CHAPTER XI
PHYSIOPATHOLOGICAL ACTION OF ACUTE PHOSGENE
POISONING a
If the effects of phosgene on the animal organism
were to be described in one phase it would be
by the words "pulmonary edema." A study of phosgene poisoning is,
therefore, of more than
passing medical interest. The work here reported was done in an attempt
to get a physiological
background for proposed forms of treatment. Various physiological
reactions have been
followed as closely as possible throughout the course of fatal phosgene
poisoning.
The general results of poisoning by lung-irritant
gases, including phosgene, have been described
in the preceding chapter, and since the experience on this point here
reported is identical, such
description need not be repeated. The division of phosgene poisoning
into three stages (see pp.
351-354) is in accord also with these findings and, although arbitrary
in certain cases, as all such
classification must be, it is of distinct advantage in locating the
various physiological
disturbances and in gaining an insight into the condition as a whole.
METHODS
Dogs were used throughout these studies. The animals
were subjected for 30 minutes to air
containing 80 to 100 parts per million of phosgene. This was
sufficient, with rare exceptions, to
produce death in the first 24 hours. The technique of this gas
administration was one gradually
evolved at the various Chemical Warfare Service laboratories. It
consisted of placing the dogs in
a 100-liter air-tight glass box through which air was drawn at the rate
of 100 liters per minute. The phosgene cylinder was connected to the
air inlet tube, the gas outflow being regulated by a
needle valve and the rate roughly determined by a flow meter. From the
gassing chamber itself
air was drawn in order to determine by chemical analysis the exact
concentration of phosgene to
which the animals were subjected.
All animals on which it was necessary to make
incisions were morphinized either before or
immediately after being gassed. A series of morphine controls had been
carefully studied, and
care was taken that none of the effects to be described could be
attributed to morphine. In order
to make observations rapidly and frequently, the animals were kept tied
to operating boards.
Since no pressure was exerted anywhere except by the cords on the
limbs, and the respiratory
passages were entirely unobstructed, this restraint seemed
unobjectionable. The animals lay
quietly and comfortably until the usual asphyxial stimulations occurred
shortly before death.
ARTERIAL BLOOD PRESSURE
By attaching a mercury manometer to the femoral
artery, arterial blood pressure records were
made in the usual way at half-hour intervals. The general course of the
blood pressure in a
typical case of phosgene poisoning
a The data
in this chapter are based, in the main, on the experimental
observations made by the
detachment of the Medical Division of the Chemical Warfare Service on
duty at the University
of Wisconsin laboratory, account of which
was published by Maj. W. J. Meek, C. W. S., and Lieut. Col. J. A. E.
Eyster, M. C.: Experiments
on the Pathological Physiology of Acute Phosgene Poisoning. American
Journal of Physiology,
Baltimore, Md., 1920, ii, No. 2, 303.
357
be seen at a glance by
referring to Chart XIX. This composite curve, in common with those that
are to follow, was made by dividing each of the experiments in the
series into 10 equal periods.
The animals lived an average of 16 hours after gassing. Each of the 10
intervals, therefore,
represents on the average a little over one hour and a half. The data
for the same period in all the
experiments were averaged and the results plotted as a composite curve.
A few
animals showed a slight fall of blood pressure after being taken from
the gassing chamber.
In most cases this was insignificant, and it did not lower the
composite curve during the first
period. As a rule the blood pressure gradually rose during the first
half of the experiment,
increasing some 10 percent above the normal. Beginning with the sixth
period, it began to fall
slowly,
CHART XIX.- Composite curve,
from ten experiments, of the changes in arterial block pressure
after acute phosgene gassing.
reaching normal at the
beginning of the eighth interval. Once having passed the normal the
decline became extremely rapid and continued without intermission until
the death of the animal.
This break in blood pressure, which occurred at the eighth period, was
an extremely striking
event in all the animals studied. It made possible a very accurate
prediction as to how much
longer the animal would survive. Until its significance was fully
appreciated, many of the
animals died before final observations could be made.
Chart XX is a reproduction
of the actual records from a typical experiment. The points just,
mentioned may be noted. The first record, at 11.10 a. m., was taken
shortly after the gassing. Tie
pressure then rose gradually for more than six hours. At 12.10 a. m.,
13 hours after gassing, the
pressure was still normal, though falling. One hour and twenty minutes
later the animal was
dead.
