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Detroit, MI
Dr. Rivers is affiliated with the Departments of Emergency Medicine and Surgery, Henry Ford Hospital.
Correspondence to: Emanuel Rivers, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202
Mixed venous oxygen saturation (S
O2) in sepsis is commonly referred to as an end point of low impact on clinical decisions in sepsis patients because of the following common refrain: "SO2 is always increased in septic ICU patients." However, there are fundamental principles that render this modality clinically useful when applying it to the supply-dependent phase of sepsis (ie, global tissue hypoxia). The presence of global tissue hypoxia not only has pathologic significance in vitro,1 but there is a pathologic link among the clinical presence of global tissue hypoxia (ie, low SO2 and cardiac index), the generation of inflammatory mediators, and mitochondrial impairment of oxygen utilization that is seen in septic ICU patients.2 Furthermore, identifying sudden episodes of supply dependency in septic ICU patients (ie, sudden decreases in SO2) has diagnostic and prognostic significance.3 With this background, the rationale for using central venous oxygen (ScvO2) saturation as a surrogate for SO2 to detect and treat global tissue hypoxia in the most proximal phase of sepsis management (supply dependency) was the basis for its use in the Early Goal Directed Therapy in Severe Sepsis and Septic Shock Study (EGDT).4
Early hemodynamic assessment using physical examination, vital signs,5 central venous pressure,6 and urinary output7 fails to detect supply dependency or persistent global tissue hypoxia. Shock patients who are resuscitated to having normal vital signs continue to exhibit evidence of global tissue hypoxia (ScvO2 < 70% and increased lactate levels) and require additional resuscitation, as shown by Rady et al.6 Similar findings were confirmed in the EGDT study as 39.8% of the control group vs 5% of the EGDT group continued to have global tissue hypoxia after 6 h of resuscitation despite the fact that all patients attained the same vital sign goals (ie, MAP, > 65 mm Hg; CVP, > 8 mm Hg; urine output, 0.5 mL/kg/h). These findings of global tissue hypoxia, or "cryptic shock," in patients8 have prognostic significance as this state was associated with a 56.5% in-hospital mortality rate. The therapeutic significance was realized as the EGDT patients received early and more aggressive therapy with fluids, RBC transfusion, and inotropic agents.
The question of whether the ScvO2 is a numeric equivalent to SO2 has been examined in a number of studies,9101112 which continues to fuel this debate. These studies, including the trial by Chawla et al,11 have consistently shown that ScvO2 values are (on average) approximately 5% higher than SO2 values, which is likely secondary to the contributions of deoxygenated blood from the coronary sinus. Recognizing this minor, yet consistent, difference allows the clinician to make an accurate assessment of global tissue hypoxia. Furthermore, the clinical utility of an end point of resuscitation is determined by whether it changes clinical practice, morbidity, and mortality in a cohort of patients under the rigors of an appropriately designed clinical trial. In other words, has this end point been calibrated to have clinical utility in the setting in which it is to be used? This was done with ScvO2 in the EGDT study,4 in which the range of ScvO2 values was 48.6 to 49.2%, with lactate levels of 6.9 to 7.7 mmol/L indicating significant supply dependency. Using the finding from Chawla et al,11 the SO2 values would be extrapolated to 43 to 45%. Thus, irrespective of whether the ScvO2 value equals the SO2 value, the presence of a low ScvO2 level in patients with early sepsis portends increased morbidity and mortality, and correcting this value according to a consensus-derived algorithm13 improves morbidity and mortality. It should be further noted that, in this well-designed study by Chawla et al,11 the majority of the 51 patients were not supply-dependent as the mean SO2 values ranged from 67.6 to 70.5, and the corresponding ScvO2 values ranged from 71.9 to 77.0 with no mention of lactate levels.
Examining studies comparing the numeric equivalency of SO2 vs ScvO2, while of important academic value, does not address clinical utility. The concept of the approximately 5% numeric difference between SO2 and ScvO2 values is not novel, and the Surviving Sepsis Campaign has acknowledged14 this by recommending obtaining an SO2 level of 65% and/or an ScvO2 level of 70% in the resuscitation portion of its management of patients with severe sepsis and septic shock bundle.
Footnotes
Dr. Rivers has done consultant work for Biosite, Inc., Chiron, the Lilly Corporation, and Edwards Lifesciences over the past year. As a consultant, he helped advise the company in developing, but holds no patent rights to, catheters used for early, goal-directed therapy.
References
This article has been cited by other articles:
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  K. M. Chin, R. N. Channick, N. H. Kim, and L. J. Rubin Central Venous Blood Oxygen Saturation Monitoring in Patients With Chronic Pulmonary Arterial Hypertension Treated With Continuous IV Epoprostenol: Correlation With Measurements of Hemodynamics and Plasma Brain Natriuretic Peptide Levels Chest, September 1, 2007; 132(3): 786 - 792. [Abstract] [Full Text] [PDF]
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