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Canadian Journal of Anesthesia 48:1011-1014 (2001)
© Canadian Anesthesiologists' Society, 2001

Cardiothoracic Anesthesia, Respiration and Airway

Hepatosplanchnic oxygenation is better preserved during mild hypothermic than during normothermic cardiopulmonary bypass

[L'oxygénation hépatosplanchnique est mieux préservée pendant la circulation extracorporelle sous légère hypothermie que sous normothermie]

Nobuhiro Okano, MD*, Haruhiko Hiraoka, MD*, Ryoichi Owada, MD*, Nao Fujita, MD*, Yuji Kadoi, MD{dagger}, Shigeru Saito, MD{dagger}, Fumio Goto, MD{dagger} and Toshihiro Morita, MD*

* From the Department of Anesthesiology, Saitama Cardiovascular and Pulmonary Center, Saitama; and
{dagger} the Department of Anesthesiology and Reanimatology, Gunma University, School of Medicine, Gunma, Japan.

Dr. Nobuhiro Okano, Department of Anesthesiology, Saitama Cardiovascular and Pulmonary Center, 1696 Itai Konan-machi Osato-gun, Saitama 360-0105, Japan. Phone: 81-48-536-9900; Fax: 81-48-536-9920; E-mail: richard{at}ka2.so-net.ne.jp


    Abstract
 TOP
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
Purpose: To assess and compare the effects of normothermic and mild hypothermic cardiopulmonary bypass (CPB) on hepatosplanchnic oxygenation.

Methods: We studied 14 patients scheduled for elective coronary artery bypass graft surgery who underwent normothermic (>35°C; group I, n=7) or mild hypothermic (32°C; group II, n=7) CPB. After induction of anesthesia, a hepatic venous catheter was inserted into the right hepatic vein to monitor hepatic venous oxygen saturation (ShvO2) and hepatosplanchnic blood flow by a constant infusion technique that uses indocyanine green.

Results: The ShvO2 decreased from a baseline value in both groups during CPB and was significantly lower at ten minutes and 60 min after the onset of CPB in group I (39.5 ± 16.2% and 40.1 ± 9.8%, respectively) than in group II (61.1 ± 16.2% and 61.0 ± 17.9%, respectively; P <0.05). During CPB, the hepatosplanchnic oxygen extraction ratio was significantly higher in group I than in group II (44.0 ± 7.2% vs 28.7 ± 13.1%; P <0.05).

Conclusion: Hepatosplanchnic oxygenation was better preserved during mild hypothermic CPB than during normothermic CPB.


    Introduction
 TOP
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
NORMOTHERMIC cardiopulmonary bypass (CPB) is now commonly used in cardiac surgery, mainly because of the lack of the adverse effects of hypothermia and rewarming.1 However, the increased oxygen demand associated with normothermia may compromise tissue oxygenation as a result of the reduced oxygen delivery caused by hemodilution. Although reports on CPB are conflicting, some studies indicated greater increases in splanchnic vs systemic oxygen extraction.2–4 We hypothesized that this imbalance between oxygen demand and supply would be greater during normothermic than mild hypothermic CPB. To test this hypothesis, we investigated changes in hepatic venous oxygen saturation (ShvO2), hepatosplanchnic blood flow, and oxygen delivery during mild hypothermic and normothermic CPB.


    Patients and methods
 TOP
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
After obtaining approval from the Ethics Committee and informed consent from the patients, we randomly allocated 14 otherwise healthy patients undergoing elective coronary artery bypass graft surgery into the normothermic (group I, n=7) and the mild hypothermic (group II, n=7) groups.

After premedication with 10 mg diazepam po, anesthesia was induced with 0.2 mg•kg–1 midazolam and 5 µg•kg–1 fentanyl; tracheal intubation was facilitated with 0.1 mg•kg–1 vecuronium. Anesthesia was maintained with 15 µg•kg–1 fentanyl, vecuronium, 4 mg•kg–1•hr–1 propofol and 50% oxygen in air. In addition to radial and pulmonary artery catheters for routine monitoring, a hepatic venous catheter (Harmac Medical Products, USA.) was inserted into the right hepatic vein via the right femoral vein under fluoroscopic guidance.

