The Kidneys and Regulation of Water and Inorganic Ions
521
Classifi cation of Acidosis
and Alkalosis
To repeat, acidosis refers to any situation in which the hydro-
gen ion concentration of arterial plasma is elevated whereas
alkalosis denotes a reduction. All such situations fi t into two
distinct categories (
Table 14–8
): (1)
respiratory acidosis
or
alkalosis;
(2)
metabolic acidosis
or
alkalosis
.
As its name implies, respiratory acidosis results from
altered alveolar ventilation. Respiratory acidosis occurs when
the respiratory system fails to eliminate carbon dioxide as fast
as it is produced. Respiratory alkalosis occurs when the respi-
ratory system eliminates carbon dioxide faster than it is pro-
duced. As described earlier, the imbalance of arterial hydrogen
ion concentrations in such cases is completely explainable in
terms of mass action. Thus, the hallmark of a respiratory aci-
dosis is an elevation in both arterial
P
CO
2
and hydrogen ion
concentration, whereas that of respiratory alkalosis is a reduc-
tion in both.
Metabolic acidosis or alkalosis includes all situations
other than those in which the primary problem is respiratory.
Some common causes of metabolic acidosis are excessive pro-
duction of lactic acid (during severe exercise or hypoxia) or of
ketone bodies (in uncontrolled diabetes mellitus or fasting, as
described in Chapter 16). Metabolic acidosis can also result
from excessive loss of bicarbonate, as in diarrhea. Another
cause of metabolic alkalosis is persistent vomiting, with its
associated loss of hydrogen ions as HCl from the stomach.
What is the arterial
P
CO
2
in metabolic acidosis or alka-
losis? By defi nition, metabolic acidosis and alkalosis must be
due to something other than excess retention or loss of carbon
dioxide, so you might have predicted that arterial
P
CO
2
would
Table 14–7
Renal Responses to Acidosis
and Alkalosis
Responses to Acidosis
1. Suffi cient hydrogen ions are secreted to reabsorb all the
fi ltered bicarbonate.
2. Still more hydrogen ions are secreted, and this contributes
new bicarbonate to the plasma as these hydrogen ions are
excreted bound to nonbicarbonate urinary buffers such as
HPO
4
2–
.
3. Tubular glutamine metabolism and ammonium excretion
are enhanced, which also contributes new bicarbonate to the
plasma.
Net result:
More new bicarbonate ions than usual are added
to the blood, and plasma bicarbonate is increased,
thereby compensating for the acidosis. The urine is
highly acidic (lowest attainable pH = 4.4).
Responses to Alkalosis
1. Rate of hydrogen ion secretion is inadequate to reabsorb
all the fi ltered bicarbonate, so signifi cant amounts of
bicarbonate are excreted in the urine, and there is little or
no excretion of hydrogen ions on nonbicarbonate urinary
buffers.
2. Tubular glutamine metabolism and ammonium excretion
are decreased so that little or no new bicarbonate is
contributed to the plasma from this source.
Net result:
Plasma bicarbonate concentration is decreased,
thereby compensating for the alkalosis. The urine
is alkaline (pH > 7.4).
Table 14–8
Changes in the Arterial Concentrations of Hydrogen Ions, Bicarbonate, and Carbon Dioxide
in Acid-Base Disorders
Primary Disorder
H
+
HCO
3
CO
2
Cause of HCO
3
Change
Cause of CO
2
Change
Respiratory acidosis
↑↑↑
ÿ
Ÿ
Renal compensation
ÿ
Ÿ
Primary abnormality
Respiratory alkalosis
↓↓↓
Metabolic acidosis
↑↓↓
ÿ
Ÿ
Primary abnormality
ÿ
Ÿ
Refl ex ventilatory compensation
Metabolic alkalosis
↓↑↑
Table 14–8
physiological
inquiry
A patient has an arterial
P
O
2
of 50 mmHg, an arterial
P
CO
2
of 60 mmHg, and an arterial pH of 7.36. Classify the acid-base disturbance and
hypothesize a cause.
Answer can be found at end of chapter.
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