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Title: DISTURBANCES OF THE HEART
Author: OLIVER T. OSBORNE, A.M., M.D.
Release Date: February, 2003 [Etext #3731]
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Project Gutenberg's Disturbances of the Heart, by Oliver T. Osborne
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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
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
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,
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
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
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.