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.
A basic system for ABG analysis
If one is specifically fixated on acid-base balance, one can skip steps 1 and 9.
1) Oxygenation
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).
2) The change in pH
Acidaemia or alkalaemia? .. Or none?
3) The change in pCO2
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
4) The change in Base Excess
Is the SBE (or ABE) positive or negative? This is the metabolic component of the acid-base disorder.
5) Assessment of compensation
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.
6) Assessment of the metabolic component of acidosis
Calculate the anion gap: AG = (Na+ + K+) - (Cl- + HCO3-)
- Normal value decreases by 1 for every 4g/L decrease in albumin, from a normal value of 40g/L.
- Use the actual bicarbonate value if the CO2 is very abnormal (i.e more than 20mmHg higher or lower than the normal range).
Calculate the delta ratio: (change in anion gap) / (change in bicarbonate)
- 0-0.4 = NAGMA;
- 0.4-0.8 = mixed;
- 0.8-2.0 = HAGMA;
- >2.0 = mixed metabolic alkalosis and acidosis
7)Assessment of the high anion gap metabolic acidosis - Osmolar gap
The osmolar gap equation: OG = (measured osmolality) - ( 2 × Na+) + Urea + Glucose
8) Assessment of the normal anion gap metabolic acidosis - Urinary anion gap
Urinary anion gap = (Na+ + K+) - Cl-
Positive UAG: renal causes of NAGMA, eg. RTA
Normal or negative UAG: gastrointestinal causes of NAGMA
9) Oxygen carrying capacity
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.
A slightly expanded system for ABG analysis
Assessment of tension-based and content-based oxygenation indices
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.
- The a/A ratio is just PaO2 divided by PAO2; it is not confused by FiO2 changes and is probably the most accurate tension-based index.
- An FShunt value is even more accurate; however one is rarely fortunate enough to have a mixed venous gas to calculate a proper arteriovenous cO2 difference.
- Typically, one ends up getting an FShunte value, which assumes a normal-ish arteriovenous cO2 difference. This is probably good enough for government work, unless there is good reason to suspect some sort os serious derangement of systemic oxygen extraction (eg. cyanide toxicity or severe uncontrolled shock).
Thus:
- A pO2(a/A) of over 75% is probably normal.
- Hypoxia with a normal pO2(a/A) suggests either alveolar hypoventilation is responsible (i.e. the PACO2 is high) or the atmospheric pressure is low.
- Hypoxia with a low a/A ratio can be any one of the following:
- V/Q mismatch, eg shunt - intrapulmonary or intracardiac
- Diffusion defect
- Increased oxygen extraction ratio
- Hypoxia with a high FShunt suggests a V/Q mismatch.
- Ideally, one would use a mixed venous sample to exclude increased oxygen extraction ratio as a possibility (i.e. a normal FShunt would suggest that the reason the arterial blood is hypoxic is the admixture of severely hypoxic venous blood via the shunt).
The change in pH
Acidaemia or alkalaemia? It is ok for this value to be normal. Chronic respiratory acidosis may be completely compensated, with a normal pH.
The change in pCO2
Is the pCO2 contributing to the change in pH, or is the pCO2 reacting to it?
The change in Standard Base Excess
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).
Assessment of compensation
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:
- For acute respiratory acid-base disturbances, the Copenhagen rules are useless (the standard bicarbonate and base excess values use a normalised CO2 value, and cannot be used to assess the efficacy of compensation). Acute variations in PaCO2 do not influence the SBE.
- For the rest, calculations can be performed, in which PaCO2 is measured in mmHg, and the change in SBE is measured from a baseline of either 2.0 or -2.0 mEq/L.
- For chronic acid-base disturbances, rise in PaCO2 = 0.4 × change in SBE
- For metabolic acidosis, rise in PaCO2 = 1.0 × change in SBE
- For metabolic alkalosis, fall in PaCO2 = 0.6 × change in SBE
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
- 1mmol increase with acute respiratory acidosis
- 4mmol increase with chronic respiratory acidosis
- 2mmol decrease with acute respiratory alkalosis
- 5mmol decrease with chronic respiratory alkalosis
Metabolic disturbance: 1.5 plus 8 and 0.7 plus 20.
- The 1.5 plus 8 rule: in metabolic acidosis, the multiplier for bicarbonate is 1.5, and 8mmHg is added
- the 0.7 plus 20 rule: in metabolic alkalosis, the multiplier for bicarbonate is 0.7, and 20mmHg is added.
Assessment of the metabolic component of acidosis
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.
Assessment of NAGMA using the urinary anion gap
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).
Optional step: Assessment of oxygen-haemoglobin dissociation mechanics
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?
- The p50(st) is abnormal in the presence of abnormal 2,3-DPG levels and in the presence of some dyshaemoglobins (eg. sulfahemoglobin or weird haemoglobin mutants) but not others (eg.methaemoglobin, foetal haemoglobin and carboxyhaemoglobin are excluded).
- A difference between the p50(st) and the p50 reflects the magnitude of Bohr's effect and temperature on the oxyhaemoglobin dissociation curve.
- Thus, in the presence of a normal p50(st) and an abnormal p50 one would conclude that the curve has shifted purely because of pH, pCO2 and T°.
- If the p50(st) and p50 are both abnormal, and approximately equal, one would conclude that the curve is shifted purely due to the effect of dyshaemoglobins and 2,3-DPG levels.