Physiological studies on acute carbon monoxide poisoning
In view of the frequent incidence of acute carbon monoxide(CO) poisoning among
air crews as well as among those who are daily using briquette, the author
undertook in past a series of stuides concerning (1) the tolerance of mice to CO,
and (2) changes in erythrocyte counts and hematocrit ratios in the CO intoxication.
In these investigations the author derived a formula which would enable us to
compute the appearance time of the respiratory arrest when one breathes various
concentrations of CO. Moreover, it was pointed out that there is a considerable
individual difference in the appearance time of the respiratory arrest for a given
CO concentration. Although it has been previously stated by various investigators
that an increase in the hemoglobin concentration during CO exposure is one of the
most important factors which increase the tolerance of animals to CO intoxication,
there was no obvious correlation between the degree of increase in the hemoglobin
concentration and the apperince time of the respiratory arrest during the acute CO
These observations led the author to undertake more systematic studies on this
problem of individual difference in order that one can understand what factors are
involved in determining the tolerance of each animal to a given CO enviroment.
Experiments were carried out on 24 anesthetized dogs. Various measurements were
made on the following 5 experimental groups:
Group A: 0.45% CO in air Group B: 0.45% CO in O^^2
Group C: 0.35% CO in air Group D: 0.12% CO in air
Group E: o.12% CO in air, but anemic(hemoglobin concentration of 6.5gm%)
The following items were determined in each group before and during the exposure
of each animal to a given CO gas mixture:
a. Changes in blood composition such as O^^2, CO^^2, CO, glucose, lactic acid,
hydrogen ion and potassium ion.
b. Changes in blood cells.
c. Changes in various cardio-pulmonary functions such as the alveolar gas
exchange, the pulmonary ventilation, the arterial blood pressure, the pulse rate
and the cardiac output.
Unless the animal died in the middle of experiment as in Groups A, C and E, the
observation was made until 280 minutes after the start of breathing CO gas mixture.
The results may be summarized as follows:
(a) Changes in blood composition;
1. Upon exposure to CO, the arterial O^^2 content of blood decreased while the CO
content increased as expected. However, the CO^^2 content was also reduced
significantly and this is attributable to the hyperventilation which takes place
during CO exposure.
In those groups in which the animal died, the arterial O^^2 content was reduced
to approximately 2 vols %.
2. The arterial blood pH was reduced significantly during CO exposure.
3. Both the blood sugar level and the lactic acid concentrationincreased during
4. The plasma concentration of potassium ion was not altered significiantly
during CO exposure.
(b) Changes in blood cells:
1. The erythroyte count, the hemoglobin concentration and the hematocrit ratio
increased in parallel during the exposure to CO.
2. The leucocyte count also increased significiantly during CO exposure. However,
there was a simultaneous eosinopenia.
(c) Changes in various cardio-pulmonary functions;
1. The minute volume as well as the O^^2 consumption and the CO^^2 output were
increased significantly during CO exposrue. The value of alveolar gas exchange
ratio increased temporarily at the beginning but subsequently returned to the
2. The blood pressure and the pulse rate somewhat increased at the very
beginning, but were soon reduced to subnormal level.
3. The cardiac output was increased variably during Co exposure.
In general, these changes were more distinct in Groups A, C and E than in Groups
B and D. In other words, when the concentration of CO is the same as in Groups A
and B or in Groups D and E, the animal with either higher O^^2 concentration (i.e.
Group B) or with higher hemoglobin concentration(i.e. Group D) has the greater
tolerance than that of the raspective control. On the basis of the above
observations, the overall sequence of acute Co poisoning may be summarized as
follows: As oon as the animal is exposed to CO, the arterial O^^2 content is
lowered as the result of formation of carboxyhemoglobin and this reduction in blood
O^^2 content stimulates the anaerobic glycolytic process which would in turn
increase the lactic acid concentration and the hydrogen ion concentration. The
increase in hydrogen ion of blood would induce hyperventilation by stimulating the
chemoreceptors. On the other hand, a sudden exposure to CO may also release
adrenaline as indicated by the increased blood sugar, the pulse rate and the blood
pressure. the increase in the hematocrit ratio may also be attributed to the
splenic contraction due to adrenaline released. However, as the arterial O^^2
ontent drops further, the central nervous system may be suppressed as a result of
which the vasomotor center and the cardiac center become less active and thus the
pulse rate and the blood pressure decrease to a subnormal level. As long as
hyperventilation lasts, the respiratory muscles have to work harder and this would
bring about the increase in O^^2 consumption. Although the greater CO^^2 output was
observed, this could be best attributed to hyperventilation as well as to the
oxidation of CO to CO^^2.
The observed increase in the cardiac output is very difficult to be interpreted
in view of the above statement that the activity of the cardiac center may be
suppressed as a result of the reduction in arterial O^^2, although this elevated
cardiac output would be of great help in prolonging the survival time of the
animal. In other words many changes take place upon exposure to CO and some(e.g.,
increases in the hematorit ratio, in the blood sugar level and in the cardiac
output) of these may undoubtedly increase the tolerance of the animal to CO while
some(e.g., increases in O^62 consumption and in hydrogen ion concentration, and in
blood pressure) may be actually detrimental to the maintenance of life in cO
environment. Hence, it is virtually impossible to single out a factor which is most
important in determining the tolerance of animal to CO.