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Pro: Low-flow cardiopulmonary bypass is the preferred technique for patients undergoing cardiac surgical procedures
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PRO AND CON Paul G. Barash, MD Section Editor
Pro: Low-Flow Cardiopulmonary Bypass Is the Preferred Technique for Patients Undergoing Cardiac Surgical Procedures James A. DiNardo, MD, and Julie A. Wegner, PhD, CCP
C
ARDIOPULMONARY BYPASS (CPB) is routinely used to facilitate most adult cardiac surgical procedures. The CPB circuit is intended to isolate the cardiopulmonary system so that optimal surgical exposure can be obtained. For this isolation to be effective, the CPB circuit must be capable of performing the functions of the intact cardiopulmonary system for a finite period. At the minimum, the circuit must be capable of adding oxygen and removing carbon dioxide from the blood and of providing adequate perfusion of all organs with this blood. In adults, low-flow CPB (30 to 40 mL/kg/min and 1.3 to 1.7 L/min/m2) in conjunction with moderate systemic hypothermia (26° to 31°C) enhances myocardial protection, provides adequate cerebral and systemic circulation, reduces fluid requirements, and allows aggressive hemoconcentration. Higher flows (2.0 to 2.4 L/min/m2) afford no tangible advantages over lower flows because there is no direct evidence that higher CPB flow rates result in better organ perfusion or better outcomes. There is no evidence that low-flow CPB is associated with any adverse outcomes.1,2 Four major criticisms of low-flow CPB in adults exist and are addressed.
MAP. There is a small positive slope to the cerebral autoregulation relationship on CPB that is less pronounced at hypothermia (0.86 mL/100 g/min increase in cerebral blood flow for each 10-mmHg increase in MAP) than at normothermia (1.78 mL/100 g/min increase in cerebral blood flow for each 10-mmHg increase in MAP).6 Cerebral blood flow is disproportionately maintained relative to systemic blood flow even at extremely low flow rates during moderatehypothermia CPB.7 At comparable MAP, alterations in pump flow rates do not produce changes in CBF.8 From a practical point of view, cerebral blood flow can be reliably maintained or increased during low-flow CPB using phenylephrine.9 The first-line therapy to increase MAP in the Gold et al3 study was phenylephrine. High-flow proponents are fond of pointing out that in theory high perfusion pressure may improve collateral blood flow to the territory of vessels occluded by emboli and reduce hypoperfusion.10 Equally likely is the possibility that a high MAP obtained by increased flow may sandblast the ascending aorta and increase the risk of embolization from preexisting atheromas.
LOW-FLOW CARDIOPULMONARY BYPASS BY NECESSITY PRODUCES LOW MEAN ARTERIAL PRESSURE DURING CARDIOPULMONARY BYPASS, WHICH IS ASSOCIATED WITH ADVERSE NEUROLOGIC OUTCOME
LOW-FLOW CARDIOPULMONARY BYPASS PREDISPOSES PATIENTS TO A GREATER RISK OF CEREBRAL EMBOLI THAN HIGH-FLOW TECHNIQUES
First, it is not clear that low perfusion pressure (mean arterial blood pressure [MAP], 50 to 60 mmHg) on CPB predisposes to adverse neurologic outcome. The oftenquoted prospective study by Gold et al3 did not show individual differences in the cardiac, neurologic, or neurocognitive complication rates 6 months after surgery when low MAP CPB (50 to 60 mm Hg) was compared with high MAP CPB (80 to 100 mmHg) for adult patients undergoing coronary artery bypass graft surgery. The study did show, however, a higher incidence of combined cardiac and neurologic complications in the low-pressure group. When a subset of the same data was analyzed, it was determined that the prevalence and severity of transesophageal echocardiography– detected atheromas in the thoracic aorta were predictors of stroke and death after coronary artery bypass graft surgery.4 The data also make it impossible, however, to exclude the possibility that differences in the prevalence and severity of aortic atheromatous disease account for the observed outcome differences between the high and low MAP groups.5 Second, cerebral blood flow in the presence of alpha-stat pH management is remarkably constant over a wide range of
