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an emergency hemostasis panel that the laboratory to provided results within 15 minutes.
24
Pharmacologic therapy such as antibrinolytic agents and
recombinant factor VIIa are used with caution in postpartum
patients because of the risk of thrombotic events. Because brinolysis is commonly seen during severe PPH, there has been
Ruptured ectopic pregnancy
Postpartum:
Uterine inversion
Uterineatony
interest in the use of tranexamic acid for hemorrhage prevention and treatment. Several small trials have shown benet in
reducing blood loss during vaginal delivery and cesarean deliv-
ANTEPARTUM MATERNAL HEMORRHAGE
ery without an increase in the incidence of adverse events.25
ere are wide variations in dosing, but most studies have
administered 1 gram intravenously over approximately 10
minutes. Alarge, multicenter international randomized, controlled trial is currently underway.
26
Recombinant Factor VIIa (NovoSeven) has become an
accepted treatment option in massive transfusion protocols
for obstetric patients. Registries in Europe27 and in Australia
and New Zealand28 have reported on large series of women
who received recombinant activated factor VII (rFVIIa) as
an o- label indication during severe postpartum hemorrhage. Both series found positive response rates of about
80% aer one dose with few side eects, although both
series had cases with subsequent thrombosis and thrombosis and embolism remain a concern in all parturients.
Additionally, its use in AFE syndrome has been challenged.
A case series of 44 reports of AFE compared those who
received rFVIIa to those who did not and found the risk
of death or permanent disability was doubled when rFVIIa
was given.29 During AFE, high circulating tissue factor concentrations can combine with rFVIIa to form intravascular
clots. Although there are methodologic problems with this
type of study, the results are concerning. Because postprocedure thromboembolism is a major concern, thromboprophylaxis is recommended once bleeding risk islow.
SPECIFIC OBSTETRIC CONDITIONS LEADING
TOSEVERE PERIPARTUM HEMORRHAGE
ABNORMAL PLACENTATION:PLACENTA PREVIA/
ACCRETA/ PERCRETA
A clear understanding of the risk factors, diagnosis, and
management of antepartum hemorrhage is necessary for all
practicing anesthesia providers. ese are discussed below.
Risk Factors
Risk factors for abnormal placentation include uterine scarring from prior cesarean delivery or myomectomy, uterine
broids, history of postpartum hemorrhage, and multiparity. Aplacenta previa exists when all or part of the placenta
lies over the cervical os in front of the fetal presenting part.
Placenta accreta (78% of accreta cases) is an abnormally
adherent placenta in which chorionic villi attach to the
myometrium. ere are three grades of placenta accreta,
depending on depth of invasion. Aplacenta increta (17%
of cases) has grown into the myometrium, while a placenta
percreta (5% of cases) has grown through the myometrium
and uterine serosa with or without invasion into other pelvic structures such as bladder, bowel or vasculature.
e greatest risk for placenta accreta is placenta previa
in the presence of prior cesarean delivery. e risk is highly
related to the number of previous uterine scars (usually cesarean sections) in the presence of a placenta previa.30 As the
number of prior cesarean deliveries goes up, a woman with
a placenta previa also faces increasing maternal morbidity
from coagulopathy, hysterectomy, thromboembolism, and
Obstetric hemorrhage can occur antepartum or postpartum,
so in some cases both mother and fetus are at risk. e following conditions contribute to peripartum hemorrhage, and are
pulmonary edema31 (Table 50.3). Perinatal morbidity is not
aected, although known diagnosis of abnormal placentation may lead to a planned late preterm delivery.
discussed in terms of their etiology or risk factors, diagnosis,
obstetric management, and anesthetic considerations.
