Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 36Gas Transport & pH in the Lung 615

PCO 2 , so that some additional H 2 CO 3 is removed. The pH thus
falls only to 7.2 or 7.3 (Figure 36–9).
There are two additional factors that make the carbonic-
acid-bicarbonate system such a good biological buffer. First,
the reaction CO 2 + H 2 O ←→ H 2 CO 3 proceeds slowly in either
direction unless the enzyme carbonic anhydrase is present.
There is no carbonic anhydrase in plasma, but there is an
abundant supply in red blood cells. Second, the presence of
hemoglobin in the blood increases the buffering of the system
by binding free H+ produced by the hydration of CO 2 and
allowing for movement of the HCO 3 – into the plasma.

ACIDOSIS & ALKALOSIS

The pH of the arterial plasma is normally 7.40 and that of
venous plasma slightly lower. A decrease in pH below the
norm (acidosis) is technically present whenever the arterial
pH is below 7.40 and an increase in pH (alkalosis) is techni-
cally present whenever pH is above 7.40. In practice, varia-
tions of up to 0.05 pH unit occur without untoward effects.
Acid–base disorders are split into four categories: respira-
tory acidosis, respiratory alkalosis, metabolic acidosis, and
metabolic alkalosis. In addition, these disorders can occur in
combination. Some examples of acid–base disturbances are
shown in Table 36–3.

RESPIRATORY ACIDOSIS

Any short-term rise in arterial PCO 2 (ie, above 40 mm Hg) due
to decreased ventilation results in respiratory acidosis. The
CO 2 that is retained is in equilibrium with H 2 CO 3 , which in
turn is in equilibrium with HCO 3 – , so that the plasma HCO 3 –
rises and a new equilibrium is reached at a lower pH. This can

be indicated graphically on a plot of plasma HCO 3 – concen-

tration versus pH (Figure 36–10). The pH change observed at

any increase in PCO 2 during respiratory acidosis is dependent

on the buffering capacity of the blood. The initial changes

shown in Figure 36–10 are those that occur independently of

any compensatory mechanism; that is, they are those of un-

compensated respiratory acidosis.

RESPIRATORY ALKALOSIS

Any short-term decrease in ventilation that lowers PCO 2 be-

low what is needed for proper CO 2 exchange (ie, below 35 mm

Hg) results in respiratory alkalosis. The decreased CO 2 shifts

the equilibrium of the carbonic acid–bicarbonate system to ef-

fectively lower the [H+] and increase the pH. As in respiratory

acidosis, initial pH changes corresponding to respiratory alka-

losis (Figure 36–10) are those that occur independently of any

compensatory mechanism and are thus uncompensated res-

piratory alkalosis.

METABOLIC ACIDOSIS & ALKALOSIS

Blood pH changes can also arise by nonrespiratory mechanism.

Metabolic acidosis (or nonrespiratory acidosis) occurs when

strong acids are added to blood. If, for example, a large amount

of acid is ingested (eg, aspirin overdose), acids in the blood are

FIGURE 36–9 Buffering by the H 2 CO 3 –HCO 3 – system in
blood. The bars are drawn as if buffering occurred in separate steps
over time (left to right) in order to show the effect of the initial reaction,
the reduction of H 2 CO 3 to its previous value, and its further reduction by
the increase in ventilation. In this case, [H 2 CO 3 ] is actually the concentra-
tion of dissolved CO 2 , so that the mEq/L values for it are arbitrary.

25

20

15

10

5

0

5

10

15

meq/L

[HCO 3 −]

meq/L

[H 2 CO 3 ]

[HCO 3 −]

[H 2 CO 3 ]

ratio 20 0.9 10 16

pH 7.4 6.0 7.1 7.3

Acid added TABLE 36–3 Plasma pH, HCO 3

• , and PCO
  2 values in
  various typical disturbances of acid–base balance.a

Arterial Plasma

Condition pH

HCO 3 –

(mEq/L)

PCO 2

(mm Hg) Cause

Normal 7.40 24.1 40

Metabolic

acidosis

7.28 18.1 40 NH 4 Cl ingestion

6.96 5.0 23 Diabetic acidosis

Metabolic

alkalosis

7.50 30.1 40 NaHCO 3 – ingestion

7.56 49.8 58 Prolonged vomiting

Respiratory

acidosis

7.34 25.0 48 Breathing 7% CO 2

7.34 33.5 64 Emphysema

Respiratory

alkalosis

7.53 22.0 27 Voluntary hyper-

ventilation

7.48 18.7 26 Three-week resi-

dence at 4000-m

altitude

aIn the diabetic acidosis and prolonged vomiting examples, respiratory compensation

for primary metabolic acidosis and alkalosis has occurred, and the Pco 2 has shifted

from 40 mm Hg. In the emphysema and high-altitude examples, renal compensation

for primary respiratory acidosis and alkalosis has occurred and has made the devia-

tions from normal of the plasma HCO 3 – larger than they would otherwise be.