Blood Gas Ninja Part 2: Basics

http://www.patchtogether.com/designs/panda-ninja-3121.htmlI know last week I said I’d talk about SIDe and SIDa, but I needed to put this groundwork in first.  As it came to over a 1000 words, we’ll save the gaps for next week.

The way we are taught to analyse blood gases comes from a miss-match of 2 slightly different schools of thought based on Henderson Hasselbach understanding of blood gas chemistry (Boston and Copenhagen).  Though the stewart hypothesis helps us understand whats going on with acid-base its utility by the bedside is limited.

Old School methods, are based on observational data, and often fall apart or get confusing when things get complicated.

Most people’s mental algorithm for blood gas analysis looks like this:

Step 1:  Look at the pH is it low or high?

Step 2:  Look at the PCO2 is it low or high?

Step 3:  Look at a Metabolic component, is it low or high?

So when we all look at a blood gas the first thing all of us do is look at the pH and then the CO2.  If the pH is low and the CO2 is high we throw up our hands and go “it’s a respiratory acidosis” and move on.  However if the patient has a low pH and a normal CO2 we claim it’s metabolic and move on.

Now if you are a Bostonian you look at the HCO3- and apply a series of rules of thumb to work out what kind of metabolic disturbance, if you are a Copenhaganite you look at the standard Base Excess.

You can do either.  I’m not judging you, but I find the Boston approach hard to reconcile as it seems you need to have the answer before you start looking at the blood gas, some people find this approach reasonable as you always have a clinical context to interpret the ABG in.  The other issue with this approach is that it uses the HCO3which we know from last week is a dependent variable.

Boston Rules of Thumb

NB: The Boston rules are AMERICAN, which means they use partial pressures in mmHg  To convert to a KPa you need to divide the American value by 7.6 (or ask google to convert).

Rule 1

1 for 10 in Acute Respiratory Acidosis

The HCO3will increase by 1 mmol/l for every 10mmHg in pCO2 over 40(mmhg)

Expected HCO3–   = 24 + [actual pCO2 – 40]/10

Effectively the higher CO2 shifts the equilibrium towards the production of more HCO3

Rule 2

4 for 10 in Chronic Respiratory Acidosis

The HCO3 will increase by 4 mmol/l for every 10mmHg in pCO2 over 40

Expected HCO3= 24 + 4 [actual pCO2 – 40]/10

Renal compensation occurs over a few days.

Rule 3

2 for 10 in Acute Respiratory Alkalosis

The HCO3will decrease by 2mmol/l for every 10mmgHg in pCO2 below 40

Expected HCO3= 24 -2 (40- Actual pCO2)/10

However you can normally not get a HCO3less than 18mmol/l because you cannot have negative values of PCO2.  So if your number here is less than 18, it suggests a co-existing metabolic acidosis.

Rule 4

The 5 for 10 Rule for a Chronic Respiratory Alkalosis

HCO3 will reduce by 5mmol/l for every 10mmHg decrease in pCO2 below 40mmHg.

Expected HCO3 = 24 -5 [40-Actual pCO2]/10

The limit of compensation is about 12-15 mmol/l

Your answer can be +/-2

Rule 5

The One and Half pluse 8 Rule for a metabolic acidosis

Expected PCO2 = 1.5 x [HCO3-] + 8

The limit of PCO2 is about 10 mmHg  Your answer can be +/-2

Rule 6

The point Seven plus Twenty Rule for a metabolic alkalosis

Expected pCO2 = 0.7 x [HCO3]  + 20

Your answer can be +/-5

There are certainly some pretty big limitations to this approach, it tends to fall down in a big heap if you have someone with a combination of acid base disorders, or has 2 of the same type (for example 2 causes of metabolic acidosis).  It’s a lot to remember for little benefit over what we were taught at medical school but here are some examples where they might be useful.  It also fails to take account of ATOT and SID in explaining acid base disturbance.

Example 1.

You’ve got Diedre, an end stage COPD patient who claims to be more short of breath than normal.  She has a PCO2 of 70 and an HCO3 of 36.  The expected HCO3 for her (rule 2) is 24 + 12 = 36.  We can see that the actual measured value is the same as the expected value so we can be pretty sure there is no evidence of another acid base disorder lying in wait for us.

