Page 98 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Development of Acidosis
–
The pH of blood is a function of the concentra- ! As the liver needs two HCO 3 ions when in-
+
–
tions of HCO 3 and CO 2 (→ p. 86). An acidosis corporating two molecules of NH 4 ; in the for-
(pH < 7.36) is caused by too high a concentra- mation of urea (→ p. 86), increased urea pro-
tion of CO 2 (hypercapnia, respiratory acidosis) duction can lead to acidosis. In this way the
–
or too low a concentration of HCO 3 (metabolic supply of NH 4 Cl can cause acidosis (→ A7).
acidosis) in blood. In certain circumstances the infusion of
Many primary or secondary diseases of the large amounts of NaCl solution can lead to an
–
respiratory system (→ p. 66–80) as well as ab- acidosis, because extracellular HCO 3 is “dilut-
Acid–Base Balance lead to respiratory acidosis (→ A3). This can extracellular space inhibits Na /H exchange
normal regulation of breathing (→ p. 82) can
ed” in this way. In addition, expansion of the
+
+
in the proximal tubules as a result of which
also be caused by inhibition of erythrocytic
+
carbonic anhydrase, because it slows the for-
not only Na absorption in the proximal tu-
–
–
+
in the lung and
bules but also H secretion and HCO 3 absorp-
mation of CO 2 from HCO 3
tion is impaired.
thus impairs the expiratory elimination of CO 2
from the lungs.
! Infusion of CaCl 2 results in the deposition of
There are several causes of metabolic aci-
Respiration, dosis: Ca 2+ in bone in the form of alkaline salts (cal-
+
cium phosphate, calcium carbonate). H ions,
formed when bicarbonate and phosphate dis-
! In hyperkalemia (→ A4) the chemical gradi-
sociate, can cause acidosis.
ent across the cell membrane is reduced. The
favors the development of acidosis (→ A2).
4 resulting depolarization diminishes the elec- – ! Mineralization of bone, even without CaCl 2 ,
trical driving force for the electrogenic HCO 3
transport out of the cell. It slows down the ef- ! Acidosis can also develop when there is in-
–
flux of HCO 3 in the proximal tubules via creased formation or decreased breakdown of
–
+
Na (HCO 3 ) 3 cotransport. The resulting intra- organic acids (→ A1). These acids are practi-
+
cellular alkalosis inhibits the luminal Na /H + cally fully dissociated at the blood pH, i.e., one
+
exchange and thus impairs H + secretion as H is formed per molecule of acid. Lactic acid is
–
well as HCO 3 production in the proximal tu- produced whenever the energy supply is pro-
bule cells. Ultimately these processes lead to vided from anaerobic glycolysis, for example,
(extracellular) acidosis. in O 2 deficiency (→ p. 84), circulatory failure
! Other causes of reduced renal excretion of (→ p. 224), severe physical exercise, fever
H + and HCO 3 – production are renal failure (→ p. 20ff.), or tumors (→ p.14ff.). The elimi-
(→ p.110ff.), transport defects in the renal nation of lactic acid by gluconeogenesis or de-
tubules (→ p. 96ff.), and hypoaldosteronism gradation is impaired in liver failure and some
(→ A5). (Normally aldosterone stimulates H + enzyme defects. Fatty acids, β-hydroxybutyric
secretion in the distal tubules; → p. 270). acid and acetoacetic acid accumulate in cer-
–
! PTH inhibits HCO 3 absorption in the proxi- tain enzyme defects but especially in in-
mal tubules; thus in hyperparathyroidism renal creased fat mobilization, for example, in star-
–
excretion of HCO 3 is raised. As PTH simulta- vation, diabetes mellitus (→ p. 286ff), and hy-
neously promotes the mobilization of alkaline perthyroidism.
minerals from bone (→ p.132), an acidosis ! A protein-rich diet promotes the develop-
only rarely results. Massive renal loss of ment of metabolic acidosis, because when
–
HCO 3 occurs if carbonic anhydrase is inhib- amino acids containing sulfur are broken
ited, because its activity is a precondition for down (methionine, cystine, cysteine), SO 4 2– +
– +
HCO 3 absorption in the proximal tubules. 2 H are generated; when lysine and arginine
+
! Loss of bicarbonate from the gut (→ A6) oc- are broken down H is produced (→ A8).
curs in vomiting of intestinal contents, diar- The extent of acidosis depends, among
rhea, or fistulas (open connections from the other factors, on the blood’s buffering capac-
gut or from excretory ducts of glands). Large ity.
88 amounts of alkaline pancreatic juice, for exam-
ple, can be lost from a pancreatic duct fistula.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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