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Discussion of the Treatment of the Heart in Its Various Disorders,
With a Chapter on Blood Pressure

Professor of Therapeutics and formerly Professor of Clinical
Medicine in Yale Medical School NEW HAVEN, CONN.

Five Hundred Thirty-Five
North Dearborn Street, Chicago


The second edition of this book is offered with the hope that it
will be as favorably received as was the former edition, The text
has been carefully revised, in a few parts deleted, and extensively
elaborated to bring the book up to the present knowledge concerning
the scientific therapy of heart disturbances. A complete section has
been added on blood pressure.


That marvelous organ which, moment by moment and year by year, keeps
consistently sending the blood on its path through the arteriovenous
system is naturally one whose structure and function need to be
carefully studied if one is to guard it when threatened by disease.
This series of articles deals with heart therapy, not discussing the
heart structurally and anatomically, but taking up in detail the
various forms of the disturbances which may affect the heart. The
cordial reception given by the readers of The Journal to this series
of articles has warranted its issue in book form so that it may be
slipped into the pocket for review at appropriate times, or kept on
the desk for convenient reference.


Preface to First Edition
Disturbances of the Heart in General
Classification of Cardiac Disturbances
Blood Pressure
Myocardial Disturbances
Chronic Diseases of the Valves
Acute Cardiac Symptoms: Acute Heart Attack
Diet and Baths in Heart Disease
Heart Disease in Children and During Pregnancy
Cardiovascular Renal Disease
Disturbances of the Heart Rate
Toxic Disturbances and Heart Rate
Miscellaneous Disturbances


Of prime importance in the treatment of diseases of the heart is a
determination of the exact, or at least approximately exact,
condition of its structures and a determination of its ability to

This is not the place to describe its anatomy or its nervous
mechanism or the newer instruments of precision in estimating the
heart function, but they may be briefly itemized. It has now been
known for some time that the primary stimulus of cardiac contraction
generally occurs at the upper part of the right auricle, near its
junction with the superior vena cava, and that this region may be
the "timer" of the heart.

This is called the sinus node, or the sino-auricular node, and
consists of a small bundle of fibers resembling muscle tissue. Lewis
[Footnote: Lewis: Lecture in the Harvey Society, New York Academy of
Medicine, Oct. 31, 1914.] describes this bundle as from 2 to 3 cm.
in length, its upper end being continuous with the muscle fibers of
the wall of the superior vena cava. Its lower end is continuous with
the muscle fibers of the right auricle. From this node "the
excitation wave is conducted radially along the muscular strands at
a uniform rate of about a thousand millimeters per second to all
portions of the auricular musculature."

Though a wonderfully tireless mechanism, this region may fall out of
adjustment, and the stimuli proceeding from it may not be normal or
act normally. It has been shown recently not only that there must be
perfection of muscle, nerve and heart circulation but also that the
various elements in solution in the blood must be in perfect amounts
and relationship to each other for the heart stimulation to be
normal. It has also been shown that if for any reason this region of
the right auricle is disturbed, a stimulus or impulse might come
from some other part of the auricle, or even from the ventricle, or
from some point between them. Such stimulations may constitute
auricular, ventricular or auriculoventricular extra contractions or
extrasystoles, as they are termed. In the last few years it has been
discovered that the auriculoventricular handle, or "bundle of His,"
has a necessary function of conductivity of auricular impulse to
ventricular contraction. A temporary disturbance of this
conductivity will cause a heart block, an intermittent disturbance
will cause intermittent heart block (Stokes-Adams disease), and a
prolonged disturbance, death. It has also been shown that
extrasystoles, meaning irregular heart action, may be caused by
impulses originating at the apex, at the base or at some point in
the right ventricle.

In the ventricles, Lewis states, the Purkinje fibers act as the
conducting agent, stimuli being conducted to all portions of the
endocardium simultaneously at a rate of from 2,000 to 1,000 mm. per
second. The ventricular muscle also aids in the conduction of the
stimuli, but at a slower rate, 300 mm. per minute. The rate of
conduction, Lewis believes, depends on the glycogen content of the
structures, the Purkinje fibers, where conduction is most rapid,
containing the largest amount of glycogen, the auricular musculature
containing the next largest amount of glycogen, and the ventricular
muscle fibers the least amount of glycogen.

Anatomists and histologists have more perfectly demonstrated the
muscle fibers of the heart and the structure at and around the
valves; the physiologic chemists have shown more clearly the action
of drugs, metals and organic solutions on the heart; and the
physiologists and clinicians with laboratory facilities have
demonstrated by various new apparatus the action of the heart and
the circulatory power under various conditions. It is not now
sufficient to state that the heart is acting irregularly, or that
the pulse is irregular; the endeavor should be to determine whit
causes the irregularity, and what kind of irregularity is present.


A moment may be spent on clinical interpretation of pulse tracings.
It has recently been shown that the permanently irregular pulse is
due to fibrillary contraction, or really auricular fibrillation--in
other words, irregular stimuli proceeding from the auricle--and that
such an irregular pulse is not due to disturbance at the
auriculoventricular node, as believed a short time ago. These little
irregular stimuli proceeding from the auricle reach the
auriculoventricular node and are transmitted to the ventricle as
rapidly as the ventricle is able to react. Such rapid stimuli may
soon cause death; or, if for any reason, medicinal or otherwise, the
ventricle becomes indifferent to these stimuli, it may not take note
of more than a certain portion of the stimuli. It then acts slowly
enough to allow prolongation of life, and even considerable
activity. If such a heart becomes more rapid from such stimuli, 110
or more, for any length of time, the condition becomes very serious.
Digitalis in such a condition is, of course, of supreme value on
account of its ability to slow the heart. Such irregularity perhaps
most frequently occurs with valvular disease, especially mitral
stenosis and in the muscular degenerations of senility, as fibrosis.

Atropin has been used to differentiate functional heart block from
that produced by a lesion. Hart [Footnote: Hart: Am. Jour. Med. Sc.,
1915, cxlix, 62.] has used atropin in three different types of heart
block. In the first the heart block is induced by digitalis. This
was entirely removed by atropin. In the second type, where there was
normal auricular activity, but where the ventricular contractions
were decreased, atropin affected an increase in the number of
ventricular contractions, but did not completely remove the heart
block. He adopted atropin where the heart block was associated with
auricular fibrillation. The number of ventricular contractions was
increased, but not enough to indicate the complete removal of the
heart block.

Lewis [Footnote: Lewis: Brit. Med. Jour., 1909, ii, 1528.] believes
that 50 percent of cardiac arrhythmia originates in muscle
disturbance or incoordination in the auricle. These stimuli are
irregular in intensity, and the contractions caused are irregular in
degree. If the wave lengths of the pulse tracing show no regularity-
-if, in fact, hardly two adjacent wave lengths are alike--the
disturbance is auricular fibrillation. Injury to the auricle, or
pressure for any reason on the auricle, may so disturb the
transmission of stimuli and contractions that the contractions of
the ventricle are very much fewer than the stimuli proceeding from
the auricle. In other words, a form of heart block may occur.
Various stimuli coming through the pneumogastric nerves, either from
above or from the peripheral endings in the stomach or intestines,
may inhibit or slow the ventricular contractions. It seems to have
been again shown, as was earlier understood, that there are
inhibitory and accelerator ganglia in the heart itself, each subject
to various kinds of stimulation and various kinds of depression.

Both auricular fibrillation and auricular flutter are best shown by
the polygraph and the electrocardiograph. The former is more exact
as to details. Auricular flutter, which has also been called
auricular tachysystole, is more common that is supposed. It consists
of rapid coordinate auricular contractions, varying from 200 to 300
per minute. Fulton [Footnote: Fulton, F. T.: "Auricular Flutter,"
with a Report of Two Cases, Arch. Int. Med., October, 1913, p. 475.]
finds in this condition that the initial stimulus arises in some
part of the auricular musculature other than the sinus node. It is
different from paroxysmal tachycardia, in which the heart rate
rarely exceeds 180 per minute. In auricular flutter there is always
present a certain amount of heart block, not all the stimuli
reaching the ventricle. There may be a ratio of auricular
contractions to ventricular contractions, according to Fulton, of
2:1, 3:1, 4:1 and 5:1, the 2:1 ratio being most common.

Of course it is generally understood that children have a higher
pulse rate than adults; that women normally have a higher pulse rate
than men at the same age; that strenuous muscular exercise,
frequently repeated, without cardiac tire while causing the pulse to
be rapid at the time, slows the pulse during the interim of such
exercise and may gradually cause a more or less permanent slow
pulse. It should be remembered that athletes have slow pulse, and
the severity of their condition must not be interpreted by the rate
of the pulse. Even with high fever the pulse of an athlete may be

Not enough investigations have been made of the rate of the pulse
during sleep under various conditions. Klewitz [Footnote: Klewitz:
Deutsch. Arch. f. klin. Med. 1913, cxii, 38.] found that the average
pulse rate of normal individuals while awake and active was 74 per
minute, but while asleep the average fell to 59 per minute. He found
also that if a state of perfect rest could be obtained during the
waking period, the pulse rate was slowed. This is also true in cases
of compensated cardiac lesions, but it was not true in decompensated
hearts. He found that irregularities such as extrasystoles and
organic tachycardia did not disappear during sleep, whereas
functional tachycardia did.

It is well known that high blood pressure slows the pulse rate; that
low blood pressure generally increases the pulse rate, and that
arteriosclerosis, or the gradual aging of the arteries, slows the
pulse, except when the cardiac degeneration of old age makes the
heart again more irritable and more rapid. The rapid heart in
hyperthyroidism is also well understood. It is not so frequently
noted that hypersecretion of the thyroid may cause a rapid heart
without any other tangible or discoverable thyroid symptom or
symptoms of hyperthyroidism. Bile in the blood almost always slows
the pulse.


The interpretation of the arterial tracing shows that the nearly
vertical tip-stroke is due to the sudden rise of blood pressure
caused by the contraction of the ventricles. The long and irregular
down-stroke means a gradual fall of the blood pressure. The first
upward rise in this gradual decline is due to the secondary
contraction and expansion of the artery; in other words, a tidal
wave. The second upward rise in the decline is called the recoil, or
the dicrotic wave, and is due to the sudden closure of the aortic
valves and the recoil of the blood wave. The interpretation of the
jugular tracing, or phlebogram as the vein tracing may be termed,
shows the apex of the rise to be due to the contraction of the
auricle. The short downward curve from the apex means relaxation of
the auricle. The second lesser rise, called the carotid wave, is
believed to be due to the impact of the sudden expansion of the
carotid artery. The drop of the wave tracing after this cartoid rise
is due to the auricular diastole. The immediate following second
rise not so high as that of the auricular contraction is known as
the ventricular wave, and corresponds to the dicrotic wave in the
radial. The next lesser decline shows ventricular diastole, or the
heart rest. A tracing of the jugular vein shows the activity of the
right side of the heart. The tracing of the carotid and radial shows
the activity of the left side of the heart. After normal tracings
have been carefully taken and studied by the clinician or a
laboratory assistant, abnormalities in these readings are readily
shown graphically. Especially characteristic are tracings of
auricular fibrillation and those of heart block.


