ANALYTIC TOOLS USED IN ACID-BASE CHEMISTRY
Textbooks and clinical practice have tended to overestimate the
importance of isolated changes in hydrogen or bicarbonate ion concentration. An
emerging body of evidence suggests that the clinical significance of acid-base perturbations
is determined by the underlying cause rather than the serum concentration of hydrogen
and hydroxyl ions. Nevertheless, acid-base chemistry remains a mainstay of clinical
data interpretation because of ubiquitous availability, low cost, and universal acceptance.
The accuracy of acid-base measurements, however, is not determined by the blood
gas value alone, which measures volatile acid and pH. Rather, measurement of each
of the strong and weak ions that influence water dissociation, although cumbersome,
is essential.
Acid-base abnormalities are best described by alterations in PCO2
,
SID, and ATOT
. Unfortunately, many approaches used to teach and describe
the acid-base status of a patient fail to adequately explain many commonly seen perioperative
acid-base abnormalities (e.g., dilutional or hyperchloremic acidosis) and mislead
us about the cause of the problem (i.e., dilutional acidosis is caused by reduced
SID, not dilution of bicarbonate). Although it is important to consider historically
used approaches, modern approaches to acid-base interrogation focus on physical chemistry
to calculate the magnitude of the disturbance in the SID or recalculate the base
deficit or excess (BDE)
using the SID and ATOT
. We next consider some of the tools that have
evolved over the past 50 years to assist in interpretation of acid-base conundrums.
None is entirely accurate, and each has a dedicated group of followers.[23]
We deal with each of these approaches chronologically and discuss the merits and
demerits.
Carbon Dioxide-Bicarbonate (Boston) Approach
Schwartz, Brackett, and others,[21A]
[21B]
at Tufts University in Boston, developed
an
approach to acid-base chemistry using acid-base maps and the mathematical relationship
between carbon dioxide tension and serum bicarbonate (or total CO2
), derived
from the Henderson-Hasselbalch equation, to predict the nature of acid-base disturbances
(see Table 41-2
). A number
of patients with known acid-base disturbances at steady states of compensation were
evaluated. The degree of compensation from what was considered normal was measured
for each disease state. The investigators were able to describe six primary states
of acid-base imbalance using linear equations or maps relating hydrogen ion concentration
to PCO2
for respiratory disturbances and
PCO2
to HCO3
-
concentration
for metabolic disturbances ( Fig. 41-2
).
For any given acid-base disturbance, an expected HCO3
-
concentration
was determined. For most simple disturbances, this is a reasonable approach.
Using these maps and equations, physicians have been able to determine
the nature of most respiratory and metabolic acid-base disturbances. Although there
is a mathematical relationship in place, alterations in H+
and HCO3
-
do not reflect cause and effect. For example, chronic hypoventilation is associated
with an increase in
Figure 41-2
Acid-base nomogram using the Boston approach. Different
acid-base disturbances can be distinguished based on the relative values of PCO2
and HCO3
-
. (Adapted from Brenner BM, Rector FC: The
Kidney, 3rd ed. Philadelphia, WB Saunders, 1986, p 473.)
PCO2
and HCO3
-
.
Many physicians have incorrectly assigned the increase in HCO3
-
as compensation for raised PCO2
. It is
not. The increased HCO3
-
concentration reflects increased
total CO2
in the body. Alterations in HCO3
-
reflect
its role as a buffer, CO2
by-product, and weak acid.
Although the PCO2
-HCO3
-
approach is relatively accurate for most disturbances, there are several inherent
pitfalls, particularly in relation to the metabolic component. First, the approach
is not as simple as it seems, requiring the clinician to refer to confusing maps
or to learn formulas and perform mental arithmetic. Second, the system neither explains
nor accounts for many of the complex acid-base abnormalities seen in perioperative
and critically ill patients, such as those with acute acidosis in the setting of
hypoalbuminemia, hyperchloremic acidosis, or dilutional acidosis or with lactic acidosis
in the setting of chronic respiratory acidosis.