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J Thorac Cardiovasc Surg 1994;107:510-0519
© 1994 Mosby, Inc.
Cardiopulmonary Bypass, Myocardial Management, and Support Techniques |
Toronto, Ontario, Canada
Supported by the Medical Research Council of Canada (Grant MT-9829). Dr. Ikonomidis is a Fellow of the Medical Research Council of Canada; Dr. Yau is a Fellow of the Heart and Stroke Foundation of Canada; Dr. Weisel is a Career Investigator of the Heart and Stroke Foundation of Ontario.
Presented at the Sixty-fifth Scientific Sessions of the American Heart Association, New Orleans, La., Nov. 16, 1992.
Received for publication Feb. 18, 1993. Accepted for publication June 29, 1993. Address for reprints: Richard D. Weisel, MD, The Toronto Hospital, EN 14-215, 200 Elizabeth St., Toronto, Ontario M5G 2C4.
Abstract
Retrograde delivery of warm blood cardioplegia may improve nutrient cardioplegic flow beyond coronary obstructions, but may not adequately perfuse the right ventricle and the posterior left ventricle. To determine the optimal flow rate for warm retrograde cardioplegia, we assessed 62 patients undergoing elective coronary artery bypass in two studies. In the low flow study, administration of 50 ml/min (n = 9), 75 ml/min (n = 11), or 100 ml/min (n = 7) was associated with high lactate production and oxygen extraction during cardioplegic administration. At 50 minutes of cardioplegic arrest, the coronary venous effluent pH was low in all groups. In the high flow study, 30 patients all received flow rates of 100, 200, and 300 ml/min in randomized order during the crossclamp period. In addition, five patients received cardioplegia at a rate of 500 ml/min for the duration of the crossclamp period. Administration of 200 ml/min or higher minimized lactate production and maintained coronary venous pH within the physiologic range, but flows of 300 ml/min or higher did not increase oxygen use or reduce lactate or acid production. Patients in the low flow groups had significantly greater myocardial lactate release during cardioplegic infusion and after removal of the crossclamp than the high flow group. Warm retrograde cardioplegia should be delivered at flow rates of at least 200 ml/min during elective coronary artery bypass operations. (J THORAC CARDIOVASC SURG1994;107:510-9)
The concept of coronary sinus cardioplegic delivery is not new. Maintenance of cardiac arrest by retrograde perfusion was suggested in 1957,
1 and this technique may provide nutritive flow to areas of myocardium that may be incompletely perfused with antegrade techniques because of coronary obstructions. 2,3 Patients with a left anterior descending coronary artery obstruction may not have adequate protection of the anterior myocardium with antegrade cardioplegia when an internal mammary artery is used for revascularization. This problem is accentuated in patients with ischemic rest angina or a recent myocardial infarction in whom adequate protective coronary collaterals have not developed. 4 The introduction of normothermic cardioplegia may allow resuscitation of the ischemic myocardium particularly in high-risk patients. 5 Therefore warm retrograde cardioplegia may resuscitate the ischemic anterior myocardium in patients with acute anterior ischemia who will receive an internal mammary artery bypass graft.
Compared with that in antegrade cardioplegia, a significant proportion of retrograde flow may be shunted away from the heart via thebesian collaterals into the ventricular cavities. 4,6-8 Further, retrograde cardioplegia may inadequately perfuse the right ventricle and posterior left ventricle or posterior interventricular septum. 7,8 We have previously reported that continuous normothermic antegrade blood cardioplegia reduces anaerobic myocardial lactate production and improves early postoperative myocardial function when given at flow rates of 80 ml/min or higher. 9,10 However, higher flow rates may be required with warm retrograde cardioplegia to meet the metabolic demands of the warm arrested myocardium. Increasing retrograde cardioplegic flow rates may be limited by the coronary sinus pressure 11 and the risk of systemic hyperkalemia and hemodilution. 12 Higher coronary sinus cardioplegic flow rates may not increase nutritive flow. 4
We report the results of two studies designed to define the optimal flow rate for delivery of retrograde normo thermic blood cardioplegia that provides sufficient nutritive flow to maintain aerobic cardiac metabolism. The first study examines the results of cardioplegia administered at low (50 to 100 ml/min) flow rates. The second study tests high flow rates (100 to 300 ml/min). An additional five patients received a flow rate of 500 ml/min.
