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


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.


DescriptionThere 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.


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.


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.


DescriptionThere 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.


Blood Gas #15
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