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DOI:
10.4103/0971-9784.124111
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Cardiopulmonary bypass during
pregnancy – Fetal demise: An enigma
Ever since the first use of cardiopulmonary
bypass (CPB) in 1959 in a pregnant woman
with a 6 weeks gestation for pulmonary
valvotomy and atrial septal defect closure,
wherein the fetus spontaneously aborted 3
months later,[1] the fetal mortality for open
cardiac surgery during pregnancy continue
to remains high at 9.5-29% with an average
of 19% over the past 25 years.[2-4] The effects
of CPB are the key factors responsible for
fetal demise. The extraordinary increases in
our knowledge of CPB, maternal and fetal
circulatory physiology and technological
advances have not been able to bring down
the fetal mortality associated with CPB. The
obstacle has been inadequate knowledge of
the effects of CPB on fetal well-being and lack
of fetal monitors that can indicate adequacy/
inadequacy of fetal needs, particularly,
circulatory needs. The most intuitive cause
of adverse fetal outcome during CPB could
be inadequate supply of O2 and nutrients to
the fetus. Considering fetal hypoxemia as
the cause of fetal demise, the interventions
are directed to increase fetal O2 delivery and
are limited to maneuvers that increase O2
delivery to fetus during CPB. The measures
include increases in CPB flow and mean
arterial pressure (MAP) and hematocrit of
prime and measures to prevent increases
in placental vascular resistance including
uterine relaxants. It is interesting to note that
a review of the Mayo Clinic surgical database
spanning 35 years (1976-2009) revealed
that only 21 pregnant patients underwent
cardiothoracic surgery during that period.
[5]
Evidently, the developed world have
effectively educated their population and CPB
during pregnancy is a rare and unimportant
issue with them. Moreover, the manifestations
of rheumatic heart disease, particularly mitral
stenosis, occur much later in developed
nations. However, the issue is relevant for
developing countries where rheumatic heart
disease still exists in sizable proportion and
the gaps in our knowledge for managing these
cases needs to be researched.
With the initiation of CPB, fetal bradycardia
is observed and fetal hypoxemia is believed
to be the prime cause of fetal bradycardia.
The supply of O2 to the fetus is dependent on
exchange of gases across the placenta and the
efficiency of fetal hemoglobin (HbF) to receive
O2 from the maternal blood, which is CPB prime
during CPB. It is noteworthy that the placental
circulation does not exhibit autoregulation,[2,5]
as a result the placental blood flow changes
directly with the changes in arterial perfusion
pressure (MAP during CPB). In an experimental
study, pulsatile flow was shown to prevent
the drop in placental perfusion and limit
the rise in placental vascular resistance.[6]
Additionally, oxygenation of the CPB prime
can only marginally increase O2 supply to the
fetus. In essence, well oxygenated blood must
be delivered to the utero-placental circulation,
at a reasonable MAP, using pulsatile flow.
The utero-placental flow may be reduced by
low CPB flows, low MAP, inferior vena cava
compression and aortic compression.[7] Even
if the uterine circulation is adequate, the
fetus still depends on utero-placental blood
flow and umbilical venous blood flow and its
characteristics for tissue oxygenation. There
are several differences in the characteristics
of fetal blood and hemodynamics vis-à-vis
an adult. The hemoglobin (Hb) concentration
is about 16 g%, which increases the total O2
carrying capacity. The predominant Hb from
10 to 12 week until delivery is HbF, which
has greater affinity to O2 because of reduced
affinity with 2, 3 diphosphoglycerate. Increased
affinity of HbF with O2 facilitates O2 transfer
Address for correspondence: Dr. Praveen Kumar Neema, Department of Anaesthesiology, AIIMS Raipur - 492 099, Chhattisgarh, India.
E-mail: [email protected]
Annals of Cardiac Anaesthesia  Vol. 17:1  Jan-Mar-2014
1
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Neema: CPB during pregnancy – Fetal demise: An enigma
across the placenta but reduces O2 release to the tissues.