An animal study showed that when an embolic load is delivered into the aortic cannula distal to the arterial filter, a greater proportion of the embolic load is delivered to the cerebral circulation relative to the systemic circulation with low-flow CPB compared with high-flow CPB.11 This study used normothermia (35°C) and alpha-stat pH management. The findings of this study cannot be used as an indictment of low-flow CPB techniques in adults for several reasons. First, the quantity of emboli delivered to the cerebral circulation in this study is not all that different at flow rates in the clinically relevant range of 1.5 to 3.0 L/min/m2. Second, in clinical practice, the periods for peak risk of cerebral emboli
From the Department of Anesthesia, Cardiac Anesthesia Service, Children’s Hospital, Boston, MA; and Sarver University Heart Center, Tucson, AZ. Address reprint requests to James A. DiNardo, MD, Department of Anesthesia, Cardiac Anesthesia Service, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail: [email protected] Copyright © 2001 by W.B. Saunders Company 1053-0770/01/1505-0022$35.00/0 doi:10.1053/jcan.2001.26550 Key words: low-flow CPB.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 15, No 5 (October), 2001: pp 649-651
649
650
DINARDO AND WEGNER
are periods when there is extensive aortic manipulation, such as during aortic clamping and unclamping and during placement of a side-biting clamp for construction of proximal anastomoses.12 If a low-flow CPB is a risk factor for cerebral distribution of aortic emboli, CPB flow could be increased during those high-risk periods without having to maintain high flows throughout CPB. Alternately, the patient could be made mildly hypocarbic (PaCO2, 25 to 30 mm Hg) at the time of peak embolic risk. An animal study by the same group showed that regional and total cerebral embolization are functions of PaCO2 at the time of embolization.13
blood cells through the microvasculature and produces heterogeneity of microvascular flow.22 Microvascular flow alterations appear to be inherent to the pathophysiology of CPB. In sepsis, it has been shown that efforts to increase cardiac output (flow) with inotropes may improve global and regional DO2 but do not improve organ microvascular flow.21 It is naive to think that increased flow during CPB can be used to correct microvascular perfusion abnormalities. Attention would be better directed toward therapies to reduce inflammation and blood trauma or to directly reverse microvascular flow heterogeneity.
INADEQUATE SYSTEMIC OXYGEN DELIVERY IS A CONSEQUENCE OF LOW-FLOW CARDIOPULMONARY BYPASS
LOW-FLOW CARDIOPULMONARY BYPASS OFFERS NO ADVANTAGES OVER HIGH-FLOW CARDIOPULMONARY BYPASS
Adequate systemic oxygen delivery (DO2) as assessed by a normal mixed venous oxygen saturation of 70% and a mixed venous PO2 of 40 mmHg has been shown to occur in adult cardiac surgical patients during moderately hypothermic CPB at low flows.14,15 This adequate DO2 is primarily the result of the reduced metabolic requirements induced by hypothermia balancing the reduced DO that accompanies low-flow CPB.16 A normal mixed venous saturation does not rule out the possibility that regional hypoperfusion exists, but regional hypoperfusion may exist during high-flow CPB as well.17 Increasing flow does not necessarily improve organ perfusion; it has been shown that under conditions of high-flow CPB a substantial portion of flow is shunted to skeletal muscle.17 Increasing flow rates is ineffective in increasing gastric mucosa oxygen delivery during CPB despite maintenance of DO2 at pre-CPB levels.18 Regional venous desaturation indicative of regional hypoperfusion may be a consequence of CPB regardless of whether high flow or low flow is used. Evidence that factors other than the quantity of blood flow influence organ perfusion on CPB is abundant. Alterations in microcirculation play an important role in the distribution of blood flow during CPB. During CPB, blood is exposed to anomalous mechanical and environmental factors that initiate intense activation of the host inflammatory response. This systemic inflammatory response when initiated is similar to that seen in sepsis and endotoxemia.19 Extensive endothelial activation leads to vasocontriction, leukocyte and platelet aggregate plugging of the microvasculature, and edema formation. One of the hallmark consequences of these