Perfusion 2002; 17: 133 139

The relationship between mixed venous and regional venous oxygen saturation during cardiopulmonary bypass
Lena Lindholm1, Vigdis Hansdottir2, Magnus Lundqvist1 and Anders Jeppsson1
1 2

Department of Cardiothoracic Surgery, Sahlgrenska University Hospital, Go teborg, Sweden; Department of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Go teborg, Sweden
ration. There was a statistical correlation between mixed venous and hepatic vein oxygen saturation (r = 0.76, p < 0.0001). Jugular vein oxygen saturation was lower than mixed venous saturation in all three measurements (21.6 1.9% during hypothermia, p < 0.001; 16.7 1.9% during rewarming, p < 0.001; and 5.6 2.2% postoperatively, p = 0.037). No significant correlation in oxygen saturation could be detected between mixed venous and jugular vein blood (r = 0.06, p = 0.65). Systemic temperature did not influence the differences in oxygen saturation between mixed venous and regional venous blood at any time point. In conclusion, regional deoxygenation occurs during CPB, in spite of normal mixed venous saturation. Mixed venous oxygen saturation correlates with hepatic, but not with jugular, vein saturation. The level of hypothermia does not influence differences in oxygen saturation between mixed venous and regional venous blood. Perfusion (2002) 17, 133 139.

The relationship between mixed venous and regional venous saturation during cardiopulmonary bypass (CPB), and whether this relationship is influenced by temperature, has been incompletely elucidated. Thirty patients undergoing valve and/or coronary surgery were included in a prospective, controlled and randomized study. The patients were allocated to two groups: a hypothermic group (28C) and a tepid group (34C). Blood gases were analysed in blood from the hepatic vein and the jugular vein and from mixed venous blood collected before surgery, during hypothermia, during rewarming, and 30 min after CPB was discontinued. Oxygen saturation in the hepatic vein was lower than in the mixed venous blood at all times of measurement (24.0 3.0% during hypothermia, 36. 5 2. 9% during r ewarm ing , and 30.5 3.0% postoperatively, p < 0.001 at all time points). In 23% of the measurements, the hepatic saturation was < 25% in spite of normal ( > 60%) mixed venous satu-

Introduction
The current recommendations for systemic blood flow during cardiopulmonary bypass (CPB) are based on measurements of whole body oxygen consumption. 1 Total oxygen consumption during clinical CPB is assessed by measuring mixed venous oxygen saturation or tension.24 Reduced mixed venous oxygenation indicates a mismatch in oxygen supply/ demand. A systemic pump index (PI) [= l/min/m2/ BSA (body surface area)] of 2.2 2.5 during normothermic CPB is considered sufficient,1,5 and this flow results generally in a mixed venous oxygen saturation of 60 70%. Postoperative vital organ dysfunction may be caused by regional hypoperfusion and subsequent ischemia. There is evidence that regional oxygen desaturation occurs regularly during CPB, and the rewarming period has been suggested to be crucial. 6,7 Even though the recommended pump flow during CPB results in an acceptable mixed venous oxygen saturation, regional desaturation may occur without obvious changes in mixed venous blood. The first aim of this study was to investigate if oxygen saturation in venous blood from two vital organs, the brain and the liver, can be predicted from mixed venous measurements during and early after CPB. Hypothermia is frequently used in heart surgery to reduce metabolic activity, and thereby protect organs and tissues during CPB.1 The second aim of the study was to investigate whether the level of hypothermia affects the relationship between regional and mixed venous oxygen saturation and tension.

Patients and methods

Patients Thirty patients with acquired heart disease undergoing open heart surgery at Sahlgrenska University
10.1191/0267659102pf54 5oa

Address for correspondence: Lena Lindholm, Heart-Centre, University Hospital, Umea S-901 85, Umea , Sweden. E-mail: lena.e.lindholm@ ulf.se

