FHR Case Presentation #3
Prolonged Deceleration / (Fetal Bradycardia)
Author:
Craig V. Towers, M.D.
Objectives: Upon the completion of this CNE article, the reader will be able to
1.
List the potential etiologies for prolonged decelerations / fetal bradycardia.
2.
Categorize the various types of prolonged decelerations (fetal bradycardia) based on
maternal versus fetal origin and state their differences.
3.
Discuss the importance of the examination and other aspects of the fetal monitor
tracing in helping to differentiate between the various causes for prolonged
decelerations (fetal bradycardia).
Case Presentation:
An 18-year-old female Gravida 1 Para 0 was admitted to labor and delivery for
induction. The patient had good prenatal care with normal prenatal laboratory results and
she was now 41 3/7 weeks gestation by good dates. Her past medical history was negative
for any major medical disorders. Her vital signs revealed a blood pressure of 112/68, pulse
of 78, and a temperature of 37.10C. The patient had undergone two prior modified
biophysical profiles that were reactive with normal amniotic fluid volumes. The initial
vaginal exam was closed, long, and -2 station. On admission, she received a prostaglandin E2
vaginal insert. Approximately 8 hours later the insert was removed and an oxytocin infusion
was started. The fetal heart monitor tracing at that time is seen in Strip #1. The infusion
began at 1 milli-unit per minute (mU/min) and was increased to 2 mU/min 20 minutes later
and then was increased by 2 mU/min increments thereafter until a good labor pattern
developed at a level of 12 mU/min. Several hours later, the patient was found to be 4 cm
dilated, completely effaced, and zero station as seen in Strip #2. About an hour later, the
fetal heart rate strip demonstrated what is seen in Strip #3 & Strip #4.
Discussion:
A prolonged deceleration is defined as a drop in the fetal heart rate from the baseline
by > 15 beats per minute (bpm) that lasts for > 2 minutes but < 10 minutes from the onset
to the return to baseline. If the fetal heart rate level stays below the baseline for > 10
minutes, it is considered a baseline change. In brief review, the normal fetal heart rate
baseline ranges between 110 beats per minute (bpm) on the lower end up to 160 bpm at the
upper end. In any 10 minute window, the baseline must be for a minimum of 2 minutes (see
ref. 1 & 2). If a prolonged deceleration lasts for more than 10 minutes and drops below 110
beats per minute (bpm), it is re-classified as a fetal bradycardia. There are cases where the
fetal heart rate baseline is constantly recorded at a level below 110 bpm in the absence of a
deceleration and these instances would also be classified as a fetal bradycardia. Several
etiologies exist as potential causes for prolonged decelerations (that may or may not lead to
fetal bradycardia), and these can be categorized into 5 basic groups or origins listed below:
1.
Maternal
 Hypotension
o position
o status-post epidural or spinal anesthetic
o drug induced
2.

hemorrhage

cardiac failure

acute hypoxia
Uterine
 hyperstimulation – excessive contraction frequency, prolonged contraction,
or increased uterine tone
o excessive oxytocin (pitocin) or other agents
o infection
o placental abruption
o status-post epidural
o spontaneous

3.
Placental
 abruption

4.
rupture
large infarct or vessel thrombosis
Umbilical cord
 compression
o frank umbilical cord prolapse
o inutero-compression
o rapid dilation and descent of the fetal head in labor
5.
Fetal
 hypovolemia / hypotension
o fetal-to-maternal hemorrhage
o ruptured fetal vessel (vasa previa)
o uterine rupture

anomalous fetus or fetal central nervous system damage
When presented with a prolonged deceleration, a rapid systematic evaluation needs to be
performed in order to potentially determine the cause. As noted in the list, there is some
overlap in the potential etiologies, and the prolonged deceleration may actually be due to
several factors. For example, a uterine rupture can lead to maternal hypotension (due to
hemorrhage), placental abruption, and fetal hemorrhage. Thus, the actual cause behind the
prolonged deceleration with a uterine rupture may be multifactorial. These multifactorial
inputs may be the explanation behind why one child that is delivered within a certain time
period is normal and another is not.
