In summary, the oxygen extraction ratio is  VO₂ / DO₂. LITFL have an excellent page on this topic, which is both concise and comprehensive. The most important literature reference would have to be the 2011 article by Keith Walley.  This topic is examined in Question 13.2 from the second paper of 2012. As far as I am able to tell, the OER has never previously, nor subsequently, appeared in the exam papers. Which is a pity, because it is fascinating; but the pragmatic candidate may safely ignore this topic in favour of more examinable material. An extensive digression about the relationship of venous oxygenation and cellular metabolism is carried out elsewhere.

In brief, the information required to answer  Question 13.2 is only the following points:

• O₂ER is VO₂ / DO₂; the normal ratio is 0.2-0.3, which corresponds to an ScVO₂ of 70-80%.
• A high O₂ER (i.e. a low ScVO₂) is a feature of "flow insufficiency" states, i.e. anything which causes a decreased cardiac output (or an increased tissue oxygen demand, for that matter)
• A low O₂ER (i.e. a high ScVO₂) demonstrates either a diminished tissue oxygen demand, or inefficient oxygen utilisation by the tissues, or some sort of pathologically increased cardiac output (well in excess of the organism's physiological requirements).

In greater detail:

Calculation of the oxygen extraction ratio

The simple O₂ER  equation can be expressed as follows:

• O₂ER  = VO₂ / DO₂
• VO₂ = CO ×(CaO₂ - CvO₂)  ...this is the global oxygen consumption
• DO₂ = CO ×CaO₂ ...this is the global oxygen delivery.

In order to calculate this, one requires the cardiac output (from the PA catheter) and the oxygen content of the blood. The oxygen carrying capacity of blood is discussed in another chapter, and remains fairly stable in ICU patients (given that the haemoglobin and arterial saturation is carefully monitored and controlled). So, really, the only variable which actually varies is the mixed venous saturation. Thus the O₂ER  equation can be simplified as follows:

• O₂ER  = (SaO₂-SvO₂) / SaO₂

Or even more simply,

• O₂ER  = 100% - SvO₂ (in percent)

(assuming that the arterial saturation is close to 100%).

Why use mixed saturation, rather then central venous saturation?  The difference between SvO₂ and ScvO₂ is explored in greater detail elsewhere. For the purposes of calculating whole-body oxygen extraction, the mixed venous measurement is theoretically best, as it incorporates the blood contributed by the cardiac veins. As the myocardium is an organ of some relevance,  one should want to included its metabolic activity in the calculation of whole-body oxygen utilisation. In fact, in the context of a paralysed sedated septic shock patient with a hyperdynamic circulation, cardiac activity may be the most oxygen-hungry process in the body. This is reflected in the finding that in severe sepsis there is no predictable agreement between SvO₂ and ScvO₂ (van Beest et al, 2010).

Oxygen extraction by the whole body and individual tissues

It would make sense to say that each individual tissue type will have a different  O₂ER at any given moment, depending on how hard it is working. It might range from 100% (in heavily exercising muscle) to 1% (in dormant ligaments at rest). LITFL quotes some numbers (eg. a myocardial O₂ER of 60%). However, in reality the oxygen extraction of each individual tissue fluctuates constantly. 

At a certain O₂ER (probably around 60-70%) probably represents some sort of critical level; studies of dying ICU patients have revealed that lactate starts rising at a critical SvO₂ value of around 40%.

Causes of an abnormal VO₂

McLellan and Walsh in their 2004 article  report a few situations where the VO₂ may be abnormal:

From this table, one can work out the answer to the question, "what might cause a markedly abnormal O₂ER".

Causes of abnormal oxygen extraction ratio

Theoretical rationale for the clinical use of O₂ER

• The O₂ER may be used to assess "flow insufficiency" in critically ill patients
• There is some evidence that high O₂ER is associated with lactic acidosis, suggesting that it could be useful as a global index of tissue oxygen delivery.
• Shock is defined as inadequate oxygen delivery; thus the O₂ER should theoretically be a perfect representation for the magnitude of shock.

Arguments in support of the clinical use of O₂ER

• Use of O₂ER to guide blood transfusion practice appears to decrease the use of blood transfusion after cardiac surgery; ...especially if one's existing practice is excessively liberal and involves some sort of haemoglobin trigger.
• The O₂ER can be used to calculate cardiac output from central venous saturation measurements, and is therefore useful as an assessment of therapy being used to alter the cardiac output.

Arguments against the routine use of the O₂ER

• The measurement of O₂ER requires a PA catheter, which carries a certain known risk.
• The measurement of O₂ER by central venous saturation may be inaccurate.
• O₂ER may identify flow insufficiency, but it does not help discriminate between causes of flow insufficiency.
• Arterial lactate is superior to O₂ER where it comes to discriminating survivors from nonsurvivors of septic shock, and its measurement does not require pulmonary arterial cannulation. Why not just stick with the lactate?