Category Archives: Acid-Base

The Lactate Conspiracy: Part 2

So in the last post I established:

  • Lactate is a base.
  • Lactate production retards cellular acidosis.
  • Lactate is produced all the time.
  • Lactate is fuel.

I have suggested that the traditional lactate hypothesis

“Lactate is a byproduct of anaerobic respiration that is produced in response to cellular hypoxia secondary to inadequate oxygen delivery.  It is a marker of tissue hypoperfusion and shock”

 Is not correct.

However we all see, and all know that when people are sick their lactates go up, and when their lactates go up they become acidotic.

Why is this?

There are two reasons.

The first is the simplest.  When people are sick they are generally metabolically very active because they are trying to deal with whatever is making them sick.  At a very basic level that means that each person’s cell is recycling ATP as fast as it can.

The extra protons come from this reaction.

However there are some points to make to this approach of ‘counting’ protons when it comes to cellular chemistry.  The first is that these reactions don’t occur in isolation, they occur in a complex network, and they occur in a solution that is mostly water.  As such this is a slightly reductive way of thinking about cellular respiration.  Water can supply and buffer excess hydrogen to a certain degree (though it’s pKa is 14 so it doesn’t do much of this).  However we upregulate this reaction enough you can see that excess protons can be produced, and they will need to go somewhere.

We can say that the acidosis associated with lactate production is due to an induced hypermetabolic state.  Once the cells own intrinsic attempts at buffering (making more lactate, bicarbonate etc etc) are exhausted those excess protons leak out and make the cell, and the surrounding tissue fluid more acidotic.

The second reason, and this I think is the best reason, is because of the laws of physics.  Essentially when we upregulate the production of lactate, we increase the strong ion difference as lactate is a anion.  Lactate sits alongside, chloride, bicarbonate, and phosphate in the buffer base, and to obey the law of electrochemical neutrality some of the buffer base has to release some free hydrogen into solution to balance things.

If you have no idea what this paragraph or image mean, then you need to read this article.

So the lactate makes you acidotic, in the same way that excess chloride infusion can make you acidotic.  It’s not ‘to blame’ it’s just the last step in a chain reaction that started when cellular metabolism got kicked into first gear and the accelerator got floored.

Now just to summarise (again):

  • Lactate is a base.
  • Lactate production retards cellular acidosis.
  • Lactate is produced all the time.
  • Lactate is fuel.

Lactate is produced as part of normal glycoylsis. An elevated lactate indicates a HYPERMETABOLIC state, IT CAUSES ACIDOSIS by INCREASING the STRONG ION DIFFERENCE.

If Lactate is produced in response to badness, and there is experimental evidence that suggests it is metabolised by the heart, lungs, kidney, and brain during times of physiological stress why oh why would we try to ‘clear’ it?

Clearing lactate essentially means doing things to increase oxygen delivery to cells, but we know that it’s not hypoxia that is really driving lactate production it is the energy demand of the cell exceeding the supply available to it, so dumping fluid, and blood into someone’s circulation isn’t necessarily going to improve things (apart from by diluting the lactate when you do your next gas)

This has interesting implications.  If lactate is a fuel.  Can it be a treatment?

Couple of interesting properties of lactate – it can be thought of as a consumable anion, this means you can give a load of cation (ie sodium) without having to give a lot of chloride, or a lot of bicarbonate.  As the cells eat the lactate and turn it into glucose, or break it down completely.

I didn’t find much out there, but I did find 5 studies.  They are recent, small, and of variable quality, but I think they point to a few uses:

In one pilot single blind RCT in Austrailia1.  Patients with pretty horrific heart failure (ICU admissions, needs inotropes, or ventilation) were given 3ml/kg bolus of half-molar sodium lactate and an infusion of 1ml/kg/24hrs versus a hartmanns bolus and infusion.  Their CO was measured by ultransonographers blinded to the treatment arm.  The results show a significant increase in CO at 24 hours.

Intervention Control
CO at baseline 4.05 +/- 1.37  L/min 4.72 +/- 1.3 L/min
CO at 24 hours 5.49 +/- 1.9 L/min 4.96 +/- 1.21 L/min
CO at 48 hours 4.87 +/- 2.38 L/min 4.76 +/- 1.58 L/min

In two studies conducted in the UK on people who has sustained TBI half molar sodium lactate infusion was shown to decrease episodes of raised ICP3, and decrease ICP2 more effectively than mannitol.

In patients with TBI and ICP monitors with the kind of brain injury we can’t do much about other than prevent secondary insult they gave either normal saline or 0.5ml/kg/hr of half molar sodium lactate for 48 hours.  There were 11 episodes of RICP in the SL group and 20 in the control group (p=<0.05).  The other interesting thing was these people’s cumulative fluid balance.  It was much lower. 