Non-pulsatile CPB used a membrane oxygenator, priming with crystalloid solution and a pump flow of 2.3–2.5 L•min–1•m–2. A mean arterial pressure (MAP) of 50–90 mmHg was maintained by phenylephrine infusion and a hematocrit greater than 20% by transfusion of packed red cells if needed. The target nasopharyngeal temperature was above 35°C for the normothermic group and at 32°C for the mild hypothermic group. After CPB, the cardiac index (CI) was maintained above 3.0 L•min–1•m–2 by administering dopamine or dobutamine or both.

Administration of 1–2 mg•kg–1•hr–1 propofol for sedation in the intensive care unit was discontinued and patients extubated when awake and their blood gas analysis comparable to that before surgery. Lactated Ringer's solution (2–3 mL•kg–1•hr–1), colloids and packed red blood cells were administered to maintain a CVP of 8–14 mmHg, a pulmonary artery occlusion pressure of 5–12 mmHg, and a hematocrit above 30%.

Hemodynamic variables, arterial, mixed venous, and hepatic venous blood gases, and hepatic venous lactate concentrations were measured: 1) after the induction of anesthesia; 2) ten minutes and; 3) 60 min after the onset of CPB; 4) at the unclamping of the aorta; 5) at the cessation of CPB; 6) at the end of the operation; 7) six hours and; 8) 24 hr after the end of the operation.

Hepatic blood flow was determined by a primed (6 mg), continuous infusion (1 mg•min–1) of indocyanine green (ICG)5 into a central venous catheter: 1) after the induction of anesthesia; 2) during the steady state of CPB; and 3) after cessation of the CPB. Arterial and hepatic venous ICG concentrations were in steady-state plateaus at each measurement.

Various oxygen-utilization variables calculated by standard formulae were systemic oxygen delivery index (DO2I), consumption index (VO2I) and extraction ratio (OER), and hepatosplanchnic oxygen delivery index (DO2splI), consumption index (VO2splI), and extraction ratio (OERspl).

All data are expressed as means ± SD. One-way analysis of variance was followed by Bonferroni test for intragroup comparisons and by Student t test for intergroup comparisons. A P value of less than 0.05 was considered significant.


    Results
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 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
No significant differences were found between groups in patient height and weight, dosage of phenylephrine and catecholamines, duration of CPB (mean, 146 min), aortic clamping (123 min), and operation (352 min). Furthermore, neither CI, MAP, nor hemoglobin concentrations differed between groups during the study period (Table IGo). In group I, mixed venous oxygen saturation (SvO2) decreased early in the course of CPB, while in group II, it decreased at the time of rewarming. The changes in both VO2I and OER during CPB also differed largely between groups: they increased in group I and decreased in group II. Postoperatively, these levels significantly increased in both groups with no differences between groups. Hepatic venous lactate concentrations were higher in group II than in group I throughout the observation period.


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TABLE I Systemic hemodynamic and oxygen-utilization variables, lactate concentrations, and nasopharyngeal temperatures
 
As shown in the FigureGo, ShvO2 decreased from a baseline value in both groups during CPB; at ten minutes and 60 min after the onset of CPB, it was lower in group I than in group II. Changes in hepatic blood flow (SBFI) and oxygen-utilization variables are summarized in Table IIGo. Changes in SBFI were not found during CPB in either group. DO2splI was significantly decreased to a similar degree during CPB in both groups. In group I, VO2splI was markedly increased from baseline value during CPB, while in group II, no increase was found at any time point studied. OERspl was increased in both groups during CPB, more in group I than in group II. The alanine aminotransferase and total bilirubin measured on postoperative days one, three, and seven did not show any major change in either group.



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FIGURE Hepatic venous oxygen saturation(ShvO2) in normothermic group (•) and in mild hypothermic group (°).

*P <0.05 compared with baseline, #P <0.05 compared with mild hypothermic group. 1) after the induction of anesthesia; 2) ten minutes after the onset of CPB; 3) 60 min after the onset of CPB; 4) at unclamping of the aorta; 5) at the cessation of CPB; 6) at the end of operation; 7) six hours after the operation; 8) 24 hr after the operation.

