Journal of Clinical Anesthesia (2005) 17, 229 – 234

Case Conference of the University of Florida

Series Editors: A. Joseph Layon, MD ! Michael E. Mahla, MD
Associate Series Editors: Lawrence Caruso, MD ! Andrea Gabrielli, MD

Cardiac arrest during pregnancyB

Carl W. Peters MD (Associate Professor)a,*,
Abraham J. Layon MD (Professor)a,
Rodney K. Edwards MD (Assistant Professor)b
a
Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA
b
Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA

Received 20 September 2004; accepted 20 September 2004

Comment by Rodney K. Edwards, MDb

Keywords:
Abstract This case involves cardiac arrest of a 29-week pregnant African American woman, occurring
Cardiac arrest;
2 days after surgical correction of an incarcerated ventral hernia with small bowel obstruction. The
Pregnancy;
patient could not be resuscitated from the arrest. Details of the case are presented, and diagnostic and
HIV infection
unique management considerations for this uncommon occurrence are set forth.

1. Introduction conditions associated with pregnancy, namely eclampsia

Cardiac arrest is an infrequent occurrence in pregnancy
[1]. The causes generally fall into 1 of 2 categories [2].
The first category includes those conditions that affect
only pregnant individuals. The other is a list of non–
pregnancy- associated potentially deadly processes that can
often be recognized and treated but are made more
complex and difficult to manage by their appearance in
the parturient. In the former group lie the familiar
B
Case conference presentations are selected and edited at the
Department of Anesthesiology, University of Florida College of Medicine.
T Corresponding author. ATTN: Editorial Office, Department of
Anesthesiology, University of Florida College of Medicine, Box 100254,
Gainesville, FL 32610-0254, USA. Tel.: +1 352 265 8012; fax: +1 352 265
8013.
E-mail address: cpeters@anest.ufl.edu (C.W. Peters).
and preeclampsia, HELLP syndrome, puerperal hemor-
rhage, peripartum cardiomyopathy, amniotic fluid embo-
lism, and anesthetic catastrophe associated with labor and
delivery. In the latter category are the traditional killers of
nonpregnant individuals such as pulmonary thromboem-
bolic events; heart disease, both congenital and acquired;
rapidly progressive infection leading to sepsis; and
endocrine and inflammatory disorders.
We present a 29-week pregnant patient who died of an
unknown event. She was a model for risk factors for several
conditions mentioned in the next sections, but the specific
cause of her death is unknown because no postmortem
examination was allowed. The clinical picture was further
clouded by the complication of HIV infection, although the
patient’s blood cell counts at the time of her death were
unknown. The case is presented in detail, including
pertinent differential diagnostic considerations.

0952-8180/$ – see front matter

doi:10.1016/j.jclinane.2004.09.003
230
2. Case report
The patient was a 34-year-old African American woman
who was positive for hepatitis C and HIV since 1998, and
29 weeks pregnant by ultrasound and by dates. She had
undergone gastric bypass surgery in 1990, but she was
morbidly obese at the time of this event. Two inguinal hernia
repairs had been done since the gastric bypass surgery. The
patient presented to labor and delivery triage with 1 day of
abdominal pain. Physical examination findings were abdom-
inal tenderness and reducible ventral hernia. An abdominal
computed tomographic (CT) scan was performed, which
showed findings consistent with a small bowel obstruction.
The patient was evaluated by the general surgery service,
which recommended conservative management. The patient
was admitted to the hospital and followed closely.
Twenty-four hours after the initial evaluation, a dilated
small bowel loop was seen on plain abdominal film with an
area of tenderness to the right of her gastric bypass incision.
On the basis of these findings, the patient was taken to the
operating room for surgical exploration and reduction of her
small bowel obstruction.
