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PARTVI.
OBSTETRICCRISES
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41.
INTRODUCTION TOPERIPARTUM URGENCIES AND EMERGENCIES
FORTHE ANESTHESIA PROVIDER
Rachel M.Kacmar
PHYSIOLOGIC CHANGES OFPREGNANCY
Pregnancy aects every organ system, and these changes
can be accelerated and more pronounced in the peripartum period. Many of the normal physiologic changes
have implications during urgent and emergent events in
the peripartum period, including initial unstable conditions to full resuscitation. Additionally, many pathophysiologic states exist as well that present specic challenges
during the pregnancy and especially in the peripartum
period. A wide range of these topics will be covered in
depth in the obstetric anesthesia chapters in this section. In this introductory chapter, the major physiologic
changes that occur during pregnancy are introduced
along with a general approach to an unstable parturient.
increased ejection fraction,
trocardiogram (ECG) and aortocaval compression from
the gravid uterus. e heart is shied superiorly, anteriorly,
and leward from diaphragmatic elevation, leading to possible ECG changes, such as shi in QRS axis (rightward in
rst trimester and leward in third trimester) and transient
ST- T wave changes.8 Flow murmurs and dysrhythmias,
such as sinus tachycardia, premature atrical or ventricular
contractions are commonly seen.
ion, or supine hypotension syndrome of pregnancy, occurs
due to compression of the descending aorta and inferior
vena cava by the gravid uterus aer 16– 20 weeks’ gestation.
Decreased venous return and subsequently decreased CO
can cause maternal symptoms as well as decreased uteroplacental perfusion. Fieen degrees of le tilt is necessary to
restore maternal cardiac output.
CARDIOVASCULARSYSTEM
Pregnant women experience profound adaptive changes in
maternal hemodynamics. Blood volume increases during pregnancy, peaking around 34 weeks gestation.
1,2
Women experience a dilutional anemia due to a greater increase in plasma
volume compared to red blood cell mass, resulting in a normal hemoglobin concentration of 11– 12 g/ dL at full term.3
Blood volume returns to prepregnancy state approximately
6 weeks postpartum. Cardiac output (CO) also increases
progressively throughout pregnancy, peaking at 40% to 50%
above baseline at 32 weeks’ gestation as a result of increases
in both stroke volume and heart rate. During labor there may
be up to an additional 40% increase in CO by the end of the
2nd stage, and immediately postpartum maternal CO can rise
75% above predelivery values.4 As pregnancy advances, the
systemic vascular resistance (SVR) decreases through a number of mechanisms5:ese include the low- resistance placental circulation, vasodilation due to elevated progesterone and
prostacyclin levels, and decreased blood viscosity.
Other pregnancy- related changes to the cardiovascu-
lar system include mild le ventricular hypertrophy and
RESPIRATORYSYSTEM
Pregnant women increase minute ventilation via increases in
both tidal volume and respiratory rate due to changes in wakefulness and central chemoreex drives for breathing, acid– base
balance, metabolic rate, and cerebral blood ow.12 Anormal
PaCO2 in a pregnant patient is 30 to 32 mmHg with partial metabolic compromise (normal pregnant bicarbonate
level 20mmHg), to give a normal pH of 7.41 to 7.44.13 As
the gravid uterus enlarges, the diaphragm elevates, leading to
altered lung volumes and capacities. Compared to the prepregnancy state, at term gestation women usually have decreased
total lung capacity (TLC) and functional residual capacity
(FRC), increased tidal volume (TV) and unchanged vital
capacity (VC).8 Pulmonary vascular resistance (PVR) also
decreases due to progesterone- induced dilation of conducting
airways. Oxygen consumption is increased 40%– 60% at term
gestation due to the high metabolic demands of the uteroplacental unit and fetus.14 Due to these changes, parturients in
the third trimester quickly become hypoxemic when the experience hypopnea or apnea. Decreased FRC, especially in the
6,7
changes in the normal elec-
9,10
Aortocaval compress-
11
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supine position, and decreased mixed venous saturation from
increased oxygen uptake by fetal hemoglobin, also contribute
to hypoxemia risk.
