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Ann Thorac Surg 2000;69:1622-1626
© 2000 The Society of Thoracic Surgeons

Current review

Cardiac operations during pregnancy: review of factors influencing fetal outcome

Ahmet Mahli, MDa, Seval Izdes, MDa, Demet Coskun, MDa

a Department of Anesthesiology and Reanimation, Medical School of Gazi University, Ankara, Turkey

Address reprint requests to Dr Mahli, Gazi Üniversitesi Tip Fakültesi, Anesteziyoloji ve Reanimasyon AD, 06510 Beevler-Ankara-Turkey
e-mail: mahli{at}behcet.tip.gazi.edu.tr


   Abstract
Top
 Abstract
Introduction
 Case presentation
 Comment
 References
 
Women with underlying rheumatic heart disease, even if well compensated, can easily be affected by acute heart failure caused by out-of-the-ordinary cardiorespiratory requirements during pregnancy. In such cases, medical therapy is not always sufficient to drive a heart, and open heart operation might be necessary. Many factors associated with cardiac operations requiring cardiopulmonary bypass, such as hypothermia, can adversely affect both the mother and the fetus, but the morbidity and mortality rates are higher for the fetus than the mother. Because fetal heart tones were lost during cardiopulmonary bypass and were reheard in the intensive care unit in our case presentation, we have presumed that the loss of fetal heart tones should not always indicate fetal death and have discussed harmful factors in relation with the fetal morbidity and mortality in light of the literature.


   Introduction
Top
 Abstract
 Introduction
Case presentation
 Comment
 References
 
Pregnancy creates a great burden on the cardiovascular system and can result in decompensation in women with underlying cardiac disease. To minimize the maternal and fetal risks, the first choice of treatment should be medical. In cases that are refractory to medical treatment, however, corrective cardiac operations should be undertaken [1].

Pregnant women who have cardiac operations requiring cardiopulmonary bypass (CPB) must face a nonphysiologic hemodynamic status where the tolerance is not clearly known, which can adversely affect both the mother and the fetus [2, 3]. Cardiopulmonary bypass has many potential side effects, including alteration of the cellular protein components of blood as well as coagulation, vasoactive substance release from leukocytes, complement activation, particulate and air embolism, nonpulsatile flow, hypotension, and hypothermia. All of these factors can hamper uteroplacental perfusion and fetal development. Furthermore, cannulation of the inferior vena cava can obstruct the blood flow and can cause reduced right ventricular filling and resultant alterations in placental perfusion [3, 4]. The effects of the pump and perfusate type used during CPB and the duration of perfusion on maternal and fetal outcome are well recognized [1]. Theoretically, factors related to CPB such as nonpulsatile perfusion, hyperoxygenation, and heparinization may have adverse effects on the placenta and the fetus [5].

Most studies of cardiac operations during pregnancy are case presentations, at times organized as literature reviews [1, 3, 5–8]. In our case presentation, we interpreted the deceleration and loss of fetal heart tones during CPB in pregnant women as not always indicating fetal death and have discussed this fact in light of the literature.


   Case presentation
Top
 Abstract
 Introduction
 Case presentation
Comment
 References
 
A 24-year-old gravida at 32 weeks’ gestation was admitted to our hospital with complaints of shortness of breath and palpitation. She was 1.58 m tall and weighed 60 kg. Her medical history revealed rheumatic valvular disease. Severe mitral stenosis was diagnosed on the basis of the physical examination and the laboratory investigations. Open mitral commissurotomy was the chosen treatment. Upon fetal checks, fetal development was found not to be consistent with the gestational age, but no pathologic signs were observed. Although open heart operations have been done in our hospital for 15 years, previously only one case had undergone CPB during pregnancy.

