Open Access

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

Critical Care201115:1005

https://doi.org/10.1186/cc10491

Published: 7 November 2011

Abstract

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 (SvO2) levels do not exclude fluid responsiveness [1]. SvO2 is assumed to reflect the balance between arterial oxygen delivery (DO2) and oxygen consumption (VO2) provided arterial blood oxygen saturation (SaO2) is normal. Indeed, the modified Fick equation states:
Sv O 2 = Sa O 2 - V O 2 / cardiac output  ×  Hb  ×  1 . 34

where Hb is the hemoglobin concentration.

Nevertheless, the interpretation of SvO2 and its changes in shock states must be cautious for at least four reasons. First, in any shock state, oxygen demand exceeds VO2 by definition such that SvO2 cannot reflect the balance between DO2 and oxygen demand, which is better assessed by markers of anaerobic metabolism such as the blood lactate level. Second, as VO2/DO2 dependency is a characteristic pattern of shock states [2], any increase in DO2 during resuscitation will be associated with a simultaneous increase in VO2 and hence with no or only a small increase in SvO2 until a critical DO2 is reached. Third, the tissue oxygen utilization is impaired in severe sepsis so VO2 may decrease relative to oxygen demand, even if DO2 is normal or high. Fourth, because of the hyperbolic relation ship between SvO2 and cardiac output (graphical representation of the modified Fick equation) [3], SvO2 should not change much in response to an increase in cardiac output in cases of hyperdynamic shock states. For all these reasons, interest in SvO2 monitoring in septic shock has been debated - although SvO2 or its surrogate, central venous oxygen saturation, has been recommended as a major hemodynamic target of early resuscitation in septic shock [4, 5].

Nevertheless, SvO2 might still play an important role in the monitoring of septic shock by identifying the patients in whom DO2 could be further augmented and then by guiding the therapy aimed at increasing DO2. This point is of particular importance since systematic maximization of DO2 is not recommended in every patient with septic shock [5].

Velissaris and colleagues showed that a given value of SvO2 cannot be used to predict a positive response to fluid challenge [1]. These 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 differs from the concept of global VO2/DO2 balance and thus from SvO2.

Patients with low SvO2 can be either fluid responsive in cases of hypovolemic shock or fluid unresponsive in cases of cardiogenic shock. In the study by Velissaris and colleagues almost two-thirds of patients with a low SvO2 (<60%) were fluid nonresponders [1], suggesting that their heart was operating on the flat part of the Frank-Starling curve. This observation suggests that in the presence of low SvO2 it is mandatory to obtain additional information to identify the cases where fluid administration should be considered the most logical therapeutic measure. Cardiac filling pressures are not appropriate to make such a therapeutic decision [7], as confirmed by Velissaris and colleagues [1]. By contrast, dynamic tests (pulse pressure variation, passive leg raising and endexpiratory occlusion tests) are far more reliable to predict fluid responsiveness/unresponsiveness [8, 9]. In cases of low SvO2 the presence of fluid responsiveness should incite infusing fluid, 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 SvO2 or central venous blood oxygen saturation can be observed [10, 11] as confirmed in the study by Velissaris and colleagues [1]. One striking finding of their study is that an increase in cardiac output with fluid infusion occurred in more than 50% of patients who exhibited a high SvO2 (>70%) at baseline [1]. This confirms that preload responsiveness can coexist with the presence of reduced oxygen extraction capacities and thus high SvO2. A reliable prediction of fluid responsiveness would also be important to obtain in cases of high SvO2. Whether the presence of preload responsiveness should lead to the decision to infuse fluid, however, is still uncertain. One should anticipate that abnormally high SvO2 is an indicator of profoundly decreased oxygen extraction capacities so that the additional increase in DO2 cannot be effectively 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 SvO2, the less likely the correction of tissue hypoxia with fluid infusion, even in the presence of indicators of preload responsiveness. Since the study by Velissaris and colleagues [1] was not designed to confirm this hypothesis, further studies are required.

