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Ann Thorac Surg 1999;68:1369-1375
© 1999 The Society of Thoracic Surgeons
a Division of Pediatric Cardiothoracic Surgery, Children’s Hospital Medical Center, Cincinnati, Ohio, USA
Address reprint requests to Dr Pearl, Division of Cardiothoracic Surgery, Children’s Hospital Medical Center, 3333 Burnet Ave, OSB-3, Cincinnati, OH 45229
e-mail: pearj0{at}chmcc.org
Presented at the Poster Session of the Thirty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Antonio, TX, Jan 25–27, 1999.
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Abstract |
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Methods. Plasma TXB2, ET-1, and LTB4 levels were measured in 34 infants undergoing CPB: 22 underwent MUF (group 1), and 12 did not (group 2). Samples were obtained at various time points. All patients underwent conventional ultrafiltration during the rewarming phase of cardiopulmonary bypass.
Results. In group 1, mean end-CPB TXB2 level was 101.2 pg/mL versus 46.9 pg/mL post-MUF (p < 0.05). The mean TXB2 level 1 hour post-CPB (54.1 pg/mL) was not significantly different from the post-MUF level. In group 2, the mean end-CPB TXB2 level was 123.6 pg/mL versus 53.2 pg/mL 1 hour post-CPB. Hence, TXB2 levels decreased by similar amounts and to similar levels by 1 hour post-CPB in both groups. ET-1 levels increased after CPB and were unaffected by MUF: 1.45, 1.80, 2.55 pg/mL at end-CPB, post-MUF, and 1 hour post-CPB, respectively, in group 1; and 1.51, and 2.73 pg/mL at end-CPB and 1 hour post-CPB in group 2. LTB4 levels post-MUF were 119% of pre-MUF values, and were similar at 1 hour post-CPB in both groups.
Conclusions. Despite reduction in TXB2 by MUF, values were similar and approached baseline 1 hour post-CPB in both groups. LTB4 levels increased slightly with MUF. ET-1 levels increased during and post-CPB and were unaffected by MUF. MUF does not appear to have a significant effect on post-CPB levels of TXB2, ET-1, and LTB4. Therefore, the improved hemodynamics observed with MUF do not appear to be related to removal of these cytokines.
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More sophisticated animal and human studies have documented improved systolic and diastolic ventricular function with MUF [3, 5]. In addition, improved pulmonary function and decreased ventilator time have been suggested [7, 8]. MUF has been shown to decrease postoperative blood loss, chest tube output, and the incidence of pleural effusions in patients undergoing cavopulmonary connections [9].
Unfortunately, in most studies to date, groups were not standardized with respect to the use or type of conventional ultrafiltration (UF) used during cardiopulmonary bypass (CPB). It is likely that conventional UF or dilutional UF during CPB would have a significant effect on myocardial edema and function, as well as on total lung water and pulmonary function. Because of variations in technique in prior nonstandardized studies, it is difficult to ascertain whether postbypass MUF is of significant additional benefit over aggressive conventional or dilutional UF.
In addition, it has been suggested that MUF and conventional UF decrease levels of various cytokines and inflammatory mediators [6, 10–12]. Elevated levels of endothelin-1 (ET-1) and thromboxane B2 (TXB2) have been correlated with postoperative pulmonary hypertension, myocardial dysfunction, and reperfusion/reoxygenation injury [10, 13]. Cardiopulmonary bypass activates circulating leukocytes, resulting in increased levels of leukotriene (LTB4). LTB4 is a potent chemotactic cytokine whose levels correlate with leukocyte-mediated injury [14]. Effective removal of these mediators could result in lower postoperative levels, which might contribute to improved cardiopulmonary function.
Due to differences in either the type of ultrafiltration used on CPB between groups, or the complete absence of conventional ultrafiltration, the contribution of cytokine removal by postbypass MUF remains unclear. In order to define the potential benefit of MUF on removal of ET-1, TXB2, and LTB4, two groups of infants with identical intraoperative ultrafiltration techniques were studied, the only difference being the addition of MUF post-CPB in one group.
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Material and methods |
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Conduct of bypass and ultrafiltration
In all infants, the pump was primed with 1 or 2 U of whole blood or packed red blood cells. Prime additives included Solumedrol (30 mg/kg), cefazolin (25 mg/kg), albumin (25 gm), heparin (2,000 U), and NaHCO3 (25 milli-equivalents). The D901 Lilliput 1 hollow-fiber membrane oxygenator (Dideco, Mirandola, Italy) was used for all patients, and circuits were constructed using similar tubing size. Total prime volume was 800 mL.