During the operative intervention, blood loss was 50 mL
and urine output was 375 mL. She received 4000 mL of
crystalloid (2 L of normal saline and 2 L of lactated Ringer’s
solution) and 2 units of packed red blood cells. Vecuronium
10 mg was given for muscle relaxation during the case, and
the patient’s trachea remained intubated in the recovery room
for approximately 60 minutes postoperatively because of
residual neuromuscular blockade. Extubation thereafter was
successful, with subsequent vital signs of blood pressure of
128/57 mm Hg, heart rate (HR) 119 bpm, temperature
35.9 8C, respiratory rate (RR) of 17 breaths/min, and pulse
oximetric saturation (Spo2) of 100% (inspired oxygen
concentration [Fio2] not specified). She remained in the
recovery room for part of the night.
Early in the morning, approximately 36 hours after arrival
at the hospital, the patient was transferred to the surgical
intensive care unit (SICU) for persistent marginal Spo2 that
had developed during her recovery room stay, namely 96%
on an Fio2 of .5. Arterial blood gas (ABG) analysis on arrival
at the SICU showed pH 7.43, Paco2 26 mm Hg, Pao2 59 mm
Hg, and sodium bicarbonate (HCO3 )16 mM/L on oxygen 7 L
by mask. One hour later, ABG showed pH 7.45, Paco2
24 mm Hg, Pao2 69 mm Hg, and HCO3 16 mM/L on 6 L O2
by mask. Serum electrolytes at that time were sodium
135 mEq/L, potassium 3.7 mEq/L, chloride 108 mEq/L,
HCO3 20 mM/L, BUN 32 mg/dL, creatinine 0.5 mg/dL,
glucose 133 mg/dL, total calcium 8.1 mg/dL, magnesium
1.4 mEq/L, and phosphate 3.2 mM/L. Hemoglobin was
10.1 gm/dL, hematocrit 32%, platelets 417 000 cells/lL, and
white blood cell count 11 000 cells/lL.
During morning rounds, the patient was found to have
very small tidal volumes. A chest radiograph showed
pulmonary edema, with the comment by the managing
physician of bimpending respiratory failure.Q Dobutamine
C.W. Peters et al.
was administered for inotropic support, and the patient was
given aggressive pulmonary toilet with emphasis on full
sitting position to assist in respiration. Diuretic medication
was administered with a target of 1 to 1.5 L of urine
production. An echocardiogram was ordered, but no record
exists in the hospital computer records as to whether it was
done. All electrolyte abnormalities were corrected during
the day. By that evening, about 48 hours after arrival, the
patient’s RR was 35 to 40 breaths/min and Spo2 was 93%
on supplementary oxygen. At that point, the patient was
started on full-face bilevel positive airway pressure, with an
inspiratory pressure of 15 cm H2O, an expiratory pressure of
10 cm H2O, and Fio2 of 0.7. This treatment improved the
patient’s Spo2 to between 95% and 97%. Lower extremity
Doppler ultrasound studies performed to evaluate for a deep
venous thrombosis (DVT) and were negative; the decision
was then made not to obtain CT studies of the pelvis or
chest. By the next morning, 60 hours after arrival in the
hospital, the patient had diuresed 3 L of fluid. The chest
radiograph, which was difficult to interpret because of the
patient’s morbid obesity, showed a picture compatible with
improving pulmonary edema. However, it did show possible
air bronchograms, and on the basis of this finding, the
original antibiotic treatment was changed to include
coverage for aspiration pneumonia. Bilevel positive airway
pressure respiratory support was increased to 23/20 cm
H2O, the patient was continued in the full upright sitting
position, and discussion was conducted about the indica-
tions for endotracheal intubation in this patient.
