Question 23.1

A 70-year-old male presents to the ED with a 2-week history of increasing dyspnoea, cough with altered sputum and fever. Past history includes chronic obstructive airways disease (COPD), lung cancer seven years ago treated with chemotherapy and radiation therapy with no sign of recurrence since.

Examination findings included RR 30 breaths/min, BP 110/70mmHg, HR 145 bpm, Temp 37.4ºC, anxious and distress but tired and peripherally cold and cyanosed.

CXR shows findings consistent with COPD and right lower lobe infiltrate.

The following arterial blood gas is taken one hour after receiving 2 litres of fluid resuscitation, antibiotics and bi-level non-invasive ventilation (NIV), at FiO₂ = 1.0.

Parameter	Patient Value			Normal Adult Range
FiO₂	1.0
pH	7.16*	7.35		– 7.45
PCO₂	33 mmHg* (4.3 kPa)*	35	–	45 (4.6 – 6.0)
PO₂	272 mmHg (38.5 kPa)
Bicarbonate	11 mmol/L*	22	–	30
Base Excess	-17 mmol/L*	-3 – +3
Sodium	138 mmol/L	135 – 145
Potassium	4.3 mmol/L	3.5 – 5.0
Chloride	121 mmol/L*	95	–	110
Glucose	13.1 mmol/L*	3.5 – 7.8
Lactate	6.4 mmol/L*	0.6 – 2.4
Haemoglobin	131 g/L*	135 – 175
Creatinine	150 micromol/L*	70	–	120

a) Give your interpretation of the arterial blood gas and outline potential causes.

(40% marks)

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College Answer

a)
ABG:

Metabolic acidosis, normal anion gap however mixed cause (hyperchloremic predominant), high lactate and renal impairment.

Respiratory compensation but less than expected (superimposed respiratory acidosis). Impaired oxygenation with moderate shunt PaO2:FiO2 272 – A-a DO2 400.
Hyperglycemia (stress response).

Dx.

Type 1 respiratory impairment secondary to pneumonia on background of COAD.
Inadequate respiratory compensation due to fatigue and reduced respiratory reserve (COAD).
Metabolic acidosis due to:

Chloride excess - fluid resuscitation
Lactate elevation – sepsis plus inadequate cardiac output.
Renal impairment

Discussion

Let us dissect these results systematically.

The A-a gradient is high:
The alveolar oxygen tension is (1.0 × 713) - (33 × 1.25) = 671.75mmHg
Thus, the A-a gradient is 399.75.
This would be consistent with a large shunt, though as has been discussed elsewhere, A-a gradient is an oxygen tension-based measure and therefore cannot be used to make the diagnosis of shunt (only to discriminate hypoventilation from all other causes of hypoxia). With the history of
There is acidaemia.
The PaCO₂ is low, which is a move in the appropriate direction given the degree of acidaemia
The SBE is -17, suggesting a metabolic acidosis.
The respiratory compensation is inadequate, whichever side of the Atlantic debate you're on.
The expected PaCO₂ (11 × 1.5) + 8 = 24.5mmHg, and so there is also a respiratory acidosis according to the Boston rules.
According to the Copenhagen rules, the the expected PaCO₂= (40 - SBE) = 23mmHg.
The anion gap is (138) - (121 + 11) = 6, or 10.3 when calculated with potassium.
Later in this same SAQ we get the albumin level (in Question 23.2) and it is 27g/L. The expected anion gap is therefore 8.75. Thus, this is a pure normal anion gap metabolic acidosis, with barely any contribution from the lactate.

In summary:

Widened A-a gradient
Normal anion gap metabolic acidosis, with minimal respiratory compensation (thus, also a respiratory acidosis).
Hyperlactataemia
Hyperglycaemia
Renal impairment

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