Conventional UF was begun as soon as rewarming was started. The AN69H Hemofilter/dialyzer (Hospal Industry, Meyzieu, France) was used in all cases. Excess volume in the CPB circuit was reduced to the lowest, safe operating level before the termination of CPB. After termination of CPB, arterio-venous MUF was carried out. Blood was drained from the aortic cannula, pumped through the ultrafiltrator and reinfused through the cardioplegia system into a venous cannula. MUF was carried out in three phases.
Phase I
Blood was drawn off the aortic cannula at approximately 30% of a 2.5-L/min/m2 cardiac index. The ultrafiltrator effluent line was attached to wall vacuum at 400 mm Hg. To maintain an adequate filling pressure left atrial (LA) or central venous pressure (CVP) while volume was being removed by the ultrafiltrator, remaining volume in the venous reservoir was transfused into the ultrafiltration circuit via the arterial pump. Once the venous reservoir was empty, an additional 200 to 400 mL of Normosol was placed into the cardiotomy reservoir, and infusion continued until the arterial boot and oxygenator were cleared of red blood cells. On average, this phase took about 10 to 15 minutes.
Phase II
After reinfusion of all residual volume in the venous reservoir and oxygenator, volume continued to be drained via the arterial cannula and ultrafiltered, but no additional volume was transfused via the arterial pump. The ultrafiltrator effluent line suction was decreased to 200 mm Hg. The "drying-out" phase of MUF was continued until the filling pressure or mean arterial pressure was as low as the surgeon felt was acceptable. This phase usually took 3 to 5 minutes.
Phase III
The goal of this final phase was to reinfuse all of the volume contained in the arterial line, cardioplegia administration set, and ultrafiltrator. The arterial cannula was removed and the arterial line was emptied to the ultrafiltrator. The vacuum was turned off while Protamine was administered, and the remaining volume in the cardioplegia administration set was transfused. Depending on the patients’ hemodynamics, the remainder of the volume was transfused as needed.
Blood samples were obtained from the patients’ arterial line pre- and postbypass, and from the venous line of the bypass circuit while on CPB. Samples were obtained prebypass, at 15 and 60 minutes of CPB, end-CPB, post-MUF (in group 1), and 1 hour post-CPB. Four milliliters of blood was obtained and placed in tubes containing EDTA and indomethacin (10 µg/mL) and immediately placed on ice. All samples were centrifuged at 4°C within 1 hour of collection and the supernatant stored at -80°C. The supernatant was assayed for TXB2 (the metabolite of thromboxane A2), ET-1, and LTB4.
ET-1 assay
A commercial ET-1 immunoassay kit (R&D Systems, Minneapolis, MN) was used to measure ET-1 (in pg/mL).
TXB2 assay and LTB4 assay
Frozen samples were thawed and underwent an extraction process. Ethanol extraction was carried out by passing samples through a C-18 Reverse Phase Column (Varian, Harbor City, CA) under a slight vacuum. Columns were then flushed with ethanol and hexane and eluted with an ethyl acetate/1% methanol solution. Samples were then evaporated under a stream of nitrogen and reconstituted. Analysis was performed using an enzyme-linked immunosorbent assay technique with kits supplied by Assay Designs (Ann Arbor, MI).
Statistical analysis
Analysis of variance and the two-tailed, paired Student’s t test were used to compared values at different time periods. A p value less than or equal to 0.05 was considered significant (Statview 4.01 software; Abacus Concepts Inc, Berkeley, CA).
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(TNF) and interleukins (IL), and increases in eicosanoids such as TXB2 and ET-1, have been demonstrated [18]. It has been theorized that in addition to the effect of extracorporeal circulation itself, part of the cardiopulmonary dysfunction associated with bypass is related to relative pulmonary ischemia and subsequent reperfusion injury while on total CPB without ventilation [13, 16]. Increased pulmonary leukocyte activity, and increased pulmonary TXB2 and ET-1, have been found after CPB [16, 19]. LTB4, a potent chemotactic cytokine, is increased by CPB and can be correlated with increased leukocyte activity, as determined by tissue myeloperoxidase activity [14]. Attempts to minimize the adverse effects of activated inflammatory mediators have included improved oxygenator and circuit design, use of heparin-bonded circuits [20], administration of antiinflammatory agents such as steroids [21, 22], use of TXB2 blockers [23] or of endothelin-converting enzyme blockers [24], and removal of mediators with a variety of methods of conventional or modified ultrafiltration [6, 7, 9, 11, 25].
