Skeletal Muscle Oxygenation in Critically Ill

Introduction

The duration and severity of tissue hypoxia have been related to increased mortality. Maintenance of adequate oxygen delivery (DO2) is essential to preserve organ function, as a sustained low DO2 is a path to organ failure and death. DO2 does not have influence on oxygen consumption (VO2) until it reaches critically low values (DO2crit), when VO2 starts to fall. Low cardiac output states (cardiogenic, hypovolemic and obstructive types of shock), anemic and hypoxic hypoxemia are characterized by a decreased DO2 but preserved oxygen extraction ratio (OER=the ratio of DO2 to VO2, VO2/ DO2) so that DO2crit remains normal. In distributive shock, the oxygen extraction capability is altered so that the critical oxygen extraction ratio is typically decreased. These situations are typically associated with an increased DO2crit, and VO2 can become dependant on DO2 even when the latter is normal or elevated. These observations help to characterize the four principal types of circulatory shock, however this classification is somewhat simplistic as several types of alternations may coexist, in particular in cardiogenic shock. Rhodes et al. reported that outcome was more favorable in septic patients whose VO2 increased after dobutamine administration. DO2 also increased in survivors. On the other hand DO2 did not increase in patients whose VO2 did not increase. In dobutamine test proposed by Rhodes et al. the hemodynamic response was influenced by cardiovascular reserve and the degree of stimulation of adrenoreceptors at baseline. Unfortunately global measurements of DO2 and VO2 may not be sensitive enough to be clinically relevant. They may fail to detect regional perfusion abnormalities as in splanchnic circulation.

Measurement of mixed venous oxygen saturation (SvO2) from the pulmonary artery is used for the calculations of the VO2 and has been advocated as an indirect index of tissue of tissue oxygenation and prognostic predictor in critically ill patients. Catheterization of pulmonary artery is costly, has inherent risks and its usefulness remains under debate. Not surprisingly the monitoring of central venous oxygen saturation (ScvO2) was suggested as a simpler and chipper assessment of global DO2 to VO2 ratio.

Near infrared spectroscopy (NIRS) is a technique for continuous, non-invasive, bedside monitoring of tissue oxygen saturation (StO2). Like pulse oximetry, NIRS uses the principles of light transmission and absorption to non-invasively measure the concentrations of oxygenated hemoglobin and reduced hemoglobin in tissue. NIRS offers greater tissue penetration and does not discriminate between compartments. Therefore it provides a global assessment of oxygenation in all vascular compartments (arterial, venous and capillary) in sample volume of underlining tissue. We have previously shown that thenar muscle tissue oxygen saturation during stagnant ischemia decreases slower in septic shock patients compared to patients with severe sepsis, localized infection and healthy volunteers. This may be due to microcirculatory or metabolic changes, and probably correlates to muscle tissue oxygen consumption. The rate of StO2 decrease correlated with SOFA score, norepinephrine requirement, and plasma lactate concentration. As recently described, StO2 in sample volume of underlining tissue depends in vivo on 3 major determinants: the concentration in oxy-hemoglobin, capillary recruitment and the vascular size (vasodilatation or constriction). The StO2 during stagnant ischemia has then to be viewed in light of these determinants. The gradual decrease (slope) of StO2 after cuff inflation-induced vascular occlusion depends mainly on the augmentation of the concentration of deoxy-hemoglobin and estimates tissue oxygen consumption and to a lesser degree on vessel de-recruitment. The StO2 upslope during reperfusion (cuff deflation) can be analyzed in light of flow papers during ischemia/reperfusion test. Vasodilatation after ischemia leads to recruitment of more vessels and increase in the local blood flow, which in turn results in a StO2 increase. It remains unclear which of the described changes is more influential, however this StO2 increase mirrors the maximal local DO2 at the time of measurement. The development on NIRS signal processing might be able to provide a clinical important tissue hemoglobin concentration index and local oxygen consumption as shown by De Blasi et al., such an index may help to clarify the mechanism(s) by which StO2 signal varies.

The aim of our study was to study skeletal muscle oxygen kinetics in low flow state due to combined cardiogenic and septic circulatory failure, relate it with central heamodynamic variables and outcome. We hypothesized that basal StO2 could relate to ScvO2, because blood flowing through upper limb muscles importantly contributes to flow through superior vena cava. The second hypothesis was that decrease of skeletal muscle OER and lower muscle oxygen consumption are more pronounced in patients with septic component of circulatory failure due to microcirculatory and metabolic changes seen in sepsis, what results in higher mortality.