Abbreviations

DO2

oxygen delivery

Hb: 

hemoglobin concentration

SaO2

arterial blood oxygen saturation

SvO2

mixed venous blood oxygen saturation

VO2

oxygen consumption.

Declarations

Authors’ Affiliations

(1)
Service de Réanimation Médicale, Hôpital de Bicêtre, Hôpitaux Universitaires Paris-Sud
(2)
Faculté de Médecine Paris-Sud, Université Paris-Sud
(3)
Service de Réanimation Médicale, Hôpital Antoine Béclère, Hôpitaux Universitaires Paris-Sud

References

  1. Velissaris D, Pierrakos C, Scolletta S, De Backer D, Vincent JL: High mixed venous oxygen saturation levels do not exclude fluid responsiveness in critically ill septic patients. Crit Care 2011, 15: R177.PubMed CentralView ArticlePubMedGoogle Scholar
  2. Schumacker PT, Cain SM: The concept of a critical oxygen delivery. Intensive Care Med 1987, 13: 223-229. 10.1007/BF00265110View ArticlePubMedGoogle Scholar
  3. Jain A, Shroff SG, Janicki JS, Reddy HK, Weber KT: Relation between mixed venous oxygen saturation and cardiac index. Nonlinearity and normalization for oxygen uptake and hemoglobin. Chest 1991, 99: 1403-1409. 10.1378/chest.99.6.1403View ArticlePubMedGoogle Scholar
  4. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M, Early Goal-Directed Therapy Collaborative Group: Early goaldirected therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001, 345: 1368-1377. 10.1056/NEJMoa010307View ArticlePubMedGoogle Scholar
  5. Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, Reinhart K, Angus DC, Brun-Buisson C, Beale R, Calandra T, Dhainaut JF, Gerlach H, Harvey M, Marini JJ, Marshall J, Ranieri M, Ramsay G, Sevransky J, Thompson BT, Townsend S, Vender JS, Zimmerman JL, Vincent JL: Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med 2008, 34: 17-60. 10.1007/s00134-007-0934-2PubMed CentralView ArticlePubMedGoogle Scholar
  6. Monnet X, Teboul JL: Volume responsiveness. Curr Opin Crit Care 2007, 13: 549-553. 10.1097/MCC.0b013e3282ec68b2View ArticlePubMedGoogle Scholar
  7. Osman D, Ridel C, Ray P, Monnet X, Anguel N, Richard C, Teboul JL: Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med 2007, 35: 64-68. 10.1097/01.CCM.0000249851.94101.4FView ArticlePubMedGoogle Scholar
  8. Marik PE, Monnet X, Teboul JL: Hemodynamic parameters to guide fluid therapy. Annals Intensive Care 2011, 1: 1. 10.1186/2110-5820-1-1View ArticleGoogle Scholar
  9. Teboul JL, Monnet X: Detecting volume responsiveness and unresponsiveness in intensive care unit patients: two different problems, only one solution. Crit Care 2009, 13: 175. 10.1186/cc7979PubMed CentralView ArticlePubMedGoogle Scholar
  10. Kraft P, Steltzer H, Hiesmayr M, Klimscha W, Hammerle AF: Mixed venous oxygen saturation in critically ill septic shock patients. The role of defined events. Chest 1993, 103: 900-906. 10.1378/chest.103.3.900View ArticleGoogle Scholar
  11. van Beest PA, Hofstra JJ, Schultz MJ, Boerma EC, Spronk PE, Kuiper MA: The incidence of low venous oxygen saturation on admission to the intensive care unit: a multi-center observational study in The Netherlands. Crit Care 2008, 12: R33. 10.1186/cc6811PubMed CentralView ArticlePubMedGoogle Scholar

Copyright

© BioMed Central Ltd 2011

Advertisement