If both systolic and diastolic blood pressure are taken, and the
heart strength is more or less accurately determined, mistakes in
the administration of cardiac drugs will be less frequent. Besides
mapping out the size of the heart by roentgenoscopy and studying the
contractions of the heart with the fluoroscope, and a detailed study
of sphygmographic and cardiographic tracings, which methods are not
available to the large majority of physicians, there are various
methods of approximately, at least, determining the strength of the
heart muscle.

Barringer [Footnote: Barringer, T. B., Jr.: The Circulatory Reaction
to Graduated Work as a Test of the Heart's Functional Capacity,
Arch. Int. Med., March, 1916, p. 363.] has experimented both with
normal persons and with patients who were suffering some cardiac
insufficiency. He used both the bicycle ergometer and dumb-bells,
and finds that there is a rise of systolic pressure after ordinary
work, but a delayed rise after very heavy work, in normal persons.
In patients with cardiac insufficiency he finds there is a delayed
rise in the systolic pressure after even slight exercise, and those
with marked cardiac insufficiency have even a lowering of blood
pressure from the ordinary level. They all have increase in pulse
rate. He quotes several authorities as showing that during muscle
work the carbon dioxid of the blood is increased in amount, which,
stimulating the nervous centers controlling the suprarenal glands,
increases the epinephrin content of the blood. The consequence is
contraction of the splanchnic blood vessels, with a rise in general
blood pressure. Also, the quickened action of the heart increases
the blood pressure. After a rest from the exercise, the extra amount
of carbon dioxid is eliminated from the blood, the suprarenal glands
decrease their activity, and the blood pressure falls.

Nicolai and Zuntz [Footnote: Nicolai anal Zuntz: Berl. klin.
Wehnschr., May 4, 1914, p. 821.] have shown that with the first
strain of heavy work the heart increases in size, but it soon
becomes normal, or even smaller, as it more strenuously contracts,
and the cavities of the heart will be completely emptied at each
systole. If the work is too heavy, and the systolic blood pressure
is rapidly increased, it may become so great as to prevent the left
ventricle from completely evacuating its content. The heart then
increases in size and may sooner or later become strained; if this
strain is severe, an acute dilatation may of course occur, even in
an otherwise well person. Such instances are not infrequent. A heart
which is already enlarged or slightly dilated and insufficient,
under the stress of muscular labor will more slowly increase its
forcefulness, and we have the delayed rise in systolic pressure.

Barringer concludes that:

The pulse rate and the blood pressure reaction to graduated work is
a valid test of the heart's functional capacity. If the systolic
pressure reaches its greatest height not immediately after work, but
from thirty to 120 seconds later, or if the pressure immediately
after work is lower than the original level, that work, whatever its
amount, has overtaxed the heart's functional capacity and may be
taken as an accurate measure of the heart's sufficiency.

In another article, Barringer [Footnote: Barringer, T. B., Jr.:
Studies of the Heart's Functional Capacity as Estimated by the
Circulatory Reaction to Graduated Work, Arch. Int. Med., May, 1916,
p. 670.] advises the use of a 5-pound dumb-bell extended upward from
the shoulder for 2 feet. Each such extension represents 10 foot-
pounds of work, although the exertion of holding the dumb-bell
during the nonextension period is not estimated. He believes that if
circulatory tire is shown with less than 100 foot-pounds per minute
exercise, other signs of cardiac insufficiency will be in evidence.
He also believes that these foot-pound tests can be made to
determine whether a patient should be up and about, and also that
such graded exercise will increase the heart strength in cardiac

Schoonmaker, [Footnote: Schoonmaker: Am. Jour. Med. Sc., October,
1915, p. 582.] after studying the blood pressure of 127 patients,
concludes that myocardial efficiency will be shown by a comparison
of the systolic and diastolic blood pressure, with the patient lying
down and standing up, after walking a short distance. Such slight
exercise should not cause any subjective symptoms, either dyspnea,
palpitation or chest pain. If the heart muscle is in good condition,
the systolic pressure should remain the same after this slight
exertion and these changes in posture. When the heart is good, there
may be slight increased pressure when the patient is standing. If,
after this slight exercise in the erect posture, the systolic
pressure is diminished, the heart muscle is defective.

Martinet [Footnote: Martinet: Presse med., Jan. 20, 1916.] tests the
heart strength as follows: He counts the pulse until for two
successive minutes there is the same number of beats, first when the
patient is lying down, and then when he is standing. He also takes
the systolic and diastolic pressures at the same time. He then
causes the person to bend rapidly at the knees twenty times. The
pulse rate and the blood pressure are then taken each minute for
from three to five minutes. The person then reclines, and the pulse
and pressure are again recorded, Martinet says that an examination
of these records in the form of a chart gives a graphic
demonstration of the heart strength. If the heart is weak, there are
likely to be asystoles, and tachycardia may occur, or a lowered
blood pressure.

Rehfisch [Footnote: Rehfisch: Berl. klin. Wehnsehr., Nov. 29, 1915]
states that when a healthy person takes even slight exercise, the
aortic closure becomes louder than the second pulmonic sound,
showing an increased systolic pressure. If the left ventricle is
unable properly to empty itself against the increased resistance
ahead, the left auricle will contain too much blood, and with the
right ventricle sufficient, there will be an accentuation of the
second pulmonic sound and it may become louder than the second
aortic sound, showing a cardiac deficiency. If, on the other hand,
the right ventricle becomes insufficient, or is insufficient, the
second pulmonic sound is weaker than normal, and the prognosis is

Barach [Footnote: Barach: Am. Jour. Med. Sc., July, 1916, p. 84]
presents what he terms "the energy index of the circulatory system."
He has examined 742 normal persons, and found that the pressure
pulse was anywhere from 20 to 80 percent of the diastolic pressure
in 80 per cent of his cases, while the average of his figures gave a
ratio of 50 percent; but he does not believe that it holds true that
in a normal person the pressure pulse equals 50 percent of the
diastolic pressure. Barach does not believe we have, as yet, any
very accurate method of determining the cardiac strength or
circulatory capacity for work. He does not believe that the estimate
of the pressure pulse is indicative of cardiac strength. He believes
that the important factors in the estimation of the circulatory
strength are the systolic pressure, which shows the power of the
left ventricle, the diastolic pressure, which shows the
intravascular tension during diastole as well as the peripheral
resistance, and the pulse rate, which designates the number of times
the heart must contract during a minute to maintain the proper flow
of blood. He thinks that these three factors are constantly adapting
themselves to each other for the needs of the individual, and he
finds, for instance, that when the left ventricle is hypertrophied
and the output of blood is therefore greater, then the pulse will be
slowed. His method of estimation is as follows: For instance, with a
systolic pressure of 120 mm. and a diastolic pressure of 80 mm.,
each pulse beat will represent an energy equal to lifting 120 mm.
plus 80 mm., which equals 200 mm. of mercury, and with seventy-two
pulse beats the force would be 72 X 200, which equals 14,400 mm. of
mercury. He finds an average circulatory strength based on examining
250 normal individuals by the index, which he terms S, D, R
(systolic, diastolic rate), to be 20,000 mm. of mercury per minute.

Katzenstein [Footnote: Katzenstein: Deutsch. med. Wehnsehr., April
15, 1915.] finds, after ten years of experience, that the following
test of the heart strength is valuable: He records the blood
pressure and pulse, and then compresses the femoral artery at
Poupart's ligament on the two sides at once. He keeps this pressure
up for from two to two and one-half minutes, and then again takes
the blood pressure. With a sound heart the blood pressure will be
higher and the pulse slower than the previous record taken. If the
blood pressure and pulse beat are not changed, it shows that the
heart is not quite normal, but not actually incompetent. When the
blood pressure is lower and the pulse accelerated, he believes that
there is distinct functional disturbance of the heart and loss of
power, relatively to the change in pressure and the increase of the
pulse rate. He further believes that a heart showing this kind of
weakness should, if possible, not be subjected to general

Stange [Footnote: Stange: Russk. Vrach, 1914, xiii. 72.] finds that
the cardiac power may be determined by a respiratory test as
follows: The patient should sit comfortably, and take a deep
inspiration; then he should be told to hold his breath, and the
physician compresses the patient's nostrils. As soon as the patient
indicates that he can hold his breath no longer, the number of
seconds is noted. A normal person should hold his breath from thirty
to forty seconds without much subsequent dyspnea, while a patient
with myocardial weakness can hold his breath only from ten to twenty
seconds, and then much temporary dyspnea will follow. Stange does
not find that pulmonary conditions, as tuberculosis, pleurisy or
bronchitis, interfere with this test.

Williamson [Footnote: Williamson: Ant. Jour. Med. Sc., April, 1915,
p. 492.] believes that we cannot determine the heart strength
accurately unless we have some method to note the exact position of
the diaphragm, and he has devised a method which he calls the
teleroentgen method. With this apparatus he finds that a normal
heart responds to exercise within its power by a diminution in size.
The same is true of a good compensating pathologic heart. He thinks
that a heart which does not so respond by reducing its size after
exercise has a damaged muscle, and compensation is more or less

Practical conclusions to draw from the foregoing suggestions are:

1. An enlargement of the heart after exercise can be well shown only
by fluoroscopic examination, and then best by some accurate method
of measurement.

2. The blood pressure should be immediately increased by exercise,
and after such exercise should soon return to the normal before the
exercise. If it goes below the normal the heart is weak, or the
exercise was excessive.

3. The pulse rate should increase with exercise, but not
excessively, and should within a reasonable time return to normal.

4. The stethoscope will show whether or not the normal sounds of the
heart become relatively abnormal after exercise. If such was the
fact, though the abnormality was not permanent, heart insufficiency
is more or less in evidence.

5. The relation of pulse rate to blood pressure should always be
noted, and the working power of the heart may be estimated according
to Barach's suggestion.

6. The dumb-bell exercise tests suggested by Barringer (only, the
dumb-bells may be of lighter weight) are valuable to note the
gradual improvement in heart strength of patients under treatment.

7. The holding the breath test is very suggestive of heart
efficiency or weakness, but a series of tests must be made before
its limitations are proved.


We can no longer neglect the seriousness of the effects of
competitive athletics on the heart, especially in youth and young
adults. Not only universities and preparatory schools, but also high
schools and even grammar schools must consider the advisability of
continuing competitive sports without more control than is now the
case. In the first place, the individual is likely to be trained in
one particular branch or in one particular line, which develops one
particular set of muscles. In the second place, competition to
exhaustion, to vomiting, faintness, and even syncope is absolutely
inexcusable. Furthermore, contests which partake of brutality should
certainly be seriously censored.

A committee appointed some time ago by the Medical Society of the
State of California [Footnote: California State Med. Jour., June,
1916 p. 220.] has recently reported its endorsement of Foster's
"Indictment of Intercollegiate Athletics." After five years of
personal observation of no less than 100 universities and colleges,
in thirty-eight states, Foster concludes that intercollegiate
athletics have proved a failure, and that they are costly and
injurious on account of an excessive physical training of a few
students, and of such students as need training least, while
healthful and moderate exercise at a small expense for all students
is most needed.

