Question 15.1

The following arterial blood gas and biochemistry results are from a patient with cardiac and respiratory disease and recent profuse vomiting.

Parameter

Patient

Reference

FiO2

0.4

pH

7.5*

7.35 – 7.45

PaO2

58.0 mmHg (7.6 kPa)

PaCO2

47 mmHg* (6.2 kPa*)    

35 – 45 (4.6 – 6.0)

HCO3

34.8 mmol/L*

22 – 27

Base Excess      

10.2 mmol/L*

-2.0 – +2.0

Sodium

137 mmol/L

135 – 145

Potassium

2.5 mmol/L*

3.5 – 5.0

Chloride

92 mmol/L*

95 – 105

a) Explain the acid-base status (1 marks)

b) List the potential causes of the acid-base abnormalities in this patient (3 marks)

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College comments

Syllabus topic/section: 2.1.5 Respiratory Intensive Care: Interpretation of arterial blood gases and 2.1.7 Renal Intensive Care: Blood gas analysis

Discussion: 

This section was relatively well answered with a metabolic alkalosis and incomplete respiratory compensation mostly recognised. Common causes of this clinical picture from volume contraction, diuretic therapy and vomiting were expected to be included for an at standard answer. Higher marks were achieved if candidates also recognised the specific causes associated with chronic cardiac and respiratory disease.

Interpretation

a) "cardiac and respiratory disease and recent profuse vomiting" already shouts "diuretics, steroids, hypovolemia and chloride loss in the gastric fluid" but let's be systematic before jumping to the obvious conclusions:

  • There is alkalaemia
  • The patient is hypoxic, which could be driving a respiratory alkalosis
  • The CO2, however, is elevated, which is completely reasonable if you have alkalaemia. 
  • The base excess and the biocarbonate are both given, which means you can pick your favourite rule of compensation and apply it. 
    The expected CO2 is therefore either (40 + 10.2 × 0.6) = 46 mmHg, or
    (0.7 × 34.8) + 20 = 44 mmHg.  In either case, this metabolic alkalosis is fairly well compensated (good enough for government work). 

b) With this exercise now behind us, we may safely conclude that the explanation is diuretics, steroids, hypovolemia and chloride loss in the gastric fluid. If one takes the stance that CO2of 44 is lower than expected, and this alkalosis is in fact incompletely compensated, then this can also be explained by the hypoxia, as it would be perfectly reasonable to have a higher respiratory rate in that context.

References

Khanna, Apurv, and Neil A. Kurtzman. "Metabolic alkalosis." studies 28 (2006): 29.