15,16
Uncontrolled maternal pain exacerbates the baseline respiratory physiologic changes. Minute ventilation can increase by
as much as 140% above prepregnant values in the rst stage
of an unmedicated labor and as much as 200% in the second
17,18
stage.
As a result, maternal PaCO2 can fall to as low as 10
to 15mmHg. is extreme degree of hypocarbia may cause
subsequent maternal hypoventilation. is doubling of ventilation by the parturient can also increase oxygen consumption
by as much as 50%.17 As a result, signicant hypoxemia can also
occur between contractions.
and may be a sign of preeclampsia. In most parturients, there
is either a moderate decrease in platelet count or no change.
e blood leukocyte count rises progressively throughout
pregnancy, increasing from 6,000/ mm3 to 9,000– 11,000/
mm3. However, white blood cell function is impaired, which
may account for the increased incidence and severity of
infection during pregnancy as well as the reduction of symptoms in some pregnant women with autoimmune disease.
25
Normal pregnancy is associated with profound alterations in the coagulation and brinolytic systems, leading to
a hypercoagulable state. While procoagulant changes serve
to minimize intrapartum blood loss, they also increase
the risk of thromboembolism during pregnancy and the
postpartum period sixfold.26 Fibrinogen levels increase
GASTROINTESTINALSYSTEM
As the uterus enlarges it displaces the stomach cephalad,
throughout pregnancy and the level at term is oen >400
mg/ dL. If the brinogen level is less than 200– 250 mg/ dL,
a pathologic process should be suspected.
changing the interaction of the lower esophageal sphincter
(LES) and diaphragm and increasing intragastric pressure.
e LES tone also decreases due to elevated progesterone
APPROACH TOTHE UNSTABLE PARTURIENT
levels and reaches its nadir at 36 weeks gestation.19 Pregnant
and laboring women are at increased risk for aspiration and
should be treated as “full stomachs” aer 16– 20 weeks gestation due to decreased gastric emptying.
20– 22
Acute care for pregnant patients includes many of the principles used in the general surgery or general medical patient
populations, but there are several unique considerations.
First, the presence of a possible second patient— the fetus or
RENALSYSTEM
Elevated progesterone levels lead to renal vasodilation as
well as dilation of the renal pelvis and ureters by the end of
the rst trimester. Renal blood ow increases by approximately 75% during pregnancy, which also contributes to
this dilation.23 As a result of increased renal blood ow, glomerular ltration rate increases from 100 to 150 mL/ min
by the second trimester, which in turn causes increased creatinine clearance. ese changes lead to a subsequent fall in
serum blood urea nitrogen (BUN) and creatinine (normal
~0.5– 0.6 mg/ dL at term). us, in a parturient, a “normal”
or slightly increased BUN and creatinine (0.8– 1.0 mg/
dL) indicates poor renal function. Reduced tubular reabsorption and increased renal excretion of glucose occurs,
contributing to the development of gestational diabetes
mellitus in some pregnant women.
24
neonate— must always be considered. In most situations, the
interests of the mother and the fetus are aligned. However,
from a legal perspective, a pregnant woman normally retains
the right to refuse obstetric or other medical interventions
(negative autonomy) even if that refusal leads to harm or loss
of the unborn fetus.27 While maternal- fetal conict most
oen occurs in nonacute settings,28 perioperative or peripartum emergencies may involve this sort ofissue.
One example of maternal- fetal conict during an emergency is a maternal cardiac arrest and subsequent need for
cardiopulmonary resuscitation (CPR). While the core
tenets of maternal CPR include le uterine displacement
during chest compressions29 and early airway management,
there should always be a consideration of perimortem cesarean delivery.30 Many authors report improved maternal
CPR eorts following delivery as aortocaval compression
is relieved and venous return and cardiac output are no longer impeded by the presence of a gravid uterus. Obstetric
HEMATOLOGICSYSTEM
As previously mentioned, pregnant women experience a
dilutional anemia. In the absence of dietary iron supplementation, hemoglobin levels of 9 to 10 g/ dL are common.3
Hemoglobin levels of >13 g/ dL suggest hemoconcentration,
advanced cardiac life support and perimortem cesarean
delivery are covered in depth in other chapters within the
obstetric emergencies section.