Experts, [Footnote: Rubner and Kraus: Vrtljsehr. f. gerichtl. Med,
1914, xlviii, 304.] appointed by the Prussian government to
investigate athletics, reported that for physical exercise to be of
real value it must be quite different from the preparation of a
specially equipped individual trained for a game. Exercise should
benefit all children and youth, while athletic prowess necessitates
taxing the organism to the limit of endurance, and hence is
dangerous and should not be allowed in schools or universities.

McKenzie [Footnote: McKenzie: Am. Jour. Med. Sc., January, 1913, p.
69.] found that exhausting tests of endurance were not adapted to
the development of children and youth, because the high blood
pressure caused by such exertion soon continued, and he found
athletes to have a prolonged increased blood pressure. As is
recognized by all, boat racing is particularly bad, especially the
4-mile row. Such severe exertion of course increases the blood
pressure, even in these athletes, and the heart increases its speed.
There is then exhilaration, later discomfort, and soon, as McKenzie
points out, a sensation of constriction in the chest and head. This
is soon followed by breathlessness, and soon by a feeling of fulness
in the head, and then syncope. The heart, of course, becomes
dilated. Heart murmurs are often found after much less severe
exertion than boat racing. They may not last long, or they may
disappear under proper treatment. He reported that after exercise
there were heart murmurs in seventy-four of 266 young men who were
in normal health, and that nearly 28 per cent of all normal young
men will show a murmur after exercise. He thinks that it is rare to
find, after a week, a heart murmur in a previously healthy heart, if
the athlete has not passed the age of 30.

There can be no doubt that even one, to say nothing of more, such
heart strains is inexcusable and may leave a more or less lasting
injury. Such heart strains and exertions are not entirely seen in
athletes. A man otherwise well may cause such a heart strain by
cranking his automobile, by pumping up a tire, by strenuous lifting,
by carrying a load too far or too rapidly, or by running, and an
elderly man may even cause such a heart strain by walking, hill
climbing, or even golfing, if he does these things. More or less
acute dilatation occurring in such persons is likely to recur on the
least exertion, unless the patient takes a prolonged rest cure and
the heart is so well that it recuperates perfectly. Any chronic
myocarditis, however, may prevent such a heart from ever being as
perfect as it was before.

Torgersen, [Footnote: Torgersen: Norsk Mag. f. Laegevidensk., April,
1914.] after making 600 examinations of 200 athletes, and 1,200
examinations of members of the rowing crew, decides that it is
absolutely essential that there should be skilled daily examinations
of every man during training, and a record kept of the condition of
his heart, urine, and blood pressure, before and after exercise.
When he found albumin in the urine it was always accompanied by a
falling of the blood pressure and a rapid heart, with loss of weight
and a general feeling of debility.

Middleton [Footnote: Middleton: Am. Jour. Med. Sc., September, 1915,
p. 426.] examined students who were training for football, both
during the training and after the training period, and found that
after the rest succeeding a training period there was an increased
systolic and diastolic blood pressure over the records of before the
training period. This would tend to indicate some hypertrophy of the

Insurance statistics seem to show that athletes are likely to have
earlier cardiovascular-renal disease than other individuals of the
same class and occupations.


1. Gymnasiums and athletic grounds in connection with all colleges,
preparatory schools, seminaries and high schools are essential, and
they should be added to grammar schools whenever possible.

2. Physical training and athletic games, and perhaps some type of
military training are valuable for the proper development of youth.

3. Some forms of competitive games and some competitive feats are
valuable in stimulating training and healthful sports.

4. All competitive sports and all hard training should be under the
advice and supervision of a medical council or a medical trainer.
Competitive sports which are generally recognized as harmful, mostly
on account of their duration as related to the age of the
competitors, should be prohibited.

5. Each boy should be carefully examined by a competent physician to
decide as to his general health, his limitations and the special
training necessary to perfect him or to overcome any defect. Such
examinations are even more essential in schools for girls.

6. In all group training, the weak individuals should be noted by
the medical trainer, and they should receive special and more
carefully graded exercise.

7. In all strenuous training or competitive athletic work, the
participators should all be examined more or less frequently and
more or less carefully for heart strain and albuminuria and also for
a too great increase of blood pressure.

8. All training and all athletic sports should be graded to the age
of the boy or girl and not necessarily to his or her size. Many an
overgrown boy is injured by athletic prowess beyond his heart


It should be remembered that a normal heart may slow to about 60
during sleep, and all nervous acceleration of the pulse may be
differentiated during sleep by the fact that if the heart does not
markedly slow, there is cardiac weakness or some general
disturbance. There is also cardiac weakness if there is a tendency
to yawn or to take long breaths after slight exertions or during
exertion, or if there is a feeling of suffocation and the person
suddenly wants the windows open, or cannot work, even for a few
minutes, in a closed room. If these disturbances are purely
functional, exercise not only may be endured, but will relieve some
nervous heart disturbances, while it will aggravate a real heart
disability. If the heart tends to increase in rapidity on lying
down, or the person cannot breathe well or feels suffocated with one
ordinary pillow, the heart shows more or less weakness.
Extrasystoles are due to abnormal irritability of the heart muscle,
and may or may not be noted by the patient. If they are noted, and
he complains of the condition, the prognosis is better than though
he does not note them.

It has long been known that asthma, emphysema, whooping cough, and
prolonged bronchitis with hard coughing will dilate the heart. It
has not been recognized until recently, as shown by Guthrie,
[Footnote: Guthrie, J. B.: Cough Dilatation Time a Measure of Heart
Function, The Journal. A. M. A., Jan. 3, 1914, p. 30.] that even one
attack of more or less hard coughing will temporarily enlarge the
heart. From these slight occurrences, however, the heart quickly
returns to its normal size; but if the coughing is frequently
repeated, the dilatation is more prolonged. This emphasizes the
necessity of supporting the heart in serious pulmonary conditions,
and also the necessity of modifying the intensity of the cough by
necessary drugs.

In deciding that a heart is enlarged by noting the apex beat,
percussion dulness, and by fluoroscopy, it should be remembered that
the apex beat may be several centimeters to the left from the actual
normal point, and yet the heart not be enlarged.

The necessity of protecting the heart in acute infections, and the
seriousness to the heart of infections are emphasized by the present
knowledge that tonsillitis, acute or chronic, and mouth and nose
infections of all kinds can injure the heart muscle. In probably
nearly every case of diphtheria, unless of the mildest type, there
is some myocardial involvement, even if not more than 25 percent of
such cases show clinical symptoms of such heart injury. Tuberculosis
of different parts of the body also, sooner or later, injures the
heart; and the effect of syphilis on the heart is now well


It is now recognized that any infection can cause weakness and
degeneration of the heart muscle. The Streptococcus rheumaticus
found in rheumatic joints is probably the cause of such heart injury
in rheumatism. That prolonged fever from any cause injures heart
muscle has long been recognized, and cardiac dilatation after severe
illness is now more carefully prevented. It is not sufficiently
recognized that chronic, slow-going infection can injure the heart.
Such infections most frequently occur in the tonsils, in the gums,
and in the sinuses around the nose. Tonsillitis, acute or chronic,
has been shown to be a menace to the heart. Acute streptococcie
tonsillitis is a very frequent disease, and the patient generally,
under proper treatment, quickly recovers. Tonsillitis in a more or
less acute form, however, sometimes so mild as to be almost
unnoticed, probably precedes most attacks of acute inflammatory
rheumatism. Chronically diseased tonsils may not cause joint pains
or acute fever, but they are certainly often the source of blood
infection and later of cardiac inflammations. The probability of
chronic inflammation and weakening of the heart muscle from such
slow-going and continuous infection must be recognized, and the
source of such infection removed.

The determination of the presence of valvular lesions is only a
small part of the physical examination of the heart. Furthermore,
the heart is too readily eliminated from the cause of the general
disturbance because murmurs are not heard. A careful decision as to
the size of the heart will often show that it has become slightly
dilated and is a cause of the general symptoms of weakness, leg
weariness, slight dyspnea, epigastric distress or actual chest
pains. Many such cases are treated for gastric disturbance because
there are some gastric symptoms. There is no question that gastric
flatulence, or hyperacidity, or a large meal causing distention of
the stomach may increase the cardiac disturbance, and the cardiac
disturbance may be laid entirely to indigestion; but treatment
directed toward the stomach, while it may ameliorate some of the
symptoms, will not remove the cause of the symptoms.

If the patient complains of pains in any part of the chest or upper
abdomen, or of leg aches, or of being weary, or exhausted, or of
sleeplessness at night, or of pains in the back of his head, we
should investigate the cardiac ability, besides ruling out all of
the more frequently recognized causes of these disturbances.

If there is more dyspnea than normally should occur in the
individual patient after walking rapidly or climbing a hill or going
upstairs, or if after a period of a little excitement one finds that
he cannot breathe quite normally, or that something feels tight in
his chest, the heart needs resting. If, after one has been driving a
motor car or even sitting at rest in one which has been going at
speed or has come unpleasantly near to hitting something or to being
run into, it is noticed that the little period of cardiac
disturbance and chest tension is greater than it should be, the
heart needs resting.

If the least excitement or exertion increases the cardiac speed
abnormally, it means that for many minutes, if not actually hours
during the twenty-four, the heart is contracting too rapidly, and
this alone means muscle tire and muscle nutrition lost, even if
there is no actual defect in the cardiac muscle or in its own blood
supply. If we multiply these extra pulsations or contractions by the
number of minutes a day that this extra amount of work is done, it
will easily be demonstrable to the physician and the patient what an
amount of good a rest, however partial, each twenty-four hours will
do to this heart. Of course anything that tends to increase the
activity of the disturbance of the heart should be corrected.
Overeating, overdrinking (even water), and overuse or perhaps any
use of alcohol, tobacco, tea and coffee should all be prevented. In
fact, we come right to the discussion of the proper treatment and
management of beginning high blood pressure, of the incipiency of
arteriosclerosis, of the prevention of chronic interstitial
nephritis, and the prevention of cardiovascular-renal disease.

When an otherwise apparently well person begins to complain of
weariness, or perhaps drowsiness in the daytime and sleeplessness at
night, or his sleep is disturbed, or be has feelings of mental
depression, or he says that he "senses" his heart, perhaps for the
first time in his life, with or without edema of the feet and legs,
or pains referred to the heart or heart region, we should presuppose
that there is weakening of the heart muscle until, by perfect
examination, we have excluded the heart as being the cause of such

Although constantly repeated by all books on the heart and by many
articles on cardiac pain, it still is often forgotten that pain due
to cardiac disturbance may be referred to the shoulders, to the
upper part of the chest, to the axillae, to the arms, and even to
the wrists, to the neck, into the head, and into the upper abdomen.
It is perhaps generally auricular disturbance that causes pain to
ascend, but disturbances of the ventricles can cause pain in the
arms and in the region of the stomach. Not infrequently disturbances
of the aorta cause pain over the right side of the chest as well as
tip into the neck. Real heart pains frequently occur without any
valvular lesion, and also when necropsies have shown that there has
been no sclerosis of the coronary vessels.

