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Cardiopulmonary bypass in pregnancy
Article in Annals of Cardiac Anaesthesia · January 2014
DOI: 10.4103/0971-9784.124133 · Source: PubMed
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Article
Cardiopulmonary bypass in pregnancy
Mukul Chandra Kapoor
Department of Anesthesia, Saket City Hospital, Saket, New Delhi, India
ABSTRACT
Received: 26‑11‑13
Accepted: 15‑12‑13
Cardiac surgery carried out on cardiopulmonary bypass (CPB) in a pregnant woman is associated with poor
neonatal outcomes although maternal outcomes are similar to cardiac surgery in non‑pregnant women. Most
adverse maternal and fetal outcomes from cardiac surgery during pregnancy are attributed to effects of CPB.
The CPB is associated with utero‑placental hypoperfusion due to a number of factors, which may translate
into low fetal cardiac output, hypoxia and even death. Better maternal and fetal outcomes may be achieved
by early pre‑operative optimization of maternal cardiovascular status, use of perioperative fetal monitoring,
optimization of CPB, delivery of a viable fetus before the operation and scheduling cardiac surgery on an
elective basis during the second trimester.
Key words: Cardiac surgery, Cardiopulmonary bypass, Fetal outcomes, Maternal outcomes, Pregnancy,
Uteroplacental perfusion
INTRODUCTION
The incidence of heart disease in pregnant
women is reported to vary from 1% to 4%,
with rheumatic mitral valve disease being
the most common etiology and accounting
for nearly 60% of the cases.[1] Cardiac disease
in pregnancy, if untreated, is responsible for
10‑15% of maternal mortality.[2] In low‑income
countries, 60‑80% of the pregnant women
with heart disease suffer from rheumatic
heart disease[3] and it is a major cause of death
related to pregnancy.[4] Indications for surgery
using CPB during pregnancy include cardiac
valve disease, prosthetic valve malfunction,
cardiac myxoma, congenital heart disease,
pulmonary embolism, aneurysm and coronary
artery disease.
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DOI:
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CPB was first used in a pregnant patient
in 1959, when a woman, with a 6 weeks
gestation, underwent a pulmonary valvotomy
and closure of an atrial septal defect. The
mother survived, but the fetus spontaneously
aborted 3 months later.[5] Maternal mortality
associated with CPB during pregnancy was
earlier reported to be 3‑15%.[6] Recent data
however suggests a maternal mortality rate
similar (1.47%) to that associated with CPB
in non‑pregnant women, unless the surgery
is emergent.[7] Fetal mortality has however
not reduced and remains at 16‑33% in recent
studies.[1,6] Cardiac surgery in pregnant patients,
as a result, must be limited to cases where
medical management fails. Various strategies
recommended to improve feto‑maternal
outcomes are summarized in Table 1.
CARDIOPULMONARY BYPASS AND THE FETO‑
MATERNAL UNIT
The fetal blood circulation differs from the
adult circulation. The arterial blood is not fully
saturated because of arteriovenous admixture.
The fetal hemoglobin is only 65% saturated and
the oxy‑fetal hemoglobin dissociation curve is
shifted to the left to improve oxygen uptake at
the placental level. Although the leftward shift
of the curve improves uptake, the dissociation of
oxygen to deliver oxygen is relatively restricted.
A reduction in oxygen carriage, due to any factor,
thus predisposes to early development of fetal
distress. Maintenance of fetal cardiac output,
fetal arterial pH and maternal hematocrit are
important to maintain adequate oxygen uptake
in the placenta and subsequent delivery to
tissues. Fetal cardiac output is rate dependent,
so fetal bradycardia results in fetal distress.
Address for correspondence: Dr. Mukul Chandra Kapoor, Department of Anesthesia, Saket City Hospital, Press Enclave Road, Saket, New Delhi ‑ 110 017,
India. E‑mail: mukulanjali@gmail.com
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Kapoor: CPB in pregnancy
Table 1: Strategies during cardiopulmonary bypass to
improve feto-maternal outcomes
Uterine tone monitoring
Fetal heart rate monitoring especially if fetus >24 weeks gestation
15° left lateral tilt using a wedge under the right hip or a left lateral tilt
of the table to prevent aortocaval compression >20 weeks gestation
Maternal hematocrit >25%
acidosis, consequent to low fetal cardiac output,
develops 6‑8 h after CPB is discontinued and this
acidosis can be associated with fetal death.
