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Ann Thorac Surg 1995;59:137-143
© 1995 The Society of Thoracic Surgeons

Normothermia Versus Hypothermia During Cardiopulmonary Bypass: A Randomized, Controlled Trial

Clinic for Cardiovascular Surgery, Institute of Anaesthesiology, Institute of Clinical Immunology, and Institute for Clinical Chemistry, University Hospital, Zurich, Switzerland

Accepted for publication July 22, 1994.

	Abstract

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
To evaluate the influence of perfusion temperature on systemic effects of cardiopulmonary bypass (CPB), 30 patients undergoing elective coronary artery bypass grafting were randomly assigned to either normothermic (warm, n = 14, 36°C) or hypothermic (cold, n = 16, 28°C) CPB. Serial hemodynamic measurements and blood samples were obtained before, during and after the CPB procedure. During CPB, there were no differences between both groups in the need for vasopressors (norepinephrine, phenylephrine), urinary output, or fluid balance. In the early postoperative period, normothermic CPB patients had significantly lower systemic vascular resistance and higher cardiac index measurements (mean ± standard error: systemic vascular resistance, 880 ± 27 versus 1,060 ± 57 dyne • s • cm^-5, p = 0.025; cardiac index, 3.6 ± 0.1 versus 2.9 ± 0.1 L • min^-1 • m^-2, p = 0.01) without differences in the administration of vasoactive drugs. Blood loss was significantly higher in patients after hypothermic CPB (median [range] body surface area: 370 [180–560] versus 490 [280–2,120] mL/m², p = 0.0006), with a greater need for transfusion of erythrocytes and fresh frozen plasma. Plasma levels of tumor necrosis factor and soluble tumor necrosis factor receptors increased during and after CPB, independent of perfusion temperature. This study suggests a significant influence of CPB temperature and respective perfusion management on postoperative hemodynamics and blood loss. Normothermic CPB is not associated with additional systemic adverse effects.

	Introduction

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Cardiopulmonary bypass (CPB) has been found to be associated with a wide variety of early postoperative physiologic and immunologic derangements, including an increase in capillary permeability with accumulation of interstitial fluid, fever, leukocytosis, bleeding diathesis, hypotension, and hepatic, cardiac, pulmonary, and renal dysfunction, with a wide spectrum of severity [1]. These events are considered to be the expression of an inflammatory reaction due to extensive cellular activation by the material of the extracorporeal circuit and the surgical trauma, with the release of inflammatory mediators. There is some evidence that at least a part of the mechanisms involved in the pathogenesis of this systemic inflammatory reaction might be dependent on systemic perfusion temperature during CPB [1, 2]. Because of a renewed interest in normothermic myocardial protection [3–6], normothermic CPB gained increasing popularity. It was the aim of this prospective, randomized study to evaluate the influence of temperature during CPB on postperfusion damages.

	Patients and Methods

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Patients
Thirty consecutive patients undergoing elective coronary artery bypass grafting procedures were studied in a prospective randomized trial. The study was approved by the local ethics committee. To guarantee identical postoperative management in the intensive care unit, only patients who were scheduled for first procedures of the day were included in the study. Patients with an ejection fraction less than 0.35, age greater than 65 years, previous cardiac procedures, or impaired lung, liver, or renal function were excluded. Informed consent was obtained before randomization. Fourteen patients were elected for normothermic CPB (warm group), 16 for hypothermic CPB (cold group). The preoperative clinical profiles of patients in the two groups are summarized in Table 1.

Postoperative Care
After the operation, patients were transported to the intensive care unit. All patients were ventilated in a volume-controlled mode until normal peripheral temperature and stable hemodynamics allowed respiratory weaning. In addition to a standard infusion of Ringer's lactate, hydroxyethylstarch, 5% human albumin, and crystalloids were given to keep filling pressures and mean arterial pressures at adequate levels. Additionally, mean arterial pressures were held between 60 and 80 mm Hg with the infusion of vasodilators (phentolamin, nitroglycerine, nifedipine) or inotropic agents (or both) when necessary. If there was evidence of increased postoperative bleeding, fresh frozen plasma was infused to improve hemostatic properties of the blood. Packed red cells were given when hematocrit level fell to less than 25%.

