Describe and interpret these blood gases:
History: 38-year-old woman post-PEA cardiac arrest, intubated and ventilated. History of major depression and alcoholic liver disease.
Venous blood gas on arrival to the ED:
| pH 7.33 | Na 116 mmol/L |
| pCO2 30 mmHg | K 2.3 mmol/L |
| pO2 308 mmHg (FiO2 1.0) | Ca 0.88 mmol/L |
| HCO3 16 mmol/L | Cl 61 mmol/L |
| Albumin 26 g/L | Glucose 9.0 mmol/L |
| Hb 104 g/L | Lactate >20 mmol/L |
[expand title=”Interpretation”]
What is the pH?
7.33 = acidaemia
What is the primary process?
HCO3 16 = primary metabolic acidosis
Is there compensation?
Expected pCO2 = 1.5 x HCO3 + 8 ± 2
= 1.5 x 16 + 8 ± 2
= 30 – 34
Therefore there is maximal respiratory compensation.
Are there other clues to diagnosis?
Anion gap = Na – (HCO3 + Cl)
= 116 – (16 + 61)
= 39
Correct anion gap = calculated anion gap + (normal albumin – measured albumin)/4
= 39 + (40 – 26)/4
= 42.5
Therefore there is an elevated anion gap and thus a high anion gap metabolic acidosis.
Delta gap = (Anion gap – 12) ÷ (24 – HCO3)
= (42.5 – 12) ÷ (24 – 16)
= 3.8
This suggests a coexisting metabolic alkalosis, OR a pre-existing compensated respiratory acidosis.
Strong ion difference: Na – Cl
= 55
This is consistent with a metabolic alkalosis.
Expected PAO2 = (713 x FiO2) – (pCO2 x 1.25)
= (713 x 1.0) – (30 x 1.25)
= 675.5
A-a gradient = PAO2 – PaO2
= 675.5 – 308
= 367.5
Expected A-a gradient = age/4 + 4 = 13.5, therefore there is a large A-a gradient.
Electrolyte clues:
Sodium, potassium, calcium, and chloride are all markedly low. Lactate is markedly elevated.
Formulation:
Description: There is primary metabolic acidosis with maximal respiratory compensation. The anion gap is markedly elevated and thus there is an anion gap metabolic acidosis. The delta gap of 3.8 suggests a coexisting metabolic alkalosis. There is a large A-a gradient. There is marked hyponatraemia, hypokalaemia, hypocalaemia, and hypochloraemia. There is a significantly elevated serum lactate, mild anaemia, hypoalbuminaemia, and normoglycaemia.
Interpretation:
The anion gap metabolic acidosis is most likely the result of the significantly elevated lactate resulting from end-organ hypoperfusion secondary to the PEA cardiac arrest due to severe hypokalaemia. Sepsis, alcohol/toxic alcohol ingestion and other poisonings (e.g. metformin, salicylate) should also be considered. Possible causes of the metabolic alkalosis include severe hypovolaemia/volume contraction, pseudohyperaldosteronism secondary to excessive liquorice ingestion, diuretic abuse/overuse, secondary hyperaldosteronism from hepatic failure, vomiting, antacid abuse, and renal bicarbonate retention secondary to chronic hypochloraemia/hypokalaemia. The elevated A-a gradient is likely the result of atelectasis or aspiration following the PEA arrest resulting in a V/Q mismatch. Other causes of an elevated A-a gradient include a diffusion defect (rare), right-to-left shunt (intrapulmonary or cardiac), or increased O2 extraction (CaO2-CvO2). The marked electrolyte disturbances suggest either renal or GI losses. The hypoalbuminaemia may be secondary to inadequate oral intake/poor nutrition, liver disease, or a combination of both.
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Arterial blood gas several hours later despite potassium replacement at 10 mmol/h:
| pH 7.55 | Na 120 mmol/L |
| pCO2 43 mmHg | K 1.4 mmol/L |
| pO2 100 mmHg (FiO2 0.3) | Ca 0.88 mmol/L |
| HCO3 38 mmol/L | Cl 80 mmol/L |
| Albumin 26 g/L | Glucose 8.5 mmol/L |
| Hb 105 g/L | Lactate 1.9 mmol/L |
[expand title=”Interpretation”]
What is the pH?
7.55 = alkalaemia
What is the primary process?
HCO3 38 = primary metabolic alkalosis
Is there compensation?
Expected pCO2 = 0.7 x HCO3 + 20 ± 5
= 0.7 x 38 + 20 ± 5
= 41.6 – 51.6
NB: patient is mechanically ventilated at this point and the ICU were reluctant to hypoventilate a patient post-cardiac arrest.
Are there other clues to diagnosis?
Strong Ion Different = Na – Cl
= 120 – 80
= 40
This is consistent with a metabolic alkalosis.
Expected PAO2 = (713 x FiO2) – (pCO2 x 1.25)
= (713 x 0.3) – (43 x 1.25)
= 160
A-a gradient = PAO2 – PaO2
= 160 – 100
= 60
Expected A-a gradient = age/4 + 4 = 13.5, therefore, although reduced from before, there remains an elevated A-a gradient.
Electrolyte clues:
Sodium, potassium, calcium, and chloride all remain markedly low. The lactate has normalised.
Formulation:
Description: There is primary metabolic alkalosis (potential causes as described above). The A-a gradient remains slightly elevated. Serum electrolytes all remain low with normalisation of the lactate.
Interpretation: Lactate clearance post-resuscitation has resulted in resolution of the anion-gap metabolic acidosis revealing the underlying primary metabolic alkalosis. Severe and worsening hypokalaemia despite potassium replacement at 10 mmol/h suggests ongoing potassium losses, either renal or extra-renal/gastrointestinal.
Additional Information: A measured urinary sodium of 112 mmol/L and a urinary potassium of 14 mmol/L suggested inappropriate renal electrolyte wasting. A collateral history from the patient’s husband revealed that he had found multiple empty containers of Coloxyl/Senna, and empty packets of frusemide at the patient’s home. The patient has a long history of eating disorders, chronic alcohol abuse, and chronic ibuprofen/codeine addiction. The persisting elevated A-a gradient may be secondary to pulmonary aspiration/collapse/atelectasis following her resuscitation from PEA-arrest.
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