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Anesthesiology:
doi: 10.1097/ALN.0b013e3181af59aa
Review Articles

Role of Central and Mixed Venous Oxygen Saturation Measurement in Perioperative Care

Shepherd, Stephen J. M.R.C.P., M.B.B.S.*; Pearse, Rupert M. F.R.C.A., M.B.B.S., M.D.†

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Abstract

Complications after major surgery are a leading cause of morbidity and mortality. The etiology of postoperative complications is complex, but poor cardiorespiratory reserve appears to be a key factor. There is increasing interest in the use of central and mixed venous oxygen saturation to guide therapeutic interventions during the perioperative period. However, a detailed understanding of the physiologic principles of venous oximetry is essential for safe and effective use in clinical practice. Venous oxygen saturation reflects the balance between global oxygen delivery and oxygen consumption, which may be affected by a wide range of factors during the perioperative period. The purpose of this article is to describe the physiology and measurement of mixed and central venous oxygen saturation and to explore the findings of clinical investigations of their use in perioperative care.
IT is estimated that 234 million major surgical procedures are performed worldwide each year.1 Complications after major surgery are a leading cause of morbidity and mortality. High-risk surgical patients account for more than 80% of deaths but less than 15% of in-patient procedures.2,3 Data from across the developed world confirms that poor outcomes after high-risk surgery are a global problem.4–6 Even for those patients who survive to leave hospital, postoperative complications remain an important determinant of long-term survival.6 It is therefore essential that we seek to improve outcomes for patients undergoing major surgery.
The etiology of postoperative complications is complex, but poor cardiorespiratory reserve appears a key factor. A number of reports indicate that poor outcomes after major surgery are strongly associated with derangements in tissue oxygen delivery that may in turn relate to impaired microvascular flow.7–10 The use of fluid and inotropic therapy to enhance tissue oxygen delivery may reduce the incidence of postoperative complications.11–14 There is an increasing body of literature describing changes in central (Scvo2) and mixed venous oxygen saturation (Svo2) during the perioperative period, which, along with a recent study in patients with severe sepsis,15 has led to interest in the use of venous saturation as a therapeutic goal for surgical patients. However, the complexities of the physiology of venous oxygen saturation are poorly recognized. A detailed understanding of these principles is essential for the safe and effective application in clinical practice. The aim of this article is to describe the physiology and measurement of Svo2 and Scvo2 and to describe the findings of the clinical investigations of the use of these variables in perioperative care.
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Materials and Methods

Searches of the MEDLINE and Cochrane CENTRAL databases from January 1968 to December 2008 were performed by both authors using the following search terms: (venous saturation OR venous oximetry OR Svo2 OR Scvo2) AND (surgery OR surgical OR \ *operative OR operation). Only articles published in English were included, but no restrictions were placed on source. A further online search was then carried out using the Google Scholar search engine by using the following key words: venous saturation, venous oximetry, surgery, Scvo2, Svo2. The resulting abstracts were screened to identify relevant investigations in adult patients undergoing major surgery. Studies were excluded if they had not been published in a peer-reviewed journal. Bibliographies of relevant articles were also screened. Manuscripts were screened initially by title and then by abstract before obtaining the full text of relevant articles.
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Physiology of Venous Oxygen Saturation
The terms central (Scvo2) and mixed venous oxygen saturation (Svo2) refer to the hemoglobin saturation of blood in the superior vena cava and proximal pulmonary artery, respectively.16 Rearrangement of the Fick equation illustrates that venous oxygen content is determined by arterial oxygen content, oxygen consumption and cardiac output.17 The quantity of dissolved oxygen is small under standard conditions; therefore, the more conveniently measured variable of hemoglobin saturation is preferred. This is summarized in the equation below, where CO refers to cardiac output, Cao2 refers to arterial oxygen content, Cvo2 refers to venous oxygen content, and Vo2 refers to oxygen consumption.
Equation (Uncited)
Equation (Uncited)
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Fig. 1
Fig. 1
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Where oxygen supply is insufficient to meet metabolic requirements, increased tissue oxygen extraction results in a decrease in the oxygen content of effluent venous blood. Venous oxygen saturation therefore reflects the balance between global oxygen delivery (Do2) and global oxygen consumption (Vo2).18 Vo2 and Do2 both fluctuate significantly during the perioperative period, and it is of particular importance to recognize that changes in venous saturation may reflect a variety of physiologic and pathologic changes (fig. 1). The safe use of venous saturation as a therapeutic goal depends on the prompt recognition of the cause of any derangement. Regional variations in Do2 and Vo2 are also commonplace and clinically relevant differences in the oxygen content of venous blood are to be expected in different parts of the circulation.19–22 In common with other global physiologic variables, the apparent simplicity of a single variable is often associated with a lack of sensitivity to detect regional abnormalities in an apparently stable patient. There is little published data describing the normal value of venous saturation in health. Although commonly quoted as 70%, the available data suggest this may vary from 70% to 80% in healthy individuals.23,24 Values of Svo2 and Scvo2 may often be as low as 65% in hospital in-patients before elective surgery.25
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Oxygen Delivery as a Determinant of Venous Oxygen Saturation
Global oxygen delivery is determined by cardiac output and the oxygen content of arterial blood as shown in the equation below,26 where Do2 refers to oxygen delivery and CO to cardiac output where the Bunsen solubility coefficient for O2 at 37°C is 0.02.27
Equation (Uncited)
Equation (Uncited)
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Adequate tissue oxygen delivery therefore depends on the adequacy of both respiratory and cardiovascular function. If oxygen consumption, hemoglobin concentration, and arterial saturation remain constant, changes in Svo2 are therefore directly proportional to those in cardiac output; this relationship has been demonstrated in several studies in man.24,28 In a study of healthy volunteers, orthostatic hypotension resulted in a decrease in cardiac output from 4.3 to 2.7 l min−1 at the onset of presyncopal symptoms.24 Over the same time period, Scvo2 decreased from 75% at baseline to 60%.24 A clinical series of patients undergoing one-lung ventilation demonstrated that cardiac output increased in response to sudden decreases in arterial saturation; as a consequence, Svo2 remained unchanged.28 Several reports describe reduced venous saturation in patients with a reduced cardiac output due to myocardial infarction and/or heart failure.29–34 Changes in Scvo2 and Svo2 in these circumstances reflect both the severity of hemodynamic disturbances and response to treatment.29–32
Fig. 2
Fig. 2
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The affinity of hemoglobin for oxygen is affected by the partial pressure of oxygen (fig. 2). It may be anticipated from the oxyhemoglobin dissociation curve that, at higher partial pressures of oxygen, increases in Po2 will result in only small increases in hemoglobin saturation. At lower partial pressures, such as those typical of venous blood, the same incremental rise in Po2 will result in a greater increase of hemoglobin saturation due to the greater oxygen affinity of deoxyhemoglobin.35 Consequently, the change in venous saturation in response to a step change in fractional inspired oxygen concentration may differ considerably from simultaneous changes in arterial hemoglobin saturation. Clinical and laboratory investigations have shown that an increase in fractional inspired oxygen concentration results in a greater increase in oxygen saturation of venous than arterial blood.36,37 The administration of supplemental oxygen may therefore be sufficient to rectify significant abnormalities in venous saturation even though these abnormalities may not specifically result from alveolar hypoxia. In situations where Scvo2 or Svo2 values are being used as hemodynamic endpoints for the administration of intravenous fluid or inotropic therapies, an increase in venous saturation resulting from an increase in fractional inspired oxygen concentration may be misinterpreted as an indication of adequate hemodynamic resuscitation. The potential for such simple interventions to mask the effects of shock emphasizes the importance of a detailed understanding of venous oximetry.
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Oxygen Consumption as a Determinant of Venous Oxygen Saturation
Few studies have explored the relationship between Vo2 and venous saturation during the perioperative period. This may reflect poor recognition of the importance of Vo2 as a determinant of venous saturation. Considerable changes in oxygen consumption may occur during the perioperative period. Increases in Vo2 resulting from pain, anxiety, or shivering may all result in a decrease in venous saturation,38–42 whereas the corresponding treatments may rectify such derangements.43 Experimental data suggests that the extent of such derangements may correlate with the magnitude of oxidative stress.44 General anesthesia results in a decrease in Vo2 through reductions in general motor activity, work of breathing, neuronal activity, and body temperature. These changes are the result of anesthesia itself as well as neuromuscular blockade and invasive ventilation.45–49 Volatile anesthetic agents decrease the basal metabolic rate, with reductions in sympathetic tone and cardiac output being more pronounced at higher doses.50 Intravenous hypnotics such as benzodiazepines appear to exert similar effects on metabolic demand by blunting the sympathetic neurohumoral response,51,52 and intravenous anesthetic agents such as propofol similarly reduce metabolic demand, with the probable exception of ketamine, which usually increases myocardial inotropy by increasing general sympathetic activity.53,54 Sympatheticolytic agents such as clonidine reduce perioperative Vo2.55,56 Reductions in neuronal oxygen consumption occur with the administration of volatile anesthetic agents, barbiturates, benzodiazepines, and propofol.57–61 Opiates may similarly reduce perioperative Vo2.62–65 Neuraxial blockade has both sympatheticolytic and analgesic effects,66,67 but we are unaware of reports specifically describing effects on Vo2.
