SvO2 to monitor resuscitation of septic patients: let's just understand the basic physiology

Real-time monitoring of mixed venous oxygen blood saturation (SvO2) or of central venous oxygen blood saturation is often used during resuscitation of septic shock. However, the meaning of these parameters is far from straightforward. In the present commentary, we emphasize that SvO2 - a global marker of tissue oxygen balance - can never be simplistically used as a marker of preload responsiveness, which is an intrinsic marker of cardiac performance. In some septic shock patients, because of profound hypovolemia or myocardial dysfunction, SvO2 can be low but obviously cannot alone indicate whether a fluid challenge would increase cardiac output. In other patients, because of a profound impairment of oxygen extraction capacities, SvO2 can be abnormally high even in patients who are still able to respond positively to fluid infusion. In any case, other reliable dynamic parameters can help to address the important question of fluid responsiveness/unresponsiveness. However, whether fluid administration in fluid responders and high SvO2 would be efficacious to reduce tissue dysoxia in the most injured tissues is still uncertain.

In a study of patients with sepsis, Velissaris and colleagues showed that high mixed venous blood oxygen saturation (SvO 2 ) levels do not exclude fl uid responsiveness [1]. SvO 2 is assumed to refl ect the balance between arterial oxygen delivery (DO 2 ) and oxygen consumption (VO 2 ) provided arterial blood oxygen saturation (SaO 2 ) is normal. Indeed, the modifi ed Fick equation states: where Hb is the hemoglobin concentration.
Nevertheless, the interpretation of SvO 2 and its changes in shock states must be cautious for at least four reasons. First, in any shock state, oxygen demand exceeds VO 2 by defi nition such that SvO 2 cannot refl ect the balance between DO 2 and oxygen demand, which is better assessed by markers of anaerobic metabolism such as the blood lactate level. Second, as VO 2 /DO 2 dependency is a characteristic pattern of shock states [2], any increase in DO 2 during resuscitation will be associated with a simul taneous increase in VO 2 and hence with no or only a small increase in SvO 2 until a critical DO 2 is reached. Th ird, the tissue oxygen utilization is impaired in severe sepsis so VO 2 may decrease relative to oxygen demand, even if DO 2 is normal or high. Fourth, because of the hyperbolic relation ship between SvO 2 and cardiac output (graphical representation of the modifi ed Fick equation) [3], SvO 2 should not change much in response to an increase in cardiac output in cases of hyperdynamic shock states. For all these reasons, interest in SvO 2 monitoring in septic shock has been debated -although SvO 2 or its surrogate, central venous oxygen saturation, has been recommended as a major hemodynamic target of early resuscitation in septic shock [4,5].
Nevertheless, SvO 2 might still play an important role in the monitoring of septic shock by identifying the patients in whom DO 2 could be further augmented and then by guiding the therapy aimed at increasing DO 2 . Th is point is of particular importance since systematic maximization of DO 2 is not recommended in every patient with septic shock [5].
Velissaris and colleagues showed that a given value of SvO 2 cannot be used to predict a positive response to fl uid challenge [1]. Th ese results are quite consistent with the basic physiology and deserve to be discussed. Preload responsiveness is an intrinsic property of cardiac performance, indicating that the heart is operating on the steep ascending part of the Frank-Starling relationship [6]. Preload responsiveness is therefore by nature a concept that diff ers from the concept of global VO 2 /DO 2 balance and thus from SvO 2 .

Abstract
Real-time monitoring of mixed venous oxygen blood saturation (SvO 2 ) or of central venous oxygen blood saturation is often used during resuscitation of septic shock. However, the meaning of these parameters is far from straightforward. In the present commentary, we emphasize that SvO 2 -a global marker of tissue oxygen balance -can never be simplistically used as a marker of preload responsiveness, which is an intrinsic marker of cardiac performance. In some septic shock patients, because of profound hypovolemia or myocardial dysfunction, SvO 2 can be low but obviously cannot alone indicate whether a fl uid challenge would increase cardiac output. In other patients, because of a profound impairment of oxygen extraction capacities, SvO 2 can be abnormally high even in patients who are still able to respond positively to fl uid infusion. In any case, other reliable dynamic parameters can help to address the important question of fl uid responsiveness/unresponsiveness. However, whether fl uid administration in fl uid responders and high SvO 2 would be effi cacious to reduce tissue dysoxia in the most injured tissues is still uncertain. Patients with low SvO 2 can be either fl uid responsive in cases of hypovolemic shock or fl uid unresponsive in cases of cardiogenic shock. In the study by Velissaris and colleagues almost two-thirds of patients with a low SvO 2 (<60%) were fl uid nonresponders [1], suggesting that their heart was operating on the fl at part of the Frank-Starling curve. Th is observation suggests that in the presence of low SvO 2 it is mandatory to obtain additional information to identify the cases where fl uid administration should be considered the most logical therapeutic measure. Cardiac fi lling pressures are not appropriate to make such a therapeutic decision [7], as confi rmed by Velissaris and colleagues [1]. By contrast, dynamic tests (pulse pressure variation, passive leg raising and endexpiratory occlu sion tests) are far more reliable to predict fl uid responsiveness/unresponsiveness [8,9]. In cases of low SvO 2 the presence of fl uid responsiveness should incite infusing fl uid, whereas its absence should rather incite consideration of other therapies (for example, inotropes) that enable one to increase cardiac output with the ultimate goal of decreasing tissue hypoxia.
Because septic shock is often characterized by high cardiac output and low extraction oxygen capacities, high values of SvO 2 or central venous blood oxygen saturation can be observed [10,11] as confi rmed in the study by Velissaris and colleagues [1]. One striking fi nding of their study is that an increase in cardiac output with fl uid infusion occurred in more than 50% of patients who exhibited a high SvO 2 (>70%) at baseline [1]. Th is confi rms that preload responsiveness can coexist with the presence of reduced oxygen extraction capacities and thus high SvO 2 . A reliable prediction of fl uid responsiveness would also be important to obtain in cases of high SvO 2 . Whether the presence of preload responsiveness should lead to the decision to infuse fl uid, however, is still uncertain. One should anticipate that abnormally high SvO 2 is an indicator of profoundly decreased oxygen extraction capacities so that the additional increase in DO 2 cannot be eff ectively distributed and/or utilized in the most injured peripheral tissues. In other words, one can reasonably postulate in cases of tissue hypoxia that the higher the SvO 2 , the less likely the correction of tissue hypoxia with fl uid infusion, even in the presence of indicators of preload responsiveness. Since the study by Velissaris and colleagues [1] was not designed to confi rm this hypothesis, further studies are required.