Example 2.

You’ve got Seth, a 27 year old space cadet who has been found unconscious by police with various white powders about his person.  His GCS is E1V2M2 and his BSL is 6.9.  His gas shows a pH of 7.2 with pCO2 of 70 and a HCO3 of 14.  His expected PCO2 [rule 5] is 1.5 x 14 + 8 = 29mmHg, as his actual CO2 is way higher than his expected we can infer that there is a respiratory component to his acidosis as well, that he’ll probably need intubating.

To be honest I think rule 2 and rule 5 are the most useful, and they are the ones I try to remember.

Copenhagen approach – Base Excess, Standard Base Excess

Base Excess was a term coined in the 1960’s by Siggaard-Anderson.  It is 0 when the pH =7.4 pCO2 = 40 mmHg and the temperature is 37°C.  If either the pH or the pCO2 are note 7.4 or 40mmHg, BE becomes the amount of Hydrogen required to bring the pH back to 7.4, while maintaining a pCO2 of 40mmHg.

If the BE is +VE it reflects the amount of Hydrogen you need to add to the solution to make it neutral that means the solution is going to be alkali.

If the BE is –VE it reflects the amount of Hydrogen you need to take out of the solution to make it neutral, that means the solution is going to be acidic.

Okay that’s the Base Excess, we tend not to use this because of a couple of things, firstly because it fails to take into account the movement of CO2 due to Gibbs-Donnan forces, and it fails to model accurately enough the effect of ATOT (specifically the effect of Haemoglobin inside red blood cells).  Standard base excess is base excess calculated at a Hb concentration of 50g/L.

SBE = 0.93 x ([HCO3] + 14.84 x (pH – 7.4) – 24.4)

We can use either for day to day analysis, but remember that normal BE becomes less accurate with big swings in pCO2 and Hb.

If the BE is -VE the solution is going to need LESS hydrogen to make it neutral, this means that there is either a primary metabolic acidosis or a compensated respiratory alkalosis (you’ll know immediately depending on if the CO2 is high or low).  This method isn’t perfect either, it still doesn’t tell you if the acid base disturbance is primarily metabolic or because of respiratory compensation.

So we can use our rules of thumb, or our BE to split our acid-base disorder into 1 of 4 diagnoses.  These are the primary acid base disorders, the ‘osis’ part dictates the direction of acid base disorder, not the actual pH of the solution.  So you can, in theory, have a respiratory alkalosis with a metabolic acidaemia.

pH

pCO2

HCO3-

BE

Interpretation

↓NEGATIVE

Metabolic Acidosis

↑POSITIVE

Metabolic Alkalosis

↑POSITIVE

Respiratory Alkalosis

NORMAL

Respiratory Acidosis

Are you compensating for something?

Compensation is the response to acidosis.  The body has 2 mechanisms for dealing with it depending on if the primary acidosis has a metabolic or respiratory origin.

Metabolic compensation occurs in response to a respiratory acid-base disturbance.  The kidneys excrete either more or less Hydrogen, they do this by altering the extracellular SID (by changing the urinary SID, by altering their Chloride excretion).  This is very effective and can compensate for swings of pCO2 from 25-80mmHg.  This process takes time, up to 5 days, this is why we can have incomplete compensation, or partial compensation for respiratory acid-base problems.

Hypercapnia –

Decrease urine SID, increase extracellular SID

Hypocapnia

Increase urine SID, decrease extracellular SID

Respiratory compensation is fast, but much less effective than metabolic compensation.  A normal pH is not normally achieved.  The increase or decrease in pCO2 is driven primarily by breathing faster or slower.  This is driven by central and peripheral chemoreceptors.  The central ones tend to kick in later, as it takes longer for the acidosis to equilibrate in the CSF.

 

A normal pH combined with an abnormal pCO2 can either mean that there are 2 opposing acid base disorders, or that there is a compensated respiratory acidosis.  A normal PCO2 combined with an abnormal pH always represents 2 primary acid base disorders.

Next week!  Gaps!

 

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