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Relationship between Svo2 And Scvo2
While the determinants of Scvo2 and Svo2 are very similar, the relationship between the two variables is complex and they cannot be used interchangeably.68–73 Regional variations in the balance between Do2 and Vo2 result in differences in the hemoglobin saturation of blood in the superior and inferior vena cavae.74 Streaming of caval blood continues within the right atrium and ventricle and complete mixing only occurs during ventricular contraction. The drainage of myocardial venous blood directly into the right atrium via the coronary sinus and cardiac chambers via the Thebesian veins results in further discrepancies.16 Consequently, Svo2 reflects the balance between oxygen supply and demand averaged across the entire body but Scvo2 is affected disproportionately by changes in the upper body.74 In healthy individuals, Scvo2 is usually 2–5% less than Svo2,16 largely because of the high oxygen content of effluent venous blood from the kidneys.22 This relationship changes during periods of hemodynamic instability because blood is redistributed to the upper body at the expense of the splanchnic and renal circulations.75 In shock states, therefore, the observed relationship between Scvo2 and Svo2 may reverse, and the absolute value of Scvo2 may exceed that of Svo2 by up to 20%.73 This lack of numerical equivalence has been demonstrated in various groups of critically ill patients, including those with cardiogenic, septic and hemorrhagic shock.31,68–70,76–78 This has also been demonstrated in patients undergoing general anesthesia for cardiac71,72,79 and noncardiac surgery.69,80 Although trends in Scvo2 may closely reflect those of Svo2, absolute values differ and the variables cannot be used interchangeably.68–72 This observation is sometimes cited in support of continued use of the pulmonary artery catheter. However, there is no evidence to suggest one variable is of greater clinical value than the other. As the use of the pulmonary artery catheter declines, measurement of Scvo2 is usually more convenient than Svo2, although Scvo2 measurements cannot be cannot be used to calculate Vo2 or shunt fraction.72
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Measurement of Venous Oxygen Saturation
Cardiac catheterization was first performed in 1929 by Werner Forssmann, a major advance that allowed the measurement of Svo2 and hence application of Fick’s principle to measure cardiac output.81,82 However, it was not until 1970 that the introduction of the balloon-tipped pulmonary artery catheter facilitated the routine clinical measurement of Svo2.81 Reports of the clinical utility of Scvo2 predate those of Svo2 by several years.29,33 Measurement of venous saturation may be performed either intermittently by blood sampling and cooximetry or continuously through the use of a spectrophotometric catheter.
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Intermittent Blood Sampling and Cooximetry
Cooximetry involves the measurement of hemoglobin saturation by spectrophotometry by using widely available blood gas analysis technology. The differences in light absorption spectra between oxygenated and deoxygenated hemoglobin allow calculation of the hemoglobin saturation of blood. This also allows the identification of other forms of hemoglobin such as methemoglobin and carboxyhemoglobin. Cooximetry is a reliable and well-established technique. However, in clinical practice it may be inconvenient to make frequent measurements by using this approach. Specific errors result from sample contamination, delayed measurement, and sampling from the incorrect site.83,84 As with any form of venous oximetry, interpretation errors may arise due to intracardiac shunts, tricuspid regurgitation, and catheter misplacement.84 When taking blood samples, syringe aspiration should be gentle enough to avoid high negative pressure that may increase the aspiration of pulmonary capillary blood and hence produce falsely high readings for oxygen saturation.
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Continuous Measurement Using an Indwelling Fiberoptic Catheter
The introduction of optical fiber technology has allowed the continuous measurement of venous saturation by spectrophotometry using indwelling pulmonary artery or central venous catheters. The major benefit of this approach is the provision of continuous data allowing the detection of sudden fluctuations in venous saturation, which are common during the perioperative period.85,86 The principle disadvantages of this technology are the additional cost and signal drift, although the latter can be addressed by recalibration. Advances in the technology have addressed the problem of interference from other optically active compounds such carboxyhemoglobin and bilirubin.
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Observational Studies of Perioperative Changes in Scvo2 and Svo2
Abnormalities of venous saturation are common during and after major surgery and are associated with an increased incidence of postoperative complications.87–91 Reductions in Scvo2 and Svo2 also have prognostic significance in heart failure, trauma, and sepsis.92–95 These observations are no surprise, given the wide range of pathologic abnormalities that affect venous saturation in the perioperative period.87–89
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Noncardiac Surgery
Fig. 3
Fig. 3
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Two studies have been performed in noncardiac surgical patients with complementary findings. In the first observational study of 117 patients, the lowest recorded value of Scvo2 in the early postoperative period was independently associated with subsequent complications, the optimal cut-off for the lowest Scvo2 value being 64.4%.87 Interestingly, a considerable decrease in Scvo2 was observed within the first hour after surgery, possibly as a consequence of increased Vo2 after the cessation of general anesthesia (fig. 3). In a further multicenter observational study of 60 patients, the mean value of Scvo2 was found to be reduced at various time points throughout the perioperative period in patients who developed complications.88 The optimal cutoff value in this study for the mean Scvo2 value was 73%. These investigations not only provide strong evidence to support the role of Scvo2 as a therapeutic target, but they are also highly consistent in suggesting the most appropriate target value to be an Scvo2 value of approximately 75%. However, these findings do not indicate how venous saturation should be used as a therapeutic goal. A range of factors influence Vo2, Do2, and therefore venous saturation during the perioperative period, not all of which are pathologic in nature. The most appropriate therapy to achieve a venous saturation endpoint may vary.
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Cardiothoracic Surgery
