Chapter 048. Acidosis and Alkalosis (Part 11) pdf

Chapter 048. Acidosis and
Alkalosis
(Part 11)

Alkali Administration
Chronic administration of alkali to individuals with normal renal function
rarely, if ever, causes alkalosis. However, in patients with coexistent
hemodynamic disturbances, alkalosis can develop because the normal capacity to
excrete HCO
3
–
may be exceeded or there may be enhanced reabsorption of HCO
3
–
.
Such patients include those who receive HCO
3
–
(PO or IV), acetate loads
(parenteral hyperalimentation solutions), citrate loads (transfusions), or antacids
plus cation-exchange resins (aluminum hydroxide and sodium polystyrene
sulfonate).
Metabolic Alkalosis Associated with ECFV Contraction, K
+
Depletion,
and Secondary Hyperreninemic Hyperaldosteronism
Gastrointestinal Origin
Gastrointestinal loss of H
+
from vomiting or gastric aspiration results in
retention of HCO

3
–
. The loss of fluid and NaCl in vomitus or nasogastric suction
results in contraction of the ECFV and an increase in the secretion of renin and
aldosterone. Volume contraction through a reduction in GFR results in an
enhanced capacity of the renal tubule to reabsorb HCO
3
–
. During active vomiting,
however, the filtered load of bicarbonate is acutely increased to the point that the
reabsorptive capacity of the proximal tubule for HCO
3
–
is exceeded. The excess
NaHCO
3
issuing out of the proximal tubule reaches the distal tubule, where H
+

secretion is enhanced by an aldosterone and the delivery of the poorly reabsorbed
anion, HCO
3
–
. Correction of the contracted ECFV with NaCl and repair of K
+

deficits corrects the acid-base disorder, and chloride deficiency.
Renal Origin
Diuretics
(See also Chap. 227) Drugs that induce chloruresis, such as thiazides and

loop diuretics (furosemide, bumetanide, torsemide, and ethacrynic acid), acutely
diminish the ECFV without altering the total body bicarbonate content. The serum
[HCO
3
–
] increases because the reduced ECFV "contracts" the [HCO
3
–
] in the
plasma (contraction alkalosis). The chronic administration of diuretics tends to
generate an alkalosis by increasing distal salt delivery, so that K
+
and H
+
secretion
are stimulated. The alkalosis is maintained by persistence of the contraction of the
ECFV, secondary hyperaldosteronism, K
+
deficiency, and the direct effect of the
diuretic (as long as diuretic administration continues). Repair of the alkalosis is
achieved by providing isotonic saline to correct the ECFV deficit.
Solute Losing Disorders: Bartter's Syndrome and Gitelman's
Syndrome
See Chap. 278.
Nonreabsorbable Anions and Magnesium Deficiency
Administration of large quantities of nonreabsorbable anions, such as
penicillin or carbenicillin, can enhance distal acidification and K
+
secretion by
increasing the transepithelial potential difference (lumen negative). Mg

2+

deficiency results in hypokalemic alkalosis by enhancing distal acidification
through stimulation of renin and hence aldosterone secretion.
Potassium Depletion
Chronic K
+
depletion may cause metabolic alkalosis by increasing urinary
acid excretion. Both NH
4
+
production and absorption are enhanced and HCO
3
–

reabsorption is stimulated. Chronic K
+
deficiency upregulates the renal H
+
, K
+
-
ATPase to increase K
+
absorption at the expense of enhanced H
+
secretion.
Alkalosis associated with severe K
+
depletion is resistant to salt administration,

but repair of the K
+
deficiency corrects the alkalosis.
After Treatment of Lactic Acidosis or Ketoacidosis
When an underlying stimulus for the generation of lactic acid or ketoacid is
removed rapidly, as with repair of circulatory insufficiency or with insulin
therapy, the lactate or ketones are metabolized to yield an equivalent amount of
HCO
3
–
. Other sources of new HCO
3
–
are additive with the original amount
generated by organic anion metabolism to create a surfeit of HCO
3
–
. Such sources
include (1) new HCO
3
–
added to the blood by the kidneys as a result of enhanced
acid excretion during the preexisting period of acidosis, and (2) alkali therapy
during the treatment phase of the acidosis. Acidosis-induced contraction of the
ECFV and K
+
deficiency act to sustain the alkalosis.
Posthypercapnia
Prolonged CO
2

retention with chronic respiratory acidosis enhances renal
HCO
3
–
absorption and the generation of new HCO
3
–
(increased net acid excretion).
If the Pa
CO2
is returned to normal, metabolic alkalosis results from the persistently
elevated [HCO
3
–
]. Alkalosis develops if the elevated Pa
CO2
is abruptly returned
toward normal by a change in mechanically controlled ventilation. Associated
ECFV contraction does not allow complete repair of the alkalosis by correction of
the Pa
CO2
alone, and alkalosis persists until Cl
–
supplementation is provided.