# Question 8.1

a) A 74-year-old man with known ischaemic heart disease was admitted to hospital for treatment of worsening heart failure (day 1). Despite treatment for heart failure he failed to improve and was referred for urgent intensive care assessment on day 5.

 Parameter Measured value Normal range Day 1 Day 5 pH 7.52 7.06 7.35-7.45 PaCO2 45 (5.9) 109* (14.3*) 35-45 mmHg (4.6-6.0 kPa) PaO2 141(18.5) 86.2 (11.3) 80-100 mmHg (10.5-13.0 kPa) Oxygen Saturation 99.7 89.4 >95% HCO3 36.5* 29.5* 22-27 mmol/l Base Excess 12.6* -0.2 -2 to +2 mmol/L Hb 94* 112* 130-150 g/L Sodium 141 132* 135-145 mmol/l Potassium 4.2 5.2* 3.2-4.5 mmol/l Chloride 97* 92* 100-110 mmol/l Glucose 6.0 19.4* 3.0-6.0 mmol/l Lactate 1.8 6.8* < 2.0 mmol/l Creatinine 83 73 50-100 μmol/l

i. Describe the acid-base abnormality on the Day 1 blood gas and give a clinical explanation that most likely caused this picture

ii. Describe the acid-base abnormality on the Day 5 blood gas and give three possible clinical explanations

i.

• Chronic metabolic alkalosis with partial respiratory compensation
• Background of chronic metabolic alkalosis with partial respiratory compensation could be due to diuretic therapy for heart failure (“contraction alkalosis")

ii.

• Superimposed acute respiratory acidosis and metabolic acidosis (raised lactate)
• Concomitant metabolic alkalosis given that the acidosis is not severe for the degree of PCO2 and lactate + BE is normal for the lactate + AG is also normal.
• The acute superimposed pathology:
• Cardiogenic shock
• Sepsis
• Respiratory depression from opiate or illness
• PE

Any other reasonable cause

## Discussion

This is another one of those "analyse this ABG" questions.

So, lets.

In the first gas, the result that stands out is the high pH, with a relatively normal (or slightly elevated) pCO2 and with a raised bicarbonate. This makes one think of metabolic alkalosis. However, is it properly compensated?

For one the pH is 7.52, and the PCO2 seems too low by gut feel.

The compensation equation for metabolic alkalosis is 0.7 x [HCO3-] + 20; so the PCOin this case should be something like 40-50. (the equation gives us 45mmHg, and it allows +/- 5mmHg error). So, in actual fact the metabolic alkalosis is properly compensated, at least according to the commonly used bedside rules.

So, I suppose we can blame this on frusemide.

Now, for the day 5 gas.

The pH is low; there is acidaemia.

The pCO2 is raised; and it was not raised on day 1, so it is an acute hypercapnea.

If this were a purely respiratory disorder, we would expect the bicarbonate to increase by 1mmol/L for every 10mmHg increase in CO2. There is an increase of 69mmHg of CO2, which should give us a bicarbonate value of 31mmol/L or so.

However, the measured bicarbonate is 29.5, which means a metabolic acidosis is also in play.

The anion gap is (141) - (97 + 36) = 8, or 12.2 when calculated with potassium - essentially normal.

There is a lactate rise, which contributes to this tiny increase in the anion gap. We know there is also a metabolic alkalosis in the background.

Thus, this is a triple disorder, where a metabolic alkalosis maintained by frusemide has been upset by an acute respiratory acidosis and an acute lactic acidosis.

The college answer does not delve too deeply into this.

They ask us then, what could have caused such a rise in lactate and such hypercapnea in this cardiac patient?

"any reasonable cause" is what they want. One can argue that this old man might have developed cardiogenic shock and his hypercapnea is due to his having lost consciousness from low cardiac output; or might have developed an aspiration pneumonia (SaO2 is 89%). Or sepsis of some unknown origin.

Any reasonable cause.