Antepartum:
Abnormal placentation:previa, accreta, and percreta
Placental abruption
Uterine rupture
Diagnosis
Placenta previa usually presents as painless vaginal bleeding
in the third trimester. e rst episode of bleeding is oen
mild (a “sentinel” bleed), but subsequent bleeds may be
catastrophic. e presence of placenta previa in the setting
of prior cesarean delivery should prompt further workup
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357
TABLE50.3 IN THEPRESENCE OFPLACENTA PREVIA,
THEASSOCIATION OFPRIOR CESAREAN DELIVERY
WITHPLACENTA ACCRETA
Number of Prior
Cesarean Deliveries
0 3% 15%
1 11% 23%
2 40% 59%
3 61% 83%
34,35
Risk of Placenta
Accreta
Composite Maternal
Morbidity
Anesthetic Management
e anesthetic management of placenta previa includes:
• evaluation of the airway in case emergency general
anesthesia is required,
• large bore IV access (preferably two 18- or 16- gauge
catheters),
• having a Level 1 or equivalent uid warmer
available,and
• verifying that cross- matched blood is available in the
for placenta accreta and preparation for potentially massive
BloodBank.
hemorrhage at the time of delivery.
Placenta accreta may be diagnosed aer delivery when
the placenta does not separate normally at vaginal or cesarean delivery, but there are usually characteristic antepartum ultrasound ndings.32 However one report found that
when ultrasounds from patients with clinically diagnosed
placenta accrete were given to blinded but experienced clinicians, there was a false negative rate of 18.3%.33 Magnetic
resonance imaging (MRI) may be helpful if ultrasound is
inconclusive or if placenta percreta is suspected.
34
ere is no evidence that regional anesthesia should be
avoided during cesarean delivery for placenta previa. Two
retrospective reviews of 514 and 350 cases of placenta previa found regional anesthesia was associated with reduced
blood loss and reduced need for transfusion compared to
general anesthesia.
38,39
Conversion from regional to general anesthesia was only required for inadequate duration
of two spinal anesthetics during hysterectomy for placenta
accreta.
e most important aspect of anesthetic manage-
Obstetric Management
Once placenta previa is diagnosed by ultrasound, an elective cesarean delivery will be scheduled. If the fetus is
immature, the patient may be managed expectantly in the
hospital until the fetus has documented lung maturity or
further bleeding occurs. Active labor or persistent bleeding
will require an urgent trip to the operatingroom.
e management of placenta accreta or percreta at
delivery requires early recognition by the obstetrician and a
prompt decision to proceed with hysterectomy. Leaving the
placenta in situ without hysterectomy is a less commonly
used approach.35 is technique has unpredictable results
and requires close follow- up because of the risk of infection or further bleeding, but may be life- saving if the patient
refuses blood transfusion or adequate blood products are not
available. Acomparison of one institution’s experience with
ment of placenta accreta or percreta is awareness of risk
factors and communication with the obstetrics team, initially in the form of a multidisciplinary care conference
that involves nursing and other surgical consultants.40
Small hospitals or institutions with insucient resources
should consider patient transfer to a tertiary perinatal care
36
center.
e risk of major blood loss in these cases necessitates
large bore IV access, arterial line placement, a pressure/
warming rapid infusion system, availability of cross- matched
blood with the ability to institute a massive transfusion protocol, and additional personnel to assist with resuscitation
if needed.41 Hysterectomy and massive transfusion will usually require general endotracheal anesthesia. If the woman
is highly motivated to be awake to see her newborn, the
case can be started using a neuraxial technique with general
anesthesia induced aer delivery.
immediate hysterectomy with the placenta in situ versus leaving both placenta and uterus in situ found that conservative
therapy reduced the hysterectomy rate from 85% to 15%, the
transfusion rate by half, and coagulopathy from 39% to 5%,
PLACENTAL ABRUPTION
Etiology
but 15% of patients in the conservative group developed sepsis.36 Hysterectomy with placenta le in situ remains the treatment of choice.36 Management of placenta percreta usually
requires a multispecialty surgical team and potentially interventional radiology with delivery in a hybrid operating suite.
Known risk factors for abruption include hypertension,
advanced age and parity, smoking, cocaine use, abdominal
trauma, premature rupture of membranes, and history of
37
previous abruption.
