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(Chest. 2004;126:1891-1896.)
© 2004 American College of Chest Physicians

Lack of Equivalence Between Central and Mixed Venous Oxygen Saturation*

Lakhmir S. Chawla, MD; Hasan Zia, MD; Guillermo Gutierrez, MD, PhD, FCCP; Nevin M. Katz, MD; Michael G. Seneff, MD, FCCP and Muhammed Shah, MD

* From the Critical Care Medicine Division (Drs. Chawla, Seneff, and Shah), Department of Anesthesiology, the Division of General Surgery (Dr. Zia), Department of Surgery, the Pulmonary and Critical Care Medicine Division (Dr. Gutierrez), Department of Medicine, and the Cardiothoracic Surgery Division (Dr. Katz), Department of Surgery, The George Washington University Medical Center, Washington, DC.

Correspondence to: Guillermo Gutierrez, MD, PhD, FCCP, Professor of Medicine and Anesthesiology, The George Washington University MFA, 2150 Pennsylvania Ave NW, Suite 5–404, Washington, DC 20037; e-mail: Ggutierrez{at}mfa.gwu.edu


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objective: We compared paired samples of central venous O2 saturation (ScvO2) and mixed venous O2 saturation (SO2) to test the hypothesis that ScvO2 is equivalent to SO2. We also compared O2 consumption (O2) computed with ScvO2 (O2cv) to that computed with SO2 (O2v).

Design: Prospective, sequential, observational study.

Setting: Combined medical-surgical ICU.

Patients: Fifty-three individuals > 18 years of age of either sex who required a pulmonary artery catheter (PAC) to guide fluid therapy. Subjects were identified as postsurgical (32 patients) or medical (21 patients) according to their ICU admission diagnosis.

Interventions: A PAC was inserted through the internal jugular or subclavian veins. Care was taken to place the PAC proximal port approximately 3 cm above the tricuspid valve. Blood samples were drawn from the proximal and distal ports in random order. An arterial blood sample also was drawn.

Measurements: Cardiac output in triplicate, systemic pressure, and central pressure. We analyzed blood samples for hemoglobin concentration and O2 saturation (SO2). Data were compared by correlation analysis and by the method of Bland and Altman.

Results: SO2 was consistently lower than ScvO2 (p < 0.0001), with a mean (±SD) bias of –5.2 ± 5.1%. Similar differences in ScvO2 and SO2 were present within each subgroup (p < 0.001). A lower SO2 resulted in O2v values that were higher than the O2cv values for all patients in the study (mean O2v, 236.7 ± 103.4 mL/min; mean O2cv, 191.1 ± 84.0 mL/min; p < 0.001) as well as for patients within each subgroup (p < 0.001).

Conclusions: Measurements of ScvO2 and SO2 were not equivalent in this sample of critically ill patients. Moreover, substituting ScvO2 for SO2 in the calculation of O2 produced unacceptably large errors. The decrease in SO2 between ScvO2 to SO2 may result from the mixing of atrial and coronary sinus blood. As such, this difference may be a marker of myocardial O2 consumption.

Key Words: central venous oxygenation • coronary sinus • mixed venous oxygenation • monitoring • myocardial metabolism • oxygen consumption • oxygen delivery • pulmonary artery catheter • resuscitation


   Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Mixed venous O2 saturation (SO2) is a clinical marker of systemic oxygen utilization,12 and its measurement is part of the routine monitoring of critically ill patients. The calculation of systemic O2 consumption (O2) and of pulmonary shunt fraction requires knowledge of SO2. Decreases in SO2 have been associated with a poor prognosis in patients with septic shock3 or heart failure,4 and therapeutic interventions that are aimed at raising SO2 have been tried during the resuscitation of critically ill patients.56

The measurement of SO2 requires access to blood from the pulmonary artery, the drawing of which is a highly invasive procedure. SO2 may be measured from a sample of blood drawn from the distal port of a pulmonary artery catheter (PAC) or by using a PAC equipped with fiberoptic infrared sensors. Alternatively, the measurement of central venous blood O2 saturation (ScvO2) offers an attractive option to the measurement of SO2, since it avoids some of the possible complications associated PACs.7 Fiberoptic catheters are commercially available for the continuous measurement of ScvO2, and decreases in mortality have been reported when, guided by a goal-oriented algorithm, they have been used to resuscitate patients.8

Given the potential advantages of using ScvO2 as a surrogate for SO2, it is important to establish the concordance between these measurements as well as the uncertainty associated with using ScvO2 as a measure of SO2.

