BACKGROUND

Cardiac surgery with extracorporeal support in a pregnant patient constitutes a more complex undertaking, because it represents the sum of anesthetic, surgical and cardiopulmonary bypass effects on two organisms under biologically distinct situations, the maternal and the fetal organisms. It is not unusual for a cardiac team to be required to manage opposite or conflicting interests between both of those organisms.

While maternal mortality for a particular operation is similar to that for nonpregnant women of the same age group, a relationship could be observed between the operation performed and fetal outcome. Complexity of an operation and CPB duration directly affects fetal mortality.

The coincidence of cardiovascular disease and pregnancy has decreased over the last two decades. An average international figure can be represented by an incidence of 1 to 4% of maternal cardiovascular disease during pregnancy.

CPB - FIRST TRIMESTER OF PREGNANCY

Although there is no proven relationship between the gestational age of the fetus and mortality, there is a potential risk of the occurrence of congenital malformations, when cardiopulmonary bypass is performed during the first trimester. The risks of teratogenesis due to drug administration and possibly due to cardiopulmonary bypass during the first trimester of pregnancy are always of concern.

CPB - SECOND TRIMESTER OF PREGNANCY

Cardiopulmonary bypass during the second trimester has been associated with less complications. Fetal development is completed and the chances of fetal malformations are reduced. Also uterine excitability seems to be at the lowest level during second trimester of pregnancy.

CPB - THRID TRIMESTER OF PREGNANCY

Operations with the use of CPB performed during the third trimester have been associated with a high incidence of premature labor. At this stage the maternal hemodynamic overload is also of a greater magnitude.

Recent progresses in neonatal care have improved survival of premature infants with gestational age over 28 weeks. For this reason a few authors have performed a cesarean section to deliver the infant after heparinization and cannulation of the mother but before commencing CPB.

In our days, at the third trimester, delivery before cardiopulmonary bypass can be advocated in order to avoid fetal distress from perfusion.

EFFECTS OF CPB ON THE PREGNANT UTERUS

Uterine contractions occur frequently during cardiopulmonary bypass and are considered to be the most important predictor of fetal death. The contractions are more prone to occur during rewarming. Hypothermia can produce acid-base changes, arrhythmias and uterine contractions. Whenever possible, normothermic cardiopulmonary bypass should be the first choice for a pregnant patient.

Contractions are prone to occur during the third trimester. The cause is still unknown but it is speculated that the contractions result from dilution of progesterone and other gestational hormones. Supplemental progesterone has been suggested to stabilize the uterus around the time of bypass. Some other authors have recommended the use of beta2-agonists agents such as ritodrine or isoxsuprine to cease the uterine contractions.

FETAL RESPONSE TO CPB

Cardiopulmonary bypass produce fetal changes that depend of alterations in the placenta as a consequence of hypotension and vasoconstriction. Both can greatly reduce fetal oxygenation. The most common fetal reaction is bradycardia, which very often occurs after a few minutes of CPB. Bradycardia is an indication of fetal distress and should be criteriously identified and managed. Bradycardia at the beginning of bypass may be related to a decreased fetal oxygenation secondary to placental hypotension or to acid-base changes. Hypothermia is another cause for bradycardia. Starting normothermic CPB with a high perfusion flow avoids the occurrence of fetal bradycardia.

Fetal bradycardia has consistently been related to hemodynamic changes and reduced efficiency of gas exchange at the placental interface. The adequate perfusion of placental tissue can avoid changes in fetal cardiac rate. The lack of an arterial pulse in addition to the arterial hypotension develops a state of placental hypoperfusion which reduces the efficiency of gas exchange with fetal blood. The fetus becomes hypoxic and the first manifestation is bradycardia.

Normal fetal heart rate is usually within the range of 120-160 bpm. Frequently, during CPB, the fetal heart rate decreases to 100-115 bpm but, occasionally this drop may be accentuated and heart rates of 70-80 bpm are encountered. This level of bradycardia represents a considerable degree of fetal distress.