Measurements
INTRAOPERATIVE DATA.
Intraoperative variables included CPB time, aortic cross-clamp time, reperfusion time, need for vasopressors and volume administered during CPB, minimal rectal temperature, urinary output, need for blood products, and number of aortocoronary bypass grafts.

POSTOPERATIVE DATA.
In the postoperative period (until the morning of the first postoperative day, ie, the first 18 postoperative hours) the following parameters were analyzed: volume administration (crystalloids, hydroxyethylstarch, 5% human albumin), need for blood products (packed red cells, fresh frozen plasma), urinary output, need for vasodilators (phentolamin, nitroglycerine, nifedipine) and diuretics, need for inotropic agent support, blood loss, rectal temperature, and postoperative intubation time. Inotropic agent support was defined as the need for more than 2 µg • kg^-1 • min^-1 of dopamine or the need for dobutamine, epinephrine, or norepinephrine in any dose.

HEMATOLOGY.
Analyses included blood hemoglobin levels, hematocrit, platelet counts, serum levels of creatine kinase and its myocardial-specific isoenzyme, liver enzymes, pancreas-specific amylase, lactic dehydrogenase, creatinine, C-reactive protein, tumor necrosis factor (TNF ), and the soluble TNF receptor (sTNFR). Serial blood samples were obtained the day before operation, after heparinization but before CPB, at 15 and 30 minutes after the initiation of CPB, and at the end of CPB (after weaning and before protamine administration). Further samples were obtained 3 and 9 hours after weaning from CPB and on the first, second, and sixth postoperative days. Blood samples for TNF and the sTNFR assay were anticoagulated with ethylenediaminetetraacetic acid and immediately centrifuged. Serum concentrations of TNF and sTNFR were determined using a commercially available enzyme-linked immunosorbent assay (TNF ELISA, Endogen, Boston, MA; sTNFR ELISA, Bender & Co GmbH, Vienna, Austria).

HEMODYNAMIC MEASUREMENTS.
In all patients a pulmonary thermodilution catheter was introduced after induction of anesthesia and baseline measurements of standard hemodynamics were taken. Thereafter, serial measurements were performed after closure of the chest, 3 and 9 hours after the end of the operation, and the next morning. Systemic vascular resistance was calculated by standard formulas.

Statistics
All values are reported as mean (± standard error of the mean) or as median with the range given in brackets. Data were analyzed by means of a statistical system (StatView 4.0, Abacus Concepts, Inc, Berkeley, CA). Differences among groups for continuous data were assessed with unpaired Student's t test or the Mann-Whitney test according to distribution; ² analysis and Fisher's exact test were employed for categorical data. Summary measures (peak values, area under the curve) were used for comparison of hemodynamic measurements, administration of vasoactive drugs, urinary output, blood hemoglobin levels, platelet counts, plasma concentrations of TNF and sTNFR, rectal temperature, and blood chemistry during the postoperative period [7]. Differences were considered significant at a probability level of p less than 0.05.

	Results

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
There were no significant differences between the groups in risk factors for coronary artery disease and risk factors for perioperative morbidity and mortality, with the exception of a lower prevalence of diabetic patients in the cold group (see Table 1).

Intraoperative Data
Patients in both groups were similar with respect to number of bypass grafts performed, use of internal thoracic artery, and modes of cardioplegia delivery (Table 2). There was no difference in the need for vasopressors to maintain defined systemic pressure during CPB (warm versus cold: cumulative dose of norepinephrine, 28 [0–280] versus 32 [0–380] µg, p = 0.61; phenylephrine, 0 [0–600] versus 0 [0–1,000] µg, p = 0.34). There was a tendency toward shorter CPB time in the group of patients operated in normothermia, although this tendency did not reach statistical significance.