Alterations in Svo2 have been described in patients undergoing cardio-thoracic surgery, although no reports of changes in Scvo2 were identified.89–91 Derangements in Svo2 occur before any changes in mean arterial pressure or heart rate are observed,96 and they appear to correlate well with changes in cardiac index.86 Early work in patients undergoing both cardiac and pulmonary surgery demonstrated that sustained reductions in Svo2 below 65% were associated with a higher incidence of complications, particularly arrhythmias.97 Increases in oxygen extraction ratio, derived through measurement of Svo2, have also been associated with postoperative organ failure and prolonged intensive care stay.90,91,98 During lung transplantation, changes in Svo2 reflected adverse clinical events, although this series is too small to support any more detailed conclusions.99 During cardiopulmonary bypass, Svo2 may prove a more specific indicator of global oxygen delivery; pump flow (or cardiac output) and metabolic rate are generally constant in these circumstances.100,101
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Trauma
The effects of hypovolemia on venous saturation have been described in both animals and humans.73,102,103 Fluctuations in Svo2 and Scvo2 closely mirror periods of hemorrhage and subsequent resuscitation in anesthetized dogs.73,102 A case series of ten victims of mainly penetrating trauma described similar changes in Svo2.103 Venous saturation may provide a useful indication of the severity of blood loss that is more reliable than conventional cardiovascular variables such as heart rate and arterial and central venous pressure.102,103 A single small case series describes the use of normal levels of Svo2 as therapeutic target in trauma patients in which the authors suggest a survival benefit.104 However, the study has a number of limitations, and the data do not appear to support such conclusions.
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Interventional Trials Utilizing Scvo2 and Svo2 as Therapeutic Targets in the Perioperative Period
Noncardiac Surgery
Our literature search identified only one interventional trial using Scvo2 as a therapeutic goal in perioperative care.105 This was a multicenter trial of 135 patients undergoing major abdominal (including aortic) surgery. All patients received fluid challenges, dobutamine up to 15 μg · kg−1 · min−1 and blood transfusions to achieve predefined goals for arterial pressure, urine output, and central venous pressure.105 These same therapies were administered in the intervention group to achieve the additional goal of an estimated oxygen extraction ratio of less than 27%, the value of which was calculated using intermittent measurements of Scvo2. Trial interventions were continued until an unspecified time on the first postoperative day. Dobutamine was administered more frequently and in greater doses to the Scvo2 group (2.6 ± 4.0 μg · kg−1 · min−1 vs. 0.4 ± 2.2 μg · kg−1 · min−1; P = 0.001). Volumes of intravenous fluid and transfused blood were similar in the two groups, although fluid challenges were commenced earlier stage in the Scvo2 group. Fewer patients in the Scvo2 group developed organ failure (8 of 68 patients [11.8%] vs. 20 of 67 patients [29.8%]; P < 0.05). The duration of hospital stay was also reduced in the Scvo2 group (11.3 ± 3.8 days vs. 13.4 ± 6.1 days; P < 0.05), whereas mortality was low in both groups (2.9% vs. 3.0%; absolute values not reported). This was an important investigation with encouraging findings. However, there are some limitations that prevent full interpretation of the results. The report provides little information regarding the standardization of interventions that are frequent confounders in trials of this size. In particular, there is little or no description of those interventions likely to limit excessive Vo2. These include anesthesia, analgesia, temperature maintenance, postoperative sedation, ventilation, and other aspects of postoperative critical care. It is unclear why the investigators chose to use estimated oxygen extraction ratio as a hemodynamic goal rather than absolute values of Scvo2. Although this may reduce the effects of alveolar hypoxemia as a confounder, the use of Scvo2 to calculate oxygen extraction ratio is considered unreliable.68,73,76,80,106 In common with a number of similar trials, the small sample size limits the generalizability of the findings.11–13 Although the multicenter design offsets this somewhat, much larger trials are clearly needed to resolve the question of effectiveness in routine clinical practice.
In an earlier study of patients undergoing peripheral vascular surgery, the use of Svo2 as a therapeutic endpoint for inotropic therapy was not associated with any change in outcome.107 Patients undergoing aortic reconstruction or limb salvage procedures were admitted to intensive care 12 hours preoperatively for pulmonary artery catheter placement. Initial values of Svo2 were surprisingly low but responded significantly in the intervention group (59.1% to 68.8%). However, final Svo2 values were similar in the two groups (70.0% vs. 70.1%) perhaps explaining the similar outcomes.
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Cardiothoracic Surgery
Polonen et al. randomized 196 patients undergoing elective cardiac surgery to a protocol involving the administration of intravenous fluid and inotropic therapy to attain a target Svo2 of at least 70% in the first 8 h after surgery.108 Dobutamine was administered in doses of up to 15 μg · kg−1 · min−1 where the target Svo2 was not achieved with intravenous fluid alone. Control group patients were administered intravenous fluid and dobutamine to meet goals for pulmonary artery occlusion pressure, cardiac index, arterial pressure, and hematocrit. Svo2 was similar in the two groups at baseline (control group 67 ± 6% vs. Svo2 group 67 ± 6%), but there were greater improvements in Svo2 in the Svo2 group (control group 69 ± 5% vs. Svo2 group 71 ± 4%; P < 0.001). Svo2-guided therapy was associated with a reduction in both hospital stay (7 [5–8] days vs. 6 [5–7] days; P < 0.05) and the number of patients developing complications (11 patients [5.6%] vs. 2 patients [1.0%]; P < 0.01). It is uncertain whether such a small mean difference in Svo2 of 2% is a true reflection of these improved clinical outcomes. In common with other trials, the intervention protocol principally targeted Svo2 by increasing Do2. In addition, the authors report measures in all patients that would have minimized excessive Vo2. These include postoperative sedation and ventilation that was discontinued only when the patient was normothermic and hemodynamically stable. Hemodynamic therapy to attain a target value for Svo2 is more appropriate in this context as confounding causes of decreased venous saturation are minimized. This treatment approach is possible after cardiac surgery where postoperative intensive care admission is a standard of care; this is not always the case for high-risk noncardiac surgery.2,3
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Conclusions
Scvo2 and Svo2 reflect important pathophysiological changes in oxygen delivery and consumption that occur during the perioperative period. The most appropriate clinical interventions to rectify abnormalities of venous saturation may therefore vary widely. Supplemental oxygen, respiratory support, blood products, intravenous fluid, inotropic therapy, anesthesia, analgesia, sedation, and rewarming are all commonly used perioperative interventions that affect venous oxygen saturation. Small clinical trials suggest that the use of venous saturation as a therapeutic goal for hemodynamic therapy may reduce postoperative complication rates. However, these studies are not large enough to demonstrate a mortality benefit and are poorly generalizable. Further research is required to establish the most appropriate treatment algorithms for the use of Scvo2 and Svo2 in perioperative care. Large, prospective, randomized control trials should then be undertaken to confirm the effects of such an approach on clinical outcomes.
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References

