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leward due to elevation of the diaphragm. Finally, caval
compression can occur depending on gestational age and
positioning of the patient, thus impeding venous return
and decreasing stroke volume. In the supine position, compression of the inferior vena cava (IVC) occurs at 20 weeks,
but can potentially occur even earlier at 13 to 16 weeks.2
Aortic compression may occur as well, but that thought
has been recently challenged by Higuchi etal.3 Intravenous
(IV) catheter placement above the level of the diaphragm
during resuscitation is recommended due to potential caval
compression from the gravid uterus.
Respiratory physiologic changes in parturients
include capillary engorgement and edema of the laryngeal, nasal, and oropharyngeal mucosa, which is exaggerated in preeclampsia. These changes potentially lead
to more friability of the upper airway tissues as well as
difficulty with airway management including mask ventilation. A relatively small endotracheal tube (ETT)
(i.e., 6.0– 7.0 mm internal diameter) may be necessary
for intubation. Both minute ventilation and oxygen consumption will also increase, but chest wall compliance
and functional residual capacity decrease, which results
in rapid hypoxemia after the onset ofapnea.
Gastrointestinal changes occur, leading to shiing of the
intra- abdominal portion of the esophagus into the thorax
with the upward displacement and rightward rotation of
the stomach.2 Decreased lower esophageal sphincter tone
during pregnancy added to decreased gastric and intestinal
motility during labor and delivery may increase the risk for
aspiration of gastric contents when airway reexes are lost
during cardiac arrest.
Obstetric hemorrhage, both postpartum and antepartum,
is one of the leading direct causes of maternal death, particularly in developing countries.6 e major source of peripartum hemorrhage is uterine atony. Other sources of signicant
obstetric hemorrhage are uterine rupture, placental abruption
with or without associated disseminated intravascular coagulation, HELLP (hemolysis, elevated liver enzymes, low platelets)
syndrome, placenta previa, and abnormal implantation of the
placenta as seen in placenta accreta, increta, and percreta. See
“Severe Peripartum Hemorrhage” chapter for detailed discussion of these conditions.
Cardiovascular etiologies have been identied as the
leading indirect cause of maternal mortality.8 is category
includes sudden adult death syndrome (SADS); acute myocardial infarction, mostly related to ischemic heart disease;
aortic dissection or rupture; congenital heart disease; pulmonary hypertension; and cardiomyopathy, specically
peripartum cardiomyopathy (PPCM). e underlying
pathophysiology of PPCM is unclear, but it has been associated with multiple risk factors such as older maternal
age, multiparity, and hypertension, to name a few.9 See the
“Peripartum Cardiomyopathy” chapter in this section for
further explanation. e maternal mortality registry from
the United Kingdom (UK) reported an increased incidence of mortality due to SADS and the presumed resultant death secondary to fatal arrhythmia when comparing
the period of 2006– 2008 to earlier in the decade.8 And
lastly, although the incidence of aortic dissection or rupture
leading to cardiac arrest is incredibly low, chance of survival
to hospital discharge is even lower.
5
Hypertensive disorders are another major contributor
to worldwide maternal mortality.6 e classication of dis-
ETIOLOGY
orders falls the following:gestational hypertension, chronic
hypertension, and preeclampsia with and without severe features. e subgroups of preeclamptic patients include those
In the United States, about 1 in 12,000 hospitalizations for
delivery is complicated by maternal cardiac arrest; however,
the leading causes of maternal cardiac arrest vary worldwide
depending on region.
4,5,6
e World Health Organization
(WHO) separates maternal cardiac arrest by direct obstetric and indirect causes. Direct causes include those resulting from obstetric complications or interventions during
pregnancy, labor, and puerperium; whereas indirect causes
include cardiac arrest secondary to diseases that were preexisting or disease states that were exacerbated by, but not due
to, pregnancy. Amnemonic to quickly remember the etiologies for maternal cardiac arrest is “BEAU- CHOPS” as
detailed in the American Heart Association (AHA) maternal cardiac arrest algorithm (Figure 42.1 and Table 42.2).
with (1)eclampsia, a condition with new- onset seizures due
to central nervous system involvement, and (2) HELLP
syndrome, a condition in which the patient develops hemolysis, elevated liver enzymes, and a low platelet count. See
the chapter “Severe Preeclampsia” for detailed discussion.