In this study, we compared the hemoglobin O2 saturation (SO2) of paired samples drawn from the proximal and distal ports of PACs in a population sample of critically ill adult patients. We took the proximal port blood sample as being representative of central venous blood. We tested the hypothesis that measurements of ScvO2 are equivalent to those of SO2 in critically ill patients, providing that the precision and bias of the SO2 estimate are within an acceptable clinical range.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
This was a prospective, sequential, observational study of patients who had been admitted to the George Washington University Hospital ICU over a period of 6 months. The study was approved by the institutional review board, and informed consent for participating in the study was obtained from the patient or from their next of kin.

We enrolled individuals of either sex who were > 18 years of age whose attending physicians determined that a PAC was required to guide fluid therapy. Enrollment in the study occurred when the patient or the nearest relative consented to the introduction of the PAC. Patients who were excluded from the study were those with uncorrected valvular incompetence or intracardiac shunting, or those requiring the insertion of the PAC through the femoral vein. Depending on their diagnosis at the time of ICU admission, patients were identified as being postsurgical (ie, in the postoperative group) or medical (ie, in the medical group).

A 7.5F, five-lumen PAC that was 110 cm in length and had the right atrial lumen positioned 30 cm from the tip (Edwards Lifesciences; Irvine, CA) was inserted through the internal jugular vein or the subclavian vein using a percutaneous 8.5F sheath introducer (Edwards Lifesciences). On the first appearance of right ventricular pressure waves in the distal port, the catheter was withdrawn until the right ventricular waves disappeared. The catheter distance at the entrance of the sheath introducer was noted. The catheter then was advanced 27 cm past this point, placing the distal port catheter in the pulmonary artery and the proximal port within the right atrium, approximately 3 to 4 cm above the tricuspid valve. A pressure tracing obtained from the proximal port was used to ascertain correct positioning in the right atrium. A portable chest radiograph and the presence of pulmonary artery pressure tracings confirmed the location of the distal port in the pulmonary artery.

Immediately after the insertion of the PAC, and prior to obtaining measures of pulmonary artery occlusion pressure (PAOP), each patient had one set of paired blood samples drawn in random order and in rapid succession from the proximal and distal port. The first 2 mL blood drawn for each sample was discarded to prevent contamination with flushing fluid. Blood samples were drawn with the catheter balloon deflated to avoid contamination of the distal port sample with pulmonary capillary blood.9 We drew a blood sample from a previously inserted arterial line immediately after drawing the paired PAC blood samples. The three blood samples were placed on ice and were taken to a central laboratory for the measurement of hemoglobin concentration (HC) and SO2 (ABL700; Radiometer America Inc; Westlake, OH). We then measured PAOP and cardiac output (CO) by the thermodilution method. Cardiac index (CI) was computed by dividing the average of three sequential measurements of CO by the patient’s body surface area.

We calculated systemic O2 by means of the Fick principle, neglecting the effect of dissolved O2 as follows: O2 = 13.4 x CO x HC x (SaO2 – venous O2 saturation), where SaO2 is arterial oxygen saturation. Calculations of O2 were made by substituting either ScvO2 (O2cv) or SO2 (O2v) for the venous O2 saturation in the calculation.

Data Analysis
Paired Student t test was used to compare ScvO2 to SO2, and O2cv to O2v. Paired samples were compared by correlation analysis,10 and also by the method of Bland and Altman.11 Demographic and hemodynamic data were compared for the postoperative and medical groups using the two-tailed Student t test with levels of significance adjusted according to the method of Bonferroni for multiple comparisons. Unless otherwise specified, data are shown as the mean ± SD, with p < 0.05 deemed to denote a significant difference.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
We enrolled 53 patients in the study, of whom 21 were women. Demographics and diagnoses for individuals are shown in Table 1 . Thirty-two patients in the study were in the postoperative group, and 21 were in the medical group. All patients in the medical group were in shock, as defined by the use of vasopressor agents to maintain mean arterial pressure. Sepsis was the predominant diagnosis in the medical group (62%). Coronary artery bypass grafting and aortic or mitral valve replacement represented the majority of the surgical procedures performed in patients in the postoperative group (84%). Only 25% of the postoperative group required vasopressor agents for the maintenance of BP. We found higher APACHE (acute physiology and chronic health evaluation) II scores, heart rates, mean pulmonary pressures, and CIs in the medical group. Systemic vascular resistance and HC were lower in the medical group.


