Disturbances of the Heart
by Oliver T. Osborne · English · Gutenberg #3731 · 545,013 chars · public domain (US)
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Title: Disturbances of the Heart
Author: Oliver T. Osborne
Release date: February 1, 2003 [eBook #3731]
Most recently updated: January 8, 2021
Language: English
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DISTURBANCES OF THE HEART
Discussion of the Treatment of the Heart in Its Various Disorders,
With a Chapter on Blood Pressure
OLIVER T. OSBORNE, A.M., M.D.
Professor of Therapeutics and formerly Professor of Clinical
Medicine in Yale Medical School NEW HAVEN, CONN.
THE JOURNAL of AMERICAN MEDICAL ASSOCIATION
Five Hundred Thirty-Five
North Dearborn Street, Chicago
PREFACE
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.
PREFACE TO THE FIRST EDITION
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.
CONTENTS
Preface
Preface to First Edition
Disturbances of the Heart in General
Classification of Cardiac Disturbances
Blood Pressure
Hypertension
Hypotension
Pericarditis
Myocardial Disturbances
Endocarditis
Chronic Diseases of the Valves
Acute Cardiac Symptoms: Acute Heart Attack
Diet and Baths in Heart Disease
Heart Disease in Children and During Pregnancy
Degenerations
Cardiovascular Renal Disease
Disturbances of the Heart Rate
Toxic Disturbances and Heart Rate
Miscellaneous Disturbances
DISTURBANCES OF THE HEART IN GENERAL
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
work.
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.
CLINICAL INTERPRETATION OF PULSE TRACINGS
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
slow.
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.
INTERPRETATION OF TRACINGS
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.
TESTS OF HEART STRENGTH
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
insufficiency.
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
bad.
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
anesthesia.
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
impaired.
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.
THE EFFECT OF ATHLETICS ON THE HEART
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
heart.
Insurance statistics seem to show that athletes are likely to have
earlier cardiovascular-renal disease than other individuals of the
same class and occupations.
SUGGESTIONS FOR THE CONTROL OF ATHLETICS
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
strength.
SIGNS OF HEART WEAKNESS
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
recognized.
SYMPTOMS AND SIGNS OF CARDIAC DISTURBANCE
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
disturbance.
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
through.
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
necessary.
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.
CLASSIFICATION OF CARDIAC DISTURBANCES
For the sake of discussing the therapy of cardiac disturbances in a
logical sequence, they may be classified as follows:
Pericarditis
Acute
Adherent
Myocarditis
Acute
Chronic
Fatty
Endocarditis
Acute, simple malignant
Chronic
Valvular Lesions
Broken compensation
Cardiac drugs
Diet
Resort treatment
Cardiac disease in children
Cardiac disease in pregnancy
Coronary sclerosis
Angina pectoris
Pseudo-angina
Stokes-Adams disease
Arterial hypertension
Cardiovascular-renal disease
Arrhythmia
Auricular fibrillation
Bradycardia
Paroxysmal tachycardia
Hyperthyroidism
Toxic disturbances
Physiologic hypertrophies
Simple dilatation
Shock
Stomach dilatation
Anesthesia in heart disease
BLOOD PRESSURE
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
improved.
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.
TECHNIC
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
abnormal.
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.
FACTORS INCREASING THE BLOOD PRESSURE
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
pressure.
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
musculature."
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.
VENOUS PRESSURE
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.
NORMAL BLOOD PRESSURE FOR ADULTS
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
pressure.
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.
BLOOD PRESSURE IN CHILDREN
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
pressure.
BLOOD PRESSURE AND INSURANCE
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
deliveries.
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
rises.
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
inexcusable.
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
pressure."
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
preventable.
ALTITUDE
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.
CONDITIONS CAUSING CHANGE IN BLOOD PRESSURE
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
hypotension.
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.
THE EFFECT OF DRUGS ON BLOOD PRESSURE
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.
THE EFFECT OF DRUGS ON VENOUS BLOOD PRESSURE
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.
HYPERTENSION
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
arteriosclerosis.
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.
ETIOLOGY
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
tension, or in great excitement, or with mental worry, all of which
tend, as long as there is health, to increase the blood pressure.
These men may add weight from the age of 40 on, or they may be thin
and wiry. Besides the hypertension there is likely to be a too
sturdily acting heart, which is often hypertrophied, and there is an
accentuated closure of the aortic valve. There may be dizziness, or
no head symptoms at all. Nicotin is likely to be an etiologic factor
in this class.
These women and these men may all be improved by proper treatment,
and the condition may not develop into arteriosclerosis or
nephritis.
Neurotic conditions, and in some instances neurasthenic conditions,
may show a blood pressure higher than normal. Lead may be a cause of
increased blood pressure, and diabetics occasionally have a high
pressure, although more frequently there is a lowering of blood
pressure in diabetes.
Richman believes that syphilis is the most common cause of
hypertension and arteriosclerosis without renal disease. When
arteriosclerosis and renal disease are combined, of course the
highest systolic readings occur. He thinks that when high tension
occurs under 40 years of age, kidney disease is generally the cause.
Of course it may be the only cause later in life.
High blood pressure due to syphilitic conditions may be greatly
improved by the proper treatment, although some one or more blood
vessels are likely to have been seriously damaged. Although these
patients may live for many years, they are likely to have an
apoplexy, cerebral disease or an aneurysm.
While hypertension is not a disease, and while it often should not
be combated, still, as it is always the forerunner of more serious
trouble, there can be no excuse for not most seriously considering
it and generally attempting its reduction. At the moment high
tension is discovered, there may be no special symptoms; but
troublesome symptoms are always pending, and while the patient need
not be unduly alarmed, there is no excuse for not rearranging the
individual's life so as to prolong it. This is not to state that
every high tension must be lowered, but every hypertension must be
studied and a safer systolic pressure caused if it is possible
without interfering with the person's efficiency. A high diastolic
pressure, one above 105, certainly must receive immediate attention,
and a diastolic pressure of 110 must be lowered, if possible. On the
other hand, a high systolic pressure without a high diastolic
pressure should not be rapidly lowered, else depression will be
caused.
SYMPTOMS
In hypertension, as long as the heart, which is probably
hypertrophied, remains perfectly competent, there are few symptoms,
and the person does not seek advice until he notices one or more of
several possible conditions. He may be dizzy, his head may feel full
and tight, he may have headaches, or he may have some cardiac pain
or distress. Other persons do not seek advice until there is a
slight weakening of the heart, showing the strain under which it is
laboring. In most of these high tension cases, the patients have
rather a slow heart, provided the heart is sufficient. Eyster and
Hooker [Footnote: Eyster and Hooker: Am. Jour. Physiol., May, 1908.]
found that the slowing of the heart in high blood pressure is due to
action through the vagus nerves either from the inhibitory center in
the medulla or reflexly by stimulation of the peripheral nerves of
the vessels.
Another symptom for which the patient frequently seeks advice is
that he is unable to relax from his business cares, when off duty.
He also finds that he works at a higher tension, and that coffee and
tea, alcohol and tobacco stimulate him more than usual. He sleeps
restlessly, and dreams at night. He has an increased frequency of
urination in the morning, especially after taking coffee, and
sometimes gets up once or twice at night to urinate. He is irritable
at times; short breathed on exertion, and sometimes has indigestion.
He may have pains or aches in his heart. He may find that he
dislikes to lie on his left side.
However much it may upset the patient and render him more nervous to
inform him that his blood pressure is too high, it is necessary to
give him this information. People now suspect the condition, and
they frequently seek their physicians to determine if the blood
pressure is too high and, from reading health journals, more or less
realize some of the things, at least, that must be done to decrease
the pressure. Consequently, the very things that are advised or
ordered give the patient the diagnosis, whether he is told directly
or not. Hence, we must talk freely with the patient, much as we do
in heart defects, and get his cooperation, stating how frequent the
condition is, how often it is readily improved, and how little it
may interfere with long life.
Wiener and Wolfner [Footnote: Wiener, Meyer, and Wolfner, M. L.: A
Reaction of the Pupil, Strongly Suggestive of Arteriosclerosis with
Increased Blood Pressure, THE JOURNAL A. M. A., July 17, 1915, p.
214.] state that they have found with blood pressure that the pupils
of the eyes are larger than normal, and that they readily contract
to the stimulus of light, but immediately return to their previous
size.
PROGNOSIS
Janeway [Footnote: Janeway, T. C.: A Clinical Study of Hypertensive
Cardiovascular Disease, Arch. Int. Med., December, 1913, p. 755.]
presented statistics of 458 patients with high blood pressure, 67
percent of whom were men. Of these 458 patients 212 had died, and he
found that the women with high blood pressure lived longer than men
with high blood pressure. They did not seem as likely to have
apoplexy or cardiac failure. About 85 percent of high tension cases
occur between the ages of 40 and 70.
While he believes that a systolic pressure of over 160 mm. is
pathologic, he does not find that any definite prognostic
conclusions can be drawn from the height of the pressure. Of course
the most important concomitant symptoms of high pressure are
cardiac, renal, and cerebral, and the typical headache, as he terms
it, is a symptom of serious import. In considering headache in
persons over 40, we must eliminate the eye headaches produced by the
need of presbyopic glasses or by the need of stronger lenses, as
this need is a frequent cause of headache. Dizziness and vertigo may
occur without headache, and drowsiness, though not so frequent a
symptom as insomnia, often occurs.
Janeway finds that all kinds of apoplectic attacks may occur from
simple transient aphasia to complete hemiplegia, and thirteen of his
patients who had died and thirteen of those living at the time of
this report showed failure of eyesight as an initial symptom of
arterial disease.
Janeway deplores the too frequent diagnosis of neurasthenia in these
patients. This diagnosis probably accounts for the frequency with
which neurasthenics have been said to have high blood pressure.
Patients with high blood pressure may show all kinds of symptoms
simulating neurasthenia, but hypertension is a much better diagnosis
than neurasthenia for such patients, and will lead to more rational
treatment.
