NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
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(10) The effect of holding the breath may occasionally cause a temporary
fall of blood-pressure after the chloroform inhalation has been stopped ◊ or
even when the animal is quite out of chloroform.† This fall is recovered from
directly the animal breathes again.
(11) Slight continuous asphyxia, such as is produced by pressure on the
n e c k b y s t r a p s , a b a d l y f i t t i n g m u z z l e , o r h i n d r a n c e o f t h e c h e s t m o v e m e n t s b y
the legs being too tightly bound down, gives rise to exaggerated and irregular
oscillations of the blood-pressure, and slowing and irregularity of the heart's
action. If it leads to, or is accompanied by, deep gasping inspiration, it is apt,
like anything else which causes this, to increase the intake of chloroform and
bring about a rapid decline of blood-pressure.
(12) Complete, or almost complete. asphyxia, as by forcibly closing the
nose and mouth‡ or closing the tracheal tube after tracheotomy,§ has an effect
similar to, but more marked than, that produced by holding the breath, and the
character of the trace corresponds precisely to that produced by irritation of the
peripheral end of the cut vagus. The pressure falls extremely rapidly, some-
times almost to zero, and the heart's action becomes excessively slow or even
stops for a few seconds. If the Fick trace of Experiment No. 148 be compared
with the photographic reproduction of trace A of the Glasgow Committee, it
will be seen that they are identical, and that the slow action of the heart with
great fall, of pressure, which the Glasgow Committee attributed to some capri-
cious action of chloroform upon the heart, was undoubtedly due to asphyxia.
(13) This effect of asphyxia is the result of stimulation of the vagi. The
proof of this is (a ) that, the trace corresponds exactly, as stated above, to that
produced by direct irritation of the vagus; ( b) division of both vagi entirely
abolishes it;||and ( c) the administration of atropine which paralyses the vagus
also abolishes it.
(14) In trace 158 (Fick 4), which was taken during asphyxia after a full
d o s e o f a t r o p i n e , i t w i l l b e s e e n t h a t t h e r e i s a n a l t e r n a t e l y s l o w a n d r a p i d p u l s e
according to the phase of the respiratory movement; but no continued slowing
of the heart as in vagus irritation. But there was still a distinct fall of pressure
after the atropine when the breath was held, and it was thought that the slow-
ing of the pulse above noted in this condition might be due to the disturbance
of the heart from tension in the pulmonary vessels in the absence of respira-
* Vide Experiment No. 157. † Vide Experiment No. 185. ‡Vide Experiment 148, 150, 151.
§ Vide Experiment No. 66. || Vide Experiment No. 150. ¶ Vide No. 158, Fick 4
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tory movement rather than to irritation of the vagi. To test this point Experi-
ment No. 184 was instituted. In this experiment the dog's chest was forcibly
inflated with bellows connected by a tube with the trachea, and the effect of
this proceeding was to cause a fall of pressure and slowing of the heart exactly
the same as in involuntary holding of the breath. The dog was then poisoned
with atropine, after which inflation of the chest, still caused a fall of pressure,
but without slowing of the heart (vide Fick Nos. 8 and 9). The fall of pressure
must be in some degree independent of vagus irritation, which however usually
accompanies it.
(15) It only remains to be considered whether the slow action or tem-
porary stoppage of the heart with great fall of pressure produced by vagus
irritation is in itself an element of danger in chloroform administration, and if
it is not, wherein the danger actually lies.
(16) The experiments in which deliberate irritation of the vagi was
carried on during anæsthesia show unmistakably that irritation of these nerves
diminishes rather than enhances the danger of anæsthetics. The effect upon
the heart is never continuous, and as the vagus becomes exhausted, or when
the irritation is taken off, the blood-pressure rises again, as it does when the
same result is produced by asphyxia. The slowing of the heart and circulation
which is produced by irritation of the vagus by any cause, such as holding the
breath in chloroform administration, retards the absorption and conveyance of
chloroform to the nerve centres just as holding the breath, whether voluntary
or involuntary, prevents chloroform from entering the lungs; and of itself slow-
ing or temporary stoppage of the heart in chloroform administration is not
dangerous.