While angina pectoris is a distinct, well recognized condition,
pains in the regions mentioned, especially if they occur after
exertion or after mental excitement or even after eating (provided a
real gastric excuse has been eliminated), are due to a disturbance
of the heart, generally to an overstrained heart muscle or to a
slight dilatation. Too much or too little blood in the cavity of the
heart may cause distress and pain; or an imperfect circulation
through the coronary arteries and the vessels of the heart,
impairing its nutrition or causing it to tire more readily, may be
the cause of these cardiac pains, distress or discomfort.

Palpating the radial artery is not absolutely reliable in all cases
of auricular fibrillation, or in another form of arrhythmia called
auricular flutter or tachysystole. James and Hart [Footnote: James
and Hart: Am. Jour. Med. Sc., 1914, cxlvii, 63.] have found that the
pulse is not a true criterion of the condition Of the circulation.
There is always a certain amount of heart block associated with
auricular fibrillation so that not all of the auricular stimuli pass
through the bundle of His. James and Hart determine the heart rate
both at the radial pulse and at the apex, the difference being
called the pulse deficit. They use this deficit as an aid in
deciding when to stop the administration of digitalis. When the
pulse deficit is zero, the digitalis is stopped. In this connection
they also find that, even though the pulse deficit may be zero,
there may be a difference in force and size of the waves at the
radial artery. This can be demonstrated by the use of a cuff around
the brachial artery and by varying the pressure. It will be found
that the greater the pressure, the fewer the number of beats coming

Besides the instruments of precision referred to above, more careful
percussion, more careful auscultation, more careful measurements,
roentgenoscopy and fluoroscopic examination of the heart, and a
study of the circulation with the patient standing, sitting, lying
and after exercise make the determination of circulatory ability a
specialty, and the physician who becomes an expert a specialist. It
is a specialization needed today almost more than in any other line
of medical science.

So frequently is the cause of these pains, disturbances and weakness
overlooked and the stomach or the intestines treated, or treatment
aimed at neuralgias, rheumatisms or rheumatic conditions, that a
careful examination of the patient, and a consideration of the part
the heart is playing in the causation of these symptoms are always

The treatment required for such a heart, unless there is some
complication, as a kidney complication or a too high blood pressure,
or arteriosclerosis (and none of these causes necessarily prohibits
energetic cardiac treatment), is digitalis. If there is doubt as to
the condition of the cardiac arteries, digitalis should be given in
small doses. If it causes distinct cardiac pain, it is not indicated
and should be stopped. If, on the other hand, improvement occurs, as
it generally does, the dose can be regulated by the results. The
minimum dose which improves the condition is the proper one. Enough
should be given; too much should not be given. Before deciding that
digitalis does not improve the condition (provided it does not cause
cardiac pain) the physician should know that a good and efficient
preparation of digitalis is being taken. Strychnin will sometimes
whip up a tired heart and tide it over periods of depression, but it
is a whip and not a cardiac tonic. While overeating, all
overexertion, and alcohol should be stopped, and the amount of
tobacco should be modified, there is no treatment so successful as
mental and physical rest and a change of climate and scene, with
good clean air.

Many persons with these symptoms of cardiac tire think that they are
house-tired, shop-tired, or office-tired, and take on a physical
exercise, such as walking, climbing, tennis playing or golf playing,
to their injury. Such tired hearts are not ready yet for added
physical exercise; they should be rested first.

The treatment of this cardiac tire is not complete until the
tonsils, gums, teeth and the nose and its accessory sinuses are in
good condition. Various other sources of chronic poisoning from
chronic infection should of course be eliminated, whether an uncured
gonorrhea, prostatitis, some chronic inflammation of the female
pelvic organs, or a chronic appendicitis.

Longcope [Footnote: Longcope, W. T.: The Effect of Repeated
Injections of Foreign Protein on the Heart Muscle, Arch. Int. Med.,
June, 1915, p. 1079.] has recently shown that repeated, and even at
times one protein poisoning can cause degeneration of the heart
muscle in rabbits. Hence it is quite possible that repeated
absorption of protein poisons from the intestines may injure the
heart muscle as well as the kidney structure; consequently, in heart
weakness, besides removing all evident sources of infection, we
should also give such food and cause such intestinal activity as to
preclude the absorption of protein poison from the bowels.


For the sake of discussing the therapy of cardiac disturbances in a
logical sequence, they may be classified as follows:



Acute, simple malignant
Valvular Lesions
Broken compensation
Cardiac drugs
Resort treatment
Cardiac disease in children
Cardiac disease in pregnancy
Coronary sclerosis
Angina pectoris
Stokes-Adams disease
Arterial hypertension
Cardiovascular-renal disease
Auricular fibrillation
Paroxysmal tachycardia
Toxic disturbances
Physiologic hypertrophies
Simple dilatation
Stomach dilatation
Anesthesia in heart disease


The study of the blood pressure has become a subject of great
importance in the practice of medicine and surgery. No condition can
be properly treated, no operation should be performed, and no
prognosis is of value without a proper consideration of the
sufficiency of the circulation, and the condition of the circulation
cannot be properly estimated without an accurate estimate of the
systolic and diastolic blood pressure. However perfectly the heart
may act, it cannot properly circulate the blood without a normal
tone of the blood vessels, both arteries and veins. Abnormal
vasodilatation seriously interferes with the normal circulation, and
causes venous congestion, abnormal increase in venous blood
pressure, and the consequent danger of shock and death. Increased
arterial tone or tonicity necessitates greater cardiac effort, to
overcome the resistance, and hypertrophy of the heart must follow.
This hypertrophy always occurs if the peripheral resistance is not
suddenly too great or too rapidly acquired. In other words, if the
peripheral resistance gradually increases, the left ventricle
hypertrophies, and remains for a long time sufficient. If, from
disease or disturbance in the lungs, the resistance in the pulmonary
circulation is increased, the right ventricle hypertrophies to
overcome it, and the circulation is sufficient as long as this
ventricle is able to do the work. If either this pulmonary increased
pressure or the systemic increased pressure persists or becomes too
great, it is only a question of how many months, in the case of the
right ventricle, and how many years, in the case of the left
ventricle, the heart can stand the strain.

If the cause of the increased systemic tension is an arterial
fibrosis, sooner or later the heart will become involved in this
general condition, and a chronic myocarditis is likely to result.
If, on the other hand, there is a continuous low systemic arterial
blood pressure, the circulation is always more or less insufficient,
nutrition is always imperfect, and the physical ability of the
individual is below par. It is evident, therefore, that an
abnormally high blood pressure is of serious import, its cause must
be studied, and effort must be made to remove as far as possible the
cause. On the other hand, a persistently low blood pressure may be
of serious import, and always diminishes physical ability. If
possible, the cause should be determined, and the condition

No physician can now properly practice medicine without having a
reliable apparatus for determining the blood pressure both in his
office and at the bedside. It is not necessary to discuss here the
various kinds of apparatus or what is essential in an apparatus for
it to give a perfect reading. It may be stated that in determining
the systolic and diastolic pressure in the peripheral arteries, the
ordinary stethoscope is as efficient as any more elaborate
auscultatory apparatus.

It is now generally agreed by all scientific clinicians that it is
as essential--almost more essential--to determine the diastolic
pressure as the systolic pressure; therefore the auscultatory method
is the simplest, as well as one of the most accurate in determining
these pressures. Of course it should be recognized that the systolic
pressure thus obtained will generally be some millimeters above that
obtained with the finger, perhaps the average being equivalent to
about 5 mm. of mercury. The diastolic pressure will often range from
10 to 15 mm. below the reading obtained by other methods. Therefore,
wider range of pressure is obtained by the auscultatory method than
by other methods. This difference of 5 or more millimeters of
systolic pressure between the auscultatory and the palpatory
readings should be remembered when one is consulting books or
articles printed more than two years ago, as many of these pressures
were determined by the palpatory method.

Sometimes the compression of the arm by the armlet leads to a rise
in blood pressure. [Footnote: MacWilliams and Melvin: Brit. Med.
Jour., Nov. 7, 1914.] It has been suggested that the diastolic
pressure be taken at the point where the sound is first heard on
gradually raising the pressure in the armlet.

In some persons the auscultatory readings cannot be made, or are
very unsatisfactory, and it becomes necessary to use the palpation
method in taking the systolic pressure. In instances in which the
auscultatory method is unsatisfactory, the artery below the bend of
the elbow at which the reading is generally taken may be misplaced,
or there may be an unusual amount of fat and muscle between the
artery and the skin.

The various sounds heard with the stethoscope, when the pressure is
gradually lowered, have been divided into phases. The first phase
begins with the first audible sound, which is the proper point at
which to read the, systolic pressure. The first phase is generally,
not always, succeeded by a second phase in which there is a
murmurish sound. The third phase is that at which the maximum sharp,
ringing note begins, and throughout this phase the sound is sharp
and intense, gradually increasing, and then gradually diminishing to
the fourth phase, where the sound suddenly becomes a duller tone.
The fourth phase lasts until what is termed the fifth phase, or that
at which all sound has disappeared. As previously stated, the
diastolic pressure may be read at the beginning of the fourth phase,
or at the end of the fourth phase, that is, the beginning of the
fifth; but the difference is from 3 to 10 mm. of mercury, with an
average of perhaps 5 mm.; therefore the difference is not very
great. When the diastolic pressure is high, for relative subsequent
readings, it is much better to read the diastolic at the beginning
of the fifth phase.

It is urged by many observers that the proper reading of the
diastolic pressure is always at the beginning of the fourth phase.
However, for general use, unless one is particularly expert, it is
better to read the diastolic pressure at the beginning of the fifth
phase. There can rarely be a doubt in the mind of the person who is
auscultating as to the point at which all sound ceases. There is
frequently a good deal of doubt, even after large experience, as to
just the moment at which the fourth phase begins. With the
understanding that the difference is only a few millimeters, which
is of very little importance, when the diastolic pressure is below
95, it seems advisable to urge the reading of the diastolic pressure
at the beginning of the fifth phase.

The incident of the first phase, or when sound begins, is caused by
the sudden distention of the blood vessel below the point of
compression by the armlet. In other words, the armlet pressure has
at this point been overcome. Young [Footnote: Young: Indiana State
Med. Assn. Jour., March, 1914.] believes that the murmurs of the
second phase, which in all normal conditions are heard during the 20
mm. drop below the point at which the systolic pressure had been
read, is "due to whirlpool eddies produced at the point of
constriction of the blood vessel by the cuff of the instrument." The
third phase is when these murmurs cease and the sound resembles the
first, lasting he thinks for only 5 mm. The third phase often lasts
much longer. He thinks the fourth phase, when the sound becomes
dull, lasts for about 6 mm.


It is essential that the patient on whom the examination is to be
made should be at rest, either comfortably seated, or lying down.
All clothing should be removed from the arm, and there should be no
constriction by sleeves, either of the upper arm or the axilla. When
the blood pressure is taken over the sleeve of a garment, the
instrument will register from 10 to 30 mm. higher than on the bare
arm. [Footnote: Rowan, J. J.: The Practical Application of Blood
Pressure Findings, The JOURNAL A. M. A., March 18, 1916, p. 873.]