CONDUCT OF EXTRACORPOREAL CIRCULATION AND
CARDIOPLEGIA DELIVERY
High maternal oxygen saturation
Normothermia
High perfusion flow rates (>2.5 L/min/m2)
High perfusion pressure (>70 mm Hg)
Minimize cardiopulmonary bypass time
Pulsatile perfusion
α-stat pH management
Tocolytic therapy (magnesium sulfate, β2-agonists, progesterone
supplementation and intravenous alcohol infusions)
Neonatologist and obstetrician on standby for emergency delivery
The use of CPB during pregnancy is associated with poor
neonatal outcomes. A review of the Mayo Clinic surgical
database, spanning 35 years (1976‑2009), revealed that
21 pregnant patients underwent cardiothoracic surgery
during that period.[8] Nearly, 52% of these pregnancies
had premature deliveries and there were 3 fetal deaths
(14%). Neonatal complications included intra‑uterine
growth retardation (5%), respiratory distress syndrome
(33%) and development delay (14%).[8]
The response of the feto‑placental unit to CPB has
been studied by experiments into fetal CPB and that
has helped improve the management of perfusion in
pregnant women.[9] Placental function is dependent not
only on the maternal side of the circulation, but also on
the fetal side with its responses to interventions.
Sustained forceful uterine contractions during cardiac
surgery and CPB are considered as the most important
contributors to fetal death. [10] Sustained uterine
contractions reduce uterine blood flow and intervillous
perfusion and the resultant feto‑placental insufficiency
can cause fetal hypoxia.
Thirty to 60 min after the fetus is removed from bypass
a severe, progressive respiratory acidosis develops due
to a rise in placental vascular resistance by activation of
eicosanoid products.[11,12] This late acidosis is potentiated
by low cardiac output secondary to an increase in fetal
systemic vascular resistance (SVR). The rise in fetal SVR
results from an increase in catecholamine levels due to
fetal stress response secondary to fetal manipulation
during surgery, anesthesia and fetal hypoperfusion.[13,14]
The increase in fetal SVR is poorly tolerated by the
immature fetal myocardium.[9] An intractable metabolic
34
Extracorporeal circulation causes significant alterations
in the mother and fetus. Hemodilution, changes
in coagulation, complement activation, release of
vasoactive substances by leukocytes, particulate/
air embolism, hypothermia and hypotension during
CPB add to the deleterious effects of extracorporeal
circulation.[9,15] Hemodilution is particularly deleterious
for the fetus as it compounds the physiological anemia of
pregnancy and reduces oxygen content of the placental
blood. These effects are relatively better tolerated by the
mother and thus the maternal mortality rate associated
with CPB in pregnant women is not worse than that seen
in non‑pregnant women who undergo similar cardiac
procedures on CPB.[9,16]
Fe t a l c i r c u l a t i o n d u r i n g C P B h a s n o t b e e n
well‑investigated.[17] CPB may result in lower placental
flow and pressure, which are worsened by hypothermia
and this results in impaired placental perfusion and
respiratory gas exchange. [18] Although increasing
CPB flow rates are preferable to improve placental
perfusion, sympathomimetic agents such as ephedrine
and phenylephrine (considered safe in pregnancy) can
be used to maintain perfusion pressure and improving
placental perfusion.[8] Vasoconstrictors reduce the
utero‑placental flow and should ideally be avoided.[19]
Pump flow and mean arterial pressure during CPB are the
most important factors influencing fetal oxygenation.[16]
Placental blood flow is an important factor to prevent
placental dysfunction. Placental blood flow has been
demonstrated to be significantly higher under pulsatile
bypass in experimental fetal cardiac surgery.[20] Pulsatile
flow for 30 min of CPB in a fetal lamb preparation was
found to prevent progressive hypoxemia observed
under non‑pulsatile CPB. [20] Non‑pulsatile CPB is
associated with alteration in uterine artery flow
velocity with resultant inability to meet the demands
of the feto‑placental circulation.[9,21] Improved fetal
outcomes have been reported when the intra‑aortic
balloon pump has been electively used with CPB, to
mimic pulsatile flow physiologically and improve
uterine perfusion. [17,22] Pulsatile flow prevents the
drop in placental perfusion and limits the rise in
placental vascular resistance that is observed with the
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non‑pulsatile flow.[23] It preserves endothelial nitric
oxide synthesis and decreases the activation of the fetal
renin‑angiotensin pathway, resulting in improved blood
flow to the feto‑placental unit.[23,24] A study of the human