UTERINE AND FETAL MONITORING DURING CPB

Cardiopulmonary bypass effects on the fetoplacental unit can contribute to interrupt pregnancy and to determine fetal death. In order to prevent fetal bradycardia and distress it is mandatory the addition of fetal monitoring to the CBP protocol. Since uterine contractions or increased tonus contribute to fetal discomfort and distress, uterine activity should also be monitored during CPB. An obstetrician should be available in the operationg room to monitor and adjust uterin and fetal parameters.

CONDUCT OF CARDIOPULMONARY BYPASS

Monitoring uterine activity and fetal heart rate can offer valuable information to the perfusionist as to the placental blood flow and perfusion. These last parameters can be optimized by adjustments of perfusion flow and arterial PO2.

POSITIONING ON THE OPERATING TABLE

Particularly during the third trimester, after induction of anesthesia, the patient should be positioned with 30 to 60 degrees right lateral pelvic tilt, to eliminate the inferior vena cava compression by the relaxed uterus, which can reduce venous return and cause arterial hypotension.

ANTICOAGULATION

Heparin does not cross fetoplacental barrier and cannot exert any anticoagulant effect on the fetus. Heparin monitoring should be closely followed and an ACT between 480 and 600 seconds is recommended for CPB on a pregnant patient. There is a small potential risk of placental bleeding.

PRIMING

Pregnant patients can have anemia and a lower oncotic pressure. Perfusate volume should be the minimum necessary to initiate bypass. Crystalloid hemodilution is used with success, but there has been reports of fetal distress with low hematocrit. A better environment for the fetus is represented by a perfusion hematocrit above 25%. Ideal hematocrit for a normothermic bypass is between 30 to 34%. Adding colloids favor tissue perfusion and contribute to avoid interstitial edema.

Mannitol crosses the placental barrier and can stimulate fetal diuresis on amniotic fluid. Diuretics should be very cautiously used during CPB. Furosemide is preferred to mannitol for its less dramatic effect on fetal diuresis.

An oncotically adjusted prime makes addition of mannitol or furosemide unnecessary and can avoid untoward effects of diuretics on the fetus.

Perfusate pH and temperature should be adjusted before starting bypass to avoid sudden reduction of placental blood flow and to preserve optimal fetal-maternal exchanges.

PUMP FLOW

Higher perfusion flow rates are recommended for CPB during pregnancy and objectives to sustain an adequate fetoplacental gas exchange during nonpulsatile flow. Pump flow varies between 2.5 and 2.7 l/min/m2 which should be equivalent to about 60 to 80 ml/kg/min. Arterial flow should essentially be 20-40% higher than flows used for routine CPB in nonpregnant patients.

MEAN ARTERIAL PRESSURE

Pump flow should be sufficient to maintain a mean arterial pressure above 70 mmHg (70-90 mmHg). However, the best demonstration of an adequate arterial pressure is the fetal response to CPB.

Fetal bradycardia is an indication to elevate perfusion flow (and pressure) in order to increase placental blood flow. During the average CPB on a pregnant patient, high perfusion flow, high mean arterial pressure and a normal cardiotocography usually present a clear correlation.

GAS FLOW

CPB during pregnancy is conducted with a higher FiO2 to produce an arterial PO2 of at least 200 mmHg.

If fetal bradycardia occurs arterial PO2 should be elevated to about 400 mmHg along with other measures such as increasing perfusion flow and pressure. This high maternal arterial PO2 does not affect fetal organs. Fetal arterial saturation will remain normal, according to the fetal pattern and will not contribute to produce any ill effect.

HYPOTHERMIA

Even mild degrees of hypothermia can increase uterine tone and contractions and elevate uterine vascular resistance. Fetal mortality is higher when CPB is conducted with hypothermia. Maternal bradycardia, ventricular arrhythmias, and fibrillation are more common during hypothermia.