Practitioners caring for unstable patients on labor and
delivery must also consider the environment. In most
cases, parturients are awake even if unstable, and clear
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communication is crucial for optimal care. Misconceptions,
REFERENCES
signicant anxiety, or patient naiveté may impede eective
clinical intervention. Patients are also oen hypervigilant
to events or conversations, and providers may benet from
multidisciplinary huddles away from the patient’s bedside
if circumstances allow. e presence of a patient’s family,
including children, also may impact initial eorts to care
for unstable parturients. Family members or support people may need to be escorted out of the operating room or
labor and delivery room during emergencies. Again, honest,
direct, and timely communication is key when it comes to
family members of critically ill obstetric patients. e presence of other nonsedated patients and their families makes
routine overhead pages or announcements dicult and
instead directed messaging of emergencies via group unit
phone messages or group pages may be a better option to
relay critical information enmasse.
Sta resources on labor and delivery units vary from a
typical operative setting. Most nurses and support sta see
emergencies such as cardiac arrest rarely, if ever, and may not
have the same comfort level as equivalent sta in the main
operating room. In addition, obstetricians and general surgeons do not possess the same training or background in
caring for critically ill patients. Finally, resources within a
labor and delivery room are oen scant, and may lack basic
tools such as supplemental oxygen delivery devices, suction
canisters, and electrocardiographic monitoring capability.
While most obstetric units maintain a code cart and debrillator that can be brought into a patient room, consideration
should be made as to whether moving the unstable parturient to an operating room is a more appropriate option.
Care of unstable pregnant patients is most oen multidisciplinary and involves obstetricians, anesthesiologists,
neonatologists, and other subspecialists. In some cases,
the dierent providers may have conicting goals or priorities based on role. For example, the neonatologist may
desire waiting to deliver a preterm fetus as long as possible
while the maternal fetal medicine physician favors delivery
at 34 weeks gestation due to risk of maternal morbidity.
Negotiating these dierences requires intense and repeated
multidisciplinary planning and teamwork so the opinions
of all sides can be considered.
Overall, caring for obstetric patients is stimulating and
extremely rewarding. When urgent or emergent events occur,
care providers must act quickly, as both mother and fetus may
be at risk. e discussion above of basic physiologic principles and the unique considerations that come with caring for
this patient population should provide the basis for the more
detailed discussions throughout the rest of this section.
1. Scott DE. Anemia in pregnancy. Obstetrics and Gynecology
Annual. 1972;1: 219– 44.
2. Ueland K. Maternal cardiovascular dynamics: VII. Intrapartum
blood volume changes. American Journal of Obstetrics and
Gynecology. 1976;126(6): 671– 7.
3. Recommendations to prevent and control iron deciency in
the United States. Centers for Disease Control and Prevention.
Morbidity and Mortality Weekly Report. 1998;47: 1– 29.
4. Clark SL, Cotton DB, Lee W, etal. Central hemodynamic assessment of normal term pregnancy. American Journal of Obstetrics and
Gynecology. 1989;161(6 Pt 1): 1439– 42.
5. Clapp JF 3rd, Capeless E. Cardiovascular function before, during,
and aer the rst and subsequent pregnancies. American Journal of
Cardiology. 1997;80(11): 1469– 73.
6. Kametas NA, McAulie F, Hancock J, Chambers J, Nicolaides
KH. Maternal le ventricular mass and diastolic function during
pregnancy. Ultrasound in Obstetrics and Gynecology. 2001;18(5):
460– 6.
7. Schannwell CM, Zimmermann T, Schneppenheim M, Plehn G,
Marx R, Strauer BE. Le ventricular hypertrophy and diastolic
dysfunction in healthy pregnant women. Cardiology. 2002;97(2):
73– 78.