Embolism is an important cause of maternal cardiac arrest.
e two subtypes associated with fatal events are venous
thromboembolism and amniotic uid embolism (AFE).
romboembolism has been identied as one of the top three
leading direct causes of maternal mortality.8 Pregnancy contributes to an increased risk for the development of deep venous
thrombosis (DVT) and pulmonary embolism (PE) due to an
increase in each of the factors of Virchow’s triad:hypercoagu-
7
lability, venous stasis, and vascular endothelial damage. e
296 SECTION A. MATERNAL COLLAPSE
Maternal Cardiac Arrest
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297
First Responder
• Activate maternal cardiac arrest team
• Document time of onset of maternal cardiac arrest
• Place the patient supine
• Start chest compressions as per BLS algorithm;
place hands slightly higher on sternum than usual
Subsequent Responders
Maternal Interventions
Treat per BLS and ACLS Algorithms
• Do not delay defibrillation
• Give typical ACLS drugs and doses
• Ventilate with 100% oxygen
• Monitor waveform capnography and CPR quality
• Provide post–cardiac arrest care as appropriate
Maternal Modifications
• Start IV above the diaphragm
• Assess for hypovolemia and give fluid bolus when required
• Anticipate difficult airway: experienced provider preferred for
advanced airway placement
• If patient receiving IV/IO magnesium prearrest, stop magnesium
and give IV/IO calcium chloride 10 mL in 10% solution, or
calcium gluconate 30 mL in 10% solution
• Continue all maternal resuscitative interventions (CPR,
positioning, defibrillation, drugs, and fluids) during and after
cesarean section
Obstetric Interventions for Patinet With
an Obvisouly Gravid Uterus*
• Perform manual left uterine displacement (LUD)–
displace uterus to the patient’s left to relieve
aortocaval compression
• Remove both internal and external fetal monitors
if present
Obstetric and neonatal teams should
immediately prepare for possible emergency
cesarean section
• If no ROSC by 4 minutes of resuscitative efforts,
consider performing immedicate emergency
cessarean section
• Aim for delivery within 5 minutes of onset of
resuscitative efforts
*An obviously gravid uterus is a uterus that is
deemed clinically to be sufficiently large to cause
aortocaval compression
Search for and Treat Possible Contributing Factors
Figur e4 2.1 AHA modications for maternal cardiac arrest. © 2010 American Heart Association
Bleeding/DIC
Embolism: coronary/pulmonary/amniotic fluid embolism
Anesthetic complications
Uterine atony
Cardiac disease (MI/ischemia/aortic dissection/cardiomyopathy)
Hypertension/preeclampsia/eclampsia
Other: differential diagnosis of standard ACLS guidelines
Placenta abruptio/previa
Sepsis
location of DVTs in pregnant patients is usually proximal in
the iliac or femoral veins compared with the distal calf vessels in
nonpregnant patients.10 e other main embolic phenomenon
that causes maternal cardiac arrest, AFE, is not a true embolic
event, but rather a systemic inammatory response to the introduction of a fetal antigen into the maternal circulation. is
condition initially presents as acute respiratory distress, agitation, cardiovascular instability, dysrhythmias, and seizure, and
may lead to subsequent coagulopathy and hemorrhage. In the
UK data registry, it was reported that AFE has a case fatality of
19% and 7% of the surviving women have permanent neurological injury.11 Lastly, although venous air embolism (VAE)
occurs frequently during cesarean deliveries, the majority of
these events are subclinical. However, in the rare instance of
massive VAE there is the potential for cardiovascular collapse
(BEAU-CHOPS)
and cardiac arrest. For an extended discussion, refer to the
“Peripartum Embolism” chapter.
Even in developed nations, sepsis continues to play an
important role in maternal mortality. As described by the
Centre for Maternal and Child Enquiries (CMACE), while
overall maternal mortality rate has decreased, the mortality rate related to sepsis, particularly genital tract sepsis, is
increasing.8 Community- acquired group A streptococcus
appears to be the main culprit in thesecases.
Finally, other less frequent indirect causes of maternal
mortality include a broad range of disease states spanning
neurological complications, such as epilepsy, intracranial
hemorrhage, or cerebral thrombosis; asthma; psychiatric
diseases; trauma; and diabetes mellitus, related to severe
hypoglycemic episodes. e less frequent direct causes of
OBSTETRIC LIFE SUPPORT 297
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TABLE42.2 COMMON CAUSES OFMATERNAL ARREST
AND MATERNAL MORTALITY
Category Specic Etiologies
and delivery care team— anesthesiology and the obstetric and neonatal resuscitation teams.13 Ideal components
of a maternal cardiac arrest team are seen in Table 42.3.
