The ED staff were struggling to intubate an elderly gentleman with hypoxic respiratory failure. This man is a 75 year old non-smoker who has had a NSTEMI at home after an elective laparoscopic cholecystectomy, and went on to develop acute pulmonary oedema which brought him to hospital.

Background is that of rheumatoid arthritis with decreased jaw opening, and C-spine fusion surgery which significantly limits neck extension. The first attempt at intubation did not go as planned; direct laryngoscopy proved fruitless and though the curved-blade videolaryngoscope revealed a nice-looking Grade 1 view, the bougie ended up poking uselessly into every recess other than the larynx, and the whole thing was abandoned after the saturation probe fell off.

With the suxamethonium wearing off, 50mg of rocuronium were administered, and bag-mask ventilation was recommenced. To restore morale, the pulse oximeter was reattached to the cold clammy finger - but the waveform was of poor quality, and the numbers it generated were scoffed at as being depressing and unrealistic ("50% sats? Pull the other one"). It can't be that low, they said; the patient wouldn't have such a vigorous pulse, they would be peri-arrest! After insistent demands from bystanders, an ABG was collected to debunk this theory. Shortly after the arterial sample was collected, the rhythm collapsed into broad complex bradycardia and asystole.

Then the gas came back.

Data to be interpreteted

Data to be interpreteted



Discussion and Interpretation

Assessment of tension-based and content-based oxygenation indices

Alveolar oxygen 519.25
A-a gradient 484.25
a/A ratio 0.07
PaO2/FiO2 ratio 35

The patient is profoundly hypoxic. The probe was right!

The change in pH

There is a profound acidaemia; the pH is 6.956.

The change in pCO2

The pCO2 is ridiculously high, suggesting that the patient has been without much alveolar ventilation for some time. Using the Henderson equation, the pH expected at this PaCO2 level should be around 6.979 which is very close to the measured pH.

The change in Base Excess

The respiratory acid-base disturbance here is so profound that it can be used to illustrate the dangers of using the Copenhagen standard bicarbonate value with the Boston compensation rules. The Boston rules demand an actual bicarbonate value, and if one is not aware that the ABG machine reports the corrected "standard" value, one can end up with some ridiculous conclusions. A rambling digression along this issue is presented in the chapter which compares the Boston and Copenhagen methods of acid-base assessment, using this ABG as an example.

Copenhagen interpretation of acid-base compensation:

The Actual Base Excess is slightly negative, but still within the normal acceptable limits. On this basis, one would be forced to conclude that this patient's acidaemia is caused primarily by a respiratory acidosis with a minor contribution from a metabolic acidosis.

Boston interpretation of acid-base compensation:

The calculated actual bicarbonate is 33.4mmol/L, which is slightly lower than the 35.5mmol/L expected from the "1 for 10" rule. Again, this suggests that the patient's acid-base disturbance is mainly respiratory, and that a metabolic acidosis is playing a minor supportive role.


Assessment of the metabolic component of acidosis

There isn't much of an acid base disturbance here, but let us analyse it anyway. The chapter dedicated to the anion gap also uses this blood gas example to illustrate one's options in choosing a bicarbonate value to calculate the aforementioned gap. In summary, one should use the actual bicarbonate rather than the standard bicarbonate. Using a bicarbonate value of 33.4mmol/L, one ends up with an anion gap of around 9.3, which is close enough to the expected AG (9.5, for an albumin of 30) to call this a normal anion gap metabolic acidosis.

Assessment of oxygen-hemoglobin dissociation mechanics

The p50 is significantly right-shifted, which makes sense given the profound hypercapnea and acidosis. This is Bohr effect taken to a ridiculous extreme. As the corrected p50(st) demonstrates, the pH and CO2 are responsible for this shift. In the absence of this respiratory acid-base disturbance, there would be a mild left shift, suggesting that the red cells have adjusted their 2,3-DPG content to compensate for a degree of chronic acidosis.


Brackett Jr, Newton C., Jordan J. Cohen, and William B. Schwartz. "Carbon dioxide titration curve of normal man: Effect of increasing degrees of acute hypercapnia on acid-base equilibrium." New England Journal of Medicine 272.1 (1965): 6-12.