Arnold 2002

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Hospital were included in the study after informed consent was obtained. The exclusion criteria were preoperative cerebral infarction, carotid disease, and laboratory evidence of renal or liver dysfunction. The characteristics of the patients are given in Table 1. The study protocol was approved by the Research Ethics Committee at the Medical Faculty, University of Go teborg. Clinical management The patients were premedicated with flunitrazepam and morphine/scopolamine. Anesthesia was induced with 3 5 mg/kg thiopental, followed by 0.1 mg/kg pancuronium. Fentanyl was given in incremental doses up to a total amount of 8 10 m g/ kg before sternotomy. The patients were normoventilated with oxygen and air (FiO2 0.4 0.5), and enflurane was used as an inhalation agent both prior to and after CPB. Midazolam was given during CPB. Before cannulation, heparin (Lo vens, Ballerup, Denmark), 300 IU/kg, was given and supplemented as required to maintain an activated clotting time (ACT) of more than 480 s. The extracorporeal circuit was primed with approximately 1700 ml of Ringer Acetate (Fresenius-Kabi, Uppsala, Sweden), 200 ml of mannitol (Fresenius-Kabi), 100 ml of tribonate (Fresenius-Kabi), and 7500 IU of heparin. CPB was performed with a hollow fiber membrane oxygenator, a hard shell venous reservoir, and roller pumps. Blood flow was nonpulsatile with a standard PI of 2.4 l/min. Blood gases were continuously monitored in venous and arterial tubings by a CDI 400 (Cardiovascular Device Instruments, Anaheim, CA, USA). Blood gas regimen was performed according to the a -stat principle. The pvO2 was kept above 4.5 kPa (34 mmHg).

Table 2 Mean arterial pressure, PI, blood hemoglobin, arterial O2, and pCO2 during hypothermia, rewarming, and after CPB Hypothermia Rewarming Post CPB Flow and pressure MAP (mmHg) PI (l/m2 BSA/min) Hemoglobin (g/dl) Arterial Mixed venous Jugular vein Hepatic vein 77 2.5 70 3.5 2.39 0.01 2.45 0.01 8.4 7.9 8.2 8.6 0.23 0.25 0.28 0.22 8.2 7.7 8.1 8.3 0.22 0.24 0.27 0.23 75 1.5

9.3 8.5 9.0 9.2

0.20 0.23 0.29 0.23

Arterial O2 Arterial pO2 (kPa) 22.6 0.8 Arterial oxygen saturation (%) 100 0 pCO2 (kPa) Arterial Mixed venous Jugular vein Hepatic vein 4.8 5.3 6.1 5.0 0.1 0.1 0,1 0.1

25.3 0.9 22.0 2.5 100 0 99.2 0.4 4.8 5.3 6.1 5.1 0.1 0.1 0,1 0.1 5.1 5.4 6.4 5.7 0.1 0.1 0,1 0.2

Mean SEM. CPB = cardiopulmonary bypass; SEM = standard error of the mean; MAP = mean arterial pressure; PI = pump index; BSA = body surface area; kPa = kilopascal.

Rewarming was performed with a maximum temperature gradient between heat exchanger water and venous blood of 10C and with a maximum water temperature of 40C. Weaning from bypass was started at a bladder temperature of 36C. A single period of aortic crossclamping was employed for valve replacement and all coronary anastomoses. Cardioprotection was achieved with intermittent cold (8C) blood cardioplegia. Study protocol Before surgery, oximetry catheters (Opticath; Abbot, Wiesbaden, Germany) for blood gas sampling were introduced into the right hepatic vein (7 French) and into the jugular bulb (4 French). The correct positioning of the catheters was verified by fluoroscopy and a small amount of contrast dye. Blood gases and hemoglobin levels were measured at four preset time points: 1) before surgery, 2) during hypothermia, 3) during rewarming (at a bladder temperature of 35C), and 4) 30 min after CPB was discontinued. Samples were collected from arterial blood, from the jugular vein, the hepatic vein, and from mixed venous blood. Mixed venous blood was collected from the venous line during CPB and from the pulmonary artery after CPB. Blood gases were analyzed with an ABL510 analyzer (Radiometer, Copenhagen, Denmark). The partial pressures of oxygen (pO2) and carbon dioxide (pCO2) are presented in kilopascals (kPa). The conversion factor to mmHg is: 1 kPa= 7.5 mmHg. The patients were randomly allocated to two groups: 1) a hypothermic group in which the naso-

Table 1 Patient characteristic s 28C n Age (years) Sex: male/female BSA (m2) Preoperative LVEF CPB time (min) Aortic clamp time (min) CABG (n) AVR (n) CABG+ AVR (n) 15 72 2 10/5 1.82 0.04 0.53 0.04 148 10 100 8 1 4 10 34C 15 69 2 13/2 1.96 0.06 0.6 0.04 124 9 86 7 5 4 6

Mean SEM. SEM = standard error of the mean; BSA = body surface area; LVEF = left ventricular ejection fraction; CPB = cardiopulmonary bypass; CABG = coronary artery bypass grafting; AVR = aortic valve replacement. There were no significant differences between the groups.