The fetal PO2 is low (30 mmHg) and is a part of the
mechanism to keep the ductus patent and pulmonary
vascular bed constricted. The blood in the umbilical
vein is about 80% saturated and in the ascending aorta
about 65%.[8] The umbilical vein blood because of
streaming effect preferentially enters the left ventricle
and is supplied to myocardium and brain,[8] whereas
the blood returning from superior and inferior vena
cava enters the right ventricle and is supplied to lower
half of body including placenta (for oxygenation) via
ductus arteriosus.
During management of a pregnant woman undergoing
cardiac surgery with CPB, the key issue to be addressed
is whether the O2 demand of the growing fetus at a
given gestation period is adequate. How do we know
that the needs of the fetus during CPB are adequately
fulfilled? In other words how does one monitor
adequacy/inadequacy of supply. Finally, what are the
measures available to fulfil fetal demands (increase O2
supply) if the supply is compromised? There is a need
to investigate a few more areas such as: does a change in
physical characteristics of CPB prime lead to a change
in characteristics of the fetal blood? Does it lead to fetal
intravascular volume expansion and fetal interstitial
edema? What are the clinical implications of such
changes? Will addition of albumin to CPB prime help?
Until recently, the only parameter available to know
adequacy/inadequacy of O2 supply to the fetus during
CPB was fetal heart rate (FHR). It should be realized
that at present, we are unable to manipulate fetal
circulation directly; we can only manipulate the CPB
flow and MAP and can assume that the increase in
CPB flow and MAP will enhance the placental flow
with well-oxygenated blood, will favorably change
the fetal oxygenation and circulation and correct the
fetal bradycardia. In this issue of Annals of Cardiac
Anaesthesia, Kapoor,[9] reviews basic principles of CPB
during pregnancy and Mishra et al.[10] describe utility
of transvaginal umbilical artery Doppler velocitymetry
indices in two pregnant women undergoing mitral
valve replacement with CPB and analyzed correlation
between FHR and resistivity index (RI) and pulsatility
index (PI) to evaluate adequacy of fetal blood flow.
The PI is defined as the difference between the peak
systolic velocity (PSV) and end diastolic velocity (EDV)
and divided by the mean velocity. The RI is defined as
the difference between the PSV and EDV divided by
the PSV. Both the indices are indicators of placental
2
resistance and their increased values indicate increased
placental vascular resistance, which may be treated
by vasodilators and uterine relaxants. Apparently, the
transvaginal umbilical artery Doppler velocitymetry
indices provide a therapeutic window. In the described
case 2, RI and PI were significantly raised, the MAP
was <50 mmHg and the FHR was <50/min. In such
a scenario, treating raised PI and RI by a vasodilator
is a difficult decision. Umbilical vasoconstriction can
occur as a part of fetal stress as a part of release of fetal
stress hormones which manifest as bradycardia and
increase in PI and RI. The management of umbilical
vasoconstriction is not clear. Perhaps, the solution lies
somewhere in the characteristics of the CPB prime and
the conduct of CPB. Hypothermia, hemoglobinopathies,
hypovolemia, hypotension, low cardiac output,
New York Heart Association functional class IV, etc.,
adversely affects fetal development and are associated
with adverse fetal outcome. 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. [11] Apparently, normothermic
CPB, pulsatile flow, keeping hematocrit and MAP at
or above preoperative basal values of the individuals,
could be the goals of CPB during pregnancy. The CPB
flow should take into account the fetal combined
ventricular cardiac output also, which is about 210 ml/
min at mid-gestation and 1900 ml/min at 38 weeks. [12]
Colloid oncotic pressure of the CPB prime may be
an important issue; however, there are no reports
available on this issue, but similar to hematocrit and
flow, it may be prudent to keep it close to basal values.