(17) To answer the second part of the last question in para. 15 is easy
enough, if it is kept in mind that the effect of vagus irritation upon the heart is
never continuous; and in chloroform administration as the pressure rises again
after the slowing of the heart and temporary fall of pressure produced by any
form of asphyxia, violent, respiratory efforts with bounding heart's action lead,
as in the case of struggling, to a rapid and dangerous inhalation of chloroform
and consequent rapid and dangerous decline in blood-pressure. It is, in fact,
the temporary exhaustion of the vagi after stimulation that is to be feared, and
not the actual stimulation as long as it is continued.
(18) In accordance with this fact it will be found that in chloroform ad-
ministration neither holding the breath, even if involuntary, or vagus inhibition
can be kept up beyond a certain time; and if the chloroform is not removed from
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the face, one or both of two things may happen : (1) when the animal breathes
again it takes deep and gasping inspirations, the lungs become filled with chloro-
form, and an over-dose is taken in with extreme rapidity ; or (2) when the
restraining influence of the vagus is taken off the heart, through the irritation
ceasing or the nerve becoming exhausted, the heart bounds on again, and the cir-
culation is accelerated in proportion. The blood then becomes quickly saturated
with chloroform, and an over-dose is at once conveyed to the nerve centres. The
theory which has hitherto been accepted is that the danger in chloroform admin-
istration consists in. the slowing or stoppage of the heart by vagus
inhibition. This is now shown to be absolutely incorrect. There is no doubt whatever that
the controlling influence of the vagus on the heart is a safeguard, and that it is
the exhaustion of the nerve which is dangerous.
(19) It can be readily understood how a condition in which the pulse is
rapid and bounding with high blood-pressure leads to more rapid absorption of
chloroform from the lungs, and a more rapid propulsion of the chloroformed blood
to the medulla oblongata, and consequently to 0 more rapid paralysis of the
respiratory and vaso motor centres and precipitous fall in the blood-pressure
Such a condition is produced in some cases by ether or by division of both vagi*
or by a full dose of atropine.† Not only is the poisoned blood carried more
swiftly to the vital centres in these cases, but added to this there is the fact, that
as the heart is already doing its utmost before the chloroform is given, it is un-
able to stave off by increased work the fall in pressure that occurs when the vaso
motor centre is paralysed. On the other hand, it seems clear front Experiment
No. 92 that, the direct action of chloroform upon the heart's substance is not the
cause of the fall of pressure that occurs when it is inhaled.
(20) In Experiment No. 92 repeated injections of 20m. of chloroform were
made into the jugular vein, and its effect was not to paralyse the heart, but to
produce anæsthesia and a gradual fall of blood-pressure exactly as if the chloro-
form had been inhaled. In Experiment No. 72, after a considerable amount of
ether had been injected into the jugular vein, and a bounding condition of pulse
had been produced, the effect of injecting chloroform into the jugulars was much
greater, and the fall of blood-pressure much more rapid and dangerous than in
the case when chloroform alone was injected. Granting then the truth of Ringer's
conclusions from experiments on the frog's heart (which have not been repeated
and confirmed by the Commission) that chloroform has a gradual paralysing
effect upon the heart's tissue, we must conclude that such an effect, in the degree
*
V i d e
N o s . 1 5 1 a n d 1 5 6 . †
V i d e
N o . 8 0 .
in which alone it could occur in the practical inhalation of chloroform, would
rather be a source of safety than of danger.
(21) The Committee discussed the advisability of cutting the vagi some
time previous to experimenting on the blood-pressure with chloroform. The
effect of this procedure is to cause continuous rapid action and tendency to
exhaustion of the heart, as well as to degeneration of the terminal branches of
the nerves in the heart if the animal live
s u f f i c i e n t l y
l o n g . S u c h e x p e r i m e n t s
might be of some interest theoretically, and also have had a practical bearing
upon the condition of the heart in certain cases of chronic alcoholism; but the
Committee decided not to perform them as it considered the end to be gained did
not justify the pain they would have inflicted.