1. Weiser TG, Regenbogen SE, Thompson KD, Haynes AB, Lipsitz SR, Berry WR, Gawande AA: An estimation of the global volume of surgery: A modelling strategy based upon available data. The Lancet 2008; 372:139–44

2. Jhanji S, Thomas B, Ely A, Watson D, Hinds C, Pearse RM: Mortality and utilisation of critical care resources amongst high-risk surgical patients in a large NHS trust. Anaesthesia 2008; 63:695–700

3. Pearse RM, Harrison D, James P, Watson D, Hinds C, Rhodes A, Grounds R, Bennett E: Identification and characterisation of the high-risk surgical population in the United Kingdom. Crit Care 2006; 10:R81

4. Haynes A, Weiser T, Berry W, Lipsiz S, Breizat A, Dellinger E, Herbosa T, Joseph S, Kibatala P, Lapital M, Merry A, Moorthy K, Reznik R, Taylor B, Gawande A: A surgical safety checklist to reduce morbidity and mortality in a global population. N Engl J Med 2009; 360:491–9

5. Juul A, Wetterslev J, Gluud C, Jensen G, Callesen T, Norgaard P, Fruergard K, Bestle M, Vedelsdal R, Miran A, Jacobsen J, Mortensen M, Jorgensen L, Jorgensen J, Rovsing M, Petersen P, Pott F, Haas M, Alvret R, Nielsen L, Jogabsson G, Stjernholm P, Molgaard T, Foss N, Elkjaer J, Dehlie B, Boysen K, Zaric D, Munksgaard A, Madsen J, Oberg B, Kganykin B, Blemmer T, Yndgaard S, Perko G, Wang L, Winksel P, Hildren J, Jensen P, Salas N: Effect of perioperative beta blockade in patients with diabetes undergroing major non-cardiac surgery: Randomised, placebo controlled, blinded multicentre trial. Br Med J 2006; 332:1482

6. Khuri S, Henderson W, DelPalma R, Mosca C, Healey N, Kumbhani D: Determinants of long-term survival after major surgery and the adverse effect of postoperative complications. Ann Surg 2005; 242:326–41

7. Clowes G, Vuvinic M, Weidner M: Circulatory and metabolic alterations associated with survival or death in peritonitis: Clinical analysis of 25 cases. Ann Surg 1966; 163:866–85

8. Kusano C, Baba M, Takao S, Sana S, Scimada M, Shirao K, Natsugoe S, Fukumoto T, Aiko T: Oxygen delivery as a factor in the development of fatal postoperative complications after oesophagectomy. Br J Surg 1997; 84:252–7

9. Shoemaker W, Montgomery E, Kaplan E, Elwyn D: Physiologic patterns in surviving and nonsurviving shock patients. Use of sequential cardiorespiratory variables in defining criteria for therapeutic goals and early warning of death. Arch Surg 1973; 106:630–6

10. Jhanji S, Lee C, Watson D, Hinds C, Pearse RM: Microvascular flow and tissue oxygenation after major abdominal surgery: Association with post-operative complications. Intensive Care Med 2008; 35:671–7

11. Boyd O, Grounds R, Bennett E: A randomised clinical trial of the effect of deliberate perioperative increase of oxygen delivery on mortality in high-risk surgical patients. JAMA 1993; 270:2699–707

12. Pearse RM, Belsey J, Cole J, Bennett E: Effect of dopexamine infusion on mortality following major surgery: Individual patient meta-regression analysis of published clinical trials. Crit Care Med 2008; 36:1323–9

13. Pearse RM, Dawson D, Fawcett J, Rhodes A, Bennett E: Early goal directed therapy after major surgery reduces complications and duration of hospital stay: A randomised controlled trial. Critical Care 2005; 9:R687–93

14. Wilson J, Woods I, Fawcett J, Whall R, Dibb W, Morris C, McManus E: Reducing the risk of major elective surgery: Randomised controlled trial of preoperative optimisation of oxygen delivery. Br Med J 1999; 318:1099–103

15. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001; 345:1368–77

16. Barratt-Boyes B, Wood E: The oxygen saturation of blood in the venae cavae, right-heart chambers and pulmonary vessels of healthy subjects. J Lab Clin Med 1957; 50:93–106

17. Fick A: Ueber die Messung des Blutquantums in den Herzventrikeln. Verh Phys Med Ges Wurzburg 1870;2:16–28

18. Reinhart K, Schäfer M, Rudolph T, Specht M: Mixed venous oxygen saturation. Appl Cardiopulm Pathophysiol 1989; 2:315–25

19. Lindholm L, Hansdottir V, Lundqvist M, Jeppson A: The relationship between mixed venous and regional venous oxygen saturation during cardiopulmonary bypass. Perfusion 2002; 17:133–9

20. McDaniel L, Zwiscehnberger J, Vertrees R, Nutt L, Uchida T, Nguyen T, Kramer G: Mixed venous oxygen saturation during cardiopulmonary bypass poorly predicts regional venous saturation. Anesth Analg 1995; 80:466–72

21. Weinrich M, Scheingraber S, Stephan B, Weiss C, Kayser A, Kopp B, MacSullivan R: Central venous oxygen saturation does not correlate with the venous oxygen saturation at the surgical site during abdominal surgery. Clin Hemorheol Microcirc 2008; 39:409–15

22. Dahn M, Lange M, Jacobs L: Central mixed and splanchnic venous oxygen saturation monitoring. Intens Care Med 1988; 14:373–8

23. Harms M, Lieshout JV, Jenstrup M, Pott F, Secher N: Postural effects on cardiac output and mixed venous oxygen saturation in humans. Exp Physiol 2003; 88:611–6

24. Madsen P, Iversen H, Secher N: Central venous oxygen saturation during hypovolaemic shock in humans. Scand J Clin Lab Invest 1993; 53:67–72

25. Jenstrup M, Eilersen E, Mogensen T, Secher N: A maximal central venous oxygen saturation (SvO2max) for the surgical patient. Acta Anaesthesiol Scand Suppl 1995; 107:29–32

26. Staub N: The respiratory system, Physiology. Edited by Levy RB, Mosby, 1998, pp 517–87

27. Christoforides C, Laasberg L, Hedley-Whyte J: Effect of temperature on solubility of O2 in human plasma. J Appl Physiol 1969; 26:56–60

28. Thys DM, Cohen E, Eisenkraft JB: Mixed venous oxygen saturation during thoracic anesthesia. Anesthesiology 1988; 69:1005–9