Ninety-seven of these patients had hemorrhages somewhere, most
frequently epistaxes, sometimes hemoptysis. Janeway did not find
that purpuric spots on the skin occurred early in the disease in any
of his patients.
Gastro-intestinal disturbances were not much in evidence unless the
kidneys were insufficient. Intermittent claudication in the legs
occasionally occurred. While angina pectoris and edema of the lungs
were not infrequent causes of death in men, it was a rare cause of
death in women. Dyspnea is a frequent symptom, and one for which
many patients seek medical advice.
A constant systolic blood pressure of over 200 shows a probability
that the patient will ultimately die either of uremia or of
apoplexy. Janeway found that those patients who are to die from
cardiac weakness show cardiac symptoms early in their disease. He
found that rapid continuous loss of weight pointed to an early fatal
termination.
Of the 212 patients who had died, seventy-one had shown cardiac
insufficiency at the time of the first examination; twenty-one
showed albumin or casts at that time. Of course it should be
repeatedly emphasized that chronic interstitial nephritis may be in
evidence with either albumin or casts alone, or without either being
present.
Janeway sums up his conclusions by stating that "from the time of
the development of symptoms indicative of cardiovascular or renal
disease, four years will witness the death of half the men and five
years of half the women. By the tenth year half the remainder will
have died, leaving one fourth both of the men and the women who have
lived beyond ten years." The causes of death he would place in the
following order: gradual cardiac failure; uremia; apoplexy; some
complicating acute infection; angina pectoris; accidental causes;
acute edema of the lungs and cachexia. An early occurrence of
myocardial weakness shows a 50 percent probability that death will
be caused by cardiac insufficiency. Heart pains comprise another
important indicator of future cardiac death, perhaps not an angina.
Nocturnal polyuria would indicate a uremic death in about 50 percent
of the patients, and typical headache or cerebral symptoms show the
probability of uremic death in more than 50 percent, and death from
apoplexy in a large number of the other 50 percent As just stated,
rapid loss of weight is a bad symptom.
Janeway [Footnote: Janeway, T. C.: A Study of the Causes of Death in
One Hundred Patients with High Blood Pressure, THE JOURNAL A. M. A.,
Dec. 14, 1912, p. 2106.] has previously reported seven patients with
hypertension who had diabetes. Diabetes generally, on the other
hand, causes a low blood pressure. Patients with this trouble and
with hypertension, and without nephritis, probably have an increased
secretion from the suprarenals.
We may sum up the prognosis in hypertension as follows: Hypertension
alone is not of unfavorable omen; if it is not readily reduced by
ordinary means, it is more serious. If associated with kidney, heart
or liver defect, it is most serious. If there are such serious
conditions as edema, ascites, lung congestion, cyanosis and great
dyspnea, the prognosis is dire.
Obesity being a cause of high blood pressure, it should be treated
more or less energetically, even if the individual does not continue
to add weight.
Stone [Footnote: Stone, W. J.: The Differentiation of Cerebral and
Cardiac Types of Hyperarterial Tension in Vascular Disease, Arch.
Int. Med., November, 1915, p. 775.] believes that the higher the
diastolic pressure the greater danger there is of cerebral death,
while a patient with a very high systolic, but a diastolic pressure
of 100 or lower, is in more danger of cardiac death. He urges a
greater consideration of the pressure pulse in determining the load
of the heart and the great danger from a sustained diastolic
pressure of over 105 as sooner or later bound to cause myocardial
symptoms. This load of the heart is also shown by an increased pulse
rate and increased respiratory efforts. In cardiac failure, as the
systolic pressure falls the diastolic is likely to be increased, and
the pressure pulse thus diminishing, allows insufficient blood to go
to the medullary centers, and death soon occurs. Therefore, in acute
illnesses a sustained pressure pulse gives a better prognosis than a
diminishing pressure pulse. The strenuous measures that should he
used to lower a high diastolic pressure are contraindicated when the
diastolic pressure is already low, even if the systolic pressure 1s
high. If a high systolic pressure begins to fall more or less
rapidly the heart shows fatigue, and should be stimulated by
digitalis or strophanthin.
Rowan [Footnote: Rowan, J. J.: The Practical Application of Blood
Pressure Findings, THE JOURNAL A. M. A., March 18, 1916, p. 873.]
finds that a diastolic reading of 100 mm. or more usually means that
there is a narrowing of the lumen of the vessels, owing to
stimulation of the vasoconstrictors, although it may mean the
existence of a true arterial fibrosis. While a real atheroma
generally causes a reduction in diastolic blood pressure, or at
least but slight increase, he has found in syphilitic cases with
arteriosclerosis a high diastolic pressure. If the blood pressure
cannot be reduced by ordinary measures, arteriosclerosis is probably
present. Several blood pressure examinations must be made, while the
patient is being treated, to establish the diagnosis.
Rowan finds the reading of the pulse pressure to be of great
importance, as this will indicate, sometimes before any other
symptom is present, that the patient is either improving or doing
badly, and it also aids in indicating the proper medicinal
treatment.
In arteriosclerosis the systolic pressure may be high while the
diastolic is low; hence there is a large pressure pulse. If the
heart becomes weak the systolic pressure will drop, and any
improvement caused, especially in aortic regurgitation, is by an
increase of the systolic pressure.
Rowan finds, as has long been recognized, that a conclusion as to
whether or not cerebral hemorrhage will occur cannot be made from
the condition of the radial arteries, as patients with soft radials
may suffer from cerebral hemorrhage, while those "with hard,
sclerosed, pipestem-like arteries may live to a great age and die of
anything rather than apoplexy."
Swan, [Footnote: Swan: Interstate Med. Jour., March, 1915, p. 186.]
has studied the blood pressure in fifty cases of disturbed thyroid,
and finds that functional myocardial tests show that the myocardium
is nearly always disturbed in these patients.
Before taking up the subject of treatment of high blood pressure, it
may be suggested that a high diastolic pressure with a falling
systolic pressure may require vasodilators on the one hand or
cardiac tonics on the other, and sometimes the decision can be made
only by proper tests. In other words, if the diastolic pressure is
lowered the heart will be relieved. On the other hand, if the
diastolic is being raised by an increased venous pressure from a
failing heart, digitalis, strychnin and caffein may be of benefit in
lowering the diastolic as well as raising the systolic. However, if
there is a high systolic and a low diastolic pressure, vasodilators
are often contraindicated.
TREATMENT
In this rapid high tension age the physician should be as energetic
in teaching prevention of arterial hypertension as he is in
preventing contagion. As infectious diseases are reduced in
frequency, more patients live to die of diseases later in life, and
(as previously stated) diseases with hypertension are on the
increase. It is therefore the duty of the physician to urge youths
and adults to abstain from all kinds of excesses so common in this
age. We live at such speed, even the children, that this caution is
almost daily needed. We must caution against severe athletic
competition, against personal "stunts," against recreation excesses,
even golfing, automobiling and dancing, against excess in the use of
tobacco, in eating, in late dinners, in coffee, tea and alcohol. We
must take better care of patients during their convalescence from
some serious illness lest they have circulatory debility by becoming
strenuous too soon after their recovery. The pregnant woman must be
more carefully watched, not only for her own sake, but also for the
sake of her child. Intestinal indigestion, while not the cause of
all disturbances that occur in man after 40, is still an important
element in his deterioration and degeneration, and it should be
prevented if possible.
The tendency for hypertension and arteriosclerosis to occur early in
life in patients who have suffered some serious acute infection,
whether blood poisoning, typhoid fever, or other, shows that in all
probability in these acute illnesses the internal secretions are so
disturbed that the suprarenal activity is greater than normal, while
the thyroid activity may be less than normal, and hypertension is
the consequence. Therefore, these infected patients who recover
should probably have a longer convalescence in order for the more
delicate structures of the body, such as the internal secreting
glands, to have a better chance to recover and become normal.
The enumeration of these causes and the causes that have been
mentioned before not only suggest, but also direct the treatment of
hypertension after it has occurred. The most important of all
treatment for hypertension is rest. That means for an individual,
well except for his hypertension, a vacation, that is, a rest from
physical and mental labor. For a patient who is in serious trouble
from hypertension, bed rest is the most important element in the
management. As has been previously shown, good sleep lowers the
blood pressure, and Brooks and Carroll [Footnote: Brooks, Harlow,
and Carroll, J. H.; A Clinical Study of the Effects of Sleep and
Rest on Blood Pressure, Arch. Int. Med., August, 1912, p. 97.]
showed that the greatest drop in blood pressure occurs in the first
part of the night's sleep. In other words, a patient who lies awake
long loses the best part of his night's rest as far as his
circulation is concerned. This is one more reason for abstinence
from tea and coffee in the evening by those patients who are at all
disturbed by the caffein. On the other hand, patients who are not
seriously ill should not remain for days in bed, as the blood
pressure does not tend to continue to fall, although the heart may
become weakened by such bed rest. This is especially true if the
patient is nervous and irritable and objects to such confinement.
A systolic pressure much over 200 probably never goes down to
normal, and if such a high systolic pressure goes down to below 170,
we should consider the treatment successful.
Every active treatment of hypertension should begin with a thorough
cleaning out of the intestinal canal by purgation, best with mercury
in some form. Then the diet should be modified to meet the
individual case and the person's activity. If the blood pressure is
dangerously high, he should receive but little nourishment, best in
the form of cereals and skimmed milk.
On the other hand, if he has edema or dropsy, or if the heart showed
signs of weakness, large amounts of liquids should certainly not be
given, and in such cases it is better that he receive small
quantities of milk if that agrees, rather than large quantities of
skimmed milk. The amount of water should also be fitted to the
circulatory ability and the condition of the kidneys.
When more or less active treatment does not soon lower the
hypertension, and especially a high diastolic pressure, the
prognosis is bad. In a patient who is in more or less immediate
danger from his hypertension, the food and liquid taken, the care of
the bowels, and the measures used to cause secretions from the skin
must all be governed by the condition of his other organs. There is
no excuse for excessive, strenuous measures when the heart is
failing or when the kidneys are becoming progressively insufficient.
Strenuosity in treatment is as objectionable in these cases as is
neglect of treatment in earlier stages of the trouble.
