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Ann Thorac Surg 1996;61:259-268
© 1996 The Society of Thoracic Surgeons
Department of Obstetrics and Gynecology, ``Università Cattolica del Sacro Cuore,'' Institute for Biomedical Technologies, National Council of Research, and Department of Neurology, University of Rome ``La Sapienza,'' Rome, Italy
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Abstract |
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 TopFootnotes Abstract IntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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Introduction |
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TopFootnotesAbstractIntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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Open heart operation implies a number of techniques that, in theory, could compromise the biological homeostasis of the fetoplacental system: hypothermia, hemodilution, inhibition of coagulation, and continuous blood flow. The patient on cardiopulmonary bypass (CPB) is in a precarious state as far as arterial pressure, hemostasis, and the acid–base status are concerned. Hemolysis and thrombocytolysis can result in the production of toxic substances, and transfusions can cause unpredictable alterations in the immune system of the fetus, which perhaps could be responsible for long-term complications.
The goal of this article is to compare, in the light of the knowledge available today, the biological, parameters of the mother–placenta–fetus system to the upset caused by CPB, to try to produce evidence of eventual incompatibilities and evaluate how these can be overcome.
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Cardiopulmonary Bypass Physiopathology and Pregnancy |
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Table 1
shows our review of the literature. The Index Medicus covering the period between 1970 and 1991 was consulted regarding the following entries: cardiopulmonary bypass; pregnancy-complication-cardiovascular; and heart surgery, hypothermiatab 1. The references of every article were examined to update the list of the reports. During the research we have also found several reviews of literature [2–11].
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does not include a case report in which Daley and co-workers [52] in 1956 subjected a 3-month pregnant woman to open pulmonary commissurotomy, without the auxiliary help of CPB. Not many facts are available about this case. The total circulatory arrest lasted 3 minutes; the esophageal temperature was 32°C. The pregnancy was carried to term and the baby delivered was normal also on follow-up.
The data in Table 1 were processed and analyzed in an attempt to show eventual statistically significant correlations. We consider the factors that regulate or influence the placental perfusion and oxygenation of fetal tissues. A number of such factors are closely linked and depend on one another.
Quantity of Pump Flow
Farmakides and co-workers [39] (patient 49) studied the blood flow of the uterine arteries using Doppler ultrasonography during CPB for open mitral commissurotomy at 23 weeks of pregnancy. After operation the pregnancy continued physiologically with a normal vaginal delivery at term. No problems were noted with the fetus. The article carries photographs of the flow velocity waves in one of the uterine arteries before, during, and after CPB. During CPB the flow does not have a constant velocity, as would be expected, but there are frequent waves of accelerated flow. A roller pump was used, which maintains a continuous flow, but transmits pulsations that might be perceived by the authors as from the Doppler. The flow wave demonstrated the presence of a ``diastolic'' flow between the peaks. It is difficult to explain the transitory increase of uterine resistance (S/D ratio) found after operation, lasting 48 hours, perhaps influenced by factors produced during CPB. The correlation between the high flow during CPB, the high mean arterial pressure (MAP) (85/95 mm Hg), and the normal cardiotocography (CTG), together with a favorable outcome for the fetus is notable (even if no long-term follow-up is reported).
Hawkins and co-workers [53] subjected lamb fetuses to extracorporeal circulation in normothermia and in hypothermia using the placenta as an oxygenator. Each animal was subjected to three different flow velocities (50, 70, and 100 mL • kg-1 • min-1) for 10 minutes. The partial gas pressures, O2 saturation, and fetal MAP were examined. As far as the fetuses examined at 37°C are concerned, there is an evident increase of carbon dioxide tension at lower flows together with a slight decrease in oxygen tension similar to an alteration in the placental functions.
From the examination of the other reports, it is not possible to obtain useful data about the quantity of flow because only a few researchers report the cardiac index so as to permit comparison between studies (Table 1).
Continuous/Pulsating Pump Flow
None of the researchers in Table 1 used a pulsating pump. There are several studies that take into consideration aortic coarctation during pregnancy. Because the flow after coarctation has a reduced differential pressure, it could be considered a continuous flow. The data reported are scarce and contrasting as far as the outcome of the pregnancy is concerned.
