Critical Care Obstetrics part 62 docx

Anaphylactic Shock in Pregnancy
599
Class of agent Specifi c agents Comments
Radiocontrast media (RCM) [48 – 51] Lower osmolarity RCM presently in use have
a very low risk of inducing anaphylactoid
reactions as compared to the high
osmolality agents used in the past.
Iso - osmolar agents make RCM reactions
extremely unlikely and can be requested
when a patient is felt to be at risk of such
a reaction
RCM causes anaphylactoid reactions but not true anaphylaxis. The
incidence of life - threatening reactions is < 0.1%. Peak incidence is
between the ages of 20 and 50 so it does occur in women of
childbearing age. Anaphylactoid reactions to RCM are more likely if it
has happened before but even with a prior history of reactions to
RCM, the incidence runs between 16% and 44% with a subsequent
exposure. Volume overload from administration of RCM can lead to
cardiogenic pulmonary edema that is not a hypersensitivity response
and is part of the differential diagnosis of respiratory failure in this
setting [52] . There is no relationship between RCM reactions and
shellfi sh allergies (which are generally due to reactions to tropomyosin
proteins and not iodine). The only association between these two
allergies is that persons who have anaphylaxis to any agent are more
likely to have anaphylaxis to other agents.
Pretreatment with steroids and an H1 atagonist such as diphenhydramine
can ameliorate or prevent reactions in patients deemed to be at risk
Unusual causes described in obstetric
patients
Seminal fl uid
Laminaria

Oxytocic agents
Administration of syntocinon has been associated with anaphylactoid
response but has generally been attributed to preservatives used in
specifi c formulations such as chlorobutanol [55 – 59]
Methotrexate
Anesthetic agents including local anesthetic
[53]
Anaphylaxis to MTX used intravenously to treat cancer has been reported
[60]
Colloids such as dextran, albumin Dextran use has been associated with both maternal and fetal morbidity
and mortality with an incidence of dextran - 70 solution - induced
anaphylactoid reactions of 1 in 383 [61 – 64]
Exercise [54] Exertion can precipitate anaphylaxis in some individuals and this includes
the exertion of labor [65]
Blood products Whole blood, serum, plasma, fractionated
serum products or immunoglobulins can
all provoke an anaphylactoid response
Blood products can cause an anaphylactoid response via type II or type III
hypersensitivity reactions
Latex Exposure to hard rubbers not usually
signifi cant
Latex exposure can occur with gloves,
intravenous tubing, Foley catheters,
endotracheal tubes, dental dams, vial
stoppers, condoms, adhesive dressings,
and balloons. Exposure can occur through
direct contact, aerosolization or inhalation
Latex allergies remain one of the leading causes of perioperative
anaphylactoid reactions. Widespread use of powder - free and low latex
protein gloves has decreased latex sensitization but it still does occur

in healthcare workers and patients who have undergone multiple
hospital procedures [26,66] . Infants with spina bifi da are at increased
risk of latex allergies and ideally should be delivered and cared for
using non - latex materials
Table 42.2
Continued
be more common with oral ingestions and in general the delayed
second phase is less severe than the initial presentation.
Diagnosis
Anaphylaxis is a clinical diagnosis. Three proposed sets of criteria
for the diagnosis of anaphylaxis are reviewed in Table 42.4 .
Approach to a naphylaxis
Acute m anagement [15 – 20]
The acute management of anaphylaxis is reviewed below and
should proceed in a stepwise manner.
1 Provide oxygen and assess airway. Equipment for intubation
and persons experienced with intubation should be brought to
Chapter 42
600
Table 42.4 Three distinct criteria for the diagnosis of anaphylaxis [15,16,26,68] .

Criterion 1

Acute onset of an illness over minutes to hours with involvement of skin,
mucosal tissue or both, e.g. hives, swollen lips/tongue/uvula, fl ushing with at
least one of the following:
– respiratory compromise, e.g. dyspnea, wheezing, stridor, hypoxemia
– reduced blood pressure or symptoms of end - organ dysfunction suggestive of
hypotension (e.g. syncope, incontinence, collapse, hypotonia)

Criterion 2

Two or more of the following after a potentially allergenic exposure:
– mucosa/skin involvement: urticaria, fl ushing, itching, tongue, lip or uvula
swelling
– respiratory involvement: dyspnea, stridor, bronchospasm, hypoxia
– gastrointestinal involvement: abdominal pain, vomiting
– hemodynamic instability: hypotension, syncope, incontinence

