The oxygen content of blood returning to the right side of the heart after perfusing the entire body is measured by venous oxygen saturation (S_vO₂) [1]. The hemoglobin saturation of blood in the superior vena cava and proximal pulmonary artery is referred to as central (Scvo₂) and mixed venous oxygen saturation (S_vO₂), respectively [2]. ScvO₂ is a vital measurement that can be performed by medical and nursing personnel in a critical care setting. It provides an understanding of the patient‘s oxygen delivery, oxygen consumption, and cardiac output [2]. When taken and evaluated properly, it plays an important role in the early goal-directed treatment and has been associated with reduced mortality [3]. A ScvO₂ > 70% or mixed venous oxygen saturation (SvO₂) >65% is indicated for septic and non-septic patients. [4]

Shock is defined as global cellular and tissue hypoxia secondary to either decreased systemic oxygen delivery (DO₂), systemic oxygen consumption (VO₂), inadequate oxygen utilization, or combined. A decrease in DO₂ is compensated for by an increase in VO₂, thereby preventing tissue hypoxia. Tissue hypoxia and lactic acidosis begin when a ‘critical’ DO₂ level is reached, and no more oxygen can be taken [1]. Untreated tissue hypoxia is associated with an increase in morbidity and mortality [5]. Therefore, an accurate diagnosis of global tissue hypoxia is critical. Physical examination, vital signs, measurement of central venous pressure, and urine output are all relevant but are still insufficient for detecting global tissue hypoxia [5].

The measurement of mixed venous oxygen saturation in the pulmonary artery (S_vO₂) has been recommended as an indirect indicator of tissue oxygenation. However, the use of the pulmonary artery catheter has become somewhat unpopular. By contrast, insertion of a central venous catheter into the superior vena cava is considered standard care in critically ill patients. The assessment of central venous oxygen saturation (ScvO₂), similar to SvO₂, has been recommended for detecting global tissue hypoxia [5, 6].

ScvO₂ levels can be monitored on an as-needed basis (intermittently) by taking blood from the central line for blood gas analysis. It may also be monitored in real-time (continuously) using a fiberoptic catheter equipped with reflection spectrophotometry. The saturation level is shown on an oximetry meter and is updated every 2 seconds [1].

Cardiac output, plasma hemoglobin concentration, blood transfusions, and blood volume are the most important factors influencing ScvO₂ and may lead to misinterpretation of SCvO_2. [7]. Therefore, this study was planned to assess the effect of different fractions of inspired oxygen (FiO₂) levels on central venous oxygen saturation for consideration during the evaluation of central venous oxygen saturation.

This interventional cross-over study included 60 critically ill, nonmechanically ventilated patients admitted to the respiratory critical care unit of the Chest Medicine Department at Mansoura University. All included patients already had a central line. This study was conducted within the required ethics guidelines of the Mansoura Institutional Research Board ethics committee (code number: R.21.10.1485). Informed written consent was obtained from the included patients.

Blood samples were repeatedly drawn from the distal end of the central venous catheter for blood gas analysis. The samples were aspirated into a heparinized blood gas syringe 30 min after administration of 30%, 40%, and 50% FiO₂ respectively. The samples were then analyzed in a blood gas analyzer, which was regularly calibrated.

Statistical analysis of the data was performed using SPSS V.16. A repeated-measure ANOVA with a Greenhouse-Geisser correction and post hoc tests using the Bonferroni correction were conducted.

A total of 60 patients (mean age 61±11 years) were included in the study. Males represented 58.6% (35) of the patients. In total, 37.9% of the patients had pneumonia, and 19% were hemodynamically unstable (Table 1). A subclavian catheter was inserted in 27 patients, and 33 patients had jugular catheters. All patients were spontaneously breathing, and oxygen was delivered via a simple facemask. We recorded ScvO₂ after 30 min of each increase in the FiO₂.

The results of this study showed that increasing FiO₂ from 30% to 40% resulted in a mean increase in ScvO₂ of 6.2%, whereas increasing FiO2 from 40% to 50% resulted in a mean increase in ScvO₂ of 3.2%. A repeated-measures ANOVA with a Greenhouse-Geisser correction determined that the mean ScvO₂ differed significantly between different levels of FiO₂ (F (1.710, 83.8) = 9.23, p < 0.001). Post hoc tests using the Bonferroni correction revealed a statistically significant increase in ScvO₂ when FiO₂increased from 30% to 40% (64.7 ± 15.85 vs. 70.998 ± 13.8, p=0.011) and from 30% to 50% (64.7 ± 15.85 vs. 74.098 ± 10.19, p = 0.003). However, the increase in ScvO₂ when FiO₂was changed from 40% to 50% (70.998 ± 13.8 vs. 74.098 ± 10.19, p = 0.33) was insignificant (Table 2).

A significant increase in ScvO₂with changes in FiO₂was found among patients in shock and those with pneumonia (from 30% to 50%; p = 0.002 in shock patients and from 30% to 40%; p = 0.02 in patients with pneumonia). However, a nonsignificant increase in ScvO₂ was found when FiO₂ was changed in hemodynamically stable and anemic patients and in those without pneumonia (Table 3).

Fig. (1). A graphical abstract that illustrates the results of the study.

Proper hemodynamic monitoring of critically ill patients is still in some way challenging.

ScvO₂ represents a surrogate parameter for the evaluation of the O₂ demand/supply adequacy. Therefore, there is extensive interest in the utilization of ScvO₂ to guide fluid and inotrope administration [8]. A previous study by Rivers et al. [9] on septic patients revealed a decline in morbidity and mortality in the early goal-directed therapy in which ScvO₂ was adjusted to more than 70%. In addition to cardiac output, ScvO₂ is also affected by a range of factors that affect blood oxygen content and tissue oxygen consumption. The effects of changing FiO₂ levelson ScvO₂, i.e. the highlight of the present study, were not considered by Rivers et al. [9].

The results of this study showed that increasing FiO₂ from 30% to 40% resulted in a mean increase in ScvO₂ of 6.2%, while increasing FiO₂ from 40% to 50% resulted in a mean increase in ScvO₂ of 3.2%. Jee and White [10] also investigated the effect of increasing FiO₂ to 100% on ScvO₂ in critically ill patients and found that the mean increase in ScvO₂ was 6.7%.

Nam et al. [ 11 ] reported that SvO ₂ increased by ≥5% in more than three-quarters of FiO ₂ increases from 30% to 80% or 50% to 100% during cardiac surgery and by ≥10% in the remaining one-quarter of FiO ₂ changes. Whereas HB remained almost fully saturated, PaO₂ changed remarkably as FiO₂ was changed. Legrand et al. [7] concluded that PaO₂ should not be overlooked while considering the ScvO₂ value as a therapeutic goal, as the author’s observed that ScvO₂ rose from 71% to 83% after increasing FiO₂ [7].

In patients with or without anemia, a nonsignificant increase in ScvO₂ was found with changing FiO₂ in this study. This result is compatible with that of Nam et al. [11], who found a nonsignificant association between Hb concentration and ΔSvO₂.

A significant increase in ScvO2 with changes in FiO₂ was found among patients in shock and those with pneumonia in this study. This observation may have significant implications for the interpretation of ScvO₂ data in clinical practice. However, the cause of the shock was not identified in this study.

Increasing FiO₂ was linked to a substantial rise in ScvO₂, which would consequently affect the interpretation of ScvO₂ data. Interpretation of variations in ScvO₂ in response to a therapeutic challenge should be performed at constant FiO₂, especially in patients with pneumonia.