Mortensen and Ellsworth [54], examining 32 pregnancies with aortic coarctation, report a 90.6% rate of ``complicated pregnancies'' of which 68.7% are due to gynecologic complications. On the other hand, regarding 21 pregnancies in which the lesion was eliminated before the onset of pregnancy, they report only a 9.5% rate of gynecologic complications and 85.5% normal pregnancies.
In contrast, Pritchard [55], in a review of 79 patients, found that fetal mortality and morbidity rate in women suffering from coarctation is not significantly compromised, but the fetal–neonatal data available are too scarce to make adequate deductions.
First Minutes of Cardiopulmonary Bypass
An important event during CPB is the initial hypotension that occurs when the circulation goes from corporeal to extracorporeal. The collapse of peripheral resistance can bring about a rapid decrease of the arterial pressure and the obvious consequences on placental perfusion.
Almost all investigators who have monitored the fetus with CTG during this phase report anomalies that are correlated to the maternal hemodynamic parameters (Tables 1 and 2)tab 2.
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). Koh and co-workers [23] reported a light fetal bradycardia decrease to 110 to 120 beats/min during CPB in their first patient (patient 30). The CTG tracing was obtained only for 3 of the 70 minutes of extracorporeal circulation. After CPB the CTG was normal. A severe fetal bradycardia to 80 beats/min was audible immediately after starting the CPB in the second patient (patient 31) by the same researchers. The loss of variability is evident from the analysis of the reported trace. By increasing the pump flow from 3.1 to 3.6 L/min, the fetal heart rate increased to 120 beats/min. After CPB there was compensatory tachycardia up to 170 beats/min for a short time and with poor fetal heart rate variability. Then the CTG returned to normal. No problem was noted in the baby at birth.
Werch and Lambert [26] (patient 34) cleared up the fetal bradycardia and the late decelerations by increasing pump flow from 2.8 to 4.6 L/min.
In 1977 Levy and co-workers [27] (patient 35) reported open mitral operation in a woman 22 weeks pregnant. During the cannulation they corrected the maternal hypotension, which had provoked fetal bradycardia, with the infusion of ephedrine. The CTG monitored during the full period of CPB showed loss of long- and short-term variability, with serious bradycardia down to 70 to 80 beats/min. The low cardiac index of 60 mL • kg-1 • min-1 and the low maternal MAP of 60 mm Hg could explain the reduced supply of O2 to the fetus and, therefore, the CTG alteration. Hypothermia at 34°C probably contributed to the reduction of the basal fetal cardiac frequency (FCF), but it is not sufficient to explain the loss of variability. Once CPB was terminated, the FCF increased uniformly and rapidly up to 190 beats/min. At birth, in spite of the low gestational age, the baby seemed to be in excellent condition. There were no follow-up data.
Other researchers (patients 31, 35, 38, 39, 40, 43, and 62) report the CTG registration of fetal bradycardia as soon as CPB is begun. The bradycardia often persists for the total duration of CPB. Almost all the reports point out that, after the bradycardia, when the normal maternal circulation is restored, there is compensatory tachycardia. The compensatory tachycardia is more pronounced if the bradycardia has been particularly serious. The analysis of the variability of CTG depends on a subjective evaluation; some authors report a decrease or its disappearance.
Contrary to the above data, during the first operation performed by Lamb and co-workers [30] (patient 38), fetal bradycardia, present at the initial phase of CPB, persisted despite an increase in flow and disappeared spontaneously at CPB termination when the maternal circulation was restored. The MAP values were not reported.
Even in the operation performed by Trimakas and co-workers [31] (patient 40), the fetal bradycardia during CPB was not modified despite the increase in the MAP from 60 to 80 mm Hg. From an analysis of the CTG reported, the baseline variability is evident.
Some investigators listed in Table 2 do not report alterations in the CTG tracing during CPB (patients 36, 49, 50, 60, 61). Unfortunately the data reported are rather different with regard to flow, MAP, temperature, duration of operation, and week of pregnancy.