By the next morning, about 84 hours after arrival in the
hospital, the patient was noted to be extremely tachypneic,
with RR as high as 47 breaths/min. Clinically, she was in
extremis from a respiratory standpoint despite Spo2 of
100%. Her HR ranged from 120 to 145 bpm despite
treatment with metoprolol. At that point, the decision was
made to intubate the patient’s trachea. As she was being
helped into the supine position for intubation, which was
performed easily, she was noted to become bradycardic. The
rhythm deteriorated into ventricular fibrillation within
3 minutes despite high-flow oxygen delivered by the bag-
valve mask and the administration of atropine; advanced
cardiac life support (ACLS) measures were begun. Simul-
taneously, the obstetric physicians were called to the bedside
for an emergency cesarean section. The time interval
between this call being placed and delivery of the fetus
was 16 minutes. The ACLS measures that were used during
this time were defibrillation (14 times with 360 joules),
bilateral chest tube placement and pericardiocentesis for
pulseless electrical activity, administration of epinephrine
29 mg in divided doses, vasopressin boluses of 40, 40, and
80 units, 2 g of calcium chloride, 150 meq of HCO3 in
divided doses, and an epinephrine infusion. Transcutaneous
cardiac pacing was attempted but was unsuccessful. The
patient’s rhythm alternated between pulseless electrical
activity and ventricular fibrillation, in spite of these
measures and continuous cardiopulmonary resuscitation
Cardiac arrest during pregnancy
(CPR). The rhythm eventually degenerated into asystole
refractory to any measure, and the patient was declared
dead. Unfortunately, the newly delivered infant had no signs
of life, and could not be revived despite the heroic efforts of
the neonatal critical care physicians. The family declined
autopsy on both individuals.
3. Discussion
Cardiac arrest is reported to occur in about 1 in every
30 000 pregnancies that are near term [1]. This fact seems
surprising, in that pregnant women are usually in the prime of
health, unfettered by the acute or chronic conditions that are
the harbinger of what is usually a fatal occurrence in older
populations (ie, those that are most often afflicted). The rate
of occurrence is consistent, however, and is predictably due to
events that fall into 2 general categories of pathology. These
categories are (1) those conditions that impact the cardiovas-
cular stability of the population in general but affect the
pregnant patient more dramatically, and (2) those entities that
are specifically related to pregnancy.
Deep venous thrombosis and pulmonary embolism (PE)
often intrude into what seems to be a stable uneventful
pregnancy [3]. Pulmonary embolism is seen in 24% of
parturients who develop DVT for which they are not
appropriately treated, whereas only 4.5% of those treated
develop a PE. In patients not treated, approximately 15% die,
whereas less than 1% of treated patients die. The likelihood of
occurrence of DVT and PE is increased in pregnant women
by the presence of the 3 major risk factors: endothelial
vascular injury, hypercoagulable state, and venous stasis [4].
The timely discovery and treatment of DVT and PE is
frustratingly difficult. The signs and symptoms of PE are
notoriously nonspecific, being seen in a host of cardiopul-
monary conditions. Furthermore, reliance on the presence of
certain findings as a signal that a DVT workup is warranted
will leave one disappointed — DVT often remains clinically
silent within the limb [5]. Laboratory or diagnostic studies to
confirm or exclude DVT or PE may either clarify or confuse
the physician. Suspicion of PE may be investigated in a
number of ways. Ventilation-perfusion scintigraphy is
considered the first-line tool by many clinicians. High
probability scan gives positive predictive value of 97%. Up
to 70% of scans warrant further investigation [6]. Continued
suspicion of PE or pelvic DVT, despite a negative ventilation-
to-perfusion study, warrants further radiological studies such
as CT pulmonary angiography, conventional pulmonary
angiography, or magnetic resonance imaging for complete
evaluation [7,8]. The implications of radiography for the
pregnant patients are obvious, and must be scrutinized and
evaluated meticulously before radiographic studies are used
in the parturient.
Primary heart disease can lead to cardiac arrest in gravid
patients. Many women with congenital heart disease are now
surviving into child-bearing years and becoming pregnant;
231
decompensation and arrest can thus occur during pregnancy.