358
One
need not attempt to interpret the arterial blood-pressure curve of
acute phosgene poisoning
until all the other data have been presented. Its resemblance to an
asphyxial vasoconstriction,
however, is obvious. That the rise may have been due to
vasoconstriction and the fall in part to
paralysis of the vasomotor center is suggested by the large vasomotor
waves which so often
occurred late in the blood-pressure tracings. (See Chart XX, the record
at 12.45 a. m.)
VENOUS BLOOD PRESSURE
In the
preceding series of
10 experiments venous pressure observations were made
simultaneously with the arterial. These were secured by inserting a
sound into the femoral vein.
The sound was connected to a manometer and a reservoir of Ringer's
solution. The pressure in
the system was raised above what the reading was likely to be. On
removing a clip the blood
pressure was balanced against that of the fluid in the manometer. The
reading could be made
before there was any tendency to clot, and the fluid added to the
bloodstream at each observation
was negligible.
CHART
XX.- Arterial blood
pressure record from a case of acute phosgene poisoning
Venous
pressure was found
to be rather variable, conforming, on the whole, however, to what
one might expect from the arterial. During the long period of increased
arterial pressure, venous
pressure was either normal or slightly below. In the terminal stages,
however, it often rose
markedly. In 2 of the 10 experiments there was a noticeable increase in
venous pressure
immediately after gassing. These were very severe cases, death
occurring within nine hours. It
would seem probable that in these animals the initial injury to the
lungs was so great that the
pulmonary circulation was obstructed and venous pressure therefore
forced to rise.
PULSE RATE
Shortly
after gassing the
pulse rate fell in practically all cases. This occurred in animals
morphined before gassing, as, well as in those that received none of
the drug. It was therefore an
expression of the action of the poison itself. The decrease in rate
brought the pulse from an
average of 95 to 70 beats per
359
minute. By the time the
experiment was half over the heart rate had returned to normal, and
following this it was very markedly accelerated. Chart XXI presents a
composite curve from 14
experiments in which the pulse rate was carefully followed. The final
determination of the curve
is the average of the highest rates obtained in the tenth period. As
death became imminent, the
heart rate became irregular and the rate then, of course, decreased.
Electrocardiograms taken at
this time showed various kinds of blocks, dropped beats and extra
systoles, features which
characterize most records taken during death by asphyxiation.
The
pulse rate offered an
excellent means of following the condition of the animal. Two of the
dogs in one series recovered. The pulse curves from these
CHART XXI.- Composite curve
from fourteen experiments, of the changes in the heart rate after
acute phosgene gassing
animals were of special
interest. There was the initial fall and the subsequent rise, but the
latter
never exceeded 120 beats per minute. A large number of observations
have confirmed the
opinion that a fatal outcome is to be expected if the heart rate
continues to rise above 125 or 130
beats.
HEMOGLOBIN DETERMINATIONS
It was
soon realized that
there were very significant changes in the hemoglobin content of the
blood in dogs suffering from phosgene poisoning. At death the blood was
viscous, even tarry in
consistency, and the hemoglobin readings showed an almost unbelievable
concentration.
Underhill 1 first pointed out that this stage of concentration was
preceded by an initial one in
which the hemoglobin content of the blood was decreased.
360
The
characteristic
hemoglobin changes during the course of the poisoning may be seen in
Chart
XXII. In an average experiment the hemoglobin readings were below
normal during the first
four periods of the experiment. This constitutes Underhill's first
stage of phosgene poisoning.
Concentration then began, and in the period preceding death the
hemoglobin readings average
over 150 percent. The periods of concentration make up Underhill's
second stage.
The
maximum decrease in
hemoglobin occurred anywhere during the first four periods; in other
words, during the first five or six hours of the experiment. Since the
maximum decrease did not
occur in the same period for all the experiments, the composite curve
does not show the lowest
limit reached in hemoglobin concentration. In the 16 cases reported, it
actually averaged
CHART XXII.- Composite
curve from sixteen experiments, of the changes in hemoglobin
concentration after acute phosgene gassing
11 percent; that is, a
hemoglobin reading of 89. The lowest reading noted was 85, although in
a
treatment series not here reported there were readings as low as 80 and
one of 78. The maximum
decrease lasted a very brief time and often there was difficulty in
making desired observations at
exactly the proper moment.