Criterion 3

Drop in blood pressure (either < 90 mmHg or > 30 mmHg drop from baseline)
minutes to hours after exposure to a known allergen for that patient
Table 42.3 Manifestations of anaphylaxis [67] .
Affected system Symptoms/signs Comments
Skin Itching, fl ushing, sensation that skin is being pulled or burned,
urticaria (hives) and angioedmea (88%)

Psychologic Sense of impending doom
Respiratory Shortness of breath, hoarseness, diffi culty breathing/swallowing/
talking, choking, lump in throat, wheezing, stridor, laryngeal
edema (50%). CXR may show hyperinfl ation, pulmonary
edema or ARDS [67] . Intubated patients may have elevated
airway pressures and increased airway resistance

Cardiovascular Faintness, palpitations, chest discomfort, syncope, tachycardia,
bradycardia, ST/T changes on EKG, multiple PVCs, hypotension
due to sudden hypovolemia. Shock will occur in up to 30%.
Eventually fatal arrhythmias may occur
Hypotension occurs due to three factors:

1 sudden hypovolemia from third spacing of intravascular fl uid from sudden
changes in vascular permeability
2 vasodilation and
3 myocardial depression [1,15] .
Although initially cardiac output may be increased, it will often decrease with
progression of the syndrome. Systemic vascular resistance (SVR) is typically
initially reduced in anaphylaxis. However, in severely hypovolemic patients
vasoconstriction can occur and be so severe that there is no additional
response to vasopresssors
Gastrointestinal Metallic taste in mouth, nausea, vomiting, diarrhea, incontinence,
abdominal bloating, abdominal and uterine cramping (30%)

Fetal Decreased fetal movement. Fetal heart rate monitor may also
show late decelerations, tachycardia, diminished variability,
bradycardia

the bedside promptly if there is any evidence of airway compro-
mise or facial or neck swelling. Pregnant women are diffi cult
to intubate because of pregnancy - related changes in the airway
and body habitus. Anaphylaxis - related airway edema may
further contribute to the diffi culty in establishing an airway in
a pregnant patient. Therefore, if intubation is performed it
should be done by the most experienced person available and
with a plan in place for what will be done should the intubation
fail (including being prepared for the possibility of emergency
cricothyroidotomy).
2 Administer aqueous epinephrine 0.5 mg (0.5 mL of a 1 : 1000
(1 mg/mL) solution) intramuscularly into the lateral or anterior
thigh. Epinephrine will both treat hypotension and help with
bronchospasm and is the cornerstone of the initial medical man-

agement of anaphylaxis. There are no absolute contraindications
to epinephrine in the setting of anaphylaxis. This dose of
epinephrine may be repeated every 5 minutes as needed.
Subcutaneous administration is acceptable but is associated
with less rapid absorption and effect than an intramuscular or
intravenous injection. If patient is on a β - blocker, the response
Anaphylactic Shock in Pregnancy
601
pressor support (see below) should be introduced. Cesarean
delivery should rarely be necessary but should be considered if
the fetus is at a gestation where delivery may lead to a viable infant
and the fetus demonstrates ongoing distress despite aggressive
maternal resuscitation.
11 If blood pressure remains below 90/60 mmHg, begin admin-
istration of intravenous vasopressors. Patients who require this
level of care or who have ongoing airway concerns after the initial
treatment should be transferred promptly to an intensive care
unit. Epinephrine can be given intravenously at a dose of 0.1 mg
(1.0 mL of a 1 : 10 000 (1 mg/10 mL) solution) over se veral minutes
and repeated every 5 – 10 minutes as needed. This medication
should be given with the patient on a cardiac monitor and ideally
through a central line to decrease the risk of tissue damage from
extravasation. It can also be administered via an endotracheal
tube (0.3 – 0.5 mg (3 – 5 mL of a 1 : 10 000 dilution)) if intravenous
access is compromised. If continued boluses of epinephrine are
needed, a continuous infusion can be given: 1 mL of 1 : 1000 dilu-
tion of epinephrine should be placed in 500 mL of normal saline
and given at a rate of 1 – 4 micrograms per minute (0.05 – 0.1 µ g/
kg/min) and titrated to response. Some concern does exist about
the effects of epinephrine use in pregnancy because of both a

