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Table of Contents
EDITORIAL  
Year : 2014  |  Volume : 17  |  Issue : 1  |  Page : 1-3
Cardiopulmonary bypass during pregnancy - Fetal demise: An enigma


Professor and Head, Department of Anaesthesiology, All India Institute of Medical Sciences Raipur, Chhattisgarh, India

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Date of Web Publication2-Jan-2014
 

How to cite this article:
Neema PK. Cardiopulmonary bypass during pregnancy - Fetal demise: An enigma. Ann Card Anaesth 2014;17:1-3

How to cite this URL:
Neema PK. Cardiopulmonary bypass during pregnancy - Fetal demise: An enigma. Ann Card Anaesth [serial online] 2014 [cited 2019 Jun 17];17:1-3. Available from: http://www.annals.in/text.asp?2014/17/1/1/124111


Ever since the first use of cardiopulmonary bypass (CPB) in 1959 in a pregnant woman with a 6 weeks gestation for pulmonary valvotomy and atrial septal defect closure, wherein the fetus spontaneously aborted 3 months later, [1] the fetal mortality for open cardiac surgery during pregnancy continue to remains high at 9.5-29% with an average of 19% over the past 25 years. [2],[3],[4] The effects of CPB are the key factors responsible for fetal demise. The extraordinary increases in our knowledge of CPB, maternal and fetal circulatory physiology and technological advances have not been able to bring down the fetal mortality associated with CPB. The obstacle has been inadequate knowledge of the effects of CPB on fetal well-being and lack of fetal monitors that can indicate adequacy/inadequacy of fetal needs, particularly, circulatory needs. The most intuitive cause of adverse fetal outcome during CPB could be inadequate supply of O 2 and nutrients to the fetus. Considering fetal hypoxemia as the cause of fetal demise, the interventions are directed to increase fetal O 2 delivery and are limited to maneuvers that increase O 2 delivery to fetus during CPB. The measures include increases in CPB flow and mean arterial pressure (MAP) and hematocrit of prime and measures to prevent increases in placental vascular resistance including uterine relaxants. It is interesting to note that a review of the Mayo Clinic surgical database spanning 35 years (1976-2009) revealed that only 21 pregnant patients underwent cardiothoracic surgery during that period. [5] Evidently, the developed world have effectively educated their population and CPB during pregnancy is a rare and unimportant issue with them. Moreover, the manifestations of rheumatic heart disease, particularly mitral stenosis, occur much later in developed nations. However, the issue is relevant for developing countries where rheumatic heart disease still exists in sizable proportion and the gaps in our knowledge for managing these cases needs to be researched.

With the initiation of CPB, fetal bradycardia is observed and fetal hypoxemia is believed to be the prime cause of fetal bradycardia. The supply of O 2 to the fetus is dependent on exchange of gases across the placenta and the efficiency of fetal hemoglobin (HbF) to receive O 2 from the maternal blood, which is CPB prime during CPB. It is noteworthy that the placental circulation does not exhibit autoregulation, [2],[5] as a result the placental blood flow changes directly with the changes in arterial perfusion pressure (MAP during CPB). In an experimental study, pulsatile flow was shown to prevent the drop in placental perfusion and limit the rise in placental vascular resistance. [6] Additionally, oxygenation of the CPB prime can only marginally increase O 2 supply to the fetus. In essence, well oxygenated blood must be delivered to the utero-placental circulation, at a reasonable MAP, using pulsatile flow. The utero-placental flow may be reduced by low CPB flows, low MAP, inferior vena cava compression and aortic compression. [7] Even if the uterine circulation is adequate, the fetus still depends on utero-placental blood flow and umbilical venous blood flow and its characteristics for tissue oxygenation. There are several differences in the characteristics of fetal blood and hemodynamics vis-à-vis an adult. The hemoglobin (Hb) concentration is about 16 g%, which increases the total O 2 carrying capacity. The predominant Hb from 10 to 12 week until delivery is HbF, which has greater affinity to O 2 because of reduced affinity with 2, 3 diphosphoglycerate. Increased affinity of HbF with O 2 facilitates O 2 transfer across the placenta but reduces O 2 release to the tissues. The fetal PO 2 is low (30 mmHg) and is a part of the mechanism to keep the ductus patent and pulmonary vascular bed constricted. The blood in the umbilical vein is about 80% saturated and in the ascending aorta about 65%. [8] The umbilical vein blood because of streaming effect preferentially enters the left ventricle and is supplied to myocardium and brain, [8] whereas the blood returning from superior and inferior vena cava enters the right ventricle and is supplied to lower half of body including placenta (for oxygenation) via ductus arteriosus.