The majority of the reports and available literature
repeatedly show occurrence of fetal bradycardia at
the initiation of CPB secondary to hypoxemia. Earlier
the author of this editorial and his colleagues have
described a method of controlled initiation of CPB in a
child with aneurysmal main and left pulmonary artery
severe right pulmonary artery stenosis and atrial septal
defect undergoing right pulmonary artery plasty and
atrial septal defect closure.[13] The method consists of
standard aortic and bicaval cannulation and partial
clamping (about two-third clamp) of the venous drain
line; initially, low flow CPB is established with the
partially occluded main venous line and the MAP is
monitored. If the MAP remains stable, the venous clamp
is released little more and in this manner, gradually, the
total bypass is established. However, if the MAP value
decrease precipitously, the venous drain line occlusion
is further increased, the partial bypass and low tidal
Annals of Cardiac Anaesthesia  Vol. 17:1  Jan-Mar-2014
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Neema: CPB during pregnancy – Fetal demise: An enigma
volume ventilation is continued. Once, hemodynamics
stabilizes, a similar exercise is repeated. This strategy
maintains the pulsatile blood flow, provides time for
mixing of CPB prime and patients’ blood and raises
the perfusion pressure. The same technique can be
applied in pregnant women for surgery under CPB and
the establishment of CPB can be guided by the FHR.
Praveen Kumar Neema
Professor and Head, Department of Anaesthesiology,
All India Institute of Medical Sciences Raipur, Chhattisgarh, India
REFERENCES
1.
Dubourg G, Broustet P, Bricaud H, Fontan F, Trarieux M, Fontanille P.
Complete correction of a triad of Fallot, in extracorporeal circulation,
in a pregnant woman. Arch Mal Coeur Vaiss 1959;52:1389-91.
2. Mahli A, Izdes S, Coskun D. Cardiac operations during pregnancy:
Review of factors influencing fetal outcome. Ann Thorac Surg
2000;69:1622-6.
3. Davies GA, Herbert WN. Congenital heart disease in pregnancy. J Obstet
Gynaecol Can 2007;29:409-14.
4. Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascular
system. Int J Cardiol 2005;98:179-89.
Annals of Cardiac Anaesthesia  Vol. 17:1  Jan-Mar-2014
5. John AS, Gurley F, Schaff HV, Warnes CA, Phillips SD, Arendt KW,
et al. Cardiopulmonary bypass during pregnancy. Ann Thorac Surg
2011;91:1191-6.
6. Vedrinne C, Tronc F, Martinot S, Robin J, Allevard AM, Vincent M, et al.
Better preservation of endothelial function and decreased activation of
the fetal renin-angiotensin pathway with the use of pulsatile flow during
experimental fetal bypass. J Thorac Cardiovasc Surg 2000;120:770-7.
7. Chandrasekhar S, Cook CR, Collard CD. Cardiac surgery in the
parturient. Anesth Analg 2009;108:777-85.
8. Dawes GS, Mott JC, Widdicombe JG. The foetal circulation in the lamb.
J Physiol 1954;126:563-87.
9. Kapoor MC. Cardiopulmonary bypass in pregnancy. Ann Card Anaesth
2014;17:33-9.
10. Mishra M, Sawhney R, Kumar A, Bapna KR, Kohli V, Wasir H, et al. Cardiac
surgery during pregnancy: Continuous fetal monitoring using umbilical
artery Doppler flow velocity indices. Ann Card Anaesth 2014;17:46-51.
11. Pomini F, Mercogliano D, Cavalletti C, Caruso A, Pomini P. Cardiopulmonary
bypass in pregnancy. Ann Thorac Surg 1996;61:259-68.
12. Rasanen J, Wood DC, Weiner S, Ludomirski A, Huhta JC. Role of the
pulmonary circulation in the distribution of human fetal cardiac output
during the second half of pregnancy. Circulation 1996;94:1068-73.
13. Neema PK, Dharan BS, Singha S, Sethuraman M, Chandran DA, Rathod
RC. Anesthetic implications of aneurysmal main pulmonary artery and
left pulmonary artery and right pulmonary artery stenosis in a child
undergoing main pulmonary artery and right pulmonary artery plasty and
atrial septal defect closure. J Cardiothorac Vasc Anesth 2012;26:280-2.
Cite this article as: Neema PK. Cardiopulmonary bypass during pregnancy
- Fetal demise: An enigma. Ann Card Anaesth 2014;17:1-3.
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