This is a suggested pattern for the interpretation of ABGs, as presented in T.J. Morgan's chapter for Oh's Manual (Chapter 92, "Acid base balance and disorders"). This method of interpretation should probably be used to answer all those ABG-related CICM Fellowship SAQs. The original version of this sequence on page 943 (7th ed.); a summary is available in one of the Required Reading chapters.

The Diagnostic Sequence uses the Socratic method, asking a series of simple-sounding questions to arrive to a new level of understanding. These questions are as follows:

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. They are presented in Table 92.3 on page 943 of Oh's Manual. That table looks similar to (but is  sufficiently distinct from) the derivative table presented below:

Primary Acid Base Disorders
pH PaCO2 Primary Process
<7.35 <35 Metabolic acidosis
<7.35 35-45 Respiratory acidosis, metabolic acidosis
<7.35 >45 Respiratory acidosis
7.35-7.45 <35 Chronic respiratory alkalosis;
OR: respiratory alkalosis, metabolic acidosis 
7.35-7.45 35-45 Normal acid-base balance.
7.35-7.45 >45 Chronic respiratory acidosis;
OR: respiratory acidosis, metabolic alkalosis
>7.45 <35 Respiratory alkalosis
>7.45 35-45 Respiratory alkalosis, metabolic alkalosis
>7.45 >45 Metabolic alkalosis

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 acceptable. The College recognises the equivalent validity of each approach. T.J. Morgan's chapter from the Manual trends more towards the Copenhagen school, using SBE to determine

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. It is unclear as to what utility this stratification has. To describe a patient as "severe metabolic acidosis" over the phone communicates the acid-base situation less descriptively than if one were to simply report an SBE value of -22.

What is the Anion Gap?

The favoured anion gap format is the Ag(c), corrected for albumin. The candidate is invited to calculate it according to the conventional equation:

Ag(c)=  [Na+ + K+] - [Cl- +HCO3-

...where the "normal" baseline value is altered by 1 for every 4g/L change in albumin.

Is the increase in Anion Gap accompanied by a reduction in SBE or HCO3-?

This appears to be the equivalent of the delta ratio, or at least the delta gap.

The College asserts that any increase in anion gap should be matched by a decrease in SBE or bicarbonate, mole for mole. Any deviation from this 1:1 ratio is to be viewed as a mixed disorder. The college seems not to care whether the actual bicarbonate or the standard base excess are used; but one might think that the SBE is the better option. Consider that the SBE is a thought experiment where the body fluid is titrated. The calculation of delta gaps and ratios is essentially the same: the body fluids are being titrated with some sort of acid.

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 memorise.

Affording all possible respect to the Manual, instead of illegally reproducing Box 92.1 on my webpage, instead I will direct the gentle reader to another (lesser) box from the metabolic acid-base disorders chapter 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:

PANDA RUSH

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