Coronary artery disease leading to myocardial infarction
complicates 0.01% of pregnancies [9]. Myocardial infarction
occurs more often in the obese, diabetic, hypertensive, or
hyperlipidemic gravid patient. Furthermore, the pregnant
woman is more likely to be older and a smoker now than in
the past. When these facts are added to the aforementioned
risk factors, management of heart disease in the pregnant
patient becomes a genuine challenge. The combination of
subtlety of ischemia-related symptoms, intolerance to fluid
overload in those with borderline cardiovascular reserve, and
difficulty in resuscitation of the pregnant woman make for a
dismal outlook for the gravid patient with coronary artery
disease who suffers a cardiac arrest. When it happens,
infarction occurs most often in the third trimester, and
mortality rates vary from 21% to 45% [10].
As to other forms of cardiac disease, valvular cardiac
pathology is variably tolerated. Regurgitant lesions may be
better handled by the parturient who is already vasodilated,
and therefore, afterload reduced by virtue of her pregnant
condition [11]. Pulmonary hypertension, primary and
secondary, is particularly difficult to manage successfully,
with death rates varying between 30% and 52%. Causes of
secondary pulmonary hypertension include recurrent pul-
monary thromboembolism, HIV, inflammatory conditions
such as vasculitis and connective tissue disorders, and
congenital heart disease. Management may include inhaled
or intravenous vasodilators and employment of pulmonary
artery catheterization in the peripartum period for early
identification of increasing pulmonary artery pressure.
Infections can complicate pregnancy and warrant aggres-
sive intensive therapy to forestall the onset of septic shock,
which occurs in 1 per 5000 pregnancies. Ninety-five percent
of the bacterial causes of septic shock in pregnancy are
gram-negative organisms [12]. The most common infectious
entities that lead to septic shock are chorioamnionitis,
pyelonephritis, endometritis, and toxic shock syndrome.
Mortality for septic shock associated with pregnancy ranges
from 33% to 66%.
Hormonal disorders complicate pregnancy, occasionally
with lethal results. Thyroid storm, pituitary apoplexy from
enlarging prolactinoma leading to Sheehan’s syndrome
(hypopituitarism from infarct of the pituitary gland from
postpartum shock or hemorrhage), hypercalcemia from
hyperparathyroidism, and cardiovascular decompensation
from pheochromocytoma can cause maternal cardiac arrest
and death. Diabetic ketoacidosis in pregnancy carries an
estimated mortality rate of about 1%. At greatest risk is the
undiagnosed woman with first manifestation of diabetes as
diabetic ketoacidosis in pregnancy [13].
An uncommon event is the occurrence of pregnancy in a
woman with one of the rheumatologic-autoimmune diseases.
The paucity of experience hinders in-depth analysis of the
impact of these diseases on the pregnancy, but a few
observations are warranted. Systemic lupus erythematosus
(SLE) occurs at a rate of 15 to 50 per 100 000 people in the
232
United States, and more than 90% of these affected
individuals are women. Morbidity in the parturient is
increased, related for the most part to the 15% to 25%
incidence of preeclampsia in those with SLE. Further
confounding the analytical picture is the difficulty in
differentiating SLE-related preeclampsia from the signs and
symptoms of lupus nephritis or lupus cerebritis. The
appearance of these conditions can be quite similar, with
severe hypertension and proteinuria, or mental status changes
and seizures, but the treatment regimens are quite different,
with the treatment of one condition being quite destructive to
a patient with the other of these conditions. The complexity of
the interactions of SLE and other collagen-vascular diseases
such as polyarteritis nodosa and rheumatoid arthritis and
their effect on pregnancy warrant specialty consultation [14].
