Page 155 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Acidosis and Alkalosis Nonrespiratory (Metabolic) Acid–Base
Disturbances
The main objective of acid–base regulation is Nonrespiratory acidosis is most commonly
to keep the pH of blood, and thus of the body, caused by (1) renal failure or isolated renal
+
constant. The normal ranges for parameters tubular H secretion defect resulting in inabil-
+
relevant to acid–base homeostasis, as ity to eliminate normal quantities of H ions
measured in plasma (arterialized capillary (renal acidosis); (2) hyperkalemia (! p. 180);
blood) are listed in the table (see table on (3) increased !-hydroxybutyric acid and ace-
–
p. 124 for erythrocyte P CO 2 and [HCO 3 ] values). toacetic acid production (diabetes mellitus,
starvation); (4) increased anaerobic conver-
Normal range of acid–base parameters in plasma
–
sion of glucose to lactic acid (! lactate + H ),
+
Women Men e.g., due to strenuous physical work (! p. 74) or
hypoxia; (5) increased metabolic production
Acid–Base Homeostasis P CO 2 (kPa) 38.9 ! 2.3 41.0 ! 2.3 take of dietary proteins; and (6) loss of HCO 3 –
39.8 ! 1.4
+
[H ] (nmol/L)
40.7 ! 1.4
of HCl and H 2SO 4 in individuals with a high in-
7.40 ! 0.015
7.39 ! 0.015
pH
5.47 ! 0.3
5.07 ! 0.3
through renal excretion (proximal renal tubu-
(mmHg)
lar acidosis, use of carbonic anhydrase inhibi-
! 2.5
! 2.5
24
24
[HCO 3 ]
–
tors) or diarrhea.
(mmol/L)
Buffering (! A1) of excess hydrogen ions
occurs in the first stage of non-respiratory
Acid–base homeostasis exists when the fol-
–
gained). Two-thirds and one-third of the buff-
+
1. (H addition or production) – (HCO 3 addi-
6 lowing balances are maintained: – acidosis (every HCO 3 lost results in an H +
ering is achieved by HCO 3 and non-bicar-
–
+ –
–
tion or production) = (H excretion) – (HCO 3 bonate buffer bases (NBB ), respectively, and
excretion) ! 60 mmol/day (diet-depend- the CO 2 arising from HCO 3 buffering is elimi-
–
ent). nated from the body by the lungs (open sys-
2. (CO 2 production) = (CO 2 excretion) tem; ! p. 140). The standard bicarbonate con-
! 15 000–20 000 mmol/day. centration [HCO 3 ] St, the actual bicarbonate
–
H production (HCl, H 2SO 4, lactic acid, H 3PO 4, concentration [HCO 3 ] Act and the buffer base
+
–
etc.) and adequate renal H + excretion concentration [BB] decrease (negative base
(! p. 174ff.) are the main factors that influence excess; ! p. 146).
the first balance. A vegetarian diet can lead to a Respiratory compensation of non-respira-
–
considerable addition of HCO 3 (metabolism: tory acidosis (! A2) occurs in the second
–
OH + CO 2 ! HCO 3 ; ! p. 138). HCO 3 is ex- stage. The total ventilation rises in response to
–
–
creted in the urine to compensate for the the reduced pH levels (via central chemosen-
added supply (the urine of vegetarians there- sors), leading to a decrease in the alveolar and
fore tends to be alkaline). arterial P CO 2 (hyperventilation; ! A2a). This
Acid–base disturbances. Alkalosis occurs not only helps to return the [HCO 3 ]/[CO 2] ratio
–
when the pH of the blood rises above the nor- towards normal (20:1), but also converts NBB-
mal range (see table), and acidosis occurs H back to NBB (due to the increasing pH)
–
when it falls below the lower limits of normal. (! A2b). The latter process also requires HCO 3 –
Respiratory acid–base disturbances occur due and, thus, further compensatory pulmonary
to primary changes in P CO 2 (! p. 144), whereas elimination of CO 2 (! A2c). If the cause of aci-
non-respiratory (metabolic) disturbances dosis persists, respiratory compensation will
occur due to a primary change in [HCO 3 ]. eventually become insufficient, and increased
–
Acid–base disturbances can be partially or al- renal excretion of H + ions will occur
most completely compensated. (! p. 174ff.), provided that the acidosis is not
of renal origin (see above, cause 1).
Nonrespiratory (metabolic) alkalosis is
caused by (1) the administration of bases (e.g.,
142 HCO 3 infusion); (2) increased breakdown of
–
!
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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