Page 30 - ANZCP Gazette APRIL 2022
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The patient measured 169 cm and weighed 97 kg with a body surface area of 2.07 m2. Using WRH’s standard cardiac index of 2.4 L/min/m2, the calculated flow would be 4.97 L/ min. Adopting a modified cardiac index of 3.0 L/min/m2, in consideration of fetal circulation, the calculated flow for this patient was 6.2 L/min.
To avoid uterine displacement the patient can be placed in a 150 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 patient with a fetus over 20 weeks gestational age to avoid impairment of utero-placental blood flow (10). As the fetus was only at 14 weeks gestation this was not required. Fetal monitoring was not used owing to the early stage of pregnancy.
The CPB circuit was primed with 1500 ml Plasmalyte which was reduced to 1000 ml after 500 ml was removed with a pre-bypass retrograde autologous prime (RAP). WRH perfusionists attempt to RAP every patient as long as they remain haemodynamically stable. As the materno-fetal unit is very sensitive to reductions in flow and pressure, there should be a low threshold to discontinue RAP if the patient begins to become even slightly unstable. 10,000 units of heparin and 1g Cephazolin are added to the prime prior to initiating CPB.
Anaesthesia aimed to maintain physiological norms for the stage of pregnancy, with slight hypocapnia and increased minute ventilation, to mimic the mild hypocapnia which can occur during pregnancy. This is from the stimulatory effects of the increased circulating progesterone and oestrogen on central and peripheral chemoreflex drivers to breathe (34). During CPB, alpha-stat pH management is recommended for the maintenance of CO2 homeostasis and uteroplacental blood flow (35) (36). This is because maternal hypocapnia causes uteroplacental vasoconstriction (9) and reduced uterine flow which can lead to fetal acidosis. Maternal hypercapnia directly results in fetal respiratory acidosis as well as increased uteroplacental blood flow. Severe fetal respiratory acidosis causes myocardial depression (37).
The patient's pre-bypass gas was unremarkable, with a haemoglobin of 122 g/L, potassium of 3.6 mmol and activated clotting time of 104 seconds. After heparinisation and a pre- bypass ACT of 537 seconds, bypass was initiated. Due to the hypercoagulable state (an adaptive mechanism to prevent postpartum bleeding) and the extra circulating volume of pregnancy, a larger dose of heparin may be required to achieve a desirable pre-bypass ACT. It may also be useful to monitor ACTs more frequently than normal during CPB. An additional 10,000 units of heparin were added to the circuit at 70 mins and 110 mins CPB time after the ACTs dropped below 480 seconds. Due to the anticipated higher circulating volume encountered during pregnancy, there was an empty bag ready to take off extra volume from the reservoir upon initiation of CPB if necessary. In actuality there were only normal volume levels seen in the venous reservoir once on CPB; this may not have been the case if the pregnancy had been closer to the end of the second trimester. After going on bypass, flows were maintained between 6.6–6.8 L/m. Almost reliably, when the mother is placed on bypass, the fetus will develop bradycardia (17). This makes it important to set high CPB flows from the onset. Additionally, the sudden hemodilution experienced upon CPB initiation may lead to uterine muscle excitability. The excitability of uterine muscle is probably enhanced by
hormonal dilution, mainly by the dilution of progesterone (30).
As soon as CPB was stable, the patient was cooled to 340C. During hypothermia, gas exchange is decreased at the placental level due to increased uterine tone and contraction (23). Normothermic perfusion during CPB is recommended when feasible (38). The rewarm can be particularly risky to the status of the fetus as uterine contractions are common at this stage. If the patient is kept relatively warm then it obviates the need for a lengthy rewarm.
Tepid blood cardioplegia was delivered into the aortic root at our standard microplegia induction dose concentration of 400 ml/hr, flowing at 350 ml/min. Due to delayed arrest, cardioplegia was delivered antegrade into the root, retrograde through the coronary sinus and directly into the left and right coronary ostia. When asystole was achieved the maintenance dose of 200 ml/hr was applied every 20 minutes or so, in a retrograde fashion, and there was no breakthrough activity.
Maternal hyperkalemia can directly lead to fetal hyperkalemia as potassium can pass across the placenta to the fetal circulation. Fetal hyperkalemia can cause conduction disturbances and may even initiate fetal cardiac arrest – for this reason serum potassium needs to be closely monitored with the goal to stay below 5 mmol/L (9). This can be difficult as during pregnancy potassium levels will rise. In a study on pregnant women, Tomala, Mercogliano and Cavaletti found that mean potassium levels were 4.25, 5.83 and 5.95 mmol/l during the first, second and third trimester respectively (39).
To prevent high serum potassium levels during CPB, zero- balance ultrafiltration (ZBUF) was used with Hemosol BO as the replacement fluid; a total of 3 L was used during the case. The arterial blood gas (ABG) serum potassium results remained below 4.2 mmol/L throughout the procedure. Another strategy to keep maternal potassium levels under control is to scavenge the cardioplegia upon delivery. Arnoni et al (7) recommend using bicaval cannulation so that the right atrium can be opened and cardioplegia scavenged. This makes sense during the more common mitral surgery associated with pregnancy, which already necessitates bicaval cannulation. Also, predominant use of antegrade cardioplegia is feasible as there is likely to be a competent aortic valve. However, as our procedure required an aortotomy, the plan was to predominantly use retrograde cardioplegia and to scavenge it from the aortic root if maternal serum potassium began to trend too high. During the case a Livanova Xtra cell saver was available which Livanova claims will remove more than 95% potassium in POPT mode and more than 92% potassium in PSTD mode. Fresenius Kabi claims that the CATSmart cell saver will remove up to 94% potassium. The potassium during the case remained under control using ZBUF, therefore cardioplegia was not scavenged.
The obvious negative of scavenging to the cell saver is the loss of factors other than red blood cells. This makes the use of Del Nido cardioplegia a useful alternative if not already used. The lower ratio of blood to cardioplegia means less blood products will be lost to the cell saver if scavenging. As a comparison, during the 109 minute cross clamp period there was roughly 3.5 L of blood given using Wellington microplegia, whereas only 300 ml of blood would be given using Del Nido cardioplegia. It would have been fine to scavenge the total amount of Del Nido, but the blood product loss with Wellington microplegia
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