Page 157 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
+
–
organic anions (e.g., lactate , α-ketoglu- creased quantities of H in form of titratable
+
tarate ); (3) loss of H ions due to vomiting acidity (! p. 174f.) of NH 4 as well and, after a
2–
+
+
(! p. 238) or hypokalemia; and (4) volume latency period of 1 to 2 days. Each NH 4 ion ex-
–
depletion. Buffering in metabolic alkalosis is creted results in the sparing of one HCO 3 ion
+
similar to that of non-respiratory acidosis (rise in the liver, and each H ion excreted results in
–
in [HCO 3 ] St, positive base excess). Nonethe- the tubular cellular release of one HCO 3 ion
–
less, the capacity for respiratory compensation into the blood (! p. 174ff.). This process con-
through hypoventilation is very limited be- tinues until the pH has been reasonably nor-
cause of the resulting O 2 deficit. malized despite the P CO 2 increase. A portion of
the HCO 3 is used to buffer the H ions liber-
–
+
Respiratory Acid–Base Disturbances ated during the reaction NBB-H ! NBB + H +
–
Respiratory alkalosis (! B) occurs when the (! B2, right panel). Because of the relatively
long latency for renal compensation, the drop
lungs eliminate more CO 2 than is produced by
Acid–Base Homeostasis decrease in plasma P CO 2 (hypocapnia). In- acidosis than in chronic respiratory acidosis. In
in pH is more pronounced in acute respiratory
metabolism (hyperventilation), resulting in a
–
the chronic form, [HCO 3 ] Act can rise by about
versely, respiratory acidosis occurs (! B)
1 mmol per 1.34 kPa (10 mmHg) increase in
when less CO 2 is eliminated than produced
(hypoventilation), resulting in an increase in
P CO 2 .
Respiratory alkalosis is usually caused by
plasma P CO 2 (hypercapnia). Whereas bicar-
hyperventilation due to anxiety or high alti-
bonate and non-bicarbonate buffer bases
–
sulting in a fall in plasma P CO 2 . This leads to a
bolic acidosis (! p. 142), the two buffer sys-
6 (NBB ) jointly buffer the pH decrease in meta- tude (oxygen deficit ventilation; ! p. 136), re-
–
slight decrease in [HCO 3 ] Act since a small por-
tems behave very differently in respiratory al-
–
+
–
kalosis (! B1). In the latter case, the HCO 3 / tion of the HCO 3 is converted to CO 2 (H +
–
–
CO 2 system is not effective because the change HCO 3 ! CO 2 + H 2O); the HCO 3 required for
+
in P CO 2 is the primary cause, not the result of this reaction is supplied by H ions from NBB’s
+
–
respiratory alkalosis. (buffering: NBB-H ! NBB + H ). This is also
–
Respiratory acidosis can occur as the result the reason for the additional drop in [HCO 3 ] Act
of lung tissue damage (e.g., tuberculosis), im- when respiratory compensation of non-respi-
pairment of alveolar gas exchange (e.g., pul- ratory acidosis occurs (! p. 143 A, bottom
monary edema), paralysis of respiratory panel, and p. 146). Further reduction of
–
muscles (e.g., polio), insufficient respiratory [HCO 3 ] Act is required for adequate pH normal-
drive (e.g., narcotic overdose), reduced chest ization (compensation). This is achieved
motility (e.g., extreme spinal curvature), and through reduced renal tubular secretion of H . +
many other conditions. The resulting increase As a consequence, increased renal excretion of
–
in plasma CO 2 ([CO 2] = α · P CO 2 ) is followed by HCO 3 will occur (renal compensation).
+
increased HCO 3 and H production (! B1, left In acute respiratory acidosis or alkalosis,
–
+
panel). The H ions are buffered by NBB bases CO 2 diffuses more rapidly than HCO 3 and H +
–
(NBB + H ! NBB-H; ! B1, right panel) while from the blood into the cerebrospinal fluid
–
+
–
[HCO 3 ] Act increases. Unlike non-respiratory (CSF). The low NBB concentrations there
–
acidosis, [HCO 3 ] St remains unchanged (at least causes relatively strong fluctuations in the pH
initially since it is defined for normal P CO 2 ; of the CSF (! p. 126), providing an adequate
! p. 146) and [BB] remains unchanged be- stimulus for central chemosensors (! p. 132).
– –
cause the [NBB ] decrease equals the [HCO 3 ] Act
increase. Since the percentage increase in
–
[HCO 3 ] Act is much lower than the rise in [CO 2],
–
the [HCO 3 ]/[CO 2] ratio and pH are lower than
normal (acidosis).
If the increased P CO 2 persists, renal compen-
sation (! B2) of the respiratory disturbance
144 will occur. The kidneys begin to excrete in-
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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