When a prolonged deceleration occurs, one of the first items to check is the mother’s
position and blood pressure. Maternal hypotension (when it occurs) is often caused by the
mother’s position (supine hypotension) or is seen following the placement of an epidural or
spinal anesthetic agent. When a mother is supine, the enlarged uterus can compress the
inferior vena cava and thereby decrease blood flow back to the heart, leading to a decrease in
cardiac output. This is one of the main reasons why patients are labored in a left or right
lateral recumbent position. A prolonged deceleration following an epidural or spinal
anesthetic may also be caused by hypotension because of vasodilation (especially at a level
below the placement of the spinal or epidural) from a sympathetic blockade. This is why
most patients are “pre-hydrated” with a liter or more of a crystalloid solution prior to the
placement of the anesthetic. However, it should also be noted that patients are often placed
in a supine position once the spinal or epidural is placed in order to obtain a uniform
distribution of the anesthetic agent. Therefore, maternal position may play a role.
Furthermore, one study demonstrated that the prolonged decelerations that occur following
the placement of an epidural are associated with a prolonged contraction or a set of
hypertonic contractions (see ref. 3). These protracted contractions occur on average about
15 minutes after the injection. Thus, a prolonged deceleration that occurs following the
placement of a spinal or epidural anesthetic agent may involve multiple causes that include
maternal blood pressure, maternal position, and uterine contractility.
Regarding regional anesthesia, epidural is popular because a catheter can be placed
and intermittent or continuous drug administration can occur that extends the duration of
anesthesia. Spinal anesthetics, on the other hand, are one-time administrations and
therefore, are most often placed when the patient is about to deliver. Spinal anesthesia is
commonly used in the operating room prior to performing a cesarean section. This is one of
the reasons why the fetal heart rate is documented in the operating room. According to the
joint statement from the American College of Obstetricians & Gynecologists (ACOG) and
the American Academy of Pediatrics (AAP), “fetal surveillance should continue until the
abdominal sterile preparation has begun” (in the case of external monitoring), or “continued
until the abdominal sterile preparation is complete” if an internal monitor is in place (see ref.
4). It should be noted, that if a decision is made to perform a cesarean section on a laboring
patient that has an internal monitor, discontinuing the internal monitor prior to going to the
operating room is not recommended. Likewise, common sense suggests that the abdominal
prep should not begin until the surgeon is ready to scrub or is scrubbing. One of the points
of fetal monitoring is knowing what the fetal heart rate is, as close to delivery as possible.
Another reason for a drop in maternal blood pressure is medications. This is
especially true if the mother has hypertension or pre-eclampsia. These patients can be very
sensitive to medications. If a mother is admitted with an elevated blood pressure that is
treated with an intravenous anti-hypertensive medication, one needs to observe the fetal
response when the mother’s blood pressure changes. Prolonged decelerations have occurred
in patients even when the change has not resulted in a blood pressure level that is considered
hypotensive. For example, if a pregnant woman with a blood pressure of 200/110 is treated
with an intravenous anti-hypertensive medication and the blood pressure drops to 135/75,
this change is good for the mother (a blood pressure value that is now in the normal range
by definition and not hypotensive by criteria) but may result in a prolonged fetal heart rate
deceleration because of maternal cardiac output changes that significantly alter uteroplacental
blood flow. Because the true response that an individual will have to a drug that is given
intravenously is unknown until after the medicine is administered, any fetal heart rate
deceleration that occurs in close proximity to the dispensing of the drug should be suspect.
This is because hypotension can be a common finding in allergic or adverse drug reactions.
For completion purposes, one other drug related prolonged fetal heart rate
deceleration that needs to be discussed is the post-paracervical block. Though this
procedure is no longer commonly performed with the advent of continuous epidural
anesthesia, prolonged decelerations were common following the placement of this form of
anesthesia. The incidence of a post-paracervical block prolonged deceleration is wide
ranging from a low of 10% to as high as 70%, which may be another reason why the
procedure has decreased in use. The decelerations often occur about 7 to 10 minutes after
placement and would last about 8 minutes on average (but some cases never recover leading
to poor fetal outcome). The cause of the deceleration is also not completely understood and
may also be multifactorial in nature. One theory is that the deceleration is caused by a direct
fetal uptake of the drug, whereas another theory relates the deceleration to uterine artery
vasospasm along with uterine hypertonus (somewhat similar to what has been reported with
decelerations seen following epidural anesthesia) (see ref. 5).