SEVERE PERIPARTUM HEMORRHAGE 357
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Diagnosis
Diagnosis
As the placenta separates from the decidua, bleeding occurs
from the exposed vessels, and fetal distress develops because
there is less area for maternal- fetal gas exchange. Although
the classic presentation is vaginal bleeding with uterine tenderness, hypertonicity and fetal distress, the presentation
can be extremely variable.
In the appropriate clinical setting, uterine rupture should
be suspected when there is fetal distress, maternal shoulder pain (due to blood in the abdomen irritating the diaphragm), vaginal bleeding, abdominal pain between
contractions and unrelieved by epidural analgesia, loss
of fetal station or change in fetal presenting part, sudden
maternal hemodynamic instability, or cessation of uterine
Obstetric Management
Initial management includes evaluation of fetal well- being,
contractions on an intrauterine pressure catheter (IUPC).
Pain is not a sensitive indicator, and fetal distress is the most
common presentingsign.
placement of large- bore intravenous lines, type- andcrossmatch of blood products, and obtaining maternal
hematocrit and coagulation studies. e maternal risks of
abruption are signicant hemorrhage and coagulopathy,
while fetal risks include hypoxia and prematurity. Although
delivery of the fetus is the denitive treatment, the route of
delivery and timing varies. Severe fetal distress or maternal
hemodynamic instability necessitates urgent cesarean delivery. However, if the fetus and mother are stable and the
Obstetric Management
Dehiscence of a prior uterine scar is far more common than
catastrophic uterine rupture.43 Suspected rupture should
prompt immediate delivery. Depending on the condi-
tion of the uterus, the obstetrician may be able to repair
the dehiscence or rupture, but hysterectomy is sometimes
required.
cervical exam is favorable, induction of labor and vaginal
delivery may be attempted.
Anesthetic Management
Anesthetic Management
ere is no contraindication to regional anesthesia for labor
or cesarean delivery if maternal volume status and coagulation studies are normal. However, if the mother is hemodynamically unstable or coagulopathic and general anesthesia
is planned, etomidate or ketamine may be preferable to
Anesthetic involvement oen begins during an emergency
cesarean delivery for fetal distress, with the uterine rupture
discovered intraoperatively. General anesthesia may be nec-
essary if (1)the case is emergent and a functioning epidural
catheter is not in place for labor analgesia, (2) if there is
hemodynamic instability due to blood loss, or (3)if hyster-
ectomy is required.
propofol for induction. Aggressive volume replacement
and invasive monitoring may be necessary. Uterine atony is
common, and additional oxytocic drugs such as methylergonovine and prostaglandins should be available.
UTERINE RUPTURE
Etiology
Conditions associated with uterine rupture include prior
uterine surgery, abdominal trauma, direct uterine trauma
following forceps delivery or curettage, grand multiparity,
RUPTURE OFAN ECTOPIC PREGNANCY
Etiology
Hemorrhage from ruptured ectopic pregnancy is the lead-
ing cause of pregnancy- related maternal death in the rst
trimester. e major risk factors for ectopic pregnancy
are previous conservative treatment for ectopic pregnancy
(15% recurrence), tubal pathology from infection or sur-
gery, and in utero diethylstilbestrol (DES) exposure, but
many patients have no documented risk factors.
and fetal macrosomia or malposition. e risk of uterine
rupture aer a low transverse uterine incision is 0.5%–
0.9%. Concern for uterine rupture during a trial of labor
aer cesarean delivery (TOLAC) has led to more stringent
practice guidelines including the immediate availability
of all personnel necessary to perform emergency cesarean
delivery.
42
Diagnosis
Patients will present with abdominal or pelvic pain and
hemorrhagic shock may develop if rupture has occurred.
Depending on gestational age, an adnexal mass may be
44
seen.