They also looked at people’s neurological outcome at 6 months, they showed no significant difference between the two groups: 12 patients (SL group) versus 15 patients (control group) had a poor outcome at 6 months. However, more survivors from the control group had poorer neurological outcome compared to the SL group: nine versus four patients, although this difference did not reach significance (P = 0.14).  Though it is an interesting signal, and were this a paper on stroke thrombolysis probably picked up as hugely significant.

When they compared sodium lactate to mannitol, the effect of the lactate solution on ICP was significantly more pronounced (7 vs. 4 mmHg, P = 0.016), more prolonged (fourth-hour-ICP decrease: −5.9 ± 1 vs. −3.2 ± 0.9 mmHg, P = 0.009) and more frequently successful (90.4 vs. 70.4%, P = 0.053)2.


Another study in Indonesia4 looked at the efficacy of lactate bolus and infusion as a treatment for the horrifically dehydrated patients with dengue shock syndrome.  50 patients aged 2-14 years old received wither 5ml/kg of sodium lactate with a 1ml/kg infusion or ringers lactate 20ml/kg bolus plus standard maintanence therapy.  They looked at the measurement of a endothelial enzyme called SVCAM 1 (they found no difference).  There was no significant difference in outcome between groups (1 death in lactate group, 3 in control group), but the cumulative fluid balance between these groups with similar outcome was vastly different – the control group was 107 ml/kg +ve in 24 hours, whereas the lactate group was 35 ml/kg +ve in 24 hours.

Just a little context for you, the current direction of travel with research into fluid resuscitation is that too much can cause problems with acidosis, acute lung injury, and renal problems so volume sparing fluids that either exert an osmotic effect or do something else (like provide fuel) might be the ‘next’ thing.  Now I’m not saying that this is anything approaching a silver bullet, but if we can resuscitate people with less volume, we probably should.

What about sepsis?  I could only find a study on pigs, it was elegantly done however.  15 pigs were given the same challenge with e-coli endotoxin, and then resucicated over 300 minutes with either 5ml/kg/hr of 11.2% Na lactate, 5ml/kg/hr N saline, or 5ml/kg/hr of 8.4% sodium bicarbonate.  They measured lots of things, but MAP was their primary outcome.  As you can see, there was a significant improvement in MAP in the sodium lactate group.

I’ve subsequently found a similar study in sheep6, that suggests that sodium lactate infusion is harmful, so I’m not raising hypertonic sodium lactate as a panacea by any means, but the research into it’s volume sparing effects, and ability to decrease ICP needs to continue.

In Summary

The general textbook understanding of lactate physiology makes a number of basic errors which lead to inaccurate assumptions by medical staff, which can lead to inappropriate or inadvisable treatment strategies which are perpetrated throughout the world by the most junior doctor to the most senior critical care physician.

That is the lactate conspiracy.

Lactate is a fuel of last resort, and it may have therapeutic uses as a volume sparing resuscitation fluid.


  1. Nalos, Marek, et al. “Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial.” Critical Care2 (2014): R48.
  2. Ichai C, Armando G, Orban JC, Berthier F, Rami L, Samat-Long C, Grimaud D, Leverve X: Sodium-lactate vs mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients. Intensive Care Med. 2009, 35: 471-479. 10.1007/s00134-008-1283-5.
  3. Ichai C, Armando G, Orban JC, Berthier F, Rami L, Samat-Long C, Grimaud D, Leverve X: Sodium-lactate vs mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients. Intensive Care Med. 2009, 35: 471-479. 10.1007/s00134-008-1283-5.
  4. Somasetia et al. Critical Care 2014, 18:466
  5. Duburcq, Thibault, et al. “Hypertonic sodium lactate improves fluid balance and hemodynamics in porcine endotoxic shock.” Critical Care 18.4 (2014): 467.
  6. Su, Fuhong, et al. “The harmful effects of hypertonic sodium lactate administration in hyperdynamic septic shock.” Shock: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches6 (2016): 663-671.



pH 7.51…lactate of 20??

Blood Gas!

This 74 year old gentleman attended the ED after phoning a friend because he ‘though he was having a stroke in both hands’.  Paramedics had to gain entry to the house, which was in a state of disrepair, cold, and unclean.  The patient was found on the floor, surrounded by vomit.  I tend to do a VBG in situations like this because I get an acid/base status and other useful information back faster than formal bloods.

