A patient recovering from a laparotomy was referred to ICU from recovery. She is a 72 year old lady with a background of CCF, who underwent a laparotomy and adhesiolysis in the context of a subacute small bowel obstruction.
Following the laparotomy, this lady was extubated and brought to recovery. There, the breathing was found to be shallow and rapid. The pulse oximeter trace was unreliable as the patient was very cool and clammy peripherally. There was a sustained failure to awaken; the lady became increasingly unresponsive, and central cyanosis developed. The anaesthetist decided to perform a blood gas. While waiting for the result (the machine was performing a two-point calibration) a rapid sequence induction and intubation were performed.
There is severe hypoxia. The FiO2 is estimated - the patient was on a non-rebreather reservoir mask at this stage, which delivers a fairly random FiO2, but 75% is a good ballpark guess.
There is a mild acidaemia; the pH is 7.295
The pCO2 is high, likely the origin of the acidosis.
Now, if we use the flawed "0.008" rule to estimate what the pH should be, we arrive at a pH value of 7.214. This is what the pH would look like if there was no protein buffering, and if the bicarbonate level did not change from the "ideal" value (remaining at 24mmol/L).
One could also calculate the "expected" pH from the Henderson-Hasselbalch equation, using a predicted bicarbonate level (using the "1 for 10" bedside rule). If the bicarbonate increases by 1mmol/L for every 10mmHg change in PaCO2, the pH should be 7.239. The measured pH is higher, making you think that some sort of metabolic alkalosis is also present.
The Actual Base Excess is normal, suggesting that there is very little contribution here from metabolic acid-base disturbance. It is actually trending towards the alkalotic range.
Copenhagen interpretation of acid-base compensation:
With this slightly alkalotic ABE, one predicts that there should be no change to PaCO2- i.e. it should be normal. Since the measured PaCO2 is high, there must be a respiratory acidosis.
Boston interpretation of acid-base compensation:
The expected bicarbonate for this scenario is 26.3mmol/L; the actual bicarbonate is slightly higher (29.8), and therefore there must be some sort of coexisting mild metabolic alkalosis.
Note that this ABG machine reports the actual bicarbonate rather than the standard bicarbonate, which saves the Boston supporter from having to calculate the actual bicarbonate themselves.
Let us imagine that this is a chronic metabolic alkalosis. Using the Boston bedside rules ("0.7 plus 20") we can estimate that if the bicarbonate is chronically 29.8, the CO2 should usually be around 40.9mmHg. Again, this confirms that a respiratory acidosis is present.
There is no p50(st) value available from this analyser, but the p50 is slightly raised. This right shift can be accounted for by the acidosis and hypercapnea, given that the dyshaemoglobin levels are within the expected range.
This patient has an acute respiratory acidosis due to the residual effects of anaesthesia, and probably also due to hypoventilation associated with post-operative abdominal pain. The hypoxia is probably due to shunting through atelectatic regions of lung. There is an underlying (very mild) metabolic alkalosis due to chronic diuretic use - the patient's CCF has been treated with regular frusemide.