placenta under physiologic conditions revealed that an
active fetal renin‑angiotensin system may modulate
placental perfusion in vivo. [25] Vasodilators have
been used to overcome this rise in placental vascular
resistance and improve placental blood flow and
prevent the development of acidosis.[26] Lactate levels
during pulsatile‑flow CPB have been shown to remain
stable, whereas a continuous increase is observed with
non‑pulsatile CPB.[23]
vasoconstriction and hypercapnia increases uterine
blood flow. Therefore, α‑Stat pH management may
be advantageous for maintenance of carbon dioxide
homeostasis and placental perfusion.[9,33]
High‑flow, high‑pressure, normothermic and a short
CPB is possibly the best perfusion strategy to ensure
adequate placental homeostasis. Perfusion strategies
to minimize fetal risks include using normothermic
CPB, minimizing CPB times, maintaining a high flow
rate (>2.4 L/min/m 2) and mean arterial pressures
>70‑75 mm Hg.[34]
FETAL HEART MONITORING
Although mild hypothermia can be tolerated because
the fetal heart is able to autoregulate heart rate, more
profound hypothermia adversely effects fetal and
placental function and thereby increases the risk of fetal
arrhythmias and cardiac arrest.[27] There are no recent
reviews on the effect of CPB temperature on outcomes
in pregnant women. However, a review of 69 reports
of open heart surgery during pregnancy, published
20 years back, found embryo‑fetal mortality to be 24%
and 0% in the hypothermic and normothermic groups,
respectively.[16] More recently, good fetal survival has
been reported after hypothermic CPB both in animals
and human pregnant patients.[28‑30]
Normothermic perfusion however may be associated
with myocardial protection difficulties related to early
rewarming of the left ventricle. In one report, a total of
3,500 ml of cardioplegia was required for satisfactory
myocardial protection.[31] Myocardial rewarming may
be avoided with the use of continuous cold pericardial
irrigation or continuous warm blood cardioplegia,
which is effective even with long cross‑clamp times.[32]
The latter may be the method of choice to prevent the
crystalloid load imposed by frequently repeated boluses
of cold crystalloid cardioplegia. Cardioplegia may
however increase serum potassium levels, especially
in cases with prolonged periods of cardioplegic arrest.
Maternal hyperkalemia causes increased potassium
diffusion into the fetal circulation through the placental
chorionic villi. Fetal hyperkalemia leads to conduction
disturbances and may even cause fetal cardiac arrest.
Discarding coronary sinus return during cardioplegia
delivery obviates the problem. Serum potassium
concentration needs to be closely monitored with the
goal to maintain it <5 mmol/L.
Changes in carbon dioxide tension can also affect
uterine blood flow as hypocapnia causes utero‑placental
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Bradycardia, because of placental hypoperfusion,
is the most frequent fetal response to CPB and is
usually reversible by increasing the perfusion.[17] Fetal
bradycardia invariably occurs at the onset of CPB
and the reason for this is not clearly defined.[35,36] The
various causes for bradycardia postulated, include
feto‑placental dysfunction; fetal hypoxia and acidosis;
maternal hypothermia; hypothermia at the onset of
CPB;[35] and drugs that cross the placental barrier,
such as β‑adrenergic blockers. Uterine arteriovenous
shunting, obstruction of venous drainage by inferior
vena caval cannulation, particulate/gaseous emboli and
uterine artery spasm with the onset of CPB can also
reduce placental circulation and lead to fetal hypoxia.[10]
Bradycardia does not appear to be related to maternal
oxygenation or acid‑base balance. The most plausible
theory regarding its etiology is that it reflects placental
hypoperfusion due to sudden hemodilution with the
onset of CPB and the consequent fetal hypoxia.[37] Fetal
bradycardia with the onset of CPB ceases once the
maternal circulation is restored and the FHR generally
surpasses the basal heart rate.[35]
Alterations in fetal heart rate may be observed even
when maternal circulation, acid‑base balance and
perfusion pressure are stable. It has been postulated
that these alterations are related to the narcotic effect
of drugs used during anesthesia.[37] Potential reasons
for fetal asphyxia during maintenance of CPB include
reduced maternal SVR, low uterine blood flow,
hemodilution, hypothermia, prolonged CPB or maternal
narcotic administration.[38] Fetal heart rate monitoring
allows analysis of fetal condition during CPB. Fetal
heart rate monitoring is essential for early detection
and management of alterations in fetal heart function.