8. Chang A. Physiologic changes of pregnancy. In: Chestnut
D, ed. Obstetric Anesthesia: Principles and Practice. 3rd ed.
Philadelphia:Elsevier Science, Mosby; 2004: 15– 36.
9. Cutforth R, MacDonald CB. Heart sounds and murmurs in pregnancy. American Heart Journal. 1966;71(6): 741– 7.
10. Shotan A, Ostrzega E, Mehra A, Johnson JV, Elkayam U. Incidence
of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. American Journal of Cardiology. 1997;79(8):
1061– 4.
11. Lee SW, Khaw KS, Ngan Kee WD, Leung TY, Critchley LA.
Haemodynamic eects from aortocaval compression at dierent
angles of lateral tilt in non- labouring term pregnant women. British
Journal of Anaesthesia. 2012;109(6): 950– 6.
12. Jensen D, Dun J, Lam YM, etal. Physiological mechanisms of
hyperventilation during human pregnancy. Respiratory Physiology
and Neurobiology. 2008;161(1): 76– 86.
13. Lim VS, Katz AI, Lindheimer MD. Acid- base regulation in pregnancy. American Journal of Physiology. 1976;231(6): 1764– 9.
14. Prowse CM, Gaensler EA. Respiratory and acid- base changes during
pregnancy. Anesthesiology. 1965;26: 381– 92.
15. McClelland SH, Bogod DG, Hardman JG. Apnoea in pregnancy:an investigation using physiological modelling. Anaesthesia.
2008;63(3): 264– 9.
16. Kambam JR, Handte RE, Brown WU, Smith BE. Eect of normal
and preeclamptic pregnancies on the oxyhemoglobin dissociation
curve. Anesthesiology. 1986;65(4): 426– 7.
17. Hagerdal M, Morgan CW, Sumner AE, Gutsche BB. Minute ventilation and oxygen consumption during labor with epidural analgesia. Anesthesiology. 1983;59(5): 425– 7.
18. Spatling L, Fallenstein F, Huch A, Huch R, Rooth G. e variability
of cardiopulmonary adaptation to pregnancy at rest and during exercise. British Journal of Obstetrics and Gynaecology. 1992;99(Suppl
8): 1– 40.
19. Shah S, Nathan L, Singh R, Fu YS, Chaudhuri G. E2 and not
P4 increases NO release from NANC nerves of the gastrointestinal tract: implications in pregnancy. American Journal of
Physiology: Regulatory, Integrative and Comparative Physiology.
2001;280(5): R1546– 54.
20. Wong CA, McCarthy RJ, Fitzgerald PC, Raiko K, Avram MJ.
Gastric emptying of water in obese pregnant women at term.
Anesthesia and Analgesia. 2007;105(3): 751– 5.
INTRODUCTION TO PERIPARTUM URGENCIES AND EMERGENCIES 291
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21. Whitehead EM, Smith M, Dean Y, O’Sullivan G. An evaluation of gastric emptying times in pregnancy and the puerperium.
Anaesthesia. 1993;48(1): 53– 57.
22. Carp H, Jayaram A, Stoll M. Ultrasound examination of the stomach contents of parturients. Anesthesia and Analgesia. 1992;74(5):
683– 7.
23. Jeyabalan A, Conrad KP. Renal function during normal pregnancy
and preeclampsia. Frontiers in Bioscience.2007;12: 2425– 37.
24. Klein P, Polidori D, Twito O, Jae A. Impaired decline in renal
threshold for glucose during pregnancy:a possible novel mechanism
for gestational diabetes mellitus. Diabetes/ Metabolism Research
and Reviews. 2014;30(2): 140– 5.
25. Stirrat GM. Pregnancy and immunity. BMJ. 1994;308(6941):
1385– 6.
26. Franchini M. Haemostasis and pregnancy. rombosis and
Haemostasis. 2006;95(3): 401– 13.
27. Minko H, Marshall MF, Liaschenko J. e fetus, the “potential
child,” and the ethical obligations of obstetricians. Obstetrics and
Gynecology. 2014;123(5): 1100– 3.