processes is enhanced heterogeneity of microvascular flow.20,21 This pathologic heterogeneity is in part the result of a defect in microvascular autoregulation that does not allow recruitment of sufficient capillary beds to meet local oxygen demands.21 There is functional shunting at the microvascular level that produces regional hypoxia in the face of normal venous PO2 values. Factors such as high shear stress, turbulence, decreased oncotic pressure caused by dilution of plasma, hyperoxia, and hypothermia present during CPB induce changes in the mechanical properties of red blood cells. In particular, CPB decreases red blood cell deformability, which in turn impedes the passage of red
High-flow CPB techniques present technical challenges not usually required with low-flow CPB. High-flow CPB necessitates the use of larger arterial and venous cannulae to prevent high arterial catheter pressures and to allow for adequate venous drainage. High-flow techniques require that volume constantly be added to the CPB circuit to make up for what is lost to the interstitial spaces.23,24 In an effort to improve venous drainage at high flow rates, a technique previously used to assist venous drainage through extrathoracic cannulation sites for minimally invasive cardiac surgery has been adapted to routine cardiac surgery and CPB. Vacuum-assisted venous drainage25 in conjunction with high-flow CPB has been shown to improve venous drainage. This technique resulted in decreased fluid requirements on CPB (250 mL v 1000 mL), reduced myocardial rewarming during the arrest interval, and reduced interstitial edema. The same goals can easily be achieved with the use of low-flow CPB. During a typical low-flow case, no volume is added to the CPB circuit, and aggressive hemoconcentration allows removal of 1000 mL of fluid from the patient. In addition to increasing the hematocrit, hemoconcentration or ultrafiltration during CPB may help ameliorate the inflammatory response.26 Low-flow CPB allows simplification of myocardial protection techniques by reducing rewarming of the heart. Low-flow CPB reduces bronchial collateral flow and flow through mediastinal and pericardial noncoronary collaterals that warm the heart and wash out cardioplegia. Low-flow CPB reduces the incidence of ventricular distention and the subsequent need for extensive cardiac venting. These problems can be addressed during high-flow CPB with enhanced venting and myocardial preservation techniques. These techniques are not without risk, however, because retrograde cardioplegia delivery may increase the risk of cerebral emboli,27 and venting always introduces the possibility of entraining air into the heart. In summary, high-flow CPB in adults offers no advantages over low-flow CPB and may be detrimental. High-flow techniques may exacerbate the inflammatory response by increasing shear forces and generating more rapid turnover of the blood–foreign surface interface. High-flow CPB predisposes to fluid retention and complicates myocardial preservation. Highflow CPB does not improve organ perfusion because it does not address the pathophysiology of CPB at the microvascular level.
PRO AND CON
651
REFERENCES 1. Kolkka R, Hilberman M: Neurologic dysfunction following cardiac operations with low-flow, low-pressure cardiopulmonary bypass. J Thorac Cardiovasc Surg 79:432-437, 1980 2. Valentine S, Barrowcliffe M, Peacock J: A comparison of effects of fixed and tailored cardiopulmonary flow rates on renal function. Anaesth Intensive Care 21:304-308, 1993 3. Gold JP, Charlson ME, Williams-Russo P, et al: Improvement of outcomes after coronary artery bypass: A randomized trial comparing intraoperative high versus low mean arterial pressure. J Thorac Cardiovasc Surg 110:1302-1311, 1995 4. Hartman GS, Yao F-SN, Bruefach M, et al: Severity of aortic atheromatous disease diagnosed by transesophageal echocardiography predicts stroke and other outcomes associated with coronary artery surgery: A prospective study. Anesth Analg 83:701-708, 1996 5. Arrowsmith JE, Grocott HP, Newman MF: Neurologic risk assessment and outcome in cardiac surgery. J Cardiothorac Vasc Anesth 13:736-743, 1999 6. Newman MF, Croughwell ND, White WD, et al: Effect of perfusion pressure on cerebral blood flow during normothermic cardiopulmonary bypass. Circulation 