Simultaneously, high- quality basic life support (BLS)
Maternal Hemorrhage (uterine atony, placental abnormalities,
placental abruption, retained products of conception,
uterine rupture, coagulopathy, surgical bleeding,
intracranial bleeding)
Maternal chronic disease state (congenital heart
disease, valvular disease, cardiomyopathy,
arrhythmia, aortic dissection, myocardial
infarction)
Maternal acute disease state (trauma, suicide,
arrhythmia, aortic dissection, myocardial infarction,
pulmonary thromboembolism, amniotic uid
embolism, venous air embolism, cerebrovascular/
intracranial event, sepsis, hypertensive disorders of
pregnancy)
should be initiated as soon as possible in order to maximize
resuscitative eorts. While there is value in gathering many
care team members to the bedside, the code should be led
by someone who is familiar with the physiologic changes
of pregnancy and implications for resuscitation.14 While
initial life support measures are started, any precipitating
causes for arrest should be actively investigated and treated.
PATIENT POSITIONING
Due to potential aortocaval compression in gravid patients
Drug- related Anaphylaxis/ allergic reaction
Intentional drug overdose (illicitdrugs)
Accidental drug overdose/ drug error (high risk with
oxytocin, magnesium, insulin)
Anesthesiarelated
SOURCE:Adapted from AHA 2015 Guidelines on Cardiac Arrest in Pregnancy.
Neuraxial block (high spinal/ epidural, severe
hypotension)
Airway (failed intubation/ loss of airway, aspiration)
Local anesthetic systemic toxicity (LAST)
14
greater than 20 weeks in the supine position, following
maternal arrest it is recommended to relieve this obstruction by one of two methods:le- lateral tilt or manual le
uterine displacement.7 Ideal position to relieve aortocaval
compression is full le lateral decubitus, but at least 30
degrees is likely needed. Twenty weeks’ gestation can be
roughly estimated to be a fundal height at the level of the
umbilicus. Positioning of patients not in cardiac arrest in
le lateral decubitus has also been shown to be important
maternal death include anesthetic complications related to
local anesthetic systemic toxicity, failed intubation, aspiration of gastric contents, or high neuraxial block as well as
magnesium toxicity and anaphylaxis.
for both improved maternal stroke volume and fetal nonstress test outcomes.15 Figure 42.3 illustrates the 30° lelateral tilt with a board under the patient.
7
However, performing compressions in the tilt position
may lead to inadequate chest compressions with decreased
MANAGEMENT OFRESUSCITATION
Although there are no randomized controlled trials comparing the ecacy of standard ACLS protocol to the
modied ACLS protocol in pregnant patients, the scientic reasoning for the modications to account for physiologic changes of pregnancy has been published.7 Figure
force or the patient sliding o the board if the angle is
greater than 30°.16 When chest compressions are required,
the American Heart Association recommends supine position14 and manual le uterine displacement with one or two
hands, as illustrated in Figure 42.4.
7,14,17
Using the manual
displacement technique, the provider should ideally displace the uterus leward and upward toward the ceiling to
relieve aortocaval compression.
42.2 describes the standard algorithm for pulseless electrical activity (PEA)/ asystole and pulseless ventricular tachycardia/ brillation; whereas Figure 42.1, delineates the
modied algorithm for maternal cardiac arrest.
12,7
Notable
adaptations are explainedbelow.
INITIATE BASIC LIFE SUPPORT
AND ACTIVATE OBSTETRIC CODETEAM
Initially, when the pregnant woman is found to be in cardiac arrest, a “Code OB” (i.e., a clearly identied obstetricoriented code team response) should be called in order
to rapidly gather the normal code team as well as labor
CIRCULATION
Chest compressions should be hard (about 5cm depth)
and fast (at least 100 per min) with minimal interruptions and full chest recoil between compressions.
12,13,14
If the patient is intubated, compressions are to be continuous, only to be briefly interrupted for pulse checks,
provider rotation, and defibrillation. If the parturient
is not intubated, 2 breaths should follow each cycle
of 30 chest compressions. The AHA modification for
pregnancy previously recommended that hand placement on the sternum should be about 2 to 3cm higher
298 SECTION A. MATERNAL COLLAPSE
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299
Figur e4 2.2 ACLS algorithm for PEA/ asystole and pulselessVT/ VF.
in third- trimester patients compared with nonpregnant patients as a result of cephalad cardiac displacement secondary to diaphragmatic elevation by the
gravid uterus,7 however the 2015 update states that
the evidence for this is poor and recommends hand
placement on the center of the patient’s chest over the
lower half of the sternum.14 If resources allow, use of
OBSTETRIC LIFE SUPPORT 299
continuous capnography allows providers to assess the
adequacy of chest compressions as well as confirm correct placement of the endotracheal tube. Intravenous
or intraosseous access should ideally be obtained above
the diaphragm to potentially avoid any increase in circulation time that may occur from IVC compression in
the gravid patient.