The three remaining maternal causes for a prolonged deceleration are less common
and include hemorrhage, cardiac failure, and acute hypoxia. The most common cause for
maternal hemorrhage prior to delivery is third trimester bleeding. If hemorrhage from a
placenta previa or placental abruption is significant, this can lead to hypovolemia and a
decrease in cardiac output. Obviously, a mother can hemorrhage for other reasons, such as
trauma (car accident, etc.), a ruptured aneurysm, or a ruptured spleen, etc., but fortunately,
these are less common. Likewise, cardiac failure can occur following a myocardial infarct
(very rare but reported in pregnancy); could be related to an underlying anomalous cardiac
condition of the mother, such as severe valvular disease, rheumatic heart disease, or
Eisenmenger syndrome (pulmonary hypertension); or caused by a cardiomyopathy related to
hypertension, myocarditis, amniotic fluid embolus, or an idiopathic / peripartum
cardiomyopathy of pregnancy. Lastly, acute maternal hypoxia can occur following sudden
severe bronchospasm as part of an allergic or anaphylactic reaction to a drug or
environmental agent, or could be due to a pulmonary embolus or amniotic fluids embolus.
Besides maternal issues, the uterus is also a common source for prolonged
decelerations. Uterine hyperstimulation (seen as excessive uterine contractions, a protracted
contraction, or an increase in baseline internal uterine pressure) has been given various
names through the years. No standardized terminology currently exists. Some of the words
that are used include tetanic contractions, uterine hypertonus, tachysystole, polysystole,
paired contractions (couplets or triplets), skewed contraction, or a prolonged, protracted, or
extended contraction (see ref. 6). In “normal” labor, the contraction frequency on average is
once every 2 to 3 minutes (or 3 to 5 contractions in a 10-minute window) with a baseline
uterine tone on average of about 8 to 15 mmHg. “Normal” labor contractions on average
range from about 30 to 90 seconds in duration (with an average of about 60 seconds).
Excessive contraction frequency in many cases is described as contractions that occur closer
than every 2 minutes (or > 6 contractions in 10 minutes for two consecutive 10-minute
periods) (see ref. 7). An elevated baseline uterine tone is often defined as one that exceeds
20 to 25 mmHg and a prolonged, protracted, or extended contraction is one that lasts more
than 2 minutes. Again, it is important to understand that there is no universally accepted
standard on these definitions and the ones just described above are relative parameters. In
addition, the fetal response in relation to these contraction patterns is also of importance.
As listed in the differential table above, uterine hyperstimulation can lead to
prolonged fetal heart rate decelerations because these entities may impair the normal
uteroplacental blood flow. Uterine hyperstimulation can be iatrogenic from excessive
oxytocin (pitocin) or other agents that may increase myometrial activity, such as
prostaglandin agents {E1 or misoprostol (Cytotec), E2 as prostaglandin gel (Prepidil), as a
vaginal insert (Cervidil), or as a prostin suppository (Dinoprostone), and 15-methyl F2
(Hemabate or Carboprost)}, or the ergot alkaloids {ergonovine (Ergotrate),
methylergonovine (Methergine), ergotamine (Cafergot or Wigraine), dihydroergotamine, and
methysergide} (see ref. 8). If uterine hyperstimulation occurs in a patient on oxytocin, then
the infusion can be decreased or temporarily discontinued. All of the other agents listed
above are not recommended for use in a pregnancy that is viable except for prostaglandin E2
gel, prostaglandin E2 vaginal insert, or prostaglandin E1 (in cervical ripening dosages). The
vaginal insert can be removed if uterine hyperstimulation occurs. If uterine hyperstimulation
develops with prostaglandin E2 gel or prostaglandin E1, some clinicians have recommended
vaginal washing, whereas others have suggested the use of a tocolytic agent, such as
terbutaline.