The
degree of subsequent
hemoglobin concentration always bore a definite relation to the
severity of the poisoning and made possible a rather accurate
prognosis. One hundred and
twenty-five per cent may be said to represent a critical point. Any
animal exceeding this figure
was pretty sure to die in the course of the next five or six hours. If
an animal was not gassed
enough to reach this concentration, or if by any means a 125 percent
concentration could be
prevented, there was an excellent chance for recovery.
361
Hemoglobin
readings are
usually interpreted in terms of the fluid content of the blood, or
blood
volume. If plasma or water has left the blood stream there is of course
a concentration of
hemoglobin, and if fluid has entered the blood stream from the tissues
or elsewhere there is
naturally a lowered hemoglobin content. While this is the general rule,
there may be exceptions.
Hemolysis or stagnation of red blood cells at any point might very
greatly modify hemoglobin
determinations and yet the blood volume would be entirely unchanged.
The
natural interpretation
of the hemoglobin curve for phosgene poisoning would be that in
stage 1 there is an increase of blood volume and in stage 2 a marked
decrease. That there is a real
decrease in stage 2 is borne out by the fact that the lungs are now
full of fluid which must, of
course, have come from the blood. There is, however, no equally obvious
explanation for an
increase of blood volume in stage 1. Underhill 1 also found in this
stage a decrease in the blood
chlorides, but the excess at the time in the urine and fluid of the
lungs might account for this
decrease.
BLOOD-VOLUME DETERMINATIONS
The
blood volume was
determined directly in eight animals during stage 1 and in three
animals
during stage 2. The technique used was the acacia method 2 which has
been developed in the
laboratory of the University of Wisconsin. In Table 26 may be seen the
results.
TABLE
26.- Blood volume in
phosgene poisoning
The
data presented give no
evidence of a blood volume increase in stage I. In a large series of
normal dogs the volume was frequently 10 and 11 percent of body weight,
with an average of
9.7 percent. The eight animals here investigated averaged, then, within
2 percent of normal.
Furthermore, of the three animals having the greatest hemoglobin
dilutions, only one had a
volume above the average.
362
In
stage 2 only three
determinations were made; unfortunately no hemoglobin readings were
made simultaneously. Red blood-cell counts, which always paralleled the
hemoglobin readings,
indicated, however, that the latter were in the neighborhood of 135
percent. Since the technique
required the removal of 20 c.c. of blood, the determinations were made
some time before the
anticipated death of the animal. The figures, particularly the first
and third, show that these
animals had a marked decrease in blood volume. Even 8.1 percent body
weight is a lower blood
volume than we have ever found in a normal dog.
Stage 1
of phosgene
poisoning, on the grounds of blood-volume data, is believed to
represent an
actual decrease in the total hemoglobin content of the blood, a point
which will be discussed
later under histological examination
CHART XXIII.- Composite
curve, from nine experiments, of the changes in the red blood cell
counts after acute phosgene
of the lungs. In stage 2
there can be no doubt that the blood volume is actually greatly
decreased.
RED BLOOD-CELL COUNT
Little
need be said
concerning the red blood-cell counts other than that they uniformly
paralleled
the hemoglobin determinations. A composite curve from nine experiments
may be seen in Chart
XXIII. As in the hemoglobin curve, stages 1 and 2 are evident, and they
occupy the same
relative positions.
HISTOLOGICAL EXAMINATION OF
THE LUNGS
Careful
histological
examinations of lung tissue were made in a series of poisoned dogs b Special methods for fixing and staining pulmonary tissues.
b These examinations were
made by Dr. W.S.Miller, of the Department of Anatomy, University
of Wisconsin.
363
were used, rather than the
routine technique of general pathology. These examinations showed
that the injury from phosgene was almost exclusively in the lower
respiratory passages. There
was constriction or spasm of the small bronchioles, with the
accompanying atelectasis and
emphysema, and edema of the connective tissue. The alveoli were
irregular, their membranes
were injured, and in many cases they contained exudate. Very important
from the point of view
of these studies was the extensive clogging of the capillaries with red
blood cells. Even small
veins were solidly plugged. In many cases these masses in the veins had
shrunk slightly and the
surrounding clear areas were filled with serum. That these changes in
the lungs were not post-mortem is substantiated by the fact that they
were characteristic of all the early stages of
poisoning and that they were found after every attempt to avoid
post-mortem clot
Furthermore,
if phosgene in
a dilution as great as 1 to 20,000-that is, 0.222 milligrams per
liter-was bubbled through a 2 percent suspension of defibrinated dog's
blood, there was in 20 minutes
a marked agglomeration of the red corpuscles. This is direct evidence
that the gas has the power
of doing just what the histological picture shows.