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TABLE42.3 IDEAL TEAM MEMBERS FORA
DEDICATED MATERNAL CARDIAC ARRESTTEAM
Team Composition
Adult resuscitation
team
Obstetrics 1 obstetrician, 1 obstetric nurse
Anesthesiology Obstetric anesthesiologist (if available) or
Neonatology 1 physician, 1 nurse, 1 neonatal respiratory
The American Heart Association supports development of dedicated teams in centers with
labor and delivery units. In facilities without obstetric or neonatal services, contingency
plans should be in place in the event of a maternal cardiac arrest.
SOURCE:Adapted from AHA 2015 Guidelines on Cardiac Arrest in Pregnancy
Critical care physicians/ nurses and/ or
emergency physicians/ nurses, respiratory
therapist or equivalent, pharmacist or
equivalent
staff anesthesiologist, anesthesia assistant or
certied nurse anesthetist if available
therapist or equivalent
14
14
Figur e4 2.4 Two- handed manual left uterine displacement.
given the risk of a full stomach situation and potential dif-
AIRWAY MANAGEMENT
Maternal oxygenation and ventilation is a priority during
obstetric basic life support (OBLS). e anesthesiologist
should prepare for airway management at the start of resuscitation eorts, and hypoxia should always be considered
as a possible cause of cardiac arrest.14 Prior to intubation,
eective ventilation with 100% oxygen is ideal; however,
signicant upper- airway obstruction may occur due to pharyngeal mucosal edema that may require jaw thrust, oral
airways, or nasal airways during bag- mask ventilation. Due
to nasopharyngeal capillary engorgement in pregnancy,
oral airways are preferable to nasal airways, and repeated
airway manipulations should be avoided.13 If possible, an
cult intubation in parturients. As in standard ACLS, the
establishment of an airway should not interrupt chest compressions, and in the event that endotracheal intubation is
dicult, placement of a laryngeal mask airway (LMA) for
oxygenation and ventilation should be considered while
readying to obtain more denitive, secure airway. Lastly,
cricoid pressure may not be eective in preventing aspiration; therefore, the Society for Obstetric Anesthesia and
Perinatology (SOAP) does not recommend its routine
use.13 See “Dicult Airway: Special Considerations in
Pregnancy” chapter for more discussion of the obstetric
airway. It must be reinforced that periods of apnea in pregnancy lead to rapid onset of hypoxemia that can contribute
to worsened fetal hypoxia and acidosis.
experienced provider should attempt airway management,
DEFIBRILLATION
Figur e4 2.3 Left lateral tilt using back board for support.
300 SECTION A. MATERNAL COLLAPSE
While performing CPR, debrillation should be readied in
the event of a shockable rhythm (i.e., pulseless ventricular
tachycardia or brillation). e energy requirement used
to perform an electrical shock in pregnancy is no dierent
from that which would be used in the same scenario in nonpregnancy.7 Additionally, removing fetal scalp electrodes
and external fetal monitors to prevent theoretical electrical burns for the fetus and mother is reasonable, but should
never be the reason to delay debrillation if appropriate.
MEDICATIONS
13
ere are no contraindications to using any of the medications in the current ACLS algorithms during ALCS in a pregnant patient. Similarly, there is no evidence to support dose
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301
adjustment of resuscitation medication during maternal cardiac arrest.7 Although the volume of distribution and clearance
of drugs dier due to physiologic changes in pregnancy, these
pharmacokinetic changes may have little to no impact during
the low- ow cardiac output state of maternal cardiac arrest.
If the patient was receiving magnesium prior to the
maternal arrest, the magnesium infusion should be discontinued and calcium should be administered to combat
potential contribution from magnesium toxicity leading to
is based on one case report of a woman at 13 weeks gestation
who arrested without PMCD and underwent post– cardiac
arrest hypothermia, who eventually went on to have a term
delivery with favorable maternal and fetal outcomes.7 Patients
13
undergoing therapeutic hypothermia should be evaluated for
the utility of continuous fetal heart rate monitoring due to the
risk for fetal bradycardia. Even in nonviable fetuses, heart rate
monitoring may help guide maternal supportive care to optimize intrauterine fetal resuscitation.
cardiac arrest.
