Index
It is used as a measure of the adequacy of total body O2 delivery.
Central venous oxygen saturation (ScvO2) shows early if there is an imbalance between oxygen consumption (VO2I) and oxygen supply (DO2I).
There is a good correlation between central venous oxygen saturation (ScvO2) and SvO2 (mixed venous oxygenation measured through a PA catheter).
Central venous oxygen saturation (ScvO2) is less invasive than the measurement of mixed venous oxygen saturation (SvO2) through the PA catheter, which has a high impact on patient outcome.
- Percentage of hemoglobin in central venous blood saturated with oxygen.
- Earlier and more sensitive oxygenation imbalance indicator.
- High impact on patient outcome.
SvO2 – ScvO2: Is it the same?
The gold standard for assessing the adequacy of oxygen supply is mixed venous oxygen saturation (SvO2), provided by the pulmonary artery catheter (also known as: Swan-Ganz catheter).
However, limitations related to insertion and placement difficulties, but also possible complications related to said catheter, lead to a substantial decrease in its use.
Meanwhile, industrialists have developed a regular central venous catheter along with a fiberoptic lumen for continuous monitoring of hemoglobin saturation.
Placed through the jugular of a subclavian vein, at the confluence of the superior vena cava and the right atrium, such catheters actually monitor central venous oxygen saturation (ScvO2).
However, one must wonder whether mixed venous oxygen saturation (SvO2) and central venous oxygen saturation (ScvO2) provide the same information.
Actually, taken in the pulmonary artery, mixed venous oxygen saturation (SvO2) is a surrogate for overall tissue oxygenation.
While the central venous oxygen saturation (ScvO2) essentially reflects the oxygenation of the upper part of the body (head, upper limbs of the neck and upper part of the trunk).
And a lower proportion of the lower body (lower trunk and lower limbs), depending on the exact position of the tip of the catheter.
However, central venous oxygen saturation (ScvO2) does not include venous blood from the coronary sinus that is commonly found in the right atrium.
Therefore, taken at the confluent of the vena cava in the right atrium (ie, upstream of the coronary sinus), central venous oxygen saturation (ScvO2) does not include myocardial oxygenation.
In contrast, mixed venous oxygen saturation (SvO2) refers to the venous blood of the pulmonary artery, that is, by definition, after the coronary venous sinus.
This difference could have a great impact on the observed values, since:
- Venous blood from the coronary sinus, with an oxygen saturation close to 40%, is the most deoxygenated venous blood in the body.
- That in critically ill patients an imbalance in myocardial oxygen supply / demand is likely to occur.
ScvO2: a validated monitoring parameter
Experimental validation
Many studies have compared central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) in the same patients.
Most of them showed a good correlation between central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) and a similar trend in time evolution.
In 1989, Reinhart et al. reported, in a dog model, a correlation coefficient between central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) of 0.96.
In this study, the two values showed a difference of less than 5% in 77% of the cases.
Later, Reinhart et al. confirmed their results in intensive care unit (ICU) patients: central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) had a similar evolution in 90% of cases and had a coefficient of correlation of 0.81 (P <0.001).
Similarly, Martin et al. reported a parallel evolution of central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) in 75% of cases.
Taking these results into account, it seems that central venous oxygen saturation (ScvO2) and especially its evolution over time could be used as an interesting substitute for monitoring mixed venous saturation (SvO2).
However, the impact of central venous oxygen saturation (ScvO2) monitoring on the prognosis of critically ill patients remains to be demonstrated.
Clinical validation
Therefore, some authors focused on evaluating the connection between central venous oxygen saturation (ScvO2) and prognosis and, especially, the reduction of benefits considering the optimization of central venous oxygen saturation (ScvO2) as an objective for resuscitation.
Pearse et al. It was observed in a cohort of 118 postoperative patients with major surgery that a decrease in central venous oxygen saturation (ScvO2) during the first 8 hours was associated with an increase in morbidity and mortality at 28 days.
Consistently, Futier et al. showed in major abdominal surgery that a central venous oxygen saturation (ScvO2) <70% was associated with postoperative complications.
Furthermore, central venous oxygen saturation (ScvO2) appears to be a reliable and sensitive parameter for detecting bleeding in trauma patients admitted to the emergency room.