View larger version (21K): [in this window] [in a new window]   Fig 1. . Cardiac index and systemic vascular resistance (SVR) after normothermic () and hypothermic () cardiopulmonary bypass (CPB). The area under the curve of cardiac index was significantly larger in patients after normothermic CPB (p = 0.01) with significantly lower SVR during the same period (p = 0.025). All values are mean ± standard error of the mean.

View larger version (18K): [in this window] [in a new window]   Fig 2. . Rectal temperature during the first postoperative hours in patients after normothermic () and hypothermic () cardiopulmonary bypass (CPB). Note that patients in the hypothermic group remained significantly colder until the first day (p = 0.002). All values are mean ± standard error of the mean.

INFLAMMATORY MEDIATORS.
TNF levels over time in both groups are summarized in Table 4. Because of a marked intrapatient variability over time, a specific postoperative course of TNF levels could not be established. In both groups, there was an increase in TNF levels during or after operation (or both) (p < 0.0001). Neither peak TNF levels nor area under the curve differed after warm or cold systemic perfusion (peak TNF: warm, 52 [11–352] versus cold, 36 [1–171] pg/mL, p = 0.63; TNF area under the curve: 12 [1–72] versus 9 [0–59] pg/mL, p = 0.87). On the first postoperative day, TNF levels returned to almost normal values in both groups (normal: 0 to 6.3 pg/mL). Soluble TNF-receptor levels rose significantly during and after the procedure and peaked at 3 hours postoperatively, independent of CPB temperature. The area under the curve of sTNFR levels were similar in both groups (warm, 0.37 [0.22–0.44]; cold, 0.35 [0.18–0.78] ng/mL, p = 0.51).

View larger version (27K): [in this window] [in a new window]   Fig 3. . Time course of serum levels of creatine kinase (CK) and its myocardial-specific isoenzyme (CK-MB), liver enzymes (GOT, GPT), lactic dehydrogenase (LDH), pancreas-specific amylase (p Amylase), creatinine, C-reactive protein (CRP) from the day of admission (Day -1) to the sixth postoperative day in patients after normothermic () and hypothermic () cardiopulmonary bypass (CPB). The area under the curve showed no significant differences between groups. All values are mean ± standard error of the mean.

	Comment

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

Tumor Necrosis Factor
Strong evidence suggests that TNF plays a central role in the development of the systemic inflammatory response syndrome, regardless of whether it is of infectious or noninfectious origin [8, 9]. It is the only cytokine identified thus far that is capable of triggering the entire spectrum of physiologic, humoral, and tissue responses characteristic of the septic shock syndrome such as fever, shock, myocardial depression, capillary leakage, pulmonary edema, adult respiratory distress syndrome, oliguric renal failure, gastrointestinal necrosis, and many more responses [10, 11]. Cells derived from the monocyte/macrophage lineage are the principal source of TNF, but TNF is also made by various other cells, ie Kupfer cells, T cells, and B cells, and is released in response to endotoxin, enterotoxin, and products of complement activation [10]. Several studies demonstrated a more or less pronounced release of TNF during and after CPB [12, 13], indicating that at least a part of the whole body inflammatory reaction might be triggered by TNF. In our study, plasma TNF levels rose significantly during and after CPB. As in other studies [14, 15], the intrapatient and interpatient variability of TNF levels was substantial and therefore impeded the analysis of an exact time course of TNF levels and reduced the statistical strength of comparisons. However, there were no differences in TNF levels in patients operated under normothermic conditions as compared with those in the hypothermia group. The same is true for plasma levels of sTNF receptors. Soluble TNF receptors are produced by cleavage of cellular receptors, and are increased after exposure to TNF itself, lipopolysaccharide, and other cytokines. They reduce the bioactivity of TNF by competitive binding. In our study, soluble TNF receptor levels rose significantly during and after the procedure, again without differences between groups. It seems therefore that the production of neither agonist nor antagonist is dependent on CPB temperature.

