Review 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. Access this article online
Website: www.annals.in PMID: *** DOI: 10.4103/0971-9784.124133 Quick Response Code:
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: [email protected]
Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
33
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 Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
Kapoor: CPB in pregnancy
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 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. 37
Kapoor: CPB in pregnancy
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Kapoor: CPB in pregnancy 48. Pavankumar P, Venugopal P, Kaul U, Iyer KS, Das B, Sampathkumar A, et al. Closed mitral valvotomy during pregnancy. A 20‑year experience. Scand J Thorac Cardiovasc Surg 1988;22:11‑5. 49. Weiss BM, von Segesser LK, Alon E, Seifert B, Turina MI. Outcome of cardiovascular surgery and pregnancy: A systematic review of the period 1984‑1996. Am J Obstet Gynecol 1998;179:1643‑53. 50. Nazarian M, McCullough GH, Fielder DL. Bacterial endocarditis in pregnancy: Successful surgical correction. J Thorac Cardiovasc Surg 1976;71:880‑3. 51. Salazar E, Zajarias A, Gutierrez N, Iturbe I. The problem of cardiac valve prostheses, anticoagulants, and pregnancy. Circulation 1984;70:I169‑77. 52. Qasqas SA, McPherson C, Frishman WH, Elkayam U. Cardiovascular pharmacotherapeutic considerations during pregnancy and lactation.
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Cardiol Rev 2004;12:240‑61. 53. Kole SD, Jain SM, Walia A, Sharma M. Cardiopulmonary bypass in pregnancy. Ann Thorac Surg 1997;63:915‑6. 54. Arnoni AS, Andrade J, Falcão HCB, Souza SCS. Cardiac Surgery in Pregnancy. Rev Bras Cir Cardiovasc 1986;1:14-9. 55. Crowther CA, Harding JE. Repeat doses of prenatal corticosteroids for women at risk of preterm birth for preventing neonatal respiratory disease. Cochrane Database Syst Rev 2007;3:CD003935. 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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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. Access this article online
Website: www.annals.in PMID: *** DOI: 10.4103/0971-9784.124133 Quick Response Code:
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: [email protected]
Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
33
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 Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
Kapoor: CPB in pregnancy
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 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. 37
Kapoor: CPB in pregnancy
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