PH = 7.30, that is mild acidaemia.
pCO2 = 65 mmHg. So, we have respiratory acidosis.
Next, we need to look at the compensation. Compensation for respiratory acidosis is different between acute and chronic cases.
For acute respiratory acidosis we expect HCO3 to increase by 1 for every 10 pCO2 above 40.
While, for chronic respiratory acidosis, HCO3 should increase by 4 for every 10 pCO2 above 40.
The best way to differentiate between acute and chronic cases is by taking good history. However, in this case the history doesn’t provide us with enough information to make that differentiation. That is why we are going to look at all the possibilities.
If the case was acute, then the expected HCO3 for this patient should be:
24 + 25 x 0.1 = 26.5, This patient’s HCO3 is higher than that (31). This can be explained by having additional metabolic alkalosis.
For the causes of metabolic alkalosis we use the mnemonic CLEVER PD.
- C – contraction (dehydration)
- L – liquorice (diuretic), laxative abuse
- E – endocrine (Conn’s, Cushing’s)
- V – vomiting, GI loss (villous adenoma)
- E – excess alkali (antacids)
- R – renal (Bartter’s), severe K depletion
- P – post hypercapnia
- D – diuretics
Second possibility, the case is chronic, then the expected HCO3 for this patient should be:
24 + 25 x 0.4 = 34. This patient’s HCO3 is less than that (31). This can be explained by having additional metabolic acidosis.
Metabolic acidosis is of 2 types.
- HAGMA = high anion gap metabolic acidosis
- NAGMA = normal anion gap metabolic acidosis
We calculate anion gap as the following: AG = Na – (Cl + HCO3) = 10. According to this, if the case is chronic respiratory acidosis then the patient has associated NAGMA.
For the causes of NAGMA we use the mnemonic USED CARP
- U = Ureteroenterostomy
- S = Small bowel fistula
- E = Extra chloride
- D = Diarrhea
- C = Carbonic anhydrase inhibitors
- A = Adrenal insufficiency/ Addison’s disease
- R = Renal tubular acidosis
- P = Pancreatic fistula.
There is a third possibility, that is acute on chronic respiratory acidosis. In which the patient has already elevated pCO2 and HCO3 then it gets worse with acute exacerbation.
For example, this patient has chronically elevated pCO2 of 55 mmHg, In this case his expected HCO3 should be: 24 + 0.4 x 15 = 30 mmol/L. Then condition exacerbated and the patient retained 10 mmHg of pCO2 acutely, for that 10 he will add 0.1 x 10 mmol/L of HCO3. The patient final HCO3 will be 31 mmol/L.
We have 3 possibilities:
- Acute respiratory acidosis with metabolic alkalosis
- Chronic respiratory acidosis with NAGMA
- Acute on chronic respiratory acidosis.
This patient’s base line creatinine level is usually around 100 umol/L. On these blood gases results it is 266 umol/L. Also his glucose level was high. On examination he looked dehydrated.
He was started on N/S intravenous hydration. His blood gases normalised the next day.
The final conclusion was Acute respiratory acidosis with metabolic alkalosis. The metabolic alkalosis was due to contraction alkalosis (Dehydration).
Special thanks to Dr Mostafa Mohamed Said Abdalla Mohamed Othman for providing the details of this case.