(22) In Experiment No. 178, the case of a dog that had had morphine,
remarkable slowing and even temporary cessation of the heart's action occurred
again and again at the same moment as the respiration stopped.* but the heart
invariably recovered itself, and began again to beat regularly before any steps
were taken to restore the animal, and without any respiration occurring.
We find in this case that it was possible to restore the animal even after un-
usually long intervals had been allowed to elapse between the cessation of the
natural, and the commencement of artificial, respiration. The failure of the
heart , if . such it can be called, instead. of being a danger to the animal, proved
to be a positive safeguard by preventing the absorption of the residual
c h l o r o f o r m a n d i t s d i s t r i b u t i o n t h r o u g h t h e s y s t e m .
(23) The effect of artificial respiration after the natural respiration has
ceased, is to cause an alternate rise and fall of small amount in the blood-pressure,
the trace thus formed upon the drum being a coarse imitation, altered some-
what by the shaking of the table, of the natural respiratory
c u r v e . T h e d i f f e r - r e n c c o n s i s t s c h i e f l y i n t h e f a c t t h a t t h e a r t i f i c i a l r i s e a n d f a l l i s m o r e a b r u p t
than in natural breathing, and that the rise always coincides with expiration or
compression of the chest. After artificial respiration has been continued for a
certain time, the blood-pressure begins to rise again, and a little later natural
respiration returns.
(24)
The effect of artificial respiration in restoring an animal after the
respiration had stopped was always marked. in a few exceptional cases, such
a s N o . 1 5 9 , a p h o s p h o r u s d o g , a n d N o . 1 4 2 , a h o r s e w h i c h h a d a n e n o r m o u s
* Vide No. 178, Fick readings 2 and 3, 8, 13, 18, and 26, and compare No.49, Fick reading 2 and 8,
and No 60, Fick reading 3, which are similar cases, but were not so carefully observed.
over-dose, although the artificial respiration was commenced as soon as possible
after the breathing was noticed to have stopped, it was not successful.
(25) Complete stoppage of the respiration always means that an over-dose
has been administered, and the over-dose may have been so great as to render
restoration impossible. It is impossible to say whether, after chloroform
has been pushed and then discontinued, the respiration will be restored spon-
t a n e o u s l y o r n o t , a n d i t i s n e v e r i n a n y c a s e c e r t a i n t h a t a r t i f i c i a l r e s p i r a t i o n w i l l
restore the natural respiration and blood-pressure, no matter how soon it is com-
menced after the respiration stops. A great deal depends upon the amount of the
alter-fall: in some cases, even after the respiration has been restored, the pressure
continues to fall and respiration again ceases, and artificial respiration then
fails. We thus find respiration restored by artificial respiration while chloroform is sti
ll being absorbed, and this tends to show that artificial respiration does not
merely pump the chloroform out of the blood, but exerts considerable influence i
n e x c i t i n g t h e n a t u r a l r e s p i r a t i o n .
(26) The time which elapses before artificial succeeds in restoring natural
respiration varies very greatly. In one case, No. 116, it was continued for eleven
minutes before the first natural gasps commenced. This period is undoubtedly
prolonged in some cases by a condition of physiological apnœa which renders it
unnecessary for the animal to breathe. Consequently, whenever the pressure rose
considerably during artificial respiration it was stopped, and the animal then
generally breathed after a few seconds.
