Page 28 - ANZCP Gazette APRIL 2022

Pre-CPB Considerations
Fetal Haemoglobin
Timing of Surgery
If surgical intervention becomes necessary during the pregnancy, the first consideration should be the timing of the operation. If viable, the fetal outcome will be best if delivery can occur before the operation rather than post surgery. The risks of fetal morbidity and mortality, if the mother is placed on CPB, are 9% and 30% respectively (6). The WRH patient had a preoperative functional status of NYHA class IV which has been associated with a 66% fetal mortality risk (7). There does not seem to be any increased maternal risk due to pregnancy over non-pregnant patients (8).
A gestational period of 24 weeks onwards can progress to a survivable delivery; however, the risk of delaying intervention may be too great for the mother. The 2nd trimester is thought to be the optimal time to perform the procedure if surgery is required prior to delivery. This is because maternal physiologic haematologic/haemodynamic changes have not peaked, uterine excitability is least, aorto-caval compression is not seen and fetal organogenesis is in an advanced safer stage (9).
At WRH the survival rate for a preterm delivery at 24 weeks is currently around 75%, with every additional day rapidly increasing this percentage, so from this stage onwards it is likely that the fetus would be delivered prior to cardiac surgery. Ideally, delivery would occur at least a couple of days prior to surgery due to the risk of bleeding upon heparinisation post caesarean section (CS). However, in a review of 21 cardiac cases performed on pregnant patients at the Mayo Clinic, seven patients underwent CS immediately prior to cardiothoracic surgery without major complication. These patients did require additional blood products, with a median blood loss during CS of 800 ml, although there was no excessive bleeding necessitating prolonged packing of the abdominal wound or hysterectomy (10).
Fetal Blood Saturation
The oxygen saturation of fetal arterial blood is typically less than that seen in adults. This is due to the differences in fetal circulation. The placenta is the site of blood oxygenation, nutrient uptake and removal of waste products rather than the lungs. Oxygenated blood leaves the placenta via the umbilical vein. A quarter of this blood goes through the first of the fetal shunts, the ductus venosus, to the IVC. The remainder of the blood goes to the liver via the portal vein and then to the IVC via the hepatic vein. Blood reaches the right atrium and bypasses the lungs via the second of the shunts, the foramen ovale, which allows blood to pass from the RA to the LA. Not all the blood leaving the RA goes via the foramen ovale, some still enters the RV and exits via the PA. The third shunt, the ductus arteriosus, permits blood to cross from the PA to the aorta due to high pulmonary vascular resistance. The loop is completed when blood leaves the internal iliac arteries and flows along the umbilical arteries back to the placenta. See Figure 1. The mixing of arterial and venous blood in the fetal circulation accounts for the lower arterial blood saturation.

Another difference to normal adult circulation is encountered in the haemoglobin of the fetus. Fetal haemoglobin has a much greater affinity for oxygen than adult haemoglobin. This is due to differences in 2-3 bisphosphoglycerate (2-3 BPG) levels. When 2-3 BPG binds to Hb it lowers the affinity for oxygen. Fetal Hb has a different amino acid present at the binding site for 2-3 BPG which creates less interaction than adult Hb. Fetal Hb shifts the oxygen dissociation curve to the left so that it can bind oxygen at a lower partial pressure. This is important because by the time the maternal blood reaches the placenta some of the oxygen has already been utilised, therefore it is less saturated than when it leaves the lungs. During pregnancy the maternal levels of 2-3 BPG increase which further exaggerates the difference in affinity for oxygen at the placenta.
Fetal Cardiac Output
In a study on fetal sheep, Gilbert tested the impact of volume changes on fetal CO (12). He found that volume increases gave only very small increases in CO, suggesting that the fetal heart is operating at the upper limit of its Starling function curve. As a result, there is very little cardiac reserve for increases in fetal CO. This means that fetal CO is rate dependent, so fetal bradycardia results in fetal stress (8).
Fetal and Uterine Monitoring
In theory, it would be beneficial to monitor the fetal heart rate and to monitor for uterine contractions during CPB. Fetal bradycardia is linked to fetal stress during CPB so fetal heart rate should be maintained between 110 and 160 beats/min (13). Sustained and forceful uterine contractions, that occur frequently during cardiac surgery and CPB, are considered as the most important contributor to fetal death (14)(15).
In practice, there are many limitations to monitoring devices that are currently available. The fetus in our patient was at 14
25 APRIL 2022 | www.anzcp.org