Fetal heart rate monitoring can be intermittently done
for fetuses at <24 weeks gestation but should be
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Kapoor: CPB in pregnancy
continuously done for fetuses at ≥ 24 weeks gestation.
Continual monitoring of the fetus postoperatively, for
at least 12‑24 h, is also recommended because there is
a risk of preterm labor in this period.
Fetal monitoring is commonly done using a
cardiotachometer.[39] Intraoperative fetal echocardiography
shows the fetal cardiac reactions more accurately and
its use is recommended.[1] Doppler transducers are
available to monitor fetal heart rate from the maternal
abdominal wall, but these probes are difficult to maintain
in place during surgery. Trans‑vaginal probes can be
used to monitor fetal heart rate and umbilical cord flow,
especially if gestational age is low, however they are
difficult to use and technically challenging.
Fetal heart rate monitoring during CPB should be
focused to maintain fetal heart rates between 110 and
160 beats/min[40] and to guide the perfusionist to adjust
the perfusion flow rate, the mean arterial pressure and
the maternal temperature.
UTERINE MONITORING
Uterine contractions occur frequently during CPB and
are considered the most important predictors of fetal
death.[41] They are more common during the rewarming
phase after moderate or profound hypothermia[39] and
occur more frequently with increasing gestational age.[9]
It has been suggested that the CPB related hemodilution
decreases the progesterone hormonal levels increasing
uterine excitability. Utero‑placental hypoperfusion can
precipitate uterine contractions and these contractions
may occur even after completion of CPB and surgery.[8]
Uterine contraction monitoring is essential for early
control because the contractions are associated with
significant fetal loss.[9] When the uterus is relaxed,
a mean arterial pressure of ≥ 70 mmHg is required
for adequate placental perfusion,[31] however when
uterine contractions occur (seen more frequently with
increasing gestational age), the blood pressure required
to ensure adequate placental perfusion increases.
Uterine contractions may cause placental insufficiency
and secondary fetal hypoxia during CPB. The use
of uterine monitoring is therefore recommended for
early identification of contractions so that they can
be adequately treated before they lead to placental
hypoperfusion and fetal bradycardia occurs.[9]
Tocolytic therapy with β2‑agonists; magnesium;
progesterone supplementation; and intravenous alcohol
36
infusions have been successfully used to stabilize the
uterus during CPB.[10,31,42] However, recent evidence
suggests that there is no benefit with the use of tocolytic
therapy.[43,44] β‑agonists increase myocardial oxygen
demand and myocardial work in a circulation that is
already physiologically compromised by the burden of
pregnancy and by the initiation of CPB.[37]
PATIENTS WITH PROSTHETIC CARDIAC VALVES
Bioprosthetic valves are implanted in women of
childbearing age, who need to complete their families
because anticoagulants can be avoided. Early reports
suggested that pregnancy favors calcification of
porcine xenografts, leading to bioprosthetic failure,[45,46]
however, recent evidence shows that pregnancy does
not increase structural deterioration or reduce the
survival of bioprosthetic valves. Rarely, such patients
with bioprosthetic valves may come for surgical
replacement of failed xenograft during pregnancy.
Women with mechanical prosthetic heart valves
are advised against pregnancy as anticoagulant
use is associated with severe teratogenic effects.
Pregnancy increases the risk of thrombosis of prosthetic
mechanical heart valves.[15,47] Pregnant women with
such valves may present as surgical emergencies due
to valve dysfunction resulting from valve thrombosis,
endocarditis, perivalvular leaks or prosthesis structure
defects. Such patients may be on oral anticoagulants
or heparin and are prone to increased blood loss.
Antifibrinolytic agents, such as tranexamic acid,
are generally not recommended as pregnancy is an
intrinsically hypercoagulable state[8] and their use must
be reserved for extreme situations.
FUNCTIONAL STATUS OF THE MOTHER
Fetal mortality was described to be higher than 50%
in patients in functional class III and IV in earlier
studies. [48] A recent study has found much lower
mortality rates in functional class III (20%), but rates
in patients in functional class IV (66.7%) continue
to remain high.[1] Careful optimization by medical
therapy and improvement in the functional status of
patient helps reduce mortality and morbidity. Other
measures to reduce maternal and fetal mortality
include avoiding functional deterioration during
pregnancy and perhaps prescribing early surgery to
prevent these patients from requiring an emergency
procedure; performing surgery as fast as possible,
with minimal CPB time; providing adequate fetal
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monitoring (cardiotachometer and intraoperative
fetal echocardiography); and preferably performing
surgery in the second trimester of pregnancy. Use of
intraoperative trans‑esophageal echocardiography
helps optimize cardiac function and maintain
adequate cardiac output apart from acting as a guide
to assess surgical repair.