METHODS
Patient population
wo patients scheduled for coronary artery bypass grafting agreed to participate in this evaluation of retrograde cardioplegia. Twenty-seven patients undergoing operation between Jan. 16, 1991, and May 3, 1991, participated in a study of low-flow normothermic blood retrograde cardioplegia. Thirty-five patients having operations between Oct. 23, 1991, and Feb. 11, 1992, participated in a study of high-flow normothermic retrograde cardioplegia. All patients signed a consent form approved by the Human Experimentation Committee. Patients admitted to the study (Table I) were primarily men aged 37 to 79 years with double- or triple-vessel coronary artery disease and preserved preoperative left ventricular function (ejection fraction greater than 30% as assessed by single-plane contrast ventriculography). No patient had a previous cardiac operation.
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Cardioplegic technique
All patients received normothermic blood cardioplegia delivered retrograde via the coronary sinus. Blood cardioplegic solutions were prepared by mixing oxygenated bypass circuit blood and a crystalloid solution in a 4:1 ratio and were delivered via the Buckberg-Shiley Plus system (Shiley Inc., Irvine, Calif.). 9 In all patients, the heart was arrested with a 500 ml infusion of high-potassium (27 mEq/L) blood cardioplegia delivered at 37° C into the aortic root at a pressure of 70 mm Hg as measured directly through a separate port of the cardioplegic cannula (Research Medical Inc., Midvale, Utah). After arrest, low-potassium (13 mEq/L) cardioplegia was infused via a retrograde cannula positioned after transatrial insertion with the balloon just inside the coronary sinus orifice. 2 The adequacy of cannula positioning was confirmed by observing distension of the posterior interventricular vein and maintenance of coronary sinus pressure (as measured through a separate port of the retrograde catheter). The pressure measured in the coronary sinus during cardioplegic administration was carefully recorded, maintained below 40 mm Hg, and used to calculate the coronary vascular resistance index.
Cardioplegic flow was interrupted for completion of distal anastomoses when adequate visualization could not be accomplished with a saline flush. Interruptions in flow were for periods less than 7 minutes. A proximal anastomosis was constructed after each distal anastomosis, and all were constructed during a single crossclamp period. 13 A left internal mammary artery graft was anastomosed to the left anterior descending coronary artery as the last anastomosis for all patients. The systemic temperature was not actively cooled but was allowed to drift to between 30° and 32° C.
In the low-flow study, 27 patients were randomized to receive low-potassium (13 mEq/L) cardioplegia infused continuously at rates of 50 (9 patients), 75 (11 patients), and 100 (7 patients) ml/min.
In the high-flow study, 30 patients received low-potassium cardioplegia (13 mEq/L) infused at rates of 100, 200, and 300 ml/min at different times during the crossclamp period. The order of the flows was determined for each patient by a randomization schedule. Five additional patients received cardioplegia at a flow rate of 500 ml/min throughout the crossclamp period. After completion of a distal anastomosis the heart was returned to the pericardial cradle and the preselected flow rate was given for 4 minutes during construction of the proximal anastomosis. During the cardioplegic infusion, the right atrium, right ventricle, and pulmonary artery were constantly monitored to ensure that they were collapsed and had a negative pressure to prevent contamination of the aortic root samples. Cardioplegic and coronary venous (aortic root) samples were obtained during the fifth minute of retrograde cardioplegia by gentle sampling from the cardioplegia line and aortic root, respectively. Care was taken during sampling to ensure that the right atrium and pulmonary artery remained collapsed. After completion of the next distal anastomosis the next flow rate on the randomization schedule was administered. The aortic effluent rate was estimated by a 1-minute timed aortic root collection during cardioplegic flow obtained from an aortic root vent connected to a gravity siphon.