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pharyngeal temperature was reduced to 28C (n = 15), and 2) a tepid group in which the nasopharyngeal temperature was reduced to 34C (n = 15). Statistical analysis The nonparametric MannWhitney test was used to establish whether the randomization had provided groups that were comparable. To evaluate total differences in oxygen saturation and tension between mixed venous blood and jugular and hepatic venous blood during the study period, an analysis of variance (ANOVA) for repeated measures was used, followed by the MannWhitney test. To evaluate overall correlation coefficients for the three time points (hypothermia, rewarming, and postoperatively), Spearmans rank sum test was used to determine r values for each individual. The r values for all the individuals were then compared with zero using the Mann Whitney test and the total p value was calculated. When correlation was analyzed separately at a single time point, Spearmans rank sum test was used. Statistical significance was defined as

p < 0.05. All the results are expressed as the mean standard error of the mean (SEM).

Results
Clinical course One patient with impaired myocardial function (preoperative ejection fraction 0.27) died 3 h after surgery because of intractable ventricular arrhythmias. Stroke was diagnosed and verified by computer tomography in three cases (all in the tepid group). The remaining 26 patients recovered normally after surgery and were discharged within 2 weeks. Systemic hemodynamic parameters Mean arterial pressure (MAP) and PI are listed in Table 2. There was a weak overall correlation between mixed venous oxygen saturation (svO2) and MAP (r = 0.31, p = 0.011). When the correlation was analyzed separately during the three measurement periods, there was only a correlation during rewarming (r = 0.66, p < 0.0001), while there was no correla-

90 80 70

+++
60 50 % 40 30 20 10 0 PRE OPERATIVE HYPOTHERMIA REWARMING POST CPB
Figure 1 Oxygen saturation in mixed venous blood (^) and blood from the jugula r (~) and hepatic ( &) veins at the four preset time points. Mean SEM. Statistical significant differences between the groups are indicated as ***p < 0.0001,+ + p = 0.0038, + + + p < 0.0001.

+++ +++ ++

***

***
+++
MIXED VENOUS HEPATIC VEIN JUGULAR VEIN

+++

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100 HEPATIC VENOUS OXYGEN SATURATION (%) 90 80 70 60 50 40 30 20 10 0 0 10 20 30 40 50 60 70 80 90 100 MIXED VENOUS OXYGEN SATURATION (%)
Figure 2 Correlation between hepatic venous oxygen saturation and mixed venous oxygen saturation at hypothermia (^), during rewarming (&), and 30 min after CPB was discontinued (~).

r = 0.76, p < 0.0001

HYPOTHERMIA REWARMING POST CPB

tion during hypothermia (r = 0.10, p = 0.57) or postoperatively (r = 0.08, p = 0.67). The relationship between mixed venous and hepatic vein oxygenation Oxygen saturation. In the hepatic vein, oxygen saturation (shvO2) increased during hypothermia and decreased during rewarming and after CPB (Figure 1). ShvO2 was lower than in mixed venous blood during all three measurements (Figure 1). The absolute mean differences between mixed venous oxygen saturation and shvO2 were 24.0 3.0% (95% confidence interval 17.8 30.3%) during hypothermia, 36.5 2.9% (30.6 42.4%) during rewarming, and 30.5 3.0% (24.3 36.6%) after CPB, corresponding to relative differences of 30%, 52%, and 48%, respectively. In 23% of all measurements, hepatic oxygen saturation was < 25% in spite of normal (> 60%) mixed venous saturation. During rewarming, 28% had a hepatic oxygen saturation of < 25% and normal mixed venous oxygen saturation. There was a statistical correlation between svO2 and shvO2 (r = 0.76, p < 0.0001) (Figure 2). When correlation was analyzed separately during the three measurement periods, correlation was strongest during rewarming (r = 0.59, p = 0.0001), followed by hypothermia (r = 0.50, p = 0.009) and the postoperative measurement (r = 0.37, p = 0.0497). There was no