Significant hypothermia should be avoided unless extended aortic clamp times are anticipated or a circulatory arrest period is required. During hypothermia there is reduced gas exchange at the placental level. Rewarming produces uterine contractions and increases amniotic fluid pressure.

VASOACTIVE DRUGS

Under a few circumstances it may become necessary to administer vasoactive drugs to adjust maternal arterial pressure or resistance. Blood flow to the uterus is under a strong alfa-adrenergic control. Vasopressors with alfa-adrenergic receptors effect can reduce uterine and placental blood flow. Efedrin does not influence uterine flow. The same occurs with a low-dose infusion of dopamine (< 5 mcg/kg/min).

Administration of isoproterenol has been recommended as the inotrope of choice, soon after bypass. This drug has also a positive effect on maternal and fetal heart rate.

Whenever a peripheral vasodilatory effect is required during CPB, an infusion of hidralazine can be administered without any untoward effect. This drug can produce a 20-30% reduction on mean arterial pressure and at the same time increase renal, uterine and placental blood flow. Recommended initial dose is 1.5 mcg/kg/min, to be adjusted according to the hemodynamic response.

ACID-BASE MANAGEMENT

Acid-base disturbances are not well tolerated by the fetus as they alter gas exchange efficiency at the placental level. Normothermic CPB favors monitoring and managing acid-base status and significant changes are less prone to occur. Metabolic acidosis as a consequence of reduced tissue perfusion and respiratory alkalosis secondary to excessive gas flow in the oxygenator are about the only changes seen. Both can easily be corrected by adjusting perfusion and gas flow without having to resort to any drugs.

MYOCARDIAL PROTECTION

Regardless of the type of cardioplegia and the administration route (antegrade, retrograde or combined), the cardioplegia efluent should be aspirated from the right atrium (or coronary ostia) to avoid its mixing to the perfusate. The hyperkalemia secondary to the cardioplegia infusion affects the fetal myocardium and produce bradycardia, conduction disturbances or cardiac arrest. High potassium levels in maternal blood accentuates diffusion to fetal blood at the placental corionic villi and originates fetal hyperkalemia. This is particularly important during long procedures and with the use of continuous cardioplegia.

MANAGEMENT OF FETAL BRADYCARDIA

During CPB the occurrence of severe fetal bradycardia indicates fetal distress. Increasing arterial pump flow and FiO2 usually is all that is necessary to correct the bradycardia. If, despite those measures fetal heart rate remains low, a small drip of efedrin may be required. Correcting any degree of metabolic acidosis will have the same result. In a few cases, despite all management, fetal bradycardia persists for the duration of CPB and reverts when normal circulation is resumed.

When the bradycardia prolongs to the immediate postoperative period, the risk of fetal death is substantially increased.

MANAGEMENT OF UTERIN CONTRACTIONS

Prolonged and intense contractions are associated with a higher incidence of fetal death. Dilution of pregnancy hormones, such as progesterone has been suggested to be responsible for the increase uterine activity. Arterial hypotension, hypothermia and rewarming can also induce uterine contractions. Excessive uterine activity produces placental insufficiency and fetal hypoxia and distress.

Some beta-agonist agents can cease uterine contractions. Ritodrin is commonly indicated in those circumstances and is very effective to abolish uterine contractions, as an infusion of 50-150 mcg/min and should be maintained for at least 12 hours. Another effective agent is terbutaline in the dose of 10 mcg/min which can be increased as necessary up to 80 mcg/min and should be continued for 4 hours. Venous infusion of alcohol is effective to abolish uterine contractions in the experimental setting but has not been clinically used.

CONCLUSIONS

Cardiopulmonary bypass during pregnancy carries a high risk of fetal morbidity and mortality. Preparation and management of CPB for a pregnant patient should be oriented towards the avoidance of any sudden changes of placental blood flow. Fetal bradycardia is the earliest indication of fetal distress and must be aggressively managed. Uterine contractions can also be detrimental to the optimal placental perfusion and should be abolished by tocolytic agents if necessary.