section
39.5
Acid-Base Balance
937
TABLE 39-1
Classification and Characteristics o f Simple Acid-Base Disorders
*
Primary Change
Compensatory Response
Expected Compensation
Metabolic
acidosis
IU H C O
3
-
iiP c o
2
P c o 2 = 1 . 5
(HCO
3
- ) +
8 ± 2.
Pco
2
falls by 1-1.3 mm Hg for each
mEq/L fall in HCO
3
- .
Last 2 digits of pH = Pco
2
(thus, if
PCo
2
= 28, pH = 7.28).
HCO
3
- +15 = last 2 digits of pH
(HC03- = 15, pH = 7.30).
Alkalosis
ÎÎÎH C O
3
-
TTPco
2
Pco
2
increases
6
mm Hg for each
10 mEq/L rise in HC03- .
HCO
3
- + 15 = last 2 digits of pH
(HCO
3
- = 35, pH = 7.50).
Respiratory
acidosis
Acute
TTTPco
2
ÎHCO
3
-
HCO
3
- increases by 1 mEq/L for each
1 0
mm Hg rise in Pco2-
Chronic
TTTPco
2
ÎÎH C O
3
-
HCO
3
- increases by 3.5 mEq/L for each
1 0
mm Hg rise in Pco2-
Alkalosis
Acute
ixUPco
2
|H C 0 3-
HCO
3
- falls by 2 mEq/L for each
1 0
mm Hg fall in Pco2-
Chronic
l i |P c o
2
U H CO
3
-
HCO
3
- falls by 5 mEq/L for each
1 0
mm Hg fall in Pco2-
T
= Increase;
l =
decrease.
*Reproduced, with permission, from R. G. Narins and L. B. Gardner: Simple acid-base disturbances.
M e d . C lin . N o r th A m .
65, 321 (1981).
muscles.
Renal compensation is slower but can be
maintained for an extended period because of induction
of glutaminase.
Treatment is by correction of the cause of the acidosis
(e.g., insulin administration in diabetic ketoacidosis)
and neutralization of the acid with NaHCC>
3
, sodium
lactate,
or
TRIS
[tris(hydroxymethyl)aminomethane]
buffer. Problems that may occur following alkali re-
placement therapy include development of respiratory
alkalosis, particularly if the low CO
2
tension persists, and
further decline in the pH of CSF, which may decrease
consciousness. The alkaline “overshoot” results from
resumption of oxidation of organic anions (e.g., lactate,
acetoacetate) with resultant production of bicarbonate
from CO
2
. Severe acidosis should be corrected slowly
over
several
hours.
Potassium
replacement
therapy
frequently is needed because of the shift of intracellular
K+ to extracellular fluid and loss of K+ in the urine.
Respiratory alkalosis
occurs when the respiratory
rate increases abnormally (hyperventilation), leading to
decrease in Pco
2
and rise in blood pH. Hyperventilation
occurs
in
hysteria,
pulmonary
irritation
(pulmonary
embolus), and head injury with damage to the respiratory
center.
The increase in blood pH is buffered by plasma HCO ,
and, to some extent, by exchange of plasma K+ for intra-
cellular H+. Renal compensation seldom occurs because
this type of alkalosis is usually transitory.
Metabolic alkalosis
is characterized by elevated plas-
ma HC0
3
level. It may result from administration of
excessive amounts of alkali (e.g., during NaHCC
>3
treat-
ment of peptic ulcer) or of acetate, citrate, lactate, and other
substrates that are oxidized to HCO
3
, and from vomiting,
which causes loss of H+ and Cl- .
In excessive loss of extracellular K+ from the kidneys,
cellular K+ diffuses out and is replaced by Na+ and H+
from the extracellular fluid. Since K+ and H+ are nor-
mally secreted by the distal tubule cells to balance Na+
uptake during Na+ reabsorption (see Figure 39-3), if ex-
tracellular K+ is depleted, more H+ is lost to permit reab-
sorption of the same amount of Na+. Loss of H+ by both
routes causes hypokalemic alkalosis. Excessive amounts