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  		Table 1. Demographic and Hemodynamic Parameters*

 
Shown in Table 2 are the SO2 values, and O2cv and O2v values. For the group as a whole, the values for SO2 were lower than those for ScvO2 (p < 0.001), with a mean difference (ie, bias) of –5.2 ± 5.1%. ScvO2 was greater than SO2 (p < 0.001) for both the medical and postoperative groups. For all patients, a lower SO2 resulted in a computed O2v that was higher than the O2cv (p < 0.001). Both the postoperative and medical groups also had higher O2v than O2cv (p < 0.001).


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  		Table 2. Oxyhemoglobin Saturation and Calculated O2 Computed Using ScvO2 and SO2*

 
Figure 1 , top, shows the linear correlation of paired ScvO2 and SO2 measurements for all patients in the study (SO2 = –2.64 + 0.97 ScvO2; r = 0.88; p < 0.0001). Figure 1, bottom, shows the Bland-Altman analysis of the paired SO2 samples. As noted previously, SO2 was lower than ScvO2, with a bias of –5.2% (95% confidence interval for the mean, –3.8 to –6.6%) and a 2-SD scatter ranging from –15.5 to 5.2%. Figure 2 , top, shows the correlation of O2cv to O2v for all patients in the study (O2v = 25.5 + 1.1 O2cv; r = 0.89; p < 0.0001). A Bland-Altman analysis of these data (Fig 2, bottom) yields a bias toward a higher O2v of 44.8 mL/min (95% confidence interval for the mean, 31.9 to 57.8 mL/min) and a 2-SD scatter ranging from –48.5 to 139.1 mL/min. Similar results were noted when analyzing the data from each subgroup (data not shown).



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  		Figure 1. Top: paired SO2 and ScvO2 measurements (percentage of saturation) for all patients in the study. The linear correlation was as follows: SO2 = –2.64 + 0.97 ScvO2; r = 0.88; p < 0.0001). Bottom: Bland-Altman analysis of the paired SO2 and ScvO2 measurements shows a bias toward a lower SO2 of –5.2%, with 95% limits of agreement ranging from –15.5 to 5.2%.

 


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  		Figure 2. Top: O2v shown as a function of O2cv for all patients in the study. The linear correlation was as follows: O2v = 25.5 + 1.1 O2cv; r = 0.89; p < 0.0001). Bottom: Bland-Altman analysis shows a bias toward a greater O2v of 44.8 mL/min, with 95% limits of agreement ranging from –48.5 to 139.1 mL/min.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In the present study, we took blood from the right atrium to be representative of central venous blood. We exercised great care during the insertion of the PAC to position the proximal port approximately 3 cm above the tricuspid valve. Presumably, this position placed the ScvO2 sampling site anterior to the coronary sinus but sufficiently distal into the right atrium to allow for the mixing of superior and inferior vena cava blood. The location of this sampling site for measuring ScvO2 differs from that of commercially available, oximetry-capable central venous catheters. In the latter, the infrared transducer lies within the superior vena cava.12

Judging from the robust linear relationship that is present between ScvO2 and SO2, it would be reasonable to conclude that these measures are equivalent. The strength of this relationship is not surprising, given that ScvO2 and SO2 are physiologically tethered. Conversely, a paired-sample comparison of ScvO2 and SO2 shows a systematic bias of 5.2% SO2, with ScvO2 higher than SO2. This bias is present throughout the span of measurement, implying a greater relative error for SO2 at lower ScvO2 values, which is precisely the SO2 range of greatest interest. Even more troublesome, is the unacceptably wide limit of agreement that exists between ScvO2 and SO2. For example, a measurement of 74% for ScvO2 corresponds to an SO2 of 68.8%, with an uncertainty of the estimate ranging from 58 to 79%. This estimate is unlikely to be suitable for clinical use, in particular when applied to protocol-guided resuscitation in which decreases in SO2 of 5 to 7% may trigger therapeutic interventions, such as the use of inotropic agents or the transfusion of blood. We also noted that predictions of O2 based on ScvO2 are biased toward a lower O2 and were associated with unacceptably wide limits of agreement.