overall correlation between MAP and shvO2 (r = 0.17, p = 0.21). Oxygen tension. In the hepatic vein, oxygen tension (phvO2) displayed the same pattern as oxygen saturation, with higher tension in mixed venous blood than in the hepatic vein during all three measurements. When measured over the whole study period ( p < 0.0001) and at all the individual measurement points, there were significant differences between pvO2 and phvO2. The average difference between pvO2 and phvO2 was 1.9 0.2 kPa (95% confidence interval 1.5 2.4 kPa) during hypothermia, 2.3 0.2 kPa (2.0 2.6 kPa) during rewarming, and 1.9 0.2 kPa (1.5 2.3 kPa) after CPB, corresponding to 31%, 46%, and 40%, respectively. As with oxygen saturation, there was an overall correlation between pvO2 and phvO2 (r = 0.64, p < 0.0001). When the correlation was tested separately during the three measurement periods, it was strongest during rewarming (r = 0.52, p = 0.004), followed by hypothermia (r = 0.50, p = 0.006) and postoperatively (r = 0.34, p = 0.07). There was no overall correlation between MAP and phvO2 (r = 0.10, p = 0.46). The relationship between mixed venous and jugular vein oxygenation Oxygen saturation. There was a significant difference between svO2 and jugular vein oxygen saturation

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JUGULAR VENOUS OXYGEN SATURATION (%)

100 90 80 70 60 50 40 30 20 10 0 0 10 20 30 40 50 60 70 80 90 100 MIXED VENOUS OXYGEN SATURATION (%) HYPOTHERMIA REWARMING POST CPB r = 0.06, p = 0.65

Figure 3 Correlation between jugular venous oxygen saturation and mixed venous oxygen saturation at hypothermia (^), during rewarming (&), and 30 min after CPB was discontinued (~).

(sjvO2) during the whole period and at each individual measurement point ( p < 0.0001, p < 0.0001, and p = 0.0037 during hypothermia, rewarming, and after CPB, respectively) (Figure 1). The mean absolute difference in svO2 and sjvO2 was 21.6 1.9% (95% confidence interval 17.8 25.5%) during hypothermia, 16.7 1.9% (12.8 20.7%) during rewarming, and 5.6 2.2% (0.9 10.2%) after CPB, corresponding to a relative difference of 27%, 23%, and 13%, respectively. No significant correlation could be detected in oxygen saturation between svO2 and sjvO2 (r = 0.06, p = 0.65) (Figure 3). There was no significant correlation between MAP and sjvO2 (r = 0.18, p = 0.16). Oxygen tension. Measured over the entire study period, there was a significant difference between

pvO2 and jugular oxygen tension (pjvO 2) ( p < 0.0001). During hypothermia and rewarming, there were significant differences between pvO2 and pjvO2 but not after CPB. The mean difference between pvO2 and pjvO2 was 1.6 0.2 kPa (95% confidence interval 1.2 2.0 kPa) during hypothermia, 0.8 0.2 kPa (0.4 1.2 kPa) during rewarming, and 0.5 0.3 kPa ( 0.2 to 0.7 kPa) after surgery, corresponding to a relative difference of 25%, 15%, and 4%, respectively. In contrast to the hepatic vein, there was no correlation between overall pvO2 and pjvO2 (r = 0.15, p = 0.27) and no correlation between MAP and pjvO2 (r = 0.01, p = 0.35). Influence of temperature The absolute and relative differences in oxygen tension and saturation between mixed venous blood and

Table 3 Differences in oxygen saturation and tension between mixed venous blood and blood from jugular and hepatic veins Hypothermia 28C Delta oxygen saturation (%) Mixed venous versus jugular venous blood Mixed venous versus hepatic venous blood Delta oxygen tension (kPa) Mixed venous versus jugular venous blood Mixed venous versus hepatic venous blood 21 3.3 18 4.1 1.7 0.4 1.6 0.4 34C 22 2.1 30 4.0 1.4 0.1 2.2 0.2 Rewarming 28C 16 3.1 34 3.9 0.9 0.2 2.2 0.2 34 C 18 2.4 39 4.2 0.7 0.3 2.4 0.2 28C 3 4.0 34 4.1 0.4 0.6 2.0 0.2 Post CPB 34 C 8 2.3 27 4.3 0.6 0.2 1.8 0.3

Mean SEM. There were no significant differences between the groups. SEM= standard error of the mean; kPa= kilopascal.

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blood from the jugular and the hepatic veins were not significantly different between the 28 and 34C group at any measurement point (Table 3). The correlation coefficients between mixed venous and hepatic and jugular vein oxygenation were similar in the 28 and 34C group.