The issue of a prolonged or protracted contraction following the placement of an
epidural has been discussed above. If an excessive contraction pattern is seen in a patient
not receiving oxytocin and who is not recently status-post epidural placement, it could be a
sign of placental abruption or chorioamnionitis. Many patients (though not all) with
placental abruption will have clinical signs of pain and vaginal bleeding and patients with
chorioamnionitis are usually febrile. Lastly, there are occasional patients that spontaneously
will have an excessive contraction pattern, naturally occurring protracted contractions, or
paired (coupled) contractions. Though this may be normal for these patients, these instances
can still lead to fetal heart rate deceleration patterns or a prolonged deceleration that requires
some form of intervention, and therefore, need to be watched closely.
The other uterine source for a prolonged deceleration is uterine rupture. Though the
overwhelming majority of these occur in patients that have a prior cesarean section, uterine
rupture has been reported to occur following myomectomy, a perforated dilatation &
curettage or D & C (that may not have been appreciated at the time), or spontaneously in an
unscarred uterus. Though numerous clinical signs have been reported with uterine rupture,
including pain, a change in contraction pattern, a sudden loss of fetal station on vaginal
exam, vaginal bleeding, and/or maternal hypotension, the most common and consistent
finding is a change in the fetal heart rate pattern to one with decelerations or a prolonged
deceleration that can lead to a bradycardia (see ref. 9)
Placental sources for a prolonged deceleration are abruption and large infarcts or
vessel thrombosis. The majority of placental infarcts or vessel thromboses will not cause a
prolonged deceleration unless the fetus happens to be on a monitor at the time of the infarct
or thrombosis. Most cases of infarcts and thromboses develop slowly and chronically over
time leading to a decrease in amniotic fluid volume, fetal growth restriction, and a fetal heart
rate pattern more consistent with uteroplacental insufficiency (late decelerations). Placental
abruption, on the other hand, is more common and can be responsible for a prolonged
deceleration. Placental abruptions vary in their appearance from those that are small, slow,
and indolent in onset to others that are sudden and large (and everything in between). The
most common etiology for placental abruption is idiopathic (meaning unknown) and this is
seen in about 60% of cases. The most common identifiable cause is hypertension (chronic
or pregnancy onset), which on average accounts for about 25% of the cases (a range of 15%
to 45%). The remaining 15% or so have been associated with trauma, drugs (such as
cocaine or amphetamine usage), hypercoagulable states (patients with lupus anticoagulant or
anticardiolipin antibodies, protein C or S deficiency, antithrombin III deficiency, Factor V
Leiden mutation, prothrombin gene 20210A mutation, and others), placental anomalies
(circumvallate placenta), uterine anomalies, multiple gestation, and sudden uterine
decompression from an over distended condition (for example, membrane rupture in a
patient with severe polyhydramnios) (see ref. 10). If a large sudden placental abruption
occurs during labor, the fetal heart rate will likely drop into a prolonged deceleration without
much prior warning, except for the possible clinical signs of maternal pain and vaginal
bleeding (but again vaginal bleeding in some cases can be concealed). If a patient were to
have a smaller placental abruption, one might see an excessive uterine contraction pattern (as
discussed above) that may be associated with periodic decelerations that over time could lead
to a prolonged deceleration.
The fourth major category in the differential for producing a prolonged deceleration
is cord compression. An obvious cause is frank umbilical cord prolapse, where the cord
descends beyond the fetal presenting part in the birth canal. This is often seen in breech
presentation (or other non-vertex presentations) but can occur in cephalic presentation as
well (especially if the patient has a contracted pelvis). Umbilical cord compression can also
occur inutero, especially in patients with minimal amniotic fluid. Usually, inutero umbilical
cord compression is intermittent and will produce variable decelerations; however, if the
cord becomes compromised to where it is compressed for a long period of time, a
prolonged deceleration will occur. A separate entity that is often listed as inutero cord
compression but has been associated with prolonged decelerations is rapid dilation and
descent of the fetal head. Others have stated that this deceleration may be due to fetal head
compression causing a vagal response that produces the deceleration. In reality, we probably
will never know if these specific decelerations are related to cord compression or a vagal
response of head compression (or a combination of the two) because they are not
predictable and no one can see inside the uterus at the time of the deceleration in order to
rule one in or out. What is important to understand is that a prolonged deceleration can be
seen in patients that have a rapid dilation and descent labor pattern.