Bie [Footnote: Bie: Ugesk. f. Laeger, March 4, 1915.] believes there
is no direct connection between the blood pressure and the anatomic
condition in the kidneys, although abnormal conditions in the two
are almost invariably found parallel.
A patient with simple hypertension and otherwise well, which means
that his diastolic pressure is at least no higher than 110, should
have his diet, tobacco, coffee and tea regulated; should have
recreation periods one or more times a week, and vacations not too
infrequently; should take some brisk purgative once or twice a week,
and may receive one or other of the physical treatments for the
reduction of blood pressure, whether Turkish baths or electric light
baths. If he does not sleep well, there is no hypnotic drug so
valuable in his case as chloral. This should not be long given, but
it will produce the purest kind of sleep and lowers the blood
pressure.
If any other drug is needed, nitroglycerin is the best. If
arteriosclerosis is present, sodium iodid in small doses, 3 grains
two or three times a day, is valuable. Larger doses of sodium iodid
are not needed, unless it is advisable to give such doses for a
short period. The value of iodid in these cases is best obtained by
small doses long continued. If the patient is obese, shall doses of
thyroid extract long continued are of value, such as 2 or 3 grains
once a day. If the thyroid extract causes the heart to become more
rapid, it should be discontinued.
Whether the diet should be meat protein free, or whether meat may be
allowed once a day, depends entirely on the individual and on his
physical activities. It is frequently a mistake to take all meat out
of his diet.
When there is obesity, the bulk of the food should be greatly
diminished, and anything that tends to stimulate the patient's
appetite should be withheld. This means all condiments, and at times
even salt. Sugar should be greatly reduced, and starches greatly
reduced, but he must have some. In other words, he should not be cut
down to a diabetic diet. No more liquid should be taken with the
meals than is essential to swallow the food. Water should be taken
between meals. There is no question that almost every one today
should have a very light breakfast, except perhaps those who labor
hard physically and are exposed for hours, daily, to the
inclemencies of the weather. Such patients probably need more food.
It is also well, in hypertension cases, to have one day a week in
which a very minimum amount of food is taken, whether that be milk,
or skimmed milk, or a small amount of carbohydrate, without protein
food.
If the foregoing management does not reduce hypertension, the
kidneys are generally beginning to become involved in the sclerotic
degeneration, whether the urine shows such a condition or not. On
the other hand, there are exceptions to this rule.
As indican in the urine gives evidence of putrefactive changes in
the intestines and the probability of the absorption of toxins from
the intestines, although we have no real proof that these toxins are
the direct cause of hypertension, our patient is undoubtedly
physically better, and will have less arterial tension when this
intestinal condition is removed. Therefore, our treatment of the
individual is not a success as long as such fermentation and
putrefaction persist. If such putrefaction cannot be removed by diet
and laxatives and mental rest and the prevention of physical
strenuosity, radical changes in diet are advisable, although it may
not be necessary to continue such a diet more than a few days at a
time. A rigid milk diet for a few days may change the flora of the
intestine completely; then a vegetable diet may be given, with
return to a mixed diet; or the various lactic acid bacilli may be
given, or one of the various fermented milks may be the diet, the
object being to change the flora in the intestine and thus modify
the ferments. So-called bowel antiseptics, such as salol, for a
short time may be of advantage. Colon washings may be of great
advantage. Liquid petroleum may be advantageous.
Besides preventing the absorption of toxins from the intestine, we
must prevent such absorption from any latent infection. The most
frequent kind of such infection is pyorrhea alveolaris.
A simple method that sometimes is an efficient aid in lowering the
blood pressure is complete muscular and mental relaxation. The
patient lies down for a while in the middle of the day and relaxes
every muscle of his body. With this he may take slow breathing
exercises. He should be in a dark room, quiet if possible, and
alone, and should teach his brain to be for a short time mentally
inert.
The physical methods of lowering the blood pressure are
hydrotherapeutic, whether by warm baths or more strenuously by
Turkish baths, by hot air baths (body baking) which is occasionally
very efficient, or, perhaps more now in vogue, by electric light
baths. The duration of these baths, and the frequency, must be
determined by the results. If the heart is made rapid, and the heart
muscle shows signs of weakness, the duration of these baths must not
be long, and they may be contraindicated. These baths are most
efficient in lowering the blood pressure when the patient reclines
for several hours after the bath. The amount of sweating that is
advisable in these cases depends on the condition of the heart. If
the heart muscle is insufficient, profuse sweating is inadvisable.
Also if the kidneys are insufficient, profuse sweating is
inadvisable as tending to concentrate the toxins in the blood. On
the other hand, when the surface of the body tends to be cool, and
there are internal congestions, the value of these baths is very
great. Sometimes the electric light baths increase the tension
instead of diminishing it, and when properly used they may be of
benefit in some cases of hypotension. The frequency of the baths and
the question of how many weeks they should be intermittently
continued, depend on the individual case. After a course of such
treatment sometimes patients have a diminished systolic blood
pressure not only for weeks, but even for months, provided they do
not break the rules laid down for them.
The Nauheim baths, while stated not to raise the blood pressure, are
not much advocated in hypertension, and Brown [Footnote: Brown:
California State Jour. Med., November, 1907, p. 279.] who made more
than 500 observations of patients of all ages, found that the full
strength Nauheim bath would raise the blood pressure in all feverish
and circulatory conditions. He also found that a fifteen minute
sodium chlorid bath, 7 pounds to 40 gallons, at a temperature of
from 94 to 98 degrees F., lowered the pressure from 10 to 15 mm.
This is not different from the effect obtained from a fifteen minute
warm bath at from 94 to 98 degrees F., or a fifteen minute mustard
bath of the same temperature. In other words, the slight irritation
of mustard or of salt in a warm bath made no special difference in
the amount of lowering of the blood pressure. On the other hand, he
found that a fifteen minute calcium chlorid bath, 1 1/2 pounds to 40
gallons, at 94 degrees F., raised the blood pressure 15 mm.
The autocondensation treatment to lower the blood pressure is not so
satisfactory as it was hoped to be. The blood pressure can thus be
lowered, but it soon again rises, and probably generally more
rapidly than after the bath treatments, and in some persons it
causes considerable depression. Van Rennselaer [Footnote: Van
Rensselaer: Month. Cycl. and Med. Bull., November, 1912, p. 643.]
has reviewed this subject of high frequency treatment, and recalls
the fact that Nicola Tesla demonstrated, in 1891, the form of
electricity which we now term high frequency. High frequency means
more than 10,000 cycles per second, at which frequency muscles do
not contract and pain is not felt, whereas in medicine the frequency
of the currents used runs up into the hundreds of thousands, or even
into the millions. The French investigator, d'Arsonval, studied the
physiologic action of these high frequency currents and found that
the respiration and heart are made more rapid and the blood pressure
is reduced, while the intake of oxygen is increased and the carbon
dioxid excretion is increased. The temperature may rise. The
excretion of the urinary solids is mostly increased. Perspiration
may be caused, and he believes the glandular activities are
increased. In a word, metabolic changes in the body are made more
active and the blood pressure is lowered.
Besides the effect of altitude on blood pressure, as previously
declared, patients with dangerously high blood pressure should, if
possible, not be subjected to intense cold. In other words, a person
with hyper-tension, if financially able, should not remain in a cold
climate during the winter. On the other hand, even if he is stout
and feels sufficiently warm with light clothing during the winter,
his skin becoming chilled adds to his tension. Therefore he should
be clothed as warmly as he will tolerate.
After a period which may be termed the normal period of hypertension
in normal life, as age advances the systolic tension may lower,
provided there is no kidney lesion. This is due to the slowly
developing chronic myocarditis and a lessening of the tension and
therefore lessening of the resistance to the heart. This may be
nature's method of lengthening the life of the individual. In other
words, as the arteries grow older the force of the heart slightly
lessens, the blood pressure lowers, and the individual is safer.
This frequently occurs in otherwise perfectly normal individuals,
without treatment.
When the blood pressure is suddenly excessively high from any cause,
venesection may be life saving, and should perhaps be more
frequently done than it is. It may save a heart that is in agony
from tension, and may prevent an apoplexy. It is of little value
except temporarily in uremic conditions, but at other times it may,
at the time, save life and allow other methods of reducing the
dangerous tension to become effective. A chronic high tension
patient may be repeatedly bled, although such treatment will not
long save life, as the blood pressure in many such cases soon
returns to its previous height.
Some very high tension cases, especially in women at the menopause,
and where there is no kidney involvement, have the blood pressure
reduced successfully only by large doses of thyroid, sometimes well
combined with bromids, especially if the thyroid causes excitation.
Such treatment persisted in for a time may cause months of
improvement, and even years.
DRUGS IN HYPERTENSION
The drugs that are mostly used to lower blood pressure are nitrites
or drugs which are like nitrites, and these are nitroglycerin,
sodium nitrite, erythroltetra nitrate and amyl nitrite, and the
frequency of their use is in the order named. Other drugs used to
lower blood pressure are iodids, thyroid, alkalies, chloral, bromids
and aconite, the latter rarely.
Amyl nitrite is required only when a sudden immediate effect is
desired in angina pectoris or in some other serious spasmodic
condition. Sodium nitrite is more likely to upset the stomach than
is nitroglycerin. It acts, however, a little longer, but not enough
to warrant its frequent selection. The dose of sodium nitrite is
from 0.03 to 0.06 gm. (1/2 grain to a grain), best in tablet form
and given with plenty of water. The tablet should of course be
dissolved or crushed with the teeth. It should not be given on an
empty stomach, as it may cause considerable irritation and pain. It
more or less actively lowers the blood pressure for about an hour.