28. Townsend SF. Ethics for the pediatrician: obstetric conict: when fetal and maternal interests are at odds. Pediatrics in
Review.2012;33(1):33– 37.
29. 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(18 Suppl 3):
S829– 861.
30. Drukker L, Hants Y, Sharon E, Sela HY, Grisaru- Granovsky S.
Perimortem cesarean section for maternal and fetal salvage:concise
review and protocol. Acta Obstetricia et Gynecologica Scandinavica.
2014;93(10): 965– 72.
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SECTIONA
MATERNAL COLLAPSE
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42.
OBSTETRIC LIFE SUPPORT
PULSELESS ELECTRICAL ACTIVITY/ ASYSTOLE AND PULSELESS
VENTRICULAR TACHYCARDIA/ FIBRILLATION
Nathaniel N. Hsu and Richard C.Month
CLINICALCASE
understanding of key modications to the advanced car-
diac life support (ACLS) protocol may still be decient.
A 40- year- old G2P1 with preeclampsia presents for an
emergent cesarean delivery for nonreassuring fetal heart
tones. e patient has a well- functioning labor epidural in
place and is undergoing the cesarean smoothly aer epidural administration of 2% lidocaine with sodium bicarbonate and epinephrine. Shortly aer incision, a healthy baby
boy is delivered, the placenta is removed, and the uterus
is exteriorized for incisional closure. Midway through closure, the patient becomes increasingly anxious and short of
breath and is noted to be more tachycardic and hypotensive, with SaO2 in the 80s. Despite oxygen and vasopressor
administration, she still feels nauseated and “wants to pass
out.” Suddenly, the ECG shows ventricular tachycardia,
the patient becomes unresponsive, and no central pulse is
palpable. e code cart is brought into the room while the
Asurvey of anesthesia, obstetric, and emergency medicine
physicians showed that between 25% and 40% of respon-
dents incorrectly answered questions on crucial dierences
between resuscitation of the pregnant and nonpregnant
patients.1 Table 42.1 describes a summary of the relevant
physiologic changes in pregnancy that necessitate adapta-
tions to the “normal” ACLS protocol when resuscitating a
pregnant patient.
Cardiovascular changes during pregnancy include
increased blood volume and cardiac output. Uterine blood
ow increases from the nongravid perfusion rate of 50 mL/
min up to 900 mL/ min at term.2 e disproportionate
increase in plasma volume relative to red blood cell volume
leads to physiologic anemia of pregnancy. Additionally, the
point of maximal cardiac impulse is displaced cephalad and
patient is being intubated. An endotracheal tube is placed
and conrmed. Pads are placed on the patient’s chest, and
she receives a 200J biphasic shock with subsequent return of
spontaneous circulation (ROSC). In the midst of obtaining
additional IV access, oozing around the patient’s previous
TABLE42.1 KEY PHYSIOLOGIC CHANGES
INPREGNANCY INFLUENCING ACLS PROTOCOL
Organ System Changes in Pregnancy
IV and incisional sites is noted. Aer closure of the abdominal incision, the patient is subsequently transferred to the
intensive care unit (ICU) intubated, on pressors, with continued transfusion of blood products.
INTRODUCTION
Cardiac arrest during pregnancy presents challenges to the
code response team that are uniquely dierent than in the
nonpregnant population. Besides taking into account the
physiologic changes in pregnancy, one must consider both
the mother and fetus as patients while performing cardiopulmonary resuscitation (CPR). Unfortunately, provider
Cardiovascular Blood volume increase
Cardiac output increase
Cephalad and leftward displacement of the point
of maximal impulse
Uterine blood ow increases to 900 mL/ min
atterm
IVC compression occurs at 20 weeks,
and possibly aortic compression too
Respiratory Upper airway edema
Minute ventilation increase
Oxygen consumption increase
Chest wall compliance decrease
FRC decrease
Gastrointestinal Lower esophageal sphincter tone decrease
Esophageal and intestinal motility decrease
Delayed gastric emptying during labor
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