The fifth and final category is fetal origin. These are less common when compared
to many of the categories listed above. Fetal hemorrhage that leads to hypovolemia and
hypotension can produce a prolonged deceleration if it is sudden and significant. If a fetus
becomes anemic slowly over time (such as Rh sensitization or a maternal parvovirus B-19
infection or a slow maternal-to fetal hemorrhage) the fetal heart rate pattern is likely to show
a sinusoidal pattern or a tracing with periodic decelerations. Acute fetal hemorrhage,
however, often produces a rapid drop in fetal volume, which then precipitates the prolonged
deceleration that often continues into a bradycardia, as defined. This type of hemorrhage
can be seen with a sudden severe fetal-to-maternal hemorrhage, a ruptured fetal vessel, or a
ruptured uterus (previously discussed above). The only way to truly determine a fetal-tomaternal hemorrhage is to have a low hemoglobin and hematocrit in the child immediately
after delivery and a mother with a positive Kleihauer-Betke test. A ruptured fetal vessel
usually occurs in a situation where fetal vessels are located on the membranes and then are
torn when the membranes rupture. If these fetal vessels happen to lie over the cervix, the
finding is called a vasa previa; however, they can actually be located anywhere inutero and
can lead to a prolonged deceleration if torn. Common findings that could lead to a situation
where the fetal vessels are found on the membranes are in cases where there is a
succenturiate lobe placenta (a small extra placental lobe that is separate from the main body
of the placenta) or a membranous umbilical cord insertion (where the cord inserts onto the
membranes instead of the placenta itself. In both of these settings, fetal vessels traverse
across the membranes in order to reach the main body of the placenta.
The second fetal category is also very rare but has been reported. Reports of
anomalous fetuses, especially central nervous system (CNS) or cardiac anomalies, as well as,
inutero fetal CNS damage from a prior non-lethal asphyxial event, or hemorrhage
(intraventricular and intraparenchymal) from ruptured aneurysms or arteriovenous (AV)
malformations or cerebral infarcts have occurred that have been associated with prolonged
decelerations in the fetal heart rate tracing. These situations often produce unusual tracings
that may include a wandering baseline, minimal to absent variability, unusual decelerations
associated with contractions, and spontaneous decelerations (some of which are prolonged
by definition).
There are cases of fetal bradycardia, where the fetal heart rate baseline is consistently
below 110 that are not connected to a prolonged deceleration. This is actually a separate
differential (and includes such items as low maternal temperature or medication usage, fetal
cardiac anomalies or arrhythmias, normal variation, and fetal hypoxia) and will be discussed
in other courses. One might argue that fetal hypoxia should be in the differential as an
etiology for prolonged deceleration. In actuality, nearly every cause in the above differential
list produces some form of fetal hypoxia, and thus it is a component of every item listed.
Nevertheless, a clinical situation where a normally oxygenated fetus suddenly becomes
hypoxic and nothing on the list has occurred is unlikely. End stage prolonged decelerations
/ bradycardias have been seen in cases of severe asphyxia just prior to fetal death. However,
these patterns are preceded by persistent periodic decelerations with absent variability.
Case Presentation Outcome and Summary:
As seen on Strip #3, the oxytocin infusion was discontinued, oxygen was started, the
patient was moved to her right, then left side and the intravenous infusion was increased. In
addition, an internal fetal scalp electrode was placed. Though not recorded on the tracing,
the mother’s blood pressure was still in the normal range and she had not recently received
an epidural or any other medications. The fetal heart rate tracing recovered and she was
later taken to the delivery room where she spontaneously delivered a 3620-gram male infant
with Apgar scores of 8 and 9 for 1 and 5 minutes, respectively. Strip #5 shows the tracing
after recovery and near delivery. The cause for the prolonged deceleration in this case was
uterine hyperstimulation (excessive contraction frequency and a prolonged contraction).
In review, when a prolonged fetal heart rate deceleration occurs, a rapid systematic
approach can be performed to help determine the etiology. This includes (though not in any
particular order) an awareness of any recent epidural placement or medication usage,
evaluating the mother’s position and checking her vital signs, quickly assessing for any
maternal symptoms of chest pain, shortness of breath, abdominal pain, or bleeding,
performing a vaginal examination to check for any evidence of a prolapsed cord or rapid
dilation and descent, and quickly analyzing the fetal monitor tracing for any evidence of
uterine hyperstimulation. If the etiology for the deceleration prior to delivery is still
uncertain, examine the placenta and check the neonate’s hemoglobin and hematocrit count
(if anemic, consider performing a Kleihauer-Betke test on the mother). Potential therapeutic
measures can include changing the mother’s position, increasing the intravenous infusion
rate, applying oxygen, discontinuing any oxytocin infusion, and assessing the need for
delivery.