Erythrol tetranitrate is preferred by some clinicians who find that
its effect lasts somewhat longer. There is probably, however, no
better nitrite or nitrate than nitroglycerin. While it acts but a
short time, it acts effectively, and although no nitrite has
vasodilating effects for any length of time from one dose, when the
doses are given repeatedly and for days at a time, the blood
pressure will generally be more or less reduced. The dose is from
1/500 to 1/100 grain, three or four times a day, or every three
hours, as desired. The best form in which to use it is in a very
soluble tablet, and the tablet should not be dissolved unless
intense immediate action is desired. It acts when absorbed from the
tongue almost as rapidly as when given hypodermically; it acts in
two or three minutes, and the blood pressure may drop from 20 to 30
mm. In experimental tests the action does not last more than from
fifteen minutes to half an hour, but clinically the effect of
repeated doses is much more satisfactory. Spirit of glyceryl
trinitrate or spirit of Nitroglycerin, dose 1 minim, keeps well if
care is taken to guard against evaporation of alcohol; tablets if
well made and kept in bottles properly corked, will retain their
activity for months.
The closer a physician is to the laboratory, the less he believes in
the value of nitroglycerin in hypertension. The nearer he is to
clinical work the more he believes in it. It is a fact that in some
instances, even with a dose as small as 1/200 grain of
nitroglycerin, three or four times in twenty-four hours, the blood
pressure will be lower, whatever the diet is and whatever the other
treatments are, than if the patient does not take the nitroglycerin.
Also the value of these short relaxation periods from the standpoint
of a strained and tired heart should not be underestimated, the same
as the value of a night's rest, or the value of a recreation period
of an hour or two. If a patient has hypotension and a systolic
pressure of 110, and is given nitroglycerin, the very unpleasant
results from its administration will be immediately noticed. Hence
nitroglycerin is one of the most valuable drugs that we possess for
the treatment of hypertension, and some patients are even benefited
by as small a dose as l/500 grain. Lawrence [Footnote: Lawrence, C.
H.: The Effect of Pressure-Lowering Drugs and Therapeutic Measures
on Systolic and Diastolic Pressure in Man, Arch. Int. Med., April,
1912, p. 409.] found that the fall of diastolic pressure from
nitrites was about half of the fall of systolic pressure. When there
is no kidney lesion a very high systolic pressure falls more under
nitroglycerin than does a medium high systolic pressure.
Alkalies, whether potassium or sodium citrate or sodium bicarbonate,
are often of advantage in so changing and aiding metabolism, or
perhaps reducing the irritation from hyperacidity or a mild
condition of acidosis, that their administration causes a lowering
of blood pressure.
While iodids may not be direct vasodilators and do not render the
blood more aplastic or diminish its viscosity, as shown by Capps
[Footnote: Capps, J. A.: Effect of Iodids on the Circulation and
Blood Vessels in Arteriosclerosis, THE JOURNAL A. M. A., Oct. 12,
1912. p. 1350.] still, iodids in small doses, 0.1 to 0.2 gm. (1-1/2
to 3 grains) given from once to three times a day, after meals
(these small doses do not disturb the stomach), will stimulate the
thyroid gland to greater activity, and when this gland secretes
properly, the blood pressure is somewhat lowered. Of course, in
syphilitic sclerosis large doses of iodids are indicated and are
valuable.
In obese patients with hypertension, in the hypertension of women at
the menopause, and in hypertension with insufficient kidneys,
thyroid medication is often of great value. Sometimes a small dose
of from 0.1 to 0.2 gm. (1 1/12 to 3 grains) once a day is all that
is needed. At other times, especially when there is no marked
arteriosclerosis and no marked kidney or liver lesion, very high
blood pressures are reduced only by very large doses, even as much
as 10 grains a day. Such treatment is often of very great benefit.
Of course, if one of the persons under consideration has symptoms of
hyperthyroidism, or if small doses of thyroid cause palpitation, the
treatment is not indicated, on the one hand, and should be stopped,
on the other. Sometimes when the blood pressure cannot be reduced,
in these cases without apparent organic lesions, and thyroid
treatment is more or less successful, but at the same time causes
great excitation, it may be combined with bromid medication, and
then the benefit is sometimes very great.
A patient who cannot sleep and who has hypertension may receive
bromids if he is very irritable or if there are symptoms of thyroid
irritability; but the most successful sleep and lowering of blood
pressure is caused by chloral. A dose of 0.5 gm. (7 1/2 grains) at
night is generally sufficient and need not be long continued.
Chloral has been frequently given to reduce pressure in 0.2 to 0.25
gm. (3 or 4 grain) doses, three times a day, after meals.
Bromids, of course, will lower the blood pressure, but they depress
all metabolism, interfere with digestion, and are not advisable for
any length of time. However, in some cases they cause a marked
improvement in the patient's condition.
Patients under treatment with chloral, bromids, and thyroid
especially, should be carefully watched and the treatment modified
to meet the varying conditions. Patients under iodid need not be
seen so frequently; those under nitroglycerin or alkalies still less
frequently. But all patients under the active management of
hypertension should be seen at from one to three week intervals, and
the urine should be repeatedly examined and the blood pressure
carefully recorded.
HYPOTENSION
A low systolic pressure and a low diastolic pressure may not cause
any symptoms or give any cause for anxiety. It does show, especially
if the systolic pressure is below normal for the age of the person,
a lack of reserve power, and such patients will not well stand
serious illnesses, operations, injuries or serious physical and
mental strains. If there is a low systolic pressure and a high
diastolic pressure, this shows impairment of the heart, whether or
not any other organic lesion is present.
Generally speaking, a low systolic pressure shows a weak acting
heart muscle, and a very low diastolic pressure shows a dilated
condition of the arterioles. In aortic regurgitation this low
diastolic pressure is constantly in evidence, and, if the systolic
pressure is not below normal, does not signify that the circulation
is insufficient. If the systolic pressure is not very low but the
diastolic is high, vasodilator drugs, by lowering the diastolic and
increasing the pulse pressure, are often of benefit. If there is
increased venous congestion and increased venous pressure and a high
diastolic pressure with a low systolic pressure, digitalis not only
will often raise the systolic pressure, but also will lower
diastolic by improving the general circulation and removing venous
congestion.
While intestinal indigestion and absorption of toxins often tend to
raise the blood pressure, some toxins thus absorbed, especially of
the ptomain variety, lower blood pressure and cause shock, perhaps
by weakening the muscle of the heart or by acting on the vasodilator
vessels; or they may cause dilation of the vessels of the abdomen
and in this manner lower blood pressure.
Very low blood pressure after exertion, after severe physical
exercise, or after competitive athletic tests shows that the heart
cannot sustain such strains and should not be again subjected to
them. In severe mental and physical strains the suprarenals may be
inhibited in their activities, and a hypotension, more or less
prolonged, may result.
Sewall [Footnote: Sewall: Am. Jour. Med. Sc., April, 1916, p. 491]
believes that hypotension is frequently due to splanchnic stasis,
and that sluggish circulation in this region, especially when the
person is in the erect posture, is an important factor in general
physiologic disturbances or lack of general tone. When the
splanchnic vessels are dilated there is also a lack of proper tone
to the cerebral vessels, and this may be a cause of mental weariness
and neurasthenia. While ptosis of organs in the abdomen and a
flaccid condition of the musculature of the abdomen are frequent
causes of this splanchlnic stasis, and therefore hypotension,
especially in women, it is quite possible that suprarenal
insufficiency will allow this condition of the splanchnic vessels to
occur frequently.
Serious illness and infections will lower the blood pressure
sometimes to a dangerous point. Of course, hemorrhages lower the
blood pressure. Shock and collapse cause lowering of blood pressure,
frequently to a fatal point, and Cornwall [Footnote: Cornwall: New
York Med. Jour. March 7, 1914, p. 470.] finds that a patient may
live several hours with a systolic pressure below 60, and several
days when it is below 70; that he may walk around with a systolic
pressure of 90, provided the pressure pulse is sufficiently large,
that is, that the diastolic pressure is low enough to cause a
circulation of blood. Of course, if the difference between the
systolic and the diastolic pressure is diminished to the vanishing
point, the patient cannot stand it, and dies. It should be
remembered that just before death venous pressure is likely to rise,
and this may raise the diastolic pressure.
With the progressive toxemia of typhoid fever the blood pressure
will become lowered from the myocardial degeneration. Of course, the
blood pressure will drop suddenly from a hemorrhage, but Piersol
[Footnote: Piersol: Pennsylvania Med. Jour., May, 1914, p. 625]
finds that with perforation the peritoneal irritation may cause a
rise of blood pressure, and he thinks that this sign may precede for
several hours more positive signs of the accident.
As in other infections, the blood pressure will fall in scarlet
fever; but if it suddenly rises, a kidney complication is to be
looked for. The blood pressure always falls in diphtheria, and
always falls in acute rheumatism; consequently, strenuous sweating
measures in the treatment of rheumatism should not be used as soon
as the blood pressure has become low.
Failing circulation in pneumonia, if accompanied by low blood
pressure, requires different treatment from the failure of
circulation in these cases when the blood pressure is high. Hence
the relationship of the systolic to the diastolic pressure in
pneumonia is of very great importance in deciding on the proper
treatment. In one instance the blood pressure must be lowered; in
the other, the heart must be stimulated.
While tobacco, in ordinary conditions, raises the blood pressure,
after the heart has been seriously injured by the nicotin, the blood
pressure is likely to be found lower, and such patients are quickly
benefited by the withdrawal of the tobacco and the administration of
digitalis.
Anemia almost invariably causes low blood pressure. Also in a
patient who has hypotension without any distinct evidence of
disease, especially if there has been any possible exposure to
tuberculosis, that disease should be suspected and every test made
to eliminate such a cause.
Serious cachexia, such as that caused by carcinoma or other growths,
gives low blood pressure. Diabetes causes low blood pressure,
provided there are no nephritis and no marked suprarenal
stimulation.
Excessive use of alcohol, while tending to promote hypertension by
the disturbances that it causes, may give, by causing a weak heart
muscle, a permanent low blood pressure. A single large dose of
alcohol always lowers the blood pressure.
Arteriosclerosis frequently reaches a stage when the blood pressure
is low, and with atheroma of the arteries of the arms a true blood
pressure is difficult to obtain. Addison's disease, or any other
organic lesion of the suprarenals, will lower the pressure, while
stimulation of the suprarenals increases the pressure. Any great
drain on the system, whether from diabetes without nephritis, or
from profuse diarrhea of any type, will cause hypotension.
