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!

 

Blood Gas Ninja part 1: Science.

http://www.fatfaceandme.com/2012/12/the-black-ninja/
Reproduced from fatfaceandme blog. Under CC licence.

Acid-base homeostasis is vital to life.  Disruptions in the balance of Hydrogen ions within the body, and within the cell cause problems that are often the symptoms of disease.  Understanding how these mechanisms work gives us two valuable insights, firstly it aids in diagnosis, and second it can guide treatment.

Everything begins with water. 

We are all approximately 60% water (though I have evidence that some ED Registrars are made entirely from gin).  Water dissociates as follows

H2O <–> H+ + OH

The dissociation of water is constant, and is dependent on temperature, at high temperatures you get more dissociation, this means you get more liberated Hydrogen ions, and so the acidity goes up.

If we are 60% water, that’s a lot of available, easily liberated hydrogen.  We don’t measure hydrogen ion concentration, we measure the negative logarithm of proton concentration (because some bright spark thought that was easier).

Normal mean INTRACELLULAR pH = 6.8

ECF [pH usually aprx > 7.3] – Contains cells, particles, dissolved gases, fully and partially dissociated ions

Normal mean ARTERIAL pH = 7.4

So it’s important to realise that what we are measuring and what we really care about, are again, different things.  We should care about the intracellular pH, but we can’t measure that, so we measure the arterial (or venous) pH of blood, and use that as a surrogate for extracellular fluid (ECF) which is, in itself, a surrogate for intracellular pH.

Determinants of pH

Numero uno; CO2

We make a lot of CO2 each day from aerobic metabolism and the trusty Krebs cycle (12 500 mEq/day).  It goes from the cell to the ECF, to the blood, to the lungs where it follows it’s partial pressure gradient out into the atmosphere.  For us to understand CO2’s effect on plasma pH we have to plug it into our formula.

CO+ H2O <–>  H2CO3 <–> H+ + HCO3

Using this, and the formula for pH we can derive the following formula

pH = 6.1 + log10([HCO3]/αPCO2)

This equation is the Henderson Hasselbach equation (not the top one!) and it is how we derive the bicarbonate in a blood gas readout.  6.1 is the pKa (another time), and α is the solubility coefficient of CO2. (which is 0.3, but we all knew that right?)

Important point:  HCO3 is a derived value.  It is not a measurement.

Numero Dos; Non-volatile weak acid dissociation

Fluid compartments have a soup of molecules that don’t generate CO2.  Some of these have acidic properties.  They predominantly have a negative charge, and this charge alters in parallel with pH.  The main constituents are albumin, and inorganic phosphate (haemoglobin is also a weak acid and does the same thing inside the red cell).  This gets expressed with the incredibly complex formula

HA <–>  H+ + A

Now one of the laws of physics comes into play here.  That law is conservation of mass

We can define the total amount of non-volatile weak acids in a fluid compartment ATOT,.

ATOT = HA + A

KEY POINT:  ATOT is a constant, it cannot vary with pH, because you would have to convert some of the mass to energy, which would cause your fluid compartment to EXPLODE [e=mc2].  A change in pH signals a shift in the balance between HA and A.

 

Numero trois; Electrical Neutrality – and strong ions.

The balance of charge of cations and anions must equal eachother in a dissolved fluid.  This is another one of the laws of physics, takes precedence over any desire for pH neutrality.

K+, Na+, Ca2+, Mg2+, Clexist as ions dissolved in fluid.  We also have lactate, sulphate, and β-hydroxybutyrate acting as strong cations in the plasma compartment.

In human plasma we do not have a balance of cations and anions, this “gap” or “difference” is the Strong Ion Difference [SID], which is expressed mEq/L (because it’s an expression of CHARGE, not concentration).

SID = [strong cations] – [strong anions]

And because of the law of electrical neutrality we can re-arrange that formula to state:

SID + [H+] –[HCO3] – [CO2-3] – [A] – [OH] = 0

Number “whats spanish for four?” –  crazy voodoo – aka Gibbs Donnon forces.

