Page 100 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Effects of Acidosis and Alkalosis
–
It is through changes in breathing and renal also bound to HCO 3 , the concentration of free
functions that the body tries to compensate Ca 2+ falls more in metabolic than in respiratory
for abnormalities of acid–base metabolism, alkalosis. Effects, especially of respiratory al-
thus to keep blood pH constant. Changes in kalosis (hypocapnia), include among others
–
pH as well as HCO 3 and CO 2 concentrations raised neuromuscular excitability with cramps,
in blood, when acid–base balance is abnormal, in part due to reduced plasma Ca 2+ concentra-
and how they are compensated can be demon- tion, but is in the first instance the result of
–
strated in graphs. HCO 3 concentration, for ex- constriction of the cerebral vessels and thus
Acid–Base Balance or the logarithm of P CO 2 is plotted as a function losis can inhibit neuromuscular excitability by
(→ A, left)
hypoperfusion of the brain. Intracellular alka-
ample, is plotted as a function of P CO 2
+
of pH (→ A, right; Siggaard-Andersen nomo-
activating the K channels. Hypocapnia also
gram: gray lines = CO 2 equilibration lines).
stimulates contraction of the bronchial muscu-
lature and thus increases airway resistance. Al-
These graphs illustrate the following abnor-
kalosis inhibits gluconeogenesis and promotes
malities and mechanisms for compensating
glycolysis so that hypoglycemia and lactacide-
them:
Respiration, ! Respiratory alkalosis (→ A1) is compensat- mia may occur. Finally, intracellular alkalosis
–
favors cell division.
ed by decreased reabsorption of HCO 3 in the
kidneys.
The effects of respiratory and metabolic
! Metabolic alkalosis (→ A2) can theoretically
acidosis (→ B, red arrows) are largely similar.
–
+
through depolarization they also lose K . In ad-
need to take up sufficient O 2 sets narrow limits
4 be compensated by hypoventilation. But the In extracellular acidosis the cells lose HCO 3 ;
+
+
to this form of compensation. dition, acidosis inhibits Na /K -ATPase. Hyper-
! Respiratory acidosis (→ A4) is compensated kalemia develops (→ p.124). On the other
+
by increased renal excretion of acids (or hand, acidosis stimulates Na /H + exchange.
+
–
through forming HCO 3 ). The increased plas- The result is not only Na uptake but also cell
–
–
ma HCO 3 results in more HCO 3 being filtered swelling.
at the glomeruli. The kidney must therefore Furthermore, intracellular acidosis inhibits
+
continually reabsorb an increased amount of K channels and has a negative inotropic effect
–
–
filtered HCO 3 if renal loss of HCO 3 is to be as well as (by blocking the intercellular con-
avoided. nections) a negative dromotropic effect on the
! Metabolic acidosis (→ A3) can be compen- cardiac muscle (→ B, right). Hypercapnia in-
duces vasodilation (fall in blood pressure, rise
sated by respiratory reduction in plasma CO 2
concentration. However, the lower the plasma in intracerebral pressure) and relaxation of the
CO 2 concentration the less CO 2 is given off with bronchial musculature. Intracellular acidosis
each breath. Thus, in order to exhale the par- inhibits the pacemaker enzymes of glycolysis
ticular amount of CO 2 , hyperventilation must and hyperglycemia occurs. Prolonged acidosis
–
be maintained until the plasma HCO 3 concen- promotes demineralization of bone (→ B, right),
tration is again normal, either through raised because alkaline bone salts are dissolved by
+
renal excretion of acid or through the break- acids (→ p.132). In intracellular acidosis H is
down of organic acids (→ p. 86). taken up by the mitochondria in exchange for
+
+
The effect of alkalosis is usually hypokale- Ca . H also inhibits adenylylcyclase and thus
–
mia, because the cells release less HCO 3 , de- impairs hormonal effects. Finally, cellular
+
+
polarize less, and thus lose less K . If H is re- acidosis inhibits cell division and favors apo-
+
+
moved from the cell by Na /H exchange, Na + ptotic cell death.
gains access to the cell, but is again pumped
out of the cell in exchange for K + (→ B).
In addition, more Ca 2+ is bound to plasma
proteins in alkalosis (→ B, right). As a result,
90 there is a fall in the concentration of ionized
Ca 2+ in plasma. As part of Ca 2+ in plasma is
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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