Year : 2014  |  Volume : 17  |  Issue : 1  |  Page : 33--39

Cardiopulmonary bypass in pregnancy

Mukul Chandra Kapoor 
 Department of Anesthesia, Saket City Hospital, Saket, New Delhi, India

Correspondence Address:
Mukul Chandra Kapoor
Department of Anesthesia, Saket City Hospital, Press Enclave Road, Saket, New Delhi - 110 017


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.

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Kapoor MC. Cardiopulmonary bypass in pregnancy.Ann Card Anaesth 2014;17:33-39

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Kapoor MC. Cardiopulmonary bypass in pregnancy. Ann Card Anaesth [serial online] 2014 [cited 2020 Oct 1 ];17:33-39
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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.

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].{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.

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 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

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]

Fetal circulation during CPB has not been 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 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]

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],[29],[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 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

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 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 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 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 13 th and 28 th 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 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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