Carbon dioxide storage in the human body

This chapter is most relevant to Section F8(ii) from the 2017 CICM Primary Syllabus, which expects the exam candidates to be able to "describe the carbon dioxide carriage in blood including the Haldane effect and the chloride shift". The specific question of CO₂ storage has never been as popular as the question of transport or carriage, and so this topic is under-represented in the CICM First Part exams. 

In summary:

Whole-body CO₂ stores

Much of one's CO₂, tied up in non-dissolved form, can be viewed as a form of storage. Strange to think of it in that way (why would one possess a capacious reserve of a waste product?) but in fact the "stored" CO₂ plays a major role in maintaining the acid-base balance.

How much CO₂ do you have stored right now? To explore this topic in detail, an excellent article by Cherniack and Longobardo can be found in Physiology Reviews (1970) - but it is paywalled. Fortunately, the free preview at deepdyve.com offers a brief glimpse. The information afforded by this glimpse has been taken by the author and again represented as one of those disgraceful gamblegrams:

Thus, the adult 70kg male has about 1.8L/kg - up to 126L in total - of "potential" CO₂ trapped inside them. A massive amount, about 1.6L/kg, is not readily accessible, as it is a part of the crystalline matrix of bone, or dissolved in the cytosol of tissues. The bony stores consist of about 30% bicarbonate, and 70% carbonate; they were revealed to researchers who heated bone and observed the release of CO₂ (which was in considerable volume). This form of storage is largely irrelevant to the minute and second timescales of respiratory acid-base physiology, but becomes more important in chronic disorders, and plays a considerable role in the certain exotic circumstances-for example, in the demineralisation of bone associated with decompression sickness.

Of this massive bony storehouse, about 9L is gradually exchanged, and forms 15% of the total daily CO₂ production; this exchange process probably plays little role in buffering because of its glacial slowness (its rate appears to be limited by blood flow to bone). The remainder is only about 3L - this is the CO₂ in circulation - is involved in routine gas exchange processes and buffering; this is the CO₂we are interested in when we discuss the compensation for acute acid-base disturbances.

So, it is possible to arrive at a volume of carbon dioxide which is available reasonably quickly. A confident-sounding radiolabelled bicarbonate study presents us with a figure of around 200 (+/- 42) ml/kg of CO₂ for adults. The average adult male therefore has about 14 litres of CO₂ on board which is fairly easy to access on the timescales involved in subacute acid-base disorders, and of these 14L about 3L are available for immediate use in buffering.

Of these 3 litres, the majority (80-90%) is stored in the form of bicarbonate anions (HCO_3^-) swimming around in extracellular fluid. About 5-10% is present as unchanged gas, dissolved in the water of extracellular fluid (predominantly in the blood). Another 5-10% or so is stored as carbamino compounds inside erythrocytes, and a minor fraction (perhaps 2-5%) is available as a free gas in the alveolar gas mixture. Lastly, the smallest fraction of all - measured probably in millilitres or microlitres- exists at any given time in the form of carbonic acid, and represents a transitional form; this is either CO₂ in the process of being turned into bicarbonate, or bicarbonate in the process of being turned into CO₂.