In
slightly later stages
than the one figured, there was evidence that compensatory paths were
being opened up for the blood stream. Capillaries which were not
plugged were widened and
others had been dilated sufficiently to allow a flow of fluid around
the obstructions.
The
importance of these
histological findings on the physiological conception of phosgene
poisoning is at once apparent. The plugged capillaries and veins at
first must have greatly
increased pulmonary resistance and the work of the right heart. Later
there was relief by the
development of compensatory passages. Just how the heart reacted to
this will be seen in the
following section. Furthermore the injuries to the alveolar walls must
have decreased the
exchange of gases between the blood and the alveolar air.
HEART SIZE
In a
large series of
experiments, stereoscopic examinations and X-ray photographs of the
thorax
were made at frequent intervals. At first the outline of the heart was
sketched in with a grease
pencil on the glass cover of the fluoroscope. Later stereoscopic plates
were made and these, of
course, proved much more reliable than the former method. To be sure
that the animal was in the
same position for each photograph, a lead cross was sewed to the chest
and the center of this
brought under a plumb bob at each exposure. Exposures were always made
during the same
phase of respiration, preferably inspiration, and the flashes were long
enough to insure that it
was the diastolic size of the heart which was secured.
These
observations showed
two interesting and important changes in heart size during acute
phosgene poisoning. There was, first, immediately after removal from
the gas chamber, an
increase in the size of the heart which varied considerably in degree,
but which was always
associated with a relative enlargement of the right auricle and
ventricle. This condition persisted
for several hours and might even increase for an hour or more.
364
By the
beginning of the
fourth period, assuming that the experiment had been divided into 10
equal intervals, a second change appeared which was a gradual reduction
in heart size. This
seemed to appear first in the left ventricle, but soon the whole heart
became distinctly smaller. It
assumed a pendular shape which was apparently identical with that
following severe
hemorrhage, as determined in control experiments. This decrease in size
continued during the
development of the extensive pulmonary edema. During the period of
asphyxial death the heart
began to enlarge, particularly the right side, and after the death
plates invariably showed a
dilated heart with relative increase of the right side.
FIG.
45.- Superimposed
outlines of three X-ray photographs taken at intervals during phosgene
poisoning to show changes in shape of the heart. The solid line
indicates the normal. The dotted
line shows the right-sided dilatation 39 minutes after gassing. The
broken line is from a photograph taken 11hours and 53 minutes after
exposure to the gas. The heart had then become
pendular in shape and much reduced in size
Figure
45 illustrates
strikingly the stages of increase and decrease in heart size. The area
of the
normal heart shadow as determined by the planimeter was 51.2 sq. cm.
Thirty-nine minutes after
gassing, the area had increased to 55.4 sq. cm. Eleven hours and
fifty-three minutes after
exposure the heart had decreased to 44.5 sq. cm. This was at a time
when the pulmonary edema
had become very marked.
CHANGES IN THE LUNGS
The
condition of the lungs
was determined in a large number of animals by means of physical,
fluoroscopic, and stereoscopic X-ray examinations. Immediately after
ramoval from the gas
clwamber there was noted a diffuse, clouding of the hings, usually most
marked in the middle
and upper lobes, but
365
sometimes involving the
lower lobes also. This was accompanied by an increase in density and
number of the streaky shadows cast by the larger bronchi and vessels at
the roots of the lungs.
For a few hours the cloudy appearance of the lungs generally increased
slowly without being
associated, however, with any constant physical signs. Occasionally
transitory fine, dry,
crackling rales were heard during expiration, and occasionally there
was a slight roughening of
the normal respiratory sounds.
After these few hours the lungs often appeared
somewhat clearer. This improvement, however,
was transient and gave way during the latter third of the experiment to
a streaky, mottled
appearance, at first marked near the roots of the lungs but later
involving the whole of both
lungs. Often the heart outline was in part lost or obscured. It was at
this time that numerous rales
of all varieties made their appearance, medium moist predominating.