29. Goldman R, Klughaupt M, Metcalf T, Spivack A, Harrison D: Measurement of central venous oxygen saturation in patients with myocardial infarction. Circulation 1968; 38:941–6

30. Hutter A, Moss A: Central venous oxygen saturations: The value of serial determinations in patients with acute myocardial infarction. JAMA 1970; 212:299–303

31. Muir A, Kirby N, King A, Miller H: Mixed venous oxygen saturation in relation to cardiac output in myocardial infarction. Br Med J 1970; 4:276–8

32. Creamer J, Edwards J, Nightingale P: Hemodynamic and oxygen transport variables in cardiogenic shock secondary to acute myocardial infarction, and response to treatment. Am J Cardiol 1990; 65:1297–300

33. Scheinman M, Brown M, Rapaport E: Critical assessment of use of central venous oxygen saturation as a mirror of mixed venous oxygen in severely ill cardiac patients. Circulation 1969; 40:165–72

34. Goldman R, Braniff B, Harrison D: The use of central venous oxygen saturation measurements in a coronary care unit. Ann Intern Med 1968; 68:1280–7

35. Antonini E, Wyman J, Brunori M, Bucci E, Fronticelli C, Rossi-Fanlli A: Studies on the relations between molecular and functional properties of hemoglobin. IV. The Bohr effect in human hemoglovin measured by proton binding. J Biol Chem 1963; 238:2950–7

36. Ho K, Harding R, Chamberlain J: The impact of arterial oxygen tension on venous oxygen saturation in circulatory failure. Shock 2008; 29:3–6

37. Jee R, White N: The effect of inspired oxygen concentration on central venous oxygen saturation. J Intens Care Soc 2007; 8:7–10

38. Guffin A, Girard D, Kaplan J: Shivering following cardiac surgery: Hemodynamic changes and reversal. J Cardiothorac Anaesth 1987; 1:24–8

39. Horvath S, Spurr G, Hutt B, Hamilton L: Metabolic cost of shivering. J Appl Physiol 1956; 8:595–602

40. Rodriguez J, Weissman C, Damask M, Askanazi J, Hyman A, Kinney J: Physiologic requirements during rewarming: Suppression of the shivering response. Crit Care Med 1983; 11:490–7

41. Roe C, Goldberg M, Blair C, Kinney J: The influence of body temperature on early postoperative oxygen consumption. Surgery 1966; 60:85–92

42. Freeman L, Nixon P, Sallabank P, Reaveley D: Psychological stress and silent myocardial ischemia. Am Heart J 1987; 114:477–82

43. Baraka A, Baroody M, Haroun S, Nawafal M, Dabbous A, SIbai A, Jamal S, Shamli S: Continuous venous oximetry during cardiopulmonary bypass: Influence of temperature changes, perfusion flow, and hematocrit levels. J Cardiothorac Anesth 1990; 4:35–8

44. van der Hoeven M, Maertzdorf W, Blanco C: Mixed venous oxygen saturation and biochemical parameters of hypoxia during progressive hypoxemia in 10 to 14 day old piglets. Paediatr Resuscitation 1997; 52:878–84

45. Colonna-Romano P, Horrow J: Dissociation of mixed venous oxygen saturation and cardiac index during opiod induction. J Clin Anesth 1994; 6:95–8

46. Freebairn R, Derrick J, Gomersall C, Young R, Joynt G: Oxygen delivery, oxygen consumption, and gastric intramucosal pH are not improved by a computer-controlled, closed-loop, vecuronium infusion in severe sepsis and septic shock. Crit Care Med 2000; 28:1569–71

47. Marik P, Kaufman D: The effects of neuromuscular paralysis on systemic and splanchnic oxygen utilization in mechanically ventilated patients. Chest 1996; 109:1038–42

48. Vernon D, Witte M: Effect of neuromuscular blockade on oxygen consumption and energy expenditure in sedated, mechanically ventilated children. Crit Care Med 2000; 28:1569–71

49. Dörges V, Wenzel V, Dix S, Kühl A, Schumann T, Hüppe M, Iven H, Gerlach K: The effect of midazolam on stress levels during simulated emergency medical service transport: A placebo-controlled, dose-response study. Anesth Analg 2002; 95:417–22

50. Scheeren T, Schwarte L, Arndt J: Metabolic regulation of cardiac output during inhalation anaesthesia in dogs. Acta Anaesthesiol Scand 1999; 43:421–30

51. Kumba C, Van der Linden P: Effects of sedative drugs on metabolic demand. Ann Fr Anaesth Reanimation 2008; 27:574–80

52. Mirzai H, Tekin I, Tarkan S, Ok G, Goktan C: Effect of propofol and clonidine on cerebral blood flow velocity and carbon dioxide reactivity in the middle cerebral artery. J Neurosurg Anesthesiol 2004; 16:1–5

53. Adams H, Parker J, Mathew B: The influence of ketamine on inotropic and chronotropic responsiveness of heart muscle. J Pharmacol Exper Ther 1977; 201:171–83

54. Folts J, Afonso S, Rowe G: Systemic and coronary haemodynamic effects of ketamine in intact anaesthetized and unanaesthetized dogs. Br J Anaesth 1975; 47:686–94

55. DeLaunay L, Bonnet F, Duval P: Clonidine decreases post-operative oxygen consumption in patients recovering from general anaesthesia. Br J Anaesth 1991; 67:397–401

56. Taittonen M, Kirvela O, Aantaa R, Kanto J: The effect of clonidine or midazolam premedication on perioperative responses during ketamine anesthesia. Anesth Analg 1998; 87:161–7