After preparations for an open heart procedure, a cardiotocograph was positioned externally by an obstetrician, and the fetal heart rate (FHR) was found to be 150 beats per minute and rhythmic. Intubation followed the induction anesthesia with relevant doses of propofol, fentanyl, and pancuronium. Anesthesia was maintained with N2O:O2 (50%:50%) inhalation, continuous propofol infusion, and fentanyl administration when required. Cardiopulmonary bypass was initiated after the cannulation of the aorta and the vena cava, and it was standardized using a crystalloid prime. Systemic mild hypothermia (30° to 32°C) was established. Maternal systolic blood pressure was set to be 70 to 80 mm Hg and the pump blood flow was set to be 2.2 to 2.4 L/m2 per minute throughout CPB. The prime solution was composed of the following: 1,500 mL of Ringer lactate solution, 20 mmol of sodium bicarbonate, and 50 mg (5000 IU) of heparin. After the aortic cross-clamp was applied, hyperkalemic buffered cold crystalloid cardioplegic solution was infused into the aortic root at 10 mL per kilogram of body weight. Myocardial protection was provided by topical cooling with ice slush as well. After initiation of CPB and at 10 minutes after application of the aortic cross- clamp, during mitral commisurotomy through a left atrial approach, progressive deceleration in the FHR and asystole was observed. The position of the CTG probe was checked and was moved to various zones over the abdomen in search of the fetal heart beat, but the fetal heart beat could not be heard. During the 15-minute aortic cross-clamp period, mitral commissurotomy was done and the patient was rewarmed. During this period, intravenous nitroglycerin was used. Cardiac activity resumed after a single defibrillation. After the pump was disconnected, protamine was administered and bleeding checks were made. The operation was completed 1 hour after disconnection from the pump. The fetus was judged to be dead by the obstetrician and the pregnancy to be terminated after maternal hemodynamic stabilization, and the patient was taken to the intensive care unit. Two hours after the patient was taken to the intensive care unit, the obstetrician was able to hear the fetal heart tones by a fetoscope and found the FHR to be within normal range and rhythmic. Therefore, the decision of termination of the pregnancy was abandoned, and the patient gave birth to a healthy male child by spontaneous vaginal delivery at term.


   Comment
Top
 Abstract
 Introduction
 Case presentation
 Comment
References
 
Organic heart disease, with an incidence of 1% to 4%, is the primary cause of maternal and fetal death during pregnancy. The underlying cause is rheumatic heart disease in 60% of these cases, and mitral stenosis is the most frequent diagnosis [3, 9–12].

Most of the pregnant women with mild to moderate mitral stenosis can tolerate the burden on the cardiovascular system caused by pregnancy. However, in cases with moderate to severe lesions, complications, such as pulmonary venous congestion, pulmonary edema, right ventricular dysfunction, pulmonary hypertension, hemoptysis, atrial fibrillation, systemic or pulmonary embolism, and infective endocarditis, can occur during pregnancy. Furthermore, atrial fibrillation in pregnant women with mitral stenosis of any severity can precipitate pulmonary edema and can result in sudden and unexpected deterioration. In such cases, emergency commissurotomy is done [12]. Likewise, the indication for the operation to be undertaken in our case was the decompensation in heart failure despite medical treatment.

In 1958, Leyse and colleagues [13] first used CPB in a heart operation during pregnancy. After the initial trials, pregnant women have been recognized to tolerate CPB as well as nonpregnant women, but the effects of CPB on the fetus have varied [2, 5, 14]. In the review articles, the maternal mortality rate has ranged from 1.5% to 5%, and the fetal mortality rate has ranged from 16% to 33% [1, 3, 5, 7, 8, 14, 15]. Pomini and colleagues [7] evaluated 69 women who had cardiac operations with CPB during pregnancy and found the embryo-fetal mortality rate to be 24% under hypothermic conditions versus 0% under normothermic conditions. They also found that maternal mortality rates did not differ at different temperatures [7]. Younger gestational age and a greater degree of hypothermia are known to increase fetal morbidity during CPB [4]. In contrast, open heart operations have been reported to be undertaken at any gestational age but are best done between 24 and 28 weeks’ gestation, after the completion of organogenesis. If a modern neonatal intensive care unit is available, just before CPB a cesarean section in the third trimester has been reported to be safe [8, 14].

Although fetal bradycardia is known to develop frequently during the initiation of extracorporeal circulation and to normalize immediately after CPB [16–19], abnormal FHR was reported not to return to normal value [1] and to continue for several hours postoperatively [20]. Fetal bradycardia can be caused by fetal hypoxia or acidosis, maternal hypothermia, or administration of drugs such as propranolol that are transferable through the placenta. Fetal hypoxia can be caused by reduced oxygen content of the maternal blood, reduced uterine perfusion pressure, or increased uterine arterial resistance [4]. Like fetal bradycardia, compensatory tachycardia that frequently follows fetal distress is also reported to indicate fetal hypoxia [7].