(27) The time which may be allowed to pass with impunity before
com-mencing artificial respiration also seems to vary considerably. This point was not
particularly attended to in the manometer experiments except in experiments 162
and 178, which were instituted to test the truth of the opinion formed by the Sub-
Committee that morphine had some slight action in impairing the efficiency
of artificial respiration. In these cases the commencement of artificial respiration
was postponed for more than two minutes after respiration ceased, and was
s u c - c e s s f u l ; b u t t h i s i s c e r t a i n l y f a r a b o v e t h e a v e r a g e i n t e r v a l t h a t c a n b e a l l o w e d
with safety. The success of artificial respiration in restoring the blood-pressure
i s , i n s o m e c a s e s , v e r y r e m a r k a b l e . I n E x p e r i m e n t N o . 4 0 t h e h e a r t h a d
apparently ceased beating* and the dog was believed by every one present to
be dead and yet recovered with artificial respiration. The success in this
instance is due to the fact that concentrated chloroform had been pushed for
t w o m i n u t e s , r e g a r d l e s s o f t h e b r e a t h i n g , a n d t h e s t o p p a g e o f t h e h e a r t w a s d u e
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to stimulation of the vagus through asphyxia. The animal was therefore easily
restored as lie was suffering more from asphyxia than from chloroform poisoning.*
(28) It corresponds to those cases, which are so often reported, in which
dangerous failure of the heart is said to have occurred some minutes after the
administration of chloroform had been discontinued, and which are sometimes
restored, and sometimes not, by artificial. respiration. There is nothing at all
sudden about, the failure of the heart in these cases, but the attention of the
chloroformist, which has been wandering. is suddenly called to the fact that the
patient is apparently dead. When the animal was really dead, it was found in
some cases that artificial respiration still maintained a small. amount Qf mean
pressure in the manometer. In others the pressure seemed to fall to the zero
line between each compression of the chest.
(29) The dangers of too vigorous artificial respiration were illustrated in
some of the accidental deaths. In one ease the liver was badly ruptured. and in
another the pleural cavity was lull of blood. In three cases. Nos. 80. 92 and.
103, rhythmical movements of the diaphragm were noticed after the heart had
ceased beating, and after the chest had been opened. It is remarkable that in two
of these cases the splanchnic nerve had been divided. The third was a case in
which chloroform had been injected into the jugular, and in this case there was a
synchronous movement of the jaw as well. In all, death and stoppage of the
heart had occurred gradually, and in No. 103 the heart was still irritable. These
movements cannot be called respiration. though the last gasp of' a dying animal,
that ineffective jerk of the diaphragm, which is such a fatal symptom, is very
likely in many cases a movement of the same character. Similar movements,
which were continued much longer, occurred in. Experiment No. 104 after the
thorax was opened, while the heart was still beating. Still more remarkable con
vulsions of the muscles of the jaws. ears. and fore-feet occurred in Experiment
No. 167 in the case of a dog that had been poisoned with nicotine. These move
ments continued at regular intervals for more than ten minutes alter death, and
were sufficiently forcible to jerk the handles of a pressure forceps fixed on the end
of the tongue off the table at each spasm. in a rabbit in Experiment. No. 153 the
auricles of the heart continued to beat rhythmically for three hours after it was
supposed to be dead from chloroform and its thorax had been laid open. Irri
tability of the heart after death was noticed in many cases, but seemed to be
most marked in cases where ether had been used.
* There was a mistake in para. 27 as it originally stood. In the observation at Fick 12 chloroform was admin
istered for two minutes and not fur a few seconds only. The error was caused by confusion in the tracing on account
of its having been carried twice round the drum at the end of the experiment.
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(30) Chloroform injected in the heart through the jugular vein did not
cause clotting of the blood as was the case when ether was injected
.
