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:
In greater detail:
The simple O2ER equation can be expressed as follows:
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:
Or even more simply,
(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).
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%.
McLellan and Walsh in their 2004 article report a few situations where the VO2 may be abnormal:
Factors which INCREASE the VO2 | Factors which DECREASE the VO2 |
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From this table, one can work out the answer to the question, "what might cause a markedly abnormal O2ER".
An abnormally HIGH O2ER | An abnormally LOW O2ER |
Inadequate oxygen delivery:
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Increased oxygen delivery:
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Increased oxygen consumption:
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Decreased oxygen consumption:
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Abnormal circulation:
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Abnormal circulation:
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Measurement artifact:
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Measurement artifact:
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Walley, Keith R. "Use of central venous oxygen saturation to guide therapy." American journal of respiratory and critical care medicine 184.5 (2011): 514-520
McLellan, S. A., and T. S. Walsh. "Oxygen delivery and haemoglobin." Continuing Education in Anaesthesia, Critical Care & Pain 4.4 (2004): 123-126.
Leach, R. M., and D. F. Treacher. "The pulmonary physician in critical care• 2: Oxygen delivery and consumption in the critically ill." Thorax 57.2 (2002): 170-177.
Ronco, Juan J., et al. "Identification of the critical oxygen delivery for anaerobic metabolism in critically ill septic and nonseptic humans." JAMA: the journal of the American Medical Association 270.14 (1993): 1724-1730.
Orlov, David, et al. "The clinical utility of an index of global oxygenation for guiding red blood cell transfusion in cardiac surgery." Transfusion 49.4 (2009): 682-688.
Bakker, Jan, et al. "Blood lactate levels are superior to oxygen-derived variables in predicting outcome in human septic shock." CHEST Journal 99.4 (1991): 956-962.
van Beest, Paul A., et al. "No agreement of mixed venous and central venous saturation in sepsis, independent of sepsis origin." Crit Care 14.6 (2010): R219.