A 46-year-o ld male presents with vomiting for the past five days.

His arterial blood gas result on room air is shown below:

Parameter

Patient Value

Adult Normal Range

pH

7.74*

7.35 -7.45

pCO2

48.5 mmHg (6.4 kPa)*

35.0 -45.0 (4.6 - 6.0)

pO2

80 mmHg (10.5 kPa)

80 - 100 (10.5 -13.0}

Bicarbonate

62 mmol/L*

20- 30

Base Excess

39.6 mmol/L*

-2.0 - +2.0

SpO2

97.6%

95.0 -98.0

Sodium

131 mmol/L*

135 - 145

Potassium

3.1 mmol/L*

3.5 - 5.0

Chloride

47 mmol/L*

95 - 105

Glucose

10.5 mmol/L*

3.5 - 6.0

Lactate

5.6 mmol/L*

< 2.0

Describe the acid-base derangements seen        (30% marks)

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College answer

  • Profound metabolic alkalosis with inadequate respiratory compensation
  • Lactic acidosis (raised anion gap)

Discussion

Let us dissect this systematically:

  1. The A-a gradient is about 10 (alveloar O2 is about 89 mmHg). There is no problem with gas exchange.
  2. There is severe alkalaemia
  3. The CO2 is appropriately elevated
  4. There is metabolic alkalosis; SBE is 39.6 mmol/L
  5. The compensation is probably inadequate, and the extreme example demonstrates the limitations of compensation. The expected CO2 by Boston rules is (62 × 0.7) + 20 = 63.4 mmHg; the SBE-based Copenhagen rules give us a number closer to 64 mmHg. Either way, the rules of compensation recommend a CO2 level which approaches the maximal possible level for compensation. With an alveolar CO2 of 64 on room air, the alveolar oxygen tension would be around 55-60 mmHg, which means hypoxia would drive the respiratory rate (alkalaemia being a relatively weak depressant of respiratory drive). 
    In any case, there is inadequate respiratory compensation.
  6. The potassium is low and the lactate is high, which is consistent with hypovolaemia. The patient is severely dehydrated and this has stimulated aldosterone secretion, worsening the alkalosis and promoting hypokalemia. 

References

References