6 research outputs found
Respiratory failure in pulmonary anoxaemia
(a) The Ventilation in Pulmonary Hypoxemia
The role played by chemical constituents of the
blood in controlling pulmonary ventilation has been the
subject of numerous investigations for over one hundred
years since Kussmaul and Tenner in 1857 showed that a
chemical stimulus was involved by experiments in which a
large increase in ventilation was produced by breathing
low oxygen mixtures and by re breathing from a bag.
The earliest theory which attempted to account
for these observations was put forward by Rosenthal in
1862, and again in 1882, He suggested that the oxygen
content of the blood determined the ventilatory response.
He discounted any place for CO2 in the regulation of
ventilation on the basis of experiments showing that
inhalation of high concentrations of CO2 (20 to 30 this chemoreceptor discharge of nervous impulses
increased.
Gesell, Lapides and Levin showed in 19^0 that
blocking these sinus nerve impulses in animals by the
application of cold to the nerves depressed the ventilation
when the animals were breathing room air at rest. These
observations were confirmed by Marshall and Rosenfeld (1936).
All of these workers agreed that hypoxaeinia was
more effective than CO^ excess in increasing the peripheral
chemoreeeptor activity, whereas CCg excess in the arterial
blood was the major factor in stimulating the central
respiratory control mechanism.
The relative importance of the central and
peripheral mechanisms in maintaining the pulmonary ventilation under varying conditions was estimated in a quantitative
way by Gesell et al. (v.s.) using the cold block technique.
The part played by the peripheral chemoreceptors in controlling the ventilation in response to a fixed degree of
hypoxaemia varied between 0 and 100 CO^
was inspired nerve blocking had no effect, showing that
in these circumstances respiration was 100 controlled by
a central mechanism which was presumably insensitive to
liypoxaenia.
Bjurstedt (19*»-6) and Gernandt (19*+6) confirmed
these observations and found that the greater the acidity
of the blood, the less was the effect upon respiration of
blocking the sinus nerves. Bjurstedt also showed that in
the early stages of acute hypoxia, the peripheral
chemoreceptors played a large part in controlling the
respiration; but this part gradually decreased with time
until, over a period of six to ten hours, it became slight
as the pK of the blood fell towards normal. The maximum
hypoxaemic stimulus to respiration coincided with the time
at which the pH was most raised due to CO,, washout. The
mechanism of the compensatory decrease in plasma bicarbonate
which resulted in the return of the blood pH towards normal
was assumed to be a renal one due to diminished tubular
reabsorption of bicarbonate. This renal compensatory
phenomenon had been studied by Haliane (J.S.), Kellas and
Kennaway in 1919 and also by Haldane (J.B.S.) in 1921.
They observed that the initial alkalinity of the blood
upon acute exposure to hypoxia gradually decreased with
time, the pH of the blood becoming less upon continued
exposure. Y. Henderson in studying the same process in
1919 showed that the 'hypocapnia \*as followed by a hypocarbia
Winterstein (1956) noted that hypoxaemie human
subjects given 100 oxygen to breath in the early stages
of the period of oxygen lack reacted by becoming apnoeic.
If the anoxaemia was continued over a longer time the
duration of apnoea due to breathing oxygen decreased.
All of these observations point to a direct
relationship between the magnitude of the hypoxaemic
stimulus to respiration and the pH of the blood. It
would appear to be reasonable to test the implication that
hypoxaemic emphysematous subjects with marked C0^ retention
and lowered blood pH should show little or no immediate
decrease in pulmonary ventilation on breathing high
concentrations of oxygen