These were heard in both
inspiration and expiration. In brief, the clinical signs were now those
of extensive pulmonary
edema and passive congestion.
In the
later stages there
was frequently an impairment of the percussion notes, most evident in
the pendant portions, and an extension of deep cardiac dullness,
especially on the right side. X-ray plates showed, however, that this
was not due to cardiac enlargement but probably to better
transmission of heart dullness by the edematous lung.
There
were thus three more
or less distinct changes to be made out by means of the X ray in the
lungs of animals fatally poisoned with phosgene. First a diffuse
cloudiness due probably to the
initial epithelial injury and to the agglomeration of the corpuscles in
the capillaries. Second, an
improvement, a decrease in the cloudiness, accounted for by a reopening
of many of the
capillary passages. Third, a marked increase in the density and extent
of all shadows cast by
bronchi and blood vessels and an extension of the mottled appearance to
all parts of the lungs. It
is worthy of mention that it was only during the third stage that the
classical clinical signs of
pulmonary edema developed. The X ray proved a much more delicate method
of following lung
lesions than the older methods of percussion and auscultation.
RESPIRATORY RATE AND
PULMONARY AERATION
One of
the earliest results
of phosgene gassing was an increase in the respiratory rate. By the end
of the fourth period, that is stage 1, the rate had usually increased
from an average of 30 to 45
per minute. This increase continued through stage 2 until the death
period itself, when the
respirations, of course, became irregular and gradually less rapid.
Respiratory
rate,
particularly in the dog where there may be much panting, gives a poor
idea of
the amount of air actually passing in and out of the lungs. To secure
such data a series of five
experiments was run, in which the dogs were placed in an air-tight
rigid chamber that inclosed
the entire animal except the head. An inflated rubber collar secured an
air-tight fit around the
neck. The box was connected by tubing to a piston recorder which not
only made a record of the
respiratory rate but on calibration gave an accurate measure of the air
passing in and out of the
lungs.
The
data thus secured, as
shown in Table 27, indicate in all cases a final marked increase in
pulmonary aeration. In all cases the amount of air respired was at
least doubled in the latter
periods of the poisoning. Even after the
366
break in arterial pressure
when respirations often slowed down, the increase in aeration was
maintained. In three cases the amount respired immediately after
gassing was definitely lower
than normal.
TABLE
27.- Pulmonary aeration during
phosgene poisoning
TEMPERATURE
The
only constant change in
temperature was a gradual fall as blood concentration increased and
death became imminent. This amounted to as much as 20 in many cases.
Very frequently there
was a slight initial rise in temperature during stage 1.
ALKALINE RESERVE
Our
studies on alkaline
reserve were very incomplete. Determinations taken at irregular
intervals
in 11 experiments seem, however, to justify the statement that there
was no change of particular
significance until the latter periods of the experiment. At about the
time blood pressure fell so
markedly there was a decided decrease in the alkaline reserve. The
tissues at that time were
undoubtedly suffering from oxygen want and the decrease in carbonate
was due to the formation
of fixed acids.
DISCUSSION
The
various pathological
physiology studies just reported are of interest chiefly in giving a
conception of phosgene poisoning as a whole. In fatal cases, and these
studies were made on
such, two rather well-marked stages were apparent. The first of these
was characterized by the
nervous reflexes due to the irritation of the gas in the respiratory
passages and by the direct
chemical action of the gas or its decomposition products on the blood.
The second stage was
characterized by well-developed pulmonary edema and its natural
consequences. The whole
subject, indeed, might well be termed a study of pulmonary edema
induced by phosgene.
The
first effect of the gas
was to injure the linings of the deep respiratory passages. Spasm of
bronchiole musculature was evidence of the stimulation produced by the
fumes. As a result of
this there was a reflex cardiac inhibition, very characteristic of many
stimulations of the
respiratory surfaces. The composite curve of heart rates shows a
decrease during the first half of
the poisoning. Another reflex from the same cause was a vasomotor one
which brought about
peripheral constriction, with a rise in blood pressure. The X ray gave
evidence of pulmonary
injury at this time although physical signs were usually entirely
absent. More important than
these nervous phenomena, however, is the direct action of the gas on
the blood in the pulmonary
capillaries. Here the red corpuscles were agglomerate(l into masses
which largely
367
filled and blocked the
capillary passages. Bubbling gas through blood showed that it might
have
just this effect. The results of this plugging of the capillaries were
twofold. In the first place
pulmonary resistance was increased and a load thrown upon the right
heart. Evidence of this was
seen in the right cardiac dilatation found in the X-ray plates. A
second result was the removal of
red cells from the circulation, which resulted in a decreased
hemoglobin content of the blood.