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359
Obstetric/ Gynecologic Management
Urgent surgical removal of the aected fallopian tube or
dissection of the ectopic pregnancy with preservation of
the tube is required. Laparoscopy is the preferred surgical
approach, but if there is extensive bleeding or poor visualization of the pelvis, laparotomy should be performed.
45
Anesthetic Management
General endotracheal anesthesia is required for this emergent laparoscopic or open abdominal procedure. If hemodynamically unstable, standard resuscitative measures
should betaken.
POSTPARTUM MATERNAL HEMORRHAGE
UTERINE INVERSION
Etiology
Uterine inversion is an uncommon problem oen associated
with fundal pressure during delivery or excessive traction on
the umbilical cord, especially if the placenta does not easily
separate. e uterine fundus collapses into the endometrial
cavity, turning the uterus partially or completely insideout.
Diagnosis
e diagnosis is usually obvious. ere will be massive hemorrhage due to atony, vasovagal shock due to traction on the
uterosacral ligaments, and a mass in the vagina or outside
the perineum. Maternal shock and hypotension develop
rapidly.
Obstetric Management
Rapid replacement of the uterus is required, followed by
oxytocic drugs to maintain uterinetone.
Anesthetic Management
epidural analgesia, uterine relaxation can be accomplished
with intravenous nitroglycerin or terbutaline (250 mcg subcutaneously or IV). Nitroglycerin has a fast onset and short
duration when used in a bolus dose as a tocolytic to accomplish replacement of the uterus.47 Since it is a vasodilator,
when used in the presence of hypovolemia it should be
accompanied by a pressor such as phenylephrine. Volume
resuscitation must occur simultaneously, and blood loss can
be massive, so large bore intravenous access and transfusion
is oen necessary.
UTERINEATONY
Etiology
Uterine contraction is the primary mechanism controlling
blood loss at delivery, and thus uterine atony is the most
common cause of postpartum hemorrhage, accounting for
80% of cases.48 Conditions associated with atony include:
Multiple gestation Chorioamnionitis
Macrosomia Precipitouslabor
Polyhydramnios Augmented labor
(exposure to oxytocin)
High parity (>5) Tocolytic agents
(includingmagnesium)
Prolonged labor Volatile anesthetics
(> 0.5MAC)
Maternal age < 20, > 40 Prior postpartum
hemorrhage
However, over 60% of cases have no recognized risk
factors.
Diagnosis
Uterine atony is diagnosed aer vaginal or cesarean delivery
by manual examination of the uterine fundus that demonstrates lack of rmness and muscletone.
Uterine relaxation is oen necessary before the uterus can
be replaced, and intense analgesia is also required.46 Rapid
induction of general anesthesia with intubation and volatile anesthetics could accomplish both of these objectives,
however this is impractical in a labor room. Intravenous
ketamine (25– 50 mg) for analgesia plus a uterine relaxant such as nitroglycerin (100– 500 mcg IV) can be used
in that setting. If the patient is already comfortable from
SEVERE PERIPARTUM HEMORRHAGE 359
Obstetric Management
In addition to infusion of oxytocin, the obstetrician will perform bimanual compression of the uterus, uterine massage,
and evaluation for retained placenta. Retained placenta can
be seen on ultrasound examination and may be removed
by a manual sweep or by curettage. Additional oxytocic
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TABLE50.4 OXYTOCIC MEDICATIONS, DOSING AND SIDE EFFECT PROFILES
Medication
Oxytocin 10- 80 units/ L as an infusion IV bolus doses cause vasodilation and hypotension, hyponatremia can occur when
Methylergonovine 0.2 mg IM Can cause widespread vasoconstriction, increased pulmonary ar tery pressures,
Prostaglandin F2α(Carboprost)
Misoprostol 800 mcg PR May cause fever in high doses
Carbetocin 100 mcg IV Not available in the United States
Dose and Route
0.25 mg IM May cause bronchospasm, increased pulmonary ar tery pressures, VQ mismatching
medications will be administered (Table 50.4). If hemorrhage continues, other strategies for obstetric management
may include placement of an intrauterine balloon catheter
for tamponade of the uterus and use of B- Lynch sutures.
