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
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.
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
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.
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.
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.
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.