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

 

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:

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.

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.


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

 

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:

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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