616 SECTION VIIRespiratory Physiology
quickly increased, lowering the available Hb–, Prot–, and
HCO 3 – buffers. The H 2 CO 3 that is formed is converted to H 2 O
and CO 2 , and the CO 2 is rapidly excreted via the lungs. This is
the situation in uncompensated metabolic acidosis (Figure
36–10). Note that in contrast to respiratory acidosis, PCO 2 is
unchanged and the shift toward metabolic acidosis occurs
along the isobar line (Figure 36–11). When the free [H+] level
falls as a result of addition of alkali, or more commonly, the re-
moval of large amounts of acid (eg, following vomiting), meta-
bolic alkalosis results. In uncompensated metabolic alkalosis
the pH rises along the isobar line (Figures 36–10 and 36–11).
RESPIRATORY & RENAL COMPENSATION
Uncompensated acidosis and alkalosis as described above are
seldom seen because of compensation systems. The two main
compensatory systems are respiratory compensation and
renal compensation.
The respiratory system compensates for metabolic acidosis
or alkalosis by altering ventilation, and consequently, the PCO 2 ,
which can directly change blood pH. Respiratory mechanisms
tend to be fast. In response to metabolic acidosis, ventilation is
increased, resulting in a decrease of PCO 2 (eg, from 40 mm Hg
to 20 mm Hg) and a subsequent increase in pH toward normal
(Figure 36–11). In response to metabolic alkalosis, ventilation
is decreased, PCO 2 is increased, and a subsequent decrease in
pH occurs. Because respiratory compensation is a quick
response, the graphical representation in Figure 36–11 over-
states the two-step adjustment in blood pH. In actuality, as
soon as metabolic acidosis begins, respiratory compensation is
invoked and pH is kept from the large shifts depicted.
For complete compensation from respiratory or metabolic
acidosis/alkalosis, renal compensatory mechanisms are invoked.
The kidney responds to acidosis by actively secreting fixed acids
while retaining filtered HCO 3 –. In contrast, the kidney responds
to alkalosis by decreasing H+ secretion and by decreasing the
retention of filtered HCO 3 –.
Renal tubule cells in the kidney have active carbonic anhy-
drase and thus can produce H+ and HCO 3 – from CO 2. In
response to acidosis, these cells secrete H+ into the tubular fluid
in exchange for Na+ while the HCO 3 – is actively reabsorbed into
the peritubular capillary; for each H+ secreted, one Na+ and one
HCO 3 – are added to the blood. The result of this renal compen-
sation for respiratory acidosis is shown graphically in the shift
from acute to chronic respiratory acidosis in Figure 36–10.
Conversely, in response to alkalosis, the kidney decreases H+
secretion and depresses HCO 3 – reabsorption. The kidney tends
to reabsorb HCO 3 – until the level in plasma exceeds 26–28
mEq/L (normal is 24 mEq/L). Above this threshold, HCO 3 –
appears in the urine. The result of this renal compensation for
respiratory alkalosis is shown graphically in the shift from acute
to chronic respiratory alkalosis in Figure 36–10. Clinical evalu-
ations of acid–base status are discussed in Clinical Box 36–2.HYPOXIA
Hypoxia is O 2 deficiency at the tissue level. It is a more cor-
rect term than anoxia, with there rarely being no O 2 at all left
in the tissues.FIGURE 36–10 Acid–base nomogram. Changes in the PCO 2
(curved lines), plasma HCO 3 – , and pH (or [H+]) of arterial blood in res-
piratory and metabolic acidosis are shown. Note the shifts in HCO 3 –
and pH as acute respiratory acidosis and alkalosis are compensated,
producing their chronic counterparts. (Reproduced with permission from
Cogan MG, Rector FC Jr.: Acid–base disorders. In: The Kidney, 4th ed. Brenner BM,
Rector FC Jr. [editors]. Saunders, 1991.)
60
56
52
48
44
40
36
32Ar terial plasma [HCO− 3
] (meq/L)28
24
20
16
12
8
4
0
7.00 7.10 7.20 7.30 7.40 7.50 7.60 7.70 7.80
Arterial blood pH100 90 80 70 60 50 40 35 30 25 20Arterial blood [H+] (nmol/L)120 100 90 80 70 60 50 4020
151035
3025
Acute
respiratory
alkalosisAcute
respiratory
acidosis
NormalChronic
respiratory
alkalosis PCO 2 (mm Hg)Metabolic
acidosisChronic
respiratory
acidosisMeta-
bolic
alkalosisFIGURE 36–11 Acid–base paths during metabolic acidosis.
Changes in true plasma pH, HCO 3 – , and PCO 2 at rest, during metabolic
acidosis and alkalosis, and following respiratory compensation are
plotted. Metabolic acidosis or alkalosis causes changes in pH along the
PCO 2 isobar line. Respiratory compensation moves pH towards normal
by altering PCO 2. (This is called a Davenport diagram and is based on Davenport
HW: The ABC of Acid–Base Chemistry, 6th ed. University of Chicago Press, 1974.)34
32
30
28
26
24
22
20
18
16
14
12
10
7.2 7.3 7.4 7.5 7.6
pHCompensated
metabolic
alkalosis,
PCO 2 48 mm HgCompensated
metabolic
acidosis,
PCO 2 21 mm HgPCO2
40 mm HgUncompensated
metabolic
alkalosis,
PCO 2
40 mm HgUncompensated
metabolic
acidosis,
PCO 2
40 mm HgNormalPlasma HCO− 3
(meq/L)