weak association with ventral hernias when used in the fi rst tri-
mester and its possible adverse effects on uterine blood fl ow.
Because of these concerns, some authors have suggested a trial of
terbutaline subcutaneously (typically 0.25 mg subcutaneously) as
an alternative to epinephrine in pregnancy. However, the data
supporting the effi cacy of terbutaline in the treatment of anaphy-
laxis are minimal and therefore most experts would recommend
the use of epinephrine as a fi rst - line agent in treating anaphylaxis
in pregnancy given the life - threatening nature of the condition.
Studies in non - pregnant patients have shown that fatality rates
are highest in patients in whom treatment with epinephrine is
delayed [24 – 26] . Other vasopressors that may be helpful in
patients with anaphylactic shock when epinephrine has failed
include dopamine (5 – 20 µ g/kg/min), norepinephrine (0.5 – 30 µ g/
min) or phenylephrine (30 – 180 µ g/min). Vasopressin 10 – 40 IU
IV has also been reported to be of assistance in refractory
cases [15] .
Management of the p atient a fter the a cute e pisode
of a naphylaxis
Management after an anaphylactic reaction typically involves
ongoing vasopressor support until the blood pressure no longer
requires it. The acute symptoms and danger should usually have
begun to resolve within 6 hours of the onset of the event. Steroids
and antihistamines are typically continued for 72 – 96 hours and
then can be discontinued.
Once the patient has been stabilized, a careful history should
be taken to identify all exposures in the hours prior to the reac-
tion. The patient should also be asked about any exertion prior
to the onset of the event, including sexual activity.
Laboratory fi ndings that may be drawn as soon as possible after

the event to help confi rm the diagnosis of an anaphylactoid
to epinephrine may be dampened, and the patient may be given
glucagon 1 mg intravenously as an alternate if epinephrine
does not produce the desired effect. This dose of glucagon
may be repeated as needed every 1 minute until a total of 5 mg
has been given. Glucagon has chronotropic and inotropic
effects on the heart that are not mediated through the β -
receptors [21] .
3 Ensure the patient has two large - bore (14 – 16 G) peripheral
intravenous lines in place for fl uid and medication administra-
tion and prepare to obtain central venous access. Typically
5 – 10 mL/kg of normal saline or Ringer ’ s lactate should be admin-
istered in the fi rst minutes of treatment although this will warrant
monitoring in patients with renal or cardiac disease [22] . Pregnant
women have a predisposition to pulmonary edema that also war-
rants extra attention to overall fl uid balance. Use fl uid boluses to
maintain blood pressure above 90/60 mmHg, especially if the
patient has not responded to epinephrine. Anaphylaxis is often
associated with sudden and massive extravasation of fl uid into
the third space and patients may have profound intravascular
volume depletion. In severe cases of anaphylaxis up to 7 L of fl uid
may need to be given to support blood pressure [23] .
4 Remove the inciting antigen when possible. Consider use of a
tourniquet to obstruct venous return from a limb that was
exposed to the probable precipitating antigen when appropriate.
The tourniquet should be released every 15 minutes to prevent
ischemia.
5 Place the patient in the reverse Trendelenburg position lying
on her left side to improve venous return.
6 Initiate cardiac and frequent blood pressure monitoring.

Initially, these parameters should be measured no less frequently
than every 5 minutes.
7 Administer an intravenous histamine H
1
blocker (typically
diphenhydramine 25 mg IV over 3 – 5 min) and histamine H
2

blocker (typically ranitidine 1 mg/kg IV over 10 – 15 min).
8 Administer intravenous steroids (typically hydrocortisone
100 mg every 6 hours or methylprednisolone 1 – 2 mg/kg per day).
These agents do not treat the acute symptoms of anaphylaxis but
may have a role in preventing late - phase reactions. Because there
are rare reports of biphasic reactions occurring as late as 72 hours
after the initial exposure, many experts would continue steroids
at a dose equivalent to this dose for a total of 4 days (typically
prednisolone 50 mg daily).
9 If wheezing is present, administration of bronchodilators such
as albuterol (2.5 – 5 mg in 3 mL saline via nebulizer) should be
considered.
10 Place a fetal monitoring device on the patient. Several anec-
dotal reports of fetal injury or death in the setting of anaphylaxis
despite prompt maternal blood pressure control have suggested
that maternal blood pressure in anaphylaxis may be maintained
at the expense of uterine (or splanchnic) fl ow. Evidence of fetal
distress should be addressed by improving oxygen delivery
through increasing oxygen administration, changing position of
the mother, and increasing fl uid administration. If there is
ongoing evidence of maternal or fetal compromise, then vaso-
Chapter 42