94:II353-II357, 1996 7. Schwartz AE, Kaplon RJ, Young WL, et al: Cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. Anesthesiology 81:959-964, 1994 8. Schwartz AE, Sandhu AA, Kaplon RJ, et al: Cerebral blood flow is determined by arterial pressure and not cardiopulmonary bypass flow rate. Ann Thorac Surg 60:165-170, 1995 9. Schwartz AE, Minanov O, Stone G, et al: Phenylephrine increases cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. Anesthesiology 85:380-384, 1996 10. Muhonen MG, Sawin PD, Loftus CM: Pressure-flow relationships in canine collateral dependent cerebrum. Stroke 23:998-994, 1992 11. Sungurtekin H, Plochl W, Cook DJ: Relationship between cardiopulmonary bypass flow rate and cerebral embolization in dogs. Anesthesiology 91:1387-1393, 1999 12. Barbut D, Hinton RB, Szatrowski TP, et al: Cerebral emboli detected during bypass surgery are associated with clamp removal. Stroke 25:2398-2402, 1994 13. Plochl W, Cook DJ: Quantification and distribution of cerebral emboli during cardiopulmonary bypass in the swine. Anesthesiology 90:183-190, 1999
14. Baraka AS, Baroody MA, Haroun St, et al: Effect of alpha-stat versus pH-stat strategy on oxyhemoglobin dissociation and whole-body oxygen consumption during hypothermic cardiopulmonary bypass. Anesth Analg 74:32-37, 1992 15. Baraka A: The effect of perfusion flow on oxidative metabolism during cardiopulmonary bypass. Anesth Analg 76:1191-1194, 1993 16. Lazenby WD, Ko W, Zelano JA, et al: Effects of temperature and flow rate on regional blood flow and metabolism during cardiopulmonary bypass. Ann Thorac Surg 53:957-964, 1992 17. McDaniel LB, Zwischenberger JB, Vertrees RA, et al: Mixed venous oxygen saturation during cardiopulmonary bypass poorly predicts regional venous saturation. Anesth Analg 80:466-472, 1995 18. Sicsis JC, Duranteau J, Corbineau H, et al: Gastric mucosal oxygen delivery decreases during cardiopulmonary bypass despite constant systemic oxygen delivery. Anesth Analg 86:455-460, 1998 19. Boyle EM, Morgan EN, Kovacich JC, et al: Microvascular responses to cardiopulmonary bypass. J Cardiothorac Vasc Anesth 14:30-35, 1999 (suppl 1) 20. Humer MF, Phang PT, Friesen BP, et al: Heterogeneity of gut capillary transit times and impaired gut oxygenation in endotoxemic pigs. J Appl Physiol 81:895-904, 1996 21. Ince C, Sinaasappel M: Microcirculatory oxygenation and shunting in sepsis and shock. Crit Care Med 27:1369-1377, 1999 22. Kameneva MV, Undar A, Antaki JF, et al: Decrease in red blood cell deformability caused by hypothermia, hemodilution, and mechanical stress: Factors related to cardiopulmonary bypass. ASAIO J 45: 307-310, 1999 23. Plochl W, Orszulak TA, Cook DJ, et al: Support of mean arterial pressure during tepid cardiopulmonary bypass: Effects of phenylephrine and pump flow on systemic oxygen supply and demand. J Cardiothorac Vasc Anesth 13:441-445, 1999 24. O’Dwyer C, Woodson LC, Conroy BP, et al: Regional perfusion abnormalities with phenylephrine during normothermic bypass. Ann Thorac Surg 63:728-735, 1997 25. Munster K, Andersen U, Mikkelsen J: Vacuum assisted venous drainage (VAVD). Perfusion 14:419-423, 1999 26. Journois D, Pouard P, Greeley WL, et al: Hemofiltration during cardiopulmonary bypass in pediatric cardiac surgery. Anesthesiology 81:1181-1189, 1994 27. Baker AJ, Naser B, Benaroia M: Cerebral microemboli during coronary artery bypass using different cardioplegia techniques. Ann Thorac Surg 59:1187-1191, 1995
PRO AND CON Paul G. Barash, MD Section Editor
Pro: Low-Flow Cardiopulmonary Bypass Is the Preferred Technique for Patients Undergoing Cardiac Surgical Procedures James A. DiNardo, MD, and Julie A. Wegner, PhD, CCP
C
ARDIOPULMONARY BYPASS (CPB) is routinely used to facilitate most adult cardiac surgical procedures. The CPB circuit is intended to isolate the cardiopulmonary system so that optimal surgical exposure can be obtained. For this isolation to be effective, the CPB circuit must be capable of performing the functions of the intact cardiopulmonary system for a finite period. At the minimum, the circuit must be capable of adding oxygen and removing carbon dioxide from the blood and of providing adequate perfusion of all organs with this blood. In adults, low-flow CPB (30 to 40 mL/kg/min and 1.3 to 1.7 L/min/m2) in conjunction with moderate systemic hypothermia (26° to 31°C) enhances myocardial protection, provides adequate cerebral and systemic circulation, reduces fluid requirements, and allows aggressive hemoconcentration. Higher flows (2.0 to 2.4 L/min/m2) afford no tangible advantages over lower flows because there is no direct evidence that higher CPB flow rates result in better organ perfusion or better outcomes. There is no evidence that low-flow CPB is associated with any adverse outcomes.1,2 Four major criticisms of low-flow CPB in adults exist and are addressed.
