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)

[Click here to toggle visibility of the answers]

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.

  1. 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
  2. There is acidaemia.
  3. The PaCO2 is low, which is a move in the appropriate direction given the degree of acidaemia
  4. The SBE is -17, suggesting a metabolic acidosis.
  5. 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.
  6. 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