In previous studies, fetal bradycardia has been described as a response to the decrease in uteroplacental perfusion and the resultant uterine contractions and can be corrected by increased maternal blood flow [16]. Hypothermia in nonresponsive cases has also been effective [21]. Hypothermia can cause alterations in the acid-base status; lead to coagulation disorders, arrhythmia, and ventricular fibrillation; and precipitate uterine contractions, thus reducing placental oxygen exchange [4, 7]. With regard to blood gases, transplacental flow, and flow to the fetal organs, the placenta exposed to hypothermia in vivo is postulated not to be a good oxygen supplier [22–24]. Although mild hypothermia can be tolerated because the fetal heart rate can be carried on with autoregulation, fetal and placental functions can decline, and the risk of fetal arrhythmia and cardiac arrest can increase at lower core temperatures [7, 25–27].

Although the cause of extensive uterine contractions during the rewarming phase after moderate or profound hypothermia during CPB is not known, the frequency of these contractions is higher with older gestational age and can result in placental failure and secondary fetal hypoxia. Furthermore, the dilution effect of CPB is thought to reduce the hormonal levels (progesterone in particular), which might augment the uterine excitability [5, 8].

Because the placental blood vessels are maximally dilated, the uterine blood flow is not autoregulated and is directly proportional to the maternal mean arterial pressure and inversely proportional to the uterine vascular resistance [28–30]. A decrease in maternal blood pressure can result in fetal bradycardia just before CPB. Maternal hypotension shortly after initiation of CPB is caused by a decrease in systemic vascular resistance affected by hemodilution, the release of vasoactive substances, or both and can result in a significant reduction in placental perfusion [7, 11, 29, 30]. Furthermore, various factors, such as poor placental perfusion during nonpulsatile flow, uterine arteriovenous shunts, the obstruction of venous drainage due to cannulation of inferior vena cava, uterine artery spasm, and particulate and gaseous embolism, can affect placental circulation and result in fetal hypoxia [31, 32] and accompanying cardiotocographic alterations [21, 33].

The heart rate deceleration observed by fetal monitoring during CPB is likely caused by reduced blood flow to the intervillous space and the resultant fetal hypoxia. The exact cause for the reduced flow is not known but is thought to be insufficient blood flow or uterine artery spasm during extracorporeal perfusion [11]. Maternal alkalosis shifts the maternal oxygen-hemoglobin dissociation curve to the left, leading to decreased fetal partial arterial oxygen pressure and oxygen content [4, 34–36]. Moreover, some authors have reported fetal arrhythmia to be caused by hypothermia rather than being related to maternal oxygenation and acid-base balance [5, 17], whereas others have reported fetal arrhythmia after use of normothermic perfusion [16].

The reduced FHR during CPB has been reported to be increased [17, 31, 37] or temporarily restored by increasing maternal blood flow (16%) [1, 7, 16, 31, 33, 37–39] and, thus, increasing perfusion pressure. However, FHR is likely to deteriorate, and prolonged CPB can result in permanent bradycardia [7]. In general, FHR is increased temporarily as a result of the restored maternal circulation after discontinuation of CPB, finally reverting to baseline values. Conversely, if maternal acid-base balance, flow rate, and perfusion pressure are within normal limits during CPB, the development of permanent fetal bradycardia despite increasing CPB flow [31, 33] is proposed to be related to fetal exposure to factors such as high doses of narcotic analgesic agents [19, 33, 40]. Furthermore, avoidance from inotropic and vasoconstrictive agents that reduce uteroplacental blood flow (other than phenylephrine and ephedrine) is recommended [41].

Despite being an indirect method for assessing the function of the fetoplacental unit, external monitoring of FHR and the uterus has been reported to reduce fetal mortality rate to 9.5% by enabling early recognition of potential problems during CPB and timely provision of the required treatment [3, 5, 7, 11, 17]. Continuous monitoring during the postoperative period is recommended, considering the possibility of premature labor in the first few postoperative days [26].

