Co-oximetry

Co-oximetry has been asked about in Question 26.3  from the second paper of 2008, and in  Question 17.2 from the first paper of 2010. Additionally, Question 19.3  from the first paper of 2009 refers to the "oxygen saturation gap" in regards to the diagnosis of intoxication. Generally, the college like to ask about the reasons for a difference between pulse oximeter readings and co-oximeter readings. In brief, one can say that low co-oximeter readings always represent true hypoxia, and high co-oximeter readings always represent true normoxia, whereas this is not the case for the pulse oximeter. The co-oximeter is not confused by ambient light,  absence of pulsatile flow, tricuspid regurgitation, carboxyhaemoglobin  or methylene blue dye. 

• The principle is similar to that of the pulse oximeter, except:
  • There are several wavelengths of light
  • There is no need for pulsatile flow
• The co-oximeter detects the following haemoglobin species:
  • Oxyhaemoglobin
  • Deoxyhaemoglobin
  • Carboxyhaemoglobin
  • Methaemoglobin

Low co-oximeter readings always represent true hypoxia. The core basic science behind the "oxygen gap" between co-oximeter readings and pulse oximeter readings comes partly from the difference between fractional and functional oxygen saturation. 

• Fractional saturation (FO₂Hb) is the fraction of total haemoglobin which happens to be oxygenated
• Functional saturation (sO₂) is the fraction of effective haemoglobin which is oxygenated, i.e. measuring 

Causes of HIGH Co-oximetery and LOW Pulse Oximetry Readings

(i.e, pulse oximeter fails to detect that the saturation is normal)

• Poor peripheral perfusion
• Ambient light
• Poor probe contact
• Dyes – methylene blue
• Tricuspid regurgitation
• Methaemoglobin

Causes of LOW Co-oximetry and HIGH Pulse Oximetry Readings

• Carboxyhaemoglobin
• Radiofrequency interference
• Leukocyte larceny (oxygen consumption by cells in the collection tube, may also occur in situations such as severe thrombocytosis)

Now, a little bit about methaemoglobinaemia here. Carboxyhaemoglobin, the bright fire-engine red species, is clearly so alike with oxyhaemoglobin in its absorption spectrum that the pulse oximeter will reliably read it as oxyhaemoglobin. The result is that the pulse oximeter reading is a predictable sum of real and "carboxygenated" haemoglobin, i.e. when your sats are 100% you could have a 70% carboxyhaemoglobin content, and your "real" haemoglbin might only be 30% saturated.

Not so with methaemoglobin. Pulse oximetry measurement of mixed normal haemoglobin and methaemoglobin will usually be depressed. When one's methaemoglobin level is in excess of 35%, the pulse oximeter will usually read 85% (Barker et al, 1989). The pulse oximeter will then continue to read this value, whether the oxygenation deteriorates or improves, i.e. at 60% methaemoglobin concentration and a fractional oxygen saturation of 30% or 100%, it will still give you an SpO2 of 85%. This is why highly respected resources report that "methemoglobinemia typically causes the pulse oximeter to report a [pulse oximeter] saturation of ~82-86% (even if the PaO2 is very high)." 

"Oxygen saturation gap"

Question 19.3  from the first paper of 2009 refers to the "oxygen saturation gap". Though not a formally accepted term to describe this phenomenon, the "gap" is a well recognised feature of dyshaemoglobinaemia. It develops when the pulse oximeter reads a certain saturation, and the ABG machine or CO-oximeter returns a different reading. The "gap" in saturation readings is vaguely representative of the concentration of the abnormal haemoglobin in the blood.