PERIMORTEM CESAREAN DELIVERY
In gravid patients without ROSC, who have a uterine
fundal height at the level of or above the umbilicus, perimortem cesarean delivery (PMCD) is a measure that may
improve maternal and fetal outcomes. Ideally, providers should strive to perform PMCD within 5 minutes of
maternal arrest.7 is means that incision should be made
CONCLUSION
While there are many barriers to successful maternal resuscitation, if the patient survives this initial arrest, the likelihood of survival to hospital discharge is much higher
compared with other patient populations.3 As with other
rare clinical events, simulation and team training can help
providers prepare for and maintain competence in maternal
cardiac arrest algorithms.
at 4 minutes in order to deliver the fetus by 5 minutes if
ROSC has not occurred, regardless of fetal viability. Acase
series in women who underwent PMCD noted sudden
and dramatic improvement in maternal response to resus-
SUMMARY OFESSENTIALS OFMATERNAL
RESUSCITATION
citation, including ROSC, upon emptying of the uterus in
12 of 20 women.18 It is plausible that delivery of the fetus
improves quality of chest compressions, increases venous
return, decreases oxygen consumption, and improves pulmonary mechanics in the mother.13 Fetal delivery within 5
minutes optimizes neonatal outcomes; however, neonatal
survival has been documented with delivery times up to 30
minutes aer onset of maternal arrest.
7,18,19
Even in the ideal simulated conditions in which providers knew they were being timed, meeting the goals listed above
is extremely challenging. One study revealed only 14% of teams
made incision for PMCD by 4 minutes following maternal cardiac
19,20
arrest.
Authors found that transporting to the operating room
instead of performing the PMCD at the site of arrest (in the labor
and delivery [L&D] room) nearly doubled the time to incision19
and is associated with decreased quality of chest compressions.21
us, the AHA recommends providers perform PMCD at the
site of arrest if it occurs on the labor and delivery oor, emergency
medicine department, or ICU.14 Amore extensive discussion of
perimortem cesarean delivery can be found in the “Perimortem
Cesarean Delivery for Maternal Cardiac Arrest” chapter.
• “Code OB” or “OB Rapid Response” should activate the
usual hospital code teams along with anesthesiology and
the obstetric and neonatal resuscitationteams
• C- A- B- U=Circulation— Airway— Breathing— Uterus
• Leward displacement of the uterus is required,
preferably with manual displacement and supine
positioning during chest compressions
• Hand placement is on the center of the chest over the
lower half of sternum during chest compressions
• IV placement above the diaphragm
• Expert provider should anticipate the potential for more
challenging airway management, smaller ETT may be
needed for intubation
• Fetal assessment should not be performed during
maternal resuscitation and fetal monitors should be
removed/ detached as soon as possible. However,
removal of fetal monitors should not delay shock or
debrillation if appropriate.
POST– CARDIAC ARRESTCARE
e current AHA guidelines recommend that therapeutic
hypothermia can be considered for the pregnant patient aer
cardiac arrest, on a case- by- case basis. is recommendation
• If patient is on magnesium prior to arrest, stop the
infusion, and administer calcium
• In gravid patients with a uterine fundus palpable at or
above the umbilicus, early preparation should be made
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for PMCD in anticipation of incision at 4 minutes
and neonatal delivery at 5 minutes aer onset of
cardiacarrest
• May consider, on an individual basis, therapeutic
hypothermia for comatose pregnant patient withROSC
CASE- BASED LEARNING DISCUSSION
1. What would the dierential for the cause of cardiac
arrest be in the case above? And what is the most likely
cause of the arrest?
2. What are current treatments for amniotic uid
embolism?
3. How would you treat cardiac arrest associated with
local anesthetic systemic toxicity in pregnancy?
4. Are there any concerns for using amiodarone,
lidocaine, or other antiarrhythmics for the treatment of
arrhythmias in pregnant patients?
5. Why is the timing for a PMCD important?
6. How would the resuscitation have diered if the arrest
occurred prior to delivery of thefetus?
REFERENCES
1. Cohen SE, Andes LC, Carvalho B. Assessment of knowledge
regarding cardiopulmonary resuscitation of pregnant women.
International Journal of Obstetric Anesthesia. 2008;17:20– 25.
2. Gaiser R . Physiologic changes of pregnancy. In:Chestnut DH, Wong
CA, Tsen LC, etal. eds. Chestnut’s Obstetric Anesthesia:Principles
and Practice. 5th ed. Philadelphia, PA:Elsevier; 2014:15– 38.