From the standpoint of obstetric conditions that can lead to
cardiac arrest, there is a host of repeat killers. Preeclampsia
and eclampsia frequently evolve into lethal events such as
intracerebral hemorrhage, cardiovascular instability, multi-
organ system failure, and uncontrolled bleeding in other body
sites from coagulopathy. The former condition is character-
ized by severe hypertension, abdominal pain, oliguria,
deteriorating renal function, headache and visual changes,
liver function test abnormalities, and pulmonary edema. The
addition of seizures to this milieu of symptoms defines the
onset of eclampsia, although up to 38% of eclamptic patients
can experience seizures without any preeclamptic symptoms
[15]. Two percent of those experiencing eclamptic seizures
die as a result of the complications of these events. At
highest risk are those with preexisting hypertension, multiple
gestations, first pregnancy, those with a family history of
preeclampsia, renal disease, and diabetes. A common
companion to eclampsia is the HELLP syndrome, consisting
of hemolysis, elevated liver enzymes, and low platelets. The
rate of occurrence is less than 1% of pregnancies, occurs in
late pregnancy (27-36 weeks’ gestation), and carries a
mortality rate of 1% to 3% [16]. Up to one third of the
fetuses delivered to women with this condition may die.
Most frequent laboratory manifestations in this condition are
a low platelet count (below 100 000 cells/lL) and serum
transaminases that are slightly elevated.
Hemorrhage, both prepartum (abruption and placenta
previa) and associated with delivery itself (natural and
surgical) and its immediate aftermath, can be massive and
may lead to death from exsanguination [2]. The hemorrhage
may be obvious or subtle. Massive hemorrhage occurs in
pregnancy for a number of reasons. It can be surprisingly
difficult to diagnose in timely fashion. Large vessels
supplying and draining the uterus provide a conduit for
major blood loss when pathological processes such as
abruption, uterine rupture or atony, or placenta previa
complicate the pregnancy or delivery. Uterine atony is the
most common cause and is treated primarily with medications
that constrict the uterine tissue and vessels. Late identification
of massive hemorrhage can lead to cardiac arrest, which is
particularly difficult to correct because of the blate startQ on
C.W. Peters et al.
resuscitation that causes the event in the first place. Treatment
involves simultaneous pathways of employment of ACLS
algorithms and repletion of intravascular blood volume. The
astute clinician must remain alert to the signs and symptoms
that are manifestations of bleeding and must provide
hemodynamic support to the hemorrhaging patient.
Peripartum cardiomyopathy affects about 1000 pregnant
women each year in the United States. The condition is
characterized by the onset of heart failure symptoms within
1 month before delivery to about 5 months after delivery.
Peripartum cardiomyopathy is a diagnosis of exclusion, and
all other etiologies of congestive heart failure must be ruled
out before its being invoked as the cause. This condition is
felt to be a form of infectious myocarditis, possibly viral in
origin, or perhaps autoimmune or idiopathic in etiology.
The clinical picture manifests typical features of heart
failure: chest pain, orthopnea and paroxysmal nocturnal
dyspnea, overt fluid overload with pedal edema, and
shortness of breath with exertion. Sinus tachycardia and
nonspecific ST-wave and T-wave changes are often seen. In
about 50% of patients, the cardiomyopathy resolves after
delivery; of those cases that do not resolve, most patients
die [17].
Amniotic fluid embolism occurs infrequently in preg-
nancy but generates high rates of morbidity and mortality.
The phenomenon was first described in 1926 by Meyer, as
noted by R.G. Mason [18] and is characterized by
respiratory distress, cardiovascular collapse, altered mental
status, and alteration of coagulation parameters [19]. The
presentation may masquerade as any of the other more
common life-threatening conditions that may happen
abruptly in the peripartum period. These conditions include
eclampsia with status-epilepticus, acute thromboembolism,
and anaphylaxis. Seventy percent of the cases of amniotic
fluid embolism occur during labor and delivery, the majority
within 5 minutes of delivery. A small percentage of cases
occurs before delivery, and 19% of cases occur during
cesarean section. A very broad estimate of overall occur-
rence is 3 per 100 000 pregnancies [20], and the fatality rate
varies from 22% to 88%.
Anesthetic complications such as an unmanageable
airway and drug-induced hemodynamic instability are well-
recognized companions to obstetric anesthesia [21]. Vasodi-
lator side effects of both regional and general anesthetic drugs
can precipitate cardiac arrest in the parturient who already is
in a barely compensated state of hypovolemia or who is
dehydrated from preeclampsia. Deaths from the consequen-
ces of the difficult obstetric airway have decreased in
frequency mainly because of greater clinician awareness
and the invention of useful airway management adjuncts.