Biochemical measurements
Blood samples were obtained before crossclamp application with the patient at 37° C during cardiopulmonary bypass, at intervals during the crossclamp period, and during reperfusion. Before crossclamp and during reperfusion, arterial blood samples were drawn from a peripheral arterial line and venous samples were obtained from a catheter in the coronary sinus. During cardioplegic administration, arterial samples were taken from the cardioplegic line and coronary venous samples were drawn from the aortic root after at least 4 minutes of cardioplegic flow. These samples were assayed for the partial pressures of oxygen (Po2) and carbon dioxide, pH (Acid-Base Laboratory, Radiometer, Copenhagen, Denmark), and oxygen saturation (Co-Oximeter, Instrumentation Laboratory Inc., Lexington, Mass.). Oxygen content (O2Con) was calculated from the formula
O2Con = 1.39 Hgb x S + 0.003 PO2
where Hgb is the hemoglobin concentration and S is the oxygen saturation. 14
Blood samples for lactate assay were mixed with a measured volume of 6% perchloric acid. Lactate concentration was measured in the protein-free supernatant by an enzymatic method (Rapid Lactate Stat Pack kit, Calbiochem-Behring, La Jolla, Calif.). 9 Myocardial lactate production and oxygen extraction were calculated as the difference between the arterial and coronary venous content.
We used an antibody inhibition technique to measure the MB isoenzyme of creatine kinase (CK-MB). 9 Integration of the time-concentration curve for CK-MB release within the first 48 hours after operation allowed calculation of the total CK-MB release, expressed as units (U) times hours per liter. 9
Statistical analysis
Statistical analysis was done with the SAS programs (SAS Institute, Cary, N. C.). Metabolic variables were analyzed by analysis of variance (ANOVA) to compare cardioplegic flow rates. When ANOVA indicated a significant difference (p < 0.05), the differences were specified with Duncan's multiple range test.
Categorical data are displayed as the absolute and percent frequency. Continuous data variables are listed as the mean and standard error of the mean. Statistical significance was assumed at a probability level of less than 0.05.
RESULTS
Clinical data
The preoperative characteristics of the patients are listed in 
Table I. The intraoperative and postoperative characteristics are shown in Tables II and III. There were no significant differences in any of the preoperative variables consistent with the random distribution of the patients. Intraoperatively (Table II), cardioplegic flow was discontinued for a greater percentage of the crossclamp period (41% ± 12%) in patients in the high-flow group than in those in the low-flow group (22% ± 14%; p = 0.0001). In the low-flow study, patients given 100 ml/min received more total cardioplegia volume than patients given 75 ml/min or 50 ml/min (p = 0.01). The total cardioplegia volume delivered to patients in the high-flow group was greater than the mean total cardioplegia volume of patients in the low-flow group (p = 0.04). Despite these differences, there were no significant differences in the highest serum potassium concentration during the crossclamp period (Table II).
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Table III).
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The coronary sinus pressures (in millimeters of mercury) during the crossclamp period were 15.1 ± 1.1 at 50 ml/min, 18.8 ± 1.6 at 75 ml/min, and 13.6 ± 0.9 at 100 ml/min (75 versus 50 minutes: p = 0.004, ANOVA). The coronary vascular resistance measurements (dynes x sec/cm5) were 23.5 ± 1.8 at 50 ml/min, 19.3 ± 1.7 at 75 ml/min, and 10.7 ± 0.7 at 100 ml/min (p = 0.0001, ANOVA).
High-flow study
Fig. 4 shows the results of the timed aortic root collections at the three high flow rates (100, 200, and 300 ml/min). An infusion of 100 ml/min was associated with recovery of 132 ml/min from the aortic root, an increase of 32 ml. In contrast, infusion of 200 or 300 ml/min resulted in decreased recovery at the aortic root (150 and 180 ml, respectively). The amount of cardioplegic shunt therefore increased with increasing flow rates. The coronary sinus pressures were lowest at 100 ml/min (11.0 ± 0.9 mm Hg) and increased significantly (p = 0.0001) with flow rates of 200 ml/min (17.5 ± 1.2 mm Hg) and 300 ml/min (19.4 ± 1.5 mm Hg), which were similar. The coronary vascular resistance measurements (100 ml/min: 8.6 ± 0.7 dynes x sec/cm5; 200 ml/min:70 ± 0.05 dynes x sec/cm5; 300 ml/min: 5.2 ± 0.4 dynes x sec/cm5) fell significantly (p = 0.0001) with each increase in flow rate.