While it may be better, for insurance examinations, to take the
blood pressure of the left arm in right handed persons as a truer
indicator of the general condition, the difference is generally not
great. The right arm of right handed persons usually registers a
full 5 mm. higher systolic pressure than the left arm.

The patient, being at rest and removed as far as possible from all
excitement, may be conversed with to take his mind away from the
fact that his blood pressure is being taken. He also should not
watch the dial, as any tensity on his part more or less raises the
systolic pressure, the diastolic not being much affected by such
nervous tension. The armlet having been carefully applied, it is
better to inflate gradually 10 mm. higher than the point at which
the pulsation ceases in the radial. The stethoscope is then firmly
applied, but with not too great pressure, to the forearm just below
the flexure of the elbow. The exact point at which the sound is
heard in the individual patient, and the exact amount of pressure
that must be applied, will be determined by the first reading, and
then thus applied to the second reading. One reading is never
sufficient for obtaining the correct blood pressure. The blood
pressure may be read by means of the stethoscope during the gradual
raising of pressure in the cuff, note being taken of the first sound
that is heard (the diastolic pressure), and the point at which all
sound disappears, as the pressure is increased (the systolic
pressure). The former method is the one most frequently used.

By taking the systolic and diastolic pressures, the difference
between the two being the pressure pulse, we learn to interpret the
pressure pulse reading. While the average pressure pulse has
frequently been stated as 30 mm., it is probable that 35 at least,
and often 40 mm. represents more nearly the normal pressure pulse,
and from 25 mm. on the one hand to 50 on the other may not be

Faught [Footnote: Faught: New York Med Jour., Feb. 27, 1915, p.
396.] states his belief that the relation of the pressure pulse to
the diastolic pressure and the systolic pressure are as 1, 2 and 3.
In other words, a normal young adult with a systolic pressure of 120
should have a diastolic pressure of 80, and therefore a pulse
pressure of 40. If these relationships become much abnormal, disease
is developing and imperfect circulation is in evidence, with the
danger of broken compensation occurring at some time in the future.

It should be remembered that the diastolic pressure represents the
pressure which the left ventricle must overcome before the blood
will begin to circulate, that is, before the aortic valve opens,
while the pressure pulse represents the power of the left ventricle
in excess of the diastolic pressure. Therefore it is easy to
understand that a high diastolic pressure is of serious import to
the heart; a diastolic pressure over 100 is significant of trouble,
and over 110 is a menace.


With normal heart and arteries, exertion and exercise should
increase the systolic pressure, and generally somewhat increase the
diastolic pressure. The pressure pulse should therefore be greater.
When there is circulatory defect or abnormal blood pressure,
exercise may not increase the systolic pressure, and the pressure
pulse may grow smaller. As a working rule it should be noted that
the diastolic pressure is not as much influenced by physiologic
factors or the varying conditions of normal life as is the systolic

In an irregularly acting heart the systolic pressure may vary
greatly, from 10 to 20 mm. or more, and a ventricular contraction
may not be of sufficient power to open the semilunar valves. Such
beats will show an intermittency in the blood pressure reading as
well as in the radial pulse. The succeeding heart beats after
abortive beats or after a contraction of less power have increased
force, and consequently give the highest blood pressure. Kilgore
urges that these highest pressures should not be taken as the true
systolic blood pressure, but the average of a series of these
varying blood pressures. In irregularly acting hearts it is best to
compress the arm at a point above which the systolic pressure is
heard, then gradually reduce the pressure until the first systolic
pressure is recorded, and then keep the pressure of the cuff at this
point and record the number of beats of the heart which are heard
during the minute. Then reduce the pressure 5 mm. and read again for
a minute, and so on down the scale until the varying systolic
pressures are recorded. The average of these pressures should be
read as the true systolic blood pressure. During an intermittency of
the pulse from a weak or intermittently acting ventricle, the
diastolic pressure will reach its lowest point, and in auricular
fibrillation the pressure pulse from the highest systolic to the
lowest diastolic may be very great.

In arteriosclerosis the systolic may be high, and the diastolic low,
and hence a large pressure pulse. When the heart begins to fail in
this condition, the systolic pressure drops and the pressure pulse
shortens, and of course any improvement in this condition will be
shown by an increase in the systolic pressure. The same is true with
aortic regurgitation and a high systolic pressure.

If the systolic pressure is low and the diastolic very low, or when
the heart is rapid, circulation through the coronary vessels of the
heart is more or less imperfect. Any increase in arterial pressure
will therefore help the coronary circulation. The compression of a
tight bandage around the abdomen, or the infusion of blood or saline
solutions, especially when combined with minute amounts of
epinephrin, will raise the blood pressure and increase the coronary
circulation and therefore the nutrition of the heart.

MacKenzie [Footnote: MacKenzie: Med Rec., New York, Dec. 18, 1915.],
from a large number of insurance examinations in normal subjects,
finds that for each increase of 5 pulse beats the pressure rises 1
mm. He also finds that the effect of height on blood pressure in
adults seems to be negligible. On the other hand, it is now
generally proved that persons with overweight have a systolic
pressure greater than is normal for individuals of the same age. He
believes that diastolic pressure may range anywhere from 60 mm. of
mercury to 105, and the person still be normal. A figure much below
60 certainly shows dangerous loss of pressure, and one far below
this, except in profound heart weakness, is almost pathognomonic of
aortic regurgitation. While the systolic range from youth to over 60
years of age gradually increases, at the younger age anything below
105 mm. of mercury should be considered abnormally low, and although
150 mm. at anything over 40 has been considered a safe blood
pressure as long as the diastolic was below 105, such pressures are
certainly a subject for investigation, and if the systolic pressure
is persistently above 150, insurance companies dislike to take the
risk. However, it should be again urged in making insurance
examinations that psychic disturbance or mental tensity very readily
raises the systolic pressure. MacKenzie believes that a diastolic
pressure over 100 under the age of 40 is abnormal, and anything over
the 110 mark above that age is certainly abnormal.

It has been shown, notably by Barach and Marks, [Footnote: Barach,
J. H., and Marks, W. L.: Effect of Change of Posture--Without Active
Muscular Exertion--on the Arterial and Venous Pressures, Arch. Int.
Med., May, 1913, p 485.] that posture changes the blood pressure.
When a normal person reclines, with the muscular system relaxed,
there is an increase in the systolic pressure and a decrease in the
diastolic pressure, with an increase in the pressure pulse from the
figures found when the person is standing. When, after some minutes
of repose, he assumes the erect posture again, the systolic pressure
will diminish and the diastolic pressure increase, and the pressure
pulse shortens.

Excitement can raise the blood pressure from 20 to 30 mm., and if
such excitement occurs in high tension cases there is often a
systolic blow in the second intercostal space at the right of the
sternum. This may not be due to narrowing of the aortic orifice; it
may be due to a sclerosis of the aorta. On the other hand, it may be
due entirely to the hastened blood stream from the nervous
excitability. This is probably the case if this sound disappears
when the patient reclines. If it increases when the heart becomes
slower and the patient is lying down, the cause is probably organic.

This psychic influence on blood pressure is stated by Maloney and
Sorapure [Footnote: Maloney and Sorapure: New York Med. Jour., May
23, 1914, p. 1021.] "to be greater than that from posture, than that
arising from carbonic acid gas control of the blood, than that
arising from mechanical action of deep breathing upon the
circulation, and than that arising from removal of spasm from the

Weysse and Lutz [Footnote: Weysse and Lutz: Am. Jour. Physiol., May,
1915.] find that the systolic pressure varies during the day in
normal persons, and is increased by the taking of food, on an
average of 8 mm. The diastolic pressure is not much affected by
food. This increased systolic pressure is the greatest about half an
hour after a meal, and then gradually declines until the next meal.

Any active, hustling man, or a man under strain, has a rise of blood
pressure during that strain, especially notable with surgeons during
operation, or with brokers or persons under high nervous tension.
Daland [Footnote: Daland: Pennsylvania Med Jour., July, 1913.]
states that a man driving an automobile through a crowded street may
have an increase of systolic pressure of 30 mm., and an increase of
15 mm. in his diastolic pressure, while the same man driving through
the country where there is little traffic will increase but 10 mm.
systolic and 5 mm. diastolic. Fear always increases the blood
pressure. This is probably largely due to the peripheral
contractions of the blood vessels and nervous chilling of the body.


The venous pressure, after a long neglect, is now again being
studied, and its determination is urged as of diagnostic and
prognostic significance.

Hooker [Footnote: Hooker: Am. Jour. Physiol., March, 1916.] says
there is a progressive rise of venous pressure from youth to old
age. He has described an apparatus [Footnote: Hooker: Am. Jour.
Physiol., 1914, xxxv, 73.] which allows of the reading of the blood
pressure in a vein of the hand when the arm is at absolute rest, and
best with the patient in bed and reclining at an angle of 45
degrees. He finds that just before death there is a rapid rise in
venous pressure, or a continuously high pressure above the 20 cm. of
water level, and he believes that a venous pressure continuously
above this 20 cm. of water limit which is not lowered by digitalis
or other means is serious; and that the heart cannot long stand such
a condition. These dangerous rises in venous pressure are generally
coincident with a fall of systolic arterial pressure, although there
may be no constant relation between the two. He also finds that with
an increase of venous pressure the urinary output decreases. This,
of course, shows venous stasis in the kidneys as well as a probable
lowering of arterial pressure.

Clark [Footnote: Clark, A. D.: A Study of the Diagnostic and
Prognostic Significance of Venous Pressure Observations in Cardiac
Disease, Arch. Int. Med., October, 1915, p. 587.] did not find that
venesection prevented a subsequent rapid rise in venous pressure in
dire cases. From his investigations he concludes that a venous
pressure of 20 cm. of water is a danger limit between compensation
and decompensation of the heart, and a rise above this point will
precede the clinical signs of decompensation.

Hooker also found that there are daily variations of venous pressure
from 10 to 20 cm. of water, with an average of 15 cm., while in
sleep it falls 7 or 8 cm.

It seems probable that there may be a special nervous mechanism of
the veins which may increase the blood pressure in them as
epinephrin solution may cause some constriction.

Wiggers [Footnote: Wiggers C. J.: The Supravascular Venous Pulse in
Man, THE JOURNAL. A.M.A., May 1, 1915, p. 1485.] describes a method
of taking and interpreting the supraclavicular venous pulse. He also
[Footnote: Wiggers C. J.: The Contour of the Normal Arterial Pulse,
THE JOURNAL. A.M.A., April 24, 1915, p. 1380.] carefully describes
the readings and the different phases of normal arterial pulse, and
urges that it should be remembered that "the pulse as palpated or
recorded from any artery is the variation in the arterial volume
produced by the intra-arterial pressure change at that point."

A quick method of estimating the venous pressure by lowering and
raising the arm has long been utilized. The dilatation of the veins
of the back of the hand when the hand is raised should disappear,
and they should practically collapse, in normal conditions, when the
hand is at the level of the apex of the heart. When the venous
pressure is increased, this collapse will not occur until the hand
is above the level of the heart. Oliver [Footnote: Oliver: Quart.
Med Jour., 1907, i, 59.] found that the venous pressure denoted by
the collapse of the veins may be shown approximately in millimeters
of mercury by multiplying by 2 each inch above the level of the
heart in which the veins collapse. When a normal person reclines
after standing there is a fall in venous pressure, and when he again
stands erect there is an increase in venous pressure.