602
Table 42.5 The differential diagnosis of anaphylaxis.
Alternative diagnoses Comments
Vasovagal response Should generally be associated with bradycardia and pallor and no fl ushing, rash, itch, hives or wheezing
Anxiety Hives and hypotension should not be present
Amniotic fl uid embolism (AFE) Initial presentation may be similar but AFE should not be associated with rash, itch or hives and is generally associated with
DIC
Pulmonary edema in pregnancy Pulmonary edema can occur in pregnancy in association with fl uid overload, pre - eclampsia, infection or tocolytic
administration. Onset will generally be gradual over several hours and not be associated with rash or hypotension
Medication effects other than allergies Vancomycin, nicotinic acid, ACE inhibitors and alcohol can all cause fl ushing in susceptible individuals
Pulmonary embolism or any other cause
of acute respiratory failure
Can cause sudden - onset tachycardia, respiratory failure (with or without wheeze) and hypotension but should not cause rash
or itch
Scromboid poisoning [68] Histamine - producing bacteria in fi sh such as spoiled tuna, mackerel and skipjack can cause gastrointestinal symptoms,
fl ushing, headache, dizziness but not usually hives. This can be diffi cult to distinguish from anaphylaxis but is suggested by
a clustering of cases related to a particular meal/restaurant
Vocal cord dysfunction Young women can present with acute inspiratory stridor related to paradoxic vocal cord motion. This is more often seen in
women with a preceding diagnosis of asthma. Stridor in this setting is typically only inspiratory which distinguishes it from
the stridor seen with true airway edema which is typically both inspiratory and expiratory. Hypotension, uvular edema, rash
should not be seen in these patients
Acute myocardial infarction, congestive
heart failure
Less likely in this patient population but it is reasonable to obtain EKG, CXR and serial cardiac enzymes (troponin) in patients
presenting with probable anaphylaxis. If concern exists for a cardiac cause, an echocardiogram should be ordered acutely
Miscellaneous Flushing syndromes (carcinoid syndrome, medullary carcinoma of the thyroid, perimenopausal symptoms) pheochromocytoma
Hemorrhagic/hypovolemic shock
Septic shock
Epiglottitis
Status asthmaticus

Foreign body aspiration
Panic attacks
Systemic mastocytosis
response include serum levels of histamine and tryptase, both of
which will be elevated in anaphylaxis [18,27] . Histamine will be
elevated for up to 60 minutes and tryptase for up to 6 hours.
Typically, several specimens should be obtained in the 6 - hour
period following the onset of anpahylaxis so that a pattern of
elevation followed by decline may be observed. The assay for
histamine can be falsely elevated from basophil activation of
clotted blood in the test tube and has a very short half - life that
limits its clinical use at many instructions. Therefore a 24 - hour
urine sample looking for the histamine metabolite N - methyl his-
tamine may be a useful additional test to consider. Assays showing
elevated levels of histamine or tryptase and its metabolites are
indicative of anaphylaxis; however a normal assay does not pre-
clude the diagnosis.
All patients who have had an anaphylactic event should be
educated as to the seriousness of their condition and its propen-
sity to recur. Patients should be provided a prescription for an
epinephrine autoinjector and educated as to its use. The impor-
tance of this should be emphasized to the patient, as many
patients will not fulfi l their prescription or be willing to self - inject
unless they clearly understand the nature of their condition
[15,28,29] . Preloaded auto - injectors marketed in the US include
EpiPen © and Twinject © . Twinject © has the advantage of offering
two - dose devices that may be necessary to treat more severe reac-
tions in adults.
Ideally, all patients who have had an episode of life - threatening
anaphylaxis should be referred to an allergist for care and coun-

