Asian Cardiovasc Thorac Ann 2005;13:17-19
© 2005 Asia Publishing EXchange Ltd
Intraoperative Hemofiltration in Adults: Prevention of Hypercirculatory Syndrome?
Theodor Tirilomis, MD,
Martin Friedrich, MD,
Horia Sîrbu, MD,
Ivan Aleksic, MD,
Thomas Busch, PhD
Department of Thoracic, Cardiac and Vascular Surgery, University of Göttingen, Göttingen, Germany
For reprint information contact: Theodor Tirilomis, MD Tel: 49 551 396 025 Fax: 49 551 396 002 Email: theodor.tirilomis{at}med.uni-goettingen.de, Department of Thoracic, Cardiac and Vascular Surgery, University of Göttingen. Robert-Koch-Str. 40, Göttingen D-37075, Germany.
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ABSTRACT
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Hypercirculatory syndrome (HCS) after cardiac surgery may be a sequela of extracorporeal circulation due to hemodilution and release of inflammatory mediators. The aim of this study was to investigate the influence of intraoperative hemofiltration (HF) on the incidence of HCS. A prospective cohort study of 80 patients scheduled for elective coronary bypass was performed. The patients were randomized to two groups: in the conventional (CONV) group 40 patients were treated conventionally and in the HF group 40 patients underwent intraoperative HF. There was no perioperative mortality. The incidence of HCS was comparable in both groups (32% in CONV group versus 40% in HF group; n.s.). Mean cardiac output was higher and systemic vascular resistance lower in CONV group patients than in HF group patients, however these differences did not reach statistical significance. According to this data intraoperative HF does not prevent postoperative HCS induced by cardiopulmonary bypass. Further studies are required to identify the etiology of HCS, and to prevent it occurring after open-heart surgery.
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INTRODUCTION
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Approximately 10% of patients undergoing open-heart surgery develop a hypercirculatory syndrome (HCS) after the procedure.1 The cause of this condition is still not clear. It is probably a component of the systemic inflammatory response syndrome (SIRS) that develops due to surgical trauma and is mainly associated with the use of cardiopulmonary bypass (CPB). Otherwise, there is evidence of induction of a hypercirculatory syndrome induced by hemodilution and fluid overload at the beginning and during extracorporeal circulation.2 Direct effects of cardioplegia solutions during surgery may also induce a hypercirculatory syndrome.3 Surgical manipulation during these operations may potentiate these effects. However, even if the etiology of postoperative hypercirculatory syndrome is unknown, it is known that the insult that initiates the response is going to occur, and that it may adversely influence patient outcome due to postoperative organ dysfunction.1,4
Experimental5 and clinical studies6 in neonates and infants have shown positive effects of filtration, mainly on the prevention of SIRS. The aim of this study was to determine if postoperative HCS in adults can be prevented by removing the fluid overload and inflammatory factors associated with CPB.
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PATIENTS AND METHODS
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A prospective cohort study of 80 patients scheduled for elective coronary bypass was performed. The patients were randomized into two equal groups of 40 patients: in the CONV group the patients were treated conventionally and in the HF group the patients underwent intraoperative hemofiltration during CPB. Patients with ejection fraction < 40%, diabetes mellitus, severe pulmonary, renal, and hepatic failure, or significant peripheral vascular disease and patients with concomitant cardiac disease or redo procedures were excluded from the study. In the CONV group 18 patients were male and 22 female, in the HF group 21 and 19 respectively. Mean age in the CONV group was 63 ± 2 years and in the HF group 65 ± 2 years.
All operations were performed through median sternotomy and all patients were connected to the CPB with venous cannulation of the right atrium using a double-stage cannula and arterial cannulation of the ascending aorta. The priming volume of the heart-lung machine consisted of 1L Ringer’s lactate solution and 0.5L hydroxyethylstarch 6%. During CPB mild systemic hypothermia of 32°C was applied. Myocardial protection was performed by topical cooling of the heart and antegrade application of 2L cold crystalloid Bretschneider’s cardioplegia. Blood suctioned from the operative field was collected by the heart-lung machine in the reservoir and returned to the patient. In the HF group zero-fluid balanced hemofiltration was performed during CPB to eliminate priming volume and cardioplegia solution. Further intraoperative and postoperative treatments did not differ between patients of both groups.
In all cases a Swan-Ganz catheter was used. Cardiac output was measured by the thermodilution method and hemodynamic variables were calculated before surgery, before CPB start, at the end of CPB, at the end of surgery, and hourly after CPB. HCS was defined as simultaneous presence of cardiac output > 6 L·min–1, systemic vascular resistance < 800 dyn s cm–5, and mean arterial pressure < 60 mm Hg.
