FOAMed question of the day 10 #FOAMedQOTD

Interpret the following blood gas and suggest a possible cause:

 pH 7.54

PCO2        12

PO2        31

HCO3–         10.5

ABG machine



  1. pH (7.54) – alkalaemia
    CO2 (12 !!)- primary respiratory alkalosis; however expected HCO3 = 24- 2x [(40-12)/10] = 24 – 2x[2.8 ] = 18.4 !!
    Therefore there is a co-existing primary metabolic acidosis !!
    Expected CO2 (for HCO3 of 10.5) = 1.5×10.5+8 = 23.75; supporting the co-existing respiratory alkalosis.

    This combination is classic for SALICYLATE poisoning !!

    However, I don’t know what to make of the pO2 of 31 (ie. is this venous or arterial) ?
    We don’t have an FiO2 to calculate the A-a gradient; but assuming room-air (at sea-level) there is a marked VQ mismatch.

    Alternatively; thinking outside the box – this could all be explained by an arterial sample taken from a patient/climber at very-high to extreme altitude …..

  2. Chris Cole (@DocOnSkis) says:

    Mixed picture.

    Resipratory alkalosis + metabolic acidosis + hypoxaemia.

    Assuming the blood hasn’t had anything weird done to it, or other oddness, I’m going to do with: Salicylate (aspirin) toxicity.

    I’d like to see the rest of the gas results, including a lactate, and know a little more about the patient.


  3. Chris Cole (@DocOnSkis) says:

    2nd guess: Really anxious person with a large PE…. :-)

  4. Chris Cole (@DocOnSkis) says:

    3rd and final guess: Patient is climbing Mt Everest… +/- too many aspirin… and might be anxious about it…

  5. Lucy Watt says:

    Resp alkalosis

  6. Vncristine says:


  7. Vincristine says:

    The PO2 falls at altitude, PCO2 falls with increased respiratory effort, the alkalosis created is corrected by excretion of bicarb in the kidney.

  8. 1. It’s not certain whether this is arterial or venous, but if it’s arterial, I’m running back to have another look at the patient and maybe tube / ventilate them.
    2. Assuming that it’s venous, the next question is: acute or chronic. There is a respiratory alkalosis. If this is acute, there is a cooexisting metabolic acidosis. If this is chronic, then the corrected bicarb of 21.7 is a touch on the low side, but would be hard to fully interpret.

    If this is venous, it’s hard to interpret that pO2, but it’s still quite low for blood taken from a major vein – perhaps there is also arterial hypoxaemia.

    For a single unifying diagnosis: acute mountain sickness, with maybe some acetazolamide use to explain the metabolic acidosis.

  9. Interesting gas, tricky to interpret without more clinical information. Assuming ABG, low pO2 raises possibility of VBG.

    pH 7.54 – moderate alkalaemia – low pCO2 & low HCO = primary respiratory alkalosis
    pCO2 – 12 – marked hypocarbia – near maximal hyperventilation
    PO2 – 31 – marked hypoxaemia – assuming ABG A-a gradient will be raised regardless of FiO2 (gradient >100 with FiO2 of 0.21)
    HCO – 10.5 – if acute respiratory alkalosis then expected HCO would be ~18 (10:2 rule) indicating associated metabolic acidosis, if chronic the HCO at expected level (10:5 rule).

    If acute resp alkalosis then associated metabolic acidosis and raised A-a gradient – multiple potential causes including central (raised ICP, SOL, CVA), toxicological esp salicylate, pulmonary (pneumonia, PE)
    If chronic resp alkalosis then casues include either longstanding CNS lesion, chronic airways disease

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