57. Van Aken H, Van Hemelrijck J: An overview of the influence of anesthesia on cerebral blood flow and cerebral metabolism. Minerva Anestesiologie 1993; 59:615–20

58. Hoffman W, Miletich D, Albrecht R: The effects of midazolam on cerebral blood flow and oxygen consumption and its interaction with nitrous oxide. Anesth Analg 1986; 65:729–33

59. Kasti K, Långsjo J, Aalto S, Oikonen V, Sipilä H, Teräs M, Hinkka S, Metsähonkala L, Scheinin H: Effects of sevoflurane, propofol, and adjunct nitrous oxide on regional cerebral blood flow, oxygen consumption, and blood volume in humans. Anesthesiology 2003; 99:603–13

60. Lenz C, Frietsch T, Futterer C, Rebel A, Ackern Kv, Kuschinsky W, Waschke K: Local coupling of cerebral blood flow to cerebral glucose metabolism during inhalational anesthesia in rats: Desflurane versus isoflurane. Anesthesiology 1999; 91:1720–3

61. Smith A, Wollman H: Cerebral blood flow and metabolism: Effects of anesthetic drugs and techniques. Anesthesiology 1972; 36:378–400

62. Bernard J, Bourreli B, Pinaud M: Effects of systemic morphine and epidural bupivacaine on postoperative oxygen consumption during rewarming. J Clin Anesth 1988; 1:81–6

63. Locker G, Mader R, Rizovski B, Knapp S, Domanovits H, Muellner M, Hoeller C, Steger G, Sterz F, Freissmuth M, Frass M, Laggner A: Negative chronotropic effects of fentanyl attenuate beneficial effects of dobutamine on oxygen metabolism: Hemodynamic and pharmacokinetic interactions. J Pharmacol Exp Ther 1999; 290:43–50

64. Westenskow D, Jordan W: Changes in oxygen consumption induced by fentanyl and thiopentone during balanced anaesthesia. Can Anaesth Soc J 1978; 25:18–21

65. Westenskow D, Jordan W, Hodges M, Stanley T: Correlation of oxygen uptake and cardiovascular dynamics during N2O-fentanyl and N2O-thiopental anesthesia in the dog. Anesth Analg 1978; 57:37–41

66. Breslow M, Jordan D, Christopherson R, Rosenfeld B, Miller C, Hanley D, Beattie C, Traystman R, Rogers M: Epidural morphine decreases postoperative hypertension by attenuating sympathetic nervous system hyperactivity. JAMA 1989; 261:3577–81

67. Liu S, Wu C: Effect of postoperative analgesia on major postoperative complications: A systematic update of the evidence. Anesth Analg 2007; 104:689–702

68. Chawla L, Zia H, Gutierrez G, Katz N, Seneff M, Shah M: Lack of equivalence between central and mixed venous oxygen saturation. Chest 2004; 126:1891–6

69. Dueck M, Klimek M, Appenrodt S, Weigand C, Boerner U: Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Anesthesiology 2005; 103:249–57

70. Ho K, Harding R, Chamberlain J, Bulsara M: A comparison of central and mixed venous oxygen saturation in circulatory failure [Jan. 17, Epub ahead of print]. J Cardiothorac Vasc Anesth 2008

71. Lorentzen A, Lindskov C, Sloth E, Jakobsen C: Central venous oxygen saturation cannot replace mixed venous saturation in patients undergoing cardiac surgery. J Cardiothorac Vasc Anesth 2008; 22:853–7

72. Sekkat H, Sohawon S, Noordally S: A comparison of mixed and central venous oxygen saturation in patients during and after cardiac surgery. J Intens Care Soc 2009; 10:99–101

73. Reinhart K, Rudolph T, Breedle D, Hannemann L, Cain S: Comparison of central-venous to mixed-venous oxygen saturations during changes in oxygen supply/demand. Chest 1989; 95:1216–21

74. Glamann D, Lange R, Hillis L: Incidence and significance of a “step-down” in oxygen saturation from superior vena cava to pulmonary artery. Am J Cardiol 1991; 68:695–7

75. Lee J, Wright F, Barber R, Stanley L: Central venous oxygen saturation in shock: A study in man. Anesthesiology 1972; 36:472–8

76. Martin C, Auffray J, Badetti C, Perrin G, Papazian L, Gouin F: Monitoring of central venous oxygen saturation versus mixed venous oxygen saturation in critically ill patients. Intens Care Med 1992; 18:101–4

77. Pieri M, Brandi L, Bertolini R, Calafa M, Giunta F: Comparison of bench central and mixed pulmonary venous oxygen saturation in critically ill patients. Minerva Anestesiologie 1995; 61:285–91

78. Varpula M, Karlsson S, Ruokonen E: Mixed venous oxygen saturation cannot be estimated by central venous oxygen saturation in septic shock. Intens Care Med 2006; 32:1336–43

79. Turnaoglu S, Tugrul M, Camci E, Cakar N, Akinci Ō, Ergin P: Clinical applicability of the substitution of mixed venous oxygen saturation with central venous oxygen saturation. J Cardiothorac Vasc Anesth 2001; 15:574–9

80. Reinhart K, Kersting T, Föhring U, Schäfer M: Can central-venous replace mixed-venous oxygen saturation measurements during anesthesia? Adv Exper Med Biol 1986; 200:67–72

81. Jhanji S, Dawson J, Pearse RM: Cardiac output monitoring: Basic science and clinical application. Anaesthesia 2008; 63:172–81

82. Meyer J: Wener Forssmann and catheterization of the heart. Ann Thorac Surg 1990; 49:497–9

83. Edwards J, Mayall R: Importance of the sampling site for measurement of mixed venous oxygen saturation in shock. Crit Care Med 1998; 26:1356–60