Discussion
The main findings in this study are: 1) marked desaturation occurs during CPB in spite of normal mixed venous saturation; 2) mixed venous oxygen saturation is a weak indicator of splanchnic and cerebral venous oxygen saturation; and 3) level of hypothermia does not influence differences in oxygenation between mixed venous, and hepatic and jugular vein blood. The relationship in oxygen saturation between mixed venous blood and hepatic venous blood has previously only been reported during non-CPB conditions. 810 Dahn et al.9 found no difference between mixed venous and hepatic venous oxygen saturation in postoperative noncardiac patients, while septic patients had a mean absolute gradient of 15%. Similar findings in septic patients were reported by MeierHellmann et al.10 Ruokonen et al.8 found a mean absolute difference of 12% in oxygen saturation between mixed venous blood and hepatic vein blood in a mixed series of postoperative open heart surgery patients, septic patients, and patients with respiratory failure. The present study demonstrates substantially greater differences during and early after CPB. The absolute mean difference between mixed venous and hepatic venous oxygen saturation was 24% during hypothermia, 36% during rewarming, and 30% during the early postoperative phase. These findings demonstrate that marked splanchnic oxygen desaturation occurs during CPB in spite of normal mixed venous blood saturation levels. Furthermore, in 23% of the measurements with apparently normal mixed venous oxygen saturation (> 60%), the hepatic oxygen saturation was below 25% (Figure 2), a level that has previously been suggested as being critical for postoperative liver function.11 Although our results clearly demonstrate that hepatic desaturation may occur during and early after CPB in spite of normal mixed venous saturation, a statistically significant correlation between svO2 and shvO2 was demonstrated. However, the correlation coefficients were calculated from changes in individual patients and cannot be used to predict shvO2 from a single svO2 measurement. The results of the correlation calculations can instead be interpreted as meaning that: perioperative adjustments (e.g., flow, temperature, Hb), resulting

in increased svO2, are also beneficial for splanchnic circulation. In contrast to hepatic vein oxygenation, jugular vein oxygenation has been extensively investigated during CPB.7,1214 In the present study, there was a marked difference in oxygen tension and saturation during hypothermia and rewarming between mixed venous and jugular vein blood. This confirms, as suggested previously,7 that a mismatch in cerebral oxygen supply and demand may occur during CPB, in spite of normal mixed venous oxygenation. We were not able to detect any correlation between jugular vein oxygen saturation and mixed venous saturation. This is in contrast to the findings of Croughwell et al.7 where a weak but statistically significant correlation was detected. The difference may be due to the fact that fewer patients were included in the present study. However, our study strongly supports the conclusion of Croughwell et al. that mixed venous saturation is a poor indicator of jugular bulb saturation and that other methods are necessary to assess cerebral oxygenation during CPB. The lack of correlation among jugular venous saturation, mixed venous saturation, and MAP argues in favor of maintained autoregulation of cerebral blood flow during CPB and implies, in contrast to splanchnic oxygenation, that perioperative adjustment in order to increase mixed venous saturation may not have any impact on cerebral oxygenation. The patients included in this study were cooled during hypothermic CPB to two different temperatures, 28 or 34C. The level of hypothermia did not influence the difference between mixed venous and regional venous oxygenation either during the hypothermic period or during the rewarming and postoperative periods. The results suggest that a temperature between 28 and 34C does not influence the relationship between mixed venous and regional venous oxygenation. However, it remains to be demonstrated that the relationship also is constant at normothermic CPB, which is currently being used with increasing frequency.15 The results of the present study indicate that even though the present flow recommendations result in acceptable mixed venous saturation, it does not protect individual vital organs from deoxygenation. One may, therefore, speculate about other strategies. One option would naturally be to increase the pump flow. Parolari et al.16 demonstrated that a higher blood flow precures perfusion of more vascular beds, which may be beneficial. On the other hand, increased flow may lead to higher pressure gradients across the oxygenator and the arterial cannula, with subsequent hemolysis. 1 Another option would be to use more profound hypothermia to protect organs and tissues. This may

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also have adverse effects with prolonged rewarming and an increased systemic inflammatory response.17 A third alternative would be to use pharmacological or metabolic vasodilating agents. We have previously demonstrated that insulin and amino acid infusion after CABG enhances postoperative renal blood flow by 50%18 and that insulin (GIK) improves hepatic venous oxygenation19 and it is also possible that regional blood flow to other organs would benefit from a similar treatment modality.

To summarize, marked hepatic and jugular venous desaturation occurs in spite of normal mixed venous saturation during CPB. New methods to assess regional oxygenation during CPB are needed.