Occasionally a girl with chlorosis who is not menstruating may have
an increased blood pressure. Many of the hemorrhagic or purpuric
conditions will show a hypotension.
Meningitis in various forms may show a hypertension from cerebral
and nervous irritation. Neurasthenic patients quite generally have
hypotension, although occasionally with suprarenal disturbance they
may have an increased tension.
In the hypotension of surgical shock and in shock during anesthesia,
Henderson's findings [Footnote: Henderson: Am. Jour. Physiol., 1910,
xxvii, 158.] that hyperoxygenation and insufficient carbon dioxid
may be partially responsible for the condition should be remembered,
and it has long been known that carbon dioxid congestion, as caused
by laughing gas anesthesia, for instance, increases the blood
pressure.
A systolic pressure of 110 mm. or lower in an adult should be
considered hypotension, anything below 105 mm. calls for treatment,
and a systolic pressure of 100 or lower in an adult calls for rest
from all active duties.
These patients are weary, they have mental and physical tire, may
get short breathed, may have palpitation of the heart, and often
have headaches and dizziness from imperfect circulation in the head.
There may be edemas of the legs and ankles toward night. If such
patients have the systolic blood pressure raised even a small
amount, or if the diastolic pressure, which is very low, is raised
even a small amount, they immediately feel better.
If the kidneys are normal, they should have meat as part of their
diet. If they are not nervous and irritable, coffee and tea should
be allowed, except at the evening meal. While sleep may tend to
lower pressure somewhat, these patients' hearts require a long bed
rest; in other words, they should go to bed at an early hour. They
should rise early, however, in the morning, and, as recommended by
Goodman, [Footnote: Goodman: Am. Jour. Med. Sc., April, 1914, p.
503.] they should perform mild calisthenic exercises before
dressing.
The increased muscle tone thus caused raises the blood pressure
somewhat, and the great depression before breakfast is not
experienced. These patients rely oil their morning coffee for
bracing. If they have much indigestion at night which keeps them
awake so that they do not get good comfortable rest, their largest
meals should be the morning and noon meals, and the evening meal
should be very light.
Pendent abdomens or ptosed abdominal organs should be held up by
proper abdominal bandages or corsets.
If the bowels are constipated, only the vegetable laxatives should
be used, if it drug is needed at all. Salines should not be allowed,
or other cathartics which cause profuse watery discharges. If a
brisk purge is required, castor oil is the best.
Plenty of fresh air, and mild exercises in the open air all tend to
increase the pressure. Graded walking, climbing, or other more
interesting exercises are advisable, as all tending to raise the
pressure, provided that at no time are they carried to the point of
exhaustion.
Forced feeding may be useful. Cool sponging in the morning, if there
is proper reaction, is often of benefit. Iron may be indicated;
bitter tonics may be indicated. Digitalis and strychnin are often of
advantage. Caffein may be used as a drug as well as given in coffee
and tea. Atropin may be of value in some forms of hypotension.
At times with a low systolic pressure, but a relatively high
diastolic pressure, nitroglycerin is valuable.
More or less actite hypotension may occur in hot weather or with
overheating, often termed heat exhaustion. Such patients should, if
possible, go to a cooler region, whether to the seashore or to the
mountains is unimportant. The treatment of dangerous sudden low
blood pressure, as shock, will be discussed elsewhere.
PERICARDITIS
ACUTE PERICARDITIS
As this inflammation is generally secondary to some other condition,
its treatment cannot be positively outlined. Furthermore, it is
often a terminal condition, and in such instances the results of
treatment are of necessity nil. The most frequent terminal cause is
nephritis; other terminal causes are pulmonary tuberculosis,
adjacent abscesses, cancer or other growth.
The most frequent infectious cause is rheumatism; other infectious
causes are cerebrospinal fever, typhoid fever, acute miliary
tuberculosis, pneumonia and Sepsis. Accidental causes are traumatism
and an adjacent inflammation of the pleura.
The result of an inflammation of the pericardium may be a fibrous
exudate, or an exudate which is both serous and fibrous, or one in
which pus is present in considerable amount.
The onset of pericarditis may be more or less acute, or it may
commence insidiously. For this reason, during severe illness, and
especially in those diseases which are known to have pericarditis
often as a sequence, frequent examination of the heart should be
made as a routine procedure.
SYMPTOMS AND SIGNS
If there is pain or much aching in the cardiac region, it tends to
disappear with the exudate, if such is to occur, in the same way as
does the pain of pleurisy. If there is much exudate, the pressure on
the heart of course increases, the cardiac dulness enlarges, dyspnea
occurs and even perhaps later cyanosis. As the exudate accumulates,
the patient must lie higher and higher in order that the fluid may
gravitate to the lowest part of the sac and give the heart the
greatest ability to work. Reflex pain may occur from disturbances of
the pneumogastric nerve, or from the weight and pressure of the
enlarged and heavy pericardium. Reflex vomiting may be a troublesome
and distressing symptom.
Acute pericarditis occurring in rheumatism, in acute infections, and
from simple injuries tends to recovery. In dry pericarditis with
serious adhesions, or if adhesions occur as a sequence of acute
pericarditis, the future prognosis is bad, as myocarditis may
develop and sudden death or acute dilatation may occur. As stated
above, if pericarditis develops during the progress of chronic
disease, such as interstitial nephritis, or during sepsis, or from
abscesses or growths in the region of the pericardium, the prognosis
is bad.
TREATMENT OF ACUTE PERICARDITIS
In acute pericarditis, absolute mental as well as physical rest is
essential. Even if the patient does not appear to be seriously ill
and has not much fever, he should not be allowed to have visitors,
to discuss business matters, or to carry on any conversation,
however little exciting. Anything which increases the heart beat
increases the irritation of the inflamed surfaces of the
pericardium. He should not be allowed to sit up, either to eat or to
attend to the calls of Nature. These rules are imperative, and when
they are followed the pain is less, the heart beats less rapidly, is
less hampered by pressure from whatever exudate may be present, and
the adhesions which are liable to form will be less in amount and
less serious for the future work of the heart.
The treatment, of course, depends largely on the cause of the
pericarditis, as, if the cause is one of those just enumerated in
which the prognosis is dire, any treatment directed toward the
pericardial inflammation is almost useless. The periearditis under
these conditions will be more or less benefited, if at all affected,
by the treatment directed toward the cause.
The indications for treatment in all other instances are:
1. To attempt to abort the inflammation.
2. To stop the pain.
3. To limit, if possible, the amount of exudate, and to diminish the
exudate already present.
4. To diminish the rapidity of the heart and to strengthen it.
1. Abortive Treatment.--For many years bloodletting was considered
of the greatest importance in the early treatment of this disease;
but owing to the fact that, except from traumatism, pericarditis
rarely occurs except as a sequela of acute disease after the patient
has been sick along time, or as a terminal condition in a patient
who has long been chronically diseased and therefore has already
lost more or less strength, venesection has been nearly abandoned.
Leeches may be used over the region of the pericardium, and cups are
sometimes used. Dry cupping is more frequently used. These measures
sometimes seem to reduce the inflammation, and certainly often
relieve pain, but the most valuable local treatment is cold, which
may be applied either in the form of an ice bag or by a small coil
through which ice water is caused to flow by siphonage. Cold may be
applied more or less continuously, depending on the sensations of
the patient. The bag or ice cap must not be overfilled and must not
be heavy, as the patient often cannot stand pressure over the
pericardium. Sometimes the relief from pain and the diminution of
the number of the heart beats is marked, and for this reason alone
the cardiac inflammation may be inhibited. If cold applications are
not tolerated by the patient (and they often are not in children)
warm applications may be used, such as an electric pad or cloths
wrung out of hot water and covered with oiled silk, and the pain
will often be relieved thus. While hot applications would not tend
to abort the inflammation, they probably do not tend to promote it.
A diminished diet, of small amount at a time, and such purging as
the patient's strength will allow are essential in attempting to
hasten recovery.
Just what can be done locally or generally to combat the
inflammation actively must depend on the cause. When the
inflammation occurs as a complication of acute rheumatism, it has
been suggested that salicylates, which arc not inhibiting rheumatism
and may be depressant to the heart, should be stopped if they are
being administered; but if the salicylates are apparently improving
the inflammation in the joints, pericarditis would not
contraindicate their continued use. Except in large doses,
salicylates probably do not depress the heart. In pericarditis it is
perhaps well always to administer an alkali in some form unless
otherwise contraindicated, whether or not the cause is rheumatism. A
diminished alkalinity of the blood would always increase the
likelihood of an augmented amount of pericardial or endocardial
inflammation. The blood must be kept strongly alkaline. It is
possible that one of the reasons why pericarditis or endocarditis
occurs so frequently in serious prolonged fevers is that the patient
has not eaten enough cereals or other carbohydrates, and the system
has become more or less endangered by acidosis. Carbohydrate
starvation is inexcusable with our present understanding of the
danger from acideinia, and even from a diminished amount of alkalies
in the blood.
The cause of pericarditis being so varied, any anti-toxin treatment
or any vaccine treatment could be indicated only if the cause of the
inflammation rendered the serum or vaccine advisable.
2. Stopping the Pain.--Nowhere else in the body should pain be so
speedily combated as when it occurs in the region of the heart.
Morphin, with or without atropin, as deemed best, should be
administered hypodermically in the amount and with the frequency
necessary to stop the pain and quiet the restlessness. As stated
above, the frequent need for morphin may be prevented by use of the
ice bag. Morphin might even be considered an abortive treatment, as
nothing tends so much to inhibit this inflammation as the quietude
of the heart caused by the absence of pain, the production of sleep
and the prevention of restlessness, muscle twitching and muscle
movements. The more quiet the patient is, the more quiet is the
heart.
If for any reason morphin is contraindicated, and if pain is not a
symptom, the patient's nerves may be quieted and rest may be given
by sodium bromid, or by veronal-sodium, the dose of the former being
2 gm. (30 grains) two or three times in twenty-four hours, according
to its action and the necessity for it, and the dose of the latter
0.2 gm. (3 grains) once in six hours, if deemed necessary.
