Question 4.1

Last updated 28/08/2021 - 00:46
 Topic: Acid-Base Disorders
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The following results were obtained from a 32-year-old female admitted with severe asthma.

Parameter Patient Value

Adult Normal Range
FiO2 0.4  
pH 6.92* 7.35 – 7.45
PO2 81 mmHg (10.8 kPa)  
PCO2 71.0 mmHg (9.5 kPa) *

35.0 – 45.0 (4.6 – 6.0)  
SpO2 95%  
Bicarbonate 14.0 mmol/L* 22.0 – 26.0
Base Excess -16.0 mmol/L* -2.0 – +2.0
Lactate 9.0 mmol/L* 0.5 – 1.6
Sodium 139 mmol/L 135 – 145
Potassium 4.2 mmol/L 3.5 – 5.0
Chloride 108 mmol/L* 95 – 105
Glucose 19.2 mmol/L* 3.5 – 6.0

a) Describe the abnormalities and give a potential reason for each.    (40% marks)

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College answer

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Discussion

Let's go through this ABG in some detail.

  • The oxygenation is impaired. The A-a gradient is elevated: the expected alveolar O2 is (713 × 0.4) - (71  / 0.8) = 196.45, which means the gradients is 115 mmHg. In the context of severe asthma, where oxygenation usually  should not be the main issue, this could represent the development of massive amounts of physiological dead space due to hyperinflation. This patient probably needs a bit of intravascular filling.
  • There is acidaemia. Boy, is there acidaemia.
  • There is a metabolic acidosis. SBE is -16.
  • The CO2 is unhelpfully high, ~81. If this elevation is completely acute, which it should be, the raised CO2 should have increased the bicarbonate by about 4.1 (1.0 mmol/L for every 10 mmHg increase in CO2 above 40). The bicarbonate should be 28.1. But it is 16. Ergo, there is a metabolic acidosis. But you already knew that from looking at the base excess.  To look at things from the other direction, the expected CO2 would be 24 by the SBE method, or (1.5×14)+8 = 29 using the Boston rules. Either way, the CO2 of 81 is preposterously high, and so there is a combined respiratory and metabolic acidosis. The explanation for the raised CO2 is obviously asthma with severe bronchospasm, poor CO2 clearance because of impaired expiratory airflow, and increased dead space due to dynamic hyperinflation.
  • The anion gap is slightly elevated (139-108-14 = 17).
  • The delta ratio is therefore (17-12)/(24-14) = 0.5, i.e. this is mostly a normal anion gap metabolic acidosis. The chloride of 108 suggests here has been some saline resuscitation.
  • The lactate is raised, which is an expected consequence of salbutamol therapy. 
  • Thus, in summary, the metabolic acidosis is partly the consequence of hyperlactatemia and partly the result of hyperchloraemia.
  • The glucose is raised, which is also an expected consequence of salbutamol therapy. Moreover, the massive CO2 excess is a potent sympathetic stimulus, which would result in systemic catecholamine release.

References

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