MAP. There is a small positive slope to the cerebral autoregulation relationship on CPB that is less pronounced at hypothermia (0.86 mL/100 g/min increase in cerebral blood flow for each 10-mmHg increase in MAP) than at normothermia (1.78 mL/100 g/min increase in cerebral blood flow for each 10-mmHg increase in MAP).6 Cerebral blood flow is disproportionately maintained relative to systemic blood flow even at extremely low flow rates during moderatehypothermia CPB.7 At comparable MAP, alterations in pump flow rates do not produce changes in CBF.8 From a practical point of view, cerebral blood flow can be reliably maintained or increased during low-flow CPB using phenylephrine.9 The first-line therapy to increase MAP in the Gold et al3 study was phenylephrine. High-flow proponents are fond of pointing out that in theory high perfusion pressure may improve collateral blood flow to the territory of vessels occluded by emboli and reduce hypoperfusion.10 Equally likely is the possibility that a high MAP obtained by increased flow may sandblast the ascending aorta and increase the risk of embolization from preexisting atheromas.
LOW-FLOW CARDIOPULMONARY BYPASS BY NECESSITY PRODUCES LOW MEAN ARTERIAL PRESSURE DURING CARDIOPULMONARY BYPASS, WHICH IS ASSOCIATED WITH ADVERSE NEUROLOGIC OUTCOME
LOW-FLOW CARDIOPULMONARY BYPASS PREDISPOSES PATIENTS TO A GREATER RISK OF CEREBRAL EMBOLI THAN HIGH-FLOW TECHNIQUES
First, it is not clear that low perfusion pressure (mean arterial blood pressure [MAP], 50 to 60 mmHg) on CPB predisposes to adverse neurologic outcome. The oftenquoted prospective study by Gold et al3 did not show individual differences in the cardiac, neurologic, or neurocognitive complication rates 6 months after surgery when low MAP CPB (50 to 60 mm Hg) was compared with high MAP CPB (80 to 100 mmHg) for adult patients undergoing coronary artery bypass graft surgery. The study did show, however, a higher incidence of combined cardiac and neurologic complications in the low-pressure group. When a subset of the same data was analyzed, it was determined that the prevalence and severity of transesophageal echocardiography– detected atheromas in the thoracic aorta were predictors of stroke and death after coronary artery bypass graft surgery.4 The data also make it impossible, however, to exclude the possibility that differences in the prevalence and severity of aortic atheromatous disease account for the observed outcome differences between the high and low MAP groups.5 Second, cerebral blood flow in the presence of alpha-stat pH management is remarkably constant over a wide range of
An animal study showed that when an embolic load is delivered into the aortic cannula distal to the arterial filter, a greater proportion of the embolic load is delivered to the cerebral circulation relative to the systemic circulation with low-flow CPB compared with high-flow CPB.11 This study used normothermia (35°C) and alpha-stat pH management. The findings of this study cannot be used as an indictment of low-flow CPB techniques in adults for several reasons. First, the quantity of emboli delivered to the cerebral circulation in this study is not all that different at flow rates in the clinically relevant range of 1.5 to 3.0 L/min/m2. Second, in clinical practice, the periods for peak risk of cerebral emboli
From the Department of Anesthesia, Cardiac Anesthesia Service, Children’s Hospital, Boston, MA; and Sarver University Heart Center, Tucson, AZ. Address reprint requests to James A. DiNardo, MD, Department of Anesthesia, Cardiac Anesthesia Service, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail: [email protected] Copyright © 2001 by W.B. Saunders Company 1053-0770/01/1505-0022$35.00/0 doi:10.1053/jcan.2001.26550 Key words: low-flow CPB.
