DISTURBANCES OF THE HEART

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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.

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