References or Suggested Reading:
1.
ACOG. Management of Intrapartum Fetal Heart Rate Tracings: American College of
Obstetrics and Gynecology Practice Bulletin #116 November 2009 – Reaffirmed
2013.
2.
Electronic fetal heart monitoring: research guidelines for interpretation. National
Institute of Child Health and Human Development Research Planning workshop.
Am J Obstet Gynecol 1997;177:1385-90.
3.
Freeman RK, Garite TJ, Nageotte MP, Miller LA. Fetal Heart Rate Monitoring 4rd
Edition. Lippincott Williams and Wilkins. Page 243. Philadelphia, PA. 2013.
4.
ACOG / AAP. Guidelines for Perinatal Care 7th Edition. American College of
Obstetrics and Gynecology and American Academy of Pediatrics. October 2012
Pages 177-180.
5.
Carlsson B-M, Johansson M, Westin B. Fetal heart rate pattern before and after
paracervical anesthesia. A prospective study. Acta Obstet Gynecol Scand
1987;66:391-5
6.
Stookey RA, Sokol RJ, Rosen MJ. Abnormal contraction patterns in patients during
labor. Obstet Gynecol 1973;42:359-65.
7.
The American College of Obstetrics & Gynecology. Prolog on Obstetrics. Fifth
Edition. Induction of labor. Page 69. 2003.
8.
Graves CR. Agents that cause contraction or relaxation of the uterus. In Goodman
& Gilman’s: The Pharmacological Basis of Therapeutics. Ninth Edition. McGRawHill, New York 1996, pp. 944-5.
9.
ACOG. Vaginal Birth After Previous Cesarean Delivery. American College of
Obstetrics & Gynecology Practice Bulletin #115 August 2010 – Reaffirmed 2013.
10.
The American College of Obstetrics & Gynecology. Prolog on Obstetrics. Fifth
Edition. Placental abruption. Page 65. 2003
About the Author
Dr. Towers is currently the Director of Maternal-Fetal Medicine at University of
Tennessee Medical Center, Knoxville, Tennessee and is a Professor in the Department of
Obstetrics & Gynecology. Dr. Towers has over 90 publications in peer review medical
journals and he has given lectures on a wide variety of obstetrical topics nationwide,
including fetal heart rate monitoring. He has authored a book for pregnant women regarding
the safety of over-the-counter medications entitled I’m Pregnant & I Have a Cold – Are Overthe-Counter Drugs Safe to Use? published by RBC Press, Inc. He is one of the new Editors of
Drugs in Pregnancy and Lactation, Williams and Wilkins. Dr. Towers reports no conflicts of
interest.
Examination:
1.
A prolonged deceleration is defined as a
A.
drop in the fetal heart rate from the baseline by > 15 bpm that lasts for > 2
minutes but < 10 minutes from the onset to the return to baseline
B.
fetal heart rate that drops below 110 for > 15 minutes
C.
drop in the fetal heart rate from the baseline by > 30 beats per minute that
lasts for > 10 minutes before it returns to the baseline
D.
fetal heart rate that drops below 110 for > 10 minutes
E.
drop in the fetal heart rate from the baseline by > 15 bpm that never returns
to the baseline
2.
If the fetal heart rate level drops below the baseline by > 15 bpm for > 10 minutes, it
is considered a
A.
bradycardia
B.
tachycardia
C.
baseline change
D.
prolonged deceleration
E.
protracted variable deceleration
3.
Maternal causes for a prolonged deceleration include all of the following EXCEPT
A.
hypotension
B.
acute hypoxia
C.
cardiac failure
D.
diabetes
E.
hemorrhage
4.
In strip #1 above, the variability for the most part is
A.
absent
B.
minimal
C.
moderate or normal
D.
marked
E.
reactive
5.