GESTATIONAL AGE
Fetal losses appear to be associated with urgent,
high‑risk cardiac surgery, maternal comorbidities and
operations performed at early gestational age.[49] Fetal
mortality declines if cardiac surgery was delayed
and the fetus is allowed to mature. Attempts to delay
surgery until an advanced gestational age minimizes
the risks associated with prematurity and fetal
demise.[8] Determining the optimal timing of cardiac
surgical intervention is one of the most challenging and
critical clinical decisions in the care of the pregnant
patient with cardiac disease and needs to be patient
specific. Early intervention will decrease maternal risk,
but may result in fetal demise.[8] The ideal gestational
age for operation is established as the period between
the 13th and 28th weeks.[50,51] There is a higher trend
towards fetal malformations in the first trimester; and
to preterm delivery, maternal hemodynamic alterations
and mortality in the third trimester. For conducting
cardiac surgery using CPB, the second trimester is
considered the safest gestational age as the maternal
physiologic hematologic/hemodynamic changes have
not peaked, uterine excitability least, aorto‑caval
compression not seen and fetal organogenesis is in an
advanced safer stage.
Delaying cardiac surgery until after delivery may result
in maternal death. If the fetus is of advanced enough
gestational age and the planned maternal surgery is
anticipated to be complicated, prolonged in length or
anticoagulation will be needed, delivery prior to CPB
should be considered.[8] Emergency Cesarean section
is advocated for women who need to have a cardiac
operation in the third trimester because the estimated
fetal risks are high during CPB.
DRUGS AND ANESTHETIC AGENTS
The pregnancy related changes in organ function
results in altered maternal drug pharmacokinetics
and pharmacodynamics. [52] The hemodilution at
the onset of CPB further alters drug pharmacology
and there is increased variability of unbound drug
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concentrations. Drug transfer across the placenta to
the fetus occurs as per drug concentration gradient
from the maternal‑to‑fetal circulation and the placental
membrane characteristics. Drugs often require more
frequent dosing, without a change in the total daily
maternal dosage.[52] All inhaled anesthetics and most
intravenous anesthetics are highly lipid soluble and
freely cross the placenta. Volatile anesthetics are also
potent uterine relaxants and decrease uterine blood
flow. Most adverse maternal and fetal outcomes from
cardiac surgery during pregnancy are attributed to
effects of CPB and the underlying cardiac status of the
mother, not the anesthetic agent used.[34]
OTHER FACTORS
A meta‑analysis of the data of a recent study found
maternal age higher than 35 years, reoperations and
emergency surgery to be independent factors for fetal
mortality.[1] Additional strategies currently in use to
minimize fetal risks include minimizing intraoperative
blood loss and maintaining uterine displacement to
avoid aorto‑caval compression.[34] During CPB, uterine
displacement can be maintained by placing patient in
a 15° left lateral recumbent position by using a wedge
under the right hip or by a left lateral tilt of the table.
This should be performed for any parturient >20 weeks
gestational age to avoid impairment of utero‑placental
blood flow.[8] Hyperoxygenation should be maintained
and hematocrit kept >25%.[15]
In addition, optimizing maternal oxygen saturation
and avoiding maternal hypoglycemia are important
for preventing fetal bradycardia.[9,53] To prevent fetal
hypoglycemia addition of hypertonic glucose to the CPB
perfusate, to increase fetal energy substrate, has been
tried.[54] Administration of maternal corticosteroids to
initiate endothelial membrane stability and maturation
of the fetal lungs must be considered as this can
substantially improve fetal outcome, should delivery
occur after CPB.[55]
To conclude, CPB management of pregnant women
should be focused toward improving outcomes in both
mother as well as the fetus. Acceptable maternal and
fetal outcomes may be achieved by early pre‑operative
optimization of maternal cardiovascular status, use of
perioperative fetal monitoring, optimization of CPB,
delivery of a viable fetus before the operation and
scheduling surgery on an elective basis during the
second trimester.
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Cite this article as: Kapoor MC. Cardiopulmonary bypass in pregnancy. Ann
Card Anaesth 2014;17:33-9.
Source of Support: Nil, Conflict of Interest: None declared.
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