While other series suggest that central venous oxygen saturation (ScvO2) could be a prognostic marker in myocardial infarction, acute heart failure, as well as in patients with severe sepsis.
But the great clinical advantage related to central venous oxygen saturation (ScvO2) has been suggested by Rivers et al.
In fact, these authors reported that, in patients with severe sepsis, an early and aggressive therapy aimed to normalize in the first hours.
Central venous oxygen saturation (ScvO2) MAP and central venous pressure (PVC) values achieved a reduction in hospital mortality from 46.5% to 30.5% (relative risk 0.58 (0.38–0.87), P = 0.009).
These results were later confirmed by two large studies conducted, respectively, in 15,022 and 330 patients that showed a reduction in mortality related to the implementation of central venous oxygen saturation (ScvO2) as a resuscitation goal.
Although the study by Levy et al. did not demonstrate any improvement in survival related specifically to the implementation of central venous oxygen saturation (ScvO2), the implementation of the global target did.
Lactate measurement, blood culture before antibiotics, broad spectrum antibiotics, fluids and vasopressors, central venous pressure> 8 mmHg and central venous oxygen saturation (ScvO2)> 70%).
This could be partly explained by the fact that, among these 6 resuscitation goals, central venous oxygen saturation (ScvO2)> 70% was the least frequently achieved, both after the first trimester of patients was included. as after the last trimester of patients (resp., in 13.3% and 24.3% of cases).
Recently, Jones et al. demonstrated, in 300 patients with septic shock, that the mortality of patients who benefited from central venous oxygen saturation (ScvO2) was low (23% (17-30%)) and similar to that of patients treated with lactate . Clearance directed to goal directed therapy (17% (11-24%)).
Central venous oxygen saturation (ScvO2) is considered an adequate prognostic factor in many clinical situations in critically ill patients.
The Surviving Sepsis Campaign , which compiles all the European guidelines on the treatment of patients with severe sepsis and sepsis shock, suggested including central venous oxygen saturation (ScvO2) as an objective parameter in the first 6 hours of treatment ( central venous oxygen saturation (ScvO2)> 70%).
ScvO2 limits
Theoretical limits
The first limit of the use of central venous oxygen saturation (ScvO2) refers to its ignorance of the saturation of the coronary sinus venous blood.
Since the end of the central venous oxygen saturation (ScvO2) catheter is generally upstream of the coronary sinus junction point in the right atrium, the central venous oxygen saturation (ScvO2) value does not take into account the adequacy / myocardial oxygen demand.
As oxygen extraction from the myocardium is physiologically basically high, coronary venous blood is one of the most deoxygenated venous blood in the body.
This explains that the value of mixed venous oxygen saturation (SvO2), which actually takes into account venous coronary blood, is usually lower than the central venous oxygen saturation (ScvO2).
Furthermore, any significant increase in myocardial oxygen consumption could lead to critical oxygen withdrawal that would have no impact on monitoring central venous oxygen saturation (ScvO2).
In addition, central venous oxygen saturation (ScvO2), like mixed venous oxygen saturation (SvO2), is a global oxygenation parameter.
Therefore, any local change in tissue oxygenation runs the risk of being “diluted” in the rest of the venous blood and becoming undetectable.
Similarly, in the case of a drop in regional venous saturation responsible for a drop in central venous oxygen saturation (ScvO2), it would not be possible to assess the affected territory without further exploration.
Then, theoretically, it is assumed that the distal end of the central venous catheter is placed at the junction of the vena cava and the right atrium to allow an adequate assessment of tissue oxygenation of the lower and upper territories.
However, verifying the position of the distal end of the catheter with a chest radiograph is not accurate enough.
Furthermore, as the venous saturation of the superior vena cava is systematically lower than the inferior vena cava, any variation in the position of the catheter tip could have a great influence on the measurements and therefore lead to misinterpretation. central venous saturation (ScvO2).
Ultimately, as previously reported, central venous oxygen saturation (ScvO2) depends on the extraction of oxygen from the tissue and the affinity of hemoglobin for oxygen.
Experiments report that septic patients may experience a decrease in oxygen extraction capacity, an increase in capillary bypass, as well as changes in the affinity of hemoglobin for oxygen.
All these changes can alter the theoretical relationship between central venous oxygen saturation (ScvO2) and cardiac output, as the interpretation of central venous oxygen saturation (ScvO2), to guide hemodynamic therapy becomes more complex.