Others have considered the issue of whether ScvO2 can be substituted for SO2.13 Experimental studies in animals show an excellent correlation between ScvO2 and SO2. Reinhart et al14 found a Spearman correlation coefficient of 0.97 in anesthetized dogs over a broad range of cardiorespiratory conditions, including hypoxia, hemorrhage, and resuscitation. Schou et al15 also found a correlation coefficient of 0.97 between ScvO2 and SO2 in pigs that had been subjected to conditions of graded hypoxemia. Of note, both studies found SO2 to be consistently lower than ScvO2.

The findings presented here agree with those of other studies1617181920212223 comparing measures of ScvO2 and SO2 in critically ill patients. Table 3 shows a compilation of prior clinical studies comparing ScvO2 to SO2, along with their Spearman correlation coefficients and 95% confidence intervals. The weighted average for ScvO2 is greater than that for SO2 by 2.4% SO2. The estimate for {rho},10 the weighted average correlation for the general population, is 0.87. These figures compare favorably with the results of the present study.


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  		Table 3. Comparison of Prior Studies Relating ScvO2 to SO2 in Critically Ill Patients*

 
A few studies192324 in healthy volunteers or in patients who were deemed not to be in shock found either no differences between ScvO2 and SO2 or even a small increase in SO2 in pulmonary artery blood with weighted mean averages of 75.4 ± 5.8% and 76.2 ± 5.7%, respectively, for ScvO2 and SO2. We did not detect this difference in behavior between the subgroups studied, even though their hemodynamic conditions appeared to be different. The medical group included a sicker group of patients with higher APACHE II scores than those in the postoperative group. The medical group also had higher CO and lower systemic vascular resistance, reflecting a high percentage of patients in septic shock. Most postoperative patients were not in shock and did not receive inotropic agents. Despite these differences, we noted similar findings for SO2 and O2 in both populations, that is, both groups showed a 5% step-down from ScvO2 measurements to SO2 measurements.

A possible explanation for the decrease in SO2 from ScvO2 to SO2 is the myocardial extraction of O2 as blood flows through the right ventricle into the pulmonary artery. Although, to our knowledge, the rate of O2 diffusion from ventricular blood into the myocardium has not been quantified, we consider this possibility unlikely.

A more likely hypothesis is that atrial blood, as it moves toward the pulmonary artery, mixes with blood of lower O2 content. A key element with regard to the significance of this hypothesis is the position of the proximal port of the PAC. The possibility exists that blood drawn from the proximal port of the PAC originated mainly from the superior vena cava. Should this have been the case, and should inferior vena cava effluent be composed of blood with a lower O2 content, then the mixing of these effluents could have resulted in a lower SO2.

It is also possible, however, that decreases in ScvO2 resulted from atrial blood mixing with blood emanating from the coronary sinus and Thebesian veins. Although coronary sinus flow may be but a fraction of total blood flow, the effluent from the coronary sinus has very low SO2, since the heart maximally extracts oxygen from the coronary blood flow. We are of the opinion that mixing with coronary sinus blood is the most likely explanation for the decrease in SO2 from ScvO2 to SO2.

We conclude that ScvO2 is not a reliable surrogate for SO2 in critically ill medical or surgical patients. Moreover, substituting ScvO2 for SO2 in the calculation of O2 is prone to unacceptably large errors. We cannot comment on the precision and repeatability of SO2 estimates, since we did not measure sequential changes in SO2 and ScvO2. It is possible that, although biased toward a larger estimate of SO2, the limits of agreement for repeated measures of ScvO2 and SO2 may be narrow enough to allow for continuous monitoring of ScvO2 as a surrogate for SO2 in individual patients.12

The step-down from ScvO2 to SO2 propounds the intriguing possibility that differences in blood SO2 measured at the proximal and distal ports of the PAC may be related to measures of myocardial O2 utilization. Further studies measuring coronary sinus blood O2 content and flow are needed to test this hypothesis.


   Footnotes
 
Abbreviations: APACHE = acute physiology and chronic health evaluation; CI = cardiac index; CO = cardiac output; HC = hemoglobin concentration; PAC = pulmonary artery catheter; PAOP = pulmonary artery occlusion pressure; ScvO2 = O2 saturation of pulmonary central venous blood; SO2 = O2 saturation; SO2 = mixed venous O2 saturation; O2 = oxygen consumption; O2cv = oxygen consumption calculated with O2 saturation of pulmonary central venous blood; O2v = O2 consumption calculated with O2 saturation of pulmonary artery blood

This study was financed in its entirety by The George Washington University Medical Center Department of Anesthesiology Research Fund.

Received for publication January 14, 2004. Accepted for publication June 22, 2004.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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