Comparison between central venous oxygen saturation and tissue oxygenation and perfusion: a case report

Editor,

It has been shown that mixed venous oxygen saturation (SvO₂), which is correlated with outcome in critically ill patients, cannot be adequately estimated from central venous oxygen saturation (ScvO₂), as measured in the vena cava superior ^[1]. However, early goal-directed therapy using a target of 70% for ScvO₂ has been shown to significantly reduce ICU and hospital mortality in patients with severe sepsis and septic shock ^[2]. Pathophysiologically, normal or supranormal mixed and thus probably also ScvO₂ in patients with severe shock might be associated with a mismatch of oxygen delivery and demand due to O₂-shunting ^[3]. With respect to ScvO₂, values below 70% may be interpreted as an undersupply in tissue oxygenation, which per se is difficult to assess clinically. For these reasons, muscle oxygen saturation (StO₂) has been suggested in critically ill patients for assessment of adequate tissue oxygenation. Here, we present two cases that question the interpretation of ScvO₂ as absolute value. As indicators of tissue perfusion and function, we measured StO₂ by a near infrared spectrometry (NIRS) sensor on the right thenar (Inspectra, Hutchinson Technology Inc, Arnhem, Netherlands), serum lactate ^[4] and indocyanine green plasma disappearance rate (ICG-PDR, LiMON, Pulsion Medical Systems AG, Munich, Germany) ^[5].

Case 1

A 54-year-old man with chronic alcohol abuse and liver cirrhosis was admitted to the emergency department because of oedematous pancreatitis and intestinal paralysis. He developed multiple organ dysfunction [the Sequential Organ Failure Assessment (SOFA) score 18], requiring endotracheal intubation and mechanical ventilation. Furthermore, vasopressor support (norepinephrine 0.64 μg kg⁻¹ min⁻¹) and renal replacement therapy became necessary. Initially, ScvO₂ was 67% and ΔSO₂ (SaO₂ – ScvO₂) was 33%, whereas StO₂ was 82% (cardiac index 2.79 l min⁻¹ m⁻²; haemoglobin 8.6 g dl⁻¹). ICG-PDR was markedly reduced (3.0% min⁻¹) and serum lactate elevated (5.2 mmol l⁻¹). After transfusion of four units of fresh frozen plasma due to liver failure (approximately 1 l of fluid), ScvO₂ was 68% (ΔSO₂ 34%), whereas StO₂ increased to 94% (cardiac index 3.09 l min⁻¹ m⁻²; haemoglobin 8.3 g dl⁻¹). ICG-PDR and serum lactate were nearly unchanged (Table 1). Thus, ScvO₂ and ICG-PDR were unchanged after increased systemic oxygen delivery (322 vs. 357 ml min⁻¹ m⁻²). However, serum lactate decreased slightly and StO₂ increased to 94%.

Table 1: Values of global haemodynamics, oxygen transport and regional oxygenation before and after fluid challenge in patient 1

Case 2

A 54-year-old man who had undergone pancreas and kidney transplantation required explantation of the pancreas because of infection. He developed peritonitis and abscess formation near the previous anastomosis of the common iliac artery. Unfortunately, spontaneous vessel rupture occurred and the patient went into haemorrhagic shock. Postoperatively, the patient was mechanically ventilated (FiO₂ 0.3). At this time point, the heart rate was 78 min⁻¹, blood pressure 100/65 mmHg and ScvO₂ 93%, whereas ΔSO₂ (SaO₂ – ScvO₂) was 5%. Furthermore, ICG-PDR was 18.7% min⁻¹ and StO₂ was 86%. After 3 l of Ringer's solution and transfusion of one pack of red blood cell concentrate, ScvO₂ and heart rate decreased, whereas blood pressure increased. However, StO₂ increased to 91%, whereas serum lactate and ICG-PDR remained unchanged. After administration of a further 1 l of Ringer's solution, ScvO₂ slightly increased to 84%, whereas StO₂ reached 96% (Table 2).

Table 2: Values of global haemodynamics, oxygen transport and regional oxygenation before and after fluid challenge in patient 2

Discussion

The two cases question the value of ScvO₂ in terms of providing adequate information on regional perfusion and oxygenation. In case 1, our findings indicate that blood flow in the organ, that is, hepatosplanchnic blood flow, was very low and did not increase during the intervention, whereas ScvO₂ was near to the target of 70%. Furthermore, the distribution of blood flow may have changed as StO₂ increased but ScvO₂ did not change in parallel. However, it needs to be borne in mind in this particular case that liver cirrhosis may have led to a decrease in ICG-PDR and increase in lactate, which makes the comparison of ScvO₂ and these parameters even more difficult or perhaps impossible.

Peripheral shunting per se may cause a low difference between arterial and central (mixed) venous oxygen saturation. In case 2, the initially very high value of ScvO₂ was difficult to interpret as a ‘shunting phenomenon’ because lactate, ICG-PDR and other organ function were normal. In this case, it may be assumed that analgesia and low cerebral oxygen extraction may have contributed to this value. Notably, ICG-PDR did not change during the course; however, the last fluid challenge led to a parallel change in StO₂. For comparison, in a patient with necrotizing fasciitis, ScvO₂ was always high, whereas ICG-PDR showed a dramatic decrease during the septic shock ^[6].

The correlation between changes in ScvO₂ and lactate is still a matter for experimental and clinical studies. For comparison, data from Rivers et al.^[2] in patients with sepsis may be used. In this study, control patients had on average a serum lactate of 6.9 ± 4.5 mmol l⁻¹, whereas ScvO₂ was 49.2 ± 13.3%. In this study, both variables changed according to the underlying hypothesis of hypoperfusion that ScvO₂ increased to 66 ± 15.5%, whereas lactate dropped to 4.9 ± 4.7 mmol l⁻¹ during the initial 6 h period.

The limitations of ScvO₂ in terms of estimating SvO₂ have been described previously ^[1]. However, the difference between these two parameters may be most pronounced in low output states, which most likely were not present in our patients. Patient 1 had a hyperdynamic circulation, and the lack of correct indication of tissue hypoperfusion by ScvO₂ may be related to shunting. However, as no further techniques were used, more detailed information cannot be given by our data and our findings remain limited.

One limitation of ScvO₂per se is right-to-left shunt, which was not present in our two cases. Consequently, one would assume that a higher oxygen supply would be associated with a higher tissue oxygenation and ScvO₂. As can be seen from global haemodynamic variables, patients responded to fluid challenges and oxygen delivery was increased.

In conclusion, ScvO₂ as a variable of global oxygen transport does not yield detailed information on regional perfusion and oxygenation. Furthermore, slight changes in regional perfusion may not be detected by ScvO₂. Further studies are warranted to assess the relation between ScvO₂ and markers of regional function and perfusion.

Acknowledgement

Dr Samir Sakka is a member of the Medical Advisory Board of Pulsion Medical Systems AG, Munich, Germany, and has received honoraria from this company for giving lectures.