Data are presented as mean ± standard deviation. For statistical analysis multiple analyses of variance for repeated measurements (MANOVA) were used. For post-hoc comparison Student’s t test was applied. A level of p < 0.05 was considered statistically significant.
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RESULTS
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The perioperative and clinical results were comparable in both groups. CPB time was 67 ± 4 minutes (min) in the CONV group and 68 ± 3 min in the HF group, aortic cross-clamp time was 47 ± 7 min and 49 ± 2 min, respectively. There were no early deaths or severe postoperative complications.
The hemodynamic data did not show statistically significant differences between the groups. In both groups cardiac output increased after surgery, systemic vascular resistance decreased at the end of CPB followed by a slight increase, and mean arterial pressure showed an initial drop immediately at the end of CPB, followed by an increase thereafter. The previously mentioned criteria of HCS were fulfilled at any time after CPB in 32% of the patients in CONV group and 40% of the patients in HF group (Figure 1
). This result is surprising, but without statistical significance. Comparing the subgroups with respect to presence of postoperative HCS, the mean values of cardiac output were lower in the HF group than in the CONV group (Figure 2) and the mean values of systemic vascular resistance were higher in HF group than in CONV group (Figure 3), although again these differences did not reach statistical significance.
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Figure 2. Mean values of cardiac output in the subgroups of CONV group and HF group with presented (HCS) or not presented (non-HCS) postoperative HCS.
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Figure 3. Mean values of systemic vascular resistance in the subgroups of CONV group and HF group with presented (HCS) or not presented (non-HCS) postoperative HCS.
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DISCUSSION
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Postoperative HCS is probably a facet of the SIRS as a result of surgical trauma, use of CPB, perioperative surgical and anesthesiological management. It may adversely influence outcome after open-heart surgery due to postoperative heart failure. The observation that the criteria for postoperative HCS were fulfilled in approximately one-third of the patients after CPB was very surprising. A possible explanation for this high incidence may be the very close monitoring of hemodynamics in this group of patients whereas previous studies reported only clinical observations.
The present study demonstrated that intraoperative HF does not prevent postoperative HCS. Although the intention of the presented study was not to identify mechanisms inducing HCS after open-heart surgery, it can be accepted that intraoperative hemodilution is not a singular cause of HCS in adults. Between patients with intraoperative HF and patients without HF there were no differences in postoperative morbidity and outcome. In accordance with our results, Babka et al7 in a prospective study found no significant differences in clinical parameters between the group of patients on whom intraoperative HF was used and the group of patients who did not receive HF, notably no difference in postoperative blood loss, transfused blood units, or length of stay after surgery.
Due to the encouraging results of modified ultrafiltration after pediatric cardiac operations, modifications of HF techniques in adults have also been applied. Tassani and colleagues8 investigated the inflammatory response in CABG patients undergoing combined zero-balanced ultrafiltration during rewarming and modified ultrafiltration immediately after the end of CPB, versus a control (not-hemofiltrated) group. The investigators found diminished concentrations of interleukin-6 and interleukin-8 only in a very limited time period immediately after the end of CPB in patients with HF compared to the not hemofiltrated patients. Clinical parameters improved slightly, with earlier extubation after surgery in the study patient cohort.
In an experimental animal study, Eising et al9 found that combined conventional and modified HFwas ineffective in reducing the inflammatory process, or improving cardiac function in the pig model. Grünenfelder et al10 reported lower levels of adhesion molecules and cytokines in adult patients with modified ultrafiltration performed after the end of CPB. However, they could not demonstrate any significant impact on the clinical outcome of patients undergoing elective coronary artery bypass grafting. In contrast to these findings, Luciani and colleagues11 found significantly lower rates of respiratory, neurological, and gastrointestinal complications and blood transfusion requirements in patients treated with modified ultrafiltration at the end of CPB, but there was no difference in cardiac morbidity.
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CONCLUSION
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Our data suggests that intraoperative hemofiltration in adults does not prevent postoperative hypercirculatory syndrome induced by cardiopulmonary bypass. Our study is in concordance with previous reports on this and similar topics, which support a strong interest in treatment preventing perioperative hemodynamic instability. Further studies are required to identify the etiology of hypercirculatory syndrome and prevent the development of such circulatory dysregulation after open-heart surgery.
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References
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ABSTRACT
INTRODUCTION