Two reports are rather peculiar. Burke and co-workers [51] (patient 63) refer to a sinusoidal pattern with the FCF oscillating between 120 and 150 beats/min. Having noticed the low MAP (25 to 30 mm Hg), in spite of the high cardiac rate of 3 L • m-2 • min-1, they proceed to increase it to 50 mm Hg with an infusion of 
-adrenergics, obtaining no modification in the CTG pattern. At the end of CPB the fetal cardiac activity returned to baseline, except for a reduced variability that persisted for several hours. The patient cardiac index, stimulated with drugs, was 3 L • m-2 • min-1.
Another case that merits attention concerns the patient of Izquierdo and co-workers [45] (patient 56), who subjected a patient suffering from early preeclampsia to open heart operation. The CTG during operation showed severe fetal distress and death of the fetus during one protracted uterine contraction.
Uterine Contractions
In some reports (patients 34, 41, 50, 55, 56, and 59), contractions during the CPB were observed. Some investigators also point out the presence of more or less serious deceleration that disappears in spite of the continuous contractions as soon as maternal circulation is restored.
The patient operated on by Lamb and co-workers [30] (patient 39), at the beginning of CPB, presented fetal bradycardia down to 70 beats/min. The basal FCF seems to increase to 160 beats/min after increasing the flow. At that point the tracing shows deep repetitive decelerations, which in their form and frequency seem to be caused by unknown uterine contractions (the CTG is not reported). Contractions are reported ``immediately after the end of the bypass.'' A clear index of O2 deficit is the presence of compensatory tachycardia after CPB.
Nagy and co-workers [40] (patient 50) report to have practiced CTG and fetal electrocardiography during CPB. In spite of the presence of contractions, they do not indicate cardiographic alterations with the exception of a decrease in the basal FCF, probably caused by a slight hypothermia. The circulatory parameters used during CPB are not recorded.
Priming
There are not many studies that allow us to make conclusions concerning the characteristics of this important parameter during CPB.
Conroy and co-workers [50] (patient 61) did not report any pathologic alteration of the CTG even if blood was not used either before or during CPB, with the hematocrit decreased to 18% due to hemodilution. The MAP values were not high. The pump flow was lower than the cardiac output measured before operation (6 L/min; after operation, 11 L/min). The only cardiographic alteration reported was a slight bradycardia. The basal FCF decreased to 110 beats/min at the beginning of CPB, then increased to 120 beats/min. When the physiologic conditions were resumed, it was 138 beats/min.
Hypothermia
There are few data available in the literature on hypothermia in pregnancy or on the effects produced on the uteroplacental circulation.
Assali and Westin [56] studied the effect of deep hypothermia in dogs at the end of pregnancy. During the cold phase a significant increase was noted in uterine resistance with a marked reduction in the hematic flow, independent of the cardiac output. The reduction of the flow can be related to the increase in the uterine tone as shown by the increase in the intraamniotic pressure. The causes of the uterine contractions are not explained.
Several recent studies have been carried out to evaluate intrauterine operation with the aid of hypothermia (ie, open heart operations on lamb fetuses placing them in CPB at the end of pregnancy but keeping the placenta as a gas exchange organ). All the studies proved that the placenta, if subjected to hypothermia in vivo, is not a good oxygenator in terms of hematic gases, transplacental flow, and flow to the fetal organs [53, 57–59].
Several operations carried out with the help of hypothermia in pregnant women have been reported. Hess and Davis [60] subjected a 37-week pregnant woman, suffering from a cerebral aneurysm, to neurosurgery with the aid of hypothermia. The time in hypothermia lasted 16 hours with the minimum temperature reaching 28°C. The FCF dropped even further after an episode of maternal hemorrhage and rose again after a transfusion and after the maternal pressure returned to normal. No abnormal conditions were found in the tone of the uterus either during or after operation. No problems were observed in bringing the pregnancy to term or when the baby was born. It is interesting to note that the fetus maintains the ability to autoregulate its cardiac activity even during hypothermia, as shown during the maternal hypotensive episode.
Vandewater and Paul [61] did not find any pathologic alterations in the pH or hematic gases in 9 sheep subjected to hypothermia. They concluded that placental functions remain intact.
In 1988, a case was reported of nephropyelitis in a 32-week pregnant woman in which the temperature decreased to 34°C. The FCF was monitored with cardiotocography showing only a serious bradycardia at 90 beats/min without the accompanying signs of fetal hypoxia and with FCF accelerations. Once the normothermia was reestablished, the FCF fell into normal values. Eventual contractile activity was not mentioned (nor was tocolytic therapy) [62].
