contraction.
3. The onset and return are gradual and smooth.
4. The drop in fetal heart rate usually varies between 10 and
20 BPM and rarely falls lower than 30 to 40 BPM.
5. Although not always, there is a correlation between the
magnitude of decelerations and the degree of fetal hypoxia.
The major cause of late decelerations is reduced placental
perfusion, as can be seen during supine hypotensive syn-
drome because of aortocaval compression, severe hypoten-
sion following regional anesthesia, abruptio placentae,
postmaturity, diabetes mellitus; pre-eclampsia/eclampsia,
etc.
Besides these three main patterns, the other patterns that have
been described are prolonged decelerations and a sinusoidal
pattern.
Prolonged decelerations may be associated with a loss of
variability and a baseline fetal heart rate below 70 BPM; once
the duration exceeds 2 to 3 minutes, urgent intervention is
usually necessary.
A sinusoidal pattern is associated with a sine wave pattern
above and below the baseline with a cyclicity of about 4 to 8
minutes. Actually, there is an increased long-term variability.
One of the major causes of this pattern is the severe fetal
anemia usually associated with Rh incompatibly. A benign
sinusoidal pattern has been associated with narcotics like
alphaprodine (Nisentil) or butorphanol (Stadol).
Besides fetal heart rate monitoring, fetal scalp pH sampling
is also very important in making an ultimate judgement of fetal
well-being.5,6 Normal fetal scalp pH varies between 7.25 and
7.32; mild acidosis is documented when the pH varies between
7.20 and 7.24; and severe acidosis is noted when the pH
becomes lower than 7.20. A good correlation has been
observed between severity of the fetal heart rate pattern and fetal
 240 240 126
210 210

180 180

150 150

120 120

90 90

60 60
FETAL MONITORING

30 30
17263 17264
100 100
MEDS MEDS
DL DL
EFF
80 EFF
80
STA STA
ROM
60 ROM
60
PH PH
O2
40 O2
40
PULSE PULSE
TEMP
20 TEMP
20
B/P B/P
0 0

Figure 10-6. Late decelerations. (Adapted from Martin R: Prepartum and intrapartum
fetal monitoring, in Datta S (ed): Anesthetic and Obstetric Management of High Risk
Pregnancy. Chicago, Mosby-Year Book, 1991.)
 FETAL MONITORING 127

acidosis as observed by fetal scalp pH. At the present, most

obstetricians are in favor of confirming fetal compromise as
shown in fetal heart rate monitoring by routine sampling of fetal
scalp pH.

Biophysical Profile
Peripartum evaluation of the high-risk fetus is done by evalu-
ation of immediate biophysical activities: (1) fetal movement,
(2) fetal tone, (3) fetal breathing movements, (4) heart rate
activity, and (5) volume of amniotic fluid.7 The first four para-
meters reflect the presence of normal fetal central nervous
system activity, whereas amniotic fluid volume is an indicator
of long-term or chronic fetal compromise. These parameters
are all measured by ultrasound except for the fetal heart rate.
The variables are scored 2 if normal and 0 if abnormal. Fetal
heart rate activity is measured by nonstress testing and the oxy-
tocin challenge test.

Nonstress Test
This involves the detection of changes in the fetal
heart rate and fetal movement in association with uterine
contraction.
Usually this test is described as reactive if there are two
fetal movements in 20 minutes with accelerations of the fetal
heart rate of at least 15 BPM. The test is described as nonre-
active in the absence of fetal movement and accelerations of
the fetal heart rate.

Contraction Stress Test

or Oxytocin Challenge Test
In the presence of a nonreactive nonstress test, the oxytocin
challenge test becomes an important issue. Intravenous oxy-
tocin is used, beginning at a rate of 0.5–1.0 units/min, to
induce three adequate uterine contractions within a 10-minute
period. The oxytocin challenge test is considered to be posi-
tive if persistent late decelerations exist, whereas the test is
interpreted as negative in the presence of normal fetal heart
128 FETAL MONITORING

rate tracings. The oxytocin challenge test is contraindicated if

there is history of classical cesarean section or placenta previa
and if the parturient is at risk of premature labor.
A poor biophysical score (5 or less out of 10) indicates that
close supervision of the fetus is necessary.

Assessment of Fetal Maturity

Phospholipids, the major components of lung surfactant, are
produced by fetal alveolar cells in a sufficient amount by 36
weeks’ gestation. The lecithin/sphingomyelin ratio (L/S) is
commonly used to predict fetal lung maturity and is said to be
normal when the ratio is 2 in normal pregnancies. For diabetic
parturients, the ratio should be at least 3.5 or higher. Mea-
surements of saturated phosphotidylcholine are occasionally
used in normal parturients; the normal value is 500 mg/dL,
whereas in diabetics it is 1,000 mg/dL.
Recently, the TDx fetal lung maturity (FLM) test has become
popular.8 It is expressed in milligrams of surfactant per gram
of albumin (the cutoff value is 50 mg/g).
A FLM value of <50 mg/g indicates immature lung, between
50 and 70 mg/g is borderline, and >70 mg/g predicts adequate
lung maturity. In the author’s institution, FLM is not used in
diabetic parturients.
In summary, an adequate knowledge of the detection of
normal uterine activity and fetal well-being is necessary so that
anesthetic techniques do not interfere with uterine activity, the
fetoplacental unit, or above all, the fetus.

References
1. Caldeyro-Barcia R, Posserio JJ: Physiology of uterine contractions.
Clin Obstet Gynecol 1960; 3:386.
2. Reynold SRM, et al: Recording uterine contraction patterns in preg-
nant women: Applications of strain gauge in multi-channel toco-
dynamometer. Science 1947; 106:427.
3. Williams EA, Stallworthy JA: A simple method of internal tocogra-
phy. Lancet 1952; 1:330.
4. Freeman RK, Gartie TJ (eds): Fetal Heart Rate Monitoring. Balti-
more, Williams & Wilkins, 1981, pp 63–83.
 FETAL MONITORING 129

5. James LS: Acid-base status of human infants in relation to birth

asphyxia and the onset of respiration. J Pediatr 1958; 52:379.
6. Saline E, Schneider D: Biochemical supervision of the foetus during
labour. J Obstet Gynaecol Br Commonw 1967; 74:799.
7. Manning FA, et al: Fetal biophysical profile scoring: A prospective
study in 1184 high-risk patients. Am J Obstet Gynecol 1981;
140:289.
8. Russell JC, et al: Multicenter evaluation of TDx test for assessing
fetal lung maturity. Clin Chem 1989; 35:1005.

View publication stats