(31)
In the course of the experiments of the Committee various drugs were
administered in order to ascertain if they had any effect in modifying the action
of chloroform. The result showed that none of them had any effect in prevent
ing the typical descent of the blood-pressure that occurs when chloroform is
inhaled. Atropine, when given in a dose sufficient to paralyse the vagi, of
course prevents the action of those nerves in asphyxia, and by increasing the
action of the heart it appears to cause a more rapid descent in the blood-pres
sure when chloroform is inhaled as has been already explained. Morphine
appeared in No. 162 to render the rise in blood-pressure that occurred when the
chloroform was discontinued slower and less complete, and to bring about a more
or less permanent condition of anæsthesia. It may be noted that the animal
used in this experiment was a monkey, and in other experiments with monkeys,
when no morphine had been given, it was remarked that the animal., after a few
inhalations of chloroform, would often lie quite quiet in a state of semi-insensi
bility for a long time without further inhalations; still this condition was much
more marked in Experiment No. 162 than in any of the others. No action of this
kind was noticed in the dog No. 178, but other experiments (Nos. 90 and 94)
showed that pariah dogs are very indifferent to the action of morphine, and it is
probable that the dose of morphine in this case was insufficient to bring about the
condition noted in the monkey. The peculiar behaviour of the heart in No. 178
was not the result of the previous administration of morphine, for a similar phe
nomenon had occurred in other cases (49 and 60) in which no morphine had
been given. Experiments Nos. 162 and 178 prove conclusively that morphine
has no effect in shortening the period that may be allowed to elapse between
the cessation of natural respiration and the commencement of artificial respiration.
(32) The other drugs used had no effect upon the action of chloroform
except when their own special. action became the leading feature in the case, as
for instance, during the vomiting from apomorphine (104, Fick 9) or the convul
sions produced by nicotine (167).
(33) In order to test the alleged danger from shock during chloroform
administration, the Committee performed a very large number of those operations
which are reputed to be particularly dangerous in this connection, such as extrac
tions of teeth, evulsion of nails, section of the muscles of the eye, snipping of the
s ki n of t he anus . &amp; c. I n many cas es t he oper at i on was per f or med when t he
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animal was merely stupefied by the chloroform and not fully insensible. In such
cases a slight variation in the blood-pressure would sometimes occur, such as one
would expect from the irritation of a sensory nerve or from the struggling that
ensued, but in no case in any stage of anæsthesia was there anything even sug-
gestive of syncope or failure of the heart's action. In thrusting a needle into the
heart, there was often a momentary, but well-marked, fall of blood-pressure;
but even this was absent in all other injuries. If chloroform really had any
power to increase the tendency to shock in operations, it is impossible to believe
that it would not have been manifested to some degree at, least in one or other
of these numerous experiments. The Commission was, however, not content
with this negative result, and determined to ascertain the effect of direct irrita-
tion of the vagi during continued chloroform administration. The result of such
experiments (Nos. 65, 117, and others)proved that inhibition of the heart's action
prevented, rather than assisted, the fatal effects of prolonged chloroform inhal-
ation. An animal that was put into a condition of extreme danger (from which
it could only be restored by means of artificial respiration) by inhalation of
chloroform for one minute, recovered spontaneously and readily after five minutes
of chloroform inhalation together with inhibition of the heart by electrical irri-
tation of the vagus carried on simultaneously. In one of these experiments, No.
117, chloroform was pushed for seven minutes; and during continued irritation
of the vagus the animals repeatedly came round without artificial respiration.
The danger really begins when the irritation is discontinued or fails to inhibit
the heart, and thus enables the chloroform in the lungs to be rapidly absorbed and
thrown into the system. This danger is certainly increased by deliberately pump
ing the chloroform into the lungs, by means of artificial respiration, for animals
in which this was done, although they showed a tendency to recover when the
chloroform and imitation o f t he vagus were discontinued, afterwards died rapidly.
(34) On another occasion, during Experiment No. 117, the animal was very
nearly killed by a comparatively short inhalation of chloroform, owing to the
electrodes becoming accidentally short-circuited and tailing to keep up the
irritation of the vagus. Something similar occurred in No. 177, the effect of
the irritation of the vagus passing off. while the chloroform was still being
pushed, and thus putting the animal into a condition of extreme and unexpected
jeopardy. Nothing could be more striking than these near approaches to
accidental death from failure to irritate the vagus efficiently.
(35) Other experiments were made to test the truth of the statement that
chloroform increases the action of electrical stimuli applied to the vagus, and