Before allowing the gentle reader to proceed, I should mention that specifically for the CICM trainees there is in fact an Official Blood Gas Diagnostic Sequence, promoted by Oh's Manual. This sequence is the nearest thing to a gold standard for blood gas interpretation and should probably be used to answer all those ABG-related CICM Fellowship SAQs.
If one is specifically fixated on acid-base balance, one can skip steps 1 and 9.
Use the Alveolar Gas Equation, or just look at the a/A ratio.
PAO2 = (FiO2 × 713) - (PaCO2 × 1.25);
a/A ratio = PaO2 / PAO2 (An a/A over 75% is normal).
Acidaemia or alkalaemia? .. Or none?
Is the pCO2 contributing to the change in pH, or is the pCO2 reacting to it?
This is the respiratory component of the acid-base disorder
Is the SBE (or ABE) positive or negative? This is the metabolic component of the acid-base disorder.
Apply the bedside rules to assess the degree of compensation:
Copenhagen interpretation:
The "0.4" and "0.6" rules, using the Standard Base Excess.
Boston interpretation:
the "1-4-2-5" and "1.5+8 or 0.7 + 20" rules, using the actual bicarbonate value.
Calculate the anion gap: AG = (Na+ + K+) - (Cl- + HCO3-)
Calculate the delta ratio: (change in anion gap) / (change in bicarbonate)
The osmolar gap equation: OG = (measured osmolality) - ( 2 × Na+) + Urea + Glucose
Urinary anion gap = (Na+ + K+) - Cl-
Positive UAG: renal causes of NAGMA, eg. RTA
Normal or negative UAG: gastrointestinal causes of NAGMA
p50: is the shift of the oxyhaemoglobin curve in the appropriate direction, i.e. what you expect from the other variables on this blood gas? If not, look at the concentration of the dyshaemoglobins
p50(st): this shift is exclusively an assessment of 2,3-DPG concentration.
Use the Alveolar Gas Equation:
PAO2 = (FiO2 × 713) - (PaCO2 × 1.25)
The A-a gradient is a pretty crude index. Either the machine has calculated the a/A ratio and Fshunt, or you have do some of it yourself.
Thus:
Acidaemia or alkalaemia? It is ok for this value to be normal. Chronic respiratory acidosis may be completely compensated, with a normal pH.
Is the pCO2 contributing to the change in pH, or is the pCO2 reacting to it?
Is the SBE positive or negative? The base excess indicates the metabolic component of the acid-base disorder, because it is measured at a standardised pCO2 (40mmHg).
By this stage one has probably decided whether the disorder is primarily metabolic or respiratory.
Now is the time to apply the bedside rules to assess the degree of compensation, to establish how much of the disorder is metabolic and how much is respiratory.
Copenhagen interpretation:
Boston interpretation:
Respiratory disturbance: the 1-4-2-5 rules
The numbers describe the change in HCO3 in response to a 10mHg change in PaCO2
Metabolic disturbance: 1.5 plus 8 and 0.7 plus 20.
If a metabolic acidosis is present, it is time to figure out how much of the metabolic component is due to unmeasured anions. At this point one calculates the anion gap (adjusting the normal value for albumin) and the delta ratio.
If a normal anion gap metabolic acidosis is present, its time to figure out whether the renal chloride excretion is adequate, or whether the kidneys are contributing to the problem by producing a renal tubular acidosis. One accomplishes this by calculating the urinary anion gap: (Na+ + K+) - Cl-
A low urinary anion gap implies that appropriate acidification of the urine is occurring.
A high (or positive) urinary anion gap suggests that there is a renal acidification defect.
Obviously, this step extents beyond the "ABG analysis" part of this system, unless you funnelled the patient's urine through the analyser (incidentally, a phone call to Radimeter has revealed that this would void the warranty unless you have bought the appropriate module).
Look at the p50(st) and the p50. Calculate the difference between the two.
Are these variables where they are expected to be, according to the other parameters? e.g. if the patient is acidotic, is the p50 appropriately increased?