If your patient affected by chronic metabolic acidosis (e.g. uremic patient) has lower HCO3 than normal , as expected, how much pCO2 decrease ? Namely how you compute expected pCO2?. Reading your answer I suppose you use winters' formula. It is rigth?
Treatment of metabolic acidosis requires treating the underlying cause. Bicarbonate is generally withheld until pH is very low (below 7.10 - 7.15). The dose of bicarbonate should not exceed 0.5 - 1 mEq/kg at a time with additional doses guided by further measurements of pH, pCO2, and HCO3, correction = 0.5 (wt in Kg) x (desired bicarbonate - measured bicarbonate) in mEq/L.
Note-: correct with 50% calculated bicarbonate deficit and recheck the serum level .
How to compute PaCO2 during chronic metabolic acidosis?
We don’t have to compute for chronic metabolic acidosis (CMA) since the PaCO2 value in mmHg is equal to the two digits of the pH value
For instance IF pH = 7.25, PaCO2 should be about 25 mmHg,
With this formula, we can immediately focus on the respiratory compensation:
For a pH value of 7.25,
If PaCO2 is significantly greater than 25 mmHg, the respiratory compensation is inadequate, thus a respiratory insufficiency is associated;
If PaCO2 is largely lower than 25 mmHg, the respiratory is higher than CMA required, therefore a respiratory alkalosis is associated to CMA.
Furthermore, according to the alveolar gas equation (Fi02 of 21%): Pa02 + PaCO2= 140 mmHg; in this case, in absence of pulmonary disease, PaO2 should be elevated, near 115 mmHg
Thus, we don’t need to compute!!
FG Brivet, FM Jacobs: Anomalies de l’Equilibre Acido-basique d’Origine Métabolique in Réanimation Médicale ; Collège National des Enseignants de Réanimation Médicale, Masson Paris 2009 PP 1356-1365.
In the same way for ACUTE Metabolic Acidosis, instead of using Narins’s formula:
PaCO2 = 1,5 × + 8 ± 2 mmHg (1)
It is easier to use Schlichtig’s formula: Delta PaCO2 (mmHg) = Standard base excess (2)
Thus in case of acute metabolic acidosis, with the same value of pH (7.25) and an SBE of 18, for instance (SBE value being systematically reported by lab but rarely used….), PaC02 should be near 22 mmHg (40- 18). If PaCO2 value is greater than the expected value, respiratory compensation is inadequate, the patient is at risk of respiratory failure, whereas if PaCO2 is lower than 18 we can claim that a respiratory alkalosis is associated.
With this approach I can say goodbye Mr. Davenport, you are too sophisticated for me at 5 in the morning…
1/ Narins RG, Emmet M. Simple and mixed acid-base disorders: a practical approach. Medicine, 1980, 59: 161-167.
2/ Schlichtig R, Grogono AW, Severinghaus JW. Human PaCO2 and standard base excess compensation for acid-base imbalance. Crit Care Med, 1998, 26:1173-1179.
TO Brivet thank you very much. I know the statement CO2 = last digits of pH but I failed to find well published references . Can I have a copy ( by mail) of your paper?
Nowaday I quickly compute pCO2 in chronic metabolic acidosis as HCO3 + 15. Again I failed to find references (however the latter is from Harrison's and from Brenner's textbooks).
On the other hand I found the statement "Delta CO2 equal to Delta SBE" easy but not accurate.
Unfortunately, most of the assesments between metabolic acidosis and PaC02 concern acute and not chronic metabolic acidosis. Being retired, i gived all my textbooks to my collaborators, so i can not find the exact reference for the two digits of the pH. Some papers reported this link in their abstract, but they are too old for an online version.
Any how, we may look at the Fulop's letter entitled" Arterial tension of PC02 during metabolic acidosis" Am J Nehrol 1998,18/351-2 ( payperview!!)
the Acid-base diagrams, maths, myths and measurements editorial in the Lancet ( 1974) is of interest
I have extensively studied this topic. Now I have the right answer: it depends to HCO3 value. I send results of my study to italian national congress of nephrology. If it will be accepted I write here the formulas
Be careful, the Fulop’s studies to predict PaCO2 values during metabolic acidosis (MA) enrolled KETOACIDOSIS and Lactic Acidosis, two acute diseases. Schlichtig R et al (CCM 1998) computed many data of metabolic acidosis series and found that for ACUTE MA Delta PaCO2 is near to the delta SBE, whereas for chronic MA they found a 0.4 coefficient.
At evidence, PCO2 during chronic MA in human being is not a main topic or a clinical problem (look at Pubmed). Indeed, patients suffering from Chronic MA secondary to chronic kidney disease are encouraged to absorb bicarbonate.
In a dog experimental model Madias et al found that “; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin”. J Appl Physiol Respir Environ Exerc Physiol. 1984 Jun;56(6):1640-6.
Thus, today, according to EBM, even if I wrote it in my review, I am not so sure, that PCO2 value is numerically close to the two-digit number of pH, in case of CHRONIC metabolic acidosis. I will change my text for the next update of our Textbook.
Thanks for this discussion which highlighted one of my personal mistake.
I have submitted a paper about these topics. Referee asked me some little changes and clarifications.
In few days I will submitt the revised paper. When paper will be accepted I would like to send it to you. Please give me your personal email. My emails are: [email protected] and [email protected]
Please, attached you find a letter (in english language too) summarizing my opinion on the use of Winters' formula. it runs well only if HCO3< 10-12 mmHg.
A full paper on this topic is under revision by a Journal
I agree with Francois Brivet that the formula available for calculating PCO2 from HCO3 is available only for acute metabolic acidosis . There are formulas available for acute & chronic respiratory acidosis . Chronic metabolic acidosis occurs in chronic kidney disease & renal tubular acidosis & there is a definite need for a formula . Whether this can be extrapolated from chronic respiratory acidosis needs to be proven .
Thank you , Marco Marano , for your valuable comments . In acute metabolic acidosis , there is no time for compensation & the acid load is high , leading to severe acidosis . The examples are DKA & Lactic acidosis , as mentioned by Francois Brivet . In chronic metabolic acidosis , the bone is a very good buffer & acidosis is reasonably compensated . In severe acute respiratory acidosis , the kidneys take time to compensate to raise bicarbonate , while in chronic acidosis , there is better compensation . Therefore , the formula for acute metabolic acidosis ,should reflect this factor as they would be misdiagnosed as mixed acid base disorder ( metabolic acidosis + respiratory acidosis ) .
I am looking for a dataset of acute metabolic acidosis, namely a series of blood gas analysis, to try to write a paper. If you have it I invite you to share with me your data and co-author a paper with me
Thank you for inviting me to write a paper . I will check up , if I have the data . I do not think , I have serial blood gas analysis data , as requested by you . I shall send you the details , if they are available .
I Will look at our database. We should have large series but mechanically ventilated patients should not be enrolled. Whitin few days i will sent the data to M Marano.
"Superimposing respiratory acid-base disorders can be promptly and effectively ruled out by computing expected pCO2 as [HCO3] + 15, a very simple formula proved to be interchangeable with the common practical rule that requires computes and assumptions, but leads to same results"