3. Higuchi H, Takagi S, Zhang K, Furui I, Ozaki M. Eect of lateral
tilt angle on the volume of the abdominal aorta and inferior vena
cava in pregnant and nonpregnant women determined by magnetic
resonance imaging. Anesthesiology. 2015;122(2):286– 93.
4. McCown A, McKay RF. Cardiopulmonary resuscitation in preg-
nancy. In: Santos AC, Epstein JN, Chaudhuri K, eds. Obstetric
Anesthesia. NewYork, NY:McGraw- Hill;2015.
5. Mhyre JM, Tsen LC, Einav S, Kuklina EV, Leert LR, Bateman
BT. Cardiac arrest during hospitalization for delivery in the United
States, 1998– 2011. Anesthesiology. 2014;120(4):810– 8.
6. Khan KS, Wojdyla D, Say L, etal. WHO analysis of causes of maternal death:a systematic review. Lancet. 2006;367:1066– 74.
7. Vanden Hoek TL, Morrison LJ, Shuster M, etal. Part12:Cardiac
arrest in special situations:2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122:S833– 8.
8. Centre for Maternal and Child Enquiries (CMACE). Saving
mothers’ lives: reviewing maternal deaths to make motherhood
safer: 2006– 08. e Eighth report on condential enquiries
into maternal deaths in the United Kingdom. British Journal of
Obstetrics and Gynecology. 2011;118(Suppl. 1):1– 203.
9. Givertz MM. Cardiology patient page:peripartum cardiomyopathy.
Circulation. 2013;127:e622– 6.
10. Chan WS, Spencer FA, Ginsberg JS. Anatomic distribution of deep
vein thrombosis in pregnancy. CMAJ. 2010;182:657– 60.
11. Fitzpatrick K, Tunell D, Kurinczuk J, Knight M. Incidence, risk
factors, management and outcomes of amniotic- uid embolism:a
population- based cohort and nested case- control study. BJOG.
2015. doi:10.1111/ 1471–0528.13300
12. Neumar RW, Otto CW, Kronick SL, etal. Part8:Adult advanced
cardiovascular life support: 2010 American Heart Association
guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122:S729– 67.
13. Lipman S, Cohen S, Einav S, et al. e Society for Obstetric
Anesthesia and Perinatology consensus statement on the
management of cardiac arrest in pregnancy. Anesth Analg.
2014;118(5):1003– 16.
14. Jeejeebhoy FM, Zelop CM, Lipman S, et al.; on behalf of the
American Heart Association Emergency Cardiovascular Care
Committee, Council on Cardiopulmonary, Critical Care,
Perioperative and Resuscitation, Council on Cardiovascular
Diseases in the Young, and Council on Clinical Cardiology. Cardiac
arrest in pregnancy:a scientic statement from the American Heart
Association. Circulation. 2015;132:1747– 73.
15. Tamás, P, Szilágyi, A, Jeges, S, et al. Eects of maternal central
hemodynamics on fetal heart rate patterns. Acta Obstetricia et
Gynecologica Scandinavica. 2007;86(6):711– 4.
16. Rees GA, Willis BA. Resuscitation in late pregnancy. Anaesthesia.
1988;43(5):347– 9.
17. Kundra P, Khanna S, Habeebullah S, Ravishankar M. Manual displacement of the uterus during caesarean section. Anaesthesia.
2007;62(5):460– 5.
18. Katz V, Balderston K, DeFreest M. Perimortem cesarean delivery: were our assumptions correct? Am J Obstet Gynecol.
2005;192(6):1916– 20.
19. Dijkman A, Huisman CM, Smit M, etal. Cardiac arrest in pregnancy:increasing use of perimortem caesarean section due to emergency skills training? BJOG. 2010;117(3):282– 7.
20. Lipman S, Daniels K, Cohen SE, Carvalho B. Labor room setting compared with the operating room for simulated perimortem
cesarean delivery: a randomized controlled trial. Obstet Gynecol.
2011;118(5):1090– 4.
21. Lipman SS, Wong JY, Arafeh J, Cohen SE, Carvalho B. Transport
decreases the quality of cardiopulmonary resuscitation during simulated maternal cardiac arrest. Anesth Analg. 2013;116:162– 7.
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43.
PERIMORTEM CESAREAN DELIVERY FORMATERNAL
CARDIACARREST
Benjamin Cobb and StevenLipman
CLINICALCASE
and gods whose births occurred miraculously with their
mother dying in childbirth.” In general, PMCD is part of
A 38- year- old term parturient in active labor reports acute
onset shortness of breath in the labor room. Shortly thereaer she becomes unresponsive and an adult code for cardiac arrest is activated by the labor nurse. e anesthesia
provider arrives as the primary nurse is transferring the role
of chest compressions to anothernurse.