Several studies have reported improved hemodynamics in addition to improved fluid balance and increased hematocrit with MUF [3–5, 9]. However, "hemodynamics" (usually reported as improved mean arterial pressure) may be influenced by many factors in the early post-CPB period. Few studies have carefully analyzed these hemodynamic changes attributed to MUF in a controlled comparison with patients not undergoing MUF. Nonetheless, this subjective observation has resulted in attempts to find objective support.
Effect of MUF on hematocrit and free water
Initial reports on MUF concluded that MUF decreased blood usage and decreased chest tube drainage in pediatric cardiac patients [2, 6]. However, despite a greater hematocrit immediately post-MUF, values 4 hours later have been shown to be identical to patients without MUF [2]. Other studies have also shown no difference in hematocrit between groups at any time during the perioperative period, suggesting increased use of blood products in non-MUF patients [6]. From these studies, it could be concluded that the combination of miniaturizing circuits and oxygenator size, along with aggressive conventional ultrafiltration and MUF, could decrease blood usage.
Effect of MUF on cardiopulmonary function: cardiac function
In one of the few controlled studies of MUF done in animals, Daggett and colleagues did demonstrate improved preload recruitable stroke work after CPB with cardioplegic arrest in animals undergoing MUF compared with either conventional UF or no UF [5]. This functional improvement was correlated with lower myocardial water content (ie, less myocardial edema). Total body weight gain was also significantly less with MUF than with either conventional UF or no UF. However, in the conventional UF group, fluid removed by UF during CPB was replaced with lactate ringers, resulting in no net fluid removal. It is not surprising that this form of zero-balance ultrafiltration (Z-BUF) did not decrease total body water.
In the only human MUF study with sophisticated analysis of ventricular function, the group from Great Ormand Street Hospital in London did demonstrate improved ventricular function in infants undergoing MUF after CPB compared with no MUF [3]. The infants undergoing MUF had a decrease in myocardial cross-sectional area, decrease in end-diastolic length, decrease in end-diastolic pressure, increase in mean ejection pressure, and an increase in the slope of the preload recruitable stroke work index. Despite a relatively small number of patients, this study has provided conclusive evidence that MUF does improve both diastolic and systolic function.
However, an important limitation of the Great Ormand Street study was that conventional UF was not done during bypass in either group. Hence, the comparison was really between some form of ultrafiltration, in this case MUF, and no ultrafiltration at all. It is likely that conventional UF would have had some effect on decreasing myocardial edema and, hence, on ventricular function. This study needs to be viewed in terms of the benefits of any ultrafiltration versus no ultrafiltration, rather than specifically in terms of MUF.
Effect of MUF on cardiopulmonary function: pulmonary function
It has also been suggested that MUF improves postoperative pulmonary function. A recent publication by Bando and colleagues showed marked decrease in post-op ventilation time in patients undergoing MUF [7]. The difference was most pronounced in patients with preoperative pulmonary hypertension, prolonged bypass times, and in neonates. However, the overall ventilator time in both groups seemed high compared with our current experience.
Unfortunately, this was not a controlled study in that the technique of ultrafiltration during CPB was quite different between the MUF and non-MUF group, adding another significant variable. MUF patients underwent dilutional UF while on CPB with a total of 42.2 mL/kg of fluid removed during CPB. In contrast, the non-MUF patients underwent only conventional UF during CPB with an average of 25.6 mL/kg removed (40% less). The amount of fluid removed by MUF was considerably greater, averaging 124.7 mL/kg. This makes comparison of the two groups difficult because MUF was not the only variable. It is possible that more aggressive conventional or dilutional UF in the non-MUF group would have minimized the reported differences between the two groups.
It is interesting that in Bando’s study the hematocrit was no different between groups at any time during the perioperative period, indicating more liberal use of blood products in the non-MUF patients. Increased blood exposure may be more of a factor in terms of ventilator time and pulmonary inflammatory response than whether patients underwent MUF or not. Once again, more aggressive ultrafiltration on CPB may also decrease blood usage and limit the resultant pulmonary injury.