Bailey [Footnote: Bailey: Am. Jour Med. Sc., May, 1911, p. 709.]
states that in interpreting pulsation in the peripheral veins, it
should not be forgotten that they may overlie pulsating arteries.
Pulsation in veins may be due also to an aneurysmal dilatation, or
to direct connection with an artery. As the etiology in many
instances of varicose veins is uncertain, he thinks that they may be
caused by incompetence of the right heart, more or less temporary
perhaps, from muscular exertion. This incompetence being frequently
repeated, peripheral veins may dilate. Moreover, the contraction of
the right heart may cause a wave in the veins of the extremities,
and he believes that incompetency of the tricuspid valve may be the
cause of varicosities in the veins of the extremities.


Woley [Footnote: Woley, II. P.: The Normal Variation of the Systolic
Blood Pressure, THE JOURNAL A. M. A., July 9, 1910, p. 121.] after
studying, the blood pressure in a thousand persons, found that the
systolic average for males at all ages was 127.5 mm., while that for
females at all ages was 120 mm. He found the average in persons from
15 to 30 years to be 122 systolic; from 30 to 40, 127 mm., and from
the ages of 40 to 50, to be 130 mm.

Lee [Footnote: Lee: Boston Med. and Surg. Jour., Oct. 7, 1915.]
examined 662 young men at the average age of 18, and found that the
average systolic blood pressure was 120 mm., and the average
diastolic 80 mm. Eighty-five of these young men, however, had a
systolic pressure of over 140. It is not unusual to find that a
young man who is very athletic has an abnormally high systolic

Barach and Marks [Footnote: Barach, J. H., and Marks, W. L.: Blood
Pressures: Their Relation to Each Other and to Physical Efficiency,
Arch. Int. Med., April, 1914, p 648.] in a series of 656 healthy
young men, found that the systolic pressure was above 150 in only 10
percent, and that in 338 cases the diastolic pressure, read at the
fifth phase, did not exceed 100 mm. in 96 percent

Nicholson [Footnote: Nicholson: Am. Jour. Med. Sc., April, 1914, p.
514.] believes that with a low systolic pressure and a large
pressure pulse there is probably a strong heart and dilated blood
vessels, while with a low systolic pressure and a small pressure
pulse the heart itself is weak, with also, perhaps, dilated blood
vessels. If there is a high systolic pressure and a correspondingly
high diastolic pressure, the balance between the vessels and the
heart is compensated as long as the heart muscle is sufficient. He
believes the velocity of the blood in the blood stream may be
roughly estimated as being equal to the pressure pulse multiplied by
the pulse rate.

Faber 44 [Footnote: Faber: Ugeskrifta f. Laeger, June 10, 1915.]
examined 211 obese patients, and in 182 of these there was no kidney
or vascular disturbance. In 52 percent of these 211 persons the
systolic pressure was under 140, while in the remaining 48 percent
it ranged from 145 to 200 mm.


May Michael, [Footnote: Michael, May: A Study of Blood Pressure in
Normal Children, Am. Jour. Dis. Child., April, 1911, p. 272.] after
a study of the blood pressure in 350 children, came to the
conclusion that the blood pressure in children increases with age
principally because of the increase in height and weight, as she
found that children of the same age but of different weights and
heights had different blood pressures. Sex in children makes no
difference in the blood pressure, it being determined by the height
and weight.

Judson and Nicholson [Footnote: Judson, C. F., and Nicholson,
Percival: Blood Pressure in Normal Children, Am. Jour. Dis. Child.,
October, 1914, p. 257.] made 2,300 observations in children of from
3 to 15 years of age, and found there was a gradual increase in the
systolic blood pressure from 3 to 10 years, and a more rapid rise
from 10 to 14, with a rapid elevation during the fourteenth year, or
the age of puberty. The systolic pressure varied from 91 mm. in the
fourth year to 105.5 in the fourteenth year, while the diastolic
pressure remained almost at a uniform level. The pressure pulse,
therefore, increased progressively with the increase of the systolic


An epitome of the consensus of opinion of the risk of accepting
persons for insurance as modified by the blood pressure is presented
by Quackenbos. [Footnote: Quackenbos: New York Med. Jour., May 15,
1915, p. 999.] Some companies have ruled that at the age of 20 they
will take a person with a systolic pressure up to 137; at the age of
30 up to 140; at the age of 40 up to 144; at 50 up to 148, and at 60
up to 153, although some companies will not accept a person who
shows a persistent systolic pressure of 150. Quackenbos says that
when persons with higher blood pressures than the foregoing have
been kept under observation for some time, they sooner or later show
albumin and casts in the urine. In other words, this stage of higher
blood pressure is too frequently followed by cardiovascular-renal
disease for insurance companies to accept the risk.

On the other hand, too low a systolic pressure in an adult, 105 mm.
or below, should cause suspicion of some serious condition, the most
frequent being a latent or quiescent tuberculosis. Such low pressure
certainly shows decreased power of resistance to any acute disease.

Statistics prove that there are more deaths between the ages of 40
and 50 from cardiovascular-renal disease, that is from heart,
arterial and kidney degenerations, than formerly. Whether this is
due to the high tension at which we all live, or to the fact that
more children are saved and live to middle life, or whether the
prevention of many infectious diseases saves deficient individuals
for this middle life period, has not been determined. Probably all
are factors in bringing about these statistics.

While the continued use of alcohol may not cause arteriosclerosis
directly, it can cause such impaired digestion of foods in the
stomach and intestine, and such impaired activity of the glands,
especially the liver, that toxins from imperfect digestion and from
waste products are more readily produced and absorbed, and these are
believed by some directly or indirectly to cause cardiovascular-
renal disease. Hence alcohol is an important factor in causing the
death of persons from 40 to 50 years of age.

The question of whether or not a person smokes too much, and what
constitutes oversmoking, will soon be asked on all insurance blanks.
As tobacco almost invariably raises the blood pressure, and when the
blood pressure again falls there is again a craving in the man for
the narcotic, it must be a factor in producing, later in life,
cardiovascular-renal disease. Hence an increased systolic blood
pressure must be in part interpreted by the amount of tobacco that
the person uses. BLOOD PRESSURE AND PREGNANCY Evans [Footnote:
Evans: Month. Cyc. and Med. Bull., November, 1912, p. 649.] of
Montreal studied thirty-eight pregnant women who had eclampsia,
albuminuria and toxic vomiting, and found the systolic pressures to
vary from 200 to 140 mm. He did not find that the highest pressures
necessarily showed the greatest insufficiency of the kidneys, but
that the blood pressure must be considered in conjunction with other
toxic symptoms. In thirty-two cases he was compelled to induce labor
when the blood pressure was 150 mm. or under, while in four cases
with a blood pressure over 150 mm., the toxic symptoms were so
slight that the patients were allowed to go to term and had natural

A rising blood pressure in pregnancy, when associated with other
toxic symptoms, is indicative of danger, and Evans believes that a
systolic pressure of 160 mm, is ordinarily the danger limit.

Newell [Footnote: Newell, h. S.: The Blood Pressure During
Pregnancy, THE JOURNAL A. M. A., Jan. 30, 1915, p. 393.] has studied
the blood pressure during normal pregnancy, and finds that when the
systolic pressure is persistently below 100, the patient is far
below par, and that the condition should be improved in order for
her to withstand the strain of parturition. When the systolic
pressure is above 130, the patient should be carefully watched, and
he thinks that 150 is the danger line. Some pregnant women have an
increasing rise in blood pressure throughout the pregnancy, without
albuminuria. In other cases this rise is followed by the appearance
of albumin in the urine. Thirty-nine of the patients studied by
Newell had albumin in the urine without increase in blood pressure;
hence he believes that a slight amount of albumin may not be
accompanied by other symptoms. Five patients had a blood pressure of
140 or over throughout their pregnancy, and in only one of these
patients was albumin found. All passed through labor normally,
showing that a blood pressure below 150 may not necessarily be
indicative of a serious condition; but a patient who has a systolic
pressure over 135 must certainly be carefully watched. A fact
brought out by Newell's investigations is very important, namely,
that a continuously increased blood pressure is not as indicative of
trouble as when a blood pressure has been low and later suddenly

Hirst [Footnote: Hirst: Pennsylvania Med. Jour., May, 1915, p. 615.]
also urges that a high blood pressure in pregnancy does not
necessarily represent a toxemia, and also that a serious toxemia can
occur with a blood pressure of 130 or lower, although such instances
are rare. Hirst believes that when a toxemia is in evidence in
pregnancy while the blood pressure is low, the cause of the toxemia
is liver disturbance rather than kidney disturbance, and he thinks
this form of toxemia is more serious and has a higher mortality than
the nephritic type. Therefore in a patient with eclamptic symptoms
and a low blood pressure, the prognosis is more unfavorable than
when the blood pressure is high. He believes that if high blood
pressure occurs early in the months of pregnancy, there is
preexisting, although perhaps latent, nephritis. In these conditions
the diastolic pressure is also likely to be high.

With the patient eclamptic and stupid, whatever the date of the
pregnancy, Hirst would do venesection immediately in amount from 16
to 24 ounces, depending on what amount seems advisable. If
venesection is done before actual convulsions have occurred, the
blood pressure falls temporarily but rapidly rises again. He finds
that if a patient is past the eighth month, rupture of the membranes
will usually bring a rapid fall of from 50 to 90 points in systolic
pressure. Usually, of course, such rupture of the membranes will
induce labor. He finds that the fluidextract of veratrum viride is
valuable when eclampsia is in evidence or imminent. He gives it
hypodermically, 15 minims at the first dose and 5 minims
subsequently, until the systolic pressure is reduced to 140 or less.
He admits that this is rather strenuous treatment. He does not speak
of treatment by thyroid extracts, which has been regarded as
valuable by some other workers.

In these patients who show eclamptic symptoms, he maintains a milk
diet, and purging and sweating. It should be remembered that
venesection or profuse bleeding during induced parturition is more
valuable than sweating in all eclamptic cases and in all nephritic
convulsions. Profuse sweating does little more than take the water
out of the blood, and even concentrates the poisons in the blood.

Hirst causes purging by 2 ounces of castor oil and a few minims of
croton oil. He also advises large doses of magnesium sulphate. In
such serious disturbances as eclampsia, it is not necessary to give
a magnesium salt, which, it has been shown, can have unpleasant
action on the nervous system. Sodium sulphate is as valuable and is
not open to this danger.

Hirst urges that whatever the blood pressure, with albuminuria, as
soon as persistent headache occurs, and especially if there are
disturbances of vision, the pregnancy must be terminated at once. On
this there can be no other opinion. Temporizing with such a case is

After labor has been induced there is an immediate fall of blood
pressure, which lasts some hours. The pressure will again rise, and
usually is the last sign of toxemia to disappear, and he finds that
this increased pressure may last from two to three weeks when there
is not much nephritis, and several months when there is nephritis.

