Editorial
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Website: www.annals.in PMID: *** DOI: 10.4103/0971-9784.124111 Quick Response Code:
Cardiopulmonary bypass during pregnancy – Fetal demise: An enigma 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.[2-4] 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 O2 and nutrients to the fetus. Considering fetal hypoxemia as the cause of fetal demise, the interventions are directed to increase fetal O2 delivery and are limited to maneuvers that increase O2 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 O2 to the fetus is dependent on exchange of gases across the placenta and the efficiency of fetal hemoglobin (HbF) to receive O2 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 O2 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 O2 carrying capacity. The predominant Hb from 10 to 12 week until delivery is HbF, which has greater affinity to O2 because of reduced affinity with 2, 3 diphosphoglycerate. Increased affinity of HbF with O2 facilitates O2 transfer
Address for correspondence: Dr. Praveen Kumar Neema, Department of Anaesthesiology, AIIMS Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
1
Neema: CPB during pregnancy – Fetal demise: An enigma
across the placenta but reduces O2 release to the tissues. The fetal PO2 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 O2 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 O2 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 O2 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 2
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
Access this article online
Website: www.annals.in PMID: *** DOI: 10.4103/0971-9784.124111 Quick Response Code:
Cardiopulmonary bypass during pregnancy – Fetal demise: An enigma 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.[2-4] 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 O2 and nutrients to the fetus. Considering fetal hypoxemia as the cause of fetal demise, the interventions are directed to increase fetal O2 delivery and are limited to maneuvers that increase O2 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 O2 to the fetus is dependent on exchange of gases across the placenta and the efficiency of fetal hemoglobin (HbF) to receive O2 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 O2 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 O2 carrying capacity. The predominant Hb from 10 to 12 week until delivery is HbF, which has greater affinity to O2 because of reduced affinity with 2, 3 diphosphoglycerate. Increased affinity of HbF with O2 facilitates O2 transfer
Address for correspondence: Dr. Praveen Kumar Neema, Department of Anaesthesiology, AIIMS Raipur - 492 099, Chhattisgarh, India. E-mail: [email protected]
Annals of Cardiac Anaesthesia Vol. 17:1 Jan-Mar-2014
1
Neema: CPB during pregnancy – Fetal demise: An enigma
across the placenta but reduces O2 release to the tissues. The fetal PO2 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 O2 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 O2 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 O2 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 2
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