Side Effects
diluted in hypotonic intravenous solutions
coronary artery vasospasm, hypertension, nausea and vomiting
with hypoxia, nausea, and diarrhea
All providers on labor and delivery should be prepared
to treat obstetric hemorrhage. e National Partnership for
Maternal Safety, a joint venture of obstetricians, anesthe-
49
siologists, midwives, pathologists, family physicians, and
nurses, has created a consensus bundle for treating obstet-
Anesthetic Management
e patient should be evaluated for hemodynamic stability
and need for analgesia. Oxygen should be applied and monitors placed for blood pressure and heart rate. If blood loss
is ongoing, additional intravenous access and baseline labs
should be obtained. If the patient does not have a regional
anesthetic and requires short- term analgesia for obstetric
ric hemorrhage that addresses “best practices” for this scenario.51 ey stress anticipation of hemorrhage risk factors,
preparation of patients at high risk, recognition and rapid
response when hemorrhage does occur, and open reporting and tracking of hemorrhage occurrence so contributing
system issues can be identied and corrected. Such initiatives and clinical practice are crucial as we continue to ght
hemorrhage- related obstetric morbidity and mortality.
maneuvers, intravenous fentanyl or ketamine may be given.
Moving to the operating room can be benecial so general
anesthesia can be induced if necessary, patient position and
CASE- BASED LEARNING DISCUSSION
lighting can be optimized for the obstetrician, and aggressive resuscitation can be more easily performed. Consider
implementing the massive transfusion protocol with ongoing blood loss.
Anesthesiologists should be aware of the dose, route,
1. What are your concerns with placenta previa and a
history of prior cesarean deliveries? What questions
would you ask the obstetrician about their ultrasound
ndings?
and major side eects of the oxytocic drugs that can be used
(Table 50.4). Oxytocin is the mainstay of the uterotonic
medications, but the optimal dose is unclear. Bolus doses
≥ 10 units can cause signicant vasodilation and hypotension, especially in the presence of hypovolemia due to
hemorrhage. Studies comparing women having cesarean
delivery without labor to those having cesarean delivery
for the indication of labor dystocia have shown the ED90
of oxytocin is increased signicantly aer labor, presumably
2. Should delivery occur immediately? What factors
would lead you to proceed with emergent cesarean and
use of general anesthesia?
3. You visit with the patient about the anesthetic plan for
her cesarean delivery. She strongly desires to be awake
for the delivery of her baby. Her prior cesareans were all
done using regional anesthesia without any problems. Is
this a reasonable request?
because of down- regulation of oxytocin receptors in the
uterus. Supplemental agents may include methylergonovine (Methergine) and prostaglandins, with selection oen
based on potential adverse eects. Carbetocin, an oxytocin
analogue, is highly eective with minimal side eects, but it
is not available in the United States.
50
4. Acare conference is planned. How would you present
the anesthetic concerns and your preparation for them?
Discuss intravenous access, invasive monitoring, choice
of anesthetic, any blood products you would have
available, additional equipment, and so forth. Should
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361
this case be done on L&D? e main operating room?
In the interventional radiologysuite?
5. During the surgery, signicant hemorrhage occurs.
Which laboratory studies will be most useful to you?
What transfusion protocol will you use? What does
it mean to institute the massive transfusion protocol?
Are there medications that can be used in a postpartum
woman to treat massive hemorrhage?
6. If the cause of her postpartum hemorrhage was uterine
atony rather than abnormal placentation, what oxytocic
drugs are available to you? What dose and route of
administration would you use? What are their side
eects?
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51. Main EK, Goman D, Scavone BM, etal. National partnership for
maternal safety:consensus bundle on obstetric hemorrhage. Anesth
Analg. 2015;121:142– 8.
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51.