seling regarding their condition. Allergists will often do skin and
serum IgE tests to confi rm or identify inciting antigens and con-
sider the need for immunotherapy. Skin testing should only be
done by allergists and should be delayed for at least 4 weeks so
that mast cells in the skin have a chance to replenish their infl am-
matory mediators. Serum testing can, however, be done imme-
diately [15] .
Patients who have had anaphylaxis should be told to wear a
MedicAlert bracelet or a similar device to avoid inadvertent expo-
sure to a precipitating allergen. Patient with anaphylaxis who
have been on a β - blocker should generally be switched to an
alternate medication if at all possible because the β - blocker may
decrease the effi cacy of epinephrine given in a subsequent attack.
Anaphylactic Shock in Pregnancy
603
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21 Fisher MM . Clinical observations on the pathophysiology and treat-
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22 Clark S , Long AA , Gaeta TJ , Camargo CA Jr . Multicenter study of
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Differential d iagnosis
The differential diagnosis of anaphylaxis is broad and is sum-
marized in Table 42.5 .
Conclusions
Anaphylaxis and anaphylactoid reactions are common in hospi-
talized patients. They are a medical emergency which warrant
prompt administration of oxygen, intravenous fl uids, epineph-
rine and removal of the inciting agent when possible. Management
in pregnancy is unchanged from that for non - pregnant patients.
The life - saving nature of epinephrine in this setting justifi es its
use even if there are concerns about its effects in general on pla-
cental fl ow. Patients who have had anaphylactic responses should
be observed for at least 8 hours and placed on steroids because
of a risk of a biphasic response in 48 – 72 hours. With prompt
identifi cation and management, both mother and fetus can

expect to do well.
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605
Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade,
M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd.
43
Fetal Considerations in the Critically Ill
Gravida

Jeffrey P. Phelan
1
& Shailen S. Shah
2


1
Department of Obstetrics and Gynecology, Citrus Valley Medical Center, West Covina and Clinical Research, Childbirth
Injury Prevention Foundation, City of Industry, Pasadena, CA, USA

2
Maternal - Fetal Medicine, Virtua Health, Voorhees, NJ and Thomas Jefferson University Hospital, Philadelphia, PA, USA
Introduction
Unlike any other medical or surgical specialty, obstetrics deals
with the simultaneous management of two – and sometimes
more – individuals. Under all circumstances, the obstetrician must
delicately balance the impact of each treatment decision on the
pregnant woman and her fetus, seeking, when possible, to mini-
mize the risks of harm to each person. Throughout this text, the
primary focus has been on the critically ill obstetric patient and,
secondarily, her fetus. Although the fetal effects of those illnesses
were reviewed in part, the goal of this chapter is to highlight,
especially for the non - obstetric clinician, the important clinical
fetal considerations encountered when caring for these compli-
cated pregnancies. To achieve that objective, this chapter reviews:
(i) current techniques for assessing fetal well - being; (ii) fetal
assessment in the intensive care unit; (iii) fetal considerations in
several maternal medical and surgical conditions; (iv) the con-
temporary management of the gravida who is brain - dead or in a
persistent vegetative state; and (v) the role of perimortem cesar-

ean delivery in modern obstetrics.
Detection of f etal d istress in the c ritically i ll
o bstetric p atient
More than four decades ago, Hon and Quilligan [1] demon-
strated the relationship between certain fetal heart rate (FHR)
patterns and fetal condition by using continuous electronic FHR
monitoring in laboring patients. Since then, continuous elec-
tronic FHR monitoring has become a universally accepted
method of assessing fetal well - being during labor [2,3] with the
goal of permitting the clinician to identify those fetuses at a
greater likelihood of intrapartum fetal death [4] and to intervene
when certain FHR abnormalities are present.
In addition to the intrapartum assessment of fetal well - being,
the fetal monitor has been used to assess fetal health before labor
[5] and attempt to identify those fetuses at risk for intrauterine
death and convert those fetuses so identifi ed from outpatient to
inpatient care. Once in labor and delivery, continuous fetal moni-
toring is used to determine whether continued expectant man-
agement or delivery by induction of labor or cesarean is the next
form of intervention. It is this area of fetal monitoring, antepar-
tum rather than intrapartum fetal assessment that is used more
frequently in the arena of the critically ill gravida. Regardless, the
focus of this chapter will be on applications of fetal monitoring
to assess fetal status both in the intensive care unit setting and
intrapartum during labor.
Although the presence of a reassuring FHR tracing is virtually
always associated with a well - perfused and oxygenated fetus
[5,6] , an “ abnormal tracing ” is not necessarily predictive of an
adverse fetal outcome. While it was anticipated that the detec-
tion of abnormal FHR patterns during labor and expeditious