Although he says he has found no bad action from ergot, either by
the mouth or hypodermically in these eclamptic cases, it would seem
inadvisable to use ergot, which may raise the blood pressure. He
finds that pituitary extract "can cause dangerous rise of blood

Pelissier [Footnote: Pelissier: Archiv. mens., d'obst. et de gynec.,
Paris, 1915, iv, No. 5.] believes that when there is prolonged
vomiting in early pregnancy, with an increase in systolic blood
pressure, and with an increased viscosity of the blood, the outlook
is serious, and active treatment should be inaugurated.

Irving [Footnote: Irving, F. C.: The Systolic Blood Pressure in
Pregnancy, THE JOURNAL A. M. A., March 25, 1916, p. 935.] reports,
after a study of 5,000 pregnant women, that in 80 percent the
systolic blood pressure varied from 100 to 130; in 9 percent it was
below 100, at least at times, but a pressure below 90 does not mean
that the woman will suffer shock; in 11 percent the pressure was
above 130, and high pressure in young pregnant women more frequently
indicates toxemia than when it occurs in older women; high pressure
is more indicative of toxemia than is albuminuria; a progressively
increasing blood pressure is of bad omen, and most cases of
eclampsia occur with a pressure of 160 or more, but eclampsia may
occur with a moderate blood pressure. Irving believes that with
proper preliminary preventive treatment most eclampsia is


It has long been known that altitude increases the heart rate and
tends to lower the systolic and diastolic blood pressures; that
these conditions, though actively present at first, gradually return
to normal, and that after a prolonged stay at the altitude may
become nearly normal for the individual. Burker [Footnote: Burker,
K.; Jooss, E.; Moll, E., and Neumann, E.: Ztschr. f. Biol., 1913,
lxi, 379. The Influence of Altitude on the Blood, editorial, THE
JOURNAL A. M. A., Nov. 1, 1913, p. 1634.] showed that altitude
increases the red blood cells from 4 to 11.5 percent, and the
hemoglobin from 7 to 10 percent The greatest increase in these
readings is in the first few days. It has also been shown that with
every 100 mm. of fall of atmospheric pressure there is an increased
hemoglobin percentage of 10 percent over that at the sea level.
[Footnote: Blood and Respiration at Moderate Altitudes, editorial,
THE JOURNAL A. M. A., Feb. 20, 1915, p. 670.]

Schneider and Havens [Footnote: Schneider and Havens: Am. Jour.
Physiol., March, 1915.] find that in low altitudes abdominal massage
increases the red corpuscles, and the percentage of hemoglobin in
the peripheral vessels. While there is thus apparently a reserve of
red corpuscles while the individual is in a low altitude, in a high
altitude they find such reserve to be absent; in other words,
abdominal massage did not cause this increase in red corpuscles in
the peripheral vessels. This absence of reserve is easily accounted
for by the fact that after one reaches the high altitude there is an
increase in red corpuscles and hemoblogin in the peripheral blood.

Schneider and Hedblom [Footnote: Schneider and Hedblom: Am. Jour.,
Physiol., November, 1908.] showed that the fall in systolic pressure
at altitudes is greater and more certain than the fall in diastolic,
some individuals even having a rise in diastolic pressure. This rise
in diastolic pressure is probably caused by dyspnea.

Schrumpf, [Footnote: Schrumpf: Deutsch. Arch. f. klin. Med., 1914,
cxiii, 466] on the other hand, finds that normal blood pressure is
not much affected by an ascent of about 6,500 feet, while patients
with arteriosclerosis and hypertension, without kidney disease, have
a fall in pressure. A patient with coronary disease should certainly
not go to any great altitude, while patients with compensated
valvular lesions, he found, were not injured by ordinary heights. He
found that altitude seemed to decrease high systolic and diastolic
pressures, while it even elevated those which were below normal, and
caused these patients to feel better.

Any person who has a circulatory disturbance, and who must or does
go to a higher altitude, should rest for a series of days, until his
blood pressure and blood have reached an equilibrium.

Smith [Footnote: Smith, F. C.: The Effect of Altitude on Blood
Pressure, THE JOURNAL A. M. A., May 29, 1915, p. 1812.] made a
series of observations on blood pressures at Fort Stanton which has
an altitude of 6,230 feet. He took the blood pressure readings in
fifty-four young adults, seventeen of whom were women, and found
that the average systolic reading in the men was 129 mm., and in the
women 121, while the average diastolic in the men was 84, and in the
women 82. Therefore he agrees with Schrumpf that the effect of
altitude on normal blood pressure has been overestimated. In
tuberculosis he found that the effect of altitude was not great. He
does not believe that this amount of altitude, namely, a little more
than 6,000 feet, makes much difference in an ordinary tuberculous
patient. He did not find that artificial pneumothorax made any
important change in the blood pressure. His findings do not quite
agree with Peters and Bullock, [Footnote: Peters, L. S.r and
Bullock, E. S.: Blood Pressure Studies in Tuberculosis at a High
Altitude, Arch. Int. Med., October, 1913, p. 456.] who studied 600
cases of tuberculosis at an altitude of 6,000 feet, and found the
blood pressure was increased, both in normal and in consumptive
individuals. They also found that the increase in blood pressure,
which kept gradually rising up to a certain limit, was indicative
that the tuberculous patient was not much toxic; therefore the
increase in blood pressure was of good prognosis.


Woolley [Footnote: Woolley, P. G.: Factors Governing Vascular
Dilatation and Slowing of the Blood Stream in Inflammation, THE
JOURNAL A. M. A., Dec. 26, 1914, p. 2279.] quotes Starling as
finding that the blood vessels dilate from physical and chemical
changes in the musculature, and that this dilatation is caused by
deficient oxidation and accumulation of the products of metabolism,
including carbon dioxid. This dilatation ordinarily is transient and
not associated with exudation, but in inflammation the dilatation is
persistent and there is exudation. The carbon dioxid increase during
exercise stimulates a greater circulation of oxygen in the tissues
which later counteracts the normal increase in acid products. In
inflammatory processes, however, the acid accumulates too rapidly to
allow of saturation. In this case the circulation becomes slowed and
the cells become affected.

Besides these charges in the blood vessels of the muscles, the
general blood pressure becomes raised on exercise, the heart more
rapid and the temperature somewhat elevated, and the breathing is
increased. This increased heart rate does not stop immediately on
cessation of the exercise, but persists for a longer or shorter
time. The better trained the individual, the sooner the speed of the
heart becomes normal.

Benedict and Cathcart [Footnote: Benedict and Cathcart: Pub. 77,
Carnegie Institute of Washington.] have found that the increased
absorption of oxygen, showing increased metabolism, persists after
exercise as long as the heart action is increased.

Newburgh and Lawrence [Footnote: Newburgh, L. H., and Lawrence C.
H.: The Effect of Heat on Blood Pressure, Arch. Int. Med., February,
1914, p. 287.] have found that increased temperature in animals,
equal to that occurring in persons suffering with infection, reduces
the blood pressure, causing a hypotension. This shows that high
temperature alone in an individual sooner or later causes

Although prolonged pain may cause a fall of blood pressure from
shock, the first acute pain may cause a rise in blood pressure, and
Curschmann [Footnote: Curschmann: Munchen. med. Wehnschr., Oct. 15,
1907.] found that the blood pressure was high in the gastro-
intestinal crises of tabes and in colic, and that the application of
faradic electricity to the thigh could raise the blood pressure from
8 to 10 mm. in normal individuals.

The positive effect of decomposition products in the intestine, more
especially such as come from meat proteins, is well recognized; but
the importance, in high pressure cases, of the absorption of toxins
derived from imperfectly digested food remaining in the bowels over
night is not sufficiently recognized. Patients with high blood
pressure should not eat a heavy evening meal, and especially should
they not eat meat. Willson [Footnote: Willson, R. N.: The
Decomposition Food Products as Cardiovascular Products, THE JOURNAL
A. M. A., Sept. 25, 1915, p. 1077.] well describes the condition
caused by the absorption of these toxins. If the heart muscle is
intact, he finds such absorption in high pressure cases will show
diastolic as well as systolic increase:

The vessels pulsate and throb; the skin is pale; the head aches;
the tongue is coated; the breath is foul; vertigo is often
distressing; and not infrequently the hands and feet feel distended
and swollen. A thorough house-cleaning of the gastro-intestinal
canal causes the expulsion of the offending substances and the
expulsion of gas, whereupon the blood pressure often resumes its
normal level and the symptoms disappear.

Wilson suggests that not only the meat proteins, but also the
oxyphenylethylamin in overripe cheese may often cause this
poisoning; and cheese is frequently eaten by these people at
bedtime. Of course if any particular fruit or article of food causes
intestinal upset in a given individual, they should be avoided.

When the heart is hypertrophied in disease, the cavities of the
ventricles are probably also generally enlarged, and therefore they
propel more blood at each contraction than in normal persons and
thus increase the blood pressure.

The blood pressure is raised not only by intestinal toxemia and
uremia, but also by lead poisoning and the conditions generally
present in gout.

It has been pointed out by Daland [Footnote: Daland: Pennsylvania
Med. Jour., July, 1913.] that nervous exhaustion may raise the blood
pressure in those who are neurotic, and he finds that this
hypertension may exist for months in some cases. On the other hand,
in neurasthenics the blood pressure is generally lowered. As he
points out, there is often a very great increase in the systolic
blood pressure at the menopause, while the diastolic pressure may
not be high. This makes a very large pressure pulse. This suggests
the possibility of disturbances of the glands of internal secretion.
This hypertension is generally improved under proper treatment.

Schwarzmann [Footnote: Schwarzmann: Zentralbl. f. inn. Med., Aug. 1,
1914.] studied the blood pressure in eighty cases of acute
infection, and found that a high diastolic blood pressure during
such illness indicates a tendency to paralysis of the abdominal
vessels, and hence a sluggish circulation in the vessels of the
abdomen. He found that in seriously ill patients this high diastolic
pressure is of bad prognosis. He also found that a lower systolic
pressure with a lower diastolic pressure is not a sign that the
heart is weakening, but only that the visceral tone is growing less.
On the other hand, when the diastolic pressure rises while the
systolic falls, this is a sign of failing heart.

Newburgh and Minot [Footnote: Newburgh, L. H. and Minot, G. II: The
Blood Pressure in Pneumonia, Arch. Int. Med., July, 1914, p. 48.]
find that the blood pressure course in pneumonia does not suggest
that there is a failure of the vasomotor center. They found that
"low systolic pressures are not invariably of evil omen." They also
found that the systolic pressure in fatal cases is often higher than
in those in which the patients recovered, and they found that the
rate of the pulse is more important in determining the treatment
than the blood pressure measurements.

The work which has been described under this section is of interest
as indicating the newer experimental work on the physiology of blood
pressure. Much of it is new, however, and it is difficult to draw
absolute therapeutic conclusions from the evidence offered.


Free catharsis is a well established and valuable method of
relieving the heart in many cases of broken compensation, and in
cases with high blood pressure even while compensation is still
good, salines administered once or twice a week assist in
elimination, and in the reduction of blood pressure.