Clinical limits
First, it could be argued that the measurement of central venous oxygen saturation (ScvO2) requires a central venous catheter, which is an invasive technique, exposing patients to complications such as infection or bleeding.
However, central venous lines are often necessary for critically ill patients and therefore could be used for monitoring central venous oxygen saturation (ScvO2).
However, in severe sepsis and septic shock, tissue hypoperfusion should lead to particularly low values of central venous oxygen saturation (ScvO2), as observed by Rivers et al. In the early stage of sepsis.
However, after the first hours of resuscitation, this situation is rarely fulfilled, and central venous oxygen saturation (ScvO2) values tend to be paradoxically normal or even increased.
This could be explained by the physiological modification induced by sepsis and described above (decreased oxygen extraction capacity of the tissue, increased capillary bypass and changes in the affinity of hemoglobin for oxygen).
Consistently, in such situations, the agreement between mixed venous blood oxygen saturation (SvO2) and central venous oxygen saturation (ScvO2) appears much less satisfactory, especially in the setting of septic shock.
Furthermore, the clinical validation of central venous oxygen saturation (ScvO2) is mainly based on a single study, which is a single center study, and its results are still controversial.
In fact, van Beest et al. In a prospective multicenter Dutch study, it was reported that only 1% of patients meeting the inclusion criteria required by Rivers et al. had a central venous oxygen saturation (ScvO2) <50%.
Ho et al. in a retrospective study, as well as in the ARISE group (Australian Resuscitation Assessment of Sepsis), in a multicenter study.
In-hospital mortality of 26 to 28% was reported in patients who did not benefit from early goal-directed therapy, but who met the inclusion criteria for the Rivers trial.
This mortality rate is much lower than that observed by Rivers in his control group.
Finally, the low values of central venous pressure (5-6 mmHg) observed by Rivers et al. suggest that their patients were probably highly hypovolemic.
Global versus regional circulation
If global hemodynamic optimization is considered an essential prerequisite to ensure adequate tissue perfusion, it may not always be sufficient to prevent the development of organ failure.
The poor precision of global venous oxygen saturation monitoring to detect changes in regional oxygenation has been well described in animal models.
For example, Legrand et al. Recently, in a rat model, it was shown that LPS-induced endotoxemia could induce alterations in microvascular perfusion and oxygenation in the renal cortex in rats, which appeared to depend only on renal and systemic macrohemodynamic alterations.
Consistently, Vallet et al. and Lagoa et al. reported, in endotoxemic dogs, that after resuscitation, skeletal VO2 is maintained when blood flow within the intestine is significantly altered by mucosal hypoxia.
In humans, as described by Sakr et al. Global hemodynamic parameters fail to discriminate survivors from non-survivors after 24 hours of intensive care in patients with septic shock.
An illustrative example is the inaccuracy of global mixed venous oxygen saturation (SvO2) to detect cerebral venous desaturations.
In this perspective, the global central venous oxygen saturation (ScvO2) could face some limitations with respect to the local insufficiency in the DO2 / VO2 balance.
In fact, local mixed venous oxygen saturation (SvO2) might not be detected by monitoring global oxygen saturation, diluting the signal between a normally saturated global venous blood.
Therefore, mixed regional venous oxygen saturation (SvO2) could be an interesting additional target parameter.
However, while regional mixed venous oxygen saturation (SvO2) monitoring may be possible at the bedside for some organs, such as jugular venous oxygen monitoring, it is much more difficult for others, such as the kidney or the intestine, for example.
In such a situation, some alternative parameters for regional monitoring could be of interest.
Conclution
In conclusion, measurement of central venous oxygen saturation (ScvO2) appears to be an interesting tool, especially in the early phase of shock, to guide fluid management and blood transfusion or inotropic support.
However, a great understanding of its determinants and the physiology of circulation appear to be essential to ensure a reliable interpretation in clinical practice.
When central venous oxygen saturation (ScvO2) is low, it reflects an adaptation mechanism to an inadequate oxygen supply and should lead clinicians to understand the reasons for it and propose an appropriate optimization strategy.
Furthermore, in clinical situations such as septic shock, after the first hours of treatment, a “normal” or even high central venous oxygen saturation (ScvO2) can be falsely reassuring.
