For blood gas interpretation, there is an official "Diagnostic Sequence" available in Oh's Manual. It is presented in T.J. Morgan's chapter for Oh's Manual (Chapter 92, "Acid base balance and disorders"); an owner of the Manual may find it on page 943 of the 7th edition. One expects that the college examiners, being the authors of the Manual, expect their exam candidates to use this ritualised approach. Therefore, one deviates from it at their peril. However some people may find it possible, or perhaps even desirable, to modify this Diagnostic Sequence. 

Below, the reader is first offered a brief summary of the canonic CICM approach. Then the author shamelessly presents his own heretical variant thereof, posing it as a valid alternative.

The Official Diagnostic Sequence

What is the primary process?
The candidate is invited to figure out whether there is only one primary disorder, or whether there are two, or none at all. This is done by looking at the pH and pCO2, and deciding whether they make sense together. The College recognizes nine possible combinations of pH and pCO2.

Is there compensation?
The candidate is asked to determine whether there is compensation for the primary disorder. Recommendations are:

  • Assess respiratory compensation according to the CO2
  • Assess metabolic compensation according to the SBE

Is the compensation adequate?
Morgan directs us to assess the adequacy of compensation by using the "Bedside Rules".  Either the Boston rules or the SBE-based Copenhagen rules are probably acceptable. The College recognises the equivalent validity of each approach. The reader is reminded that though chronic acid-base disorders may compensate the pH fully, this will never happen in acute respiratory disorders, or in metabolic acid-base disorders.

If a metabolic acidosis/alkalosis is present, how severe is it?
The candidate is asked to stratify the severity of the acid-base disturbance according to the magnitude of the SBE derangement. The specific numbers are 4, 10 and 14 (or -4, -10 and -14) corresponding to mild, moderate and severe categories.

What is the Anion Gap?
In Oh's Manual, the favoured anion gap format is the Ag(c), corrected for albumin. The candidate is invited to calculate it according to the conventional equation, where 

Is the increase in Anion Gap accompanied by a reduction in SBE or HCO3-?
This appears to be the equivalent of the delta ratio. The College asserts that any increase in anion gap should be matched by a decrease in SBE or bicarbonate, mole for mole. Therefore any deviation from this rule is to be viewed as a mixed disorder.

What is the cause of the increased Anion Gap?
The candidate is invited to consider the osmolal gap as a means of discriminating between different causes of high anion gap metabolic acidosis. The College directs us to Box 92.1 which lists the various causes of metabolic acidosis, and which the Fellowship Candidate should probably commit to memory.

Affording all possible respect to the holy Manual, instead of illegally reproducing Box 92.1 on my website, I will direct the gentle reader to another (lesser) box from the metabolic acidosis  and metabolic alkalosis chapters in the "Required Reading" exam summary section.

To simplify revision, this box is reproduced below:

Causes of Metabolic Acid-Base Disorders

Metabolic Acidosis

Metabolic Alkalosis

High anion gap metabolic acidosis:

Normal anion gap metabolic acidosis:


Chloride depletion

  • Gastric losses by vomiting or drainage
  • Diuretics: loop or thiazides
  • Diarrhoea
  • Posthypercapneic state
  • Dietary chloride deprivation
  • Gastrocystoplasty
  • Cystic fibrosis (loss due to high sweat chloride content)

Bicarbonate excess (real or apparent)

  • Iatrogenic alkalinisation
  • Recovery from starvation
  • Hypoalbuminemia

Potassium depletion

  • Primary hyperaldosteronism
  • Mineralocorticoid oversupplementation
  • Licorice (glycyrrhizic acid)
  • β-lactam antibiotics
  • Liddle syndrome
  • Severe hypertension
  • Bartter and Gitelman syndromes
  • Laxative abuse
  • Clay ingestion

Calcium excess

  • Hypercalcemia of malignancy
  • Milk-alkali syndrome

The Unofficial Systematic Approach to ABG interpretation

One of the disadvantages of the official system is its failure to somehow incorporate the interpretation of oxygen carriage. To be sure, it is a "acid-base interpretation" system, but too frequently the college asks the candidate to comment on the abnormalities  in the presented gas sample, and it would be amiss not to comment on the grossly abnormal oxygenation. Furthermore, issues of osmolality and urinary electrolytes are often raised, which call for additional optional steps. At risk of further complicating an already over-complex process, the author's thoughts on this issue are offered in the form of a systematic approach to ABG interpretation. In the discussion sections of the past paper SAQs, this approach has been followed.

A further note on the anion gap and delta ratio. In July 2019, Jeremy Cohen (the CICM Chair of the Second Part Exam) issued a decree via the official college newsletter, stating that

"unless otherwise specified in the question stem, anion gap calculations should be made without inclusion of potassium or correction to albumin."

Furthermore, judging from the college answers, The One True Gap value is  12, at least for the purposes of calculating the delta ratio in CICM SAQs. Logically, it would follow that if one insisted on continuing to use potassium in the equations, the normal value would be 16 or so. These values are consistent across early CICM literature, most notably seen in Data Interpretation in Critical Care Medicine which was written by the former college president and a group of similarly rockstar-level ICU celebrities.  Because the Chair's statement is definitive, all debate regarding which formula to use and what normal values to accept is meaningless to the Fellowship exam candidate, and has been accordingly demoted to the Part One resource section.

Step 1: The A-a gradient: use the Alveolar Gas Equation:

PAO2 = (FiO2 x 713) - (PaCO2 x 1.25)

  • Normal = 10mmHg; +1mmHg for every decade of life

PaO2/FiO2 ratios in ARDS:

  • 300-200 = "mild" ARDS, ~ 27% mortality
  • 200-100 = "moderate" ARDS ~32% mortality
  • under 100 = "Severe" ARDS, ~ 45% mortality

2) The change in pH: acidaemia or alkalaemia?

3) The change in pCO2: is the pCO2 contributing to the change in pH, or is the pCO2 reacting to it?

4)The change in Standard Base Excess: metabolic acidosis or alkalosis?

5)The compensation:

  • HCO3- change with respiratory disorders:
    • 1mmol increase with acute respiratory acidosis
    • 4mmol increase with chronic respiratory acidosis
    • 2mmol decrease with acute respiratory alkalosis
    • 5mmol decrease with chronic respiratory alkalosis
  • CO2 change with metabolic disorders:
    • PaCO2 = (1.5 × HCO3) + 8 for metabolic acidosis
    • PaCO2 = (0.7 × HCO3) + 20 for metabolic alkalosis
  • Other formulae:
    • Metabolic acidosis: Change in PaCO2 = SBE (or 1.2 × SBE)
    • Metabolic alkalosis: Change in PaCO2 = 0.7 × SBE

6) The Anion Gap and delta ratio

  • Anion gap: (Na+ ) - (Cl- + HCO3-)
    • Normal value (12) drops by 1 for every 4g/L of albumin lost (counting from a normal albumin of 40)
  • Delta ratio= (change in anion gap) / (change in bicarbonate)

7) Osmolar gap for high anion gap metabolic acidosis

  • Osmolar gap= measured osmolality - (2× Na+ + glucose + urea)

8) Urinary anion gap for normal aniong gap metabolic acidosis

  • Urinary anion gap = (Na+ + K+) - Cl-
    • Low or negative UAG = appropriate acidification of the urine
    • High UAG = renal acidification defect.