Journal of Cardiothoracic and Vascular Anesthesia, Vol 15, No 5 (October), 2001: pp 649-651
649
650
DINARDO AND WEGNER
are periods when there is extensive aortic manipulation, such as during aortic clamping and unclamping and during placement of a side-biting clamp for construction of proximal anastomoses.12 If a low-flow CPB is a risk factor for cerebral distribution of aortic emboli, CPB flow could be increased during those high-risk periods without having to maintain high flows throughout CPB. Alternately, the patient could be made mildly hypocarbic (PaCO2, 25 to 30 mm Hg) at the time of peak embolic risk. An animal study by the same group showed that regional and total cerebral embolization are functions of PaCO2 at the time of embolization.13
blood cells through the microvasculature and produces heterogeneity of microvascular flow.22 Microvascular flow alterations appear to be inherent to the pathophysiology of CPB. In sepsis, it has been shown that efforts to increase cardiac output (flow) with inotropes may improve global and regional DO2 but do not improve organ microvascular flow.21 It is naive to think that increased flow during CPB can be used to correct microvascular perfusion abnormalities. Attention would be better directed toward therapies to reduce inflammation and blood trauma or to directly reverse microvascular flow heterogeneity.
INADEQUATE SYSTEMIC OXYGEN DELIVERY IS A CONSEQUENCE OF LOW-FLOW CARDIOPULMONARY BYPASS
LOW-FLOW CARDIOPULMONARY BYPASS OFFERS NO ADVANTAGES OVER HIGH-FLOW CARDIOPULMONARY BYPASS
Adequate systemic oxygen delivery (DO2) as assessed by a normal mixed venous oxygen saturation of 70% and a mixed venous PO2 of 40 mmHg has been shown to occur in adult cardiac surgical patients during moderately hypothermic CPB at low flows.14,15 This adequate DO2 is primarily the result of the reduced metabolic requirements induced by hypothermia balancing the reduced DO that accompanies low-flow CPB.16 A normal mixed venous saturation does not rule out the possibility that regional hypoperfusion exists, but regional hypoperfusion may exist during high-flow CPB as well.17 Increasing flow does not necessarily improve organ perfusion; it has been shown that under conditions of high-flow CPB a substantial portion of flow is shunted to skeletal muscle.17 Increasing flow rates is ineffective in increasing gastric mucosa oxygen delivery during CPB despite maintenance of DO2 at pre-CPB levels.18 Regional venous desaturation indicative of regional hypoperfusion may be a consequence of CPB regardless of whether high flow or low flow is used. Evidence that factors other than the quantity of blood flow influence organ perfusion on CPB is abundant. Alterations in microcirculation play an important role in the distribution of blood flow during CPB. During CPB, blood is exposed to anomalous mechanical and environmental factors that initiate intense activation of the host inflammatory response. This systemic inflammatory response when initiated is similar to that seen in sepsis and endotoxemia.19 Extensive endothelial activation leads to vasocontriction, leukocyte and platelet aggregate plugging of the microvasculature, and edema formation. One of the hallmark consequences of these processes is enhanced heterogeneity of microvascular flow.20,21 This pathologic heterogeneity is in part the result of a defect in microvascular autoregulation that does not allow recruitment of sufficient capillary beds to meet local oxygen demands.21 There is functional shunting at the microvascular level that produces regional hypoxia in the face of normal venous PO2 values. Factors such as high shear stress, turbulence, decreased oncotic pressure caused by dilution of plasma, hyperoxia, and hypothermia present during CPB induce changes in the mechanical properties of red blood cells. In particular, CPB decreases red blood cell deformability, which in turn impedes the passage of red
