Oxygen Extraction Ratio

Created on Tue, 07/21/2015 - 23:25
Last updated on Sat, 10/10/2015 - 00:18

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:

Factors which INCREASE the VO2 Factors which DECREASE the VO2
  • Surgery
  • Trauma
  • Burns
  • Inflammation
  • Sepsis
  • Pyrexia
  • Shivering
  • Seizures
  • Agitation/anxiety/pain
  • Adrenergic drugs
  • Weaning from ventilation
  • Sedation/analgesics
  • Muscle paralysis
  • Shock/hypovolaemia
  • Hypothermia/cooling
  • Mechanical ventilation
  • Antipyretics
  • Starvation/hyponutrition

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

An abnormally HIGH O2ER An abnormally LOW O2ER

Inadequate oxygen delivery:

  • Hypoxia
  • Anaemia
  • Blood flow insufficiency: shock states of all sorts

Increased oxygen delivery:

  • Hyperbaric oxygen
  • Polycythaemia
  • Hyperdynamic circulation
    • Artificial circulation, eg. ECMO
    • High cardiac output state, eg.  sepsis, cirrhosis, anxiety,

Increased oxygen consumption:

  • Increased muscle activity:
    • Exercise, including respiratory effort
    • Shivering
    • Seizures
  • States of inflammation, eg. sepsis
  • Increased metabolic rate:
    • Hyperthermia
    • Hyperthyroidism
    • Catecholamine excess
    • Response to massive injury or burns

Decreased oxygen consumption:

  • Decreased muscle activity:
    • Sedation
    • Paralysis
    • Atrophy
    • Mechanical ventilation
  • Decreased metabolic rate:
    • Hypothermia
    • Hypothyroidism
    • Starvation
  • Failure of oxygen utilisation
    • Mitochondrial dysfunction in sepsis
    • Cyanide toxicity (among others)

Abnormal circulation:

  • Right-to-left shunt (cyanotic defect)
  • Arteriovenous malformations
  • Portosystemic shunts (in liver disease)

Abnormal circulation:

  • Left-to-right shunt (non-cyanotic defect)
  • Microcirculatory shunt (eg. in sepsis)
  • Tourniquet (large fraction of the circulation excluded by occlusion, eg. aortic crossclamp)

Measurement artifact:

  • Post-collection error in the VBG (prolonged sample-to-machine transit time)

Measurement artifact:

  • Central venous rather than mixed venous samples (SvO2 is frequently higher)
  • Inadequate mixing of blood (PA catheter in the wrong position)

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

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?

 

References

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.