His observations were essentially normal, apart from his 3 lead which was a veritable soup of short lived atrial arrhythmias, and PVCs.  He was also a bit cold 34 degrees C.  What is your interpretation of this gas?

pH 7.51
pCO2 60
pO2 28
BE 22
Na 145
K 2.2
AG 55.4
Cl 44
iCa 0.74
Gluc 9.8
Lac 20.0
HCO3- 40.8


My interpretation:

So starting from the top the patient is Alkalotic, with an elevated CO2.  This means they have to have a metabolic alkalosis with respiratory compensation.  Lets looks more closely at the metabolic component, the BE is 22, which means we have ‘22’ more bases than normal, we can also see that his bicarbonate is 40.8. (thats where they are coming from).

There are clues here.  We know that bicarbonate takes time to respond to problems.  This man must have a chronic problem causing his bicarbonate to go up.  We can infer this is a chronic metabolic alkalosis with a degree of respiratory compensation which is probably new.

Lets examine the AG – the gap is 55.4! Which is the highest gap I have EVER seen.  Remember that AG is calculated by adding the Na and K, and taking the chloride from bicarbonate.  Where is the source of the gap.  It’s predominantly from the Chloride.  Look it’s 44!  That’s less than HALF what it should be, I suspect that it’s not the only cause of the Gap here,  as we’ve got a lactate of 20 , pushing in the other direction and perversely helping to correct the alkalosis.

If you fancy you can calculate his SID which is 96!  High SID alkalosis is usually caused by gastric outlet obstruction, vomiting, excessive NG suctioning, diuretic mistakes,  primary hypoaldosteronism, or volume depletion.

This man has pyloric stenosis from untreated chronic H pylori, and acute renal failure secondary to volume depletion.  I think his gas shows a chronic metabolic alkalosis with respiratory compensation and a hyperlactaemia.   I have never seen this pattern in an adult before!


Na 147
K 2.1
Cl 51
Urea 33.8
Creat 542
Ca2+corr 2.1
Mg2+ 2.0
CRP <3




Blood Gas Ninja III : Mind The Gaps

cuteninjNow we’ve covered the easy bits of acid base, the determinants of pH, and compensation. This week I’m covering all the weird and wonderful calculations you can do to help you potentially whittle down the diagnostic options.   You don’t have to calculate SID, SIG, or OG for every gas, but its useful to know how to, so when you need to, you can.

Anion Gap

anion gap

So a metabolic acidosis is caused by a decrease in SID, making the buffer base contract to maintain the law electrochemical neutrality.  This is usually because strong anions accumulate.  Now we don’t normally measure the strong anions, so we find them by calculating ‘gaps’.  Most of these ‘gaps’ were introduced before we started routinely measuring lactates, so I think it’s a point of contention whether lactate still counts as an ‘unmeasured’ anion, but for the purposes of what we’re talking about let’s call it a measured, unmeasured one!

Take your measured anions and subtract them from your measured cations.

Anion Gap = [Na+] + [K+] – [Cl-] – [HCO3]

If the anion gap is really large (>30) you have a metabolic acidosis.  Anion gaps get bigger if you have less HCO3, Cl.  Now the ‘gap’ itself, is this unmeasured component.  The anion gaps is affected by fluctuations in ATOT because A- which makes up ATOT is usually the biggest component of the gap in healthy individuals.  This means that if someone’s albumin, and sometimes phosphate are low, the size of their anion gap may be less, or normal, when in fact they’re got a rip roaring metabolic acidosis.

We can correct for albumin;

AGc  = AG + 2.5 (normal albumin in g/dl – observed albumin in g/dl)

 The normal range for Anion Gap and AGc is between 10 and 18 mEq/L

Causes of a high anion gap metabolic acidosis can be remembered by the mnemonic MUDPILESCAT and causes of a normal anion gap acidosis can be remembered by USED CRAP

Low Anion Gap Normal Anion GapUSED CRAP Elevated Anion GapMUDPILESCAT
  • Decreased albumin
  • Dilution
  • Multiple Myeloma
  • Hypercalcaemia
  • Hypermagnesaemia
  • Lithium OD
  • Polymixin B
  • Increased lipids
  • Iodide ingestion


  • Ureterenterostomy/Uretersigmoid  connection
  • Small Bowel fistula, steroid excess
  • Extra Chloride
  • Diarrhoea


  • Carbonic Anhydrase inhibitors, CaCl ingestion, cholestytramine ingestion
  • Renal Tubular Acidosis
  • Adrenal insufficicney, Ammonium Chloride ingestion
  • Pancreatic fistula, Parenteral nutrition
  • Methanol
  • Uraemia
  • DKA
  • Paraldehyde
  • Iron, Isoniazid
  • Lactate
  • Ethylene Glycol
  • Salicylates
  • Carbon Monoxide, Cyanide
  • Alcoholic Keotacidosis
  • Toluene


Strong Ion Difference:  [Na+] – [Cl]

This is a quick by the bedside estimate.  If you wanted to calculate a proper SID, you’d need a whole host of other measured values, but as you now know was makes up SID you can use this quick and dirty measure.