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Improved methods of myocardial protection may reduce the morbidity and mortality of high-risk patients undergoing cardiac operations. In recent reviews from our institution, the overall operative mortality of elective bypass operation (1.5%) has not changed in recent years, despite an increase in the number of high-risk patients. 15,16 However, emergency operation, previous bypass operation, and left main coronary artery disease remain strong predictors of outcome and suggest the requirement for improved techniques to resuscitate the ischemic myocardium in these high-risk patients.
Hypothermia has many undesirable consequences. These include detrimental effects on enzyme function, 17 membrane stability, 18 calcium sequestration, 19 glucose utilization, 20 adenosine triphosphate generation, 21 tissue oxygen uptake, 22 hydrogen ion regulation, 23 and maintenance of osmotic homeostasis. 24 Further, we have shown that cardiac hypothermia delays the recovery of the oxidative metabolism of fatty acids and lactate 25,26 and reduces mitochondrial state 3 oxidation and citrate synthetase activity. 27 These changes may prevent early postischemic intracellular adenosine triphosphate repletion. 28
Warm cardioplegic induction and terminal warm cardioplegic infusions permit restoration of oxidative metabolism and myocardial energy stores before reperfusion. 29 Therefore continuous warm blood cardioplegia may allow maintenance of aerobic cardiac metabolism and resuscitate the arrested heart by channeling all available energy toward cellular repair and regeneration. 9
The normothermic, arrested heart requires at least three times the oxygen of the cold arrested heart. 30 Therefore warm cardioplegia must be given at flow rates sufficient to meet the higher metabolic demands of the warm arrested heart. We have previously shown that warm antegrade cardioplegia should be delivered at flow rates greater than 80 ml/min. 9 However, in the common case of use of the internal mammary artery as the last bypass to a critically stenosed left anterior descending coronary artery, the anterior myocardium may be ischemic during most of the crossclamp period. Prolonged ischemia may result in infarction, especially in patients with acute coronary insufficiency in whom adequate coronary collaterals have not developed. A solution to this problem is the delivery of warm blood cardioplegia retrograde into the coronary sinus, inasmuch as published evidence indicates that retrograde infusions supply the left anterior descending artery territory more effectively than antegrade infusions with a coronary stenosis or occlusion. 2,4,8 Menasche and colleagues 3 have reported excellent clinical results in patients with coronary artery obstructions with hypothermic retrograde cardioplegia at a flow rate of 100 ml/min, suggesting excellent myocardial protection beyond the coronary occlusions. However, because of the higher metabolic demand of the normothermic arrested heart, 30 the cardioplegia flow rate under conditions of normothermia would likely have to be increased. This postulate is confirmed by our study, which indicates that delivery of warm retrograde cardioplegia should occur at flow rates greater than 200 ml/min. We evaluated the metabolic consequences of different warm retrograde cardioplegic flow rates in low-risk patients. We did not anticipate and we did not find differences in the clinical outcome in these low-risk patients.
The reasons for the requirement of higher flow rates with retrograde than with antegrade infusions are conceptualized in Fig. 7. Retrograde cardioplegia enters the coronary sinus and could be distributed to three "compartments." One compartment represents myocardium, which receives adequate flow to maintain aerobic myocardial metabolism (usually the anterolateral portion of the left ventricle). A second compartment represents underperfused myocardium, which results in anaerobic metabolism and lactate production. Animal studies have suggested that retrograde infusions do not adequately perfuse the right ventricle, posterior left ventricle, and posterior interventricular septum. 2,4,8 Insertion of the retrograde cannula deep into the coronary sinus may further augment this problem. 2 A recent study by Aronson and colleagues 31 assessed retrograde cardioplegic distribution with the use of sonicated microbubbles in patients undergoing cardiac operations. They reported distribution of flow to the right ventricle that was significantly less than flow to the left ventricle at perfusion pressures similar to those used with delivery of high flows in this study.