Especially if there are cerebral symptoms, as typically presented in
cerebrospinal meningitis, and especially if the arterial tension is
low, the subcutaneous administration of an aseptic ergot will quiet
the central nervous system, increase the blood pressure, quiet the
heart, and prolong the action of a single dose of morphin. It is the
best plan to administer ergot deep into the muscles, with the
deltoid as the place of choice. If the skin is properly cleansed,
the syringe clean and the preparation of the drug aseptic, no
inflammation or abscess will ever occur. If there is any painful
swelling, a wet alcohol dressing to the part will soon relieve it.
The frequence with which ergot should be so administered depends on
the results and the indications. Once in twelve hours for several
doses is generally the best method for its use.
3. The Exudate.--When a fluid exudate into the pericardium has
occurred from inflammation that is, when it is not an exudate from
disturbed kidneys or circulation--it will continue to increase to
some extent in spite of any treatment. Just how much this exudate
may be prevented by the use of small blisters over or around the
heart, and just how much watery stools and diuresis may prevent the
advance of the exudate is difficult to determine. Small blisters,
properly applied, have many times seemed to be the determining
factor in stopping the increase in the fluid, or to have been the
starting cause of the resorption of the exudate.
The amount of purging that should be caused by saline cathartics
such as sodium sulphate (Glauber salt), potassium and sodium
tartrate (Rochelle salt), or the official compound jalap powder
cannot be declared dogmatically. Saline purging should be governed
by the character of the circulation. If the heart is strong, the
pulse not weak, and the blood pressure good, nothing is more
valuable in this condition. Portal depletion is of great advantage,
especially if the amount of liquid ingested is kept as low as
possible, so that the blood vessels may become thirsty and thus tend
to absorb an exudate wherever they find it. Much harm has been done,
however, and death has been caused by saline purgatives in
endeavoring to relieve edemas from a failing heart or to prevent a
uremia from kidney inflammation. The depression following such
purging is often serious. If the circulation is weak, dependence
should be placed on purgation by some of the simple vegetable
cathartics or a small dose of calomel. While it is advisable to give
a saline in concentrated solution, it should not be so strong as to
cause vomiting. With our better understanding of magnesium
absorption and the depressant effect of magnesium on the nervous
system, magnesium salts should not be used in serious conditions.
Diuretics often do not act well when most needed. The simplest
diuretic is potassium citrate, given in wintergreen or peppermint
water, in doses of 2 gm. (30 grains), three or four tunes in twenty-
four hours. One or more of the vegetable, nonirritant diuretics may
be tried if preferred. If the sickness preceding the pericarditis
was not a long fever, and the heart muscle is considered in good
condition, digitalis in small doses may be the best possible
diuretic. Incidentally it will slow the heart, if there is not much
elevation of temperature, and will give some cardiac rest.
Although the patient's diet should be limited in bulk, and
especially in amount of liquids, good nutrition should soon be
given. Systemic weakness certainly tends to increase the exudate;
systemic strength aids in absorption of the exudate.
Iron is early indicated, and nothing is better than 5 drops of the
tincture of chlorid of iron in a little lemonade or orangeade,
administered once in eight hours.
If the exudate tends to decrease, it perhaps may be hastened by the
local application of tincture of iodin over the cardiac region. Also
the administration of small doses of an iodid, as 0.3 gm. (5 grains)
of sodium iodid, given in plenty of water three times a day, is
useful. An iodid circulating in the blood seems to aid absorption.
It has long been believed that iodin in the blood tends to promote
absorption of thickened, left-over material from exudates, and to
prevent the formation of strong fibrous adhesions. Until our
knowledge is more exact in this matter, it is advisable to use iodid
as suggested. If the above-named dose is not tolerated, less should
be given.
If in spite of all the therapeutic measures suggested, the fluid
increases and the pericardium becomes more distended and the heart's
action more labored, paracentesis must be done. The point at which
the aspirating needle should be inserted into the pericardium
depends somewhat on the conditions in each individual case. It is
often best to insert an exploratory needle first. This will
determine the fluidity and character of the exudate. If pus is
found, a more radical surgical procedure than simple paracentesis
must be done immediately. The point of puncture for aspiration most
frequently chosen is in the fourth or fifth intercostal space, about
an inch to the left of the sternal margin. Paracentesis is also
often done in the region of the normal apex beat. The position of
the patient is determined by his dyspnea; he should lie in the
position most comfortable for him. The fluid should be withdrawn
slowly and the pulse carefully watched. The withdrawal of a small
amount of fluid may later seem to be the starting cause of
resorption of the rest of the fluid. On the other hand, it may often
be not of more value than the simple removal of the immediate
pressure, the fluid may again accumulate, and more radical surgery
must be performed.
4. To Strengthen the Heart.--Most of the methods of meeting this
indication have already been stated, namely, absolute rest; absolute
quiet; the use of the bed pan; any movement that must be made should
be deliberate; the nurse and other attendants must be quiet;
necessary conversation must be brief, and every method must be used
to quiet and prevent the heart's action from becoming rapid. The
food taken should be small in amount and nonstimulating; that is, no
tea or coffee should be given, and nothing too hot or too cold.
Movements of the bowels should be caused with the least possible
general disturbance. If the patient does not sleep, he must be made
to sleep. The whole body and the nervous system must have periods of
rest. If the heart is very weak, small closes of morphin may be
used. If the heart is not weak, bromids or chloral may be given. If
the blood pressure is high, such hypnotics will lower it, or if the
heart is strong and the condition does not contraindicate it,
aconite may be used in small doses, for a day or two, unless the
fever is high and it seems advisable to use one of the coal-tar
antipyretics, which reduce the blood tension and the heart activity.
As stated above, pain must not be allowed. Sometimes, when the heart
has not been injured by prolonged fever, digitalis in small doses
may slow the heart and act for good.
Convalescence.--The convalescence should be prolonged as in any
other cardiac inflammation. The patient should be given more and
more nourishing food, and the iron tonic may be changed to a capsule
containing 0.05 gm. of quinin and 0.05 gm. of reduced iron, three
times a day.
It is a question as to when patients convalescent from pericarditis
should be permitted exercise. It has been thought that gentle
movements and possibly exercise, sooner than theoretically
justified, might cause the heart to beat a little more actively and
possibly prevent the formation of tight adhesions between the two
layers of the pericardium. Whether such activity of the heart will
prevent adhesions is something that has not been determined.
The small doses of sodium iodid, perhaps 0.2 gm. (3 grains) two or
three times a day, should be continued for some time. Iodid in this
dosage does no harm and may do a great deal of good.
ADHERENT PERICARDITIS
Following dry pericarditis or pericarditis with an exudate,
especially when the exudate is fibrinous in character, the fibrous
substance which is not absorbed or resorbed may develop into
connective tissue, and the two pericardial surfaces become
permanently grown together, causing the so-called adherent
pericarditis. These adhesions between the two surfaces of the
pericardium may be general throughout the entire pericardial sac, or
they may be limited to some one or more parts of the pericardium.
Perhaps one of the most frequent points of adhesion is the anterior
part of the pericardium, while the apex is the part most likely to
be free, even when other parts of the pericardium have grown
together. This freedom of the apex is probably due to the constant
and more extensive motion of the apical portion of the heart, and is
the reason that it has been suggested, as referred to under acute
pericarditis, that, other conditions not contraindicating, the
patient may be allowed to move about a little during convalescence
to cause the heart to beat more actively. Sometimes the surfaces of
the pericardium are not closely adherent to each other, but bands of
adhesion stretch from one surface to the other.
After adhesions have taken place between the two layers of the
pericardium, the action of the heart is impaired, serious
interference with the cardiac action may develop, and sudden death
may occur. If the heart is given all the rest possible during the
acute phase of the disease, there will be less likelihood of the
surfaces becoming so irritated that adhesions readily form. Anything
which permits complete absorption and resorption of tile exudate
will tend to prevent these hampering adhesions. If the adhesions are
such as to cause irregular heart, recurrent pain and the danger of
sudden death, surgical help has been suggested. This surgical
procedure is to remove a portion of the ribs, perhaps of the third,
fourth and fifth, to allow the heart more freedom of action to
compensate for the impairment of its activity from the adhesions.
Such an operation was first suggested by Brauer of Heidelberg in
1902.
The question of the best method of producing anesthesia in this
condition of the heart is a serious one. A patient might die during
the anesthesia; but he might also die at any time from cardiac
spasm. In certain instances, in adults, local anesthesia might be
sufficient. Pain reflexes, however, would be serious. Such an
operation would be indicated when the apex is fixed so that there is
a constant sensation of hugging of the heart at the fourth and fifth
ribs, with paroxysms of pain and cardiac weakness.
MYOCARDIAL DISTURBANCES
While the myocardium is the most important muscle structure of the
body, it has but recently been studied carefully or well understood
clinically or pathologically. A heart was "hypertrophied" or
"dilated" or perhaps "fatty." It suffered from "pain," "angina
pectoris," from some "serious weakness" or from "coronary disease,"
and that ended the pathology and the clinical diagnosis. This is the
age of heart defects; no one can understand a patient's condition
now, whatever ails him, without studying his heart. No one can treat
a patient properly now without considering the management of the
circulation. No one should administer a drug now without considering
what it will do to the patient's heart.
Although we are scientifically interested in the administration of
specific treatments, antitoxins and vaccines; although we have a
better understanding of food values, and order diets with more
careful consideration of the exact needs of the individual, and
although we are using various physical methods to promote
elimination of toxins, poisons and products of metabolism, we have
until lately forgotten the physical fact that one thirteenth of the
weight of a normal adult is blood. A man who weighs 170 pounds has
13 pounds of blood. This proportion is not true in the obese, and is
not true in children. Whether the person is sick in bed, miserable
though up and about, or beginning to feel the first sensations of
slight incapacity for his life work, his ability properly to
circulate this one thirteenth of his weight through the various
arterial and venous channels and capillary tracts must, with the
increasing tension and speed of our lives, be taken into
consideration.