Hemodynamics
Several studies report lower systemic vascular resistance during normothermic as compared with hypothermic CPB, necessitating the infusion of large volumes of crystalloid fluids or the infusion of high doses of vasopressors (eg, phenylephrine) or both [16, 17]. We could not confirm these results, either in our retrospective study [18] or in this prospective study. There was no difference in the need for norepinephrine or phenylephrine (or both) during CPB. Fluid balance after CPB and urinary output during CPB were equal in normothermic and hypothermic patients. These clinical findings are consistent with our blood chemistry data, which showed no difference in TNF production during CPB with the two temperature managements. There might be several reasons for the different results in our and the above-mentioned studies. First, all patients (independent of CPB temperature) received cold intermittent blood cardioplegia. Therefore a volume and potassium overload due to continuous administration of cardioplegic solution in the normothermic group, as observed in the Toronto study [17], could be avoided. Second, in contrast with other groups [16, 17], pump flow had been adjusted to the perfusion temperature during CPB.

During the early postoperative period, however, patients after normothermic CPB showed significantly lower systemic vascular resistances and higher cardiac indices. Whether cardiac index was higher due to lower systemic resistances or vice versa could not be clearly established. However, as myocardial protection was equal in both groups, it has to be supposed that high cardiac index was probably a consequence of low systemic vascular resistance. Lower systemic vascular resistance may be explained partly by the fact that body temperature was consistently higher in patients after normothermic CPB. In any case, in our patients with ejection fractions above 35%, lower systemic vascular resistance did not result in an increased need for vasopressors, as observed by other authors [19]. We may therefore exclude concern about jeopardizing flow through arterial grafts in the postoperative period as a consequence of normothermic CPB in these patients. As during CPB, there was no clear sign of increased capillary leakage in the warm group. Neither total volume need nor total fluid balance were significantly different in the two groups during the first 18 postoperative hours.

Blood Loss
An increased bleeding tendency after cardiac operations is attributed to the damaging effects of CPB [20]. It may be further affected by hypothermia due to induction of a reversible platelet dysfunction [21]. A first clinical study [20] showed a decreased blood loss during the first 12 postoperative hours in patients operated on under normothermia as compared with hypothermia; in that study there were no differences with regard to the total amount of transfused packed red blood cells. Our study results confirm these findings. Normothermic patients bled less during the first 18 postoperative hours and received significantly less erythrocyte and fresh frozen plasma transfusions. As there were no differences in postoperative platelet count and quick ratio between groups, some improved platelet function after normothermic bypass can be presumed.

Organ Dysfunction
Multiple organ dysfunction after CPB is associated with substantial mortality [22]. Several theoretical considerations might presume increased organ damage during normothermic CPB independent of the cytokine production. Ischemic tolerance of inhomogenousely perfused organs is decreased in normothermia, and higher blood flow rates during warm CPB lead to additional blood trauma. However, our serial measurements of serum enzyme levels during the first postoperative week did not reveal any difference between patients in warm and cold groups. There was no evidence of increased liver, pancreas, or muscle damage, nor was there an increase in hemolysis or impaired renal function. The reasons for these findings may include (1) a shorter CPB time in the warm group, and (2) no need for rewarming normothermic patients, thus avoiding rewarming injury.

At present it appears that normothermic CPB offers a good alternative to traditional hypothermic CPB for selected indications. There is no evidence that normothermia per se is associated with increased systemic adverse effects; however, there have been objections to the lesser safety limits in cases of pump failure during normothermic CPB and to the not yet clearly established effects of normothermic CPB on cerebral protection [23, 24]. In addition, it has to be considered that our patient population was at rather low risk. The influence of CPB temperature in high-risk patients remains to be investigated.

	Footnotes

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Address reprint requests to Dr Tönz, Clinic for Pediatric Surgery, University Hospital, 3010 Bern, Switzerland.

	References

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 

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