ScvO2 as an Alternative Transfusion Trigger

${\mathrm{VO}}_2=\mathrm{SV}\times \mathrm{HR}\times \left[{\mathrm{CaO}}_2-\left(\mathrm{Hb}\times 1.34\times {\mathrm{SvO}}_2+0.003\times {\mathrm{PvO}}_2\right)\right]=\mathrm{CO}\times \left[{\mathrm{CaO}}_2-{\mathrm{CvO}}_2\right]$

DO₂, oxygen delivery; SV, stroke volume; HR, heart rate; Hb, haemoglobin; SaO₂, arterial haemoglobin oxygen saturation; PaO₂, arterial oxygen partial pressure; CO, cardiac output; CaO₂, arterial oxygen content; VO₂, oxygen consumption; SvO₂, mixed venous haemoglobin oxygen saturation; PvO₂, mixed venous oxygen partial pressure; CvO₂, mixed venous oxygen content

From the above formulae, oxygen delivery for an average adult at rest can be calculated:

$\mathrm{CO}=70\;\mathrm{mL}\times 72/ \min =5\;\mathrm{L}/ \min$

${\mathrm{CaO}}_2=\left(150\;\mathrm{g}/\mathrm{L}\times 1.34\;\mathrm{mL}\times 1\right)+\left(0.003\times 100\;\mathrm{mmHg}\right)=201.3\;\mathrm{mL}/\mathrm{L}$

${\mathrm{DO}}_2\sim 1000\;\mathrm{mL}/ \min$

Oxygen consumption at rest is

${\mathrm{CvO}}_2=\left(150\;\mathrm{g}/\mathrm{L}\times 1.34\;\mathrm{mL}\times 0.75\right)+\left(0.003\times 40\;\mathrm{mmHg}\right)=150.87$

${\mathrm{VO}}_2=5\;\mathrm{L}/ \min \times \left(\;201.3\;\mathrm{mL}/\mathrm{L}-150.87\;\mathrm{mL}/\mathrm{L}\right)\sim 250\;\mathrm{mL}/ \min$

$\mathrm{Oxygen}\;\mathrm{extraction}\;\left({\mathrm{VO}}_2/{\mathrm{DO}}_2\times 100\right)=250\;\mathrm{mL}/ \min\;/\;1000\;\mathrm{mL}/ \min \times 100=25\;\%$

In the critically ill, there is often an imbalance between delivery and consumption: DO₂ may be too low for several reasons (hypovolaemia, bleeding, pump failure, etc.) and frequently accompanied by increased VO₂ (agitation, fever, pain, etc.). The circulation can compensate to some extent, but after a critical threshold severe oxygen debt and shock may occur [8].

One of the most common causes of inadequate DO₂ in the intensive care unit is anaemia requiring red blood cell transfusions [9]. It has recently been suggested that haemoglobin level should not be the only factor on which the indication of transfusion is based [5, 6]. Clinicians utilise different tools from simple clinical signs (confusion, tachycardia, ST segment elevation/depression, diuresis) to invasive haemodynamic measurements (central venous oxygen saturation, oxygen extraction, central venous-to-arterial carbon dioxide difference) in order to have information on anaemia-related altered oxygen extraction and hence the need for blood administration [10]. One of the potentially useful physiological parameters is the central venous oxygen saturation (ScvO₂).

8.3 Central Venous Oxygen Saturation (ScvO₂) as a Transfusion Trigger

ScvO₂ is an easily obtained parameter via the central venous catheter already in situ in most critically ill patients, and it is often used as a marker of the balance between oxygen delivery and consumption. The normal value of ScvO₂ varies between 73 and 82 % [6, 7]. It is slightly higher than mixed venous oxygen saturation (SvO₂) and is considered a reasonable surrogate marker in the clinical setting [10]. The main factors which influence ScvO₂ are haemoglobin, arterial oxygen saturation of haemoglobin, cardiac output and oxygen consumption (Fig. 8.1).

Fig. 8.1

Factors affecting ScvO₂

It was found during haemorrhage in animal and human experimental models that ScvO₂ may be useful for the identification of patients with occult or ongoing clinically significant blood loss [11, 12]. In bleeding conditions, a ScvO₂ value of ~70 % has been used as a goal to therapeutic intervention in attempts at improving oxygen delivery [10]. In a prospective human interventional study, it was found that acute isovolaemic anaemia with a haemoglobin of 5 g/dL in conscious healthy resting humans did not produce haemodynamic instability, but oxygen imbalance was accompanied by a significant drop in mixed venous saturation [13]. These results were reinforced by a retrospective analysis of a prospective observational study in which ScvO₂ was found to be a good indicator of transfusion [14]. The results of our recent animal study on isovolaemic haemodilution gave further evidence that anaemia-induced change in oxygen balance can be monitored by ScvO₂ [15]. We found a strong, negative correlation between VO₂/DO₂ and ScvO₂ (r = −0.71, p < 0.001). Taking >30 % as the critical threshold of VO₂/DO₂ for indicating oxygen debt, the area under the curve (AUC) for ScvO₂ was compelling (AUC = 0.768 ± 0.056 (0.657–0.878) p < 0.001).

Only gold members can continue reading. Log In or Register to continue