200
U N I T 2
Integrative Body Functions
ventilation, metabolic alkalosis may develop due to a
rapid drop in PCO
2
, while serum HCO
3
–
, which must be
eliminated through the kidney, remains elevated.
Maintenance of Metabolic Alkalosis.
Maintenance
of metabolic alkalosis resides within the kidney and its
inability to rid the body of the excess HCO
3
–
. Many of
the conditions that accompany the development of met-
abolic alkalosis, such as contraction of the ECF volume,
hypochloremia, and hypokalemia, also increase reab-
sorption of HCO
3
–
by the kidney, thereby contributing
to its maintenance.
Manifestations.
Metabolic alkalosis is characterized by
a serum pH above 7.45, serum HCO
3
–
above 29 mEq/L
(29 mmol/L), and base excess above 3.0 mEq/L
(3 mmol/L). Persons with metabolic alkalosis often
are asymptomatic or have signs related to ECF volume
depletion or hypokalemia. The manifestations of meta-
bolic alkalosis are summarized in Table 8-10.
Neurologic signs and symptoms (e.g., hyperexcitabil-
ity) occur less frequently with metabolic alkalosis than
with other acid–base disorders because HCO
3
–
enters
the cerebrospinal fluid (CSF) more slowly than CO
2
.
When neurologic manifestations do occur, as in acute
and severe metabolic alkalosis, they include mental
confusion, hyperactive reflexes, tetany, and carpopedal
spasm. Metabolic alkalosis also leads to a compensatory
hypoventilation with development of various degrees of
hypoxemia and respiratory acidosis. Significant mor-
bidity occurs with severe metabolic alkalosis, including
respiratory failure, arrhythmias, seizures, and coma.
Treatment.
The treatment of metabolic alkalosis usu-
ally is directed toward correcting the cause of the condi-
tion. A chloride deficit requires correction. Potassium
chloride usually is the treatment of choice when there
is an accompanying potassium deficit. When potassium
chloride is used as a therapy, the Cl
–
anion replaces the
HCO
3
–
anion and the K
+
corrects the potassium deficit,
allowing the kidneys to retain H
+
while eliminating K
+
.
Fluid replacement is used in the treatment of volume
contraction alkalosis.
Respiratory Acidosis
Respiratory acidosis represents a decrease in pH caused
by an elevation in arterial PCO
2
, usually due to con-
ditions that impair alveolar ventilation. It can present
as an acute or chronic condition, and can occur as the
result of decreased ventilatory drive, lung disease, or
disorders of the chest wall or respiratory muscles.
72,73
Less commonly, it results from excess CO
2
production.
Acute Disorders ofVentilation.
Acute respiratory fail-
ure is associated with a rapid rise in arterial PCO
2
along
with a minimal increase in serum HCO
3
–
and a large
decrease in pH. It can be caused by impaired function
of the respiratory center in the medulla (as in narcotic
overdose), lung disease, chest injury, weakness of the
respiratory muscles, or airway obstruction. Almost all
persons with acute respiratory acidosis become hypox-
emic when breathing room air. In many cases, signs of
hypoxemia develop prior to those of respiratory acido-
sis because CO
2
diffuses across the alveolar capillary
membrane 20 times more rapidly than oxygen.
2,4
Chronic Disorders of Ventilation.
Chronic respiratory
acidosis is characterized by a sustained increase in arterial
PCO
2
, resulting in renal adaptation with a more marked
increase in serum HCO
3
–
and a lesser decrease in pH.
72,73
It is a relatively common disturbance in persons with
chronic obstructive pulmonary disease (COPD). In these
persons, the persistent elevation of PCO
2
stimulates renal
H
+
secretion and HCO
3
–
reabsorption. The effectiveness
of these compensatory mechanisms can often return the
pH to near-normal values as long as oxygen levels are
maintained within a range that does not unduly suppress
chemoreceptor control of respirations.
An acute episode of respiratory acidosis can develop
in persons with chronic lung disease who receive oxy-
gen therapy at a flow rate that raises their PO
2
to a level
that produces a decrease in ventilation (see Chapter
23). In these persons, the medullary respiratory center
has adapted to the elevated levels of CO
2
and no longer
Vomiting
Decreased GFR
Cl - depletion
K
+
depletion
Renin release
Aldosterone
secretion
HCO
3
-
reabsorption
HCO
3
-
reabsorption
Alkalosis
HCO
3
-
filtration
HCO
3
-
reabsorption
Extracellular fluid depletion
FIGURE 8-19.
Renal mechanisms for bicarbonate (HCO
3
–
)
reabsorption and maintenance of metabolic alkalosis following
depletion of extracellular fluid volume, chloride (Cl
–
), and
potassium (K
+
) due to vomiting. GFR, glomerular filtration rate.