During management of a pregnant woman undergoing cardiac surgery with CPB, the key issue to be addressed is whether the O 2 demand of the growing fetus at a given gestation period is adequate. How do we know that the needs of the fetus during CPB are adequately fulfilled? In other words how does one monitor adequacy/inadequacy of supply. Finally, what are the measures available to fulfil fetal demands (increase O 2 supply) if the supply is compromised? There is a need to investigate a few more areas such as: does a change in physical characteristics of CPB prime lead to a change in characteristics of the fetal blood? Does it lead to fetal intravascular volume expansion and fetal interstitial edema? What are the clinical implications of such changes? Will addition of albumin to CPB prime help?

Until recently, the only parameter available to know adequacy/inadequacy of O 2 supply to the fetus during CPB was fetal heart rate (FHR). It should be realized that at present, we are unable to manipulate fetal circulation directly; we can only manipulate the CPB flow and MAP and can assume that the increase in CPB flow and MAP will enhance the placental flow with well-oxygenated blood, will favorably change the fetal oxygenation and circulation and correct the fetal bradycardia. In this issue of Annals of Cardiac Anaesthesia, Kapoor, [9] reviews basic principles of CPB during pregnancy and Mishra et al. [10] describe utility of transvaginal umbilical artery Doppler velocitymetry indices in two pregnant women undergoing mitral valve replacement with CPB and analyzed correlation between FHR and resistivity index (RI) and pulsatility index (PI) to evaluate adequacy of fetal blood flow. The PI is defined as the difference between the peak systolic velocity (PSV) and end diastolic velocity (EDV) and divided by the mean velocity. The RI is defined as the difference between the PSV and EDV divided by the PSV. Both the indices are indicators of placental resistance and their increased values indicate increased placental vascular resistance, which may be treated by vasodilators and uterine relaxants. Apparently, the transvaginal umbilical artery Doppler velocitymetry indices provide a therapeutic window. In the described case 2, RI and PI were significantly raised, the MAP was <50 mmHg and the FHR was <50/min. In such a scenario, treating raised PI and RI by a vasodilator is a difficult decision. Umbilical vasoconstriction can occur as a part of fetal stress as a part of release of fetal stress hormones which manifest as bradycardia and increase in PI and RI. The management of umbilical vasoconstriction is not clear. Perhaps, the solution lies somewhere in the characteristics of the CPB prime and the conduct of CPB. Hypothermia, hemoglobinopathies, hypovolemia, hypotension, low cardiac output, New York Heart Association functional class IV, etc., adversely affects fetal development and are associated with adverse fetal outcome. A review of 69 reports of open-heart surgery during pregnancy, published 20 years back, found embryo-fetal mortality to be 24% and 0% in the hypothermic and normothermic groups, respectively. [11] Apparently, normothermic CPB, pulsatile flow, keeping hematocrit and MAP at or above preoperative basal values of the individuals, could be the goals of CPB during pregnancy. The CPB flow should take into account the fetal combined ventricular cardiac output also, which is about 210 ml/min at mid-gestation and 1900 ml/min at 38 weeks. [12] Colloid oncotic pressure of the CPB prime may be an important issue; however, there are no reports available on this issue, but similar to hematocrit and flow, it may be prudent to keep it close to basal values. The majority of the reports and available literature repeatedly show occurrence of fetal bradycardia at the initiation of CPB secondary to hypoxemia. Earlier the author of this editorial and his colleagues have described a method of controlled initiation of CPB in a child with aneurysmal main and left pulmonary artery severe right pulmonary artery stenosis and atrial septal defect undergoing right pulmonary artery plasty and atrial septal defect closure. [13] The method consists of standard aortic and bicaval cannulation and partial clamping (about two-third clamp) of the venous drain line; initially, low flow CPB is established with the partially occluded main venous line and the MAP is monitored. If the MAP remains stable, the venous clamp is released little more and in this manner, gradually, the total bypass is established. However, if the MAP value decrease precipitously, the venous drain line occlusion is further increased, the partial bypass and low tidal volume ventilation is continued. Once, hemodynamics stabilizes, a similar exercise is repeated. This strategy maintains the pulsatile blood flow, provides time for mixing of CPB prime and patients' blood and raises the perfusion pressure. The same technique can be applied in pregnant women for surgery under CPB and the establishment of CPB can be guided by the FHR.

