College answer

Primary respiratory acidosis – likely secondary to asthma, 
Secondary high anion gap metabolic acidosis – shock, sepsis 
Concomitant non-anion gap metabolic acidosis – fluid resuscitation, (delta ratio 0.5) 
Increased Aa gradient – pulmonary sepsis 
Elevated lactate – sepsis, B2 agonist use 
Elevated glucose – pre-existing diabetes, stress, B2 agonist, steroids 
 

Discussion

The abnormalities addressed systematically are as follows:

1) There is no hypoxia per se, but the A-a gradient is widened (114)

2) There is profound acidaemia.

3) The CO₂ is a major contributor to the acid-base disturbance.

4) There is a metabolic acidosis; the SBE is -16. As such, the expected CO₂ is 28. To use the Boston rules,  the expected CO₂ = (14 ×1.5) + 8 = 29, close enough for government work. Regardless of which acid-base church you follow, we should all be convinced that there is a combination of a severe metabolic acidosis with a severe respiratory acidosis.

5) The anion gap is (139 + 4.2) - (108 + 14) = 21.2, or 17 if you omit the potassium as the college frequently do.

6) The delta ratio is therefore either 0.92 or 0.5; depending on whether or not you included the potassium you could come to the conclusion that either there is a minor contribution from NAGMA, or that the contribution is substantial. Either way, the delta ratio points to a mixed acidosis. The lactate on its own certainly does not explain all of the base deficit.

Thus:

• There is a mixed respiratory and metabolic acidosis
• The metabolic acidosis is a mixed high and normal anion gap acidosis
• There is also hyperglycaemia

Explanations? "Potential reasons for each"?

• The respiratory acidosis is due to the failure of CO₂ clearance associated with severe asthma
• The A-a gradient is raised- this could be due to increased shunt resulting from a high intrinsic PEEP, or there may be pneumonia.
• The lactate component of the acidosis is likely due to salbutamol administration
• The hyperglycaemia is another phenomenon associated with β2-adrenoceptor stimulation (Dawson et al, 1995)
• The hyperchloraemia is likely due to normal saline resuscitation or the reverse chloride shift which occurs in the arterial circulation (where chloride moves out of RBCs in exchange for bicarbonate)