Acknowledgement
n, PhD, Statistical advice was given by Anders Ode Kunga lv, Sweden.

References
1 Kirklin JW, Barrat-Boyes BG. Hypothermia, circulatory arrest and cardiopulmonar y bypass. In Kirklin JW, Barrat-Boyes BG eds. Cardiac surgery. New York: Livingstone, 1993: 61 128. 2 Swan H, Sanchez M, Tyndall M, Koch C. Quality control of perfusion: monitoring venous blood oxygen tension to prevent hypoxic acidosis. J Thorac Cardiovasc Surg 1990; 99: 868 72. 3 Stanley TH, Isern-Amaral JI. Periodic analysis of mixed venous oxygen tension to monitor the adequacy of perfusion during and after cardiopulmonar y bypass. Can Anaesth Soc J 1974; 21: 454 60. 4 Galletti PM, Brecher GA. Heart lung bypass principles and techniques of extracorporeal circulation. New York: Grune and Stratton, 1962. 5 Davis RF, Dobbs JL, Casson H. Conduct and monitoring of cardiopulmonar y bypass. In Gravlee GP, Davis RF, Utley JR eds. Cardiopulmonar y bypass principles and practice . Baltimore, MD: Williams and Wilkins, 1993: 578 602. 6 Jeppsson A, Andersson LG, Ekroth R, Joachimsson PO. Renal hypoxanthine balance in cardiac surgery: effects of felodipine. J Cardiothorac Vasc Anesth 1999; 13: 715 19. 7 Croughwell ND, Frasco P, Blumenthal JA, Leone BJ, White WD, Reves JG. Warming during cardiopulmonary bypass is associated with jugular bulb desaturation. Ann Thorac Surg 1992; 53: 827 32. 8 Ruokonen E, Takala J, Uusaro A. Effect of vasoactive treatment on the relationship between mixed venous and regional oxygen saturation. Crit Care Med 1991; 19: 1365 69. 9 Dahn MS, Lange PM, Jacobs LA. Central mixed and splanchnic venous oxygen saturation monitoring. Intensive Care Med 1988; 14: 373 78. 10 Meier-Hellmann A, Hannemann L, Specht M, Schaffartzik W, Spies C. The relationship between mixed venous and hepatic venous O2 saturation in patients with septic shock. Adv Exp Med Biol 1994; 345: 701 707. 11 Takano H, Matsuda H, Kadoba K et al. Monitoring of hepatic venous oxygen saturation for predicting acute liver dysfunction after Fontan operations. J Thorac Cardiovasc Surg 1994; 108: 700 708. 12 van der Linden J, Ekroth R, Lincoln C, Pugsley W, Scal n H. Is cerebral blood flow/metabolic mislan M, Tyde match during rewarming a risk factor after profound hypothermic procedures in small children? Eur J Cardiothorac Surg 1989; 3: 209 15. 13 Croughwell ND, White WD, Smith LR et al. Jugular bulb saturation and mixed venous saturation during cardiopulmonary bypass. J Cardiovasc Surg 1995; 10(suppl 4): 503 508. 14 Nakajima T, Kuro M, Hayashi Y, Kitaguchi K, Uchida O, Takaki O. Clinical evaluation of cerebral oxygen balance during cardiopulmonary bypass: on-line continuous monitoring of jugular venous oxyhemoglobin saturation. Anesth Analg 1992; 74: 630 35. 15 Christenson JT, Maurice J, Simonet F et al. Normothermic versus hypothermic perfusion during primary coronary artery bypass grafting. Cardiovasc Surg 1995; 3: 519 24. 16 Parolari A, Alamanni F, Gherli T et al. Cardiopulmonary bypass and oxygen consumption: oxygen delivery and hemodynamics . Ann Thorac Surg 1999; 67: 1320 27. 17 Ohata T, Sawa Y, Kadoba K et al. Normothermia has beneficial effects in cardiopulmonar y bypass attenuating inflammatory reactions. ASAIO J 1995; 41: M288 91. 18 Jeppsson A, Ekroth R, Kirno K et al. Insulin and amino acid infusion after cardiac operations: effects on systemic and renal perfusion. J Thorac Cardiovasc Surg 1997; 113: 594 602. 19 Lindholm L, Bengtsson A, Hansdottir V, Westerlind A, Jeppsson A. Insulin (GIK) improves central mixed and hepatic venous oxygenation in clinical cardiac surgery. Scand Cardiovasc J 2001; 35: 347 52.

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