VALVULAR DISEASE
SPECIFIC CONSIDERATIONS FORMANAGEMENT DURING LABOR AND DELIVERY
Shobana Chandrasekhar and C. LaToyaMason
CLINICALCASE
MATERNAL RISK ASSESSMENT AND
MONITORING
A 30- year- old G2P0 with moderate mitral stenosis is admitted to labor and delivery with mild uterine contractions at
37 weeks gestation. She has a history of atrial brillation at
28 weeks, which was treated with digoxin and beta blockers.
Currently, she is painfully contracting and is seeking labor
analgesia. Vital signs are stable, but intermittent premature
atrial contractions (PACs) and short runs of supraventricular tachycardia (SVT) are present on telemetry monitoring.
Cardiovascular disease occurs in only 1%– 3% of pregnancies but accounts for 10%– 15% of maternal mortality.6
Identifying parturients at increased risk for catastrophic
cardiovascular complication is paramount. Factors that
may predict increased maternal cardiac risk include history
of prior cardiac events or arrhythmias, signicant le ventricular obstruction and/ or dysfunction, functional status,
and degree of symptoms present. Women with no or very
mild symptoms (New York Heart Association [NYHA]
INTRODUCTION
Classes Iand II) tolerate pregnancy reasonably well, while
those with marked congestive symptoms (NYHA Classes
Cardiovascular disease is a leading cause of maternal morbidity and mortality.
1,2
In the United States, cardiovascular conditions ranked rst among categorical contributors
to an overall increased pregnancy- related mortality ratio
during the years 2006– 2010.3 Complex valvular heart
disease accounts for approximately 30% to 50% of all cardiac diseases of pregnancy, and management of aected
parturients can be quite challenging.
4,5
Determination
of disease severity and maternal risk assessment are especially important to development of appropriate plans of
care and to prevent adverse maternal and fetal outcomes
during the labor, delivery, and immediate postpartum
periods. An understanding of the pathophysiology of the
various causative lesions, thorough evaluation, and a multidisciplinary approach are key components to the successful management of these patients, allowing for selection
of an anesthetic technique that balances the benets and
consequences to both mother and infant, thereby leading
to optimal patient outcomes. More detailed background
information about each lesion for the general adult population is presented in the “Severe Valvular Disease” chapter
in the “Cardiac Crises” section.
III and IV) are at risk for major morbidity and mortality.7 In
women with valvular cardiac disease, risk assessment should
ideally be initiated at a preconception visit and continued
throughout pregnancy. e Task Force on the Management
of Cardiovascular Disease during Pregnancy of the European
Society of Cardiology (ESC) currently recommends use
of integrated risk stratication.8 e ESC’s stratication
scheme, a modication of the World Health Organization’s
approach that incorporates all known maternal cardiovascular risk factors, represents the most comprehensive risk
assessment system available to date (Figure51.1).
At the minimum, standard ASA monitoring should
be utilized in the management of parturients with valvular disease. Electrocardiogram allows for ongoing evaluation of heart rate and detection of arrhythmias. Labor,
delivery, and the immediate postpartum periods are
highly dynamic states; invasive blood pressure monitoring
oers the benets of beat- to- beat assessment and a conduit whereby specimens may be easily obtained for laboratory studies. Parturients with severe valvular disease
only rarely require central venous catheter +/ - pulmonary
artery catheterization. Notably, technological advances
363
364
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WHO I WHO II
Mild or uncomplicated Mild or uncomplicated - Mechanical valve- Severe mitral stenosis
- pulmonary stenosis
- patent ductus
arteriosus
- mitral valve proplapse
Repaired simple
lesions (PDA, ASD,
VSD, total anomalous
pulmonary venous
drainage).
Isolated atrial or
ventricular ectopic
beats
Patient can be considered
very low risk, with no
increased mortality and
no/mild increase in
maternal morbitdity.
Patient’s follow up with
cardiologist can be
limited to one or two
visits during pregnancy.