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6 reported that the shunt may divert up to 74% of coronary sinus perfusates away from nutritive flow. More recent reports have demonstrated that approximately 30% of retrogradely infused solutions are shunted away via thebesian collaterals to the ventricular cavities (predominantly the right ventricular cavity). 4,7,8Fig. 7 also illustrates that the aortic root also receives a systemic arterial contribution, likely from bronchial collaterals. This collateral contribution is significant at flow rates of 100 ml/min, because the aortic root recovery at this flow rate is 132 ml/min. The collateral contribution results in underestimation of myocardial lactate production, oxygen extraction, and acid production because systemic arterial blood has lower lactate and acid and higher oxygen contents than those found in coronary venous effluent. Flow rates higher than 200 ml/min improved myocardial aerobic metabolism with less lactate release and higher coronary effluent pH after crossclamp removal. However, the shunt fraction also increased at flow rates greater than 200 ml/min so that the increase in aortic effluent became less than the increase in cardioplegic flow rate. Previous studies have confirmed our finding that increasing cardioplegic delivery increases the shunt flow. 7,8 Increasing the cardioplegic flow to 300 or 500 ml/min did not further increase myocardial oxygen utilization or decrease cardiac lactate or acid release. Higher cardioplegic flows increase the amount of potassium infused, necessitating treatment for hyperkalemia with insulin or furosemide or the delivery of blood without crystalloid cardioplegia. Our study has some limitations. First, the aortic root effluent samples accurately reflect the nutritive flow through the coronary capillaries, but do not represent all of the cardioplegia delivered into the coronary sinus. Second, the aortic root samples were contaminated with systemic arterial blood with low lactate and acid concentrations, which resulted in underestimation of myocardial lactate and acid production. Third, aortic root samples were occasionally collected after brief (less than 7 minutes) interruptions in cardioplegic flow, which were necessary to allow excellent visualization for completion of distal anastomoses. We have noted that the washout of lactate and acid stabilizes 2 to 3 minutes after the restoration of flow after such interruptions (unpublished data). We incorporated this knowledge into the design of this study such that the aortic root samples were obtained after 4 minutes of restoration of flow.
Inhomogeneous antegrade cardioplegic delivery may reduce perioperative myocardial protection. 32,33 Increasing the retrograde perfusion rate to 300 or 500 ml/min did not prevent lactate production, a finding that suggests that warm retrograde cardioplegia cannot eliminate anaerobic metabolism at any flow rate. Therefore this technique may not provide adequate myocardial protection and should be used with caution. To reduce anaerobic metabolism, a technique that combines antegrade and retrograde cardioplegic infusion may be required. However, retrograde perfusion at flow rates greater than 200 ml/min (with coronary sinus pressures greater than 17 mm Hg) did not improve tissue perfusion or reduce anaerobic metabolism. Cardioplegia delivery at lower flow rates may not afford acceptable myocardial protection and may result in inadequate clinical outcomes.
We thank the perfusionists of The Toronto Hospital for their assistance in this study: Michael P. Courtenay, RRT, CPC, EMCA; Janet E. Cox, RRT, CPC; Edith L. Lacroix, RRT, CPC; Theresa M. Liedke, RN, CCP, CPC; Mindy M. Madonik, BSc, RRT, CCP, CPC; Arthur F. Melo, BSc, RRT, CPC; Lance B. Mitchell, BPhE, CPC, EMCA; Lee M. Noble, RRT, CCP, CPC; and Nancy G. Pretty, RN, CCP, CPC. We also thank Susette Schacherl, BA, for her assistance in the preparation of this manuscript.
References
This article has been cited by other articles:
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|
|
 |
|
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|
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|
|
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|
|
|
|
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|
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|
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|
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|
|
|
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|
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