This frequency, however, has not dropped to zero.
If cardiac arrest does occur, a number of issues arise. All
ACLS measures must begin immediately, as in any episode
of cardiac arrest. The pregnant state, however, complicates
matters. Airway management is complicated by the gastric
hypokinesis of pregnancy; cricoid pressure should be
Cardiac arrest during pregnancy
maintained until the airway is secured to prevent the higher
risk of aspiration of gastric contents. Efficient ventilation
and oxygenation are more difficult to accomplish because of
the increased oxygen requirements and decreased chest wall
compliance of pregnancy [1]. Venous return to the heart
from the lower extremities will occur only when compres-
sion of the inferior vena cava is released by rolling the
patient toward her left side with support from a wedge, an
overturned chair, or the knees of an assistant kneeling on the
floor on the patient’s right side. Cardiopulmonary resusci-
tation and mask ventilation can be efficiently accomplished
when the patient is turned no more than 308 to the left.
Cardiopulmonary resuscitation and ACLS measures are
seldom needed on the labor and delivery ward, so frequent
rehearsals of mock scenarios involving cardiac arrest will
shorten the response times and heighten the awareness of
correct ACLS procedures when these procedures are
warranted. In addition, the literature is replete with guidance
for successful perimortem and postmortem cesarean section
for emergency delivery of an infant from a dying mother,
both to save the infant or the mother [22 - 24].
In the case of maternal cardiac arrest and possible
perimortem cesarean section (from the ancient Roman legal
code known as Lex Caesare [25]), time obviously is the
most crucial issue. For arrests that occur in the labor and
delivery suite, the obstetrician is immediately at hand to
perform the operation. At more distant sites, recognition of
the potential need for surgical intervention for delivery of
the fetus must be immediate so as to summon the
appropriate individual for surgical assistance. In Great
Britain, between 1972 and 1996, 56 postmortem cesarean
sections yielded 6 neurologically normal children. A
10-year survey of perimortem cesarean sections yielded
25 healthy survivors from 40 deliveries. In the most
comprehensive review of the literature on the subject,
93% of the surviving infants were born within 15 minutes
of the maternal death, and only 2 had neurological defects;
70% of the survivors were delivered within 5 minutes [25].
One final consideration that fits into neither large category
mentioned above, but that sits in the background of any
analysis of this patient’s management and outcome, is the
influence of her HIV infection on her cardiovascular
condition. There is an evolving body of literature defining
the influence of HIV infection on cardiovascular status. Eight
to 10% of the new HIV patients develop symptomatic heart
failure over a 2- to 5-year period. However, there is little
information addressing HIV infection as a predictor of sudden
cardiac decompensation and cardiac arrest, specifically in the
parturient. It has been well demonstrated that HIV can
profoundly affect cardiovascular integrity in a number of
ways. These ways include the association of HIV infection
with myocarditis, with nutritional deficiencies that affect
contractility, and with side affects of medications used to treat
HIV infection [26] All of these processes may lead to dilated
cardiomyopathy. In addition, HIV infection is associated with
pericardial effusions that may progress to tamponade, with
233
bacterial, fungal, and marantic endocarditis; with pulmonary
hypertension; and with vasculitic, atheromatous, and hyper-
tensive cardiac conditions. The mental jump from occult
HIV-related cardiac pathology to the sudden pregnancy-
related cardiovascular decompensation of this unfortunate
individual is easy to make, although we remain unsure of the
precise cause of her death.