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Comment |
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TopFootnotesAbstractIntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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tab 3. The year 1975 was selected because it is the median of the year range when the operations were performed.
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). With regard to the fetus, considering only the more recent cases, the combined rate of abortion and intrauterine death is low. The embryofetal morbidity rate is handicapped by incomplete follow-up data in many reports.
Quantity of Pump Flow
In the case of a pregnant woman who has to undergo operation with the help of CPB, the flow must be regulated higher than in a patient who is not pregnant so as to maintain an adequate perfusion to that sort of arteriovenous fistula that is the placenta [63]. To determine the correct quantity of flow, it is necessary to calculate the cardiac output of the patient at that particular moment of pregnancy. Because the influence of the CPB on the fetus is not 100% known [64], it cannot be presumed that it is possible to maintain an identical perfusion to the periphery of the fetus regulating a cardiac index during CPB identical to the situation before operation. To be certain of keeping the fetus in the proper physiologic conditions during CPB, therefore, it is necessary to: (1) evaluate the flow in the uterine arteries comparing it with normal values; (2) evaluate the degree of oxygenation of the fetal tissues; and (3) evaluate if a certain quantity of flow has or has not caused structural or functional alterations in the organs or the systems of the fetus in a long-term follow-up. All of the above should be done to eliminate the influence of eventual confusing factors that are in themselves capable of changing the placental or fetal perfusion.
From the reported data, it is not possible to extrapolate the optimal increase from the baseline flow of the patient to set the CPB. Because several fetuses did well during CPB and after delivery, we must assume that it is possible to maintain the fetus in good conditions. Due to the lack of data reported, especially regarding cardiac index, we have not been capable of determining any correlation between the quantity of flow during CPB and CTG or neonatal outcome.
Continuous/Pulsating Pump Flow
There are no experimental data on the type of flow to the placenta that would allow deductions concerning respiratory exchanges. Data extrapolated from patients with aortic coarctation are doubtful [54, 55]. The pulsations within the intervillous space may favor the exchanges of respiratory gases. The only advantage would seem to be that it is possible to remain close to the physiology of the fetus.
Cardiotocography
There are very few researchers who report data regarding fetal monitoring conditions and maternal metabolism, and all our knowledge has to be extrapolated from CTG.
The CTG analysis can be biased from false-positive data in several situations [65]. One fact that validates the criteria defining hypoxia is the compensatory tachycardia that often follows the fetal distress. It strongly suggests that during bradycardia the pH and O2 supply really decrease below normal conditions, so as to force the fetus to compensate.
Some of the investigators listed in Table 2 (patients 34, 36, 49, 50, 60, and 61) did not report serious CTG alteration caused by hypoxia during CPB. Data are too scant for a comparison and to determine rules in conducting CPB, but in these cases moderate or no hypothermia, high pump flow, and high maternal MAP were used.
Werch and Lambert [26] (patient 34) report ``a direct correlation between flow rate and fetal heart rate.'' After the considerable increase in pump flow, in spite of uterine contractions, a physiologic fetal heart rate pattern is manifest in the reported photograms.
The work of Levy and co-workers [27] (patient 35) shows progressive reduced variability without decelerations; a pattern that can be influenced by hypothermia and not only by low flow and low MAP. The compensatory tachycardia after CPB strongly suggests a reduced support of O2. At birth, the baby was well, but we do not have a long-term follow-up.
In the reports of Lamb [30] and Trimakas [31] and their co-workers (patients 38, 39, and 40), they do not find any improvement in oxygenation while raising the pump flow and the maternal MAP.
In the report by Burke and co-workers [51] (patient 63), the causes that brought about the manifestation of a sinusoidal pattern are not known. A notable fact is that the MAP at 50 mm Hg was too low to supply an adequate placental flow.
In the other case reported by Izquierdo and co-workers [45] (patient 56), it is not surprising that the sum of different negative factors influencing the placental flow, such as the uterine hypertone, visible in the tracings, and others linked to the CPB could contribute to cutting off the O2 supply causing the death of the fetus.