Effect of MUF on inflammatory mediators
Increased levels of TXB2 have been documented in humans undergoing CPB [26, 27]. The major source of this increase is thought to be from pulmonary tissue [27], although release from activated platelets may also contribute. Additionally, increases in the levels of TNF, IL-1 and IL-6, leukotrienes, and ET-1 have been demonstrated [10, 17, 28].
Substances that are stored and released such as TXB2 have a very short half-life. Therefore, removal of the stimulus for their production (ie, CPB) should result in a fairly rapid fall in levels, such has been demonstrated with TXB2 in this study. Other mediators, such as ET-1, require gene activation with increased transcription and translation for increased levels. Gene activation may persist for some time after CPB. Hence, either conventional or modified ultrafiltration would not be expected to significantly influence production or levels of these substances. The molecular regulation behind production of some cytokines, therefore, creates a conceptual problem regarding the ability of MUF to effectively decrease their levels. If bypass is the stimulus for continued synthesis and release of these substances, continued circulation of blood through the bypass circuit during MUF would continue to perpetuate this process.
Conventional versus modified ultrafiltration
In a study similar to ours, Wang and colleagues found no difference between conventional and modified ultrafiltration in terms of removing the inflammatory mediators IL-6, IL-8, TNF-, and leukocyte elastase. In fact, plasma concentrations of all of these substances increased after UF or MUF, despite passage of these mediators into the ultrafiltrate. Ultrafiltration was more efficient at removing TNF- than the other mediators, yet levels still increased post-MUF [11]. Similarly, in a pig model of endotoxic shock, veno-venous hemofiltration did not significantly reduce plasma concentration of TNF, PGE2, PGF1, or TXB2 [29]. In contrast to Wang’s findings, these investigators found that TNF did not move across the membrane into the filtrate, although the other mediators were found in the filtrate. While the presence or absence of these cytokines in the effluent is important, the exact concentrations are not helpful due to the large and variable amount of effluent. Measurement can be difficult due to the sensitivity of the assays in relationship to the diluted concentrations.
Assuming that MUF could remove certain inflammatory cytokines such as complement and interleukins, then ultrafiltration during the rewarming phase of bypass would be expected to as well. Indeed, in a study of 20 children, a reduction in TNF, IL-10, and C3A was demonstrated with conventional ultrafiltration, which resulted in lower levels of IL-1, IL-6, and IL-8 24 hours postbypass [25].
In another study of 32 patients undergoing Tetralogy of Fallot (TOF) repair, aggressive ultrafiltration on CPB decreased plasma concentrations of C3A, C5a, IL-6, and TNF [30]. Patients undergoing conventional UF demonstrated improved hemodynamics, reduced blood loss, improved aveolar-arterial (A-a) gradient, and decreased ventilator time. Despite removal of some inflammatory mediators in this study, the improved cardiopulmonary function was attributed primarily to decreasing total body water (TBW). MUF was not used.
Our own data demonstrate removal of between 214 and 373 mL/kg of fluid by UF, and an additional 138 mL/kg when MUF was used. These volumes are much greater than that reported by others. Prime volumes may vary considerably among centers, accounting for some of the wide variation in the amount of fluid removed by conventional UF. In addition, the amount of crystalloid added to the bypass circuit from cardioplegia and iced saline/slush is unknown. It is clear, however, that significant net fluid removal can be accomplished with conventional ultrafiltration. In many instances, this amount may be greater than that which can be removed by MUF, as in our experience. The ability to remove volume by conventional UF may negate some of the benefits ascribed by MUF.
ET-1 and ultrafiltration
ET-1 is a potent pulmonary vasoconstrictor and is responsible for the later phases of hypoxic or endotoxin-induced pulmonary hypertension. ET-1 is also a myocardial depressant and is involved with leukocyte adhesion and activation. Increased levels of ET-1 have been demonstrated in acute hypoxia-reoxygenation, chronic hypoxia, and after CPB [10, 24]. Both ET-1 receptor expression and pulmonary ET-1 production increase in the lung after CPB [19]. In patients with low-flow pulmonary hypertension, preoperative ET-1 levels have been shown to be significantly higher, and to increase further postoperatively, peaking at 6 hours [10]. Due to the very short half-life of ET-1, this peak can only be from continued production and release of ET-1.