4. Comment by Rodney K. Edwards, MD, MS
The authors provide an interesting case report and a
thorough review of the potential causes of cardiac arrest
during pregnancy. As stated, no postmortem examination
was conducted, and this fact makes determination of the
cause of this particular patient’s death impossible to
ascertain. Fortunately, such an occurrence during pregnancy
is quite uncommon. However, when pregnant women do
suffer cardiac arrest, prompt action is needed from
individuals skilled with the provision of CPR, knowledge-
able about the physiologic changes associated with
pregnancy, and experienced with emergent cesarean deliv-
ery. Otherwise, mortality for both mother and fetus is the
likely outcome.
The authors discuss the fact that the gravid uterus impairs
venous return to the heart during CPR. However, left lateral
tilt does not completely alleviate the problem. Tilting the
patient helps to relieve this obstruction. However, it also
decreases the effectiveness of chest compressions, because
this lateral tilt causes the trunk to roll [27,28]. Because
emptying the uterus will alleviate some of this obstruction to
venous return, perimortem cesarean delivery has been
advocated as a way not only to attempt to salvage a viable
fetus but also to improve the effectiveness of CPR in
pregnant women with cardiac arrest.
In 1986, Katz et al [29] reviewed reports of successful
results with perimortem cesarean delivery. They found that
infant survival was most likely if delivery occurred within
5 minutes of cardiac arrest, and that infant survival without
serious neurological impairment was unlikely if delivery
occurred more than 15 minutes after cardiac arrest.
Therefore, these authors and several texts recommend
initiating delivery within 4 minutes of cardiac arrest.
This recommendation — that delivery should be initiated
within 4 minutes after cardiac arrest — assumes that delivery
of the infant can be effected in approximately 1 minute.
Because of several factors present in this patient, this
interval may not have been achievable. Because of her
morbid obesity and recent surgery, abdominal entry would
require more time than for the usual emergent cesarean
delivery. Furthermore, for obvious reasons, this patient’s
hepatitis C and HIV infections would understandably result
in care to avoid injury to the surgeon or any assistants.
Another factor that could result in delay in initiating a
perimortem cesarean delivery is the location of the patient at
the time of arrest. This woman was located in the SICU at the
234
time of her cardiac arrest. It likely would require more time to
summon obstetricians to this unit than to an emergent
delivery in the labor and delivery unit. If a pregnant woman
is critically ill, locating a pack containing the instruments
necessary to perform a cesarean delivery at her bedside and
notifying the obstetrics team of any deterioration in status
before cardiac arrest would decrease the interval from cardiac
arrest to delivery.
In the case report, there is no mention of whether the fetal
HR tracing was being monitored. The ABG reports indicate
that maternal, and therefore fetal, oxygenation was margin-
al. Monitoring the fetal HR tracing can provide some insight
as to the status of the fetus in a pregnant woman with
respiratory distress. Oxygen delivery to the fetus is
inadequate with maternal Po2 values at or below 60 mm
Hg, and efforts to improve oxygenation of the mother are
needed. Fetal HR tracing analysis may suggest a need for
increased oxygen delivery to the pregnant woman, even if
measures of her Spo2 are reassuring.
Furthermore, fetal condition before maternal cardiac arrest
can predict the likelihood of intact neonatal survival. As an
example, unlike the case reported herein, if the etiology of
cardiac arrest were massive hemorrhage, maternal circulation
would be directed preferentially to the brain, heart, and
adrenal glands. Therefore, the uteroplacental circulation
would be diminished long before cardiac arrest, and intact
neonatal survival would be unlikely, regardless of the time
interval from cardiac arrest to delivery.
In summary, cardiac arrest during pregnancy is an
uncommon event. When it does occur during the latter
part of pregnancy, perimortem cesarean delivery may
improve the outcome for both the fetus/neonate and the
pregnant woman. Provision of care by a multidisciplinary
health care team and optimal communication between the
members of this team will maximize the likelihood of
survival for both patients. Beyond 24 weeks’ gestation, the
standard ABCs of CPR (airway, breathing, and circulation)
should also include a bDQ — for delivery [30]. Unfortu-
nately, even under ideal circumstances, mortality is the
usual outcome for both the pregnant woman who experi-
ences cardiac arrest and her fetus.
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