MATERNAL CARDIACARREST
medical lore, and the utility of this procedure was debated
throughout the 19th century, given the preponderance
of maternal death in childbirth (2%– 4% at that time).
4,5
Physician skepticism about fetal survival aer such eorts6
and the ecacy of CPR in pregnancy prevented widespread
consideration of PMCD as a potential resuscitative maneu-
ver for the parturient until more recently.
4
Evolving obstetric practices and patient demographics
inuenced the role of PMCD in maternal/ fetal resuscitation. A population- based study from 1998– 2011 high-
Resuscitation in the setting of maternal cardiac arrest
requires multiple modications to account for the anatomic
and physiologic changes of pregnancy. e impact of these
changes on the success of maternal resuscitation is a topic
of ongoing inquiry. Current American Heart Association
(AHA) guidelines for cardiac arrest in pregnancy include
lights a shi in the underlying causes of maternal cardiac
arrest in the United States from maternal sepsis and dehydration in the 1800s6 to hemorrhage, heart failure, and
thromboembolic disease.7 As infection became a less frequent cause of maternal death (Table 43.1) and women
increasingly labored in settings where emergency care was
immediate activation of the cardiac arrest and neonatal
teams, chest compressions rendered on a supine patient
with manual uterine displacement, rapid debrillation if
applicable, ventilation with 100% oxygen, and use of wave-
TABLE43.1 CHANGING CAUSES OFMATERNAL DEATH
INCASES WITHSURVIVING INFANTS INTHE SETTING
OFPERIMORTEM CESAREAN DELIVERY
6
form capnography if available to assess quality of cardiopulmonary resuscitation (CPR). If these interventions fail
to result in a return of spontaneous circulation (ROSC)
within 4 minutes, emergent cesarean delivery might be
life- saving for both mother and fetus.
1,2
Unfortunately, up
to one- third of pregnant women remain undelivered at the
Years
1879– 1956 HTN Diseases 39
Causes of Maternal Death
Infection 37
Other 24
Percent
time of death.3 Advanced life support during pregnancy is
covered in depth in a subsequent chapter.
1956– 1970 HTN Diseases 23
Infection 9
HISTORY OFPERIMORTEM CESAREAN
DELIVERY
e role of a perimortem cesarean delivery (PMCD) in
maternal resuscitation has evolved over time. Katz writes,
“almost all ancient mythologies have references to heroes
Anesthesia 18
Embolism 18
Cardiac 16
Other 16
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readily available, the ecacy of a PMCD as a resuscitative maneuver was reconsidered. is culminated in the
American Heart Association’s adoption of PMCD into the
1986 algorithm for maternal cardiac arrest
4,8
(Figure43.1).
patients, but even optimal chest compressions during CPR
in the later stages of pregnancy may only result in 10% of
normal CO.
4,9,10
e gravid uterus (>20 weeks gestation)
may contribute to this observed decrease in CO by impairing blood return to the heart secondary to inferior vena cava
PHYSIOLOGIC BASIS OFPERIMORTEM
CESAREAN DELIVERY
(IVC) compression in the supine position.2 e decrease in
preload can be compounded by increased aerload due to
aortic compression, again by the gravid uterus.
Le uterine tilt, a technique widely used in pregnant
Perimortem cesarean delivery has a broad physiologic
impact. e ultimate goal during maternal resuscitative
eorts is maintenance of adequate cerebral blood ow and
restoration of spontaneous circulation to avoid a hypoxic
neurologic injury. Cardiac output (CO) during superb
CPR is approximately 30% of normal in nonpregnant
women to avoid the phenomenon of uterine aortocaval
compression, may further compromise cardiac output by
aecting the ecacy of chest compressions.2 Arecent study
suggests a quite signicant degree of tilt may be necessary
to alleviate hemodynamic compromise from the uterus.11
Providers may not be able to generate adequate chest
Figur e4 3.1 Cardiac arrest in pregnancy in- hospital (ACLS) algorithm. SOURCE:Reprinted with permission. Circulation. 2015;132:1747– 73. ©2015 American Heart
Association,Inc.
304 SECTION A. MATERNAL COLLAPSE
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305
compressions not only due to the angle of tilt but also the
lack of a rm surface behind the patient. In addition, the le
tilt may have ramications on establishing airway control
and upper extremity venous access, which limits oxygenation of the patient and delivery of resuscitation medications. Evacuation of the uterus may relieve IVC and aortic
compression, eliminating the need for le uterine displacement and improving the ecacy of chest compressions and
likelihood of adequate cerebral perfusion.