 
   References Top

1.Dubourg G, Broustet P, Bricaud H, Fontan F, Trarieux M, Fontanille P. Complete correction of a triad of Fallot, in extracorporeal circulation, in a pregnant woman. Arch Mal Coeur Vaiss 1959;52:1389-91.  Back to cited text no. 1
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2.Mahli A, Izdes S, Coskun D. Cardiac operations during pregnancy: Review of factors influencing fetal outcome. Ann Thorac Surg 2000;69:1622-6.  Back to cited text no. 2
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3.Davies GA, Herbert WN. Congenital heart disease in pregnancy. J Obstet Gynaecol Can 2007;29:409-14.  Back to cited text no. 3
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4.Abbas AE, Lester SJ, Connolly H. Pregnancy and the cardiovascular system. Int J Cardiol 2005;98:179-89.  Back to cited text no. 4
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5.John AS, Gurley F, Schaff HV, Warnes CA, Phillips SD, Arendt KW, et al. Cardiopulmonary bypass during pregnancy. Ann Thorac Surg 2011;91:1191-6.  Back to cited text no. 5
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6.Vedrinne C, Tronc F, Martinot S, Robin J, Allevard AM, Vincent M, et al. Better preservation of endothelial function and decreased activation of the fetal renin-angiotensin pathway with the use of pulsatile flow during experimental fetal bypass. J Thorac Cardiovasc Surg 2000;120:770-7.  Back to cited text no. 6
    
7.Chandrasekhar S, Cook CR, Collard CD. Cardiac surgery in the parturient. Anesth Analg 2009;108:777-85.  Back to cited text no. 7
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8.Dawes GS, Mott JC, Widdicombe JG. The foetal circulation in the lamb. J Physiol 1954;126:563-87.  Back to cited text no. 8
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9.Kapoor MC. Cardiopulmonary bypass in pregnancy. Ann Card Anaesth 2014;17:33-9.  Back to cited text no. 9
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10.Mishra M, Sawhney R, Kumar A, Bapna KR, Kohli V, Wasir H, et al. Cardiac surgery during pregnancy: Continuous fetal monitoring using umbilical artery Doppler flow velocity indices. Ann Card Anaesth 2014;17:46-51.  Back to cited text no. 10
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11.Pomini F, Mercogliano D, Cavalletti C, Caruso A, Pomini P. Cardiopulmonary bypass in pregnancy. Ann Thorac Surg 1996;61:259-68.  Back to cited text no. 11
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12.Rasanen J, Wood DC, Weiner S, Ludomirski A, Huhta JC. Role of the pulmonary circulation in the distribution of human fetal cardiac output during the second half of pregnancy. Circulation 1996;94:1068-73.  Back to cited text no. 12
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13.Neema PK, Dharan BS, Singha S, Sethuraman M, Chandran DA, Rathod RC. Anesthetic implications of aneurysmal main pulmonary artery and left pulmonary artery and right pulmonary artery stenosis in a child undergoing main pulmonary artery and right pulmonary artery plasty and atrial septal defect closure. J Cardiothorac Vasc Anesth 2012;26:280-2.  Back to cited text no. 13
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Correspondence Address:
Praveen Kumar Neema
Department of Anaesthesiology, AIIMS Raipur - 492 099, Chhattisgarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.124111

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