The more and more frequently repeated statements that the operation
was successfully performed but that the patient died of shock, and
that the typhoid fever and the pneumonia were being successfully
combated, but that the patient died of heart failure, together with
the increase in arteriosclerosis, cardiac disturbances and renal
disease, emphatically present the necessity of more carefully
studying the circulation. A better understanding and the constant
study of the blood pressure shows nothing but the necessity of the
age. The unwillingness of the patient to suffer pain, even for a few
minutes, without some narcotic, generally a cardiac debilitating
drug, means that, if he is a sufferer from chronic or recurrent
pain, he has taken a great deal of medicine which has done his heart
no good. Repeated high tension of life raises the blood pressure and
puts more work on the heart. Therefore the heart is found weary, if
not actually degenerated, when any serious accident, medical or
surgical, happens to the patient.
The requirements of the age have, then, necessitated that the heart
be more carefully studied, and therefore the heart strength and its
disturbances are better understood. The mere determination as to
where the apex beat is located, and as to what murmurs may be
present is not sufficient; we must attempt to determine the probable
condition of the myocardium. The following conditions are
recognized: (1) acute myocarditis, (2) chronic myocarditis
(fibrosis, cardiosclerosis), (3) fatty degeneration, and (4) fatty
heart.
ACUTE MYOCARDITIS
Probably most acute infections cause more or less myocarditis,
depending on their intensity and their prolongation. This
disturbance of the heart is often unrecognized, and has been simply
referred to as "the heart growing weaker from the fever process."
The acute infections most likely to cause a myocarditis are
rheumatism, influenza, sepsis, cerebrospinal meningitis, diphtheria,
typhoid fever, scarlet fever, and mouth and throat infections. It is
probably rare when acute endocarditis occurs that more or less
myocarditis is not present. The acute myocarditis may develop some
fatty degeneration, and with this softening and weakening of the
heart muscle acute dilatation readily occurs, which may be a cause
of sudden death, or, if less serious, may be the cause of prolonged
disability, if the heart ever recovers its original size and
strength.
The symptoms are often indefinite, and the diagnosis of the
condition hardly possible. It may be taken for granted, however,
that hardly any serious illness can long continue without cardiac
muscle disturbance. If endocarditis is present, soft systolic
murmurs soon appear. With the acute myocarditis developing, the apex
beat is less positive, less accentuated, and later it becomes
diffuse and even feeble. The closure of the aortic valve is less
typically sharp, showing that the blood vessels are not so
thoroughly filled. The peripheral circulation is not so active, the
blood pressure falls, and the heart becomes more rapid, especially
on the least exertion. All of these signs indicate myocardial
weakness.
The treatment of this condition is largely preventive. It should be
well recognized that prolonged high fever, prolonged insufficient or
improper nutrition, prolonged acute pain, and especially prolonged
septic processes will always cause myocardial degeneration. It
should be recognized that after ether and chloroform anesthesia,
especially after chloroform, the heart muscle may be disturbed and
the tonicity be lost. Therefore after anesthesia, after operations,
and after all illnesses which have lasted more than a few days, the
convalescence of the patient must be more or less deliberate. Sudden
rising, sudden erect posture, the exertion of walking too early,
going up stairs too early or taking moderate, and later severe
exercise too early, may cause dilatation of the heart muscle that
has become weakened by acute myocarditis. If acute myocarditis is
believed or known to be present, cardiac tonics such as digitalis
should not be given; large doses of strychnin should not be given;
vasocontractors such as ergot should not be given; large amounts of
food or large bulks of liquid should not be taken into the stomach
at one time; in fact, unless there is some special indication, the
twenty-four hour amount of fluid should be diminished. The surface
circulation and the muscle circulation should be improved by such
cold or warm water applications as the disease or condition calls
for. Massage should be early inaugurated to promote the return
circulation. The heart should be treated as though it were the
frailest of Venetian glass and would crack with the least rough
handling, or even with a rapid change of temperature, great cold or
too much heat. A prolonged, tedious convalescence, with the return
to activity so graded as to give the heart no strain, and to keep
its work always just below what it is able to do, will often mean
return to perfect strength and health.
No cardiac debilitating drug should be administered when myocarditis
has been surmised or diagnosed. The safest hypnotic, if one is
needed, is morphin in small doses. If there are weakening
perspirations, atropin should be given, especially as it is also a
circulatory stimulant. Calcium in almost any form seems to be of
value in the majority of heart conditions. It is a sedative to the
nervous system, and is certainly indicated in acute myocarditis.
Calcium lactate is perhaps the best salt to administer, in doses of
0.25 gm. (4 grains), three or four times in twenty-four hours.
Calcium glycerophosphate may be used, in powder form or in capsule,
in doses of 0.30 gm. (5 grains) three or four times in twenty-four
hours; or lime-water may be given.
An exact prognosis of this inflammation is impossible. We do not
know how far an acute myocarditis may progress and entire recovery
take place; we do not know how slight a myocarditis may cause
serious symptoms. Clinically we know that many patients after
serious illness never again have perfect circulatory strength. Other
patients almost die of heart failure and yet apparently absolutely
recover their ability to do hard physical work.
CHRONIC MYOCARDITIS: FIBROUS
Chronic myocarditis may develop on an acute myocarditis, but is
generally a slowly progressive chronic process from the beginning;
it occurs mostly in persons past middle life, and as a rule is not
primarily associated with rheumatism or valvular disease of the
heart. Perhaps generally the term "chronic myocarditis" is
incorrect, as a real inflammatory condition is not present and has
not been present; it is really a degenerative process with the
development of connective tissue, a fibrosis and more or less
hardening of the arterioles, a cardiosclerosis. In many instances
this fibrosis is associated with fat deposits or fatty degeneration.
The disease is often caused by a narrowing or obstruction or
calcareous degeneration of the coronary arteries, thus diminishing
the blood supply to the heart muscle. This chronic myocardial
degeneration is often a part of the general arteriosclerosis, and is
an important factor in what is termed cardiovascular-renal disease.
In simple chronic renal diseases the heart first normally
hypertrophies to overcome the increased blood tension and increased
resistance.
The principal causes of this degeneration are normal old age, or
premature age caused by various conditions. In other words, anything
which hastens arteriosclerosis will cause myocardial degeneration.
The causes recognized as most frequently producing this condition
are syphilis; gout; repeated attacks of rheumatism; excess in the
use of alcohol (meaning repeated daily too large amounts, as well as
actual dipsomania); the overuse of tobacco; excess in drinking tea
or coffee; general overeating, and excessive eating of meat in
particular, if the organs of elimination do not work perfectly and
if such eating causes or allows putrefactive changes in the
intestines; and progressive, prolonged wasting diseases, such as
tuberculosis and cancer. It has also seemed in some cases that the
only cause was excessive, hard physical labor, including excessive
athletic work, and in other cases that prolonged anxiety and worry
have been causes of cardiac degeneration and actual cardiac failure.
Prolonged absorption of toxins from mouth and tonsil infections may
be a not infrequent cause.
These myocardial changes are sometimes associated with chronic
pericarditis and chronic endocarditis, and may accompany or follow
valvular disease of the heart. Failure of compensation in valvular
disease and dilatation of the heart are sequences which occur sooner
or later.
SYMPTOMS AND SIGNS
The symptoms of chronic myocardial degeneration are progressive
weakness, slight at first, noticeable on exertion (and what was not
considered exertion becomes such), as evidenced by slight
palpitation, slight shortness of breath, leg weariness and mental
tire. The heart frequently becomes more rapid, not only with
exertion and change of position to the erect, but even after eating.
Slight cardiac stimulants, as coffee, affect the heart more than
previously; there is some sleeplessness, more or less troublesome,
and more or less indigestion. There may be mental irritability and
some mental deterioration, as shown in various ways. There are
likely to be slight edemas of the lower extremities toward night.
The amount of urine may diminish. A previously high blood pressure
becomes lower. The pulse may be occasionally intermittent, and later
actually irregular.
The physical signs often show an enlargement of the heart, with
increased activity at first, from irritability of the heart and a
lack of perfect coordination; later the heart may show typical signs
of weakness. Not infrequently a heart suffering from fibrosis acts
perfectly until some sudden exertion, as lifting, running or serious
illness causes it suddenly to become weak. Such a heart rarely
regains its former strength. This occurs frequently to those who
have supposed themselves to be in perfect physical health. Some
sudden strain which they have previously been able to endure without
injury, such as carrying a weight upstairs, cranking a refractory
engine, pumping up a series of tires, or walking rapidly with a
younger or more active companion, will suddenly give cardiac
distress signals, serious exhaustion and more or less lengthy
prostration, perhaps for an hour or so, or perhaps for several days.
Permanent cardiac weakness may follow, or compensation may again
occur, to be more easily broken later. Slight cardiac pains and
sensations referred to the cardiac region become frequent. Disliking
to lie on the left side, when previously the patient has been able
to sleep on this side without discomfort, is an evidence of cardiac
disturbance. There may be no real pains, but the patient becomes
conscious of his heart, perhaps for the first time in his life. This
alone is an indication of coming trouble.
If these signs and symptoms develop late in life, or at any age with
other symptoms of sclerosis or senility, little can be done
therapeutically except to afford temporary relief and to prevent the
occurrence of acute attacks of cardiac distress or dyspnea. If the
disturbance is really due to chronic cardiac degeneration, the
sooner the patient learns that his ability is restricted, that his
life is narrowed, the better for his future.
MANAGEMENT
The advice he should receive is well understood: to avoid physical
efforts; to avoid mental tire; to avoid overeating or overdrinking
of any foods or liquids; to reduce or abstain from alcohol, coffee,
tea and tobacco, depending on what seems advisable in the individual
case; to reduce the amount of meat eaten, especially if there is
intestinal indigestion; to relieve intestinal indigestion; to cause
free daily movements of the bowels; to abstain from any food which
tends to cause gastric or intestinal flatulence; to abstain from
such foods as contain nucleins, if the patient is gouty; to take
frequent warm baths (not too hot) to promote the secretions and the
circulation in the skin, and to take such daily exercise as seems
advisable. If the patient cannot take exercise, simple calisthenics
or massage should be instituted.
