The following results were obtained from a 23-year-old female admitted with severe asthma.


Patient Value

Adult Normal Range





7.35 -7 45


81 mmHg 10.8 kPa)


71.0 mmHg (9.5

350- . 45 0 . 4.6 — 6 0)




14.0 mmol/L*

22.0 - 26.0

Base Excess

-16.0 mmol/L*

_2.0 _ +2.0


9.0 mmol/L*

0.5 - 1.6


139 mmol/L

135 - 145


4.2 mmol/L

3.5-5 0


108 mmol/L*

95 - 105


19.2 mmol/L*

3.5 - 6.0

      a) Describe the abnormalities and give a potential reason for each.                           (30% marks)

[Click here to toggle visibility of the answers]

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 


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 CO= (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.


  • 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)



Dawson, K. P., A. C. Penna, and P. Manglick. "Acute asthma, salbutamol and hyperglycaemia.Acta Paediatrica 84.3 (1995): 305-307.

Westen, Edward A., and Henry D. Prange. "A reexamination of the mechanisms underlying the arteriovenous chloride shift." Physiological and Biochemical Zoology 76.5 (2003): 603-614.