C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
195
controlling HCO
3
–
loss is the
chloride/bicarbonate
anion
exchange that occurs in association with Na
+
reabsorp-
tion. Chloride is absorbed along with Na
+
throughout
the tubules. In situations of volume depletion due to
vomiting and Cl
–
depletion, the kidney is forced to sub-
stitute HCO
3
–
for the Cl
–
anion, thereby increasing its
absorption of HCO
3
–
.
Both reabsorption of HCO
3
–
and excretion of acid
are accomplished through H
+
secretion as the urine fil-
trate moves through the tubular structure of the kidney.
The epithelial cells of the proximal tubule, the thick
ascending limb of Henle, and distal tubule all secrete H
+
nto the tubular fluid by the Na
+
/H
+
counter-transport
mechanism (see Chapter 24). The
potassium/hydrogen
exchange system in the collecting tubules functions in
H
+
secretion by substituting the reabsorption of K
+
for
excretion of H
+
Acidosis tends to increase H
+
elimi-
nation and decrease K
+
elimination, with a resultant
increase in serum potassium levels, whereas alkalosis
tends to decrease H
+
elimination and increase K
+
elimi-
nation, with a resultant decrease in serum potassium
levels.
64–66
Generation of New Bicarbonate.
Another impor-
tant but more complex buffer system that facilitates the
excretion of H
+
and generation of new HCO
3
–
is the
ammonia buffer system.
Renal tubular cells are able to
use the amino acid glutamine to synthesize ammonia
(NH
3
) and secrete it into the tubular fluid. Hydrogen
ions then combine with the NH
3
to form ammonium
ions (NH
4
+
). The NH
4
+
ions, in turn, combine with
Cl
–
ions that are present in the tubular fluid to form
ammonium chloride (NH
4
Cl), which is then excreted
in the urine. Under normal conditions, the amount of
H
+
ion eliminated by the ammonia buffer system is
about 50% of the acid excreted and new HCO
3
–
regen-
erated. However, with chronic acidosis, it can become
the dominant mechanism for H
+
excretion and new
HCO
3
–
generation.
Phosphate Buffer System.
Because extremely acidic
urine (pH 4.0 to 4.5) would be damaging to structures
in the urinary tract, the elimination of H
+
requires a buf-
fer system. There are two important intratubular buffer
systems: the phosphate buffer system and the previously
described ammonia buffer system. The
phosphate buf-
fer system
uses HPO
4
2–
and H
2
PO
4
–
that are present in
the tubular filtrate to buffer H
+
. Because HPO
4
2–
and
H
2
PO
4
–
are poorly absorbed, they become more concen-
trated as they move through the tubules.
LaboratoryTests
Laboratory tests that are used in assessing acid–base
balance include arterial blood gases and serum electro-
lytes, base excess or deficit, and anion gap. Although
useful in determining whether acidosis or alkalosis is
present, the pH measurements of the blood provide
little information about the cause of an acid–base
disorder.
Arterial blood gases
provide a means of assessing the
respiratory component of acid–base balance. H
2
CO
3
levels are determined from arterial PCO
2
levels and the
solubility coefficient for CO
2
(normal arterial PCO
2
is
38 to 42 mm Hg). Arterial blood gases are used because
venous blood gases
are highly variable, depending on
metabolic demands of the various tissues that empty
into the vein from where the sample is being drawn.
Laboratory tests are used to measure serum electro-
lytes, CO
2
content, and HCO
3
–
. These measurements are
determined by adding a strong acid to a blood sample
and measuring the amount of CO
2
that is produced.
More than 70% of the CO
2
in the blood is in the form of
bicarbonate. The serum bicarbonate is then determined
from the total CO
2
content of the blood.
Base excess
or
deficit
is a measure of the HCO
3
–
excess or deficit. It
describes the amount of a fixed acid or base that must
be added to a blood sample to achieve a pH of 7.4 (nor-
mal ± 2.0 mEq/L).
60
A base excess indicates metabolic
alkalosis, and a base deficit indicates metabolic acidosis.
The
anion gap
describes the difference between the
serum concentration of the major measured cation (Na
+
)
and the sum of the measured anions (Cl
–
and HCO
3
–
).
This difference represents the concentration of unmea-
sured anions, such as phosphates, sulfates, organic acids,
and proteins (Fig. 8-18). Normally, the anion gap ranges
between 8 and 12 mEq/L (a value of 16 mEq/L is normal
if both Na
+
and K
+
concentrations are used in the calcu-
lation). The anion gap is increased in conditions such as
lactic acidosis and ketoacidosis that result in a decrease
in HCO
3
, and it is normal in hyperchloremic acidosis,
where Cl
–
replaces the HCO
3
–
anion.
1
Disorders of Acid–Base Balance
The terms
acidosis
and
alkalosis
describe the clinical
conditions that arise as a result of changes in dissolved
CO
2
and HCO
3
–
concentrations.
64
There are two types
100
110
120
130
140
150
Normal
Acidosis
due to excess
organic acids
Acidosis
due to excess
chloride levels
mEq/L
Sodium 142 mEq/L
Sodium 142 mEq/L
Sodium 142 mEq/L
Chloride 103 mEq/L
Bicarbonate 27 mEq/L
Chloride 103 mEq/L
Bicarbonate 14 mEq/L
Chloride 116 mEq/L
Bicarbonate 14 mEq/L
Anion gap 25 mEq/L
Anion gap
12 mEq/L
Anion gap
12 mEq/L
FIGURE 8-18.
The anion gap in acidosis due to excess
metabolic acids and excess serum chloride levels. Unmeasured
anions such as phosphates, sulfates, and organic acids
increase the anion gap because they replace bicarbonate.This
assumes there is no change in sodium content.
