Question 20.1

College Answer

Severe metabolic alkalosis (raised SID)
Respiratory compensation (incomplete)

High anion gap (approx. 31) metabolic acidosis
Profound hypochloraemia

Gastric losses and fluid depletion causing chloride loss and metabolic alkalosis

Metabolic acidosis secondary to renal failure (acute? Acute on chronic?) +/- sepsis from pancreatitis and/or gastro-enteritis
CO2 retention as compensation for severe metabolic alkalosis

Discussion

Let us dissect these results systematically.

1. The A-a gradient is high:
   The alveolar oxygen tension is (0.4 × 713) - (62 × 1.25) = 207.7;
   thus the A-a gradient is 74.7.
2. There is alkalaemia.
3. The PaCO₂ is high, which is a move in the appropriate direction given the degree of alkalaemia.
4. The SBE is  over 30 mmol/L, suggesting a severe metabolic alkalosis.
   If the SBE was not available, the bicarbonate of 65 would have been impressive enough.
5. The respiratory compensation is adequate. Only to the Boston rules apply, as the precise value of SBE is not given.
   The expected PaCO₂ (65 × 0.7) + 20 = 65.5mmHg, and so there is totally appropriate respiratory compensation.
6. The anion gap is raised: (149) - (53  + 65) = 31, or 34.3 when calculated with potassium.
7. The delta ratio cannot be calculated, as there is a metabolic alkalosis instead of a metabolic acidosis here.

So, in summary, the blood abnormalities are:

• Hypoxia
• Alkalaemia
• Metabolic alkalosis with hypochloraemia
• Hypernatremia
• Hyperlactataemia
• A high anion gap, which is not completely accounted for by the raised lactate, and which could represent ketones or non-volatile acids associated with renal failure.
• Ionised hypocalcemia
• Renal failure (impossible to say, acute or chronic)

The college make a few strange statements here. For instance, the respiratory compensataion for this metabolic alkalosis is complete, but they think it is not. Are we using the same Boston equations? If we were to use the Copenhagen rules instead, we would expect the PaCO₂ to be 40 + (30 ×0.6) = 58mmHg, and that would still be withing 4mmHg of the measured value.

So, it is difficult to tell exactly why the college think the compensation is incomplete. Certainly, complete compensation does not mean the normalisation of pH has been achieved.

In 1984, in his educational article for Kidney International  John Harrington explored this issue, and concluded that the relationship between PaCO₂ and HCO₃^- remains stable and near-linear for a broad range of values, extending even into the ridiculous.  Every 1mmol/L rise in bicarbonate was matched by a 0.7mmHg increase in PaCO_2. in a series of cruel human experiments on alkalotic volunteers who were either fed bicarbonate and THAM for many days  by Goldring et al (1962), or had acetate administered via dialysis circuits by De Strihou et al (1973). If one plugs this rate of rise into an online calculator, one observes a rise of pH by about 0.01 for ever 1mmol increase in bicarbonate.

So, the pH will inevitably trend to alkalaemia. Furthermore, it is possible to demonstrate that the correction of pH back to 7.45 would require a PaCO₂ of around 94mmHg, and this cannot be viewed as a physiologically beneficial move by any sane person. For this very sensible reason, respiratory compensation for truly severe metabolic alkalosis could never take place outside of mathematical models. To achieve a stable PaCO₂ of 94mmHg the alkalotic person would have to be severely hypoxic on room air (with an alveolar oxygen tension no greater than 34 mmHg), and breathing at a rate of around 2 breaths per minute.

Goldring, Roberta M., et al. "Respiratory adjustment to chronic metabolic alkalosis in man." Journal of Clinical Investigation 47.1 (1968): 188.

De Strihou, C. Van Ypersele, and A. Frans. "The respiratory response to chronic metabolic alkalosis and acidosis in disease." Clinical Science 45.4 (1973): 439-448.

Harrington, John T. "Metabolic alkalosis." Kidney international 26.1 (1984): 88-97.