Whether nitroglycerin or other nitrite is advisable depends on the
peripheral blood pressure. If the blood pressure is low, or not
higher than is best for the patient, such treatment would be
inadvisable. If, from the supposed cause, iodid seems to be
indicated, it should be given in small doses and continued for some
time. It is often wise, however, to give small doses, as 0.10 or
0.20 gm. (2 or 3 grains) once or twice in twenty-four hours, for a
long period, to any patient who leas fibrosis or selerosis in any
form. Iodid tends to prevent the progress of connective tissue
formation. It is quite possible that some of its value is in
activating a sluggish or imperfectly acting thyroid gland. If the
patient is old, his thyroid is subinvoluting, and a little more of
its activity will be of advantage. Many diseases which cause chronic
myocarditis also cause, later, subactivity of the thyroid. Thyroid
extract may be indicated if the patient is obese.
If, in spite of this management and treatment, the patient has
cardiac asthma attacks, with or without pain, especially if there
are pendent edemas, the question arises as to whether or not
digitalis should be given. In such cases one cannot tell without
trying whether digitalis will be of benefit or will cause more
discomfort. 11 small dose of an active preparation should be given
at first twice in twenty-four hours, and after a week once in
twenty-four hours, its action being carefully watched and the
decision as to whether the dose is too large or too small arrived
at. It may do a great amount of good; it can cause increased cardiac
pains. If used carefully and stopped when it appears not to be
acting well, it will do no harm.
Chilling of the surface of the body should be avoided; sudden cold
or sustained severe cold, which increases the contraction of the
peripheral blood vessels and puts more strain on the heart muscle,
is to be avoided if possible. More hours in bed at night and lying
down after the heavier meals of the day will tend to give the heart
the kind of rest it needs. Also complete rest for one day a week, or
a rest of several days at a time, and a rest, both mental and
physical, with such walking, golfing or riding as seems advisable,
for at least one month every year, will prolong the lives of these
patients, and may make an imperfect heart act well for months and
years. If the patient is anemic he should, of course, receive some
nonastringent iron; a. tablet of saccharated ferric oxid
(Eisenzucker), in small doses, 0.20 gm. (3 grains), once or twice in
twenty-four hours, is sufficient.
The prognosis of a case diagnosed as chronic myocarditis or chronic
degeneration of the heart is doubtful, as one cannot tell until
several weeks or months of observation whether this particular heart
also has fatty degeneration or not. If there is fatty degeneration,
the prognosis is bad. If there is no serious fatty degeneration, the
patient, with the modified life outlined, may live for a long time.
Acute dilatation from any serious strain on the heart may occur, and
if there is fatty degeneration it is liable to occur at any time.
Attacks of cardiac asthma are always serious, and always damage the
heart a little more.
FATTY DEGENERATION
Fatty degeneration of the heart muscle may be caused by acute
poisoning (as phosphorus, arsenic, etc.), by serious infections, or
it may follow fibrosis of the heart or coronary artery disease. The
symptoms are those of serious circulatory weaicnens, which does not
seem to improve under any ordinary management. It is difficult, if
the heart is enlarged, to determine whether there is more or less
serious acute dilatation or whether the heart muscle has suffered
fatty degenration.
The treatment of such a patient requires the best of judgment as to
the amount of food and liquid that should be given, the regulation
of the administration of laxatives, the sponging of the body, the
means of producing sleep if there is insomnia, how much reading,
conversation or amusements should be allowed, how much stimulation
by stryclmin or other stimulating drug should be given, and whether
or not very small doses of digitalis should he tried. These are all
matters for individualizing, and for the best medical judgment which
we are called on to give. How much repair can take place in a heart
muscle when fatty degeneration has started we do not know. Such
treatment will give the heart the only chance it has to recuperate,
but the prognosis is bad.
FATTY HEART
The cause of deposits of fat around the heart or in between its
chambers is the same as the cause of general obesity. These patients
are likely to be obese, or at least to have large abdomens with
large deposits of fat around the abdomen. This fat in itself will
interfere somewhat with abdominal respiration. This tends to cause
dyspnea, and the heart tends to be disturbed from these causes, if
much fat is not really in the pericardium. The symptoms are those of
imperfect heart action; the patient is dyspneic on exertion or in
leaning over, the heart acts rapidly on such exertion, the patient
puffs, perspires easily, and becomes leg weary, sedentary in his
habits, and more or less incapacitated for work. He may not be a
large eater; if he is, and his eating habit is corrected, the
prognosis is better than if he is putting on weight in spite of
eating sparingly.
The general treatment is that for obesity, and if the heart muscle
is intact, various depletion methods may be inaugurated. More and
more exercise, sweatings from Turkish baths, electric-light baths,
body baking, vigorous massage and more or less purging are all
valuable. Anything which reduces the general weight will help the
heart. The prognosis is often good.
ENDOCARDITIS
It should be understood that especially in acute conditions a
positive separation of endocarditis from myocarditis is incorrect.
Acute endocarditis can probably not occur without some inyocarditis,
and myocarditis probably does not occur without some endocardial
disturbance and perhaps some pericardial irritation. This is
especially true in endocarditis which occurs during any acute
infection, even in rheumatism. The greater the amount of
pericarditis, the more serious is the acute condition. The greater
the amount of myocarditis, the more doubtful is the heart strength
in the near future. The greater the amount of endocarditis, the
greater the doubt of freedom from future permanent valvular lesions.
Endocarditis may be divided into: acute mild (simple) endocarditis,
acute malignant (ulcerative, infective) endocarditis, chronic
endocarditis and valvular disease.
ACUTE MILD ENDOCARDITIS
This inflammation of the endocardium is generally confined to the
region of the valves, and the valves most frequently so inflamed are
the mitral and aortic. There may be a slight inflammation or actual
ulceration and loss of tissue. Vegetations more or less constantly
occur on the inflamed surfaces, with more or less danger of
particles becoming loosened and moving free in the blood stream,
causing embolic obstruction in different parts of the body. There is
also more or less probability of serious adhesions or contractions
occurring from the healing of the ulcerated surfaces. The future
health and welfare of the valves depend on the fact that the
inflammation has healed without contractions or adhesions.
It is often difficult to decide when acute endocarditis has
developed; but with the knowledge that the endocardium often becomes
inflamed during almost any of the acute infections, the physician
should repeatedly examine the heart for murmurs, for muffled closure
of the valves, or for other evidences of endocarditis or myocarditis
during the acute infective process.
It has been shown positively that acute endocarditis is due to
micro-organisms, generally streptococci, staphylococci or
pneumococci, and, more frequently than once believed, gonococci. The
most frequent causes are acute rheumatic fever, diphtheria,
pneumonia, cerebrospinal meningitis, scarlet fever, erysipelas,
influenza, chorea, gonorrhea, sepsis and typhoid fever. It may also
follow a follicular tonsillitis or some infection of the mouth or
throat with or without arthritis. Tuberculosis may also occasionally
cause an endocarditis. Organisms may be found in a terminal simple
endocarditis due to a chronic disease, as tuberculosis or cancer;
such inflammations may have been caused by circulating toxins.
It will be noticed by the foregoing classification that the terms
"mild" and "malignant" endocarditis are used. The purpose is to
convey the fact that there may be no etiologic distinction between
the two forms, and it is impossible to decide clinically in the
beginning of an endocardial inflammation which form is present. In
the malignant form the infection is probably more serious or the
infective germs are more active, the ulcerations deeper, and the
likelihood of emboli and the seriousness of such embolic infarcts
more serious and more dangerous. The differences in inflammation in
the two cases is really one of degree, and the classification is
made to coincide with this probable fact. it is, of course,
clinically recognized that endocarditis following certain diseases,
especially rheumatism, is of the simple or mild type, while that
termed ulcerative endocarditis may occur apparently as a primary or
general infection, and the causative bacteria, as a rule, are
readily discovered in the blood. The Streptococcus viridans is one
of the most dangerous of these bacteria.
A SECONDARY AFFECTION
Mild endocarditis is rarely a primary affection, and is almost
invariably secondary to one of the diseases named above. Nearly 75
percent of secondary endocarditis occurs as a complication of acute
articular rheumatism and chorea, or subsequently. On the other hand,
about 40 percent of all patients with acute articular rheumatism
develop endocarditis, sometimes perhaps so mild as to be hardly
discoverable. This complication is most likely to occur during the
second or third week of rheumatic fever. It is not sufficiently
recognized that a subacute arthritis, recurring tonsillitis, open
and concealed infections in the mouth, and even a condition of the
system with acute, changeable and varying joint and muscle pains may
all develop a mild endocarditis, even with subsequent valvular
lesions. Therefore in all of these conditions the decision can be
made only as to how much rest the patient must have or how serious
the condition is to be considered by careful examination of the
heart in every instance.
Children are more liable than adults to this complication,
especially with rheumatism. Therefore, acute mild endocarditis with
future valvular lesions occurs most frequently during childhood and
adolescence, and if one attack has occurred, a subsequent infection,
especially of rheumatism, is liable to cause another acute
endocarditis.
PATHOLOGY
The part of the heart most affected is the part which has the most
work to do--the left side of the heart--and of this side the left
ventricle and therefore the mitral and aortic valves; the most
frequent valve to be inflamed and to stiffer permanent disability is
the a mitral valve, the valve which in its inflamed condition is
subjected to the greatest amount of pressure and therefore
irritation. Not infrequently soft systolic murmurs are heard at the
pulmonary and tricuspid valves during acute endocarditis. It is
rare, however, that these valves are so affected during childhood or
adult life as to be permanently disabled.
Whether a diminished alkalinity of the blood in rheumatism has
anything to do with the cause of the frequent complication of
endocarditis has not been determined. Whether the administration of
alkalies to the point of increasing the alkalinity of the blood is
any protection against the complication of endocarditis has also not
been positively demonstrated, although clinically such treatment is
believed by a large number of practitioners to be wise.
A chronic endocarditis wi
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