Question 11.2

A 64-year-old female patient is admitted to ICU following lung volume reduction surgery for bullous emphysematous lung disease. She is an ex-smoker with 40 pack year history, with a background history of hypertension and cor pulmonale. She was extubated post-procedure, prior to ICU admission. Her medications include amlodipine, frusemide, and bronchodilators. The following blood gas analysis was done on day 2 post-operative.

Parameter Patient Value Adult Normal Range
FiO2 0.25  
pH 7.40 7.35 – 7.45
pO2 57 mmHg (7.6 kPa)  
pCO2 64.0 mmHg (8.5 kPa)*    35.0 – 45.0 (4.6 – 6.0)
SpO2 88%  
Bicarbonate      39.0 mmol/L* 22.0 – 26.0
Base Excess 12.3 mmol/L* -2.0 – +2.0
Lactate 0.8 mmol/L 0.5 – 1.6
Sodium 134 mmol/L* 135 – 145
Potassium 4.4 mmol/L 3.5 – 5.0
Chloride 101 mmol/L 95 – 105
Glucose 7.7 mmol/L* 3.5 – 6.0

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College answer

Not available.

Discussion

Let us dissect these results systematically:

  1. The A-a gradient is slightly raised:
    PAO2 = (0.25 × 713) - (64× 1.25) = 98
    Thus, A-a = (98 - 57) = 41 mmHg.
  2. There is no acid-base disturbance. The pH is perfect.
  3. The PaCO2 is elevated.
  4. The SBE is 12.3, suggesting a metabolic alkalosis. The bicarbonate is 39.
  5. If we assume the primary disorder is metabolic alkalosis, then there is also a mild respiratory acidosis: the expected CO2 is 40+(0.7 × 12.3) = 48.6, or (0.7 × 39) + 20 = 47.3 mmHg. 
    If we assume that the hypercapnia is the primary disorder, then the expected bicarbonate would be (2.4 × 4) + 24, or 33.6. In other words, there would be a mild respiratory alkalosis.  
  6. This disturbance does not call for a calculation of the anion gap, but if you tried to calculate it, you'd find that it is negative (134-101-39 = -6). 

So. This is a double disorder, a metabolic alkalosis as well as a respiratory acidosis. This heavy smoker has just had some of her gas exchange surface removed, and is under the effects of opiates following surgery, which explains this underwhelming respiratory performance. The metabolic alkalosis could be explained by some degree of chronic renal adaptation to hypercapnia, as well as the effects of long-term frusemide therapy.

References