- Uncorrected ASD or
VSD
- Tetralogy of Fallot
(repaired)
- Arrhythmias
WHO II or III
(Varies based on individual patient)
- Mild compromised left ventricular function
- Hypertrophic cardiomyopathy
- Valvular heart disease not considered WHO I or
IV
- Marfan syndrome with normal aortic diameter
- Bicuspid aortic valve associated with aortic
dilatation not >45 mm
- Repaired aortic coarctation with bicuspid
aortic valve
Patient can be considered at
low to moderate risk with
mild increase in maternal
mortality and moderate
increase in morbidity.
Patient’s follow up with
cardiologist should be every
trimester.
WHO III WHO IV
- Systemic right ventricle
- Fontan circulation
- Tetrology of Fallot
(unrepaired)
- Other complex
congenital heart disease
- Aortic dilatation 40–45
mm in Marfan syndrome
or 45–50 mm in patients
with bicuspid
aortic valve
Patient can be considered
high risk with significantly
increased morbidity and
mortality.
Patient should be cared for
by expert multispecialty
interdisciplinary team
Monthly or bimonthly
cardiac and obstetric
monitoring if pregnancy
pursued.
- Severe symptomatic aortic
stenosis
- Pulmonary arterial
hypertension
- Severe left ventricular
dysfunction (LVEF <30%,
NYHA Class III-IV)
- History or peripartum
cardiomyopathy with
residually impaired left
ventricular function.
- Uncorrected severe
coarctation
- Marfan syndrome with
aorta dilated >45 mm or
aortic dilatation >50 mm
with bicuspid aortic valve
Patient should be
considered extremely high
risk and pregnancy is
contraindicated secondary
to high risk of maternal
mortality and severe
morbidity.
If pregnancy does occur,
close monthly or
bimonthly followup is
necessary.
Figure51.1 Risk stratication:the modied World Health Organization (WHO) approach. © 2014 Michael Nanna and Kathleen Stergiopoulos. Journal of the American Heart
Association. 2014;3:e000712.
including noninvasive cardiac output monitoring modalities (e.g., Edwards EV1000 and Cheetah NICOM) and
serial transthoracic echocardiography have largely replaced
the use of highly invasive monitors in obstetric anesthesia.
Intraoperative transesophageal echocardiography (TEE)
can be used in parturients undergoing cesarean delivery
with general anesthesia.
TYPES OFVALVULAR HEART
DISEASE:PATHOPHYSIOLOGY AND
MANAGEMENT
A clear understanding of each of the dierent valvular
lesions and the accompanying pathophysiology is needed
for optimal patient outcome.
AORTIC STENOSIS
Aortic stenosis (AS) is an abnormal narrowing of the aortic
valve’s orice that obstructs blood ow from the le ventricle (LV). e occurrence of AS in pregnancy is rare, yet
signicant, given that pregnancy is a high- risk period for
patients with aortic pathology. Aortic pathology is noted
to be one of the leading causes of maternal mortality in the
2003– 2005 report of the UK Condential Enquiry into
Maternal and Child Health.
8,9
Women with AS may tolerate the hemodynamic changes of pregnancy well and may
potentially be asymptomatic when the obstruction is of mild
or moderate severity as quantied by an aortic valve area
greater than 1.0cm2. In critical AS, with valvular area less
than 0.5cm2 and ow gradient greater than 60mmHg, the
patient may experience dyspnea, angina, and/ or syncope.
364 SECTION B. CARDIAC CRISES
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365
Symptomatology indicates considerable risk for arrhythmias, myocardial decompensation, pulmonary edema, and
LV failure.10 e incidence of complications for both mother
and fetus directly increases with severity of AS. Women with
a bicuspid aortic valve etiology of severe AS are also at risk
for aortic dilation and dissection, hypertension- related disorders, and premature labor, and infants born to women
pregnancy, catheter- based valvuloplasty, and surgical valve
replacement.4 If denitive surgical intervention is required
early in pregnancy, the risk of fetal mortality may be as high
as 30%.15 e inammatory and nonpulsatile nature of cardiopulmonary bypass have profoundly negative eects on
uteroplacental blood ow and the fetus that may be exaggerated by concurrent hypotension and hypothermia.