delivery of such fetuses would impact the subsequent develop-
ment of cerebral palsy, this expectation has not been realized
because the number of fetuses injured during labor was highly
overestimated and the number of fetuses injured before labor
were highly underestimated [7] . However, with the ubiquitous
use of electronic FHR monitoring during labor and a rise in the
cesarean delivery rate for the past two decades from 5% to over
25%, a decline in the rate of asphyxia - induced cerebral palsy
among singleton term infants has been observed [8,9] . For
example, Smith and associates [9] documented a 56% decline
over two decades in the incidence of hypoxic ischemic encepha-
lopathy (HIE) among singleton term infants. During this time,
the incidence of HIE dropped from 1 per 8000 to 1 per 12 500
births.
While the specifi c entity of cerebral palsy is, in most cases,
unrelated to the events associated with labor and delivery, it is
more often related to prenatal developmental events, infection,
or complications of prematurity. Nevertheless, the basic physio-
logic observations relating to specifi c FHR patterns remain, for
the most part, valid. The critically ill mother will necessarily shunt
blood from the splanchnic bed (including the uterus) in response
Chapter 43
606
hypoxic event, such as those depicted in Table 43.1 , the FHR
suddenly drops and remains at a lower level unresponsive to
remedial measures and/or terbutaline therapy. In the critical care
setting, a sudden, rapid, and sustained deterioration of the FHR
or a prolonged FHR deceleration may arise from a partial or
complete abruption in cases of markedly elevated maternal blood
pressures or an aggressive lowering of maternal BP with antihy-

pertensive agents [17] . This type of FHR pattern may also herald
a sudden maternal hypoxic event, such as amniotic fl uid embolus
syndrome [18] , acute respiratory insuffi ciency, or an eclamptic
seizure [17,19] . Prolonged FHR decelerations have also been
associated with maternal operative procedures such as cardiopul-
monary bypass with inadequate maternal fl ow rates [20,21] , and
brain surgery during hypothermia [22] .
In a patient with a prior normal baseline FHR, the abrupt
occurrence and persistence of a fetal heart rate of less than
110 bpm for an extended period of time unresponsive to remedial
measures and/or terbutaline therapy constitutes an obstetric
emergency. Under these circumstances, and assuming the preg-
nant woman is hemodynamically and clinically stable and the
fetus is potentially viable, these patients should be managed as if
the fetus has had a cardiac arrest and be delivered as rapidly as it
is technically feasible for the level of the institution.
Tachycardia
Fetal tachycardia is defi ned as a baseline FHR of 160 bpm or
greater. Most commonly, this type of baseline FHR abnormality
can be associated with prematurity, maternal pyrexia, or chorio-
amnionitis. In addition, betamimetic administration, hyperthy-
roidism, or fetal cardiac arrhythmias may also be responsible. The
clinical observation of a FHR tachycardia, in and of itself, is prob-
ably not an ominous fi nding but probably refl ects a normal physi-
ologic adjustment to an underlying maternal or fetal condition.
Although operative intervention is rarely required, a search for
the underlying basis for the tachycardia and a reanalysis of the
admission FHR pattern may be helpful.
For example , the patient with a previously reactive FHR pattern
with a normal baseline rate (Figure 43.1 ) who develops the Hon

pattern of intrapartum asphyxia or ischemia [11] which is char-
acterized by a substantial rise in the baseline rate often to a level
of tachycardia (Figures 43.2 & 43.3 ) in association with an inabil-
ity to accelerate or non - reactivity, repetitive FHR decelerations,
to shock. Because of this and the fact that the fetus operates on
the steep portion of the oxyhemoglobin dissociation curve, any
degree of maternal hypoxia or hypoperfusion may fi rst be mani-
fested as an abnormality of the FHR. In this sense, the late
second - and third - trimester fetus serves as a physiologic oximeter
and cardiac output computer. Observation of FHR changes, thus,
may assist or alert the clinician to subtle degrees of physiologic
instability, which would be unimportant in a non - pregnant adult
but may have potentially detrimental effects to the fetus [10] .
The next few pages present an overview of FHR patterns per-
tinent to the critically ill gravida. Interpretations of FHR patterns,
like all diagnostic tests, depend on the index population, and
consequently, certain of these observations may not be applicable
to the laboring but otherwise well mother. For a more detailed
description of antepartum and intrapartum FHR tracings associ-
ated with fetal brain injury the reader is referred to the classic
descriptions by Phelan and Ahn [11] , Phelan and Kim [12] ,
Phelan [13] and Phelan and associates [14] .
Baseline f etal h eart r ate
The baseline FHR is the intrinsic heart rate of the fetus. A normal
baseline FHR is between 110 beats per minute (bpm) and
160 bpm. A baseline FHR below 110 bpm is termed a bradycardia
and 160 bpm or higher is considered a tachycardia.
Bradycardia
Bradycardia is defi ned as the intrinsic heart rate of the fetus of
less than 110 bpm, as opposed to a sudden, rapid, and sustained