This first stage of phosgene poisoning, as shown by Underhill, is most
easily determined by
following the hemoglobin, and it may be spoken of as the stage of
decreased hemoglobin
concentration.
Underhill
explained the
decreased hemoglobin concentration on the basis of blood dilution by
body fluids. Just how or why blood volume should be increased at this
time is not clear. That this
interpretation is probably not sufficient is shown by direct
determinations which indicate no
increase in blood volume, and by the histological examination which
show the red cells
agglomerated in the capillaries.
Long
before the end of the
first stage pulmonary edema was under way. The direct cause of this
was undoubtedly the increased permeability of alveolar and capillary
walls, due to direct injury
from the gaseous fumes. The increased pulmonary blood pressure
resulting from the capillary
plugging greatly favored the condition.
The
second stage of acute
phosgene poisoning was characterized by rapid development of the
pulmonary edema with all its physical signs. This resulted in a
decreased blood volume and
increased hemoglobin concentration and a smaller diastolic size of the
heart. The essential thing
was the greatly reduced blood volume, which is almost entirely
accounted for by the increased
fluid in the lungs.
Death
under such conditions
obviously may be accounted for in either one of two ways. The
edematous condition of the lungs may interfere with the gaseous
exchanges to such an extent
that the animal asphyxiates, or the blood volume may be so reduced that
even though the
hemoglobin is oxygenated there is not enough fluid to secure its proper
distribution to and
circulation in the tissues. So far as the tissues themselves were
concerned the result was the
same. They died of oxygen starvation. Death was probably due to a
combination of the two
causes. This belief is based on a series of experiments in which gassed
animals were
immediately placed in chambers containing 40 to 60 percent oxygen. The
carbon dioxide content
was of course kept within physiological limits and oxygen supplied
automatically so as to keep
the amount constant. The majority of these animals lived from 48 to 72
hours instead of the
average 16 and seemed to be recovering. On being released the usual
occurrence was for each
dog to walk across the room and fall into an asphyxial convulsion,
which quickly terminated in
death. Several of the animals were hurried back into the oxygen chamber
and resuscitated. These
animals were edematous with reduced blood volumes, but in an atmosphere
of 40 percent oxygen
life was preserved, one is tempted to believe, because of complete
hemoglobin saturation and
physical absorption of oxygen. That decreased blood volume is a
cardinal part of the syndrome,
and possibly by far the most important part, need not be questioned.
368
SUMMARY
1. A
study of the
pathological physiology of acute phosgene poisoning shows a well-marked
succession of events which finally results in typical pulmonary edema.
The microscope and the
X ray both show an early injury to the linings of the deep respiratory
passages. Irritation from
this results in a certain amount of reflex cardiac inhibition and
vasoconstriction. Coincident with
these changes there is a direct action of the gas on the red blood
cells, which causes them to
agglomerate and obstruct the pulmonary capillaries.The removal of red
blood cells from the
active circulation in this way results in a decreased hemoglobin
percentage. The plugging of the
capillaries throws a strain on the right heart and a right-sided
cardiac dilatation is apparent.
These are the chief characteristics of stage 1.
2. Even
during stage 1 the
injury to the alveolar membranes and the increased pressure have
initiated the transfusion of fluid from the blood into the tissue
spaces and later into the air
passages of the lungs. The rapid development of the edema is the chief
characteristic of stage 2.
It results in hemoglobin concentration, reduction in blood volume and
decrease in heart size, all
three of which proceed to extreme degrees. Death ultimately results
from decreased oxygenation
of the pulmonary blood and from oxygen starvation of the tissues due to
decreased blood
volume, the latter being probably the more important.
REFERENCES
(1) Underhill, Frank P.:
The Lethal War Gases. New Haven, Conn., Yale University Press, 1920.
(2) Meek, W. J., Gasser, H.
S., and Erlanger, J.: Studies in Secondary Traumatic Shock American
Journal of Physiology, Baltimore, Md., October, 1919, 1, No. 1, 31.
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