Maternal hypotension that may occur when a mother is supine is due to
A.
an increase in cardiac output
B.
the enlarged uterus compressing the inferior vena cava
C.
a lack of pre-hydration
D.
an increase in blood flow back to the heart
E.
the enlarged uterus compressing the aorta
6.
A prolonged deceleration that occurs status-post epidural placement may be caused
by any of the below factors EXCEPT
A.
maternal hypotension
B.
C.
D.
E.
a prolonged contraction
maternal supine position
a set of hypertonic contractions
maternal hypoxia
7.
According to the joint statement from ACOG and the AAP, when an internal fetal
scalp monitor is in place and the patient moves to the operating room,
A.
fetal surveillance should continue until the abdominal sterile preparation has
begun
B.
the monitor should be removed and changed to an external monitor
C.
fetal surveillance should continue until the surgeon begins to scrub
D.
the monitor should be removed and intermittent auscultation performed
E.
fetal surveillance should continue until the abdominal sterile preparation is
complete
8.
The most common cause for maternal hemorrhage prior to delivery is
A.
trauma
B.
third trimester bleeding
C.
ruptured aneurysm
D.
ruptured spleen
E.
car accident
9.
In the case presentation, the fetal heart rate dropped below 110 bpm and the
deceleration lasted for 11.5 minutes, which
A.
makes it reactive
B.
reclassifies it as a tachycardia
C.
classifies it as a moderate deceleration
D.
reclassifies it as a bradycardia
E.
results in no change in definition
10.
Normal baseline uterine tone on average is about _______ .
A.
8 to 15 mmHg
B.
15 to 25 mmHg
C.
> 25 mmHg
D.
8 to 15 cm2 H2O
E.
15 to 25 cm2 H2O
11.
All of the following medications may cause uterine hyperstimulation EXCEPT
A.
prostaglandin 15-methyl F2
B.
methylergonovine
C.
indomethacin
D.
ergotamine
E.
misoprostol
12.
The most common and consistent finding in patients with uterine rupture is
A.
maternal hypotension
B.
a sudden loss of fetal station on vaginal exam
C.
D.
E.
a fetal heart rate pattern with decelerations or a prolonged deceleration
vaginal bleeding
a change in contraction pattern
13.
The most common etiology for placental abruption is
A.
cocaine or amphetamine usage
B.
hypertension
C.
hypercoagulable states
D.
idiopathic
E.
trauma
14.
Usually, inutero umbilical cord compression is intermittent and will produce
A.
early decelerations
B.
variable decelerations
C.
late decelerations
D.
prolonged decelerations
E.
a sinusoidal pattern bradycardias
15.
If a fetus becomes anemic slowly over time, the fetal heart rate pattern is likely to
show
A.
early decelerations
B.
variable decelerations
C.
a bradycardia
D.
prolonged decelerations
E.
a sinusoidal pattern
16.
In the setting of a prolonged deceleration, if the neonate following delivery is found
to be anemic, the best test to verify a fetal-to-maternal hemorrhage would be a
A.
Kleihauer-Betke
B.
parvovirus B-19 antibody titer
C.
maternal antibody screen
D.
urine drug screen
E.
C-reactive protein
17.
An anomaly that could lead to a situation where the fetal vessels are found on the
membranes is a
A.
succenturiate lobe placenta
B.
circummarginate placenta
C.
Couvelaire uterus
D.
circumvallate placenta
E.
unicornuate uterus
18.
The cause for a fetal heart rate baseline that is consistently below 110 (unrelated to a
prolonged deceleration) includes all of the following EXCEPT
A.
fetal cardiac anomalies
B.
elevated maternal temperature
C.
normal variations
D.
fetal cardiac arrhythmias
E.
fetal hypoxia
19.
When faced with a prolonged deceleration of uncertain origin, potential therapeutic
measures can include all of the following EXCEPT
A.
discontinuing any oxytocin infusion
B.
changing the mother’s position
C.
increasing the intravenous infusion rate
D.
applying oxygen
E.
administering a dose of terbutaline
20.
In strip #5 above, the tocodynamometer is an external monitor. Which of the
following statements is true?
A.
The baseline uterine tone is normal.
B.
The contraction pattern would be considered excessive.
C.
The contraction strength is elevated.
D.
The contraction pattern would be considered normal.
E.
The baseline uterine tone is elevated.