# Blood Gas #18

Describe and interpret this arterial blood gas:

History: A 50-year-old man with systemic sclerosis and altered bowel habit presents with dyspnoea and hypotension.

 pH 7.18 Na 141 mmol/L pCO2 48 mmHg K 1.5 mmol/L pO2 74.7 mmHg (FiO2 0.8) Cl 110 mmol/L HCO3 17.3 mmol/L Glucose 7.7 mmol/L Lactate 4.3 mmol/L

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What is the pH?

7.18 = acidaemia

What is the primary process?

pCO2 = 48 mmHg = primary respiratory acidosis

Is there compensation?

Expected HCO3 = 24 + (pCO2 – 40)/10

= 24 + 0.8

= 24.8

Measured HCO3 = 17.3 mmol/L, therefore there is a coexisting primary metabolic acidosis.

Are there other clues to diagnosis?

Anion gap = Na – (HCO3 + Cl)

= 141 – (17.3 + 110)

= 13.7

Therefore this is a non-anion gap metabolic acidosis.

Delta gap = (Anion gap – 12) ÷ (24 – HCO3)

= (13.7 – 12) ÷ (24 – 17.3)

= 0.25

This is consistent with a pure NAGMA.

Strong Ion Difference (SID) = Na – Cl

= 141 – 110

= 31

This is consistent with a NAGMA.

Expected PAO2 = (713 x FiO2) – (pCO2 x 1.25)

= (713 x 0.8) – (48 x 1.25)

= 570.4 – 60

= 510.4

A-a gradient = PAO2 – PaO2

= 510.4 – 74.7

= 435.7

Normal A-a gradient = Age/4 + 4

= 50/4 + 4

= 16.5

Therefore there is a significantly elevated A-a gradient with relative hypoxia.

Electrolyte clues:

There is an elevated lactate, normoglycaemia, hyperchloraemia, and severe hyperkalaemia.

Description: This arterial blood gas shows an an acidaemia due to coexisting primary respiratory and non-anion gap metabolic acidoses. There is a markedly elevated A-a gradient with significant hypoxia. There is hyperlactataemia, normoglycaemia, hyperchloraemia, and severe hyperkalaemia.

Interpretation: In the clinical context, the  non-anion gap metabolic acidosis may be due to diarrhoea resulting in potassium and bicarbonate loss. The non-anion gap metabolic acidosis may also be the result of chronic adrenal insufficiency in the context of long-term steroids for systemic sclerosis. This would be especially true in the context of hypotension that is unresponsive to intravenous fluid replacement and/or vasopressors. Type 1 renal tubular acidosis could also result in this biochemical picture. In addition there is hypoxaemic and hypercarbic respiratory failure with an elevated A-a gradient and significant hypoxia suggesting an additional primary lung pathology which may have contributed to  a decompensation of chronic disease process. The hyperlactataemia suggests inadequate end-organ perfusion and oxygenation from hypotension and/or sepsis. Management should include judicious fluid resuscitation with commencement of inopressor therapy as required to maintain a mean arterial pressure ≥ 65 mmHg, intravenous antibiotic treatment of suspected underlying infection ± sepsis, intravenous potassium replacement, and consideration of intravenous steroid therapy if suspected adrenal insufficiency.

Additional information: Patient had chronic diarrhoea for 2-3 months and acute decompensation due to severe aspiration pneumonia.

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