deterioration of the FHR from a previously normal or tachycardic
rate that lasts until delivery. As such, a FHR bradycardia may be
associated with an underlying congenital fetal abnormality, such
as a structural defect of the fetal heart. In addition, congenital
bradyarrhythmias may involve fetal heart block secondary to a
prior maternal infection, a structural defect of the fetal heart, or
systemic lupus erythematosus with anti - Ro/SSA antibodies [15] .
In these circumstances, the FHR bradycardia is not usually a
threat to the fetus. But, alternative methods of fetal assessment,
such as the fetal biophysical profi le (FBP) [16] , are necessary in
this select group of patients to assure fetal well - being before
and during labor. Given the inherent diffi culties in providing
continuous fetal monitoring and assuring fetal well - being in
fetuses with a bradyarrhythmia, cesarean delivery may well rep-
resent the preferred route of delivery for these patients. Obviously,
the decision to proceed directly to a cesarean will depend on the
overall clinical circumstances and appropriate patient informed
consent.
Prolonged f etal h eart r ate d eceleration or a s udden,
r apid and s ustained d eterioration of the f etal h eart r ate
Prolonged FHR deceleration is distinctly different from a brady-
cardia. In the former, the fetal monitor strip is typically reactive
with a normal or tachycardic baseline rate; but, due to a sentinel
Table 43.1 Sentinel hypoxic events associated with a sudden, rapid, and
sustained deterioration of the fetal heart rate that was unresponsive to remedial
measures and/or terbutaline lasting until delivery from a previously reactive fetal
heart rate.
Umbilical cord prolapse
Uterine rupture
Placental abruption

Maternal arrest, e.g. AFE syndrome
Fetal exsanguination
AFE, amniotic fl uid embolus.
607
Figure 43.1 Admission FHR of this term pregnancy with spontaneously ruptured membranes exhibits a baseline rate around 120 bpm and numerous FHR accelerations
or a reactive FHR pattern.
Figure 43.2 Some time later, the fetus exhibits an FHR tachycardia around 160 bpm, repetitive FHR decelerations and non - reactivity.
Chapter 43
608
Fetal h eart r ate v ariability
Fetal heart rate variability (FHRV) is defi ned as the beat - to - beat
variation in the FHR resulting from the continuous interaction
of the parasympathetic and sympathetic nervous systems on the
fetal heart. For clinical purposes, normal FHRV may be viewed
as a beat - to - beat variation of the FHR of 6 bpm or more above
and below the baseline FHR.
Currently, two approaches, the National Institutes of Child
Health and Human Development (NICHD) [25] and the
Childbirth Injury Prevention Foundation (CIPF) [11,14] are
available to classify FHRV. The NICHD and CIPF approaches
subclassify FHRV into 4 and 2 categories, respectively. This
means that the CIPF classifi cation incorporates the NICHD cri-
teria of undetectable (absent FHRV) and minimal (more than
and usually a loss of FHR variability, fl ags fetal brain injury [23]
and the fetus is at risk for hypoxic ischemic brain injury [11 – 13] .
In this clinical setting, assessment of the usual causes of FHR
tachycardia should be undertaken. If the mother does not have a
fever to account for the change in fetal status, assessment of fetal
acid – base status with scalp or acoustic stimulation [6,12] or
delivery as soon as it is practical, in keeping with the capability

of the hospital, should be considered. If the gravida has a fever,
she should be cultured, and treated with antibiotics and anti-
pyretics. If the FHR pattern does not return to normal (i.e. the
same FHR pattern the fetus had on admission – normal baseline
FHR and reactive) within approximately an hour of the initiation
of medical therapy and regardless of whether the fetal heart rate
variability is average [11 – 13,24] , the patient should be delivered
as expeditiously as possible.
Figure 43.3 Later in the labor, the baseline FHR reaches 180 bpm and continues to exhibit repetitive FHR decelerations, non - reactivity, and diminished variability. The
fetus was born with spastic quadriplegia due to hypoxic ischemic encephalopathy.