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 |
[expand title=”Interpretation”]
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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