Maternal neurologic injury from anoxia occurs aer
approximately 5 minutes.6 Pregnancy incrementally
increases both maternal metabolic rate and oxygen consumption and reduces pulmonary functional residual
capacity (FRC), all of which increase the risk of maternal
hypoxemia. e presence of the placenta and fetus further
deplete maternal oxygen content. While the fetal metabolism is down- regulated in the setting of maternal compromise, maternal cardiac arrest is not surprisingly associated
with a high fetal mortality rate.12 Uterine evacuation may
contribute to improved maternal oxygenation by decreasing
overall metabolic demands, improving FRC and permitting
improved positive pressure ventilation, and increased car-
Activation of a “code blue” immediately upon recognition of maternal cardiac arrest is essential to ensure delivery
of the fetus within 5 minutes (or earlier). e “maternal code
blue” responders should include a provider capable of performing PMCD and the adult code team, as well as a neonatal intensive care (NICU) team.
2,14
Essential equipment, as
listed in Box 43.1, for delivery of the neonate should be immediately available. While the guidelines recommend starting a
PMCD at 4 minutes to facilitate delivery by 5 minutes given
the incremental risk of maternal anoxic brain injury, waiting to perform a PMCD is not mandated. Delivery may be
initiated in the absence of a return of spontaneous circulation earlier than 4 minutes aer initial resuscitative measures based on clinical circumstances and the discretion of
the team.
15,16
Both vertical and Pfannenstiel incisions have
been reported in the literature, and the quickest approach
should be employed.
4,8
Alternatively, vaginal delivery may be
considered at the discretion of the provider, but should take
place within the same guidelines to maximize maternal/ fetal
outcomes.14 In the event of successful ROSC, hemostasis,
analgesia, and anxiolysis may be necessary; disposition to
the intensive care unit should be arranged.
diac output and oxygen delivery. Delivery of the fetus also
allows the neonatal team to begin resuscitative measures. In
this circumstance, PMCD in a timely manner may physiologically lend itself to both maternal and fetal survival.
4,8
REFLECTIONS ONMODERN PERIMORTEM
CESAREAN DELIVERY
PERIMORTEM CESAREAN DELIVERY
LOGISTICS
e ecacy of performing a PMCD in the published literature is limited to case reports/ series, given the rarity of
the event. Katz etal. performed a literature review from
1986– 2004 of maternal cardiac arrest and found 38 cases of
e 2013 AHA guidelines recommend consideration of
emergency PMCD when maternal hemodynamics are
impacted due to uterine aortocaval compression regardless
of gestational age and fetal viability.2 Twenty weeks of gestational age is commonly accepted as the point where aortocaval
compression may hinder maternal resuscitative eorts, while
in most states a fetus is not considered viable until 23– 24
weeks gestational age. e exact gestational age at which aortocaval compression becomes relevant remains unclear, may
vary by patient even prior to 20 weeks13 and in situations such
as polyhydramnios and multiple gestation, where the uterine
volume is greater than otherwise expected.14 Approximation
of gestational age may be attempted by palpating the fundal
height (20 weeks corresponding with a periumbilical fundal
level), albeit unreliable, especially in the chaotic setting of
maternal cardiac arrest.
1,2,4
us, when in doubt about gestational age, err on the side of le uterine displacement and the
consideration of PMCD if maternal resuscitation is required.
PMCD. In this review, the most common causes of maternal cardiac arrest were trauma, cardiac disease, and embolic
disease. Of 20 cases with potentially reversible causes,
13/20 reported maternal survival to discharge. Twelve cases
out of 18 documenting hemodynamic status demonstrated
return of maternal pulse and blood pressure following
cesarean delivery. In addition, 30/ 38 PMCDs reported the
delivery of a surviving infant (all between 25 and 42 weeks
gestation). e author concluded that PMCD is strongly
supported “within 4 minutes of maternal cardiac arrest if
resuscitation is ineective” and in no case was maternal
hemodynamic status worsened aer PMCD.
16
More recently, Dijkman et al. performed an impact
assessment in the Netherlands of the Managing Obstetric
Emergencies and Trauma (MOET) course that included
maternal and neonatal outcomes from 1993 to 2008 in
the setting of a PMCD. Twelve PMCDs of 55 maternal
cardiac arrests were included in the analysis (29– 40 weeks
PERIMORTEM CESAREAN DELIVERY 305
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