The approach to evaluation of acid-base disorders used in this on-line text is known as the Boston approach. The researchers promoting this approach are from Boston. An alternative method of evaluation promoted by Astrup and Siggaard-Anderson from Copenhagen uses the ‘Base Excess’ approach. At times the differences between the two groups has stirred controversy (called the 'Great Trans-Atlantic Acid-Base Debate' by Bunker in 1965). Many of the differences between the two groups persist and it is important to have some understanding of the issues involved. The controversy has recently been stirred again by Severinghaus (1993) who favours the Copenhagen approach.
The basic idea is that we need a way to quantify the various acid-base disorders. This tells us the severity of the acid-base disturbance and this is important clinical information. We also need to determine whether the body's compensation for the acid-base disorder is appropriate. If not, this indicates the presence of a second acid-base disorder.
Acid-base disorders are classified as being of respiratory origin (primary change in pCO2) or of metabolic origin (primary change in fixed acids). Some basic questions to be answered by any approach are:
Respiratory disorders are quantified by the amount of change in pCO2 in the arterial blood. If the pCO2 is further away from its normal value, then a larger disorder is present. This seems simple enough as CO2 is the ‘respiratory acid’ and can be easily measured.
Metabolic disorders are quantified by the amount of excess fixed acids (the ‘metabolic acids’) present in the blood. If more fixed acids are present, then a disorder of larger magnitude is present. This is clear enough but in a particular metabolic disorder, we may not know what are the particular fixed acids that are causing the acidosis. Indeed there may be more than one type involved.
No. BUT we can estimate the total amount of excess fixed acid present indirectly.
The argument goes like this:
1. Buffering of fixed acids in the extracellular fluid is predominantly by bicarbonate.
2. One bicarbonate molecule will react with one H+ molecule produced by one molecule of fixed acid.
3. So [HCO3] will decrease by one molecule for every molecule of fixed acid present.
4. The total amount of excess fixed acids should therefore be equal to the amount by which the bicarbonate concentration drops from its usual value.
Conclusion: The magnitude of the metabolic disorder (in the ECF) can be quantified indirectly by the amount of change in the [HCO3]. This seems an improvement because now there is only one quantity to measure and also it is easy to 'measure' (Bicarbonate is not actually measured in a blood-gas machine but instead is calculated, using the Henderson-Hasselbalch equation, by substituting into this equation the measured values of pH & pCO2).
As stated above, the pCO2 and the [HCO3] are not independent of one another as the argument so far has tacitly assumed. An increase in pCO2 will cause an increase in [HCO3]. This occurs because of the Law of Mass Action in the following equation:
CO2 + H2O <=> H2CO3 <=> H+ + HCO3-
This is a problem because a change in respiratory acid is changing the baseline used for assessment of the metabolic disorder. What we need is some way of assessing the metabolic disorder that corrects or allows for this interaction between CO2 and HCO3.
Several pCO2-independent indices have been proposed as being suitable for this purpose:
Standard bicarbonate is the bicarbonate concentration of a sample when the pCO2 has been adjusted (or ‘standardised’) to 40 mmHg at a temperature of 37C. This would remove the influence of changes in pCO2 by seeing what the [HCO3] would be if the respiratory component was made the same for all measurements. The term was introduced by Jorgensen & Astrup in 1957 but is conceptually the same as the idea of a 'standard pH' (at pCO2 of 40mmHg & temperature of 37C) introduced by Henderson much earlier.
Buffer base is a measure of the concentration of all the buffers present in either plasma or blood.
Base Excess (BE) is a measure of how far Buffer Base has changed from its normal value & was introduced by Astrup and Siggaard-Andersen in 1958. BE in whole blood is independent of pCO2 in the sample when measured in the blood gas machine. BE is proposed as a measure of the magnitude of the metabolic disorder because it assesses all the extracellular buffers (in the blood sample) and is independent of pCO 2 (in vitro). Unfortunately, there are several problems with the use of BE in this way. For example:
If BE is calculated for a haemoglobin concentration of 30 or 50 g/l instead of the actual haemoglobin, the differences between in vitro and in vivo behaviour can be mostly eliminated (See Severinghaus, 1976). This lower [Hb] is considered to be the ‘effective [Hb]’ of the whole ECF (ie what the [Hb] would be if the haemoglobin was distributed throughout the whole ECF rather than just the intravascular compartment). This attempts to eliminate the error introduced by the incorrect assumption that the buffering of blood is the same as the buffering by the whole ECF.
The Radiometer range of blood gas machines are made in Copenhagen and are very successfully used worldwide. These machines provides a printout with the full family of 'derived' (or 'contrived', depending on your perspective) Copenhagen-type blood gas variables for those who are interested. Other brands of machine have usually followed this practice so they can survive in the competitive marketplace. This assists in the survival of the Copenhagen approach.
The alternative method of quantifying acid-base disorders has been developed by investigators from Boston (eg Schwartz & Relman). This ‘Boston approach’ is the method used so far in this book and the six bedside rules have been outlined in section 9.3
This approach is based on actual experimental work in humans (eg whole body titrations) rather than on blood samples in a machine.
These results are based on buffering and compensatory processes that affect the whole body rather than just the blood. Additionally, appropriate compensation for both acute and chronic disorders can be determined and corrected for when interpreting the blood gas results. The results are presented in a couple of different ways: as graphs with 90% confidence intervals, or as a set of calculation rules. This book uses the rules method because these can be easily committed to memory and can be easily used at the bedside when assessing patients with acid-base disorders.
This does not require the introduction of new terms like Base Excess and Buffer Base. The assessment of the magnitude of metabolic disturbances is based on a comparison of the ‘actual’ (ie measured) and the ‘expected’ values of [HCO3]. The determination of the ‘expected ‘ value (using clinical knowledge and the rules of section 9.3) incorporates the corrections necessary to adjust for the interaction between pCO2 and HCO3.
Within the traditional approach to acid-base analysis, the Boston 'bicarbonate method' is preferable to the Copenhagen 'base excess method' because:
Despite the above, it should be noted that the quantitative approach pioneered by Stewart may be a better approach. It has great strength in aiding understanding about what is going on but unfortunately it is difficult to use clinically. It is very limited in usefulness for routine clinical application and interpretation of blood-gas results. An introduction to this alternative approach is presented in Chapter 10.