Multicenter Study of Central Venous Oxygen Saturation (ScvO2) as a Predictor of Mortality in Patients With Sepsis
Received 6 February 2009; received in revised form 30 May 2009 and 19 July 2009; accepted 6 August 2009. published online 26 October 2009.
Study objective
Abnormal (both low and high) central venous saturation (ScvO2) is associated with increased mortality in emergency department (ED) patients with suspected sepsis.
Methods
This was a secondary analysis of 4 prospectively collected registries of ED patients treated with early goal-directed therapy–based sepsis resuscitation protocols from 4 urban tertiary care hospitals. Inclusion criteria were sepsis, hypoperfusion defined by systolic blood pressure less than 90 mm Hg or lactate level greater than or equal to 4 mmol/L, and early goal-directed therapy treatment. ScvO2 levels were stratified into 3 groups: hypoxia (ScvO2 <70%); normoxia (ScvO2 71% to 89%); and hyperoxia (ScvO2 90% to 100%). The primary exposures were initial ScvO2 and maximum ScvO2 achieved, with the primary outcome as inhospital mortality. Multivariate analysis was performed.
Results
There were 619 patients who met criteria and were included. For the maximum ScvO2, compared with the mortality rate in the normoxia group of 96 of 465 (21%; 95% confidence interval [CI] 17% to 25%), both the hypoxia mortality rate, 25 of 62 (40%; 95% CI 29% to 53%) and hyperoxia mortality rate, 31 of 92 (34%; 95% CI 25% to 44%) were significantly higher, which remained significant in a multivariate modeling. When the initial ScvO2 measurement was analyzed in a multivariate model, only hyperoxia was significantly higher.
Conclusion
The maximum ScvO2 value achieved in the ED (both abnormally low and high) was associated with increased mortality. In multivariate analysis for initial ScvO2, the hyperoxia group was associated with increased mortality, but not the hypoxia group. This study suggests that future research aimed at targeting methods to normalize high ScvO2 values by therapies that improve microcirculatory flow or mitochondrial dysfunction may be warranted.
aHarvard Affiliated Emergency Medicine Residency, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA
bCenter for Vascular Biology Research and Division of Molecular and Vascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA
cDepartment of Emergency Medicine, Carolinas Medical Center, Charlotte, NC
dDepartment of Emergency Medicine, Cooper University Hospital, Camden, NJ
eDepartment of Emergency Medicine, Hospital of the University of Pennsylvania, Camden, NJ
fDivision of Critical Care Medicine, Cooper University Hospital, Camden, NJ
Address for correspondence: Nathan I. Shapiro, MD, MPH, Beth Israel Deaconess Medical Center, 1 Deaconess Road, CC2-W, Boston, MA 02215; 617-754-2323, fax 617-754-2350
Supervising editor: Gregory J. Moran, MD
Author contributions: All authors participated in the conception of the study, study design, and data collection. JVP and NIS oversaw the final data compilation and statistical analysis. All authors participated in the drafting of the article into its final form. All authors take responsibility for the paper as a whole.
Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement. This study was supported in part by National Institutes of Health grants HL091757 and GM076659 (Dr. Shapiro), the National Institutes of Health/National Institute of General Medical Sciences: K23GM83211 (Dr. Trzeciak), National Institutes of Health/National Institute of General Medical Sciences: K23GM076652 (Dr. Jones), and a research endowment from the Beatrice Wind Gift Foundation (Dr. Gaieski). Dr. Trzeciak has received research support from Novo Nordisk, Biosite, and Eli Lilly. Dr. Jones has received research support from Critical Biologics and Hutchinson Technology. Dr. Shapiro receives research grants from Hutchinson Technologies, Eli Lilly, and Inverness Medical and is on the Eli Lilly speaker's bureau.
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Please see page 41 for the Editor's Capsule Summary of this article.
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