Uterine Contraction
Uterine contractile activity seems to be an important problem in patients subjected to CPB.
The contractions during CPB can be evaluated in a manner similar to a ``stress test.'' The presence of decelerations would seem to indicate that the flow supplied by the CPB is inadequate to overcome the obstacle created by contractions. Therefore, the contractions complicate the reading of the CTG tracing. They create a temporary O2 deficit that can alter the underlying basal tracing. It can only be supposed that in many of the above-mentioned cases, the basal FCF was in the normal range, suggesting an adequate supply of O2 to the fetus. The presence of contractions also alters the analysis of the variability.
The CPB seems to be a strong stimulus to contraction genesis. Numerous researchers report its appearance during or immediately after the end of CPB. It is probable that some factors produced during CPB (prostaglandins?) provoke uterine contractions. The use of hypothermia, especially in the warming phase, can also provoke contractile uterine activity.
Prime
The supply of O2 to the fetus is one of the crucial factors of the CPB (the uptake of CO2 should not be influenced significantly by the quality of the prime). The prime does not seem to be an important problem for the fetoplacental unit, because no problem was found in respect to the different hemodilution in the previously examined reports.
Hypothermia
Several data confirm that hypothermia during CPB should be avoided, because the fetal mortality is higher if the temperature is below 35°C (Table 3)Au: table 3 OK? No table 4.
Hypothermia can cause uterine contractions. The placental functions are seriously reduced by hypothermia and the problem seems to derive from the increase of uterine tone, and thus, a reduced blood flow. We do not know if the fetal cardiocirculatory system could be damaged by hypothermia. Fetal function does not seem to be excessively reduced by hypothermia. In fact, the fetus maintains the capability to autoregulate its heart rate during light hypothermia [60]. In deep hypothermia, fetal and placental functions seem more reduced.
Heparinization
No maternal mortality and morbidity was due to coagulation problems. No problems with respect to total inhibition of coagulation are reported, nor on placental disruption during or after CPB.
Vasoactive Drugs
It does not seem that vasoactive or cardioactive drugs such as -adrenergic drugs caused negative effects on placental perfusion. Epinephrine and dopamine are safe agents in pregnancy and can be used during operation to avoid hypotension.
The effects of ß2-agonists for tocolytic therapy during CPB should be evaluated.
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Practical Advice |
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TopFootnotesAbstractIntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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The following facts should be pointed out:
The CPB must be performed at high flow. In any case, a 2.7 L • m-2 • min-1 index is desirable.
If gestational age is more than 20 weeks, during operation the patient must be positioned in the left lateral recumbent position.
Hypothermia should be avoided for the following three reasons: (1) the cold phase, and particularly the warm phase, seem to trigger mechanisms capable of increasing uterine irritability and unleashing uterine contractions. (2) The exchanges of respiratory gases, especially O2, through the placenta seem to be negatively influenced by a decrease in temperature. (3) Theoretically, the warming phase can provoke anomalies in fetal myocardic conduction; anomalies that are difficult to diagnose and/or to treat without resorting to invasive fetal monitoring.
Uterine contractile activity must be monitored continuously and treated immediately. Halothane at high doses has tocolytic properties. Some possible drugs are ß2-agonists, nitric oxide donors such us nitroglycerin, and inhibitors of the synthesis of prostaglandins. The use of nitroglycerin is still in the experimental stage. The inhibitors of the synthesis of prostaglandins would be effective, especially if administered before operation, because this kind of contractile activity could be caused by prostanoid molecules.
Even if not mentioned by any of the investigators, the hyperkalemic cardioplegia, if not recovered, can reach the placenta and the fetus. It would be prudent to avoid this potentially damaging factor.
The time necessary for CPB must be kept to a minimum. The operating room must be prepared and ready to perform urgent cesarean section and provide neonatal assistance.
A monitor for CTG is mandatory. It would be useful to monitor the fetus with Doppler ultrasonography. A transvaginal examination would improve the quality, at the same time keeping the echographist away from the operating field.
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Acknowledgments |
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Footnotes |
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TopFootnotesAbstractIntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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TopFootnotesAbstractIntroductionCardiopulmonary Bypass...CommentPractical AdviceAcknowledgmentsReferences |
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