This is the name given to the forces that compel dissolved ions to alter their equilibria across semi-permeable membranes (if you want to draw some circles with a dotted line across the middle and talk about concentration gradients…you can, I won’t stop you).  The 3 fluid compartments that we are concerned about in this model are the ones inside red blood cells, as well in the plasma, and the ECF.  Each compartment contains big molecules which have a charge, and will not diffuse (haemoglobin and albumin I’m looking at you).  Red blood cells harbour a lot of negative charge (as they’re packed with Hb) so they attract Na+ and K+, if it wasn’t for the Na/K+ ATPase working against that electrochemical gradient, they’d swell up, pop, and we would all die.  Chloride is the major anion, and it is shuttled around by this affect a lot.

Putting this all together.

There are 6 equations that govern, and predict how much H+ there is in the plasma.  They are as follows.

Water dissociation equilibrium [H+] x [OH] = Kw

Weak acid dissociation equilibrium [H+] x [A] = Ka x [HA]

Conservation of mass for weak acids [HA] + [A] = [ATOT]

Bicarbonate Ion formation equilibrium [H+] x [HCO3] = Kc x PCO2

Carbonate ion formation equilibrium [H+] x [CO32-] = K3 x [HCO3]

Electrical neutrality SID + [H+] –[HCO3] – [CO2-3] – [A] – [OH] = 0

Stewart proved (using sexy maths) that 6 of the variables in these equations (HA, A, HCO3, CO32-, OH and H+) are reliant on just 3 independent variables: SID, ATOT and PCO2

The Strong Ion Difference.

stewart

SID is the gap between anions and cations on this bar chart.  It is a ‘charge space’ – that is filled by weak ions dissociating in varying combinations to keep the charge in solution equal.  The majority of this work is completed by just 2 components, the weak acids (A) and the HCO3 .  If we add more cations to the mix, the buffer base has to get larger to obey the law of electrical neutrality.  If we add more anions, the buffer base has to get smaller to obey the same law.

In conclusion

The pH of human plasma is based on 3 things:

  • ATOT – the concentration of non volatile weak acids
  • PCO2 – the partial pressure of CO2
  • SID – the charge space between cations and anions dissolved in the plasma.

Next week – we’ll talk about “apparent SID” Vs “effective SID”, anion gaps, and what clinical applications all this has!

For more on SID – have a look at this youtube lecture, it really helped me understand this.

How to nail the ARCP

You’ve heard your consultants tell you that the ARCP isn’t about ‘passing’ or ‘failing’, that they aren’t looking to ‘catch you out’, but there is a lot of stuff to get ready, and it can often feel like the ARCP meeting is a bit of a grilling.

nailedThey key to passing the ED ARCP is preparation, from my limited understanding the Anaesthetic ARCP is like a group hug.

Your deanery will have hidden a document which has a list of ‘competencies’ you need to prove you’ve achieved.  Get hold of this (it’s normally stuck on the deanery website somewhere).  Look at it in the first few weeks of your placement.

You need to register with the college to access the eportfolio.  This is expensive (£90 or thereabouts each year), but you can phone up and do it.  The people at the college are pretty quick at doing this most of the time.

Now that you’ve got that document and the eportfolio you can capture assessments whenever the opportunity arises.  Get assessments filled in as soon as you’ve done whatever it is you’ve been assessed on, the web forms take a few minutes to fill in.

I also annotate the document from the deanery whenever I got a CEX/CBD etc thats relevant, and I upload it to my portfolio as a guide.

It’s also good to keep a list of all of the interesting cases you see while you are just working normally.  These cases should be used for CBDs.

Your ARCP assessors have to go through 30-40 of these eportfolios each year, the easier you make it for them, the easier it is for you to get an outcome 1.  The other thing to do is to link assessments together, and link them to the curriculum part of the eportfolio.  It’s important to do this as you go.  If you are struggling to get access to cases that you need to ‘tick off’ then the earlier you can identify them, the earlier you can flag it with your supervisor and they can do something about it (cherry pick, simulate, or CBD it!).

So just to summarize:

  • Prepare, as soon as possible get eportfolio and ‘how to pass’ document.
  • Add things to your eportfolio as they happen
  • Link the heck out of things
  • Annotate your how to pass document with every piece of evidence you get.
  • Identify gaps early, and get help to fill them!

On ARCP day:

  • The dress code is ‘job interview’
  • Take a paper copy of your ‘how to pass document’, if the assessors have not been able to find things, and you can tell them exactly where your evidence is, you can snatch victory from the jaws of defeat.

Here is the document I made for my CT3 ARCP,  – ARCP, make your own.

Good Luck!