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CHAPTER TWENTY-ONE
Water, Electrolyte, and Acid-Base Balance
These acids may also combine with bicarbonate ions
in the urine. Excess bicarbonate ions are excreted, interfer-
ing with the function of the bicarbonate acid-base buffer
system.
Whatever the cause, metabolic acidosis shifts pH down-
ward. However, the following factors resist this shift: chemi-
cal buffer systems, which accept excess hydrogen ions; the
respiratory center, which increases breathing rate and depth;
and the kidneys, which excrete more hydrogen ions.
Alkalosis
Respiratory alkalosis develops as a result of
hyperventilation,
described in chapter 19 (p. 758). Hyperventilation is accom-
panied by too great a loss of carbon dioxide and consequent
decreases in carbonic acid and hydrogen ion concentrations
(f
g. 21.17)
.
Hyperventilation may happen during periods of anxiety.
It may also accompany fever or poisoning from salicylates,
such as aspirin. At high altitudes, hyperventilation may be
a response to low oxygen pressure. Also, musicians, such as
bass tuba players, who must provide a large volume of air
when playing sustained passages, sometimes hyperventilate.
In each case, rapid, deep breathing depletes carbon dioxide,
and the pH of body fl
uids increases.
Chemical buffers, such as hemoglobin, that release
hydrogen ions resist this pH change. Also, the lower levels of
carbon dioxide and hydrogen ions stimulate the respiratory
center to a lesser degree. This inhibits hyperventilation, thus
reducing further carbon dioxide loss. At the same time, the
kidneys decrease their secretion of hydrogen ions, and the
urine becomes alkaline as bases are excreted.
Chemical buffers, such as hemoglobin, may resist this shift
in pH. At the same time, increasing levels of carbon dioxide
and hydrogen ions stimulate the respiratory center, increas-
ing breathing rate and depth and thereby lowering carbon
dioxide levels. Also, the kidneys may begin to excrete more
hydrogen ions.
Eventually, thanks to these chemical and physiologi-
cal buffers, the pH of the body fl uids may return to normal.
When this happens, the acidosis is said to be
compensated
.
The symptoms of respiratory acidosis result from depres-
sion of central nervous system function and include drowsi-
ness, disorientation, and stupor. Evidence of respiratory
insufficiency, such as labored breathing and cyanosis, is
usually also evident. In
uncompensated acidosis,
the person
may become comatose and die.
Metabolic acidosis is due to either accumulation of non-
respiratory acids or loss of bases
(f
g. 21.16)
. Factors that
may lead to this condition include
1. Kidney disease that reduces glomerular ±
ltration and
fails to excrete the acids produced in metabolism
(uremic acidosis).
2. Prolonged vomiting that loses the alkaline contents of
the upper intestine and stomach contents. (Losing only
the stomach contents produces metabolic alkalosis.)
3. Prolonged diarrhea, in which excess alkaline intestinal
secretions are lost (especially in infants).
4. Diabetes mellitus, in which some fatty acids react to
produce ketone bodies, such as
acetoacetic acid, beta-
hydroxybutyric acid,
and
acetone.
Normally, these
molecules are scarce, and cells oxidize them as energy
sources. However, if fats are being used at an abnormally
high rate, as may occur in diabetes mellitus, ketone
bodies may accumulate faster than they can be oxidized,
and spill over into the urine (ketonuria); in addition,
the lungs may release acetone, which is volatile and
imparts a fruity odor to the breath. More seriously, the
accumulation of acetoacetic acid and beta-hydroxybutyric
acid may lower pH (ketonemic acidosis).
FIGURE 21.15
Some of the factors that lead to respiratory acidosis.
FIGURE 21.16
Some of the factors that lead to metabolic acidosis.
Accumulation of CO
2
Respiratory
acidosis
Decreased rate
and depth of
breathing
Obstruction of
air passages
Decreased
gas exchange
Accumulation of nonrespiratory acids
Metabolic acidosis
Excessive loss of bases
Kidney failure
to excrete acids
Excessive production of acidic
ketones as in diabetes mellitus
Prolonged diarrhea
with loss of alkaline
intestinal secretions
Prolonged vomiting
with loss of intestinal
secretions
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