However, profuse purging in heart disease may be followed by
unfavorable symptoms, especially when the systolic blood pressure is
low. When there is hypotension, or when the diastolic pressure is
high and the venous pressure is high, and when there is edema or
effusion, watery catharsis should be caused only after due
consideration, and always with a careful watching of the effect on
the heart and blood pressure. The blood pressure is lowered by such
catharsis, and the heart is often slowed. Neilson and Hyland
[Footnote: Neilson, C. H., and Hyland, R. F.: The Effect of Strong
Purging on Blood Pressure and the Heart, THE JOURNAL A. M. A., Feb.
8, 1913, p. 436.] studied the effect of purging on the heart and
blood pressure, and were inclined to the view that in serious heart
conditions brisk purging should not be done. They think that the
slowing of the heart after such purging may be, due to an increased
viscosity of the blood, or perhaps to a reflex irritation from the
purgative on the intestinal canal.

Pilcher and Sollmann [Footnote: Pilcher and Sollmann: Jour.
Pharmacol. and Exper. Therap., 1913, vi, 323.] have shown that the
fall of blood pressure after the administration of nitrites is
mostly due to the action of these drugs on the peripheral vessels.
Chloroform, of course, depressed the vasomotor center, but ether had
no effect on this center, or slightly stimulated it. Such
stimulation, however, Pilcher and Sollmann believe may be secondary
to asphyxia. Nicotin they found to cause intense stimulation of the
vasomotor center. Ergot and hydrastis and its alkaloids seem to have
no effect on the vasomotor center. Strophanthus acted on this center
only moderately, and digitalis very slightly, if at all. Camphor in
doses large enough to cause convulsions stimulated the vasomotor
center. In smaller doses it generally stimulated the center
moderately, but not always. Even when this center was stimulated,
however, the camphor did not necessarily increase the blood
pressure. The rise in blood pressure from epinephrin is due entirely
to its action on the peripheral blood vessels and the heart. It has
no action on the vasomotor center. They found that strychnin in
large doses may stimulate the vasomotor center moderately, but
usually it did not act on this center unless the patient was
asphyxiated; then it acted intensely. The conclusion to be drawn
from their experiments is that when there is asphyxia, increased
venous pressure, and also a rising blood pressure from the
stimulation of carbon dioxid, strychnin is contraindicated.

It should be recognized that digitalis very frequently not only does
not raise blood pressure, but also may lower it; especially in
aortic insufficiency and when there is cyanosis. Even with some
forms of angina pectoris, digitalis in small doses may reduce the
frequency of the pain. This decrease of pain following the use of
digitalis has in some cases been ascribed to the improvement of
coronary circulation and resulting better nutrition of heart muscle.
Of course under these conditions the action of digitalis must be
carefully watched, and it should not be given too long.

Although sodium nitrite and nitroglycerin have but a short period of
action, in laboratory experimentation, in lowering the blood
pressure, when given repeatedly four or five times a day the blood
pressure is lowered in very many instances by these drugs. Sometimes
when the blood pressure is not lowered, there is relief of tension
in the head from high pressure, and the patient feels better. There
is also relief of the heart when it is laboring to overcome a high
resistance. One drop of the official spirit of nitroglycerin on the
tongue will cause a lowering in the peripheral pressure pulse, the
radial pulse becoming larger and fuller. This effect begins in three
minutes or less, reaches its maximum in about five minutes, and the
effect passes off in fifteen minutes or more. [Footnote: Hewlett, A.
W., and Zwaluwenburg, J. G. Van: The Pulse Flow in the Brachial
Artery, Arch. Int. Med., July, 1913, p. 1.]

It has been stated that iodids are of no value except in syphilitic
arteriosclerosis, but iodids in small doses are stimulant to the
thyroid gland, and the thyroid secretes a vasodilating substance.
Therefore, the use of either iodids or thyroid would seem to be
justified in many instances of high blood pressure.

Fairlee [Footnote: Fairlee: Lancet, London, Feb. 28, 1914.] has
studied the effect of chloroform and ether on blood pressure, and
finds that there is a fall of pressure throughout the administration
of chloroform, and but little alteration of the blood pressure
during the administration of ether. It may cause a slight rise, or
it may cause a slight fall, but changes in pressure with ether are
not marked. When there is slight surgical shock present, as from
some injury, they found that chloroform would lower the pressure
considerably. Hence it would seem that chloroform should not be used
as an anesthetic after serious injuries.


Capps and Matthews [Footnote: Capps, J. A., and Matthews, S. A.:
Venous Blood Pressure as influenced by the Drugs Employed in
Cardiovascular Therapy, THE JOURNAL A. M. A., Aug. 9, 1913, p. 388.]
have shown that even with first class preparations of digitalis,
there may be only a moderate gradual rise in arterial pressure, but
not much change in venous pressure. Venous pressure was not much
affected by small doses of epinephrin, but with large doses it rose
from 10 to 80 mm. Pituitary extract acts somewhat similarly to
epinephrin. Caffein, though raising the arterial pressure, did not
influence the venous pressure. Strychnin did not raise either
pressure until the dose was sufficient to cause muscular
contractions. They found that the nitrites caused a fall in venous
pressure as well as arterial pressure, although the heart might be
accelerated and more regular. They think that the nitrites act by
depressing the nerve endings in the veins as well as the arteries.
Morphin they found did not act on the venous pressure, although it
lowered arterial tension, in ordinary doses of 1/8 or 1/6 grain; but
with doses of from 1/4 to 1/2 grain, both arterial and venous
pressures were lowered. They found that alcohol in ordinary doses
did not influence the venous pressure, although it lowered the
arterial pressure; but very large doses lowered the arterial and
raised the venous pressure. They think that when the venous pressure
is increased only by large doses of epinephrin, pituitary extract
and alcohol, the effect is due to failure of the heart, although it
may be due to an increase of carbon dioxid in the blood, in other
words, to asphyxia.


Arterial hypertension may be divided into stages. In the first stage
the arteries are healthy, but the tone, owing to contraction of the
muscular walls, is too great. This condition or stage has been
termed "chronic arterial hypertension." This condition may be due to
irritants circulating in the blood, to nervous tension, to incipient
chronic interstitial nephritis, or may be the first stage of
sclerosis of the arteries. If from any cause this hypertension
persists, the muscular coats of the arteries will become more or
less hypertrophied, and sooner or later degenerative changes begin
in the intima, and finally fibrosis occurs in the external coat of
the arteries; in other words, arteriosclerosis is in evidence. If
the patient lives with this arteriosclerosis, a later stage of the
arterial disease may occur which has been termed atheroma, with
thickening, and possibly calcareous deposits in some parts of the
walls of the vessels, while in other parts the coats become thinner
and insufficient. At this stage the heart, which has already shown
some trouble, becomes unable to force the blood properly against
this enormous resistance of inelastic vessels and the blood pressure
begins to fail as the left ventricle weakens.

Edema, failing heart, perhaps aneurysms, peripheral obstruction, or
hemorrhages are the final conditions in this chronic disease of

Riesman [Footnote: Riesman: Pennsylvania Med. Jour., December, 1911,
p. 193.] divides hypertension into four classes hypertension without
apparent nephritis or arterial disease; hypertension with
arteriosclerosis; hypertension with nephritis, and hypertension with
both arteriosclerosis and nephritis. These classes are given here in
the order of the seriousness of the prognosis.


One of the most common causes of hypertension is clue to excess of
eating and drinking. The products caused by maldigestion of
proteins, and the toxins formed and absorbed especially from meat
proteins, particularly when the excretions are insufficient, are the
most frequent causes of hypertension. Whatever other element or
condition may have caused increased blood pressure, the first step
toward improving and lowering this pressure is to diminish the
amount of meat eaten or to remove it entirely from the diet. In
pregnancy where there is increased metabolic change, when the
proteins are not well or properly cared for in gout, and when there
is intestinal fermentation or putrefaction, hypertension is likely
to occur. The increased blood pressure in these cases is directly
due to irritation of the toxins on the blood vessel walls.

While alcohol does not tend to raise arterial blood pressure, in
large amounts it may raise the venous pressure. Also, by causing an
abundant appetite and thus increasing the amount of food taken, by
interfering with the activity of the liver, and by impairing the
intestinal digestion, it can indirectly disturb the metabolism and
cause enough toxin to be produced to raise the blood pressure.

Any drug or substance that raises the blood pressure by stimulating
the vasomotor center or the arterioles, when constantly repeated,
will be a cause of hypertension. This is particularly true of
caffein and nicotin. Also, anything that might stimulate, or that
does stimulate, the suprarenal glands will cause a continued high
blood pressure. It is quite probable that in many cases of gout the
suprarenals are hypersecreting and it has been shown by Cannon, Aub
and Binger [Footnote: Cannon, Aub and Binger: Jour. Pharmacol. and
Exper. Therap., March, 1912.] that nicotin in small closes increases
the suprarenal secretion. Therefore, nicotin becomes a decided cause
of hypertension and arteriosclerosis.

Thayer found that heavy work is the cause of about two thirds of all
cases of arteriosclerosis, and one of the functions of the
suprarenals is to destroy the waste products of muscular activity;
hence these glands, in these cases, are hypersecreting. Furthermore,
the reason that many infections are followed later by arterio-
sclerosis may be the fact that the suprarenals have been stimulated
to hypertrophy and hypersecrete.

Many persons in middle life, and especially women at the time of the
menopause, show hypertension without arterial or kidney reason. At
this time of life the thyroid is disturbed, and often, especially if
weight is added, it is not secreting sufficiently. Whether, with the
polyglandular disturbance of the menopause the suprarenals are
excited and hypersecreting, or whether they are simply relatively
secreting more vasopressor substance than is combated by the
vasodilator substance from the thyroid, cannot be determined. These
women are energetic, and look full of health and full of strength,
but their faces frequently flush, sometimes they are dizzy, and the
systolic blood pressure is too high. Reisman has pointed out that
these patients are likely to have very large breasts, and there is
reason to believe that we must begin to study more carefully the
effect of large breasts on the metabolism of girls and women. There
certainly is an internal secretion of some importance furnished by
these glands.

In hyperthyroidism at first the blood pressure may be lowered on
account of the increased physiologic secretion of the thyroid gland.
Later the blood pressure may be raised by stimulation of the
suprarenals, or it may become raised from the irritated and
stimulated heart becoming hypertrophied. If the heart is normal the
ventricles should hypertrophy with the increased work that they are
under; and the blood pressure could increase for this reason. Later
in exophthalmic goiter the heart muscle may become degenerated, a
chronic myocarditis, and the ventricles may slightly dilate. At this
time the blood pressure is lowered. When such a condition has
occurred, the heart bears thyroidectomy badly; hence an operation on
this gland should, if possible, be performed before the heart muscle
has become injured. If the heart shows signs of loss of power, minor
operations to cut off the blood supply of the thyroid should first
be done, and the patient's heart allowed to improve before a
thyroidectomy is performed.

Men with hypertension without kidney or arterial excuse are likely
to have been athletes, or to have done some severe competitive work,
or, as above stated, to have labored hard, or to have worked at high

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