6
with severe AS may have intrauterine growth restriction
resulting in premature birth and low birth weight.
Women with AS should undergo echocardiography
to assess aortic valve parameters, and, even if asymptomatic, antepartum exercise testing is recommended. Surgical
intervention prior to pregnancy is recommended for symptomatic patients with severe AS.12 For patients who develop
signs and symptoms of heart failure during pregnancy, there
is no optimal medical treatment, but therapy may include
restriction of activities and cautious administration of
diuretics to improve congestive symptoms. Beta blockers or
calcium channel antagonists may help achieving the overall
management goals of avoiding tachycardia, preserving preload and circulating blood volume, and maintaining SVR.
Phenylephrine, an alpha- adrenergic agonist, is the vasopressor of choice in patients with AS, as it helps preserve
coronary perfusion pressure.
13,14
Cardiac surgery is reserved
for when medical management fails, because cardiac surgical morbidity and mortality in parturients is higher versus
nonpregnant patients.6 If a severely symptomatic pregnant
patient does not respond to medical therapy, depending
on gestational age, providers should discuss termination of
11
Anesthesia forLabor and Delivery inParturients
withAortic Stenosis
Obstetric indications and maternal severity of disease
strongly inuence mode and timing of delivery. Labor
with or without assisted vaginal delivery is preferred and
may be safely pursued in the asymptomatic patient with
mild- moderate AS who has tolerated pregnancy very well.
Assisted second stage is more commonly used in patients
with moderate- severe AS and those patients with dilated
aorticroots.
Hemodynamic management principles for the parturient with AS are listed in Table 51.1 and include the following:(1)avoidance of aortocaval compression, (2)avoidance
of tachycardia, (3)avoidance of decreases in systemic vascular
resistance, and (4)maintenance of venous return and le ventricular lling.13 Anesthetic strategies during labor and delivery include early placement of an epidural catheter to allow
gradual titration of analgesia using an epidural solution composed of low- concentration local anesthetic and narcotic (Box
51.1). Acombined spinal- epidural technique with intrathecal
TABLE51.1 HEMODYNAMIC GOALS OFVALVULAR LESIONS MOST COMMONLY ENCOUNTERED INPREGNANCY
Valvular Lesion
Mitral Stenosis • Avoid tachycardia, as it causes decrease inw LV lling time and underlling of LV
Mitral Regurgitation • Avoid bradycardia. Maintenance of normal to elevated heart rate is advocated.
Aortic Stenosis • Maintain normal sinus rhythm.
Aortic Regurgitation • Maintenance of normal to elevated hear t rate is advocated.
LV=left ventricle; SVR=systemic vascular resistance
SOURCE:Reprinted with permission from Chandrasekhar S, Suresh MS. Chapter45:Anesthetic management of critically ill parturient with cardiac disease. In:Belfort M, Saade GR, etal.,
eds., Critical Care Obstetrics. 5th ed. NewYork:Blackwell- Wiley; 2010:639– 55.
VALVULAR DISEASE 365
Hemodynamic Principles of Anesthetic Management
• Maintain preload
• Maintain normal sinus rhythm. Atrial brillation can precipitate pulmonary edema
• Avoid myocardial depression. As LV impairment usually accompanies mitral insufciency, even
minimal myocardial depression may cause signicant compromise.
• Avoid increase in SVR, as it will increase the regurgitant ow and decrease forward ow.
• Avoid decrease inSVR.
• Maintain preload and LV lling
• Avoid myocardial depression. As LV impairment usually accompanies aortic insufciency, even
minimal myocardial depression may cause signicant compromise.
• Avoid increase in SVR as it will increase the regurgitant ow and decrease forward ow.
Preferred First- Line
Vasopressor
Phenylephrine
Ephedrine
Phenylephrine
Ephedrine
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