Skeletal muscle oxygen saturation does not estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock

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Abstract
Introduction: Low cardiac output states such as left heart failure are characterized by preserved oxygen extraction ratio, which is in contrast to severe sepsis. Near infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of the study was to determine the relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock. Methods: Sixty-five patients with severe left heart failure due to primary heart disease were divided into two groups: groups A (n = 24) and B (n = 41) included patients without and with additional severe sepsis/septic shock, respectively. Thenar muscle StO2 was measured using NIRS in the patients and in 15 healthy volunteers. Results: StO2 was lower in group A than in group B and in healthy volunteers (58 ± 13%, 90 ± 7% and 84 ± 4%, respectively; P < 0.001). StO2 was higher in group B than in healthy volunteers (P = 0.02). In group A StO2 correlated with SvO2 (r = 0.689, P = 0.002), although StO2 overestimated SvO2 (bias -2.3%, precision 4.6%). In group A changes in StO2 correlated with changes in SvO2 (r = 0.836, P < 0.001; ΔSvO2 = 0.84 × ΔStO2 - 0.67). In group B important differences between these variables were observed. Plasma lactate concentrations correlated negatively with StO2 values only in group A (r = -0.522, P = 0.009; lactate = -0.104 × StO2 + 10.25). Conclusion: Skeletal muscle StO2 does not estimate SvO2 in patients with severe left heart failure and additional severe sepsis or septic shock. However, in patients with severe left heart failure without additional severe sepsis or septic shock, StO2 values could be used to provide rapid, noninvasive estimation of SvO2; furthermore, the trend in StO2 may be considered a surrogate for the trend in SvO2. Trial Registration: NCT00384644