In patients with preoperative pulmonary hypertension, Bando and colleagues demonstrated that the combination of dilutional UF and MUF resulted in significantly lower ET-1 levels at end surgery, 3, 6, and 12 hours postoperatively compared with patients undergoing conventional ultrafiltration [31]. However, as mentioned previously, conventional ultrafiltration was used in the non-MUF group, whereas dilutional ultrafiltration, which removed twice the volume during CPB, was used in the MUF group. ET-1 levels, which were fairly high at end-CPB, fell from 8 to 3 pg/mL during MUF, and continued to fall postoperatively. In the non-MUF group, ET-1 levels remained elevated at 6 to 12 hours postoperatively.
The significant and persistent decrease in ET-1 with MUF seen in Bando’s study [7] is difficult to explain. ET-1 is not stored in significant quantities and requires transcription and translation to increase blood levels. Assuming this process is activated by hypoxia-reoxygenation and/or CPB, increased ET-1 production should occur to a similar degree in both groups. Increased levels postoperatively reflect ongoing production and should be unrelated to whatever blood levels were present at end-CPB or end-MUF. Such a striking difference between these two groups could only be related to marked differences in ongoing ET-1 production, rather than whether ET-1 was removed by ultrafiltration or not.
In contrast to Bando’s findings, we have demonstrated both in humans and in an animal model [32] a steady increase in arterial ET-1 levels during CPB including during ultrafiltration and MUF. Even if ET-1 can pass into the ultrafiltrate, the ongoing production is likely to replenish systemic levels rapidly once UF or MUF is stopped. Decreased pulmonary hypertension as a result of MUF may be explained by decreased lung edema, or preservation of the nitric oxide pathway, rather than by removal of ET-1.
Leukotriene B4
Our results show a consistent increase in LTB4 during bypass, with a further slight increase during MUF. Levels begin to fall postbypass. It does not appear that UF or MUF have a significant effect on LTB4 levels, and in fact, levels increase by 24% during MUF. Continued activation of leukocytes by the bypass circuit, oxygenator, and/or ultrafiltrator undoubtedly leads to continued production and release of LTB4 and continued high levels. This effect may persist for considerable time postoperatively. Gadaleta and associates demonstrated increased LTB4 generation by neutrophils 24 hours post-CPB [14]. As the primary stimulus is removed with the termination of any form of extracorporeal circulation (CPB or MUF), leukocyte production of LTB4 eventually decreases and levels fall. Even if MUF could acutely decrease levels of LTB4, it is likely that they would rapidly increase again secondary to continued release by activated neutrophils.
Thromboxane B2
Levels of TXB2 more than triple on CPB. TXB2 has been correlated with pulmonary hypertension, pulmonary cellular sequestration, and increased capillary leak [23]. Pulmonary tissue and platelets are the main known sources of TXB2. Platelet activation from CPB and pulmonary ischemia as a consequence of decreased pulmonary blood flow during CPB bypass result in marked increases in TXB2 levels. TXB2 falls rapidly once extracorporeal circulation ceases. Although ultrafiltration can remove TXB2, levels by 1 hour post-CPB are similar whether MUF is used or not. It is unlikely that a slightly earlier decrease in levels of TXB2 with MUF is of clinical significance.
Conclusion
It is likely that much of the improvement in hemodynamics seen with MUF, or with UF, is a consequence of increased hematocrit, decreased myocardial edema, and decreased lung water. In fact, in a piglet study looking at the effect of MUF on cerebral metabolic recovery, animals that did not undergo MUF, but were transfused to similar hematocrits, had comparable hemodynamics [33]. MUF may have advantages in terms of decreasing myocardial edema and lung water when conventional UF is either not performed, or done only minimally. Effective removal of TXB2, LTB4, and ET-1 does not appear to be a significant component of the improvement in hemodynamics and pulmonary function seen with MUF. It is possible that removal of complement or other cytokines such as TNF may be of clinical significance. However, the decrease of other mediators such as ET-1 can only occur by downregulation of ET-1 production once the stimulus (ie, CPB) is stopped. It is likely that the most significant benefit of either ultrafiltration or MUF is from reversal of hemodilution and decreasing total body water. The improvement in cardiopulmonary function associated with MUF is not related to removal of ET-1, TXB2, or LTB4. Critical analysis of the available data does not support a significant additive benefit for MUF, when aggressive ultrafiltration is carried out on CPB.
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