To prevent the deleterious effects caused by the reduction in perfusion of the placental intervillous space during CPB, high flow rate (> 2.5 L/m2 per minute) and high pressure (mean arterial pressure > 70 mm Hg) are recommended in parallel to the physiologic increase in maternal cardiac output accompanying the increase in gestational age [5, 14, 37, 42]. Short periods of normothermic and pulsatile perfusions, where possible, are thought to be beneficial as well [1, 4, 5, 7, 8, 16, 17, 37, 42]. In two previously published case presentations, fetal bradycardia observed after initiation of CPB was corrected by increasing the blood flow rate from 3.1 to 3.6 L/minute in one case [17] and from 2.8 to 4.6 L/minute in the other [37]. In contrast, in another case presentation, fetal bradycardia was reported not to be restored by increasing blood flow rate but to cease spontaneously upon the restoration of maternal flow after discontinuation of CPB [31]. Permanent fetal bradycardia despite a perfusion flow rate of 3 L/m2 per minute was reported to indicate fetal acidosis [20].

Although hypothermia is believed to protect the fetus by reducing fetal oxygen requirement, the application of normothermic or mild hypothermic perfusion is recommended unless the aortic clamp time is unexpectedly long, because the rewarming period can be a risk for premature labor due to the augmentation of the uterine contractions [5, 43].

Upon correction of maternal hypotension, which is known to cause fetal bradycardia during cannulation or after initiation of extracorporeal circulation and cooling to 32°C, an increase in fetal heart rate was reported after ephedrine infusion [21, 44]. Because of the ongoing fetal distress findings on cardiotocograph for several hours during and after the operation in a patient with a CPB flow rate of 3 L/m2 per minute and mean arterial pressure held at 50 mm Hg after intravenous phenylephrine infusion, the perfusion flow rate was reported to be more important than the perfusion pressure to maintain fetal blood flow [20]. The uterine contractions during CPB, the cause of which is not known but is presumed to be related to hypothermia and rewarming [5], affect the uterine blood flow and reduce the placental flow [45]. This might explain the continued fetal distress despite increased perfusion pressure and pump flow [11, 16, 19, 37, 46]. For this reason, some authors suggest no treatment for the contractions [19], but others suggest aggressive treatment with tocolytic agents [11, 16, 39, 43, 47, 48].

Several case presentations report fetal death despite appropriate conditions during CPB. After mitral valve replacement using mild hypothermic CPB during the 23rd gestational week, the fetal heart beat could not be detected and the fetus was reported to be stillborn [42]. Of 23 women who had open mitral commissurotomies with mild hypothermic CPB, the loss of fetal heart tones after transfer to the intensive care unit and subsequent spontaneous abortion was reported in only one case [5]. In another patient who had deep hypothermic total circulatory arrest at 19°C with a mean bypass flow rate of 2.4 L/m2 per minute and a mean perfusion pressure of 60 mm Hg, fetal heart tones were lost at 24°C and then reheard upon continuation of the operation followed by transfer to the intensive care unit [49].

The fetal core temperature is only 0.5°C higher than the maternal colon temperature and approximately 0.2°C higher than the amniotic fluid temperature, and the amniotic fluid temperature is different from the uterine wall temperature only by 0.1°C. The thermal diffusion capacity of the placental villous surface is known to be superior to that of the fetal body surface. These low fetomaternal temperature gradients indicate that almost all fetal temperature loss is through the umbilical blood flow toward the placenta [50].

In our case, fetal death was suspected upon the observation of fetal bradycardia and subsequent loss of fetal heart beat at 15 minutes after initiation of CPB. However, after rehearing the fetal heart tones 2 hours after the operation two possible explanations were considered. First, there might have been a temporary, or unrecognized, condition of fetal acidosis and/or reduction in fetal perfusion flow despite normal CPB flow. Second, there might have been deficient delivery of heat to the fetus during the maternal rewarming period caused by vasoconstriction in the umbilical vessels as well as the peripheral vessels. Hence, we presume the heat of the organs near the uterus was slowly transferred to the fetus and the umbilical vasoconstriction was abolished upon stabilization of the maternal hemodynamic and metabolic status at 2 hours postoperatively.

Besides appropriate selection and dosage of anesthetic agents and supportive agents, the maintenance of acid-base balance during open heart operations in pregnant women, the use of high flow rate, high perfusion pressure, and normothermia or mild hypothermia during CPB, minimization of the duration of CPB and the aortic cross-clamp time, and continuous cardiotocographic monitoring during and after the entire procedure is suggested in the studies cited above. In addition, because the fetal heart tones were lost during CPB and reheard in the intensive care unit in our case, we presume that the loss of fetal heart tones should not always indicate fetal death, and we suggest that enough time should be taken postoperatively to make a precise determination of fetal death.


   References
Top
 Abstract
 Introduction
 Case presentation
 Comment
 References
 

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