High-flow CPB techniques present technical challenges not usually required with low-flow CPB. High-flow CPB necessitates the use of larger arterial and venous cannulae to prevent high arterial catheter pressures and to allow for adequate venous drainage. High-flow techniques require that volume constantly be added to the CPB circuit to make up for what is lost to the interstitial spaces.23,24 In an effort to improve venous drainage at high flow rates, a technique previously used to assist venous drainage through extrathoracic cannulation sites for minimally invasive cardiac surgery has been adapted to routine cardiac surgery and CPB. Vacuum-assisted venous drainage25 in conjunction with high-flow CPB has been shown to improve venous drainage. This technique resulted in decreased fluid requirements on CPB (250 mL v 1000 mL), reduced myocardial rewarming during the arrest interval, and reduced interstitial edema. The same goals can easily be achieved with the use of low-flow CPB. During a typical low-flow case, no volume is added to the CPB circuit, and aggressive hemoconcentration allows removal of 1000 mL of fluid from the patient. In addition to increasing the hematocrit, hemoconcentration or ultrafiltration during CPB may help ameliorate the inflammatory response.26 Low-flow CPB allows simplification of myocardial protection techniques by reducing rewarming of the heart. Low-flow CPB reduces bronchial collateral flow and flow through mediastinal and pericardial noncoronary collaterals that warm the heart and wash out cardioplegia. Low-flow CPB reduces the incidence of ventricular distention and the subsequent need for extensive cardiac venting. These problems can be addressed during high-flow CPB with enhanced venting and myocardial preservation techniques. These techniques are not without risk, however, because retrograde cardioplegia delivery may increase the risk of cerebral emboli,27 and venting always introduces the possibility of entraining air into the heart. In summary, high-flow CPB in adults offers no advantages over low-flow CPB and may be detrimental. High-flow techniques may exacerbate the inflammatory response by increasing shear forces and generating more rapid turnover of the blood–foreign surface interface. High-flow CPB predisposes to fluid retention and complicates myocardial preservation. Highflow CPB does not improve organ perfusion because it does not address the pathophysiology of CPB at the microvascular level.
PRO AND CON
651
REFERENCES 1. Kolkka R, Hilberman M: Neurologic dysfunction following cardiac operations with low-flow, low-pressure cardiopulmonary bypass. J Thorac Cardiovasc Surg 79:432-437, 1980 2. Valentine S, Barrowcliffe M, Peacock J: A comparison of effects of fixed and tailored cardiopulmonary flow rates on renal function. Anaesth Intensive Care 21:304-308, 1993 3. Gold JP, Charlson ME, Williams-Russo P, et al: Improvement of outcomes after coronary artery bypass: A randomized trial comparing intraoperative high versus low mean arterial pressure. J Thorac Cardiovasc Surg 110:1302-1311, 1995 4. Hartman GS, Yao F-SN, Bruefach M, et al: Severity of aortic atheromatous disease diagnosed by transesophageal echocardiography predicts stroke and other outcomes associated with coronary artery surgery: A prospective study. Anesth Analg 83:701-708, 1996 5. Arrowsmith JE, Grocott HP, Newman MF: Neurologic risk assessment and outcome