Ganong's Review of Medical Physiology, 23rd Edition

630
SECTION VII
Respiratory Physiology

VENTILATORY RESPONSES TO CO
2

The arterial P
CO 2
is normally maintained at 40 mm Hg. When
arterial P
CO 2
rises as a result of increased tissue metabolism,
ventilation is stimulated and the rate of pulmonary excretion
of CO
2
increases until the arterial P
CO 2
falls to normal, shut-
ting off the stimulus. The operation of this feedback mecha-
nism keeps CO
2
excretion and production in balance.
When a gas mixture containing CO
2
is inhaled, the alveolar
P
CO 2
rises, elevating the arterial P
CO 2
and stimulating ventila-
tion as soon as the blood that contains more CO
2
reaches the
medulla. CO
2
elimination is increased, and the alveolar P
CO 2
drops toward normal. This is why relatively large increments
in the P
CO 2
of inspired air (eg, 15 mm Hg) produce relatively
slight increments in alveolar P
CO 2
(eg, 3 mm Hg). However,
the P
CO 2
does not drop to normal, and a new equilibrium is
reached at which the alveolar P
CO 2
is slightly elevated and the
hyperventilation persists as long as CO
2
is inhaled. The essen-
tially linear relationship between respiratory minute volume
and the alveolar P
CO 2
is shown in Figure 37–8.
Of course, this linearity has an upper limit. When the P
CO 2
of the inspired gas is close to the alveolar P
CO 2
, elimination of
CO
2
becomes difficult. When the CO
2
content of the inspired
gas is more than 7%, the alveolar and arterial P
CO 2
begin to rise

abruptly in spite of hyperventilation. The resultant accumula-

tion of CO

2

in the body

(hypercapnia)

depresses the central

nervous system, including the respiratory center, and produces

headache, confusion, and eventually coma

(CO

2

narcosis).

VENTILATORY RESPONSE

TO OXYGEN LACK

When the O 2 content of the inspired air is decreased, respira-

tory minute volume is increased. The stimulation is slight

when the PO 2 of the inspired air is more than 60 mm Hg, and

marked stimulation of respiration occurs only at lower PO 2 val-

ues (Figure 37–9). However, any decline in arterial PO 2 below

100 mm Hg produces increased discharge in the nerves from

the carotid and aortic chemoreceptors. There are two reasons

why this increase in impulse traffic does not increase ventila-

tion to any extent in normal individuals until the PO 2 is less

than 60 mm Hg. Because Hb is a weaker acid than HbO 2 , there

is a slight decrease in the H+ concentration of arterial blood

when the arterial PO 2 falls and hemoglobin becomes less satu-

rated with O 2. The fall in H+ concentration tends to inhibit res-

piration. In addition, any increase in ventilation that does

FIGURE 37–8 Responses of normal subjects to inhaling O 2
and approximately 2, 4, and 6% CO 2. The relatively linear increase
in respiratory minute volume in response to increased CO 2 is due to an
increase in both the depth and rate of respiration. (Reproduced with
permission from Lambertsen CJ in: Medical Physiology, 13th ed. Mountcastle VB
[editor]. Mosby, 1974.)

32

28

24

20

16

12

8

4

38 40 42 44 46 48 50

± 1 SE

Alveolar PCO 2 (mm Hg)

Respiratory minute volume (L / min)

FIGURE 37–9 Top: Average respiratory minute volume during

the first half hour of exposure to gases containing various amounts of

O 2. Marked changes in ventilation occur at PO 2 values lower than 60

mm Hg. The horizontal line in each case indicates the mean; the verti-

cal bar indicates one standard deviation. Bottom: Alveolar PO 2 and

PCO 2 values when breathing air at various barometric pressures. The

two graphs are aligned so that the PO 2 of the inspired gas mixtures in

the upper graph correspond to the PO 2 at the various barometric pres-

sures in the lower graph. (Courtesy of RH Kellogg.)

40

30

20

10

0

120

100

80

60

40

20

0

21

160

20

152

%O 2 in insp gas

PO 2 in insp gas

15

114

10

76

5

38

Ventilation (L /min)

Pressure (mm Hg)

760700 600 500 400 300 200

Alveolar PCO 2

Alveolar PO 2

Barometric pressure (mm Hg)