Question 20.3

The following arterial blood gas result was obtained from a 65-year-old lady with exacerbation of chronic obstructive pulmonary disease (COPD), day 7 in ICU following intubation and ventilation for respiratory failure.

Parameter	Patient Value		Normal Adult Range
FiO₂	0.3
pH	7.48*	7.35		– 7.45
PCO₂	42 mmHg (5.5 kPa)	35	–	45 (4.6 – 6.0)
PO₂	104 mmHg (13.7 kPa)
Total haemoglobin	122 g/L	115 – 165
SpO₂	98%	95	–	100
Base Excess	7.0 mmol/L*	-3.0 – +3.0
Bicarbonate	31 mmol/L	22	–	32

a) Interpret the arterial blood gas. (10% marks)

b) Give four possible reasons for the acid-base disturbance seen. (10% marks)

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College Answer

Metabolic alkalosis

Raised A-a gradient

Diuretics

Steroids

NG losses

Post hypercapnia

Discussion

A systematic approach to this problem would resemble the following:

The A-a gradient is high:
The alveolar oxygen tension is (0.3 × 713) - (42 × 1.25) = 161.4
thus the A-a gradient is 57.4
There is alkalaemia.
The PaCO₂ is on the high end of normal, which is a move in the appropriate direction given the presence of alkalaemia
The SBE is 7.0 mmol/L, suggesting a mild metabolic alkalosis
If the SBE was not available, the bicarbonate of 31 would have been enough to call this a metabolic alkalosis
The respiratory compensation is adequate.
According to the Boston rules, the expected PaCO₂ is (31 × 0.7) + 20 = 41.7mmHg, and so there is totally appropriate respiratory compensation.
With the Copenhagen rules, we can expect a PaCO₂of 44.2mmHg, which is close enough.
The anion gap cannot be calculated, and it is in any case irrelevant.

In summary:

Raised A-a gradient
Metabolic alkalosis

Why would this be? One may refer to the list of causes for metabolic alkalosis. In a ventilated COPD patient with a normal-looking PaCO₂ one could very easily point the blame at a posthypercapneic state.In fact, that is the only thing you can conclude from the bare minimum history the college has given. However, the question asks for four possible reasons. The college model answer offers diuretics, steroids and NG losses as potential contributors. Because of how little history is given, rhese differentials are at least as likely as the use of β-lactam antibiotics, Liddle's syndrome or clay ingestion.

References

Banga, Amit, and G. C. Khilnani. "Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay." COPD: Journal of Chronic Obstructive Pulmonary Disease 6.6 (2009): 437-440.

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