[SID] = [Na+] + [K+] + [Ca2+] + [MG2+] – [CL] – [Other Strong Anions].


<38  Low SID >38  High SID
Strong ion acidosis (probably hyperchloraemic acidosis).Renal Tubular AcidosisDiarrhoea Metabolic AlkalosisNG SuctionDiureticsHyperaldosteronism

Volume depletion


Strong Ion Gap

Remember Stewart?  Good.  In 1990 Jones proposed using Strong Ion Gap as a scanning tool for acid base disturbance.  This is found by taking SIDa, (apparent SID), from SIDe(effective SID)

SIDa = [Na+] + [K+] + [Ca2+] + [Mg2+] – [Cl-] – [Lactate]

SIDe = [A-] + [HCO3-]


What you are doing here is taking your strong ion difference, and taking it away from the buffer base, if you do this.  The normal SIG should be close to zero.  The SIG is NOT the AG, and it is not the same as the Standard Base Excess.

High SIG  (> than 2) Low SIG (less than -<2)
Increase in unmeasured strong anions

  • D –lactate
  • Ketoacids
  • Salicylate


Increase in unmeasured weak anions

  • Polygelinate (Gelspan etc)
  • Myeloma IgA


Increase in unmeasured strong cations (lithium)Increase in unmeasured weak cations

  • Myeloma
  • IgG

Increased Chloride

Increased Sodium


I think SIG is quite difficult to use, one of its big limitations is quite small errors in the lab will affect the SIG.  It’s also not really been studied enough to make it easy to work out routinely by the bedside.  Whereas things like the AGc have been around for decades.  Now some studies have shown that a high SIG is a very strong predictor of mortality [ROC 0.991 (95% I 0.972-0.998) ] but this was in penetrating trauma patients requiring vascular surgery (quite a narrow population).

[citation – Kaplan, Lewis J., and John A. Kellum. “Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury*.” Critical care medicine 32.5 (2004): 1120-1124.]


Osmolar Gap

Anion Gaps, SIDs, and SIGs can be useful for estimating charged particle concentrations within plasma.  What about uncharged molecules?  For this we need a different gap.

The osmolar gap is calculated by taking measured osmolality from the calculated osmolality.  It should normally be less than 10.  The osmolality is the measured.  You can use an osmolar gap calculation to look for molecules dissolved in the plasma that do not have a charge.

Osmole: A unit of osmotic pressure, the amount of a solute that dissolves in solution to form one mole of particles.

Osmolality:  number of osmoles dissolved in a kg of solvent [mass] (This is measured)

Osmolarity: number of osmoles dissolved in a litre of solvent [volume] (This is calculated)

Calculated Osmolarity =  (2 X Na+)  + Glucose + Urea

Osmolar Gap = Osmolality – Osmolarity

If we have a high osmolar gap, we can infer there is an excess of a weird dissolved molecule in the blood.  If you work in a department that doesn’t routinely measure ETOH, an elevated osmolar gap metabolic acidosis might be your only blood result that tells you they are sloshed (you may have worked this out in other ways).  Some calculators or equations add in alcohol to this equation too.

Causes of high osmolar gap:

  • Ethanol
  • Mannitol
  • Methanol
  • Ethylene Gylcol
  • Sorbitol
  • Polyethylene glycol
  • Propylene glycol (used to suspend lorazapam and diazepam IV solutions)
  • Glycine (think TURP)
  • Maltose
  • Lithium

Three words of caution

  • There are 2 types of osmometers, one works by using vapour pressure, the other using freezing point depression.  Only the freezing point depression method works accurately with volatile chemicals like methanol and ethanol.  Your lab could use either.  If they use vapour pressure osmometry you might get falsely normal results.
  • There are many different formulae for the OG, depending on local units of measurement. None of them are wrong, but all of them produce slightly different results.
  • An obtunded patient, with a high osmolar gap could have ingested more than one thing.


So in conclusion

We can use the Anion Gap to give us a better idea of the causes of metabolic acidosis.  SID and SIG can give us some further clarity in certain situations but there utility is nowhere near as good as the anion gap.  The Osmolar Gap gives us an indication of unmeasured uncharged molecules, but doesn’t tell us what they are.

Blood Gas Ninja Part 2: Basics 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.







Metabolic Acidosis


Metabolic Alkalosis


Respiratory Alkalosis


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


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!