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)

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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 due to alveolar hypoventilation, also in the context of asthma with gas trapping
  • 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 HCO3-  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.