 

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TABLE II Hepatosplanchnic blood flow and oxygen-utilization variables
 

    Discussion
 TOP
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
We observed that oxygen consumption exceeded oxygen delivery specifically in the hepatosplanchnic region (Table IIGo), resulting in a marked reduction in ShvO2 (FigureGo). In addition, we could demonstrate that a small difference in systemic temperature had an important effect on the hepatosplanchnic oxygen balance; normothermic CPB further exacerbated the imbalance of oxygen demand and supply.

The lactate concentrations in the hepatic vein were higher during mild hypothermia. Anaerobic metabolism in the hepatosplanchnic region may have been more pronounced during mild hypothermic than during normothermic CPB. However, other contributors to these high concentrations of lactate may include a decrease in lactate metabolism secondary to systemic hypothermia and an increase in lactate production outside the splanchnic region.6.7 Thus, the increased lactate concentrations may not always indicate the presence of hepatosplanchnic hypoperfusion.

Liver dysfunction does not constitute a major cause of morbidity after CPB. Despite the presence of severe hepatic venous oxygen desaturation, postoperative liver function tests did not show any major abnormalities in either group. Possible explanations include a very transient decrease in ShvO2, the limited number of patients studied and their relatively low-risk, preservation of hepatosplanchnic blood flow during CPB, and fully developed compensation mechanisms in the liver.8.9 However, a perioperative decrease in ShvO2 to below 30% during liver resection is associated with postoperative liver dysfunction.10 In the present study, hepatosplanchnic oxygenation was better preserved during mild hypothermic than normothermic CPB. However, the limits of compensation and the duration of tolerance for hepatic venous hypoxia are not yet known.


    Acknowledgments
 
We thank Mr. Kamiyashiki and Mr. Someya for their technical assistance (Division of Medical Engineering in our institute). This work was supported by the institutional research fund of Saitama Cardiovascular and Pulmonary Center.

Revision received July 27, 2001. Accepted for publication May 31, 2001.


    References
 TOP
 Abstract
 Introduction
 Patients and methods
 Results
 Discussion
 References
 
1 Cook DJ. Changing temperature management for cardiopulmonary bypass. Anesth Analg 1999; 88: 1254–71.[Free Full Text]

2 Thorén A, Elam M, Ricksten S-E. Jejunal mucosal perfusion is well maintained during mild hypothermic cardiopulmonary bypass in humans. Anesth Analg 2001; 92: 5–11.[Abstract/Free Full Text]

3 McNicol L, Andersen LW, Liu G, Doolan L, Baek L. Markers of splanchnic perfusion and intestinal translocation of endotoxins during cardiopulmonary bypass: effects of dopamine and milrinone. J Cardiothorac Vasc Anesth 1999; 13: 292–8.[Medline]

4 Okano N, Fujita N, Kadoi Y, Saito S, Goto F. Disturbances in hepatocellular function during cardiopulmonary bypass using propofol anesthesia. Eur J Anaesth 2001; 18: 1–7.

5 Bradley SE, Ingelfinger FJ, Bradley GP, Curry JJ. The estimation of hepatic blood flow in man. J Clin Invest 1945; 24: 890–7.

6 Landow L, Phillips DA, Heard SO, Prevost D, Vandersalm TJ, Fink MP. Gastric tonometry and venous oximetry in cardiac surgery patients. Crit Care Med 1991; 19: 1226–33.[Medline]

7 Haisjackl M, Birnbaum J, Redlin M, et al. Splanchnic oxygen transport and lactate metabolism during normothermic cardiopulmonary bypass in humans. Anesth Analg 1998; 86: 22–7.[Abstract]

8 Takala J. Determinants of splanchnic blood flow. Br J Anaesth 1996; 77: 50–8.[Free Full Text]

9 Pastor CM, Suter PM. Hepatic hemodynamics and cell functions in human and experimental sepsis. Anesth Analg 1999; 89: 344–52.[Free Full Text]

10 Kainuma M, Fujiwara Y, Kimura N, Shitaokoshi A, Nakashima K, Shimada Y. Monitoring hepatic venous hemoglobin oxygen saturation in patients undergoing liver surgery. Anesthesiology 1991; 74: 49–52.[Medline]




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This Article
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