84. Suter P, Lindauer J, Fairley H, Schlobohm R: Errors in data derived from pulmonary artery blood gas values. Crit Care Med 1975; 3:175–81

85. Pond C, Blessios G, Lappas D, McCawley C: Perioperative evaluation of a new mixed venous saturation catheter in cardiac surgical patients. J Cardiothorac Vasc Anesth 1992; 6:280–2

86. Waller J, Kaplan J, Bauman D, Craver J: Clinical evaluation of a new fiberoptic catheter oximeter during cardiac surgery. Anesth Analg 1982; 61:676–9

87. Pearse R, Dawson D, Fawcett J, Rhodes A, Grounds R, Bennett E: Changes in central venous saturation after major surgery and association with outcome. Critical Care 2005; 9:R694–9

88. Jakob S, Bracht H, Eigenmann V, Haenggi M, Inderbitzin D, Loher S, Raeber C, Takala J, Vogt A, Mäkinen K, Miettinen P, Niskanen M, Parviainen I, Leppikangas H, Nunes S, Ruokonen E: Multicentre study on peri- and postoperative central venous oxygen saturation in high-risk surgical patients. Crit Care 2006; 10:R158

89. Poeze M, Ramsay G, Greve JW, Singer M: Prediction of postoperative cardiac surgical morbidity and organ failure within 4 hours of intensive care unit admission using esophageal Doppler ultrasonography. Crit Care Med 1999; 27:1288–94

90. Polonen P, Hippelainen M, Takala R, Ruokonen E, Takala J: Relationship between intra- and postoperative oxygen transport and prolonged intensive care after cardiac surgery: A prospective study. Acta Anaesthesiol Scand 1997; 41:810–7

91. Routsi C, Vincent J, Bakker J, Backer D, Lejeune P, d’Hollander A, Clerc JL, Kahn R: Relation between oxygen consumption and oxygen delivery in patients after cardiac surgery. Anesth Analg 1993; 77:1104–10

92. Ander D, Jaggi M, Rivers E, Rady M, Levine T, Levine A, Masura J, Gryzbowski M: Undetected cardiogenic shock in patients with congestive heart failure presenting to the emergency department. Am J Cardiol 1998; 82:888–91

93. Krafft P, Steltzer H, Hiesmayr M, Klimscha W, Hammerle A: Mixed venous oxygen saturation in critically ill septic shock patients. The role of defined events. Chest 1993; 103:900–6

94. Moomey C, Melton S, Croce M, Timothy C, Proctor K: Prognostic value of blood lactate, base deficit and oxygen-derived variables in an LD50 model of penetrating trauma. Crit Care Med 1999; 27:154–61

95. Scalea T, Hartnett R, Duncan A, Atweh N, Phillips T, Sclafani S, Furotes M, Shaftan G: Central venous oxygen saturation: A useful clinical tool in trauma patients. J Trauma 1990; 30:1539–43

96. Jamieson W, Turnbull K, Larrieu A, Dodds W, Allison J, Tyers G: Continuous monitoring of mixed venous oxygen saturation in cardiac surgery. Can J Surg 1982; 25:538–43

97. Krauss X, Verdouw P, Hughenholtz P, Nauta J: On-line monitoring of mixed venous oxygen saturation after cardiothoracic surgery. Thorax 1975: 636–43

98. Schmidt C, Frank L, Forsythe S, Estafanous F: Continuous SvO2 measurement and oxygen transport patterns in cardiac surgery patients. Crit Care Med 1984; 12:523–7

99. Conacher I, Paes M: Mixed venous oxygen saturation during lung transplantation. J Cardiothorac Vasc Anesth 1994; 8:671–4

100. McArthur K, Clark L, Lyons C, Edwards S: Continous recording of blood oxygen saturation in open-heart operations. Surgery 1962; 51:121–6

101. Stanley T, Isern-Amaral J: Periodic analysis of mixed venous oxygen tension to monitor the adequacy of perfusion during and after cardiopulmonary bypass. Can Anaesth Soc J 1974; 21:454–60

102. Scalea T, Holman M, Fuortes M, Baron B, Philips T, Goldstein A, Sclafani S, Shaftan G: Central venous blood oxygen saturation: An early, accurate measurement of volume during hemorrhage. J Trauma 1988; 28:725–32

103. Kazarian K, Guercio LD: The use of mixed venous blood gas determinations in traumatic shock. Ann Emerg Med 1980; 9:179–82

104. Kremzar, Spec-Marn A, Kompan L, Cerovic O: Normal values of SvO2 as therapeutic goal in patients with multiple injuries. Intens Care Med 1996; 23:65–70

105. Donati A, Loggi S, Preiser J, Orsetti G, Munch C, Gabbanelli V, Pelaia P, Pietropaoli P: Goal-directed intraoperative therapy reduces morbidity and length of hospital-stay in high-risk surgical patients. Chest 2007; 132:1817–24

106. Ladakis C, Myrianthefs P, Karabinis A, Karatzas G, Dosios T, Fildissis G, Gogas J, Baltopoulos G: Central venous and mixed venous oxygen saturation in critically ill patients. Respiration 2001; 68:279–85

107. Ziegler D, Wright J, Choban P, Flancbaum L: A prospective randomised trial of preoperative ‘optimisation’ of cardiac function in patients undergoing elective peripheral vascular surgery. Surgery 1997; 122:584–92

108. Pölönen P, Ruokonen E, Hippeläinen M, Pöyhönen M, Takala J: A prospective, randomized study of goal-oriented hemodynamic therapy in cardiac surgical patients. Anesth Analg 2000; 90:1052–9

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