in cardiac surgery. J Cardiothorac Vasc Anesth 13:736-743, 1999 6. Newman MF, Croughwell ND, White WD, et al: Effect of perfusion pressure on cerebral blood flow during normothermic cardiopulmonary bypass. Circulation 94:II353-II357, 1996 7. Schwartz AE, Kaplon RJ, Young WL, et al: Cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. Anesthesiology 81:959-964, 1994 8. Schwartz AE, Sandhu AA, Kaplon RJ, et al: Cerebral blood flow is determined by arterial pressure and not cardiopulmonary bypass flow rate. Ann Thorac Surg 60:165-170, 1995 9. Schwartz AE, Minanov O, Stone G, et al: Phenylephrine increases cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. Anesthesiology 85:380-384, 1996 10. Muhonen MG, Sawin PD, Loftus CM: Pressure-flow relationships in canine collateral dependent cerebrum. Stroke 23:998-994, 1992 11. Sungurtekin H, Plochl W, Cook DJ: Relationship between cardiopulmonary bypass flow rate and cerebral embolization in dogs. Anesthesiology 91:1387-1393, 1999 12. Barbut D, Hinton RB, Szatrowski TP, et al: Cerebral emboli detected during bypass surgery are associated with clamp removal. Stroke 25:2398-2402, 1994 13. Plochl W, Cook DJ: Quantification and distribution of cerebral emboli during cardiopulmonary bypass in the swine. Anesthesiology 90:183-190, 1999
14. Baraka AS, Baroody MA, Haroun St, et al: Effect of alpha-stat versus pH-stat strategy on oxyhemoglobin dissociation and whole-body oxygen consumption during hypothermic cardiopulmonary bypass. Anesth Analg 74:32-37, 1992 15. Baraka A: The effect of perfusion flow on oxidative metabolism during cardiopulmonary bypass. Anesth Analg 76:1191-1194, 1993 16. Lazenby WD, Ko W, Zelano JA, et al: Effects of temperature and flow rate on regional blood flow and metabolism during cardiopulmonary bypass. Ann Thorac Surg 53:957-964, 1992 17. McDaniel LB, Zwischenberger JB, Vertrees RA, et al: Mixed venous oxygen saturation during cardiopulmonary bypass poorly predicts regional venous saturation. Anesth Analg 80:466-472, 1995 18. Sicsis JC, Duranteau J, Corbineau H, et al: Gastric mucosal oxygen delivery decreases during cardiopulmonary bypass despite constant systemic oxygen delivery. Anesth Analg 86:455-460, 1998 19. Boyle EM, Morgan EN, Kovacich JC, et al: Microvascular responses to cardiopulmonary bypass. J Cardiothorac Vasc Anesth 14:30-35, 1999 (suppl 1) 20. Humer MF, Phang PT, Friesen BP, et al: Heterogeneity of gut capillary transit times and impaired gut oxygenation in endotoxemic pigs. J Appl Physiol 81:895-904, 1996 21. Ince C, Sinaasappel M: Microcirculatory oxygenation and shunting in sepsis and shock. Crit Care Med 27:1369-1377, 1999 22. Kameneva MV, Undar A, Antaki JF, et al: Decrease in red blood cell deformability caused by hypothermia, hemodilution, and mechanical stress: Factors related to cardiopulmonary bypass. ASAIO J 45: 307-310, 1999 23. Plochl W, Orszulak TA, Cook DJ, et al: Support of mean arterial pressure during tepid cardiopulmonary bypass: Effects of phenylephrine and pump flow on systemic oxygen supply and demand. J Cardiothorac Vasc Anesth 13:441-445, 1999 24. O’Dwyer C, Woodson LC, Conroy BP, et al: Regional perfusion abnormalities with phenylephrine during normothermic bypass. Ann Thorac Surg 63:728-735, 1997 25. Munster K, Andersen U, Mikkelsen J: Vacuum assisted venous drainage (VAVD). Perfusion 14:419-423, 1999 26. Journois D, Pouard P, Greeley WL, et al: Hemofiltration during cardiopulmonary bypass in pediatric cardiac surgery. Anesthesiology 81:1181-1189, 1994 27. Baker AJ, Naser B, Benaroia M: Cerebral microemboli during coronary artery bypass using different cardioplegia techniques. Ann Thorac Surg 59:1187-1191, 1995