albumin and Atot
fortunately for our mathematical efforts, there are but a few "weak ions" in body fluids with
concentrations that are high enough to be relevant for acidbase analysis.
the best known one is HCO3-; because it is tightly related to
H2CO3 / CO2
it is considered as a special case, with H2CO3 as a "volatile acid".
fortunately again, all of the other "weak ions" are the anions of incompletely dissociating acids
("weak bases" are very rare, and our programme indicates,
when these ought to be considered). and there are only two such acids to be reckoned with:
albumin and phosphate
both together are often called Atot,
with the corresponding anion A-.
the effect of albumin is by far the dominating one, typically contributing about 10mEq/l of negative charges,
while phosphate's contribution tends to be less than 2mEq/l.
their ionisation is dependent on the pH they are exposed to and which they in turn influence -
this kind of circular mathematics makes calculations on a piece of paper a formidable challenge,
but is no match even for an outdated computer (i have been testrunning on a 100MHz, 48MB RAM machine :-) ).
you can calculate the negative ionisation of albumin and phosphate for different pH values
by following this link! - with a lot more information about the calculations.
a good rule of thumb is to calculate 1mEq/l negative charge per 4g/l albumin (or 0,4g/dl or 1,5mmol/l). so a patient with a normal pH, PCO2 and BE but an albumin of 10g/l (or 0,1g/dl or 0,4mmol/l) must have an unrecognised metabolic acidosis of 7,5mEq/l. this is not a trifle amount!
conversely your patient with a high PCO2 and BE may not be one of those "carbon-dioxide retainers", but simply compensating a low albumin metabolic alkalosis.
everything else - globulins or citric acid cycle intermediates come to mind - has no practical
significance.
is albumin a buffer?
read more via this link!
and what about haemoglobin?
haemoglobin gets often mentioned in the context of "buffer bases", to use this common expression from
the Siggaard-Andersen terminology.
according to the Stewart approach, haemoglobin cannot possibly contribute to the acid-base
status of extracellular fluid (ECF), because it is found almost exclusively inside of erythrocytes, unable to
influence the electrolyte composition of the fluid surrounding them, and the PCO2 has already
been measured, independently of what the influence of haemoglobin may be. the basic chemical principles behind
the Stewart approach dictate that it is the ECF composition which determines the plasma pH.
there is a very Salomonic solution to these seemingly irreconciliable positions, though. and it dates back to the pioneering times
of acid-base research, when Stewart still was in his diapers, and Ole Siggaard-Andersen had yet to be born:
